{"id": "5d8c934a2048-0", "page_content": "DIAGNOSTIC AND STATISTICAL \nMANUAL OF\nMENTAL DISORDERS\nFIFTH EDITION\nDSM-5\u2122", "source": "dsm5.pdf"} {"id": "415a51d548ec-0", "page_content": "American Psychiatric Association\nOfficers 2012\u20132013\nPRESIDENT DILIP V. J ESTE , M.D.\nPRESIDENT -ELECT JEFFREY A. L IEBERMAN , M.D.\nTREASURER DAVID FASSLER , M.D.\nSECRETARY ROGER PEELE , M.D.\nAssembly\nSPEAKER R. S COTT BENSON , M.D.\nSPEAKER -ELECT MELINDA L. Y OUNG , M.D.\nBoard of Trustees\nJEFFREY AKAKA , M.D.\nCAROL A. B ERNSTEIN , M.D.\nBRIAN CROWLEY , M.D.\nANITA S. E VERETT , M.D.\nJEFFREY GELLER , M.D., M.P.H.\nMARC DAVID GRAFF , M.D.\nJAMES A. G REENE , M.D.\nJUDITH F. K ASHTAN , M.D.\nMOLLY K. M CVOY, M.D.\nJAMES E. N ININGER , M.D.\nJOHN M. O LDHAM , M.D.\nALAN F. S CHATZBERG , M.D.\nALIK S. W IDGE , M.D., P H.D.\nERIK R. V ANDERLIP , M.D., \nMEMBER -IN-TRAINING TRUSTEE -ELECT", "source": "dsm5.pdf"} {"id": "31f28e62a544-0", "page_content": "Washington, DC\nLondon, EnglandDIAGNOSTIC AND STATISTICAL \nMANUAL OF\nMENTAL DISORDERS\nFIFTH EDITION\nDSM-5\u2122", "source": "dsm5.pdf"} {"id": "2c134e9439dc-0", "page_content": "Copyright \u00a9 2013 American Psychiatric Association\nDSM and DSM-5 are trademarks of the American Psychiatric Association. Use of these terms\nis prohibited without perm ission of the American Psychiatric Association.\nALL RIGHTS RESERVED. Unless auth orized in writing by the APA, no part of this book may\nbe reproduced or used in a manner inconsistent with the APA\u2019s copyright. This prohibition\napplies to unauthorized uses or reproductions in any form, including electronic applications.\nCorrespondence regarding copyright permissions should be directed to DSM Permissions,\nAmerican Psychiatric Publishing, 1000 Wilso n Boulevard, Suite 1825, Arlington, VA 22209-\n3901.\nManufactured in the United States of America on acid-free paper.\nISBN 978-0-89042-554-1 (Hardcover) 2nd printing June 2013\nISBN 978-0-89042-555-8 (Paperba ck) 2nd prin ting June 2013\nAmerican Psychiatric Association\n1000 Wilson Boulevard\nArlington, VA 22209-3901\nwww.psych.org\nThe correct citation for this book is American Psychiatric Association: Diagnostic and Statisti-\ncal Manual of Mental Disorders, Fifth Edition. Arlington, VA, American Psychiatric Associa-\ntion, 2013.\nLibrary of Congress Cataloging-in-Publication Data\nDiagnostic and statistical manual of mental disorders : DSM-5. \u2014 5th ed.\np. ; cm.\nDSM-5\nDSM-V\nIncludes index.\nISBN 978-0-89042-554-1 (hardcover : alk. paper) \u2014 ISBN 978-0-89042-555-8 (pbk. : alk. paper)\nI. American Psychiatric Association. II. American Psychiatric Association. DSM-5 Task Force.", "source": "dsm5.pdf"} {"id": "2c134e9439dc-1", "page_content": "III. Title: DSM-5. IV. Title: DSM-V. \n[DNLM: 1. Diagnostic and statistical manual of mental disorders. 5th ed. 2. Mental Disorders\u2014\nclassification. 3. Mental Disorders\u2014diagnosis. WM 15]\nRC455.2.C4\n616.89'075\u2014dc23\n2013011061\nBritish Library Cataloguing in Publication Data\nA CIP record is available from the British Library.\nText Design\u2014Tammy J. Cordova\nManufacturing\u2014R.R. Donnelley", "source": "dsm5.pdf"} {"id": "d37ebd147212-0", "page_content": "Contents\nDSM-5 Classification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii\nPreface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xli\n Section I\nDSM-5 Basics\nIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5\nUse of the Manual . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19\nCautionary Statement for Forensic Us e of DSM-5 . . . . . . . . . . . .25\n Section II\nDiagnostic Criteria and Codes\nNeurodevelopmental Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . .31\nSchizophrenia Spectrum and Other Psychotic Disorders . . . . . .87\nBipolar and Related Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . .123\nDepressive Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .155\nAnxiety Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .189", "source": "dsm5.pdf"} {"id": "d37ebd147212-1", "page_content": "Obsessive-Compulsive and Re lated Disorders . . . . . . . . . . . . .235\nTrauma- and Stressor-Related Disorders . . . . . . . . . . . . . . . . . .265\nDissociative Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .291\nSomatic Symptom and Related Disorders . . . . . . . . . . . . . . . . .309\nFeeding and Eating Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . .329\nElimination Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .355\nSleep-Wake Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .361\nSexual Dysfunctions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .423\nGender Dysphoria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .451", "source": "dsm5.pdf"} {"id": "2c0cb3036a0f-0", "page_content": "Disruptive, Impulse-Control, and Con duct Disorders . . . . . . . . 461\nSubstance-Related and Addictive Disord ers . . . . . . . . . . . . . . . 481\nNeurocognitive Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 591\nPersonality Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 645\nParaphilic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 685\nOther Mental Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 707\nMedication-Induced Movement Disorders \nand Other Adverse Effects of Medication . . . . . . . . . . . . . . . . 709\nOther Conditions That May Be a Fo cus of Clinical Attention . . 715\n Section III\nEmerging Measures and Models\nAssessment Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 733\nCultural Formulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 749\nAlternative DSM-5 Model for Personality Disorder s . . . . . . . . . 761", "source": "dsm5.pdf"} {"id": "2c0cb3036a0f-1", "page_content": "Conditions for Further Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . 783\n Appendix\nHighlights of Ch anges From DSM-IV to DSM-5 . . . . . . . . . . . . . 809\nGlossary of Technical Terms . . . . . . . . . . . . . . . . . . . . . . . . . . . . 817\nGlossary of Cultural Concepts of Dist ress . . . . . . . . . . . . . . . . . 833\nAlphabetical Listing of DSM-5 Diagno ses and Codes \n(ICD-9-CM and ICD-10-CM). . . . . . . . . . . . . . . . . . . . . . . . . . . . 839\nNumerical Listing of DS M-5 Diagnoses and Codes\n (ICD-9-CM) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 863\nNumerical Listing of DS M-5 Diagnoses and Codes\n (ICD-10-CM) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 877\nDSM-5 Advisors and Other Contributors . . . . . . . . . . . . . . . . . . 897", "source": "dsm5.pdf"} {"id": "2c0cb3036a0f-2", "page_content": "Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 917", "source": "dsm5.pdf"} {"id": "6001a2cc7a68-0", "page_content": "DSM-5 Task Force\nDAVID J. K UPFER , M.D.\nTask Force Chair\nDARREL A. R EGIER , M.D., M.P.H.\nTask Force Vice-Chair\nWilliam E. Narrow, M.D., M.P.H., \nResearch DirectorSusan K. Schultz, M.D., Text Editor\nEmily A. Kuhl, Ph.D., APA Text Editor\nDan G. Blazer, M.D., Ph.D., M.P.H.\nJack D. Burke Jr., M.D., M.P.H.\nWilliam T. Carpenter Jr., M.D. \nF. Xavier Castellanos, M.D.\nWilson M. Compton, M.D., M.P.E.\nJoel E. Dimsdale, M.D.\nJavier I. Escobar, M.D., M.Sc.\nJan A. Fawcett, M.D.\nBridget F. Grant, Ph.D., Ph.D. (2009\u2013)\nSteven E. Hyman, M.D. (2007\u20132012)\nDilip V. Jeste, M.D. (2007\u20132011)\nHelena C. Kraemer, Ph.D.\nDaniel T. Mamah, M.D., M.P.E.\nJames P. McNulty, A.B., Sc.B.\nHoward B. Moss, M.D. (2007\u20132009)Charles P. O\u2019Brien, M.D., Ph.D.\nRoger Peele, M.D.\nKatharine A. Phillips, M.D. \nDaniel S. Pine, M.D.\nCharles F. Reynolds III, M.D.\nMaritza Rubio-Stipec, Sc.D.\nDavid Shaffer, M.D.\nAndrew E. Skodol II, M.D.\nSusan E. Swedo, M.D.", "source": "dsm5.pdf"} {"id": "6001a2cc7a68-1", "page_content": "Susan E. Swedo, M.D.\nB. Timothy Walsh, M.D. \nPhilip Wang, M.D., Dr.P.H. (2007\u20132012)\nWilliam M. Womack, M.D.\nKimberly A. Yonkers, M.D.\nKenneth J. Zucker, Ph.D. \nNorman Sartorius, M.D., Ph.D., Consultant\nAPA Division of Research Staff on DSM-5\nDarrel A. Regier, M.D., M.P.H., \nDirector, Division of Research\nWilliam E. Narrow, M.D., M.P.H., \nAssociate Director\nEmily A. Kuhl, Ph.D., Senior Science \nWriter; Staff Text Editor\nDiana E. Clarke, Ph.D., M.Sc., Research \nStatistician\nLisa H. Greiner, M.S.S.A., DSM-5 Field \nTrials Project Manager\nEve K. Moscicki, Sc.D., M.P.H., \nDirector, Practice Research Network\nS. Janet Kuramoto, Ph.D. M.H.S., \nSenior Scientific Research Associate, \nPractice Research Network\nAmy Porfiri, M.B.A. \nDirector of Finance and AdministrationJennifer J. Shupinka, Assistant Director, \nDSM Operations\nSeung-Hee Hong, DSM Senior Research \nAssociate\nAnne R. Hiller, DSM Research Associate\nAlison S. Beale, DSM Research Associate\nSpencer R. Case, DSM Research Associate\nJoyce C. West, Ph.D., M.P.P., \nHealth Policy Research Director, Practice \nResearch Network\nFarifteh F. Duffy, Ph.D., \nQuality Care Research Director, Practice \nResearch Network\nLisa M. Countis, Field Operations \nManager, Practice Research Network\nChristopher M. Reynolds, \nExecutive Assistant", "source": "dsm5.pdf"} {"id": "6001a2cc7a68-2", "page_content": "Manager, Practice Research Network\nChristopher M. Reynolds, \nExecutive Assistant\nAPA Office of the Medical Director\nJAMES H. S CULLY JR., M.D.\nMedical Director and CEO", "source": "dsm5.pdf"} {"id": "92cb8317dce6-0", "page_content": "Editorial and Coding Consultants\nMichael B. First, M.D. Maria N. Ward, M.Ed., RHIT, CCS-P\nDSM-5 Work Groups\nADHD and Disruptive Behavior Disorders\nDAVID SHAFFER , M.D.\nChair\nF. X AVIER CASTELLANOS , M.D.\nCo-Chair\nPaul J. Frick, Ph.D., Text Coordinator \nGlorisa Canino, Ph.D. \nTerrie E. Moffitt, Ph.D. \nJoel T. Nigg, Ph.D. Luis Augusto Rohde, M.D., Sc.D.\nRosemary Tannock, Ph.D. \nEric A. Taylor, M.B.\nRichard Todd, Ph.D., M.D. (d. 2008)\nAnxiety, Obsessive-Compulsive Spectrum, Posttraumatic, \nand Dissociative Disorders\nKATHARINE A. P HILLIPS , M.D.\nChair\nMichelle G. Craske, Ph.D., Text \nCoordinator\nJ. Gavin Andrews, M.D.\nSusan M. B\u00f6gels, Ph.D.\nMatthew J. Friedman, M.D., Ph.D.\nEric Hollander, M.D. (2007\u20132009)\nRoberto Lewis-Fern\u00e1ndez, M.D., M.T.S.\nRobert S. Pynoos, M.D., M.P.H.Scott L. Rauch, M.D.\nH. Blair Simpson, M.D., Ph.D.\nDavid Spiegel, M.D.\nDan J. Stein, M.D., Ph.D.\nMurray B. Stein, M.D.\nRobert J. Ursano, M.D.\nHans-Ulrich Wittchen, Ph.D.\nChildhood and Adolescent Disorders\nDANIEL S. P INE, M.D.\nChair", "source": "dsm5.pdf"} {"id": "92cb8317dce6-1", "page_content": "DANIEL S. P INE, M.D.\nChair\nRonald E. Dahl, M.D.\nE. Jane Costello, Ph.D. (2007\u20132009)\nRegina Smith James, M.D.\nRachel G. Klein, Ph.D.James F. Leckman, M.D.\nEllen Leibenluft, M.D.\nJudith H. L. Rapoport, M.D.\nCharles H. Zeanah, M.D.\nEating Disorders\nB. T IMOTHY WALSH , M.D. \nChair\nStephen A. Wonderlich, Ph.D., \nText Coordinator\nEvelyn Attia, M.D.\nAnne E. Becker, M.D., Ph.D., Sc.M.\nRachel Bryant-Waugh, M.D.\nHans W. Hoek, M.D., Ph.D.Richard E. Kreipe, M.D.\nMarsha D. Marcus, Ph.D.\nJames E. Mitchell, M.D.\nRuth H. Striegel-Moore, Ph.D.\nG. Terence Wilson, Ph.D.\nBarbara E. Wolfe, Ph.D. A.P.R.N.", "source": "dsm5.pdf"} {"id": "bc0226764c4c-0", "page_content": "Mood Disorders \nJAN A. F AWCETT , M.D.\nChair\nEllen Frank, Ph.D., Text Coordinator\nJules Angst, M.D. (2007\u20132008)\nWilliam H. Coryell, M.D.\nLori L. Davis, M.D.\nRaymond J. DePaulo, M.D.\nSir David Goldberg, M.D.\nJames S. Jackson, Ph.D.Kenneth S. Kendler, M.D. \n(2007\u20132010)\nMario Maj, M.D., Ph.D.\nHusseini K. Manji, M.D. (2007\u20132008)\nMichael R. Phillips, M.D.\nTrisha Suppes, M.D., Ph.D.\nCarlos A. Zarate, M.D.\nNeurocognitive Disorders\nDILIP V. J ESTE , M.D. (2007\u20132011)\nChair Emeritus\nDAN G. B LAZER , M.D., P H.D., M.P.H.\nChair\nRONALD C. P ETERSEN , M.D., P H.D.\nCo-Chair\nMary Ganguli, M.D., M.P.H., \nText Coordinator\nDeborah Blacker, M.D., Sc.D.\nWarachal Faison, M.D. (2007\u20132008)Igor Grant, M.D.\nEric J. Lenze, M.D.\nJane S. Paulsen, Ph.D.\nPerminder S. Sachdev, M.D., Ph.D.\nNeurodevelopmental Disorders\nSUSAN E. S WEDO , M.D. \nChair\nGillian Baird, M.A., M.B., B.Chir., \nText Coordinator\nEdwin H. Cook Jr., M.D.", "source": "dsm5.pdf"} {"id": "bc0226764c4c-1", "page_content": "Text Coordinator\nEdwin H. Cook Jr., M.D.\nFrancesca G. Happ\u00e9, Ph.D.\nJames C. Harris, M.D.\nWalter E. Kaufmann, M.D.\nBryan H. King, M.D.\nCatherine E. Lord, Ph.D.Joseph Piven, M.D.\nSally J. Rogers, Ph.D.\nSarah J. Spence, M.D., Ph.D.\nRosemary Tannock, Ph.D.\nFred Volkmar, M.D. (2007\u20132009)\nAmy M. Wetherby, Ph.D.\nHarry H. Wright, M.D.\nPersonality and Personality Disorders1\nANDREW E. S KODOL , M.D.\nChair \nJOHN M. O LDHAM , M.D.\nCo-Chair \nRobert F. Krueger, Ph.D., Text \nCoordinator\nRenato D. Alarcon, M.D., M.P.H.\nCarl C. Bell, M.D.\nDonna S. Bender, Ph.D.Lee Anna Clark, Ph.D.\nW. John Livesley, M.D., Ph.D. (2007\u20132012)\nLeslie C. Morey, Ph.D.\nLarry J. Siever, M.D.\nRoel Verheul, Ph.D. (2008\u20132012)\n1The members of the Personality and Personality Disorders Work Group are responsible for the\nalternative DSM-5 model for personality disorders that is included in Section III. The Section II\npersonality disorders criteria and text (with upda ting of the text) are retained from DSM-IV-TR.", "source": "dsm5.pdf"} {"id": "1605fc581f0f-0", "page_content": "Psychotic Disorders\nWILLIAM T. C ARPENTER JR., M.D.\nChair\nDeanna M. Barch, Ph.D., Text \nCoordinator\nJuan R. Bustillo, M.D.\nWolfgang Gaebel, M.D.\nRaquel E. Gur, M.D., Ph.D.\nStephan H. Heckers, M.D.Dolores Malaspina, M.D., M.S.P.H.\nMichael J. Owen, M.D., Ph.D.\nSusan K. Schultz, M.D.\nRajiv Tandon, M.D.\nMing T. Tsuang, M.D., Ph.D.\nJim van Os, M.D.\nSexual and Gender Identity Disorders \nKENNETH J. Z UCKER , PH.D.\nChair \nLori Brotto, Ph.D., Text Coordinator\nIrving M. Binik, Ph.D.\nRay M. Blanchard, Ph.D.\nPeggy T. Cohen-Kettenis, Ph.D.\nJack Drescher, M.D.\nCynthia A. Graham, Ph.D.Martin P. Kafka, M.D.\nRichard B. Krueger, M.D.\nNiklas L\u00e5ngstr\u00f6m, M.D., Ph.D.\nHeino F.L. Meyer-Bahlburg, Dr. rer. nat.\nFriedemann Pf\u00e4fflin, M.D.\nRobert Taylor Segraves, M.D., Ph.D.\nSleep-Wake Disorders\nCHARLES F. R EYNOLDS III, M.D.\nChair\nRuth M. O\u2019Hara, Ph.D., Text Coordinator\nCharles M. Morin, Ph.D.\nAllan I. Pack, Ph.D.Kathy P. Parker, Ph.D., R.N.\nSusan Redline, M.D., M.P.H.", "source": "dsm5.pdf"} {"id": "1605fc581f0f-1", "page_content": "Susan Redline, M.D., M.P.H.\nDieter Riemann, Ph.D.\nSomatic Symptom Disorders\nJOEL E. D IMSDALE , M.D.\nChair\nJames L. Levenson, M.D., Text \nCoordinator\nArthur J. Barsky III, M.D.\nFrancis Creed, M.D.\nNancy Frasure-Smith, Ph.D. (2007\u20132011)Michael R. Irwin, M.D.\nFrancis J. Keefe, Ph.D. (2007\u20132011)\nSing Lee, M.D.\nMichael Sharpe, M.D.\nLawson R. Wulsin, M.D.\nSubstance-Related Disorders\nCHARLES P. O\u2019B RIEN , M.D., P H.D.\nChair\nTHOMAS J. C ROWLEY , M.D.\nCo-Chair \nWilson M. Compton, M.D., M.P.E., \nText Coordinator\nMarc Auriacombe, M.D.\nGuilherme L. G. Borges, M.D., Dr.Sc.\nKathleen K. Bucholz, Ph.D.\nAlan J. Budney, Ph.D.\nBridget F. Grant, Ph.D., Ph.D.\nDeborah S. Hasin, Ph.D.Thomas R. Kosten, M.D. (2007\u20132008)\nWalter Ling, M.D.\nSpero M. Manson, Ph.D. (2007-2008)\nA. Thomas McLellan, Ph.D. (2007\u20132008)\nNancy M. Petry, Ph.D.\nMarc A. Schuckit, M.D.\nWim van den Brink, M.D., Ph.D. \n(2007\u20132008)", "source": "dsm5.pdf"} {"id": "e76234ec1ce7-0", "page_content": "DSM-5 Study Groups\nDiagnostic Spect ra and DSM/ICD Harmonization\nSTEVEN E. H YMAN , M.D.\nChair (2007\u20132012)\nWilliam T. Carpenter Jr., M.D.\nWilson M. Compton, M.D., M.P.E.\nJan A. Fawcett, M.D.\nHelena C. Kraemer, Ph.D.\nDavid J. Kupfer, M.D.William E. Narrow, M.D., M.P.H.\nCharles P. O\u2019Brien, M.D., Ph.D.\nJohn M. Oldham, M.D.\nKatharine A. Phillips, M.D.\nDarrel A. Regier, M.D., M.P.H.\nLifespan Developmental Approaches\nERIC J. L ENZE , M.D.\nChair\nSUSAN K. S CHULTZ , M.D.\nChair Emeritus\nDANIEL S. P INE, M.D.\nChair Emeritus\nDan G. Blazer, M.D., Ph.D., M.P.H.\nF. Xavier Castellanos, M.D.\nWilson M. Compton, M.D., M.P.E.Daniel T. Mamah, M.D., M.P.E.\nAndrew E. Skodol II, M.D.\nSusan E. Swedo, M.D.\nGender and Cross-Cultural Issues\nKIMBERLY A. Y ONKERS , M.D.\nChair\nROBERTO LEWIS -FERN\u00c1NDEZ , M.D., M.T.S.\nCo-Chair, Cross-Cultural Issues\nRenato D. Alarcon, M.D., M.P.H.\nDiana E. Clarke, Ph.D., M.Sc.\nJavier I. Escobar, M.D., M.Sc.", "source": "dsm5.pdf"} {"id": "e76234ec1ce7-1", "page_content": "Javier I. Escobar, M.D., M.Sc.\nEllen Frank, Ph.D.\nJames S. Jackson, Ph.D.\nSpiro M. Manson, Ph.D. (2007\u20132008)\nJames P. McNulty, A.B., Sc.B.Leslie C. Morey, Ph.D.\nWilliam E. Narrow, M.D., M.P.H.\nRoger Peele, M.D.\nPhilip Wang, M.D., Dr.P.H. (2007\u20132012)\nWilliam M. Womack, M.D.\nKenneth J. Zucker, Ph.D.\nPsychiatric/General Medical Interface\nLAWSON R. W ULSIN , M.D.\nChair\nRonald E. Dahl, M.D.\nJoel E. Dimsdale, M.D.\nJavier I. Escobar, M.D., M.Sc.\nDilip V. Jeste, M.D. (2007\u20132011)\nWalter E. Kaufmann, M.D.Richard E. Kreipe, M.D.\nRonald C. Petersen, Ph.D., M.D.\nCharles F. Reynolds III, M.D.\nRobert Taylor Segraves, M.D., Ph.D.\nB. Timothy Walsh, M.D.", "source": "dsm5.pdf"} {"id": "db835f9be4b5-0", "page_content": "Impairment and Disability\n JANE S. P AULSEN , PH.D.\nChair\nJ. Gavin Andrews, M.D.\nGlorisa Canino, Ph.D.\nLee Anna Clark, Ph.D.\nDiana E. Clarke, Ph.D., M.Sc.\nMichelle G. Craske, Ph.D.Hans W. Hoek, M.D., Ph.D.\nHelena C. Kraemer, Ph.D.\nWilliam E. Narrow, M.D., M.P.H.\nDavid Shaffer, M.D.\nDiagnostic Assessm ent Instruments\nJACK D. B URKE JR., M.D., M.P.H.\nChair\nLee Anna Clark, Ph.D.\nDiana E. Clarke, Ph.D., M.Sc.\nBridget F. Grant, Ph.D., Ph.D.Helena C. Kraemer, Ph.D.\nWilliam E. Narrow, M.D., M.P.H.\nDavid Shaffer, M.D.\nDSM-5 Research Group\nWILLIAM E. N ARROW , M.D., M.P.H.\nChair\nJack D. Burke Jr., M.D., M.P.H.\nDiana E. Clarke, Ph.D., M.Sc.\nHelena C. Kraemer, Ph.D.David J. Kupfer, M.D.\nDarrel A. Regier, M.D., M.P.H.\nDavid Shaffer, M.D.\nCourse Specifiers and Glossary\nWOLFGANG GAEBEL , M.D.\nChair\nEllen Frank, Ph.D.\nCharles P. O\u2019Brien, M.D., Ph.D.\nNorman Sartorius, M.D., Ph.D., \nConsultant\nSusan K. Schultz, M.D.Dan J. Stein, M.D., Ph.D.\nEric A. Taylor, M.B.", "source": "dsm5.pdf"} {"id": "db835f9be4b5-1", "page_content": "Eric A. Taylor, M.B.\nDavid J. Kupfer, M.D.\nDarrel A. Regier, M.D., M.P.H.", "source": "dsm5.pdf"} {"id": "6d36277c0179-0", "page_content": "xiiiDSM-5\n Classification\nBefore each disorder name, ICD-9-CM code s are provided, followe d by ICD-10-CM codes\nin parentheses. Blank lines indicate that eith er the ICD-9-CM or the ICD-10-CM code is not\napplicable. For some disorders, the code can be indicated only according to the subtype or\nspecifier.\nICD-9-CM codes are to be used for coding purposes in the United States through Sep-\ntember 30, 2014. ICD-10-CM codes are to be used starting October 1, 2014.\nFollowing chapter titles and disorder name s, page numbers for the corresponding text\nor criteria are incl uded in parentheses.\nNote for all mental disorders due to another medical condition: Indicate the name of\nthe other medical condition in the name of th e mental disorder due to [the medical condi-\ntion]. The code and name for the other medica l condition should be listed first immedi-\nately before the mental disorder due to the medical condition.\nNeurodevelopmental Disorders (31)\nIntellectual Disabilities (33)\n___.__ (___.__) Intellectual Disability (Intelle ctual Developmental Disorder) (33)\nSpecify current severity:\n317 (F70) Mild\n318.0 (F71) Moderate\n318.1 (F72) Severe\n318.2 (F73) Profound\n315.8 (F88) Global Developmental Delay (41)\n319 (F79) Unspecified Intellectual Disability (Intellectual Developmental \nDisorder) (41)\nCommunication Disorders (41)\n315.32 (F80.2) Language Disorder (42)\n315.39 (F80.0) Speech Sound Disorder (44)", "source": "dsm5.pdf"} {"id": "6d36277c0179-1", "page_content": "315.39 (F80.0) Speech Sound Disorder (44)\n315.35 (F80.81) Childhood-Onset Fluency Disorder (Stuttering) (45)\nNote: Later-onset cases are diagnosed as 307.0 (F98.5) adult-onset fluency\ndisorder.\n315.39 (F80.89) Social (Pragmatic) Communication Disorder (47)\n307.9 (F80.9) Unspecified Communication Disorder (49)", "source": "dsm5.pdf"} {"id": "88e5281eaa4e-0", "page_content": "xiv DSM-5 Classification\nAutism Spectrum Disorder (50)\n299.00 (F84.0) Autism Spectrum Disorder (50)\nSpecify if: Associated with a known medic al or genetic condition or envi-\nronmental factor; Associ ated with another neurodevelopmental, men-\ntal, or behavioral disorder\nSpecify current severity for Criterion A and Criterion B: Requiring very\nsubstantial support, Requiring substantial support, Requiring support\nSpecify if: With or without accompanyi ng intellectual impairment, With\nor without accompanying language impairment, With catatonia (use\nadditional code 293.89 [F06.1])\nAttention-Deficit/Hyperactivity Disorder (59)\n___.__ (___.__) Attention-Deficit/Hyperactivity Disorder (59)\nSpecify whether:\n314.01 (F90.2) Combined presentation\n314.00 (F90.0) Predominantly inattentive presentation\n314.01 (F90.1) Predominantly hyperactive/impulsive presentation\nSpecify if: In partial remission\nSpecify current severity: Mild, Moderate, Severe\n314.01 (F90.8) Other Specified Attention-Deficit/Hyperactivity Disorder (65)\n314.01 (F90.9) Unspecified Attention-Deficit/Hyperactivity Disorder (66)\nSpecific Learning Disorder (66)\n___.__ (___.__) Specific Learning Disorder (66)\nSpecify if:\n315.00 (F81.0) With impairment in reading (specify if with word reading \naccuracy, reading rate or fluency, reading comprehension)\n315.2 (F81.81) With impairment in written expression ( specify if with spelling \naccuracy, grammar and punctu ation accuracy, clarity or \norganization of written expression)", "source": "dsm5.pdf"} {"id": "88e5281eaa4e-1", "page_content": "accuracy, grammar and punctu ation accuracy, clarity or \norganization of written expression)\n315.1 (F81.2) With impairment in mathematics ( specify if with number sense, \nmemorization of arithmetic facts, accurate or fluent \ncalculation, accurate math reasoning)\nSpecify current severity: Mild, Moderate, Severe\nMotor Disorders (74)\n315.4 (F82) Developmental Coordination Disorder (74)\n307.3 (F98.4) Stereotypic Movement Disorder (77)\nSpecify if: With self-injurious behavior , Without self-injurious behavior\nSpecify if: Associated with a known medical or genetic condition, neuro-\ndevelopmental disorder, or environmental factor\nSpecify current severity: Mild, Moderate, Severe\nTic Disorders\n307.23 (F95.2) Tourette's Disorder (81)\n307.22 (F95.1) Persistent (Chronic) Motor or Vocal Tic Disorder (81)\nSpecify if: With motor tics only, With vocal tics only", "source": "dsm5.pdf"} {"id": "ae3692a494c9-0", "page_content": "DSM-5 Classification xv\n307.21 (F95.0) Provisional Tic Disorder (81)\n307.20 (F95.8) Other Specified Tic Disorder (85)\n307.20 (F95.9) Unspecified Tic Disorder (85)\nOther Neurodevelopmental Disorders (86)\n315.8 (F88) Other Specified Neurodevelopmental Disorder (86)\n315.9 (F89) Unspecified Neurodevelopmental Disorder (86)\nSchizophrenia Spectrum \nand Other Psychotic Disorders (87)\nThe following specifiers apply to Schizophre nia Spectrum and Othe r Psychotic Disorders\nwhere indicated:\naSpecify if: The following course specifiers are only to be used after a 1-year duration of the dis-\norder: First episode, currently in acute episode; First episode, currently in partial remission;\nFirst episode, currently in full remission; Multiple episodes, currently in acute episode; Mul-\ntiple episodes, currently in partial remission; Multiple episodes, currently in full remission;\nContinuous; Unspecified\nbSpecify if: With catatonia (use additional code 293.89 [F06.1])\ncSpecify current severity of delusions, hallucinations, disorganized speech, abnormal psycho-\nmotor behavior, negative symptoms, impaired cognition, depression, and mania symptoms\n301.22 (F21) Schizotypal (Personality) Disorder (90)\n297.1 (F22) Delusional Disordera, c (90)\nSpecify whether: Erotomanic type, Grandiose type, Jealous type, Persecu-\ntory type, Somatic type, Mi xed type, Unspecified type\nSpecify if: With bizarre content", "source": "dsm5.pdf"} {"id": "ae3692a494c9-1", "page_content": "Specify if: With bizarre content\n298.8 (F23) Brief Psychotic Disorderb, c (94)\nSpecify if: With marked stressor(s), Without marked stressor(s), With\npostpartum onset\n295.40 (F20.81) Schizophreniform Disorderb, c (96)\nSpecify if: With good prognostic featur es, Without good prognostic fea-\ntures\n295.90 (F20.9) Schizophreniaa, b, c (99)\n___.__ (___.__) Schizoaffective Disordera, b, c (105)\nSpecify whether:\n295.70 (F25.0) Bipolar type\n295.70 (F25.1) Depressive type\n___.__ (___.__) Substance/Medication-Ind uced Psychotic Disorderc (110)\nNote: See the criteria set and corresponding recording procedures for\nsubstance-specific codes and ICD-9-CM and ICD-10-CM coding.\nSpecify if: With onset during intoxicatio n, With onset during withdrawal\n___.__ (___.__) Psychotic Disorder Due to Another Medical Conditionc (115)\nSpecify whether:\n293.81 (F06.2) With delusions\n293.82 (F06.0) With hallucinations", "source": "dsm5.pdf"} {"id": "6611a946fb19-0", "page_content": "xvi DSM-5 Classification\n293.89 (F06.1) Catatonia Associated With Anothe r Mental Disorder (Catatonia \nSpecifier) (119)\n293.89 (F06.1) Catatonic Disorder Due to Another Medical Condition (120)\n293.89 (F06.1) Unspecified Catatonia (121)\nNote: Code first 781.99 (R29.818) other symptoms involving nervous and\nmusculoskeletal systems.\n298.8 (F28) Other Specified Schizophrenia Spectrum and Other Psychotic \nDisorder (122)\n298.9 (F29) Unspecified Schizophrenia Spectrum and Other Psychotic \nDisorder (122)\nBipolar and Related Disorders (123)\nThe following specifiers apply to Bipolar and Related Disorders where indicated:\naSpecify: With anxious distress ( specify current severity: mild, modera te, moderate-severe, severe);\nWith mixed features; With rapid cycling; With melancholic features; With atypical features;\nWith mood-congruent psychotic features; With mood-incongruent psychotic features; With\ncatatonia (use additional code 293.89 [F06.1]); With peripartum onset; With seasonal pattern\n___.__ (___.__) Bipolar I Disordera (123)\n___.__ (___.__) Current or most recent episode manic\n296.41 (F31.11) Mild\n296.42 (F31.12) Moderate\n296.43 (F31.13) Severe\n296.44 (F31.2) With psychotic features\n296.45 (F31.73) In partial remission\n296.46 (F31.74) In full remission", "source": "dsm5.pdf"} {"id": "6611a946fb19-1", "page_content": "296.46 (F31.74) In full remission\n296.40 (F31.9) Unspecified\n296.40 (F31.0) Current or most recent episode hypomanic\n296.45 (F31.71) In partial remission\n296.46 (F31.72) In full remission\n296.40 (F31.9) Unspecified\n___.__ (___.__) Current or most recent episode depressed\n296.51 (F31.31) Mild\n296.52 (F31.32) Moderate\n296.53 (F31.4) Severe\n296.54 (F31.5) With psychotic features\n296.55 (F31.75) In partial remission\n296.56 (F31.76) In full remission\n296.50 (F31.9) Unspecified\n296.7 (F31.9) Current or most recent episode unspecified\n296.89 (F31.81) Bipolar II Disordera (132)\nSpecify current or most recent ep isode: Hypomanic, Depressed\nSpecify course if full criteria for a mood episode are not currently met: In\npartial remission, In full remission\nSpecify severity if full criteria for a mood episode are currently met:\nMild, Moderate, Severe", "source": "dsm5.pdf"} {"id": "94e968134e15-0", "page_content": "DSM-5 Classification xvii\n301.13 (F34.0) Cyclothymic Disorder (139)\nSpecify if: With anxious distress\n___.__ (___.__) Substance/Medication-Induced Bipo lar and Related Disorder (142)\nNote: See the criteria set and corresponding recording procedures for\nsubstance-specific codes and ICD-9-CM and ICD-10-CM coding.\nSpecify if: With onset during intoxicatio n, With onset during withdrawal\n293.83 (___.__) Bipolar and Related Disorder Due to Another Medical Condition \n(145)\nSpecify if: \n(F06.33) With manic features\n(F06.33) With manic- or hypomanic-like episode\n(F06.34) With mixed features\n296.89 (F31.89) Other Specified Bipolar and Related Disorder (148)\n296.80 (F31.9) Unspecified Bipolar and Related Disorder (149)\nDepressive Disorders (155)\nThe following specifiers apply to Depressive Disorders where indicated:\naSpecify: With anxious distress ( specify current severity: mild, moderate, moderate-severe,\nsevere); With mixed features; With melancholic features; With atypical features; With mood-\ncongruent psychotic features; With mood-incongruent psych otic features; Wi th catatonia\n(use additional code 293.89 [F06.1]); With peripartum on set; With seasonal pattern\n296.99 (F34.8) Disruptive Mood Dysregulation Disorder (156)\n___.__ (___.__) Major Depressive Disordera (160)\n___.__ (___.__) Single episode\n296.21 (F32.0) Mild\n296.22 (F32.1) Moderate", "source": "dsm5.pdf"} {"id": "94e968134e15-1", "page_content": "296.22 (F32.1) Moderate\n296.23 (F32.2) Severe\n296.24 (F32.3) With psychotic features\n296.25 (F32.4) In partial remission\n296.26 (F32.5) In full remission\n296.20 (F32.9) Unspecified\n___.__ (___.__) Recurrent episode\n296.31 (F33.0) Mild\n296.32 (F33.1) Moderate\n296.33 (F33.2) Severe\n296.34 (F33.3) With psychotic features\n296.35 (F33.41) In partial remission\n296.36 (F33.42) In full remission\n296.30 (F33.9) Unspecified\n300.4 (F34.1) Persistent Depressive Disorder (Dysthymia)a (168)\nSpecify if: In partial remission, In full remission\nSpecify if: Early onset, Late onset\nSpecify if: With pure dysthymic syndrome ; With persistent major depres-\nsive episode; With intermittent ma jor depressive epis odes, with current", "source": "dsm5.pdf"} {"id": "99e4df7fe792-0", "page_content": "xviii DSM-5 Classification\nepisode; With intermittent major depressive episodes, without current\nepisode\nSpecify current severity: Mild, Moderate, Severe\n625.4 (N94.3) Premenstrual Dysphoric Disorder (171)\n___.__ (___.__) Substance/Medication-Induced Depressive Disorder (175)\nNote: See the criteria set and corresponding recording procedures for\nsubstance-specific codes and IC D-9-CM and ICD-10-CM coding.\nSpecify if: With onset during intoxication, With onset during withdrawal\n293.83 (___.__) Depressive Disorder Due to Another Medical Condition (180)\nSpecify if: \n(F06.31) With depressive features\n(F06.32) With major depressive-like episode\n(F06.34) With mixed features\n311 (F32.8) Other Specified Depressive Disorder (183)\n311 (F32.9) Unspecified Depressive Disorder (184)\nAnxiety Disorders (189)\n309.21 (F93.0) Separation Anxiety Disorder (190)\n313.23 (F94.0) Selective Mutism (195)\n300.29 (___.__) Specific Phobia (197)\nSpecify if:\n(F40.218) Animal\n(F40.228) Natural environment\n(___.__) Blood-injection-injury\n(F40.230) Fear of blood\n(F40.231) Fear of injections and transfusions\n(F40.232) Fear of other medical care\n(F40.233) Fear of injury\n(F40.248) Situational\n(F40.298) Other\n300.23 (F40.10) Social Anxiety Disorder (Social Phobia) (202)\nSpecify if: Performance only", "source": "dsm5.pdf"} {"id": "99e4df7fe792-1", "page_content": "Specify if: Performance only\n300.01 (F41.0) Panic Disorder (208)\n___.__ (___.__) Panic Attack Specifier (214)\n300.22 (F40.00) Agoraphobia (217)\n300.02 (F41.1) Generalized Anxiety Disorder (222)\n___.__ (___.__) Substance/Medication-Induced Anxiety Disorder (226)\nNote: See the criteria set and corresponding recording procedures for\nsubstance-specific codes and IC D-9-CM and ICD-10-CM coding.\nSpecify if: With onset during intoxicatio n, With onset during withdrawal,\nWith onset after medication use", "source": "dsm5.pdf"} {"id": "91b9d89bc31f-0", "page_content": "DSM-5 Classification xix\n293.84 (F06.4) Anxiety Disorder Due to Anot her Medical Condition (230)\n300.09 (F41.8) Other Specified Anxiety Disorder (233)\n300.00 (F41.9) Unspecified Anxiety Disorder (233)\nObsessive-Compulsive and Related Disorders (235)\nThe following specifier applies to Obsessive-Compulsive and Rela ted Disorders where indicated:\naSpecify if: With good or fair insight, With poor insight, With absent insight/delusional beliefs\n300.3 (F42) Obsessive-Compulsive Disordera (237)\nSpecify if: Tic-related\n300.7 (F45.22) Body Dysmorphic Disordera (242)\nSpecify if: With muscle dysmorphia\n300.3 (F42) Hoarding Disordera (247)\nSpecify if: With excessive acquisition\n312.39 (F63.3) Trichotillomania (Hair-Pulling Disorder) (251)\n698.4 (L98.1) Excoriation (Skin-Picking) Disorder (254)\n___.__ (___.__) Substance/Medication-Induced Obsessive-Compulsive and \nRelated Disorder (257)\nNote: See the criteria set and corresponding recording procedures for\nsubstance-specific codes and ICD-9-CM and ICD-10-CM coding.\nSpecify if: With onset during intoxicatio n, With onset during withdrawal,\nWith onset after medication use\n294.8 (F06.8) Obsessive-Compulsive and Related Disorder Due to Another \nMedical Condition (260)\nSpecify if: With obsessive-compulsive disorder\u2013like symptoms, With", "source": "dsm5.pdf"} {"id": "91b9d89bc31f-1", "page_content": "Specify if: With obsessive-compulsive disorder\u2013like symptoms, With \nappearance preoccupations, With hoarding symptoms, With hair-\npulling symptoms, With skin-picking symptoms\n300.3 (F42) Other Specified Obsessive-Compulsive and Related Disorder \n(263)\n300.3 (F42) Unspecified Obsessive-Compulsive and Related Disorder (264)\nTrauma- and Stressor-Related Disorders (265)\n313.89 (F94.1) Reactive Attachment Disorder (265)\nSpecify if: Persistent\nSpecify current severity: Severe\n313.89 (F94.2) Disinhibited Social Enga gement Disorder (268)\nSpecify if: Persistent\nSpecify current severity: Severe\n309.81 (F43.10) Posttraumatic Stress Disorder (includes Posttraumatic Stress \nDisorder for Children 6 Years and Younger) (271)\nSpecify whether: With dissociative symptoms\nSpecify if: With delayed expression\n308.3 (F43.0) Acute Stress Disorder (280)", "source": "dsm5.pdf"} {"id": "a829f62eda84-0", "page_content": "xx DSM-5 Classification\n___.__ (___.__) Adjustment Disorders (286)\nSpecify whether:\n309.0 (F43.21) With depressed mood\n309.24 (F43.22) With anxiety\n309.28 (F43.23) With mixed anxiety and depressed mood\n309.3 (F43.24) With disturbance of conduct\n309.4 (F43.25) With mixed disturbance of emotions and conduct\n309.9 (F43.20) Unspecified\n309.89 (F43.8) Other Specified Trauma- and Stressor-Related Disorder (289)\n309.9 (F43.9) Unspecified Trauma- and Stress or-Related Disorder (290)\nDissociative Disorders (291)\n300.14 (F44.81) Dissociative Identity Disorder (292)\n300.12 (F44.0) Dissociative Amnesia (298)\nSpecify if: \n300.13 (F44.1) With dissociative fugue\n300.6 (F48.1) Depersonalization/Derealization Disorder (302)\n300.15 (F44.89) Other Specified Dissociative Disorder (306)\n300.15 (F44.9) Unspecified Dissocia tive Disorder (307)\nSomatic Symptom and Related Disorders (309)\n300.82 (F45.1) Somatic Symptom Disorder (311)\nSpecify if: With predominant pain\nSpecify if: Persistent\nSpecify current severity: Mild, Moderate, Severe\n300.7 (F45.21) Illness Anxiety Disorder (315)\nSpecify whether: Care seeking type, Care avoidant type", "source": "dsm5.pdf"} {"id": "a829f62eda84-1", "page_content": "Specify whether: Care seeking type, Care avoidant type\n300.11 (___.__) Conversion Disorder (Functional Neurological Symptom \nDisorder) (318)\nSpecify symptom type:\n(F44.4) With weakness or paralysis\n(F44.4) With abnormal movement\n(F44.4) With swallowing symptoms\n(F44.4) With speech symptom\n(F44.5) With attacks or seizures\n(F44.6) With anesthesia or sensory loss\n(F44.6) With special sensory symptom\n(F44.7) With mixed symptoms\nSpecify if: Acute episode, Persistent\nSpecify if: With psychological stressor (s pecify stressor), Without psycho-\nlogical stressor", "source": "dsm5.pdf"} {"id": "22d0388ebb9e-0", "page_content": "DSM-5 Classification xxi\n316 (F54) Psychological Factors Affecting Other Medical Conditions (322)\nSpecify current severity: Mild, Moderate, Severe, Extreme\n300.19 (F68.10) Factitious Disorder (includes Fact itious Disorder Imposed on Self, \nFactitious Disorder Imposed on Another) (324)\nSpecify Single episode, Recurrent episodes\n300.89 (F45.8) Other Specified Somatic Symptom and Related Disorder (327)\n300.82 (F45.9) Unspecified Somatic Symptom and Related Disorder (327)\nFeeding and Eating Disorders (329)\nThe following specifiers apply to Feedin g and Eating Disorders where indicated:\naSpecify if: In remission\nbSpecify if: In partial remission, In full remission\ncSpecify current severity: Mild, Moderate, Severe, Extreme\n307.52 (___.__) Picaa (329)\n(F98.3) In children\n(F50.8) In adults\n307.53 (F98.21) Rumination Disordera (332)\n307.59 (F50.8) Avoidant/Restrictive Food Intake Disordera (334)\n307.1 (___.__) Anorexia Nervosab, c (338)\nSpecify whether:\n(F50.01) Restricting type\n(F50.02) Binge-eating/purging type\n307.51 (F50.2) Bulimia Nervosab, c (345)\n307.51 (F50.8) Binge-Eating Disorderb, c (350)\n307.59 (F50.8) Other Specified Feeding or Eating Disorder (353)", "source": "dsm5.pdf"} {"id": "22d0388ebb9e-1", "page_content": "307.50 (F50.9) Unspecified Feeding or Eating Disorder (354)\nElimination Disorders (355)\n307.6 (F98.0) Enuresis (355)\nSpecify whether: Nocturnal only, Diur nal only, Nocturnal and diurnal\n307.7 (F98.1) Encopresis (357)\nSpecify whether: With constipation an d overflow incontinence, Without\nconstipation and overflow incontinence\n___.__ (___.__) Other Specified Elimination Disorder (359)\n788.39 (N39.498) With urinary symptoms\n787.60 (R15.9) With fecal symptoms\n___.__ (___.__) Unspecified Elimination Disorder (360)\n788.30 (R32) With urinary symptoms\n787.60 (R15.9) With fecal symptoms", "source": "dsm5.pdf"} {"id": "539821d96d12-0", "page_content": "xxii DSM-5 Classification\nSleep-Wake Disorders (361)\nThe following specifiers apply to Sl eep-Wake Disorders where indicated:\naSpecify if: Episodic, Persistent, Recurrent\nbSpecify if: Acute, Subacute, Persistent\ncSpecify current severity: Mi ld, Moderate, Severe\n307.42 (F51.01) Insomnia Disordera (362)\nSpecify if: With non\u2013sleep disorder mental comorbidity, With other \nmedical comorbidity, With other sleep disorder\n307.44 (F51.11) Hypersomnolence Disorderb, c (368)\nSpecify if: With mental disorder, With medical condition, With another\nsleep disorder\n___.__ (___.__) Narcolepsyc (372)\nSpecify whether:\n347.00 (G47.419) Narcolepsy without cataplexy bu t with hypocretin deficiency\n347.01 (G47.411) Narcolepsy with cataplexy but without hypocretin deficiency \n347.00 (G47.419) Autosomal dominant cerebellar ataxia, deafness, and \nnarcolepsy\n347.00 (G47.419) Autosomal dominant narcolepsy, obesity, and type 2 diabetes\n347.10 (G47.429) Narcolepsy secondary to another medical condition\nBreathing-Related Sleep Disorders (378)\n327.23 (G47.33) Obstructive Sleep Apnea Hypopneac (378)\n___.__ (___.__) Central Sleep Apnea (383)\nSpecify whether:\n327.21 (G47.31) Idiopathic central sleep apnea\n786.04 (R06.3) Cheyne-Stokes breathing", "source": "dsm5.pdf"} {"id": "539821d96d12-1", "page_content": "786.04 (R06.3) Cheyne-Stokes breathing\n780.57 (G47.37) Central sleep apnea comorbid with opioid use\nNote: First code opioid use disorder, if present.\nSpecify current severity\n___.__ (___.__) Sleep-Related Hypoventilation (387)\nSpecify whether:\n327.24 (G47.34) Idiopathic hypoventilation\n327.25 (G47.35) Congenital central alve olar hypoventilation\n327.26 (G47.36) Comorbid sleep-related hypoventilation\nSpecify current severity\n___.__ (___.__) Circadian Rhythm Sleep-Wake Disordersa (390)\nSpecify whether:\n307.45 (G47.21) Delayed sleep phase type (391)\nSpecify if: Familial, Overlapping with non-24-hour sleep-wake type\n307.45 (G47.22) Advanced sleep phase type (393)\nSpecify if: Familial\n307.45 (G47.23) Irregular sleep-wake type (394)\n307.45 (G47.24) Non-24-hour sleep-wake type (396)", "source": "dsm5.pdf"} {"id": "98c9e33f87f0-0", "page_content": "DSM-5 Classification xxiii\n307.45 (G47.26) Shift work type (397)\n307.45 (G47.20) Unspecified type\nParasomnias (399)\n___.__ (__.__) Non\u2013Rapid Eye Movement Sleep Arousal Disorders (399)\nSpecify whether:\n307.46 (F51.3) Sleepwalking type\nSpecify if: With sleep-related eating , With sleep-related sexual \n behavior (sexsomnia)\n307.46 (F51.4) Sleep terror type\n307.47 (F51.5) Nightmare Disorderb, c (404)\nSpecify if: During sleep onset\nSpecify if: With associated non\u2013sleep disorder, With associated other\nmedical condition, With associated other sleep disorder\n327.42 (G47.52) Rapid Eye Movement Sleep Behavior Disorder (407)\n333.94 (G25.81) Restless Legs Syndrome (410)\n___.__ (___.__) Substance/Medication-Induc ed Sleep Disorder (413)\nNote: See the criteria set and corresponding recording procedures for\nsubstance-specific codes and ICD-9-CM and ICD-10-CM coding.\nSpecify whether: Insomnia type, Dayt ime sleepiness type, Parasomnia\ntype, Mixed type\nSpecify if: With onset during intoxicatio n, With onset during discontinua-\ntion/withdrawal\n780.52 (G47.09) Other Specified Insomnia Disorder (420)\n780.52 (G47.00) Unspecified Insomnia Disorder (420)\n780.54 (G47.19) Other Specified Hypersomnolence Disorder (421)\n780.54 (G47.10) Unspecified Hypersomnolence Disorder (421)", "source": "dsm5.pdf"} {"id": "98c9e33f87f0-1", "page_content": "780.59 (G47.8) Other Specified Sleep-Wake Disorder (421)\n780.59 (G47.9) Unspecified Sleep-Wake Disorder (422)\nSexual Dysfunctions (423)\nThe following specifiers apply to Sexual Dysfunctions where indicated:\naSpecify whether: Lifelong, Acquired\nbSpecify whether: Generalized, Situational\ncSpecify current severity: Mi ld, Moderate, Severe\n302.74 (F52.32) Delayed Ejaculationa, b, c (424)\n302.72 (F52.21) Erectile Disordera, b, c (426)\n302.73 (F52.31) Female Orgasmic Disordera, b, c (429)\nSpecify if: Never experienced an orgasm under any situation\n302.72 (F52.22) Female Sexual Interest/Arousal Disordera, b, c (433)\n302.76 (F52.6) Genito-Pelvic Pain/Penetration Disordera, c (437)", "source": "dsm5.pdf"} {"id": "fe90bf07c27e-0", "page_content": "xxiv DSM-5 Classification\n302.71 (F52.0) Male Hypoactive Sexual Desire Disordera, b, c (440)\n302.75 (F52.4) Premature (Early) Ejaculationa, b, c (443)\n___.__ (___.__) Substance/Medication-Induc ed Sexual Dysfunctionc (446)\nNote: See the criteria set and corresponding recording procedures for\nsubstance-specific codes and IC D-9-CM and ICD-10-CM coding.\nSpecify if: With onset during intoxicatio n, With onset during withdrawal,\nWith onset after medication use\n302.79 (F52.8) Other Specified Sexual Dysfunction (450)\n302.70 (F52.9) Unspecified Sexual Dysfunction (450)\nGender Dysphoria (451)\n___.__ (__.__) Gender Dysphoria (452)\n302.6 (F64.2) Gender Dysphoria in Children\nSpecify if: With a disorder of sex development\n302.85 (F64.1) Gender Dysphoria in Adolescents and Adults\nSpecify if: With a disorder of sex development\nSpecify if: Posttransition\nNote: Code the disorder of sex develo pment if present, in addition to \ngender dysphoria.\n302.6 (F64.8) Other Specified Gender Dysphoria (459)\n302.6 (F64.9) Unspecified Gender Dysphoria (459)\nDisruptive, Impulse-Contro l, and Conduct Disorders (461)\n313.81 (F91.3) Oppositional Defi ant Disorder (462)\nSpecify current severity: Mild, Moderate, Severe", "source": "dsm5.pdf"} {"id": "fe90bf07c27e-1", "page_content": "Specify current severity: Mild, Moderate, Severe\n312.34 (F63.81) Intermittent Explosive Disorder (466)\n___.__ (__.__) Conduct Disorder (469)\nSpecify whether:\n312.81 (F91.1) Childhood-onset type\n312.82 (F91.2) Adolescent-onset type\n312.89 (F91.9) Unspecified onset\nSpecify if: With limited prosocial emotions\nSpecify current severity: Mild, Moderate, Severe\n301.7 (F60.2) Antisocial Personality Disorder (476)\n312.33 (F63.1) Pyromania (476)\n312.32 (F63.2) Kleptomania (478)\n312.89 (F91.8) Other Specified Disruptive, Impulse-Control, and Conduct \nDisorder (479)\n312.9 (F91.9) Unspecified Disruptive, Impulse-Control, and Conduct Disorder \n(480)", "source": "dsm5.pdf"} {"id": "fee7ba06bff9-0", "page_content": "DSM-5 Classification xxv\nSubstance-Related and Addictive Disorders (481)\nThe following specifiers and note apply to Substance-Related and Addictive Disorders where\nindicated:\naSpecify if: In early remission, In sustained remission\nbSpecify if: In a controlled environment\ncSpecify if: With perceptual disturbances\ndThe ICD-10-CM code indicates the comorbid pres ence of a moderate or severe substance use\ndisorder, which must be present in order to apply the code for substance withdrawal.\nSubstance-Related Disorders (483)\nAlcohol-Related Disorders (490)\n___.__ (___.__) Alcohol Use Disordera, b (490)\nSpecify current severity:\n305.00 (F10.10) Mild\n303.90 (F10.20) Moderate\n303.90 (F10.20) Severe\n303.00 (___.__) Alcohol Intoxi cation (497)\n(F10.129) With use disorder, mild\n(F10.229) With use disorder, moderate or severe\n(F10.929) Without use disorder\n291.81 (___.__) Alcohol Withdrawalc, d (499)\n(F10.239) Without perceptual disturbances\n(F10.232) With perceptual disturbances\n___.__ (___.__) Other Alcohol-Induced Disorders (502)\n291.9 (F10.99) Unspecified Alcohol-Related Disorder (503)\nCaffeine-Related Disorders (503)\n305.90 (F15.929) Caffeine Intoxication (503)\n292.0 (F15.93) Caffeine Withdrawal (506)\n___.__ (___.__) Other Caffeine-Induc ed Disorders (508)", "source": "dsm5.pdf"} {"id": "fee7ba06bff9-1", "page_content": "___.__ (___.__) Other Caffeine-Induc ed Disorders (508)\n292.9 (F15.99) Unspecified Caffeine-Related Disorder (509)\nCannabis-Related Disorders (509)\n___.__ (___.__) Cannabis Use Disordera, b (509)\nSpecify current severity:\n305.20 (F12.10) Mild\n304.30 (F12.20) Moderate\n304.30 (F12.20) Severe", "source": "dsm5.pdf"} {"id": "9bf6239863ce-0", "page_content": "xxvi DSM-5 Classification\n292.89 (___.__) Cannabis Intoxicationc (516)\nWithout perceptual disturbances\n(F12.129) With use disorder, mild\n(F12.229) With use disorder, moderate or severe\n(F12.929) Without use disorder\nWith perceptual disturbances\n(F12.122) With use disorder, mild\n(F12.222) With use disorder, moderate or severe\n(F12.922) Without use disorder\n292.0 (F12.288) Cannabis Withdrawald (517)\n___.__ (___.__) Other Cannabis-Induced Disorders (519)\n292.9 (F12.99) Unspecified Cannabis-Related Disorder (519)\nHallucinogen-Related Disorders (520)\n___.__ (___.__) Phencyclidine Use Disordera, b (520)\nSpecify current severity:\n305.90 (F16.10) Mild\n304.60 (F16.20) Moderate\n304.60 (F16.20) Severe\n___.__ (___.__) Other Hallucinogen Use Disordera, b (523)\nSpecify the particular hallucinogen\nSpecify current severity:\n305.30 (F16.10) Mild\n304.50 (F16.20) Moderate\n304.50 (F16.20) Severe\n292.89 (___.__) Phencyclidine Intoxication (527)\n(F16.129) With use disorder, mild\n(F16.229) With use disorder, moderate or severe\n(F16.929) Without use disorder\n292.89 (___.__) Other Hallucinogen Intoxication (529)\n(F16.129) With use disorder, mild\n(F16.229) With use disorder, moderate or severe", "source": "dsm5.pdf"} {"id": "9bf6239863ce-1", "page_content": "(F16.229) With use disorder, moderate or severe\n(F16.929) Without use disorder\n292.89 (F16.983) Hallucinogen Persisting Pe rception Disorder (531)\n___.__ (___.__) Other Phencyclidine-Induced Disorders (532)\n___.__ (___.__) Other Hallucinogen-Induced Disorders (532)\n292.9 (F16.99) Unspecified Phencyclidine-Related Disorder (533)\n292.9 (F16.99) Unspecified Hallucinogen-R elated Disorder (533)\nInhalant-Related Disorders (533)\n___.__ (___.__) Inhalant Use Disordera, b (533)\nSpecify the particular inhalant\nSpecify current severity:\n305.90 (F18.10) Mild", "source": "dsm5.pdf"} {"id": "8d34144e671d-0", "page_content": "DSM-5 Classification xxvii\n304.60 (F18.20) Moderate\n304.60 (F18.20) Severe\n292.89 (___.__) Inhalant Intoxication (538)\n(F18.129) With use disorder, mild\n(F18.229) With use disorder, moderate or severe\n(F18.929) Without use disorder\n___.__ (___.__) Other Inhalant-Induced Disorders (540)\n292.9 (F18.99) Unspecified Inhalant-Related Disorder (540)\nOpioid-Related Disorders (540)\n___.__ (___.__) Opioid Use Disordera (541)\nSpecify if: On maintenance therapy, In a controlled environment\nSpecify current severity:\n305.50 (F11.10) Mild\n304.00 (F11.20) Moderate\n304.00 (F11.20) Severe\n292.89 (___.__) Opioid Intoxicationc (546)\nWithout perceptual disturbances\n(F11.129) With use disorder, mild\n(F11.229) With use disorder, moderate or severe\n(F11.929) Without use disorder\nWith perceptual disturbances\n(F11.122) With use disorder, mild\n(F11.222) With use disorder, moderate or severe\n(F11.922) Without use disorder\n292.0 (F11.23) Opioid Withdrawald (547)\n___.__ (___.__) Other Opioid-Induced Disorders (549)\n292.9 (F11.99) Unspecified Opioid-Related Disorder (550)\nSedative-, Hypnotic-, or Anxiolytic-Related Disorders (550)", "source": "dsm5.pdf"} {"id": "8d34144e671d-1", "page_content": "Sedative-, Hypnotic-, or Anxiolytic-Related Disorders (550)\n___.__ (___.__) Sedative, Hypnotic, or Anxiolytic Use Disordera, b (550)\nSpecify current severity:\n305.40 (F13.10) Mild\n304.10 (F13.20) Moderate\n304.10 (F13.20) Severe\n292.89 (___.__) Sedative, Hypnotic, or Anxi olytic Intoxication (556)\n(F13.129) With use disorder, mild\n(F13.229) With use disorder, moderate or severe\n(F13.929) Without use disorder\n292.0 (___.__) Sedative, Hypnotic, or Anxiolytic Withdrawalc, d (557)\n(F13.239) Without perceptual disturbances\n(F13.232) With perceptual disturbances", "source": "dsm5.pdf"} {"id": "759d006edab3-0", "page_content": "xxviii DSM-5 Classification\n___.__ (___.__) Other Sedative-, Hypnotic-, or Anxiolytic-Induced Disorders \n(560)\n292.9 (F13.99) Unspecified Sedative-, Hypnotic-, or Anxiolytic-Related Disorder \n(560)\nStimulant-Related Disorders (561)\n___.__ (___.__) Stimulant Use Disordera, b (561)\nSpecify current severity:\n___.__ (___.__) Mild\n305.70 (F15.10) Amphetamine-type substance\n305.60 (F14.10) Cocaine\n305.70 (F15.10) Other or unspecified stimulant\n___.__ (___.__) Moderate\n304.40 (F15.20) Amphetamine-type substance\n304.20 (F14.20) Cocaine\n304.40 (F15.20) Other or unspecified stimulant\n___.__ (___.__) Severe\n304.40 (F15.20) Amphetamine-type substance\n304.20 (F14.20) Cocaine\n304.40 (F15.20) Other or unspecified stimulant\n292.89 (___.__) Stimulant Intoxicationc (567)\nSpecify the specific intoxicant\n292.89 (___.__) Amphetamine or other stimulant, Without perceptual \ndisturbances\n(F15.129) With use disorder, mild\n(F15.229) With use disorder, moderate or severe\n(F15.929) Without use disorder\n292.89 (___.__) Cocaine, Without perceptual disturbances\n(F14.129) With use disorder, mild\n(F14.229) With use disorder, moderate or severe\n(F14.929) Without use disorder", "source": "dsm5.pdf"} {"id": "759d006edab3-1", "page_content": "(F14.929) Without use disorder\n292.89 (___.__) Amphetamine or other stimulant, With perceptual \ndisturbances\n(F15.122) With use disorder, mild\n(F15.222) With use disorder, moderate or severe\n(F15.922) Without use disorder\n292.89 (___.__) Cocaine, With perceptual disturbances\n(F14.122) With use disorder, mild\n(F14.222) With use disorder, moderate or severe\n(F14.922) Without use disorder\n292.0 (___.__) Stimulant Withdrawald (569)\nSpecify the specific substance causing the withdrawal syndrome\n(F15.23) Amphetamine or other stimulant\n(F14.23) Cocaine\n___.__ (___.__) Other Stimulant-Induced Disorders (570)", "source": "dsm5.pdf"} {"id": "c9df4f365e78-0", "page_content": "DSM-5 Classification xxix\n292.9 (___.__) Unspecified Stimulant-Related Disorder (570)\n(F15.99) Amphetamine or other stimulant\n(F14.99) Cocaine\nTobacco-Related Disorders (571)\n___.__ (___.__) Tobacco Use Disordera (571)\nSpecify if: On maintenance therapy, In a controlled environment\nSpecify current severity:\n305.1 (Z72.0) Mild\n305.1 (F17.200) Moderate\n305.1 (F17.200) Severe\n292.0 (F17.203) Tobacco Withdrawald (575)\n___.__ (___.__) Other Tobacco-Induced Disorders (576)\n292.9 (F17.209) Unspecified Tobacco-Related Disorder (577)\nOther (or Unknown) Substance\u2013Related Disorders (577)\n___._ (___.__) Other (or Unknown) Substance Use Disordera, b (577)\nSpecify current severity:\n305.90 (F19.10) Mild\n304.90 (F19.20) Moderate\n304.90 (F19.20) Severe\n292.89 (___.__) Other (or Unknown) Substance Intoxication (581)\n(F19.129) With use disorder, mild\n(F19.229) With use disorder, moderate or severe\n(F19.929) Without use disorder\n292.0 (F19.239) Other (or Unknown) Substance Withdrawald (583)\n___.__ (___.__) Other (or Unknown) Substance\u2013Induced Disorders (584)\n292.9 (F19.99) Unspecified Other (or Unknown) Su bstance\u2013Related Disorder (585)\nNon-Substance-Related Disorders (585)", "source": "dsm5.pdf"} {"id": "c9df4f365e78-1", "page_content": "Non-Substance-Related Disorders (585)\n312.31 (F63.0) Gambling Disordera (585)\nSpecify if: Episodic, Persistent\nSpecify current severity: Mild, Moderate, Severe\nNeurocognitive Disorders (591)\n___.__ (___.__) Delirium (596)\naNote: See the criteria set and corresponding recording procedures for\nsubstance-specific codes and ICD-9-CM and ICD-10-CM coding.\nSpecify whether:\n___.__ (___.__) Substance intoxication deliriuma\n___.__ (___.__) Substance withdrawal deliriuma\n292.81 (___.__) Medication-induced deliriuma\n293.0 (F05) Delirium due to another medical condition", "source": "dsm5.pdf"} {"id": "ba5a0451f257-0", "page_content": "xxx DSM-5 Classification\n293.0 (F05) Delirium due to multiple etiologies\nSpecify if: Acute, Persistent\nSpecify if: Hyperactive, Hypoacti ve, Mixed level of activity\n780.09 (R41.0) Other Specified Delirium (602)\n780.09 (R41.0) Unspecified Delirium (602)\nMajor and Mild Neurocognitive Disorders (602)\nSpecify whether due to: Alzheimer\u2019s disease, Frontotemporal lobar degeneration, Lewy body\ndisease, Vascular disease, Traumatic brain injury, Substance/medication use, HIV infection,\nPrion disease, Parkinson\u2019s disease, Huntington\u2019s disease, Another medical condition, Multi-\nple etiologies, Unspecified\naSpecify Without behavioral disturbance, With behavioral disturbance. For possible major neuro-\ncognitive disorder and for mild ne urocognitive disorder, behavioral disturbanc e cannot be coded but\nshould still be indicated in writing.\nbSpecify current severity: Mild, Moderate, Severe. This specifier applies only to major neurocogni-\ntive disorders (i ncluding probable and possible).\nNote: As indicated for each subtype, an additional medical code is needed for probable major\nneurocognitive disorder or majo r neurocognitive disorder. An additional medical code should\nnot be used for possible major neurocognitive disorder or mild neur ocognitive disorder.\nMajor or Mild Neurocognitive Disorder Due to Alzheimer\u2019s Disease (611)\n___.__ (___.__) Probable Major Neurocognitive Disorder Due to Alzheimer\u2019s \nDiseaseb\nNote: Code first 331.0 (G30.9) Alzheimer\u2019s disease.\n294.11 (F02.81) With behavioral disturbance", "source": "dsm5.pdf"} {"id": "ba5a0451f257-1", "page_content": "294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance\n331.9 (G31.9) Possible Major Neurocognitive Disorder Due to Alzheimer\u2019s \nDiseasea, b\n331.83 (G31.84) Mild Neurocognitive Disorder Due to Alzheimer\u2019s Diseasea\nMajor or Mild Frontotemporal Neurocognitive Disorder (614)\n___.__ (___.__) Probable Major Neurocognitive Di sorder Due to Frontotemporal \nLobar Degenerationb\nNote: Code first 331.19 (G31.09) frontotemporal disease.\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance\n331.9 (G31.9) Possible Major Neurocognitive Disorder Due to Frontotemporal \nLobar Degenerationa, b\n331.83 (G31.84) Mild Neurocognitive Disorder Due to Frontotemporal Lobar \nDegenerationa\nMajor or Mild Neurocognitive Disorder With Lewy Bodies (618)\n___.__ (___.__) Probable Major Neurocognitive Disorder With Lewy Bodiesb\nNote: Code first 331.82 (G31.83) Lewy body disease.\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance", "source": "dsm5.pdf"} {"id": "d79501ac5e3f-0", "page_content": "DSM-5 Classification xxxi\n331.9 (G31.9) Possible Major Neurocognitive Disorder With Lewy Bodiesa, b\n331.83 (G31.84) Mild Neurocognitive Disorder With Lewy Bodiesa\nMajor or Mild Vascular Neurocognitive Disorder (621)\n___.__ (___.__) Probable Major Vascular Neurocognitive Disorderb\nNote: No additional medical code for vascular disease.\n290.40 (F01.51) With behavioral disturbance\n290.40 (F01.50) Without behavioral disturbance\n331.9 (G31.9) Possible Major Vascular Neurocognitive Disordera, b\n331.83 (G31.84) Mild Vascular Neur ocognitive Disordera\nMajor or Mild Neurocognitive Disorder Due to Traumatic Brain Injury (624)\n___.__ (___.__) Major Neurocognitive Disorder Due to Traumatic Brain Injuryb\nNote: For ICD-9-CM, code first 907.0 late effect of intracranial injury without\nskull fracture. For IC D-10-CM, code first S06.2X9S diffuse traumatic brain\ninjury with loss of consciousness of unspecified duration, sequela.\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance\n331.83 (G31.84) Mild Neurocognitive Disorder Due to Traumatic Brain Injurya\nSubstance/Medication-Induced Major or Mild Neurocognitive Disordera (627)\nNote: No additional medical code. See the criter ia set and corresponding recording procedures\nfor substance-specific codes and ICD-9-CM and ICD-10-CM coding.\nSpecify if: Persistent", "source": "dsm5.pdf"} {"id": "d79501ac5e3f-1", "page_content": "Specify if: Persistent\nMajor or Mild Neurocognitive Disorder Due to HIV Infection (632)\n___.__ (___.__) Major Neurocognitive Disorder Due to HIV Infectionb\nNote: Code first 042 (B20) HIV infection.\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance\n331.83 (G31.84) Mild Neurocognitive Disorder Due to HIV Infectiona\nMajor or Mild Neurocognitive Disorder Due to Prion Disease (634)\n___.__ (___.__) Major Neurocognitive Disord er Due to Prion Diseaseb\nNote: Code first 046.79 (A81.9) prion disease.\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance\n331.83 (G31.84) Mild Neurocognitive Disorder Due to Prion Diseasea\nMajor or Mild Neurocognitive Disorder Due to Parkinson\u2019s Disease (636)\n___.__ (___.__) Major Neurocognitive Disorder Probably Due to Parkinson\u2019s \nDiseaseb\nNote: Code first 332.0 (G20) Parkinson\u2019s disease.\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance", "source": "dsm5.pdf"} {"id": "b242bdd7d8d4-0", "page_content": "xxxii DSM-5 Classification\n331.9 (G31.9) Major Neurocognitive Disorder Possibly Due to Parkinson\u2019s \nDiseasea, b\n331.83 (G31.84) Mild Neurocognitive Disorder Due to Parkinson\u2019s Diseasea\nMajor or Mild Neurocognitive Disorder Due to Huntington\u2019s Disease (638)\n___.__ (___.__) Major Neurocognitive Disorder Due to Huntington\u2019s Diseaseb\nNote: Code first 333.4 (G10) Huntington\u2019s disease.\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance\n331.83 (G31.84) Mild Neurocognitive Disorder Due to Huntington\u2019s Diseasea\nMajor or Mild Neurocognitive Disorder Due to Another Medical Condition (641)\n___.__ (___.__) Major Neurocognitive Disord er Due to Another Medical \nConditionb\nNote: Code first the other medical condition.\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance\n331.83 (G31.84) Mild Neurocognitive Disorder Due to Another Medical \nConditiona\nMajor or Mild Neurocognitive Disorder Due to Multiple Etiologies (642)\n___.__ (___.__) Major Neurocognitive Disorder Due to Multiple Etiologiesb\nNote: Code first all the etiological medical conditions (with the exception\nof vascular disease).\n294.11 (F02.81) With behavioral disturbance\n294.10 (F02.80) Without behavioral disturbance\n331.83 (G31.84) Mild Neurocognitive Disorder Due to Multiple Etiologiesa\nUnspecified Neurocognit ive Disorder (643)", "source": "dsm5.pdf"} {"id": "b242bdd7d8d4-1", "page_content": "Unspecified Neurocognit ive Disorder (643)\n799.59 (R41.9) Unspecified Neurocognitive Disordera\nPersonality Disorders (645)\nCluster A Personality Disorders\n301.0 (F60.0) Paranoid Personality Disorder (649)\n301.20 (F60.1) Schizoid Personality Disorder (652)\n301.22 (F21) Schizotypal Personality Disorder (655)\nCluster B Personality Disorders\n301.7 (F60.2) Antisocial Personality Disorder (659)\n301.83 (F60.3) Borderline Personality Disorder (663)\n301.50 (F60.4) Histrionic Personality Disorder (667)\n301.81 (F60.81) Narcissistic Personality Disorder (669)", "source": "dsm5.pdf"} {"id": "df9dfe94c6b9-0", "page_content": "DSM-5 Classification xxxiii\nCluster C Personality Disorders\n301.82 (F60.6) Avoidant Personality Disorder (672)\n301.6 (F60.7) Dependent Personalit y Disorder (675)\n301.4 (F60.5) Obsessive-Compulsive Personality Disorder (678)\nOther Personality Disorders\n310.1 (F07.0) Personality Change Due to Another Medical Condition (682)\nSpecify whether: Labile type, Disinhibited type, Aggressive type, Apathetic\ntype, Paranoid type, Other type, Combined type, Unspecified type\n301.89 (F60.89) Other Specified Personality Disorder (684)\n301.9 (F60.9) Unspecified Personality Disorder (684)\nParaphilic Disorders (685)\nThe following specifier applies to Pa raphilic Disorders where indicated:\naSpecify if: In a controlled environment, In full remission\n302.82 (F65.3) Voyeuristic Disordera (686)\n302.4 (F65.2) Exhibitionistic Disordera (689)\nSpecify whether: Sexually aroused by exposing genitals to prepubertal\nchildren, Sexually aroused by exposi ng genitals to physically mature\nindividuals, Sexually aroused by exposing genitals to prepubertal chil-\ndren and to physically mature individuals\n302.89 (F65.81) Frotteuristic Disordera (691)\n302.83 (F65.51) Sexual Masochism Disordera (694)\nSpecify if: With asphyxiophilia\n302.84 (F65.52) Sexual Sadism Disordera (695)\n302.2 (F65.4) Pedophilic Disorder (697)", "source": "dsm5.pdf"} {"id": "df9dfe94c6b9-1", "page_content": "302.2 (F65.4) Pedophilic Disorder (697)\nSpecify whether: Exclusive type, Nonexclusive type\nSpecify if: Sexually attracted to males, Se xually attracted to females, Sexu-\nally attracted to both\nSpecify if: Limited to incest\n302.81 (F65.0) Fetishistic Disordera (700)\nSpecify: Body part(s), Nonliving object(s), Other\n302.3 (F65.1) Transvestic Disordera (702)\nSpecify if: With fetishism, With autogynephilia\n302.89 (F65.89) Other Specified Paraphilic Disorder (705)\n302.9 (F65.9) Unspecified Paraphilic Disorder (705)\nOther Mental Disorders (707)\n294.8 (F06.8) Other Specified Mental Disorder Due to Another Medical \nCondition (707)\n294.9 (F09) Unspecified Mental Disorder Due to Another Medical Condition \n(708)\n300.9 (F99) Other Specified Mental Disorder (708)\n300.9 (F99) Unspecified Mental Disorder (708)", "source": "dsm5.pdf"} {"id": "40d97c1e5546-0", "page_content": "xxxiv DSM-5 Classification\nMedication-Induced Movement Disorders and \nOther Adverse Effects of Medication (709)\n332.1 (G21.11) Neuroleptic-Induced Parkinsonism (709)\n332.1 (G21.19) Other Medication-Induced Parkinsonism (709)\n333.92 (G21.0) Neuroleptic Malignant Syndrome (709)\n333.72 (G24.02) Medication-Induced Acute Dystonia (711)\n333.99 (G25.71) Medication-Induced Acute Akathisia (711)\n333.85 (G24.01) Tardive Dyskinesia (712)\n333.72 (G24.09) Tardive Dystonia (712)\n333.99 (G25.71) Tardive Akathisia (712)\n333.1 (G25.1) Medication-Induced Postural Tremor (712)\n333.99 (G25.79) Other Medication-Induced Movement Disorder (712)\n___.__ (___.__) Antidepressant Disconti nuation Syndrome (712)\n995.29 (T43.205A) Initial encounter\n995.29 (T43.205D) Subsequent encounter\n995.29 (T43.205S) Sequelae\n___.__ (___.__) Other Adverse Effect of Medication (714)\n995.20 (T50.905A) Initial encounter\n995.20 (T50.905D) Subsequent encounter\n995.20 (T50.905S) Sequelae\nOther Conditions That May Be a Focus \nof Clinical Attention (715)\nRelational Problems (715)", "source": "dsm5.pdf"} {"id": "40d97c1e5546-1", "page_content": "of Clinical Attention (715)\nRelational Problems (715)\nProblems Related to Fa mily Upbringing (715)\nV61.20 (Z62.820) Parent-Child Relational Problem (715)\nV61.8 (Z62.891) Sibling Relational Problem (716)\nV61.8 (Z62.29) Upbringing Away From Parents (716)\nV61.29 (Z62.898) Child Affected by Parental Relationship Distress (716)\nOther Problems Related to Primary Support Group (716)\nV61.10 (Z63.0) Relationship Distress With Spouse or Intimate Partner (716)\nV61.03 (Z63.5) Disruption of Family by Se paration or Divorce (716)\nV61.8 (Z63.8) High Expressed Emotion Level Within Family (716)\nV62.82 (Z63.4) Uncomplicated Bereavement (716)", "source": "dsm5.pdf"} {"id": "3d061eda7bc2-0", "page_content": "DSM-5 Classification xxxv\nAbuse and Neglect (717)\nChild Maltreatment and Neglect Problems (717)\nChild Physical Abuse (717)\nChild Physical Abuse, Confirmed (717)\n995.54 (T74.12XA) Initial encounter\n995.54 (T74.12XD) Subsequent encounter\nChild Physical Abuse, Suspected (717)\n995.54 (T76.12XA) Initial encounter\n995.54 (T76.12XD) Subsequent encounter\nOther Circumstances Related to Child Physical Abuse (718)\nV61.21 (Z69.010) Encounter for mental health serv ices for victim of child abuse \nby parent\nV61.21 (Z69.020) Encounter for mental health services for victim of nonparental \nchild abuse\nV15.41 (Z62.810) Personal history (past history) of physical abuse in childhood\nV61.22 (Z69.011) Encounter for mental health services for perpetrator of parental \nchild abuse\nV62.83 (Z69.021) Encounter for mental health services for perpetrator of \nnonparental child abuse\nChild Sexual Abuse (718)\nChild Sexual Abuse, Confirmed (718)\n995.53 (T74.22XA) Initial encounter\n995.53 (T74.22XD) Subsequent encounter\nChild Sexual Abuse, Suspected (718)\n995.53 (T76.22XA) Initial encounter\n995.53 (T76.22XD) Subsequent encounter\nOther Circumstances Related to Child Sexual Abuse (718)\nV61.21 (Z69.010) Encounter for mental health services for victim of child sexual \nabuse by parent", "source": "dsm5.pdf"} {"id": "3d061eda7bc2-1", "page_content": "abuse by parent\nV61.21 (Z69.020) Encounter for mental health services for victim of nonparental \nchild sexual abuse\nV15.41 (Z62.810) Personal history (past history) of sexual abuse in childhood\nV61.22 (Z69.011) Encounter for mental health services for perpetrator of parental \nchild sexual abuse\nV62.83 (Z69.021) Encounter for mental health services for perpetrator of \nnonparental child sexual abuse\nChild Neglect (718)\nChild Neglect, Confirmed (718)\n995.52 (T74.02XA) Initial encounter\n995.52 (T74.02XD) Subsequent encounter", "source": "dsm5.pdf"} {"id": "bbbac78fd743-0", "page_content": "xxxvi DSM-5 Classification\nChild Neglect, Suspected (719)\n995.52 (T76.02XA) Initial encounter\n995.52 (T76.02XD) Subsequent encounter\nOther Circumstances Related to Child Neglect (719)\nV61.21 (Z69.010) Encounter for mental health services for victim of child neglect \nby parent\nV61.21 (Z69.020) Encounter for mental health services for victim of nonparental \nchild neglect\nV15.42 (Z62.812) Personal history (past histor y) of neglect in childhood\nV61.22 (Z69.011) Encounter for mental health services for perpetrator of parental \nchild neglect\nV62.83 (Z69.021) Encounter for mental health services for perpetrator of \nnonparental child neglect\nChild Psychological Abuse (719)\nChild Psychological Abuse, Confirmed (719)\n995.51 (T74.32XA) Initial encounter\n995.51 (T74.32XD) Subsequent encounter\nChild Psychological Abuse, Suspected (719)\n995.51 (T76.32XA) Initial encounter\n995.51 (T76.32XD) Subsequent encounter\nOther Circumstances Related to Child Psychological Abuse (719)\nV61.21 (Z69.010) Encounter for mental health se rvices for victim of child \npsychological abuse by parent\nV61.21 (Z69.020) Encounter for mental health services for victim of nonparental \nchild psychological abuse\nV15.42 (Z62.811) Personal history (past history) of psychological abuse in \nchildhood\nV61.22 (Z69.011) Encounter for mental health services for perpetrator of parental \nchild psychological abuse", "source": "dsm5.pdf"} {"id": "bbbac78fd743-1", "page_content": "child psychological abuse\nV62.83 (Z69.021) Encounter for mental health services for perpetrator of \nnonparental child psychological abuse\nAdult Maltreatment and Neglect Problems (720)\nSpouse or Partner Violence, Physical (720)\nSpouse or Partner Violence, Physical, Confirmed (720)\n995.81 (T74.11XA) Initial encounter\n995.81 (T74.11XD) Subsequent encounter\nSpouse or Partner Violence, Physical, Suspected (720)\n995.81 (T76.11XA) Initial encounter\n995.81 (T76.11XD) Subsequent encounter\nOther Circumstances Related to Spouse or Partner Violence, Physical (720)\nV61.11 (Z69.11) Encounter for mental health serv ices for victim of spouse or \npartner violence, physical", "source": "dsm5.pdf"} {"id": "bd7aa62861e6-0", "page_content": "DSM-5 Classification xxxvii\nV15.41 (Z91.410) Personal history (past history) of spouse or partner violence, \nphysical\nV61.12 (Z69.12) Encounter for mental health serv ices for perpetrator of spouse \nor partner violence, physical\nSpouse or Partner Violence, Sexual (720)\nSpouse or Partner Violence, Sexual, Confirmed (720)\n995.83 (T74.21XA) Initial encounter\n995.83 (T74.21XD) Subsequent encounter\nSpouse or Partner Violence, Sexual, Suspected (720)\n995.83 (T76.21XA) Initial encounter\n995.83 (T76.21XD) Subsequent encounter\nOther Circumstances Related to Spouse or Partner Violence, Sexual (720)\nV61.11 (Z69.81) Encounter for mental health serv ices for victim of spouse or \npartner violence, sexual\nV15.41 (Z91.410) Personal history (past history) of spouse or partner violence, \nsexual\nV61.12 (Z69.12) Encounter for mental health serv ices for perpetrator of spouse \nor partner violence, sexual\nSpouse or Partner, Neglect (721)\nSpouse or Partner Neglect, Confirmed (721)\n995.85 (T74.01XA) Initial encounter\n995.85 (T74.01XD) Subsequent encounter\nSpouse or Partner Neglect, Suspected (721)\n995.85 (T76.01XA) Initial encounter\n995.85 (T76.01XD) Subsequent encounter\nOther Circumstances Related to Spouse or Partner Neglect (721)", "source": "dsm5.pdf"} {"id": "bd7aa62861e6-1", "page_content": "Other Circumstances Related to Spouse or Partner Neglect (721)\nV61.11 (Z69.11) Encounter for mental health serv ices for victim of spouse or \npartner neglect\nV15.42 (Z91.412) Personal history (past history) of spouse or partner neglect\nV61.12 (Z69.12) Encounter for mental health serv ices for perpetrator of spouse \nor partner neglect\nSpouse or Partner Abuse, Psychological (721)\nSpouse or Partner Abuse, Psychological, Confirmed (721)\n995.82 (T74.31XA) Initial encounter\n995.82 (T74.31XD) Subsequent encounter\nSpouse or Partner Abuse, Psychological, Suspected (721)\n995.82 (T76.31XA) Initial encounter\n995.82 (T76.31XD) Subsequent encounter\nOther Circumstances Related to Spouse or Partner Abuse, Psychological (721)\nV61.11 (Z69.11) Encounter for mental health serv ices for victim of spouse or \npartner psychological abuse", "source": "dsm5.pdf"} {"id": "2ee3a96eefeb-0", "page_content": "xxxviii DSM-5 Classification\nV15.42 (Z91.411) Personal history (past history) of spouse or partner \npsychological abuse\nV61.12 (Z69.12) Encounter for mental health services for perpetrator of spouse \nor partner psychological abuse \nAdult Abuse by Nonspouse or Nonpartner (722)\nAdult Physical Abuse by Nonspous e or Nonpartner, Confirmed (722)\n995.81 (T74.11XA) Initial encounter\n995.81 (T74.11XD) Subsequent encounter\nAdult Physical Abuse by Nonspouse or Nonpartner, Suspected (722)\n995.81 (T76.11XA) Initial encounter\n995.81 (T76.11XD) Subsequent encounter\nAdult Sexual Abuse by Nonspouse or Nonpartner, Confirmed (722)\n995.83 (T74.21XA) Initial encounter\n995.83 (T74.21XD) Subsequent encounter\nAdult Sexual Abuse by Nonspouse or Nonpartner, Suspected (722)\n995.83 (T76.21XA) Initial encounter\n995.83 (T76.21XD) Subsequent encounter\nAdult Psychological Abuse by Nonspo use or Nonpartner, Confirmed (722)\n995.82 (T74.31XA) Initial encounter\n995.82 (T74.31XD) Subsequent encounter\nAdult Psychological Abuse by Nonspouse or Nonpartner, Suspected (722)\n995.82 (T76.31XA) Initial encounter\n995.82 (T76.31XD) Subsequent encounter\nOther Circumstances Related to Adult Ab use by Nonspouse or Nonpartner (722)\nV65.49 (Z69.81) Encounter for mental health services for victim of nonspousal", "source": "dsm5.pdf"} {"id": "2ee3a96eefeb-1", "page_content": "adult abuse\nV62.83 (Z69.82) Encounter for mental health services for perpetrator of \nnonspousal adult abuse\nEducational and Occupational Problems (723)\nEducational Problems (723)\nV62.3 (Z55.9) Academic or Educational Problem (723)\nOccupational Problems (723)\nV62.21 (Z56.82) Problem Related to Current Military Deployment Status (723)\nV62.29 (Z56.9) Other Problem Related to Employment (723)\nHousing and Economic Problems (723)\nHousing Problems (723)\nV60.0 (Z59.0) Homelessness (723)\nV60.1 (Z59.1) Inadequate Housing (723)", "source": "dsm5.pdf"} {"id": "f7a91ceec96a-0", "page_content": "DSM-5 Classification xxxix\nV60.89 (Z59.2) Discord With Neighbor, Lodger, or Landlord (723)\nV60.6 (Z59.3) Problem Related to Living in a Residential Institution (724)\nEconomic Problems (724)\nV60.2 (Z59.4) Lack of Adequate Food or Safe Drinking Water (724)\nV60.2 (Z59.5) Extreme Poverty (724)\nV60.2 (Z59.6) Low Income (724)\nV60.2 (Z59.7) Insufficient Social Insurance or Welfare Support (724)\nV60.9 (Z59.9) Unspecified Housing or Economic Problem (724)\nOther Problems Related to the Social Environment (724)\nV62.89 (Z60.0) Phase of Life Problem (724)\nV60.3 (Z60.2) Problem Related to Living Alone (724)\nV62.4 (Z60.3) Acculturation Difficulty (724)\nV62.4 (Z60.4) Social Exclusion or Rejection (724)\nV62.4 (Z60.5) Target of (Perceived) Adverse Disc rimination or Persecution (724)\nV62.9 (Z60.9) Unspecified Problem Related to Social Environment (725)\nProblems Related to Crime or Interaction With the Legal System (725)\nV62.89 (Z65.4) Victim of Crime (725)\nV62.5 (Z65.0) Conviction in Civil or Criminal Proceedings Without \nImprisonment (725)\nV62.5 (Z65.1) Imprisonment or Other Incarceration (725)", "source": "dsm5.pdf"} {"id": "f7a91ceec96a-1", "page_content": "V62.5 (Z65.2) Problems Related to Release From Prison (725)\nV62.5 (Z65.3) Problems Related to Other Legal Circumstances (725)\nOther Health Service Encounters for Counseling and Medical Advice (725)\nV65.49 (Z70.9) Sex Counseling (725)\nV65.40 (Z71.9) Other Counseling or Consultation (725)\nProblems Related to Other Psychosocial, Personal, and Environmental \nCircumstances (725)\nV62.89 (Z65.8) Religious or Spiritual Problem (725)\nV61.7 (Z64.0) Problems Related to Unwanted Pregnancy (725)\nV61.5 (Z64.1) Problems Related to Multiparity (725)\nV62.89 (Z64.4) Discord With Social Service Provider, Including Probation \nOfficer, Case Manager, or So cial Services Worker (725)\nV62.89 (Z65.4) Victim of Terrorism or Torture (725)\nV62.22 (Z65.5) Exposure to Disaster, War, or Other Hostilities (725)\nV62.89 (Z65.8) Other Problem Related to Psyc hosocial Circumstances (725)\nV62.9 (Z65.9) Unspecified Problem Related to Unspecified Psychosocial \nCircumstances (725)", "source": "dsm5.pdf"} {"id": "0f43c9ecf557-0", "page_content": "xl DSM-5 Classification\nOther Circumstances of Personal History (726)\nV15.49 (Z91.49) Other Personal History of Psychological Trauma (726)\nV15.59 (Z91.5) Personal History of Self-Harm (726)\nV62.22 (Z91.82) Personal History of Mili tary Deployment (726)\nV15.89 (Z91.89) Other Personal Risk Factors (726)\nV69.9 (Z72.9) Problem Related to Lifestyle (726)\nV71.01 (Z72.811) Adult Antisocial Behavior (726)\nV71.02 (Z72.810) Child or Adolescent Antisocial Behavior (726)\nProblems Related to Access to Medical and Other Health Care (726)\nV63.9 (Z75.3) Unavailability or Inaccessibility of Health Care Facilities (726)\nV63.8 (Z75.4) Unavailability or Inaccessibility of Other Helping Agencies (726)\nNonadherence to Medical Treatment (726)\nV15.81 (Z91.19) Nonadherence to Medical Treatment (726)\n278.00 (E66.9) Overweight or Obesity (726)\nV65.2 (Z76.5) Malingering (726)\nV40.31 (Z91.83) Wandering Associated With a Mental Disorder (727)\nV62.89 (R41.83) Borderline Intellectual Functioning (727)", "source": "dsm5.pdf"} {"id": "cba4fc540fe6-0", "page_content": "xliPreface\nThe American Psychiatric Association\u2019s Diagnostic and Statistical Manual of\nMental Disorders (DSM) is a classification of mental di sorders with associ ated criteria de-\nsigned to facilitate more reliable diagnoses of these disorders. With successive editions\nover the past 60 years, it has become a standard reference for clinical practice in the mental\nhealth field. Since a complete description of the underlying pathological processes is not\npossible for most mental diso rders, it is important to emph asize that the current diagnos-\ntic criteria are the best available descriptio n of how mental disord ers are expressed and\ncan be recognized by trained clinicians. DSM is intended to serve as a practical, functional,\nand flexible guide for organizing information that can aid in the accurate diagnosis and\ntreatment of mental disorders. It is a tool for clinicians, an essential educational resource\nfor students and practitioners, and a reference for researchers in the field.\nAlthough this edition of DSM was designed fi rst and foremost to be a useful guide to\nclinical practice, as an official nomenclature it must be applicable in a wide diversity of\ncontexts. DSM has been used by clinicians and researchers from diff erent orientations (bi-\nological, psychodynamic, cognitive, behavior al, interpersonal, family/systems), all of\nwhom strive for a common language to commu nicate the essential ch aracteristics of men-\ntal disorders presented by their patients. The information is of value to all professionals\nassociated with various aspects of mental health care, including psychiatrists, other\nphysicians, psychologists, social workers, nu rses, counselors, forensic and legal special-\nists, occupational and rehabilitation therapists , and other health professionals. The criteria\nare concise and explicit and intended to fac ilitate an objective asse ssment of symptom pre-", "source": "dsm5.pdf"} {"id": "cba4fc540fe6-1", "page_content": "sentations in a variety of clinical settings\u2014inpatient, outpatient, partial hospital, consul-\ntation-liaison, clinical, private practice, an d primary care\u2014as well in general community\nepidemiological studies of mental disorders. DSM-5 is also a tool for collecting and com-\nmunicating accurate public health statistics on mental disorder morbidity and mortality\nrates. Finally, the criteria and corresponding text serve as a textbook for students early in\ntheir profession who need a structured way to understand and diagnose mental disorders\nas well as for seasoned professionals encounteri ng rare disorders for the first time. Fortu-\nnately, all of these uses are mutually compatible.\nThese diverse needs and interests were take n into consideration in planning DSM-5.\nThe classification of disorders is harmoniz ed with the World Health Organization\u2019s Inter-\nnational Classification of Diseases (ICD), the official coding system used in the United States,\nso that the DSM criteria define disorders identified by ICD diagnostic names and code\nnumbers. In DSM-5, both ICD-9-CM and ICD- 10-CM codes (the latter scheduled for adop-\ntion in October 2014) are attached to the relevant disorders in the classification.\nAlthough DSM-5 remains a catego rical classification of sepa rate disorders, we recog-\nnize that mental disorders do not always fit completely within the boundaries of a single\ndisorder. Some symptom domains, such as de pression and anxiety, involve multiple di-\nagnostic categories and may reflect common underlying vulnerabilities for a larger group\nof disorders. In recognition of this reality, the disorders in cluded in DSM-5 were reordered\ninto a revised organizational structure meant to stimulate new clinical perspectives. This\nnew structure corresponds with the organizational arrangement of disorders planned for", "source": "dsm5.pdf"} {"id": "cba4fc540fe6-2", "page_content": "new structure corresponds with the organizational arrangement of disorders planned for\nICD-11 scheduled for release in 2015. Other enhancements have been introduced to pro-\nmote ease of use across all settings:", "source": "dsm5.pdf"} {"id": "3ad635fe837f-0", "page_content": "xlii Preface\n\u2022Representation of developmental issues related to diagnosis. The change in chapter\norganization better reflects a lifespan approach, with disorders more frequently diag-\nnosed in childhood (e.g., neurodevelopmental disorders) at the beginning of the man-\nual and disorders more applicable to olde r adulthood (e.g., neurocognitive disorders)\nat the end of the manual. Also, within the text, subheadings on development and course\nprovide descriptions of how disorder pr esentations may change across the lifespan.\nAge-related factors specific to diagnosis (e.g., symptom presentation and prevalence\ndifferences in certain age groups) are also included in the text. For added emphasis,\nthese age-related factors have been added to the criteria themselves where applicable\n(e.g., in the criteria sets for insomnia di sorder and posttraumati c stress disorder, spe-\ncific criteria describe how symptoms might be expressed in children). Likewise, gender\nand cultural issues have been integrat ed into the disorders where applicable.\n\u2022Integration of scientific findings from th e latest research in genetics and neuroimag-\ning. The revised chapter structure was informed by recent research in neuroscience and\nby emerging genetic linkages between diag nostic groups. Genetic and physiological\nrisk factors, prognostic indicators, and so me putative diagnostic markers are high-\nlighted in the text. This new structure shoul d improve clinicians\u2019 ability to identify di-\nagnoses in a disorder spectrum based on common neurocircuitry, genetic vulnerability,\nand environmental exposures. \n\u2022Consolidation of autistic disorder, Asperg er\u2019s disorder, and pervasive developmen-\ntal disorder into autism spectrum disorder. Symptoms of these disorders represent a\nsingle continuum of mild to severe impair ments in the two domains of social commu-\nnication and restrictive repetitive behaviors/ interests rather than being distinct disor-", "source": "dsm5.pdf"} {"id": "3ad635fe837f-1", "page_content": "nication and restrictive repetitive behaviors/ interests rather than being distinct disor-\nders. This change is designed to improve the se nsitivity and specificity of the criteria for\nthe diagnosis of autism spectrum disorder and to identify more focused treatment tar-\ngets for the specific impairments identified.\n\u2022Streamlined classification of bi polar and depressive disorders. Bipolar and depres-\nsive disorders are the most co mmonly diagnosed conditions in psychiatry. It was there-\nfore important to streamline th e presentation of these disorders to enhance both clinical\nand educational use. Rather than separating the definition of ma nic, hypomanic, and\nmajor depressive episodes from the definition of bipolar I disorder, bipolar II disorder,\nand major depressive disorder as in the prev ious edition, we included all of the com-\nponent criteria within the respective criteria for each disorder. This approach will facil-\nitate bedside diagnosis and treatment of these important disorders. Likewise, the\nexplanatory notes for differentiating bereav ement and major depres sive disorders will\nprovide far greater clinical guidance than was previously provided in the simple be-\nreavement exclusion criterion. The new specifiers of anxious distress and mixed fea-\ntures are now fully described in the narrativ e on specifier variations that accompanies\nthe criteria for these disorders.\n\u2022Restructuring of substance use diso rders for consistency and clarity. The categories\nof substance abuse and substance dependence have been eliminated and replaced with\nan overarching new category of substance use disorders\u2014with the specific substance\nused defining the specific disorders. \u201cDepen dence\u201d has been easily confused with the\nterm \u201caddiction\u201d when, in fa ct, the tolerance and withdrawal that previously defined\ndependence are actually very normal responses to prescr ibed medications that affect\nthe central nervous system and do not necessar ily indicate the presence of an addiction.", "source": "dsm5.pdf"} {"id": "3ad635fe837f-2", "page_content": "the central nervous system and do not necessar ily indicate the presence of an addiction.\nBy revising and clarifying these criteria in DSM-5, we hope to alleviate some of the\nwidespread misunderstanding about these issues.", "source": "dsm5.pdf"} {"id": "8108bfa5b8ff-0", "page_content": "By revising and clarifying these criteria in DSM-5, we hope to alleviate some of the\nwidespread misunderstanding about these issues.\n\u2022Enhanced specificity for major and mild neurocognitive disorders. Given the explo-\nsion in neuroscience, neuropsychology, and br ain imaging over the pa st 20 years, it was\ncritical to convey the current state-of-the-art in the diagnosis of specific types of disor-\nders that were previously referred to as the \u201cdementias\u201d or organic brain diseases. Bi-\nological markers identified by imaging for vascular and traumatic brain disorders and", "source": "dsm5.pdf"} {"id": "068c5f9d5c12-0", "page_content": "Preface xliii\nspecific molecular genetic fi ndings for rare variants of Alzheimer\u2019s disease and Hun-\ntington\u2019s disease have greatly advanced cl inical diagnoses, and these disorders and\nothers have now been separated into specific subtypes. \n\u2022Transition in conceptualizing personality disorders. Although the benefits of a more\ndimensional approach to personality disorder s have been identified in previous edi-\ntions, the transition from a ca tegorical diagnostic system of individual disorders to one\nbased on the relative distribution of personality traits ha s not been widely accepted. In\nDSM-5, the categorical personality disorder s are virtually unchan ged from the previous\nedition. However, an alternative \u201chybrid\u201d model has been proposed in Section III to\nguide future research that separates interp ersonal functioning assessments and the ex-\npression of pathological personality traits for six specific disorders. A more dimensional\nprofile of personality trait expression is also proposed for a trait-specified approach. \n\u2022Section III: new disorders and features. A new section (Section III) has been added to\nhighlight disorders that requir e further study but are not sufficiently well established to\nbe a part of the official classification of me ntal disorders for routine clinical use. Dimen-\nsional measures of symptom severity in 13 symptom domains have also been incorpo-\nrated to allow for the measurement of symp tom levels of varying severity across all\ndiagnostic groups. Likewise, the WHO Di sability Assessment Schedule (WHODAS), a\nstandard method for assessing global disabilit y levels for mental disorders that is based\non the International Classification of Functi oning, Disability and Health (ICF) and is ap-\nplicable in all of medicine, has been provid ed to replace the more limited Global As-\nsessment of Functioning scale. It is our hope that as these measures are implemented", "source": "dsm5.pdf"} {"id": "068c5f9d5c12-1", "page_content": "sessment of Functioning scale. It is our hope that as these measures are implemented\nover time, they will provide greater accuracy and flexibility in the clinical description of\nindividual symptomatic presen tations and associated disability during diagnostic as-\nsessments.\n\u2022Online enhancements. DSM-5 features online supplemental information.\nAdditional cross-cutting and diagnostic severity measures are available online\n(www.psychiatry.org/dsm5), linked to the re levant disorders. In addition, the Cul-\ntural Formulation Interview, Cultural Formulation Interview\u2014Informant Version, and\nsupplementary modules to the core Cultural Formulation Interview are also included\nonline at www.psychiatry.org/dsm5.\nThese innovations were designed by the leadin g authorities on mental disorders in the\nworld and were implemented on the basis of their expert review, public commentary, and\nindependent peer review. The 13 work group s, under the direction of the DSM-5 Task\nForce, in conjunction with other review bodi es and, eventually, the APA Board of Trust-\nees, collectively represent the gl obal expertise of the specialty. This effort was supported\nby an extensive base of advisors and by the professional staff of the APA Division of Re-\nsearch; the names of everyone involved are to o numerous to mention here but are listed in\nthe Appendix. We owe tremendous thanks to those who devoted countless hours and in-\nvaluable expertise to this effort to improve the diagno sis of mental disorders. \nWe would especially like to acknowledge th e chairs, text coordinators, and members of\nthe 13 work groups, listed in the front of th e manual, who spent many hours in this vol-\nunteer effort to improve the scientific basis of clinical practice over a sustained 6-year pe-", "source": "dsm5.pdf"} {"id": "068c5f9d5c12-2", "page_content": "unteer effort to improve the scientific basis of clinical practice over a sustained 6-year pe-\nriod. Susan K. Schultz, M.D., who served as text editor, worked tirelessly with Emily A.\nKuhl, Ph.D., senior science writer and DSM-5 st aff text editor, to coordinate the efforts of\nthe work groups into a cohesive whole. Willia m E. Narrow, M.D., M. P.H., led the research\ngroup that developed the overall research stra tegy for DSM-5, including the field trials,", "source": "dsm5.pdf"} {"id": "c91f7b845ba2-0", "page_content": "the work groups into a cohesive whole. Willia m E. Narrow, M.D., M. P.H., led the research\ngroup that developed the overall research stra tegy for DSM-5, including the field trials,\nthat greatly enhanced the eviden ce base for this revision. In addition, we are grateful to\nthose who contributed so much time to the in dependent review of the revision proposals,\nincluding Kenneth S. Ke ndler, M.D., and Robert Freedman , M.D., co-chairs of the Scien-\ntific Review Committee; John S. McIntyre, M.D., and Joel Ya ger, M.D., co-chairs of the\nClinical and Public Health Committee; and Glenn Martin, M.D., chair of the APA Assem-", "source": "dsm5.pdf"} {"id": "c421fc68cce3-0", "page_content": "xliv Preface\nbly review process. Special thanks go to Helena C. Kraemer, Ph.D., fo r her expert statistical\nconsultation; Michael B. First, M.D., for his valuable input on the coding and review of cri-\nteria; and Paul S. Appelbau m, M.D., for feedback on forensic issues. Maria N. Ward,\nM.Ed., RHIT, CCS-P, also helped in verifying all ICD coding. The Summit Group, which\nincluded these consultants, the chairs of all review groups, the task force chairs, and the\nAPA executive officers, chaired by Dilip V. Jeste, M.D., provided le adership and vision in\nhelping to achieve compromise and consensus. This level of commitment has contributed\nto the balance and objectivity that we feel are hallmarks of DSM-5.\nWe especially wish to recognize the outst anding APA Division of Research staff\u2014\nidentified in the Task Force and Work Grou p listing at the front of this manual\u2014who\nworked tirelessly to interact with the task force, work groups, advisors, and reviewers to\nresolve issues, serve as liaison s between the groups, direct and manage the academic and\nroutine clinical practice field trials, and record decisions in this important process. In par-\nticular, we appreciate the support and guidan ce provided by James H. Scully Jr., M.D.,\nMedical Director and CEO of the APA, throug h the years and travails of the development\nprocess. Finally, we thank the editorial and pr oduction staff of American Psychiatric Pub-\nlishing\u2014specifically, Rebecca Rinehart, Publish er; John McDuffie, Edit orial Director; Ann\nEng, Senior Editor; Greg Kuny, Managing Editor; and Tammy Cordova, Graphics Design", "source": "dsm5.pdf"} {"id": "c421fc68cce3-1", "page_content": "Manager\u2014for their guidance in bringing this all together and creating the final product. It\nis the culmination of efforts of many talented individuals who dedicated their time, exper-\ntise, and passion that made DSM-5 possible.\nDavid J. Kupfer, M.D.\n DSM-5 Task Force Chair\nDarrel A. Regi er, M.D., M.P.H.\n DSM-5 Task Force Vice-Chair\nDecember 19, 2012", "source": "dsm5.pdf"} {"id": "eb474c814cbb-0", "page_content": "SECTION I\nDSM-5 Basics\nIntroduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5\nUse of the Manual . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .19\nCautionary Statement for Forensic Use of DSM-5 . . . . . . . . . . . . . . . . . .25", "source": "dsm5.pdf"} {"id": "077f1c3bb444-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "7d0721f12729-0", "page_content": "This section is a basic orientation to the purpose, structure, content, and\nuse of DSM-5. It is not intended to provide an exhaustive account of the evo-\nlution of DSM-5, but rather to give readers a succinct overview of its key ele-\nments. The introductory section descr ibes the public, professional, and expert\nreview process that was used to extensively evaluate the diagnostic criteria\npresented in Section II. A summary of t he DSM-5 structure, harmonization with\nICD-11, and the transition to a non-axial system with a new approach to as-\nsessing disability is also presented. \u201cUse of the Manual\u201d includes \u201cDefinition of\na Mental Disorder,\u201d forensic considerations, and a brief overview of the diag-\nnostic process and use of coding and recording procedures.", "source": "dsm5.pdf"} {"id": "5bbfc55fdaf0-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "da632e691166-0", "page_content": "5Introduction\nThe creation of the fifth edition of Diagnostic and Statistical Manual of Mental Disorders\n(DSM-5) was a massive undertaking that involv ed hundreds of peop le working toward a\ncommon goal over a 12-year process. Much thought and deliberation were involved in\nevaluating the diagnostic criter ia, considering the organization of every aspect of the man-\nual, and creating new features believed to be mo st useful to clinicians. All of these efforts\nwere directed toward the goal of enhancing th e clinical usefulness of DSM-5 as a guide in\nthe diagnosis of mental disorders.\nReliable diagnoses are essential for guidin g treatment recommendations, identifying\nprevalence rates for mental health service pl anning, identifying patient groups for clinical\nand basic research, and documenting importan t public health information such as mor-\nbidity and mortality rates. As the understand ing of mental disorders and their treatments\nhas evolved, medical, scientific, and clinical professionals have focused on the character-\nistics of specific disorders and their im plications for treatment and research. \nWhile DSM has been the cornerstone of substant ial progress in reliability, it has been well\nrecognized by both the American Psychiatric Association (APA) and the broad scientific com-\nmunity working on mental diso rders that past science was no t mature enough to yield fully\nvalidated diagnoses\u2014that is, to provide consistent, strong, and objective scientific validators\nof individual DSM disorders. The science of mental disorders continues to evolve. However,\nthe last two decades since DSM-IV was released have seen real and durable progress in such\nareas as cognitive neuroscience , brain imaging, epidemiology, and genetics. The DSM-5 Task\nForce overseeing the new edition recognized that research advances will require careful, iter-\native changes if DSM is to maintain its place as the touchstone classifi cation of mental disor-", "source": "dsm5.pdf"} {"id": "da632e691166-1", "page_content": "ders. Finding the right balance is critical. Speculative results do not belong in an official\nnosology, but at the same time, DSM must evolve in the context of other clinical research ini-\ntiatives in the field. One important aspect of this transition derives from the broad recognition\nthat a too-rigid categorical system does not capt ure clinical experience or important scientific\nobservations. The results of nu merous studies of comorbidity and disease transmission in fam-\nilies, including twin studies and molecular genetic studies, make strong arguments for what\nmany astute clinicians have long observed: the boundaries between many disorder \u201ccatego-\nries\u201d are more fluid over the li fe course than DSM-IV recognized, and many symptoms as-\nsigned to a single disorder may occur, at vary ing levels of severity, in many other disorders.\nThese findings mean that DSM, like other medi cal disease classifications, should accommo-\ndate ways to introduce dimens ional approaches to mental di sorders, including dimensions\nthat cut across current categories. Such an appr oach should permit a more accurate description\nof patient presentations and increase the validity of a diagnosis (i.e., the degree to which diag-\nnostic criteria reflect the comprehensive mani festation of an underlying psychopathological\ndisorder). DSM-5 is designed to better fill the need of clinicians, patients, families, and re-\nsearchers for a clear and concise description of ea ch mental disorder organized by explicit di-\nagnostic criteria, supplemented, when approp riate, by dimensional measures that cross\ndiagnostic boundaries, and a brie f digest of information about th e diagnosis, risk factors, as-\nsociated features, research advances, and various expressions of the disorder. \nClinical training and experience are needed to use DSM for determining a diagnosis. The\ndiagnostic criteria identify symptoms, behavior s, cognitive functions, personality traits, phys-", "source": "dsm5.pdf"} {"id": "5d5b1d6a8926-0", "page_content": "Clinical training and experience are needed to use DSM for determining a diagnosis. The\ndiagnostic criteria identify symptoms, behavior s, cognitive functions, personality traits, phys-\nical signs, syndrome combinations, and durations that require clinical expertise to differenti-\nate from normal life variation and transient responses to stress. To facilitate a thorough", "source": "dsm5.pdf"} {"id": "8cfc1978f0db-0", "page_content": "6 Introduction\nexamination of the range of symptoms present, DSM can serve clinicians as a guide to identify\nthe most prominent symptoms that should be assessed when diagnosing a disorder. Although\nsome mental disorders may have well-defined boundaries around symptom clusters, scien-\ntific evidence now places many, if not most, disorders on a spectrum with closely related dis-\norders that have shared symptoms, shared genetic and environmental risk factors, and\npossibly shared neural substrates (perhaps most strongly established for a subset of anxiety\ndisorders by neuroimaging and animal models). In short, we have come to recognize that the\nboundaries between disorders are more porous than originally perceived.\nMany health profession and educational groups have been involved in the development\nand testing of DSM-5, including physicians, psychologists, social workers, nurses, counselors,\nepidemiologists, statisticians, neuroscientists, and neuropsychologists. Finally, patients, fam-\nilies, lawyers, consumer organizations, and advoca cy groups have all participated in revising\nDSM-5 by providing feedback on the mental di sorders described in this volume. Their moni-\ntoring of the descriptions and explanatory text is essential to improve understanding, reduce\nstigma, and advance the treatment and eventual cures for these conditions.\nA Brief History\nThe APA first published a predecessor of DSM in 1844, as a statistical classification of in-\nstitutionalized mental patients. It was designed to improve co mmunication about the\ntypes of patients cared for in these hospitals. This forerunner to DSM also was used as a\ncomponent of the full U.S. census. After World War II, DSM evolved through four major\neditions into a diagnostic classification system for psychiatrists, other physicians, and\nother mental health professionals that descri bed the essential features of the full range of", "source": "dsm5.pdf"} {"id": "8cfc1978f0db-1", "page_content": "other mental health professionals that descri bed the essential features of the full range of\nmental disorders. The current ed ition, DSM-5, builds on the go al of its predecessors (most\nrecently, DSM-IV-TR, or Text Revision, published in 2000) of providing guidelines for di-\nagnoses that can inform treatment and management decisions. \nDSM-5 Revision Process\nIn 1999, the APA launched an evaluation of the strengths and weaknesses of DSM based on\nemerging research that did not support the bo undaries established for some mental disor-\nders. This effort was coordinated with the World Health Organization (WHO) Division of\nMental Health, the World Psychiatric Associat ion, and the National Institute of Mental\nHealth (NIMH) in the form of several conferen ces, the proceedings of which were published\nin 2002 in a monograph entitled A Research Agenda for DSM-V. Thereafter, from 2003 to 2008,\na cooperative agreement with the APA and th e WHO was supported by the NIMH, the Na-\ntional Institute on Drug Abuse (NIDA), and the National Institute on Alcoholism and Alco-\nhol Abuse (NIAAA) to convene 13 internatio nal DSM-5 research planning conferences,\ninvolving 400 participants from 39 countries, to review the world litera ture in specific diag-\nnostic areas to prepare for revision s in developing both DSM-5 and the International Classi-\nfication of Diseases, 11th Revision (ICD-11). Reports from these conferences formed the basis\nfor future DSM-5 Task Force reviews and set the stage for the new edition of DSM.", "source": "dsm5.pdf"} {"id": "8cfc1978f0db-2", "page_content": "for future DSM-5 Task Force reviews and set the stage for the new edition of DSM.\nIn 2006, the APA named David J. Kupfer, M.D., as Chair and Darrel A. Regier, M.D.,\nM.P.H., as Vice-Chair of the DSM-5 Task Fo rce. They were char ged with recommending\nchairs for the 13 diagnostic work groups and additional task force members with a multi-\ndisciplinary range of expertise who would oversee the development of DSM-5. An addi-\ntional vetting process was init iated by the APA Board of Trus tees to disclose sources of\nincome and thus avoid conflicts of interest by task force and work group members. The full\ndisclosure of all income and research grants from commercial sources, including the phar-", "source": "dsm5.pdf"} {"id": "340140add8fb-0", "page_content": "income and thus avoid conflicts of interest by task force and work group members. The full\ndisclosure of all income and research grants from commercial sources, including the phar-\nmaceutical industry, in the previous 3 years, the imposition of an income cap from all com-\nmercial sources, and the publication of disclosu res on a Web site set a new standard for the", "source": "dsm5.pdf"} {"id": "4974d3a6ff2a-0", "page_content": "Introduction 7\nfield. Thereafter, the task force of 28 memb ers was approved in 2007, and appointments of\nmore than 130 work group members were approved in 2008. More than 400 additional\nwork group advisors with no voting authority were also approved to participate in the pro-\ncess. A clear concept of the next evolutionary stage for the classification of mental disorders\nwas central to the efforts of the task force an d the work groups. This vision emerged as the\ntask force and work groups recounted the history of DSM-IV\u2019s classification, its current\nstrengths and limitations, and strategic directio ns for its revision. An intensive 6-year pro-\ncess involved conducting liter ature reviews and secondary an alyses, publishing research\nreports in scientific journals, developing dr aft diagnostic criteria, posting preliminary\ndrafts on the DSM-5 Web site for public comme nt, presenting preliminary findings at pro-\nfessional meetings, performing field tr ials, and revising criteria and text. \nProposals for Revisions \nProposals for the revision of DSM-5 diagnostic criteria were develo ped by members of the\nwork groups on the basis of ra tionale, scope of change, expected impact on clinical man-\nagement and public health, strength of the su pporting research evidence, overall clarity,\nand clinical utility. Proposals encompassed chan ges to diagnostic criteria; the addition of\nnew disorders, subtypes, an d specifiers; and the deleti on of existing disorders. \nIn the proposals for revisions, strengths and weaknesses in the current criteria and no-\nsology were first identified. Novel scientific findings over the previous two decades were\nconsidered, leading to the creation of a resear ch plan to assess potential changes through\nliterature reviews and se condary data analyses. Four princi ples guided the draft revisions:", "source": "dsm5.pdf"} {"id": "4974d3a6ff2a-1", "page_content": "1) DSM-5 is primarily intended to be a manual to be used by clinicians, and revisions must\nbe feasible for routine clinical practice; 2) recommendations for revisions should be guided\nby research evidence; 3) where possible, co ntinuity should be maintained with previous\neditions of DSM; and 4) no a priori constraints should be placed on the degree of change\nbetween DSM-IV and DSM-5. \nBuilding on the initial lite rature reviews, work groups identified key issues within\ntheir diagnostic areas. Work groups also examined broa der methodological concerns,\nsuch as the presence of contra dictory findings within the literature; development of a re-\nfined definition of mental disorder; cross-cutting issues relevant to all disorders; and the\nrevision of disorders categorized in DSM-IV as \u201cnot otherwise specified.\u201d Inclusion of a\nproposal for revision in Section II was informed by consideration of its advantages and\ndisadvantages for public health and clinical ut ility, the strength of the evidence, and the\nmagnitude of the change. New diagnoses and d isorder subtypes and specifiers were sub-\nject to additional stipulations, such as demons tration of reliability (i.e., the degree to which\ntwo clinicians could independently arrive at the same diagnosis for a given patient). Dis-\norders with low clinical utility and weak valid ity were considered for deletion. Placement\nof conditions in \u201cConditions for Further Study\u201d in Section III was contingent on the\namount of empirical evidence generated on the diagnosis, diagnostic reliability or valid-\nity, presence of clear clinical need, an d potential benefit in advancing research.\nDSM-5 Field Trials\nThe use of field trials to empirically demonstrat e reliability was a noteworthy improvement in-\ntroduced in DSM-III. The design and implemen tation strategy of the DSM-5 Field Trials rep-", "source": "dsm5.pdf"} {"id": "4974d3a6ff2a-2", "page_content": "resent several changes over approaches used for DSM-III and DSM-IV, particularly in\nobtaining data on the precision of kappa reliabil ity estimates (a statistical measure that assesses\nlevel of agreement between raters that corrects for chance agreement due to prevalence rates)", "source": "dsm5.pdf"} {"id": "1f3ffec36cb5-0", "page_content": "obtaining data on the precision of kappa reliabil ity estimates (a statistical measure that assesses\nlevel of agreement between raters that corrects for chance agreement due to prevalence rates)\nin the context of clinical settings with high leve ls of diagnostic comorbidity. For DSM-5, field\ntrials were extended by using two distinctive designs: one in large, diverse medical-academic\nsettings, and the other in routine clinical practice s. The former capitalized on the need for large\nsample sizes to test hypotheses on reliability and clinical utility of a range of diagnoses in a", "source": "dsm5.pdf"} {"id": "b2497028fd6a-0", "page_content": "8 Introduction\nvariety of patient populations; the latter su pplied valuable information about how proposed\nrevisions performed in everyday clinical settings among a diverse sample of DSM users. It is\nanticipated that future clinical and basic research studies will focus on the validity of the re-\nvised categorical diagnostic criteria and the underlying dimensional features of these disor-\nders (including those now being explored by th e NIMH Research Domain Criteria initiative).\nThe medical-academic field trials were cond ucted at 11 North American medical-academic\nsites and assessed the reliability, feasibility, and clinical utility of select revisions, with priority\ngiven to those that represented the greatest degree of change from DSM-IV or those potentially\nhaving the greatest public health impact. The fu ll clinical patient populations coming to each\nsite were screened for DSM-IV diagnoses or qu alifying symptoms likely to predict several spe-\ncific DSM-5 disorders of interest. Stratified sample s of four to seven specific disorders, plus a\nstratum containing a representative sample of all other diagnoses, were id entified for each site.\nPatients consented to the study and were randomly assigned for a clinical interview by a cli-\nnician blind to the diagnosis, followed by a se cond interview with a clinician blind to previous\ndiagnoses. Patients first filled out a computer-assisted inventory of cross-cutting symptoms in\nmore than a dozen psychological domains. These inventories were scored by a central server,\nand results were provided to clinicians before they conducted a typical clinical interview (with\nno structured protocol). Clinicians were required to score the presence of qualifying criteria on\na computer-assisted DSM-5 diagnostic checklist, de termine diagnoses, score the severity of the\ndiagnosis, and submit all data to the central Web-based server. This study design allowed the\ncalculation of the degree to wh ich two independent clinicians could agree on a diagnosis (us-", "source": "dsm5.pdf"} {"id": "b2497028fd6a-1", "page_content": "calculation of the degree to wh ich two independent clinicians could agree on a diagnosis (us-\ning the intraclass kappa statistic) and the agreement of a single patient or two different clini-\ncians on two separate ratings of cross-cutting symptoms, pers onality traits, disability, and\ndiagnostic severity meas ures (using intraclass correlation coefficients) along with information\non the precision of these estimates of reliabilit y. It was also possible to assess the prevalence\nrates of both DSM-IV and DSM-5 conditions in the respective clinical populations.\nThe routine clinical practice field trials in volved recruitment of individual psychiatrists\nand other mental health clinicians. A volunteer sample was recruited that included gener-\nalist and specialty psychiatrists, psychologists, licensed clinical social workers, counselors,\nmarriage and family therapists , and advanced practice psychiatric mental health nurses.\nThe field trials provided exposure of the proposed DSM-5 diagnoses and dimensional mea-\nsures to a wide range of clinicians to assess their feasibility and clinical utility. \nPublic and Professional Review\nIn 2010, the APA launched a unique Web site to facilitate public and professional input into\nDSM-5. All draft diagnostic criteria and prop osed changes in organization were posted on\nwww.dsm5.org for a 2-month co mment period. Feedback totaled more than 8,000 submis-\nsions, which were systematically reviewed by each of the 13 work groups, whose members,\nwhere appropriate, integrated questions and comments into discussions of draft revisions\nand plans for field trial testing. After revisions to the initial draft criteria and proposed\nchapter organization, a second posting occurred in 2011. Wo rk groups considered feedback\nfrom both Web postings and the results of th e DSM-5 Field Trials when drafting proposed", "source": "dsm5.pdf"} {"id": "b2497028fd6a-2", "page_content": "from both Web postings and the results of th e DSM-5 Field Trials when drafting proposed\nfinal criteria, which were posted on the Web si te for a third and final time in 2012. These\nthree iterations of external review produced more than 13 ,000 individually signed com-", "source": "dsm5.pdf"} {"id": "c489c1d05429-0", "page_content": "final criteria, which were posted on the Web si te for a third and final time in 2012. These\nthree iterations of external review produced more than 13 ,000 individually signed com-\nments on the Web site that were received and reviewed by the work groups, plus thousands\nof organized petition signers for and against so me proposed revisions, all of which allowed\nthe task force to actively address concerns of DSM users, as well as patients and advocacy\ngroups, and ensure that clinical utility remained a high priority.\nExpert Review\nThe members of the 13 work groups, representi ng expertise in their respective areas, col-\nlaborated with advisors and reviewers unde r the overall direction of the DSM-5 Task", "source": "dsm5.pdf"} {"id": "8d3aa4f5d07e-0", "page_content": "Introduction 9\nForce to draft the diagnostic criteria and ac companying text. This effort was supported by\na team of APA Division of Research staff an d developed through a network of text coor-\ndinators from each work group. The preparation of the text was coordinated by the text\neditor, working in close collaboration with th e work groups and under the direction of the\ntask force chairs. The Scientific Review Comm ittee (SRC) was established to provide a sci-\nentific peer review process that was external to that of the work groups. The SRC chair,\nvice-chair, and six committee members were charged with reviewing the degree to which\nthe proposed changes from DSM-IV could be supported with scientific evidence. Each\nproposal for diagnostic revi sion required a memorandum of evidence for change pre-\npared by the work group and accompanied by a summary of supportive data organized\naround validators for the proposed diagnostic criteria (i.e., antecedent validators such as\nfamilial aggregation, concurrent validators such as biological markers, and prospective\nvalidators such as response to treatment or course of illness). The submissions were re-\nviewed by the SRC and scored according to the strength of the supportive scientific data.\nOther justifications for change, such as those arising from clinical experience or need or\nfrom a conceptual reframing of diagnostic ca tegories, were generall y seen as outside the\npurview of the SRC. The reviewers\u2019 scores, wh ich varied substantially across the different\nproposals, and an accompanying brief commen tary were then returned to the APA Board\nof Trustees and the work groups for consideration and response.\nThe Clinical and Public Health Committee (CPH C), composed of a chair, vice-chair, and\nsix members, was appointed to consider additi onal clinical utility, public health, and log-", "source": "dsm5.pdf"} {"id": "8d3aa4f5d07e-1", "page_content": "ical clarification issues for criteria that ha d not yet accumulated the type or level of evi-\ndence deemed sufficient for change by the SRC. This review process was particularly\nimportant for DSM-IV disorders with known deficiencies for whic h proposed remedies\nhad neither been previously considered in the DSM revision process nor been subjected to\nreplicated research studies. These selected d isorders were evaluated by four to five exter-\nnal reviewers, and the blinded results were reviewed by CPHC members, who in turn\nmade recommendations to the APA Boar d of Trustees and the work groups. \nForensic reviews by the members of the APA Council on Psychiatry and Law were con-\nducted for disorders frequently appearing in forensic environments and ones with high\npotential for influencing civil and criminal judgments in courtroom settings. Work groups\nalso added forensic experts as advisors in pertinent areas to complement expertise pro-\nvided by the Council on Psychiatry and Law. \nThe work groups themselves were charged with the responsib ility to review the entire re-\nsearch literature surrounding a diagnostic area, including old, revised, and new diagnostic cri-\nteria, in an intensive 6-year re view process to assess the pros and cons of making either small\niterative changes or major conceptual changes to address the inevitable reification that occurs\nwith diagnostic conceptual approaches that pe rsist over several decades. Such changes in-\ncluded the merger of previously separate diagno stic areas into more dimensional spectra, such\nas that which occurred with autism spectrum disorder, substance use disorders, sexual dys-\nfunctions, and somatic symptom and related di sorders. Other changes included correcting\nflaws that had become apparent over time in th e choice of operational criteria for some disor-\nders. These types of changes po sed particular challenges to the SRC and CPHC review pro-", "source": "dsm5.pdf"} {"id": "8d3aa4f5d07e-2", "page_content": "cesses, which were not constructed to evaluate the validity of DSM-IV diagnostic criteria.\nHowever, the DSM-5 Task Force, which had re viewed proposed changes and had responsi-", "source": "dsm5.pdf"} {"id": "b43e41d3a106-0", "page_content": "cesses, which were not constructed to evaluate the validity of DSM-IV diagnostic criteria.\nHowever, the DSM-5 Task Force, which had re viewed proposed changes and had responsi-\nbility for reviewing the text describing each disorder contemporaneously with the work\ngroups during this period, was in a unique positio n to render an informed judgment on the sci-\nentific merits of such revisions. Furthermore, ma ny of these major changes were subject to field\ntrial testing, although comprehensive testing of all proposed changes could not be accommo-\ndated by such testing because of time limitations and availa bility of resources.\nA final recommendation from the task forc e was then provided to the APA Board of\nTrustees and the APA Assembly\u2019s Committee on DSM-5 to consider some of the clinical\nutility and feasibility features of the propos ed revisions. The assembly is a deliberative", "source": "dsm5.pdf"} {"id": "d67613b13a62-0", "page_content": "10 Introduction\nbody of the APA representing the district branches and wider membership that is com-\nposed of psychiatrists from throughout the United States who provide geographic, prac-\ntice size, and interest-based diversity. The Committee on DSM-5 is a committee made up\nof a diverse group of assembly leaders.\nFollowing all of the preceding review steps, an executive \u201csummit committee\u201d session\nwas held to consolidate input from review and assembly committee chairs, task force\nchairs, a forensic advisor, and a statistical ad visor, for a preliminary review of each disor-\nder by the assembly and APA Board of Trus tees executive committees. This preceded a\npreliminary review by the full APA Board of Trustees. The assembly voted, in November\n2012, to recommend that the bo ard approve the publication of DSM-5, and the APA Board\nof Trustees approved its publication in December 2012. The ma ny experts, re viewers, and\nadvisors who contributed to this pr ocess are listed in the Appendix.\nOrganizational Structure\nThe individual disorder definitions that cons titute the operationali zed sets of diagnostic\ncriteria provide the core of DSM-5 for clinic al and research purpos es. These criteria have\nbeen subjected to scientific re view, albeit to varying degrees , and many disorders have un-\ndergone field testing for interrater reliability. In contrast, the classification of disorders (the\nway in which disorders are grou ped, which provides a high-level organization for the man-\nual) has not generally been thought of as scientif ically significant, despite the fact that judg-\nments had to be made when disorders were initially divided into chapters for DSM-III.\nDSM is a medical classification of disorders and as such serves as a historically deter-\nmined cognitive schema imposed on clinical an d scientific informatio n to increase its com-", "source": "dsm5.pdf"} {"id": "d67613b13a62-1", "page_content": "mined cognitive schema imposed on clinical an d scientific informatio n to increase its com-\nprehensibility and utility. Not surprisingly, as th e foundational science that ultimately led\nto DSM-III has approached a half-century in ag e, challenges have begun to emerge for cli-\nnicians and scientists alike that are inherent in the DSM structure rather than in the de-\nscription of any single disorder. These challenges include high rates of comorbidity within\nand across DSM chapters, an exce ssive use of and need to rely on \u201cnot otherwise specified\u201d\n(NOS) criteria, and a growing inability to integrate DSM disorders with the results of ge-\nnetic studies and other scientific findings. \nAs the APA and the WHO began to plan their respective revisions of the DSM and the\nInternational Classification of Disorders (ICD), both cons idered the possibility of improving\nclinical utility (e.g., by helping to explain a pparent comorbidity) and facilitating scientific\ninvestigation by rethinking the organizational structures of both publications in a linear\nsystem designated by alphanume ric codes that sequence chap ters according to some ra-\ntional and relational structure. It was critical to both th e DSM-5 Task Force and the WHO\nInternational Advisory Group on the revision of the ICD-10 Section on Mental and Behav-\nioral Disorders that the revisions to the or ganization enhance clinical utility and remain\nwithin the bounds of well-replicated scientific information. Although the need for reform\nseemed apparent, it was import ant to respect the state of the science as well as the chal-\nlenge that overly rapid change would pose for the clinical and research communities. In\nthat spirit, revision of the organization was approached as a conservative, evolutionary di-\nagnostic reform that would be guided by emer ging scientific evidence on the relationships", "source": "dsm5.pdf"} {"id": "d67613b13a62-2", "page_content": "agnostic reform that would be guided by emer ging scientific evidence on the relationships\nbetween disorder groups. By reordering and regrouping the existing disorders, the re-\nvised structure is meant to stim ulate new clinical perspectives and to encourage research-\ners to identify the psychological and physiologi cal cross-cutting factors that are not bound\nby strict categorical designations.", "source": "dsm5.pdf"} {"id": "2891d7104673-0", "page_content": "ers to identify the psychological and physiologi cal cross-cutting factors that are not bound\nby strict categorical designations. \nThe use of DSM criteria has the clear virtue of creating a common language for com-\nmunication between clinicians about the diagno sis of disorders. The official criteria and\ndisorders that were determined to have accepted clinical applicability are located in Sec-\ntion II of the manual. However, it should be noted that these diagnostic criteria and their", "source": "dsm5.pdf"} {"id": "cd9717cb22b2-0", "page_content": "Introduction 11\nrelationships within the classification are ba sed on current research and may need to be\nmodified as new evidence is gathered by fu ture research both within and across the do-\nmains of proposed disorders. \u201cConditions for Further Study,\u201d described in Section III, are\nthose for which we determined that the scient ific evidence is not yet available to support\nwidespread clinical use. These diagnostic crit eria are included to highlight the evolution\nand direction of scientific advances in these areas to stimulate further research. \nWith any ongoing review proces s, especially one of this co mplexity, different viewpoints\nemerge, and an effort was made to consider various viewpoints and, when warranted, ac-\ncommodate them. For example, personality diso rders are included in both Sections II and\nIII. Section II represents an update of the te xt associated with the same criteria found in\nDSM-IV-TR, whereas Section III includes the proposed research model for personality dis-\norder diagnosis and conceptualization developed by the DSM-5 Personality and Personality\nDisorders Work Group. As this field evolves, it is hoped that both versions will serve clin-\nical practice and research initiatives.\nHarmonization With ICD-11\nThe groups tasked with revising the DSM and ICD systems shared the overarching goal of\nharmonizing the two classifications as much as possible, for the following reasons: \n\u2022 The existence of two major classifications of mental disorders hinders the collection and\nuse of national health statistics, the design of clinical trials aimed at developing new\ntreatments, and the consideration of global ap plicability of the results by international\nregulatory agencies.\n\u2022 More broadly, the existence of two classificat ions complicates attempts to replicate sci-\nentific results across national boundaries. \n\u2022 Even when the intention was to identify identical patient populations, DSM-IV and", "source": "dsm5.pdf"} {"id": "cd9717cb22b2-1", "page_content": "\u2022 Even when the intention was to identify identical patient populations, DSM-IV and\nICD-10 diagnoses did not always agree.\nEarly in the course of the revisions, it be came apparent that a shared organizational\nstructure would help harmonize the classificatio ns. In fact, the use of a shared framework\nhelped to integrate the work of DSM and ICD work groups and to focus on scientific is-\nsues. The DSM-5 organization and the proposed linear structure of the ICD-11 have been\nendorsed by the leadership of the NIMH Resear ch Domain Criteria (RDoC) project as con-\nsistent with the initial overa ll structure of that project.\nOf course, principled disagreements on th e classification of psychopathology and on\nspecific criteria for certain disorders were expected given the current state of scientific\nknowledge. However, most of the salient differences betw een the DSM and the ICD classi-\nfications do not reflect real sc ientific differences, but rather represent historical by-products\nof independent committee processes. \nTo the surprise of participants in both revi sion processes, large sections of the content\nfell relatively easily into place, reflecting real strengths in some areas of th e scientific lit-\nerature, such as epidem iology, analyses of comorbidity, twin studies, and certain other ge-\nnetically informed designs. When disparities emerged, they almost always reflected the\nneed to make a judgment about where to plac e a disorder in the face of incomplete\u2014or,\nmore often, conflicting\u2014d ata. Thus, for example, on the ba sis of patterns of symptoms, co-\nmorbidity, and shared risk factors, attentio n-deficit/hyperactivity disorder (ADHD) was\nplaced with neurodevelopmental disorders, but the same data also supported strong ar-", "source": "dsm5.pdf"} {"id": "cd9717cb22b2-2", "page_content": "placed with neurodevelopmental disorders, but the same data also supported strong ar-\nguments to place ADHD within disruptive , impulse-control, and conduct disorders.\nThese issues were settled with the preponderance of evidence (most notably validators ap-\nproved by the DSM-5 Task Force). The work gr oups recognize, however, that future dis-\ncoveries might change the placement as well as the contours of individual disorders and,", "source": "dsm5.pdf"} {"id": "6fee9c50d491-0", "page_content": "proved by the DSM-5 Task Force). The work gr oups recognize, however, that future dis-\ncoveries might change the placement as well as the contours of individual disorders and,\nfurthermore, that the simple and linear organi zation that best supports clinical practice", "source": "dsm5.pdf"} {"id": "95542eff6d35-0", "page_content": "12 Introduction\nmay not fully capture the complexity and hete rogeneity of mental di sorders. The revised\norganization is coordinated with the mental and behavioral disorders chapter (Chapter V)\nof ICD-11, which will utilize an expanded numeric\u2013alphanumeric coding system. How-\never, the official coding system in use in the Un ited States at the time of publication of this\nmanual is that of the International Classificatio n of Diseases, Ninth Revi sion, Clinical Modifica-\ntion (ICD-9-CM)\u2014the U.S. adaptation of ICD-9. International Classificat ion of Diseases, Tenth\nRevision, Clinical Modification (ICD-10-CM), adapted from IC D-10, is scheduled for imple-\nmentation in the United States in October 2014. Given the impending release of ICD-11, it\nwas decided that this iteration, and not ICD-10, would be the most relevant on which to focus\nharmonization. However, given that adoption of the ICD-9-CM coding system will remain\nat the time of the DSM-5 releas e, it will be necessary to use the ICD-9-CM codes. Further-\nmore, given that DSM-5\u2019s organizational stru cture reflects the an ticipated structure of\nICD-11, the eventual ICD-11 co des will follow the sequential order of diagnoses in the\nDSM-5 chapter structure more closely. At present, both the ICD-9-CM and the ICD-10-CM\ncodes have been indicated for each disorder. These codes will not be in sequential order\nthroughout the manual because they were assigned to complement earlier organizational\nstructures.\nDimensional Approach to Diagnosis\nStructural problems rooted in the basic de sign of the previous DSM classification, con-", "source": "dsm5.pdf"} {"id": "95542eff6d35-1", "page_content": "Structural problems rooted in the basic de sign of the previous DSM classification, con-\nstructed of a large number of narrow diagnostic categories, have emerged in both clinical\npractice and research. Relevant evidence come s from diverse sources, including studies of\ncomorbidity and the substantia l need for not otherwise specified diagnoses, which repre-\nsent the majority of diagnoses in areas such as eating disorders, personality disorders, and\nautism spectrum disorder. Stud ies of both genetic and environmental risk factors, whether\nbased on twin designs, familial transmission , or molecular analyses, also raise concerns\nabout the categorical structure of the DSM system. Because the previous DSM approach\nconsidered each diagnosis as categorically sepa rate from health and from other diagnoses,\nit did not capture the widespread sharing of symptoms and risk factors across many dis-\norders that is apparent in studies of comorb idity. Earlier editions of DSM focused on ex-\ncluding false-positive results fr om diagnoses; thus, its categories were overly narrow, as is\napparent from the widespread need to use NO S diagnoses. Indeed, the once plausible goal\nof identifying homogeneous populations for trea tment and research resu lted in narrow di-\nagnostic categories that did not capture clinical reality, symptom heterogeneity within dis-\norders, and significant sharing of symptoms across multiple disorders. The historical\naspiration of achieving diagnostic homogene ity by progressive subt yping within disorder\ncategories no longer is sensible; like most common human ills, mental disorders are het-\nerogeneous at many levels, ranging fr om genetic risk factors to symptoms. \nRelated to recommendations about alteration s in the chapter structure of DSM-5, mem-\nbers of the diagnostic spectra study group examined whether scientific validators could\ninform possible new groupings of related diso rders within the existing categorical frame-\nwork. Eleven such indicators were recommended for this purpose: shared neural sub-", "source": "dsm5.pdf"} {"id": "95542eff6d35-2", "page_content": "work. Eleven such indicators were recommended for this purpose: shared neural sub-\nstrates, family traits, genetic risk factors, sp ecific environmen tal risk factors, biomarkers,\ntemperamental antecedents, abnormalities of emotional or cognitive processing, symptom\nsimilarity, course of illness, high comorbidit y, and shared treatmen t response. These indi-\ncators served as empirical guidelines to info rm decision making by the work groups and", "source": "dsm5.pdf"} {"id": "cf31cfa3d4eb-0", "page_content": "similarity, course of illness, high comorbidit y, and shared treatmen t response. These indi-\ncators served as empirical guidelines to info rm decision making by the work groups and\nthe task force about how to cluster disorders to maximize their validity and clinical utility. \nA series of papers was developed and published in a prominent international journal\n(Psychological Medicine, Vol. 39, 2009) as part of both the DSM-5 and the ICD-11 develop-\nmental processes to document that such valid ators were most useful for suggesting large\ngroupings of disorders rather th an for \u201cvalidating\u201d individual disorder diagnostic criteria.\nThe regrouping of mental disorders in DSM-5 is intended to enable future research to en-", "source": "dsm5.pdf"} {"id": "8a685ad62edd-0", "page_content": "Introduction 13\nhance understanding of disease origins and pathophysiological commonalities between\ndisorders and provide a base for future replication wherein data can be reanalyzed over\ntime to continually assess validity. Ongoing revisions of DSM-5 will make it a \u201cliving doc-\nument,\u201d adaptable to future discoveries in neurobiology, genetics, and epidemiology.\nOn the basis of the published findings of this common DSM-5 and ICD-11 analysis, it\nwas demonstrated that clustering of diso rders according to what has been termed internal-\nizing and externalizing factors represents an empirically supported framework. Within both\nthe internalizing group (representing disorder s with prominent anxiety, depressive, and\nsomatic symptoms) and the externalizing group (representing disorders with prominent\nimpulsive, disruptive conduct, and substance use symptoms), the sh aring of genetic and\nenvironmental risk factor s, as shown by twin studies, like ly explains much of the system-\natic comorbidities seen in both clinical an d community samples. The adjacent placement of\n\u201cinternalizing disorders,\u201d characterized by de pressed mood, anxiety, and related physio-\nlogical and cognitive symptoms, should aid in developing new diagnostic approaches, in-\ncluding dimensional approaches, while facilitati ng the identification of biological markers.\nSimilarly, adjacencies of the \u201cexternalizing group,\u201d including disord ers exhibiting antiso-\ncial behaviors, conduct disturbances, addictio ns, and impulse-control disorders, should en-\ncourage advances in identifying diagnoses, markers, and underlying mechanisms.\nDespite the problem posed by categorical diagnoses, the DSM-5 Task Force recognized\nthat it is premature scientifically to propose alternative definitions fo r most disorders. The\norganizational structure is meant to serve as a bridge to new diagnostic approaches with-\nout disrupting current clinical practice or research. With support from DSM-associated", "source": "dsm5.pdf"} {"id": "8a685ad62edd-1", "page_content": "out disrupting current clinical practice or research. With support from DSM-associated\ntraining materials, the National Institutes of Health other funding agencies, and scientific\npublications, the more dimensional DSM-5 approach and organizational structure can fa-\ncilitate research across current diagnostic ca tegories by encouraging broad investigations\nwithin the proposed chapters and across adja cent chapters. Such a reformulation of re-\nsearch goals should also keep DSM-5 central to the development of dimensional approaches\nto diagnosis that will likely supplement or supersede current categorical approaches in\ncoming years.\nDevelopmental and Life span Considerations\nTo improve clinical utility, DSM-5 is organi zed on developmental and lifespan consider-\nations. It begins with diagnoses thought to reflect developmental processes that manifest\nearly in life (e.g., neurodevelopmental and schizophrenia spectrum and other psychotic\ndisorders), followed by diagnoses that more commonly manifest in adolescence and\nyoung adulthood (e.g., bipolar, depressive, and anxiety disorders), an d ends with diagno-\nses relevant to adulthood and later life (e.g., neurocognitive disord ers). A similar approach\nhas been taken, where possible, within each chapter. This organizational structure facili-\ntates the comprehensive use of lifespan informat ion as a way to assist in diagnostic deci-\nsion making. \nThe proposed organization of chapters of DSM-5, after the neurodevelopmental disor-\nders, is based on groups of internalizing (emoti onal and somatic) disorders, externalizing\ndisorders, neurocognitive disorders, and other disorders. It is hoped that this organization\nwill encourage furthe r study of underlying pathophysiological processes that give rise to\ndiagnostic comorbidity and sy mptom heterogeneity. Furthermore, by arranging disorder\nclusters to mirror clinical reality, DSM-5 shou ld facilitate identifica tion of potential diag-", "source": "dsm5.pdf"} {"id": "8a685ad62edd-2", "page_content": "noses by non\u2013mental health specialist s, such as primary care physicians.", "source": "dsm5.pdf"} {"id": "977befe874da-0", "page_content": "clusters to mirror clinical reality, DSM-5 shou ld facilitate identifica tion of potential diag-\nnoses by non\u2013mental health specialist s, such as primary care physicians. \nThe organizational structure of DSM-5, alon g with ICD harmonization, is designed to\nprovide better and more flexible diagnostic concepts for the next epoch of research and to\nserve as a useful guide to clinicians in explai ning to patients why they might have received\nmultiple diagnoses or why they might have re ceived additional or altered diagnoses over\ntheir lifespan.", "source": "dsm5.pdf"} {"id": "8b36867f395a-0", "page_content": "14 Introduction\nCultural Issues\nMental disorders are defined in relation to cultural, social, and familial norms and values.\nCulture provides interpretive frameworks that shape the experience and expression of the\nsymptoms, signs, and behaviors that are criter ia for diagnosis. Culture is transmitted, re-\nvised, and recreated within the family and other social systems and institutions. Diagnostic\nassessment must therefore consider whether an individual\u2019s experiences, symptoms, and\nbehaviors differ from sociocultural norms and lead to difficult ies in adaptation in the cul-\ntures of origin and in specific social or familial contexts. Key aspects of culture relevant to di-\nagnostic classification and assessment have been considered in the development of DSM-5.\nIn Section III, the \u201cCultural Formulation\u201d contains a detailed discussion of culture and\ndiagnosis in DSM-5, including tools for in-dep th cultural assessment. In the Appendix, the\n\u201cGlossary of Cultural Concepts of Distress \u201d provides a description of some common cul-\ntural syndromes, idioms of distress, and causal explanations relevant to clinical practice.\nThe boundaries between normalit y and pathology vary across cultures for specific types\nof behaviors. Thresholds of tolerance for spec ific symptoms or behaviors differ across cul-\ntures, social settings, and fami lies. Hence, the level at which an experience becomes prob-\nlematic or pathological will differ. The judgment that a given behavior is abnormal and\nrequires clinical attention depends on cultural norms that are internalized by the individual\nand applied by others around them, including family members and clinicians. Awareness of\nthe significance of culture may correct mistaken interpretations of ps ychopathology, but cul-\nture may also contribute to vulnerability and suffering (e.g., by amplif ying fears that main-\ntain panic disorder or health anxiety). Cultural meanings, habits, and traditions can also", "source": "dsm5.pdf"} {"id": "8b36867f395a-1", "page_content": "tain panic disorder or health anxiety). Cultural meanings, habits, and traditions can also\ncontribute to either stigma or support in the social and familial response to mental illness.\nCulture may provide coping strategies that enhance resilience in response to illness, or sug-\ngest help seeking and options for accessing heal th care of various types, including alterna-\ntive and complementary health systems. Culture may influence acceptance or rejection of a\ndiagnosis and adherence to treatments, affecting the course of illness and recovery. Culture\nalso affects the conduct of the cl inical encounter; as a result, cultural differences between the\nclinician and the patient have implications fo r the accuracy and acceptance of diagnosis as\nwell as for treatment decisions, prognost ic considerations, and clinical outcomes.\nHistorically, the construct of the culture- bound syndrome has been a key interest of\ncultural psychiatry. In DSM-5, this construct h as been replaced by three concepts that offer\ngreater clinical utility: \n1.Cultural syndrome is a cluster or group of co-occurr ing, relatively invariant symptoms\nfound in a specific cultural gr oup, community, or context (e.g., ataque de nervios ). The\nsyndrome may or may not be recognized as an illness within the culture (e.g., it might\nbe labeled in various ways), but such cultural patterns of distress and features of illness\nmay nevertheless be recognizab le by an outside observer. \n2.Cultural idiom of distress is a linguistic term, phrase, or way of talking about suffering\namong individuals of a cultural group (e.g., similar ethnicity and religion) referring to\nshared concepts of pathology and ways of expressing, communicating, or naming es-\nsential features of distress (e.g., kufungisisa ). An idiom of distress need not be associated", "source": "dsm5.pdf"} {"id": "8b36867f395a-2", "page_content": "with specific symptoms, syndromes, or perceived causes. It may be used to convey a\nwide range of discomfort, including everyd ay experiences, subclinical conditions, or\nsuffering due to social circumstances rather than mental disorders. For example, most", "source": "dsm5.pdf"} {"id": "8fcd78abd5e8-0", "page_content": "wide range of discomfort, including everyd ay experiences, subclinical conditions, or\nsuffering due to social circumstances rather than mental disorders. For example, most\ncultures have common bodily idioms of dist ress used to express a wide range of suf-\nfering and concerns.\n3.Cultura l explanation or perceived cause is a label , attribution, or feature of an explanatory\nmodel that provides a culturally conceived etiology or cause for symptoms, illness, or\ndistress (e.g., maladi moun ). Causal explanations may be salient features of folk classi-\nfications of disease used by laypersons or healers.", "source": "dsm5.pdf"} {"id": "c87140ae05f5-0", "page_content": "Introduction 15\nThese three concepts (for whic h discussion and examples are provided in Section III\nand the Appendix) suggest cultural ways of understanding and describing illness experi-\nences that can be elicited in the clinical encounter. They influence symptomatology, help\nseeking, clinical presentations, expectations of treatment, illness adaptation, and treat-\nment response. The same cultur al term often serves more than one of these functions. \nGender Differences\nSex and gender differences as they relate to th e causes and expression of medical conditions\nare established for a number of diseases, including selected mental disorders. Revisions to\nDSM-5 included review of potential differenc es between men and women in the expression\nof mental illness. In terms of nomenclature, sex differences are variations attributable to an\nindividual\u2019s reproductive organs an d XX or XY chromosomal complement. Gender differ-\nences are variations that result from biological sex as well as an individual\u2019s self-represen-\ntation that includes the psychological, be havioral, and social consequences of one\u2019s\nperceived gender. The term gender differences is used in DSM-5 because, more commonly,\nthe differences between men and women are a re sult of both biological sex and individual\nself-representation. However, some of the di fferences are based on only biological sex. \nGender can influence illness in a variety of ways. First, it may exclusively determine\nwhether an individual is at risk for a disord er (e.g., as in premenstrual dysphoric disor-\nder). Second, gender may moderate the overa ll risk for development of a disorder as\nshown by marked gender differences in the prevalence and incidence rates for selected\nmental disorders. Third, gender may influence the likelihood that particular symptoms of\na disorder are experienced by an individual . Attention-deficit/hype ractivity disorder is", "source": "dsm5.pdf"} {"id": "c87140ae05f5-1", "page_content": "a disorder are experienced by an individual . Attention-deficit/hype ractivity disorder is\nan example of a disorder with differences in presentation that are most commonly expe-\nrienced by boys or girls. Gender likely has other effects on the experience of a disorder that\nare indirectly relevant to psychiatric diagnosis. It may be that certain symptoms are more\nreadily endorsed by men or women, and that this contributes to differences in service pro-\nvision (e.g., women may be more likely to recognize a depr essive, bipolar, or anxiety dis-\norder and endorse a more comprehen sive list of symptoms than men). \nReproductive life cycle events, including estr ogen variations, also contribute to gender\ndifferences in risk and expression of illness. Thus, a specifier for postpartum onset of mania\nor major depressive episode denotes a time frame wherein women may be at increased risk\nfor the onset of an illness episode. In the case of sleep and energy, alterations are often nor-\nmative postpartum and thus may have lower diagnostic reliability in postpartum women. \nThe manual is configured to include information on gender at multiple levels. If there\nare gender-specific symptoms, th ey have been added to the di agnostic criteria. A gender-\nrelated specifier, such as perinatal onset of a mood episode, provides additional informa-\ntion on gender and diagnosis. Finally, other issues that are pertinent to diagnosis and gen-\nder considerations can be found in the se ction \u201cGender-Related Diagnostic Issues.\u201d\nUse of Other Specified and Unspecified Disorders\nTo enhance diagnostic specificity, DSM-5 repl aces the previous NOS designation with two\noptions for clinical use: other specified disorder and unspecified disorder. The other specified\ndisorder category is provided to allow the clinician to communicate the specific reason", "source": "dsm5.pdf"} {"id": "c87140ae05f5-2", "page_content": "disorder category is provided to allow the clinician to communicate the specific reason\nthat the presentation does not meet the criteria for any specific category within a diagnos-\ntic class. This is done by recording the name of the category, followed by the specific rea-\nson. For example, for an in dividual with clin ically significant depressive symptoms", "source": "dsm5.pdf"} {"id": "db95bedd1419-0", "page_content": "tic class. This is done by recording the name of the category, followed by the specific rea-\nson. For example, for an in dividual with clin ically significant depressive symptoms\nlasting 4 weeks but whose symptomatology falls short of the diagnostic threshold for a\nmajor depressive episode, the clinician would re cord \u201cother specified depressive disorder,\ndepressive episode with insufficient symptoms.\u201d If the clinician chooses not to specify the", "source": "dsm5.pdf"} {"id": "bb79122665cd-0", "page_content": "16 Introduction\nreason that the criteria are not met for a sp ecific disorder, then \u201cunspecified depressive\ndisorder\u201d would be diagnosed. Note that th e differentiation between other specified and\nunspecified disorders is based on the clinic ian\u2019s decision, providing maximum flexibility\nfor diagnosis. Clinicians do not have to diff erentiate between other specified and unspec-\nified disorders based on some feature of the presentation itself. When the clinician deter-\nmines that there is evidence to specify the na ture of the clinical presentation, the other\nspecified diagnosis can be given. When the clinician is not able to further specify and de-\nscribe the clinical presentation, the unspecifie d diagnosis can be given. This is left entirely\nup to clinical judgment.\nFor a more detailed discussion of how to us e other specified and unspecified designa-\ntions, see \u201cUse of the Manual\u201d in Section I.\nThe Multiaxial System\nDespite widespread use and its adoption by certain insurance and governmental agencies,\nthe multiaxial system in DSM-IV was not requ ired to make a mental disorder diagnosis. A\nnonaxial assessment system was also included that simply listed the appropriate Axis I, II,\nand III disorders and conditio ns without axial designations. DSM-5 has moved to a nonax-\nial documentation of diagnosis (formerly Axes I, II, and III), with separate notations for\nimportant psychosocial and contextual factors (formerly Ax is IV) and disability (formerly\nAxis V). This revision is consistent with the DSM-IV text that states, \u201cThe multiaxial dis-\ntinction among Axis I, Axis II, and Axis III disorders does not imply that there are funda-\nmental differences in their conceptualizatio n, that mental disorders are unrelated to\nphysical or biological factors or processes, or that general medical conditions are unrelated", "source": "dsm5.pdf"} {"id": "bb79122665cd-1", "page_content": "physical or biological factors or processes, or that general medical conditions are unrelated\nto behavioral or psychosocial factors or processes.\u201d The approa ch of separately noting di-\nagnosis from psychosocial and contextual fact ors is also consistent with established WHO\nand ICD guidance to consider the individual\u2019s functional status separately from his or her\ndiagnoses or symptom status. In DSM-5, Axis III has been combined with Axes I and II.\nClinicians should continue to list medical cond itions that are import ant to the understand-\ning or management of an individual\u2019s mental disorder(s).\nDSM-IV Axis IV covered psychosocial and en vironmental problems that may affect the\ndiagnosis, treatment, and prognosis of ment al disorders. Although this axis provided\nhelpful information, even if it was not us ed as frequently as intended, the DSM-5 Task\nForce recommended that DSM-5 should not deve lop its own classification of psychosocial\nand environmental problems, bu t rather use a selected set of the ICD-9-CM V codes and\nthe new Z codes contained in ICD-10-CM. Th e ICD-10 Z codes were examined to deter-\nmine which are most relevant to mental disorders and also to identify gaps. \nDSM-IV Axis V consisted of the Global Assessment of Functionin g (GAF) scale, repre-\nsenting the clinician's judgment of the individu al\u2019s overall level of \u201cfunctioning on a hy-\npothetical continuum of ment al health\u2013illness.\u201d It was recommended that the GAF be\ndropped from DSM-5 for several reasons, including its conceptual lack of clarity (i.e., in-\ncluding symptoms, suicide risk, and disabilities in its descriptors) and questionable psy-", "source": "dsm5.pdf"} {"id": "bb79122665cd-2", "page_content": "cluding symptoms, suicide risk, and disabilities in its descriptors) and questionable psy-\nchometrics in routine practice. In order to provide a global measur e of disability, the WHO\nDisability Assessment Schedule (WHODAS) is included, for further stud y, in Section III of\nDSM-5 (see the chapter \u201cAssessment Measure s\u201d). The WHODAS is based on the Interna-\ntional Classification of Functioning, Disability and Health (ICF) for use across all of medicine\nand health care. The WHODAS (version 2.0), and a modification developed for children/\nadolescents and their parents by the Impairment and Disability Study Group were in-\ncluded in the DSM-5 field trial.", "source": "dsm5.pdf"} {"id": "e68ae608f796-0", "page_content": "Introduction 17\nOnline Enhancements\nIt was challenging to determine what to incl ude in the print version of DSM-5 to be most\nclinically relevant and useful and at the same time maintain a manageable size. For this\nreason, the inclusion of clinical rating scales and measures in the pr int edition is limited to\nthose considered most relevant. Additional as sessment measures used in the field trials\nare available online (www.psychiatry.org/dsm5 ), linked to the relevant disorders. The\nCultural Formulation Interview, Cultural Fo rmulation Interview\u2014Informant Version, and\nsupplementary modules to the core Cultural Formulation Interview are also available on-\nline at www.psychiatry.org/dsm5.\nDSM-5 is available as an online subscription at PsychiatryOnline.org as well as an e-\nbook. The online component contains modules and assessment tools to enhance the diag-\nnostic criteria and text. Also available online is a complete set of supportive references as\nwell as additional helpful information. The organizational structure of DSM-5, its use of\ndimensional measures, and compatibility with ICD codes will allow it to be readily adapt-\nable to future scientific discoveries and refinements in its c linical utility. DSM-5 will be an-\nalyzed over time to continually assess its validity and enhance its value to clinicians.", "source": "dsm5.pdf"} {"id": "3a465716c25e-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "b22ee51623f2-0", "page_content": "19Use of the Manual\nThe introduction contains much of the history and developmental process of the\nDSM-5 revision. This section is designed to prov ide a practical guide to using DSM-5, par-\nticularly in clinical practice. The primary purp ose of DSM-5 is to assist trained clinicians\nin the diagnosis of their patients\u2019 mental diso rders as part of a case formulation assess-\nment that leads to a fully informed treatmen t plan for each individual. The symptoms con-\ntained in the respective diagnostic criter ia sets do not constitute comprehensive\ndefinitions of underlying disorders, which encompass cognitive, emotional, behavioral,\nand physiological processes that are far more co mplex than can be described in these brief\nsummaries. Rather, they are intended to summa rize characteristic syndromes of signs and\nsymptoms that point to an underlying disord er with a characteristic developmental his-\ntory, biological and environmental risk factors, neuropsychological and physiological cor-\nrelates, and typical clinical course.\nApproach to Clinical Case Formulation\nThe case formulation for any given patient must involve a careful clinical history and con-\ncise summary of the social, psychological, and biological factors that may have contrib-\nuted to developing a given mental disorder. Hence, it is not sufficient to simply check off\nthe symptoms in the diag nostic criteria to make a mental disorder diagnosis. Although a\nsystematic check for the presence of these crit eria as they apply to each patient will assure\na more reliable assessment, the relative severity and valence of in dividual criteria and\ntheir contribution to a diagnosis require clin ical judgment. The symptoms in our diagnos-\ntic criteria are part of the relatively limited repertoire of human emotional responses to in-\nternal and external stresses that are genera lly maintained in a homeostatic balance without", "source": "dsm5.pdf"} {"id": "b22ee51623f2-1", "page_content": "ternal and external stresses that are genera lly maintained in a homeostatic balance without\na disruption in normal functioning. It requires clinical training to recognize when the com-\nbination of predisposing, precipitating, perpetuating, and protective factors has resulted\nin a psychopathological condition in which physical signs and symptoms exceed normal\nranges. The ultimate goal of a clinical case formulation is to use the available contextual\nand diagnostic information in developing a comprehensive treatment plan that is in-\nformed by the individual\u2019s cultural and social context. However, recommendations for the\nselection and use of the most appropriate ev idence-based treatment options for each dis-\norder are beyond the scope of this manual.\nAlthough decades of scientific effort have go ne into developing the diagnostic criteria\nsets for the disorders included in Section II, it is well recognized that this set of categorical\ndiagnoses does not fully describe the full rang e of mental disorders that individuals ex-\nperience and present to clinicians on a daily basis throughout the world. As noted previ-\nously in the introduction, the range of genetic/environmental interactions over the course\nof human development affecting cognitive, em otional and behavioral function is virtually\nlimitless. As a result, it is impossible to capt ure the full range of psychopathology in the\ncategorical diagnostic categories that we are now using. Hence, it is also necessary to in-\nclude \u201cother specified/unspecified\u201d disorder options for presentations that do not fit\nexactly into the diagnostic boundaries of disorders in each chapter. In an emergency de-\npartment setting, it may be possible to id entify only the most prominent symptom ex-\npressions associated with a particular chap ter\u2014for example, delusions, hallucinations,", "source": "dsm5.pdf"} {"id": "da9c8d8cf983-0", "page_content": "20 Use of the Manual\nmania, depression, anxiety, substance intoxi cation, or neurocognitive symptoms\u2014so that\nan \u201cunspecified\u201d disorder in that category is identified until a fuller differential diagnosis\nis possible.\nDefinition of a Mental Disorder\nEach disorder identified in Section II of the manual (excluding those in the chapters enti-\ntled \u201cMedication-Induced Movement Disord ers and Other Adverse Effects of Medica-\ntion\u201d and \u201cOther Conditions That May Be a Fo cus of Clinical Attention\u201d) must meet the\ndefinition of a mental disorder. Although no definition can capture all aspects of all dis-\norders in the range contained in DSM-5, the following elements are required:\nA mental disorder is a syndrome characte rized by clinically significant distur-\nbance in an individual\u2019s cognition, emotion regulation, or behavior that reflects\na dysfunction in the psychological, biological, or developmental processes un-\nderlying mental functioning. Mental disorders are usually associated with signif-\nicant distress or disability in social, occupational, or other important activities.\nAn expectable or culturally approved response to a common stressor or loss,\nsuch as the death of a loved one, is not a mental disorder. Socially deviant be-\nhavior (e.g., political, religious, or sex ual) and conflicts that are primarily be-\ntween the individual and society are not mental disorders unless the deviance\nor conflict results from a dysfuncti on in the individual, as described above.\nThe diagnosis of a mental disorder should have clinical utility: it should help clinicians\nto determine prognosis, treatment plans, and potential treatment outcomes for their pa-\ntients. However, the diagnosis of a mental disorder is not equivalent to a need for treat-\nment. Need for treatment is a complex clinic al decision that takes into consideration", "source": "dsm5.pdf"} {"id": "da9c8d8cf983-1", "page_content": "ment. Need for treatment is a complex clinic al decision that takes into consideration\nsymptom severity, symptom salience (e.g., the pr esence of suicidal ideation), the patient\u2019s\ndistress (mental pain) associated with the sy mptom(s), disability related to the patient\u2019s\nsymptoms, risks and benefits of available trea tments, and other factors (e.g., psychiatric\nsymptoms complicating other illness). Clinicians may thus encounter individuals whose\nsymptoms do not meet full crit eria for a mental disorder bu t who demonstrate a clear need\nfor treatment or care. The fact that some in dividuals do not show all symptoms indicative\nof a diagnosis should not be used to justify limiting their access to appropriate care.\nApproaches to validating diagnostic criteria for discrete categorical mental disorders\nhave included the following types of evidence: antecedent validators (similar genetic mark-\ners, family traits, temperament, and environmen tal exposure), concurrent validators (simi-\nlar neural substrates, biomarkers, emotional and cognitive processing, and symptom\nsimilarity), and predictive validators (simila r clinical course and treatment response). In\nDSM-5, we recognize that the current diagnostic criteria for any single disorder will not nec-\nessarily identify a homogeneous group of patients who can be characterized reliably with all\nof these validators. Available evidence shows that these va lidators cross existing diagnostic\nboundaries but tend to congregate more frequently within and across adjacent DSM-5 chap-\nter groups. Until incontrovertible etiological or pathophysiological mechanisms are identi-\nfied to fully validate specific disorders or disorder spectra, the most important standard for\nthe DSM-5 disorder criteria will be their clin ical utility for the assessment of clinical course\nand treatment response of individuals groupe d by a given set of diagnostic criteria.", "source": "dsm5.pdf"} {"id": "da9c8d8cf983-2", "page_content": "and treatment response of individuals groupe d by a given set of diagnostic criteria.\nThis definition of mental disorder was developed for clinical, public health, and re-\nsearch purposes. Additional information is usua lly required beyond that contained in the\nDSM-5 diagnostic criteria in or der to make legal judgments on such issues as criminal re-", "source": "dsm5.pdf"} {"id": "d8fdf437f39a-0", "page_content": "search purposes. Additional information is usua lly required beyond that contained in the\nDSM-5 diagnostic criteria in or der to make legal judgments on such issues as criminal re-\nsponsibility, eligibility for disability compen sation, and competency (see \u201cCautionary\nStatement for Forensic Use of DSM-5\u201d elsewhere in this manual).", "source": "dsm5.pdf"} {"id": "315ebc073db9-0", "page_content": "Use of the Manual 21\nCriterion for Clinical Significance\nThere have been substantial e fforts by the DSM-5 Task Force and the World Health Orga-\nnization (WHO) to separate the concepts of mental disorder and disability (impairment in\nsocial, occupational, or other important areas of functioning). In the WHO system, the In-\nternational Classification of Diseases (ICD) c overs all diseases and disorders, while the In-\nternational Classification of Functioning, Disability and Health (ICF) provides a separate\nclassification of global disability. The WHO Disability Assessment Schedule (WHODAS)\nis based on the ICF and has proven useful as a standardized measure of disability for men-\ntal disorders. However, in the absence of clea r biological markers or clinically useful mea-\nsurements of severity for many mental disord ers, it has not been possible to completely\nseparate normal and pathological symptom expressions contained in diagnostic criteria.\nThis gap in information is particularly problematic in clinical situations in which the pa-\ntient\u2019s symptom presentation by itself (particu larly in mild forms) is not inherently path-\nological and may be encountered in individuals for whom a diagnosis of \u201cmental\ndisorder\u201d would be inappropriat e. Therefore, a generic diagno stic criterion requiring dis-\ntress or disability has been used to establish disorder thresholds, usually worded \u201cthe dis-\nturbance causes clinically significant distre ss or impairment in social, occupational, or\nother important areas of functioning.\u201d The text following the revised definition of a mental\ndisorder acknowledges that this criterion may be especially helpful in determining a pa-\ntient\u2019s need for treatment. Use of informatio n from family members and other third parties\n(in addition to the individual) regarding the individual\u2019s perf ormance is recommended\nwhen necessary.\nElements of a Diagnosis", "source": "dsm5.pdf"} {"id": "315ebc073db9-1", "page_content": "when necessary.\nElements of a Diagnosis\nDiagnostic Criteria and Descriptors\nDiagnostic criteria are offered as guidelines for making diagnoses, and their use should be\ninformed by clinical judgment. Text descript ions, including introductory sections of each\ndiagnostic chapter, can help support diagnosis (e.g., providing differential diagnoses; de-\nscribing the criteria more fully under \u201cDiagnostic Features\u201d). \nFollowing the assessment of diagnostic criter ia, clinicians should consider the applica-\ntion of disorder subtypes and/ or specifiers as appropriate. Severity and course specifiers\nshould be applied to denote the individual\u2019s current presentation, but only when the full\ncriteria are met. When full criteria are no t met, clinicians should consider whether the\nsymptom presentation meets crit eria for an \u201cother specified\u201d or \u201cunspecified\u201d designa-\ntion. Where applicable, specific criteria for defining disorder severity (e.g., mild, moder-\nate, severe, extreme), descriptive features (e.g., with good to fair insight; in a controlled\nenvironment), and course (e.g., in partial remi ssion, in full remission, recurrent) are pro-\nvided with each diagnosis. On the basis of the clinical interview, text descriptions, criteria,\nand clinician judgment, a final diagnosis is made.\nThe general convention in DSM-5 is to allo w multiple diagnoses to be assigned for\nthose presentations that meet criteria for more than one DSM-5 disorder.\nSubtypes and Specifiers\nSubtypes and specifiers (some of which are code d in the fourth, fifth, or sixth digit) are\nprovided for increased specificity. Subtypes define mutually exclusive and jointly exhaus-\ntive phenomenological subgroupings within a diagnosis and are indicated by the instruc-\ntion \u201c Specify whether\u201d in the criteria set. In contrast, specifiers are not intended to be", "source": "dsm5.pdf"} {"id": "315ebc073db9-2", "page_content": "mutually exclusive or jointly exhaustive, and as a consequence, more than one specifier\nmay be given. Specifiers are indicated by the instruction \u201c Specify \u201d or \u201cSpecify if\u201d in the cri-\nteria set. Specifiers provide an opportunity to define a more homogeneous subgrouping of", "source": "dsm5.pdf"} {"id": "082bfdfabf2b-0", "page_content": "22 Use of the Manual\nindividuals with the disorder who share certai n features (e.g., major depressive disorder,\nwith mixed features) and to conv ey information that is relevant to the management of the\nindividual\u2019s disorder, such as the \u201cwith other medical comorbidity\u201d specifier in sleep-\nwake disorders. Although a fifth digit is sometimes assigned to code a subtype or specifier\n(e.g., 294.11 [F02.81] major neurocognitive disorder due to Alzheimer\u2019s disease, with be-\nhavioral disturbance) or severity (296.21 [F32. 0] major depressive disorder, single episode,\nmild), the majority of subtypes and specifie rs included in DSM-5 cannot be coded within\nthe ICD-9-CM and ICD-10-CM systems and are indicated only by including the subtype or\nspecifier after the name of the disorder (e.g., social anxiety disorder [social phobia], per-\nformance type). Note that in some cases, a specifier or subtype is codable in ICD-10-CM\nbut not in ICD-9-CM. Accordingly, in some c ases the 4th or 5th character codes for the sub-\ntypes or specifiers are provided only for the ICD-10-CM coding designations.\nA DSM-5 diagnosis is usually applied to the individual\u2019s current presentation; previ-\nous diagnoses from which the individual has recovered shoul d be clearly noted as such.\nSpecifiers indicating course (e.g., in partial remission, in full remission) may be listed after\nthe diagnosis and are indicated in a numb er of criteria sets. Where available, severity spec-\nifiers are provided to guide clinicians in rating the intensity, frequency, duration, symptom\ncount, or other severity indicator of a disorder . Severity specifiers are indicated by the in-", "source": "dsm5.pdf"} {"id": "082bfdfabf2b-1", "page_content": "count, or other severity indicator of a disorder . Severity specifiers are indicated by the in-\nstruction \u201c Specify current severity\u201d in the criteria se t and include disorder-specific defini-\ntions. Descriptive features specifiers have also been provided in the criteria set and convey\nadditional information that can inform trea tment planning (e.g., obsessive-compulsive\ndisorder, with poor insight). Not all disorders include course , severity, and/or descriptive\nfeatures specifiers. \nMedication-Induced Movement Disorders and Other \nConditions That May Be a Fo cus of Clinical Attention\nIn addition to important psychosocial and en vironmental factors (see \u201cThe Multiaxial Sys-\ntem\u201d in the \u201cIntroduction\u201d elsewhere in this ma nual), these chapters in Section II also con-\ntain other conditions that are not mental disorders but may be encountered by mental\nhealth clinicians. These conditions may be listed as a reason for clinical visit in addition to,\nor in place of, the mental disorders listed in Section II. A separate chapter is devoted to\nmedication-induced disorders and other adverse effects of medication that may be as-\nsessed and treated by clinicians in mental health practice such as akathisia, tardive dyski-\nnesia, and dystonia. The description of neurol eptic malignant syndrome is expanded from\nthat provided in DSM-IV-TR to highlight the em ergent and potentially life-threatening na-\nture of this condition, and a new entry on an tidepressant discontinuation syndrome is pro-\nvided. An additional chapter discusses other conditions that may be a focus of clinical\nattention. These include relational problems, problems related to abuse and neglect, prob-\nlems with adherence to treatment regimens, obesity, antisocial behavior, and malingering.\nPrincipal Diagnosis", "source": "dsm5.pdf"} {"id": "082bfdfabf2b-2", "page_content": "Principal Diagnosis\nWhen more than one diagnosis for an individual is given in an inpatient setting, the prin-\ncipal diagnosis is the condition established after study to be chiefly responsible for occa-\nsioning the admission of the individual. When more than one diagnosis is given for an\nindividual in an outpatient setting, the reason for visit is the condition that is chiefly re-\nsponsible for the ambulatory care medical servic es received during the visit. In most cases,\nthe principal diagnosis or the reason for visit is also the main focus of attention or treat-\nment. It is often difficult (and somewhat ar bitrary) to determine which diagnosis is the", "source": "dsm5.pdf"} {"id": "3c171e167b17-0", "page_content": "the principal diagnosis or the reason for visit is also the main focus of attention or treat-\nment. It is often difficult (and somewhat ar bitrary) to determine which diagnosis is the\nprincipal diagnosis or the reason for visit, especially when, for example, a substance-\nrelated diagnosis such as alcohol use disorder is accompanied by a non-substance-related\ndiagnosis such as schizophrenia. For example, it may be unclear which diagnosis should", "source": "dsm5.pdf"} {"id": "bb1302393c73-0", "page_content": "Use of the Manual 23\nbe considered \u201cprincipal\u201d for an individual hospitalized with both schizophrenia and al-\ncohol use disorder, because each condition ma y have contributed equally to the need for\nadmission and treatment. The principal diagnosis is indicated by listing it first, and the re-\nmaining disorders are listed in order of focu s of attention and treatment. When the prin-\ncipal diagnosis or reason for visit is a ment al disorder due to another medical condition\n(e.g., major neurocognitive disorder due to Alzheimer\u2019s disease, psychotic disorder due to\nmalignant lung neoplasm), ICD coding rules re quire that the etiological medical condition\nbe listed first. In that case, the principal diagnosis or reason for visit would be the mental\ndisorder due to the medical condition, the seco nd listed diagnosis. In most cases, the dis-\norder listed as the principal diagnosis or the reason for visit is followed by the qualifying\nphrase \u201c(principal diagnosis)\u201d or \u201c(reason for visit).\u201d\nProvisional Diagnosis\nThe specifier \u201cprovisional\u201d can be used when there is a strong presumption that the full\ncriteria will ultimately be met for a disord er but not enough information is available to\nmake a firm diagnosis. The clinician can indi cate the diagnostic uncertainty by recording\n\u201c(provisional)\u201d following the diagnosis. For example, this diagnosis might be used when\nan individual who appears to ha ve a major depressive disorder is unable to give an ade-\nquate history, and thus it canno t be established that the full cr iteria are met. Another use of\nthe term provisional is for those situations in which differential diagnosis depends exclu-\nsively on the duration of illness. For example, a diagnosis of schizophreniform disorder re-\nquires a duration of less than 6 months bu t of at least 1 month and can only be given", "source": "dsm5.pdf"} {"id": "bb1302393c73-1", "page_content": "provisionally if assigned before remission has occurred.\nCoding and Reporting Procedures\nEach disorder is accompanied by an identify ing diagnostic and statistical code, which is\ntypically used by institutions and agencies for data collection and billing purposes. There\nare specific recording protocol s for these diagnostic codes (i dentified as coding notes in\nthe text) that were established by WHO, the U.S. Centers fo r Medicare and Medicaid Ser-\nvices (CMS), and the Centers for Disease Cont rol and Prevention\u2019s National Center for\nHealth Statistics to ensure co nsistent international recordin g of prevalence and mortality\nrates for identified health conditions. For most clinicians, the codes are used to identify the\ndiagnosis or reason for visit for CMS and private insurance servic e claims. The official\ncoding system in use in the United States as of publication of this ma nual is ICD-9-CM. Of-\nficial adoption of ICD-10-CM is scheduled to take place on October 1, 2014, and these\ncodes, which are shown parenthetically in this manual, should not be used until the offi-\ncial implementation occurs. Both ICD-9-CM and ICD-10-CM codes have been listed 1) pre-\nceding the name of the disorder in the classification and 2) accompanying the criteria set\nfor each disorder. For some diagnoses (e.g ., neurocognitive and substance/medication-\ninduced disorders), the appropriate code depe nds on further specification and is listed\nwithin the criteria set for the disorder, as coding notes, and, in some cases, further clarified\nin a section on recording proc edures. The names of some di sorders are followed by alter-\nnative terms enclosed in parentheses, which, in most cases, were the DSM-IV names for\nthe disorders.\nLooking to the Future:", "source": "dsm5.pdf"} {"id": "bb1302393c73-2", "page_content": "the disorders.\nLooking to the Future:\nAssessment and Monitoring Tools\nThe various components of DSM-5 are provided to facilitate patient assessment and to aid\nin developing a comprehensive case formulation. Whereas the diagnostic criteria in Sec-\ntion II are well-established measures that have undergone extensive review, the assess-", "source": "dsm5.pdf"} {"id": "78cfa0444ca9-0", "page_content": "24 Use of the Manual\nment tools, a cultural formul ation interview, and conditions for further study included in\nSection III are those for which we determined that the scientific evidence is not yet avail-\nable to support widespread clinical use. These diagnostic aids and criteria are included to\nhighlight the evolution and direction of scientif ic advances in these areas and to stimulate\nfurther research.\nEach of the measures in Section III is provi ded to aid in a compre hensive assessment of\nindividuals that will contribute to a diagnosi s and treatment plan tailored to the individ-\nual presentation and clinical context. Where cultural dynamics are particularly important\nfor diagnostic assessment, the cultural formulation interview should be considered as a\nuseful aid to communication with the individual. Cross-cutting symptom and diagnosis-\nspecific severity measures provide quantitative ratings of important clinical areas that are\ndesigned to be used at the initial evaluation to establish a baseline for comparison with rat-\nings on subsequent encounters to monito r changes and inform treatment planning.\nThe use of such measures will undoubtedly be facilitated by digital applications, and\nthe measures are included in Section III to provide for further evaluation and develop-\nment. As with each DSM edition, the diagnostic criteria and the DSM-5 classification of\nmental disorders reflect the current consensu s on the evolving knowledge in our field.", "source": "dsm5.pdf"} {"id": "14605ba66d16-0", "page_content": "25Cautionary Statement for\nForensic Use of DSM-5\nAlthough the DSM-5 diagnostic criteria and text are primarily designed to assist\nclinicians in conducting clinical assessment, case formulation, an d treatment planning,\nDSM-5 is also used as a reference for the cour ts and attorneys in assessing the forensic con-\nsequences of mental disorders. As a result, it is important to note that the definition of\nmental disorder included in DSM-5 was developed to meet the needs of clinicians, public\nhealth professionals, and research investigators rather than all of the technical needs of the\ncourts and legal professionals. It is also im portant to note that DSM-5 does not provide\ntreatment guidelines for any given disorder.\nWhen used appropriately, diagnoses and di agnostic information can assist legal deci-\nsion makers in their determinations. For exampl e, when the presence of a mental disorder\nis the predicate for a su bsequent legal determination (e.g ., involuntary civil commitment),\nthe use of an established system of diagnosi s enhances the value and reliability of the de-\ntermination. By providing a co mpendium based on a review of the pertinent clinical and\nresearch literature, DSM-5 may facilitate legal decision makers\u2019 understanding of the rel-\nevant characteristics of mental disorders. The literature related to di agnoses also serves as\na check on ungrounded speculation about ment al disorders and about the functioning of a\nparticular individual. Finally, diagnostic in formation about longitud inal course may im-\nprove decision making when the legal issue co ncerns an individual\u2019s mental functioning\nat a past or future point in time.\nHowever, the use of DSM-5 should be inform ed by an awareness of the risks and lim-\nitations of its use in forensic settings. When DSM-5 categories, criteria, and textual descrip-", "source": "dsm5.pdf"} {"id": "14605ba66d16-1", "page_content": "tions are employed for forensic purposes, ther e is a risk that diagnostic information will be\nmisused or misunderstood. These dangers aris e because of the imperfect fit between the\nquestions of ultimate concern to the law and the information contained in a clinical diagno-\nsis. In most situations, the clinical diagnosis of a DSM-5 mental disorder such as intellec-\ntual disability (intellectual developmental di sorder), schizophrenia , major neurocognitive\ndisorder, gambling disorder, or pedophilic di sorder does not imply that an individual\nwith such a condition meets legal criteria for the presence of a mental disorder or a speci-\nfied legal standard (e.g., for co mpetence, criminal responsibility , or disability). For the latter,\nadditional information is usually required beyond that contained in the DSM-5 diagnosis,\nwhich might include information about the individual\u2019s functional impairments and how\nthese impairments affect the particular abilities in question. It is precisely because impair-\nments, abilities, and disabilities vary widely wi thin each diagnostic category that assign-\nment of a particular diagnosis does not imply a specific level of im pairment or disability.\nUse of DSM-5 to assess for th e presence of a mental diso rder by nonclinical, nonmed-\nical, or otherwise insufficiently trained indi viduals is not advised. Nonclinical decision\nmakers should also be cautioned that a di agnosis does not carry any necessary implica-\ntions regarding the etiology or causes of the individual\u2019s mental di sorder or the individ-\nual\u2019s degree of control over behaviors that may be associat ed with the disorder. Even\nwhen diminished control over one\u2019s behavior is a feature of the disorder, having the diag-\nnosis in itself does not demons trate that a particular individu al is (or was) unable to con-", "source": "dsm5.pdf"} {"id": "14605ba66d16-2", "page_content": "trol his or her behavior at a particular time.", "source": "dsm5.pdf"} {"id": "95173330c629-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "3da53fb8d2fb-0", "page_content": "SECTION II\nDiagnostic Criteria and Codes\nNeurodevelopmental Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .31\nSchizophrenia Spectrum and Other Psychotic Disorders . . . . . . . . . . . .87\nBipolar and Related Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .123\nDepressive Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .155\nAnxiety Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .189\nObsessive-Compulsive and Related Disorders. . . . . . . . . . . . . . . . . . . .235\nTrauma- and Stressor-Related Disorders . . . . . . . . . . . . . . . . . . . . . . . .265\nDissociative Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .291\nSomatic Symptom and Related Disorders . . . . . . . . . . . . . . . . . . . . . . .309\nFeeding and Eating Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .329", "source": "dsm5.pdf"} {"id": "3da53fb8d2fb-1", "page_content": "Elimination Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .355\nSleep-Wake Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .361\nSexual Dysfunctions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .423\nGender Dysphoria. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .451\nDisruptive, Impulse-Control, and Conduct Disorders. . . . . . . . . . . . . . .461\nSubstance-Related and Addictive Disorders . . . . . . . . . . . . . . . . . . . . .481\nNeurocognitive Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .591\nPersonality Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .645\nParaphilic Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .685", "source": "dsm5.pdf"} {"id": "3da53fb8d2fb-2", "page_content": "Other Mental Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .707\nMedication-Induced Movement Disorders and \nOther Adverse Effects of Medication. . . . . . . . . . . . . . . . . . . . . . . . . .709\nOther Conditions That May Be a Focus of Clinical Attention. . . . . . . . .715", "source": "dsm5.pdf"} {"id": "ac3927f61133-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "51bb052844af-0", "page_content": "This section contains the diagnostic criteria approved for routine clinical\nuse along with the ICD-9-CM codes (ICD-10 codes are shown parenthetically).\nFor each mental disorder, the diagnostic criteria are followed by descriptive\ntext to assist in diagnostic decision making. Where needed, specific recording\nprocedures are presented with the diagnostic criteria to provide guidance in\nselecting the most appropriate code. In some cases, separate recording pro-\ncedures for ICD-9-CM and ICD-10-CM are provided. Although not considered\nas official DSM-5 disorders, medication -induced movement disorders and other\nadverse effects of medication, as well as other conditions that may be a focus\nof clinical attention (including additi onal ICD-9-CM V codes and forthcoming\nICD-10-CM Z codes), are provided to indicate other reasons for a clinical visit\nsuch as environmental factors and relational problems. These codes are adapted\nfrom ICD-9-CM and ICD-10-CM and we re neither reviewed nor approved as\nofficial DSM-5 diagnoses, but can provide additional context for a clinical for-\nmulation and treatment plan. These three components\u2014the criteria and their\ndescriptive text, the medication-i nduced movement disorders and other ad-\nverse effects of medication, and the descriptions of other conditions that may\nbe a focus of clinical attention\u2014represent the key elements of the clinical di-\nagnostic process and thus are presented together.", "source": "dsm5.pdf"} {"id": "6415ef16a5e1-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "8a3f407e06cf-0", "page_content": "31Neurodevelopmental\nDisorders\nThe neurodevelopmental disorders are a group of co nditions with onset in the\ndevelopmental period. The diso rders typically manifest early in development, often be-\nfore the child enters grade school, and are characterized by developmental deficits that\nproduce impairments of person al, social, academic, or occupational functioning. The\nrange of developmental deficits varies from very specific limitations of learning or control\nof executive functions to glob al impairments of social skills or intelligence. The neurode-\nvelopmental disorders frequent ly co-occur; for example, in dividuals with autism spec-\ntrum disorder often have intellectual disability (intellectual developmental disorder), and\nmany children with attention-deficit/hyperactivity disorder (ADHD) also have a specific\nlearning disorder. For some diso rders, the clinical presentation includes symptoms of ex-\ncess as well as deficits and delays in achiev ing expected milestones. For example, autism\nspectrum disorder is diagnose d only when the characteristic deficits of social communi-\ncation are accompanied by excessively repetitive behaviors, restricted interests, and insis-\ntence on sameness. \nIntellectual disability (intel lectual developmental disorder) is characterized by deficits\nin general mental abilities, such as reasoning, problem solving, planning, abstract thinking,\njudgment, academic learning, and learning from experience. The deficits result in impair-\nments of adaptive functioning, such that the individual fails to meet standards of personal\nindependence and social responsibility in one or more aspects of daily life, including com-\nmunication, social participation, academic or occupational functionin g, and personal inde-\npendence at home or in community settings . Global developmental delay, as its name\nimplies, is diagnosed when an individual fa ils to meet expected developmental milestones", "source": "dsm5.pdf"} {"id": "8a3f407e06cf-1", "page_content": "implies, is diagnosed when an individual fa ils to meet expected developmental milestones\nin several areas of intellectual functioning. The diagnosis is used for individuals who are\nunable to undergo systematic assessments of intellectual functioning, including children\nwho are too young to participate in standardiz ed testing. Intellectual disability may result\nfrom an acquired insult during the developm ental period from, for example, a severe head\ninjury, in which case a neurocognitive disorder also may be diagnosed.\nThe communication disorders include language disorder, speech sound disorder, so-\ncial (pragmatic) communication disorder, and childhood-onset fluency disorder (stutter-\ning). The first three disorders are characterize d by deficits in the development and use of\nlanguage, speech, and social communication, respectively. Childhood -onset fluency dis-\norder is characterized by disturbances of the normal fluency an d motor production of\nspeech, including repetitive sounds or syllables, prolongation of consonants or vowel\nsounds, broken words, blocking, or words pr oduced with an exce ss of physical tension.\nLike other neurodevelopmental disorders, communication di sorders begin early in life\nand may produce lifelong functional impairments.\nAutism spectrum disorder is characterized by persistent deficits in social communica-\ntion and social interaction across multiple cont exts, including deficits in social reciprocity,\nnonverbal communicative behavior s used for social interaction, and skills in developing,\nmaintaining, and understandin g relationships. In addition to the social communication\ndeficits, the diagnosis of autism spectrum disorder requires th e presence of restricted, re-\npetitive patterns of behavior, interests, or activities. Because symptoms change with de-\nvelopment and may be masked by compensator y mechanisms, the diagnostic criteria may", "source": "dsm5.pdf"} {"id": "cce0c9b6d498-0", "page_content": "32 Neurodevelopmental Disorders\nbe met based on historical information, although the current presentation must cause sig-\nnificant impairment.\nWithin the diagnosis of autism spectrum disorder, individual clinical characteristics\nare noted through the use of specifiers (with or without accompanying intellectual impair-\nment; with or without accompan ying structural language im pairment; associated with a\nknown medical/genetic or environmental/acquired condition; associated with another\nneurodevelopmental, mental, or behavioral disorder), as well as specifiers that describe\nthe autistic symptoms (age at first concern; wi th or without loss of established skills; sever-\nity). These specifiers provide clinicians with an opportunity to individualize the diagnosis\nand communicate a richer clinical description of the affected individuals. For example, many\nindividuals previously diagnosed with Asperg er\u2019s disorder would now receive a diagnosis\nof autism spectrum disorder without language or intellectual impairment.\nADHD is a neurodevelopmental disorder defined by impairing levels of inattention, dis-\norganization, and/or hyperactivity-impulsivity. Inattention and disorganization entail inabil-\nity to stay on task, seeming not to listen, and lo sing materials, at leve ls that are inconsistent\nwith age or developmental level. Hyperactivity-impulsivity entails overactivity, fidgeting, in-\nability to stay seated, intruding into other people\u2019s activities , and inability to wait\u2014symptoms\nthat are excessive for age or developmental level. In childhood, ADHD frequently overlaps\nwith disorders that are often considered to be \u201cexternalizing disorders,\u201d such as oppositional\ndefiant disorder and conduct di sorder. ADHD often persists in to adulthood, with resultant\nimpairments of social, academic and occupational functioning.\nThe neurodevelopmental motor disorders in clude developmental coordination disor-\nder, stereotypic movement disorder, and tic disorders. Developmen tal coordination dis-", "source": "dsm5.pdf"} {"id": "cce0c9b6d498-1", "page_content": "der, stereotypic movement disorder, and tic disorders. Developmen tal coordination dis-\norder is characterized by deficits in the acquisition and execution of coordinated motor\nskills and is manifested by clumsiness and slow ness or inaccuracy of performance of mo-\ntor skills that cause interference with activiti es of daily living. St ereotypic movement dis-\norder is diagnosed when an individual has repetitive, seemingly driven, and apparently\npurposeless motor behaviors, such as hand fl apping, body rocking, head banging, self-\nbiting, or hitting. The movements interfere with social, academic, or other activities. If the\nbehaviors cause self-injury, this should be specified as part of the diagnostic description.\nTic disorders are characterized by the presen ce of motor or vocal tics, which are sudden,\nrapid, recurrent, nonrhythmic, sterotyped motor movements or vocalizations. The dura-\ntion, presumed etiology, and clinical presentation define the specific tic disorder that is di-\nagnosed: Tourette\u2019s disorder, persistent (chronic) motor or vocal tic disorder, provisional\ntic disorder, other specified tic disorder, and unspecified tic disorder . Tourette\u2019s disorder\nis diagnosed when the individual has multiple motor and vocal tics that have been present\nfor at least 1 year and that have a waxing-waning symptom course.\nSpecific learning disorder, as the name implie s, is diagnosed when there are specific defi-\ncits in an individual\u2019s ability to perceive or process information efficiently and accurately. This\nneurodevelopmental disorder first manifests during the years of formal schooling and is\ncharacterized by persistent and impairing diffi culties with learning foundational academic\nskills in reading, writing, and/ or math. The individual\u2019s perfor mance of the affected academic", "source": "dsm5.pdf"} {"id": "cce0c9b6d498-2", "page_content": "skills is well below average for age, or acceptable performance levels are achieved only with\nextraordinary effort. Specific learning disorder may occur in individuals identified as intellec-", "source": "dsm5.pdf"} {"id": "7051fbdf9c70-0", "page_content": "skills is well below average for age, or acceptable performance levels are achieved only with\nextraordinary effort. Specific learning disorder may occur in individuals identified as intellec-\ntually gifted and manifest only when the le arning demands or assessment procedures (e.g.,\ntimed tests) pose barriers that cannot be overcome by their innate intelligence and c ompensa-\ntory strategies. For all individuals, specific le arning disorder can produce lifelong impairments\nin activities dependent on the skills , including occupational performance.\nThe use of specifiers for the neurodevelopme ntal disorder diagnoses enriches the clin-\nical description of the individual\u2019s clinical course and current symptomatology. In addi-\ntion to specifiers that describe the clinical presentation, such as age at onset or severity\nratings, the neurodevelopmental disorders ma y include the specifier \u201cassociated with a\nknown medical or genetic condition or environmental factor.\u201d This specifier gives clini-", "source": "dsm5.pdf"} {"id": "2afb2ef251d3-0", "page_content": "Intellectual Disability (Intellectual Developmental Disorder) 33\ncians an opportunity to document factors that may have played a role in the etiology of the\ndisorder, as well as those that might affect the clinical course. Examples include genetic\ndisorders, such as fragile X syndrome, tuberous sclerosis, and Rett syndrome; medical con-\nditions such as epilepsy; and environmental fa ctors, including very low birth weight and\nfetal alcohol exposure (even in the absence of stigmata of fetal alcohol syndrome).\nIntellectual Disabilities\nIntellectual Disability\n (Intellectual Developmental Disorder)\nDiagnostic Criteria\nIntellectual disability (intellectual development al disorder) is a disorder with onset during\nthe developmental period that includes both intellectual and adaptive functioning deficits\nin conceptual, social, and practical domains. The following three criteria must be met:\nA. Deficits in intellectual functions, such as reasoning, problem solving, planning, abstract\nthinking, judgment, academic learning, and learning from experience, confirmed by\nboth clinical assessment and individualized, standardized intelligence testing.\nB. Deficits in adaptive functioning that result in failure to meet developmental and socio-\ncultural standards for personal independence and social responsibility. Without ongo-\ning support, the adaptive deficits limit functioning in one or more activities of daily life,\nsuch as communication, social participation, and independent living, across multiple\nenvironments, such as home, school, work, and community.\nC. Onset of intellectual and adaptive deficits during the developmental period.\nNote: The diagnostic term intellectual disability is the equivalent term for the ICD-11 diag-\nnosis of intellectual developmental disorders. Although the term intellectual disability is\nused throughout this manual, both terms are used in the title to clarify relationships with\nother classification systems. Moreover, a federal statute in the United States (Public Law", "source": "dsm5.pdf"} {"id": "2afb2ef251d3-1", "page_content": "other classification systems. Moreover, a federal statute in the United States (Public Law\n111-256, Rosa\u2019s Law) replaces the term mental retardation with intellectual disability, and\nresearch journals use the term intellectual disability. Thus, intellectual disability is the\nterm in common use by medical, educational, and other professions and by the lay public\nand advocacy groups.\nSpecify current severity (see Table 1): \n317 (F70) Mild\n318.0 (F71) Moderate\n318.1 (F72) Severe\n318.2 (F73) Profound\nSpecifiers\nThe various levels of severity are defined on the basis of adaptive functioning, and not IQ\nscores, because it is adaptive functioning that determines the level of supports required.\nMoreover, IQ measures ar e less valid in the lower end of the IQ range.", "source": "dsm5.pdf"} {"id": "f957343119ee-0", "page_content": "34 Neurodevelopmental DisordersTABLE 1 Severity levels for intellectual disability (intellectual developmental disorder)\nSeverity \nlevel Conceptual domain Social domain Practical domain\nMild For preschool children, there \nmay be no obvious conceptual \ndifferences. Fo r school-age \nchildren and adults, there are \ndifficulties in learning aca-\ndemic skills involving reading, \nwriting, arithmetic, time, or \nmoney, with support needed \nin one or more areas to meet \nage-related expectations. In \nadults, abstract thinking, exec-\nutive function (i.e., planning, \nstrategizing, priority setting, \nand cognitive flexibility), and \nshort-term memory, as well as \nfunctional use of academic \nskills (e.g., reading, money \nmanagement), are impaired. \nThere is a somewhat concrete \napproach to problems and \nsolutions compared with \nage-mates. Compared with typically developing age-\nmates, the individual is immature in social \ninteractions. For example, there may be diffi-\nculty in accurately perceiving peers\u2019 social \ncues. Communication, conversation, and lan-\nguage are more concrete or immature than \nexpected for age. There may be difficulties reg-\nulating emotion and behavior in age-appropri-\nate fashion; these difficulties are noticed by \npeers in social situations. There is limited \nunderstanding of risk in social situations; \nsocial judgment is immature for age, and \nthe person is at risk of being manipulated \nby others (gullibility).The individual may functi on age-appropriately in \npersonal care. Individuals need some support with \ncomplex daily living tasks in comparison to peers. In \nadulthood, supports typicall y involve grocery shop-", "source": "dsm5.pdf"} {"id": "f957343119ee-1", "page_content": "adulthood, supports typicall y involve grocery shop-\nping, transportation, home and child-care organiz-\ning, nutritious food preparation, and banking and \nmoney management. Recreati onal skills resemble \nthose of age-mates, although judgment related to \nwell-being and organization around recreation \nrequires support. In adulthood, competitive \nemployment is often seen in jobs that do not empha-\nsize conceptual skills.\u00a0Individuals generally need \nsupport to make health care decisions and legal \ndecisions, and to learn to perform a skilled vocation \ncompetently. Support is typically needed to raise a \nfamily.", "source": "dsm5.pdf"} {"id": "801af9e4acb0-0", "page_content": "Intellectual Disability (Intellectual Developmental Disorder) 35Moderate All through development, the \nindividual\u2019s conceptual skills \nlag markedly behind those of \npeers. For preschoolers, lan-\nguage and pre-academic skills \ndevelop slowly. For school-age \nchildren, progress in reading, \nwriting, mathematics, and \nunderstanding of time and \nmoney occurs slowly across \nthe school years and is mark-\nedly limited compared with \nthat of peers. For adults, aca-\ndemic skill development is \ntypically at an elementary \nlevel, and support is required \nfor all use of academic skills in \nwork and personal life. Ongo-\ning assistance on a daily basis \nis needed to complete concep-\ntual tasks of day-to-day life, \nand others may take over these \nresponsibilities fully for the \nindividual.The individual shows marked differences from \npeers in social and communicative behavior \nacross development. Spoken language is typi-\ncally a primary tool for social communication \nbut is much less complex than that of peers. \nCapacity for relationships is evident in ties to \nfamily and friends, and the individual may \nhave successful friendships across life and \nsometimes romantic relations in adulthood. \nHowever, individuals may not perceive or \ninterpret social cues ac curately. Social judg-\nment and decision-making abilities are lim-\nited, and caretakers must assist the person \nwith life decisions.\u00a0Friendships with typically \ndeveloping peers are often affected by com-\nmunication or social limitations. Significant \nsocial and communicative support is needed \nin work settings for success. The individual can care for personal needs involving \neating, dressing, elimination, and hygiene as an", "source": "dsm5.pdf"} {"id": "801af9e4acb0-1", "page_content": "eating, dressing, elimination, and hygiene as an \nadult, although an extended period of teaching and \ntime is needed for the individual to become indepen-\ndent in these areas, and reminders may be needed. \nSimilarly, participation in all household tasks can be \nachieved by adulthood, although an extended \nperiod of teaching is ne eded, and ongoing supports \nwill typically occur for adult-level performance. \nIndependent employment in jobs that require lim-\nited conceptual and communication skills can be \nachieved, but considerable support from co-work-\ners, supervisors, and others is needed to manage \nsocial expectations, job co mplexities, and ancillary \nresponsibilities such as scheduling, transportation, \nhealth benefits, and mone y management. A variety \nof recreational skills can be developed. These typi-\ncally require additional supports and learning \nopportunities over an ex tended period of time. \nMaladaptive behavior is present in a significant \nminority and causes social problems.TABLE 1 Severity levels for intellectual disability (intellectual developmental disorder) (continued)\nSeverity \nlevel Conceptual domain Social domain Practical domain", "source": "dsm5.pdf"} {"id": "03bdb76f9f7c-0", "page_content": "36 Neurodevelopmental DisordersSevere Attainment of conceptual skills \nis limited. The individual gen-\nerally has little understanding \nof written language or of con-\ncepts involving numbers, \nquantity, time, and money. \nCaretakers provide extensive \nsupports for problem solving \nthroughout life. Spoken language is quit e limited in terms of \nvocabulary and grammar. Speech may be sin-\ngle words or phrases and may be supple-\nmented through augmentative means. Speech \nand communication are focused on the here \nand now within everyday events.\u00a0Language is \nused for social communication more than for \nexplication. Individuals understand simple \nspeech and gestural communication. Relation-\nships with family members and familiar others \nare a source of pleasure and help. The individual requires suppo rt for all activities of \ndaily living, including meals, dressing, bathing, and \nelimination. The individual requires supervision at \nall times. The individual cannot make responsible \ndecisions regarding\u00a0well-being of self or others. In \nadulthood, participation in tasks at home, recre-\nation, and work requires ongoing support and assis-\ntance. Skill acquisition in all domains involves long-\nterm teaching and ongoing support. Maladaptive \nbehavior, including self-injury, is present in a signif-\nicant minority.\u00a0\nProfound Conceptual skills generally \ninvolve the physical world \nrather than symbolic pro-\ncesses. The individual may use \nobjects in goal-directed fashion \nfor self-care, work, and recre-\nation. Certain visuospatial \nskills, such as matching and \nsorting based on physical char-\nacteristics, may be acquired. \nHowever, co-occ urring motor \nand sensory impairments may", "source": "dsm5.pdf"} {"id": "03bdb76f9f7c-1", "page_content": "However, co-occ urring motor \nand sensory impairments may \nprevent functional use of \nobjects. The individual has very limited understanding \nof symbolic communication in speech or ges-\nture. He or she may understand some simple \ninstructions or gestures. The individual \nexpresses his or her own desires and emotions \nlargely through nonverbal, nonsymbolic com-\nmunication. The individu al enjoys relation-\nships with well-known family members, \ncaretakers, and familiar others, and initiates \nand responds to social interactions through \ngestural and emotional cues. Co-occurring \nsensory and physical impairments may pre-\nvent many social activities. The individual is dependent on others for all aspects of \ndaily physical care, health, and safety, although he or \nshe may be able to participat e in some of these activi-\nties as well. Individuals without severe physical \nimpairments may assist with some daily work tasks at \nhome, like carrying dishes to the table. Simple actions \nwith objects may be the basi s of participation in some \nvocational activities with high levels of ongoing sup-\nport. Recreational activities may involve, for example, \nenjoyment in listening to music, watching movies, \ngoing out for walks, or part icipating in water activi-\nties, all with the support of others. Co-occurring \nphysical and sensory impairments are frequent \nbarriers to participation (beyond watching) in home, \nrecreational, and vocational activities. Maladaptive \nbehavior is present in a significant minority.TABLE 1 Severity levels for intellectual disability (intellectual developmental disorder) (continued)\nSeverity \nlevel Conceptual domain Social domain Practical domain", "source": "dsm5.pdf"} {"id": "5b78f9981019-0", "page_content": "Intellectual Disability (Intellectual Developmental Disorder) 37\nDiagnostic Features\nThe essential features of intellectual disab ility (intellectual developmental disorder) are\ndeficits in general mental abilities (Criteri on A) and impairment in everyday adaptive\nfunctioning, in comparison to an individual \u2019s age-, gender-, and socioculturally matched\npeers (Criterion B). Onset is during the developmental period (Criterion C). The diagnosis\nof intellectual disability is based on both clinical assessment and standardized testing of\nintellectual and adaptive functions.\nCriterion A refers to intellectual function s that involve reasoning, problem solving,\nplanning, abstract thinking, judgment, lear ning from instruction and experience, and\npractical understanding. Critical componen ts include verbal comprehension, working\nmemory, perceptual reasoning, quantitative reasoning, abstract thought, and cognitive ef-\nficacy. Intellectual functioning is typically me asured with individually administered and\npsychometrically valid, comprehensive, cultur ally appropriate, psychometrically sound\ntests of intelligence. Individuals with intellec tual disability have scores of approximately\ntwo standard deviations or more below the population mean, including a margin for mea-\nsurement error (generally +5 points). On te sts with a standard deviation of 15 and a mean\nof 100, this involves a score of 65\u201375 (70 \u00b1 5). Clinical training and judgment are required\nto interpret test results and assess intellectual performance.\nFactors that may affect test scores include practice effects and the \u201cFlynn effect\u2019 (i.e.,\noverly high scores due to out- of-date test norms). Invalid scores may result from the use of\nbrief intelligence screening tests or group tests; highly discrepant individual subtest scores\nmay make an overall IQ score invalid. Instrume nts must be normed for the individual\u2019s so-", "source": "dsm5.pdf"} {"id": "5b78f9981019-1", "page_content": "ciocultural background and native language. Co-occurring disorders that affect communi-\ncation, language, and/or motor or sensory fu nction may affect test scores. Individual\ncognitive profiles based on ne uropsychological testing are mo re useful for understanding\nintellectual abilities than a single IQ score. Such testing may identify areas of relative\nstrengths and weaknesses, an assessment import ant for academic and vocational planning.\nIQ test scores are approximat ions of conceptual function ing but may be insufficient to\nassess reasoning in real-life situations and ma stery of practical task s. For example, a per-\nson with an IQ score above 70 may have such severe adaptive behavi or problems in social\njudgment, social understanding, and other area s of adaptive functioning that the person\u2019s\nactual functioning is comparable to that of in dividuals with a lower IQ score. Thus, clinical\njudgment is needed in interpre ting the results of IQ tests.\nDeficits in adaptive functioning (Criterion B) refer to how well a person meets community\nstandards of personal independen ce and social responsibility, in comparison to others of sim-\nilar age and sociocultural background. Adaptive functioning involves adaptive reasoning in\nthree domains: conceptual, social, and practical. The conceptual (academic) domain involves\ncompetence in memory, language, reading, writing, math reasoning, acquisition of practical\nknowledge, problem solving, and judgment in novel situations , among others. The social do-\nmain involves awareness of others\u2019 thoughts, feelings, and experiences; empathy; interper-\nsonal communication skills; friendship abilit ies; and social judgment, among others. The\npractical domain involves learning and self-management across life settings, including personal\ncare, job responsibilities, money management, recreation, self-management of behavior, and", "source": "dsm5.pdf"} {"id": "5b78f9981019-2", "page_content": "care, job responsibilities, money management, recreation, self-management of behavior, and\nschool and work task organization, among others . Intellectual capacity, education, motivation,\nsocialization, personality features, vocational opportunity, cultural experience, and coexisting", "source": "dsm5.pdf"} {"id": "e7afe38a24d2-0", "page_content": "school and work task organization, among others . Intellectual capacity, education, motivation,\nsocialization, personality features, vocational opportunity, cultural experience, and coexisting\ngeneral medical conditions or mental di sorders influence adaptive functioning.\nAdaptive functioning is assessed using both clinical evaluation and individualized,\nculturally appropriate, psychometrically sound measures. Standardized measures are\nused with knowledgeable informants (e.g., pa rent or other f amily member; teacher; coun-\nselor; care provider) and the individual to th e extent possible. Additional sources of infor-\nmation include educational, developmental, medical, and mental health evaluations.\nScores from standardized measures and interv iew sources must be interpreted using clin-\nical judgment. When standardized testing is di fficult or impossible, because of a variety of", "source": "dsm5.pdf"} {"id": "db605dcece2b-0", "page_content": "38 Neurodevelopmental Disorders\nfactors (e.g., sensory impairme nt, severe problem behavior), the individual may be diag-\nnosed with unspecified intellectual disability. Adaptive functioning may be difficult to\nassess in a controlled setting (e.g., prisons, dete ntion centers); if poss ible, corrob orative in-\nformation reflecting functioning outsid e those settings should be obtained.\nCriterion B is met when at least one domain of adaptive functioning\u2014conceptual, so-\ncial, or practical\u2014is sufficiently impaired th at ongoing support is needed in order for the\nperson to perform adequately in one or more life settings at school, at work, at home, or in\nthe community. To meet diagnostic criteria for intellectual disability, the deficits in adap-\ntive functioning must be directly related to the intellectual impairments described in Cri-\nterion A. Criterion C, onset during the deve lopmental period, refers to recognition that\nintellectual and adaptive deficits are pr esent during childhood or adolescence.\nAssociated Features Supporting Diagnosis\nIntellectual disability is a heterogeneous condition with multiple causes. There may be\nassociated difficulties with social judgment; assessment of risk; self-management of behav-\nior, emotions, or interpersonal relationships; or motivation in school or work environments.\nLack of communication skills may predispose to disruptive and aggressive behaviors. Gull-\nibility is often a feature, involving naivet\u00e9 in social situations and a tendency for being easily\nled by others. Gullibility and lack of awareness of risk may result in exploitation by others\nand possible victimization, fraud, unintentional criminal involvement, false confessions,\nand risk for physical and sexual abuse. These associated features can be important in crim-\ninal cases, including Atkins-type hearings involving the death penalty.\nIndividuals with a diagnosis of intellectual disability with co-occurring mental disor-", "source": "dsm5.pdf"} {"id": "db605dcece2b-1", "page_content": "Individuals with a diagnosis of intellectual disability with co-occurring mental disor-\nders are at risk for suicide. They think about suicide, make suicide attempts, and may die\nfrom them. Thus, screening for su icidal thoughts is essential in the assessment process. Be-\ncause of a lack of awareness of risk and dang er, accidental injury rates may be increased.\nPrevalence\nIntellectual disability has an overall general population prevalence of approximately 1%,\nand prevalence rates vary by age. Prevalence for severe intellectual disability is approxi-\nmately 6 per 1,000.\nDevelopment and Course\nOnset of intellectual disability is in the de velopmental period. The age and characteristic\nfeatures at onset depend on the etiology and severity of brain dysfunction. Delayed motor,\nlanguage, and social milestones may be identifi able within the first 2 years of life among\nthose with more severe intellectual disability, while mild levels may not be identifiable un-\ntil school age when difficulty with academic learning becomes appare nt. All criteria (in-\ncluding Criterion C) must be fulfilled by hi story or current presentation. Some children\nunder age 5 years whose presentation will even tually meet criteria for intellectual disabil-\nity have deficits that meet criter ia for global developmental delay.\nWhen intellectual disability is associated with a genetic syndrome, there may be a char-\nacteristic physical appearance (as in, e.g., Down syndrome). Some syndromes have a\nbehavioral phenotype, which refers to specific behaviors that are characteristic of particular\ngenetic disorder (e.g., Lesch-Nyhan syndro me). In acquired forms, the onset may be\nabrupt following an illness such as meningitis or encephalitis or head trauma occurring\nduring the developmental period. When intellectual disability results from a loss of pre-", "source": "dsm5.pdf"} {"id": "db605dcece2b-2", "page_content": "during the developmental period. When intellectual disability results from a loss of pre-\nviously acquired cognitive skills, as in severe traumatic brain injury , the diagnoses of in-\ntellectual disability and of a neurocognitive disorder may both be assigned.\nAlthough intellectual disability is generally nonprogressive, in certain genetic disor-", "source": "dsm5.pdf"} {"id": "2f21b41d4fbd-0", "page_content": "tellectual disability and of a neurocognitive disorder may both be assigned.\nAlthough intellectual disability is generally nonprogressive, in certain genetic disor-\nders (e.g., Rett syndrome) there are periods of worsening, followed by stabilization, and in", "source": "dsm5.pdf"} {"id": "09361f3ee53f-0", "page_content": "Intellectual Disability (Intellectual Developmental Disorder) 39\nothers (e.g., San Phillippo synd rome) progressive worsening of intellectual function. After\nearly childhood, the disorder is generally lifelong, although severity levels may change\nover time. The course may be influenced by underlying medical or genetic conditions and\nco-occurring conditions (e.g., hearing or visual impairments, epilepsy). Early and ongoing in-\nterventions may improve adap tive functioning throughout childhood and adulthood. In\nsome cases, these result in significant improve ment of intellectual functioning, such that\nthe diagnosis of intellectual disability is no lo nger appropriate. Thus, it is common practice\nwhen assessing infants and young children to de lay diagnosis of intellectual disability un-\ntil after an appropriate course of intervention is provided. For olde r children and adults,\nthe extent of support provided may allow for fu ll participation in all activities of daily liv-\ning and improved adaptive function. Diagnost ic assessments must determine whether im-\nproved adaptive skills are the result of a st able, generalized new skill acquisition (in which\ncase the diagnosis of intellectual disability may no longer be appropriate) or whether the\nimprovement is contingent on the presence of supports and ongoing interventions (in\nwhich case the diagnosis of intellectua l disability may still be appropriate).\nRisk and Prognostic Factors \nGenetic and physiological. Prenatal etiologies include genetic syndromes (e.g., se-\nquence variations or copy number variants involving one or more genes; chromosomal\ndisorders), inborn errors of metabolism, brai n malformations, maternal disease (including\nplacental disease), and environmental influences (e.g., alcohol, other drugs, toxins, terato-\ngens). Perinatal causes include a variety of labor and delivery-related events leading to", "source": "dsm5.pdf"} {"id": "09361f3ee53f-1", "page_content": "gens). Perinatal causes include a variety of labor and delivery-related events leading to\nneonatal encephalopathy. Postnatal causes include hypoxic ischemic injury, traumatic\nbrain injury, infections, demyelinating disorder s, seizure disorders (e .g., infantile spasms),\nsevere and chronic social deprivation, and toxic metabolic syndromes and intoxications\n(e.g., lead, mercury).\nCulture-Related Diagnostic Issues \nIntellectual disability occurs in all races and cultures. Cultural sen sitivity and knowledge\nare needed during assessment, and the individu al\u2019s ethnic, cultural, and linguistic back-\nground, available experiences, and adaptive functioning within his or her community and\ncultural setting must be taken into account.\nGender-Related Diagnostic Issues\nOverall, males are more likely than female s to be diagnosed with both mild (average\nmale:female ratio 1.6:1) and severe (average male:female ratio 1.2:1) forms of intellectual\ndisability. However, gender ratios vary widely in reported studies. Sex-linked genetic fac-\ntors and male vulnerability to brain insult ma y account for some of the gender differences.\nDiagnostic Markers\nA comprehensive evaluation includes an assess ment of intellectual capacity and adaptive\nfunctioning; identification of genetic and nongenetic etiolo gies; evaluation for associated\nmedical conditions (e.g., cerebral palsy, seiz ure disorder); and eval uation for co-occurring\nmental, emotional, and behavior al disorders. Components of the evaluation may include\nbasic pre- and perinatal medical history, three- generational family pedigree, physical exam-\nination, genetic evaluation (e.g., karyotype or chromosomal microarray analysis and testing\nfor specific genetic syndromes), and metabo lic screening and neuroimaging assessment.\nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "09361f3ee53f-2", "page_content": "Differential Diagnosis\nThe diagnosis of intellectual disability should be made whenever Criteria A, B, and C are\nmet. A diagnosis of intellectual disability should not be assumed because of a particular", "source": "dsm5.pdf"} {"id": "9cf2f32a17d0-0", "page_content": "40 Neurodevelopmental Disorders\ngenetic or medical condition. A genetic syndro me linked to intellec tual disability should\nbe noted as a concurrent diagnosi s with the intellectual disability.\nMajor and mild neurocognitive disorders. Intellectual disability is categorized as a neu-\nrodevelopmental disorder and is distinct from the neurocognitive disorders, which are\ncharacterized by a loss of cognitive function ing. Major neurocognitive disorder may co-\noccur with intellectual disability (e.g., an individual with Down syndrome who develops\nAlzheimer\u2019s disease, or an individual with intellectual disability who loses further cogni-\ntive capacity following a head injury). In such cases, the diagnoses of intellectual disability\nand neurocognitive disorder may both be given.\nCommunication disorders and specific learning disorder. These neurodevelopmental\ndisorders are specific to the communication and learning domains and do not show defi-\ncits in intellectual an d adaptive behavior. They may co-o ccur with intellectual disability.\nBoth diagnoses are made if full criteria are met for intellectual disability and a communi-\ncation disorder or specific learning disorder.\nAutism spectrum disorder. Intellectual disability is common among individuals with\nautism spectrum disorder. Assessment of intellectual ability may be complicated by so-\ncial-communication and behavior deficits inherent to auti sm spectrum disorder, which\nmay interfere with understanding and comply ing with test procedures. Appropriate as-\nsessment of intellectual functioning in autism spectrum disorder is essential, with reas-\nsessment across the developmental period, becaus e IQ scores in auti sm spectrum disorder\nmay be unstable, particularly in early childhood.\nComorbidity\nCo-occurring mental, neurodevelopmental, me dical, and physical conditions are frequent\nin intellectual disability, with rates of some conditions (e.g., ment al disorders, cerebral", "source": "dsm5.pdf"} {"id": "9cf2f32a17d0-1", "page_content": "in intellectual disability, with rates of some conditions (e.g., ment al disorders, cerebral\npalsy, and epilepsy) three to fo ur times higher than in the ge neral population. The prognosis\nand outcome of co-occurring diagnoses may be influenced by the presence of intellectual\ndisability. Assessment procedur es may require modifications because of associated disor-\nders, including communication disorders, autism spectrum disorder, and motor, sensory,\nor other disorders. Knowledgeable informan ts are essential for identifying symptoms\nsuch as irritability, mood dysregulation, aggression, eating problems, and sleep problems,\nand for assessing adaptive functioning in various community settings.\nThe most common co-occurring mental an d neurodevelopmental disorders are atten-\ntion-deficit/hyperactivity disorder; depressi ve and bipolar disorders; anxiety disorders;\nautism spectrum disorder; stereotypic movement d isorder (with or without self-injurious\nbehavior); impulse-control disorders; and ma jor neurocognitive disorder. Major depres-\nsive disorder may occur througho ut the range of severity of intellectual disability. Self-\ninjurious behavior requires pr ompt diagnostic attention and may warrant a separate di-\nagnosis of stereotypic movement disorder. Individuals with intellectual disability, partic-\nularly those with more severe intellectual disability, may also exhibit aggression and\ndisruptive behaviors, including harm of others or property destruction.\nRelationship to Ot her Classifications\nICD-11 (in development at the time of this publication) uses the term intellectual develop-\nmental disorders to indicate that these are disorders that involve impaired brain functioning\nearly in life. These disorders are described in ICD-11 as a metasyndrome occurring in the\ndevelopmental period analogous to dementia or neurocognitive disorder in later life.", "source": "dsm5.pdf"} {"id": "9cf2f32a17d0-2", "page_content": "developmental period analogous to dementia or neurocognitive disorder in later life.\nThere are four subtypes in ICD-11: mild, moderate, severe, and profound.\nThe American Association on Intellectual and Developmental Disabilities (AAIDD)\nalso uses the term intellectual disability with a similar meaning to the term as used in this", "source": "dsm5.pdf"} {"id": "814539b93e49-0", "page_content": "Global Developmental Delay 41\nmanual. The AAIDD\u2019s classification is multidimensional rather than categorical and is\nbased on the disability construc t. Rather than listing specifie rs as is done in DSM-5, the\nAAIDD emphasizes a profile of supports based on severity.\nGlobal Developmental Delay\n315.8 (F88)\nThis diagnosis is reserved for individuals under the age of 5 years when the clinical severity\nlevel cannot be reliably assessed during early childhood. This category is diagnosed when\nan individual fails to meet expected developmental milestones in several areas of intellec-\ntual functioning, and applies to individuals who are unable to undergo systematic assess-\nments of intellectual functioning, including children who are too young to participate in\nstandardized testing. This category requires reassessment after a period of time.\nUnspecified Intellectual Disability\n(Intellectual Developmental Disorder)\n319 (F79)\nThis category is rese rved for individuals over the age of 5 years when assessment of the\ndegree of intellectual disabi lity (intellectual developmental disorder) by means of locally\navailable procedures is rendered difficult or impossible because of associated sensory or\nphysical impairments, as in blindness or prel ingual deafness; locomotor disability; or pres-\nence of severe problem behaviors or co-occurring mental disorder. This category should\nonly be used in exceptional circumstances and requires reassessment after a period of time. \nCommunication Disorders\nDisorders of communication include deficits in language, speech, and communication.\nSpeech is the expressive production of sounds and includes an indivi dual\u2019s articulation,\nfluency, voice, and resonance quality. Language includes the form, fu nction, and use of a\nconventional system of symbol s (i.e., spoken words, sign language, written words, pic-", "source": "dsm5.pdf"} {"id": "814539b93e49-1", "page_content": "tures) in a rule -governed manner for communication. Communication includes any verbal\nor nonverbal behavior (whether intentional or unintentional) that influences the behavior,\nideas, or attitudes of another individual. Assessments of speech, language and communi-\ncation abilities must take into account the individual's cultural and language context,\nparticularly for individuals growing up in bilingual environments. The standardized mea-\nsures of language development and of nonverba l intellectual capacity must be relevant for\nthe cultural and linguistic group (i.e., tests developed and standardized for one group may\nnot provide appropriate norms for a different group). The diagnostic category of commu-\nnication disorders includes the following: language disorder, speech sound disorder,\nchildhood-onset fluency disord er (stuttering), social (pra gmatic) communication disor-\nder, and other specified and unspecified communica tion disorders.", "source": "dsm5.pdf"} {"id": "91e164b0f061-0", "page_content": "42 Neurodevelopmental Disorders\nLanguage Disorder\nDiagnostic Criteria 315.32 (F80.2)\nA. Persistent difficulties in the acquisition and use of language across modalities (i.e.,\nspoken, written, sign language, or other) due to deficits in comprehension or produc-\ntion that include the following:\n1. Reduced vocabulary (word knowledge and use).\n2. Limited sentence structure (ability to put words and word endings together to form\nsentences based on the rules of grammar and morphology).\n3. Impairments in discourse (ability to use vocabulary and connect sentences to ex-\nplain or describe a topic or series of events or have a conversation).\nB. Language abilities are substantially and quantifiably below those expected for age, re-\nsulting in functional limitations in effective communication, social participation, aca-\ndemic achievement, or occupational performance, individually or in any combination.\nC. Onset of symptoms is in the early developmental period.\nD. The difficulties are not attributable to hearing or other sensory impairment, motor dys-\nfunction, or another medical or neurological condition and are not better explained by in-\ntellectual disability (intellectual developmental disorder) or global developmental delay.\nDiagnostic Features\nThe core diagnostic features of language disorder are difficulties in the acquisition and use\nof language due to deficits in the comprehe nsion or production of vocabulary, sentence\nstructure, and discourse. The language defi cits are evident in spoken communication,\nwritten communication, or sign language. La nguage learning and use is dependent on\nboth receptive and expressive skills. Expressive ability refers to the production of vocal, ges-\ntural, or verbal signals, while receptive ability refers to the process of receiving and com-\nprehending language messages. Language skills need to be assessed in both expressive", "source": "dsm5.pdf"} {"id": "91e164b0f061-1", "page_content": "prehending language messages. Language skills need to be assessed in both expressive\nand receptive modalities as these may differ in severity. For example, an individual\u2019s ex-\npressive language may be seve rely impaired, while his recept ive language is hardly im-\npaired at all.\nLanguage disorder usually affects vocabulary and grammar, and these effects then\nlimit the capacity for discourse. The child\u2019s fi rst words and phrases are likely to be delayed\nin onset; vocabulary size is smaller and less varied than expected; and sentences are\nshorter and less complex with grammatical errors , especially in past tense. Deficits in com-\nprehension of language are fr equently underestimated, as children may be good at using\ncontext to infer meaning. There may be word-finding problems, impoverished verbal def-\ninitions, or poor understand ing of synonyms, multiple meanings, or word play appro-\npriate for age and culture. Problems with remembering new words and sentences are\nmanifested by difficulties following instructions of increasing length, difficulties rehears-\ning strings of verbal information (e.g., remembering a phone number or a shopping list),\nand difficulties remembering novel sound se quences, a skill that may be important for\nlearning new words. Difficulties with discour se are shown by a reduced ability to provide\nadequate information abou t the key events and to narrate a coherent story.\nThe language difficulty is manifest by abilities substantially and quantifiably below\nthat expected for age and significantly inte rfering with academic achievement, occupa-\ntional performance, effective communication, or socialization (Criterion B). A diagnosis of\nlanguage disorder is made based on the synthesis of the individual\u2019s history, direct clinical\nobservation in different contexts (i.e., home, school, or work), and scores from standard-\nized tests of language ability that can be used to guide estimates of severity.", "source": "dsm5.pdf"} {"id": "537892e08f43-0", "page_content": "Language Disorder 43\nAssociated Features Supporting Diagnosis\nA positive family history of language disorders is often present. Individuals, even chil-\ndren, can be adept at accommodating to their limited language. They may appear to be shy\nor reticent to talk. Affected individuals may prefer to communicate only with family mem-\nbers or other familiar individuals. Although these social indicators are not diagnostic of a\nlanguage disorder, if they are notable and pers istent, they warrant referral for a full lan-\nguage assessment. Language d isorder, particularly expressiv e deficits, may co-occur with\nspeech sound disorder.\nDevelopment and Course\nLanguage acquisition is marked by changes from onset in toddlerhood to the adult level of\ncompetency that appears during adolescence. Changes appear across the dimensions of\nlanguage (sounds, words, grammar, narrati ves/expository texts, and conversational\nskills) in age-graded increments and synchron ies. Language disorder emerges during the\nearly developmental period; however, there is considerable variation in early vocabulary\nacquisition and early word combinations, an d individual differenc es are not, as single\nindicators, highly predictive of later outcomes. By age 4 years, individual differences in\nlanguage ability are more stable, with bette r measurement accuracy, and are highly pre-\ndictive of later outcomes. Language disorder diagnosed from 4 years of age is likely to be\nstable over time and typically persists into adulthood, although the particular profile of\nlanguage strengths and deficits is likely to change over the course of development.\nRisk and Prognostic Factors\nChildren with receptive language impairment s have a poorer prognosis than those with\npredominantly expressive impairments. They are more resistant to treatment, and diffi-\nculties with reading comprehe nsion are frequently seen.\nGenetic and physiological. Language disorders are highly heritable, and family mem-", "source": "dsm5.pdf"} {"id": "537892e08f43-1", "page_content": "Genetic and physiological. Language disorders are highly heritable, and family mem-\nbers are more likely to have a history of language impairment.\nDifferential Diagnosis\nNormal variations in language. Language disorder needs to be distinguished from nor-\nmal developmental variations, and this distinctio n may be difficult to make before 4 years\nof age. Regional, social, or cultural/ethnic va riations of language (e.g., dialects) must be\nconsidered when an individual is being assessed for language impairment.\nHearing or other sensory impairment. Hearing impairment needs to be excluded as the\nprimary cause of language difficulties. Langua ge deficits may be associated with a hearing\nimpairment, other sensory deficit, or a speech-motor deficit. When language deficits are in\nexcess of those usually associ ated with these problems, a di agnosis of language disorder\nmay be made.\nIntellectual disability (intell ectual developmental disorder). Language delay is often the\npresenting feature of intellect ual disability, and the definitive diagnosis may not be made\nuntil the child is able to complete standard ized assessments. A separate diagnosis is not\ngiven unless the language deficits are clearl y in excess of the intellectual limitations.\nNeurological disorders. Language disorder can be acquired in association with neuro-\nlogical disorders, including epilepsy (e.g., ac quired aphasia or Landau-Kleffner syndrome).\nLanguage regression. Loss of speech and language in a child younger than 3 years may\nbe a sign of autism spectrum disorder (with developmental regression) or a specific neuro-\nlogical condition, such as Landau-Kleffner syndrome. Among children older than 3 years,\nlanguage loss may be a symptom of seizures, and a diagnostic assessment is necessary to\nexclude the presence of epilepsy (e.g., routine and sleep electroencephalogram).", "source": "dsm5.pdf"} {"id": "650a54de0eaf-0", "page_content": "44 Neurodevelopmental Disorders\nComorbidity\nLanguage disorder is strongly associated with other neurodevelopmental disorders in\nterms of specific learning d isorder (literacy and numeracy), attention-deficit/hyperactiv-\nity disorder, autism spectrum disorder, and developmental coordination disorder. It is\nalso associated with social (pragmatic) commu nication disorder. A positive family history\nof speech or language disorders is often present.\nSpeech Sound Disorder\nDiagnostic Criteria 315.39 (F80.0)\nA. Persistent difficulty with speech sound production that interferes with speech intelligi-\nbility or prevents verbal communication of messages. \nB. The disturbance causes limitations in effect ive communication that interfere with social\nparticipation, academic achievement, or occupational performance, individually or in\nany combination.\nC. Onset of symptoms is in the early developmental period.\nD. The difficulties are not attributable to congenital or acquired conditions, such as cere-\nbral palsy, cleft palate, deafness or hearing loss, traumatic brain injury, or other medi-\ncal or neurological conditions. \nDiagnostic Features \nSpeech sound production descri bes the clear articulation of the phonemes (i.e., individual\nsounds) that in combination make up spoken words. Speech sound production requires both\nthe phonological knowledge of speech sounds and the ability to coordinate the movements of\nthe articulators (i.e., the jaw, tongue, and lips ,) with breathing and vocalizing for speech. Chil-\ndren with speech production difficulties may experience difficulty with phonological knowl-\nedge of speech sounds or the ability to coordi nate movements for speech in varying degrees.\nSpeech sound disorder is thus heterogeneous in its underlying mechanisms and includes pho-\nnological disorder and articulation disorder . A speech sound disorder is diagnosed when", "source": "dsm5.pdf"} {"id": "650a54de0eaf-1", "page_content": "nological disorder and articulation disorder . A speech sound disorder is diagnosed when\nspeech sound production is not what would be expected based on the child\u2019s age and devel-\nopmental stage and when the deficits are not the result of a physical, st ructural, neurological,\nor hearing impairment. Among typically develo ping children at age 4 years, overall speech\nshould be intelligible, whereas at age 2 years, only 50% may be understandable.\nAssociated Features Supporting Diagnosis\nLanguage disorder, particularly expressive de ficits, may be found to co-occur with speech\nsound disorder. A positive family history of speech or language disorders is often present. \nIf the ability to rapidly coordinate the articu lators is a particular aspect of difficulty,\nthere may be a history of delay or incoordinati on in acquiring skills that also utilize the\narticulators and related facial musculature; among others, these sk ills include chewing,\nmaintaining mouth closure, and blowing the no se. Other areas of motor coordination may\nbe impaired as in developm ental coordination disorder. Verbal dyspraxia is a term also\nused for speech prod uction problems.\nSpeech may be differentially impaired in ce rtain genetic conditions (e.g., Down syn-\ndrome, 22q deletion, FoxP2 gene mutation). If present, these should also be coded.\nDevelopment and Course\nLearning to produce speech sounds clearly and accurately and learning to produce con-\nnected speech fluently are developmental skills. Articulation of speech sounds follows a", "source": "dsm5.pdf"} {"id": "812c4ba7956b-0", "page_content": "Childhood-Onset Fluency Disorder (Stuttering) 45\ndevelopmental pattern, which is reflected in the age norms of standardized tests. It is not\nunusual for typically developing children to use developmental processes for shortening\nwords and syllables as they are learning to talk, but their progression in mastering speech\nsound production should result in mostly in telligible speech by age 3 years. Children with\nspeech sound disorder continue to use immature phonological simplification processes\npast the age when most children can produce words clearly.\nMost speech sounds should be produced cl early and most words should be pronounced\naccurately according to age an d community norms by age 7 years. The most frequently mis-\narticulated sounds also tend to be learned later, leading them to be called the \u201clate eight\u201d ( l, r,\ns, z, th, ch, dzh, and zh). Misarticulation of an y of these sounds by it self could be considered\nwithin normal limits up to age 8 years. When multiple sounds are involved, it may be appro-\npriate to target some of those sounds as part of a plan to improve intelligibility prior to the age\nat which almost all children can produce them a ccurately. Lisping (i.e., misarticulating sibi-\nlants) is particularly common and may involve fr ontal or lateral patterns of airstream direc-\ntion. It may be associated with an ab normal tongue-thrust swallowing pattern.\nMost children with speech sound disorder re spond well to treatment, and speech dif-\nficulties improve over time, and thus the diso rder may not be lifelong. However, when a\nlanguage disorder is also present, the spee ch disorder has a poorer prognosis and may be\nassociated with specific learning disorders.\nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "812c4ba7956b-1", "page_content": "associated with specific learning disorders.\nDifferential Diagnosis\nNormal variations in speech. Regional, social, or cultural/ethnic variations of speech\nshould be considered before making the diagnosis.\nHearing or other sensory impairment. Hearing impairment or deafness may result in\nabnormalities of speech. Defici ts of speech sound production may be associated with a\nhearing impairment, other sensory deficit, or a speech-mo tor deficit. When speech deficits\nare in excess of those usually associated with these problems, a diagnosis of speech sound\ndisorder may be made.\nStructural deficits. Speech impairment may be due to stru ctural deficits (e.g., cleft palate).\nDysarthria. Speech impairment may be attributable to a motor disorder, such as cerebral\npalsy. Neurological signs, as well as distinct ive features of voice, differentiate dysarthria\nfrom speech sound disorder, although in young children (under 3 years) differentiation\nmay be difficult, particularly when there is no or minima l general body motor involve-\nment (as in, e.g., Worster-Drought syndrome).\nSelective mutism. Limited use of speech may be a sign of selective mutism, an anxiety\ndisorder that is characterized by a lack of sp eech in one or more contexts or settings. Se-\nlective mutism may develop in children with a speech disorder because of embarassment\nabout their impairments, but many children with selective mutism exhibit normal speech\nin \u201csafe\u201d settings, such as at home or with close friends. \nChildhood-Onset Fluency Disorder (Stuttering)\nDiagnostic Criteria 315.35 (F80.81)\nA. Disturbances in the normal fluency and time patterning of speech that are inappropri-\nate for the individual\u2019s age and language skills, persist over time, and are characterized", "source": "dsm5.pdf"} {"id": "812c4ba7956b-2", "page_content": "ate for the individual\u2019s age and language skills, persist over time, and are characterized\nby frequent and marked occurrences of one (or more) of the following:\u00a0\n1. Sound and syllable repetitions.\n2. Sound prolongations of consonants as well as vowels.", "source": "dsm5.pdf"} {"id": "38ab5f601a0b-0", "page_content": "46 Neurodevelopmental Disorders\n3. Broken words (e.g., pauses within a word).\n4. Audible or silent blocking (filled or unfilled pauses in speech).\n5. Circumlocutions (word substitutions to avoid problematic words).\n6. Words produced with an excess of physical tension.\n7. Monosyllabic whole-word repetitions (e.g., \u201cI-I-I-I see him\u201d).\nB. The disturbance causes anxiety about speaking or limitations in effective communica-\ntion, social participation, or academic or occupational performance, individually or in\nany combination.\nC. The onset of symptoms is in the early developmental period. ( Note: Later-onset cases\nare diagnosed as 307.0 [F98.5] adult-onset fluency disorder.)\nD. The disturbance is not attributable to a s peech-motor or sensory deficit, dysfluency as-\nsociated with neurological insult (e.g., stroke, tumor, trauma), or another medical con-\ndition and is not better explained by another mental disorder.\nDiagnostic Features\nThe essential feature of childho od-onset fluency disorder (stu ttering) is a disturbance in\nthe normal fluency and time patterning of spee ch that is inappropriate for the individual\u2019s\nage. This disturbance is characterized by freq uent repetitions or prolongations of sounds\nor syllables and by other types of speech dysfluencies, including broken words (e.g.,\npauses within a word), audible or silent blocki ng (i.e., filled or unfilled pauses in speech),\ncircumlocutions (i.e., word su bstitutions to avoid proble matic words), words produced\nwith an excess of physical tension, and mono syllabic whole-word repetitions (e.g., \u201cI-I-I-I\nsee him\u201d). The disturbance in fluency interferes with academic or occupational achieve-", "source": "dsm5.pdf"} {"id": "38ab5f601a0b-1", "page_content": "see him\u201d). The disturbance in fluency interferes with academic or occupational achieve-\nment or with social communication. The extent of the disturbance varies from situation to\nsituation and often is more severe when there is special pressure to communicate (e.g., giv-\ning a report at school, interviewing for a job) . Dysfluency is often absent during oral read-\ning, singing, or talking to inanimate objects or to pets.\nAssociated Features Supporting Diagnosis\nFearful anticipation of the problem may develop. The speaker may attempt to avoid dys-\nfluencies by linguistic mechanisms (e.g., al tering the rate of sp eech, avoiding certain\nwords or sounds) or by avoiding certain speec h situations, such as telephoning or public\nspeaking. In addition to being features of the condition, stress and anxiety have been\nshown to exacerbate dysfluency.\nChildhood-onset fluency diso rder may also be accompanied by motor movements\n(e.g., eye blinks, tics, tremors of the lips or face, jerking of the head, breathing movements,\nfist clenching). Children with fluency disorder show a range of language abilities, and the\nrelationship between fluency disorder and language abilities is unclear.\nDevelopment and Course\nChildhood-onset fluency disord er, or developmental stutteri ng, occurs by age 6 for 80%\u2013\n90% of affected individuals, with age at onset ranging from 2 to 7 years. The onset can be\ninsidious or more sudden. Typically, dysfluencies start gradually, with repetition of initial\nconsonants, first words of a phrase, or long words. The child may not be aware of dysflu-\nencies. As the disorder progresses, the dysfluencies become more frequent and interfering,", "source": "dsm5.pdf"} {"id": "38ab5f601a0b-2", "page_content": "encies. As the disorder progresses, the dysfluencies become more frequent and interfering,\noccurring on the most meaningful words or phr ases in the utterance. As the child becomes\naware of the speech difficulty, he or she may develop mechanisms for avoiding the dys-\nfluencies and emotional responses, including avoidance of public speaking and use of\nshort and simple utterances. Longitudinal research shows that 65%\u201385% of children re-", "source": "dsm5.pdf"} {"id": "e6539f7c215a-0", "page_content": "Social (Pragmatic) Communication Disorder 47\ncover from the dysfluency, with severity of fl uency disorder at age 8 years predicting re-\ncovery or persistence into adolescence and beyond.\nRisk and Prognostic Factors\nGenetic and physiological. The risk of stuttering among first-degree biological rela-\ntives of individuals wi th childhood-onset fluency disorder is more than three times the\nrisk in the general population.\nFunctional Consequences of \nChildhood-Onset Fluency Disorder (Stuttering)\nIn addition to being features of the condit ion, stress and anxiety can exacerbate dysflu-\nency. Impairment of social function ing may result from this anxiety.\nDifferential Diagnosis\nSensory deficits. Dysfluencies of speech may be associated with a hearing impairment\nor other sensory deficit or a sp eech-motor deficit. When the speech dysfluencies are in ex-\ncess of those usually associated with these problems, a diagnosis of childhood-onset flu-\nency disorder may be made.\nNormal speech dysfluencies. The disorder must be distinguished from normal dysflu-\nencies that occur frequently in young children, which include whole-word or phrase rep-\netitions (e.g., \u201cI want, I want ice cream\u201d), incomplete phrases, in terjections, unfilled\npauses, and parenthetical remarks. If these difficulties increase in frequency or complexity\nas the child grows older, a diagnosis of child hood-onset fluency diso rder is appropriate.\nMedication side effects. Stuttering may occur as a side effect of medication and may be\ndetected by a temporal relationship with exposure to the medication.\nAdult-onset dysfluencies. If onset of dysfluencies is during or after adolescence, it is an", "source": "dsm5.pdf"} {"id": "e6539f7c215a-1", "page_content": "\u201cadult-onset dysfluency\u201d rather than a neurodevelopmental disorder . Adult-onset dysflu-\nencies are associated with specific neurologic al insults and a variety of medical conditions\nand mental disorders and may be specified with them, but they are not a DSM-5 diagnosis. \nTourette\u2019s disorder. Vocal tics and repetitive vocalizations of Tourette\u2019s disorder\nshould be distinguishable from the repetitive sounds of childhood-onset fluency disorder\nby their nature and timing. \nSocial (Pragmatic) Communication Disorder\nDiagnostic Criteria 315.39 (F80.89)\nA. Persistent difficulties in the social use of verbal and nonverbal communication as man-\nifested by all of the following:\n1. Deficits in using communication for social purposes, such as greeting and sharing\ninformation, in a manner that is appropriate for the social context.\n2. Impairment of the ability to change communication to match context or the needs of\nthe listener, such as speaking differently in a classroom than on a playground, talk-\ning differently to a child than to an adul t, and avoiding use of overly formal language.\n3. Difficulties following rules for conversation and storytelling, such as taking turns in\nconversation, rephrasing when misunderstoo d, and knowing how to use verbal and\nnonverbal signals to regulate interaction.", "source": "dsm5.pdf"} {"id": "a1425b210997-0", "page_content": "48 Neurodevelopmental Disorders\n4. Difficulties understanding what is not explicitly stated (e.g., making inferences) and\nnonliteral or ambiguous meanings of language (e.g., idioms, humor, metaphors,\nmultiple meanings that depend on the context for interpretation).\nB. The deficits result in functional limitations in effective communication, social participa-\ntion, social relationships, academic achievement, or occupational performance, indi-\nvidually or in combination.\nC. The onset of the symptoms is in the ear ly developmental period (but deficits may not\nbecome fully manifest until social communication demands exceed limited capacities).\nD. The symptoms are not attributable to another medical or neurological condition or to low\nabilities in the domains of word structure and grammar, and are not better explained by\nautism spectrum disorder, intellectual dis ability (intellectual developmental disorder),\nglobal developmental delay, or another mental disorder.\nDiagnostic Features\nSocial (pragmatic) communication disorder is characterized by a primary difficulty with\npragmatics, or the social use of language an d communication, as manifested by deficits in\nunderstanding and following social rules of verbal and nonverbal communication in nat-\nuralistic contexts, changing language accordin g to the needs of the listener or situation,\nand following rules for conversations and stor ytelling. The deficits in social communica-\ntion result in functional limitations in effective communicatio n, social participation, devel-\nopment of social relationships, academic ac hievement, or occupational performance. The\ndeficits are not better explaine d by low abilities in the domains of structural language or\ncognitive ability.\nAssociated Features Supporting Diagnosis\nThe most common associated feat ure of social (pragmatic) co mmunication disorder is lan-\nguage impairment, which is characterized by a history of delay in reaching language mile-", "source": "dsm5.pdf"} {"id": "a1425b210997-1", "page_content": "guage impairment, which is characterized by a history of delay in reaching language mile-\nstones, and historical, if not current, structur al language problems (see \u201cLanguage Disorder\u201d\nearlier in this chapter). Individuals with social communication deficits may avoid social inter-\nactions. Attention-deficit/hype ractivity disorder (ADHD), beha vioral problems, and specific\nlearning disorders are also more common among affected individuals.\nDevelopment and Course \nBecause social (pragmatic) co mmunication depends on adeq uate developmental progress\nin speech and language, diagnosis of social (pragmatic) communication disorder is rare\namong children younger than 4 years. By ag e 4 or 5 years, most children should possess\nadequate speech and language abilities to permit identification of specific deficits in social\ncommunication. Milder forms of the disorder may not become apparent until early ado-\nlescence, when language and social interactions become more complex.\nThe outcome of social (pragmatic) communicat ion disorder is variable, with some chil-\ndren improving substantially over time and othe rs continuing to have difficulties persist-\ning into adulthood. Even am ong those who have significant improvements, the early\ndeficits in pragmatics may cause lasting impa irments in social relationships and behavior\nand also in acquisition of other rela ted skills, such as written expression. \nRisk and Prognostic Factors\nGenetic and physiological. A family history of autism spectrum disorder, communica-\ntion disorders, or specific learning disorder appears to increase the risk for social (prag-\nmatic) communication disorder.", "source": "dsm5.pdf"} {"id": "90809a9439fd-0", "page_content": "Unspecified Communication Disorder 49\nDifferential Diagnosis\nAutism spectrum disorder. Autism spectrum disorder is the primary diagnostic con-\nsideration for individuals presenting with social communication de ficits. The two disor-\nders can be differentiated by the presence in autism spectrum disorder of restricted/\nrepetitive patterns of behavior , interests, or activities and their absence in social (prag-\nmatic) communication disorder. Individuals wi th autism spectrum disorder may only dis-\nplay the restricted/repetitive patterns of behavi or, interests, and activities during the early\ndevelopmental period, so a co mprehensive history should be obtained. Current absence of\nsymptoms would not preclude a diagnosis of autism spectrum disorder, if the restricted\ninterests and repetitive behaviors were present in the past. A diagnosis of social (prag-\nmatic) communication disorder should be considered only if the developmental history\nfails to reveal any evidence of restricted/repetitive patterns of behavior, interests, or ac-\ntivities.\nAttention-deficit/hyperactivity disorder. Primary deficits of AD HD may cause impair-\nments in social communication and functional limitations of effectiv e communication, so-\ncial participation, or academic achievement.\nSocial anxiety disorder (social phobia). The symptoms of social communication disor-\nder overlap with those of social anxiety diso rder. The differentiating feature is the timing\nof the onset of symptoms. In social (pragm atic) communication di sorder, the individual\nhas never had effective social communication; in social anxiety disorder, the social com-\nmunication skills developed appr opriately but are not utilized because of anxiety, fear, or\ndistress about social interactions.\nIntellectual disability (intellectual developm ental disorder) and global developmental\ndelay. Social communication skills may be deficient among individuals with global de-", "source": "dsm5.pdf"} {"id": "90809a9439fd-1", "page_content": "delay. Social communication skills may be deficient among individuals with global de-\nvelopmental delay or in tellectual disability, but a separa te diagnosis is not given unless\nthe social communication deficits are clearl y in excess of the intellectual limitations.\nUnspecified Communication Disorder\n307.9 (F80.9)\nThis category applies to presentations in which symptoms characteristic of communication\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of func tioning predominate but do not meet the full criteria for com-\nmunication disorder or for any of the disorders in the neurodevelopmental disorders diag-\nnostic class. The unspecified communication disorder category is used in situations in\nwhich the clinician chooses not to specify the reason that the criteria are not met for com-\nmunication disorder or for a specific neurodevelopmental disorder, and includes presen-\ntations in which there is insufficient information to make a more specific diagnosis.", "source": "dsm5.pdf"} {"id": "928b7e631f71-0", "page_content": "50 Neurodevelopmental Disorders\nAutism Spectrum Disorder\nAutism Spectrum Disorder\nDiagnostic Criteria 299.00 (F84.0)\nA. Persistent deficits in social communication and social interaction across multiple con-\ntexts, as manifested by the following, currently or by history (examples are illustrative,\nnot exhaustive; see text):\n1. Deficits in social-emotional reciprocit y, ranging, for example, from abnormal social\napproach and failure of normal back-and-fort h conversation; to reduced sharing of\ninterests, emotions, or affect; to failure to initiate or respond to social interactions.\n2. Deficits in nonverbal communicative behavi ors used for social interaction, ranging,\nfor example, from poorly integrated ver bal and nonverbal communication; to abnor-\nmalities in eye contact and body language or deficits in understanding and use of\ngestures; to a total lack of facial expressions and nonverbal communication.\n3. Deficits in developing, maintaining, and understanding relationships, ranging, for ex-\nample, from difficulties adjusting behavior to suit various social contexts; to difficulties\nin sharing imaginative play or in making friends; to absence of interest in peers.\nSpecify current severity:\nSeverity is based on social communicat ion impairments and restricted, re-\npetitive patterns of behavior (seeTable 2).\nB. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at\nleast two of the following, currently or by history (examples are illustrative, not exhaus-\ntive; see text):\n1. Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple\nmotor stereotypies, lining up toys or flipping objects, echolalia, idiosyncratic\nphrases).", "source": "dsm5.pdf"} {"id": "928b7e631f71-1", "page_content": "phrases).\n2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns of\nverbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties\nwith transitions, rigid thinking patterns, greeting rituals, need to take same route or\neat same food every day).\n3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g.,\nstrong attachment to or preoccupation with unusual objects, excessively circum-\nscribed or perseverative interests).\n4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of\nthe environment (e.g., apparent indifference to pain/temperature, adverse re-\nsponse to specific sounds or textures, excessive smelling or touching of objects,\nvisual fascination with lights or movement).\nSpecify current severity:\nSeverity is based on social communicat ion impairments and restricted, re-\npetitive patterns of behavior (see Table 2).\nC. Symptoms must be present in the early developmental period (but may not become\nfully manifest until social demands exceed limited capacities, or may be masked by\nlearned strategies in later life). \nD. Symptoms cause clinically significant impai rment in social, occupat ional, or other im-\nportant areas of current functioning.", "source": "dsm5.pdf"} {"id": "df070b821d57-0", "page_content": "Autism Spectrum Disorder 51\nE. These disturbances are not better explained by intellectual disability (intellectual devel-\nopmental disorder) or global developmental delay. Intellectual disability and autism\nspectrum disorder frequently co-occur; to make comorbid diagnoses of autism spec-\ntrum disorder and intellectual disability, social communication should be below that ex-\npected for general developmental level.\nNote: Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger\u2019s\ndisorder, or pervasive developmental disorder not otherwise specified should be given the\ndiagnosis of autism spectrum disorder. Individuals who have marked deficits in social\ncommunication, but whose symptoms do not ot herwise meet criteria for autism spectrum\ndisorder, should be evaluated for social (pragmatic) communication disorder.\nSpecify if:\nWith or without accompanying intellectual impairment\nWith or without accompan ying language impairment\nAssociated with a known medical or gene tic condition or en vironmental factor\n(Coding note: Use additional code to identify the associated medical or genetic condition.)\nAssociated with another neurodevelopmen tal, mental, or behavioral disorder\n(Coding note: Use additional code[s] to identify the associated neurodevelopmental,\nmental, or behavioral disorder[s].)\nWith catatonia (refer to the criteria for catatonia associated with another mental dis-\norder, pp. 119\u2013120, for definition) ( Coding note: Use additional code 293.89 [F06.1]\ncatatonia associated with autism spectrum disorder to indicate the presence of the co-\nmorbid catatonia.)\nRecording Procedures\nFor autism spectrum disorder th at is associated with a known medical or genetic condition\nor environmental factor, or with another ne urodevelopmental, mental , or behavioral dis-\norder, record autism spectrum disorder associated with (name of condition, disorder, or", "source": "dsm5.pdf"} {"id": "df070b821d57-1", "page_content": "order, record autism spectrum disorder associated with (name of condition, disorder, or\nfactor) (e.g., autism spectrum disorder associated with Rett syndrome). Severity should be\nrecorded as level of support needed for ea ch of the two psychopa thological domains in\nTable 2 (e.g., \u201crequiring very substantial support for deficits in social communication and\nrequiring substantial support fo r restricted, repetitive behaviors\u201d). Specification of \u201cwith\naccompanying intellectual impairment\u201d or \u201cwithout accompanying intellectual impair-\nment\u201d should be recorded next. Language im pairment specification should be recorded\nthereafter. If there is accompan ying language impairment, the current level of verbal func-\ntioning should be recorded (e.g., \u201cwith accompanying language impairment\u2014no intelligi-\nble speech\u201d or \u201cwith accompanying language impairment\u2014phrase speech\u201d). If catatonia is\npresent, record separately \u201ccatatonia asso ciated with autism spectrum disorder.\u201d\nSpecifiers\nThe severity specifiers (see Table 2) may be used to describe succinctly the current symp-\ntomatology (which might fall below level 1), with the recognition that severity may vary by\ncontext and fluctuate over time. Severity of social communication difficulties and re-\nstricted, repetitive behaviors sh ould be separately rated. The descriptive severity categories\nshould not be used to determine eligibility fo r and provision of services; these can only be\ndeveloped at an individual level and through di scussion of personal priorities and targets.\nRegarding the specifier \u201cwith or without ac companying intellectual impairment,\u201d un-\nderstanding the (often uneven) intellectual prof ile of a child or adult with autism spectrum\ndisorder is necessary for interpre ting diagnostic features. Separate estimates of verbal and\nnonverbal skill are necessary (e.g., using untimed nonverbal tests to assess potential\nstrengths in individuals with limited language).", "source": "dsm5.pdf"} {"id": "f121b3329c0e-0", "page_content": "52 Neurodevelopmental DisordersTABLE 2 Severity levels for autism spectrum disorder\nSeverity level Social communication Restricted, repetitive behaviors\nLevel 3 \n\u201cRequiring very substantial support\u201dSevere deficits in verbal and nonverbal social com-\nmunication skills cause severe impairments in func-\ntioning, very limited initiation of social \ninteractions, and minimal response to social over-\ntures from others. For example, a person with few \nwords of intelligible speech who rarely initiates \ninteraction and, when he or she does, makes \nunusual approaches to meet needs only and \nresponds to only very direct social approaches.Inflexibility of behavior, extreme difficulty coping \nwith change, or other restricted/repetitive behav-\niors markedly interfere with functioning in all \nspheres. Great distress/difficulty changing focus \nor action.\nLevel 2\n\u201cRequiring substantial support\u201dMarked deficits in verbal and nonverbal social com-\nmunication skills; social impairments apparent \neven with supports in place; limited initiation of \nsocial interactions; an d reduced or abnormal \nresponses to social overtures from others. For \nexample, a person who sp eaks simple sentences, \nwhose interaction is limited to narrow special inter-\nests, and who has markedly odd nonverbal com-\nmunication.Inflexibility of behavior , difficulty coping with \nchange, or other restricted/repetitive behaviors \nappear frequently enough to be obvious to the \ncasual observer and inte rfere with functioning \nin a variety of contexts. Distress and/or difficulty \nchanging focus or action.\nLevel 1 \n\u201cRequiring support\u201dWithout supports in place, deficits in social communi-\ncation cause noticeable impairments.\nDifficulty initiating social interactions, and clear \nexamples of atypical or unsuccessful responses to", "source": "dsm5.pdf"} {"id": "f121b3329c0e-1", "page_content": "Difficulty initiating social interactions, and clear \nexamples of atypical or unsuccessful responses to \nsocial overtures of others. May appear to have \ndecreased interest in social interactions. For example, \na person who is able to speak in full sentences and \nengages in communication but whose to-and-fro con-\nversation with others fails, and whose attempts to \nmake friends are odd and typically unsuccessful.Inflexibility of behavior causes significant interfer-\nence with functioning in one or more contexts. Dif-\nficulty switching between activities. Problems of \norganization and planning hamper independence.", "source": "dsm5.pdf"} {"id": "8d590ac5f292-0", "page_content": "Autism Spectrum Disorder 53\nTo use the specifier \u201cwith or without acco mpanying language impairment,\u201d the cur-\nrent level of verbal functioning should be ass essed and described. Ex amples of the specific\ndescriptions for \u201cwith accompanying language impairment\u201d might include no intelligible\nspeech (nonverbal), single words only, or phrase speech. Language level in individuals\n\u201cwithout accompanying language impairment\u201d might be further described by speaks in\nfull sentences or has fluent speech. Since receptive language may lag behind expressive\nlanguage development in autism spectrum disorder, receptive and expressive language\nskills should be considered separately.\nThe specifier \u201cassociated with a known medica l or genetic condition or environmental fac-\ntor\u201d should be used when the individual has a known genetic disorder (e.g., Rett syndrome,\nFragile X syndrome, Down syndrome), a medical disorder (e.g. epilepsy), or a history of envi-\nronmental exposure (e.g., valproate, fetal alcohol syndrome, very low birth weight).\nAdditional neurodevelopmental, mental or be havioral conditions should also be noted\n(e.g., attention-deficit/hypera ctivity disorder; developmenta l coordination disorder; dis-\nruptive behavior, impulse-control, or conduct disorders; anxiety, depressive, or bipolar\ndisorders; tics or Tourette\u2019s disorder; self-inj ury; feeding, eliminatio n, or sleep disorders).\nDiagnostic Features\nThe essential features of autism spectrum diso rder are persistent impairment in reciprocal\nsocial communication and social interaction (Criterion A), and restricted, repetitive pat-\nterns of behavior, interests, or activities (Criterion B). These symptoms are present from\nearly childhood and limit or impair everyday functioning (Criteria C and D). The stage at\nwhich functional impairment becomes obvious will vary according to characteristics of", "source": "dsm5.pdf"} {"id": "8d590ac5f292-1", "page_content": "which functional impairment becomes obvious will vary according to characteristics of\nthe individual and his or her environment. Co re diagnostic features are evident in the\ndevelopmental period, but intervention, co mpensation, and current supports may mask\ndifficulties in at least some contexts. Manifestations of the disorder also vary greatly de-\npending on the severity of the autistic condit ion, developmental level, and chronological age;\nhence, the term spectrum. Autism spectrum disorder enco mpasses disorders previously re-\nferred to as early infantile autism, childhood autism, Ka nner\u2019s autism, high-functioning\nautism, atypical autism, pervasive developmen tal disorder not otherw ise specified, child-\nhood disintegrative disorder , and Asperger\u2019s disorder.\nThe impairments in communicat ion and social interaction specified in Criterion A are\npervasive and sustained. Diagnoses are most valid and reliable when based on multiple\nsources of information, including clinician\u2019s observations, caregiver history, and, when\npossible, self-report. Verbal and nonverbal deficits in social communication have varying\nmanifestations, depending on the individual\u2019s age, intellectual level, and language ability,\nas well as other factors such as treatment history and current support. Many individuals\nhave language deficits, ranging from complete lack of speech through language delays,\npoor comprehension of speech, echoed speech, or stilted and overly literal language. Even\nwhen formal language skills (e.g ., vocabulary, grammar) are intact, the use of language for\nreciprocal social communication is im paired in autism spectrum disorder.\nDeficits in social-emotional reciprocity (i.e., the ability to engage with others and share\nthoughts and feelings) are cl early evident in young children with the disorder, who may\nshow little or no initiation of social interaction and no sharing of emotions, along with re-", "source": "dsm5.pdf"} {"id": "8d590ac5f292-2", "page_content": "show little or no initiation of social interaction and no sharing of emotions, along with re-\nduced or absent imitation of others\u2019 behavior . What language exists is often one-sided,\nlacking in social reciprocity, and used to re quest or label rather th an to comment, share\nfeelings, or converse. In adults without inte llectual disabilities or language delays, deficits", "source": "dsm5.pdf"} {"id": "329e12926e8c-0", "page_content": "lacking in social reciprocity, and used to re quest or label rather th an to comment, share\nfeelings, or converse. In adults without inte llectual disabilities or language delays, deficits\nin social-emotional reciprocity may be most apparent in difficulties processing and re-\nsponding to complex social cues (e.g., when and how to join a conversation, what not to\nsay). Adults who have developed compensation strategies for some social challenges still\nstruggle in novel or un supported situations and suffer fr om the effort and anxiety of con-\nsciously calculating what is social ly intuitive for most individuals.", "source": "dsm5.pdf"} {"id": "a1e421104243-0", "page_content": "54 Neurodevelopmental Disorders\nDeficits in nonverbal communicative behavi ors used for social interaction are mani-\nfested by absent, reduced, or atypical use of eye contact (relative to cultural norms), ges-\ntures, facial expressions, body orientation, or speech intona tion. An early feature of autism\nspectrum disorder is impaired joint attention as manifested by a lack of pointing, showing,\nor bringing objects to share interest with others, or failure to follow someone\u2019s pointing or\neye gaze. Individuals may learn a few functional gestures, but their re pertoire is smaller\nthan that of others, and they often fail to use expressive gestures spontaneously in com-\nmunication. Among adults with fluent language, the difficulty in coordinating nonverbal\ncommunication with speech may give the impr ession of odd, wooden, or exaggerated\n\u201cbody language\u201d during interactions. Impairme nt may be relatively subtle within indi-\nvidual modes (e.g., someone may have relati vely good eye contact when speaking) but\nnoticeable in poor integration of eye contact, gesture, body posture, prosody, and facial ex-\npression for social communication.\nDeficits in developing, maintaining, an d understanding relationships should be\njudged against norms for age, gender, and culture. There may be absent, reduced, or atyp-\nical social interest, manifested by rejectio n of others, passivity, or inappropriate ap-\nproaches that seem aggressive or disruptive . These difficulties are particularly evident in\nyoung children, in whom there is often a lack of shared social play and imagination (e.g.,\nage-appropriate flexible pretend play) and, late r, insistence on playing by very fixed rules.\nOlder individuals may struggle to understand what behavior is considered appropriate in", "source": "dsm5.pdf"} {"id": "a1e421104243-1", "page_content": "Older individuals may struggle to understand what behavior is considered appropriate in\none situation but not another (e.g., casual beha vior during a job interview), or the different\nways that language may be used to communic ate (e.g., irony, white lies). There may be an\napparent preference for solitary activities or for interacting with much younger or older\npeople. Frequently, there is a de sire to establish friendships wi thout a complete or realistic\nidea of what friendship entails (e.g., one-sid ed friendships or friendships based solely on\nshared special interests). Relationships with siblings, co-workers, and caregivers are also\nimportant to consider (i n terms of reciprocity).\nAutism spectrum disorder is also defined by restricted, repetitive patterns of behavior,\ninterests, or activities (as specified in Criterion B), which show a range of manifestations\naccording to age and ability, intervention, and current supports. Stereotyped or repetitive\nbehaviors include simple motor stereotypies (e.g., hand flappi ng, finger flicking), repeti-\ntive use of objects (e.g., spinning coins, linin g up toys), and repetitive speech (e.g., echola-\nlia, the delayed or immediate parroting of heard words; use of \u201cyou\u201d when referring to\nself; stereotyped use of words, phrases, or pr osodic patterns). Exce ssive adherence to rou-\ntines and restricted patterns of behavior may be manifest in resistance to change (e.g., dis-\ntress at apparently small changes, such as in packaging of a favorite food; insistence on\nadherence to rules; rigidity of thinking) or ri tualized patterns of ve rbal or nonverbal be-\nhavior (e.g., repetitive questioning, pacing a perimeter). Highly restricted, fixated interests", "source": "dsm5.pdf"} {"id": "a1e421104243-2", "page_content": "havior (e.g., repetitive questioning, pacing a perimeter). Highly restricted, fixated interests\nin autism spectrum disorder tend to be ab normal in intensity or focus (e.g., a toddler\nstrongly attached to a pan; a child preoccupied with vacuum cleaners; an adult spending\nhours writing out timetables). Some fascinations and routines may relate to apparent hy-\nper- or hyporeactivity to sensory input, ma nifested through extreme responses to specific\nsounds or textures, excessive smelling or touc hing of objects, fascination with lights or\nspinning objects, and sometimes apparent indi fference to pain, heat, or cold. Extreme re-", "source": "dsm5.pdf"} {"id": "b59290269ad9-0", "page_content": "sounds or textures, excessive smelling or touc hing of objects, fascination with lights or\nspinning objects, and sometimes apparent indi fference to pain, heat, or cold. Extreme re-\naction to or rituals involving taste, smell, te xture, or appearance of food or excessive food\nrestrictions are common and ma y be a presenting feature of autism spectrum disorder.\nMany adults with autism spectrum disord er without intellectual or language disabili-\nties learn to suppress repetitive behavior in public . Specia l interests may be a source of\npleasure and motivation and provide avenues for education and employment later in life.\nDiagnostic criteria may be met when restricted, repetitive patterns of behavior, interests,\nor activities were clearly pres ent during childhood or at some time in the past, even if\nsymptoms are no longer present.", "source": "dsm5.pdf"} {"id": "8b0480b516e7-0", "page_content": "Autism Spectrum Disorder 55\nCriterion D requires that the features must ca use clinically significant impairment in so-\ncial, occupational, or other impo rtant areas of current function ing. Criterion E specifies that\nthe social communication defici ts, although sometime s accompanied by intellectual disabil-\nity (intellectual developmental disorder), are not in line with the individual\u2019s developmental\nlevel; impairments exceed difficulties expected on the basis of developmental level.\nStandardized behavioral diagnostic instruments with good psychometric properties,\nincluding caregiver interviews, questionnair es and clinician observation measures, are\navailable and can improve re liability of diagnosis over time and across clinicians.\nAssociated Features Supporting Diagnosis\nMany individuals with autism spectrum disorder also have intellectual impairment and/or\nlanguage impairment (e.g., slow to talk, language comprehension behind production). Even\nthose with average or high inte lligence have an uneven profil e of abilities. The gap between\nintellectual and adaptive function al skills is often large. Moto r deficits are often present, in-\ncluding odd gait, clumsiness, and other abnormal motor signs (e.g., walk ing on tiptoes). Self-\ninjury (e.g., head banging, biting the wris t) may occur, and disr uptive/challenging behav-\niors are more common in children and adoles cents with autism spectrum disorder than\nother disorders, including intellectual disabili ty. Adolescents and adults with autism spec-\ntrum disorder are prone to anxiety and depres sion. Some individuals develop catatonic-like\nmotor behavior (slowing and \u201cf reezing\u201d mid-action), but thes e are typically not of the mag-\nnitude of a catatonic episode. However, it is possible for individuals with autism spectrum\ndisorder to experience a marked deterioratio n in motor symptoms an d display a full cata-", "source": "dsm5.pdf"} {"id": "8b0480b516e7-1", "page_content": "disorder to experience a marked deterioratio n in motor symptoms an d display a full cata-\ntonic episode with symptoms such as mutism, posturing, grimacing and waxy flexibility.\nThe risk period for comorbid catatonia appears to be greate st in the adolescent years.\nPrevalence \nIn recent years, reported frequencies for au tism spectrum disorder across U.S. and non-\nU.S. countries have approached 1% of the po pulation, with similar estimates in child and\nadult samples. It remains unclear whether high er rates reflect an expansion of the diag-\nnostic criteria of DSM-IV to include subthreshold cases, increased awareness, differences\nin study methodology, or a true increase in the frequency of autism spectrum disorder.\nDevelopment and Course\nThe age and pattern of onset also should be noted for autism spectr um disorder. Symptoms\nare typically recognized during th e second year of life (12\u201324 months of age) but may be seen\nearlier than 12 months if developmental delays are severe, or noted later than 24 months if\nsymptoms are more subtle. The pattern of onset description might include information\nabout early developmental delays or any losses of social or language skills. In cases where\nskills have been lost, parents or caregivers may give a history of a gradual or relatively\nrapid deterioration in social behaviors or lang uage skills. Typically, this would occur be-\ntween 12 and 24 months of age and is distinguished from the rare instances of developmen-\ntal regression occurring after at least 2 years of normal development (previously described\nas childhood disintegrative disorder).\nThe behavioral features of autism spectrum disorder first become evident in early\nchildhood, with some cases presenting a lack of interest in social interaction in the first\nyear of life. Some children with autism spectrum disorder experience developmental pla-", "source": "dsm5.pdf"} {"id": "8b0480b516e7-2", "page_content": "year of life. Some children with autism spectrum disorder experience developmental pla-\nteaus or regression, with a gradual or relatively rapid deterioration in social behaviors or\nuse of language, often du ring the first 2 years of life. Such losses are rare in other disor-\nders and may be a useful \u201cred flag\u201d for autism spectrum disorder. Much more unusual", "source": "dsm5.pdf"} {"id": "f8af85d6bd33-0", "page_content": "use of language, often du ring the first 2 years of life. Such losses are rare in other disor-\nders and may be a useful \u201cred flag\u201d for autism spectrum disorder. Much more unusual\nand warranting more extensive medical invest igation are losses of skills beyond social\ncommunication (e.g., loss of se lf-care, toileting, motor skills) or those occurring after the", "source": "dsm5.pdf"} {"id": "418b5d8cdfe6-0", "page_content": "56 Neurodevelopmental Disorders\nsecond birthday (see also Rett syndrome in the section \u201cDifferential Diagnosis\u201d for this\ndisorder).\nFirst symptoms of autism spectrum disorder frequently involve delayed language de-\nvelopment, often accompanied by lack of social interest or unusual social interactions (e.g.,\npulling individuals by the hand without any a ttempt to look at them ), odd play patterns\n(e.g., carrying toys around but never pl aying with them), and unusual communication\npatterns (e.g., knowing the alphabet but not responding to own name). Deafness may be\nsuspected but is typically ruled out. During the second year, odd and repetitive behaviors\nand the absence of typical play become more apparent. Since many typically developing\nyoung children have strong preferences and en joy repetition (e.g., eating the same foods,\nwatching the same vide o multiple times), dist inguishing restricted and repetitive behav-\niors that are diagnostic of autism spectrum disorder can be difficult in preschoolers. The\nclinical distinction is based on the type, freq uency, and intensity of the behavior (e.g., a\nchild who daily lines up objects for hours an d is very distressed if any item is moved).\nAutism spectrum disorder is not a degenera tive disorder, and it is typical for learning\nand compensation to continue throughout life. Symptoms are often most marked in early\nchildhood and early school years, with deve lopmental gains typical in later childhood in\nat least some areas (e.g., increa sed interest in social interact ion). A small proportion of in-\ndividuals deteriorate behaviorally during adolescence, whereas most others improve.\nOnly a minority of individuals with autism spectrum disorder live and work indepen-\ndently in adulthood; those who do tend to have superior lang uage and intellectual abilities", "source": "dsm5.pdf"} {"id": "418b5d8cdfe6-1", "page_content": "dently in adulthood; those who do tend to have superior lang uage and intellectual abilities\nand are able to find a niche that matches thei r special interests and skills. In general, indi-\nviduals with lower levels of impairment may be better able to function independently.\nHowever, even these individuals may remain socially naive and vulnerable, have difficul-\nties organizing practical dema nds without aid, and are pron e to anxiety and depression.\nMany adults report using compensation strate gies and coping mechanisms to mask their\ndifficulties in public but suffer from the stress and effort of maintaining a socially accept-\nable facade. Scarcely anything is known ab out old age in autism spectrum disorder.\nSome individuals come for first diagnosis in adulthood, perhaps prompted by the diagno-\nsis of autism in a child in the family or a breakdown of relations at work or home. Obtaining de-\ntailed developmental history in such cases may be difficult, and it is important to consider self-\nreported difficulties. Where clinical observat ion suggests criteria are currently met, autism\nspectrum disorder may be diagno sed, provided there is no evidence of good social and com-\nmunication skills in childhood. For example, the re port (by parents or another relative) that the\nindividual had ordinary and sustained recipr ocal friendships and good nonverbal communi-\ncation skills throughout childhood would rule out a diagnosis of autism spectrum disorder;\nhowever, the absence of de velopmental information in itself should not do so.\nManifestations of the social and communication impairments and restricted/repeti-\ntive behaviors that define autism spectrum d isorder are clear in th e developmental period.\nIn later life, intervention or compensation, as well as current supports, may mask these dif-", "source": "dsm5.pdf"} {"id": "418b5d8cdfe6-2", "page_content": "In later life, intervention or compensation, as well as current supports, may mask these dif-\nficulties in at least some co ntexts. However, symptoms remain sufficient to cause current\nimpairment in social, occupational, or other important areas of functioning.\nRisk and Prognostic Factors\nThe best established prognostic factors for individual outcome wi thin autism spectrum\ndisorder are presence or absence of associa ted intellectual disability and language impair-", "source": "dsm5.pdf"} {"id": "9929c43392f3-0", "page_content": "The best established prognostic factors for individual outcome wi thin autism spectrum\ndisorder are presence or absence of associa ted intellectual disability and language impair-\nment (e.g., functional language by age 5 years is a good prognostic sign) and additional\nmental health problems. Epilepsy, as a comorb id diagnosis, is associated with greater in-\ntellectual disability and lower verbal ability.\nEnvironmental. A variety of nonspecific risk factors, such as advanced parental age, low\nbirth weight, or fetal exposure to valproate, may contribute to risk of autism spectrum dis-\norder.", "source": "dsm5.pdf"} {"id": "6db2b248ec56-0", "page_content": "Autism Spectrum Disorder 57\nGenetic and physiological. Heritability estimates for au tism spectrum disorder have\nranged from 37% to higher than 90%, based on twin concordance rates. Currently, as many\nas 15% of cases of autism spec trum disorder appear to be associated with a known genetic\nmutation, with different de novo copy number variants or de novo mutations in specific\ngenes associated with the disorder in differ ent families. However, even when an autism\nspectrum disorder is associated with a know n genetic mutation, it does not appear to be\nfully penetrant. Risk for the remainder of case s appears to be polygenic, with perhaps hun-\ndreds of genetic loci making relatively small contributions.\nCulture-Related Diagnostic Issues \nCultural differences will exist in norms for social interaction, no nverbal communication,\nand relationships, but individuals with auti sm spectrum disorder are markedly impaired\nagainst the norms for their cultural context. Cultural and socioeconomic factors may affect\nage at recognition or diagnosis; for example, in the United Stat es, late or underdiagnosis of\nautism spectrum disorder among Af rican American children may occur.\nGender-Related Diagnostic Issues\nAutism spectrum disorder is di agnosed four times more often in males than in females. In\nclinic samples, females tend to be more li kely to show accompanying intellectual disabil-\nity, suggesting that girls without accompan ying intellectual impairments or language\ndelays may go unrecognized, perhaps because of subtler manifestatio n of social and com-\nmunication difficulties.\nFunctional Consequences of Autism Spectrum Disorder\nIn young children with autism spectrum diso rder, lack of social and communication abil-\nities may hamper learning, especially learning through social interaction or in settings", "source": "dsm5.pdf"} {"id": "6db2b248ec56-1", "page_content": "ities may hamper learning, especially learning through social interaction or in settings\nwith peers. In the home, insistence on rout ines and aversion to change, as well as sensory\nsensitivities, may interfere with eating and sleeping and make routine care (e.g., haircuts,\ndental work) extremely difficult. Adaptive skills are typically below measured IQ. Ex-\ntreme difficulties in planning, organization , and coping with change negatively impact\nacademic achievement, even fo r students with above-average intelligence. During adult-\nhood, these indivi duals may have difficulties establishing independence because of con-\ntinued rigidity and difficulty with novelty.\nMany individuals with autism spectrum d isorder, even without intellectual disability,\nhave poor adult psychosocial functioning as indexed by measures such as independent\nliving and gainful employment. Functional cons equences in old age are unknown, but so-\ncial isolation and communication problems (e .g., reduced help-seeking) are likely to have\nconsequences for health in older adulthood.\nDifferential Diagnosis \nRett syndrome. Disruption of social interaction ma y be observed during the regressive\nphase of Rett syndrome (typic ally between 1\u20134 years of age); thus, a substantial proportion\nof affected young girls may ha ve a presentation that meets diagnostic criteria for autism\nspectrum disorder. Howe ver, after this period, most individuals with Rett syndrome im-\nprove their social communication skills, and auti stic features are no longer a major area of\nconcern. Consequently, autism spectrum disorder should be considered only when all di-\nagnostic criteria are met.\nSelective mutism. In selective mutism, early develo pment is not typically disturbed.\nThe affected child usually exhibits appropriate communication skills in certain contexts\nand settings. Even in settings where the child is mute, social reciprocity is not impaired,", "source": "dsm5.pdf"} {"id": "6db2b248ec56-2", "page_content": "and settings. Even in settings where the child is mute, social reciprocity is not impaired,\nnor are restricted or repetitive patterns of behavior present.", "source": "dsm5.pdf"} {"id": "f337bcf2678c-0", "page_content": "58 Neurodevelopmental Disorders\nLanguage disorders and social (p ragmatic) communi cation disorder. In some forms\nof language disorder, there may be problems of communication an d some secondary so-\ncial difficulties. However, specific language disorder is not usually associated with abnor-\nmal nonverbal communication, no r with the presence of restricted, repetitive patterns of\nbehavior, interests, or activities.\nWhen an individual shows impairment in social communication and social interactions\nbut does not show restricted and repetitive beha vior or interests, criteria for social (prag-\nmatic) communication disorder, instead of autism spectrum disorder, may be met. The di-\nagnosis of autism spectrum disorder supersedes that of so cial (pragmatic) communication\ndisorder whenever the criteria for autism spectrum disorder are met, and care should be\ntaken to enquire carefully regarding past or current restricted/repetitive behavior.\nIntellectual disability (intellectual developmental disorder) wit hout autism spectrum\ndisorder. Intellectual disability without autism spectrum disorder may be difficult to\ndifferentiate from autism spectrum disorder in very young children. Individuals with in-\ntellectual disability who have not developed language or symbolic skills also present a\nchallenge for differential diagnos is, since repetitive behavior often occurs in such individ-\nuals as well. A diagnosis of autism spectrum disorder in an indivi dual with intellectual\ndisability is appropriate when social communi cation and interaction are significantly im-\npaired relative to the developmental level of the individual\u2019s nonverbal skills (e.g., fine\nmotor skills, nonverbal problem solving). In cont rast, intellectual disability is the appropri-\nate diagnosis when there is no apparent di screpancy between the le vel of social-commu-\nnicative skills and other intellectual skills.\nStereotypic movement disorder. Motor stereotypies are among the diagnostic charac-", "source": "dsm5.pdf"} {"id": "f337bcf2678c-1", "page_content": "Stereotypic movement disorder. Motor stereotypies are among the diagnostic charac-\nteristics of autism spectrum disorder, so an additional diagnosis of stereotypic movement\ndisorder is not given when such repetitive be haviors are better explained by the presence\nof autism spectrum disorder. However, when stereotypies cause self-injury and become a\nfocus of treatment, both diagnoses may be appropriate.\nAttention-deficit/hyperactivity disorder. Abnormalities of attention (overly focused or\neasily distracted) are common in individuals with autism spectrum disorder, as is hy-\nperactivity. A diagnosi s of attention-deficit/hyperactivity disord er (ADHD) should be\nconsidered when attentional difficulties or hyperactivity exceeds that typically seen in in-\ndividuals of comparable mental age.\nSchizophrenia. Schizophrenia with childhood onset usually develops after a period of\nnormal, or near normal, development. A prod romal state has been described in which so-\ncial impairment and atypical interests and belie fs occur, which could be confused with the\nsocial deficits seen in autism spectrum d isorder. Hallucinations and delusions, which are\ndefining features of schizophrenia, are not features of autism spectrum disorder. How-\never, clinicians must take into account the potential for individual s with autism spectrum\ndisorder to be concrete in their interpretati on of questions regarding the key features of\nschizophrenia (e.g., \u201cDo you he ar voices when no one is th ere?\u201d \u201dYes [on the radio]\u201d).\nComorbidity\nAutism spectrum disorder is frequently assoc iated with intellectual impairment and struc-\ntural language disorder (i.e., an inability to comprehend and construc t sentences with proper\ngrammar), which should be noted under the relevant specifiers when applicable. Many in-", "source": "dsm5.pdf"} {"id": "f337bcf2678c-2", "page_content": "grammar), which should be noted under the relevant specifiers when applicable. Many in-\ndividuals with autism spectrum disorder have psychiatric sympto ms that do not form part of\nthe diagnostic criteria for the disorder (about 70% of individuals with autism spectrum dis-\norder may have one comorbid mental disord er, and 40% may have two or more comorbid", "source": "dsm5.pdf"} {"id": "e46025fc34c8-0", "page_content": "the diagnostic criteria for the disorder (about 70% of individuals with autism spectrum dis-\norder may have one comorbid mental disord er, and 40% may have two or more comorbid\nmental disorders). When criteria for both ADHD and autism spectrum disorder are met, both\ndiagnoses should be given. This same principle applies to concurrent diagnoses of autism\nspectrum disorder and developmental coordina tion disorder, anxiety disorders, depressive", "source": "dsm5.pdf"} {"id": "cfc653ac8a63-0", "page_content": "Attention-Deficit/Hyperactivity Disorder 59\ndisorders, and other comorbid diagnoses. Among individuals who are nonverbal or have\nlanguage deficits, observable si gns such as changes in sleep or eating and increases in chal-\nlenging behavior should trigger an evaluation fo r anxiety or depression. Specific learning dif-\nficulties (literacy and numeracy ) are common, as is developm ental coordination disorder.\nMedical conditions commonly associated with autism spectrum disorder should be noted\nunder the \u201cassociated with a known medical/ge netic or environmental/acquired condition\u201d\nspecifier. Such medical conditions include epilepsy, sleep proble ms, and constipation.\nAvoidant-restrictive food intake disorder is a fairly frequent presenting feature of autism\nspectrum disorder, and extreme and na rrow food preferences may persist. \nAttention-Deficit/Hyperactivity \nDisorder\nAttention-Deficit/Hyperactivity Disorder\nDiagnostic Criteria \nA. A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with\nfunctioning or development, as characterized by (1) and/or (2):\n1.Inattention: Six (or more) of the following symptoms have persisted for at least\n6 months to a degree that is inconsistent with developmental level and that nega-\ntively impacts directly on social and academic/occupational activities:\nNote: The symptoms are not solely a manifestation of oppositional behavior, defi-\nance, hostility, or failure to understand tasks or instructions. For older adolescents\nand adults (age 17 and older), at least five symptoms are required.\na. Often fails to give close attention to details or makes careless mistakes in\nschoolwork, at work, or during other activities (e.g., overlooks or misses details,\nwork is inaccurate).", "source": "dsm5.pdf"} {"id": "cfc653ac8a63-1", "page_content": "work is inaccurate).\nb. Often has difficulty sustaining attention in tasks or play activities (e.g., has diffi-\nculty remaining focused during lectures, conversations, or lengthy reading).\nc. Often does not seem to listen when spoken to directly (e.g., mind seems else-\nwhere, even in the absence of any obvious distraction).\nd. Often does not follow through on instructions and fails to finish schoolwork,\nchores, or duties in the workplace (e.g., starts tasks but quickly loses focus and\nis easily sidetracked).\ne. Often has difficulty organizing tasks and activities (e.g., difficulty managing se-\nquential tasks; difficulty keeping materials and belongings in order; messy, dis-\norganized work; has poor time management; fails to meet deadlines).\nf. Often avoids, dislikes, or is reluctant to engage in tasks that require sustained\nmental effort (e.g., schoolwork or hom ework; for older adolescents and adults,\npreparing reports, completing form s, reviewing lengthy papers).\ng. Often loses things necessary for tasks or activities (e.g., school materials, pen-\ncils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones). \nh. Is often easily distracted by extraneous stimuli (for older adolescents and\nadults, may include unrelated thoughts).\ni. Is often forgetful in daily activities (e.g., doing chores, running errands; for older\nadolescents and adults, returning calls, paying bills, keeping appointments).", "source": "dsm5.pdf"} {"id": "1759ec07f2ce-0", "page_content": "60 Neurodevelopmental Disorders\n2.Hyperactivity and impulsivity: Six (or more) of the following symptoms have per-\nsisted for at least 6 months to a degree that is inconsistent with developmental level\nand that negatively impacts directly on social and academic/occupational activities:\nNote: The symptoms are not solely a manifestation of opposition al behavior, defi-\nance, hostility, or a failure to understand tasks or instructions. For older adolescents\nand adults (age 17 and older), at least five symptoms are required.\na. Often fidgets with or taps hands or feet or squirms in seat.\nb. Often leaves seat in situations when remaining seated is expected (e.g., leaves\nhis or her place in the classroom, in the office or other workplace, or in other\nsituations that require remaining in place).\nc. Often runs about or climbs in situations where it is inappropriate. ( Note: In ad-\nolescents or adults, may be limited to feeling restless.)\nd. Often unable to play or engage in leisure activities quietly.\ne. Is often \u201con the go,\u201d acting as if \u201cdriven by a motor\u201d (e.g., is unable to be or un-\ncomfortable being still for extended time, as in restaurants, meetings; may be\nexperienced by others as being restless or difficult to keep up with).\nf. Often talks excessively.\ng. Often blurts out an answer before a question has been completed (e.g., com-\npletes people\u2019s sentences; cannot wait for turn in conversation).\nh. Often has difficulty waiting his or her turn (e.g., while waiting in line).\ni. Often interrupts or intrudes on others (e.g., butts into conversations, games, or\nactivities; may start using other people\u2019s things without asking or receiving per-", "source": "dsm5.pdf"} {"id": "1759ec07f2ce-1", "page_content": "activities; may start using other people\u2019s things without asking or receiving per-\nmission; for adolescents and adults, may intrude into or take over what others\nare doing).\nB. Several inattentive or hyperactive-impulsive symptoms were present prior to age\n12 years.\nC. Several inattentive or hyperactive-impulsive symptoms are present in two or more set-\ntings (e.g., at home, school, or work; with friends or relatives; in other activities).\nD. There is clear evidence that the symptoms interfere with, or reduce the quality of, so-\ncial, academic, or occupational functioning.\nE. The symptoms do not occur exclusively during the course of schizophrenia or another\npsychotic disorder and are not better explai ned by another mental disorder (e.g., mood\ndisorder, anxiety disorder, dissociative diso rder, personality disorder, substance intox-\nication or withdrawal).\nSpecify whether:\n314.01 (F90.2) Combined presentation: If both Criterion A1 (inattention) and Crite-\nrion A2 (hyperactivity-impulsivity) are met for the past 6 months.\n314.00 (F90.0) Predominantly inattentive presentation: If Criterion A1 (inattention)\nis met but Criterion A2 (hyperactivity-impulsivity) is not met for the past 6 months.\n314.01 (F90.1) Predominantly hyperactive/impulsive presentation: If Criterion A2 (hy-\nperactivity-impulsivity) is met and Criterion A1 (inattention) is not met for the past 6 months.\nSpecify if:\nIn partial remission: When full criteria were previously met, fewer than the full criteria", "source": "dsm5.pdf"} {"id": "1759ec07f2ce-2", "page_content": "In partial remission: When full criteria were previously met, fewer than the full criteria\nhave been met for the past 6 months, and the symptoms still result in impairment in\nsocial, academic, or occupational functioning.\nSpecify current severity:\nMild: Few, if any, symptoms in excess of those required to make the diagnosis are\npresent, and symptoms result in no more than minor impairments in social or occupa-\ntional functioning.\nModerate: Symptoms or functional impairment between \u201cmild\u201d and \u201csevere\u201d are present.", "source": "dsm5.pdf"} {"id": "763292c725d1-0", "page_content": "Attention-Deficit/Hyperactivity Disorder 61\nSevere: Many symptoms in excess of those required to make the diagnosis, or several\nsymptoms that are particularly severe, are present, or the symptoms result in marked\nimpairment in social or occupational functioning.\nDiagnostic Features\nThe essential feature of attent ion-deficit/hyperactivity disorder (ADHD) is a persistent\npattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or\ndevelopment. Inattention manifests behaviorally in ADHD as wandering off task, lacking\npersistence, having difficulty sustaining focus, and being disorganized and is not due to\ndefiance or lack of comprehension. Hyperactivity refers to excessive motor activity (such as\na child running about) when it is not appropriat e, or excessive fidgeting, tapping, or talk-\nativeness. In adults, hyperactivity may manife st as extreme restlessness or wearing others\nout with their activity. Impulsivity refers to hasty actions that occur in the moment without\nforethought and that have high potential for harm to the individual (e.g., darting into the\nstreet without looking). Impulsivity may reflec t a desire for immediate rewards or an in-\nability to delay gratification. Impulsive behaviors may manifest as social intrusiveness\n(e.g., interrupting others excessively) and/ or as making important decisions without con-\nsideration of long-term consequences (e.g., taking a job without ad equate information).\nADHD begins in childhood. The requirement that several symptoms be present before\nage 12 years conveys the importance of a substantial clinical presentation during child-\nhood. At the same time, an earlier age at onset is not specified because of difficulties in es-\ntablishing precise childhood onset retrospectively. Adult recall of childhood symptoms", "source": "dsm5.pdf"} {"id": "763292c725d1-1", "page_content": "tablishing precise childhood onset retrospectively. Adult recall of childhood symptoms\ntends to be unreliable, and it is bene ficial to obtain ancillary information.\nManifestations of the disorder must be presen t in more than one setting (e.g., home and\nschool, work). Confirmation of substantial symptoms across settings typically cannot be\ndone accurately without consulting informants who have seen the individual in those set-\ntings. Typically, symptoms vary depending on context within a given setting. Signs of the\ndisorder may be minimal or absent when the individual is receiving frequent rewards for\nappropriate behavior, is under close supervision, is in a novel setting, is engaged in espe-\ncially interesting activities, has consistent exte rnal stimulation (e.g., via electronic screens),\nor is interacting in one-on-one situa tions (e.g., the clinician's office).\nAssociated Features Supporting Diagnosis\nMild delays in language, motor, or social development are not specific to ADHD but often co-\noccur. Associated features may in clude low frustration tolerance, irritability, or mood lability.\nEven in the absence of a specific learning disorder, academic or work performance is often im-\npaired. Inattentive behavior is associated with various underlying cognit ive processes, and in-\ndividuals with ADHD may exhibit cognitive pr oblems on tests of attention, executive\nfunction, or memory, although these tests are not suff iciently sensitive or specific to serve as di-\nagnostic indices. By early adulthood, ADHD is a ssociated with an increased risk of suicide at-\ntempt, primarily when comorbid with mood, conduct, or substance use disorders.\nNo biological marker is diagnostic for AD HD. As a group, compared with peers, chil-\ndren with ADHD display incr eased slow wave electroenc ephalograms, reduced total", "source": "dsm5.pdf"} {"id": "763292c725d1-2", "page_content": "dren with ADHD display incr eased slow wave electroenc ephalograms, reduced total\nbrain volume on magnetic resonance imaging, and possibly a delay in posterior to anterior\ncortical maturation, but thes e findings are not diagnostic . In the uncommon cases where\nthere is a known genetic cause (e.g., Fragile X syndrome, 22q11 deletion syndrome), the\nADHD presentation should still be diagnosed.\nPrevalence\nPopulation surveys sugge st that ADHD occurs in most cultures in about 5% of children", "source": "dsm5.pdf"} {"id": "0bae126498f6-0", "page_content": "ADHD presentation should still be diagnosed.\nPrevalence\nPopulation surveys sugge st that ADHD occurs in most cultures in about 5% of children\nand about 2.5% of adults.", "source": "dsm5.pdf"} {"id": "10f7006fd014-0", "page_content": "62 Neurodevelopmental Disorders\nDevelopment and Course\nMany parents first observe excessive motor activity when the child is a toddler, but symp-\ntoms are difficult to distinguish from highly variable normative be haviors before age 4\nyears. ADHD is most often identified during elementary school years, and inattention be-\ncomes more prominent and impairing. The disord er is relatively stable through early ad-\nolescence, but some individuals have a worsened course wi th development of antisocial\nbehaviors. In most individuals with ADHD , symptoms of motoric hyperactivity become\nless obvious in adolescence and adulthood, bu t difficulties with restlessness, inattention,\npoor planning, and impulsivity persist. A subs tantial proportion of children with ADHD\nremain relatively impa ired into adulthood.\nIn preschool, the main manifestation is hyperactivity. Inattentio n becomes more prom-\ninent during elementary school. During adoles cence, signs of hypera ctivity (e.g., running\nand climbing) are less common and may be conf ined to fidgetiness or an inner feeling of\njitteriness, restlessness, or im patience. In adulthood, along wi th inattention and restless-\nness, impulsivity may remain problematic ev en when hyperactivity has diminished.\nRisk and Prognostic Factors \nTemperamental. ADHD is associated with reduced be havioral inhibition, effortful con-\ntrol, or constraint; negative emotionality; an d/or elevated novelty seeking. These traits\nmay predispose some children to ADHD bu t are not specific to the disorder.\nEnvironmental. Very low birth weight (less than 1,500 grams) conveys a two- to three-\nfold risk for ADHD, but most children with low birth weig ht do not develop ADHD. Al-\nthough ADHD is correlated with smoking du ring pregnancy, some of this association", "source": "dsm5.pdf"} {"id": "10f7006fd014-1", "page_content": "though ADHD is correlated with smoking du ring pregnancy, some of this association\nreflects common genetic risk. A minority of c ases may be related to reactions to aspects of\ndiet. There may be a history of child abuse, neglect, multiple foster placements, neurotoxin\nexposure (e.g., lead), infectio ns (e.g., encephalitis), or alcohol exposure in utero. Exposure\nto environmental toxicants has been correlat ed with subsequent ADHD, but it is not\nknown whether these associations are causal.\nGenetic and physiological. ADHD is elevated in the firs t-degree biological relatives of\nindividuals with ADHD. The heritability of AD HD is substantial. While specific genes\nhave been correlated with ADHD, they are ne ither necessary nor sufficient causal factors.\nVisual and hearing impairments, metabolic abnormalities, sleep disorders, nutritional de-\nficiencies, and epilepsy should be considered as possible influences on ADHD symptoms.\nADHD is not associated with specific physic al features, although rates of minor phys-\nical anomalies (e.g., hypertelorism, highly arched palate, low-set ears) may be relatively\nelevated. Subtle motor delays and other neur ological soft signs may occur. (Note that\nmarked co-occurring clumsiness and motor delays should be coded separately [e.g., de-\nvelopmental coordina tion disorder].)\nCourse modifiers. Family interaction patterns in ea rly childhood are unlikely to cause\nADHD but may influence its course or contri bute to secondary development of conduct\nproblems.\nCulture-Related Diagnostic Issues\nDifferences in ADHD prevalence rates across re gions appear attributable mainly to differ-\nent diagnostic and methodological practices. However, there also may be cultural varia-\ntion in attitudes toward or interpretations of children\u2019s behaviors. Clinical identification", "source": "dsm5.pdf"} {"id": "10f7006fd014-2", "page_content": "tion in attitudes toward or interpretations of children\u2019s behaviors. Clinical identification\nrates in the United States for African Americ an and Latino populations tend to be lower\nthan for Caucasian populations. Informant symptom ratings may be influenced by cul-\ntural group of the child and the informant, su ggesting that culturally appropriate practices\nare relevant in assessing ADHD.", "source": "dsm5.pdf"} {"id": "8e16b8bfc4a2-0", "page_content": "Attention-Deficit/Hyperactivity Disorder 63\nGender-Related Diagnostic Issues\nADHD is more frequent in males than in fema les in the general population, with a ratio of\napproximately 2:1 in children and 1.6:1 in ad ults. Females are more likely than males to\npresent primarily with inattentive features.\nFunctional Consequences of \nAttention-Deficit/Hy peractivity Disorder\nADHD is associated with reduced school performance and academic attainment, social re-\njection, and, in adults, poorer occupation al performance, attainment, attendance, and\nhigher probability of unemployment as well as elevated interpersonal conflict. Children\nwith ADHD are significantly more likely than their peers without ADHD to develop con-\nduct disorder in adolescence and antisocial personality disorder in adulthood, conse-\nquently increasing the likelihood for substance use disorders and incarceration. The risk of\nsubsequent substance use disorders is elevated, especially when conduct disorder or an-\ntisocial personality disorder develops. Individuals with ADHD are more likely than peers\nto be injured. Traffic accidents and violatio ns are more frequent in drivers with ADHD.\nThere may be an elevated likelihood of obesity among individuals with ADHD.\nInadequate or variable self-app lication to tasks that require sustained effort is often in-\nterpreted by others as laziness , irresponsibility, or failure to cooperate. Family relation-\nships may be characterized by discord and ne gative interactions. Peer relationships are\noften disrupted by peer rejection, neglect, or teasing of the individual with ADHD. On av-\nerage, individuals with ADHD obtain less schooling, have poorer vocational achievement,\nand have reduced intellectual scores than their peers, although there is great variability. In\nits severe form, the disorder is markedly impairing, affecting social, familial, and scholas-\ntic/occupational adjustment.", "source": "dsm5.pdf"} {"id": "8e16b8bfc4a2-1", "page_content": "tic/occupational adjustment.\nAcademic deficits, school-relat ed problems, and peer neglect tend to be most associ-\nated with elevated symptoms of inattention, whereas peer reje ction and, to a lesser extent,\naccidental injury are most salient with mark ed symptoms of hyperactivity or impulsivity.\nDifferential Diagnosis\nOppositional defiant disorder. Individuals with oppositional defiant disorder may re-\nsist work or school tasks that require self-application because they resist conforming to\nothers' demands. Their behavior is characte rized by negativity, hostility, and defiance.\nThese symptoms must be differentiated from aversion to school or mentally demanding\ntasks due to difficulty in sustaining mental effort, forgetting instructions, and impulsivity\nin individuals with ADHD. Complicating the di fferential diagnosis is the fact that some\nindividuals with ADHD may develop secondary oppositional attitudes toward such tasks\nand devalue their importance.\nIntermittent explosive disorder. ADHD and intermittent expl osive disorder share high\nlevels of impulsive behavior. However, indi viduals with intermitte nt explosive disorder\nshow serious aggression toward others, which is not characteristic of ADHD, and they do\nnot experience problems with sustaining atte ntion as seen in ADHD. In addition, intermit-\ntent explosive disorder is rare in childhood. Intermittent explosive disorder may be diag-\nnosed in the presence of ADHD.\nOther neurodevelopmental disorders. The increased motoric acti vity that may occur in\nADHD must be distinguished from the repetiti ve motor behavior that characterizes stereo-\ntypic movement disorder and some cases of autism spectr um disorder. In stereotypic\nmovement disorder, the motoric be havior is generally fixed and repetitive (e.g., body rock-\ning, self-biting), whereas the fidgetiness and restlessness in ADHD are typically general-", "source": "dsm5.pdf"} {"id": "8e16b8bfc4a2-2", "page_content": "ized and not characterized by repetitive ster eotypic movements. In Tourette\u2019s disorder,", "source": "dsm5.pdf"} {"id": "0f12257d85fc-0", "page_content": "64 Neurodevelopmental Disorders\nfrequent multiple tics can be mistaken for the generalized fidgetiness of ADHD. Prolonged\nobservation may be needed to differentiate fidgetiness from bouts of multiple tics.\nSpecific learning disorder. Children with specific learning disorder may appear inat-\ntentive because of frustration, lack of interest, or limited ab ility. However, inattention in\nindividuals with a specific learning disorder who do not have ADHD is not impairing out-\nside of academic work.\nIntellectual disability (intell ectual developmental disorder). Symptoms of ADHD are\ncommon among children placed in academic sett ings that are inappropriate to their intel-\nlectual ability. In such cases, the symptoms are not evident during non-academic tasks. A\ndiagnosis of ADHD in intellectual disability requires that inattention or hyperactivity be\nexcessive for mental age.\nAutism spectrum disorder. Individuals with ADHD and those with autism spectrum\ndisorder exhibit inattention, social dysfunction, and difficult-to-manage behavior. The so-\ncial dysfunction and peer rejection seen in individuals with ADHD must be distinguished\nfrom the social disengagement, isolation, an d indifference to facial and tonal communica-\ntion cues seen in individuals with autism sp ectrum disorder. Childr en with autism spec-\ntrum disorder may display tantru ms because of an inability to tolerate a change from their\nexpected course of events. In contrast, child ren with ADHD may misbehave or have a tan-\ntrum during a major transition because of impulsivity or poor self-control.\nReactive attachment disorder. Children with reactive attachment disorder may show\nsocial disinhibition, but not the full ADHD symptom cluster, and display other features\nsuch as a lack of enduring relationship s that are not characteristic of ADHD.\nAnxiety disorders. ADHD shares symptoms of inattent ion with anxiety disorders. Indi-", "source": "dsm5.pdf"} {"id": "0f12257d85fc-1", "page_content": "Anxiety disorders. ADHD shares symptoms of inattent ion with anxiety disorders. Indi-\nviduals with ADHD are inattentive because of their attraction to external stimuli, new\nactivities, or preoccupation with enjoyable activities. This is distinguished from the inat-\ntention due to worry and rumination seen in anxiety disorders. Restlessness might be seen\nin anxiety disorders. Howeve r, in ADHD, the symptom is not associated with worry and\nrumination.\nDepressive disorders. Individuals with depressive diso rders may present with inabil-\nity to concentrate. However, poor concentration in mood disorders becomes prominent\nonly during a depressive episode.\nBipolar disorder. Individuals with bipola r disorder may have increased activity, poor\nconcentration, and increased impulsivity, bu t these features are episodic, occurring sev-\neral days at a time. In bipolar disorder, increased impulsivity or inattention is accompa-\nnied by elevated mood, grandiosity, and ot her specific bipolar features. Children with\nADHD may show significant changes in mood within the same day; such lability is dis-\ntinct from a manic episode, which must last 4 or more days to be a clinical indicator of bi-\npolar disorder, even in childre n. Bipolar disorder is rare in preadolescents, even when\nsevere irritability and anger are prominent, whereas ADHD is common among children\nand adolescents who display excessive anger and irritability.\nDisruptive mood dysregulation disorder. Disruptive mood dysregulation disorder is\ncharacterized by pervasive irritability, and intolerance of frustratio n, but impulsiveness\nand disorganized attention are not essential features. However, most children and adoles-\ncents with the disorder have symptoms that also meet crit eria for ADHD, which is diag-\nnosed separately.", "source": "dsm5.pdf"} {"id": "0f12257d85fc-2", "page_content": "nosed separately.\nSubstance use disorders. Differentiating ADHD from su bstance use disorders may be\nproblematic if the first presentation of ADHD symptoms follows the onset of abuse or fre-\nquent use. Clear evidence of ADHD before su bstance misuse from informants or previous\nrecords may be essential for differential diagnosis.", "source": "dsm5.pdf"} {"id": "73cb3e37e925-0", "page_content": "Other Specified Attention-Deficit/Hyperactivity Disorder 65\nPersonality disorders. In adolescents and adults, it may be difficult to distinguish ADHD\nfrom borderline, narcissistic, and other person ality disorders. All these disorders tend to\nshare the features of disorganization, social intrusiveness, emotional dysregulation, and\ncognitive dysregulation. Howe ver, ADHD is not characterized by fear of abandonment,\nself-injury, extreme ambivalence, or other fe atures of personality disorder. It may take\nextended clinical observation, informant interview, or detailed history to distinguish im-\npulsive, socially intrusive, or inappropriate behavior from narcissist ic, aggressive, or dom-\nineering behavior to make this differential diagnosis.\nPsychotic disorders. ADHD is not diagnosed if the symp toms of inattention and hyperac-\ntivity occur exclusively during the course of a psychotic disorder.\nMedication-induced symptoms of ADHD. Symptoms of inattention, hyperactivity, or\nimpulsivity attributable to the use of medication (e.g., bron chodilators, isoniazid, neuro-\nleptics [resulting in akathisia], thyroid replacement medication) are diagnosed as other\nspecified or unspecified other (or un known) substance\u2013related disorders.\nNeurocognitive disorders. Early major neurocognitive disorder (dementia) and/or\nmild neurocognitive disorder are not known to be associated with ADHD but may present\nwith similar clinical features. These conditions are distinguished from ADHD by their late\nonset.\nComorbidity\nIn clinical settings, comorbid disorders are frequent in individuals whose symptoms meet\ncriteria for ADHD. In the general population, oppositional defiant di sorder co-occurs with\nADHD in approximately half of children wi th the combined presentation and about a\nquarter with the predominantly inattentive presentation. Conduct disorder co-occurs in", "source": "dsm5.pdf"} {"id": "73cb3e37e925-1", "page_content": "quarter with the predominantly inattentive presentation. Conduct disorder co-occurs in\nabout a quarter of children or adolescents with the combined presentation, depending on\nage and setting. Most children and adolescent s with disruptive mood dysregulation dis-\norder have symptoms that also meet criteria for ADHD; a lesser percentage of children\nwith ADHD have symptoms that meet criter ia for disruptive mood dysregulation disor-\nder. Specific learning disorder commonly co-occurs with ADHD. Anxiety disorders and\nmajor depressive disorder occur in a minority of individuals with ADHD but more often\nthan in the general population. Intermittent explosive disorder occu rs in a minority of\nadults with ADHD, but at rates above population levels. Although substance use disor-\nders are relatively more frequent among adul ts with ADHD in the general population, the\ndisorders are present in only a minority of adults with AD HD. In adults, antisocial and\nother personality disorders may co-occur with ADHD. Other disorders that may co-occur\nwith ADHD include obsessive-compulsive diso rder, tic disorders, and autism spectrum\ndisorder.\nOther Specified Attention-Deficit/\nHyperactivity Disorder\n314.01 (F90.8)\nThis category applies to presentations in wh ich symptoms characteristic of attention-\ndeficit/hyperactivity disorder that cause clinic ally significant distress or impairment in so-\ncial, occupational or other important areas of functioning predominate but do not meet the\nfull criteria for attention-deficit/hyperactivity disorder or any of the disorders in the neuro-\ndevelopmental disorders diagnostic class. The other specified attention-deficit/hyperactiv-\nity disorder category is used in situations in which the clinician chooses to communicate", "source": "dsm5.pdf"} {"id": "899ad7767549-0", "page_content": "66 Neurodevelopmental Disorders\nthe specific reason that the presentation does not meet the criteria for attention-deficit/\nhyperactivity disorder or any specific neur odevelopmental disorder. This is done by re-\ncording \u201cother specified attention-deficit/hyperactivity disorder\u201d followed by the specific\nreason (e.g., \u201cwith insufficient inattention symptoms\u201d). \nUnspecified Attention-Deficit/\nHyperactivity Disorder\n314.01 (F90.9)\nThis category applies to presentations in wh ich symptoms characteristic of attention-\ndeficit/hyperactivity disorder that cause clinic ally significant distress or impairment in so-\ncial, occupational, or other important areas of functioning predominate but do not meet the\nfull criteria for attention-deficit/hyperactivity disorder or any of the disorders in the neuro-\ndevelopmental disorders diagnostic class. The unspecified attention-deficit/hyperactivity\ndisorder category is used in situations in which the clinician chooses not to specify the rea-\nson that the criteria are not met for attention- deficit/hyperactivity disorder or for a specific\nneurodevelopmental disorder, and includes presentations in which there is insufficient in-\nformation to make a more specific diagnosis. \nSpecific Learning Disorder\nSpecific Learning Disorder\nDiagnostic Criteria \nA. Difficulties learning and using academic skills, as indicated by the presence of at least\none of the following symptoms that have persisted for at least 6 months, despite the\nprovision of interventions that target those difficulties:\n1. Inaccurate or slow and effortful word reading (e.g., reads single words aloud incor-\nrectly or slowly and hesitantly, frequently guesses words, has difficulty sounding\nout words).\n2. Difficulty understanding the meaning of what is read (e.g., may read text accurately\nbut not understand the sequence, relationships, inferences, or deeper meanings of\nwhat is read).", "source": "dsm5.pdf"} {"id": "899ad7767549-1", "page_content": "what is read).\n3. Difficulties with spelling (e.g., may add, omit, or substitute vowels or consonants).\n4. Difficulties with written expression (e.g., makes multiple grammatical or punctua-\ntion errors within sentences; employs poor paragraph organization; written expres-\nsion of ideas lacks clarity).\n5. Difficulties mastering number sense, number facts, or calculation (e.g., has poor\nunderstanding of numbers, their magnitude, and relationships; counts on fingers to\nadd single-digit numbers instead of recalling the math fact as peers do; gets lost in\nthe midst of arithmetic computation and may switch procedures).\n6. Difficulties with mathematical reasoning (e.g., has severe difficulty applying math-\nematical concepts, facts, or procedures to solve quantitative problems).", "source": "dsm5.pdf"} {"id": "35cb18c67380-0", "page_content": "Specific Learning Disorder 67\nB. The affected academic skills are substantially and quantifiably below those expected\nfor the individual\u2019s chronological age, and cause significant interference with academic\nor occupational performance, or with activiti es of daily living, as confirmed by individu-\nally administered standardized achievement measures and comprehensive clinical\nassessment. For individuals age 17 years and older, a documented history of impairing\nlearning difficulties may be substituted for the standardized assessment.\nC. The learning difficulties begin during school-age years but may not become fully man-\nifest until the demands for those affected academic skills exceed the individual\u2019s lim-\nited capacities (e.g., as in timed tests, reading or writing lengthy complex reports for a\ntight deadline, excessively heavy academic loads).\nD. The learning difficulties are not better accounted for by intellectual disabilities, uncor-\nrected visual or auditory acuity, other mental or neurological disorders, psychosocial\nadversity, lack of proficiency in the language of academic instruction, or inadequate\neducational instruction.\nNote: The four diagnostic criteria are to be met based on a clinical synthesis of the indi-\nvidual\u2019s history (developmental, medical, fa mily, educational), school reports, and psycho-\neducational assessment.\nCoding note: Specify all academic domains and subskills that are impaired. When more\nthan one domain is impaired, each one should be coded individually according to the fol-\nlowing specifiers.\nSpecify if:\n315.00 (F81.0) With impairment in reading:\nWord reading accuracy\nReading rate or fluency\nReading comprehension\nNote: Dyslexia is an alternative term used to refer to a pattern of learning difficulties\ncharacterized by problems with accurate or fluent word recognition, poor decoding,\nand poor spelling abilities. If dyslexia is used to specify this particular pattern of dif-", "source": "dsm5.pdf"} {"id": "35cb18c67380-1", "page_content": "and poor spelling abilities. If dyslexia is used to specify this particular pattern of dif-\nficulties, it is important also to specify any additional difficulties that are present,\nsuch as difficulties with reading comprehension or math reasoning.\n315.2 (F81.81) With impairme nt in written expression:\nSpelling accuracy\nGrammar and punctuation accuracy\nClarity or organization of written expression\n315.1 (F81.2) With impairment in mathematics:\nNumber sense\nMemorization of arithmetic facts\nAccurate or fluent calculation\nAccurate math reasoning\nNote: Dyscalculia is an alternative term used to refer to a pattern of difficulties char-\nacterized by problems processing numerical information, learning arithmetic facts,\nand performing accurate or fluent calculations. If dyscalculia is used to specify this\nparticular pattern of mathematic difficulties, it is important also to specify any addi-\ntional difficulties that are present, such as difficulties with math reasoning or word rea-\nsoning accuracy.\nSpecify current severity:\nMild: Some difficulties learning skills in one or two academic domains, but of mild enough\nseverity that the individual may be able to compensate or function well when provided with\nappropriate accommodations or support services, especially during the school years.", "source": "dsm5.pdf"} {"id": "28ec65346476-0", "page_content": "68 Neurodevelopmental Disorders\nModerate: Marked difficulties learning skills in one or more academic domains, so that\nthe individual is unlikely to become proficient without some intervals of intensive and\nspecialized teaching during the school years. Some accommodations or supportive\nservices at least part of the day at school, in the workplace, or at home may be needed\nto complete activities accurately and efficiently.\nSevere: Severe difficulties learning skills, affecting several academic domains, so that\nthe individual is unlikely to learn those skills without ongoing intensive individualized\nand specialized teaching for most of the school years. Even with an array of appropri-\nate accommodations or services at home, at school, or in the workplace, the individual\nmay not be able to complete all activities efficiently.\nRecording Procedures\nEach impaired academic domain and subskill of specific learning disorder should be re-\ncorded. Because of ICD coding requirements, im pairments in reading, impairments in writ-\nten expression, and impairments in mathematics, with their corresponding impairments in\nsubskills, must be coded sepa rately. For example, impairments in reading and mathematics\nand impairments in the subskills of reading rate or fluency, reading comprehension, accu-\nrate or fluent calculation, and accurate math reasoning would be coded and recorded as\n315.00 (F81.0) specific learning disorder with impairment in reading, with impairment in\nreading rate or fluency and impairment in reading comprehension; 315.1 (F81.2) specific\nlearning disorder with impairment in mathemat ics, with impairment in accurate or fluent\ncalculation and impairment in accurate math reasoning.\nDiagnostic Features\nSpecific learning disorder is a neurodevelopmental disorder with a biological origin that is\nthe basis for abnormalities at a cognitive level that are associated with the behavioral signs", "source": "dsm5.pdf"} {"id": "28ec65346476-1", "page_content": "the basis for abnormalities at a cognitive level that are associated with the behavioral signs\nof the disorder. The biological origin includes an interaction of geneti c, epigenetic, and en-\nvironmental factors, which affect the brain\u2019s ab ility to perceive or process verbal or non-\nverbal information efficiently and accurately.\nOne essential feature of specific learning diso rder is persistent diff iculties learning key-\nstone academic skills (Criterion A), with onset duri ng the years of formal schooling (i.e., the de-\nvelopmental period). Key academic skills incl ude reading of single words accurately and\nfluently, reading comprehension, written expression and spelling, arithmetic calculation, and\nmathematical reasoning (solving mathematical problems). In contrast to talking or walking,\nwhich are acquired developmenta l milestones that emerge wi th brain maturation, academic\nskills (e.g., reading, spelling, writing, mathematic s) have to be taught and learned explicitly.\nSpecific learning disorder disrupts the normal pa ttern of learning academ ic skills; it is not sim-\nply a consequence of lack of o pportunity of learning or inadeq uate instruction. Difficulties\nmastering these key academic skills may also impe de learning in other academic subjects (e.g.,\nhistory, science, social studies) , but those problems are attributable to difficulties learning the\nunderlying academic skills. Difficulties learning to map letters with the sounds of one\u2019s lan-\nguage\u2014to read printed words (often called dyslexia)\u2014is one of the most common manifesta-\ntions of specific learning disord er. The learning difficulties manifest as a range of observable,\ndescriptive behaviors or symptoms (as listed in Criteria A1\u2013A6). These clinical symptoms may\nbe observed, probed by means of the clinical interview, or ascert ained from school reports, rat-", "source": "dsm5.pdf"} {"id": "28ec65346476-2", "page_content": "ing scales, or descriptions in previous educational or psychological assessments. The learning\ndifficulties are persistent, not transitory. In ch ildren and adolescents, persistence is defined as\nrestricted progress in learning (i.e., no evidence that the individual is catching up with class-", "source": "dsm5.pdf"} {"id": "43223ec68bbb-0", "page_content": "difficulties are persistent, not transitory. In ch ildren and adolescents, persistence is defined as\nrestricted progress in learning (i.e., no evidence that the individual is catching up with class-\nmates) for at least 6 months despite the provision of extra help at home or school. For example,\ndifficulties learning to read si ngle words that do not fully or rapidly remit with the provision of\ninstruction in phonological skills or word iden tification strategies may indicate a specific", "source": "dsm5.pdf"} {"id": "3edcdd2462f2-0", "page_content": "Specific Learning Disorder 69\nlearning disorder. Evidence of persistent learning difficulties may be derived from cumulative\nschool reports, portfolios of the child\u2019s evalua ted work, curriculum-based measures, or clinical\ninterview. In adults, persistent difficulty refers to ongoing difficulties in literacy or numeracy\nskills that manifest during childhood or adol escence, as indicated by cumulative evidence\nfrom school reports, evaluated portfo lios of work, or previous assessments.\nA second key feature is that the individual\u2019s performance of the affected academic skills is\nwell below average for age (Criterion B). One robust clinical indicator of difficulties learning\nacademic skills is low academic achievement for age or average achievement that is sustain-\nable only by extraordinarily high levels of effort or support. In children, the low academic skills\ncause significant interference in school performance (as indicated by school reports and\nteacher\u2019s grades or ratings). Another clinical indicator, particularly in adults, is avoidance of\nactivities that require the academic skills. Also in adulthood, low academic skills interfere with\noccupational performance or everyday activities requiring those skills (as indicated by self-re-\nport or report by others). However, this criterion also requires psycho metric evidence from an\nindividually administered, psychometrically s ound and culturally appropriate test of aca-\ndemic achievement that is norm -referenced or criter ion-referenced. Academic skills are dis-\ntributed along a continuum, so there is no natural cutpoint that can be used to differentiate\nindividuals with and without spec ific learning disorder. Thus, any threshold used to specify\nwhat constitutes significantly low academic achi evement (e.g., academic skills well below age\nexpectation) is to a large extent arbitrary. Lo w achievement scores on one or more standard-\nized tests or subtests within an academic domain (i.e., at least 1.5 standard deviations [SD] be-", "source": "dsm5.pdf"} {"id": "3edcdd2462f2-1", "page_content": "low the population mean for age, which translates to a standard score of 78 or less, which is\nbelow the 7th percentile) are need ed for the greatest diagnostic certainty. However, precise\nscores will vary according to the particular standardized tests that are used. On the basis of\nclinical judgment, a more leni ent threshold may be used (e.g., 1.0\u20132.5 SD below the pop-\nulation mean for age), when learning diffic ulties are supported by converging evidence\nfrom clinical assessment, academic history, school reports, or test scores. Moreover, since\nstandardized tests are not available in all languages, the diagnosis may then be based in\npart on clinical judgment of sc ores on available test measures.\nA third core feature is that the learning di fficulties are readily apparent in the early\nschool years in most individuals (Criterion C) . However, in others, the learning difficulties\nmay not manifest fully until later school year s, by which time learning demands have in-\ncreased and exceed the individual\u2019s limited capacities.\nAnother key diagnostic feature is that the learning difficulties are considered \u201cspe-\ncific,\u201d for four reasons. First, they are not attr ibutable to intellectual disabilities (intellec-\ntual disability [intellectual developmenta l disorder]); global developmental delay;\nhearing or vision disorders, or neurological or motor disorders) (Criterion D). Specific\nlearning disorder affects lear ning in individuals who othe rwise demonstrate normal lev-\nels of intellectual functioning (generally estima ted by an IQ score of greater than about 70\n[\u00b15 points allowing for measurement error ]). The phrase \u201cunexpected academic under-\nachievement\u201d is often cited as the defining ch aracteristic of specific learning disorder in\nthat the specific learning disabilities are not part of a more general learning difficulty as", "source": "dsm5.pdf"} {"id": "3edcdd2462f2-2", "page_content": "that the specific learning disabilities are not part of a more general learning difficulty as\nmanifested in intellectual disability or global developmental delay. Specific learning dis-", "source": "dsm5.pdf"} {"id": "5fe51d6522b7-0", "page_content": "that the specific learning disabilities are not part of a more general learning difficulty as\nmanifested in intellectual disability or global developmental delay. Specific learning dis-\norder may also occur in individuals identified as intellectually \u201cgifted.\u201d These individuals\nmay be able to sustain apparently adequate academic functioning by using compensatory\nstrategies, extraordinarily high effort, or su pport, until the learning demands or assess-\nment procedures (e.g., timed tests) pose barri ers to their demonstrating their learning or\naccomplishing required tasks. Second, the lear ning difficulty cannot be attributed to more\ngeneral external factors, such as economic or environmental disadvantage, chronic absen-\nteeism, or lack of education as typically prov ided in the individual\u2019s community context.\nThird, the learning difficulty canno t be attributed to a neurol ogical (e.g., pediatric stroke)\nor motor disorders or to vision or hearing di sorders, which are often associated with prob-\nlems learning academic skills but are distinguishable by presence of neurological signs.", "source": "dsm5.pdf"} {"id": "f2174f787d27-0", "page_content": "70 Neurodevelopmental Disorders\nFinally, the learning difficulty may be restricted to one academic skill or domain (e.g., read-\ning single words, retrieving or calculating number facts).\nComprehensive assessment is required. Specifi c learning disorder can only be diagnosed\nafter formal education starts bu t can be diagnosed at any point afterward in children, adoles-\ncents, or adults, providing there is evidence of onset during the years of formal schooling (i.e.,\nthe developmental period). No sing le data source is sufficient fo r a diagnosis of specific learn-\ning disorder. Rather, specific learning disorder is a clinical diagnosis based on a synthesis of\nthe individual\u2019s medical, develo pmental, educational, and family history; the history of the\nlearning difficulty, including it s previous and current manifestat ion; the impact of the diffi-\nculty on academic, occupational, or social functioning; previo us or current school reports;\nportfolios of work requiring academic skills; curriculum-based assessments; and previous or\ncurrent scores from individual standardized test s of academic achievemen t. If an intellectual,\nsensory, neurological, or motor disorder is susp ected, then the clinical assessment for specific\nlearning disorder should also include methods appropriate for these disorders. Thus, compre-\nhensive assessment will involve professionals with expertise in specific learning disorder and\npsychological/cognitive assessment. Since specific learning disorder typically persists into\nadulthood, reassessment is rarely necessary, un less indicated by marked changes in the learn-\ning difficulties (amelioration or worsenin g) or requested for specific purposes.\nAssociated Features Supporting Diagnosis\nSpecific learning disorder is frequently but not invariably preceded, in preschool years, by\ndelays in attention, language, or motor skills that may pers ist and co-occur with specific\nlearning disorder. An uneven profile of abilities is common , such as above-average abili-", "source": "dsm5.pdf"} {"id": "f2174f787d27-1", "page_content": "learning disorder. An uneven profile of abilities is common , such as above-average abili-\nties in drawing, design, and other visuospatial abilities, but slow, effortful, and inaccurate\nreading and poor reading comprehension and written expression. Individuals with spe-\ncific learning disorder typica lly (but not invariably) exhibit poor performance on psycho-\nlogical tests of cognitive processing. However, it remains unclear whether these cognitive\nabnormalities are the caus e, correlate, or consequence of th e learning difficulties. Also, al-\nthough cognitive deficits associated with diff iculties learning to read words are well doc-\numented, those associated with other manifestations of specific learning disorder (e.g.,\nreading comprehension, arithmetic computat ion, written expression) are underspecified\nor unknown. Moreover, individu als with similar behavioral sy mptoms or test scores are\nfound to have a variety of cognitive deficits, and many of these processing deficits are also\nfound in other neurodevelopmental disorders (e.g., attention-deficit/hyperactivity disor-\nder [ADHD], autistic spectrum disorder, communication diso rders, developmental coor-\ndination disorder). Thus, asses sment of cognitive processing deficits is not required for\ndiagnostic assessment. Specific le arning disorder is associated with increased risk for sui-\ncidal ideation and suicide attempts in children, adolescents, and adults.\nThere are no known biological markers of spec ific learning disorder. As a group, indi-\nviduals with the disorder show circumscribe d alterations in cognitive processing and\nbrain structure and func tion. Genetic differences are also evident at the group level. But\ncognitive testing, neuroimaging, or genetic test ing are not useful for diagnosis at this time.\nPrevalence\nThe prevalence of specific learning disorder across the academic domains of reading, writ-", "source": "dsm5.pdf"} {"id": "f2174f787d27-2", "page_content": "Prevalence\nThe prevalence of specific learning disorder across the academic domains of reading, writ-\ning, and mathematics is 5%\u201315% among school-age children across different languages\nand cultures. Prevalence in adults is unknown but appear s to be approximately 4%.", "source": "dsm5.pdf"} {"id": "0bf09f2ef085-0", "page_content": "ing, and mathematics is 5%\u201315% among school-age children across different languages\nand cultures. Prevalence in adults is unknown but appear s to be approximately 4%.\nDevelopment and Course\nOnset, recognition, and diagnosis of specific learning disorder usually occurs during the\nelementary school years when children are requir ed to learn to read, sp ell, write, and learn", "source": "dsm5.pdf"} {"id": "b49a6945955e-0", "page_content": "Specific Learning Disorder 71\nmathematics. However, precursors such as la nguage delays or defi cits, difficulties in\nrhyming or counting, or difficulties with fine motor skills required for writing commonly\noccur in early childhood before the start of formal schooling. Manifestations may be be-\nhavioral (e.g., a reluctance to engage in le arning; oppositional beha vior). Specific learning\ndisorder is lifelong, but the course and clinical expression are variable, in part depending\non the interactions among the task demands of the environment, the range and severity of\nthe individual\u2019s learning difficulties, the indi vidual\u2019s learning abilities, comorbidity, and\nthe available support systems and intervention . Nonetheless, problems with reading flu-\nency and comprehension, spelling, written expr ession, and numeracy sk ills in everyday life\ntypically persist into adulthood.\nChanges in manifestation of symptoms occur with age, so that an individual may have\na persistent or shifting array of learning difficulties across the lifespan.\nExamples of symptoms that may be observed among preschool-age children include a lack\nof interest in playing games with language s ounds (e.g., repetition, rhyming), and they may\nhave trouble learning nursery rhymes. Preschool children with sp ecific learning disorder may\nfrequently use baby talk, mispronounce words, and have trouble remembering names of let-\nters, numbers, or days of the week. They may fa il to recognize letters in their own names and\nhave trouble learning to count. Kindergarten-age children with specific learning disorder may\nbe unable to recognize and write letters, may be unable to write their own names, or may use\ninvented spelling. They may have trouble brea king down spoken words into syllables (e.g.,", "source": "dsm5.pdf"} {"id": "b49a6945955e-1", "page_content": "\u201ccowboy\u201d into \u201ccow\u201d and \u201cboy\u201d) and trouble reco gnizing words that rhyme (e.g., cat, bat, hat).\nKindergarten-age children also may have trouble connecting letters with their sounds (e.g., let-\nter b makes the sound /b/) and may be unable to recognize phonemes (e.g., do not know\nwhich in a set of words [e.g., dog, man, car] starts with the same sound as \u201ccat\u201d).\nSpecific learning disorder in elementary school\u2013age children typically manifests as\nmarked difficulty learning letter-sound corres pondence (particularly in English-speaking\nchildren), fluent word decoding, spelling, or ma th facts; reading aloud is slow, inaccurate,\nand effortful, and some childr en struggle to understand the magnitude that a spoken or\nwritten number represents. Children in prim ary grades (grades 1\u20133) may continue to have\nproblems recognizing and manipulating phon emes, be unable to read common one-sylla-\nble words (such as mat or top), and be un able recognize common irregularly spelled\nwords (e.g., said, two). They may commit read ing errors that indicate problems in con-\nnecting sounds and letters (e.g., \u201cbig\u201d for \u201cg ot\u201d) and have difficult y sequencing numbers\nand letters. Children in grades 1-3 also may have difficulty remembering number facts or\narithmetic procedures for addi ng, subtracting, and so forth, and may complain that read-\ning or arithmetic is hard and avoid doing it. Ch ildren with specific learning disorder in the\nmiddle grades (grades 4\u20136) may mispronounce or skip parts of long, multisyllable words\n(e.g., say \u201cconible\u201d for \u201cconvertible,\u201d \u201caminal\u201d for \u201canimal\u201d) and confuse words that", "source": "dsm5.pdf"} {"id": "b49a6945955e-2", "page_content": "sound alike (e.g., \u201ctornado\u201d for \u201cvolcano\u201d) . They may have trouble remembering dates,\nnames, and telephone numbers and may have trouble completing homework or tests on\ntime. Children in the middle grades also may have poor comprehension with or without\nslow, effortful, and inaccurate reading, and they may have trouble reading small function\nwords (e.g., that, the, an, in). They may ha ve very poor spelling and poor written work.\nThey may get the first part of a word correctly , then guess wildly (e.g., read \u201cclover\u201d as\n\u201cclock\u201d), and may express fear of read ing aloud or refuse to read aloud.", "source": "dsm5.pdf"} {"id": "5c887ced64b0-0", "page_content": "They may get the first part of a word correctly , then guess wildly (e.g., read \u201cclover\u201d as\n\u201cclock\u201d), and may express fear of read ing aloud or refuse to read aloud.\nBy contrast, adolescents may have mastered word decoding, but reading remains slow\nand effortful, and they are likely to show ma rked problems in reading comprehension and\nwritten expression (including poor spelling) and poor master y of math facts or mathemat-\nical problem solving. During adolescence an d into adulthood, indi viduals with specific\nlearning disorder may continue to make nu merous spelling mistakes and read single\nwords and connected text slowly and with mu ch effort, with trou ble pronouncing multi-\nsyllable words. They may frequently need to reread material to understand or get the main\npoint and have trouble making inferences fr om written text. Adolescents and adults may", "source": "dsm5.pdf"} {"id": "eb83ae00d57a-0", "page_content": "72 Neurodevelopmental Disorders\navoid activities that demand reading or arit hmetic (reading for pl easure, reading instruc-\ntions). Adults with specific learning disord er have ongoing spelling problems, slow and\neffortful reading, or problems making impo rtant inferences from numerical information\nin work-related written documents. They ma y avoid both leisure and work-related activ-\nities that demand reading or writing or use alternative approaches to access print (e.g.,\ntext-to-speech/speech-to-text softwa re, audiobooks, audiovisual media).\nAn alternative clinical expression is that of circumscribed learning difficulties that per-\nsist across the lifespan, such as an inability to master the basic sense of number (e.g., to\nknow which of a pair of number s or dots represents the larger magnitude), or lack of pro-\nficiency in word identification or spelling. Av oidance of or reluctance to engage in activi-\nties requiring academic skills is common in ch ildren, adolescents, and adults. Episodes of\nsevere anxiety or anxiety disorders, including somatic complaints or panic attacks, are\ncommon across the lifespan and accompany both the circumscribed and the broader ex-\npression of learning difficulties.\nRisk and Prognostic Factors \nEnvironmental. Prematurity or very low birth weight increases the risk for specific\nlearning disorder, as does pr enatal exposure to nicotine.\nGenetic and physiological. Specific learning disorder a ppears to aggregate in families,\nparticularly when affecting reading, mathemat ics, and spelling. The relative risk of spe-\ncific learning disorder in reading or mathematics is substantially higher (e.g., 4\u20138 times\nand 5\u201310 times higher, respectively) in first- degree relatives of individuals with these\nlearning difficulties compared with those wi thout them. Family hist ory of reading diffi-", "source": "dsm5.pdf"} {"id": "eb83ae00d57a-1", "page_content": "learning difficulties compared with those wi thout them. Family hist ory of reading diffi-\nculties (dyslexia) and parental literacy skills predict literacy problems or specific learning\ndisorder in offspring, indicating the combin ed role of genetic and environmental factors.\nThere is high heritability for both reading ab ility and reading disability in alphabetic and\nnonalphabetic languages, including high heritabi lity for most manifestations of learning abil-\nities and disabilities (e.g., heritability estimate values greater than 0. 6). Covariation between\nvarious manifestations of learning difficulties is high, suggesting that genes related to one\npresentation are highly co rrelated with genes related to another manifestation.\nCourse modifiers. Marked problems with inattentive be havior in preschool years is pre-\ndictive of later difficulties in reading and ma thematics (but not necessarily specific learn-\ning disorder) and nonresponse to effective academic interventions. Delay or disorders in\nspeech or language, or impaired cognitive processing (e.g., phonological awareness,\nworking memory, rapid serial naming) in presch ool years, predicts la ter specific learning\ndisorder in reading and writ ten expression. Comorbidity wi th ADHD is predictive of\nworse mental health outcome than that associ ated with specific learning disorder without\nADHD. Systematic, intensive, individualized instruction, using evidence-based interven-\ntions, may improve or ameliorate the learning difficulties in some individuals or promote\nthe use of compensatory strategies in others , thereby mitigating the otherwise poor out-\ncomes.\nCulture-Related Diagnostic Issues\nSpecific learning disorder oc curs across languages, cultures, races, and socioeconomic\nconditions but may vary in its manifestation according to the nature of the spoken and\nwritten symbol systems and cultural and educational practices. For example, the cognitive", "source": "dsm5.pdf"} {"id": "eb83ae00d57a-2", "page_content": "written symbol systems and cultural and educational practices. For example, the cognitive\nprocessing requirements of reading and of wo rking with numbers vary greatly across or-\nthographies. In the English language, the observable hallmark clinical symptom of diffi-\nculties learning to read is inaccurate and slow reading of single words; in other alphabetic", "source": "dsm5.pdf"} {"id": "86420277f8a1-0", "page_content": "thographies. In the English language, the observable hallmark clinical symptom of diffi-\nculties learning to read is inaccurate and slow reading of single words; in other alphabetic\nlanguages that have more direct mapping be tween sounds and letters (e.g., Spanish, Ger-\nman) and in non-alphabetic la nguages (e.g., Chinese, Japanese), the hallmark feature is", "source": "dsm5.pdf"} {"id": "fb00795416df-0", "page_content": "Specific Learning Disorder 73\nslow but accurate reading. In English-language learners, assessment should include con-\nsideration of whether the source of reading difficulties is a limited proficiency with Eng-\nlish or a specific learning disorder. Risk fact ors for specific learning disorder in English-\nlanguage learners include a family history of specific learning disorder or language delay\nin the native language, as well as learning difficulties in English and failure to catch up\nwith peers. If there is suspicio n of cultural or language differences (e.g., as in an English-\nlanguage learner), the assessment needs to ta ke into account the individual\u2019s language\nproficiency in his or her first or native lang uage as well as in the second language (in this\nexample, English). Also, assessment should co nsider the linguistic and cultural context in\nwhich the individual is living, as well as his or her educational and learning history in the\noriginal culture and language.\nGender-Related Diagnostic Issues\nSpecific learning disorder is more common in males than in fema les (ratios range from\nabout 2:1 to 3:1) and cannot be attributed to factors such as ascertainment bias, definitional\nor measurement variation, language , race, or socioeconomic status.\nFunctional Consequences of\nSpecific Learning Disorder\nSpecific learning disorder can have negative functional consequences across the lifespan,\nincluding lower academic attainment, higher ra tes of high school dropout, lower rates of\npostsecondary education, high levels of psyc hological distress and poorer overall mental\nhealth, higher rates of unemployment and under-employment, and lower incomes. School\ndropout and co-occurring depressive symptoms increase the risk for poor mental health\noutcomes, including suicidality, whereas high levels of social or emotional support predict\nbetter mental health outcomes.\nDifferential Diagnosis\nNormal variations in academic attainment. Specific learning disorder is distinguished", "source": "dsm5.pdf"} {"id": "fb00795416df-1", "page_content": "Differential Diagnosis\nNormal variations in academic attainment. Specific learning disorder is distinguished\nfrom normal variations in academic attainment due to external factors (e.g., lack of edu-\ncational opportunity, consistently poor instru ction, learning in a second language), be-\ncause the learning difficulties persist in the presence of adequate educational opportunity\nand exposure to the same instruction as the p eer group, and competency in the language of\ninstruction, even when it is different from one\u2019s primary spoken language.\nIntellectual disability (intelle ctual developmental disorder). Specific learning disorder\ndiffers from general learning difficulties assoc iated with intellectual disability, because the\nlearning difficulties occur in the presence of normal levels of intellectual functioning (i.e.,\nIQ score of at least 70 \u00b1 5). If intellectual disa bility is present, specific learning disorder can\nbe diagnosed only when the learning difficult ies are in excess of those usually associated\nwith the intellectual disability.\nLearning difficulties due to neurological or sensory disorders. Specific learning dis-\norder is distinguished from lear ning difficulties due to neurological or sensory disorders\n(e.g., pediatric stroke, traumatic brain injury , hearing impairment, vi sion impairment), be-\ncause in these cases there are abnormal findings on neurological examination.\nNeurocognitive disorders. Specific learning disorder is distinguished from learning\nproblems associated with neurodegenerative cognitive disorders, because in specific\nlearning disorder the clinical expression of specific learning difficulties occurs during the\ndevelopmental period, and the difficulties do not manifest as a mark ed decline from a for-\nmer state.", "source": "dsm5.pdf"} {"id": "e8ab6b9e5b94-0", "page_content": "74 Neurodevelopmental Disorders\nAttention-deficit/hyperactivity disorder. Specific learning disorder is distinguished from\nthe poor academic performance associated with ADHD, because in the latter condition the\nproblems may not necessarily reflect specific difficulties in learning academic skills but\nrather may reflect difficulties in performing those skills. However, the co-occurrence of\nspecific learning disorder and ADHD is more fr equent than expected by chance. If criteria\nfor both disorders are met, both diagnoses can be given.\nPsychotic disorders. Specific learning disorder is dist inguished from the academic and\ncognitive-processing difficulties associated wi th schizophrenia or psychosis, because with\nthese disorders there is a decline (often rapid) in these functional domains.\nComorbidity \nSpecific learning disorder commonly co-occ urs with neurodevelopmental (e.g., ADHD,\ncommunication disorders, developmental coordi nation disorder, autistic spectrum disor-\nder) or other mental disorders (e.g., anxiety disorders, depressive and bipolar disorders).\nThese comorbidities do not necessarily exclud e the diagnosis specific learning disorder\nbut may make testing and differential diagnosis more difficult, because each of the co-\noccurring disorders independentl y interferes with the executio n of activities of daily liv-\ning, including learning. Thus, clinical judgment is required to attrib ute such impairment to\nlearning difficulties. If there is an indication that another diagnosis could account for the\ndifficulties learning keystone academic skills described in Criterion A, specific learning\ndisorder should not be diagnosed. \nMotor Disorders\nDevelopmental Coordination Disorder\nDiagnostic Criteria 315.4 (F82)\nA. The acquisition and execution of coordinated motor skills is substantially below that ex-\npected given the individual\u2019s chronological age and opportunity for skill learning and\nuse. Difficulties are manifested as clumsi ness (e.g., dropping or bumping into objects)", "source": "dsm5.pdf"} {"id": "e8ab6b9e5b94-1", "page_content": "as well as slowness and inaccuracy of performance of motor skills (e.g., catching an\nobject, using scissors or cutlery, handwriting, riding a bike, or participating in sports). \nB. The motor skills deficit in Criterion A significantly and persistently interferes with activ-\nities of daily living appropriate to chronological age (e.g., self-care and self-mainte-\nnance) and impacts academic/school pr oductivity, prevocational and vocational\nactivities, leisure, and play.\nC. Onset of symptoms is in the early developmental period.\nD. The motor skills deficits are not better explained by intellectual disability (intellectual devel-\nopmental disorder) or visual impairment and are not attributable to a neurological condi-\ntion affecting movement (e.g., cerebral palsy, muscular dystrophy, degenerative disorder).\nDiagnostic Features\nThe diagnosis of developmental coordination diso rder is made by a clinical synthesis of the\nhistory (developmental and medical), physical ex amination, school or workplace report, and\nindividual assessment using psychometrically sound and culturally appropriate standardized\ntests. The manifestation of impaired skills re quiring motor coordination (Criterion A) varies", "source": "dsm5.pdf"} {"id": "d29d35802989-0", "page_content": "Developmental Coordination Disorder 75\nwith age. Young children may be delayed in achi eving motor milestones (i.e., sitting, crawling,\nwalking), although many achieve typical motor milestones. They also may be delayed in de-\nveloping skills such as negotiating stairs, peda ling, buttoning shirts, completing puzzles, and\nusing zippers. Even when the skill is achiev ed, movement executio n may appear awkward,\nslow, or less precise than that of peers. Older children and adults may display slow speed or in-\naccuracy with motor aspects of activities such as assembling puzzles, building models, playing\nball games (especially in teams), handwriting, ty ping, driving, or carrying out self-care skills.\nDevelopmental coordination di sorder is diagnosed only if the impairment in motor\nskills significantly interferes with the performanc e of, or participation in, daily activities in\nfamily, social, school, or community life (Criteri on B). Examples of such activities include\ngetting dressed, eating meals with age-appropriate utensils and without mess, engaging\nin physical games with others, using specific t ools in class such as rulers and scissors, and\nparticipating in team exercise activities at sc hool. Not only is ability to perform these ac-\ntions impaired, but also marked slowness in execution is common. Handwriting compe-\ntence is frequently affected, consequently affe cting legibility and/or speed of written output\nand affecting academic achievement (the impact is distinguished from specific learning\ndifficulty by the emphasis on the motoric comp onent of written output skills). In adults,\neveryday skills in education and work, especially those in which speed and accuracy are\nrequired, are affected by coordination problems.\nCriterion C states that the onset of sympto ms of developmental coordination disorder\nmust be in the early developmental period. However, developmental coordination disorder is", "source": "dsm5.pdf"} {"id": "d29d35802989-1", "page_content": "must be in the early developmental period. However, developmental coordination disorder is\ntypically not diagnosed before age 5 years because there is considerable variation in the age at\nacquisition of many motor skills or a lack of st ability of measurement in early childhood (e.g.,\nsome children catch up) or because other causes of motor delay may not have fully manifested.\nCriterion D specifies that the diagnosis of developmental coordination disorder is\nmade if the coordination difficulties are not better explained by visual impairment or at-\ntributable to a neurological condition. Thus, visual functi on examination and neurological\nexamination must be included in the diagnost ic evaluation. If intellectual disability (intel-\nlectual developmental disorder) is present, the motor difficulties are in excess of those ex-\npected for the mental age; ho wever, no IQ cut-off or disc repancy criterion is specified.\nDevelopmental coordination disorder does no t have discrete subtypes; however, indi-\nviduals may be impaired predominantly in gro ss motor skills or in fine motor skills, in-\ncluding handwriting skills.\nOther terms used to describe developm ental coordination disorder include childhood\ndyspraxia, specific developmental disorder of motor function, and clumsy child syndrome.\nAssociated Features Supporting Diagnosis\nSome children with developmental coordination disorder sh ow additional (usually sup-\npressed) motor activity, such as choreiform movements of unsupported limbs or mirror\nmovements. These \u201coverflow\u201d movements are referred to as neurodevelopment al immaturities or\nneurological soft signs rather than neurological abnormalit ies. In both current literature and\nclinical practice, their role in diagnosis is still unclear, requiring further evaluation.\nPrevalence\nThe prevalence of developmental coordination disorder in children ages 5\u201311 years is 5%\u2013\n6% (in children age 7 years, 1.8% are diagnosed with severe developmental coordination", "source": "dsm5.pdf"} {"id": "d29d35802989-2", "page_content": "disorder and 3% with probable developmental coordination disorder). Males are more of-\nten affected than females, with a male:female ratio between 2:1 and 7:1.", "source": "dsm5.pdf"} {"id": "a7f36fafa5db-0", "page_content": "disorder and 3% with probable developmental coordination disorder). Males are more of-\nten affected than females, with a male:female ratio between 2:1 and 7:1.\nDevelopment and Course\nThe course of developmental coordination disord er is variable but stable at least to 1 year\nfollow-up. Although there may be improvement in the longer term, problems with coor-", "source": "dsm5.pdf"} {"id": "57293b5ccb19-0", "page_content": "76 Neurodevelopmental Disorders\ndinated movements continue th rough adolescence in an esti mated 50%\u201370% of children.\nOnset is in early childhood. Delayed motor mile stones may be the first signs, or the disor-\nder is first recognized when the child attempts tasks such as holding a knife and fork, but-\ntoning clothes, or playing ball games. In middle childhood, there are difficulties with\nmotor aspects of assembling puzzles, building models, playing ball, and handwriting, as\nwell as with organizing belongings, when mo tor sequencing and co ordination are re-\nquired. In early adulthood, there is continuing difficulty in learning new tasks involving\ncomplex/automatic motor skills, including drivin g and using tools. Inability to take notes\nand handwrite quickly may affect performance in the workplace. Co-occurrence with\nother disorders (see the sectio n \u201cComorbidity\u201d for this disorder) has an additional impact\non presentation, course, and outcome.\nRisk and Prognostic Factors \nEnvironmental. Developmental coordination disorder is more common following pre-\nnatal exposure to alcohol and in pr eterm and low-birth-weight children.\nGenetic and physiological. Impairments in underlying neurodevelopmental processes\u2014\nparticularly in visual-motor sk ills, both in visual-motor perception and spatial mentalizing\u2014\nhave been found and affect the ability to make rapid motoric adjustments as the complexity of\nthe required movements increases. Cerebellar dysfunction has been proposed, but the neural\nbasis of developmental coordination disorder remains unclear. Because of the co-occurrence of\ndevelopmental coordination disorder with atte ntion-deficit/hyperactiv ity disorder (ADHD),\nspecific learning disabilities, and autism spectr um disorder, shared genetic effect has been pro-\nposed. However, consistent co-occurrence in twins appears only in severe cases.", "source": "dsm5.pdf"} {"id": "57293b5ccb19-1", "page_content": "posed. However, consistent co-occurrence in twins appears only in severe cases.\nCourse modifiers. Individuals with ADHD and with developmental coordination dis-\norder demonstrate more impair ment than individuals with ADHD without developmen-\ntal coordination disorder.\nCulture-Related Diagnostic Issues\nDevelopmental coordination disorder occurs across cultures, races, and socioeconomic\nconditions. By definition, \u201cacti vities of daily living\u201d implie s cultural differences necessi-\ntating consideration of the context in whic h the individual child is living as well as\nwhether he or she has had appropriate opportun ities to learn and practice such activities. \nFunctional Consequences of \nDevelopmental Coordination Disorder \nDevelopmental coordination disorder leads to impaired functional performance in activ-\nities of daily living (Criterion B), and the impairment is increased with co-occurring con-\nditions. Consequences of developmental coordination disorder include reduced\nparticipation in team play and sports; poor self-esteem and sense of self-worth ; emotional\nor behavior problems; impair ed academic achievement; p oor physical fitness; and re-\nduced physical activity and obesity.\nDifferential Diagnosis\nMotor impairments due to another medical condition. Problems in coordination may\nbe associated with visual function impairme nt and specific neurological disorders (e.g.,\ncerebral palsy, progressive lesions of the cerebellum, neuromuscula r disorders). In such\ncases, there are additional findin gs on neurological examination. \nIntellectual disability (intell ectual developmental disorder). If intellectual disability is\npresent, motor competences may be impaired in accordance with the intellectual disabil-", "source": "dsm5.pdf"} {"id": "185dd6a01c65-0", "page_content": "Stereotypic Movement Disorder 77\nity. However, if the motor difficulties are in excess of what could be accounted for by the\nintellectual disability, and crit eria for developmental coordination disorder are met, de-\nvelopmental coordination disorder can be diagnosed as well. \nAttention-deficit/hyperactivity disorder. Individuals with ADHD may fall, bump into\nobjects, or knock things over. Careful observat ion across different contexts is required to\nascertain if lack of motor competence is at tributable to distract ibility and impulsiveness\nrather than to developmental coordination disorder. If criteria for both ADHD and devel-\nopmental coordination disorder are met, both diagnoses can be given.\nAutism spectrum disorder. Individuals with autism spectrum disorder may be uninter-\nested in participating in task s requiring complex coordination skills, such as ball sports,\nwhich will affect test performance and function but not reflect core motor competence. Co-\noccurrence of developmental coordination disorder and autism spectr um disorder is com-\nmon. If criteria for both disorders are met, both diagnoses can be given.\nJoint hypermobility syndrome. Individuals with syndrome s causing hyperextensible\njoints (found on ph ysical examination; often with a complaint of pain) may present with\nsymptoms similar to those of deve lopmental coordination disorder.\nComorbidity\nDisorders that commonly co-occur with deve lopmental coordination disorder include\nspeech and language disorder; specific learning disorder (especially reading and writing);\nproblems of inattention, incl uding ADHD (the most frequent coexisting condition, with\nabout 50% co-occurrence); autism spectrum disord er; disruptive and emotional behavior\nproblems; and joint hypermobility syndrome. Different clusters of co-occurrence may be\npresent (e.g., a cluster with severe reading di sorders, fine motor problems, and handwriting", "source": "dsm5.pdf"} {"id": "185dd6a01c65-1", "page_content": "problems; another cluster with impaired movement control and motor planning). Presence\nof other disorders does not exclude develo pmental coordination disorder but may make\ntesting more difficult and may independently interfere with th e execution of activities of\ndaily living, thus requiring examiner judgment in ascribing impairment to motor skills. \nStereotypic Movement Disorder\nDiagnostic Criteria 307.3 (F98.4)\nA. Repetitive, seemingly driven, and apparently purposeless motor behavior (e.g., hand\nshaking or waving, body rocking, head banging, self-biting, hitting own body).\nB. The repetitive motor behavior interferes wit h social, academic, or other activities and\nmay result in self-injury.\nC. Onset is in the early developmental period.\nD. The repetitive motor behavior is not attributable to the physiological effects of a sub-\nstance or neurological condition and is no t better explained by another neurodevel-\nopmental or mental disorder (e.g., trichotillomania [hair-pulling disorder], obsessive-\ncompulsive disorder).\nSpecify if:\nWith self-injurious behavior (or behavior that would result in an injury if preventive\nmeasures were not used)\nWithout self-injurious behavior\nSpecify if:\nAssociated with a known medical or genetic condition, neurodevelopmental dis-\norder, or environmental factor (e.g., Lesch-Nyhan syndrome, intellectual disability\n[intellectual developmental disorder], intrauterine alcohol exposure)", "source": "dsm5.pdf"} {"id": "183bae2f7d78-0", "page_content": "78 Neurodevelopmental Disorders\nCoding note: Use additional code to identify the associated medical or genetic\ncondition, or neurodevelopmental disorder.\nSpecify current severity:\nMild: Symptoms are easily suppressed by sensory stimulus or distraction.\nModerate: Symptoms require explicit protective measures and behavioral modification.\nSevere: Continuous monitoring and protective m easures are required to prevent seri-\nous injury.\nRecording Procedures\nFor stereotypic movement diso rder that is associated with a known medical or genetic\ncondition, neurodevelopmental disorder, or environmental factor, record stereotypic\nmovement disorder associated with (name of condition, disorder, or factor) (e.g., stereo-\ntypic movement disorder associat ed with Lesch-Nyhan syndrome).\nSpecifiers\nThe severity of non-self-injurious stereotypi c movements ranges from mild presentations\nthat are easily suppressed by a sensory stimul us or distraction to continuous movements\nthat markedly interfere with all activities of da ily living. Self-injurious behaviors range in se-\nverity along various dimensions, including the frequency, impact on adaptive functioning,\nand severity of bodily injury (from mild bruising or erythema from hitting hand against\nbody, to lacerations or amputa tion of digits, to retinal detachment from head banging).\nDiagnostic Features\nThe essential feature of stereotypic movement disorder is repetitive, seemingly driven,\nand apparently purposeless motor behavior (Criterion A). These behaviors are often\nrhythmical movements of the head, hands, or body without obvious adaptive function.\nThe movements may or may not respond to efforts to stop them. Among typically devel-\noping children, the repetitive movements may be stopped when attention is directed to\nthem or when the child is distracted from performing them. Among children with neuro-\ndevelopmental disorders, the behaviors are typically less responsive to such efforts. In", "source": "dsm5.pdf"} {"id": "183bae2f7d78-1", "page_content": "developmental disorders, the behaviors are typically less responsive to such efforts. In\nother cases, the individual demonstrates self-restraining beha viors (e.g., sitting on hands,\nwrapping arms in clothing, finding a protective device).\nThe repertoire of behaviors is variable; each individual presents with his or her own in-\ndividually patterned, \u201csignat ure\u201d behavior. Examples of no n-self-injurious stereotypic\nmovements include, but are not limited to, bo dy rocking, bilateral flapping or rotating\nhand movements, flicking or fl uttering fingers in front of the face, arm waving or flapping,\nand head nodding. Stereotyped self-injurious behaviors include, but are not limited to, re-\npetitive head banging, face slapping, eye poki ng, and biting of hands, lips, or other body\nparts. Eye poking is particularly concerning; it occurs more freq uently among children\nwith visual impairment. Multiple movements may be combined (e.g., cocking the head,\nrocking the torso, waving a small string repetitively in front of the face).\nStereotypic movements may oc cur many times during a da y, lasting a few seconds to\nseveral minutes or longer. Frequency can vary from many occurrences in a single day to\nseveral weeks elapsing between episodes. The behaviors vary in context, occurring when\nthe individual is engrossed in other activities , when excited, stressed, fatigued, or bored.\nCriterion A requires that the movements be \u201capparently\u201d purposeless. However, some\nfunctions may be served by the movements. For example, stereotypic movements might\nreduce anxiety in response to external stressors.\nCriterion B states that the stereotypic mo vements interfere with social, academic, or", "source": "dsm5.pdf"} {"id": "183bae2f7d78-2", "page_content": "Criterion B states that the stereotypic mo vements interfere with social, academic, or\nother activities and, in some children, may resu lt in self-injury (or would if protective mea-\nsures were not used). If self-injury is present, it should be coded using the specifier. Onset", "source": "dsm5.pdf"} {"id": "7202e199b462-0", "page_content": "Stereotypic Movement Disorder 79\nof stereotypic movements is in the early deve lopmental period (Criterion C). Criterion D\nstates that the repetitive, stereotyped behavior in stereotypic movement disorder is not at-\ntributable to the physiological effects of a su bstance or neurological condition and is not\nbetter explained by another ne urodevelopmental or mental disorder. The presence of\nstereotypic movements may indicate an unde tected neurodevelopmental problem, espe-\ncially in children ages 1\u20133 years.\nPrevalence \nSimple stereotypic movements (e.g., rocking) ar e common in young typically developing chil-\ndren. Complex stereoty pic movements are much less common (occurring in approximately\n3%\u20134%). Between 4% and 16% of individuals with intellectual disability (intellectual develop-\nmental disorder) engage in stereotypy and self-injury. The risk is greater in individuals with\nsevere intellectual disability. Among individual s with intellectual disability living in res-\nidential facilities, 10%\u201315% may have stereo typic movement disord er with self-injury.\nDevelopment and Course \nStereotypic movements typically begin within the first 3 years of life. Simple stereotypic move-\nments are common in infancy and may be involve d in acquisition of motor mastery. In chil-\ndren who develop complex motor stereotypies, approximately 80% exhibit symptoms before\n24 months of age, 12% between 24 and 35 months, and 8% at 36 months or older. In most typ-\nically developing children, these movements resolve over time or can be suppressed. Onset of\ncomplex motor stereotypies may be in infancy or later in the develo pmental period. Among", "source": "dsm5.pdf"} {"id": "7202e199b462-1", "page_content": "individuals with intellectual disability, the ster eotyped, self-injurious behaviors may persist\nfor years, even though the typography or pattern of self-injury may change.\nRisk and Prognostic Factors\nEnvironmental. Social isolation is a risk factor for self-stimulation that may progress to\nstereotypic movements with repetitive self-inj ury. Environmental stress may also trigger\nstereotypic behavior. Fear may alter physiological state, resulting in increased frequency\nof stereotypic behaviors.\nGenetic and physiological. Lower cognitive functioning is link ed to greater risk for stereo-\ntypic behaviors and poorer response to interv entions. Stereotypic movements are more fre-\nquent among individuals with moderate-to-se vere/profound intellectual disability, who by\nvirtue of a particular syndrome (e.g., Rett syndrome) or environmental factor (e.g., an environ-\nment with relatively insufficient stimulation) se em to be at higher risk for stereotypies. Repet-\nitive self-injurious behavior ma y be a behavioral phenotype in neurogenetic syndromes. For\nexample, in Lesch-Nyhan syndrome, there are bo th stereotypic dystonic movements and self-\nmutilation of fingers, lip biti ng, and other forms of self-injury unless the individual is re-\nstrained, and in Rett syndrome and Cornelia de Lange syndrome, self-i njury may result from\nthe hand-to-mouth st ereotypies. Stereotypic behaviors may result from a painful medical con-\ndition (e.g., middle ear infection, de ntal problems, gastro esophageal reflux).\nCulture-Related Diagnostic Issues\nStereotypic movement disorder, wi th or without self-injury, occurs in all races and cultures.\nCultural attitudes toward unusual behaviors may result in delayed diagnosis. Overall cultural", "source": "dsm5.pdf"} {"id": "7202e199b462-2", "page_content": "Cultural attitudes toward unusual behaviors may result in delayed diagnosis. Overall cultural\ntolerance and attitudes toward stereotypic movement vary and mu st be considered.\nDifferential Diagnosis\nNormal development. Simple stereotypic movements ar e common in infancy and early\nchildhood. Rocking may occur in the transition from sleep to awake, a behavior that usu-", "source": "dsm5.pdf"} {"id": "bbc476de6522-0", "page_content": "80 Neurodevelopmental Disorders\nally resolves with age. Complex stereotypi es are less common in typically developing\nchildren and can usually be suppressed by dist raction or sensory stimulation. The indi-\nvidual\u2019s daily routine is rarely affected, and the movements generally do not cause the\nchild distress. The diagno sis would not be appropriat e in these circumstances.\nAutism spectrum disorder. Stereotypic movements may be a presenting symptom of\nautism spectrum disorder and should be con sidered when repetitive movements and be-\nhaviors are being evaluated. Deficits of soci al communication and re ciprocity manifesting\nin autism spectrum disorder are generally ab sent in stereotypic mo vement disorder, and\nthus social interaction, social communication , and rigid repetitive behaviors and interests\nare distinguishing features. Wh en autism spectrum disorder is present, stereotypic move-\nment disorder is diagnosed only when there is self-injury or when the stereotypic behav-\niors are sufficiently severe to become a focus of treatment.\nTic disorders. Typically, stereotypies have an earlier age at onset (before 3 years) than\ndo tics, which have a mean age at onset of 5\u20137 years. They are consistent and fixed in their\npattern or topography compared with tics, which are variable in their presentation. Ste-\nreotypies may involve arms, hands, or the entire body, while tics commonly involve eyes,\nface, head, and shoulders. Stereotypies are more fixed, rhythmic, and prolonged in dura-\ntion than tics, which, generally, are brief, ra pid, random, and fluctuating. Tics and stereo-\ntypic movements are both reduced by distraction.\nObsessive-compulsive and related disorders. Stereotypic movement disorder is dis-", "source": "dsm5.pdf"} {"id": "bbc476de6522-1", "page_content": "Obsessive-compulsive and related disorders. Stereotypic movement disorder is dis-\ntinguished from obsessive-co mpulsive disorder (OCD) by the absence of obsessions, as\nwell as by the nature of the repetitive behaviors. In OCD the individual feels driven to per-\nform repetitive behaviors in response to an ob session or according to rules that must be ap-\nplied rigidly, whereas in stereotypic movement disorder the behaviors are seemingly\ndriven but apparently purposeless. Trichot illomania (hair-pulling disorder) and excoria-\ntion (skin-picking) disorder are characterize d by body-focused repetitive behaviors (i.e.,\nhair pulling and skin picking) that may be seemingly driven but th at are not apparently\npurposeless, and that may not be patterned or rhythmical. Furthermore, onset in tricho-\ntillomania and excoriation disord er is not typically in the early developmental period, but\nrather around puberty or later.\nOther neurological and medical conditions. The diagnosis of stereotypic movements\nrequires the exclusion of habits, mannerisms, pa roxysmal dyskinesias, and benign he-\nreditary chorea. A neurological history and examination are required to assess features\nsuggestive of other disorders, such as myoclo nus, dystonia, tics, and chorea. Involuntary\nmovements associated with a neurological co ndition may be distinguished by their signs\nand symptoms. For example, repetitive, stereotypic movements in tardive dyskinesia can\nbe distinguished by a history of chronic neuroleptic use and characteristic oral or facial\ndyskinesia or irregular trunk or limb movements. These type s of movements do not result\nin self-injury. A diagnosis of stereotypic mo vement disorder is not appropriate for repet-", "source": "dsm5.pdf"} {"id": "bbc476de6522-2", "page_content": "itive skin picking or scratching associated with amphetamine intoxi cation or abuse (e.g.,\npatients are diagnosed with substance/medication-induced obsessi ve-compulsive and re-\nlated disorder) and repetitive choreoathetoid movements associated with other neurolog-\nical disorders.\nComorbidity\nStereotypic movement d isorder may occur as a primary diagnosis or secondary to another\ndisorder. For example, stereotypies are a common manifestation of a variety of neuro-\ngenetic disorders, such as Lesch-Nyhan syndrome, Rett syndrome, fragile X syndrome,\nCornelia de Lange syndrome, and Smith-Magenis syndrome. When stereotypic move-", "source": "dsm5.pdf"} {"id": "0ef6ed49968e-0", "page_content": "genetic disorders, such as Lesch-Nyhan syndrome, Rett syndrome, fragile X syndrome,\nCornelia de Lange syndrome, and Smith-Magenis syndrome. When stereotypic move-\nment disorder co-occurs with another me dical condition, both should be coded.", "source": "dsm5.pdf"} {"id": "67a69c33e9bf-0", "page_content": "Tic Disorders 81\nTic Disorders\nDiagnostic Criteria \nNote: A tic is a sudden, rapid, recurrent, nonrhythmic motor movement or vocalization.\nTourette\u2019s Disorder 307.23 (F95.2)\nA. Both multiple motor and one or more vocal tics have been present at some time during\nthe illness, although not necessarily concurrently.\nB. The tics may wax and wane in frequency but have persisted for more than 1 year since\nfirst tic onset.\nC. Onset is before age 18 years.\nD. The disturbance is not attributable to the physiological effects of a substance (e.g., co-\ncaine) or another medical condition (e.g., Huntington\u2019s disease, postviral encephalitis).\nPersistent (Chronic) Motor or Vocal Tic Disorder 307.22 (F95.1)\nA. Single or multiple motor or vocal tics have been present during the illness, but not both\nmotor and vocal.\nB. The tics may wax and wane in frequency but have persisted for more than 1 year since\nfirst tic onset.\nC. Onset is before age 18 years.\nD. The disturbance is not attributable to the physiological effects of a substance (e.g., co-\ncaine) or another medical condition (e.g., Huntington\u2019s disease, postviral encephalitis).\nE. Criteria have never been met for Tourette\u2019s disorder.\nSpecify if:\nWith motor tics only\nWith vocal tics only\nProvisional Tic Disorder 307.21 (F95.0)\nA. Single or multiple motor and/or vocal tics.\nB. The tics have been present for less than 1 year since first tic onset.\nC. Onset is before age 18 years.", "source": "dsm5.pdf"} {"id": "67a69c33e9bf-1", "page_content": "C. Onset is before age 18 years.\nD. The disturbance is not attributable to the physiological effects of a substance (e.g., co-\ncaine) or another medical condition (e.g., Huntington\u2019s disease, postviral encephalitis).\nE. Criteria have never been met for Tourette\u2019s disorder or persistent (chronic) motor or\nvocal tic disorder.\nSpecifiers \nThe \u201cmotor tics only\u201d or \u201cvocal tics only\u201d spec ifier is only required for persistent (chronic)\nmotor or vocal tic disorder.\nDiagnostic Features\nTic disorders comprise four diagnostic categori es: Tourette\u2019s disorder, persistent (chronic)\nmotor or vocal tic disorder, pr ovisional tic disorder, and the other specified and unspecified\ntic disorders. Diagnosis for any tic disorder is based on the presence of motor and/or vocal\ntics (Criterion A), dura tion of tic symptoms (C riterion B), age at onse t (Criterion C), and ab-\nsence of any known cause such as another medical condition or substance use (Criterion D).\nThe tic disorders are hierarchical in order (i .e., Tourette\u2019s disorder, followed by persistent\n[chronic] motor or vocal tic disorder, followed by provisional tic disorder, followed by the", "source": "dsm5.pdf"} {"id": "203c455d24bf-0", "page_content": "82 Neurodevelopmental Disorders\nother specified and unspecified tic disorders), such that once a tic disorder at one level of the\nhierarchy is diagnosed, a lower hierarchy diagnosis cannot be made (Criterion E).\nTics are sudden, rapid, recurrent, nonrhythmic motor movements or vocalizations. An\nindividual may have various tic symptoms over time, but at any point in time, the tic rep-\nertoire recurs in a characteristic fashion. Although tics can include almost any muscle group\nor vocalization, certain tic symptoms, such as eye blinking or throat clearing, are common\nacross patient populations. Tics are generall y experienced as involun tary but can be vol-\nuntarily suppressed for varying lengths of time.\nTics can be either simple or complex. Simple motor tics are of short duration (i.e., milli-\nseconds) and can include eye blinking, should er shrugging, and extension of the extrem-\nities. Simple vocal tics include throat clea ring, sniffing, and grunting often caused by\ncontraction of the diaphragm or muscles of the oropharynx. Complex motor tics are of lon-\nger duration (i.e., seconds) and often include a combination of simple tics such as simul-\ntaneous head turning and shoulder shrugging . Complex tics can appear purposeful, such\nas a tic-like sexual or obscene gesture ( copropraxia ) or a tic-like imitation of someone else\u2019s\nmovements ( echopraxia). Similarly, complex vocal tics include repeating one\u2019s own sounds\nor words ( palilalia ), repeating the last-heard word or phrase ( echolalia ), or uttering socially\nunacceptable words, including obscenities, or ethnic, racial, or religious slurs ( coprolalia ).", "source": "dsm5.pdf"} {"id": "203c455d24bf-1", "page_content": "Importantly, coprolalia is an abrupt, sharp ba rk or grunt utterance and lacks the prosody\nof similar inappropriate speech observed in human interactions.\nThe presence of motor and/or vocal tics varies across the four tic disorders (Criterion\nA). For Tourette\u2019s disorder, both motor and vo cal tics must be present, whereas for per-\nsistent (chronic) motor or vocal tic disorder, on ly motor or only vocal tics are present. For\nprovisional tic disorder, motor and/or vocal tics may be presen t. For other specified or un-\nspecified tic disorders, the movement disorder symptoms are best characterized as tics but\nare atypical in presentation or age at onset, or have a known etiology.\nThe 1-year minimum duration criterion (Cri terion B) assures that individuals diag-\nnosed with either Tourette\u2019s disorder or pe rsistent (chronic) moto r or vocal tic disorder\nhave had persistent symptoms. Tics wax and wa ne in severity, and some individuals may\nhave tic-free periods of weeks to months; ho wever, an individual who has had tic symp-\ntoms of greater than 1 year\u2019s duration since fi rst tic onset would be considered to have per-\nsistent symptoms regardless of duration of ti c-free periods. For an individual with motor\nand/or vocal tics of less than 1 year since firs t tic onset, a provisional tic disorder diagnosis\ncan be considered. There is no duration specif ication for other specif ied and unspecified tic\ndisorders. The onset of tics mu st occur prior to age 18 year s (Criterion C). Tic disorders\ntypically begin in the prepubertal period, with an average age at onset between 4 and 6\nyears, and with the incidence of new-onset tic disorders decreasing in the teen years. New", "source": "dsm5.pdf"} {"id": "203c455d24bf-2", "page_content": "years, and with the incidence of new-onset tic disorders decreasing in the teen years. New\nonset of tic symptoms in adulthood is exceedin gly rare and is often associated with expo-\nsures to drugs (e.g., excessive cocaine use) or is a result of a central nervous system insult\n(e.g., postviral encephalitis). Although tic onse t is uncommon in teenagers and adults, it is\nnot uncommon for adolescents an d adults to present for an initial diagnostic assessment\nand, when carefully evaluated, provide a histor y of milder symptoms dating back to child-\nhood. New-onset abnormal move ments suggestive of tics out side of the us ual age range\nshould result in evaluation for other move ment disorders or for specific etiologies.", "source": "dsm5.pdf"} {"id": "2d8d7afa4985-0", "page_content": "hood. New-onset abnormal move ments suggestive of tics out side of the us ual age range\nshould result in evaluation for other move ment disorders or for specific etiologies.\nTic symptoms cannot be attributable to the physiologica l effects of a substance or an-\nother medical condition (Criterion D). When there is strong eviden ce from the history,\nphysical examination, and/or laboratory resu lts to suggest a plausible, proximal, and\nprobable cause for a tic disorder, a diagnosis of other specified tic disorder should be used.\nHaving previously met diagnostic criteria fo r Tourette\u2019s disorder negates a possible di-\nagnosis of persistent (chronic) motor or vocal ti c disorder (Criterion E). Similarly, a previ-\nous diagnosis of persistent (chronic) motor or vocal tic disorder negates a diagnosis of\nprovisional tic disorder or ot her specified or unspecified tic disorder (Criterion E).", "source": "dsm5.pdf"} {"id": "6e001d788060-0", "page_content": "Tic Disorders 83\nPrevalence\nTics are common in childhood but transient in most cases. The estimated prevalence of\nTourette\u2019s disorder ranges from 3 to 8 per 1,000 in school-age children.\u00a0Males are more\ncommonly affected than females, with the rati o varying from 2:1 to 4:1.\u00a0A national survey\nin the United States estimated 3 per 1,000 for the prevalence of clinically identified cases.\nThe frequency of identified cases was lower among African Americans and Hispanic\nAmericans, which may be related to differences in access to care.\nDevelopment and Course\nOnset of tics is typically between ages 4 and 6 years. Peak severity occurs between ages 10\nand 12 years, with a decline in severity during adolescence. Many adults with tic disorders\nexperience diminished sympto ms. A small percentage of in dividuals will have persis-\ntently severe or worsening symptoms in adulthood.\nTic symptoms manifest similarly in all age groups and across the lifespan. Tics wax and\nwane in severity and change in affected muscle groups an d vocalizations over time. As\nchildren get older, they begin to report th eir tics being associated with a premonitory\nurge\u2014a somatic sensation that precedes the tic\u2014and a feeling of tension reduction follow-\ning the expression of the tic. Tics associated with a premonitory urge may be experienced\nas not completely \u201cinvoluntary\u201d in that the ur ge and the tic can be resisted. An individual\nmay also feel the need to perform a tic in a specific way or repeat it until he or she achieves\nthe feeling that the tic has been done \u201cjust right.\u201d\nThe vulnerability toward developing co-occurring conditions changes as individuals\npass through the age of risk for various co-o ccurring conditions. For example, prepubertal", "source": "dsm5.pdf"} {"id": "6e001d788060-1", "page_content": "children with tic disorders are more likely to experience attention-deficit/hyperactivity\ndisorder (ADHD), obsessive-co mpulsive disorder (OCD), and separation anxiety disorder\nthan are teenagers and adults, who are more li kely to experience the new onset of major\ndepressive disorder, substance use disorder, or bipolar disorder.\nRisk and Prognostic Factors \nTemperamental. Tics are worsened by anxiety, excitement, and exhaustion and are better\nduring calm, focused activities. Individuals ma y have fewer tics when engaged in schoolwork\nor tasks at work than when relaxing at home after school or in the evening. Stressful/exciting\nevents (e.g., taking a test, participating in exciting activities) often make tics worse. \nEnvironmental. Observing a gesture or sound in another person may result in an indi-\nvidual with a tic disorder making a simila r gesture or sound, which may be incorrectly\nperceived by others as purposeful. This can be a particular problem when the individual is\ninteracting with authority figures (e .g., teachers, supe rvisors, police).\nGenetic and physiological. Genetic and environmental factors influence tic symptom\nexpression and severity. Important risk allele s for Tourette\u2019s disorder and rare genetic\nvariants in families with tic disorders have been identified. Obstetrical complications,\nolder paternal age, lower birth weight, and maternal smoking during pregnancy are as-\nsociated with worse tic severity.\nCulture-Related Diagnostic Issues\nTic disorders do not appear to vary in clinical characteristics, course , or etiology by race,\nethnicity, and culture. However, race, ethnici ty, and culture may impa ct how tic disorders\nare perceived and managed in the family an d community, as well as influencing patterns\nof help seeking, and choices of treatment.", "source": "dsm5.pdf"} {"id": "251cd75eadf1-0", "page_content": "84 Neurodevelopmental Disorders\nGender-Related Diagnostic Issues\nMales are more commonly affected than females, but there are no gender differences in the\nkinds of tics, age at onset, or course. Wome n with persistent tic disorders may be more\nlikely to experience anxiety and depression.\nFunctional Consequenc es of Tic Disorders\nMany individuals with mild to moderate tic se verity experience no distress or impairment\nin functioning and may even be unaware of their tics. Individuals with more severe symp-\ntoms generally have more impairment in daily living, but ev en individuals with moderate\nor even severe tic disorders may function we ll. The presence of a co-occurring condition,\nsuch as ADHD or OCD, can have greater impa ct on functioning. Less commonly, tics dis-\nrupt functioning in daily activities and result in social isolation, interpersonal conflict,\npeer victimization, inab ility to work or to go to school, and lower quality of life. The indi-\nvidual also may experience substantial psycho logical distress. Rare complications of Tou-\nrette\u2019s disorder include physical injury, such as eye injury (from hitting oneself in the face),\nand orthopedic and neurological injury (e.g., disc disease related to forceful head and neck\nmovements).\nDifferential Diagnosis\nAbnormal movements that may accompany other medical conditions and stereotypic\nmovement disorder. Motor stereotypies are defined as involuntary rhythmic, repetitive,\npredictable movements that appe ar purposeful but serve no obvious adaptive function or\npurpose and stop with distraction. Examples include repetitive hand waving/rotating,\narm flapping, and finger wiggling. Motor stereo typies can be differentiated from tics based\non the former\u2019s earlier age at onset (younger than 3 years), prolonged duration (seconds to", "source": "dsm5.pdf"} {"id": "251cd75eadf1-1", "page_content": "minutes), constant repetitive fixed form and location, exacer bation when engrossed in ac-\ntivities, lack of a premonitory urge, and ce ssation with distraction (e.g., name called or\ntouched). Chorea represents rapid, random, continua l, abrupt, irregular, unpredictable,\nnonstereotyped actions that are usually bilatera l and affect all parts of the body (i.e., face,\ntrunk, and limbs). The timing, direction, and dist ribution of movements vary from mo-\nment to moment, and movements usually worsen during attempted voluntary action. Dys-\ntonia is the simultaneous sustained contracture of both agonist and antagonist muscles,\nresulting in a distorted posture or movement of parts of the bo dy. Dystonic postures are of-\nten triggered by attempts at voluntary movements and are not seen during sleep.\nSubstance-induced and paroxysmal dyskinesias. Paroxysmal dyskinesias usually oc-\ncur as dystonic or choreoathetoid movement s that are precipitated by voluntary move-\nment or exertion and less commonly arise from normal background activity.\nMyoclonus. Myoclonus is characterized by a sudden unidirectional movement that is\noften nonrhythmic. It may be worsened by movement and occur du ring sleep. Myoclonus\nis differentiated from tics by its rapidity, la ck of suppressibility, and absence of a premon-\nitory urge.\nObsessive-compulsive and related disorders. Differentiating obsessive-compulsive\nbehaviors from tics may be difficult. Clues fa voring an obsessive-compulsive behavior in-\nclude a cognitive-based drive (e.g., fear of co ntamination) and the n eed to perform the ac-", "source": "dsm5.pdf"} {"id": "251cd75eadf1-2", "page_content": "tion in a particular fashion a certain number of times, equally on both sides of the body, or\nuntil a \u201cjust right\u201d feeling is achieved. Impulse-control proble ms and other repetitive be-\nhaviors, including persistent hair pulling, skin picking, and nail biting, appear more goal\ndirected and complex than tics.", "source": "dsm5.pdf"} {"id": "b7beb1eb01f7-0", "page_content": "Other Specified Tic Disorder 85\nComorbidity\nMany medical and psychiatric conditions have been described as co-occurring with tic disor-\nders, with ADHD and obsessive-compulsive and related disorders be ing particularly com-\nmon. The obsessive-compulsive symptoms observed in tic disorder tend to be characterized\nby more aggressive symmetry and order symptoms and poorer response to pharmacotherapy\nwith selective serotonin reuptake inhibitors. Children with ADHD ma y demonstrate disrup-\ntive behavior, social immaturi ty, and learning difficulties th at may interfere with academic\nprogress and interpersonal relationships and lead to greater impairment than that caused by a\ntic disorder. Individuals with tic disorders can also have other movement disorders and other\nmental disorders, such as depressive, bipolar, or substance use disorders.\nOther Specified Tic Disorder\n307.20 (F95.8)\nThis category applies to presentations in which symptoms characteristic of a tic disorder\nthat cause clinically significant distress or impairment in social, occupational, or other im-\nportant areas of functioning predominate but do not meet the full criteria for a tic disorder\nor any of the disorders in the neurodevelopmental disorders diagnostic class. The other\nspecified tic disorder category is used in situations in which the clinician chooses to com-\nmunicate the specific reason that the presentation does not meet the criteria for a tic disor-\nder or any specific neurodevelopmental disorder. This is done by recording \u201cother specified\ntic disorder\u201d followed by the specific reason (e.g., \u201cwith onset after age 18 years\u201d). \nUnspecified Tic Disorder\n307.20 (F95.9)\nThis category applies to presentations in whic h symptoms characteristic of a tic disorder\nthat cause clinically significant distress or impairment in social, occupational, or other im-\nportant areas of functioning predominate but do not meet the full criteria for a tic disorder", "source": "dsm5.pdf"} {"id": "b7beb1eb01f7-1", "page_content": "or for any of the disorders in the neurodevelopmental disorders diagnostic class. The un-\nspecified tic disorder category is used in situations in which the clinician chooses not to\nspecify the reason that the criteria are not met for a tic disorder or for a specific neurode-\nvelopmental disorder, and includes presentations in which there is insufficient information\nto make a more specific diagnosis.", "source": "dsm5.pdf"} {"id": "15618ee427fb-0", "page_content": "86 Neurodevelopmental Disorders\nOther Neurodevelopmental Disorders\nOther Specified Neurodevelopmental Disorder\n315.8 (F88)\nThis category applies to presentations in which symptoms characteristic of a neurodevel-\nopmental disorder that cause impairment in social, occupational, or other important areas\nof functioning predominate but do not meet the full criteria for any of the disorders in the\nneurodevelopmental disorders diagnostic clas s. The other specified neurodevelopmental\ndisorder category is used in situations in which the clinician chooses to communicate the\nspecific reason that the presentation does not meet the criteria for any specific neurode-\nvelopmental disorder. This is done by recording \u201cother specified neurodevelopmental dis-\norder\u201d followed by the specific reason (e.g., \u201cneurodevelopmental disorder associated with\nprenatal alcohol exposure\u201d).\nAn example of a presentation that can be specified using the \u201cother specified\u201d desig-\nnation is the following:\nNeurodevelopmental disord er associated with pren atal alcohol exposure: Neu-\nrodevelopmental disorder associated with prenatal alcohol exposure is characterized\nby a range of developmental disabilities following exposure to alcohol in utero.\nUnspecified Neurodevelopmental Disorder\n315.9 (F89)\nThis category applies to presentations in which symptoms characteristic of a neurodevel-\nopmental disorder that cause impairment in social, occupational, or other important areas\nof functioning predominate but do not meet the full criteria for any of the disorders in the\nneurodevelopmental disorders diagnostic class. The unspecified neurodevelopmental dis-\norder category is used in situations in which the clinician chooses not to specify the reason\nthat the criteria are not met for a specific neurodevelopmental disorder, and includes pre-\nsentations in which there is insufficient information to make a more specific diagnosis\n(e.g., in emergency room settings).", "source": "dsm5.pdf"} {"id": "11f9d338a0e2-0", "page_content": "87Schizophrenia Spectrum and\nOther Psychotic Disorders\nSchizophrenia spectrum and other psychotic disorders include schizophrenia,\nother psychotic disorders, and schizotypal (per sonality) disorder. They are defined by ab-\nnormalities in one or more of the following fi ve domains: delusions, hallucinations, disor-\nganized thinking (speech), grossly disorganiz ed or abnormal moto r behavior (including\ncatatonia), and negative symptoms.\nKey Features That Define the Psychotic Disorders\nDelusions\nDelusions are fixed beliefs that are not amenable to change in light of conflicting evidence.\nTheir content may include a variety of themes (e.g., persecutory, referential, somatic, reli-\ngious, grandiose). Persecutory delusions (i.e., belief that one is going to be harmed, harassed,\nand so forth by an individual, organizat ion, or other group) are most common. Referential\ndelusions (i.e., belief that certain gestures, comm ents, environmental cues, and so forth are\ndirected at oneself) are also common. Grandiose delusions (i.e., when an individual believes\nthat he or she has exceptional abilities, wealth, or fame) and erotomanic delusions (i.e., when\nan individual believes falsely that another person is in love with him or her) are also seen.\nNihilistic delusions involve the conviction that a ma jor catastrophe will occur, and somatic\ndelusions focus on preoccupations regarding health and organ function.\nDelusions are deemed bizarre if they are clearly implausible and not understandable to\nsame-culture peers and do not derive from or dinary life experiences. An example of a bi-\nzarre delusion is the belief that an outside forc e has removed his or her internal organs and", "source": "dsm5.pdf"} {"id": "11f9d338a0e2-1", "page_content": "replaced them with someone else\u2019s organs wi thout leaving any wounds or scars. An ex-\nample of a nonbizarre delusion is the belief that one is under surveilla nce by the police, de-\nspite a lack of convincing evidence. Delusion s that express a loss of control over mind or\nbody are generally considered to be bizarre; these include th e belief that one\u2019s thoughts\nhave been \u201cremoved\u201d by some outside force (thought withdrawal ), that alien thoughts have\nbeen put into one\u2019s mind ( thought insertion ), or that one\u2019s body or actions are being acted on\nor manipulated by so me outside force ( delusions of control ). The distinction between a de-\nlusion and a strongly held idea is sometimes di fficult to make and depends in part on the\ndegree of conviction with which the belief is held despite clear or reasonable contradictory\nevidence regarding its veracity. \nHallucinations\nHallucinations are perception-like experiences that occur without an external stimulus.\nThey are vivid and clear, with the full force and impact of normal perceptions, and not\nunder voluntary control. They may occur in any sensory modality, but auditory halluci-\nnations are the most common in schizophrenia and related disorders. Auditory hallucina-\ntions are usually experienced as voices, whethe r familiar or unfamiliar, that are perceived\nas distinct from the individual\u2019s own though ts. The hallucinations must occur in the con-\ntext of a clear sensorium; those that occur while falling asleep ( hypnagogic ) or waking up", "source": "dsm5.pdf"} {"id": "3edb2c58041a-0", "page_content": "88 Schizophrenia Spectrum and Other Psychotic Disorders\n(hypnopompic ) are considered to be within the rang e of normal experience. Hallucinations\nmay be a normal part of religious expe rience in certain cultural contexts. \nDisorganized Thinking (Speech)\nDisorganized thinking (formal thought disorder ) is typically inferred from the individual\u2019s\nspeech. The individual may switch from one topic to another ( derailment or loose associa-\ntions ). Answers to questions may be oblique ly related or completely unrelated ( tangential-\nity). Rarely, speech may be so severely disorgan ized that it is nearly incomprehensible and\nresembles receptive aphasia in its linguistic disorganization ( incoherence or \u201cword salad\u201d).\nBecause mildly disorganized speech is common and nonspecific, the symptom must be se-\nvere enough to substantially impair effective communication. The severity of the impair-\nment may be difficult to evaluate if the person making the diagnosis comes from a\ndifferent linguistic background than that of the person being examin ed. Less severe dis-\norganized thinking or speech may occur du ring the prodromal and residual periods of\nschizophrenia.\nGrossly Disorganized or Abnormal Motor Behavior \n(Including Catatonia)\nGrossly disorganized or abnormal motor behavior may manifest itself in a variety of ways,\nranging from childlike \u201csilliness\u201d to unpred ictable agitation. Problems may be noted in\nany form of goal-directed behavior, leading to difficulties in performing activities of daily\nliving.\nCatatonic behavior is a marked decrease in reactivity to the environment. This ranges\nfrom resistance to instructions ( negativism ); to maintaining a rigid, inappropriate or bi-\nzarre posture; to a complete lack of verbal and motor responses ( mutism and stupor ). It can", "source": "dsm5.pdf"} {"id": "3edb2c58041a-1", "page_content": "also include purposeless and excessive motor activity without obvious cause ( catatonic\nexcitement ). Other features are repeated stereo typed movements, staring, grimacing,\nmutism, and the echoing of speech. Although catatonia has historically been associated\nwith schizophrenia, catatonic symptoms are nonspecific and may occur in other mental\ndisorders (e.g., bipolar or depressive disorder s with catatonia) and in medical conditions\n(catatonic disorder due to another medical condition).\nNegative Symptoms\nNegative symptoms account for a substantial portion of the morbidity associated with\nschizophrenia but are less prominent in other psychotic disorders. Two negative symp-\ntoms are particularly prominent in schizophrenia: diminished emotional expression and\navolition. Diminished emotional expression includes reductions in the expression of emo-\ntions in the face, eye contact, intonation of speech (prosody), and movements of the hand,\nhead, and face that normally give an emotional emphasis to speech. Avolition is a decrease\nin motivated self-initiated purposeful activities. The individual may sit for long periods of\ntime and show little interest in participating in work or so cial activities. Other negative\nsymptoms include alogia, anhedonia, and asociality. Alogia is manifested by diminished\nspeech output. Anhedonia is the decreased ability to ex perience pleasure from positive\nstimuli or a degradation in the recollection of pleasure previously experienced. Asociality\nrefers to the apparent lack of interest in so cial interactions and may be associated with avo-\nlition, but it can also be a ma nifestation of limited opportunities for social interactions. \nDisorders in This Chapter\nThis chapter is organized along a gradient of psychopathology. Clinicians should first con-\nsider conditions that do not re ach full criteria for a psychotic disorder or are limited to one", "source": "dsm5.pdf"} {"id": "9a96ec81c94a-0", "page_content": "Schizophrenia Spectrum and Other Psychotic Disorders 89\ndomain of psychopathology. Then they should consider time-limited conditions. Finally,\nthe diagnosis of a schizophrenia spectrum diso rder requires the exclusion of another con-\ndition that may give rise to psychosis.\nSchizotypal personality disorder is noted within this chapter as it is considered within\nthe schizophrenia spectrum, although its full description is found in the chapter \u201cPerson-\nality Disorders.\u201d The diagnosis schizotypal pers onality disorder captures a pervasive pat-\ntern of social and interpersonal deficits, including reduced capacity for close relationships;\ncognitive or perceptual distor tions; and eccentricities of behavior, usually beginning by\nearly adulthood but in some cases first becoming apparent in childhood and adolescence.\nAbnormalities of beliefs, thinki ng, and perception are below the threshold for the diagno-\nsis of a psychotic disorder.\nTwo conditions are defined by abnormalities limited to one domain of psychosis: delu-\nsions or catatonia. Delusional disorder is characterized by at least 1 month of delusions but\nno other psychotic symptoms. Catatonia is desc ribed later in the chapter and further in this\ndiscussion.\nBrief psychotic disorder lasts more than 1 day and remits by 1 month. Schizophreni-\nform disorder is characterized by a symptomatic presentation equivalent to that of schizo-\nphrenia except for its duration (less than 6 months) and the absence of a requirement for a\ndecline in functioning.\nSchizophrenia lasts for at least 6 months an d includes at least 1 month of active-phase\nsymptoms. In schizoaffective disorder, a mood episode and the active-phase symptoms of\nschizophrenia occur together an d were preceded or are followe d by at least 2 weeks of de-", "source": "dsm5.pdf"} {"id": "9a96ec81c94a-1", "page_content": "lusions or hallucinations with out prominent mood symptoms.\nPsychotic disorders may be induced by anot her condition. In substance/medication-\ninduced psychotic disorder, the psychotic symp toms are judged to be a physiological con-\nsequence of a drug of abuse, a medication, or toxin exposure and cease after removal of the\nagent. In psychotic disorder due to anothe r medical condition, the psychotic symptoms\nare judged to be a direct physiological consequence of another medical condition.\nCatatonia can occur in severa l disorders, including neurod evelopmental, psychotic, bi-\npolar, depressive, and other mental disorders. This chapter also includes the diagnoses\ncatatonia associated with anot her mental disorder (catatonia specifier), catatonic disorder\ndue to another medical condition, and unspecifie d catatonia, and the diagnostic criteria for\nall three conditions are described together.\nOther specified and unspecified schizophrenia spectrum and other psychotic disor-\nders are included for classifyin g psychotic presentations that do not meet the criteria for\nany of the specific psychotic disorders, or psychotic symptomatology about which there is\ninadequate or contra dictory information.\nClinician-Rated Assessment of Symptoms and\n Related Clinical Phenomena in Psychosis\nPsychotic disorders are heterogeneous, and th e severity of symptoms can predict impor-\ntant aspects of the illness, such as the degree of cognitive or neur obiological deficits. To\nmove the field forward, a detailed framework fo r the assessment of severity is included in\nSection III \u201cAssessment Measures,\u201d which may help with treatment planning, prognostic\ndecision making, and research on patho physiological mechanisms. Section III \u201cAssess-\nment Measures\u201d also contains dimensional as sessments of the primary symptoms of psy-\nchosis, including hallucinations, delusions, disorganized speech (except for substance/", "source": "dsm5.pdf"} {"id": "9a96ec81c94a-2", "page_content": "chosis, including hallucinations, delusions, disorganized speech (except for substance/\nmedication-induced psychotic disorder and psychotic disorder due to another medical\ncondition), abnormal psychomotor behavior, and negative symptoms, as well as dimen-\nsional assessments of depression and mania. Th e severity of mood symptoms in psychosis", "source": "dsm5.pdf"} {"id": "c1ad587c38f3-0", "page_content": "condition), abnormal psychomotor behavior, and negative symptoms, as well as dimen-\nsional assessments of depression and mania. Th e severity of mood symptoms in psychosis\nhas prognostic value and guides treatment. There is growing evidence that schizoaffective", "source": "dsm5.pdf"} {"id": "24aead66716f-0", "page_content": "90 Schizophrenia Spectrum and Other Psychotic Disorders\ndisorder is not a distinct nosological catego ry. Thus, dimensional assessments of depres-\nsion and mania for all psychotic disorders alert clinicians to mood pathology and the need\nto treat where appropriate. The Section III sc ale also includes a dimensional assessment of\ncognitive impairment. Many individuals with psychotic disorders have impairments in a\nrange of cognitive domains that predict functi onal status. Clinical neuropsychological as-\nsessment can help guide diagnosis and treatm ent, but brief assessments without formal\nneuropsychological assessment can provide us eful information that can be sufficient for\ndiagnostic purposes. Formal neuropsychological testing, when conducted, should be ad-\nministered and scored by personnel trained in the use of testing instruments. If a formal\nneuropsychological assessment is not conducted, the clinician should use the best avail-\nable information to make a judgment. Furthe r research on these assessments is necessary\nin order to determine their c linical utility; thus, the assessments available in Section III\nshould serve as a prototype to stimulate such research.\nSchizotypal (Personality) Disorder\nCriteria and text for schizotypal personality disorder can be found in the chapter \u201cPerson-\nality Disorders.\u201d Because this disorder is cons idered part of the schizophrenia spectrum of\ndisorders, and is labeled in this section of ICD-9 and ICD-10 as schizotypal disorder, it is\nlisted in this chapter and disc ussed in detail in the DSM-5 chapter \u201cPersonality Disorders.\u201d\nDelusional Disorder\nDiagnostic Criteria 297.1 (F22)\nA. The presence of one (or more) delusions with a duration of 1 month or longer.\nB. Criterion A for schizophrenia has never been met.", "source": "dsm5.pdf"} {"id": "24aead66716f-1", "page_content": "B. Criterion A for schizophrenia has never been met. \nNote: Hallucinations, if present, are not prominent and are related to the delusional\ntheme (e.g., the sensation of being infested with insects associated with delusions of\ninfestation).\nC. Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly\nimpaired, and behavior is not obviously bizarre or odd.\nD. If manic or major depressive episodes have occurred, these have been brief relative\nto the duration of the delusional periods.\nE. The disturbance is not attributable to the physiological effects of a substance or an-\nother medical condition and is not better ex plained by another mental disorder, such\nas body dysmorphic disorder or obsessive-compulsive disorder.\nSpecify whether:\nErotomanic type: This subtype applies when the central theme of the delusion is that\nanother person is in love with the individual.\nGrandiose type: This subtype applies when the central theme of the delusion is the\nconviction of having some great (but unrecognized) talent or insight or having made\nsome important discovery.\nJealous type: This subtype applies when the central theme of the individual\u2019s delusion\nis that his or her spouse or lover is unfaithful.\nPersecutory type: This subtype applies when the central theme of the delusion in-\nvolves the individual\u2019s belief that he or she is being conspired against, cheated, spied\non, followed, poisoned or drugged, maliciously maligned, harassed, or obstructed in\nthe pursuit of long-term goals.\nSomatic type: This subtype applies when the central theme of the delusion involves\nbodily functions or sensations.", "source": "dsm5.pdf"} {"id": "d52cc5fba628-0", "page_content": "Delusional Disorder 91\nMixed type: This subtype applies when no one delusional theme predominates.\nUnspecified type: This subtype applies when the dominant delusional belief cannot\nbe clearly determined or is not described in the specific types (e.g., referential delu-\nsions without a prominent persecutory or grandiose component). \nSpecify if:\nWith bizarre content: Delusions are deemed bizarre if they are clearly implausible, not\nunderstandable, and not derived from ordinary li fe experiences (e.g., an individual\u2019s be-\nlief that a stranger has removed his or her internal organs and replaced them with some-\none else\u2019s organs without leaving any wounds or scars).\nSpecify if:\nThe following course specifiers are only to be used after a 1-year duration of the disorder:\nFirst episode, currentl y in acute episode: First manifestation of the disorder meet-\ning the defining diagnostic symptom and time criteria. An acute episode is a time pe-\nriod in which the symptom criteria are fulfilled.\nFirst episode, currently in partial remission: Partial remission is a time period dur-\ning which an improvement after a previous episode is maintained and in which the de-\nfining criteria of the disorder are only partially fulfilled.\nFirst episode, currently in full remission: Full remission is a period of time after a\nprevious episode during which no disorder-specific symptoms are present.\nMultiple episodes, curr ently in acute episode\nMultiple episodes, currently in partial remission\nMultiple episodes, currently in full remission\nContinuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder are\nremaining for the majority of the illness course, with subthreshold symptom periods be-\ning very brief relative to the overall course.\nUnspecified\nSpecify current severity:\nSeverity is rated by a quantitative assessment of the primary symptoms of psychosis,", "source": "dsm5.pdf"} {"id": "d52cc5fba628-1", "page_content": "Specify current severity:\nSeverity is rated by a quantitative assessment of the primary symptoms of psychosis,\nincluding delusions, hallucinations, disorganized speech, abnormal psychomotor be-\nhavior, and negative symptoms. Each of these symptoms may be rated for its current\nseverity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)\nto 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom\nSeverity in the chapter \u201cAssessment Measures.\u201d)\nNote: Diagnosis of delusional disorder can be made without using this severity specifier.\nSubtypes\nIn erotomanic type, the central theme of the delusion is that another person is in love with\nthe individual. The person about whom this conviction is held is usually of higher status\n(e.g., a famous individual or a superior at work) but can be a complete stranger. Efforts to\ncontact the object of the delusion are common. In grandiose type, the central theme of the de-\nlusion is the conviction of having some great talent or insight or of having made some im-\nportant discovery. Less commo nly, the individual may have the delusion of having a\nspecial relationship with a prominent individu al or of being a prominent person (in which\ncase the actual individual may be regarded as an impostor). Grandiose delusions may\nhave a religious content. In jealous type, the central theme of the delusion is that of an un-\nfaithful partner. This belief is arrived at with out due cause and is based on incorrect infer-\nences supported by small bits of \u201cevidence\u201d (e.g., disarrayed clothing). The individual\nwith the delusion usually conf ronts the spouse or lover and at tempts to intervene in the", "source": "dsm5.pdf"} {"id": "d52cc5fba628-2", "page_content": "imagined infidelity. In persecutory type, the central theme of the delusion involves the in-", "source": "dsm5.pdf"} {"id": "3944bae69a55-0", "page_content": "92 Schizophrenia Spectrum and Other Psychotic Disorders\ndividual\u2019s belief of being conspired against, cheated, spied on, followed, poisoned, mali-\nciously maligned, harassed, or obstructed in the pursuit of long-term goals. Small slights\nmay be exaggerated and become the focus of a delusional system. The affected individual\nmay engage in repeated attempts to obtain sat isfaction by legal or legislative action. Indi-\nviduals with persecutory delusions are often resentful and angry and may resort to vio-\nlence against those they believe are hurting them. In somatic type, the central theme of the\ndelusion involves bodily functi ons or sensations. Somatic de lusions can occur in several\nforms. Most common is the belief that the indi vidual emits a foul odor ; that there is an in-\nfestation of insects on or in the skin; that ther e is an internal parasite; that certain parts of\nthe body are misshapen or ugly; or that parts of the body are not functioning.\nDiagnostic Features\nThe essential feature of delusional disorder is the presence of one or more delusions that\npersist for at least 1 month (Criterion A). A diagnosis of delusional disorder is not given if\nthe individual has ever had a symptom presen tation that met Criterion A for schizophre-\nnia (Criterion B). Apart from the direct impact of the delusions, impairments in psychoso-\ncial functioning may be more circumscribed th an those seen in other psychotic disorders\nsuch as schizophrenia,\u00a0and behavior is not obviously bizarre or odd (Criterion C).\u00a0If mood\nepisodes occur concurrently with the delusions , the total duration of these mood episodes\nis brief relative to the total duration of the delusional periods (Criterion D). The delusions", "source": "dsm5.pdf"} {"id": "3944bae69a55-1", "page_content": "are not attributable to the physiological effects of a su bstance (e.g., cocaine) or another\nmedical condition (e.g., Alzheimer\u2019s disease) and are not better explained by another men-\ntal disorder, such as body dy smorphic disorder or obsessive- compulsive disorder (Crite-\nrion E).\nIn addition to the five symptom domain areas identified in the diagnostic criteria, the\nassessment of cognition, depression, and mani a symptom domains is vital for making crit-\nically important distinctions between the va rious schizophrenia spectrum and other psy-\nchotic disorders.\nAssociated Features Supporting Diagnosis\nSocial, marital, or work problems can result from the delusional beliefs of delusional dis-\norder. Individuals with delusional disorder ma y be able to factually describe that others\nview their beliefs as irrational but are unable to accept this themselves (i.e., there may be\n\u201cfactual insight\u201d but no true insight). Many individuals de velop irritable or dysphoric\nmood, which can usually be understood as a re action to their delusional beliefs. Anger and\nviolent behavior can occur with persecutory, jealous, and erotomanic types. The individ-\nual may engage in litigious or antagonistic behavior (e.g., sending hundreds of letters of\nprotest to the government). Legal difficulties can occur, particularly in jealous and eroto-\nmanic types. \nPrevalence\nThe lifetime prevalence of delusional disorder has been estimated at around 0.2%, and the\nmost frequent subtype is persecutory. Delu sional disorder, jealous type, is probably more\ncommon in males than in females, but there ar e no major gender differences in the overall\nfrequency of delu sional disorder.\nDevelopment and Course\nOn average, global function is generally better than that observed in schizophrenia. Al-", "source": "dsm5.pdf"} {"id": "3944bae69a55-2", "page_content": "On average, global function is generally better than that observed in schizophrenia. Al-\nthough the diagnosis is generally stable, a pr oportion of individuals go on to develop", "source": "dsm5.pdf"} {"id": "072f0422ff52-0", "page_content": "Delusional Disorder 93\nschizophrenia. Delusional disorder has a significant familial relationship with both\nschizophrenia and schizotypal personality diso rder. Although it can occur in younger age\ngroups, the condition may be more prevalent in older individuals.\nCulture-Related Diagnostic Issues\nAn individual\u2019s cultural and religious backgr ound must be taken into account in evaluat-\ning the possible presence of delusional di sorder. The content of delusions also varies\nacross cultural contexts.\nFunctional Consequences of Delusional Disorder\nThe functional impairment is usually more ci rcumscribed than that seen with other psy-\nchotic disorders, although in some cases, the impairment may be substantial and include\npoor occupational functioning and social isola tion. When poor psychosocial functioning is\npresent, delusional beliefs themselves ofte n play a significant role. A common character-\nistic of individuals with delusional disorder is the apparent normality of their behavior\nand appearance when their delusional idea s are not being discussed or acted on. \nDifferential Diagnosis\nObsessive-compulsive and related disorders. If an individual wi th obsessive-compul-\nsive disorder is completely convinced that his or her obsessive-comp ulsive disorder beliefs\nare true, then the diagnosis of obsessive-compulsive disorder, with absent insight/delu-\nsional beliefs specifier, should be given rath er than a diagnosis of delusional disorder.\nSimilarly, if an individual with body dysm orphic disorder is completely convinced that\nhis or her body dysmorphic disorder beliefs are true, then the diagnosis of body dysmor-\nphic disorder, with absent insight/delusional beliefs specifier, should be given rather than\na diagnosis of delusional disorder. \nDelirium, major neurocognitive disorder, psychotic disorder due to another medical con-", "source": "dsm5.pdf"} {"id": "072f0422ff52-1", "page_content": "Delirium, major neurocognitive disorder, psychotic disorder due to another medical con-\ndition, and substance/medicati on-induced psychotic disorder. Individuals with these\ndisorders may present with symptoms that su ggest delusional disorder. For example, sim-\nple persecutory delusions in the context of major neurocognitive di sorder would be di-\nagnosed as major neurocognitive disorder, with behavioral disturbance. A substance/\nmedication-induced psychotic disorder cross-sectionally may be identical in symptom-\natology to delusional disorder but can be di stinguished by the chronological relationship\nof substance use to the onset and remission of the delusional beliefs.\nSchizophrenia and schizophreniform disorder. Delusional disorder can be distinguished\nfrom schizophrenia and schizophreniform disord er by the absence of the other character-\nistic symptoms of the active phase of schizophrenia. \nDepressive and bipolar disorders and schizoaffective disorder. These disorders may\nbe distinguished from delusional disorder by the temporal relationship between the mood\ndisturbance and the delusions and by the severi ty of the mood symptoms. If delusions oc-\ncur exclusively during mood episodes, the diag nosis is depressive or bipolar disorder with\npsychotic features. Mood sympto ms that meet full criteria for a mood episode can be su-\nperimposed on delusional disorder. Delusional di sorder can be diagnose d only if the total\nduration of all mood episodes remains brief rela tive to the total duration of the delusional\ndisturbance. If not, then a diagnosis of othe r specified or unspecified schizophrenia spec-\ntrum and other psychotic diso rder accompanied by other sp ecified depressi ve disorder,\nunspecified depressive disorder, other specif ied bipolar and related disorder, or unspeci-", "source": "dsm5.pdf"} {"id": "072f0422ff52-2", "page_content": "fied bipolar and related disorder is appropriate.", "source": "dsm5.pdf"} {"id": "4ff66033d673-0", "page_content": "94 Schizophrenia Spectrum and Other Psychotic Disorders\nBrief Psychotic Disorder\nDiagnostic Criteria 298.8 (F23)\nA. Presence of one (or more) of the following symptoms. At least one of these must be\n(1), (2), or (3):\n1. Delusions.\n2. Hallucinations.\n3. Disorganized speech (e.g., frequent derailment or incoherence).\n4. Grossly disorganized or catatonic behavior.\nNote: Do not include a symptom if it is a culturally sanctioned response. \nB. Duration of an episode of the disturbance is at least 1 day but less than 1 month, with\neventual full return to premorbid level of functioning.\nC. The disturbance is not better explained by major depressive or bipolar disorder with\npsychotic features or another psychotic disorder such as schizophrenia or catatonia,\nand is not attributable to the physiological effects of a substance (e.g., a drug of abuse,\na medication) or another medical condition.\nSpecify if:\nWith marked stressor(s) (brief reactive psychosis): If symptoms occur in response to\nevents that, singly or together, would be markedly stressful to almost anyone in similar\ncircumstances in the individual\u2019s culture.\nWithout marked stressor(s): If symptoms do not occur in response to events that,\nsingly or together, would be markedly stressful to almost anyone in similar circum-\nstances in the individual\u2019s culture.\nWith postpartum onset: If onset is during pregnancy or within 4 weeks postpartum.\nSpecify if:\nWith catatonia (refer to the criteria for catatonia associated with another mental dis-\norder, pp. 119\u2013120, for definition)\nCoding note: Use additional code 293.89 (F06.1) catatonia associated with brief", "source": "dsm5.pdf"} {"id": "4ff66033d673-1", "page_content": "psychotic disorder to indicate the presence of the comorbid catatonia.\nSpecify current severity:\nSeverity is rated by a quantitative assessment of the primary symptoms of psychosis,\nincluding delusions, hallucinations, disorganized speech, abnormal psychomotor be-\nhavior, and negative symptoms. Each of these symptoms may be rated for its current\nseverity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)\nto 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom\nSeverity in the chapter \u201cAssessment Measures.\u201d)\nNote: Diagnosis of brief psychotic disorder can be made without using this severity\nspecifier.\nDiagnostic Features\nThe essential feature of brief psychotic disorder is a disturba nce that involves the sudden\nonset of at least one of the following positive psychotic symptoms: delusions, hallucina-\ntions, disorganized speech (e.g., frequent de railment or incoherence), or grossly abnormal\npsychomotor behavior, includin g catatonia (Criterion A). Sudden onset is defined as\nchange from a nonpsychotic state to a clearly psychotic state within 2 weeks, usually with-\nout a prodrome. An episode of the disturbance lasts at least 1 day but less than 1 month,\nand the individual eventually has a full return to the premorbid level of functioning (Cri-", "source": "dsm5.pdf"} {"id": "02d4f7fadef4-0", "page_content": "Brief Psychotic Disorder 95\nterion B). The disturbance is not better explai ned by a depressive or bipolar disorder with\npsychotic features, by schizoaffective disorder , or by schizophrenia and is not attributable\nto the physiological effects of a substance (e .g., a hallucinogen) or another medical condi-\ntion (e.g., subdural hematoma) (Criterion C).\nIn addition to the five symptom domain areas identified in the diagnostic criteria, the\nassessment of cognition, depression, and mani a symptom domains is vital for making crit-\nically important distinctions between the va rious schizophrenia spectrum and other psy-\nchotic disorders.\nAssociated Features Supporting Diagnosis\nIndividuals with brief psychoti c disorder typically experience emotional turmoil or over-\nwhelming confusion. They may have rapid sh ifts from one intense affect to another.\nAlthough the disturbance is brief, the level of impairment may be severe, and supervision\nmay be required to ensure that nutritional and hygienic needs are met and that the indi-\nvidual is protected from the consequences of poor judgment, cognitive impairment, or act-\ning on the basis of delusions. There appears to be an increased risk of suicidal behavior,\nparticularly during the acute episode.\nPrevalence\nIn the United States, brief psychotic disorder may account for 9% of cases of first-onset\npsychosis. Psychotic disturbances that meet Crit eria A and C, but not Criterion B, for brief\npsychotic disorder (i.e., duration of active symptoms is 1\u20136 months as opposed to remis-\nsion within 1 month) are more common in developing countries than in developed coun-\ntries. Brief psychotic diso rder is twofold more common in females than in males.\nDevelopment and Course\nBrief psychotic disorder may appear in adolescence or early adulthood, and onset can oc-", "source": "dsm5.pdf"} {"id": "02d4f7fadef4-1", "page_content": "Brief psychotic disorder may appear in adolescence or early adulthood, and onset can oc-\ncur across the lifespan, with the average age at onset being the mid 30s. By definition, a\ndiagnosis of brief psychotic disorder requir es a full remission of all symptoms and an\neventual full return to the premorbid level of functioning within 1 mont h of the onset of the\ndisturbance. In some individuals, the duration of psychotic symptoms may be quite brief\n(e.g., a few days).\nRisk and Prognostic Factors \nTemperamental. Preexisting personality disorders an d traits (e.g., schizotypal person-\nality disorder; borderline personality disorder; or traits in the psychoticism domain, such\nas perceptual dysregulation, and the negative affectivity domain, such as suspiciousness)\nmay predispose the individual to the development of the disorder.\nCulture-Related Diagnostic Issues\nIt is important to distinguish symptoms of br ief psychotic disorder from culturally sanc-\ntioned response patterns. For example, in so me religious ceremonies, an individual may\nreport hearing voices, but these do not genera lly persist and are not perceived as abnormal\nby most members of the indivi dual\u2019s community. In addition , cultural and religious back-\nground must be taken into account when considering whether be liefs are delusional. \nFunctional Consequences of Brief Psychotic Disorder\nDespite high rates of relapse, for most indivi duals, outcome is excellent in terms of social\nfunctioning and symptomatology.", "source": "dsm5.pdf"} {"id": "ad697cd928fa-0", "page_content": "96 Schizophrenia Spectrum and Other Psychotic Disorders\nDifferential Diagnosis\nOther medical conditions. A variety of medical disorders can manifest with psychotic\nsymptoms of short duration. Psychotic disorder due to another medica l condition or a de-\nlirium is diagnosed when there is evidence from the history, physical examination, or lab-\noratory tests that the delusions or hallucinati ons are the direct physiological consequence\nof a specific medical condition (e.g., Cushing\u2019s syndrome, brain tumor) (see \u201cPsychotic\nDisorder Due to Another Medical Co ndition\u201d later in this chapter). \nSubstance-related disorders. Substance/medication-induced psychotic disorder, sub-\nstance-induced delirium, and substance intoxication are distinguished from brief psychotic\ndisorder by the fact that a substance (e.g., a drug of abuse, a medication, exposure to a toxin)\nis judged to be etiologically related to the psychotic symp toms (see \u201cSubstance/Medication-\nInduced Psychotic Disorder\u201d later in this chapte r). Laboratory tests, such as a urine drug\nscreen or a blood alcohol level, may be helpful in making this determination, as may a care-\nful history of substance use with attention to temporal relationships between substance in-\ntake and onset of the symp toms and to the nature of the substance being used.\nDepressive and bipolar disorders. The diagnosis of brief psychotic disorder cannot be\nmade if the psychotic symptoms are better explained by a mood episode (i.e., the psychotic\nsymptoms occur exclusively during a full major depressive, manic, or mixed episode). \nOther psychotic disorders. If the psychotic symptoms pers ist for 1 month or longer, the\ndiagnosis is either schizophr eniform disorder, delusional disorder, depressive disorder\nwith psychotic features, bipolar disorder with psychotic fe atures, or other specified or un-", "source": "dsm5.pdf"} {"id": "ad697cd928fa-1", "page_content": "with psychotic features, bipolar disorder with psychotic fe atures, or other specified or un-\nspecified schizophrenia spectrum and other psychotic disorder, depending on the other\nsymptoms in the presentation. The differentia l diagnosis between brief psychotic disorder\nand schizophreniform disorder is difficult wh en the psychotic symptoms have remitted be-\nfore 1 month in response to successful trea tment with medication. Careful attention should\nbe given to the possibility that a recurrent diso rder (e.g., bipolar disorder, recurrent acute ex-\nacerbations of schizophrenia) may be respon sible for any recurring psychotic episodes.\nMalingering and factitious disorders. An episode of factitious disorder, with predomi-\nnantly psychological signs and symptoms, may have the appearance of brief psychotic\ndisorder, but in such cases there is evidence that the symptoms are intentionally produced.\nWhen malingering involves apparently psyc hotic symptoms, there is usually evidence\nthat the illness is being feigned for an understandable goal.\nPersonality disorders. In certain individual s with personality disorders, psychosocial\nstressors may precipitate brief periods of psychotic symptoms. These symptoms are usu-\nally transient and do not warrant a separate diagnosis. If psychotic symptoms persist for at\nleast 1 day, an additional diagnosis of br ief psychotic disorder may be appropriate.\nSchizophreniform Disorder\nDiagnostic Criteria 295.40 (F20.81)\nA. Two (or more) of the following, each present for a significant portion of time during a\n1-month period (or less if successfully treated). At least one of these must be (1), (2),\nor (3):\n1. Delusions.\n2. Hallucinations.\n3. Disorganized speech (e.g., frequent derailment or incoherence).\n4. Grossly disorganized or catatonic behavior.", "source": "dsm5.pdf"} {"id": "ad697cd928fa-2", "page_content": "4. Grossly disorganized or catatonic behavior.\n5. Negative symptoms (i.e., diminished emotional expression or avolition).", "source": "dsm5.pdf"} {"id": "98efe277d2a2-0", "page_content": "Schizophreniform Disorder 97\nB. An episode of the disorder lasts at least 1 month but less than 6 months. When the\ndiagnosis must be made without waiting for recovery, it should be qualified as \u201cprovi-\nsional.\u201d\nC. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have\nbeen ruled out because either 1) no major depressive or manic episodes have occurred\nconcurrently with the active-phase symptoms, or 2) if mood episodes have occurred dur-\ning active-phase symptoms, they have been present for a minority of the total duration\nof the active and residual periods of the illness. \nD. The disturbance is not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication) or another medical condition.\nSpecify if:\nWith good prognostic features: This specifier requires the presence of at least two\nof the following features: onset of prominent psychotic symptoms within 4 weeks of the\nfirst noticeable change in usual behavior or f unctioning; confusion or perplexity; good\npremorbid social and occupational functioning; and absence of blunted or flat affect.\nWithout good prognostic features: This specifier is applied if two or more of the\nabove features have not been present.\nSpecify if:\nWith catatonia (refer to the criteria for catatonia associated with another mental disor-\nder, pp. 119\u2013120, for definition).\nCoding note: Use additional code 293.89 (F06.1) catatonia associated with schizo-\nphreniform disorder to indicate the presence of the comorbid catatonia.\nSpecify current severity:\nSeverity is rated by a quantitative assessment of the primary symptoms of psychosis,\nincluding delusions, hallucinations, disorganized speech, abnormal psychomotor be-", "source": "dsm5.pdf"} {"id": "98efe277d2a2-1", "page_content": "including delusions, hallucinations, disorganized speech, abnormal psychomotor be-\nhavior, and negative symptoms. Each of these symptoms may be rated for its current\nseverity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)\nto 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom\nSeverity in the chapter \u201cAssessment Measures.\u201d)\nNote: Diagnosis of schizophreniform disorder can be made without using this severity\nspecifier.\nNote: For additional information on Associated Features Supp orting Diagnosis, Develop-\nment and Course (age-related factors), Culture-Related Diag nostic Issues, Gender-Related\nDiagnostic Issues, Differential Diagnosis, and Comorbidity, see the corresponding sec-\ntions in schizophrenia.\nDiagnostic Features\nThe characteristic symptoms of schizophreniform disorder are identical to those of schizo-\nphrenia (Criterion A). Schizophreniform disorder is distinguish ed by its difference in du-\nration: the total duration of the illness, includ ing prodromal, active, and residual phases, is\nat least 1 month but less than 6 months (Crite rion B). The duration requirement for schizo-\nphreniform disorder is intermediate between th at for brief psychotic disorder, which lasts\nmore than 1 day and remits by 1 month, and schizophrenia, which lasts for at least 6 months.\nThe diagnosis of schizophreniform disorder is made under two conditions. 1) when an ep-\nisode of illness lasts between 1 and 6 months and the individual has already recovered,\nand 2) when an individual is symptomatic for less than the 6 months\u2019 duration required for\nthe diagnosis of schizophrenia but has not yet recovered. In this case, the diagnosis should", "source": "dsm5.pdf"} {"id": "98efe277d2a2-2", "page_content": "the diagnosis of schizophrenia but has not yet recovered. In this case, the diagnosis should\nbe noted as \u201cschizophreniform disorder (provisional)\u201d because it is uncertain if the indi-\nvidual will recover from the disturbance within the 6-month period. If the disturbance per-\nsists beyond 6 months, the diagnosis should be changed to schizophrenia.", "source": "dsm5.pdf"} {"id": "a0ae5cc0ad03-0", "page_content": "98 Schizophrenia Spectrum and Other Psychotic Disorders\nAnother distinguishing feature of schizophren iform disorder is the lack of a criterion\nrequiring impaired social and occupational functioning. While such impairments may po-\ntentially be present, they are not necessary for a diagnosis of schizophreniform disorder. \nIn addition to the five symptom domain areas identified in the diagnostic criteria, the\nassessment of cognition, depression, and mani a symptom domains is vital for making crit-\nically important distinctions between the va rious schizophrenia spectrum and other psy-\nchotic disorders.\nAssociated Features Supporting Diagnosis\nAs with schizophrenia, currently there are no laboratory or psychometric tests for schizo-\nphreniform disorder. There are multiple brain regions where ne uroimaging, neuropa-\nthological, and neurophy siological research has indicated abnormalities, but none are\ndiagnostic.\nPrevalence\nIncidence of schizophreniform disorder across sociocultural settings is likely similar to\nthat observed in schizophrenia. In the United States and other developed countries, the in-\ncidence is low, possibly fivefold less than th at of schizophrenia. In developing countries,\nthe incidence may be higher, especially for th e specifier \u201cwith good prognostic features\u201d;\nin some of these settings schizophreniform disorder may be as common as schizophrenia. \nDevelopment and Course\nThe development of schizophreniform disorder is similar to that of schizophrenia. About\none-third of individuals with an initial di agnosis of schizophreniform disorder (provi-\nsional) recover within the 6-mo nth period and schizophreniform disorder is their final di-\nagnosis. The majority of the remaining two-th irds of individuals will eventually receive a\ndiagnosis of schizophrenia or schizoaffective disorder. \nRisk and Prognostic Factors \nGenetic and physiological. Relatives of individuals with schizophreniform disorder", "source": "dsm5.pdf"} {"id": "a0ae5cc0ad03-1", "page_content": "Genetic and physiological. Relatives of individuals with schizophreniform disorder\nhave an increased risk for schizophrenia. \nFunctional Consequences of \nSchizophreniform Disorder\nFor the majority of individuals with schizo phreniform disorder who eventually receive a\ndiagnosis of schizophrenia or schizoaffective disorder, the functional consequences are\nsimilar to the consequences of those disorder s. Most individuals ex perience dysfunction in\nseveral areas of daily functioning, such as sc hool or work, interperso nal relationships, and\nself-care. Individuals who recover from schi zophreniform disorder ha ve better functional\noutcomes. \nDifferential Diagnosis \nOther mental disorders and medical conditions. A wide variety of mental and medical\nconditions can manifest with psychotic sympto ms that must be considered in the differ-\nential diagnosis of schizophreniform disord er. These include psychotic disorder due to\nanother medical condition or its treatment; delirium or major neurocognitive disorder;\nsubstance/medication-induced psychotic diso rder or delirium; depressive or bipolar\ndisorder with psychotic features; schizoaffectiv e disorder; other specified or unspecified bi-\npolar and related disorder; depressive or bipola r disorder with catatonic features; schizophre-", "source": "dsm5.pdf"} {"id": "9469656578e9-0", "page_content": "Schizophrenia 99\nnia; brief psychotic disorder; delusional diso rder; other specified or unspecified schizo-\nphrenia spectrum and other psychotic diso rder; schizotypal, schizoid, or paranoid\npersonality disorders; autism spectrum disorder; disorders presenting in childhood with\ndisorganized speech; attention-deficit/hype ractivity disorder; ob sessive-compulsive dis-\norder; posttraumatic stress diso rder; and traumatic brain injury.\nSince the diagnostic criteria for schizophreniform disorder and schizophrenia differ\nprimarily in duration of illness, the discussion of the differential diagnosis of schizophre-\nnia also applies to schizophreniform disorder.\nBrief psychotic disorder. Schizophreniform disorder differs in duration from brief psy-\nchotic disorder, which has a duration of less than 1 month.\nSchizophrenia\nDiagnostic Criteria 295.90 (F20.9)\nA. Two (or more) of the following, each present for a significant portion of time during a\n1-month period (or less if successfully treated). At least one of these must be (1), (2), or (3):\n1. Delusions.\n2. Hallucinations.\n3. Disorganized speech (e.g., frequent derailment or incoherence).\n4. Grossly disorganized or catatonic behavior.\n5. Negative symptoms (i.e., diminished emotional expression or avolition).\nB. For a significant portion of the time since the onset of the disturbance, level of function-\ning in one or more major areas, such as work, interpersonal relations, or self-care, is\nmarkedly below the level achieved prior to the onset (or when the onset is in childhood\nor adolescence, there is failure to achieve expected level of interpersonal, academic,\nor occupational functioning).", "source": "dsm5.pdf"} {"id": "9469656578e9-1", "page_content": "or occupational functioning).\nC. Continuous signs of the disturbance persist for at least 6 months. This 6-month period\nmust include at least 1 month of symptoms (or less if successfully treated) that meet Cri-\nterion A (i.e., active-phase symptoms) and may include periods of prodromal or residual\nsymptoms. During these prodromal or residual periods, the signs of the disturbance may\nbe manifested by only negative symptoms or by two or more symptoms listed in Criterion\nA present in an attenuated form (e.g., odd beliefs, unusual perceptual experiences).\nD. Schizoaffective disorder and depressive or bipolar disorder with psychotic features\nhave been ruled out because either 1) no major depressive or manic episodes have\noccurred concurrently with the active-phas e symptoms, or 2) if mood episodes have\noccurred during active-phase symptoms, they have been present for a minority of the\ntotal duration of the active and residual periods of the illness.\nE. The disturbance is not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication) or another medical condition.\nF. If there is a history of autism spectrum disorder or a communication disorder of child-\nhood onset, the additional diagnosis of schizophrenia is made only if prominent delu-\nsions or hallucinations, in addition to the other required symptoms of schizophrenia,\nare also present for at least 1 month (or less if successfully treated).\nSpecify if:\nThe following course specifiers are only to be used after a 1-year duration of the disorder\nand if they are not in contradiction to the diagnostic course criteria.\nFirst episode, currentl y in acute episode: First manifestation of the disorder meet-\ning the defining diagnostic symptom and time criteria. An acute episode is a time pe-\nriod in which the symptom criteria are fulfilled.", "source": "dsm5.pdf"} {"id": "ea107d949bd4-0", "page_content": "100 Schizophrenia Spectrum and Other Psychotic Disorders\nFirst episode, currently in partial remission: Partial remission is a period of time\nduring which an improvement after a previous episode is maintained and in which the\ndefining criteria of the disorder are only partially fulfilled.\nFirst episode, currently in full remission: Full remission is a period of time after a\nprevious episode during which no disorder-specific symptoms are present.\nMultiple episodes, currently in acute episode: Multiple episodes may be deter-\nmined after a minimum of two episodes (i.e., after a first episode, a remission and a\nminimum of one relapse). \nMultiple episodes, currently in partial remission\nMultiple episodes, currently in full remission\nContinuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder are\nremaining for the majority of the illness course, with subthreshold symptom periods be-\ning very brief relative to the overall course.\nUnspecified\nSpecify if:\nWith catatonia (refer to the criteria for catatonia associated with another mental disorder,\npp. 119\u2013120, for definition).\nCoding note: Use additional code 293.89 (F06.1) catatonia associated with\nschizophrenia to indicate the presence of the comorbid catatonia.\nSpecify current severity:\nSeverity is rated by a quantitative assessment of the primary symptoms of psychosis,\nincluding delusions, hallucinations, disorganized speech, abnormal psychomotor be-\nhavior, and negative symptoms. Each of these symptoms may be rated for its current\nseverity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)\nto 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom\nSeverity in the chapter \u201cAssessment Measures.\u201d)", "source": "dsm5.pdf"} {"id": "ea107d949bd4-1", "page_content": "Severity in the chapter \u201cAssessment Measures.\u201d)\nNote: Diagnosis of schizophrenia can be made without using this severity specifier.\nDiagnostic Features \nThe characteristic symptoms of schizophrenia involve a range of cogn itive, behavioral, and\nemotional dysfunctions, but no single sympto m is pathognomonic of the disorder. The di-\nagnosis involves the recognition of a constellation of sign s and symptoms associated with\nimpaired occupational or social functioning. Individuals with the disorder will vary sub-\nstantially on most features, as schizophrenia is a heterogeneous clinical syndrome.\nAt least two Criterion A symptoms must be present for a significant portion of time\nduring a 1-month period or longer. At least one of these symptoms must be the clear pres-\nence of delusions (Criterion A1), hallucinati ons (Criterion A2), or disorganized speech\n(Criterion A3). Grossly disorganized or ca tatonic behavior (Criterion A4) and negative\nsymptoms (Criterion A5) may also be present. In those situations in which the active-\nphase symptoms remit within a mo nth in response to treatment, Criterion A is still met if the\nclinician estimates that they would have persisted in the absence of treatment. \nSchizophrenia involves impairment in one or more major areas of functioning (Crite-\nrion B). If the disturbance begins in childhood or adolescence, the expected level of func-\ntion is not attained. Co mparing the individual with unaffected siblings may be helpful. The\ndysfunction persists for a substantial period du ring the course of the disorder and does not\nappear to be a direct result of any single feature. Avolition (i.e., reduced drive to pursue\ngoal-directed behavior; Criterion A5) is linked to the social dysfunction described under\nCriterion B. There is also strong evidence for a relationship betw een cognitive impairment", "source": "dsm5.pdf"} {"id": "ea107d949bd4-2", "page_content": "Criterion B. There is also strong evidence for a relationship betw een cognitive impairment\n(see the section \u201cAssociated Features Supporting Diagnosis\u201d for this disorder) and func-\ntional impairment in individuals with schizophrenia.", "source": "dsm5.pdf"} {"id": "c19d9f0883e0-0", "page_content": "Schizophrenia 101\nSome signs of the disturbance must persist for a continuous period of at least 6 months\n(Criterion C). Prodromal symptoms often prec ede the active phase, and residual symp-\ntoms may follow it, characterized by mild or subthreshold forms of hallucinations or\ndelusions. Individuals may express a variety of unusual or odd beliefs that are not of de-\nlusional proportions (e.g., ideas of reference or magical thinking); they may have unusual\nperceptual experiences (e.g., sensing the pres ence of an unseen person); their speech may\nbe generally understandable but vague; and their behavior may be unusual but not grossly\ndisorganized (e.g., mumbling in public). Negative symptoms are common in the pro-\ndromal and residual phases and can be seve re. Individuals who had been socially active\nmay become withdrawn from previous routines . Such behaviors are often the first sign of\na disorder.\nMood symptoms and full mood episodes ar e common in schizophrenia and may be con-\ncurrent with active-phase symptomatology. However, as distinct from a psychotic mood dis-\norder, a schizophrenia diagnosis requires the presence of delusions or hallucinations in the\nabsence of mood episodes. In addition, mood ep isodes, taken in total, should be present for\nonly a minority of the total duration of th e active and residual periods of the illness.\nIn addition to the five symptom domain areas identified in the diagnostic criteria, the\nassessment of cognition, depression, and mani a symptom domains is vital for making crit-\nically important distinctions between the va rious schizophrenia spectrum and other psy-\nchotic disorders.\nAssociated Features Supporting Diagnosis\nIndividuals with schizophrenia may display inappropriate affect (e.g., laughing in the ab-\nsence of an appropriate stimulus); a dysphoric mood that can take the form of depression,", "source": "dsm5.pdf"} {"id": "c19d9f0883e0-1", "page_content": "anxiety, or anger; a disturbed sleep pattern (e.g., daytime sleeping and nighttime activity);\nand a lack of interest in eating or food refu sal. Depersonalization, derealization, and so-\nmatic concerns may occur and sometimes reac h delusional proportions. Anxiety and pho-\nbias are common. Cognitive deficits in schi zophrenia are common and are strongly linked\nto vocational and functional impairments. Thes e deficits can include decrements in declar-\native memory, working memory, language function, and other executive functions, as well\nas slower processing speed. Ab normalities in sensory processing and inhibitory capacity,\nas well as reductions in attention, are also found. Some individuals with schizophrenia\nshow social cognition deficits, including deficits in the ability to infer the intentions of\nother people (theory of mind), and may attend to and then interpret irrelevant events or\nstimuli as meaningful, perhaps leading to th e generation of explanatory delusions. These\nimpairments frequently persist during symptomatic remission.\nSome individuals with psychosis may lack insi ght or awareness of their disorder (i.e.,\nanosognosia). This lack of \u201cinsight\u201d includes unawareness of symptoms of schizophrenia\nand may be present throughout the entire cour se of the illness. Unawareness of illness is\ntypically a symptom of schizophrenia itself rath er than a coping strategy. It is comparable\nto the lack of awareness of neurological deficits following brain damage, termed anoso-\ngnosia. This symptom is the most common predicto r of non-adherence to treatment, and it\npredicts higher relapse rates, increased numb er of involuntary trea tments, poorer psycho-\nsocial functioning, aggression, and a poorer course of illness. \nHostility and aggression can be associated with schizophrenia, although spontaneous", "source": "dsm5.pdf"} {"id": "c19d9f0883e0-2", "page_content": "Hostility and aggression can be associated with schizophrenia, although spontaneous\nor random assault is uncommon. Aggression is more frequent for younger males and for\nindividuals with a past history of violence, non-adherenc e with treatment, substance\nabuse, and impulsivity. It should be noted that the vast majority of persons with schizo-", "source": "dsm5.pdf"} {"id": "74d276b3e419-0", "page_content": "individuals with a past history of violence, non-adherenc e with treatment, substance\nabuse, and impulsivity. It should be noted that the vast majority of persons with schizo-\nphrenia are not aggressive and are more frequently victimized than are individuals in the\ngeneral population. \nCurrently, there are no radiological, laborato ry, or psychometric tests for the disorder.\nDifferences are evident in multiple brain regions between groups of healthy individuals", "source": "dsm5.pdf"} {"id": "eced39f8285e-0", "page_content": "102 Schizophrenia Spectrum and Other Psychotic Disorders\nand persons with schizophrenia, including ev idence from neuroimaging, neuropatholog-\nical, and neurophysiological studies. Differences are also evident in cellular architecture,\nwhite matter connectivity, and gray matter volume in a vari ety of regions such as the pre-\nfrontal and temporal cortices. Reduced overall brain volume has been observed, as well as\nincreased brain volume reduction with age. Brain volume reductions with age are more\npronounced in individuals with schizophrenia than in healthy individuals. Finally, indi-\nviduals with schizophrenia appear to differ from individuals withou t the disorder in eye-\ntracking and electrophysiological indices.\nNeurological soft signs common in individuals with schizophrenia include impairments\nin motor coordination, sensory integration, and motor sequencing of complex movements;\nleft-right confusion; and disinhibition of associated mo vements. In addition, minor phys-\nical anomalies of the face and limbs may occur.\nPrevalence\nThe lifetime prevalence of schizophrenia appears to be approximately 0.3%\u20130.7%, al-\nthough there is reported variation by race/ethnicity, across countries, and by geographic\norigin for immigrants and children of immigr ants. The sex ratio differs across samples and\npopulations: for example, an emphasis on nega tive symptoms and longer duration of dis-\norder (associated with poorer outcome) show s higher incidence rates for males, whereas\ndefinitions allowing for the inclusion of more mood symptoms and brief presentations\n(associated with better outcome) show equivalent risks for both sexes. \nDevelopment and Course\nThe psychotic features of schizophrenia typically emerge between the late teens and the\nmid-30s; onset prior to adolescence is rare. The peak age at onset for the first psychotic ep-", "source": "dsm5.pdf"} {"id": "eced39f8285e-1", "page_content": "isode is in the early- to mid-20s for males and in the late-20s for females. The onset may be\nabrupt or insidious, but the majority of individuals manifest a slow and gradual develop-\nment of a variety of clinically significant signs and symptoms. Half of these individuals\ncomplain of depressive symptoms. Earlier age at onset has traditionally been seen as a pre-\ndictor of worse prognosis. However, the effect of age at onset is likely related to gender,\nwith males having worse premorbid adjustment, lower educational achievement, more\nprominent negative symptoms and cognitiv e impairment, and in general a worse out-\ncome. Impaired cognition is common, and altera tions in cognition are present during de-\nvelopment and precede the emergence of psycho sis, taking the form of stable cognitive\nimpairments during adulthood. Cognitive impairments may persist when other symptoms\nare in remission and contribute to the disability of the disease. \nThe predictors of course and outcome are la rgely unexplained, and course and outcome\nmay not be reliably predicted. The course appears to be favorable in about 20% of those\nwith schizophrenia, and a small number of indi viduals are reported to recover completely.\nHowever, most individuals with schizophrenia still require formal or informal daily living\nsupports, and many remain chronically ill, with exacerbations and remissions of active\nsymptoms, while others have a course of progressive deterioration.\nPsychotic symptoms tend to diminish over the life course, perhaps in association with\nnormal age-related declines in dopamine activity. Negative symptoms are more closely re-\nlated to prognosis than are positive symptoms and tend to be the most persistent. Further-\nmore, cognitive deficits associated with the illness may not improve over the course of the\nillness.\nThe essential features of schizophrenia are th e same in childhood, but it is more diffi-", "source": "dsm5.pdf"} {"id": "eced39f8285e-2", "page_content": "The essential features of schizophrenia are th e same in childhood, but it is more diffi-\ncult to make the diagnosis. In children, delu sions and hallucinations may be less elaborate\nthan in adults, and visual hallucinations are more common and should be distinguished", "source": "dsm5.pdf"} {"id": "eb32c323cbc0-0", "page_content": "cult to make the diagnosis. In children, delu sions and hallucinations may be less elaborate\nthan in adults, and visual hallucinations are more common and should be distinguished\nfrom normal fantasy play. Disorganized speec h occurs in many disorders with childhood\nonset (e.g., autism spectrum disorder), as does disorganized behavior (e.g., attention-deficit/", "source": "dsm5.pdf"} {"id": "63b4d0880221-0", "page_content": "Schizophrenia 103\nhyperactivity disord er). These symptoms should not be attributed to schizophrenia with-\nout due consideration of the more common disorders of childhood. Childhood-onset cases\ntend to resemble poor-outcome adult cases, with gradual onset and prominent negative\nsymptoms. Children who later receive the diag nosis of schizophrenia are more likely to\nhave experienced nonspecific emotional-behavioral distur bances and psychopathology,\nintellectual and language alterati ons, and subtle motor delays.\nLate-onset cases (i.e., onset after age 40 ye ars) are overrepresent ed by females, who\nmay have married. Often, the course is ch aracterized by a predom inance of psychotic\nsymptoms with preservation of affect and soci al functioning. Such late-onset cases can still\nmeet the diagnostic crit eria for schizophrenia, but it is not yet clear whether this is the\nsame condition as schizophrenia diagnosed prio r to mid-life (e.g., prior to age 55 years).\nRisk and Prognostic Factors\nEnvironmental. Season of birth has been linked to the incidence of schizophrenia, in-\ncluding late winter/early spring in some locations and summer for the deficit form of the\ndisease. The incidence of schizophrenia and related disorders is high er for children grow-\ning up in an urban environment an d for some minority ethnic groups. \nGenetic and physiological. There is a strong contribution for genetic factors in deter-\nmining risk for schizophrenia, although most individuals who have been diagnosed with\nschizophrenia have no family history of psyc hosis. Liability is conferred by a spectrum of\nrisk alleles, common and rare, with each allele contributing only a small fraction to the to-\ntal population variance. The risk alleles identi fied to date are also associated with other\nmental disorders, including bipolar disorder, depression, an d autism spectrum disorder.", "source": "dsm5.pdf"} {"id": "63b4d0880221-1", "page_content": "mental disorders, including bipolar disorder, depression, an d autism spectrum disorder.\nPregnancy and birth complications with hypoxia and greater paternal age are associated\nwith a higher risk of schizophrenia for the developing fetus. In addition, other prenatal\nand perinatal adversities, including stress, in fection, malnutrition, maternal diabetes, and\nother medical conditions, have been linked wi th schizophrenia. However, the vast major-\nity of offspring with these risk factors do not deve lop schizophrenia. \nCulture-Related Diagnostic Issues \nCultural and socioeconomic factors must be considered, particularly when the individual\nand the clinician do not share the same cult ural and socioeconomic background. Ideas that\nappear to be delusional in one culture (e.g., witchcraft) may be commonly held in another.\nIn some cultures, visual or auditory halluci nations with a religious content (e.g., hearing\nGod\u2019s voice) are a normal part of religious experience. In addition, the assessment of dis-\norganized speech may be made difficult by lin guistic variation in narrative styles across\ncultures. The assessment of affect requires sens itivity to differences in styles of emotional\nexpression, eye contact, and body language, wh ich vary across cultures. If the assessment\nis conducted in a language that is differen t from the individual\u2019s primary language, care\nmust be taken to ensure that alogia is not rela ted to linguistic barriers. In certain cultures,\ndistress may take the form of hallucinations or pseudo -hallucinations and overvalued\nideas that may present clinically similar to true psychosis but are normative to the pa-\ntient\u2019s subgroup.\nGender-Related Diagnostic Issues \nA number of features distinguish the clinical expression of schizophrenia in females and\nmales. The general incidence of schizophrenia tends to be slightly lower in females, par-", "source": "dsm5.pdf"} {"id": "63b4d0880221-2", "page_content": "males. The general incidence of schizophrenia tends to be slightly lower in females, par-\nticularly among treated cases. The age at onset is later in females, with a second mid-life\npeak as described earlier (see the section \u201cD evelopment and Course\u201d for this disorder).\nSymptoms tend to be more affect-laden am ong females, and there are more psychotic", "source": "dsm5.pdf"} {"id": "9ea8eac72281-0", "page_content": "peak as described earlier (see the section \u201cD evelopment and Course\u201d for this disorder).\nSymptoms tend to be more affect-laden am ong females, and there are more psychotic\nsymptoms, as well as a greater propensity for psychotic symptoms to worsen in later life.", "source": "dsm5.pdf"} {"id": "7af50984cace-0", "page_content": "104 Schizophrenia Spectrum and Other Psychotic Disorders\nOther symptom differences include less freque nt negative symptoms and disorganization.\nFinally, social functioning tends to remain better preserved in females. There are, how-\never, frequent exceptions to these general caveats. \nSuicide Risk \nApproximately 5%\u20136% of individuals with schizophrenia die by suicide, about 20% attempt\nsuicide on one or more occasions, and many mo re have significant suicidal ideation. Suicidal\nbehavior is sometimes in response to command hallucinations to harm oneself or others.\nSuicide risk remains high over the whole lifespan for males an d females, although it may be\nespecially high for younger males with comorb id substance use. Other risk factors include\nhaving depressive symptoms or feelings of hopelessness and being unemployed, and the\nrisk is higher, also, in the period after a psychotic episode or hospital discharge.\nFunctional Consequences of Schizophrenia \nSchizophrenia is associated with significant social and occupational dysfunction. Making\neducational progress and maintaining employment are frequently impaired by avolition\nor other disorder manifestatio ns, even when the cognitive sk ills are sufficient for the tasks\nat hand. Most individuals are employed at a lower level than their parents, and most, par-\nticularly men, do not marry or have limited social contacts outside of their family.\nDifferential Diagnosis \nMajor depressive or bipolar disorder with psychotic or catatonic features. The distinc-\ntion between schizophrenia and major depre ssive or bipolar disorder with psychotic\nfeatures or with catatonia depends on the te mporal relationship between the mood distur-\nbance and the psychosis, and on the severity of the depressive or manic symptoms. If de-\nlusions or hallucinations occur exclusively during a major depressive or manic episode,\nthe diagnosis is depressive or bipolar disorder with ps ychotic features.", "source": "dsm5.pdf"} {"id": "7af50984cace-1", "page_content": "the diagnosis is depressive or bipolar disorder with ps ychotic features. \nSchizoaffective disorder. A diagnosis of schizoaffective disorder requires that a major\ndepressive or manic episode occur concurrently with the active-phase symptoms and that\nthe mood symptoms be present for a majority of the total duration of the active periods.\nSchizophreniform disorder an d brief psychotic disorder. These disorders are of shorter\nduration than schizophrenia as specified in Cr iterion C, which requires 6 months of symp-\ntoms. In schizophreniform disorder, the disturbance is present less than 6 months, and in\nbrief psychotic disorder, symp toms are present at least 1 day but less than 1 month. \nDelusional disorder. Delusional disorder can be distinguished from schizophrenia by\nthe absence of the other symptoms characteristic of schizophrenia (e.g., delusions, prom-\ninent auditory or visual halluc inations, disorganized speech, grossly disorganized or cata-\ntonic behavior, negative symptoms).\nSchizotypal personality disorder. Schizotypal personality disorder may be distinguished\nfrom schizophrenia by subthres hold symptoms that are associ ated with persistent person-\nality features.\nObsessive-compulsive disorder and body dysmorphic disorder. Individuals with\nobsessive-compulsive disorder and body dysmorphic disorder may present with poor or\nabsent insight, and the preoccupations may reach delusional proportions. But these\ndisorders are distinguished from schizophren ia by their prominent obsessions, compul-\nsions, preoccupations with appearance or bo dy odor, hoarding, or body-focused repeti-\ntive behaviors.\nPosttraumatic stress disorder. Posttraumatic stress disorder may include flashbacks that\nhave a hallucinatory quality, and hypervigilanc e may reach paranoid proportions. But a trau-", "source": "dsm5.pdf"} {"id": "4d2109eb97ae-0", "page_content": "Schizoaffective Disorder 105\nmatic event and characteristic symptom features relating to reliving or reacting to the event\nare required to make the diagnosis. \nAutism spectrum disorder or communication disorders. These disorders may also have\nsymptoms resembling a psychotic episode but are distinguished by their respective defi-\ncits in social interaction with repetitive an d restricted behaviors and other cognitive and\ncommunication deficits. An individual with autism spectrum disord er or communication\ndisorder must have symptoms that meet fu ll criteria for schizophrenia, with prominent\nhallucinations or delusions for at least 1 mont h, in order to be diagnosed with schizophre-\nnia as a comorbid condition.\nOther mental disorders associated with a psychotic episode. The diagnosis of schizo-\nphrenia is made only when the psychotic episode is persistent and not attributable to the\nphysiological effects of a subs tance or another medical condit ion. Individuals with a de-\nlirium or major or minor neurocognitive disorder may present with psychotic symptoms,\nbut these would have a temporal relationship to the onset of cognit ive changes consistent\nwith those disorders. Individuals with subs tance/medication-induced psychotic disorder\nmay present with symptoms char acteristic of Criterion A for schizophrenia, but the sub-\nstance/medication-induced psyc hotic disorder can usually be distinguished by the chron-\nological relationship of subs tance use to the onset and remi ssion of the psychosis in the\nabsence of substance use. \nComorbidity \nRates of comorbidity with substance-relate d disorders are high in schizophrenia. Over\nhalf of individuals with schizophrenia have tobacco use disorder and smoke cigarettes\nregularly. Comorbidity with anxiety disorder s is increasingly recognized in schizophre-\nnia. Rates of obsessive-compulsive disorder and panic disorder are elevated in individuals", "source": "dsm5.pdf"} {"id": "4d2109eb97ae-1", "page_content": "nia. Rates of obsessive-compulsive disorder and panic disorder are elevated in individuals\nwith schizophrenia compared with the general population. Schizotypal or paranoid per-\nsonality disorder may sometimes pr ecede the onset of schizophrenia.\nLife expectancy is reduced in individual s with schizophrenia because of associated\nmedical conditions. Weight gain, diabetes, metabolic syndrome, and cardiovascular and\npulmonary disease are more common in schi zophrenia than in the general population.\nPoor engagement in health maintenance behavi ors (e.g., cancer screening, exercise) in-\ncreases the risk of chronic disease, but other disorder factors, including medications, life-\nstyle, cigarette smoking, and diet, may also play a role. A shared vulnerability for\npsychosis and medical disorders may explain so me of the medical comorbidity of schizo-\nphrenia. \nSchizoaffective Disorder\nDiagnostic Criteria \nA. An uninterrupted period of illness during which there is a major mood episode (major\ndepressive or manic) concurrent with Criterion A of schizophrenia.\nNote: The major depressive episode must include Criterion A1: Depressed mood.\nB. Delusions or hallucinations for 2 or more weeks in the absence of a major mood epi-\nsode (depressive or manic) during the lifetime duration of the illness. \nC. Symptoms that meet criteria for a major mood episode are present for the majority of\nthe total duration of the active and residual portions of the illness.\nD. The disturbance is not attributable to the effects of a substance (e.g., a drug of abuse,\na medication) or another medical condition.", "source": "dsm5.pdf"} {"id": "a3837512136a-0", "page_content": "106 Schizophrenia Spectrum and Other Psychotic Disorders\nSpecify whether:\n295.70 (F25.0) Bipolar type: This subtype applies if a manic episode is part of the pre-\nsentation. Major depressive episodes may also occur.\n295.70 (F25.1) Depressive type: This subtype applies if only major depressive epi-\nsodes are part of the presentation.\nSpecify if:\nWith catatonia (refer to the criteria for catatonia associated with another mental disorder,\npp. 119\u2013120, for definition).\nCoding note: Use additional code 293.89 (F06.1) catatonia associated with\nschizoaffective disorder to indicate the presence of the comorbid catatonia.\nSpecify if:\nThe following course specifiers are only to be used after a 1-year duration of the disorder\nand if they are not in contradiction to the diagnostic course criteria.\nFirst episode, currentl y in acute episode: First manifestation of the disorder meet-\ning the defining diagnostic symptom and time criteria. An acute episode is a time pe-\nriod in which the symptom criteria are fulfilled.\nFirst episode, currently in partial remission: Partial remission is a time period dur-\ning which an improvement after a previous episode is maintained and in which the de-\nfining criteria of the disorder are only partially fulfilled.\nFirst episode, currently in full remission: Full remission is a period of time after a\nprevious episode during which no disorder-specific symptoms are present.\nMultiple episodes, currently in acute episode: Multiple episodes may be deter-\nmined after a minimum of two episodes (i.e., after a first episode, a remission and a\nminimum of one relapse). \nMultiple episodes, currently in partial remission", "source": "dsm5.pdf"} {"id": "a3837512136a-1", "page_content": "minimum of one relapse). \nMultiple episodes, currently in partial remission\nMultiple episodes, currently in full remission\nContinuous: Symptoms fulfilling the diagnostic symptom criteria of the disorder are\nremaining for the majority of the illness course, with subthreshold symptom periods be-\ning very brief relative to the overall course.\nUnspecified\nSpecify current severity:\nSeverity is rated by a quantitative assessment of the primary symptoms of psychosis,\nincluding delusions, hallucinations, disorganized speech, abnormal psychomotor be-\nhavior, and negative symptoms. Each of these symptoms may be rated for its current\nseverity (most severe in the last 7 days) on a 5-point scale ranging from 0 (not present)\nto 4 (present and severe). (See Clinician-Rated Dimensions of Psychosis Symptom\nSeverity in the chapter \u201cAssessment Measures.\u201d)\nNote: Diagnosis of schizoaffective disorder can be made without using this severity\nspecifier.\nNote: For additional information on Developmen t and Course (age-related factors), Risk\nand Prognostic Factors (environmental risk factors), Culture-Related Diagnostic Issues,\nand Gender-Related Diagnostic Issues, see th e corresponding sections in schizophrenia,\nbipolar I and II disorders, an d major depressive disorder in their respective chapters.\nDiagnostic Features\nThe diagnosis of schizoaffective disorder is based on the assessment of an uninterrupted\nperiod of illness during which the individual co ntinues to display active or residual symp-\ntoms of psychotic illness. The diagnosis is usually, but not necessarily, made during the\nperiod of psychotic illness. At some time during the period, Criterion A for schizophrenia", "source": "dsm5.pdf"} {"id": "103421508ea7-0", "page_content": "Schizoaffective Disorder 107\nhas to be met. Criteria B (soc ial dysfunction) and F (exclusion of autism sp ectrum disorder\nor other communication disorder of childhood onset) for schizophrenia do not have to be\nmet. In addition to meeting Criterion A for schizophrenia, there is a major mood episode\n(major depressive or manic) (Criterion A for schizoaffective disorder). Because loss of in-\nterest or pleasure is common in schizophrenia, to meet Criterion A for schizoaffective dis-\norder, the major depressive episode must in clude pervasive depressed mood (i.e., the\npresence of markedly diminished interest or pleasure is not sufficie nt). Episodes of de-\npression or mania are present for the majority of the total duration of the illness (i.e., after\nCriterion A has been met) (Criterion C for schi zoaffective disorder). To separate schizoaf-\nfective disorder from a depressive or bipola r disorder with psychotic features, delusions\nor hallucinations must be present for at least 2 weeks in the absence of a major mood epi-\nsode (depressive or manic) at some point duri ng the lifetime duration of the illness (Cri-\nterion B for schizoaffective disorder). The symptoms must not be attributable to the effects\nof a substance or another medical condition (Criterion D for schi zoaffective disorder).\nCriterion C for schizoaf fective disorder specifies that mood symptoms meeting criteria\nfor a major mood episode must be present for the majority of the total duration of the ac-\ntive and residual portion of the illness. Criter ion C requires the asses sment of mood symp-\ntoms for the entire course of a psychotic illnes s, which differs from th e criterion in DSM-IV,", "source": "dsm5.pdf"} {"id": "103421508ea7-1", "page_content": "which required only an assessment of the curr ent period of illness. If the mood symptoms\nare present for only a relative ly brief period, the diagnosis is schizophrenia, not schizoaf-\nfective disorder. When deciding whether an individual\u2019s presentation meets Criterion C,\nthe clinician should review the total duration of psychotic illness (i.e., both active and re-\nsidual symptoms) and determine when significa nt mood symptoms (untreated or in need\nof treatment with antidepressant and/or mo od-stabilizing medication) accompanied the\npsychotic symptoms. This determination requir es sufficient histor ical information and\nclinical judgment. For example, an individual with a 4-year history of active and residual\nsymptoms of schizophrenia develops depressi ve and manic episodes that, taken together,\ndo not occupy more than 1 year during the 4- year history of psycho tic illness. This presen-\ntation would not meet Criterion C.\nIn addition to the five symptom domain areas identified in the diagnostic criteria, the\nassessment of cognition, depression, and mani a symptom domains is vital for making crit-\nically important distinctions between the va rious schizophrenia spectrum and other psy-\nchotic disorders.\nAssociated Features Supporting Diagnosis\nOccupational functioning is frequently impair ed, but this is not a defining criterion (in\ncontrast to schizophrenia). Restricted social contact and difficulties with self-care are as-\nsociated with schizoaffective disorder, but negative symptoms may be less severe and less\npersistent than those seen in schizophrenia. Anosognosia (i.e., poor insight) is also com-\nmon in schizoaffective disorder, but the deficits in insight may be less severe and perva-\nsive than those in schizophrenia. Individual s with schizoaffective disorder may be at\nincreased risk for later developing episodes of major depressive disorder or bipolar disor-", "source": "dsm5.pdf"} {"id": "103421508ea7-2", "page_content": "increased risk for later developing episodes of major depressive disorder or bipolar disor-\nder if mood symptoms contin ue following the remission of symptoms meeting Criterion A\nfor schizophrenia. There may be associated al cohol and other substance-related disorders. \nThere are no tests or biological measures that can assist in making the diagnosis of\nschizoaffective disorder. Whether schizoaffe ctive disorder differs from schizophrenia", "source": "dsm5.pdf"} {"id": "58ff9185b91b-0", "page_content": "There are no tests or biological measures that can assist in making the diagnosis of\nschizoaffective disorder. Whether schizoaffe ctive disorder differs from schizophrenia\nwith regard to associated features such as structural or function al brain abnormalities,\ncognitive deficits, or geneti c risk factors is not clear.\nPrevalence\nSchizoaffective disorder appe ars to be about one-third as common as schizophrenia. Life-\ntime prevalence of schizoaffective disorder is estimated to be 0.3%. The incidence of", "source": "dsm5.pdf"} {"id": "db1f4694bf97-0", "page_content": "108 Schizophrenia Spectrum and Other Psychotic Disorders\nschizoaffective disorder is higher in females than in males, mainly due to an increased in-\ncidence of the depressive type among females.\nDevelopment and Course\nThe typical age at onset of schizoaffective di sorder is early adulthood, although onset can\noccur anywhere from adolescence to late in lif e. A significant number of individuals diag-\nnosed with another psychotic illness initially will receive the diagnosis schizoaffective dis-\norder later when the pattern of mood epis odes has become more apparent. With the\ncurrent diagnostic Criterion C, it is expected that the diagnosis for some individuals will\nconvert from schizoaffective d isorder to another disorder as mood symptoms become less\nprominent. The prognosis for schizoaffective di sorder is somewhat better than the prog-\nnosis for schizophrenia but worse than the prognosis for mood disorders. \nSchizoaffective disorder may occur in a variety of temporal patterns. The following is\na typical pattern: An individual may have pronounced auditory hallucinations and per-\nsecutory delusions for 2 months before the onset of a prom inent major depressive episode.\nThe psychotic symptoms and the full major depr essive episode are then present for 3 months.\nThen, the individual recovers completely fr om the major depressive episode, but the psy-\nchotic symptoms persist for another month be fore they too disappear. During this period\nof illness, the individual\u2019s symptoms concurre ntly met criteria for a major depressive ep-\nisode and Criterion A for schizophrenia, and during this same period of illness, auditory\nhallucinations and delusions were present both before and after the depressive phase. The\ntotal period of illness lasted for about 6 mo nths, with psychotic sy mptoms alone present\nduring the initial 2 months, both depressive and psychotic symptoms present during the", "source": "dsm5.pdf"} {"id": "db1f4694bf97-1", "page_content": "during the initial 2 months, both depressive and psychotic symptoms present during the\nnext 3 months, and psychotic symptoms alone pr esent during the last month. In this in-\nstance, the duration of the depressive episode was not brief relative to the total duration of\nthe psychotic disturbance, and thus the presen tation qualifies for a diagnosis of schizoaf-\nfective disorder.\nThe expression of psychotic symptoms across the lifespan is variable. Depressive or\nmanic symptoms can occur before the onset of psychosis, during acute psychotic episodes,\nduring residual periods, and after cessation of psychosis. For example, an individual\nmight present with prominent mood symptoms during the prodromal stage of schizo-\nphrenia. This pattern is not necessarily indicative of schizoaffective disorder, since it is the\nco-occurrence of psychotic and mood symptoms that is diagnostic. For an individual with\nsymptoms that clearly meet the criteria for sc hizoaffective disorder but who on further fol-\nlow-up only presents with residual psychoti c symptoms (such as subthreshold psychosis\nand/or prominent negative symptoms), the diagnosis may be changed to schizophrenia,\nas the total proportion of psychotic illness compared with mood symptoms becomes more\nprominent. Schizoaffective diso rder, bipolar type, may be more common in young adults,\nwhereas schizoaffective disorder, depressive type, may be more common in older adults. \nRisk and Prognostic Factors\nGenetic and physiological. Among individuals with schizophrenia, there may be an in-\ncreased risk for schizoaffective disorder in first-degree relatives. The risk for schizoaffec-\ntive disorder may be increased among indivi duals who have a first- degree relative with\nschizophrenia, bipolar disorder, or schizoaffective disorder. \nCulture-Related Diagnostic Issues", "source": "dsm5.pdf"} {"id": "db1f4694bf97-2", "page_content": "Culture-Related Diagnostic Issues \nCultural and socioeconomic factors must be considered, particularly when the individual\nand the clinician do not share the same cultur al and economic backgr ound. Ideas that ap-\npear to be delusional in one culture (e.g., witchcraft) may be commonly held in another.", "source": "dsm5.pdf"} {"id": "5fb2f8216eb8-0", "page_content": "and the clinician do not share the same cultur al and economic backgr ound. Ideas that ap-\npear to be delusional in one culture (e.g., witchcraft) may be commonly held in another.\nThere is also some evidence in the literature for the overdiagnosis of schizophrenia com-", "source": "dsm5.pdf"} {"id": "b9c3b0af1ef9-0", "page_content": "Schizoaffective Disorder 109\npared with schizoaffective disorder in Afri can American and Hispanic populations, so\ncare must be taken to ensure a culturally appropri ate evaluation that includes both psy-\nchotic and affective symptoms.\nSuicide Risk \nThe lifetime risk of suicide for schizophreni a and schizoaffective disorder is 5%, and the\npresence of depressive symptoms is correlated with a higher risk for suicide. There is ev-\nidence that suicide rates are higher in North American populations than in European,\nEastern European, South American, and Indian populations of individuals with schizo-\nphrenia or schizoaffective disorder.\nFunctional Consequences of Schizoaffective Disorder\nSchizoaffective disorder is associated with social and occupational dysfunction, but dys-\nfunction is not a diagnostic criterion (as it is for schizophrenia), an d there is substantial\nvariability between individuals diagno sed with schizoaffective disorder.\nDifferential Diagnosis\nOther mental disorders and medical conditions. A wide variety of psychiatric and med-\nical conditions can manifest with psychotic and mood symptoms that must be considered\nin the differential diagnosis of schizoaffective disorder. Th ese include psychotic disorder\ndue to another medical condition; delirium; major neurocognitive disorder; substance/\nmedication-induced psychotic disorder or neurocognitive disorder; bipolar disorders\nwith psychotic features; major depressive diso rder with psychotic features; depressive or\nbipolar disorders with catatonic features; schi zotypal, schizoid, or paranoid personality\ndisorder; brief psychotic disorder; schizophre niform disorder; schizophrenia; delusional\ndisorder; and other specified and unspecified schizophrenia spectrum and other psychotic\ndisorders. Medical conditions and substance use can present with a combination of psy-\nchotic and mood symptoms, and thus psychoti c disorder due to another medical condition", "source": "dsm5.pdf"} {"id": "b9c3b0af1ef9-1", "page_content": "chotic and mood symptoms, and thus psychoti c disorder due to another medical condition\nneeds to be excluded. Distinguishing schizoaffective disorder from schizophrenia and\nfrom depressive and bipolar diso rders with psychotic features is often difficult. Criterion\nC is designed to separate schizoaffective di sorder from schizophrenia, and Criterion B is\ndesigned to distinguish schizoaffective diso rder from a depressive or bipolar disorder\nwith psychotic features. More specifically, schizoaffective disorder can be distinguished\nfrom a depressive or bipolar disorder with psyc hotic features due to the presence of prom-\ninent delusions and/or hallucinations for at least 2 weeks in the absence of a major mood\nepisode. In contrast, in depressive or bipo lar disorders with psychotic features, the psy-\nchotic features primarily occur during the mo od episode(s). Because the relative propor-\ntion of mood to psychotic symptoms may ch ange over time, the appropriate diagnosis\nmay change from and to schizoaffective disord er (e.g., a diagnosis of schizoaffective dis-\norder for a severe and prominent major depre ssive episode lasting 3 months during the\nfirst 6 months of a persistent psychotic illnes s would be changed to schizophrenia if active\npsychotic or prominent residual symptoms pe rsist over several years without a recurrence\nof another mood episode).\nPsychotic disorder due to another medical condition. Other medical conditions and\nsubstance use can manifest with a combinat ion of psychotic and mood symptoms, and\nthus psychotic disorder due to another medical condition needs to be excluded. \nSchizophrenia, bipolar, and depressive disorders. Distinguishing schizoaffective dis-\norder from schizophrenia and from depressiv e and bipolar disorders with psychotic fea-\ntures is often difficult. Criterion C is design ed to separate schizoaffective disorder from", "source": "dsm5.pdf"} {"id": "b9c3b0af1ef9-2", "page_content": "tures is often difficult. Criterion C is design ed to separate schizoaffective disorder from\nschizophrenia, and Criterion B is designed to distinguish schi zoaffective disorder from a", "source": "dsm5.pdf"} {"id": "01ea4c60d76e-0", "page_content": "110 Schizophrenia Spectrum and Other Psychotic Disorders\ndepressive or bipolar disorder with psychoti c features. More specifically, schizoaffective\ndisorder can be distinguished from a depressive or bipolar disorder with psychotic features\nbased on the presence of prom inent delusions and/or hallucinations for at least 2 weeks in\nthe absence of a major mood episode. In cont rast, in depressive or bipolar disorder with\npsychotic features, the psychoti c features primarily occur duri ng the mood episode(s). Be-\ncause the relative proportion of mood to ps ychotic symptoms may change over time, the\nappropriate diagnosis may change from and to schizoaffective disorder. (For example, a\ndiagnosis of schizoaffective disorder for a se vere and prominent major depressive episode\nlasting 3 months during the first 6 months of a chronic psychotic illness would be changed\nto schizophrenia if active ps ychotic or prominent residual symptoms persist over several\nyears without a recurrence of another mood episode.) \nComorbidity\nMany individuals diagnosed with schizoaffect ive disorder are also diagnosed with other\nmental disorders, especially substance use d isorders and anxiety disorders. Similarly, the\nincidence of medical conditions is increase d above base rate for the general population\nand leads to decre ased life expectancy.\nSubstance/Medication-Induced\n Psychotic Disorder\nDiagnostic Criteria \nA. Presence of one or both of the following symptoms:\n1. Delusions.\n2. Hallucinations.\nB. There is evidence from the history, physical examination, or laboratory findings of both\n(1) and (2):\n1. The symptoms in Criterion A developed during or soon after substance intoxication\nor withdrawal or after exposure to a medication.\n2. The involved substance/medication is capable of producing the symptoms in Crite-\nrion A.", "source": "dsm5.pdf"} {"id": "01ea4c60d76e-1", "page_content": "rion A.\nC. The disturbance is not better explained by a psychotic disorder that is not substance/\nmedication-induced. Such evidence of an independent psychotic disorder could in-\nclude the following: \nThe symptoms preceded the onset of the substance/medication use; the symptoms\npersist for a substantial period of time (e.g., about 1 month) after the cessation of\nacute withdrawal or severe intoxication; or there is other evidence of an indepen-\ndent non-substance/medication-induced psychotic disorder (e.g., a history of recur-\nrent non-substance/medication-related episodes).\nD. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nNote: This diagnosis should be made instead of a diagnosis of substance intoxication or\nsubstance withdrawal only when the symptoms in Criterion A predominate in the clinical\npicture and when they are sufficiently severe to warrant clinical attention.", "source": "dsm5.pdf"} {"id": "52e3bfbd543c-0", "page_content": "Substance/Medication-Induced Psychotic Disorder 111\nCoding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-\ntion]-induced psychotic disorders are indicated in the table below. Note that the ICD-10-\nCM code depends on whether or not there is a comorbid substance use disorder present\nfor the same class of substance. If a mild substance use disorder is comorbid with the sub-\nstance-induced psychotic disorder, the 4th position character is \u201c1,\u201d and the clinician should\nrecord \u201cmild [substance] use disorder\u201d before the substance-induced psychotic disorder\n(e.g., \u201cmild cocaine use diso rder with cocaine-induced ps ychotic disorder\u201d). If a m oderate or\nsevere substance use disorder is comorbid with the substance-induced psychotic disor-\nder, the 4th position character is \u201c2,\u201d and the clinician should record \u201cmoderate [substance]\nuse disorder\u201d or \u201csevere [substance] use disorder,\u201d depending on the severity of the co-\nmorbid substance use disorder. If there is no comorbid substance use disorder (e.g., after\na one-time heavy use of the substance), then the 4th position character is \u201c9,\u201d and the cli-\nnician should record only the substance-induced psychotic disorder.\nSpecify if (see Table 1 in the chapter \u201cSubstance-Related and Addictive Disorders\u201d for diag-\nnoses associated with substance class):\nWith onset during intoxication: If the criteria are met for intoxication with the sub-\nstance and the symptoms develop during intoxication.\nWith onset during withdrawal: If the criteria are met for withdrawal from the sub-\nstance and the symptoms develop during, or shortly after, withdrawal.\nSpecify current severity:", "source": "dsm5.pdf"} {"id": "52e3bfbd543c-1", "page_content": "stance and the symptoms develop during, or shortly after, withdrawal.\nSpecify current severity:\nSeverity is rated by a quantitative assessment of the primary symptoms of psychosis,\nincluding delusions, hallucinations, abnormal psychomotor behavior, and negative\nsymptoms. Each of these symptoms may be rated for its current severity (most severe\nin the last 7 days) on a 5-point scale ranging from 0 (not present) to 4 (present and\nsevere). (See Clinician-Rated Dimensions of Psychosis Symptom Severity in the chap-\nter \u201cAssessment Measures.\u201d)\nNote: Diagnosis of substance/medication-induced psychotic disorder can be made\nwithout using this severity specifier.ICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate \nor severeWithout \nuse \ndisorder\nAlcohol 291.9 F10.159 F10.259 F10.959\nCannabis 292.9 F12.159 F12.259 F12.959\nPhencyclidine 292.9 F16.159 F16.259 F16.959\nOther hallucinogen 292.9 F16.159 F16.259 F16.959\nInhalant 292.9 F18.159 F18.259 F18.959\nSedative, hypnotic, or \nanxiolytic292.9 F13.159 F13.259 F13.959\nAmphetamine (or other \nstimulant)292.9 F15.159 F15.259 F15.959\nCocaine 292.9 F14.159 F14.259 F14.959\nOther (or unknown) substance 292.9 F19.159 F19.259 F19.959", "source": "dsm5.pdf"} {"id": "ba3375431b8e-0", "page_content": "112 Schizophrenia Spectrum and Other Psychotic Disorders\nRecording Procedures\nICD-9-CM. The name of the substance/medication -induced psychotic disorder begins\nwith the specific substance (e.g., cocaine, de xamethasone) that is presumed to be causing\nthe delusions or hallucinations. The diagnostic code is selected from the table included in\nthe criteria set, which is based on the drug clas s. For substances that do not fit into any of\nthe classes (e.g., dexamethasone), the code for \u201cother substance\u201d should be used; and in\ncases in which a substance is judged to be an etiological factor but the specific class of sub-\nstance is unknown, the category \u201cu nknown substance\u201d should be used.\nThe name of the disorder is followed by the sp ecification of onset (i.e., onset during in-\ntoxication, onset during with drawal). Unlike the recording procedures for ICD-10-CM,\nwhich combine the substance-induced disorder and substance use disorder into a single\ncode, for ICD-9-CM a separate diagnostic code is given for the substance use disorder. For\nexample, in the case of delusio ns occurring during intoxication in a man with a severe co-\ncaine use disorder, the diagnosis is 292.9 cocaine-induced psychotic disorder, with onset\nduring intoxication. An additional diagnosis of 304.20 severe cocaine use disorder is also\ngiven. When more than one subs tance is judged to play a significant role in the development\nof psychotic symptoms, each should be listed separately (e.g., 292.9 cannabis-induced psy-\nchotic disorder with onset during intoxicati on, with severe cannabis use disorder; 292.9\nphencyclidine-induced psychotic disorder, wi th onset during intoxication, with mild\nphencyclidine use disorder).", "source": "dsm5.pdf"} {"id": "ba3375431b8e-1", "page_content": "phencyclidine use disorder).\nICD-10-CM. The name of the substance/medication-induced psychotic disorder begins\nwith the specific substance (e.g., cocaine, de xamethasone) that is presumed to be causing\nthe delusions or hallucinations. The diagnostic code is selected from the table included in\nthe criteria set, which is based on the drug class and presence or absence of a comorbid\nsubstance use disorder. For substances that do not fit into an y of the classes (e.g., dexa-\nmethasone), the code for \u201cother substance\u201d with no comorbid substance use should be\nused; and in cases in which a substance is judged to be an etiological factor but the specific\nclass of substance is unknown, the category \u201cunknown substance\u201d wi th no comorbid sub-\nstance use should be used.\nWhen recording the name of the disorder, th e comorbid substance use disorder (if any)\nis listed first, followed by the word \u201cwith,\u201d followed by the name of the substance-induced\npsychotic disorder, followed by the specification of onset (i .e., onset during intoxication,\nonset during withdrawal). For example, in the case of delusions occurring during intoxi-\ncation in a man with a severe cocaine use d isorder, the diagnosis is F14.259 severe cocaine\nuse disorder with cocaine-induced psychotic disorder, with onset during intoxication. A\nseparate diagnosis of the comorbid severe co caine use disorder is not given. If the sub-\nstance-induced psychotic disorder occurs without a comorbid substance use disorder\n(e.g., after a one-time heavy use of the substance), no accompanying substance use disor-\nder is noted (e.g., F16.959 phencyclidine-induce d psychotic disorder, with onset during in-", "source": "dsm5.pdf"} {"id": "ba3375431b8e-2", "page_content": "toxication). When more than one substance is judged to play a significant role in the\ndevelopment of psychotic symptoms, each should be listed separately (e.g., F12.259 severe\ncannabis use disorder with cannabis-induced ps ychotic disorder, with onset during intox-\nication; F16.159 mild phencyclidine use diso rder with phencyclidine-induced psychotic\ndisorder, with onset during intoxication).\nDiagnostic Features\nThe essential features of substance/medicati on-induced psychotic disorder are prominent\ndelusions and/or hallucinations (Criterion A) that are judged to be due to the physiolog-", "source": "dsm5.pdf"} {"id": "8de4408ebc9b-0", "page_content": "Diagnostic Features\nThe essential features of substance/medicati on-induced psychotic disorder are prominent\ndelusions and/or hallucinations (Criterion A) that are judged to be due to the physiolog-\nical effects of a substance/medication (i.e., a drug of abuse, a medication, or a toxin expo-\nsure) (Criterion B). Hallucinations that the individual realizes are substance/medication-\ninduced are not included here and instead w ould be diagnosed as substance intoxication", "source": "dsm5.pdf"} {"id": "c8c1878d78cc-0", "page_content": "Substance/Medication-Induced Psychotic Disorder 113\nor substance withdrawal with the accompanyi ng specifier \u201cwith perceptual disturbances\u201d\n(applies to alcohol withdrawal; cannabis into xication; sedative, hypnotic, or anxiolytic\nwithdrawal; and stimulant intoxication).\nA substance/medication-induced psychotic di sorder is distinguished from a primary\npsychotic disorder by considering the onset, course, and other factors. For drugs of abuse,\nthere must be evidence from the history, physical examination, or laboratory findings of\nsubstance use, intoxication, or withdrawal . Substance/medication-induced psychotic\ndisorders arise during or soon after exposure to a medication or after substance intoxica-\ntion or withdrawal but can persist for week s, whereas primary psychotic disorders may\nprecede the onset of substance/ medication use or may occur during times of sustained ab-\nstinence. Once initiated, the psychotic symp toms may continue as long as the substance/\nmedication use continues. Anothe r consideration is the presence of features that are atyp-\nical of a primary psychotic disord er (e.g., atypical age at onse t or course). For example, the\nappearance of delusions de novo in a person older than 35 years without a known history\nof a primary psychotic disorder should sugge st the possibility of a substance/medication-\ninduced psychotic disorder. Even a prior history of a primary psychotic disorder does not\nrule out the possibility of a substance/medicati on-induced psychotic disorder. In contrast,\nfactors that suggest that the psychotic symp toms are better accounted for by a primary\npsychotic disorder include persistence of ps ychotic symptoms for a substantial period of\ntime (i.e., a month or more) after the end of substance intoxication or acute substance with-", "source": "dsm5.pdf"} {"id": "c8c1878d78cc-1", "page_content": "drawal or after cessation of medication use; or a history of prior recurrent primary psy-\nchotic disorders. Other causes of psychoti c symptoms must be considered even in an\nindividual with substance into xication or withdrawal, because substance use problems are\nnot uncommon among individuals with non- substance/medication-induced psychotic\ndisorders. \nIn addition to the four symptom domain areas identified in the diagnostic criteria, the\nassessment of cognition, depression, and mani a symptom domains is vital for making crit-\nically important distinctions between the va rious schizophrenia spectrum and other psy-\nchotic disorders.\nAssociated Features Supporting Diagnosis \nPsychotic disorders can occur in association wi th intoxication with the following classes of\nsubstances: alcohol; cannabis; hallucinoge ns, including phencyclidine and related sub-\nstances; inhalants; sedatives, hypnotics, and anxiolytics; stimulants (including cocaine);\nand other (or unknown) substances. Psychotic disorders can occur in association with with-\ndrawal from the following classes of substanc es: alcohol; sedatives, hypnotics, and anxio-\nlytics; and other (or unknown) substances. \nSome of the medications reported to evoke psychotic symptoms include anesthetics\nand analgesics, anticholinergic agents, anticonvulsants, antihistamines, antihypertensive\nand cardiovascular medications, antimicrobial medications, antiparkinsonian medica-\ntions, chemotherapeutic agents (e.g., cyclosporine, procarbazine), corticosteroids, gastro-\nintestinal medications, muscle relaxants, nonsteroidal anti-inf lammatory medications,\nother over-the-counter medicati ons (e.g., phenylephrine, ps eudoephedrine), antidepres-", "source": "dsm5.pdf"} {"id": "c8c1878d78cc-2", "page_content": "sant medication, and disulfiram . Toxins reported to induce psychotic symptoms include\nanticholinesterase, organophosphate insectic ides, sarin and other nerve gases, carbon\nmonoxide, carbon dioxide, and volatile substances such as fuel or paint.\nPrevalence\nPrevalence of substance/medi cation-induced psychotic disorder in the general popula-\ntion is unknown. Between 7% and 25% of in dividuals presenting with a first episode of", "source": "dsm5.pdf"} {"id": "c4bd4d084ceb-0", "page_content": "Prevalence\nPrevalence of substance/medi cation-induced psychotic disorder in the general popula-\ntion is unknown. Between 7% and 25% of in dividuals presenting with a first episode of\npsychosis in different settings are reported to have substance/medication-induced psy-\nchotic disorder.", "source": "dsm5.pdf"} {"id": "71f5cb638282-0", "page_content": "114 Schizophrenia Spectrum and Other Psychotic Disorders\nDevelopment and Course\nThe initiation of the disorder may vary co nsiderably with the substance. For example,\nsmoking a high dose of cocaine may produce psychosis within minutes, whereas days or\nweeks of high-dose alcohol or sedative use ma y be required to produce psychosis. Alco-\nhol-induced psychotic disorder, with hallucina tions, usually occurs only after prolonged,\nheavy ingestion of alcohol in individuals who have moderate to severe alcohol use disorder,\nand the hallucinations are generally auditory in nature.\nPsychotic disorders induced by amphetamine and cocaine share similar clinical fea-\ntures. Persecutory delusions may rapidly develop shortly af ter use of amphetamine or a\nsimilarly acting sympathomimetic. The hallucination of bugs or vermin crawling in or un-\nder the skin (formication) can lead to scratchi ng and extensive skin excoriations. Cannabis-\ninduced psychotic disorder may develop shortl y after high-dose cannabis use and usually\ninvolves persecutory delusions, marked anxiety, emotional lability, and depersonalization.\nThe disorder usually remits within a day bu t in some cases may persist for a few days.\nSubstance/medication-induced psychotic disord er may at times persist when the offend-\ning agent is removed, such that it may be difficult initially to distinguish it from an indepen-\ndent psychotic disorder. Agents such as amph etamines, phencyclidine, and cocaine have been\nreported to evoke temporary ps ychotic states that can someti mes persist for weeks or longer\ndespite removal of the agent and treatment with neuroleptic medication. In later life, poly-\npharmacy for medical conditions and exposure to medications for parkinsonism, cardiovas-\ncular disease, and other medi cal disorders may be associated with a greater likelihood of", "source": "dsm5.pdf"} {"id": "71f5cb638282-1", "page_content": "cular disease, and other medi cal disorders may be associated with a greater likelihood of\npsychosis induced by prescription medicati ons as opposed to substances of abuse.\nDiagnostic Markers\u00a0\nWith substances for which relevant blood le vels are available (e.g., blood alcohol level,\nother quantifiable blood levels su ch as digoxin), the presence of a level consistent with tox-\nicity may increase diagnostic certainty.\nFunctional Consequences of \nSubstance/Medication-Indu ced Psychotic Disorder\nSubstance/medication-induced psychotic diso rder is typically severely disabling and\nconsequently is observed most frequently in emergency rooms, as individuals are often\nbrought to the acute-care setting when it occu rs. However, the disability is typically self-\nlimited and resolves upon removal of the offending agent.\nDifferential Diagnosis\nSubstance intoxication or substance withdrawal. Individuals intoxicated with stimu-\nlants, cannabis, the opioid meperidine, or phe ncyclidine, or those withdrawing from alco-\nhol or sedatives, may experience altered percep tions that they recognize as drug effects. If\nreality testing for these experiences remains inta ct (i.e., the individual recognizes that the\nperception is substance induced and neither believe s in nor acts on it), the diagnosis is not\nsubstance/medication-induced psychotic disorder. Instead, substance intoxication or\nsubstance withdrawal, with perceptual disturbances, is diagnosed (e.g., cocaine intoxica-\ntion, with perceptual disturba nces). \u201cFlashback\u201d hallucinations that can occur long after\nthe use of hallucinogens has stopped are diag nosed as hallucinogen persisting perception\ndisorder. If substance/medication-induced psychotic symptoms oc cur exclusively during\nthe course of a delirium, as in severe forms of alcohol withdrawal, the psychotic symptoms", "source": "dsm5.pdf"} {"id": "71f5cb638282-2", "page_content": "the course of a delirium, as in severe forms of alcohol withdrawal, the psychotic symptoms\nare considered to be an associated feature of the delirium and are not diagnosed sepa-\nrately. Delusions in the context of a major or mild neurocognitive disorder would be di-\nagnosed as major or mild neurocognitive disorder, with behavioral disturbance.", "source": "dsm5.pdf"} {"id": "bdf7999bcfc2-0", "page_content": "Psychotic Disorder Due to Another Medical Condition 115\nPrimary psychotic disorder. A substance/medication-induc ed psychotic disorder is\ndistinguished from a primary psychotic disord er, such as schizophrenia, schizoaffective\ndisorder, delusional disorder, brief psychotic disorder, other specified schizophrenia\nspectrum and other psychotic disorder, or un specified schizophrenia spectrum and other\npsychotic disorder, by the fact that a substance is judged to be etiologically related to the\nsymptoms.\nPsychotic disorder due to another medical condition. A substance/medication-induced\npsychotic disorder due to a prescribed trea tment for a mental or medical condition must\nhave its onset while the individual is receiv ing the medication (or during withdrawal, if\nthere is a withdrawal syndrome associated with the medication). Because individuals with\nmedical conditions often take medications fo r those conditions, the clinician must con-\nsider the possibility that the psychotic symptoms are caused by the physiological conse-\nquences of the medical condition rather than the medication, in which case psychotic\ndisorder due to another medical condition is diagnosed. The hist ory often provides the\nprimary basis for such a judgme nt. At times, a change in the treatment for the medical con-\ndition (e.g., medication substitution or disc ontinuation) may be needed to determine em-\npirically for that individual whether the medica tion is the causative agent. If the clinician\nhas ascertained that the distur bance is attributable to both a medical condition and sub-\nstance/medication use, both diagnoses (i.e., psychotic disorder due to another medical\ncondition and substance/medication-induced psychotic disorder) may be given.\nPsychotic Disorder\n Due to Another Medical Condition\nDiagnostic Criteria \nA. Prominent hallucinations or delusions.", "source": "dsm5.pdf"} {"id": "bdf7999bcfc2-1", "page_content": "Diagnostic Criteria \nA. Prominent hallucinations or delusions.\nB. There is evidence from the history, physical examination, or laboratory findings that the\ndisturbance is the direct pathophysiological consequence of another medical condi-\ntion.\nC. The disturbance is not better explained by another mental disorder.\nD. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nSpecify whether:\nCode based on predominant symptom:\n293.81 (F06.2) With delusions: If delusions are the predominant symptom.\n293.82 (F06.0) With hallucinations: If hallucinations are the predominant symptom.\nCoding note: Include the name of the other medical condition in the name of the mental\ndisorder (e.g., 293.81 [F06.2] psychotic disorder due to malignant lung neoplasm, with de-\nlusions). The other medical condition should be coded and listed separately immediately\nbefore the psychotic disorder due to the medical condition (e.g., 162.9 [C34.90] malignant\nlung neoplasm; 293.81 [F06.2] psychotic disorder due to malignant lung neoplasm, with\ndelusions).\nSpecify current severity:\nSeverity is rated by a quantitative assessment of the primary symptoms of psychosis,\nincluding delusions, hallucinations, abnormal psychomotor behavior, and negative\nsymptoms. Each of these symptoms may be rated for its current severity (most severe\nin the last 7 days) on a 5-point scale ranging from 0 (not present) to 4 (present and", "source": "dsm5.pdf"} {"id": "0715e2fd5a26-0", "page_content": "116 Schizophrenia Spectrum and Other Psychotic Disorders\nsevere). (See Clinician-Rated Dimensions of Psychosis Symptom Severity in the chap-\nter \u201cAssessment Measures.\u201d)\nNote: Diagnosis of psychotic disorder due to another medical condition can be made\nwithout using this severity specifier.\nSpecifiers\nIn addition to the symptom domain areas identified in the diagnostic criteria, the assess-\nment of cognition, depressio n, and mania symptom domains is vital for making critically\nimportant distinctions between the various schizophrenia spectrum and other psychotic\ndisorders.\nDiagnostic Features\nThe essential features of psychotic disorder due to another medical condition are promi-\nnent delusions or hallucinations that are judged to be attributable to the physiological ef-\nfects of another medical condition and are not better explained by another mental disorder\n(e.g., the symptoms are not a psychologically mediated response to a severe medical con-\ndition, in which case a diagnosis of brief psychotic disorder, with ma rked stressor, would\nbe appropriate). \nHallucinations can occur in any sensory modalit y (i.e., visual, olfactory, gustatory, tac-\ntile, or auditory), but certai n etiological factors are likely to evoke specific hallucinatory\nphenomena. Olfactory hallucinations are suggest ive of temporal lobe epilepsy. Hallucina-\ntions may vary from simple and unformed to highly comp lex and organized, depending\non etiological and environmental factors. Ps ychotic disorder due to another medical con-\ndition is generally not diagnosed if the individual maintains reality testing for the hallu-\ncinations and appreciates that they result from the medical conditio n. Delusions may have\na variety of themes, including somatic, gran diose, religious, and, most commonly, perse-", "source": "dsm5.pdf"} {"id": "0715e2fd5a26-1", "page_content": "cutory. On the whole, however, associations between delusions and particular medical\nconditions appear to be less specific than is the case for hallucinations.\nIn determining whether the ps ychotic disturbance is attributable to another medical\ncondition, the presence of a medical condition must be identified and considered to be the\netiology of the psychosis through a physiol ogical mechanism. Although there are no\ninfallible guidelines for determining whether th e relationship between the psychotic distur-\nbance and the medical condition is etiological, several considerations provide some guidance.\nOne consideration is the presen ce of a temporal association between the onset, exacerba-\ntion, or remission of the medical condition an d that of the psychotic disturbance. A second\nconsideration is the presence of features that are atypical for a psychotic disorder (e.g.,\natypical age at onset or presence of visual or olfactory hallucinations). The disturbance must\nalso be distinguished from a substance/medication-induced psychotic disorder or an-\nother mental disorder (e.g., an adjustment disorder). \nAssociated Features Supporting Diagnosis\nThe temporal association of th e onset or exacerbation of th e medical condition offers the\ngreatest diagnostic certainty that the delusions or hallucinations are attributable to a med-\nical condition. Additional factors may incl ude concomitant treatments for the underlying\nmedical condition that confer a risk for psychosis independently, such as steroid treatment\nfor autoimmune disorders.\nPrevalence\nPrevalence rates for psychotic di sorder due to another medical condition are difficult to es-\ntimate given the wide variety of underlying medical etiologies. Life time prevalence has", "source": "dsm5.pdf"} {"id": "e102c9e00a81-0", "page_content": "Psychotic Disorder Due to Another Medical Condition 117\nbeen estimated to range from 0.21% to 0.54%. When the prevalence findings are stratified\nby age group, individuals older than 65 years have a significantly greater prevalence of\n0.74% compared with those in younger age grou ps. Rates of psychosis also vary according\nto the underlying medical condition; cond itions most commonly associated with psy-\nchosis include untreated endocrine and metabo lic disorders, autoim mune disorders (e.g.,\nsystemic lupus erythematosus, N-methyl- D-aspartate (NMDA) receptor autoimmune en-\ncephalitis), or temporal lobe epilepsy. Psycho sis due to epilepsy has been further differ-\nentiated into ictal, postictal, and interictal psychosis. The most common of these is postictal\npsychosis, observed in 2%\u20137.8% of epilepsy patients. Among older individuals, there may\nbe a higher prevalence of the disorder in fe males, although additional gender-related fea-\ntures are not clear and vary considerably with the gender distributions of the underlying\nmedical conditions.\nDevelopment and Course\nPsychotic disorder due to another medical condition may be a single transient state or it\nmay be recurrent, cycling with exacerbations and remissions of the underlying medical\ncondition. Although treatment of the underlyi ng medical condition often results in a res-\nolution of the psychosis, this is not always the case, and psychotic symptoms may persist\nlong after the medical event (e.g ., psychotic disorder due to fo cal brain injury). In the con-\ntext of chronic conditions such as multiple sc lerosis or chronic interictal psychosis of epi-\nlepsy, the psychosis may assume a long-term course.\nThe expression of psychotic disorder due to another medical cond ition does not differ", "source": "dsm5.pdf"} {"id": "e102c9e00a81-1", "page_content": "The expression of psychotic disorder due to another medical cond ition does not differ\nsubstantially in phenomenology depending on age at occurrence. However, older age\ngroups have a higher prevalence of the disorder, which is most likely due to the increasing\nmedical burden associated with advanced ag e and the cumulative effects of deleterious\nexposures and age-related processes (e.g., athe rosclerosis). The nature of the underlying\nmedical conditions is likely to change across the lifespan, with younger age groups more\naffected by epilepsy, head trauma, autoimmune , and neoplastic diseas es of early to mid-\nlife, and older age groups more affected by stroke disease, anoxic events, and multiple sys-\ntem comorbidities. Underlying factors with in creasing age, such as preexisting cognitive\nimpairment as well as vision and hearing impairments, may incur a greater risk for psy-\nchosis, possibly by serving to lower th e threshold for experiencing psychosis. \nRisk and Prognostic Factors \nCourse modifiers. Identification and treatment of the underlying medical condition has\nthe greatest impact on course, although pr eexisting central nervou s system injury may\nconfer a worse course outcome (e.g., head trauma, cerebr ovascular disease).\nDiagnostic Markers\nThe diagnosis of psychotic disorder due to an other medical condition depends on the clin-\nical condition of each individual, and the diag nostic tests will vary according to that con-\ndition. A variety of medical conditions ma y cause psychotic symp toms. These include\nneurological condit ions (e.g., neoplasms, cerebrovascular disease, Huntington's disease,\nmultiple sclerosis, epilepsy, auditory or visual nerve injury or impairment, deafness,\nmigraine, central nervous system infections), endocrine co nditions (e.g., hyper- and hypo-", "source": "dsm5.pdf"} {"id": "e102c9e00a81-2", "page_content": "thyroidism, hyper- and hypopa rathyroidism, hyper- and hypo adrenocorticism), metabolic\nconditions (e.g., hypoxia, hypercarbia, hypoglycemia), fluid or electrolyte imbalances,\nhepatic or renal diseases, and autoimmune di sorders with central nervous system involve-\nment (e.g., systemic lupus er ythematosus). The associated physical examination findings,\nlaboratory findings, and patterns of prevalen ce or onset reflect th e etiological medical\ncondition.", "source": "dsm5.pdf"} {"id": "a16e31e91b39-0", "page_content": "118 Schizophrenia Spectrum and Other Psychotic Disorders\nSuicide Risk \nSuicide risk in the context of psychotic diso rder due to another me dical condition is not\nclearly delineated, although certain conditions such as epilepsy and multiple sclerosis are\nassociated with increased rates of suicide, which may be further increased in the presence\nof psychosis. \nFunctional Consequences of Psychotic Disorder \nDue to Another Medical Condition\nFunctional disability is typically severe in the context of psychotic di sorder due to another\nmedical condition but will vary considerably by the type of condition and likely improve\nwith successful resolution of the condition.\nDifferential Diagnosis\nDelirium. Hallucinations and delusions commonly occur in the context of a delirium;\nhowever, a separate diagnosis of psychotic disorder due to another medical condition is\nnot given if the disturbance occurs exclusively during the co urse of a delirium. Delusions\nin the context of a major or mild neurocogni tive disorder would be diagnosed as major or\nmild neurocognitive disorder, with behavioral disturbance. \nSubstance/medication-induced psychotic disorder. If there is evidence of recent or\nprolonged substance use (including medicati ons with psychoactive effects), withdrawal\nfrom a substance, or exposure to a toxin (e.g ., LSD [lysergic acid diethylamide] intoxica-\ntion, alcohol withdrawal), a substance/medica tion-induced psychotic disorder should be\nconsidered. Symptoms that occur during or shor tly after (i.e., within 4 weeks) of substance\nintoxication or withdrawal or after medication use may be es pecially indicative of a sub-\nstance-induced psychotic disorder, depending on the character, duration, or amount of\nthe substance used. If the clin ician has ascertained that the disturbance is due to both a", "source": "dsm5.pdf"} {"id": "a16e31e91b39-1", "page_content": "medical condition and substance use, both diag noses (i.e., psychotic disorder due to an-\nother medical condition and substance/medication-induced psychotic disorder) can be\ngiven.\nPsychotic disorder. Psychotic disorder due to another medical condition must be distin-\nguished from a psychotic disord er (e.g., schizophrenia, delusi onal disorder, schizoaffective\ndisorder) or a depressive or bipolar disorder , with psychotic featur es. In psychotic disor-\nders and in depressive or bipolar disorders, wi th psychotic features, no specific and direct\ncausative physiological mechanisms associated with a medical condition can be demon-\nstrated. Late age at onset and the absence of a personal or family history of schizophrenia\nor delusional disorder suggest the need for a thorough ass essment to rule out the diagno-\nsis of psychotic disorder due to another medical condition. Auditory hallucinations that\ninvolve voices speaking complex sentences ar e more characteristic of schizophrenia than\nof psychotic disorder due to a medical condition. Other types of hallucinations (e.g., vi-\nsual, olfactory) commonly signal a psychotic disorder due to another medical condition or\na substance/medication-induced psychotic disorder.\nComorbidity\nPsychotic disorder due to another medical co ndition in individuals older than 80 years is\nassociated with concurrent major neurocognitive disorder (dementia).", "source": "dsm5.pdf"} {"id": "deea2ca93dc1-0", "page_content": "Catatonia Associated With Another Mental Disorder (Catatonia Specifier) 119\nCatatonia\nCatatonia can occur in the context of several disorders, including neurodevelopmental,\npsychotic, bipolar, depressive disorders, and other medical cond itions (e.g., cerebral folate\ndeficiency, rare autoimmune and paraneoplastic disorders. The manual does not treat\ncatatonia as an independent class but recognizes a) catatonia associated with another men-\ntal disorder (i.e., a neurodevelopmental, psychotic disord er, a bipolar disorder, a depres-\nsive disorder, or other mental disorder), b) catatonic disorder due to another medical\ncondition, and c) unspecified catatonia.\nCatatonia is defined by the pres ence of three or more of 12 psychomotor features in the\ndiagnostic criteria for catatoni a associated with another mental disorder and catatonic dis-\norder due to another medical condition. The es sential feature of cata tonia is a marked psy-\nchomotor disturbance that may involve decr eased motor activity, decreased engagement\nduring interview or physical examination, or excessive and peculiar motor activity. The\nclinical presentation of ca tatonia can be puzzling, as th e psychomotor disturbance may\nrange from marked unresponsiveness to marked agitation. Motoric immobility may be se-\nvere (stupor) or moderate (catalepsy and waxy flexibility). Similarly, decreased engage-\nment may be severe (mutism) or moderate (negativism). Excessive and peculiar motor\nbehaviors can be complex (e.g., stereotypy) or simple (agitation) and may include echola-\nlia and echopraxia. In extreme cases, the same individual may wax and wane between de-", "source": "dsm5.pdf"} {"id": "deea2ca93dc1-1", "page_content": "creased and excessive motor activity. The se emingly opposing clinical features and\nvariable manifestations of the diagnosis cont ribute to a lack of awareness and decreased\nrecognition of catatonia. During severe stages of catatonia, the individual may need care-\nful supervision to avoid self-h arm or harming others. There are potential risks from mal-\nnutrition, exhaustion, hyperpyr exia and self-inflicted injury. \nCatatonia Associated With Another\nMental Disorder (Catatonia Specifier)\n293.89 (F06.1)\nA. The clinical picture is dominated by three (or more) of the following symptoms:\u00a0\n1. Stupor (i.e., no psychomotor activity; not actively relating to environment).\n2. Catalepsy (i.e., passive induction of a posture held against gravity).\n3. Waxy flexibility (i.e., slight, even resistance to positioning by examiner).\n4. Mutism (i.e., no, or very little, verbal response [exclude if known aphasia]).\n5. Negativism (i.e., opposition or no response to instructions or external stimuli).\n6. Posturing (i.e., spontaneous and active maintenance of a posture against gravity).\n7. Mannerism (i.e., odd, circumstantial caricature of normal actions).\n8. Stereotypy (i.e., repetitive, abnormally frequent, non-goal-directed movements).\n9. Agitation, not influenced by external stimuli.\n10. Grimacing.\n11. Echolalia (i.e., mimicking another\u2019s speech).\n12. Echopraxia (i.e., mimicking another\u2019s movements).\nCoding note: Indicate the name of the associated mental disorder when recording the", "source": "dsm5.pdf"} {"id": "deea2ca93dc1-2", "page_content": "Coding note: Indicate the name of the associated mental disorder when recording the\nname of the condition (i.e., 293.89 [F06.1] catatonia associated with major depressive dis-\norder). Code first the associated mental disorder (e.g., neurodevelopmental disorder, brief", "source": "dsm5.pdf"} {"id": "a46ade8b3b53-0", "page_content": "120 Schizophrenia Spectrum and Other Psychotic Disorders\npsychotic disorder, schizophreniform disorder, schizophrenia, schizoaffective disorder,\nbipolar disorder, major depressive disorder, or other mental disorder) (e.g., 295.70 [F25.1]\nschizoaffective disorder, depressive type; 293.89 [F06.1] catatonia associated with\nschizoaffective disorder).\nDiagnostic Features\nCatatonia associated with another mental diso rder (catatonia specifier) may be used when\ncriteria are met for catatonia during the course of a neurodevelopmental, psychotic, bipo-\nlar, depressive, or other mental disorder. The catatonia specifier is appropriate when the\nclinical picture is characterized by marked ps ychomotor distur bance and involves at least\nthree of the 12 diagnostic features listed in Cr iterion A. Catatonia is typically diagnosed in\nan inpatient setting and occurs in up to 35% of individuals with schizophrenia, but the ma-\njority of catatonia cases invol ve individuals with depressive or bipolar disorders. Before\nthe catatonia specifier is used in neurodevel opmental, psychotic, bipolar, depressive, or\nother mental disorders, a wide variety of ot her medical conditions need to be ruled out;\nthese conditions include, but are not limited to, medical cond itions due to infectious, met-\nabolic, or neurological conditions (see \u201cCatatonic Disorder Due to Another Medical Con-\ndition\u201d). Catatonia can also be a side effect of a medication (see the chapter \u201cMedication-\nInduced Movement Disorders and Other Advers e Effects of Medication\u201d). Because of the\nseriousness of the complications, particular attention should be paid to the possibility that\nthe catatonia is attributable to 333.92 (G21.0) neuroleptic malignant syndrome.", "source": "dsm5.pdf"} {"id": "a46ade8b3b53-1", "page_content": "Catatonic Disorder Due to\nAnother Medical Condition\nDiagnostic Criteria 293.89 (F06.1)\nA. The clinical picture is dominated by three (or more) of the following symptoms:\u00a0\n1. Stupor (i.e., no psychomotor activity; not actively relating to environment).\n2. Catalepsy (i.e., passive induction of a posture held against gravity).\n3. Waxy flexibility (i.e., slight, even resistance to positioning by examiner).\n4. Mutism (i.e., no, or very little, verbal response [ Note: not applicable if there is an\nestablished aphasia]).\n5. Negativism (i.e., opposition or no response to instructions or external stimuli).\n6. Posturing (i.e., spontaneous and active maintenance of a posture against gravity).\n7. Mannerism (i.e., odd, circumstantial caricature of normal actions).\n8. Stereotypy (i.e., repetitive, abnormally frequent, non-goal-directed movements).\n9. Agitation, not influenced by external stimuli.\n10. Grimacing.\n11. Echolalia (i.e., mimicking another\u2019s speech).\n12. Echopraxia (i.e., mimicking another\u2019s movements).\nB. There is evidence from the history, physical examination, or laboratory findings that the\ndisturbance is the direct pathophysiological consequence of another medical condition.\nC. The disturbance is not better explained by another mental disorder (e.g., a manic episode). \nD. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.", "source": "dsm5.pdf"} {"id": "752e3a2b7209-0", "page_content": "Unspecified Catatonia 121\nCoding note: Include the name of the medical condition in the name of the mental disor-\nder (e.g., 293.89 [F06.1]) catatonic disorder due to hepatic encephalopathy). The other\nmedical condition should be coded and listed separately immediately before the cata-\ntonic disorder due to the medical condition (e.g., 572.2 [K71.90] hepatic encephalopathy;\n293.89 [F06.1] catatonic disorder due to hepatic encephalopathy).\nDiagnostic Features\nThe essential feature of catato nic disorder due to another me dical condition is the presence\nof catatonia that is judged to be attributed to the physiological effects of another medical\ncondition. Catatonia can be diagnosed by the pres ence of at least three of the 12 clinical fea-\ntures in Criterion A. There must be evidence from the history, physical examination, or\nlaboratory findings that the catatonia is attr ibutable to another medical condition (Crite-\nrion B). The diagnosis is not given if the ca tatonia is better explained by another mental\ndisorder (e.g., manic episode) (Criterion C) or if it occurs exclusivel y during the course of\na delirium (Criterion D).\nAssociated Features Supporting Diagnosis\nA variety of medical conditions may cause catatonia, especially neurological conditions\n(e.g., neoplasms, head trauma, cerebrovascular disease, encephalitis) and metabolic con-\nditions (e.g., hypercalcemia, hepatic encepha lopathy, homocystinuria , diabetic ketoacido-\nsis). The associated physical examination find ings, laboratory findings, and patterns of\nprevalence and onset reflect those of the etiological medical condition.", "source": "dsm5.pdf"} {"id": "752e3a2b7209-1", "page_content": "prevalence and onset reflect those of the etiological medical condition.\nDifferential Diagnosis\nA separate diagnosis of catatonic disorder due to another medical condition is not given if\nthe catatonia occurs exclusively during the course of a delirium or neuroleptic malignant\nsyndrome. If the individual is currently taking neurolep tic medication, consideration\nshould be given to medication -induced movement disorders (e.g., abnormal positioning\nmay be due to neuroleptic-induced acute dy stonia) or neuroleptic malignant syndrome\n(e.g., catatonic-like features may be present, along with associated vital sign and/or labo-\nratory abnormalities). Catatonic symptoms ma y be present in any of the following five\npsychotic disorders: brief psychotic disorder , schizophreniform disorder, schizophrenia,\nschizoaffective disorder, and substance/medication-induced psychotic disorder. It may\nalso be present in some of the neurodevelopme ntal disorders, in all of the bipolar and de-\npressive disorders, and in other mental disorders. \nUnspecified Catatonia\n \nThis category applies to presentations in which symptoms characteristic of catatonia\ncause clinically significant distress or impairm ent in social, occupational, or other impor-\ntant areas of functioning but either the nature of the underlying mental disorder or other\nmedical condition is unclear, full criteria for catatonia are not met, or there is insufficient\ninformation to make a more specific diagnosis (e.g., in emergency room settings). \nCoding note: Code first 781.99 (R29.818) other symptoms involving nervous and muscu-\nloskeletal systems, followed by 293.89 (F06.1) unspecified catatonia.", "source": "dsm5.pdf"} {"id": "8b95f5c383a0-0", "page_content": "122 Schizophrenia Spectrum and Other Psychotic Disorders\nOther Specified Schizophrenia Spectrum and\nOther Psychotic Disorder\n298.8 (F28)\nThis category applies to presentations in which symptoms characteristic of a schizophre-\nnia spectrum and other psychotic disorder that cause clinically significant distress or im-\npairment in social, occupational, or other important areas of functioning predominate but\ndo not meet the full criteria for any of the disorders in the schizophrenia spectrum and other\npsychotic disorders diagnostic class. The other specified schizophrenia spectrum and oth-\ner psychotic disorder category is used in situations in which the clinician chooses to com-\nmunicate the specific reason that the presentation does not meet the criteria for any\nspecific schizophrenia spectrum and other psychotic disorder. This is done by recording \u201coth-\ner specified schizophrenia spectrum and other psychotic disorder\u201d followed by the specific\nreason (e.g., \u201cpersistent auditory hallucinations\u201d). \nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Persistent auditory hallucinations occurring in the absence of any other features.\n2.Delusions with significant overlapping mood episodes: This includes persistent\ndelusions with periods of overlapping mood episodes that are present for a substantial\nportion of the delusional disturbance (such that the criterion stipulating only brief mood\ndisturbance in delusional disorder is not met).\n3.Attenuated psychosis syndrome: This syndrome is characterized by psychotic-like\nsymptoms that are below a threshold for full psychosis (e.g., the symptoms are less\nsevere and more transient, and insight is relatively maintained).\n4.Delusional symptoms in partner of individual with delusional disorder: In the\ncontext of a relationship, the delusional ma terial from the dominant partner provides\ncontent for delusional belief by the individual who may not otherwise entirely meet cri-", "source": "dsm5.pdf"} {"id": "8b95f5c383a0-1", "page_content": "content for delusional belief by the individual who may not otherwise entirely meet cri-\nteria for delusional disorder.\nUnspecified Schizophrenia Spectrum and\nOther Psychotic Disorder\n298.9 (F29)\nThis category applies to presentations in which symptoms characteristic of a schizophre-\nnia spectrum and other psychotic disorder that cause clinically significant distress or im-\npairment in social, occupational, or other important areas of functioning predominate but\ndo not meet the full criteria for any of the disorders in the schizophrenia spectrum and oth-\ner psychotic disorders diagnostic class. The unspecified schizophrenia spectrum and oth-\ner psychotic disorder category is used in situations in which the clinician chooses not to\nspecify the reason that the criteria are not met for a specific schizophrenia spectrum and\nother psychotic disorder, and includes presentatio ns in which there is insufficient informa-\ntion to make a more specific diagnosis (e.g., in emergency room settings).", "source": "dsm5.pdf"} {"id": "dc75db26cfa2-0", "page_content": "123Bipolar and\n Related Disorders\nBipolar and related disorders are separated from the depressive disorders in\nDSM-5 and placed between the chapters on schizophrenia spectrum and other psychotic\ndisorders and depressive disord ers in recognition of their place as a bridge between the\ntwo diagnostic classes in terms of symptomato logy, family history, and genetics. The di-\nagnoses included in this chapter are bipola r I disorder, bipolar II disorder, cyclothymic\ndisorder, substance/medication-induced bipo lar and related disorder, bipolar and relat-\ned disorder due to another medical condition, other specified bipolar and related disor-\nder, and unspecified bipolar and related disorder.\nThe bipolar I disorder criter ia represent the modern understanding of the classic\nmanic-depressive disorder or affective psycho sis described in the ni neteenth century, dif-\nfering from that classic description only to th e extent that neither psychosis nor the lifetime\nexperience of a major depressive episode is a requirement. However, the vast majority of\nindividuals whose symptoms meet the criter ia for a fully syndromal manic episode also\nexperience major depressive episodes during the course of their lives.\nBipolar II disorder, requiring the lifetime experience of at least one episode of major de-\npression and at least one hypomanic episode, is no longer thought to be a \u201cmilder\u201d condition\nthan bipolar I disorder, largely because of th e amount of time individuals with this con-\ndition spend in depression and because the in stability of mood experienced by individuals\nwith bipolar II disorder is typically accompanied by serious impairment in work and social\nfunctioning.\nThe diagnosis of cyclothymic disorder is give n to adults who experience at least 2 years\n(for children, a full year) of both hypomanic and depressive periods without ever fulfilling", "source": "dsm5.pdf"} {"id": "dc75db26cfa2-1", "page_content": "(for children, a full year) of both hypomanic and depressive periods without ever fulfilling\nthe criteria for an episode of mani a, hypomania, or major depression.\nA large number of substances of abuse, some prescribed medi cations, and several\nmedical conditions can be associated with manic-like phenomena. This fact is recognized\nin the diagnoses of substance/medication-induced bipolar and related disorder and bipo-\nlar and related disorder due to another medical condition.\nThe recognition that many individuals, partic ularly children and, to a lesser extent, ad-\nolescents, experience bipolar-like phenomena that do not meet the criteria for bipolar I, bi-\npolar II, or cyclothymic disorder is reflected in the availability of the other specified\nbipolar and related disorder category. Indeed, specific criteria for a disorder involving\nshort-duration hypomania are provided in Section III in the hope of encouraging further\nstudy of this disorder.\nBipolar I Disorder\nDiagnostic Criteria\nFor a diagnosis of bipolar I disorder, it is nece ssary to meet the following criteria for a manic\nepisode. The manic episode may have been preceded by and may be followed by hypo-\nmanic or major depressive episodes.", "source": "dsm5.pdf"} {"id": "3fa67d7f1b86-0", "page_content": "124 Bipolar and Related Disorders\nManic Episode\nA. A distinct period of abnormally and persistently elevated, expansive, or irritable mood\nand abnormally and persistently increased goal-d irected activity or energy, lasting at\nleast 1 week and present most of the day, nearly every day (or any duration if hospi-\ntalization is necessary).\nB. During the period of mood disturbance and increased energy or activity, three (or\nmore) of the following symptoms (four if the mood is only irritable) are present to a sig-\nnificant degree and represent a notic eable change from usual behavior: \n1. Inflated self-esteem or grandiosity.\n2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).\n3. More talkative than usual or pressure to keep talking.\n4. Flight of ideas or subjective experience that thoughts are racing.\n5. Distractibility (i.e., attention too easily dr awn to unimportant or irrelevant external\nstimuli), as reported or observed.\n6. Increase in goal-directed activity (either socially, at work or school, or sexually) or\npsychomotor agitation (i.e., purposeless non-goal-directed activity).\n7. Excessive involvement in activities that have a high potential for painful conse-\nquences (e.g., engaging in unrestrained buyin g sprees, sexual indiscretions, or\nfoolish business investments).\nC. The mood disturbance is sufficiently severe to cause marked impairment in social or\noccupational functioning or to necessitate hospitalization to prevent harm to self or oth-\ners, or there are psychotic features.\nD. The episode is not attributable to the physiological effects of a substance (e.g., a drug\nof abuse, a medication, other treatm ent) or to another medical condition.", "source": "dsm5.pdf"} {"id": "3fa67d7f1b86-1", "page_content": "of abuse, a medication, other treatm ent) or to another medical condition.\nNote: A full manic episode that emerges during antidepressant treatment (e.g., medi-\ncation, electroconvulsive therapy) but persists at a fully syndromal level beyond the\nphysiological effect of that treatment is sufficient evidence for a manic episode and,\ntherefore, a bipolar I diagnosis.\nNote: Criteria A\u2013D constitute a manic episode. At least one lifetime manic episode is re-\nquired for the diagnosis of bipolar I disorder.\nHypomanic Episode\nA. A distinct period of abnormally and persistently elevated, expansive, or irritable mood\nand abnormally and persistently increased activity or energy, lasting at least 4 consec-\nutive days and present most of the day, nearly every day.\nB. During the period of mood disturbance and increased energy and activity, three (or\nmore) of the following symptoms (four if the mood is only irritable) have persisted, rep-\nresent a noticeable change from usual behavior, and have been present to a significant\ndegree:\n1. Inflated self-esteem or grandiosity.\n2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).\n3. More talkative than usual or pressure to keep talking.\n4. Flight of ideas or subjective experience that thoughts are racing.\n5. Distractibility (i.e., attention too easily dr awn to unimportant or irrelevant external\nstimuli), as reported or observed.\n6. Increase in goal-directed activity (either socially, at work or school, or sexually) or\npsychomotor agitation.\n7. Excessive involvement in activities that have a high potential for painful conse-\nquences (e.g., engaging in unrestrained buyin g sprees, sexual indiscretions, or\nfoolish business investments).", "source": "dsm5.pdf"} {"id": "9a590d2c41df-0", "page_content": "Bipolar I Disorder 125\nC. The episode is associated with an unequivocal change in functioning that is uncharac-\nteristic of the individual when not symptomatic.\nD. The disturbance in mood and the change in functioning are observable by others.\nE. The episode is not severe enough to cause marked impairment in social or occupa-\ntional functioning or to necessitate hospitalization. If there are psychotic features, the\nepisode is, by definition, manic.\nF. The episode is not attributable to the physiological effects of a substance (e.g., a drug\nof abuse, a medication, other treatment).\nNote: A full hypomanic episode that emerges during antidepressant treatment (e.g.,\nmedication, electroconvulsive therapy) but persists at a fully syndromal level beyond\nthe physiological effect of that treatment is sufficient evidence for a hypomanic episode\ndiagnosis. However, caution is indicated so that one or two symptoms (particularly in-\ncreased irritability, edginess, or agitation following antidepressant use) are not taken\nas sufficient for diagnosis of a hypomanic episode, nor necessarily indicative of a bi-\npolar diathesis.\nNote: Criteria A\u2013F constitute a hypomanic episode. Hypomanic episodes are common in\nbipolar I disorder but are not required for the diagnosis of bipolar I disorder.\nMajor Depressive Episode\nA. Five (or more) of the following symptoms have been present during the same 2-week\nperiod and represent a change from previous functioning; at least one of the symptoms\nis either (1) depressed mood or (2) loss of interest or pleasure.\nNote: Do not include symptoms that are clearly attributable to another medical condi-\ntion.\n1. Depressed mood most of the day, nearly every day, as indicated by either subjec-", "source": "dsm5.pdf"} {"id": "9a590d2c41df-1", "page_content": "tive report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g.,\nappears tearful). ( Note: In children and adolescents, can be irritable mood.)\n2. Markedly diminished interest or pleasure in al l, or almost all, activities most of the\nday, nearly every day (as indicated by either subjective account or observation).\n3. Significant weight loss when not dieting or weight gain (e.g., a change of more than\n5% of body weight in a month), or dec rease or increase in appetite nearly every\nday. ( Note: In children, consider failure to make expected weight gain.)\n4. Insomnia or hypersomnia nearly every day.\n5. Psychomotor agitation or retardation nearly every day (observable by others; not\nmerely subjective feelings of restlessness or being slowed down).\n6. Fatigue or loss of energy nearly every day.\n7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delu-\nsional) nearly every day (not merely self-reproach or guilt about being sick).\n8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (ei-\nther by subjective account or as observed by others).\n9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation with-\nout a specific plan, or a suicide attempt or a specific plan for committing suicide.\nB. The symptoms cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nC. The episode is not attributable to the physiological effects of a substance or another\nmedical condition. \nNote: Criteria A\u2013C constitute a major depressive episode. Major depressive episodes are\ncommon in bipolar I disorder but are not requi red for the diagnosis of bipolar I disorder.", "source": "dsm5.pdf"} {"id": "9a590d2c41df-2", "page_content": "common in bipolar I disorder but are not requi red for the diagnosis of bipolar I disorder.\nNote: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a\nnatural disaster, a serious medical illness or disability) may include the feelings of intense", "source": "dsm5.pdf"} {"id": "ba92b8bba53d-0", "page_content": "126 Bipolar and Related Disorders\nsadness, rumination about the loss, insomnia, poor appetite, and weight loss noted in Cri-\nterion A, which may resemble a depressive episode. Although such symptoms may be un-\nderstandable or considered appropriate to the loss, the presence of a major depressive\nepisode in addition to the normal response to a significant loss should also be carefully\nconsidered. This decision inevitably requires the exercise of clinical judgment based on\nthe individual\u2019s history and the cultural norms for the expression of distress in the context\nof loss.1\nBipolar I Disorder\nA. Criteria have been met for at least one manic episode (Criteria A\u2013D under \u201cManic Ep-\nisode\u201d above).\nB. The occurrence of the manic and major depressive episode(s) is not better explained\nby schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional dis-\norder, or other specified or unspecified schizophrenia spectrum and other psychotic\ndisorder.\nCoding and Recording Procedures\nThe diagnostic code for bipolar I disorder is based on type of current or most recent epi-\nsode and its status with respect to current severity, presence of psychotic features, and\nremission status. Current severity and psychotic features are only indicated if full criteria\nare currently met for a manic or major depressive episode. Remission specifiers are only\nindicated if the full criteria are not current ly met for a manic, hypomanic, or major depres-\nsive episode. Codes are as follows:\n1In distinguishing grief from a major depressive episode (MDE), it is useful to consider that in\ngrief the predominant affect is feelings of emptiness and loss, while in MDE it is persistent\ndepressed mood and the inability to anticipate happiness or pleasure. The dysphoria in grief is", "source": "dsm5.pdf"} {"id": "ba92b8bba53d-1", "page_content": "depressed mood and the inability to anticipate happiness or pleasure. The dysphoria in grief is\nlikely to decrease in intensity over days to weeks and occurs in waves, the so-called pangs of\ngrief. These waves tend to be associated with thoughts or reminder s of the deceased. The\ndepressed mood of a MDE is more persistent and not tied to specific thoughts or preoccupations.\nThe pain of grief may be accompanied by positi ve emotions and humor th at are uncharacteristic\nof the pervasive unhappiness and misery charac teristic of a major depressive episode. The\nthought content associated with grief generally features a preoccupation with thoughts and\nmemories of the deceased, rather than the self-c ritical or pessimistic ruminations seen in a MDE.\nIn grief, self-esteem is generally preserved, whereas in a MDE, feelings of worthlessness and self-\nloathing are common. If self-derog atory ideation is present in grief, it typically involves per-\nceived failings vis-\u00e0-vis the deceased (e.g., no t visiting frequently enough, not telling the\ndeceased how much he or she was loved). If a be reaved individual thinks about death and dying,\nsuch thoughts are generally focu sed on the deceased and possibl y about \u201cjoining\u201d the deceased,\nwhereas in a major depressive episode such th oughts are focused on ending one\u2019s own life\nbecause of feeling worthless, undeserving of life, or unable to cope with the pain of depression.Bipolar I disorderCurrent or \nmost recent \nepisode \nmanicCurrent or \nmost recent \nepisode \nhypomanic* Current or \nmost recent \nepisode \ndepressedCurrent or \nmost recent \nepisode \nunspecified**\nMild (p. 154) 296.41", "source": "dsm5.pdf"} {"id": "ba92b8bba53d-2", "page_content": "unspecified**\nMild (p. 154) 296.41 \n(F31.11)NA 296.51 \n(F31.31)NA\nModerate (p. 154) 296.42 \n(F31.12)NA 296.52 \n(F31.32)NA\nSevere (p. 154) 296.43 \n(F31.13)NA 296.53 \n(F31.4)NA", "source": "dsm5.pdf"} {"id": "9d5b7f951624-0", "page_content": "Bipolar I Disorder 127\nIn recording the name of a diagnosis, terms should be listed in the following order: bipolar\nI disorder, type of current or most recent episode, severity/psychotic/remission specifiers,\nfollowed by as many specifiers without codes as apply to the current or most recent epi-\nsode.\nSpecify:\nWith anxious distress (p. 149)\nWith mixed features (pp. 149\u2013150)\nWith rapid cycling (pp. 150\u2013151)\nWith melancholic features (p. 151)\nWith atypical features (pp. 151\u2013152)\nWith mood-congruent psychotic features (p. 152)\nWith mood-incongruent psychotic features (p. 152)\nWith catatonia (p. 152). Coding note: Use additional code 293.89 (F06.1).\nWith peripartum onset (pp. 152\u2013153)\nWith seasonal pattern (pp. 153\u2013154)\nDiagnostic Features\nThe essential feature of a manic episode is a distinct period during which there is an ab-\nnormally, persistently elevated, expansive, or irritable mood and persistently increased\nactivity or energy that is present for most of the day, nearly every day, for a period of at\nleast 1 week (or any duration if hospitalizatio n is necessary), accompanied by at least three\nadditional symptoms from Criterion B. If the mo od is irritable rather than elevated or ex-\npansive, at least fo ur Criterion B symptoms must be present.\nMood in a manic episode is often described as euphoric, excessively cheerful, high, or\n\u201cfeeling on top of the world.\u201d In some cases, the mood is of such a highly infectious quality", "source": "dsm5.pdf"} {"id": "9d5b7f951624-1", "page_content": "that it is easily recognized as excessive and may be characterized by unlimited and hap-\nhazard enthusiasm for interpersonal, sexual, or occupational inte ractions. For example,\nthe individual may spontaneously start extens ive conversations with strangers in public.\nOften the predominant mood is irritable rather than elevated, particularly when the indi-\nvidual\u2019s wishes are denied or if the individu al has been using substances. Rapid shifts in\nmood over brief periods of time may occur and are referred to as lability (i.e., the alterna-With psychotic \nfeatures*** \n(p. 152)296.44 \n(F31.2)NA 296.54 \n(F31.5)NA\nIn partial \nremission (p. 154)296.45 \n(F31.73)296.45 \n(F31.71)296.55 \n(F31.75)NA\nIn full remission \n(p. 154)296.46 \n(F31.74)296.46 \n(F31.72)296.56 \n(F31.76)NA\nUnspecified 296.40 \n(F31.9)296.40 \n(F31.9)296.50 \n(F31.9)NA\n*Severity and psychotic specifiers do not apply; code 296.40 (F31.0) for cases not in remission.\n**Severity, psychotic, and remission specif iers do not apply. Code 296.7 (F31.9).\n***If psychotic features are present, code the \u201cwith psychotic features\u201d specifier irrespective of epi-\nsode severity.Bipolar I disorderCurrent or \nmost recent \nepisode \nmanicCurrent or \nmost recent \nepisode \nhypomanic* Current or \nmost recent \nepisode", "source": "dsm5.pdf"} {"id": "9d5b7f951624-2", "page_content": "episode \nhypomanic* Current or \nmost recent \nepisode \ndepressedCurrent or \nmost recent \nepisode \nunspecified**", "source": "dsm5.pdf"} {"id": "37557336bcea-0", "page_content": "128 Bipolar and Related Disorders\ntion among euphoria, dysphoria, and irritability). In children, happiness, silliness and\n\u201cgoofiness\u201d are normal in the context of spec ial occasions; however, if these symptoms are\nrecurrent, inappropriate to the context, and beyond what is expected for the developmen-\ntal level of the child, they may meet Criterion A. If the happiness is unusual for a child (i.e.,\ndistinct from baseline), and the mood change occurs at the same ti me as symptoms that\nmeet Criterion B for mania, diagnostic certainty is increased; however, the mood change\nmust be accompanied by persistently increased activity or energy levels that are obvious\nto those who know the child well.\nDuring the manic episode, the individual may engage in multiple overlapping new\nprojects. The projects are often initiated with little knowledge of the topic, and nothing seems\nout of the individual\u2019s reach. The increased activity levels may manife st at unusual hours of\nthe day.\nInflated self-esteem is typicall y present, ranging from uncritical self-confidence to marked\ngrandiosity, and may reach delusi onal proportions (Criterion B1). Despite lack of any partic-\nular experience or talent, the individual may embark on comple x tasks such as writing a novel\nor seeking publicity for some im practical invention. Grandiose delusions (e.g., of having a\nspecial relationship to a famous person) are co mmon. In children, overe stimation of abilities\nand belief that, for example, they are the best at a sport or the smartest in the class is normal;\nhowever, when such beliefs are present despite cl ear evidence to the contrary or the child at-\ntempts feats that are clearly dangerous and, most important, represent a change from the\nchild\u2019s normal behavior, the grandiosity criterion should be considered satisfied.", "source": "dsm5.pdf"} {"id": "37557336bcea-1", "page_content": "child\u2019s normal behavior, the grandiosity criterion should be considered satisfied. \nOne of the most common features is a decreased need for sleep (Criterion B2) and is\ndistinct from insomnia in which the individual wants to sleep or feels the need to sleep but\nis unable. The individual may sleep little, if at all, or may awaken several hours earlier than\nusual, feeling rested and full of energy. When the sleep disturbance is severe, the individ-\nual may go for days without sleep, yet not feel tired. Often a decreased need for sleep her-\nalds the onset of a manic episode.\nSpeech can be rapid, pressured, loud, and diff icult to interrupt (Criterion B3). Individ-\nuals may talk continuously and without regard for others\u2019 wi shes to communicate, often\nin an intrusive manner or without concern for the relevance of what is said. Speech is\nsometimes characterized by jokes, puns, amus ing irrelevancies, and theatricality, with\ndramatic mannerisms, singing, and excessive gesturing. Loudness and forcefulness of\nspeech often become more important than what is conveyed. If the individual\u2019s mood is\nmore irritable than expansive, speech may be marked by complaints, hostile comments, or\nangry tirades, particularly if attempts are ma de to interrupt the individual. Both Criterion\nA and Criterion B symptoms may be accompanie d by symptoms of the opposite (i.e., de-\npressive) pole (see \u201cwith mixed features\u201d specifier, pp. 149\u2013150).\nOften the individual\u2019s thoughts race at a rate faster than they can be expressed through\nspeech (Criterion B4). Frequently there is flight of\u00a0ideas evidenced by a nearly continuous flow\nof accelerated speech, with abrupt shifts from one topic to another. When flight of ideas is se-", "source": "dsm5.pdf"} {"id": "37557336bcea-2", "page_content": "vere, speech may become disorganized, incoherent , and particularly distressful to the individ-\nual. Sometimes thoughts are experienced as so crowded that it is very difficult to speak.\nDistractibility (Criterion B5) is evidenced by an inability to censor immaterial external\nstimuli (e.g., the interviewer\u2019s attire, backgr ound noises or conversations, furnishings in\nthe room) and often prevents individuals expe riencing mania from holding a rational con-\nversation or attending to instructions.", "source": "dsm5.pdf"} {"id": "fe7a4faa57cb-0", "page_content": "the room) and often prevents individuals expe riencing mania from holding a rational con-\nversation or attending to instructions.\nThe increase in goal -directed ac tivity often consists of excessive planning and partici-\npation in multiple activities, including sexual, occupational, political, or religious activi-\nties. Increased sexual drive, fantasies, and be havior are often present. Individuals in a manic\nepisode usually show increased sociability (e.g ., renewing old acquaintances or calling or\ncontacting friends or even strangers), without regard to the intrusive, domineering, and\ndemanding nature of these interactions. They often display psychomotor agitation or rest-\nlessness (i.e., purposeless acti vity) by pacing or by holding multiple conversations simulta-", "source": "dsm5.pdf"} {"id": "cec81fcbf351-0", "page_content": "Bipolar I Disorder 129\nneously. Some individuals write excessive letters , e-mails, text messages, and so forth, on\nmany different topics to friends, public figures, or the media. \nThe increased activity criterion can be diffic ult to ascertain in children; however, when\nthe child takes on many tasks simultaneously, starts devising elaborate and unrealistic\nplans for projects, develops previously abse nt and developmentally inappropriate sexual\npreoccupations (not accounted for by sexual abuse or exposure to sexually explicit mate-\nrial), then Criterion B might be met based on clinical judgment. It is essential to determine\nwhether the behavior represents a change from the child\u2019s baseline behavior; occurs most\nof the day, nearly every day for the requisite time period; and occurs in temporal associa-\ntion with other symptoms of mania. \nThe expansive mood, excessive optimism, gr andiosity, and poor judgment often lead\nto reckless involvement in activities such as spending sprees, giving away possessions,\nreckless driving, foolish business investments, and sexual promiscuity that is unusual for\nthe individual, even though these activities ar e likely to have catastrophic consequences\n(Criterion B7). The individual may purchase many unneeded items without the money to\npay for them and, in some cases, give them away. Sexual behavior may include infidelity\nor indiscriminate sexual encounters with strangers, often disregarding the risk of sexually\ntransmitted diseases or in terpersonal consequences.\nThe manic episode must result in marked impairment in social or occupational func-\ntioning or require hospitalizatio n to prevent harm to self or others (e.g., financial losses, il-\nlegal activities, loss of employment, self-injur ious behavior). By definition, the presence of\npsychotic features during a manic episode also satisfies Criterion C.", "source": "dsm5.pdf"} {"id": "cec81fcbf351-1", "page_content": "psychotic features during a manic episode also satisfies Criterion C.\nManic symptoms or syndromes that are attrib utable to the physiological effects of a\ndrug of abuse (e.g., in the context of cocaine or amphetamine intoxication), the side effects\nof medications or treatments (e.g., steroids, L-dopa, antidepressants, stimulants), or an-\nother medical condition do not count toward the diagnosis of bipolar I disorder. However,\na fully syndromal manic episode that arises duri ng treatment (e.g., with medications, elec-\ntroconvulsive therapy, light ther apy) or drug use and persists beyond the physiological ef-\nfect of the inducing agent (i.e., after a medica tion is fully out of the individual\u2019s system or\nthe effects of electroconvulsive therapy would be expected to have dissipated completely)\nis sufficient evidence for a manic episode di agnosis (Criterion D). Caution is indicated so\nthat one or two symptoms (particularly increa sed irritability, edginess, or agitation follow-\ning antidepressant use) are not taken as suffi cient for diagnosis of a manic or hypomanic\nepisode, nor necessarily an indication of a bi polar disorder diathesis. It is necessary to\nmeet criteria for a manic episode to make a diag nosis of bipolar I disorder, but it is not re-\nquired to have hypomanic or major depressi ve episodes. However, they may precede or\nfollow a manic episode. Full descriptions of the diagnostic features of a hypomanic epi-\nsode may be found within the text for bipola r II disorder, and the features of a major de-\npressive episode are described within th e text for major depressive disorder.\nAssociated Features Supporting Diagnosis\nDuring a manic episode, individuals often do not perceive that they are ill or in need of treat-", "source": "dsm5.pdf"} {"id": "cec81fcbf351-2", "page_content": "ment and vehemently resist efforts to be treated. Individuals may change their dress, makeup,\nor personal appearance to a more sexually su ggestive or flamboyant style. Some perceive a\nsharper sense of smell, hearing, or vision. Gambling and antisocial behaviors may accompany\nthe manic episode. Some individuals may become hostile and physically threatening to others", "source": "dsm5.pdf"} {"id": "37ea22905df2-0", "page_content": "sharper sense of smell, hearing, or vision. Gambling and antisocial behaviors may accompany\nthe manic episode. Some individuals may become hostile and physically threatening to others\nand, when delusional, may become physically assaultive or suicidal. Catastrophic conse-\nquences of a manic episode (e.g., involuntary hospitalization, difficulties with the law, serious\nfinancial difficulties) often result from poor judgment, loss of insight, and hyperactivity. \nMood may shift very rapidly to anger or depression. Depressive symptoms may occur\nduring a manic episode and, if present, may last moments, hour s, or, more rarely, days (see\n\u201cwith mixed features\u201d specifier, pp. 149\u2013150).", "source": "dsm5.pdf"} {"id": "63fb37784426-0", "page_content": "130 Bipolar and Related Disorders\nPrevalence\nThe 12-month prevalence estimate in the contin ental United States was 0.6% for bipolar I\ndisorder as defined in DSM-IV. Twelve-month prevalence of bipolar I disorder across 11\ncountries ranged from 0.0% to 0.6%. The life time male-to-female prevalence ratio is ap-\nproximately 1.1:1. \nDevelopment and Course\nMean age at onset of the first manic, hypomanic, or major depressive episode is approxi-\nmately 18 years for bipola r I disorder. Special considerations are necessary to detect the di-\nagnosis in children. Since children of the same chronological age may be at different\ndevelopmental stages, it is difficult to defi ne with precision what is \u201cnormal\u201d or \u201cex-\npected\u201d at any given point. Therefore, each ch ild should be judged according to his or her\nown baseline. Onset occurs throughout the life cycle, including firs t onsets in the 60s or\n70s. Onset of manic symptoms (e.g., sexual or so cial disinhibition) in late mid-life or late-\nlife should prompt consideratio n of medical conditions (e.g., frontotemporal neurocogni-\ntive disorder) and of substance ingestion or withdrawal. \nMore than 90% of individuals who have a sin gle manic episode go on to have recurrent\nmood episodes. Approximately 60% of manic episodes occur immediately before a major\ndepressive episode. Individuals with bipolar I disorder who have multiple (four or more)\nmood episodes (major depressi ve, manic, or hypomanic) within 1 year receive the speci-\nfier \u201cwith rapid cycling.\u201d \nRisk and Prognostic Factors", "source": "dsm5.pdf"} {"id": "63fb37784426-1", "page_content": "fier \u201cwith rapid cycling.\u201d \nRisk and Prognostic Factors\nEnvironmental. Bipolar disorder is mo re common in high-income than in low-income\ncountries (1.4 vs. 0.7%). Separated, divorced, or widowed individuals have higher rates of\nbipolar I disorder than do individuals who ar e married or have neve r been married, but\nthe direction of the association is unclear. \nGenetic and physiological. A family history of bipolar diso rder is one of the strongest and\nmost consistent risk factors for bipolar disord ers. There is an average 10-fold increased risk\namong adult relatives of individuals with bipo lar I and bipolar II disorders. Magnitude of\nrisk increases with degree of kinship. Schizophrenia and bipolar disorder likely share a ge-\nnetic origin, reflected in familial co-aggregat ion of schizophrenia and bipolar disorder. \nCourse modifiers. After an individual has a manic episode with psychotic features, subse-\nquent manic episodes are more likely to in clude psychotic featur es. Incomplete inter-\nepisode recovery is more common when th e current episode is accompanied by mood-\nincongruent psychotic features.\nCulture-Related Diagnostic Issues\nLittle information exists on specific cultural differences in the expression of bipolar I dis-\norder. One possible explanation for this ma y be that diagnostic instruments are often\ntranslated and applied in diff erent cultures with no transcultural validation. In one U.S.\nstudy, 12-month prevalence of bipolar I diso rder was significantly lower for Afro-Carib-\nbeans than for African Americans or whites. \nGender-Related Diagnostic Issues\nFemales are more likely to experience rapid cycling and mixed states, and to have patterns of\ncomorbidity that differ from th ose of males, including higher rates of lifetime eating disor-", "source": "dsm5.pdf"} {"id": "63fb37784426-2", "page_content": "ders. Females with bipolar I or II disorder are more likely to experience depressive symptoms\nthan males. They also have a higher lifetime risk of alcohol use disorder than are males and a\nmuch greater likelihood of alcohol use disorder than do females in the general population.", "source": "dsm5.pdf"} {"id": "e41a90a3e437-0", "page_content": "Bipolar I Disorder 131\nSuicide Risk\nThe lifetime risk of suicide in individuals with bipolar disorder is estimated to be at least\n15 times that of the general population. In fa ct, bipolar disorder may account for one-quar-\nter of all completed su icides. A past history of suicide attempt and percent days spent de-\npressed in the past year are associated with gr eater risk of suicide attempts or completions.\nFunctional Consequences of Bipolar I Disorder\nAlthough many individuals with bipolar disord er return to a fully functional level be-\ntween episodes, approximately 30% show severe impairment in work role function. Func-\ntional recovery lags substantially behind reco very from symptoms, especially with respect\nto occupational recovery, resulting in lower socioeconomic status despite equivalent lev-\nels of education when compared with the ge neral population. Individuals with bipolar I\ndisorder perform more poorly than healthy in dividuals on cognitive tests. Cognitive im-\npairments may contribute to vocational and interpersonal difficulties and persist through\nthe lifespan, even during euthymic periods.\nDifferential Diagnosis\nMajor depressive disorder. Major depressive disorder may also be accompanied by hy-\npomanic or manic symptoms (i.e., fewer symptoms or for a shorter duration than required\nfor mania or hypomania). When the individual presents in an episode of major depression,\none must depend on corroborating history re garding past episodes of mania or hypoma-\nnia. Symptoms of irritability may be associated with either major depressive disorder or\nbipolar disorder, adding to diagnostic complexity.\nOther bipolar disorders. Diagnosis of bipolar I disorder is differentiated from bipolar II\ndisorder by determining whether there have be en any past episodes of mania. Other spec-\nified and unspecified bipolar and related disord ers should be differentiated from bipolar I", "source": "dsm5.pdf"} {"id": "e41a90a3e437-1", "page_content": "ified and unspecified bipolar and related disord ers should be differentiated from bipolar I\nand II disorders by considering whether eith er the episodes invol ving manic or hypo-\nmanic symptoms or the episodes of depressive symptoms fail to meet the full criteria for\nthose conditions.\nBipolar disorder due to another medical co ndition may be distinguished from bipolar\nI and II disorders by identifying, based on best clinical evidence, a causally related medical\ncondition.\nGeneralized anxiety disorder, panic disorder , posttraumatic stress disorder, or other\nanxiety disorders. These disorders need to be consider ed in the differential diagnosis as\neither the primary disorder or, in some case s, a comorbid disorder. A careful history of\nsymptoms is needed to differentiate generalized anxiety disorder from bipolar disorder,\nas anxious ruminations may be mistaken for ra cing thoughts, and efforts to minimize anx-\nious feelings may be taken as impulsive beha vior. Similarly, sympto ms of posttraumatic\nstress disorder need to be differentiated from bipolar disorder. It is helpful to assess the ep-\nisodic nature of the symptoms described, as well as to consider symptom triggers, in mak-\ning this differential diagnosis.\nSubstance/medication-induced bipolar disorder. Substance use disorders may mani-\nfest with substance.medicati on-induced manic symptoms th at must be distinguished\nfrom bipolar I disorder; response to mood stabilizers during a substance/medication-\ninduced mania may not necessarily be diagnost ic for bipolar disorder. There may be sub-\nstantial overlap in view of the tendency for individuals with bipolar I disorder to overuse\nsubstances during an episode. A primary diagnosis of bipolar disorder must be estab-\nlished based on symptoms that remain once substances are no longer being used.\nAttention-deficit/hyperactivity disorder. This disorder may be misdiagnosed as bipolar", "source": "dsm5.pdf"} {"id": "e41a90a3e437-2", "page_content": "Attention-deficit/hyperactivity disorder. This disorder may be misdiagnosed as bipolar\ndisorder, especially in adolescents and children. Many symptoms overlap with the symp-", "source": "dsm5.pdf"} {"id": "0319127e3d91-0", "page_content": "132 Bipolar and Related Disorders\ntoms of mania, such as rapid speech, racing thoughts, distra ctibility, and less need for\nsleep. The \u201cdouble counting\u201d of symptoms toward both ADHD and bipolar disorder can\nbe avoided if the clinician clarifies whether the symptom(s) represents a distinct episode. \nPersonality disorders. Personality disorders such as borderline personality disorder\nmay have substantial symptomatic overlap wi th bipolar disorders, since mood lability\nand impulsivity are common in both conditions . Symptoms must represent a distinct ep-\nisode, and the noticeable increase over baseline required for the diagnosis of bipolar dis-\norder must be present. A diagnosis of a personality disorder should not be made during an\nuntreated mood episode.\nDisorders with prominent irritability. In individuals with severe irritability, particularly\nchildren and adolescents, care must be take n to apply the diagnosis of bipolar disorder\nonly to those who have had a clear episode of mania or hypomania\u2014tha t is, a distinct time\nperiod, of the required duration, during which the irritability was clearly different from\nthe individual\u2019s baseline and was accompan ied by the onset of Criterion B symptoms.\nWhen a child\u2019s irritability is persistent and pa rticularly severe, the diagnosis of disruptive\nmood dysregulation disorder wo uld be more appropriate. Indeed, when any child is being\nassessed for mania, it is essential that th e symptoms represent a clear change from the\nchild\u2019s typical behavior.\nComorbidity\nCo-occurring mental disorders are common, wi th the most frequent disorders being any\nanxiety disorder (e.g., pa nic attacks, social anxiety disorder [social phobia], specific pho-\nbia), occurring in approximatel y three-fourths of individuals; ADHD, any disruptive, im-\npulse-control, or conduct disorder (e.g., intermittent explosive disorder, oppositional", "source": "dsm5.pdf"} {"id": "0319127e3d91-1", "page_content": "pulse-control, or conduct disorder (e.g., intermittent explosive disorder, oppositional\ndefiant disorder, conduct disorder), and any su bstance use disorder (e.g., alcohol use dis-\norder) occur in over half of individuals with bipolar I disorder. Adults with bipolar I dis-\norder have high rates of serious and/or untreated co-occurring medical conditions.\nMetabolic syndrome and migraine are more common among individuals with bipolar dis-\norder than in the general population. More than half of individuals whose symptoms meet\ncriteria for bipolar disorder have an alcoho l use disorder, and those with both disorders\nare at greater risk for suicide attempt.\nBipolar II Disorder\nDiagnostic Criteria 296.89 (F31.81)\nFor a diagnosis of bipolar II disorder, it is necessary to meet the following criteria for a cur-\nrent or past hypomanic episode and the following criteria for a current or past major de-\npressive episode:\nHypomanic Episode\nA. A distinct period of abnormally and persistently elevated, expansive, or irritable mood\nand abnormally and persistently increased activity or energy, lasting at least 4 consec-\nutive days and present most of the day, nearly every day.\nB. During the period of mood disturbance and in creased energy and activity, three (or more)\nof the following symptoms have persisted (four if the mood is only irritable), represent a no-\nticeable change from usual behavior, and have been present to a significant degree:\n1. Inflated self-esteem or grandiosity.\n2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).\n3. More talkative than usual or pressure to keep talking.", "source": "dsm5.pdf"} {"id": "30f094cc2d6c-0", "page_content": "Bipolar II Disorder 133\n4. Flight of ideas or subjective experience that thoughts are racing.\n5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external\nstimuli), as reported or observed.\n6. Increase in goal-directed activity (either socially, at work or school, or sexually) or\npsychomotor agitation.\n7. Excessive involvement in activities that have a high potential for painful conse-\nquences (e.g., engaging in unrestrained buyin g sprees, sexual indiscretions, or\nfoolish business investments).\nC. The episode is associated with an unequivocal change in functioning that is uncharac-\nteristic of the individual when not symptomatic. \nD. The disturbance in mood and the change in functioning are observable by others.\nE. The episode is not severe enough to cause marked impairment in social or occupa-\ntional functioning or to necessitate hospitalization. If there are psychotic features, the\nepisode is, by definition, manic.\nF. The episode is not attributable to the physiological effects of a substance (e.g., a drug\nof abuse, a medication or other treatment).\nNote: A full hypomanic episode that emerges during antidepressant treatment (e.g.,\nmedication, electroconvulsive therapy) but persists at a fully syndromal level beyond\nthe physiological effect of that treatment is sufficient evidence for a hypomanic episode\ndiagnosis. However, caution is indicated so that one or two symptoms (particularly in-\ncreased irritability, edginess, or agitation following antidepressant use) are not taken\nas sufficient for diagnosis of a hypomanic episode, nor necessarily indicative of a bi-\npolar diathesis.\nMajor Depressive Episode\nA. Five (or more) of the following symptoms have been present during the same 2-week", "source": "dsm5.pdf"} {"id": "30f094cc2d6c-1", "page_content": "period and represent a change from previous functioning; at least one of the symptoms\nis either (1) depressed mood or (2) loss of interest or pleasure.\nNote: Do not include symptoms that are clearly attributable to a medical condition.\n1. Depressed mood most of the day, nearly every day, as indicated by either subjec-\ntive report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g.,\nappears tearful). ( Note: In children and adolescents, can be irritable mood.)\n2. Markedly diminished interest or pleasure in al l, or almost all, activities most of the\nday, nearly every day (as indicated by either subjective account or observation).\n3. Significant weight loss when not dieting or weight gain (e.g., a change of more than\n5% of body weight in a month), or dec rease or increase in appetite nearly every\nday. ( Note: In children, consider failure to make expected weight gain.)\n4. Insomnia or hypersomnia nearly every day.\n5. Psychomotor agitation or retardation nearly every day (observable by others; not\nmerely subjective feelings of restlessness or being slowed down).\n6. Fatigue or loss of energy nearly every day.\n7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delu-\nsional) nearly every day (not merely self-reproach or guilt about being sick).\n8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (ei-\nther by subjective account or as observed by others).\n9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation with-\nout a specific plan, a suicide attempt, or a specific plan for committing suicide.", "source": "dsm5.pdf"} {"id": "30f094cc2d6c-2", "page_content": "out a specific plan, a suicide attempt, or a specific plan for committing suicide.\nB. The symptoms cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning. \nC. The episode is not attributable to the physiological effects of a substance or another\nmedical condition.", "source": "dsm5.pdf"} {"id": "6adf6a23d178-0", "page_content": "134 Bipolar and Related Disorders\nNote: Criteria A\u2013C above constitute a major depressive episode.\nNote: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a nat-\nural disaster, a serious medical illness or disability) may include the feelings of intense sad-\nness, rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion\nA, which may resemble a depressive episode. Although such symptoms may be under-\nstandable or considered appropriate to the loss, the presence of a major depressive episode\nin addition to the normal response to a significant loss should be carefully considered. This\ndecision inevitably requires the ex ercise of clinical judgment ba sed on the individual\u2019s history\nand the cultural norms for the expression of distress in the context of loss.1 \nBipolar II Disorder\nA. Criteria have been met for at least one hypomanic episode (Criteria A\u2013F under \u201cHypo-\nmanic Episode\u201d above) and at least one major depressive episode (Criteria A\u2013C under\n\u201cMajor Depressive Episode\u201d above).\nB. There has never been a manic episode.\nC. The occurrence of the hypomanic episode( s) and major depressive episode(s) is not\nbetter explained by schizoaffective disorder, schizophrenia, schizophreniform disor-\nder, delusional disorder, or other specified or unspecified schizophrenia spectrum and\nother psychotic disorder.\nD. The symptoms of depression or the unpredictability caused by frequent alternation be-\ntween periods of depression and hypomania caus es clinically significant distress or im-\npairment in social, occupational, or other important areas of functioning.\nCoding and Recording Procedures\nBipolar II disorder has one diagnostic code: 296.89 (F31.81). Its status with respect to cur-", "source": "dsm5.pdf"} {"id": "6adf6a23d178-1", "page_content": "rent severity, presence of psychotic features, course, and other specifiers cannot be\ncoded but should be indicated in writing (e.g., 296.89 [F31.81] bipolar II disorder, current\nepisode depressed, moderate severity, with mi xed features; 296.89 [F31.81] bipolar II dis-\norder, most recent episode depressed, in partial remission).\nSpecify current or most recent episode: \nHypomanic \nDepressed\nSpecify if:\nWith anxious distress (p. 149)\nWith mixed features (pp. 149\u2013150)\n1In distinguishing grief from a major depressive episode (MDE), it is useful to consider that in grief\nthe predominant affect is feelings of emptiness an d loss, while in a MDE it is persistent depressed\nmood and the inability to anticipate happiness or pleasure. The dysphoria in grief is likely to\ndecrease in intensity over days to weeks and occurs in waves, the so-called pangs of grief. These\nwaves tend to be associated with thoughts or re minders of the deceased. The depressed mood of a\nMDE is more persistent and not tied to specific thoughts or preoccupations. The pain of grief may\nbe accompanied by positive emotions and humor th at are uncharacteristic of the pervasive unhap-\npiness and misery characteristic of a MDE. The thought content associated with grief generally fea-\ntures a preoccupation with thoughts and memories of the deceased, rather than the self-critical or\npessimistic ruminations seen in a MDE. In grief, self-esteem is generally preserved, whereas in a\nMDE feelings of worthlessness and self-loathing ar e common. If self-derogatory ideation is present\nin grief, it typically involves pe rceived failings vis-\u00e0-vis the deceased (e.g., not visiting frequently", "source": "dsm5.pdf"} {"id": "6adf6a23d178-2", "page_content": "enough, not telling the deceased how much he or she was loved). If a bereaved individual thinks\nabout death and dying, such thoughts are genera lly focused on the deceased and possibly about\n\u201c'joining\u201d the deceased, whereas in a MDE such thoughts are focused on ending one\u2019s own life\nbecause of feeling worthless, undeserving of life, or unable to cope with the pain of depression.", "source": "dsm5.pdf"} {"id": "7e21fb7696f3-0", "page_content": "Bipolar II Disorder 135\nWith rapid cycling (pp. 150\u2013151)\nWith mood-congruent psychotic features (p. 152)\nWith mood-incongruent psychotic features (p. 152)\nWith catatonia (p. 152). Coding note: Use additional code 293.89 (F06.1).\nWith peripartum onset (pp. 152\u2013153)\nWith seasonal pattern (pp. 153\u2013154): Applies only to the pattern of major depressive\nepisodes.\nSpecify course if full criteria for a mood episode are not currently met:\nIn partial remission (p. 154)\nIn full remission (p. 154)\nSpecify severity if full criteria for a mood episode are currently met:\nMild (p. 154)\nModerate (p. 154)\nSevere (p. 154)\nDiagnostic Features\nBipolar II disorder is characterized by a clin ical course of recurr ing mood episodes con-\nsisting of one or more majo r depressive episodes (Criteria A\u2013C under \u201cMajor Depressive\nEpisode\u201d) and at least one hypomanic epis ode (Criteria A\u2013F under \u201cHypomanic Epi-\nsode\u201d). The major depressive episode must last at least 2 weeks, and the hypomanic epi-\nsode must last at least 4 days, to meet the di agnostic criteria. During the mood episode(s),\nthe requisite number of symptoms must be present most of th e day, nearly every day, and\nrepresent a noticeable change from usual behavior and functioning. The presence of a\nmanic episode during the course of illness pr ecludes the diagnosis of bipolar II disorder\n(Criterion B under \u201cBipolar II Disorder\u201d). Episodes of substance/medication-induced de-", "source": "dsm5.pdf"} {"id": "7e21fb7696f3-1", "page_content": "pressive disorder or substance/medication-i nduced bipolar and related disorder (repre-\nsenting the physiological effects of a medicati on, other somatic treatments for depression,\ndrugs of abuse, or toxin exposure) or of de pressive and related disorder due to another\nmedical condition or bipolar and related disord er due to another medi cal condition do not\ncount toward a diagnosis of bi polar II disorder unless they persist beyond the physiolog-\nical effects of the treatment or substance and then meet duration criteria for an episode. In\naddition, the episodes must not be better acco unted for by schizoaffective disorder and are\nnot superimposed on schizophrenia, schizophreniform disorder, delusional disorder, or\nother specified or unspecified schizophrenia spectrum or other psychotic disorders (Cri-\nterion C under \u201cBipolar II Disorder\u201d). The de pressive episodes or hypomanic fluctuations\nmust cause clinically significant distress or impairment in social, occupational, or other\nimportant areas of functioning (Criterion D under \u201cBipolar II Disorder \u201d); however, for hy-\npomanic episodes, this requirement does not have to be met. A hypomanic episode that\ncauses significant impairment would likely qu alify for the diagnosis of manic episode and,\ntherefore, for a lifetime diagnosis of bipolar I disorder. The recurrent major depressive ep-\nisodes are often more frequent and lengthier than those occurring in bipolar I disorder.\nIndividuals with bipolar II d isorder typically present to a clinician during a major de-\npressive episode and are unlikely to complain initially of hypomania. Typically, the hy-\npomanic episodes themselves do not cause im pairment. Instead, th e impairment results\nfrom the major depressive episodes or from a persistent pattern of unpredictable mood\nchanges and fluctuating, unreliable interperso nal or occupational functioning. Individu-", "source": "dsm5.pdf"} {"id": "7e21fb7696f3-2", "page_content": "changes and fluctuating, unreliable interperso nal or occupational functioning. Individu-\nals with bipolar II disorder may not view the hypomanic episodes as pathological or dis-\nadvantageous, although others may be troubled by the indi vidual\u2019s erratic behavior.\nClinical information from other informants, such as close friends or relatives, is often use-\nful in establishing the diagnosis of bipolar II disorder.", "source": "dsm5.pdf"} {"id": "95ba534cb46d-0", "page_content": "136 Bipolar and Related Disorders\nA hypomanic episode should not be confused wi th the several days of euthymia and re-\nstored energy or activity that may follow remiss ion of a major depressive episode. Despite the\nsubstantial differences in duration and severi ty between a manic and hypomanic episode, bi-\npolar II disorder is not a \u201cmilder form\u201d of bipo lar I disorder. Compared with individuals with\nbipolar I disorder, individuals with bipolar II di sorder have greater chronicity of illness and\nspend, on average, more time in the depressive phase of their illness, which can be severe and/\nor disabling. Depressive symptoms co-occurr ing with a hypomanic episode or hypomanic\nsymptoms co-occurring with a depressive episod e are common in individuals with bipolar II\ndisorder and are overrepresented in females, pa rticularly hypomania with mixed features. In-\ndividuals experiencing hypomania with mixed fe atures may not label their symptoms as hy-\npomania, but instead experience them as depr ession with increased energy or irritability.\nAssociated Features Supporting Diagnosis\nA common feature of bipolar II disorder is impulsivity, which can contribute to suicide at-\ntempts and substance use disorders. Impulsivit y may also stem from a concurrent person-\nality disorder, substance use disorder, anxiet y disorder, another mental disorder, or a\nmedical condition. There may be heightened levels of creativity in some individuals with\na bipolar disorder. However, that relationship may be nonlinear; th at is, greater lifetime\ncreative accomplishments have been associated with milder forms of bipolar disorder, and\nhigher creativity has been f ound in unaffected family members. The individual\u2019s attach-\nment to heightened creativity during hypomanic episodes may contribute to ambivalence", "source": "dsm5.pdf"} {"id": "95ba534cb46d-1", "page_content": "ment to heightened creativity during hypomanic episodes may contribute to ambivalence\nabout seeking treatment or undermine adherence to treatment. \nPrevalence\nThe 12-month prevalence of bipolar II disord er, internationally, is 0.3%. In the United\nStates, 12-month prevalence is 0.8%. The prevalence rate of pediatric bipolar II disorder is\ndifficult to establish. DSM-IV bipolar I, bipola r II, and bipolar disorder not otherwise spec-\nified yield a combined prevalence rate of 1. 8% in U.S. and non-U.S. community samples,\nwith higher rates (2.7% inclusive) in youths age 12 years or older. \nDevelopment and Course\nAlthough bipolar II disorder can begin in late adolescence and throughout adulthood, av-\nerage age at onset is the mid-20s, which is slight ly later than for bipolar I disorder but ear-\nlier than for major depressive disorder. The illness most of ten begins with a depressive\nepisode and is not recognized as bipolar II d isorder until a hypomanic episode occurs; this\nhappens in about 12% of individuals with the initial diagnosis of major depressive disor-\nder. Anxiety, substance use, or eating diso rders may also precede the diagnosis, compli-\ncating its detection. Many individuals expe rience several episodes of major depression\nprior to the first recognized hypomanic episode. \nThe number of lifetime episodes (both hypomanic and major depressive episodes)\ntends to be higher for bipolar II disorder than for major depressive disorder or bipolar I\ndisorder. However, individuals with bipolar I disorder are actually more likely to experi-\nence hypomanic symptoms than are individuals with bipolar II disorder.The interval\nbetween mood episodes in the co urse of bipolar II disorder tends to decrease as the indi-", "source": "dsm5.pdf"} {"id": "95ba534cb46d-2", "page_content": "vidual ages. While the hypomanic episode is the feature that defines bipolar II disorder,\ndepressive episodes are more enduring and disabling over time. Despite the predomi-\nnance of depression, once a hypomanic epis ode has occurred, the diagnosis becomes bi-\npolar II disorder and never reve rts to major depressive disorder.\nApproximately 5%\u201315% of individuals with bipolar II disorder ha ve multiple (four or\nmore) mood episodes (hypomanic or major depressive) within the previous 12 months. If", "source": "dsm5.pdf"} {"id": "518c94f1398f-0", "page_content": "Bipolar II Disorder 137\nthis pattern is present, it is noted by the specifier \u201cwith rapid cycling.\u201d By definition, psy-\nchotic symptoms do not occur in hypomanic episodes, and they appear to be less frequent\nin the major depressive episodes in bipolar II di sorder than in those of bipolar I disorder. \nSwitching from a depressive episode to a manic or hypomanic episode (with or with-\nout mixed features) may occur, both spontane ously and during treatment for depression.\nAbout 5%\u201315% of individuals with bipolar II disorder will ultimately develop a manic ep-\nisode, which changes the diagnosis to bipolar I disorder, regardless of subsequent course. \nMaking the diagnosis in children is often a challenge, especially in those with irritabil-\nity and hyperarousal that is nonepisodic (i.e., lacks the well-demarcated periods of altered\nmood). Nonepisodic irritability in youth is associated with an elevated risk for anxiety dis-\norders and major depressive disorder, but not bipolar disorder, in ad ulthood. Persistently\nirritable youths have lower familial rates of bipolar disorder than do youths who have bi-\npolar disorder. For a hypomanic episode to be diagnosed, the child\u2019s symptoms must ex-\nceed what is expected in a given environment and culture for the child\u2019s developmental\nstage. Compared with adult onset of bipolar II disorder, childhood or adolescent onset of\nthe disorder may be associated with a more severe lifetime course. The 3-year incidence\nrate of first-onset bipolar II disorder in adults older than 60 years is 0.34%. However, dis-\ntinguishing individuals older than 60 years with bipolar II disorder by late versus early\nage at onset does not appear to have any clinical utility.\nRisk and Prognostic Factors", "source": "dsm5.pdf"} {"id": "518c94f1398f-1", "page_content": "Risk and Prognostic Factors\nGenetic and physiological. The risk of bipolar II disorder tends to be highest among rel-\natives of individuals with bipolar II disorder, as opposed to individuals with bipolar I dis-\norder or major depressive disorder. There ma y be genetic factors influencing the age at\nonset for bipolar disorders.\nCourse modifiers. A rapid-cycling pattern is associated with a poorer prognosis. Return\nto previous level of social fu nction for individuals with bipolar II disorder is more likely\nfor individuals of younger age and with less severe depression, sugge sting adverse effects\nof prolonged illness on recovery. More education, fewer ye ars of illness, and being mar-\nried are independently associated with functi onal recovery in individuals with bipolar\ndisorder, even after diagnostic type (I vs. II), current depressive symptoms, and presence\nof psychiatric comorbidity are taken into account.\nGender-Related Diagnostic Issues\nWhereas the gender ratio for bipolar I disorder is equal, findings on gender differences in\nbipolar II disorder are mixed, differing by type of sample (i.e., registry, community, or\nclinical) and country of origin. There is little to no evidence of bipolar gender differences,\nwhereas some, but not all, clinical samples su ggest that bipolar II disorder is more com-\nmon in females than in males, which may refl ect gender differences in treatment seeking\nor other factors. \nPatterns of illness and comorbidity, however, seem to differ by gender, with females\nbeing more likely than males to report hypomania with mixed depressive features and a\nrapid-cycling course. Childbirth may be a spec ific trigger for a hypomanic episode, which\ncan occur in 10%\u201320% of females in nonclinical populations and most typically in the early", "source": "dsm5.pdf"} {"id": "518c94f1398f-2", "page_content": "postpartum period. Distinguishing hypomani a from the elated mood and reduced sleep\nthat normally accompany the birth of a chil d may be challenging. Postpartum hypomania\nmay foreshadow the onset of a depression that occurs in abou t half of females who expe-\nrience postpartum \u201chighs.\u201d Accurate detectio n of bipolar II disorder may help in estab-\nlishing appropriate treatment of the depression , which may reduce the risk of suicide and\ninfanticide.", "source": "dsm5.pdf"} {"id": "f6c5579dbc6b-0", "page_content": "138 Bipolar and Related Disorders\nSuicide Risk\nSuicide risk is high in bipolar II disorder. Approximately one-third of individuals with bi-\npolar II disorder report a lifetime history of suicide attempt. The prev alence rates of life-\ntime attempted suicide in bipolar II and bipola r I disorder appear to be similar (32.4% and\n36.3%, respectively). However, the lethality of attempts, as defined by a lower ratio of at-\ntempts to completed suicides, may be higher in individuals with bipolar II disorder com-\npared with individuals with bipolar I disorder. There may be an association between\ngenetic markers and increased risk for suicidal behavior in individuals with bipolar dis-\norder, including a 6.5-fold higher risk of su icide among first-degree relatives of bipolar II\nprobands compared with those with bipolar I disorder. \nFunctional Consequences of Bipolar II Disorder\nAlthough many in dividuals with bipolar II disorder return to a fully functional level be-\ntween mood episodes, at least 15% continue to have some in ter-episode dysfunction, and\n20% transition directly into another mood episode without inter-ep isode recovery. Func-\ntional recovery lags substantially behind recovery from symptoms of bipolar II disorder,\nespecially in regard to occupational recovery , resulting in lower socioeconomic status de-\nspite equivalent levels of education with the general population. Individuals with bipolar\nII disorder perform more poorly than healthy individuals on cognitive tests and, with the\nexception of memory and semantic fluency, ha ve similar cognitive impairment as do in-\ndividuals with bipolar I disord er. Cognitive impairments associ ated with bipolar II disor-\nder may contribute to vocational difficulti es. Prolonged unemployment in individuals\nwith bipolar disorder is associated with more episodes of depression, older age, increased", "source": "dsm5.pdf"} {"id": "f6c5579dbc6b-1", "page_content": "with bipolar disorder is associated with more episodes of depression, older age, increased\nrates of current panic disorder, and lif etime history of alcohol use disorder.\nDifferential Diagnosis \nMajor depressive disorder. Perhaps the most challenging differential diagnosis to con-\nsider is major depressive di sorder, which may be accompanied by hypomanic or manic\nsymptoms that do not meet full criteria (i.e., either fewer symptoms or a shorter duration\nthan required for a hypomanic episode). This is especially true in evaluating individuals\nwith symptoms of irritability, which may be associated with either major depressive dis-\norder or bipolar II disorder. \nCyclothymic disorder. In cyclothymic disorder, there are numerous periods of hypo-\nmanic symptoms and numerous periods of depr essive symptoms that do not meet symp-\ntom or duration criteria for a major depressive episode. Bipolar II disorder is distinguished\nfrom cyclothymic disorder by the presence of one or more major depressive episodes. If a\nmajor depressive episode occurs after the firs t 2 years of cyclothymic disorder, the addi-\ntional diagnosis of bipolar II disorder is given.\nSchizophrenia spectrum and other related psychotic disorders. Bipolar II disorder must\nbe distinguished from psychotic disorders (e .g., schizoaffective disorder, schizophrenia,\nand delusional disorder). Sc hizophrenia, schizoaffective di sorder, and delusional disor-\nder are all characterized by periods of psychotic symptoms that occur in the absence of\nprominent mood symptoms. Other helpful considerations incl ude the accompanying\nsymptoms, previous cour se, and family history.\nPanic disorder or other anxiety disorders. Anxiety disorders need to be considered in\nthe differential diagnosis and may frequent ly be present as co-occurring disorders.", "source": "dsm5.pdf"} {"id": "f6c5579dbc6b-2", "page_content": "the differential diagnosis and may frequent ly be present as co-occurring disorders.\nSubstance use disorders. Substance use disorders are included in the differential diag-\nnosis. \nAttention-deficit/hype ractivity disorder. Attention-deficit/hypera ctivity disorder (ADHD)\nmay be misdiagnosed as bipolar II disorder, especially in adolescents and children. Many", "source": "dsm5.pdf"} {"id": "4059d82127c0-0", "page_content": "Cyclothymic Disorder 139\nsymptoms of ADHD, such as rapid speech, racing thoughts, distractibility, and less need\nfor sleep, overlap with the symp toms of hypomania. The double counting of symptoms to-\nward both ADHD and bipolar II disorder can be avoided if the clinician clarifies whether\nthe symptoms represent a distin ct episode and if the noticeab le increase over baseline re-\nquired for the diagnosis of bipo lar II disorder is present. \nPersonality disorders. The same convention as applies for ADHD also applies when\nevaluating an individual for a personality disorder such as borderline personality disor-\nder, since mood lability and impulsivity are common in both personality disorders and bi-\npolar II disorder. Symptoms must represent a di stinct episode, and the noticeable increase\nover baseline required for the diagnosis of bipo lar II disorder must be present. A diagnosis\nof a personality disorder should not be made during an untreated mood episode unless\nthe lifetime history supports the pr esence of a personality disorder.\nOther bipolar disorders. Diagnosis of bipolar II disorder should be differentiated from\nbipolar I disorder by carefully considering whether there have been any past episodes of\nmania and from other specified and unspecifie d bipolar and related disorders by confirm-\ning the presence of fully synd romal hypomania and depression.\nComorbidity\nBipolar II disorder is more often than not associated with one or more co-occurring mental\ndisorders, with anxiety disorders being the most common. Approximately 60% of individ-\nuals with bipolar II disorder have three or more co-occurr ing mental disorders; 75% have\nan anxiety disorder; and 37% have a substa nce use disorder. Children and adolescents\nwith bipolar II disorder have a higher rate of co-occurring anxiety disorders compared", "source": "dsm5.pdf"} {"id": "4059d82127c0-1", "page_content": "with bipolar II disorder have a higher rate of co-occurring anxiety disorders compared\nwith those with bipolar I diso rder, and the anxiety disorder most often predates the bi-\npolar disorder. Anxiety and substance use diso rders occur in individuals with bipolar II\ndisorder at a higher rate than in the genera l population. Approximately 14% of individuals\nwith bipolar II disorder have at least one lif etime eating disorder, with binge-eating dis-\norder being more common than bulim ia nervosa and anorexia nervosa.\nThese commonly co-occurring disorders do no t seem to follow a course of illness that\nis truly independent from that of the bipolar disorder, but rather have strong associations\nwith mood states. For example, anxiety and ea ting disorders tend to associate most with\ndepressive symptoms, and substance use disord ers are moderately associated with manic\nsymptoms. \nCyclothymic Disorder\nDiagnostic Criteria 301.13 (F34.0)\nA. For at least 2 years (at least 1 year in children and adolescents) there have been nu-\nmerous periods with hypomanic symptoms that do not meet criteria for a hypomanic\nepisode and numerous periods with depressive sym ptoms that do not meet criteria for\na major depressive episode.\nB. During the above 2-year period (1 year in children and adolescents), the hypomanic\nand depressive periods have been present for at least half the time and the individual\nhas not been without the symptoms for more than 2 months at a time.\nC. Criteria for a major depressive, manic, or hypomanic episode have never been met. \nD. The symptoms in Criterion A are not better explained by schizoaffective disorder,\nschizophrenia, schizophreniform disorder, delusional disorder, or other specified or un-", "source": "dsm5.pdf"} {"id": "4059d82127c0-2", "page_content": "schizophrenia, schizophreniform disorder, delusional disorder, or other specified or un-\nspecified schizophrenia spectrum and other psychotic disorder.\nE. The symptoms are not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication) or another medical condition (e.g., hyperthyroidism).", "source": "dsm5.pdf"} {"id": "aac952916c88-0", "page_content": "140 Bipolar and Related Disorders\nF. The symptoms cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nSpecify if:\nWith anxious distress (see p. 149)\nDiagnostic Features\nThe essential feature of cyclot hymic disorder is a chronic, fluctuating mood disturbance\ninvolving numerous periods of hypomanic symptoms and periods of depressive symp-\ntoms that are distinct from each other (Criterion A). The hypomanic symptoms are of\ninsufficient number, severity, pervasiveness, or duration to meet full criteria for a hypo-\nmanic episode, and the depressive symptoms ar e of insufficient nu mber, severity, perva-\nsiveness, or duration to meet full criteria for a major depressive episode. During the initial\n2-year period (1 year for children or adolescents), the symptoms must be persistent (pres-\nent more days than not), and any symptom-fr ee intervals last no longer than 2 months\n(Criterion B). The diagnosis of cyclothymic disorder is made only if the criteria for a major\ndepressive, manic, or hypomanic episode have never been met (Criterion C).\nIf an individual with cyclothymic disorder su bsequently (i.e., after the initial 2 years in\nadults or 1 year in children or adolescents) experiences a major depressive, manic, or hy-\npomanic episode, the diagnosis changes to majo r depressive disorder , bipolar I disorder,\nor other specified or unspecified bipolar and related disorder (subclassified as hypomanic\nepisode without prior major depressive episod e), respectively, and the cyclothymic disor-\nder diagnosis is dropped.\nThe cyclothymic disorder diagnosis is not made if the pattern of mood swings is better\nexplained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delu-", "source": "dsm5.pdf"} {"id": "aac952916c88-1", "page_content": "explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delu-\nsional disorder, or other specified and un specified schizophrenia spectrum and other\npsychotic disorders (Criterion D), in which c ase the mood symptoms are considered asso-\nciated features of the psychoti c disorder. The mood disturbanc e must also not be attribut-\nable to the physiological effe cts of a substance (e.g., a dr ug of abuse, a medication) or\nanother medical condition (e.g., hyperthyroidis m) (Criterion E). Although some individ-\nuals may function particularly well during some of the pe riods of hypomania, over the\nprolonged course of the disorder , there must be clinically significant distress or impair-\nment in social, occupational, or other import ant areas of functioning as a result of the\nmood disturbance (Criterion F). The impairment may develop as a result of prolonged pe-\nriods of cyclical, often unpredictable mood ch anges (e.g., the individual may be regarded\nas temperamental, moody, unpredicta ble, inconsistent , or unreliable).\nPrevalence\nThe lifetime prevalence of cyclothymic diso rder is approximately 0.4%\u20131%. Prevalence in\nmood disorders clinics may rang e from 3% to 5%. In the general population, cyclothymic\ndisorder is apparently equally common in males and females. In clinical settings, females\nwith cyclothymic disorder may be more lik ely to present for tr eatment than males.\nDevelopment and Course\nCyclothymic disorder usually begins in adolescence or early adult life and is sometimes\nconsidered to reflect a temperamental predispo sition to other disorders in this chapter.\nCyclothymic disorder usually has an insidious onset and a persistent course. There is a", "source": "dsm5.pdf"} {"id": "aac952916c88-2", "page_content": "15%\u201350% risk that an individual with cyclothy mic disorder will subsequently develop bi-\npolar I disorder or bipolar II disorder. Onset of persistent, fluctuating hypomanic and de-\npressive symptoms late in adult life needs to be clearly differentiated from bipolar and", "source": "dsm5.pdf"} {"id": "e035a6102965-0", "page_content": "Cyclothymic Disorder 141\nrelated disorder due to another medical condition and depressi ve disorder due to another\nmedical condition (e.g., multiple sclerosis) before the cyclothymic disorder diagnosis is as-\nsigned. Among children with cyclothymic diso rder, the mean age at onset of symptoms is\n6.5 years of age.\nRisk and Prognostic Factors\nGenetic and physiological. Major depressive disorder, bipolar I disorder, and bipolar II\ndisorder are more common among first-degree bi ological relatives of individuals with cyclo-\nthymic disorder than in the general population. There may also be an increased familial risk of\nsubstance-related disorders. Cyclothymic disord er may be more common in the first-degree\nbiological relatives of individuals with bipolar I disorder than in the general population. \nDifferential Diagnosis\nBipolar and related disorder due to anothe r medical condition and depressive disorder\ndue to another medical condition. The diagnosis of bipolar and related disorder due to\nanother medical condition or depressive disorder due to another medical condition is\nmade when the mood disturbance is judged to be attributable to the physiological effect of\na specific, usually chronic medical condition (e.g., hyperthyroidism). This determination\nis based on the history, physical examination, or laboratory findings. If it is judged that the\nhypomanic and depressive symptoms are not the physiological consequence of the med-\nical condition, then the primary mental disorder (i.e., cyclothymi c disorder) and the med-\nical condition are coded. For example, this would be the case if the mood symptoms are\nconsidered to be the psychological (not the physiological) consequence of having a chronic\nmedical condition, or if there is no etiological relationship between the hypomanic and de-\npressive symptoms and the medical condition.", "source": "dsm5.pdf"} {"id": "e035a6102965-1", "page_content": "pressive symptoms and the medical condition.\nSubstance/medication-induced bipolar and related disorder and substance/medica-\ntion-induced depressive disorder. Substance/medication-induced bipolar and related\ndisorder and substance/medica tion-induced depressive diso rder are distinguished from\ncyclothymic disorder by the judgment that a substance/medication (especially stimu-\nlants) is etiologically related to the mood disturbance. The fr equent mood swings in these\ndisorders that are suggestive of cyclothymic disorder usually resolv e following cessation\nof substance/medication use.\nBipolar I disorder, with rapid cycling, an d bipolar II disorder, with rapid cycling.\nBoth disorders may resemble cyclothymic disorder by virtue of the frequent marked shifts\nin mood. By definition, in cyclothymic disord er the criteria for a major depressive, manic,\nor hypomanic episode has never been met, wh ereas the bipolar I di sorder and bipolar II\ndisorder specifier \u201cwith rapid cycling\u201d requ ires that full mood ep isodes be present. \nBorderline person ality disorder. Borderline personality diso rder is associated with\nmarked shifts in mood that may suggest cyclothymic disorder. If the criteria are met for\nboth disorders, both borderline personality disorder and cyclothymic disorder may be di-\nagnosed.\nComorbidity\nSubstance-related disorders and sleep disorder s (i.e., difficulties in initiating and main-\ntaining sleep) may be present in individuals with cyclothy mic disorder. Most children\nwith cyclothymic disorder treated in outpati ent psychiatric settings have comorbid mental\nconditions; they are more likely than other pediatric patients with mental disorders to\nhave comorbid attention-defi cit/hyperactivity disorder.", "source": "dsm5.pdf"} {"id": "c7abf631a7f5-0", "page_content": "142 Bipolar and Related Disorders\nSubstance/Medication-Induced\n Bipolar and Related Disorder\nDiagnostic Criteria\nA. A prominent and persistent disturbance in mood that predominates in the clinical picture\nand is characterized by elevated, expansive, or irritable mood, with or without depressed\nmood, or markedly diminished interest or plea sure in all, or almost all, activities.\nB. There is evidence from the history, physical examination, or laboratory findings of both\n(1) and (2):\n1. The symptoms in Criterion A developed during or soon after substance intoxication\nor withdrawal or after exposure to a medication.\n2. The involved substance/medication is capable of producing the symptoms in Crite-\nrion A.\nC. The disturbance is not better explained by a bipolar or related disorder that is not sub-\nstance/medication-induced. Such evidence of an independent bipolar or related disor-\nder could include the following:\nThe symptoms precede the onset of the substance/medication use; the symptoms per-\nsist for a substantial period of time (e.g., about 1 month) after the cessation of acute\nwithdrawal or severe intoxication; or there is other evidence suggesting the existence\nof an independent non-substance/medication-induced bipolar and related disorder\n(e.g., a history of recurrent non-substance/medication-related episodes). \nD. The disturbance does not occur exclusively during the course of a delirium. \nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nCoding note: The ICD-9-CM and ICD-10-CM codes fo r the [specific substance/medication]-\ninduced bipolar and related disorders are indicated in the table below. Note that the ICD-10-", "source": "dsm5.pdf"} {"id": "c7abf631a7f5-1", "page_content": "CM code depends on whether or not there is a co morbid substance use disorder present for\nthe same class of substance. If a mild substance use disorder is comorbid with the substance-\ninduced bipolar and related disorder, the 4th position character is \u201c1,\u201d and the clinician should\nrecord \u201cmild [substance] use disorder\u201d before the substance-induced bipolar and related dis-\norder (e.g., \u201cmild cocaine use disorder with coca ine-induced bipolar and related disorder\u201d). If a\nmoderate or severe substance use disorder is comorbid with the substance-induced bipolar\nand related disorder, the 4th position character is \u201c2,\u201d and the clinician should record \u201cmoder-\nate [substance] use disorder\u201d or \u201csevere [subs tance] use disorder,\u201d depending on the severity\nof the comorbid substance use disorder. If there is no comorbid substance use disorder (e.g.,\nafter a one-time heavy use of the substance), then the 4th position character is \u201c9,\u201d and the\nclinician should record only the substance-induced bipolar and related disorder.\nICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate \nor severeWithout \nuse \ndisorder\nAlcohol 291.89 F10.14 F10.24 F10.94\nPhencyclidine 292.84 F16.14 F16.24 F16.94\nOther hallucinogen 292.84 F16.14 F16.24 F16.94", "source": "dsm5.pdf"} {"id": "8065aed924b9-0", "page_content": "Substance/Medication-Induced Bipolar and Related Disorder 143\nSpecify if (see Table 1 in the chapter \u201cSubstance-Related and Addictive Disorders\u201d for di-\nagnoses associated with substance class):\nWith onset during intoxication: If the criteria are met for intoxication with the sub-\nstance and the symptoms develop during intoxication.\nWith onset during withdrawal: If criteria are met for withdrawal from the substance\nand the symptoms develop during, or shortly after, withdrawal.\nRecording Procedures\nICD-9-CM. The name of the substance/medication -induced bipolar and related disor-\nder begins with the specific su bstance (e.g., cocaine, dexame thasone) that is presumed to\nbe causing the bipolar mood symptoms. The diag nostic code is selected from the table in-\ncluded in the criteria set, which is based on the drug class. For substances that do not fit\ninto any of the classes (e.g., dexamethason e), the code for \u201cother substance\u201d should be\nused; and in cases in which a substance is judged to be an etiological factor but the specific\nclass of substance is unknown, the category \u201cunknown substance\u201d should be used.\nThe name of the disorder is followed by the sp ecification of onset (i.e., onset during in-\ntoxication, onset during with drawal). Unlike the recording procedures for ICD-10-CM,\nwhich combine the substance-induced disorder and substance use disorder into a single\ncode, for ICD-9-CM a separate diagnostic code is given for the substance use disorder. For\nexample, in the case of irritable symptoms oc curring during intoxica tion in a man with a\nsevere cocaine use disorder, the diagnosis is 292.84 cocaine-induced bipolar and related", "source": "dsm5.pdf"} {"id": "8065aed924b9-1", "page_content": "severe cocaine use disorder, the diagnosis is 292.84 cocaine-induced bipolar and related\ndisorder, with onset during intoxication. An additional diagnosis of 304.20 severe cocaine\nuse disorder is also given. When more than one substance is judged to play a significant\nrole in the development of bipolar mood symp toms, each should be listed separately (e.g.,\n292.84 methylphenidate-induced bipolar and re lated disorder, with onset during intoxi-\ncation; 292.84 dexamethasone-induced bipolar and related disorder, with onset during in-\ntoxication).\nICD-10-CM. The name of the substance/medication -induced bipolar and related disor-\nder begins with the specific su bstance (e.g., cocaine, dexame thasone) that is presumed to\nbe causing the bipolar mood symptoms. The diag nostic code is selected from the table in-\ncluded in the criteria set, whic h is based on the drug class and presence or absence of a co-\nmorbid substance use disorder. For substances th at do not fit into any of the classes (e.g.,\ndexamethasone), the code for \u201cother substanc e\u201d should be used; and in cases in which a\nsubstance is judged to be an etiological factor but the specific class of substance is un-\nknown, the category \u201cunknown substance\u201d should be used.\nWhen recording the name of the disorder, th e comorbid substance use disorder (if any)\nis listed first, followed by the word \u201cwith,\u201d followed by the name of the substance-inducedSedative, hypnotic, or anxiolytic 292.84 F13.14 F13.24 F13.94\nAmphetamine (or other \nstimulant)292.84 F15.14 F15.24 F15.94", "source": "dsm5.pdf"} {"id": "8065aed924b9-2", "page_content": "stimulant)292.84 F15.14 F15.24 F15.94\nCocaine 292.84 F14.14 F14.24 F14.94\nOther (or unknown) substance 292.84 F19.14 F19.24 F19.94ICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate \nor severeWithout \nuse \ndisorder", "source": "dsm5.pdf"} {"id": "270c3393380d-0", "page_content": "144 Bipolar and Related Disorders\nbipolar and related disorder, foll owed by the specification of onset (i.e., onset during in-\ntoxication, onset during withdrawal). For exam ple, in the case of irritable symptoms oc-\ncurring during intoxica tion in a man with a severe coca ine use disorder, the diagnosis is\nF14.24 severe cocaine use disorder with co caine-induced bipolar and related disorder,\nwith onset during intoxication . A separate diagnosis of the comorbid severe cocaine use\ndisorder is not given. If the substance-induce d bipolar and related disorder occurs without\na comorbid substance use disorder (e.g., afte r a one-time heavy use of the substance), no\naccompanying substance use disorder is note d (e.g., F15.94 amphetamine-induced bipolar\nand related disorder, with onset during into xication). When more than one substance is\njudged to play a significant role in the development of bipolar mood symptoms, each\nshould be listed separately (e.g., F15.24 severe methylphenidate use disorder with meth-\nylphenidate-induced bipolar and related disorder, with onset during intoxication; F19.94\ndexamethasone-induced bipolar and related di sorder, with onset during intoxication).\nDiagnostic Features\nThe diagnostic features of substance/medication -induced bipolar and related disorder are es-\nsentially the same as those for mania, hypomania, or depression . A key exception to the diag-\nnosis of substance/medication-induced bipolar an d related disorder is the case of hypomania\nor mania that occurs after antidepressant medi cation use or other treatments and persists be-\nyond the physiological effects of the medication. This condition is considered an indicator of", "source": "dsm5.pdf"} {"id": "270c3393380d-1", "page_content": "yond the physiological effects of the medication. This condition is considered an indicator of\ntrue bipolar disorder, not substance/medication -induced bipolar and re lated disorder. Simi-\nlarly, individuals with apparent electroconvulsive therapy\u2013induced manic or hypomanic ep-\nisodes that persist beyond th e physiological effects of the treatment are diagnosed with\nbipolar disorder, not substance/medication -induced bipolar and related disorder. \nSide effects of some antidepressants and ot her psychotropic drugs (e.g., edginess, ag-\nitation) may resemble the primary symptoms of a manic syndrome, but they are funda-\nmentally distinct from bipolar symptoms and are insufficient for the diagnosis. That is, the\ncriterion symptoms of mania/hypomania have specificity (simple agitation is not the same\nas excess involvement in purposeful activiti es), and a sufficient number of symptoms\nmust be present (not just one or two symptoms ) to make these diagnoses. In particular, the\nappearance of one or two nons pecific symptoms\u2014irri tability, edginess, or agitation during\nantidepressant treatment\u2014in the absence of a full manic or hypomanic syndrome should\nnot be taken to support a diagnosis of a bipolar disorder.\nAssociated Features Supporting Diagnosis\nEtiology (causally related to the use of psychotropic medications or substances of abuse\nbased on best clinical evidence) is the key variab le in this etiologically specified form of bi-\npolar disorder. Substances/medications that are typically considered to be associated\nwith substance/medication-induced bipolar and related diso rder include the stimulant\nclass of drugs, as well as phencyclidine and steroids; however, a numb er of potential sub-\nstances continue to emerge as new compounds are synthesized (e.g., so-calle d bath salts).", "source": "dsm5.pdf"} {"id": "270c3393380d-2", "page_content": "A history of such substance use may help increase diagnostic certainty.\nPrevalence\nThere are no epidemiological studies of substance/medication-induced mania or bipolar\ndisorder. Each etiological substance may have its own individual risk of inducing a bipo-\nlar (manic/hypomanic) disorder.\nDevelopment and Course\nIn phencyclidine-induced mania, the initial pres entation may be one of a delirium with af-\nfective features, which then becomes an atyp ically appearing manic or mixed manic state.", "source": "dsm5.pdf"} {"id": "d0d28d2d6fcb-0", "page_content": "Bipolar and Related Disorder Due to Another Medical Condition 145\nThis condition follows the ingestion or inhalati on quickly, usually within hours or, at the\nmost, a few days. In stimulant-induced manic or hypomanic states, the response is in min-\nutes to 1 hour after one or several ingestions or injections. The episode is very brief and\ntypically resolves over 1\u20132 days. With co rticosteroids and some immunosuppressant\nmedications, the mania (or mixed or depressed state) usually follows several days of in-\ngestion, and the higher doses appear to have a much greate r likelihood of producing bi-\npolar symptoms. \nDiagnostic Markers\nDetermination of the substance of use can be made through markers in the blood or urine\nto corroborate diagnosis.\nDifferential Diagnosis\nSubstance/medication-induced bipolar and related disorder should be differentiated\nfrom other bipolar disorders, substance into xication or substance-induced delirium, and\nmedication side effects (as noted earlier). A full manic episode that emerges during anti-\ndepressant treatment (e.g., medication, electr oconvulsive therapy) but persists at a fully\nsyndromal level beyond the physiological effect of that treatment is sufficient evidence for\na bipolar I diagnosis. A full hypomanic episode that emerges during antidepressant treat-\nment (e.g., medication, electroconvulsive therap y) but persists at a fully syndromal level\nbeyond the physiological effect of that treatme nt is sufficient evidence for a bipolar II di-\nagnosis only if preceded by a major depressive episode.\nComorbidity\nComorbidities are those associated with the use of illicit substances (in the case of illegal\nstimulants or phencyclidine) or diversion of prescribed stimulants. Comorbidities related", "source": "dsm5.pdf"} {"id": "d0d28d2d6fcb-1", "page_content": "to steroid or immunosuppre ssant medications are those medical indications for these\npreparations. Delirium can occur before or along with manic symptoms in individuals in-\ngesting phencyclidine or those who are prescr ibed steroid medications or other immuno-\nsuppressant medications.\nBipolar and Related Disorder\n Due to Another Medical Condition\nDiagnostic Criteria\nA. A prominent and persistent period of abnormall y elevated, expansive, or irritable mood\nand abnormally increased activity or energy that predominates in the clinical picture. \nB. There is evidence from the history, physical ex amination, or laboratory findings that the dis-\nturbance is the direct pathophysiological consequence of another medical condition. \nC. The disturbance is not better explained by another mental disorder.\nD. The disturbance does not occur exclusively during the course of a delirium. \nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioni ng, or necessitates hospitalization to pre-\nvent harm to self or others, or there are psychotic features.\nCoding note: The ICD-9-CM code for bipolar and related disorder due to another medical\ncondition is 293.83, which is assigned regardless of the specifier. The ICD-10-CM code\ndepends on the specifier (see below).", "source": "dsm5.pdf"} {"id": "38461f4b925b-0", "page_content": "146 Bipolar and Related Disorders\nSpecify if: \n(F06.33) With manic features: Full criteria are not met for a manic or hypomanic ep-\nisode.\n(F06.33) With manic- or hypomanic-like episode: Full criteria are met except Crite-\nrion D for a manic episode or except Criterion F for a hypomanic episode.\n(F06.34) With mixed features: Symptoms of depression are also present but do not\npredominate in the clinical picture.\nCoding note: Include the name of the other medical condition in the name of the mental\ndisorder (e.g., 293.83 [F06.33] bipolar disorder due to hyperthyroidism, with manic fea-\ntures). The other medical condition should also be coded and listed separately immedi-\nately before the bipolar and related disorder due to the medical condition (e.g., 242.90\n[E05.90] hyperthyroidism; 293.83 [F06.33] bipol ar disorder due to hyperthyroidism, with\nmanic features).\nDiagnostic Features\nThe essential features of bipolar and related disorder due to anothe r medical condition are\npresence of a prominent and persistent period of abnormally elevated, expansive, or irri-\ntable mood and abnormally increased activity or energy predominating in the clinical pic-\nture that is attributable to another medical condition (Criterion B). In most cases the manic\nor hypomanic picture may appear during the in itial presentation of the medical condition\n(i.e., within 1 month); howeve r, there are exceptions, especi ally in chronic medical condi-\ntions that might worsen or relapse and herald the appearance of the manic or hypomanic\npicture. Bipolar and related disorder due to another medical condition would not be diag-", "source": "dsm5.pdf"} {"id": "38461f4b925b-1", "page_content": "picture. Bipolar and related disorder due to another medical condition would not be diag-\nnosed when the manic or hypomanic episodes definitely preceded the medical condition,\nsince the proper diagnosis would be bipolar disorder (except in the unusual circumstance\nin which all preceding manic or hypomanic episodes\u2014or, when only one such episode has\noccurred, the preceding manic or hypomanic episode\u2014were associated with ingestion of\na substance/medication). The diagnosis of bipolar and related disorder due to another\nmedical condition should not be made during the course of a delirium (Criterion D). The\nmanic or hypomanic episode in bipolar and related disorder due to another medical con-\ndition must cause clinically significant dist ress or impairment in social, occupational, or\nother important areas of fu nctioning to qualify for this diagnosis (Criterion E).\nAssociated Features Supporting Diagnosis\nEtiology (i.e., a causal relationship to anothe r medical condition based on best clinical ev-\nidence) is the key variable in this etiologically specified form of bipolar disorder. The list-\ning of medical conditions that are said to be able to induce mania is never complete, and\nthe clinician\u2019s best judgment is the essence of this diagnosis. Among the best known of the\nmedical conditions that can cause a bipolar manic or hypomanic co ndition are Cushing\u2019s\ndisease and multiple sclerosis, as well as stroke and traumatic brain injuries. \nDevelopment and Course \nBipolar and related disorder due to another me dical condition usually has its onset acutely\nor subacutely within the firs t weeks or month of the onset of the associated medical con-\ndition. However, this is not always the case, as a worsening or later relapse of the associ-\nated medical condition may precede the onset of the manic or hypomanic syndrome. The", "source": "dsm5.pdf"} {"id": "38461f4b925b-2", "page_content": "ated medical condition may precede the onset of the manic or hypomanic syndrome. The\nclinician must make a clinical judgment in these situations about whether the medical con-\ndition is causative, based on temporal sequence as well as plausibility of a causal relation-", "source": "dsm5.pdf"} {"id": "70e4e1d2c6cc-0", "page_content": "Bipolar and Related Disorder Due to Another Medical Condition 147\nship. Finally, the condition may remit before or just after the medi cal condition remits,\nparticularly when treatment of the ma nic/hypomanic symptoms is effective. \nCulture-Related Diagnostic Issues\nCulture-related differences, to the extent that there is any evidence, pertain to those asso-\nciated with the medical condition (e.g., rates of multiple sclerosis and stroke vary around\nthe world based on dietary, genetic fact ors, and other environmental factors).\nGender-Related Diagnostic Issues\nGender differences pertain to those associat ed with the medical condition (e.g., systemic\nlupus erythematosus is more common in fema les; stroke is somewhat more common in\nmiddle-age males compared with females).\nDiagnostic Markers\nDiagnostic markers pertain to those associated with the medical condition (e.g., steroid\nlevels in blood or urine to help corroborate the diagnosis of Cushing\u2019s disease, which can\nbe associated with manic or depressive synd romes; laboratory test s confirming the diag-\nnosis of multiple sclerosis).\nFunctional Consequences of Bipolar and Related \nDisorder Due to Anot her Medical Condition\nFunctional consequences of the bipolar sy mptoms may exacerbate impairments associ-\nated with the medical condit ion and may incur worse outcom es due to interference with\nmedical treatment. In general, it is believed, but not established, that the illness, when in-\nduced by Cushing\u2019s disease, will not recur if the Cushing\u2019s disease is cured or arrested.\nHowever, it is also suggested, but not establ ished, that mood syndromes, including de-\npressive and manic/hypomanic ones, may be episod ic (i.e., recurring) with static brain in-\njuries and other central nervous system diseases.\nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "70e4e1d2c6cc-1", "page_content": "juries and other central nervous system diseases.\nDifferential Diagnosis\nSymptoms of delirium, catatonia, and acute anxiety. It is important to differentiate\nsymptoms of mania from excite d or hypervigilant delirious symptoms; from excited cata-\ntonic symptoms; and from agitation related to acute anxiety states. \nMedication-induced depre ssive or manic symptoms. An important differential diag-\nnostic observation is that the other medica l condition may be treated with medications\n(e.g., steroids or alpha-interferon) that can induce depressive or manic symptoms. In these\ncases, clinical judgment using all of the eviden ce in hand is the best way to try to separate\nthe most likely and/or the most important of two etiological factors (i.e., association with\nthe medical condition vs. a substance/medicati on-induced syndrome). The differential di-\nagnosis of the associated medical conditions is relevant but largely beyond the scope of the\npresent manual. \nComorbidity\nConditions comorbid with bipolar and relate d disorder due to anot her medical condition\nare those associated with the medical conditio ns of etiological relevance. Delirium can oc-\ncur before or along with manic symptoms in individuals with Cushing\u2019s disease.", "source": "dsm5.pdf"} {"id": "57787ab45ad6-0", "page_content": "148 Bipolar and Related Disorders\nOther Specified Bipolar and Related Disorder\n296.89 (F31.89)\nThis category applies to presentations in which symptoms characteristic of a bipolar and\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any of the disorders in the bipolar and related disorders diagnostic class. The other\nspecified bipolar and related disorder category is used in situations in which the clinician\nchooses to communicate the specific reason that the presentation does not meet the cri-\nteria for any specific bipolar and related disorder. This is done by recording \u201cother speci-\nfied bipolar and related disorder\u201d followed by the specific reason (e.g., \u201cshort-duration\ncyclothymia\u201d).\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Short-duration hypomanic episodes (2\u20133 days) and ma jor depressive episodes: A\nlifetime history of one or more major depressive episodes in individuals whose presenta-\ntion has never met full criteria for a manic or hypomanic episode but who have experienced\ntwo or more episodes of short-duration hypoma nia that meet the full symptomatic criteria\nfor a hypomanic episode but that only last for 2\u20133 days. The episodes of hypomanic symp-\ntoms do not overlap in time with the major depressive episodes, so the disturbance does\nnot meet criteria for major depressive episode, with mixed features.\n2.Hypomanic episodes with insufficient symptoms and major depressive epi-\nsodes: A lifetime history of one or more major depressive episodes in individuals\nwhose presentation has never met full criteria for a manic or hypomanic episode but\nwho have experienced one or more episodes of hypomania that do not meet full symp-", "source": "dsm5.pdf"} {"id": "57787ab45ad6-1", "page_content": "who have experienced one or more episodes of hypomania that do not meet full symp-\ntomatic criteria (i.e., at least 4 consecutive days of elevated mood and one or two of\nthe other symptoms of a hypomanic episode, or irritable mood and two or three of the\nother symptoms of a hypomanic episode). The episodes of hypomanic symptoms do\nnot overlap in time with the major depressive episodes, so the disturbance does not\nmeet criteria for major depressive episode, with mixed features.\n3.Hypomanic episode without pr ior major depressive episode: One or more hypo-\nmanic episodes in an individual whose presentation has never met full criteria for a ma-\njor depressive episode or a manic episode. If this occurs in an individual with an\nestablished diagnosis of persistent depressive disorder (dysthymia), both diagnoses\ncan be concurrently applied during the periods when the full criteria for a hypomanic\nepisode are met.\n4.Short-duration cyclothymia (less than 24 months): Multiple episodes of hypomanic\nsymptoms that do not meet criteria for a hypomanic episode and multiple episodes of de-\npressive symptoms that do not meet criteria for a major depressive episode that persist\nover a period of less than 24 months (less than 12 months for children or adolescents)\nin an individual whose presen tation has never met full criteria for a major depressive,\nmanic, or hypomanic episode and does not meet criteria for any psychotic disorder. Dur-\ning the course of the disorder, the hypomanic or depressive symptoms are present for\nmore days than not, the individual has not been without symptoms for more than 2 months\nat a time, and the symptoms cause clinically significant distress or impairment.", "source": "dsm5.pdf"} {"id": "1ce4555bb057-0", "page_content": "Unspecified Bipolar and Related Disorder 149\nUnspecified Bipolar and Related Disorder\n296.80 (F31.9)\nThis category applies to presentations in which symptoms characteristic of a bipolar and\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any of the disorders in the bipolar and related disorders diagnostic class. The unspec-\nified bipolar and related disorder category is used in situations in which the clinician choos-\nes not to specify the reason that the criteria are not met for a specific bipolar and related\ndisorder, and includes presentations in which there is insufficient information to make a\nmore specific diagnosis (e.g., in emergency room settings).\nSpecifiers for Bipolar and Related Disorders\nSpecify if:\nWith anxious distress: The presence of at least two of the following symptoms during\nthe majority of days of the current or most recent episode of mania, hypomania, or de-\npression:\n1. Feeling keyed up or tense.\n2. Feeling unusually restless.\n3. Difficulty concentrating because of worry.\n4. Fear that something awful may happen.\n5. Feeling that the individual might lose control of himself or herself.\nSpecify current severity:\nMild: Two symptoms.\nModerate: Three symptoms.\nModerate-severe: Four or five symptoms.\nSevere: Four or five symptoms with motor agitation.\nNote: Anxious distress has been noted as a prominent feature of both bipolar and\nmajor depressive disorder in both primary care and specialty mental health set-\ntings. High levels of anxiety have been associated with higher suicide risk, longer\nduration of illness, and greater likelihood of treatment nonresponse. As a result, it\nis clinically useful to specify accurately the presence and severity levels of anxious", "source": "dsm5.pdf"} {"id": "1ce4555bb057-1", "page_content": "is clinically useful to specify accurately the presence and severity levels of anxious\ndistress for treatment planning and monitoring of response to treatment.\nWith mixed features: The mixed features specifier can apply to the current manic, hy-\npomanic, or depressive episode in bi polar I or bipolar II disorder:\nManic or hypomanic episode, with mixed features:\nA. Full criteria are met for a manic episode or hypomanic episode, and at least\nthree of the following symptoms are present during the majority of days of the\ncurrent or most recent episode of mania or hypomania:\n1. Prominent dysphoria or depressed mood as indicated by either subjective\nreport (e.g., feels sad or empty) or observation made by others (e.g., ap-\npears tearful).\n2. Diminished interest or pleasure in all, or almost all, activities (as indicated by\neither subjective account or observation made by others).\n3. Psychomotor retardation nearly every day (observable by others; not merely\nsubjective feelings of being slowed down).", "source": "dsm5.pdf"} {"id": "6f016b1aab2d-0", "page_content": "150 Bipolar and Related Disorders\n4. Fatigue or loss of energy.\n5. Feelings of worthlessness or excessive or inappropriate guilt (not merely\nself-reproach or guilt about being sick).\n6. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ide-\nation without a specific plan, or a suicide attempt or a specific plan for com-\nmitting suicide.\nB. Mixed symptoms are observable by others and represent a change from the\nperson\u2019s usual behavior.\nC. For individuals whose symptoms meet full episode criteria for both mania and\ndepression simultaneously, the diagnosis should be manic episode, with mixed\nfeatures, due to the marked impairment and clinical severity of full mania.\nD. The mixed symptoms are not attributable to the physiological effects of a sub-\nstance (e.g., a drug of abuse, a medication, other treatment).\nDepressive episode, wit h mixed features: \nA. Full criteria are met for a major depressive episode, and at least three of the fol-\nlowing manic/hypomanic symptoms are present during the majority of days of\nthe current or most recent episode of depression:\n1. Elevated, expansive mood.\n2. Inflated self-esteem or grandiosity.\n3. More talkative than usual or pressure to keep talking.\n4. Flight of ideas or subjective experience that thoughts are racing.\n5. Increase in energy or goal-directed activity (either socially, at work or school,\nor sexually).\n6. Increased or excessive involvement in activities that have a high potential\nfor painful consequences (e.g., engaging in unrestrained buying sprees,\nsexual indiscretions, or foolish business investments).\n7. Decreased need for sleep (feeling rested despite sleeping less than usual;\nto be contrasted with insomnia).\nB. Mixed symptoms are observable by others and represent a change from the", "source": "dsm5.pdf"} {"id": "6f016b1aab2d-1", "page_content": "B. Mixed symptoms are observable by others and represent a change from the\nperson\u2019s usual behavior.\nC. For individuals whose symptoms meet full episode criteria for both mania and\ndepression simultaneously, the diagnosis should be manic episode, with mixed\nfeatures.\nD. The mixed symptoms are not attributable to the physiological effects of a sub-\nstance (e.g., a drug of abuse, a medication, or other treatment).\nNote: Mixed features associated with a major depressive episode have been found\nto be a significant risk factor for the development of bipolar I or bipolar II disorder.\nAs a result, it is clinically useful to note the presence of this specifier for treatment\nplanning and monitoring of response to treatment.\nWith rapid cycling (can be applied to bipolar I or bipolar II disorder): Presence of at\nleast four mood episodes in the previous 12 months that meet the criteria for manic,\nhypomanic, or major depressive episode.\nNote: Episodes are demarcated by either partial or full remissions of at least 2 months\nor a switch to an episode of the opposite polarity (e.g., major depressive episode to\nmanic episode).\nNote: The essential feature of a rapid-cycli ng bipolar disorder is the occurrence of\nat least four mood episodes during the previous 12 months. These episodes can\noccur in any combination and order. The episodes must meet both the duration and", "source": "dsm5.pdf"} {"id": "2f5a27e0948d-0", "page_content": "Specifiers for Bipolar and Related Disorders 151\nsymptom number criteria for a major depressive, manic, or hypomanic episode and\nmust be demarcated by either a period of full remission or a switch to an episode\nof the opposite polarity. Manic and hypomanic episodes are counted as being on\nthe same pole. Except for the fact that they occur more frequently, the episodes that\noccur in a rapid-cycling pattern are no different from those that occur in a non-rapid-\ncycling pattern. Mood episodes that count toward defining a rapid-cycling pattern\nexclude those episodes directly caused by a substance (e.g., cocaine, corticoste-\nroids) or another medical condition.\nWith melancholic features:\nA. One of the following is present during the most severe period of the current episode:\n1. Loss of pleasure in all, or almost all, activities.\n2. Lack of reactivity to usually pleasurable stimuli (does not feel much better, even\ntemporarily, when something good happens).\nB. Three (or more) of the following:\n1. A distinct quality of depressed mood characterized by profound despondency,\ndespair, and/or moroseness or by so-called empty mood.\n2. Depression that is regularly worse in the morning.\n3. Early-morning awakening (i.e., at least 2 hours before usual awakening).\n4. Marked psychomotor agitation or retardation.\n5. Significant anorexia or weight loss.\n6. Excessive or inappropriate guilt.\nNote: The specifier \u201cwith melancholic features\u201d is applied if these features are pres-\nent at the most severe stage of the episode. There is a near-complete absence of\nthe capacity for pleasure, not merely a diminution. A guideline for evaluating the\nlack of reactivity of mood is that even highly desired events are not associated with", "source": "dsm5.pdf"} {"id": "2f5a27e0948d-1", "page_content": "lack of reactivity of mood is that even highly desired events are not associated with\nmarked brightening of mood. Either mood does not brighten at all, or it brightens\nonly partially (e.g., up to 20%\u201340% of normal for only minutes at a time). The \u201cdis-\ntinct quality\u201d of mood that is characteristic of the \u201cwith melancholic features\u201d speci-\nfier is experienced as qualitatively different from that during a nonmelancholic\ndepressive episode. A depressed mood that is described as merely more severe,\nlonger lasting, or present without a reason is not considered distinct in quality. Psy-\nchomotor changes are nearly always present and are observable by others.\nMelancholic features exhibit only a modest tendency to repeat across episodes\nin the same individual. They are more frequent in inpatients, as opposed to outpa-\ntients; are less likely to occur in milder than in more severe major depressive epi-\nsodes; and are more likely to occur in those with psychotic features.\nWith atypical features: This specifier can be applied when these features predomi-\nnate during the majority of days of the current or most recent major depressive epi-\nsode. \nA. Mood reactivity (i.e., mood brightens in response to actual or potential positive\nevents).\nB. Two (or more) of the following features: \n1. Significant weight gain or increase in appetite.\n2. Hypersomnia.\n3. Leaden paralysis (i.e., heavy, leaden feelings in arms or legs).\n4. A long-standing pattern of interpersonal rejection sensitivity (not limited to epi-\nsodes of mood disturbance) that results in significant social or occupational\nimpairment.", "source": "dsm5.pdf"} {"id": "92833b75624f-0", "page_content": "152 Bipolar and Related Disorders\nC. Criteria are not met for \u201cwith melancholic features\u201d or \u201cwith catatonia\u201d during the\nsame episode.\nNote: \u201cAtypical depression\u201d has historical significance (i.e., atypical in contradis-\ntinction to the more classical agitated, \u201cendogenous\u201d presentations of depression\nthat were the norm when depression was rarely diagnosed in outpatients and al-\nmost never in adolescents or younger adults) and today does not connote an un-\ncommon or unusual clinical presentation as the term might imply.\nMood reactivity is the capacity to be cheered up when presented with positive\nevents (e.g., a visit from children, compliments from others). Mood may become\neuthymic (not sad) even for extended periods of time if the external circumstances\nremain favorable. Increased appetite may be manifested by an obvious increase in\nfood intake or by weight gain. Hypersomnia may include either an extended period\nof nighttime sleep or daytime napping that totals at least 10 hours of sleep per day\n(or at least 2 hours more than when not depressed). Leaden paralysis is defined as\nfeeling heavy, leaden, or weighted down, usually in the arms or legs. This sensation\nis generally present for at least an hour a day but often lasts for many hours at a\ntime. Unlike the other atypical features, pathological sensitivity to perceived inter-\npersonal rejection is a trait that has an early onset and persists throughout most of\nadult life. Rejection sensitivity occurs both when the person is and is not depressed,\nthough it may be exacerbated during depressive periods.\nWith psychotic features: Delusions or hallucinations are present at any time in the\nepisode. If psychotic features are present, specify if mood-congruent or mood-incon-\ngruent:\nWith mood-congruent psychotic features: During manic episodes, the con-", "source": "dsm5.pdf"} {"id": "92833b75624f-1", "page_content": "gruent:\nWith mood-congruent psychotic features: During manic episodes, the con-\ntent of all delusions and hallucinations is consistent with the typical manic\nthemes of grandiosity, invulnerability, etc., but may also include themes of sus-\npiciousness or paranoia, especially with respect to others\u2019 doubts about the in-\ndividual\u2019s capacities, accomplishments, and so forth.\nWith mood-incongruent psychotic features: The content of delusions and\nhallucinations is inconsistent with the episode polarity themes as described\nabove, or the content is a mixture of mood-incongruent and mood-congruent\nthemes.\nWith catatonia: This specifier can apply to an episode of mania or depression if cata-\ntonic features are present during most of the episode. See criteria for catatonia asso-\nciated with a mental disorder in the chapter \u201cSchizophrenia Spectrum and Other\nPsychotic Disorders.\u201d\nWith peripartum onset: This specifier can be applied to the current or, if the full crite-\nria are not currently met for a mood episode, most recent episode of mania, hypoma-\nnia, or major depression in bipolar I or bipol ar II disorder if onset of mood symptoms\noccurs during pregnancy or in the 4 weeks following delivery.\nNote: Mood episodes can have their onset either during pregnancy or postpartum.\nAlthough the estimates differ according to the period of follow-up after delivery, be-\ntween 3% and 6% of women will experience the onset of a major depressive epi-\nsode during pregnancy or in the weeks or months following delivery. Fifty percent\nof \u201cpostpartum\u201d major depressive episodes actually begin prior to delivery. Thus,\nthese episodes are referred to collectively as peripartum episodes. Women with", "source": "dsm5.pdf"} {"id": "92833b75624f-2", "page_content": "these episodes are referred to collectively as peripartum episodes. Women with\nperipartum major depressive episodes often have severe anxiety and even panic\nattacks. Prospective studies have demonstrated that mood and anxiety symptoms\nduring pregnancy, as well as the \u201cbaby blues,\u201d increase the risk for a postpartum\nmajor depressive episode.", "source": "dsm5.pdf"} {"id": "b9c1e8465bfb-0", "page_content": "Specifiers for Bipolar and Related Disorders 153\nPeripartum-onset mood episodes can pres ent either with or without psychotic\nfeatures. Infanticide is most often associated with postpartum psychotic episodes\nthat are characterized by command hallucinations to kill the infant or delusions that\nthe infant is possessed, but psychotic symptoms can also occur in severe postpar-\ntum mood episodes without such specific delusions or hallucinations.\nPostpartum mood (major depressive or manic) episodes with psychotic features\nappear to occur in from 1 in 500 to 1 in 1,000 deliveries and may be more common\nin primiparous women. The risk of postpartum episodes with psychotic features is\nparticularly increased for women with prior postpartum mood episodes but is also\nelevated for those with a prior history of a depressive or bipolar disorder (especially\nbipolar I disorder) and those with a family history of bipolar disorders.\nOnce a woman has had a postpartum episode with psychotic features, the risk\nof recurrence with each subsequent delivery is between 30% and 50%. Postpartum\nepisodes must be differentiated from delirium occurring in the postpartum period,\nwhich is distinguished by a fluctuating level of awareness or attention. The postpar-\ntum period is unique with respect to the degree of neuroendocrine alterations and\npsychosocial adjustments, the potential impact of breast-feeding on treatment plan-\nning, and the long-term implications of a history of postpartum mood disorder on sub-\nsequent family planning.\nWith seasonal pattern: This specifier applies to the lifetime pattern of mood episodes.\nThe essential feature is a regular seasonal pattern of at least one type of episode (i.e.,\nmania, hypomania, or depression). The other types of episodes may not follow this pat-", "source": "dsm5.pdf"} {"id": "b9c1e8465bfb-1", "page_content": "tern. For example, an individual may have seasonal manias, but his or her depressions\ndo not regularly occur at a specific time of year.\nA. There has been a regular temporal relationship between the onset of manic, hypo-\nmanic, or major depressive episodes and a particular time of the year (e.g., in the\nfall or winter) in bipolar I or bipolar II disorder.\nNote: Do not include cases in which there is an obvious effect of seasonally related\npsychosocial stressors (e.g., regularly being unemployed every winter). \nB. Full remissions (or a change from major depression to mania or hypomania or vice\nversa) also occur at a characteristic time of the year (e.g., depression disappears\nin the spring).\nC. In the last 2 years, the individual\u2019s manic, hypomanic, or major depressive episodes\nhave demonstrated a temporal seasonal relationship, as defined above, and no\nnon-seasonal episodes of that polarity have occurred during that 2-year period.\nD. Seasonal manias, hypomanias, or depressions (as described above) substantially\noutnumber any nonseasonal manias, hypomanias, or depressions that may have\noccurred over the individual\u2019s lifetime.\nNote: This specifier can be applied to the pattern of major depressive episodes in\nbipolar I disorder, bipolar II disorder, or major depressive disorder, recurrent. The\nessential feature is the onset and remission of major depressive episodes at char-\nacteristic times of the year. In most cases, the episodes begin in fall or winter and\nremit in spring. Less commonly, there may be recurrent summer depressive epi-\nsodes. This pattern of onset and remission of episodes must have occurred during\nat least a 2-year period, without any nonseasonal episodes occurring during this", "source": "dsm5.pdf"} {"id": "b9c1e8465bfb-2", "page_content": "at least a 2-year period, without any nonseasonal episodes occurring during this\nperiod. In addition, the seasonal depressi ve episodes must substantially outnum-\nber any nonseasonal depressive episodes over the individual\u2019s lifetime.\nThis specifier does not apply to those situations in which the pattern is better ex-\nplained by seasonally linked psychosocial stressors (e.g., seasonal unemployment\nor school schedule). Major depressive episodes that occur in a seasonal pattern", "source": "dsm5.pdf"} {"id": "ebf473c1e74d-0", "page_content": "154 Bipolar and Related Disorders\nare often characterized by prominent energy, hypersomnia, overeating, weight\ngain, and a craving for carbohydrates. It is unclear whether a seasonal pattern is\nmore likely in recurrent major depressive di sorder or in bipolar disorders. However,\nwithin the bipolar disorders group, a seasonal pattern appears to be more likely in\nbipolar II disorder than in bipolar I disorder. In some individuals, the onset of manic\nor hypomanic episodes may also be linked to a particular season.\nThe prevalence of winter-type seasonal pattern appears to vary with latitude,\nage, and sex. Prevalence increases with higher latitudes. Age is also a strong pre-\ndictor of seasonality, with younger persons at higher risk for winter depressive epi-\nsodes.\nSpecify if:\nIn partial remission: Symptoms of the immediately previous manic, hypomanic, or\ndepressive episode are present, but full criteria are not met, or there is a period lasting\nless than 2 months without any significant symptoms of a manic, hypomanic, or major\ndepressive episode following the end of such an episode.\nIn full remission: During the past 2 months, no significant signs or symptoms of the\ndisturbance were present.\nSpecify current severity: \nSeverity is based on the number of criterion symptoms, the severity of those symptoms,\nand the degree of functional disability.\nMild: Few, if any, symptoms in excess of those required to meet the diagnostic criteria\nare present, the intensity of the symptoms is distressing but manageable, and the\nsymptoms result in minor impairment in social or occupational functioning.\nModerate: The number of symptoms, intensity of symptoms, and/or functional impair-\nment are between those specified for \u201cmild\u201d and \u201csevere.\u201d", "source": "dsm5.pdf"} {"id": "ebf473c1e74d-1", "page_content": "ment are between those specified for \u201cmild\u201d and \u201csevere.\u201d\nSevere: The number of symptoms is substantially in excess of those required to make\nthe diagnosis, the intensity of the symptoms is seriously distressing and unmanage-\nable, and the symptoms markedly interfere with social and occupational functioning.", "source": "dsm5.pdf"} {"id": "32955d78f17a-0", "page_content": "155Depressive\nDisorders\nDepressive disorders include disruptive mood dysregulation disorder, major\ndepressive disorder (including major depressive episode), persistent depressive disorder\n(dysthymia), premenstrual dysphoric disord er, substance/medication-induced depres-\nsive disorder, depressive disord er due to another medical co ndition, other specified de-\npressive disorder, and unspec ified depressive disorder. Unlike in DSM-IV, this chapter\n\u201cDepressive Disorders\u201d has been separated fr om the previous chapter \u201cBipolar and Re-\nlated Disorders.\u201d The common feature of all of these disorders is the presence of sad,\nempty, or irritable mood, accompanied by somatic and cognitive changes that signifi-\ncantly affect the individual\u2019s capacity to function. What differs among them are issues of\nduration, timing, or presumed etiology. \nIn order to address concerns about the pote ntial for the overdiagnosis of and treatment\nfor bipolar disorder in children, a new diagno sis, disruptive mood dysregulation disorder,\nreferring to the presentation of children wi th persistent irritability and frequent episodes\nof extreme behavioral dyscontrol, is added to the depressive disorders for children up to\n12 years of age. Its placement in this chapter reflects the finding that children with this\nsymptom pattern typica lly develop unipolar depressive disorders or anxiety disorders,\nrather than bipolar disorders, as they mature into adolescence and adulthood.\nMajor depressive disorder represents the clas sic condition in this gr oup of disorders. It\nis characterized by discrete episodes of at least 2 weeks\u2019 duration (although most episodes\nlast considerably longer) involving clear-cut changes in affect, cogn ition, and neurovege-\ntative functions and inter-episode remissions. A diagnosis based on a single episode is", "source": "dsm5.pdf"} {"id": "32955d78f17a-1", "page_content": "tative functions and inter-episode remissions. A diagnosis based on a single episode is\npossible, although the disorder is a recurrent one in the majori ty of cases. Careful consid-\neration is given to the delineation of normal sadness and grief from a major depressive ep-\nisode. Bereavement may induce great suffering, but it does not typically induce an episode\nof major depressive disorder. When they do occur together, the depressive symptoms and\nfunctional impairment tend to be more seve re and the prognosis is worse compared with\nbereavement that is not accompanied by majo r depressive disorder. Bereavement-related\ndepression tends to occur in persons with other vulnerabilities to depressive disorders,\nand recovery may be facilitated by antidepressant treatment.\nA more chronic form of depression, persiste nt depressive disorder (dysthymia), can be\ndiagnosed when the mood disturbance continues for at least 2 years in adults or 1 year in\nchildren. This diagnosis, new in DSM-5, includes both the DSM-IV diagnostic categories of\nchronic major depression and dysthymia.\nAfter careful scientific review of the evid ence, premenstrual dy sphoric disorder has\nbeen moved from an appendix of DSM-IV (\u201c Criteria Sets and Axes Provided for Further\nStudy\u201d) to Section II of DSM-5. Almost 20 years of additional of research on this condition\nhas confirmed a specific and treatment-responsi ve form of depressive disorder that begins\nsometime following ovulation and remits within a few days of menses and has a marked\nimpact on functioning.\nA large number of substances of abuse, some prescribed medi cations, and several\nmedical conditions can be associated with de pression-like phenomena. This fact is recog-\nnized in the diagnoses of substance/medicati on-induced depressive disorder and depres-", "source": "dsm5.pdf"} {"id": "32955d78f17a-2", "page_content": "nized in the diagnoses of substance/medicati on-induced depressive disorder and depres-\nsive disorder due to an other medical condition.", "source": "dsm5.pdf"} {"id": "24d4edec834b-0", "page_content": "156 Depressive Disorders\nDisruptive Mood Dysregulation Disorder\nDiagnostic Criteria 296.99 (F34.8)\nA. Severe recurrent temper outbursts manifested verbally (e.g., verbal rages) and/or be-\nhaviorally (e.g., physical aggression toward people or property) that are grossly out of\nproportion in intensity or duration to the situation or provocation. \nB. The temper outbursts are inconsistent with developmental level.\nC. The temper outbursts occur, on aver age, three or more times per week.\nD. The mood between temper outbursts is persistently irritable or angry most of the day,\nnearly every day, and is observable by others (e.g., parents, teachers, peers).\nE. Criteria A\u2013D have been present for 12 or more months. Throughout that time, the indi-\nvidual has not had a period lasting 3 or more consecutive months without all of the\nsymptoms in Criteria A\u2013D.\nF. Criteria A and D are present in at least two of three settings (i.e., at home, at school,\nwith peers) and are severe in at least one of these.\nG. The diagnosis should not be made for the first time before age 6 years or after age 18\nyears. \nH. By history or observation, the age at onset of Criteria A\u2013E is before 10 years.\nI. There has never been a distinct period lasting more than 1 day during which the full\nsymptom criteria, except duration, fo r a manic or hypomanic episode have been met.\nNote: Developmentally appropriate mood elevation, such as occurs in the context of a\nhighly positive event or its anticipation, should not be considered as a symptom of ma-\nnia or hypomania.", "source": "dsm5.pdf"} {"id": "24d4edec834b-1", "page_content": "nia or hypomania.\nJ. The behaviors do not occur exclusively during an episode of major depressive disorder\nand are not better explained by another mental disorder (e.g., autism spectrum disor-\nder, posttraumatic stress disorder, separat ion anxiety disorder, persistent depressive\ndisorder [dysthymia]).\nNote: This diagnosis cannot coexist with oppositional defiant disorder, intermittent ex-\nplosive disorder, or bipolar disorder, though it can coexist with others, including major\ndepressive disorder, attention-deficit/hy peractivity disorder, conduct disorder, and\nsubstance use disorders. Individuals whose symptoms meet criteria for both disruptive\nmood dysregulation disorder and oppositional defiant disorder should only be given the\ndiagnosis of disruptive mood dysregulation disorder. If an individual has ever experi-\nenced a manic or hypomanic episode, the diagnosis of disruptive mood dysregulation\ndisorder should not be assigned. \nK. The symptoms are not attributable to the physiological effects of a substance or to an-\nother medical or neurological condition.\nDiagnostic Features\nThe core feature of disruptive mood dysregulat ion disorder is chronic, severe persistent ir-\nritability. This severe irritability has two prominent clinical mani festations, the first of\nwhich is frequent temper outbursts. These ou tbursts typically occur in response to frus-\ntration and can be verbal or behavioral (the la tter in the form of aggression against prop-\nerty, self, or others). They must occur frequent ly (i.e., on average, three or more times per\nweek) (Criterion C) over at least 1 year in at least two settings (Criteria E and F), such as in\nthe home and at school, and th ey must be developmentally inappropriate (Criterion B).", "source": "dsm5.pdf"} {"id": "24d4edec834b-2", "page_content": "the home and at school, and th ey must be developmentally inappropriate (Criterion B).\nThe second manifestation of severe irritability consists of chronic, persistently irritable or\nangry mood that is present between the severe temper outbursts. This irritable or angry\nmood must be characteristic of the child, bein g present most of the day, nearly every day,\nand noticeable by others in the child\u2019s environment (Criterion D).", "source": "dsm5.pdf"} {"id": "65d8bb6ba44b-0", "page_content": "Disruptive Mood Dysregulation Disorder 157\nThe clinical presentation of disruptive mo od dysregulation disord er must be carefully\ndistinguished from presentations of other, re lated conditions, particularly pediatric bi-\npolar disorder. In fact, disruptive mood dy sregulation disorder was added to DSM-5 to\naddress the considerable concern about the appropriate classification and treatment of\nchildren who present with chronic, persistent irritability relative to children who present\nwith classic (i.e., episo dic) bipolar disorder. \nSome researchers view severe, non-episodic ir ritability as characteristic of bipolar dis-\norder in children, although both DSM-IV and DSM-5 require that both children and adults\nhave distinct episodes of mania or hypomania to qualify for the diagnosis of bipolar I dis-\norder. During the latter decades of the 20th century, this contention by researchers that\nsevere, nonepisodic irritability is a manifestat ion of pediatric mania coincided with an up-\nsurge in the rates at which clinicians assigned the diagnosis of bipolar disorder to their\npediatric patients. This sharp increase in rates appears to be attributab le to clinicians com-\nbining at least two clinical presentations into a single category. That is, both classic, epi-\nsodic presentations of mania and non-episodic presentations of severe irritability have\nbeen labeled as bipolar disorder in children. In DSM-5, the term bipolar disorder is explicitly\nreserved for episodic presentations of bipolar symptoms. DSM-IV did not include a diagno-\nsis designed to capture youths whose hallmar k symptoms consisted of very severe, non-\nepisodic irritability, whereas DSM-5, with the inclusion of disruptive mood dysregulation\ndisorder, provides a distinct ca tegory for such presentations. \nPrevalence", "source": "dsm5.pdf"} {"id": "65d8bb6ba44b-1", "page_content": "disorder, provides a distinct ca tegory for such presentations. \nPrevalence\nDisruptive mood dysregulatio n disorder is common among children presenting to pedi-\natric mental health clinics. Prevalence estima tes of the disorder in the community are un-\nclear. Based on rates of chronic and severe pe rsistent irritability, which is the core feature\nof the disorder, the overall 6-month to 1-year period-prevale nce of disruptive mood dys-\nregulation disorder among children and adolescents probably falls in the 2%\u20135% range.\nHowever, rates are expected to be higher in males and school-age children than in females\nand adolescents. \nDevelopment and Course\nThe onset of disruptive mood dysregulation diso rder must be before age 10 years, and the\ndiagnosis should not be applied to children with a developmental age of less than 6 years.\nIt is unknown whether the condition presents only in this age-delimited fashion. Because\nthe symptoms of disruptive mood dysregulat ion disorder are likely to change as children\nmature, use of the diagnosis shou ld be restricted to age grou ps similar to those in which\nvalidity has been established (7\u201318 years). A pproximately half of children with severe,\nchronic irritability will have a presentation that continues to meet crit eria for the condition\n1 year later. Rates of conversion from seve re, nonepisodic irritability to bipolar disorder\nare very low. Instead, children with chronic irritability are at risk to develop unipolar de-\npressive and/or anxiety disorders in adulthood. \nAge-related variations also differentiate cl assic bipolar disorder and disruptive mood\ndysregulation disorder. Rates of bipolar disorder generally are very low prior to adoles-", "source": "dsm5.pdf"} {"id": "65d8bb6ba44b-2", "page_content": "dysregulation disorder. Rates of bipolar disorder generally are very low prior to adoles-\ncence (<1%), with a steady increase into early adulthood (1%\u20132% prevalence). Disruptive\nmood dysregulation disorder is more common th an bipolar disorder prior to adolescence,\nand symptoms of the condition generally be come less common as children transition into\nadulthood. \nRisk and Prognostic Factors \nTemperamental. Children with chronic irritability typically exhibit complicated psy-\nchiatric histories. In such children, a relati vely extensive history of chronic irritability is", "source": "dsm5.pdf"} {"id": "e250f6d47ecf-0", "page_content": "158 Depressive Disorders\ncommon, typically manifesting be fore full criteria for the syndrome are met. Such predi-\nagnostic presentations may have qualified for a diagnosis of oppositional defiant disorder.\nMany children with disruptive mood dysregulation disorder have symptoms that also\nmeet criteria for atte ntion-deficit/hyperactivity disorder (ADHD) and for an anxiety dis-\norder, with such diagnoses often being presen t from a relatively early age. For some chil-\ndren, the criteria for major depres sive disorder may also be met. \nGenetic and physiological. In terms of familial aggregat ion and genetics, it has been\nsuggested that children presenting with chronic, non-episodic irritability can be differen-\ntiated from children with bipolar disorder in their family-based risk. However, these two\ngroups do not differ in familial rates of anxi ety disorders, unipolar depressive disorders,\nor substance abuse. Compared with children with pediatric bipolar disorder or other men-\ntal illnesses, those with disruptive mood dy sregulation disorder exhibit both commonal-\nities and differences in information-proce ssing deficits. For example, face-emotion\nlabeling deficits, as well as perturbed decision making and cognitive control, are present in\nchildren with bipolar disorder and chronica lly irritable children, as well as in children\nwith some other psychiatric conditions. There is also evidence for disorder-specific dys-\nfunction, such as during tasks assessing atte ntion deployment in response to emotional\nstimuli, which has demonstrated unique signs of dysfunction in children with chronic ir-\nritability. \nGender-Related Diagnostic Issues\nChildren presenting to clinics with features of disruptive mood dysr egulation disorder are\npredominantly male. Among co mmunity samples, a male pr eponderance appears to be", "source": "dsm5.pdf"} {"id": "e250f6d47ecf-1", "page_content": "supported. This difference in prevalence betw een males and females differentiates disrup-\ntive mood dysregulation disord er from bipolar disorder, in which there is an equal gender\nprevalence.\nSuicide Risk\nIn general, evidence documenting suicidal be havior and aggression, as well as other se-\nvere functional consequences, in disruptive mood dysregulation diso rder should be noted\nwhen evaluating children with chronic irritability. \nFunctional Consequences of \nDisruptive Mood Dy sregulation Disorder\nChronic, severe irritability, su ch as is seen in disruptive mood dysregulation disorder, is\nassociated with marked disruption in a child\u2019 s family and peer relationships, as well as in\nschool performance. Because of their extrem ely low frustration tole rance, such children\ngenerally have difficulty succeeding in school; they are often unable to participate in the\nactivities typically enjoyed by healthy children; their family life is severely disrupted by\ntheir outbursts and irritability; and they have trouble initiating or sustaining friendships.\nLevels of dysfunction in childr en with bipolar disorder and disruptive mood dysregulation\ndisorder are generally comparable. Both condit ions cause severe disruption in the lives of\nthe affected individual and their families. In both disruptive mood dysregulation disorder\nand pediatric bipolar disorder, dangerous behavi or, suicidal ideation or suicide attempts,\nsevere aggression, and psychiatric hospitalization are common.\nDifferential Diagnosis\nBecause chronically irritable children and adolescents typically present with complex histo-\nries, the diagnosis of disruptive mood dysreg ulation disorder must be made while consid-\nering the presence or absence of multiple ot her conditions. Despite the need to consider", "source": "dsm5.pdf"} {"id": "8eda742a2f8c-0", "page_content": "Disruptive Mood Dysregulation Disorder 159\nmany other syndromes, differentiation of disr uptive mood dysregulation disorder from bi-\npolar disorder and oppositional defiant disorder requires pa rticularly careful assessment. \nBipolar disorders. The central feature differentiating disruptive mood dysregulation disor-\nder and bipolar disorders in children involves the longitudinal course of the core symptoms. In\nchildren, as in adults, bipolar I disorder and bipo lar II disorder manifest as an episodic illness\nwith discrete episodes of mood perturbation that can be differentiated from the child\u2019s typical\npresentation. The mood perturbation that occurs during a manic episode is distinctly different\nfrom the child\u2019s usual mood. In addition, during a manic episode, the change in mood must be\naccompanied by the onset, or worsening, of associated cognitive, behavioral, and physical\nsymptoms (e.g., distractibility, increased goal-dir ected activity), which are also present to a de-\ngree that is distinctly different from the child\u2019s usual baseline. Thus, in the case of a manic ep-\nisode, parents (and, depending on developmental level, children) should be able to identify a\ndistinct time period during which the child\u2019s mood and behavior were markedly different\nfrom usual. In contrast, the irritability of disr uptive mood dysregulation disorder is persistent\nand is present over many months; while it may wax and wane to a certain degree, severe irri-\ntability is characteristic of the child with disr uptive mood dysregulation disorder. Thus, while\nbipolar disorders are episodic conditions, disrup tive mood dysregulation disorder is not. In\nfact, the diagnosis of di sruptive mood dysregulation disorder cannot be assi gned to a child", "source": "dsm5.pdf"} {"id": "8eda742a2f8c-1", "page_content": "who has ever experienced a full-duration hypoma nic or manic episode (irritable or euphoric)\nor who has ever had a manic or hypomanic epis ode lasting more than 1 day. Another central\ndifferentiating feature between bipolar disorder s and disruptive mood dysregulation disorder\nis the presence of elevated or expansive mood and grandiosity. These symptoms are common\nfeatures of mania but are not characteristic of disruptive mood dy sregulation disorder. \nOppositional defiant disorder. While symptoms of opposition al defiant disorder typi-\ncally do occur in children with disruptive mood dysregulation disorder, mood symptoms\nof disruptive mood dysregulation disorder ar e relatively rare in children with opposi-\ntional defiant disorder. The key features that warrant the diagnosis of disruptive mood\ndysregulation disorder in children whose sympto ms also meet criteria for oppositional de-\nfiant disorder are the presence of severe an d frequently recurrent outbursts and a persis-\ntent disruption in mood betw een outbursts. In addition, the diagnosis of disruptive mood\ndysregulation disorder requires severe impairment in at least one setting (i.e., home,\nschool, or among peers) and mild to moderate impairment in a second setting. For this rea-\nson, while most children whose symptoms meet criteria for disrup tive mood dysregula-\ntion disorder will also have a presentation that meets criteria fo r oppositional defiant\ndisorder, the reverse is not the case. That is, in only approximately 15% of individuals with\noppositional defiant disorder would criteria for disruptive mood dysregulation disorder\nbe met. Moreover, even for child ren in whom criteria for both disorders are met, only the\ndiagnosis of disruptive mood dysregulation disorder should be made. Finally, both the", "source": "dsm5.pdf"} {"id": "8eda742a2f8c-2", "page_content": "diagnosis of disruptive mood dysregulation disorder should be made. Finally, both the\nprominent mood symptoms in disruptive mood dysregulation disorder and the high risk\nfor depressive and anxiety disorders in follow -up studies justify placement of disruptive\nmood dysregulation disorder among the depr essive disorders in DSM-5. (Oppositional\ndefiant disorder is included in the chapter \u201cDisruptive, Impulse-Control, and Conduct\nDisorders.\u201d) This reflects the more prominent mood comp onent among individuals with", "source": "dsm5.pdf"} {"id": "f18fda3aeb89-0", "page_content": "defiant disorder is included in the chapter \u201cDisruptive, Impulse-Control, and Conduct\nDisorders.\u201d) This reflects the more prominent mood comp onent among individuals with\ndisruptive mood dysregulation disorder, as compared with individuals with oppositional\ndefiant disorder. Nevertheless, it also should be noted that disruptive mood dysregulation\ndisorder appears to carry a high risk for be havioral pr oblems as well as mood problems.\nAttention-deficit/hyperactivity disorder, ma jor depressive disorder, anxiety disorders,\nand autism spectrum disorder. Unlike children diagnosed with bipolar disorder or op-\npositional defiant disorder, a child whose sy mptoms meet criteria for disruptive mood\ndysregulation disorder also can receive a co morbid diagnosis of ADHD, major depressive\ndisorder, and/or anxiety disorder. However, children whose irritability is present only in\nthe context of a major depressive episode or persistent depressive disorder (dysthymia)", "source": "dsm5.pdf"} {"id": "2e6a060f38ca-0", "page_content": "160 Depressive Disorders\nshould receive one of those di agnoses rather than disrupti ve mood dysregulation disor-\nder. Children with disruptive mood dysregul ation disorder may have symptoms that also\nmeet criteria for an anxiety disorder and can receive both diagnoses, but children whose ir-\nritability is manifest only in the context of exacerbation of an anxiety disorder should re-\nceive the relevant anxiety disorder diagnosis rather than disruptive mood dysregulation\ndisorder. In addition, children with autism spectrum diso rders frequently present with\ntemper outbursts when, for example, their rout ines are disturbed. In that instance, the\ntemper outbursts would be considered secondary to the au tism spectrum disorder, and\nthe child should not receive the diagnosis of disruptive mood dysregulation disorder. \nIntermittent explosive disorder. Children with symptoms su ggestive of intermittent\nexplosive disorder present with instances of severe temper outburst s, much like children\nwith disruptive mood dysregulation disorder. However, unlike disruptive mood dysreg-\nulation disorder, intermittent explosive disorder does not re quire persistent disruption in\nmood between outbursts. In addition, intermittent explosive disorder requires only 3 months\nof active symptoms, in contrast to the 12- month requirement for disruptive mood dys-\nregulation disorder. Thus, these two diagnoses should not be made in the same child. For\nchildren with outbursts and intercurrent, persis tent irritability, only the diagnosis of dis-\nruptive mood dysregulation disorder should be made. \nComorbidity\nRates of comorbidity in disruptive mood dysr egulation disorder are extremely high. It is\nrare to find individuals whose symptoms meet criteria for disrupti ve mood dysregulation\ndisorder alone. Comorbidity between disrupti ve mood dysregulatio n disorder and other", "source": "dsm5.pdf"} {"id": "2e6a060f38ca-1", "page_content": "DSM-defined syndromes appears higher than for many other pediatric mental illnesses;\nthe strongest overlap is with oppositional de fiant disorder. Not only is the overall rate of\ncomorbidity high in disruptive mood dysregul ation disorder, but also the range of comor-\nbid illnesses appears particularly diverse. These children typically present to the clinic\nwith a wide range of disruptive behavior , mood, anxiety, and even autism spectrum\nsymptoms and diagnoses. Howe ver, children with disruptive mood dysregulation disor-\nder should not have symptoms that meet criter ia for bipolar disorder, as in that context,\nonly the bipolar disorder di agnosis should be made. If children have symptoms that meet\ncriteria for oppositional defiant disorder or intermittent explosive disorder and disruptive\nmood dysregulation disorder, only the diagnosis of disruptive mood dysregulation disor-\nder should be assigned. Also, as noted earlier, the diagnosis of disruptive mood dysregu-\nlation disorder should not be assigned if the symptoms occur only in an anxiety-\nprovoking context, when the routines of a ch ild with autism spectrum disorder or obses-\nsive-compulsive disorder are disturbed, or in the context of a major depressive episode.\nMajor Depressive Disorder\nDiagnostic Criteria\nA. Five (or more) of the following symptoms have been present during the same 2-week\nperiod and represent a change from previous functioning; at least one of the symptoms\nis either (1) depressed mood or (2) loss of interest or pleasure.\nNote: Do not include symptoms that are clearly attributable to another medical condition.\n1. Depressed mood most of the day, nearly every day, as indicated by either subjec-\ntive report (e.g., feels sad, empty, hopeless) or observation made by others (e.g.,", "source": "dsm5.pdf"} {"id": "2e6a060f38ca-2", "page_content": "appears tearful). ( Note: In children and adolescents, can be irritable mood.)\n2. Markedly diminished interest or pleasure in al l, or almost all, activities most of the\nday, nearly every day (as indicated by either subjective account or observation).", "source": "dsm5.pdf"} {"id": "947b12979bba-0", "page_content": "Major Depressive Disorder 161\n3. Significant weight loss when not dieting or weight gain (e.g., a change of more than\n5% of body weight in a month), or decreas e or increase in appetite nearly every day.\n(Note: In children, consider failure to make expected weight gain.)\n4. Insomnia or hypersomnia nearly every day.\n5. Psychomotor agitation or retardation nearly every day (observable by others, not\nmerely subjective feelings of restlessness or being slowed down).\n6. Fatigue or loss of energy nearly every day.\n7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delu-\nsional) nearly every day (not merely self-reproach or guilt about being sick).\n8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (ei-\nther by subjective account or as observed by others).\n9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation with-\nout a specific plan, or a suicide attempt or a specific plan for committing suicide.\nB. The symptoms cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nC. The episode is not attributable to the physiological effects of a substance or to another\nmedical condition. \nNote: Criteria A\u2013C represent a major depressive episode.\nNote: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a nat-\nural disaster, a serious medical illness or disa bility) may include the feelings of intense sad-\nness, rumination about the loss, insomnia, poor appetite, and weight loss noted in Criterion A,\nwhich may resemble a depressive episode. Although such symptoms may be understand-\nable or considered appropriate to the loss, the presence of a major depressive episode in", "source": "dsm5.pdf"} {"id": "947b12979bba-1", "page_content": "able or considered appropriate to the loss, the presence of a major depressive episode in\naddition to the normal response to a significant loss should also be carefully considered. This\ndecision inevitably requires the ex ercise of clinical judgment ba sed on the individual\u2019s history\nand the cultural norms for the expression of distress in the context of loss.1\nD. The occurrence of the major depressive episode is not better explained by schizoaf-\nfective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or\nother specified and unspecified schizophrenia s pectrum and other psychotic disorders.\nE. There has never been a manic episode or a hypomanic episode.\nNote: This exclusion does not apply if all of the manic-like or hypomanic-like episodes\nare substance-induced or are attributable to the physiological effects of another med-\nical condition.\n1In distinguishing grief from a major depressive episode (MDE), it is useful to consider that in\ngrief the predominant affect is feelings of emptiness and loss, while in MDE it is persistent\ndepressed mood and the inability to anticipate happiness or pleasure. The dysphoria in grief is\nlikely to decrease in intensity over days to weeks and occurs in waves, the so-called pangs of\ngrief. These waves tend to be associated with thoughts or reminders of the deceased. The\ndepressed mood of MDE is more persistent and not tied to specific thoughts or preoccupations.\nThe pain of grief may be accompanied by positi ve emotions and humor th at are uncharacteristic\nof the pervasive unhappiness and misery characteristic of MDE. The thought content associated\nwith grief generally features a preoccupation with thoughts and memories of the deceased,\nrather than the self-critical or pessimistic ruminati ons seen in MDE. In grief, self-esteem is gener-", "source": "dsm5.pdf"} {"id": "947b12979bba-2", "page_content": "ally preserved, whereas in MDE feelings of wort hlessness and self-loathing are common. If self-\nderogatory ideation is present in grief, it ty pically involves perceived failings vis-\u00e0-vis the\ndeceased (e.g., not visiting frequently enough, no t telling the deceased how much he or she was\nloved). If a bereaved individual thinks abou t death and dying, such thoughts are generally\nfocused on the deceased and possibly about \u201cjoining\u201d the de ceased, whereas in MDE such", "source": "dsm5.pdf"} {"id": "b028e9d3f6a2-0", "page_content": "loved). If a bereaved individual thinks abou t death and dying, such thoughts are generally\nfocused on the deceased and possibly about \u201cjoining\u201d the de ceased, whereas in MDE such\nthoughts are focused on ending one\u2019s own life because of feeling worthless, undeserving of life,\nor unable to cope with the pain of depression.", "source": "dsm5.pdf"} {"id": "46fa251e8519-0", "page_content": "162 Depressive Disorders\nCoding and Recording Procedures\nThe diagnostic code for major depressive disorder is based on whether this is a single or\nrecurrent episode, current severity, presence of psychotic features, and remission status.\nCurrent severity and psychotic features are only indicated if full criteria are currently met\nfor a major depressive episode. Remission specifiers are only indicated if the full criteria\nare not currently met for a major depressive episode. Codes are as follows: \nIn recording the name of a diagnosis, terms should be listed in the following order: major\ndepressive disorder, single or recurrent epis ode, severity/psychotic/remission specifiers,\nfollowed by as many of the following specifiers without codes that apply to the current\nepisode.\nSpecify:\nWith anxious distress (p. 184)\nWith mixed features (pp. 184\u2013185)\nWith melancholic features (p. 185)\nWith atypical features (pp. 185\u2013186)\nWith mood-congruent psychotic features (p. 186)\nWith mood-incongruen t psychotic features (p. 186)\nWith catatonia (p. 186). Coding note: Use additional code 293.89 (F06.1).\nWith peripartum onset (pp. 186\u2013187)\nWith seasonal pattern (recurrent episode only) (pp. 187\u2013188)\nDiagnostic Features \nThe criterion symptoms for majo r depressive disorder must be present nearly every day to\nbe considered present, with the exception of weight change and suicidal ideation. De-\npressed mood must be present for most of the day, in addition to being present nearly ev-\nery day. Often insomnia or fatigue is the presenting complaint, and failure to probe for\naccompanying depressive symptoms will result in underdiagnosis. Sadness may be de-", "source": "dsm5.pdf"} {"id": "46fa251e8519-1", "page_content": "accompanying depressive symptoms will result in underdiagnosis. Sadness may be de-\nnied at first but may be elicit ed through interview or inferred from facial expression and\ndemeanor. With individuals wh o focus on a somatic complaint, clinicians should de-\ntermine whether the distress from that comp laint is associated with specific depressive\nsymptoms. Fatigue and sleep disturbance are present in a high propor tion of cases; psy-\nchomotor disturbances are much less common but are indicative of greater overall sever-\nity, as is the presence of delu sional or near-delusional guilt.Severity/course specifier Single episode Recurrent episode*\nMild (p. 188) 296.21 (F32.0) 296.31 (F33.0)\nModerate (p. 188) 296.22 (F32.1) 296.32 (F33.1)\nSevere (p. 188) 296.23 (F32.2) 296.33 (F33.2)\nWith psychotic features** (p. 186) 296.24 (F32.3) 296.34 (F33.3)\nIn partial remission (p. 188) 296.25 (F32.4) 296.35 (F33.41)\nIn full remission (p. 188) 296.26 (F32.5) 296.36 (F33.42)\nUnspecified 296.20 (F32.9) 296.30 (F33.9)\n*For an episode to be considered recurrent, there must be an interval of at least 2 consecutive months\nbetween separate episodes in which criteria are no t met for a major depressive episode. The defini-", "source": "dsm5.pdf"} {"id": "46fa251e8519-2", "page_content": "tions of specifiers are found on the indicated pages.\n**If psychotic features are present, code the \u201cwith psychotic features \u201d specifier irrespective of epi-\nsode severity.", "source": "dsm5.pdf"} {"id": "a5830c3a88a0-0", "page_content": "Major Depressive Disorder 163\nThe essential feature of a major depressive episode is a period of at least 2 weeks during\nwhich there is either depressed mood or the loss of interest or pleasure in nearly all activi-\nties (Criterion A). In children and adolescents, the mood may be irritable rather than sad.\nThe individual must also expe rience at least four additional symptoms drawn from a list\nthat includes changes in appetite or weigh t, sleep, and psychomotor activity; decreased en-\nergy; feelings of worthlessness or guilt; difficulty thinking, co ncentrating, or making deci-\nsions; or recurrent thoughts of death or suicid al ideation or suicide plans or attempts. To\ncount toward a major depressive episode, a sy mptom must either be newly present or must\nhave clearly worsened compared with the person\u2019s pre- episode status. The symptoms\nmust persist for most of the day, nearly every day, for at least 2 consecutive weeks. The ep-\nisode must be accompanied by clinically signif icant distress or impairment in social, occu-\npational, or other important areas of func tioning. For some in dividuals with milder\nepisodes, functioning may appear to be normal but requires markedly increased effort.\nThe mood in a major depressive episode is of ten described by the person as depressed,\nsad, hopeless, discouraged, or \u201cdown in the du mps\u201d (Criterion A1). In some cases, sadness\nmay be denied at first but may subsequently be elicited by interview (e.g., by pointing out\nthat the individual looks as if he or she is ab out to cry). In some individuals who complain\nof feeling \u201cblah,\u201d having no feelings, or feeling anxious, the presence of a depressed mood\ncan be inferred from the pers on\u2019s facial expression and de meanor. Some individuals em-", "source": "dsm5.pdf"} {"id": "a5830c3a88a0-1", "page_content": "can be inferred from the pers on\u2019s facial expression and de meanor. Some individuals em-\nphasize somatic complaints (e.g., bodily aches and pains) rather than reporting feelings of\nsadness. Many individuals report or exhibit in creased irritability (e.g., persistent anger, a\ntendency to respond to events with angry outbursts or blaming ot hers, an exaggerated\nsense of frustration over minor matters). In ch ildren and adolescents, an irritable or cranky\nmood may develop rather than a sad or dejected mood. This presenta tion should be dif-\nferentiated from a pattern of irritability when frustrated.\nLoss of interest or pleasure is nearly always present, at least to some degree. Individ-\nuals may report feeling less interested in hobb ies, \u201cnot caring anymore,\u201d or not feeling any\nenjoyment in activities that were previously considered pleasurable (Criterion A2). Family\nmembers often notice social withdrawal or ne glect of pleasurable avocations (e.g., a for-\nmerly avid golfer no longer plays, a child who used to enjoy soccer finds excuses not to\npractice). In some individuals, there is a significant reduction from previous levels of sex-\nual interest or desire.\nAppetite change may involve either a redu ction or increase. Some depressed individ-\nuals report that they have to force themselv es to eat. Others may eat more and may crave\nspecific foods (e.g., sweets or other carbohydrates). When appetite changes are severe (in\neither direction), there may be a significant loss or gain in weight, or , in children, a failure\nto make expected weight gains may be noted (Criterion A3).\nSleep disturbance may take the form of either difficulty sleepin g or sleeping exces-", "source": "dsm5.pdf"} {"id": "a5830c3a88a0-2", "page_content": "Sleep disturbance may take the form of either difficulty sleepin g or sleeping exces-\nsively (Criterion A4). When insomnia is presen t, it typically takes the form of middle in-\nsomnia (i.e., waking up during the night an d then having difficulty returning to sleep) or\nterminal insomnia (i.e., waking too early and be ing unable to return to sleep). Initial in-\nsomnia (i.e., difficulty falling asleep) may al so occur. Individuals who present with over-\nsleeping (hypersomn ia) may experience prolonged sleep episodes at night or increased\ndaytime sleep. Sometimes the reason that the individual seeks trea tment is for the dis-\nturbed sleep.", "source": "dsm5.pdf"} {"id": "4ee483f5a9ad-0", "page_content": "sleeping (hypersomn ia) may experience prolonged sleep episodes at night or increased\ndaytime sleep. Sometimes the reason that the individual seeks trea tment is for the dis-\nturbed sleep.\nPsychomotor changes include agitation (e.g., the inabili ty to sit still, pacing, hand-\nwringing; or pulling or rubbing of the skin, cl othing, or other objects) or retardation (e.g.,\nslowed speech, thinking, and body movements; increased pauses before answering;\nspeech that is decreased in vo lume, inflection, amount, or variety of content, or muteness)\n(Criterion A5). The psychomotor agitation or retardation must be severe enough to be ob-\nservable by others and not repres ent merely subjective feelings.\nDecreased energy, tiredness, and fatigue are common (Criterion A6). A person may re-\nport sustained fatigue without physical exertion . Even the smallest ta sks seem to require", "source": "dsm5.pdf"} {"id": "b180da74186b-0", "page_content": "164 Depressive Disorders\nsubstantial effort. The efficiency with whic h tasks are accomplished may be reduced. For\nexample, an individual may complain that washing and dressing in the morning are ex-\nhausting and take twice as long as usual.\nThe sense of worthlessness or guilt associated with a major depressive episode may in-\nclude unrealistic negative evaluations of one\u2019 s worth or guilty preoccupations or rumina-\ntions over minor past failings (Criterion A7). Such individu als often misinterpret neutral\nor trivial day-to-day events as evidence of personal defects and have an exaggerated sense\nof responsibility for untoward events. The sens e of worthlessness or guilt may be of delu-\nsional proportions (e.g., an individual who is convinced that he or she is personally re-\nsponsible for world poverty). Blaming oneself for being sick and for failing to meet\noccupational or interpersonal responsibilities as a result of the depression is very common\nand, unless delusional, is not consider ed sufficient to meet this criterion.\nMany individuals report impaired ability to think, concentrate, or make even minor\ndecisions (Criterion A8). They may appear ea sily distracted or complain of memory diffi-\nculties. Those engaged in cogn itively demanding pursuits are often unable to function. In\nchildren, a precipitous drop in grades may reflect poor concentratio n. In elderly individ-\nuals, memory difficulties may be the chief co mplaint and may be mistaken for early signs\nof a dementia (\u201cpseudodementia\u201d). When th e major depressive ep isode is successfully\ntreated, the memory problems often fully abate. However, in some individuals, particu-\nlarly elderly persons, a major depressive ep isode may sometimes be the initial presenta-\ntion of an irreve rsible dementia.", "source": "dsm5.pdf"} {"id": "b180da74186b-1", "page_content": "tion of an irreve rsible dementia.\nThoughts of death, suicidal ideation, or suicide attempts (Cri terion A9) are common.\nThey may range from a passive wish not to aw aken in the morning or a belief that others\nwould be better off if the individual were dead , to transient but recurrent thoughts of com-\nmitting suicide, to a specific suicide plan. Mo re severely suicidal individuals may have put\ntheir affairs in order (e.g., up dated wills, settled debts), acqu ired needed materials (e.g., a\nrope or a gun), and chosen a location and time to accomplish the suicide. Motivations for\nsuicide may include a desire to give up in th e face of perceived insurmountable obstacles,\nan intense wish to end what is perceived as an unending and excruciatingly painful emo-\ntional state, an inability to fo resee any enjoyment in life, or the wish to not be a burden to\nothers. The resolution of such thinking may be a more meaningful measure of diminished\nsuicide risk than denial of further plans for suicide.\nThe evaluation of the symptoms of a major depressive episode is especially difficult\nwhen they occur in an indivi dual who also has a general me dical condition (e.g., cancer,\nstroke, myocardial infarction, diabetes, pregna ncy). Some of the criterion signs and symp-\ntoms of a major depressive episode are iden tical to those of general medical conditions\n(e.g., weight loss with untreated diabetes; fatigue with cancer; hypersomnia early in preg-\nnancy; insomnia later in pregnancy or the postpartum). Such symp toms count toward a\nmajor depressive diagnosis except when they are clearly and fully attributable to a general\nmedical condition. Nonv egetative symptoms of dysphoria, anhedonia, guilt or worthless-", "source": "dsm5.pdf"} {"id": "b180da74186b-2", "page_content": "ness, impaired concentration or indecision, an d suicidal thoughts should be assessed with\nparticular care in such cases. Definitions of major depressive episodes that have been mod-\nified to include only these nonvegetative sympto ms appear to identify nearly the same in-\ndividuals as do the full criteria.\nAssociated Features Supporting Diagnosis \nMajor depressive disorder is a ssociated with high mortality, much of which is accounted", "source": "dsm5.pdf"} {"id": "cd155e39440c-0", "page_content": "dividuals as do the full criteria.\nAssociated Features Supporting Diagnosis \nMajor depressive disorder is a ssociated with high mortality, much of which is accounted\nfor by suicide; however, it is not the only cause. For example, depressed individuals ad-\nmitted to nursing homes have a markedly increased likelihood of death in the first year. In-\ndividuals frequently present with tearfulness, irritability, brooding , obsessive rumination,\nanxiety, phobias, excessive worry over physical he alth, and complaints of pain (e.g., head-\naches; joint, abdominal, or other pains). In children, separation anxiety may occur.", "source": "dsm5.pdf"} {"id": "c22fe879c387-0", "page_content": "Major Depressive Disorder 165\nAlthough an extensive literature exists de scribing neuroanatomi cal, neuroendocrino-\nlogical, and neurophysiological correlates of major depressive disord er, no laboratory test\nhas yielded results of sufficient sensitivity and specificity to be used as a diagnostic tool for\nthis disorder. Until recently, hypothalamic-pit uitary-adrenal axis hyperactivity had been\nthe most extensively investigated abnormalit y associated with major depressive episodes,\nand it appears to be associated with melancho lia, psychotic features, and risks for eventual\nsuicide. Molecular studies have also implicated peripheral factors, including genetic vari-\nants in neurotrophic factors and pro-inflammatory cytokines. A dditionally, functional\nmagnetic resonance imaging stud ies provide evidence for functional ab normalities in spe-\ncific neural systems supporting emotion processing, reward seeking, and emotion regula-\ntion in adults with major depression. \nPrevalence\nTwelve-month prevalence of major depressive disorder in the United States is approximately\n7%, with marked differences by age group such th at the prevalence in 18- to 29-year-old indi-\nviduals is threefold higher than the prevalence in individuals age 60 years or older. Females ex-\nperience 1.5- to 3-fold higher rates th an males beginning in early adolescence.\nDevelopment and Course\nMajor depressive disorder may first appear at any age, but the likelihood of onset in-\ncreases markedly with puberty. In the United States, incidence appears to peak in the 20s;\nhowever, first onset in la te life is not uncommon. \nThe course of major depressive disorder is quite variable, such that some individuals\nrarely, if ever, experience re mission (a period of 2 or more months with no symptoms, or", "source": "dsm5.pdf"} {"id": "c22fe879c387-1", "page_content": "only one or two symptoms to no more than a mild degree), while others experience many\nyears with few or no symptoms between discrete episodes. It is important to distinguish\nindividuals who present for treatment during an exacerbation of a chronic depressive ill-\nness from those whose symptoms developed recently. Chronicity of depressive symptoms\nsubstantially increases the likelihood of underlying personality, anxiety, and substance\nuse disorders and decreases the likelihood that treatment will be followed by full symp-\ntom resolution. It is therefore useful to ask individuals presenting with depressive symp-\ntoms to identify the last period of at least 2 months during wh ich they were entirely free of\ndepressive symptoms. \nRecovery typically begins within 3 months of onset for two in five individuals with ma-\njor depression and within 1 year for four in five individuals. Recency of onset is a strong\ndeterminant of the likelihood of near-term recovery, and many individuals who have been\ndepressed only for several months can be expe cted to recover sponta neously. Features as-\nsociated with lower recovery rates, other th an current episode duration, include psychotic\nfeatures, prominent anxiety, persona lity disorders, and symptom severity.\nThe risk of recurrence become s progessively lower over time as the duration of re-\nmission increases. The risk is higher in in dividuals whose preceding episode was severe,\nin younger individuals, and in individuals who have already experienced multiple epi-\nsodes. The persistence of even mild depressive symptoms du ring remission is a powerful\npredictor of recurrence.\nMany bipolar illnesses begin with one or mo re depressive episodes, and a substantial\nproportion of individuals who initially appear to have ma jor depressive disorder will\nprove, in time, to instead have a bipolar disorder. This is more likely in individuals with", "source": "dsm5.pdf"} {"id": "c22fe879c387-2", "page_content": "prove, in time, to instead have a bipolar disorder. This is more likely in individuals with\nonset of the illness in adolescence, those with psychotic features, and those with a family\nhistory of bipolar illness. The presence of a \u201cwith mixed feat ures\u201d specifier also increases\nthe risk for future manic or hypomanic diagnosis. Major depr essive disorder, particularly", "source": "dsm5.pdf"} {"id": "e1a2f32ab711-0", "page_content": "history of bipolar illness. The presence of a \u201cwith mixed feat ures\u201d specifier also increases\nthe risk for future manic or hypomanic diagnosis. Major depr essive disorder, particularly\nwith psychotic features, may al so transition into schizophre nia, a change that is much\nmore frequent than the reverse.", "source": "dsm5.pdf"} {"id": "d3cb3e787c6f-0", "page_content": "166 Depressive Disorders\nDespite consistent differences between gender s in prevalence rates for depressive disor-\nders, there appear to be no clear differences by gender in phenomenology, course, or treat-\nment response. Similarly, there are no clear effe cts of current age on the course or treatment\nresponse of major depressive disorder. Some symptom differe nces exist, though, such that\nhypersomnia and hyperphagia ar e more likely in younger individuals, and melancholic\nsymptoms, particularly psychomotor disturbances, are more common in older individuals.\nThe likelihood of suicide attempts lessens in mi ddle and late life, although the risk of com-\npleted suicide does not. Depressions with ea rlier ages at onset are more familial and more\nlikely to involve personality disturbances. The course of major depressive disorder within\nindividuals does not generally change with aging. Mean times to recovery appear to be sta-\nble over long periods, and the likelihood of be ing in an episode does not generally increase\nor decrease with time. \nRisk and Prognostic Factors\nTemperamental. Neuroticism (negative affectivity) is a well-established risk factor for the\nonset of major depressive disorder, and high le vels appear to render individuals more likely\nto develop depressive episodes in re sponse to stressful life events.\nEnvironmental. Adverse childhood experiences, part icularly when there are multiple\nexperiences of diverse types, constitute a set of potent risk factors for major depressive dis-\norder. Stressful life events are well recognized as precipitants of major depressive epi-\nsodes, but the presence or absence of adverse life events near the onset of episodes does\nnot appear to provide a useful guide to prognosis or treatment selection.\nGenetic and physiological. First-degree family members of individuals with major de-", "source": "dsm5.pdf"} {"id": "d3cb3e787c6f-1", "page_content": "Genetic and physiological. First-degree family members of individuals with major de-\npressive disorder have a risk for major depres sive disorder two- to fourfold higher than\nthat of the general population. Relative risks appear to be higher for early-onset and re-\ncurrent forms. Heritability is a pproximately 40%, and the personality trait neuroticism ac-\ncounts for a substantial port ion of this genetic liability.\nCourse modifiers. Essentially all major nonm ood disorders increase the risk of an indi-\nvidual developing depression. Major depressive episodes th at develop against the back-\nground of another disorder of ten follow a more refractory course. Substance use, anxiety,\nand borderline personality diso rders are among the most common of these, and the pre-\nsenting depressive symptoms may obscure an d delay their recognition. However, sus-\ntained clinical improvement in depressive symptoms may depend on the appropriate\ntreatment of underlying illnesses. Chronic or disabling medical conditions also increase\nrisks for major depressive episod es. Such prevalent illnesses as diabetes, morbid obesity,\nand cardiovascular disease are often complicated by depressive episodes, and these epi-\nsodes are more likely to become chronic than are depressive episodes in medically healthy\nindividuals.\nCulture-Related Diagnostic Issues\nSurveys of major depressive disorder across diverse cultures have shown sevenfold dif-\nferences in 12-month prevalen ce rates but much more consistency in female-to-male ratio,\nmean ages at onset, and the degree to which presence of the disorder raises the likelihood\nof comorbid substance abuse. While these findings suggest substantial cultural differences\nin the expression of major depressive disord er, they do not permit simple linkages be-\ntween particular cultures and the likelihoo d of specific symptoms. Rather, clinicians", "source": "dsm5.pdf"} {"id": "d3cb3e787c6f-2", "page_content": "tween particular cultures and the likelihoo d of specific symptoms. Rather, clinicians\nshould be aware that in most countries the majority of cases of depression go unrecog-\nnized in primary care settings and that in ma ny cultures, somatic sy mptoms are very likely\nto constitute the presenting complaint. Among the Criterion A symptoms, insomnia and\nloss of energy are the most uniformly reported.", "source": "dsm5.pdf"} {"id": "58a6beb89293-0", "page_content": "Major Depressive Disorder 167\nGender-Related Diagnostic Issues\nAlthough the most reproducible finding in th e epidemiology of major depressive disorder\nhas been a higher prevalence in females, th ere are no clear differences between genders in\nsymptoms, course, treatment response, or functional consequences. In women, the risk for\nsuicide attempts is higher, and the risk for suicide completion is lower. The disparity in\nsuicide rate by gender is not as great among th ose with depressive disorders as it is in the\npopulation as a whole. \nSuicide Risk\nThe possibility of suicidal behavior exists at all times during major depressive episodes.\nThe most consistently described risk factor is a past history of suicide attempts or threats,\nbut it should be remembered that most comp leted suicides are not preceded by unsuccess-\nful attempts. Other features associated with an increased risk for completed suicide\ninclude male sex, being single or living alone, and having prominent feelings of hopeless-\nness. The presence of borderline personality disorder markedly increases risk for future\nsuicide attempts. \nFunctional Consequences of \nMajor Depressive Disorder\nMany of the functional consequences of major depressive disorder derive from individual\nsymptoms. Impairment can be very mild, such th at many of those who interact with the af-\nfected individual are unaware of depressive symptoms. Impairment may, however, range\nto complete incapacity such that the depressed individual is unable to attend to basic self-\ncare needs or is mute or catatonic. Among individuals seen in ge neral medical settings,\nthose with major depressive disorder have more pain and physical illness and greater de-\ncreases in physical, social, and role functioning.\nDifferential Diagnosis\nManic episodes with irritable mood or mixed episodes. Major depressive episodes\nwith prominent irritable mood may be difficu lt to distinguish from manic episodes with", "source": "dsm5.pdf"} {"id": "58a6beb89293-1", "page_content": "with prominent irritable mood may be difficu lt to distinguish from manic episodes with\nirritable mood or from mixed episodes. This di stinction requires a careful clinical evalua-\ntion of the presence of manic symptoms.\nMood disorder due to another medical condition. A major depressive episode is the\nappropriate diagnosis if the mood disturbance is not judged, based on individual history,\nphysical examination, and laboratory findings, to be the direct pathophysiological conse-\nquence of a specific medical condition (e.g., multiple sclerosis, st roke, hypothyroidism).\nSubstance/medication-induced de pressive or bipolar disorder. This disorder is distin-\nguished from major depressive disorder by the fact that a substance (e.g., a drug of abuse,\na medication, a toxin) appears to be etiologically related to the mood disturbance. For ex-\nample, depressed mood that occurs only in the context of withdrawal from cocaine would\nbe diagnosed as cocaine-induced depressive disorder. \nAttention-deficit/hyperactivity disorder. Distractibility and low frustration tolerance\ncan occur in both attention-deficit/ hypera ctivity disorder and a major depressive epi-\nsode; if the criteria are met for both, attention-deficit/hyperactivity disorder may be diag-\nnosed in addition to the mood disorder. However, the clinic ian must be cautious not to\noverdiagnose a major depressive episode in ch ildren with attention-deficit/hyperactivity\ndisorder whose disturbance in mood is characte rized by irritability rather than by sadness\nor loss of interest.", "source": "dsm5.pdf"} {"id": "fb805e6fe8bb-0", "page_content": "168 Depressive Disorders\nAdjustment disorder with depressed mood. A major depressive episode that occurs in\nresponse to a psychosocial stressor is distin guished from adjustment disorder with de-\npressed mood by the fact that the full criteria for a major depressive episode are not met in\nadjustment disorder.\nSadness. Finally, periods of sadness are inhere nt aspects of the human experience.\nThese periods should not be diagnosed as a major depressive episod e unless criteria are\nmet for severity (i.e., five out of nine symptoms), duration (i.e., most of the day, nearly ev-\nery day for at least 2 weeks), and clinically significant distress or impairment. The diagno-\nsis other specified depressive disorder may be appropriate for presentations of depressed\nmood with clinically significant impairment that do not meet criteria for duration or se-\nverity.\nComorbidity\nOther disorders with which majo r depressive disorder frequently co-occurs are substance-\nrelated disorders, panic diso rder, obsessive-compulsive diso rder, anorexia nervosa, buli-\nmia nervosa, and borderlin e personality disorder.\nPersistent Depressive Disorder (Dysthymia)\nDiagnostic Criteria 300.4 (F34.1)\nThis disorder represents a consolidation of DSM-IV-defined chronic major depressive dis-\norder and dysthymic disorder.\nA. Depressed mood for most of the day, for more days than not, as indicated by either\nsubjective account or observation by others, for at least 2 years.\nNote: In children and adolescents, mood can be irritable and duration must be at least\n1 year.\nB. Presence, while depressed, of two (or more) of the following:\n1. Poor appetite or overeating.\n2. Insomnia or hypersomnia.", "source": "dsm5.pdf"} {"id": "fb805e6fe8bb-1", "page_content": "1. Poor appetite or overeating.\n2. Insomnia or hypersomnia.\n3. Low energy or fatigue.\n4. Low self-esteem.\n5. Poor concentration or difficulty making decisions.\n6. Feelings of hopelessness.\nC. During the 2-year period (1 year for children or adolescents) of the disturbance, the individ-\nual has never been without the symptoms in Criteria A and B for more than 2 months at a\ntime.\nD. Criteria for a major depressive disorder may be continuously present for 2 years. \nE. There has never been a manic episode or a hypomanic episode, and criteria have\nnever been met for cyclothymic disorder.\nF. The disturbance is not better explained by a persistent schizoaffective disorder,\nschizophrenia, delusional disorder, or other specified or unspecified schizophrenia\nspectrum and other psychotic disorder.\nG. The symptoms are not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication) or another medical condition (e.g. hypothyroidism).\nH. The symptoms cause clinically significant distress or impairment in social, occupational,\nor other important areas of functioning.\nNote: Because the criteria for a major depressive episode include four symptoms that are\nabsent from the symptom list for persistent depressive disorder (dysthymia), a very limited", "source": "dsm5.pdf"} {"id": "7a96bc0857c5-0", "page_content": "Persistent Depressive Disorder (Dysthymia) 169\nnumber of individuals will have depressive symptoms that have persisted longer than 2 years\nbut will not meet criteria for persistent depressive disorder. If full criteria for a major de-\npressive episode have been met at some point during the current episode of illness, they\nshould be given a diagnosis of major depressive disorder. Otherwise, a diagnosis of other\nspecified depressive disorder or unspecified depressive disorder is warranted. \nSpecify if:\nWith anxious distress (p. 184)\nWith mixed features (pp. 184\u2013185)\nWith melancholic features (p. 185)\nWith atypical features (pp. 185\u2013186)\nWith mood-congruent psychotic features (p. 186)\nWith mood-incongruent psychotic features (p. 186)\nWith peripartum onset (pp. 186\u2013187)\nSpecify if:\nIn partial remission (p. 188)\nIn full remission (p. 188)\nSpecify if:\nEarly onset: If onset is before age 21 years.\nLate onset: If onset is at age 21 years or older.\nSpecify if (for most recent 2 years of persistent depressive disorder):\nWith pure dysthymic syndrome: Full criteria for a major depressive episode have not\nbeen met in at least the preceding 2 years.\nWith persistent major depressive episode: Full criteria for a major depressive epi-\nsode have been met throughout the preceding 2-year period.\nWith intermittent major depressi ve episodes, with current episode: Full criteria for\na major depressive episode are currently met, but there have been periods of at least\n8 weeks in at least the preceding 2 years with symptoms below the threshold for a full\nmajor depressive episode.", "source": "dsm5.pdf"} {"id": "7a96bc0857c5-1", "page_content": "major depressive episode.\nWith intermittent major depressive episodes, without current episode: Full crite-\nria for a major depressive episode are not currently met, but there has been one or\nmore major depressive episodes in at least the preceding 2 years.\nSpecify current severity:\nMild (p. 188)\nModerate (p. 188)\nSevere (p. 188)\nDiagnostic Features\nThe essential feature of persistent depressive disorder (dysthymia) is a depressed mood\nthat occurs for most of the day, for more days th an not, for at least 2 ye ars, or at least 1 year\nfor children and adolescents (Criterion A). Th is disorder represents a consolidation of\nDSM-IV-defined chronic major depressive di sorder and dysthymic disorder. Major de-\npression may precede persistent depressive disorder, and major de pressive episodes may\noccur during persistent depressive disorder. Individuals whose symptoms meet major de-\npressive disorder criter ia for 2 years should be given a diagnosis of persistent depressive\ndisorder as well as majo r depressive disorder.\nIndividuals with persistent depressive diso rder describe their mood as sad or \u201cdown\nin the dumps.\u201d During periods of depressed mood, at least two of the six symptoms from\nCriterion B are present. Because these sympto ms have become a part of the individual\u2019s\nday-to-day experience, particular ly in the case of early onse t (e.g., \u201cI\u2019ve always been this", "source": "dsm5.pdf"} {"id": "3876ba28bba7-0", "page_content": "170 Depressive Disorders\nway\u201d), they may not be reported unless the indi vidual is directly prom pted. During the 2-year\nperiod (1 year for children or adolescents), any symptom-free intervals last no longer than\n2 months (Criterion C). \nPrevalence\nPersistent depressive disorder is effectively an amalgam of DSM-IV dysthymic disorder and\nchronic major depressive episode. The 12-month prevalence in the United States is approxi-\nmately 0.5% for persistent depre ssive disorder and 1.5% for chro nic major depressive disorder.\nDevelopment and Course\nPersistent depressive disorder often has an early and insidious onset (i.e., in childhood,\nadolescence, or early adult life) and, by de finition, a chronic course. Among individuals\nwith both persistent depressiv e disorder and borderline pers onality disorder, the covari-\nance of the corresponding features over ti me suggests the operatio n of a common mecha-\nnism. Early onset (i.e., before age 21 years) is associated with a higher likelihood of\ncomorbid personality disorder s and substance use disorders.\nWhen symptoms rise to the level of a major depressive episode, they are likely to sub-\nsequently revert to a lower level. However, depressive symptoms are much less likely to\nresolve in a given period of time in the context of persistent depressive disorder than they\nare in a major depressive episode.\nRisk and Prognostic Factors\nTemperamental. Factors predictive of poorer long -term outcome include higher levels\nof neuroticism (negative affect ivity), greater symptom severity, poorer global functioning,\nand presence of anxiety disorders or conduct disorder.\nEnvironmental. Childhood risk factors include parental loss or separation.\nGenetic and physiological. There are no clear differences in illness development, course,", "source": "dsm5.pdf"} {"id": "3876ba28bba7-1", "page_content": "Genetic and physiological. There are no clear differences in illness development, course,\nor family history between DSM-IV dysthymi c disorder and chronic major depressive dis-\norder. Earlier findings pertaining to either disorder are therefore likely to apply to per-\nsistent depressive disorder. It is thus likel y that individuals with persistent depressive\ndisorder will have a higher pr oportion of first-degree relatives with persistent depressive\ndisorder than do individuals with major de pressive disorder, and more depressive disor-\nders in general.\nA number of brain regions (e.g., prefrontal cortex, anterior cing ulate, amygdala, hip-\npocampus) have been implicated in persiste nt depressive disorder. Possible polysomno-\ngraphic abnormalities exist as well.\nFunctional Consequences of \nPersistent Depressive Disorder\nThe degree to which persistent depressive diso rder impacts social and occupational func-\ntioning is likely to vary widely, but effects can be as great as or greater than those of major\ndepressive disorder.\nDifferential Diagnosis\nMajor depressive disorder. If there is a depressed mood plus two or more symptoms\nmeeting criteria for a persistent depressive ep isode for 2 years or more, then the diagnosis of\npersistent depressive disorder is made. Th e diagnosis depends on the 2-year duration,\nwhich distinguishes it from episodes of depressi on that do not last 2 years. If the symptom", "source": "dsm5.pdf"} {"id": "aea118f9446e-0", "page_content": "Premenstrual Dysphoric Disorder 171\ncriteria are sufficient for a diagnosis of a major depressive episode at any time during this pe-\nriod, then the diagnosis of major depression shou ld be noted, but it is coded not as a separate\ndiagnosis but rather as a specifie r with the diagnosis of persistent depressive disorder. If the\nindividual\u2019s symptoms currently meet full crit eria for a major depressive episode, then the\nspecifier of \u201cwith intermittent major depressi ve episodes, with current episode\u201d would be\nmade. If the major depressive episode has pers isted for at least a 2-year duration and re-\nmains present, then the specifie r \u201cwith persistent major depressive episode\u201d is used. When\nfull major depressive episode cr iteria are not currently met but there has been at least one\nprevious episode of major depression in the cont ext of at least 2 years of persistent depres-\nsive symptoms, then the specifier of \u201cwith in termittent major depres sive episodes, without\ncurrent episode\u201d is used. If the individual ha s not experienced an episode of major depres-\nsion in the last 2 years, then the specifier \u201cwith pure dysthymic syndrome\u201d is used.\nPsychotic disorders. Depressive symptoms are a common associated feature of chronic\npsychotic disorders (e.g., schi zoaffective disorder, schizophrenia, delusional disorder). A\nseparate diagnosis of persistent depressive disorder is not made if the symptoms occur\nonly during the course of the psychoti c disorder (including residual phases).\nDepressive or bipolar and related diso rder due to another medical condition. Persistent\ndepressive disorder must be distinguished from a depressive or bipolar and related dis-\norder due to another medical co ndition. The diagnosis is depressive or bipolar and related", "source": "dsm5.pdf"} {"id": "aea118f9446e-1", "page_content": "order due to another medical co ndition. The diagnosis is depressive or bipolar and related\ndisorder due to another medical condition if the mood disturbance is judged, based on his-\ntory, physical examination, or laboratory findin gs, to be attributable to the direct patho-\nphysiological effects of a specific, usually chronic, medical condition (e.g., multiple\nsclerosis). If it is judged that the depressive symptoms are not attrib utable to the physiolog-\nical effects of another medical condition, then the primary ment al disorder (e.g., persistent\ndepressive disorder) is recorded, and the medi cal condition is noted as a concomitant med-\nical condition (e.g., diabetes mellitus).\nSubstance/medication-induced depressive or bipolar disorder. A substance/medi-\ncation-induced depressive or bipolar and rela ted disorder is distin guished from persis-\ntent depressive disorder when a substance (e.g ., a drug of abuse, a medication, a toxin) is\njudged to be etiologically re lated to the mood disturbance.\nPersonality disorders. Often, there is evidence of a co existing personality disturbance.\nWhen an individual\u2019s presentation meets the cr iteria for both persis tent depressive disor-\nder and a personality disorder , both diagnoses are given.\nComorbidity \nIn comparison to individuals with major depressive disorder, those with persistent de-\npressive disorder are at higher risk for psychiatric comorbidit y in general, and for anxiety\ndisorders and substance use disorders in partic ular. Early-onset persistent depressive dis-\norder is strongly associated with DSM-IV Cluster B and C personality disorders.\nPremenstrual Dysphoric Disorder\nDiagnostic Criteria 625.4 (N94.3)\nA. In the majority of menstrual cycles, at least five symptoms must be present in the final", "source": "dsm5.pdf"} {"id": "aea118f9446e-2", "page_content": "A. In the majority of menstrual cycles, at least five symptoms must be present in the final\nweek before the onset of menses, start to improve within a few days after the onset of\nmenses, and become minimal or absent in the week postmenses.\nB. One (or more) of the following symptoms must be present:\n1. Marked affective lability (e.g., mood swings; feeling suddenly sad or tearful, or in-\ncreased sensitivity to rejection).", "source": "dsm5.pdf"} {"id": "b9a9473d47b4-0", "page_content": "172 Depressive Disorders\n2. Marked irritability or anger or increased interpersonal conflicts.\n3. Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts.\n4. Marked anxiety, tension, and/or feelings of being keyed up or on edge.\nC. One (or more) of the following symptoms must additionally be present, to reach a total\nof five symptoms when combined with sym ptoms from Criterion B above.\n1. Decreased interest in usual activities (e.g., work, school, friends, hobbies).\n2. Subjective difficulty in concentration.\n3. Lethargy, easy fatigability, or marked lack of energy.\n4. Marked change in appetite; overeating; or specific food cravings.\n5. Hypersomnia or insomnia.\n6. A sense of being overwhelmed or out of control.\n7. Physical symptoms such as breast tenderness or swelling, joint or muscle pain, a\nsensation of \u201cbloating,\u201d or weight gain.\nNote: The symptoms in Criteria A\u2013C must have been met for most menstrual cycles that\noccurred in the preceding year.\nD. The symptoms are associated with clinically significant distress or interference with\nwork, school, usual social activities, or relationships with others (e.g., avoidance of so-\ncial activities; decreased productivity and efficiency at work, school, or home).\nE. The disturbance is not merely an exacerbation of the symptoms of another disorder,\nsuch as major depressive disorder, panic disorder, persistent depressive disorder\n(dysthymia), or a personality disorder (a lthough it may co-occur with any of these dis-\norders).\nF. Criterion A should be confirmed by prospect ive daily ratings during at least two symptom-\natic cycles. ( Note: The diagnosis may be made provisionally prior to this confirmation.)", "source": "dsm5.pdf"} {"id": "b9a9473d47b4-1", "page_content": "atic cycles. ( Note: The diagnosis may be made provisionally prior to this confirmation.)\nG. The symptoms are not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication, other treatment ) or another medical condition (e.g., hy-\nperthyroidism).\nRecording Procedures\nIf symptoms have not been confirmed by prospective daily ratings of at least two symp-\ntomatic cycles, \u201cprovisional\u201d should be noted after the name of the diagnosis (i.e., \u201cpre-\nmenstrual dysphoric disorder, provisional\u201d).\nDiagnostic Features\nThe essential features of premenstrual dyspho ric disorder are the expression of mood la-\nbility, irritability, dysphoria, and anxiety symptoms that occur repeatedly during the pre-\nmenstrual phase of the cycle and remit around the onset of me nses or shortl y thereafter.\nThese symptoms may be accompanied by behavioral and physical symptoms. Symptoms\nmust have occurred in most of the menstrual cycles during the past year and must have an\nadverse effect on work or social functioning. The intensity and/or expressivity of the ac-\ncompanying symptoms may be closely related to social and cultural background charac-\nteristics of the affected female, family pers pectives, and more specific factors such as\nreligious beliefs, social tolerance, and female gender role issues.\nTypically, symptoms peak around the time of the onset of menses. Although it is not\nuncommon for symptoms to linger into the first few days of menses, the individual must\nhave a symptom-free period in the follicular phase after the menstrual period begins.\nWhile the core symptoms include mood and anxiety symptoms, behavioral and somatic\nsymptoms commonly also occur. However, the presence of physic al and/or behavioral", "source": "dsm5.pdf"} {"id": "b9a9473d47b4-2", "page_content": "symptoms commonly also occur. However, the presence of physic al and/or behavioral\nsymptoms in the absence of mood and/or anxious symptoms is not sufficient for a diag-", "source": "dsm5.pdf"} {"id": "e397df75b41b-0", "page_content": "Premenstrual Dysphoric Disorder 173\nnosis. Symptoms are of comparab le severity (but not duration) to those of another mental\ndisorder, such as a major depressive episode or generalized anxiety disorder. In order to\nconfirm a provisional diagnosis, daily pros pective symptom ratings are required for at\nleast two symptomatic cycles.\nAssociated Features Supporting Diagnosis\nDelusions and hallucinations have been described in the late luteal phase of the menstrual\ncycle but are rare. The premenstrual phase has b een considered by some to be a risk period\nfor suicide. \nPrevalence\nTwelve-month prevalence of premenstrual dy sphoric disorder is between 1.8% and 5.8%\nof menstruating women. Estimates are substant ially inflated if they are based on retro-\nspective reports rather than prospective da ily ratings. However, estimated prevalence\nbased on a daily record of symptoms for 1\u20132 months may be less representative, as indi-\nviduals with the most severe symptoms may be unable to sustain the rating process. The\nmost rigorous estimate of premenstrual dy sphoric disorder is 1.8% for women whose\nsymptoms meet the full criteria without fu nctional impairment and 1.3% for women\nwhose symptoms meet the current criteria wi th functional impairment and without co-oc-\ncurring symptoms from another mental disorder. \nDevelopment and Course\nOnset of premenstrual dysphoric disorder ca n occur at any point after menarche. Inci-\ndence of new cases over a 40-month follow-up period is 2.5% (95% confidence interval =\n1.7\u20133.7). Anecdotally, many individuals, as th ey approach menopause, report that symp-", "source": "dsm5.pdf"} {"id": "e397df75b41b-1", "page_content": "toms worsen. Symptoms cease after menopaus e, although cyclical hormone replacement\ncan trigger the re-expression of symptoms.\nRisk and Prognostic Factors \nEnvironmental. Environmental factors associated with the expression of premenstrual\ndysphoric disorder include stress, history of interpersonal trauma, seasonal changes, and\nsociocultural aspects of female sexual behavior in general, and female gender role in par-\nticular. \nGenetic and physiological. Heritability of prem enstrual dysphoric disorder is unknown.\nHowever, for premenstrual sy mptoms, estimates for heritability range between 30% and\n80%, with the most stable component of premenstrual symptoms es timated to be about\n50% heritable. \nCourse modifiers. Women who use oral contraceptiv es may have fewer premenstrual\ncomplaints than do women who do not use oral contraceptives. \nCulture-Related Diagnostic Issues\nPremenstrual dysphoric disord er is not a culture-bound syndrome and has been observed\nin individuals in the United States, Europe, India, and Asia. It is unclear as to whether rates\ndiffer by race. Nevertheless, fr equency, intensity, and expres sivity of symptoms and help-\nseeking patterns may be significantl y influenced by cultural factors. \nDiagnostic Markers\nAs indicated earlier, the diagnosis of premenstrual dysphoric disorder is appropriately\nconfirmed by 2 months of pros pective symptom ratings. A number of scales, including the", "source": "dsm5.pdf"} {"id": "e4188197f0dd-0", "page_content": "174 Depressive Disorders\nDaily Rating of Severity of Problems and the Visual Analogue Sc ales for Premenstrual\nMood Symptoms, have undergone validation and are commonly used in clinical trials for\npremenstrual dysphoric disorder. The Premenst rual Tension Syndrome Rating Scale has a\nself-report and an observer vers ion, both of which have been validated and used widely to\nmeasure illness severity in women who ha ve premenstrual dysphoric disorder.\nFunctional Consequences of \nPremenstrual Dysphoric Disorder\nSymptoms must be associated with clinically meaningful distress and/or an obvious and\nmarked impairment in the ability to function so cially or occupationally in the week prior\nto menses. Impairment in social functionin g may be manifested by marital discord and\nproblems with children, other family members, or friends. Chronic marital or job prob-\nlems should not be confused with dysfunction that occurs only in association with pre-\nmenstrual dysphoric disorder. \nDifferential Diagnosis\nPremenstrual syndrome. Premenstrual syndrome differs from premenstrual dysphoric\ndisorder in that a minimum of five symptoms is not required, and there is no stipulation of\naffective symptoms for individuals who have premenstrual syndrome. This condition\nmay be more common than premenstrual dy sphoric disorder, although the estimated\nprevalence of premenstrual syndrome varies. While premen strual syndrome shares the\nfeature of symptom expression during the premenstrual phase of the menstrual cycle, it is\ngenerally considered to be less severe than premenstrual dysphoric disorder. The pres-\nence of physical or behavioral symptoms in the pr emenstruum, without the required\naffective symptoms, likely meet s criteria for prem enstrual syndrome and not for premen-", "source": "dsm5.pdf"} {"id": "e4188197f0dd-1", "page_content": "strual dysphoric disorder.\nDysmenorrhea. Dysmenorrhea is a syndrome of painful menses, but this is distinct from a\nsyndrome characterized by affective changes. Moreover, symptoms of dysmenorrhea begin\nwith the onset of menses, whereas symptoms of premenstrual dysphoric disorder, by defini-\ntion, begin before the onset of menses, even if they linger into the first few days of menses. \nBipolar disorder, major depressive disord er, and persistent depressive disorder\n(dysthymia). Many women with (either naturally occurring or substance/medication-\ninduced) bipolar or major depressive disorder or persistent depressive disorder believe\nthat they have premenstrual dysphoric disorder. However, when they chart symptoms,\nthey realize that the symptoms do not follo w a premenstrual pattern. Women with an-\nother mental disorder may experience chronic symptoms or interm ittent symptoms that\nare unrelated to menstrual cycle phase. Howeve r, because the onset of menses constitutes\na memorable event, they may report that symptoms occur only during the premenstruum\nor that symptoms worsen premenstrually. This is one of the rationales for the requirement\nthat symptoms be confirmed by daily prospect ive ratings. The process of differential di-\nagnosis, particularly if the clinician relies on retrospective symptoms only, is made more\ndifficult because of the overlap between sy mptoms of premenstrual dysphoric disorder\nand some other diagnoses. The overlap of symp toms is particularly salient for differenti-\nating premenstrual dysphoric disorder from major depressive episodes, persistent de-\npressive disorder, bipolar disorders, and bo rderline personality di sorder. However, the", "source": "dsm5.pdf"} {"id": "e4188197f0dd-2", "page_content": "pressive disorder, bipolar disorders, and bo rderline personality di sorder. However, the\nrate of personality disorders is no higher in individuals with premenstrual dysphoric dis-\norder than in those without the disorder.\nUse of hormonal treatments. Some women who present with moderate to severe pre-\nmenstrual symptoms may be using hormonal treatments, including hormonal contracep-\ntives. If such symptoms occur after initia tion of exogenous hormone use, the symptoms", "source": "dsm5.pdf"} {"id": "86f0397ae2b9-0", "page_content": "Substance/Medication-Induced Depressive Disorder 175\nmay be due to the use of hormones rather th an to the underlying condition of premen-\nstrual dysphoric disorder. If the woman stops hormones and the symptoms disappear,\nthis is consistent with substance/medi cation-induced depressive disorder.\nComorbidity\nA major depressive episode is the most frequent ly reported previous disorder in individuals\npresenting with premenstrual dysphoric disorder. A wide range of medical (e.g., migraine,\nasthma, allergies, seizure disorders) or other mental disorders (e.g., depressive and bipolar\ndisorders, anxiety disorders, bulimia nervosa, substance use disorders) may worsen in the\npremenstrual phase; however, the absence of a symptom-free period during the postmen-\nstrual interval obviates a diagnosis of premenstrual dysphoric disorder. These conditions\nare better considered premenstrual exacerbation of a current mental or medical disorder. Al-\nthough the diagnosis of premenstrual dysphoric disorder should not be assigned in situa-\ntions in which an individual only experien ces a premenstrual exacerbation of another\nmental or physical disorder, it can be considered in addition to the diagnosis of another men-\ntal or physical disorder if the individual experiences symptoms and changes in level of func-\ntioning that are characteristic of premenstrual dysphoric disorder and markedly different\nfrom the symptoms experienced as part of the ongoing disorder. \nSubstance/Medication-Induced\nDepressive Disorder\nDiagnostic Criteria \nA. A prominent and persistent disturbance in mood that predominates in the clinical pic-\nture and is characterized by depressed mood or markedly diminished interest or plea-\nsure in all, or almost all, activities.", "source": "dsm5.pdf"} {"id": "86f0397ae2b9-1", "page_content": "sure in all, or almost all, activities.\nB. There is evidence from the history, physical examination, or laboratory findings of both\n(1) and (2):\n1. The symptoms in Criterion A developed during or soon after substance intoxication\nor withdrawal or after exposure to a medication.\n2. The involved substance/medication is capable of producing the symptoms in Crite-\nrion A.\nC. The disturbance is not better explained by a depressive disorder that is not substance/\nmedication-induced. Such evidence of an independent depressive disorder could in-\nclude the following:\nThe symptoms preceded the onset of the substance/medication use; the symptoms\npersist for a substantial period of time (e.g., about 1 month) after the cessation of acute\nwithdrawal or severe intoxication; or there is other evidence suggesting the existence\nof an independent non-substance/medication-i nduced depressive disorder (e.g., a his-\ntory of recurrent non-substance/medication-related episodes).\nD. The disturbance does not occur exclusively during the course of a delirium. \nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nNote: This diagnosis should be made instead of a diagnosis of substance intoxication or\nsubstance withdrawal only when the symptoms in Criterion A predominate in the clinical\npicture and when they are sufficiently severe to warrant clinical attention.\nCoding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-\ntion]-induced depressive disorders are indicate d in the table below. Note that the ICD-10-", "source": "dsm5.pdf"} {"id": "728228b95f75-0", "page_content": "176 Depressive Disorders\nCM code depends on whether or not there is a comorbid substance use disorder present for\nthe same class of substance. If a mild substance use disorder is comorbid with the substance-\ninduced depressive disorder, the 4th position character is \u201c1,\u201d and the clinician should record\n\u201cmild [substance] use disorder\u201d before the substance-induced depressive disorder (e.g.,\n\u201cmild cocaine use di sorder with cocain e-induced depressive disorder\u201d). If a moderate or se-\nvere substance use disorder is comorbid with the substance-induced depressive disorder,\nthe 4th position character is \u201c2,\u201d and the clinician should record \u201cmoderate [substance] use\ndisorder\u201d or \u201csevere [substance] use disorder,\u201d depending on the severity of the comorbid\nsubstance use disorder. If there is no comorbid substance use disorder (e.g., after a one-\ntime heavy use of the substance), then the 4th position character is \u201c9,\u201d and the clinician should\nrecord only the substance-induced depressive disorder.\nSpecify if (see Table 1 in the chapter \u201cSubstance-Related and Addictive Disorders\u201d for di-\nagnoses associated with substance class):\nWith onset during intoxication: If criteria are met for intoxication with the substance\nand the symptoms develop during intoxication.\nWith onset during withdrawal: If criteria are met for withdrawal from the substance\nand the symptoms develop during, or shortly after, withdrawal.\nRecording Procedures\nICD-9-CM. The name of the substance/medication -induced depressive disorder begins\nwith the specific substance (e.g., cocaine, de xamethasone) that is presumed to be causing\nthe depressive symptoms. The diagnostic code is selected from the table included in the", "source": "dsm5.pdf"} {"id": "728228b95f75-1", "page_content": "the depressive symptoms. The diagnostic code is selected from the table included in the\ncriteria set, which is based on the drug class. For substances that do not fit into any of the\nclasses (e.g., dexamethasone), th e code for \u201cother substance\u201d should be used; and in cases\nin which a substance is judged to be an etiologi cal factor but the specific class of substance\nis unknown, the category \u201cunknown substance\u201d should be used.\nThe name of the disorder is followed by the sp ecification of onset (i.e., onset during in-\ntoxication, onset during with drawal). Unlike the recording procedures for ICD-10-CM,\nwhich combine the substance-induced disorder and substance use disorder into a singleICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate \nor severeWithout \nuse \ndisorder\nAlcohol 291.89 F10.14 F10.24 F10.94\nPhencyclidine 292.84 F16.14 F16.24 F16.94\nOther hallucinogen 292.84 F16.14 F16.24 F16.94\nInhalant 292.84 F18.14 F18.24 F18.94\nOpioid 292.84 F11.14 F11.24 F11.94\nSedative, hypnotic, or anxiolytic 292.84 F13.14 F13.24 F13.94\nAmphetamine (or other \nstimulant)292.84 F15.14 F15.24 F15.94\nCocaine 292.84 F14.14 F14.24 F14.94", "source": "dsm5.pdf"} {"id": "728228b95f75-2", "page_content": "Cocaine 292.84 F14.14 F14.24 F14.94\nOther (or unknown) substance 292.84 F19.14 F19.24 F19.94", "source": "dsm5.pdf"} {"id": "3ac1a2367c57-0", "page_content": "Substance/Medication-Induced Depressive Disorder 177\ncode, for ICD-9-CM a separate diagnostic code is given for the substance use disorder. For\nexample, in the case of depressive symptoms occurring during withdrawal in a man with\na severe cocaine use disorder, the diagnosis is 292.84 cocaine-induced depressive disorder,\nwith onset during with drawal. An additional diagnosis of 304.20 severe cocaine use dis-\norder is also given. When more than one substance is judged to play a significant role in\nthe development of depressive mood symptoms , each should be listed separately (e.g.,\n292.84 methylphenidate-induced depressive disorder, with onset during withdrawal;\n292.84 dexamethasone-induced depressive diso rder, with onset during intoxication).\nICD-10-CM. The name of the substance/medication -induced depressive disorder begins\nwith the specific substance (e.g., cocaine, de xamethasone) that is presumed to be causing\nthe depressive symptoms. The diagnostic code is selected from the table included in the\ncriteria set, which is based on the drug class and presence or absence of a comorbid sub-\nstance use disorder. For substances that do no t fit into any of the cl asses (e.g., dexameth-\nasone), the code for \u201cother substance\u201d should be used; and in cases in which a substance is\njudged to be an etiological factor but the spec ific class of substance is unknown, the category\n\u201cunknown substance\u201d should be used.\nWhen recording the name of the disorder, the comorbid substance use disorder (if any) is\nlisted first, followed by the word \u201cwith,\u201d follo wed by the name of the substance-induced de-\npressive disorder, followed by the specification of onset (i.e., onset during intoxication, onset", "source": "dsm5.pdf"} {"id": "3ac1a2367c57-1", "page_content": "pressive disorder, followed by the specification of onset (i.e., onset during intoxication, onset\nduring withdrawal). For example, in the case of depressive sy mptoms occurring during with-\ndrawal in a man with a severe cocaine use disorder, the diagnosis is F14.24 severe cocaine use\ndisorder with cocaine-induced depressive disorder, with onset during withdrawal. A separate\ndiagnosis of the comorbid severe cocaine use disorder is not given. If the substance-induced\ndepressive disorder occurs without a comorbid substance use disorder (e.g., after a one-time\nheavy use of the substance), no accompanying substance use disorder is noted (e.g., F16.94\nphencyclidine-induced depr essive disorder, with onset during intoxication). When more than\none substance is judged to play a significant role in the development of depressive mood\nsymptoms, each should be listed separately (e .g., F15.24 severe methylphenidate use disorder\nwith methylphenidate-induced depressive diso rder, with onset during withdrawal; F19.94\ndexamethasone-induced depressive disord er, with onset during intoxication).\nDiagnostic Features\nThe diagnostic features of substance/medication-induced depressive disorder include the\nsymptoms of a depressive disorder, such as major depressive disorder; however, the de-\npressive symptoms are associated with the ingestion, injection, or inhalation of a sub-\nstance (e.g., drug of abuse, toxin, psychotropic medicati on, other medication), and the\ndepressive symptoms persist be yond the expected length of physiological effects, intoxi-\ncation, or withdrawal period. As evidenced by clinical history, phy sical examination, or\nlaboratory findings, th e relevant depressive disorder should have developed during or\nwithin 1 month after use of a substance that is capable of producing the depressive disor-", "source": "dsm5.pdf"} {"id": "3ac1a2367c57-2", "page_content": "within 1 month after use of a substance that is capable of producing the depressive disor-\nder (Criterion B1). In additi on, the diagnosis is not better explained by an independent\ndepressive disorder. Evidence of an indepe ndent depressive disorder includes the de-\npressive disorder preceded the onset of inge stion or withdrawal from the substance; the\ndepressive disorder persists beyo nd a substantial period of ti me after the cessation of sub-\nstance use; or other evidence suggests th e existence of an independent non-substance/\nmedication-induced depressive disorder (Criterion C). This diagnosis should not be made", "source": "dsm5.pdf"} {"id": "27b42d04e614-0", "page_content": "stance use; or other evidence suggests th e existence of an independent non-substance/\nmedication-induced depressive disorder (Criterion C). This diagnosis should not be made\nwhen symptoms occur exclusivel y during the course of a delirium (Criterion D). The de-\npressive disorder associated with the substance use, intoxication, or withdrawal must\ncause clinically significant distress or impairment in social, occupa tional, or other impor-\ntant areas of functioning to qualify for this diagnosis (Criterion E).\nSome medications (e.g., stimulants, steroids, L-dopa, antibiotics, central nervous\nsystem drugs, dermatological agents, chem otherapeutic drugs, immunological agents)", "source": "dsm5.pdf"} {"id": "ce93683860c7-0", "page_content": "178 Depressive Disorders\ncan induce depressive mood di sturbances. Clinical judgment is essential to determine\nwhether the medication is truly associated with inducing the depressive disorder or\nwhether a primary depressive disorder happen ed to have its onset while the person was\nreceiving the treatment. For example, a depres sive episode that developed within the first\nseveral weeks of beginning alpha-methyldopa (an antihypertensive agent) in an individ-\nual with no history of major depressive diso rder would qualify for the diagnosis of med-\nication-induced depressive diso rder. In some cases, a prev iously established condition\n(e.g., major depressive disorder , recurrent) can recur while th e individual is coincidentally\ntaking a medication that has the capacity to cause depressive symptoms (e.g., L-dopa, oral\ncontraceptives). In such cases, the clinicia n must make a judgment as to whether the med-\nication is causative in this particular situation.\nA substance/medication-induced depressive disorder is distinguished from a primary\ndepressive disorder by considering the onset, course, and other factors associated with the\nsubstance use. There must be evidence from the history, phy sical examination, or labora-\ntory findings of substance use, abuse, intoxication, or withdrawal prior to the onset of the\ndepressive disorder. The withdrawal state for some substances can be relatively pro-\ntracted, and thus intense depressive symptoms can last for a long period after the cessation\nof substance use. \nPrevalence\nIn a nationally representative U.S. adult po pulation, the lifetime pr evalence of substance/\nmedication-induced depressive disorder is 0.26%.\nDevelopment and Course\nA depressive disorder associated with the use of substance (i.e., alcoho l, illicit drugs, or a", "source": "dsm5.pdf"} {"id": "ce93683860c7-1", "page_content": "prescribed treatment for a mental disorder or another medical condition) must have its on-\nset while the individual is using the substanc e or during withdrawal, if there is a with-\ndrawal syndrome associated with the substanc e. Most often, the de pressive disorder has\nits onset within the first few weeks or 1 month of use of the substance. Once the substance\nis discontinued, the depressive symptoms usually remit within days to several weeks, de-\npending on the half-life of the substance/medication and the presence of a withdrawal\nsyndrome. If symptoms persist 4 weeks beyond the expected time course of withdrawal of\na particular substance/medi cation, other causes for th e depressive mood symptoms\nshould be considered.\nAlthough there are a few prospective controlle d trials examining the association of de-\npressive symptoms with use of a medication, most report s are from postmarketing sur-\nveillance studies, retrospective observational studies, or case reports, making evidence of\ncausality difficult to determine. Substances implicated in medication-induced depressive\ndisorder, with varying degrees of evidence, in clude antiviral agents (efavirenz), cardio-\nvascular agents (clonidine, guanethidine, me thyldopa, reserpine), re tinoic acid deriva-\ntives (isotretinoin), antidepressants, antico nvulsants, anti-migraine agents (triptans),\nantipsychotics, hormonal agents (corticost eroids, oral contrace ptives, gonadotropin-\nreleasing hormone agonists, tamoxifen), smoking cessation agents (varenicline), and im-\nmunological agents (interferon) . However, other potential su bstances continue to emerge\nas new compounds are synthesized. A history of such substance use may help increase di-\nagnostic certainty.", "source": "dsm5.pdf"} {"id": "ce93683860c7-2", "page_content": "agnostic certainty.\nRisk and Prognostic Factors \nTemperamental. Factors that appear to increase the risk of substance/medication-\ninduced depressive disorder can be conceptualized as pertaining to the specific type of\ndrug or to a group of individuals with underlying alcohol or drug use disorders. Risk fac-", "source": "dsm5.pdf"} {"id": "47514f369eb8-0", "page_content": "Substance/Medication-Induced Depressive Disorder 179\ntors common to all drugs incl ude history of major depressive disorder, history of drug-\ninduced depression, and psychosocial stressors.\nEnvironmental. There are also risks factors pertaini ng to a specific type of medication\n(e.g., increased immune activation prior to treatment for hepatitis C associated with inter-\nferon-alfa-induced depression); high doses (greater than 80 mg/day prednisone-equiva-\nlents) of corticosteroids or high plasma conc entrations of efavirenz; and high estrogen/\nprogesterone content in oral contraceptives.\nCourse modifiers. In a representative U.S. adult popu lation, compared with individuals\nwith major depressive disorder who did not have a substance use disorder, individuals\nwith substance-induced depressive disorder were more likely to be male, to be black, to\nhave at most a high school diploma, to lack insurance, and to have lower family income.\nThey were also more likely to report higher family history of substance use disorders and\nantisocial behavior, higher 12-month history of stressful life events, and a greater number\nof DSM-IV major depressive diso rder criteria. They were more likely to report feelings of\nworthlessness, insomnia/hypersomnia, and thoughts of deat h and suicide attempts, but\nless likely to report depressed mood and parental loss by death before age 18 years.\nDiagnostic Markers\nDetermination of the substance of use can so metimes be made through laboratory assays\nof the suspected substance in the blood or urine to corroborate the diagnosis.\nSuicide Risk\nDrug-induced or treatment-emergent suicidality represents a marked change in thoughts\nand behavior from the person\u2019s baseline, is us ually temporally associated with initiation of", "source": "dsm5.pdf"} {"id": "47514f369eb8-1", "page_content": "and behavior from the person\u2019s baseline, is us ually temporally associated with initiation of\na substance, and must be distinguished from the underlying prim ary mental disorders.\nIn regard to the treatment-emergent suicida lity associated with antidepressants, a U.S.\nFood and Drug Administration (FDA) adviso ry committee considered meta-analyses of\n99,839 participants enrolled in 372 randomized clin ical trials of antidepressants in trials for\nmental disorders. The analyses showed that when the data were pooled across all adult\nage groups, there was no perceptible increased risk of suicidal behavior or ideation. How-\never, in age-stratified analyses , the risk for patients ages 18\u201324 years was elevated, albeit\nnot significantly (odds ratio [OR] = 1.55; 95% confidence interval [CI] = 0.91\u20132.70). The\nFDA meta-analyses reveal an absolute risk of suicide in patients taking investigational an-\ntidepressants of 0.01%. In conc lusion, suicide is clearly an extremely rare treatment-emer-\ngent phenomenon, but the outcome of suicid e was serious enough to prompt the FDA to\nissue an expanded black-box warning in 2007 regarding the importance of careful moni-\ntoring of treatment-emergent suicidal ideati on in patients receiving antidepressants.\nDifferential Diagnosis\nSubstance intoxication and withdrawal. Depressive symptoms occur commonly in sub-\nstance intoxication and substance withdrawal, and the diagnosis of the substance-specific\nintoxication or withdrawal will usually suffice to categorize the symptom presentation. A\ndiagnosis of substance-induced depressive di sorder should be made instead of a diag-\nnosis of substance intoxicati on or substance withdrawal when the mood symptoms are\nsufficiently severe to warrant independent clinical attention. For example, dysphoric", "source": "dsm5.pdf"} {"id": "47514f369eb8-2", "page_content": "sufficiently severe to warrant independent clinical attention. For example, dysphoric\nmood is a characteristic feature of coca ine withdrawal. Substance/medication-induced\ndepressive disorder should be diagnosed inst ead of cocaine withdrawal only if the mood\ndisturbance is substantially more intense or longer lasting than what is usually encountered\nwith cocaine withdrawal and is sufficiently seve re to be a separate focus of attention and\ntreatment.", "source": "dsm5.pdf"} {"id": "a78e47444ad3-0", "page_content": "180 Depressive Disorders\nPrimary depressive disorder. A substance/medication-induc ed depressive disorder is\ndistinguished from a primary de pressive disorder by the fact that a substance is judged to\nbe etiologically related to the symptoms, as described earlier (see section \u201cDevelopment\nand Course\u201d for this disorder).\nDepressive disorder due to another medical condition. Because individuals with other\nmedical conditions often take medications for th ose conditions, the clinician must consider the\npossibility that the mood symptoms are caused by the physiological consequences of the med-\nical condition rather than the medication, in which case depres sive disorder due to another\nmedical condition is diagnosed. The history often provides the primary basis for such a judg-\nment. At times, a change in the treatment for the other medical condition (e.g., medication sub-\nstitution or discontinuation) may be needed to determine empirically whether the medication\nis the causative agent. If the clinician has ascertained that the disturbance is a function of both\nanother medical condition and su bstance use or withdrawal, both diagnoses (i.e., depressive\ndisorder due to another medical condition and substance/medication-induced depressive\ndisorder) may be given. When there is insuffic ient evidence to determine whether the depres-\nsive symptoms are associated with substance (including a medication) ingestion or with-\ndrawal or with another medical condition or are primary (i.e., not a function of either a\nsubstance or another medical condition), a diagno sis of other specified depressive disorder or\nunspecified depressive diso rder would be indicated.\nComorbidity\nCompared with individuals with major depre ssive disorder and no comorbid substance\nuse disorder, those with substance/medicati on-induced depressive disorder have higher", "source": "dsm5.pdf"} {"id": "a78e47444ad3-1", "page_content": "use disorder, those with substance/medicati on-induced depressive disorder have higher\nrates of comorbidity with any DSM-IV mental disorder; are more likely to have specific\nDSM-IV disorders of pathological gambling and paranoid, histrionic, and antisocial per-\nsonality disorders; and are less likely to have persistent depressive disorder (dysthymia).\nCompared with individuals with major depressive disorder and a comorbid substance use\ndisorder, individuals with substance/medication-induced depressive disorder are more\nlikely to have alcohol use disorder, any othe r substance use disorder, and histrionic per-\nsonality disorder; however, they are less likely to have persistent depressive disorder.\nDepressive Disorder\n Due to Another Medical Condition\nDiagnostic Criteria\nA. A prominent and persistent period of depressed mood or markedly diminished interest\nor pleasure in all, or almost all, activiti es that predominates in the clinical picture.\nB. There is evidence from the history, physical examination, or laboratory findings that the\ndisturbance is the direct pathophysiological consequence of another medical condi-\ntion.\nC. The disturbance is not better explained by another mental disorder (e.g., adjustment\ndisorder, with depressed mood, in which the stressor is a serious medical condition).\nD. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nCoding note: The ICD-9-CM code for depressive di sorder due to another medical condi-\ntion is 293.83, which is assigned regardless of the specifier. The ICD-10-CM code de-\npends on the specifier (see below).", "source": "dsm5.pdf"} {"id": "2fa01854ceeb-0", "page_content": "Depressive Disorder Due to Another Medical Condition 181\nSpecify if: \n(F06.31) With depressive features: Full criteria are not met for a major depressive\nepisode.\n(F06.32) With major depressive\u2013like episode: Full criteria are met (except Criterion\nC) for a major depressive episode.\n(F06.34) With mixed features: Symptoms of mania or hypomania are also present but\ndo not predominate in the clinical picture.\nCoding note: Include the name of the other medical condition in the name of the mental dis-\norder (e.g., 293.83 [F06.31] depressive disorder due to hypothyroidism, with depressive fea-\ntures). The other medical condition should al so be coded and listed separately immediately\nbefore the depressive disorder due to the medical condition (e.g., 244.9 [E03.9] hypothyroid-\nism; 293.83 [F06.31] depressive disorder due to hypothyroidism, with depressive features).\nDiagnostic Features\nThe essential feature of depressive disorder due to another medical condition is a promi-\nnent and persistent period of depressed mood or markedly diminished interest or plea-\nsure in all, or almost all, ac tivities that predominates in th e clinical picture (Criterion A)\nand that is thought to be related to the direct physiological effects of another medical con-\ndition (Criterion B). In determining whethe r the mood disturbance is due to a general\nmedical condition, the clinician must first establish the presence of a general medical con-\ndition. Further, the clinician mu st establish that the mood di sturbance is etiologically re-\nlated to the general medical condition through a physiological mechanism. A careful and\ncomprehensive assessment of multiple factor s is necessary to make this judgment. Al-", "source": "dsm5.pdf"} {"id": "2fa01854ceeb-1", "page_content": "comprehensive assessment of multiple factor s is necessary to make this judgment. Al-\nthough there are no infallible guidelines for determining whether the relationship\nbetween the mood disturbance and the general medical condition is etiological, several\nconsiderations provide some guidance in this area. One consideration is the presence of a\ntemporal association between th e onset, exacerbation, or remission of the general medical\ncondition and that of the mood disturbance. A second consideration is the presence of fea-\ntures that are atypical of prim ary Mood Disorders (e.g., atypic al age at onset or course or\nabsence of family history). Evidence from the literature that suggests th at there can be a di-\nrect association between the general medical condition in question and the development\nof mood symptoms can provide a useful contex t in the assessment of a particular situation.\nAssociated Features Supporting Diagnosis\nEtiology (i.e., a causal relationship to anothe r medical condition based on best clinical ev-\nidence) is the key variable in depressive di sorder due to another medical condition. The\nlisting of the medical conditions that are said to be able to in duce major depression is never\ncomplete, and the clinician\u2019s best judg ment is the essence of this diagnosis.\nThere are clear associations, as well as some neuroanatomical correlates, of depression\nwith stroke, Huntington\u2019s dise ase, Parkinson\u2019s disease, and traumatic brain injury. Among\nthe neuroendocrine conditions most closely associated with depression are Cushing\u2019s dis-\nease and hypothyroidism. There are numerous other conditions thought to be associated\nwith depression, such as multiple sclerosis. However, the literature\u2019s support for a causal\nassociation is greater with some conditions , such as Parkinson\u2019s disease and Huntington\u2019s\ndisease, than with others, for which the differ ential diagnosis may be adjustment disorder,\nwith depressed mood.", "source": "dsm5.pdf"} {"id": "2fa01854ceeb-2", "page_content": "with depressed mood.\nDevelopment and Course\nFollowing stroke, the onset of depression appear s to be very acute, occurring within 1 day\nor a few days of the cerebrovascular accident (CVA) in the largest case series. However, in", "source": "dsm5.pdf"} {"id": "0179b39c1bd9-0", "page_content": "182 Depressive Disorders\nsome cases, onset of the depression is weeks to months following the CVA. In the largest\nseries, the duration of the major depressive episode follo wing stroke was 9\u201311 months on\naverage. Similarly, in Huntington\u2019s disease the depressive state comes quite early in the\ncourse of the illness. With Parkinson\u2019s disease and Huntington\u2019s disease, it often precedes\nthe major motor impairments and cognitive impairments associ ated with each condition.\nThis is more prominently the case for Huntin gton\u2019s disease, in which depression is con-\nsidered to be the first neuropsychiatric symptom. There is some observational evidence\nthat depression is less common as the dementia of Huntington\u2019s disease progresses. \nRisk and Prognostic Factors\nThe risk of acute onset of a major depressive disorder following a CVA (within 1 day to a\nweek of the event) appears to be strongly correlated with lesion location, with greatest risk\nassociated with left frontal strokes and least risk apparently associated with right frontal\nlesions in those individuals who present within days of the stroke. The association with\nfrontal regions and laterality is not observed in depressive states that occur in the 2\u20136 months\nfollowing stroke.\nGender-Related Diagnostic Issues\nGender differences pertain to those associat ed with the medical condition (e.g., systemic\nlupus erythematosus is more common in fema les; stroke is somewhat more common in\nmiddle-age males compared with females).\nDiagnostic Markers\nDiagnostic markers pertain to those associated with the medical condition (e.g., steroid\nlevels in blood or urine to help corroborate the diagnosis of Cushing\u2019s disease, which can\nbe associated with manic or depressive syndromes).\nSuicide Risk\nThere are no epidemiological stud ies that provide evidence to differentiate the risk of sui-", "source": "dsm5.pdf"} {"id": "0179b39c1bd9-1", "page_content": "There are no epidemiological stud ies that provide evidence to differentiate the risk of sui-\ncide from a major depressive episode due to another medical conditio n compared with the\nrisk from a major depressive episode in general. There are case reports of suicides in\nassociation with major depressive episodes associated with another medical condition.\nThere is a clear association between serious medical illnesses and suicide, particularly\nshortly after onset or diagnosis of the illness. Thus, it would be prudent to assume that the\nrisk of suicide for major depressive episodes associated with medical conditions is not less\nthan that for other forms of major depres sive episode, and might even be greater.\nFunctional Consequences of Depressive Disorder \nDue to Another Medical Condition\nFunctional consequences pertain to those asso ciated with the medical condition. In gen-\neral, it is believed, but not es tablished, that a major depres sive episode induced by Cush-\ning\u2019s disease will not recur if the Cushing\u2019s dise ase is cured or arrested. However, it is also\nsuggested, but not established, that mood syndromes, including depressive and manic/\nhypomanic ones, may be episodic (i.e., recurring ) in some individuals with static brain in-\njuries and other central nervous system diseases.\nDifferential Diagnosis\nDepressive disorders not due to another medical condition. Determination of whether\na medical condition accompanying a depressive disorder is causing the disorder depends\non a) the absence of an episode(s) of depressive episodes prior to the onset of the medical", "source": "dsm5.pdf"} {"id": "be216c2afdf0-0", "page_content": "Other Specified Depressive Disorder 183\ncondition, b) the probability that the associ ated medical condition has a potential to pro-\nmote or cause a depressive disorder, and c) a course of the depressive symptoms shortly\nafter the onset or worsening of the medical condition, especially if the depressive symp-\ntoms remit near the time that the medical disorder is effectively treated or remits.\nMedication-induced depressive disorder. An important caveat is that some medical con-\nditions are treated with medications (e.g., steroi ds or alpha-interferon) that can induce depres-\nsive or manic symptoms. In these cases, clinical judgment, based on all the evidence in hand, is\nthe best way to try to separate the most likely and/or the most important of two etiological fac-\ntors (i.e., association with the medical condition vs. a substance-induced syndrome).\nAdjustment disorders. It is important to differentiate a depressive episode from an ad-\njustment disorder, as the onset of the medical co ndition is in itself a life stressor that could\nbring on either an adjustment disorder or an episode of major depression. The major dif-\nferentiating elements are the pervasiveness the depressive picture and the number and\nquality of the depressive symptoms that the pa tient reports or demonstrates on the mental\nstatus examination. The differential diagnosis of the associated medical conditions is rel-\nevant but largely beyond the scope of the present manual. \nComorbidity\nConditions comorbid with depressive disorder due to another medical condition are those\nassociated with the medical conditions of etio logical relevance. It has been noted that de-\nlirium can occur before or along with depres sive symptoms in individuals with a variety\nof medical conditions, such as Cushing\u2019s di sease. The association of anxiety symptoms,", "source": "dsm5.pdf"} {"id": "be216c2afdf0-1", "page_content": "of medical conditions, such as Cushing\u2019s di sease. The association of anxiety symptoms,\nusually generalized symptoms, is common in depressive disorders, regardless of cause.\nOther Specified Depressive Disorder\n311 (F32.8)\nThis category applies to presentations in which symptoms characteristic of a depressive\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the depressive disorders di agnostic class. The other specified depressive\ndisorder category is used in situations in which the clinician chooses to communicate the\nspecific reason that the presentation does not meet the criteria for any specific depressive\ndisorder. This is done by recording \u201cother specified depressive disorder\u201d followed by the\nspecific reason (e.g., \u201cshort-duration depressive episode\u201d).\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Recurrent brief depression: Concurrent presence of depressed mood and at least\nfour other symptoms of depression for 2\u201313 days at least once per month (not associ-\nated with the menstrual cycle) for at least 12 consecutive months in an individual\nwhose presentation has never met criteria for any other depressive or bipolar disorder\nand does not currently meet active or residual criteria for any psychotic disorder.\n2.Short-duration depressi ve episode (4\u201313 days): Depressed affect and at least four\nof the other eight symptoms of a major depressive episode associated with clinically\nsignificant distress or impairment that persists for more than 4 days, but less than 14 days,\nin an individual whose presentation has never met criteria for any other depressive or\nbipolar disorder, does not currently meet active or residual criteria for any psychotic dis-\norder, and does not meet criteria for recurrent brief depression.", "source": "dsm5.pdf"} {"id": "be216c2afdf0-2", "page_content": "order, and does not meet criteria for recurrent brief depression.\n3.Depressive episode with insufficient symptoms: Depressed affect and at least one\nof the other eight symptoms of a major depressive episode associated with clinically", "source": "dsm5.pdf"} {"id": "95618da71b32-0", "page_content": "184 Depressive Disorders\nsignificant distress or impairment that persist for at least 2 weeks in an individual\nwhose presentation has never met criteria for any other depressive or bipolar disorder,\ndoes not currently meet active or residual criteria for any psychotic disorder, and does\nnot meet criteria for mixed anxiety and depressive disorder symptoms.\nUnspecified Depressive Disorder\n311 (F32.9)\nThis category applies to presentations in whic h symptoms characteristic of a depressive dis-\norder that cause clinically significant distress or impairment in social, occupational, or other im-\nportant areas of functioning predominate but do not meet the full criteria for any of the disorders\nin the depressive disorders diagnostic class. Th e unspecified depressive disorder category is\nused in situations in which the clinician chooses not to specify the reason that the criteria are\nnot met for a specific depressive disorder, and includes presentations for which there is insuf-\nficient information to make a more specific diagnosis (e.g., in emergency room settings).\nSpecifiers for Depressive Disorders\nSpecify if:\nWith anxious distress: Anxious distress is defined as the presence of at least two of\nthe following symptoms during the majority of days of a major depressive episode or\npersistent depressive disorder (dysthymia):\n1. Feeling keyed up or tense.\n2. Feeling unusually restless.\n3. Difficulty concentrating because of worry.\n4. Fear that something awful may happen.\n5. Feeling that the individual might lose control of himself or herself.\nSpecify current severity:\nMild: Two symptoms.\nModerate: Three symptoms.\nModerate-severe: Four or five symptoms.\nSevere: Four or five symptoms and with motor agitation.\nNote: Anxious distress has been noted as a prominent feature of both bipolar and ma-\njor depressive disorder in both primary care and specialty mental health settings. High", "source": "dsm5.pdf"} {"id": "95618da71b32-1", "page_content": "jor depressive disorder in both primary care and specialty mental health settings. High\nlevels of anxiety have been associated with higher suicide risk, longer duration of ill-\nness, and greater likelihood of treatment nonresponse. As a result, it is clinically useful\nto specify accurately the presence and severity levels of anxious distress for treatment\nplanning and monitoring of response to treatment.\nWith mixed features: \nA. At least three of the following manic/hypomanic symptoms are present nearly every\nday during the majority of days of a major depressive episode:\n1. Elevated, expansive mood.\n2. Inflated self-esteem or grandiosity.\n3. More talkative than usual or pressure to keep talking.\n4. Flight of ideas or subjective experience that thoughts are racing.\n5. Increase in energy or goal-directed activity (either socially, at work or school, or\nsexually).", "source": "dsm5.pdf"} {"id": "0e3adeeda861-0", "page_content": "Specifiers for Depressive Disorders 185\n6. Increased or excessive involvement in activities that have a high potential for\npainful consequences (e.g., engaging in unrestrained buying sprees, sexual in-\ndiscretions, foolish business investments).\n7. Decreased need for sleep (feeling rested despite sleeping less than usual; to be\ncontrasted with insomnia).\nB. Mixed symptoms are observable by others and represent a change from the per-\nson\u2019s usual behavior.\nC. For individuals whose symptoms meet full criteria for either mania or hypomania,\nthe diagnosis should be bipolar I or bipolar II disorder.\nD. The mixed symptoms are not attributable to the physiological effects of a substance\n(e.g., a drug of abuse, a medication or other treatment).\nNote: Mixed features associated with a major depressive episode have been found\nto be a significant risk factor for the development of bipolar I or bipolar II disorder.\nAs a result, it is clinically useful to note the presence of this specifier for treatment\nplanning and monitoring of response to treatment.\nWith melancholic features:\nA. One of the following is present during the most severe period of the current epi-\nsode:\n1. Loss of pleasure in all, or almost all, activities.\n2. Lack of reactivity to usually pleasurable stimuli (does not feel much better, even\ntemporarily, when something good happens).\nB. Three (or more) of the following:\n1. A distinct quality of depressed mood characterized by profound despondency,\ndespair, and/or moroseness or by so-called empty mood.\n2. Depression that is regularly worse in the morning.\n3. Early-morning awakening (i.e., at least 2 hours before usual awakening).\n4. Marked psychomotor agitation or retardation.\n5. Significant anorexia or weight loss.", "source": "dsm5.pdf"} {"id": "0e3adeeda861-1", "page_content": "5. Significant anorexia or weight loss.\n6. Excessive or inappropriate guilt.\nNote: The specifier \u201cwith melancholic features\u201d is applied if these features are present\nat the most severe stage of the episode. There is a near-complete absence of the ca-\npacity for pleasure, not merely a diminution. A guideline for evaluating the lack of reac-\ntivity of mood is that even highly desired events are not associated with marked\nbrightening of mood. Either mood does not bri ghten at all, or it brightens only partially\n(e.g., up to 20%\u201340% of normal for only minutes at a time). The \u201cdistinct quality\u201d of mood\nthat is characteristic of the \u201cwith melancholic features\u201d specifier is experienced as qual-\nitatively different from that during a nonm elancholic depressive episode. A depressed\nmood that is described as merely more severe, longer lasting, or present without a rea-\nson is not considered distinct in quality. Psychomotor changes are nearly always pres-\nent and are observable by others.\nMelancholic features exhibit only a modest tendency to repeat across episodes in the\nsame individual. They are more frequent in inpatients, as opposed to outpatients; are\nless likely to occur in milder than in more severe major depressive episodes; and are\nmore likely to occur in those with psychotic features.\nWith atypical features: This specifier can be applied when these features predomi-\nnate during the majority of days of the current or most recent major depressive episode\nor persistent depressive disorder. \nA. Mood reactivity (i.e., mood brightens in response to actual or potential positive\nevents).", "source": "dsm5.pdf"} {"id": "9163d7e2c083-0", "page_content": "186 Depressive Disorders\nB. Two (or more) of the following: \n1. Significant weight gain or increase in appetite.\n2. Hypersomnia.\n3. Leaden paralysis (i.e., heavy, leaden feelings in arms or legs).\n4. A long-standing pattern of interpersonal rejection sensitivity (not limited to epi-\nsodes of mood disturbance) that results in significant social or occupational im-\npairment.\nC. Criteria are not met for \u201cwith melancholic features\u201d or \u201cwith catatonia\u201d during the\nsame episode.\nNote: \u201cAtypical depression\u201d has historical significance (i.e., atypical in contradistinction\nto the more classical agitated, \u201cendogenous\u201d presentations of depression that were the\nnorm when depression was rarely diagnosed in outpatients and almost never in ado-\nlescents or younger adults) and today does not connote an uncommon or unusual clin-\nical presentation as the term might imply.\nMood reactivity is the capacity to be cheered up when presented with positive events\n(e.g., a visit from children, compliments from others). Mood may become euthymic (not\nsad) even for extended periods of time if the external circumstances remain favorable.\nIncreased appetite may be manifested by an obvious increase in food intake or by\nweight gain. Hypersomnia may include either an extended period of nighttime sleep or\ndaytime napping that totals at least 10 hours of sleep per day (or at least 2 hours more\nthan when not depressed). Leaden paralysis is defined as feeling heavy, leaden, or\nweighted down, usually in the arms or legs. This sensation is generally present for at\nleast an hour a day but often lasts for many hours at a time. Unlike the other atypical\nfeatures, pathological sensitivity to perceived interpersonal rejection is a trait that has", "source": "dsm5.pdf"} {"id": "9163d7e2c083-1", "page_content": "features, pathological sensitivity to perceived interpersonal rejection is a trait that has\nan early onset and persists throughout most of adult life. Rejection sensitivity occurs\nboth when the person is and is not depressed, though it may be exacerbated during\ndepressive periods.\nWith psychotic features: Delusions and/or hallucinations are present.\nWith mood-congruent psychotic features: The content of all delusions and hal-\nlucinations is consistent with the typical depressive themes of personal inade-\nquacy, guilt, disease, death, nihilism, or deserved punishment.\nWith mood-incongruent psychotic features: The content of the delusions or hal-\nlucinations does not involve typical depressive themes of personal inadequacy,\nguilt, disease, death, nihilism, or deserved punishment, or the content is a mixture\nof mood-incongruent and mood-congruent themes.\nWith catatonia: The catatonia specifier can apply to an episode of depression if cata-\ntonic features are present during most of the episode. See criteria for catatonia asso-\nciated with a mental disorder (for a description of catatonia, see the chapter\n\u201cSchizophrenia Spectrum and Other Psychotic Disorders\u201d).\nWith peripartum onset: This specifier can be applied to the current or, if full criteria\nare not currently met for a major depressive episode, most recent episode of major de-\npression if onset of mood symptoms occurs during pregnancy or in the 4 weeks follow-\ning delivery.\nNote: Mood episodes can have their onset either during pregnancy or postpartum.\nAlthough the estimates differ according to the period of follow-up after delivery, be-\ntween 3% and 6% of women will experience the onset of a major depressive epi-\nsode during pregnancy or in the weeks or months following delivery. Fifty percent", "source": "dsm5.pdf"} {"id": "9163d7e2c083-2", "page_content": "sode during pregnancy or in the weeks or months following delivery. Fifty percent\nof \u201cpostpartum\u201d major depressive episodes actually begin prior to delivery. Thus,\nthese episodes are referred to collectively as peripartum episodes. Women with\nperipartum major depressive episodes often have severe anxiety and even panic", "source": "dsm5.pdf"} {"id": "fe602c6633d7-0", "page_content": "Specifiers for Depressive Disorders 187\nattacks. Prospective studies have demonstrated that mood and anxiety symptoms\nduring pregnancy, as well as the \u201cbaby blues,\u201d increase the risk for a postpartum\nmajor depressive episode.\nPeripartum-onset mood episodes can pres ent either with or without psychotic\nfeatures. Infanticide is most often associated with postpartum psychotic episodes\nthat are characterized by command hallucinations to kill the infant or delusions that\nthe infant is possessed, but psychotic symptoms can also occur in severe postpar-\ntum mood episodes without such specific delusions or hallucinations.\nPostpartum mood (major depressive or manic) episodes with psychotic features\nappear to occur in from 1 in 500 to 1 in 1,000 deliveries and may be more common\nin primiparous women. The risk of postpartum episodes with psychotic features is\nparticularly increased for women with prior postpartum mood episodes but is also\nelevated for those with a prior history of a depressive or bipolar disorder (especially\nbipolar I disorder) and those with a family history of bipolar disorders.\nOnce a woman has had a postpartum episode with psychotic features, the risk\nof recurrence with each subsequent delivery is between 30% and 50%. Postpartum\nepisodes must be differentiated from delirium occurring in the postpartum period,\nwhich is distinguished by a fluctuating level of awareness or attention. The postpar-\ntum period is unique with respect to the degree of neuroendocrine alterations and\npsychosocial adjustments, the potential impact of breast-feeding on treatment\nplanning, and the long-term implications of a history of postpartum mood disorder\non subsequent family planning.\nWith seasonal pattern: This specifier applies to recurrent major depressive disorder.\nA. There has been a regular temporal relationship between the onset of major depres-", "source": "dsm5.pdf"} {"id": "fe602c6633d7-1", "page_content": "A. There has been a regular temporal relationship between the onset of major depres-\nsive episodes in major depressive disorder and a particular time of the year (e.g.,\nin the fall or winter).\nNote: Do not include cases in which there is an obvious effect of seasonally related\npsychosocial stressors (e.g., regularly being unemployed every winter).\nB. Full remissions (or a change from major depression to mania or hypomania) also\noccur at a characteristic time of the year (e.g., depression disappears in the spring).\nC. In the last 2 years, two major depressive episodes have occurred that demonstrate\nthe temporal seasonal relationships defined above and no nonseasonal major de-\npressive episodes have occurred during that same period.\nD. Seasonal major depressive episodes (as described above) substantially outnum-\nber the nonseasonal major depressive episodes that may have occurred over the\nindividual\u2019s lifetime.\nNote: The specifier \u201cwith seasonal pattern\u201d can be applied to the pattern of major de-\npressive episodes in major depressive disor der, recurrent. The essential feature is the\nonset and remission of major depressive episodes at characteristic times of the year.\nIn most cases, the episodes begin in fall or winter and remit in spring. Less commonly,\nthere may be recurrent summer depressive episodes. This pattern of onset and remis-\nsion of episodes must have occurred during at least a 2-year period, without any non-\nseasonal episodes occurring during this period. In addition, the seasonal depressive\nepisodes must substantially outnumber any nonseasonal depressive episodes over\nthe individual\u2019s lifetime.\nThis specifier does not apply to those situations in which the pattern is better ex-\nplained by seasonally linked psychosocial stressors (e.g., seasonal unemployment or\nschool schedule). Major depressive episodes that occur in a seasonal pattern are often", "source": "dsm5.pdf"} {"id": "fe602c6633d7-2", "page_content": "school schedule). Major depressive episodes that occur in a seasonal pattern are often\ncharacterized by prominent energy, hypersomn ia, overeating, weight gain, and a crav-\ning for carbohydrates. It is unclear whether a seasonal pattern is more likely in recur-\nrent major depressive disorder or in bipol ar disorders. However, within the bipolar", "source": "dsm5.pdf"} {"id": "388583b4aa1d-0", "page_content": "ing for carbohydrates. It is unclear whether a seasonal pattern is more likely in recur-\nrent major depressive disorder or in bipol ar disorders. However, within the bipolar\ndisorders group, a seasonal pattern appears to be more likely in bipolar II disorder than", "source": "dsm5.pdf"} {"id": "e7c880db477c-0", "page_content": "188 Depressive Disorders\nin bipolar I disorder. In some individuals, the onset of manic or hypomanic episodes\nmay also be linked to a particular season.\nThe prevalence of winter-type seasonal pattern appears to vary with latitude, age,\nand sex. Prevalence increases with higher latitudes. Age is also a strong predictor of\nseasonality, with younger persons at higher risk for winter depressive episodes.\nSpecify if:\nIn partial remission: Symptoms of the immediately previous major depressive episode\nare present, but full criteria are not met, or there is a period lasting less than 2 months\nwithout any significant symptoms of a major depressive episode following the end of\nsuch an episode.\nIn full remission: During the past 2 months, no significant signs or symptoms of the\ndisturbance were present.\nSpecify current severity:\nSeverity is based on the number of criterion symptoms, the severity of those symptoms,\nand the degree of functional disability.\nMild: Few, if any, symptoms in excess of those required to make the diagnosis are\npresent, the intensity of the symptoms is distressing but manageable, and the symp-\ntoms result in minor impairment in social or occupational functioning.\nModerate: The number of symptoms, intensity of symptoms, and/or functional impair-\nment are between those specified for \u201cmild\u201d and \u201csevere.\u201d\nSevere: The number of symptoms is substantially in excess of that required to make\nthe diagnosis, the intensity of the symptoms is seriously distressing and unmanage-\nable, and the symptoms markedly interfere with social and occupational functioning.", "source": "dsm5.pdf"} {"id": "7feb66b68292-0", "page_content": "189Anxiety\n Disorders\nAnxiety disorders include disorders that share feat ures of excessive fear and anxi-\nety and related behavioral disturbances. Fear is the emotional response to real or per-\nceived imminent threat, whereas anxiety is anticipation of future threat. Obviously, these\ntwo states overlap, but they a lso differ, with fear more ofte n associated with surges of au-\ntonomic arousal necessary for fight or flight , thoughts of immediate danger, and escape\nbehaviors, and anxiety more often associated with muscle tension and vigilance in prep-\naration for future danger and cautious or avoidant behavior s. Sometimes the level of fear\nor anxiety is reduced by pervasive avoidance behaviors. Panic attacks feature prominently\nwithin the anxiety disorders as a particular ty pe of fear response. Panic attacks are not lim-\nited to anxiety disorders but rather can be seen in other mental disorders as well.\nThe anxiety disorders differ from one anothe r in the types of objects or situations that\ninduce fear, anxiety, or avoidance behavior, and the associated cognitive ideation. Thus,\nwhile the anxiety disorders tend to be highly comorbid with each other, they can be dif-\nferentiated by close examination of the types of situations that are feared or avoided and\nthe content of the associated thoughts or beliefs. \nAnxiety disorders differ from developmentally normative fear or anxiety by being ex-\ncessive or persisting beyond developmentally appropriate periods. They differ from tran-\nsient fear or anxiety, often st ress-induced, by being persistent (e.g., typically lasting 6 months\nor more), although the criterion for duration is intended as a general guide with allowance\nfor some degree of flexibility and is sometimes of shorter duration in children (as in sepa-\nration anxiety disorder and selective mutism). Since in dividuals with anxiety disorders", "source": "dsm5.pdf"} {"id": "7feb66b68292-1", "page_content": "ration anxiety disorder and selective mutism). Since in dividuals with anxiety disorders\ntypically overestimate the danger in situations they fear or avoid, the primary determina-\ntion of whether the fear or anxiety is excessive or out of proportion is made by the clinician,\ntaking cultural contextual fa ctors into account. Many of the anxiety disorders develop in\nchildhood and tend to persist if not treated. Most occur more frequent ly in females than in\nmales (approximately 2:1 ratio). Each anxiety disorder is diagnosed only when the symp-\ntoms are not attributable to th e physiological effects of a substance/medication or to another\nmedical condition or are not better explained by another mental disorder. \nThe chapter is arranged developmentally, with disord ers sequenced according to the\ntypical age at onset. The individual with sepa ration anxiety disorder is fearful or anxious\nabout separation from attachment figures to a degree that is developmentally inappro-\npriate. There is persistent fear or anxiety about harm coming to attachment figures and\nevents that could lead to loss of or separati on from attachment figures and reluctance to go\naway from attachment figures, as well as nightmares and physical symptoms of distress. Al-\nthough the symptoms often deve lop in childhood, they can be expressed throughout adult-\nhood as well.\nSelective mutism is characterized by a consiste nt failure to speak in social situations in\nwhich there is an expectation to speak (e.g., school) even though the individual speaks in\nother situations. The failure to speak has significant consequences on achievement in aca-\ndemic or occupational settings or otherwise interferes with normal social communication. \nIndividuals with specific phobia are fearful or anxious about or avoidant of circum-\nscribed objects or situations. A specific cognitive ideation is not featured in this disorder,", "source": "dsm5.pdf"} {"id": "7feb66b68292-2", "page_content": "scribed objects or situations. A specific cognitive ideation is not featured in this disorder,\nas it is in other anxiety diso rders. The fear, anxiety, or av oidance is almost always imme-", "source": "dsm5.pdf"} {"id": "a54189a66626-0", "page_content": "190 Anxiety Disorders\ndiately induced by the phobic situation, to a de gree that is persistent and out of proportion\nto the actual risk posed. There are various ty pes of specific phobias: animal; natural envi-\nronment; blood-injectio n-injury; situational; and other situations. \nIn social anxiety disorder (social phobia), the individual is fearful or anxious about or\navoidant of social interactions and situations that involve the possi bility of being scruti-\nnized. These include social interactions such as meeting unfamiliar people, situations in\nwhich the individual may be observed eating or drinking, and situations in which the in-\ndividual performs in front of others. The cogn itive ideation is of being negatively evalu-\nated by others, by being em barrassed, humiliated, or re jected, or offending others.\nIn panic disorder, the individual experiences recurrent unexpected panic attacks and is\npersistently concerned or worr ied about having more panic attacks or changes his or her\nbehavior in maladaptive ways because of the pa nic attacks (e.g., avoidance of exercise or of\nunfamiliar locations). Panic attacks are abrupt surges of intense fear or intense discomfort\nthat reach a peak within minutes, accompan ied by physical and/or cognitive symptoms.\nLimited-symptom panic attacks include fewer than four symptoms. Panic attacks may be\nexpected, such as in response to a typically feared object or situation, or unexpected, meaning\nthat the panic attack occurs for no apparent reason. Panic attacks function as a marker and\nprognostic factor for severity of diagnosis, co urse, and comorbidity ac ross an array of dis-\norders, including, but not limit ed to, the anxiety disorders (e.g., substance use, depressive\nand psychotic disorders). Panic attack may therefore be used as a descriptive specifier for", "source": "dsm5.pdf"} {"id": "a54189a66626-1", "page_content": "and psychotic disorders). Panic attack may therefore be used as a descriptive specifier for\nany anxiety disorder as well as other mental disorders. \nIndividuals with agoraphobia are fearful and anxious about two or more of the follow-\ning situations: using public transportation; being in open spaces; being in enclosed places;\nstanding in line or being in a crowd; or bein g outside of the home alone in other situations.\nThe individual fears these situations because of thoughts that escape might be difficult or\nhelp might not be available in the event of developing panic-like symptoms or other inca-\npacitating or embarrassing symptoms. These situ ations almost always induce fear or anx-\niety and are often avoided and requ ire the presence of a companion. \nThe key features of generalized anxiety diso rder are persistent and excessive anxiety\nand worry about various domains, including work and school performance, that the indi-\nvidual finds difficult to contro l. In addition, the individual experiences physical symptoms,\nincluding restlessness or feeling keyed up or on edge; being easily fatigued; difficulty con-\ncentrating or mind going blank; irritabilit y; muscle tension; and sleep disturbance. \nSubstance/medication-induced anxiety disord er involves anxiety due to substance in-\ntoxication or withdrawal or to a medication treatment. In anxiety di sorder due to another\nmedical condition, anxiety symptoms are th e physiological consequence of another med-\nical condition.\nDisorder-specific scales are available to bette r characterize the seve rity of each anxiety\ndisorder and to capture change in severity over time. For ease of use, particularly for in-\ndividuals with more than one anxiety disorder, these scales have been developed to have\nthe same format (but different focus) across the anxiety disorders, with ratings of behav-", "source": "dsm5.pdf"} {"id": "a54189a66626-2", "page_content": "the same format (but different focus) across the anxiety disorders, with ratings of behav-\nioral symptoms, cognitive idea tion symptoms, and physical symptoms relevant to each\ndisorder.\nSeparation Anxiety Disorder\nDiagnostic Criteria 309.21 (F93.0)\nA. Developmentally inappropriate and excessive fear or anxiety concerning separation from\nthose to whom the individual is attached, as evidenced by at least three of the following:", "source": "dsm5.pdf"} {"id": "f8b1aee41302-0", "page_content": "A. Developmentally inappropriate and excessive fear or anxiety concerning separation from\nthose to whom the individual is attached, as evidenced by at least three of the following:\n1. Recurrent excessive distress when antic ipating or experiencing separation from\nhome or from major attachment figures.", "source": "dsm5.pdf"} {"id": "2b1a067340a5-0", "page_content": "Separation Anxiety Disorder 191\n2. Persistent and excessive worry about losing major attachment figures or about pos-\nsible harm to them, such as illness, injury, disasters, or death.\n3. Persistent and excessive worry about experiencing an untoward event (e.g., getting\nlost, being kidnapped, having an accident, becoming ill) that causes separation\nfrom a major attachment figure.\n4. Persistent reluctance or refusal to go out, away from home, to school, to work, or\nelsewhere because of fear of separation.\n5. Persistent and excessive fear of or reluctance about being alone or without major\nattachment figures at home or in other settings.\n6. Persistent reluctance or refusal to sleep away from home or to go to sleep without\nbeing near a major attachment figure.\n7. Repeated nightmares involving the theme of separation.\n8. Repeated complaints of physical symptoms (e.g., headaches, stomachaches, nau-\nsea, vomiting) when separation from major attachment figures occurs or is antici-\npated.\nB. The fear, anxiety, or avoidance is persistent, lasting at least 4 weeks in children and\nadolescents and typically 6 months or more in adults.\nC. The disturbance causes clinically significant distress or impairment in social, aca-\ndemic, occupational, or other im portant areas of functioning.\nD. The disturbance is not better explained by another mental disorder, such as refusing\nto leave home because of excessive resistance to change in autism spectrum disorder;\ndelusions or hallucinations concerning separation in psychotic disorders; refusal to go\noutside without a trusted companion in agoraphobia; worries about ill health or other\nharm befalling significant others in generalized anxiety disorder; or concerns about\nhaving an illness in illness anxiety disorder.\nDiagnostic Features\nThe essential feature of separation anxiety disorder is excessive fear or anxiety concerning", "source": "dsm5.pdf"} {"id": "2b1a067340a5-1", "page_content": "Diagnostic Features\nThe essential feature of separation anxiety disorder is excessive fear or anxiety concerning\nseparation from home or attachment figures. The anxiety exceeds what may be expected\ngiven the person\u2019s developmental level (Criteri on A). Individuals with separation anxiety\ndisorder have symptoms that meet at least th ree of the following criteria: They experience\nrecurrent excessive distress when separation fr om home or major atta chment figures is an-\nticipated or occurs (Criterion A1). They wo rry about the well-being or death of attachment\nfigures, particularly when separated from them, and they need to know the whereabouts\nof their attachment figures and want to stay in touch with them (Criterion A2). They also\nworry about untoward events to themselves, such as getting los t, being kidnapped, or\nhaving an accident, that would keep them fr om ever being reunited with their major at-\ntachment figure (Criterion A3). Individuals with separation anxiety disorder are reluctant\nor refuse to go out by themselves because of separation fears (Criterion A4). They have\npersistent and excessive fear or reluctance about being alone or without major attachment\nfigures at home or in other settings. Children with separa tion anxiety disorder may be un-\nable to stay or go in a room by themselv es and may display \u201cclinging\u201d behavior, staying\nclose to or \u201cshadowing\u201d the parent around the house, or requiring someone to be with\nthem when going to another room in the house (Criterion A5). They have persistent reluc-\ntance or refusal to go to sleep without bein g near a major attachme nt figure or to sleep\naway from home (Criterion A6). Children with this disorder often have difficulty at bed-\ntime and may insist that someone stay with them until they fall asleep. During the night,", "source": "dsm5.pdf"} {"id": "2b1a067340a5-2", "page_content": "time and may insist that someone stay with them until they fall asleep. During the night,\nthey may make their way to their parents\u2019 bed (or that of a significant other, such as a sib-\nling). Children may be reluctant or refuse to at tend camp, to sleep at friends\u2019 homes, or to\ngo on errands. Adults may be uncomfortable when traveling independently (e.g., sleeping\nin a hotel room). There may be repeated nightmares in which the content expresses the in-", "source": "dsm5.pdf"} {"id": "54dcee17128b-0", "page_content": "192 Anxiety Disorders\ndividual\u2019s separation anxiety (e.g., destructio n of the family through fire, murder, or other\ncatastrophe) (Criterion A7). Physical sympto ms (e.g., headaches, abdominal complaints,\nnausea, vomiting) are common in children when separation from major attachment fig-\nures occurs or is anticipated (Criterion A8). Cardiovascular symptoms such as palpitations,\ndizziness, and feeling faint are rare in youn ger children but may occur in adolescents and\nadults.\nThe disturbance must last for a period of at least 4 weeks in children and adolescents\nyounger than 18 years and is typically 6 months or longer in adults (Criterion B). However,\nthe duration criterion for adults should be used as a general guide, with allowance for\nsome degree of flexibilit y. The disturbance must cause clinically significant distress or im-\npairment in social, academic, occupational, or other important areas of functioning (Cri-\nterion C). \nAssociated Features Supporting Diagnosis\nWhen separated from major attachment figure s, children with separation anxiety disorder\nmay exhibit social withdrawal, apathy, sadne ss, or difficulty concentrating on work or\nplay. Depending on their age, individuals may have fears of animals, monsters, the dark,\nmuggers, burglars, kidnappers, car accidents, plane travel, and other situations that are\nperceived as presenting danger to the family or themselves. So me individuals become\nhomesick and uncomfortable to the point of misery when away from home. Separation\nanxiety disorder in children may lead to school refusal, which in turn may lead to academic\ndifficulties and social isolation. When extrem ely upset at the prospect of separation, chil-\ndren may show anger or occasionally aggres sion toward someone who is forcing separa-", "source": "dsm5.pdf"} {"id": "54dcee17128b-1", "page_content": "dren may show anger or occasionally aggres sion toward someone who is forcing separa-\ntion. When alone, especially in the evening or the dark, youn g children may report unusual\nperceptual experiences (e.g., seeing people p eering into their room, frightening creatures\nreaching for them, feeling eyes staring at them ). Children with this disorder may be de-\nscribed as demanding, intrusive, and in need of constant attention, and, as adults, may ap-\npear dependent and overprotective. The indi vidual\u2019s excessive de mands often become a\nsource of frustration fo r family members, leading to resent ment and conflict in the family.\nPrevalence\nThe 12-month prevalence of separation anxiety disorder among adults in the United States\nis 0.9%\u20131.9%. In children, 6- to 12-month prevalence is estima ted to be approximately 4%.\nIn adolescents in the United States, the 12-mo nth prevalence is 1.6%. Separation anxiety\ndisorder decreases in prevalence from child hood through adolescence and adulthood and\nis the most prevalent anxiety diso rder in children younger than 12 years. In clinical sam-\nples of children, the disorder is equally common in males and females. In the community,\nthe disorder is more frequent in females.\nDevelopment and Course\nPeriods of heightened separation anxiety from attachment figures are part of normal early\ndevelopment and may indicate the development of secure attachment relationships (e.g.,\naround 1 year of age, when infants may suffe r from stranger anxiety). Onset of separation\nanxiety disorder may be as early as preschoo l age and may occur at any time during child-\nhood and more rarely in adolescence. Typica lly there are periods of exacerbation and re-", "source": "dsm5.pdf"} {"id": "54dcee17128b-2", "page_content": "mission. In some cases, both the anxiety ab out possible separation and the avoidance of\nsituations involving separation from the home or nuclear family (e.g., going away to col-\nlege, moving away from attachment figure s) may persist through adulthood. However,\nthe majority of children with separation anxiety disorder are free of impairing anxiety dis-\norders over their lifetimes. Many adults with separation anxi ety disorder do not recall a\nchildhood onset of separation anxiety disorder, although they may recall symptoms.", "source": "dsm5.pdf"} {"id": "59a324f75bcb-0", "page_content": "Separation Anxiety Disorder 193\nThe manifestations of separation anxiety di sorder vary with age. Younger children are\nmore reluctant to go to school or may avoi d school altogether. Younger children may not\nexpress worries or specific fears of definite th reats to parents, home, or themselves, and the\nanxiety is manifested only when separation is experienced. As children age, worries\nemerge; these are often worries about specific dangers (e.g., accidents, kidnapping, mug-\nging, death) or vague concerns about not being reunited with attachment figures. In adults,\nseparation anxiety disorder may limit their ability to cope with changes in circumstances\n(e.g., moving, getting married). Adults with the disorder are typically overconcerned about\ntheir offspring and spouses and experience ma rked discomfort when separated from them.\nThey may also experience significant disruption in work or social experiences because of\nneeding to continuously check on the whereabouts of a significant other. \nRisk and Prognostic Factors \nEnvironmental. Separation anxiety disorder often deve lops after life stress, especially a\nloss (e.g., the death of a\u00a0relative or pet; an illness of the individual or a relative; a change of\nschools; parental divorce; a move to a new neighborhood; immigratio n; a disaster that in-\nvolved periods of separation from attachment figures). In young adults, other examples of\nlife stress include leaving the parental home, en tering into a romantic relationship, and be-\ncoming a parent. Parental overprotection and intrusiveness may be associated with sepa-\nration anxiety disorder.\nGenetic and physiological. Separation anxiety disorder in children may be heritable.\nHeritability was estimated at 73% in a communi ty sample of 6-year-old twins, with higher\nrates in girls. Children with separation an xiety disorder display particularly enhanced", "source": "dsm5.pdf"} {"id": "59a324f75bcb-1", "page_content": "rates in girls. Children with separation an xiety disorder display particularly enhanced\nsensitivity to respirat ory stimulation using CO2-enriched air.\nCulture-Related Diagnostic Issues\nThere are cultural variations in the degree to which it is co nsidered desirable to tolerate\nseparation, so that demands and opportunit ies for separation between parents and chil-\ndren are avoided in some cultures. For exampl e, there is wide variation across countries\nand cultures with respect to the age at which it is expected that offspring should leave the\nparental home. It is important to differenti ate separation anxiety disorder from the high\nvalue some cultures place on strong interdependence among family members.\nGender-Related Diagnostic Issues\nGirls manifest greater reluctance to attend or avoidance of school th an boys. Indirect ex-\npression of fear of separation may be more common in males than in females, for example,\nby limited independent activity , reluctance to be away from home alone, or distress when\nspouse or offspring do things independently or when contact with spouse or offspring is\nnot possible.\nSuicide Risk\nSeparation anxiety disorder in children may be associated with an increased risk for sui-\ncide. In a community sample, the presence of mood disorders, anxiety disorders, or sub-\nstance use has been associated with suicidal ideation and attempts. However, this\nassociation is not specific to separation anxi ety disorder and is found in several anxiety\ndisorders.\nFunctional Consequences of Separation Anxiety Disorder\nIndividuals with separation anxiety disorder often limit independent activities away from\nhome or attachment figures (e.g., in children, avoiding school, not going to camp, having", "source": "dsm5.pdf"} {"id": "27318411bd45-0", "page_content": "194 Anxiety Disorders\ndifficulty sleeping alone; in adol escents, not going away to coll ege; in adults, not leaving the\nparental home, not tr aveling, not working outside the home). \nDifferential Diagnosis\nGeneralized anxiety disorder. Separation anxiety disorder is distinguished from gener-\nalized anxiety disorder in that the anxiety predominantly concerns separation from attach-\nment figures, and if other wo rries occur, they do not pred ominate the clinical picture. \nPanic disorder. Threats of separation may lead to extreme anxiety and even a panic at-\ntack. In separation anxiety disorder, in contr ast to panic disorder, the anxiety concerns the\npossibility of being away from attachment figures and worry about untoward events be-\nfalling them, rather than being incapacitated by an unexpected panic attack. \nAgoraphobia. Unlike individuals with agoraphobia, those with separation anxiety dis-\norder are not anxious about being trapped or incapacitated in situations from which es-\ncape is perceived as difficult in the event of panic-like sy mptoms or other incapacitating\nsymptoms.\nConduct disorder. School avoidance (truancy) is common in conduct disorder, but anx-\niety about separation is not responsible for school absences, and the child or adolescent\nusually stays away from, rather than returns to, the home. \nSocial anxiety disorder. School refusal may be due to soci al anxiety disorder (social pho-\nbia). In such instances, the school avoidance is due to fear of being judged negatively by oth-\ners rather than to worries about being separated from the attachment figures. \nPosttraumatic stress disorder. Fear of separation from loved ones is common after trau-\nmatic events such as a disasters, particularly when periods of separation from loved ones", "source": "dsm5.pdf"} {"id": "27318411bd45-1", "page_content": "matic events such as a disasters, particularly when periods of separation from loved ones\nwere experienced during the traumatic event. In posttraumatic stress disorder (PTSD), the\ncentral symptoms concern intr usions about, and avoidance of, memories associated with\nthe traumatic event itself, whereas in separa tion anxiety disorder, the worries and avoid-\nance concern the well-being of attachme nt figures and separation from them.\nIllness anxiety disorder. Individuals with illness anxiety disorder worry about specific\nillnesses they may have, but the main concer n is about the medical diagnosis itself, not\nabout being separated fr om attachment figures.\nBereavement. Intense yearning or longing for th e deceased, intense sorrow and emo-\ntional pain, and preoccupation with the deceased or the circumstances of the death are ex-\npected responses occurring in bereavement, whereas fear of separation from other\nattachment figures is central in separation anxiety disorder.\nDepressive and bipolar disorders. These disorders may be associated with reluctance\nto leave home, but the main concern is not wo rry or fear of untoward events befalling at-\ntachment figures, but rather low motivation for engaging with the outside world. How-\never, individuals with separation anxiety disorder may become depressed while being\nseparated or in anticipation of separation.\nOppositional defiant disorder. Children and adolescents with separation anxiety disor-\nder may be oppositional in the context of being forced to separate from attachment figures.\nOppositional defiant disorder should be considered only wh en there is persistent opposi-\ntional behavior unrelated to the anticipation or occurrence of separation from attachment\nfigures.\nPsychotic disorders. Unlike the hallucinations in psychotic disorders, the unusual per-\nceptual experiences that may occur in separati on anxiety disorder are usually based on a", "source": "dsm5.pdf"} {"id": "27318411bd45-2", "page_content": "ceptual experiences that may occur in separati on anxiety disorder are usually based on a\nmisperception of an actual stimulus, occur only in certain situations (e.g., nighttime), and\nare reversed by the presence of an attachment figure.", "source": "dsm5.pdf"} {"id": "86eec59a62e7-0", "page_content": "Selective Mutism 195\nPersonality disorders. Dependent personality disorder is characterized by an indis-\ncriminate tendency to rely on others, wherea s separation anxiety disorder involves con-\ncern about the proximity and safety of main attachment figures. Bo rderline personality\ndisorder is characterized by fear of abandonm ent by loved ones, but problems in identity,\nself-direction, interpersonal fu nctioning, and impulsivity are additionally central to that\ndisorder, whereas they are not centra l to separation anxiety disorder. \nComorbidity\nIn children, separation anxiety disorder is hi ghly comorbid with ge neralized anxiety dis-\norder and specific phobia. In adults, comm on comorbidities include specific phobia,\nPTSD, panic disorder, generalized anxiety diso rder, social anxiety disorder, agoraphobia,\nobsessive-compulsive disorder, and personality disorders. Depressive and bipolar disor-\nders are also comorbid with separation anxiety disorder in adults.\nSelective Mutism\nDiagnostic Criteria 313.23 (F94.0)\nA. Consistent failure to speak in specific social situations in which there is an expectation\nfor speaking (e.g., at school) despite speaking in other situations.\nB. The disturbance interferes with educational or occupational achievement or with social\ncommunication.\nC. The duration of the disturbance is at least 1 month (not limited to the first month of\nschool).\nD. The failure to speak is not attributable to a lack of knowledge of, or comfort with, the\nspoken language required in the social situation.\nE. The disturbance is not better explained by a communication disorder (e.g., childhood-\nonset fluency disorder) and does not occur exclusively during the course of autism\nspectrum disorder, schizophrenia, or another psychotic disorder.\nDiagnostic Features", "source": "dsm5.pdf"} {"id": "86eec59a62e7-1", "page_content": "spectrum disorder, schizophrenia, or another psychotic disorder.\nDiagnostic Features\nWhen encountering other individuals in social interactions, children with selective mut-\nism do not initiate speech or reciprocally respond when spoken to by others. Lack of\nspeech occurs in social interactions with chil dren or adults. Children with selective mut-\nism will speak in their home in the presence of immediate family members but often not\neven in front of close friends or second-degr ee relatives, such as grandparents or cousins.\nThe disturbance is often marked by high social anxiety. Children with selective mutism of-\nten refuse to speak at school, leading to ac ademic or educational impairment, as teachers\noften find it difficult to assess skills such as reading. The lack of speech may interfere with\nsocial communication, although children wi th this disorder sometimes use nonspoken or\nnonverbal means (e.g., grunting, pointing, wr iting) to communicate and may be willing or\neager to perform or engage in social encounters when speech is not required (e.g., nonver-\nbal parts in school plays). \nAssociated Features Supporting Diagnosis\nAssociated features of selectiv e mutism may include excessive shyness, fear of social em-\nbarrassment, social isolation and withdrawal , clinging, compulsive traits, negativism,\ntemper tantrums, or mild oppositional beha vior. Although children with this disorder\ngenerally have normal language skills, ther e may occasionally be an associated commu-", "source": "dsm5.pdf"} {"id": "571cc5e9cd25-0", "page_content": "196 Anxiety Disorders\nnication disorder, although no particular association with a specific communication dis-\norder has been identified. Even when these disorders are present, anxiety is present as\nwell. In clinical settings, children with select ive mutism are almost always given an addi-\ntional diagnosis of another anxiety disorder\u2014most commonly, social anxiety disorder (so-\ncial phobia).\nPrevalence\nSelective mutism is a relatively rare disorder and has not been included as a diagnostic cat-\negory in epidemiological studies of prevalen ce of childhood disorders. Point prevalence\nusing various clinic or school samples ranges between 0.03% and 1% depending on the set-\nting (e.g., clinic vs. school vs. general population) and ages of the individual s in the sample.\nThe prevalence of the disorder does not seem to vary by sex or race/ethnicity. The disor-\nder is more likely to manifest in young children than in adolescents and adults.\nDevelopment and Course\nThe onset of selective mutism is usually befo re age 5 years, but the disturbance may not\ncome to clinical attention until entry into scho ol, where there is an increase in social inter-\naction and performance tasks, such as readin g aloud. The persistence of the disorder is\nvariable. Although clinical reports suggest that many individuals \u201coutgrow\u201d selective\nmutism, the longitudinal course of the disorder is unknown. In some cases, particularly in\nindividuals with social anxiety disorder, selective mutism may disappear, but symptoms\nof social anxiety disorder remain. \nRisk and Prognostic Factors \nTemperamental. Temperamental risk factors for sele ctive mutism are not well identi-\nfied. Negative affectivity (neuroticism) or be havioral inhibition may play a role, as may", "source": "dsm5.pdf"} {"id": "571cc5e9cd25-1", "page_content": "parental history of shyness, social isolation, and social anxiety. Children with selective\nmutism may have subtle receptive language difficulties compared wi th their peers, al-\nthough receptive language is still within the normal range. \nEnvironmental. Social inhibition on the part of parents may serve as a model for social\nreticence and selective mutism in children. Furthermore, parents of children with selective\nmutism have been described as overprotective or more cont rolling than parents of chil-\ndren with other anxiety d isorders or no disorder.\nGenetic and physiological factors. Because of the significant overlap between selective\nmutism and social anxiety disorder, there may be shared genetic factors between these\nconditions.\nCulture-Related Diagnostic Issues\nChildren in families who have immigrated to a country where a different language is spo-\nken may refuse to speak the new language beca use of lack of knowledge of the language.\nIf comprehension of the new language is adequa te but refusal to speak persists, a diagno-\nsis of selective mutism may be warranted.\nFunctional Consequences of Selective Mutism \nSelective mutism may result in social impairment, as childr en may be too anxious to en-\ngage in reciprocal social interaction with other children. As children with selective mutism\nmature, they may face increasing social isolation. In school settings, these children may\nsuffer academic impairment, because often th ey do not communicate with teachers re-\ngarding their academic or personal needs (e.g ., not understanding a class assignment, not", "source": "dsm5.pdf"} {"id": "5331c0e8b4bd-0", "page_content": "Specific Phobia 197\nasking to use the restroom). Severe impairment in school and social functioning, including\nthat resulting from teasing by peers, is co mmon. In certain instances, selective mutism\nmay serve as a compensatory strategy to decr ease anxious arousal in social encounters.\nDifferential Diagnosis\nCommunication disorders. Selective mutism should be di stinguished from speech dis-\nturbances that are better explained by a communication disorder, such as language\ndisorder, speech sound disorder (previously phonological disorder), childhood-onset\nfluency disorder (stuttering), or pragmatic (social) communication disorder. Unlike selec-\ntive mutism, the speech disturbance in these cond itions is not restricted to a specific social\nsituation. \nNeurodevelopmental disorders and schizo phrenia and other psychotic disorders.\nIndividuals with an autism spectrum disord er, schizophrenia or another psychotic disor-\nder, or severe intellectual disability may ha ve problems in social communication and be\nunable to speak appropriately in social situations. In contrast, selective mutism should be\ndiagnosed only when a child has an established capacity to speak in some social situations\n(e.g., typically at home).\nSocial anxiety disorder (social phobia). The social anxiety and social avoidance in so-\ncial anxiety disorder may be associated with selective mutism. In such cases, both diagno-\nses may be given.\nComorbidity\nThe most common comorbid conditions are other anxiety disorders, most commonly so-\ncial anxiety disorder, followed by separation anxiety diso rder and specific phobia. Oppo-\nsitional behaviors have been noted to occur in children with selective mutism, although\noppositional behavior may be limited to sit uations requiring speech. Communication de-\nlays or disorders also may appear in some children with selective mutism.\nSpecific Phobia", "source": "dsm5.pdf"} {"id": "5331c0e8b4bd-1", "page_content": "Specific Phobia\nDiagnostic Criteria\nA. Marked fear or anxiety about a specific object or situation (e.g., flying, heights, animals,\nreceiving an injection, seeing blood). \nNote: In children, the fear or anxiety may be expressed by crying, tantrums, freezing,\nor clinging.\nB. The phobic object or situation almost always provokes immediate fear or anxiety.\nC. The phobic object or situation is actively avoided or endured with intense fear or anxiety.\nD. The fear or anxiety is out of proportion to the actual danger posed by the specific object\nor situation and to the sociocultural context.\nE. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more. \nF. The fear, anxiety, or avoidance causes clin ically significant distress or impairment in\nsocial, occupational, or other important areas of functioning.\nG. The disturbance is not better explained by the symptoms of another mental disorder,\nincluding fear, anxiety, and avoidance of situations associated with panic-like symptoms\nor other incapacitating symptoms (as in agoraphobia); objects or situations related to\nobsessions (as in obsessive-compulsive disorder); reminders of traumatic events (as in\nposttraumatic stress disorder); separation from home or attachment figures (as in sep-\naration anxiety disorder); or social situations (as in social anxiety disorder).", "source": "dsm5.pdf"} {"id": "9750697b225a-0", "page_content": "198 Anxiety Disorders\nSpecify if:\nCode based on the phobic stimulus:\n300.29 (F40.218) Animal (e.g., spiders, insects, dogs).\n300.29 (F40.228) Natural environment (e.g., heights, storms, water).\n300.29 (F40.23x) Blood-injection-injury (e.g., needles, invasive medical procedures).\nCoding note: Select specific ICD-10-CM code as follows: F40.230 fear of blood;\nF40.231 fear of injections and transfusions; F40.232 fear of other medical care; or\nF40.233 fear of injury.\n300.29 (F40.248) Situational (e.g., airplanes, elevators, enclosed places).\n300.29 (F40.298) Other (e.g., situations that may lead to choking or vomiting; in chil-\ndren, e.g., loud sounds or costumed characters).\nCoding note: When more than one phobic stimulus is present, code all ICD-10-CM codes\nthat apply (e.g., for fear of snakes and flying, F40.218 specific phobia, animal, and\nF40.248 specific phobia, situational).\nSpecifiers\nIt is common for individuals to have multiple specific phobias. The average individual with\nspecific phobia fears three objects or situatio ns, and approximately 75% of individuals with\nspecific phobia fear more than on e situation or object. In such cases, multiple specific phobia\ndiagnoses, each with its own diagnostic code reflecting the phobic stimulus, would need to be\ngiven. For example, if an individual fears thunderstorms and flying , then two diagnoses\nwould be given: specific phobia, natural en vironment, and specific phobia, situational.", "source": "dsm5.pdf"} {"id": "9750697b225a-1", "page_content": "Diagnostic Features\nA key feature of this disorder is that the fear or anxiety is circumscribed to the presence of a\nparticular situation or object (Criterion A), which may be termed the phobic stimulus. The cat-\negories of feared situations or objects are provi ded as specifiers. Many individuals fear objects\nor situations from more than one category, or phobic stimulus. For th e diagnosis of specific\nphobia, the response must differ from normal, transient fears that commonly occur in the pop-\nulation. To meet the criteria for a diagnosis, the fear or anxiety must be intense or severe (i.e.,\n\u201cmarked\u201d) (Criterion A). The amount of fear experienced may vary wi th proximity to the\nfeared object or situation and may occur in anticipa tion of or in the actual presence of the object\nor situation. Also, the fear or anxiety may take the form of a full or limited symptom panic at-\ntack (i.e., expected panic attack). Another characteri stic of specific phobias is that fear or anxi-\nety is evoked nearly every time the individual comes into contact with the phobic stimulus\n(Criterion B). Thus, an indivi dual who becomes anxious only occasionally upon being con-\nfronted with the situation or object (e.g., become s anxious when flying only on one out of every\nfive airplane flights) would not be diagnosed with specific phobia. However, the degree of fear\nor anxiety expressed may vary (from anticipatory anxiety to a full panic attack) across different\noccasions of encountering the phobic object or situation because of various contextual factors\nsuch as the presence of others, duration of exposure, and other threat ening elements such as\nturbulence on a flight for indi viduals who fear flying. Fear and anxiety are often expressed dif-", "source": "dsm5.pdf"} {"id": "9750697b225a-2", "page_content": "ferently between children and adults. Also, the fear or anxiety occurs as soon as the phobic ob-\nject or situation is encountered (i.e., immediately rather than being delayed). \nThe individual actively avoids the situation, or if he or she either is unable or decides\nnot to avoid it, the situation or object evok es intense fear or anxiety (Criterion C). Active\navoidance means the individual intentionally behave s in ways that are designed to prevent\nor minimize contact with phobic objects or situ ations (e.g., takes tunnels instead of bridges\non daily commute to work for fear of heights; avoids entering a dark room for fear of spi-\nders; avoids accepting a job in a locale wh ere a phobic stimulus is more common). Avoid-", "source": "dsm5.pdf"} {"id": "a2fc7fa3c798-0", "page_content": "Specific Phobia 199\nance behaviors are often obvious (e.g., an indi vidual who fears blood refusing to go to the\ndoctor) but are sometimes less obvious (e.g., an individual who fears snakes refusing to\nlook at pictures that resemble the form or shape of snakes). Many individuals with specific\nphobias have suffered over many years and have changed their living circumstances in\nways designed to avoid the phobic object or si tuation as much as possible (e.g., an indi-\nvidual diagnosed with specific phobia, animal , who moves to reside in an area devoid of\nthe particular feared animal). Therefore, they no longer experience fear or anxiety in their\ndaily life. In such instances, avoidance behavi ors or ongoing refusal to engage in activities\nthat would involve exposure to the phobic object or situation (e.g., repeated refusal to ac-\ncept offers for work-related travel because of fear of flying) may be helpful in confirming\nthe diagnosis in the absence of overt anxiety or panic. \nThe fear or anxiety is out of proportion to th e actual danger that the object or situation\nposes, or more intense than is deemed necess ary (Criterion D). Although individuals with\nspecific phobia often recognize their reactions as disproportionate, th ey tend to overesti-\nmate the danger in their feared situations, an d thus the judgment of being out of propor-\ntion is made by the cl inician. The individual \u2019s sociocultural contex t should also be taken\ninto account. For example, fears of the dark may be reasonable in a context of ongoing\nviolence, and fear of insects may be more di sproportionate in settings where insects are\nconsumed in the diet. The fear, anxiety, or avoidance is persistent, typically lasting for\n6 months or more (Criterion E), which helps distinguish the disorder from transient fears", "source": "dsm5.pdf"} {"id": "a2fc7fa3c798-1", "page_content": "6 months or more (Criterion E), which helps distinguish the disorder from transient fears\nthat are common in the popu lation, particularly among children. However, the duration\ncriterion should be used as a general guide, with allowance for so me degree of flexibility.\nThe specific phobia must cause clinically sign ificant distress or impairment in social, oc-\ncupational, or other important areas of functioning in order for the disorder to be diag-\nnosed (Criterion F).\nAssociated Features Supporting Diagnosis\nIndividuals with specific phobia typically experience an increase in physiological arousal\nin anticipation of or during exposure to a phobic object or situation. However, the physi-\nological response to the feared situation or object varies. Whereas individuals with situa-\ntional, natural environment, an d animal specific phobias are likely to show sympathetic\nnervous system arousal, individuals with bloo d-injection-injury specific phobia often\ndemonstrate a vasovagal fainting or near-faint ing response that is marked by initial brief\nacceleration of heart rate an d elevation of blood pressure followed by a deceleration of\nheart rate and a drop in blood pressure. Curr ent neural systems models for specific phobia\nemphasize the amygdala and related structures, much as in other anxiety disorders.\nPrevalence\nIn the United States, the 12-month community prevalence estimate for specific phobia is\napproximately 7%\u20139%. Prevalence rates in European countrie s are largely similar to those\nin the United States (e.g., about 6%), but rate s are generally lower in Asian, African, and\nLatin American countries (2%\u20134%). Prevalence rates are approximately 5% in children and\nare approximately 16% in 13- to 17-year-olds. Prevalence rates are lower in older individ-", "source": "dsm5.pdf"} {"id": "a2fc7fa3c798-2", "page_content": "uals (about 3%\u20135%), possibly reflecting diminishing severity to subclinical levels. Females\nare more frequently affected than males, at a rate of approximately 2:1, although rates vary\nacross different phobic stimuli. That is, animal, natural envi ronment, and situational spe-\ncific phobias are predominantly experienced by females, whereas blood-injection-injury\nphobia is experienced nearly equally by both genders. \nDevelopment and Course", "source": "dsm5.pdf"} {"id": "74e93956470b-0", "page_content": "cific phobias are predominantly experienced by females, whereas blood-injection-injury\nphobia is experienced nearly equally by both genders. \nDevelopment and Course\nSpecific phobia sometimes develops following a traumatic event (e.g., being attacked by\nan animal or stuck in an elevat or), observation of others going through a traumatic event (e.g.,", "source": "dsm5.pdf"} {"id": "750cb9f5177b-0", "page_content": "200 Anxiety Disorders\nwatching someone drown), an unexpected panic attack in the to be feared situation (e.g.,\nan unexpected panic attack while on the subway), or informational transmission (e.g., ex-\ntensive media coverage of a plane crash). However, many individuals with specific phobia\nare unable to recall the specific reason for the onset of their phobias. Specific phobia usu-\nally develops in early childho od, with the majority of case s developing prior to age 10\nyears. The median age at onset is between 7 and 11 years, with the mean at about 10 years.\nSituational specific phobias tend to have a later age at onset than natural environment, an-\nimal, or blood-injection-injury specific phob ias. Specific phobias that develop in child-\nhood and adolescence are likely to wax and wane during that period. However, phobias\nthat do persist into adulthood are unlikely to remit for the majority of individuals. \nWhen specific phobia is being diagnosed in children, two issues sh ould be considered.\nFirst, young children may express their fear and anxiety by crying, tantrums, freezing,\nor clinging. Second, young children typically are not able to understand the concept of\navoidance. Therefore, the clinician should assemble additional information from parents,\nteachers, or others who know the child well. Excessive fears are quite common in young\nchildren but are usually transitory and only m ildly impairing and thus considered devel-\nopmentally appropriate. In such cases a diag nosis of specific phobia would not be made.\nWhen the diagnosis of specific phobia is being considered in a child, it is important to\nassess the degree of im pairment and the duration of the fear, anxiety, or avoidance, and", "source": "dsm5.pdf"} {"id": "750cb9f5177b-1", "page_content": "whether it is typical for the child\u2019s particular developmental stage. \nAlthough the prevalence of specific phobia is lower in older populations, it remains\none of the more commonly experienced disorders in late life. Several issues should be con-\nsidered when diagnosing specific phobia in older populations. Fi rst, older individuals\nmay be more likely to endorse natural envi ronment specific phobias, as well as phobias of\nfalling. Second, specific phobia (like all anxiet y disorders) tends to co-occur with medical\nconcerns in older individuals, including co ronary heart disease and chronic obstructive\npulmonary disease. Third, older individuals may be more likely to attribute the symptoms\nof anxiety to medical conditions. Fourth, olde r individuals may be more likely to manifest\nanxiety in an atypical manner (e.g., involvin g symptoms of both anxiety and depression)\nand thus be more likely to warrant a diagnosis of unspecified anxiety disorder. Addition-\nally, the presence of specific phobia in olde r adults is associated with decreased quality of\nlife and may serve as a risk factor for major neurocognitive disorder. \nAlthough most specific phobias develop in ch ildhood and adolescence, it is possible for a\nspecific phobia to develop at any age, often as the result of expe riences that are traumatic. For\nexample, phobias of choking almost always follow a near-choking event at any age. \nRisk and Prognostic Factors \nTemperamental. Temperamental risk factors for specif ic phobia, such as negative affec-\ntivity (neuroticism) or behavioral inhibition, are risk factors for ot her anxiety disorders as\nwell. \nEnvironmental. Environmental risk factors for specif ic phobias, such as parental over-", "source": "dsm5.pdf"} {"id": "750cb9f5177b-2", "page_content": "Environmental. Environmental risk factors for specif ic phobias, such as parental over-\nprotectiveness, parental loss and separation, and physical and sexual abuse, tend to pre-\ndict other anxiety disorders as well. As note d earlier, negative or traumatic encounters\nwith the feared object or situation sometime s (but not always) precede the development of\nspecific phobia. \nGenetic and physiological. There may be a genetic suscepti bility to a certain category of\nspecific phobia (e.g., an individual with a first-degree relative with a specific phobia of an-", "source": "dsm5.pdf"} {"id": "ee870cc6af54-0", "page_content": "Genetic and physiological. There may be a genetic suscepti bility to a certain category of\nspecific phobia (e.g., an individual with a first-degree relative with a specific phobia of an-\nimals is significantly more likely to have the same specific phobia than any other category\nof phobia). Individuals with blood-injection- injury phobia show a unique propensity to\nvasovagal syncope (fainting) in th e presence of the phobic stimulus.", "source": "dsm5.pdf"} {"id": "75394a3607ff-0", "page_content": "Specific Phobia 201\nCulture-Related Diagnostic Issues\nIn the United States, Asians and Latinos report significantly lower rates of specific phobia\nthan non-Latino whites, African Americans, an d Native Americans. In addition to having\nlower prevalence rates of specific phobia, some countries outside of the United States, par-\nticularly Asian and African countries, show differing phobia content, age at onset, and\ngender ratios. \nSuicide Risk \nIndividuals with specific phobia are up to 60 % more likely to make a suicide attempt than\nare individuals without the diagnosis. However, it is likely that these elevated rates are\nprimarily due to como rbidity with personality disorder s and other anxiety disorders. \nFunctional Consequences of Specific Phobia\nIndividuals with specific phobia show simi lar patterns of impairment in psychosocial\nfunctioning and decreased quality of life as individuals with other anxiety disorders and\nalcohol and substance use disorders, includ ing impairments in occupational and inter-\npersonal functioning. In older adults, impair ment may be seen in caregiving duties and\nvolunteer activities. Also, fear of falling in older adults can lead to reduced mobility and\nreduced physical and social functioning, an d may lead to receiving formal or informal\nhome support. The distress and impairment caused by specif ic phobias tend to increase\nwith the number of feared objects and situat ions. Thus, an individual who fears four ob-\njects or situations is likely to have more im pairment in his or her occupational and social\nroles and a lower quality of life than an indivi dual who fears only one object or situation.\nIndividuals with blood-injection-injury specif ic phobia are often reluctant to obtain med-\nical care even when a medical concern is present. Additionally, fear of vomiting and chok-\ning may substantially reduce dietary intake.", "source": "dsm5.pdf"} {"id": "75394a3607ff-1", "page_content": "ing may substantially reduce dietary intake. \nDifferential Diagnosis\nAgoraphobia. Situational specific phobia may resemble agoraphobia in its clinical pre-\nsentation, given the overlap in feared situations (e.g., flying, enclosed places, elevators). If\nan individual fears only one of the agorapho bia situations, then sp ecific phobia, situa-\ntional, may be diagnosed. If two or more agoraphobic situations are feared, a diagnosis of\nagoraphobia is likely warranted. For example, an individual who fears airplanes and ele-\nvators (which overlap with the \u201cpublic transportation\u201d ag oraphobic situation) but does\nnot fear other agoraphobic situations would be diagnosed with specific phobia, situa-\ntional, whereas an individual who fears airplanes, elevators, and crowds (which overlap\nwith two agoraphobic situations, \u201cusing public transportation\u201d and \u201cstanding in line and\nor being in a crowd\u201d) would be diagnosed wi th agoraphobia. Criterion B of agoraphobia\n(the situations are feared or avoided \u201cbecause of thoughts that escape might be difficult or\nhelp might not be available in the event of developing panic-like symptoms or other inca-\npacitating or embarrassing symptoms\u201d) can also be useful in differentiating agoraphobia\nfrom specific phobia. If the situations are fe ared for other reasons, such as fear of being\nharmed directly by the object or situations (e.g ., fear of the plane crashing, fear of the an-\nimal biting), a specific phobia diagnosis may be more appropriate. \nSocial anxiety disorder. If the situations are feared because of negative evaluation, so-\ncial anxiety disorder should be di agnosed instead of specific phobia.\nSeparation anxiety disorder. If the situations are feared because of separation from a", "source": "dsm5.pdf"} {"id": "75394a3607ff-2", "page_content": "Separation anxiety disorder. If the situations are feared because of separation from a\nprimary caregiver or attachment figure, separation anxiety disorder should be diagnosed\ninstead of specific phobia.", "source": "dsm5.pdf"} {"id": "3b79fb0d21b1-0", "page_content": "202 Anxiety Disorders\nPanic disorder. Individuals with specific phobia may experience panic attacks when con-\nfronted with their feared situation or object. A diagnosis of specific phobia would be given if\nthe panic attacks only occurred in response to the specific obje ct or situation, whereas a di-\nagnosis of panic disorder woul d be given if the individual also experienced panic attacks\nthat were unexpected (i.e., not in response to the specific phobia object or situation).\nObsessive-compulsive disorder. If an individual\u2019s primary fear or anxiety is of an ob-\nject or situation as a result of obsessions (e.g., fear of bloo d due to obsessive thoughts about\ncontamination from blood-borne pathogens [i.e., HIV]; fear of driving due to obsessive im-\nages of harming others), and if other diagnostic criteria for obsess ive-compulsive disorder\nare met, then obsessive-compulsive disorder should be diagnosed. \nTrauma- and stressor-related disorders. If the phobia develops following a traumatic\nevent, posttraumatic stress disorder (PTSD) should be considered as a diagnosis. How-\never, traumatic events ca n precede the onset of PTSD and sp ecific phobia. In this case, a di-\nagnosis of specific phobia would be assigned only if all of the criteria for PTSD are not met. \nEating disorders. A diagnosis of specific phobia is not given if the avoidance behavior is\nexclusively limited to avoidance of food and food-related cues, in which case a diagnosis\nof anorexia nervosa or bulimia nervosa should be considered.\nSchizophrenia spectrum and other psychotic disorders. When the fear and avoidance\nare due to delusional thinking (as in schizo phrenia or other schizophrenia spectrum and\nother psychotic disorders), a diagnosis of specific phobia is not warranted. \nComorbidity", "source": "dsm5.pdf"} {"id": "3b79fb0d21b1-1", "page_content": "other psychotic disorders), a diagnosis of specific phobia is not warranted. \nComorbidity\nSpecific phobia is rarely seen in medical-clinical settings in the absence of other psycho-\npathology and is more frequently seen in nonm edical mental health settings. Specific pho-\nbia is frequently associated with a range of ot her disorders, especially depression in older\nadults. Because of early onset, specific phobia is typically the temporally primary disorder.\nIndividuals with specific phobia are at incr eased risk for the development of other dis-\norders, including other anxiety disorders, de pressive and bipolar disorders, substance-\nrelated disorders, somatic symptom and relate d disorders, and personality disorders (par-\nticularly dependent personality disorder).\nSocial Anxiety Disorder (Social Phobia)\nDiagnostic Criteria 300.23 (F40.10)\nA. Marked fear or anxiety about one or more social situations in which the individual is\nexposed to possible scrutiny by others. Examples include social interactions (e.g., hav-\ning a conversation, meeting unfamiliar people), being observed (e.g., eating or drink-\ning), and performing in front of others (e.g., giving a speech).\nNote: In children, the anxiety must occur in peer settings and not just during interac-\ntions with adults.\nB. The individual fears that he or she will act in a way or show anxiety symptoms that will\nbe negatively evaluated (i.e., will be humiliating or embarrassing; will lead to rejection\nor offend others).\nC. The social situations almost always provoke fear or anxiety.\nNote: In children, the fear or anxiety may be expressed by crying, tantrums, freezing,\nclinging, shrinking, or failing to speak in social situations.\nD. The social situations are avoided or endured with intense fear or anxiety.", "source": "dsm5.pdf"} {"id": "439b2c3e1673-0", "page_content": "Social Anxiety Disorder (Social Phobia) 203\nE. The fear or anxiety is out of proportion to t he actual threat posed by the social situation\nand to the sociocultural context.\nF. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more. \nG. The fear, anxiety, or avoidance causes clin ically significant distress or impairment in\nsocial, occupational, or other important areas of functioning.\nH. The fear, anxiety, or avoidance is not attributable to the physiological effects of a sub-\nstance (e.g., a drug of abuse, a medication) or another medical condition.\nI. The fear, anxiety, or avoidance is not better explained by the symptoms of another\nmental disorder, such as panic disorder, bod y dysmorphic disorder, or autism spectrum\ndisorder.\nJ. If another medical condition (e.g., Parkinson\u2019 s disease, obesity, disfigurement from burns\nor injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive. \nSpecify if: \nPerformance only: If the fear is restricted to speaking or performing in public.\nSpecifiers\nIndividuals with the performanc e only type of social anxiety disorder have performance\nfears that are typically most impairing in thei r professional lives (e.g., musicians, dancers,\nperformers, athletes) or in roles that requir e regular public speaking. Performance fears\nmay also manifest in work, school, or academic settings in which regular public presenta-\ntions are required. Individuals with performance only social anxiety disorder do not fear\nor avoid nonperformanc e social situations. \nDiagnostic Features\nThe essential feature of social an xiety disorder is a marked, or in tense, fear or anxiety of so-\ncial situations in which the individual may be scrutinized by others. In children the fear or", "source": "dsm5.pdf"} {"id": "439b2c3e1673-1", "page_content": "cial situations in which the individual may be scrutinized by others. In children the fear or\nanxiety must occur in p eer settings and not just during in teractions with adults (Criterion\nA). When exposed to such social situations, the individual fears that he or she will be neg-\natively evaluated. The individu al is concerned that he or she will be judged as anxious,\nweak, crazy, stupid, boring, intimidating, dirt y, or unlikable. The individual fears that\nhe or she will act or appear in a certain way or show anxiety symptoms, such as blushing,\ntrembling, sweating, stumbling over one\u2019s words, or staring, that will be negatively eval-\nuated by others (Criterion B). Some individuals fear offending others or being rejected as\na result. Fear of offending others\u2014for exampl e, by a gaze or by showing anxiety symp-\ntoms\u2014may be the predominant fear in individu als from cultures with strong collectivistic\norientations. An individual with fear of tr embling of the hands ma y avoid drinking, eat-\ning, writing, or pointing in public; an individual with fear of sweating may avoid shaking\nhands or eating spicy foods; and an individual with fear of blushing may avoid public per-\nformance, bright lights, or discussion about intimate to pics. Some individuals fear and\navoid urinating in public restrooms when other individuals are present (i.e., paruresis, or\n\u201cshy bladder syndrome\u201d). \nThe social situations almost always provoke fear or anxiety (Criterion C). Thus, an in-\ndividual who becomes anxious only occasionally in the social situatio n(s) would not be di-\nagnosed with social anxiety di sorder. However, the degree an d type of fear and anxiety\nmay vary (e.g., anticipatory anxiety, a panic attack) across different occasions. The antici-", "source": "dsm5.pdf"} {"id": "439b2c3e1673-2", "page_content": "patory anxiety may occur sometimes far in adva nce of upcoming situations (e.g., worrying\nevery day for weeks before attending a social ev ent, repeating a speech for days in advance).\nIn children, the fear or anxiety may be expre ssed by crying, tantrums, freezing, clinging, or\nshrinking in social situations. The individual will often avoid the feared social situations.\nAlternatively, the situations are endured with intense fear or anxiety (Criterion D). Avoid-", "source": "dsm5.pdf"} {"id": "9d9fe281824d-0", "page_content": "204 Anxiety Disorders\nance can be extensive (e.g., not going to partie s, refusing school) or subtle (e.g., overpre-\nparing the text of a speech, diverting at tention to others, limiting eye contact). \nThe fear or anxiety is judged to be out of proportion to the actual risk of being nega-\ntively evaluated or to the consequences of su ch negative evaluation (Criterion E). Some-\ntimes, the anxiety may not be judged to be excessive, because it is related to an actual\ndanger (e.g., being bullied or tormented by ot hers). However, individuals with social anx-\niety disorder often overestimate the negative consequences of social situations, and thus\nthe judgment of being out of proportion is ma de by the clinician. The individual\u2019s socio-\ncultural context needs to be taken into account when this judgment is being made. For ex-\nample, in certain cultures, behavior that mi ght otherwise appear socially anxious may be\nconsidered appropriate in social situations (e .g., might be seen as a sign of respect).\nThe duration of the disturbance is typically at least 6 months (Criterion F). This dura-\ntion threshold helps distinguish the disorder from transient social fears that are com-\nmon, particularly among children and in the community. However, th e duration criterion\nshould be used as a general guide, with allowance for some degree of flexibility. The fear,\nanxiety, and avoidance must interfere significa ntly with the individual\u2019s normal routine,\noccupational or academic functioning, or social activities or relation ships, or must cause\nclinically significant distress or impairment in social, occupational, or other important ar-\neas of functioning (Criterion G). For example, an individual who is afraid to speak in pub-\nlic would not receive a diagnosis of social anxi ety disorder if this activity is not routinely", "source": "dsm5.pdf"} {"id": "9d9fe281824d-1", "page_content": "lic would not receive a diagnosis of social anxi ety disorder if this activity is not routinely\nencountered on the job or in classroom work, an d if the individual is not significantly dis-\ntressed about it. However, if the individual avoi ds, or is passed over for, the job or educa-\ntion he or she really wants because of so cial anxiety symptoms, Criterion G is met. \nAssociated Features Supporting Diagnosis\nIndividuals with social anxiety disorder may be inadequately assertive or excessively sub-\nmissive or, less commonly, highly controlling of the conversation. They may show overly\nrigid body posture or inadequate eye contact, or speak with an overly soft voice. These in-\ndividuals may be shy or withdrawn, and they may be less open in conversations and dis-\nclose little about themselves. They may seek em ployment in jobs that do not require social\ncontact, although this is not the case for indi viduals with social anxiety disorder, perfor-\nmance only. They may live at home longer. Men may be delayed in marrying and having\na family, whereas women who would want to work outside the home may live a life as\nhomemaker and mother. Self-medication with substances is common (e.g., drinking be-\nfore going to a party). Social anxiety among older adults may also include exacerbation of\nsymptoms of medical illnesses, such as increa sed tremor or tachycardia. Blushing is a hall-\nmark physical response of social anxiety disorder.\nPrevalence\nThe 12-month prevalence estimate of social an xiety disorder for the United States is ap-\nproximately 7%. Lower 12-month prevalence esti mates are seen in much of the world us-\ning the same diagnostic instrument, clusteri ng around 0.5%\u20132.0%; median prevalence in", "source": "dsm5.pdf"} {"id": "9d9fe281824d-2", "page_content": "Europe is 2.3%. The 12-month prevalence rates in children and adolescents are comparable\nto those in adults. Prevalence rates decrease with age. The 12-mont h prevalence for older\nadults ranges from 2% to 5%. In general, high er rates of social anxiety disorder are found\nin females than in males in the general popu lation (with odds ratios ranging from 1.5 to\n2.2), and the gender difference in prevalen ce is more pronounced in adolescents and\nyoung adults. Gender rates are equivalent or slightly higher for males in clinical samples,", "source": "dsm5.pdf"} {"id": "0559a0298760-0", "page_content": "2.2), and the gender difference in prevalen ce is more pronounced in adolescents and\nyoung adults. Gender rates are equivalent or slightly higher for males in clinical samples,\nand it is assumed that gender roles and social expectations play a significant role in ex-\nplaining the heightened help-seeking behavior in male patients. Prevalence in the United\nStates is higher in American Indians and lowe r in persons of Asian, Latino, African Amer-\nican, and Afro-Caribbean descent compared with non-Hispanic whites.", "source": "dsm5.pdf"} {"id": "a9aa5ac6bef8-0", "page_content": "Social Anxiety Disorder (Social Phobia) 205\nDevelopment and Course\nMedian age at onset of social anxiety disorder in the United States is 13 years, and 75% of\nindividuals have an age at onset between 8 and 15 years. The disord er sometimes emerges\nout of a childhood history of social inhibition or shyness in U.S. and European studies. On-\nset can also occur in early childhood. Onset of social anxiety disorder may follow a stress-\nful or humiliating experience (e.g., being bu llied, vomiting during a public speech), or it\nmay be insidious, developing slowly. First onse t in adulthood is relatively rare and is more\nlikely to occur after a stressful or humiliating event or after life changes that require new\nsocial roles (e.g., marrying someone from a different social class, receiving a job promo-\ntion). Social anxiety disorder may diminish after an individual with fear of dating marries\nand may reemerge after divorce. Among individu als presenting to clinical care, the disor-\nder tends to be particularly persistent. \nAdolescents endorse a broader pattern of fe ar and avoidance, including of dating,\ncompared with younger children . Older adults express social anxiety at lower levels but\nacross a broader range of situations, whereas younger adults express higher levels of so-\ncial anxiety for specific situations. In older adults, social anxiet y may concern disability\ndue to declining sensory functioning (hearing , vision) or embarrassment about one\u2019s ap-\npearance (e.g., tremor as a symptom of Parkin son\u2019s disease) or functioning due to medical\nconditions, incontinence, or cogn itive impairment (e.g., forgetting people\u2019s names). In the\ncommunity approximately 30% of individuals with social anxiety disorder experience re-", "source": "dsm5.pdf"} {"id": "a9aa5ac6bef8-1", "page_content": "community approximately 30% of individuals with social anxiety disorder experience re-\nmission of symptoms within 1 year, and about 50% expe rience remission within a few\nyears. For approximately 60% of individuals wi thout a specific treatment for social anxiety\ndisorder, the course takes several years or longer.\nDetection of social anxiety disorder in olde r adults may be challenging because of sev-\neral factors, including a focus on somatic symptoms, comorbid me dical illness, limited\ninsight, changes to social environment or roles that may obscure impairment in social\nfunctioning, or reticence about de scribing psychological distress.\nRisk and Prognostic Factors\nTemperamental. Underlying traits that predispose individuals to social anxiety disor-\nder include behavioral inhibition and fear of negative evaluation.\nEnvironmental. There is no causative role of increa sed rates of childhood maltreatment or\nother early-onset psychosocial adversity in th e development of social anxiety disorder. How-\never, childhood maltreatment an d adversity are risk factors for social anxiety disorder. \nGenetic and physiological. Traits predisposing individual s to social anxiety disorder,\nsuch as behavioral inhibition, are strongly genetically influenced. The genetic influence is\nsubject to gene-environment interaction; that is, children with high behavioral inhibition\nare more susceptible to environmental influe nces, such as socially anxious modeling by\nparents. Also, social anxiety disorder is heritable (but performance-only anxiety less so).\nFirst-degree relatives have a two to six times greater chance of having social anxiety dis-\norder, and liability to the disord er involves the interplay of di sorder-specific (e.g., fear of\nnegative evaluation) and nonspecific (e.g., neuroticism) genetic factors.\nCulture-Related Diagnostic Issues", "source": "dsm5.pdf"} {"id": "a9aa5ac6bef8-2", "page_content": "Culture-Related Diagnostic Issues\nThe syndrome of taijin kyofusho (e.g., in Japan and Korea) is often characterized by social-\nevaluative concerns, fulfilling criteria for social anxiety di sorder, that are associated with\nthe fear that the individual makes other people uncomfortable (e.g., \u201cMy gaze upsets peo-\nple so they look away and avoid me\u201d), a fear that is at times experienced with delusional\nintensity. This symptom may also be found in non-Asian settings. Other presentations", "source": "dsm5.pdf"} {"id": "f6b0b8dfeddf-0", "page_content": "ple so they look away and avoid me\u201d), a fear that is at times experienced with delusional\nintensity. This symptom may also be found in non-Asian settings. Other presentations\nof taijin kyofusho may fulfill criteria fo r body dysmorphic disorder or delusional disorder.", "source": "dsm5.pdf"} {"id": "09e7c3ccf998-0", "page_content": "206 Anxiety Disorders\nImmigrant status is associated with significan tly lower rates of social anxiety disorder in\nboth Latino and non-Latino white groups. Prev alence rates of social anxiety disorder may\nnot be in line with self-reported social anxiety levels in the same cult ure\u2014that is, societies\nwith strong collectivistic orientations may report high levels of social anxiety but low prev-\nalence of social anxiety disorder.\nGender-Related Diagnostic Issues\nFemales with social anxiety disorder report a greater number of social fears and comorbid\ndepressive, bipolar, and anxiety disorders, wh ereas males are more likely to fear dating,\nhave oppositional defiant disorder or conduct disorder, and use alcohol and illicit drugs to\nrelieve symptoms of the disorder. Paruresis is more common in males.\nFunctional Consequences of Social Anxiety Disorder\nSocial anxiety disorder is asso ciated with elevated rates of school dropout and with de-\ncreased well-being, employment , workplace productivity, soci oeconomic status, and quality\nof life. Social anxiety disorder is also associated with being single, unmarried, or divorced\nand with not having children, particularly amon g men. In older adults, there may be impair-\nment in caregiving duties and volunteer activi ties. Social anxiety disorder also impedes lei-\nsure activities. Despite the extent of distress and social impairment associated with social\nanxiety disorder, only about half of individuals with the diso rder in Western societies ever\nseek treatment, and they tend to do so only after 15\u201320 years of experiencing symptoms. Not\nbeing employed is a strong predictor for th e persistence of social anxiety disorder.\nDifferential Diagnosis\nNormative shyness. Shyness (i.e., social reticence) is a common personality trait and is\nnot by itself pathological. In some societies, shyness is even evaluated positively. How-", "source": "dsm5.pdf"} {"id": "09e7c3ccf998-1", "page_content": "not by itself pathological. In some societies, shyness is even evaluated positively. How-\never, when there is a significant adverse impa ct on social, occupational, and other impor-\ntant areas of functioning, a di agnosis of social anxiety disord er should be considered, and\nwhen full diagnostic criteria for social anxiety disorder are met, the disorder should be di-\nagnosed. Only a minority (12%) of self-identif ied shy individuals in the United States have\nsymptoms that meet diagnostic crit eria for social anxiety disorder.\nAgoraphobia. Individuals with agoraphobia may fear an d avoid social situations (e.g., go-\ning to a movie) because escape might be difficult or help might not be available in the event of\nincapacitation or panic-like sy mptoms, whereas individuals with social anxiety disorder are\nmost fearful of scrutiny by others. Moreover, in dividuals with social anxiety disorder are likely\nto be calm when left entirely alone, wh ich is often not the case in agoraphobia.\nPanic disorder. Individuals with social anxiety disord er may have panic attacks, but the\nconcern is about fear of negative evaluati on, whereas in panic disorder the concern is\nabout the panic attacks themselves. \nGeneralized anxiety disorder. Social worries are common in generalized anxiety disorder,\nbut the focus is more on the nature of ongoing relationships rather than on fear of negative\nevaluation. Individuals with generalized anxiety disorder, particularly children, may have ex-\ncessive worries about the quality of their social performance, bu t these worries also pertain to\nnonsocial performance and when the individual is not being evaluated by others. In social anx-\niety disorder, the worries focus on social performance and others\u2019 evaluation. \nSeparation anxiety disorder. Individuals with separation anxiety disorder may avoid", "source": "dsm5.pdf"} {"id": "09e7c3ccf998-2", "page_content": "Separation anxiety disorder. Individuals with separation anxiety disorder may avoid\nsocial settings (including school refusal) because of concerns about being separated from\nattachment figures or, in childre n, about requiring the presence of a parent when it is not\ndevelopmentally appropriate. Individuals with separation anxiety disorder are usually", "source": "dsm5.pdf"} {"id": "a7c092b6c643-0", "page_content": "attachment figures or, in childre n, about requiring the presence of a parent when it is not\ndevelopmentally appropriate. Individuals with separation anxiety disorder are usually\ncomfortable in social settings when their attachment figure is present or when they are at", "source": "dsm5.pdf"} {"id": "5a953d30b0e3-0", "page_content": "Social Anxiety Disorder (Social Phobia) 207\nhome, whereas those with social anxiety diso rder may be uncomforta ble when social sit-\nuations occur at home or in the presence of attachment figures.\nSpecific phobias. Individuals with specific phobias may fear embarrassment or humil-\niation (e.g., embarrassment about fainting wh en they have their blood drawn), but they do\nnot generally fear negative evalua tion in other social situations.\nSelective mutism. Individuals with selective mutism ma y fail to speak because of fear of\nnegative evaluation, but they do not fear nega tive evaluation in social situations where no\nspeaking is required (e.g., nonverbal play). \nMajor depressive disorder. Individuals with major depre ssive disorder may be con-\ncerned about being negatively evaluated by ot hers because they feel they are bad or not\nworthy of being liked. In contrast, individuals with social anxiety disorder are worried\nabout being negatively evaluated because of ce rtain social behaviors or physical symptoms.\nBody dysmorphic disorder. Individuals with body dysmorphic disorder are preoccu-\npied with one or more perceived defects or fl aws in their physical appearance that are not\nobservable or appear slight to others; this preoccupation often causes social anxiety and\navoidance. If their social fears and avoidance are caused only by their beliefs about their\nappearance, a separate diagnosis of soci al anxiety disorder is not warranted.\nDelusional disorder. Individuals with delusional disorder may have nonbizarre delu-\nsions and/or hallucinations related to the delu sional theme that focus on being rejected by\nor offending others. Although extent of insi ght into beliefs about social situations may\nvary, many individuals with social anxiety diso rder have good insight that their beliefs are\nout of proportion to the actual th reat posed by the social situation.", "source": "dsm5.pdf"} {"id": "5a953d30b0e3-1", "page_content": "out of proportion to the actual th reat posed by the social situation.\nAutism spectrum disorder. Social anxiety and social comm unication deficits are hall-\nmarks of autism spectrum disorder. Individu als with social anxiety disorder typically\nhave adequate age-appropriate social relationships and social communication capacity,\nalthough they may appear to have impairment in these areas when first interacting with\nunfamiliar peers or adults.\nPersonality disorders. Given its frequent onset in childhood and its persistence into and\nthrough adulthood, social anxiety disorder may resemble a personality disorder. The most\napparent overlap is with avoidant personalit y disorder. Individuals with avoidant person-\nality disorder have a broader avoidance pattern than those with social anxiety disorder.\nNonetheless, social anxiety disorder is typica lly more comorbid with avoidant personality\ndisorder than with other personality disorders, and avoidant personality disorder is more\ncomorbid with social anxiety disorder than with other anxiety disorders. \nOther mental disorders. Social fears and discomfort can occur as part of schizophrenia,\nbut other evidence for psychotic symptoms is usually present. In individuals with an eat-\ning disorder, it is important to determine th at fear of negative evaluation about eating\ndisorder symptoms or behaviors (e.g., purging and vomiting) is not the sole source of so-\ncial anxiety before applying a diagnosis of social anxiety disorder. Similarly, obsessive-\ncompulsive disorder may be asso ciated with social anxiety, but the additional diagnosis of\nsocial anxiety disorder is used only when social fears and avoidance are independent of\nthe foci of the obsessions and compulsions. \nOther medical conditions. Medical conditions may produce symptoms that may be em-\nbarrassing (e.g. trembling in Parkinson\u2019s dise ase). When the fear of negative evaluation\ndue to other medical conditions is excessive, a diagnosis of social anxiety disorder should\nbe considered.", "source": "dsm5.pdf"} {"id": "5a953d30b0e3-2", "page_content": "be considered.\nOppositional defiant disorder. Refusal to speak due to oppo sition t o authorit y figures", "source": "dsm5.pdf"} {"id": "7ab47f9456b1-0", "page_content": "due to other medical conditions is excessive, a diagnosis of social anxiety disorder should\nbe considered.\nOppositional defiant disorder. Refusal to speak due to oppo sition t o authorit y figures\nshould be differentiated from failure to speak due to fear of negative evaluation.", "source": "dsm5.pdf"} {"id": "9c449021efe9-0", "page_content": "208 Anxiety Disorders\nComorbidity\nSocial anxiety disorder is often comorbid wi th other anxiety disorders, major depressive\ndisorder, and substance use diso rders, and the onset of social anxiety disorder generally\nprecedes that of the other disorders, except for specific phobia and separation anxiety dis-\norder. Chronic social isolation in the course of a social anxiety disorder may result in major\ndepressive disorder. Comorbidity with depression is high also in older adults. Substances\nmay be used as self-medication for social fe ars, but the symptoms of substance intoxica-\ntion or withdrawal, such as trembling, may also be a source of (further) social fear. Social\nanxiety disorder is frequently comorbid with bipolar disorder or body dysmorphic disor-\nder; for example, an individual has body dysmorphic disorder co ncerning a preoccupa-\ntion with a slight irregularity of her nose, as well as social anxiety disorder because of a\nsevere fear of sounding unintelligent. The mo re generalized form of social anxiety disor-\nder, but not social anxiety di sorder, performance only, is often comorbid with avoidant\npersonality disorder. In children, comorbidities with high-functioning autism and selec-\ntive mutism are common.\nPanic Disorder\nDiagnostic Criteria 300.01 (F41.0)\nA. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear\nor intense discomfort that reaches a peak within minutes, and during which time four\n(or more) of the following symptoms occur:\nNote: The abrupt surge can occur from a calm state or an anxious state.\n1. Palpitations, pounding heart, or accelerated heart rate.\n2. Sweating.\n3. Trembling or shaking.", "source": "dsm5.pdf"} {"id": "9c449021efe9-1", "page_content": "2. Sweating.\n3. Trembling or shaking.\n4. Sensations of shortness of breath or smothering.\n5. Feelings of choking.\n6. Chest pain or discomfort.\n7. Nausea or abdominal distress.\n8. Feeling dizzy, unsteady, light-headed, or faint.\n9. Chills or heat sensations.\n10. Paresthesias (numbness or tingling sensations).\n11. Derealization (feelings of unreality) or depersonalization (being detached from one-\nself).\n12. Fear of losing control or \u201cgoing crazy.\u201d\n13. Fear of dying.\nNote: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncontrol-\nlable screaming or crying) may be seen. Such symptoms should not count as one of\nthe four required symptoms.\nB. At least one of the attacks has been followed by 1 month (or more) of one or both of\nthe following: \n1. Persistent concern or worry about additional panic attacks or their consequences\n(e.g., losing control, having a heart attack, \u201cgoing crazy\u201d).\n2. A significant maladaptive change in behavior related to the attacks (e.g., behaviors\ndesigned to avoid having panic attacks, such as avoidance of exercise or unfamiliar\nsituations).", "source": "dsm5.pdf"} {"id": "a4c6852a3570-0", "page_content": "Panic Disorder 209\nC. The disturbance is not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication) or another medi cal condition (e.g., hyperthyroidism, car-\ndiopulmonary disorders).\nD. The disturbance is not better explained by another mental disorder (e.g., the panic at-\ntacks do not occur only in response to feared social situations, as in social anxiety dis-\norder; in response to circumscribed phobic objec ts or situations, as in specific phobia;\nin response to obsessions, as in obsessive-compulsive disorder; in response to re-\nminders of traumatic events, as in posttraumatic stress disorder; or in response to sep-\naration from attachment figures, as in separation anxiety disorder). \nDiagnostic Features\nPanic disorder refers to recurrent unexpected panic attacks (Criterion A). A panic attack is\nan abrupt surge of intense fear or intense di scomfort that reaches a peak within minutes,\nand during which time four or more of a lis t of 13 physical and cognitive symptoms occur.\nThe term recurrent literally means more than one un expected panic attack. The term unex-\npected refers to a panic attack for which there is no obvious cue or trigger at the time of oc-\ncurrence\u2014that is, the attack appears to occu r from out of the blue, such as when the\nindividual is relaxing or emerging from sleep (nocturnal panic attack). In contrast, expected\npanic attacks are attacks for which there is an ob vious cue or trigger, such as a situation in\nwhich panic attacks typically occur. The determination of whether panic attacks are ex-\npected or unexpected is made by the clinicia n, who makes this judgment based on a com-\nbination of careful questioning as to the sequence of events preceding or leading up to the", "source": "dsm5.pdf"} {"id": "a4c6852a3570-1", "page_content": "bination of careful questioning as to the sequence of events preceding or leading up to the\nattack and the individual\u2019s own judgment of wh ether or not the attack seemed to occur for\nno apparent reason. Cultural interpretation s may influence the assignment of panic at-\ntacks as expected or unexpected (see section \u201cCulture-Related Diagnostic Issues\u201d for this\ndisorder). In the United States and Europe , approximately one-half of individuals with\npanic disorder have expected panic attacks as well as unexpected panic attacks. Thus, the\npresence of expected panic attacks does not rule out the diagnosis of panic disorder. For\nmore details regarding expected versus unexpected panic attacks, see the text accompa-\nnying panic attacks (pp. 214\u2013217).\nThe frequency and severity of panic attacks vary widely. In terms of frequency, there\nmay be moderately frequent a ttacks (e.g., one per week) for months at a time, or short\nbursts of more frequent attacks (e.g., daily) separated by weeks or months without any at-\ntacks or with less frequent attacks (e.g., two per month) over many years. Persons who\nhave infrequent panic attacks resemble person s with more frequent panic attacks in terms\nof panic attack symptoms, demographic charac teristics, comorbidity with other disorders,\nfamily history, and biological data. In terms of severity, individuals with panic disorder\nmay have both full-symptom (four or more symptoms) and limited-symptom (fewer than\nfour symptoms) attacks, and the number and type of panic attack symptoms frequently\ndiffer from one panic attack to the next. However, more th an one unexpected full-symp-\ntom panic attack is required for the diagnosis of panic disorder. \nThe worries about panic attacks or their co nsequences usually pertain to physical con-", "source": "dsm5.pdf"} {"id": "a4c6852a3570-2", "page_content": "The worries about panic attacks or their co nsequences usually pertain to physical con-\ncerns, such as worry that panic attacks refl ect the presence of life-threatening illnesses\n(e.g., cardiac disease, seizure disorder); social concerns, such as embarrassment or fear of\nbeing judged negatively by others because of visible panic symptoms; and concerns about\nmental functioning, such as \u201cgoing crazy\u201d or losing control (Criterion B). The maladaptive\nchanges in behavior represent attempts to mi nimize or avoid panic attacks or their conse-", "source": "dsm5.pdf"} {"id": "21b3718f59e2-0", "page_content": "mental functioning, such as \u201cgoing crazy\u201d or losing control (Criterion B). The maladaptive\nchanges in behavior represent attempts to mi nimize or avoid panic attacks or their conse-\nquences. Examples include avoiding physical exertion, reorganizing daily life to ensure\nthat help is available in the event of a pani c attack, restricting usual daily activities, and\navoiding agoraphobia-type situations, such as leaving home, using pu blic transportation,\nor shopping. If agoraphobia is present, a separate diagnosis of agoraphobia is given.", "source": "dsm5.pdf"} {"id": "f3430406c30d-0", "page_content": "210 Anxiety Disorders\nAssociated Features Supporting Diagnosis\nOne type of unexpected panic attack is a nocturnal panic attack (i.e., waking from sleep in\na state of panic, which differs from panicking after fully waking from sleep). In the United\nStates, this type of panic attack has been es timated to occur at leas t one time in roughly\none-quarter to one-third of individuals with panic disorder, of whom the majority also\nhave daytime panic attacks. In addition to worry about panic attacks and their conse-\nquences, many individuals with panic disorder report constant or intermittent feelings of\nanxiety that are more broadly related to heal th and mental health concerns. For example,\nindividuals with panic disorder often antici pate a catastrophic outc ome from a mild phys-\nical symptom or medication side effect (e.g., thinking that they may have heart disease or\nthat a headache means presence of a brain tumo r). Such individuals often are relatively in-\ntolerant of medication side effects. In ad dition, there may be pe rvasive concerns about\nabilities to complete daily tasks or withstand daily stressors, excessive use of drugs (e.g.,\nalcohol, prescribed medications or illicit drugs) to control panic attacks, or extreme behav-\niors aimed at controlling panic attacks (e.g., seve re restrictions on food intake or avoidance\nof specific foods or medications because of concerns about physical symptoms that pro-\nvoke panic attacks). \nPrevalence\nIn the general population, the 12-month prevalen ce estimate for panic disorder across the\nUnited States and several European countries is about 2%\u20133% in adults and adolescents. In\nthe United States, significantly lower rates of panic disorder are reported among Latinos,\nAfrican Americans, Caribbean blacks, and As ian Americans, compared with non-Latino", "source": "dsm5.pdf"} {"id": "f3430406c30d-1", "page_content": "African Americans, Caribbean blacks, and As ian Americans, compared with non-Latino\nwhites; American Indians, by contrast, have significantly higher rates. Lower estimates\nhave been reported for Asian, African, and Latin American countries, ranging from 0.1%\nto 0.8%. Females are more frequently affected than males, at a rate of approximately 2:1. The\ngender differentiation occurs in adolescence and is already observable before age 14 years.\nAlthough panic attacks occur in children, the overall prevalence of panic disorder is low\nbefore age 14 years (<0.4%). The rates of panic disorder show a gradua l increase during ad-\nolescence, particularly in females, and possibly following the onset of puberty, and peak dur-\ning adulthood. The prevalence rates decline in older individuals (i.e., 0.7% in adults over\nthe age of 64), possibly reflecting diminishing severity to subclinical levels. \nDevelopment and Course\nThe median age at onset for panic disorder in the United States is 20\u201324 years. A small\nnumber of cases begin in childhood, and onse t after age 45 years is unusual but can occur.\nThe usual course, if the disorder is untreated, is chronic but waxing and waning. Some in-\ndividuals may have episodic outbreaks with years of remission in between, and others\nmay have continuous severe symptomatology. Only a minority of individuals have full\nremission without subsequent relapse within a few years. The course of panic disorder\ntypically is complicated by a range of other disorders, in particular other anxiety disor-\nders, depressive disorders, and substance us e disorders (see section \u201cComorbidity\u201d for\nthis disorder). \nAlthough panic disorder is very rare in child hood, first occurrence of \u201cfearful spells\u201d is", "source": "dsm5.pdf"} {"id": "f3430406c30d-2", "page_content": "often dated retrospectively back to childhood. As in adults, panic disorder in adolescents\ntends to have a chronic course and is frequent ly comorbid with othe r anxiety, depressive,\nand bipolar disorders. To date, no differences in the clinical presentation between adoles-\ncents and adults have been fo und. However, adolescents may be less worried about addi-\ntional panic attacks than are young adults. Lower prevalence of panic disorder in older", "source": "dsm5.pdf"} {"id": "d25d43d99634-0", "page_content": "cents and adults have been fo und. However, adolescents may be less worried about addi-\ntional panic attacks than are young adults. Lower prevalence of panic disorder in older\nadults appears to be attributable to age- related \u201cdampening\u201d of the autonomic nervous\nsystem response. Many older individuals with \u201cpanicky feelings\u201d are observed to have a\n\u201chybrid\u201d of limited-symptom panic attacks and generalized anxiety. Also, older adults", "source": "dsm5.pdf"} {"id": "145dc74b2ffc-0", "page_content": "Panic Disorder 211\ntend to attribute their panic attacks to certai n stressful situations, such as a medical pro-\ncedure or social setting.\u00a0Older individuals may retrospectively endorse explanations for\nthe panic attack (which would preclude the diagnosis of panic disorder), even if an attack\nmight actually have been unexpected in the moment (and thus qualify as the basis for a\npanic disorder diagnosis).\u00a0This may result in under-endorsem ent of unexpected panic at-\ntacks in older individuals. Thus, careful questioning of older adults is required to assess\nwhether panic attacks were expected before entering the situation, so that unexpected\npanic attacks and the diagnosis of panic disorder are not overlooked.\nWhile the low rate of panic disorder in child ren could relate to difficulties in symptom\nreporting, this seems unlikely given that child ren are capable of reporting intense fear or\npanic in relation to separation and to phobic objects or phobic si tuations. Adolescents\nmight be less willing than adul ts to openly discuss panic a ttacks. Therefore, clinicians\nshould be aware that unexpected panic attacks do occur in adolescents, much as they do in\nadults, and be attuned to this possibility when encountering adolescents presenting with\nepisodes of intense fear or distress. \nRisk and Prognostic Factors\nTemperamental. Negative affectivity (neuroticism) (i .e., proneness to experiencing neg-\native emotions) and anxiety sensitivity (i.e., the disposition to believe that symptoms of\nanxiety are harmful) are risk factors for the onset of panic attacks and, separately, for\nworry about panic, although thei r risk status for the diagnosis of panic disorder is un-\nknown. History of \u201cfearful spe lls\u201d (i.e., limited-symptom atta cks that do not meet full cri-", "source": "dsm5.pdf"} {"id": "145dc74b2ffc-1", "page_content": "teria for a panic attack) may be a risk factor for later panic attacks and panic disorder.\nAlthough separation anxiety in childhood, espe cially when severe, may precede the later\ndevelopment of panic disorder, it is not a consistent risk factor. \nEnvironmental. Reports of childhood experiences of sexual and physical abuse are more\ncommon in panic disorder than in certain othe r anxiety disorders. Smoking is a risk factor\nfor panic attacks and panic disorder. Most individuals report identifiable stressors in the\nmonths before their first panic attack (e.g., interpersonal stressors and stressors related to\nphysical well-being, such as negative experiences with illicit or prescription drugs, dis-\nease, or death in the family). \nGenetic and physiological. It is believed that multiple genes confer vulnerability to panic\ndisorder. However, the exact genes, gene prod ucts, or functions related to the genetic re-\ngions implicated remain unknown. Current ne ural systems models for panic disorder em-\nphasize the amygdala and related structures, mu ch as in other anxiety disorders. There is\nan increased risk for panic d isorder among offspring of pare nts with anxiety, depressive,\nand bipolar disorders. Respiratory disturbance, such as asthma, is associated with panic\ndisorder, in terms of past history, comorbidity, and family history. \nCulture-Related Diagnostic Issues \nThe rate of fears about mental and somatic symptoms of anxiety ap pears to vary across\ncultures and may influence the rate of panic attacks and panic disorder. Also, cultural ex-\npectations may influence the classification of panic attacks as expected or unexpected. For\nexample, a Vietnamese individual who has a panic attack after walking out into a windy\nenvironment ( tr\u00fang gi\u00f3; \u201chit by the wind\u201d) may attribut e the panic attack to exposure to", "source": "dsm5.pdf"} {"id": "145dc74b2ffc-2", "page_content": "wind as a result of the cultural syndrome that links these two experiences, resulting in clas-\nsification of the panic attack as expected. Various other cultural syndromes are associated\nwith panic disorder, including ataque de nervios (\u201cattack of nerves\u201d) among Latin Ameri-\ncans and khy\u00e2l attacks and \u201csoul loss\u201d among Cambodians. Ataque de nervios may involve", "source": "dsm5.pdf"} {"id": "a9f80778e459-0", "page_content": "with panic disorder, including ataque de nervios (\u201cattack of nerves\u201d) among Latin Ameri-\ncans and khy\u00e2l attacks and \u201csoul loss\u201d among Cambodians. Ataque de nervios may involve\ntrembling, uncontrollable screaming or crying , aggressive or suicidal behavior, and deper-\nsonalization or derealization, which may be ex perienced longer than the few minutes typical", "source": "dsm5.pdf"} {"id": "2c4c876d1ff7-0", "page_content": "212 Anxiety Disorders\nof panic attacks. Some c linical presentations of ataque de nervios fulfill criteria for condi-\ntions other than panic attack (e.g., other spec ified dissociative disorder). These syndromes\nimpact the symptoms and frequency of panic disorder, including the individual\u2019s attribu-\ntion of unexpectedness, as cultural syndromes may create fear of certain situations, rang-\ning from interpersonal arguments (associated with ataque de nervios), to types of exertion\n(associated with khy\u00e2l attacks), to atmospheri c wind (associated with tr\u00fang gi\u00f3 attacks).\nClarification of the details of cultural attributions may aid in distinguishing expected and\nunexpected panic attacks. For more information regarding cultural syndromes, refer to the\n\u201cGlossary of Cultural Concepts of Distress\u201d in the Appendix.\nThe specific worries about panic attacks or their consequences are likely to vary from\none culture to another (and across different age groups and gender). For panic disorder,\nU.S. community samples of non- Latino whites have significantly less functional impair-\nment than African Americans. There are also hi gher rates of objectively defined severity in\nnon-Latino Caribbean blacks with panic disord er, and lower rates of panic disorder over-\nall in both African American and Afro-Carib bean groups, suggesting that among individ-\nuals of African descent, the criteria for pa nic disorder may be met only when there is\nsubstantial severity and impairment.\nGender-Related Diagnostic Issues \nThe clinical features of panic disorder do not appear to differ between males and females.\nThere is some evidence for sexual dimorphi sm, with an association between panic disor-\nder and the catechol-O-methyltransferase (COMT) gene in females only.\nDiagnostic Markers", "source": "dsm5.pdf"} {"id": "2c4c876d1ff7-1", "page_content": "Diagnostic Markers\nAgents with disparate mechanisms of action, such as sodium lactate, caffeine, isoprotere-\nnol, yohimbine, carbon dioxide, and cholecys tokinin, provoke panic attacks in individuals\nwith panic disorder to a much greater extent than in healthy control subjects (and in some\ncases, than in individuals with other anxiet y, depressive, or bipo lar disorders without\npanic attacks). Also, for a proportion of indi viduals with panic disorder, panic attacks are\nrelated to hypersensitive medullary carbon di oxide detectors, resulting in hypocapnia and\nother respiratory irregularities . However, none of these labo ratory findings are consid-\nered diagnostic of panic disorder.\nSuicide Risk\nPanic attacks and a diagnosis of panic disorder in the past 12 months are related to a higher\nrate of suicide attempts and suicidal ideation in the past 12 months even when comorbid-\nity and a history of childhood abuse and other suicide risk factors are taken into account.\nFunctional Consequences of Panic Disorder\nPanic disorder is associated with high levels of social, occupational, and physical disabil-\nity; considerable economic co sts; and the highest number of medical visits among the anx-\niety disorders, although the effects are st rongest with the presence of agoraphobia.\nIndividuals with panic disorder may be freque ntly absent from work or school for doctor\nand emergency room visits, which can lead to unemployment or dropping out of school.\nIn older adults, impairment may be seen in caregiving duties or volunteer activities. Full-\nsymptom panic attacks typically are associated with greater morbidity (e.g., greater health\ncare utilization, more disabilit y, poorer quality of life) than limited-symptom attacks. \nDifferential Diagnosis\nOther specified anxiety disorder or unspecified anxiety disorder. Panic disorder should", "source": "dsm5.pdf"} {"id": "2c4c876d1ff7-2", "page_content": "Differential Diagnosis\nOther specified anxiety disorder or unspecified anxiety disorder. Panic disorder should\nnot be diagnosed if full-symptom (unexpected) panic attacks ha ve never been experienced. In", "source": "dsm5.pdf"} {"id": "253f8c372f04-0", "page_content": "Panic Disorder 213\nthe case of only limited-symptom unexpected panic attacks, an other specified anxiety dis-\norder or unspecified anxiety disord er diagnosis should be considered.\nAnxiety disorder due to another medical condition. Panic disorder is not diagnosed if\nthe panic attacks are judged to be a direct physiological consequence of another medical\ncondition. Examples of medica l conditions that can cause panic attacks include hyperthy-\nroidism, hyperparathyroidism, pheochromocytoma, vestibular dysfunctions, seizure dis-\norders, and cardiopulmonary conditions (e.g., arrhythmias, supraventricular tachycardia,\nasthma, chronic obstructive pulmonary diseas e [COPD]). Appropriate laboratory tests\n(e.g., serum calcium levels for hyperparathy roidism; Holter monitor for arrhythmias) or\nphysical examinations (e.g., for cardiac conditions) may be helpful in determining the eti-\nological role of another medical condition. \nSubstance/medication-induced anxiety disorder. Panic disorder is not diagnosed if\nthe panic attacks are judged to be a direct physiological consequence of a substance. In-\ntoxication with central nervou s system stimulants (e.g., co caine, amphetamines, caffeine)\nor cannabis and withdraw al from central nervous system depressants (e.g., alcohol, bar-\nbiturates) can precipitate a panic attack. Howe ver, if panic attacks continue to occur out-\nside of the context of substance use (e.g., long after the effects of intoxication or withdrawal\nhave ended), a diagnosis of panic disorder should be cons idered. In addition, because\npanic disorder may precede substance use in some individuals and may be associated\nwith increased substance use, especially for pu rposes of self-medicat ion, a detailed history", "source": "dsm5.pdf"} {"id": "253f8c372f04-1", "page_content": "should be taken to determine if the individual had panic at tacks prior to excessive sub-\nstance use. If this is the case, a diagnosis of pa nic disorder should be considered in addition\nto a diagnosis of substance use disorder. Features such as onset after age 45 years or the\npresence of atypical symptoms during a panic attack (e.g., vertigo, loss of consciousness,\nloss of bladder or bowel control, slurred speech, amnesia) suggest the possibility that an-\nother medical condition or a substance may be causing the panic attack symptoms.\nOther mental disorders with panic attacks as an associated feature (e.g., other anxiety\ndisorders and psychotic disorders). Panic attacks that occur as a symptom of other anx-\niety disorders are expected (e.g., triggered by social situations in social anxiety disorder, by\nphobic objects or situations in specific phobia or agoraphobia, by worry in generalized anx-\niety disorder, by separation from home or atta chment figures in separation anxiety disorder)\nand thus would not meet crit eria for panic disorder. ( Note: Sometimes an unexpected panic\nattack is associated with the onset of another anxi ety disorder, but then the attacks become\nexpected, whereas panic disorder is characterized by recurrent unexpected panic attacks.) If\nthe panic attacks occur only in response to spec ific triggers, then only the relevant anxiety\ndisorder is assigned. However, if the individual experiences unexpected panic attacks as\nwell and shows persistent concern and worry or behavioral change because of the attacks,\nthen an additional diagnosis of pa nic disorder should be considered.\nComorbidity\nPanic disorder infrequently occurs in clinic al settings in the absence of other psychopa-\nthology. The prevalence of panic disorder is elevated in individuals with other disorders,\nparticularly other anxiety disorders (and espe cially agoraphobia), major depression, bipo-", "source": "dsm5.pdf"} {"id": "253f8c372f04-2", "page_content": "lar disorder, and possibly mild alcohol use di sorder. While panic disorder often has an ear-\nlier age at onset than the comorbid disorder(s), onset sometimes occurs after the comorbid\ndisorder and may be seen as a severi ty marker of the comorbid illness. \nReported lifetime rates of comorbidity between major depressive disorder and panic", "source": "dsm5.pdf"} {"id": "4e854eb8ee67-0", "page_content": "disorder and may be seen as a severi ty marker of the comorbid illness. \nReported lifetime rates of comorbidity between major depressive disorder and panic\ndisorder vary widely, ranging from 10% to 65% in individuals with panic disorder. In ap-\nproximately one-third of indivi duals with both disorders, the depression precedes the on-\nset of panic disorder. In the remaining two-th irds, depression occurs coincident with or\nfollowing the onset of panic disorder. A subset of individuals with panic disorder develop\na substance-related disorder, wh ich for some represents an a ttempt to treat their anxiety", "source": "dsm5.pdf"} {"id": "9393ae00bd12-0", "page_content": "214 Anxiety Disorders\nwith alcohol or medications. Comorbidity wi th other anxiety disorders and illness anxiety\ndisorder is also common. \nPanic disorder is significantly comorbid with numerous general medical symptoms\nand conditions, including, but not limited to, dizziness, ca rdiac arrhythmias, hyperthy-\nroidism, asthma, COPD, and ir ritable bowel syndrome. However, the nature of the asso-\nciation (e.g., cause and effect) between pani c disorder and these conditions remains\nunclear. Although mitral valve prolapse and thyroid disease are more common among in-\ndividuals with panic disorder than in the ge neral population, the differences in prevalence\nare not consistent.\nPanic Attack Specifier\n \nNote: Symptoms are presented for the purpose of identifying a panic attack; however,\npanic attack is not a mental disorder and cannot be coded. Panic attacks can occur in the\ncontext of any anxiety disorder as well as other mental disorders (e.g., depressive disor-\nders, posttraumatic stress disorder, substanc e use disorders) and some medical condi-\ntions (e.g., cardiac, respiratory, vestibular, gastrointestinal). When the presence of a panic\nattack is identified, it should be noted as a specifier (e.g., \u201cposttraumatic stress disorder\nwith panic attacks\u201d). For panic disorder, the pr esence of panic attack is contained within\nthe criteria for the disorder and panic attack is not used as a specifier.\nAn abrupt surge of intense fear or intense discomfort that reaches a peak within minutes,\nand during which time four (or more) of the following symptoms occur:\nNote: The abrupt surge can occur from a calm state or an anxious state.\n1. Palpitations, pounding heart, or accelerated heart rate.\n2. Sweating.\n3. Trembling or shaking.", "source": "dsm5.pdf"} {"id": "9393ae00bd12-1", "page_content": "2. Sweating.\n3. Trembling or shaking.\n4. Sensations of shortness of breath or smothering.\n5. Feelings of choking.\n6. Chest pain or discomfort.\n7. Nausea or abdominal distress.\n8. Feeling dizzy, unsteady, light-headed, or faint.\n9. Chills or heat sensations.\n10. Paresthesias (numbness or tingling sensations).\n11. Derealization (feelings of unreality) or de personalization (being detached from oneself).\n12. Fear of losing control or \u201cgoing crazy.\u201d\n13. Fear of dying.\nNote: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncontrollable\nscreaming or crying) may be seen. Such sym ptoms should not count as one of the four\nrequired symptoms.\nFeatures\nThe essential feature of a panic attack is an abru pt surge of intense fear or intense discomfort\nthat reaches a peak within minutes and during wh ich time four or more of 13 physical and cog-\nnitive symptoms occur. Eleven of these 13 sy mptoms are physical (e.g., palpitations, sweat-\ning), while two are cognitive (i.e., fear of losing control or going crazy, fe ar of dying). \u201cFear of\ngoing crazy\u201d is a colloquialism often used by indivi duals with panic atta cks and is not in-\ntended as a pejorative or diagnostic term. The term within minutes means that the time to peak", "source": "dsm5.pdf"} {"id": "386d2616b34f-0", "page_content": "Panic Attack Specifier 215\nintensity is literally only a few minutes. A panic attack can arise from either a calm state or an\nanxious state, and time to peak intensity shou ld be assessed independently of any preceding\nanxiety. That is, the start of the panic attack is the point at which there is an abrupt increase in\ndiscomfort rather than the point at which anxiet y first developed. Likew ise, a panic attack can\nreturn to either an anxious state or a calm stat e and possibly peak again. A panic attack is dis-\ntinguished from ongoing anxiety by its time to pe ak intensity, which occurs within minutes; its\ndiscrete nature; and its typically greater severity. Attacks that meet all other criteria but have\nfewer than four physical and/or cogn itive symptoms are referred to as limited-symptom attacks. \nThere are two characteristic types of pa nic attacks: expected and unexpected. Expected\npanic attacks are attacks for which there is an obvious cue or trigger, such as situations in\nwhich panic attacks have typically occurred. Unexpected panic attacks are those for which\nthere is no obvious cue or trigger at the time of occurrence (e.g., wh en relaxing or out of\nsleep [nocturnal panic attack]). The determination of whether panic attacks are expected\nor unexpected is made by the clinician, who makes this judgment based on a combination\nof careful questioning as to the sequence of events preceding or leading up to the attack\nand the individual\u2019s own judgment of whether or not the attack seemed to occur for no ap-\nparent reason. Cultural interp retations may influence their determination as expected or\nunexpected. Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncon-\ntrollable screaming or crying) may be seen; however, such symptoms should not count as", "source": "dsm5.pdf"} {"id": "386d2616b34f-1", "page_content": "trollable screaming or crying) may be seen; however, such symptoms should not count as\none of the four required symptoms. Panic attacks can occur in the context of any mental\ndisorder (e.g., anxiety disorder s, depressive disorders, bipola r disorders, eating disorders,\nobsessive-compulsive and related disorders, personality di sorders, psychotic disorders,\nsubstance use disorders) and some medical cond itions (e.g., cardiac, respiratory, vestibu-\nlar, gastrointestinal), with the majority ne ver meeting criteria for panic disorder. Recur-\nrent unexpected panic attacks are requir ed for a diagnosis of panic disorder. \nAssociated Features \nOne type of unexpected panic attack is a nocturnal panic attack (i.e., waking from sleep in a\nstate of panic), which differs from panicking after fully waking from sleep. Panic attacks\nare related to a higher rate of suicide attempts and suicidal ideation even when comorbid-\nity and other suicide risk fa ctors are taken into account.\nPrevalence\nIn the general population, 12-month prevalen ce estimates for panic attacks in the United\nStates is 11.2% in adults. Twelve-month preval ence estimates do not appear to differ sig-\nnificantly among African Americans, Asian Americans, and Latinos. Lower 12-month\nprevalence estimates for European countries ap pear to range from 2.7% to 3.3%. Females\nare more frequently affected than males, al though this gender difference is more pro-\nnounced for panic disorder. Panic attacks can oc cur in children but are relatively rare until\nthe age of puberty, when the prevalence rates increase. The prevalence rates decline in\nolder individuals, possibly reflecting diminishing severity to subclinical levels.\nDevelopment and Course\nThe mean age at onset for panic attacks in the United States is approximately 22\u201323 years", "source": "dsm5.pdf"} {"id": "386d2616b34f-2", "page_content": "The mean age at onset for panic attacks in the United States is approximately 22\u201323 years\namong adults. However, the course of panic at tacks is likely influenced by the course of\nany co-occurring mental disorder(s) and stre ssful life events. Panic attacks are uncommon,\nand unexpected panic attacks are rare, in preadolescent children . Adolescents might be\nless willing than adults to openly discuss panic attacks, even though they present with ep-\nisodes of intense fear or discom fort. Lower prevalence of pani c attacks in older individuals", "source": "dsm5.pdf"} {"id": "575c61600e71-0", "page_content": "less willing than adults to openly discuss panic attacks, even though they present with ep-\nisodes of intense fear or discom fort. Lower prevalence of pani c attacks in older individuals\nmay be related to a weaker autonomic response to emotional states re lative to younger in-\ndividuals. Older individuals may be less inclin ed to use the word \u201cfear\u201d and more inclined", "source": "dsm5.pdf"} {"id": "c2e035e48fcf-0", "page_content": "216 Anxiety Disorders\nto use the word \u201cdiscomfort\u201d to describe pa nic attacks. Older individuals with \u201cpanicky\nfeelings\u201d may have a hybrid of limited-sym ptom attacks and generalized anxiety. In\naddition, older individuals tend to attribute panic attacks to certain situations that are\nstressful (e.g., medical procedures, social se ttings) and may retrospectively endorse expla-\nnations for the panic attack even if it was un expected in the moment. This may result in un-\nder-endorsement of unexpected panic attacks in older individuals. \nRisk and Prognostic Factors \nTemperamental. Negative affectivity (neuroticism) (i .e., proneness to experiencing neg-\native emotions) and anxiety sensitivity (i.e., the disposition to believe that symptoms of\nanxiety are harmful) are risk factors for the onset of panic attacks. History of \u201cfearful\nspells\u201d (i.e., limited-symptom attacks that do not meet full criteria for a panic attack) may\nbe a risk factor for later panic attacks. \nEnvironmental. Smoking is a risk factor for panic atta cks. Most individu als report iden-\ntifiable stressors in the months before their first panic attack (e.g., interpersonal stressors\nand stressors related to physical well-being, such as negative experiences with illicit or\nprescription drugs, disease, or death in the family). \nCulture-Related Diagnostic Issues\nCultural interpretations may in fluence the determination of panic attacks as expected or\nunexpected. Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, and un-\ncontrollable screaming or crying) may be seen ; however, such symptoms should not count\nas one of the four required symptoms. Frequency of each of the 13 symptoms varies cross-", "source": "dsm5.pdf"} {"id": "c2e035e48fcf-1", "page_content": "as one of the four required symptoms. Frequency of each of the 13 symptoms varies cross-\nculturally (e.g., higher rates of paresthesias in African Americans and of dizziness in sev-\neral Asian groups). Cultural syndromes also influence the cross-cultural presentation of\npanic attacks, resulting in different symptom profiles across different cultural groups. Ex-\namples include khy\u00e2l (wind) attacks, a Cambodian cultural syndrome involving dizziness,\ntinnitus, and neck soreness; and tr\u00fang gi\u00f3 (wind-related) attacks, a Vietnamese cultural\nsyndrome associated with headaches. Ataque de nervios (attack of nerves) is a cultural syn-\ndrome among Latin Americans that may invo lve trembling, uncontrollable screaming or\ncrying, aggressive or suicidal behavior, and depersonalization or derealization, and which\nmay be experienced for longer than only a few minutes. Some clinical presentations of\nataque de nervios fulfill criteria for conditions other than panic attack (e.g., other specified\ndissociative disorder). Also, cu ltural expectations may influe nce the classification of panic\nattacks as expected or unexpected, as cultural syndromes may create fear of certain situa-\ntions, ranging from interpersonal arguments (associated with ataque de nervios ), to types of\nexertion (associated with khy\u00e2l attacks), to atmospheric wind (associated with tr\u00fang gi\u00f3 at-\ntacks). Clarification of the details of cultural attributions may aid in distinguishing ex-\npected and unexpected panic attacks. For more information ab out cultural syndromes, see\n\u201cGlossary of Cultural Concepts of Distress\u201d in the Appendix to this manual.\nGender-Related Diagnostic Issues\nPanic attacks are more common in females than in males, but clinical features or symp-", "source": "dsm5.pdf"} {"id": "c2e035e48fcf-2", "page_content": "Panic attacks are more common in females than in males, but clinical features or symp-\ntoms of panic attacks do not di ffer between males and females.\nDiagnostic Markers\nPhysiological recordings of naturally occurring panic attacks in individuals with panic\ndisorder indicate abrupt surges of arousal, usually of heart rate, that reach a peak within\nminutes and subside within minu tes, and for a proportion of these individu als the panic\nattack may be preceded by cardiorespiratory instabilities.", "source": "dsm5.pdf"} {"id": "a8e5a26d3966-0", "page_content": "Agoraphobia 217\nFunctional Consequenc es of Panic Attacks\nIn the context of co-occurring mental disord ers, including anxiety disorders, depressive\ndisorders, bipolar disorder, substance use disorders, psychoti c disorders, and personality\ndisorders, panic attacks are associated with increased symptom severity, higher rates of\ncomorbidity and suicidality, and poorer trea tment response. Also, full-symptom panic at-\ntacks typically are associated wi th greater morbidity (e.g., gr eater health care utilization,\nmore disability, poorer quality of life) than limited-symptom attacks. \nDifferential Diagnosis\nOther paroxysmal episodes (e.g., \u201canger attacks\u201d). Panic attacks should not be diag-\nnosed if the episodes do not involve the essent ial feature of an abrupt surge of intense fear\nor intense discomfort, but rather other emotional states (e.g ., anger, grief).\nAnxiety disorder due to another medical condition. Medical conditions that can cause\nor be misdiagnosed as panic attacks include hyperthyroidism, hyperparathyroidism, pheo-\nchromocytoma, vestibular dysfunctions, se izure disorders, and cardiopulmonary con-\nditions (e.g., arrhythmias, supraventricular tachycardia, asthma, chronic obstructive\npulmonary disease). Appropriate laboratory tests (e.g., serum calcium levels for hyperpara-\nthyroidism; Holter monitor for arrhythmias) or physical examinations (e.g., for cardiac con-\nditions) may be helpful in determining the etiological role of another medical condition. \nSubstance/medication-induced anxiety disorder. Intoxication with central nervous\nsystem stimulants (e.g., coca ine, amphetamines, caffeine) or cannabis and withdrawal", "source": "dsm5.pdf"} {"id": "a8e5a26d3966-1", "page_content": "from central nervous system depressants (e.g ., alcohol, barbiturat es) can precipitate a\npanic attack. A detailed histor y should be taken to determin e if the indivi dual had panic\nattacks prior to excessiv e substance use. Features such as onset after age 45 years or the\npresence of atypical symptoms during a panic attack (e.g., vertigo, loss of consciousness,\nloss of bladder or bowel contro l, slurred speech, or amnesia) suggest the possibility that a\nmedical condition or a substance may be causing the panic attack symptoms.\nPanic disorder. Repeated unexpected panic attacks are required but are no t sufficient for\nthe diagnosis of panic disorder (i .e., full diagnostic criteria fo r panic disorder must be met). \nComorbidity\nPanic attacks are associated with increased likelihood of various comorbid mental dis-\norders, including anxiety disorders, depressi ve disorders, bipolar disorders, impulse-\ncontrol disorders, and substanc e use disorders. Panic attacks are associated with increased\nlikelihood of later developing anxiety disorder s, depressive disorders, bipolar disorders,\nand possibly other disorders.\nAgoraphobia\nDiagnostic Criteria 300.22 (F40.00)\nA. Marked fear or anxiety about two (or more) of the following five situations: \n1. Using public transportation (e.g., automobiles, buses, trains, ships, planes).\n2. Being in open spaces (e.g., parking lots, marketplaces, bridges).\n3. Being in enclosed places (e.g., shops, theaters, cinemas).\n4. Standing in line or being in a crowd.\n5. Being outside of the home alone.\nB. The individual fears or avoids these situations because of thoughts that escape might\nbe difficult or help might not be available in the event of developing panic-like symp-", "source": "dsm5.pdf"} {"id": "8c728c5cc946-0", "page_content": "218 Anxiety Disorders\ntoms or other incapacitating or embarrassing symptoms (e.g., fear of falling in the el-\nderly; fear of incontinence).\nC. The agoraphobic situations almost always provoke fear or anxiety. \nD. The agoraphobic situations are actively avoi ded, require the presence of a companion,\nor are endured with intense fear or anxiety. \nE. The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic\nsituations and to the sociocultural context.\nF. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more. \nG. The fear, anxiety, or avoidance causes clin ically significant distress or impairment in\nsocial, occupational, or other important areas of functioning.\nH. If another medical condition (e.g., inflammato ry bowel disease, Parkinson\u2019s disease)\nis present, the fear, anxiety, or avoidance is clearly excessive. \nI. The fear, anxiety, or avoidance is not better explained by the symptoms of another men-\ntal disorder\u2014for example, the symptoms are not confined to specific phobia, situational\ntype; do not involve only social situations (as in social anxiety disorder); and are not re-\nlated exclusively to obsessions (as in obsessive-compulsive disorder), perceived defects\nor flaws in physical appearance (as in body dysmorphic disorder), reminders of traumatic\nevents (as in posttraumatic stress disorder), or fear of separation (as in separation anx-\niety disorder).\nNote: Agoraphobia is diagnosed irrespective of the presence of panic disorder. If an indi-\nvidual\u2019s presentation meets criteria for panic disorder and agoraphobia, both diagnoses\nshould be assigned.\nDiagnostic Features\nThe essential feature of agoraphobia is marked, or intense, fear or anxiety triggered by the", "source": "dsm5.pdf"} {"id": "8c728c5cc946-1", "page_content": "real or anticipated exposure to a wide range of situations (Criterion A). The diagnosis re-\nquires endorsement of symptoms occurring in at least two of the following five situations:\n1) using public transporation, such as automobiles, buses, trains, ships, or planes; 2) being\nin open spaces, such as parking lots, marketplac es, or bridges; 3) being in enclosed spaces,\nsuch as shops, theaters, or cine mas; 4) standing in line or being in a crowd; or 5) being out-\nside of the home alone. The examples for each situation are not exha ustive; other situations\nmay be feared. When experienci ng fear and anxiety cued by such situations, individuals\ntypically experience thoughts that something terrible might happen (Criterion B). Individ-\nuals frequently believe that esca pe from such situations might be difficult (e.g., \u201ccan\u2019t get\nout of here\u201d) or that help might be unavaila ble (e.g., \u201cthere is nobody to help me\u201d) when\npanic-like symptoms or other incapacitating or embarrassing symptoms occur. \u201cPanic-like\nsymptoms\u201d refer to any of the 13 symptoms incl uded in the criteria for panic attack, such as\ndizziness, faintness, and fear of dying. \u201cOther incapacitating or embarrassing symptoms\u201d\ninclude symptoms such as vomiting and inflammatory bowel symptoms, as well as, in\nolder adults, a fear of falling or, in children, a sense of disorientation and getting lost. \nThe amount of fear experience d may vary with proximity to the feared situation and\nmay occur in anticipation of or in the actual presence of the agoraphobic situation. Also,\nthe fear or anxiety may take the form of a full- or limited-symp tom panic attack (i.e., an ex-", "source": "dsm5.pdf"} {"id": "8c728c5cc946-2", "page_content": "pected panic attack). Fear or anxiety is evoked nearly every time the individual comes into\ncontact with the feared situation (Criterion C). Thus, an individual who becomes anxious\nonly occasionally in an agoraphobic situation (e.g., becomes anxious when standing in line\non only one out of every five occasions) would not be diagnosed with agoraphobia. The in-\ndividual actively avoids the situation or, if he or she either is unable or decides not to avoid\nit, the situation evokes intense fear or anxiety (Criterion D). Active avoidance means the in-", "source": "dsm5.pdf"} {"id": "7044eb27228d-0", "page_content": "dividual actively avoids the situation or, if he or she either is unable or decides not to avoid\nit, the situation evokes intense fear or anxiety (Criterion D). Active avoidance means the in-\ndividual is currently behaving in ways that are intentionally designed to prevent or min-\nimize contact with agoraphobi c situations. Avoidance can be behavioral (e.g., changing", "source": "dsm5.pdf"} {"id": "5efabb82566a-0", "page_content": "Agoraphobia 219\ndaily routines, choosing a job nearby to avoi d using public transportation, arranging for\nfood delivery to avoid entering shops and su permarkets) as well as cognitive (e.g., using\ndistraction to get through agoraphobic situations) in nature. The avoidance can become so\nsevere that the person is completely homebound. Often, an individual is better able to con-\nfront a feared situation when accompanied by a companion, such as a partner, friend, or\nhealth professional.\nThe fear, anxiety, or avoidance must be out of proportion to the actual danger posed by\nthe agoraphobic situations and to the sociocul tural context (Criterion E). Differentiating\nclinically significant agoraphobic fears from reasonable fears (e.g., leaving the house dur-\ning a bad storm) or from situations that ar e deemed dangerous (e.g ., walking in a parking\nlot or using public transportation in a high-cri me area) is important for a number of reasons.\nFirst, what constitutes av oidance may be difficul t to judge across cult ures and sociocultural\ncontexts (e.g., it is sociocultu rally appropriate for orthodox Muslim women in certain parts\nof the world to avoid leaving the house alone, and thus such avoidance would not be con-\nsidered indicative of agoraphobia). Second, older adults are likely to overattribute their\nfears to age-related constraints and are less likely to judge their fears as being out of pro-\nportion to the actual risk. Th ird, individuals with agoraphobia are likely to overestimate\ndanger in relation to panic-like or other bodily symptoms. Agora phobia should be diag-\nnosed only if the fear, anxiety, or avoidance pers ists (Criterion F) and if it causes clinically", "source": "dsm5.pdf"} {"id": "5efabb82566a-1", "page_content": "significant distress or impairment in social, occupational, or other important areas of func-\ntioning (Criterion G). Th e duration of \u201ctypically lasting for 6 months or more\u201d is meant to\nexclude individuals with short-lived, transien t problems. However, the duration criterion\nshould be used as a general guide, with allowance for some degree of flexibility. \nAssociated Features Supporting Diagnosis\nIn its most severe forms, agoraphobia can ca use individuals to become completely home-\nbound, unable to leave their home and dependent on others for services or assistance to pro-\nvide even for basic needs. Demoralization and depressive symptoms, as well as abuse of\nalcohol and sedative medication as inappropriate self-medication st rategies, are common. \nPrevalence\nEvery year approximately 1.7% of adolescents and adults have a diagnosis of agoraphobia.\nFemales are twice as likely as males to expe rience agoraphobia. Agoraphobia may occur in\nchildhood, but incidence peaks in late ad olescence and early adulthood. Twelve-month\nprevalence in individuals older than 65 year s is 0.4%. Prevalence rates do not appear to\nvary systematically across cultural/racial groups.\nDevelopment and Course\nThe percentage of individuals with agorapho bia reporting panic attacks or panic disorder\npreceding the onset of agoraphobia ranges fr om 30% in community samples to more than\n50% in clinic samples. The majority of individuals with panic disorder show signs of anx-\niety and agoraphobia before the onset of panic disorder.\nIn two-thirds of all cases of agoraphobia, initial onset is before age 35 years. There is a\nsubstantial incidence risk in late adolescence and early adulthood, with indications for", "source": "dsm5.pdf"} {"id": "5efabb82566a-2", "page_content": "substantial incidence risk in late adolescence and early adulthood, with indications for\na second high incidence risk phase after age 40 years. First onset in childhood is rare. The\noverall mean age at onset for agoraphobia is 17 years, although the age at onset without\npreceding panic attacks or panic disorder is 25\u201329 years. \nThe course of agoraphobia is typically pers istent and chronic. Complete remission is\nrare (10%), unless the agoraphobia is treated. With more severe agoraphobia, rates of full\nremission decrease, whereas rates of relapse and chronicity increase. A range of other dis-", "source": "dsm5.pdf"} {"id": "f13e5e3520c5-0", "page_content": "rare (10%), unless the agoraphobia is treated. With more severe agoraphobia, rates of full\nremission decrease, whereas rates of relapse and chronicity increase. A range of other dis-\norders, in particular other anxiety disorders, depressive disorders, substance use disor-\nders, and personality disorders, may complicat e the course of agoraphobia. The long-term", "source": "dsm5.pdf"} {"id": "23f9574f5cd3-0", "page_content": "220 Anxiety Disorders\ncourse and outcome of agoraphobia are associate d with substantially elevated risk of sec-\nondary major depressive disorder, persistent depressive disorder (dysthymia), and sub-\nstance use disorders.\nThe clinical features of agoraphobia are rela tively consistent across the lifespan, although\nthe type of agoraphobic situations triggering fear, anxiety, or avoidance, as well as the type of\ncognitions, may vary. For example, in children, being outside of the home alone is the most fre-\nquent situation feared, whereas in older adults, being in shops, standing in line, and being in\nopen spaces are most often feared. Also, cognitio ns often pertain to beco ming lost (in children),\nto experiencing panic-like symptoms (in adults), to falling (in older adults).\nThe low prevalence of agoraphobia in childre n could reflect difficulties in symptom re-\nporting, and thus assessments in young child ren may require solicitation of information\nfrom multiple sources, includ ing parents or teachers. Adolescents, particularly males,\nmay be less willing than adults to openly discuss agoraphobic fears and avoidance; how-\never, agoraphobia can occur prior to adulthood and should be assessed in children and\nadolescents. In older adults, comorbid somatic symptom disord ers, as well as motor dis-\nturbances (e.g., sense of fall ing or having medical compli cations), are frequently men-\ntioned by individuals as the reason for their fear and avoidance. In these instances, care is\nto be taken in evaluating whether the fear and avoidance are out of proportion to the real\ndanger involved. \nRisk and Prognostic Factors \nTemperamental. Behavioral inhibition and neurotic disposition (i.e., negative affectivity", "source": "dsm5.pdf"} {"id": "23f9574f5cd3-1", "page_content": "Temperamental. Behavioral inhibition and neurotic disposition (i.e., negative affectivity\n[neuroticism] and anxiety sensit ivity) are closely associated with agoraphobia but are rel-\nevant to most anxiety disorders (phobic disord ers, panic disorder, generalized anxiety dis-\norder). Anxiety sensitivity (t he disposition to believe that symptoms of anxiety are\nharmful) is also characteristic of individuals with agoraphobia.\nEnvironmental. Negative events in childhood (e.g., se paration, death of parent) and other\nstressful events, such as being attacked or mugge d, are associated with the onset of agorapho-\nbia. Furthermore, individuals with agoraphobia describe the family climate and child-rearing\nbehavior as being characterized by redu ced warmth and increased overprotection.\nGenetic and physiological. Heritability for agoraphobia is 61%. Of the various phobias,\nagoraphobia has the strongest and most specific association with the genetic factor that\nrepresents proneness to phobias. \nGender-Related Diagnostic Issues\nFemales have different patterns of comorbid disorders than males. Consistent with gender\ndifferences in the prevalence of mental diso rders, males have higher rates of comorbid\nsubstance use disorders. \nFunctional Consequences of Agoraphobia\nAgoraphobia is associated with considerable impairment and disability in terms of role\nfunctioning, work productivity, and disability days. Agoraphobia severity is a strong de-\nterminant of the degree of disab ility, irrespective of the pres ence of comorbid panic disor-\nder, panic attacks, and other comorbid cond itions. More than one- third of individuals\nwith agoraphobia are completely homebound and unable to work. \nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "23f9574f5cd3-2", "page_content": "Differential Diagnosis \nWhen diagnostic criteria for agoraphobia and an other disorder are full y met, both diagnoses\nshould be assigned, unless the fear, anxiety, or av oidance of agoraphobia is attributable to the\nother disorder. Weighting of crit eria and clinical judgment may be helpful in some cases.", "source": "dsm5.pdf"} {"id": "590047543808-0", "page_content": "Agoraphobia 221\nSpecific phobia, situational type. Differentiating agoraphobia from situational specific\nphobia can be challenging in some cases, because these conditions share several symptom\ncharacteristics and criteria. Specific phobia, sit uational type, should be diagnosed versus ago-\nraphobia if the fear, anxiety, or avoidance is limited to one of the agoraphobic situations.\nRequiring fears from two or more of the agorapho bic situations is a robust means for differen-\ntiating agoraphobia from specific phobias, partic ularly the situational subtype. Additional dif-\nferentiating features include the cognitive ideati on. Thus, if the situation is feared for reasons\nother than panic-like symptoms or other incapaci tating or embarrassing symptoms (e.g., fears\nof being directly harmed by the situation itself, such as fear of the plane crashing for individ-\nuals who fear flying), then a diagnosis of specific phobia may be more appropriate. \nSeparation anxiety disorder. Separation anxiety disorder can be best differentiated\nfrom agoraphobia by examining cognitive ideation. In separation anxiety disorder, the\nthoughts are about detachment from signific ant others and the home environment (i.e.,\nparents or other attachment figures), whereas in agoraphobia the focus is on panic-like\nsymptoms or other incapacitating or embarr assing symptoms in the feared situations.\nSocial anxiety disorder (social phobia). Agoraphobia should be differentiated from so-\ncial anxiety disorder based primarily on the si tuational clusters that trigger fear, anxiety,\nor avoidance and the cognitive ideation. In soci al anxiety disorder, the focus is on fear of\nbeing negatively evaluated. \nPanic disorder. When criteria for panic disorder are met, agoraphobia should not be di-", "source": "dsm5.pdf"} {"id": "590047543808-1", "page_content": "agnosed if the avoidance behaviors associated wi th the panic attacks do not extend to avoid-\nance of two or more agoraphobic situations.\nAcute stress disorder and post traumatic stress disorder. Acute stress disorder and\nposttraumatic stress disorder (PTSD) can be differentiated from agoraphobia by examin-\ning whether the fear, anxiety, or avoidance is related only to situations that remind the\nindividual of a traumatic event. If the fear, anxiety, or avoidanc e is restricted to trauma re-\nminders, and if the avoidance behavior does not extend to two or more agoraphobic situ-\nations, then a diagnosis of agoraphobia is not warranted. \nMajor depressive disorder. In major depressive disorder, the individual may avoid leav-\ning home because of apathy, loss of energy, low self-esteem, and anhe donia. If the avoid-\nance is unrelated to fears of panic-like or other incapacitating or embarrassing symptoms,\nthen agoraphobia should not be diagnosed.\nOther medical conditions. Agoraphobia is not diagnosed if the avoidance of situations\nis judged to be a physiological consequence of a medical condition. This determination is\nbased on history, laboratory findings, and a physical examination. Other relevant medical\nconditions may include neurod egenerative disorders with associated moto r disturbances\n(e.g., Parkinson\u2019s disease, multiple sclerosis), as well as cardiovascular disorders. Individ-\nuals with certain medical conditions may av oid situations because of realistic concerns\nabout being incapacitate d (e.g., fainting in an individual with transient ischemic attacks)\nor being embarrassed (e.g., diarrhea in an individual with Crohn\u2019s disease). The diagnosis\nof agoraphobia should be given only when the fear or avoidance is clearly in excess of that\nusually associated with these medical conditions. \nComorbidity", "source": "dsm5.pdf"} {"id": "590047543808-2", "page_content": "usually associated with these medical conditions. \nComorbidity\nThe majority of individuals with agoraphobia also have other mental disorders. The most\nfrequent additional diagnoses are other anxiety disorders (e.g., specific phobias, panic dis-\norder, social anxiety disorder), depressive disorders (major depre ssive disorder), PTSD,\nand alcohol use disorder. Where as other anxiety disorders (e.g., separation anxiety disor-", "source": "dsm5.pdf"} {"id": "ed1cb593b83e-0", "page_content": "order, social anxiety disorder), depressive disorders (major depre ssive disorder), PTSD,\nand alcohol use disorder. Where as other anxiety disorders (e.g., separation anxiety disor-\nder, specific phobias, panic disorder) frequent ly precede onset of agoraphobia, depressive\ndisorders and substance use disorders ty pically occur secondary to agoraphobia.", "source": "dsm5.pdf"} {"id": "dded9d8a1dda-0", "page_content": "222 Anxiety Disorders\nGeneralized Anxiety Disorder\nDiagnostic Criteria 300.02 (F41.1)\nA. Excessive anxiety and worry (apprehensive expectation), occurring more days than\nnot for at least 6 months, about a number of events or activities (such as work or school\nperformance). \nB. The individual finds it difficult to control the worry. \nC. The anxiety and worry are associated with three (or more) of the following six symp-\ntoms (with at least some symptoms having been present for more days than not for the\npast 6\u00a0months):\nNote: Only one item is required in children.\n1. Restlessness or feeling keyed up or on edge.\n2. Being easily fatigued.\n3. Difficulty concentrating or mind going blank.\n4. Irritability.\n5. Muscle tension.\n6. Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying\nsleep).\nD. The anxiety, worry, or physical symptoms cause clinically significant distress or impair-\nment in social, occupational, or other important areas of functioning.\nE. The disturbance is not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication) or another medical condition (e.g., hyperthyroidism).\nF. The disturbance is not better explained by another mental disorder (e.g., anxiety or\nworry about having panic attacks in panic disorder, negative evaluation in social anxi-\nety disorder [social phobia], contamination or other obsessions in obsessive-compul-\nsive disorder, separation from attachment figures in separation anxiety disorder,\nreminders of traumatic events in posttraumatic stress disorder, gaining weight in an-\norexia nervosa, physical complaints in somatic symptom disorder, perceived appear-\nance flaws in body dysmorphic disorder, having a serious illness in illness anxiety", "source": "dsm5.pdf"} {"id": "dded9d8a1dda-1", "page_content": "ance flaws in body dysmorphic disorder, having a serious illness in illness anxiety\ndisorder, or the content of delusional beliefs in schizophrenia or delusional disorder).\nDiagnostic Features\nThe essential feature of generalized anxiety disorder is excessive anxiety and worry (ap-\nprehensive expectation) about a number of events or activities. The intensity, duration, or\nfrequency of the anxiety and worry is out of pr oportion to the actual likelihood or impact\nof the anticipated event. The individual finds it difficult to control the worry and to keep\nworrisome thoughts from interfering with attention to tasks at hand. Adults with gener-\nalized anxiety disorder often worry about everyday, routine life circumstances, such as\npossible job responsibilities, health and fina nces, the health of family members, misfor-\ntune to their children, or minor matters (e.g., doing household chores or being late for ap-\npointments). Children with generalized anxiet y disorder tend to worry excessively about\ntheir competence or the quality of their perf ormance. During the co urse of the disorder,\nthe focus of worry may shift from one concern to another.\nSeveral features distinguish generalized anxi ety disorder from no npathological anxiety.\nFirst, the worries associated with generalized anxiety disorder are excessive and typically in-\nterfere significantly with psychosocial functi oning, whereas the worries of everyday life\nare not excessive and are perceived as more manageable and may be put off when more\npressing matters arise. Second, the worries associated with generalized anxiety disorder are", "source": "dsm5.pdf"} {"id": "32dedb64f52f-0", "page_content": "Generalized Anxiety Disorder 223\nmore pervasive, pronounced, and distressing; have longer du ration; and frequently occur\nwithout precipitants. The greater the range of life circumstances about which a person\nworries (e.g., finances, children\u2019s safety, job performance), the more likely his or her symp-\ntoms are to meet criteria for generalized anxi ety disorder. Third, everyday worries are much\nless likely to be accompanied by physical symp toms (e.g., restlessness or feeling keyed up\nor on edge). Individuals with generalized anxiety disorder report subjective distress due\nto constant worry and related impairment in social, occupational, or other important areas\nof functioning.\nThe anxiety and worry are accompanied by at least three of the following additional\nsymptoms: restlessness or feeling keyed up or on edge, being easily fatigued, difficulty\nconcentrating or mind going bl ank, irritability, muscle tens ion, and disturbed sleep, al-\nthough only one additional symptom is required in children. \nAssociated Features Supporting Diagnosis\nAssociated with muscle tension, there may be trembling, twitching, feeling shaky, and\nmuscle aches or soreness. Many individuals wi th generalized anxiety disorder also expe-\nrience somatic symptoms (e.g., sweating, naus ea, diarrhea) and an exaggerated startle re-\nsponse. Symptoms of autonomic hyperarousal (e.g., accelerated heart rate, shortness of\nbreath, dizziness) are less prominent in genera lized anxiety disorder than in other anxiety\ndisorders, such as panic disorder. Other conditions that may be associated with stress (e.g.,\nirritable bowel syndrome, headaches) frequently accompany generalized anxiety disorder. \nPrevalence\nThe 12-month prevalence of generalized anxiet y disorder is 0.9% among adolescents and", "source": "dsm5.pdf"} {"id": "32dedb64f52f-1", "page_content": "2.9% among adults in the general communit y of the United Stat es. The 12-month preva-\nlence for the disorder in other countries ranges from 0.4% to 3.6%. The lifetime morbid risk\nis 9.0%. Females are twice as likely as males to experience generalized anxiety disorder. The\nprevalence of the diagnosis peak s in middle age and declines across the later years of life.\nIndividuals of European descent tend to ex perience generalized anxiety disorder more\nfrequently than do individuals of non-Euro pean descent (i.e., Asian, African, Native\nAmerican and Pacific Islander ). Furthermore, individuals from developed countries are\nmore likely than individuals from nondeveloped countries to report that they have expe-\nrienced symptoms that meet criteria for ge neralized anxiety disorder in their lifetime.\nDevelopment and Course\nMany individuals with generalized anxiety disord er report that they have felt anxious and\nnervous all of their lives. The median age at onset for generalized anxiety disorder is 30\nyears; however, age at onset is spread over a very broad range. The median age at onset is\nlater than that for the other anxiety disorder s. The symptoms of excessive worry and anx-\niety may occur early in life but are then ma nifested as an anxious temperament. Onset of\nthe disorder rarely occurs prior to adolesce nce. The symptoms of generalized anxiety dis-\norder tend to be chronic and wax and wane across the lifespan, fluctuating between syn-\ndromal and subsyndromal forms of the diso rder. Rates of full re mission are very low.\nThe clinical expression of generalized anxiet y disorder is relatively consistent across\nthe lifespan. The primary difference across age groups is in the content of the individual\u2019s", "source": "dsm5.pdf"} {"id": "32dedb64f52f-2", "page_content": "the lifespan. The primary difference across age groups is in the content of the individual\u2019s\nworry. Children and adolescents tend to worr y more about school and sporting perfor-\nmance, whereas older adults report greater co ncern about the well-bein g of family or their\nown physical heath. Thus, the content of an in dividual\u2019s worry tends to be age appropri-\nate. Younger adults experience greater severity of symptoms than do older adults.\nThe earlier in life individuals have symptoms that meet criteria for generalized anxiety", "source": "dsm5.pdf"} {"id": "a8c986d5dc28-0", "page_content": "ate. Younger adults experience greater severity of symptoms than do older adults.\nThe earlier in life individuals have symptoms that meet criteria for generalized anxiety\ndisorder, the more comorbidity they tend to have and the more impaired they are likely to", "source": "dsm5.pdf"} {"id": "02d105e2bdb7-0", "page_content": "224 Anxiety Disorders\nbe. The advent of chronic physical disease can be a potent issue for excessive worry in the\nelderly. In the frail elderly, worries abou t safety\u2014and especially about falling\u2014may limit\nactivities. In those with early cognitive impairment, what appears to be excessive worry\nabout, for example, the whereabouts of things is probably better regarded as realistic\ngiven the cognitive impairment.\nIn children and adolescents with generalized anxiety disorder, the anxieties and wor-\nries often concern the quality of their performance or competen ce at school or in sporting\nevents, even when their performance is not being evaluated by others. There may be ex-\ncessive concerns about punctuality. They ma y also worry about ca tastrophic events, such\nas earthquakes or nuclear war. Children with the disorder may be overly conforming, per-\nfectionist, and unsure of themselves and tend to redo tasks because of excessive dissatis-\nfaction with less-than-perfect performance. They are typi cally overzealous in seeking\nreassurance and approval and require exces sive reassurance about their performance and\nother things they are worried about.\nGeneralized anxiety disorder may be overdiagnosed in children. When this diagnosis\nis being considered in children, a thorough ev aluation for the presence of other childhood\nanxiety disorders and other mental disorders should be done to determine whether the\nworries may be better explained by one of thes e disorders. Separation anxiety disorder, so-\ncial anxiety disorder (social phobia), and obsessive-compulsive disorder are often accom-\npanied by worries that may mimic those described in generalized anxiety disorder. For\nexample, a child with social anxiety disorder may be concerned abou t school performance\nbecause of fear of humiliation. Worries about illness may also be better explained by sep-\naration anxiety disorder or obsessive-compulsive disorder.", "source": "dsm5.pdf"} {"id": "02d105e2bdb7-1", "page_content": "aration anxiety disorder or obsessive-compulsive disorder.\nRisk and Prognostic Factors\nTemperamental. Behavioral inhibition, negative affectivity (neuroticism), and harm\navoidance have been associated wi th generalized anxiety disorder.\nEnvironmental. Although childhood adversities and parental overprotection have been\nassociated with generalized anxiety disorder, no environmental factors have been identi-\nfied as specific to generalized anxiety disorder or necessary or sufficient for making the di-\nagnosis.\nGenetic and physiological. One-third of the risk of expe riencing generalized anxiety\ndisorder is genetic, and these genetic factors overlap with the risk of neuroticism and are\nshared with other anxiety and mood disorder s, particularly major depressive disorder.\nCulture-Related Diagnostic Issues\nThere is considerable cultural variation in th e expression of generalized anxiety disorder.\nFor example, in some cultures, somatic symptoms predominat e in the expression of the\ndisorder, whereas in other cult ures cognitive symptoms tend to predominate. This differ-\nence may be more evident on initial presentation than su bsequently, as more symptoms\nare reported over time. There is no information as to whether the propensity for excessive\nworrying is related to culture, although the topic being worried about can be culture spe-\ncific. It is important to consider the social and cultural context when evaluating whether\nworries about certain situations are excessive.\nGender-Related Diagnostic Issues\nIn clinical settings, generalized anxiety diso rder is diagnosed somewhat more frequently\nin females than in males (about 55%\u201360% of those presenting wi th the disorder are\nfemale). In epidemiological studies, approx imately two-thirds are female. Females and\nmales who experience generalized anxiety diso rder appear to have similar symptoms but", "source": "dsm5.pdf"} {"id": "99abdc0cf6e0-0", "page_content": "Generalized Anxiety Disorder 225\ndemonstrate different patterns of comorbidity consistent with gender differences in the\nprevalence of disorders. In females, comorbidity is largely confined to the anxiety disor-\nders and unipolar depression, whereas in male s, comorbidity is more likely to extend to\nthe substance use disorders as well.\nFunctional Consequences of \nGeneralized Anxiety Disorder\nExcessive worrying impairs the individual\u2019s capa city to do things quickly and efficiently,\nwhether at home or at work. The worrying takes time and energy; the associated symp-\ntoms of muscle tension and feeling keyed up or on edge, tiredness, difficulty concentrat-\ning, and disturbed sleep contri bute to the impairment. Importantly the excessive worrying\nmay impair the ability of individuals with ge neralized anxiety disorder to encourage con-\nfidence in their children.\nGeneralized anxiety disorder is associated with significant disability and distress that is\nindependent of comorbid disorders, and most non-institutionalized adults with the disorder\nare moderately to seriously di sabled. Generalized anxiety di sorder accounts for 110 mil-\nlion disability days per annum in the U.S. population.\nDifferential Diagnosis\nAnxiety disorder due to another medical condition. The diagnosis of anxiety disorder\nassociated with another medical condition should be assigned if the individual\u2019s anxiety\nand worry are judged, based on history, labora tory findings, or physical examination, to\nbe a physiological effect of another specific medical condition (e.g., pheochromocytoma,\nhyperthyroidism). \nSubstance/medication-induced anxiety disorder. A substance/medication-induced\nanxiety disorder is distinguished from generaliz ed anxiety disorder by the fact that a sub-", "source": "dsm5.pdf"} {"id": "99abdc0cf6e0-1", "page_content": "anxiety disorder is distinguished from generaliz ed anxiety disorder by the fact that a sub-\nstance or medication (e.g., a drug of abuse, ex posure to a toxin) is judged to be etiologically\nrelated to the anxiety. For example, severe anxi ety that occurs only in the context of heavy\ncoffee consumption would be diagnosed as caffeine-induced anxiety disorder.\nSocial anxiety disorder. Individuals with social anxiety disorder often have anticipa-\ntory anxiety that is focused on upcoming social situations in which they must perform or\nbe evaluated by others, whereas individuals with generalized anxiety disorder worry,\nwhether or not they are being evaluated. \nObsessive-compulsive disorder. Several features distinguish the excessive worry of\ngeneralized anxiety disorder fr om the obsessional thoughts of obsessive-compulsive dis-\norder. In generalized anxiety disorder the focus of the worry is about forthcoming prob-\nlems, and it is the excessivene ss of the worry about future events that is abnormal. In\nobsessive-compulsive disorder, the obsessions are inappropriate ideas that take the form of\nintrusive and unwanted thou ghts, urges, or images. \nPosttraumatic stress disorder and adjustment disorders. Anxiety is invariably pres-\nent in posttraumatic stress disorder. Generali zed anxiety disorder is not diagnosed if the\nanxiety and worry are better explained by sy mptoms of posttraumatic stress disorder.\nAnxiety may also be present in adjustment di sorder, but this residual category should be\nused only when the criteria are not met for any other disorder (including generalized anx-\niety disorder). Moreover, in adjustment disorders, the anxi ety occurs in response to an\nidentifiable stressor within 3 months of the onset of the stressor and does not persist for\nmore than 6 months after the terminatio n of the stressor or its consequences.", "source": "dsm5.pdf"} {"id": "99abdc0cf6e0-2", "page_content": "Depressive, bipolar, and psychotic disorders. Generalized anxiety/worry is a common\nassociated feature of depressive, bipolar, an d psychotic disorders and should not be di-", "source": "dsm5.pdf"} {"id": "6e22897dbcbe-0", "page_content": "226 Anxiety Disorders\nagnosed separately if the excessive worry h as occurred only during the course of these\nconditions.\nComorbidity\nIndividuals whose presen tation meets criteria for genera lized anxiety disorder are likely\nto have met, or currently meet, criteria for other anxiety and unip olar depressive disor-\nders. The neuroticism or emotional liability th at underpins this pattern of comorbidity is\nassociated with temperamental antecedents and genetic and environmental risk factors\nshared between these disorders, although in dependent pathways are also possible. Co-\nmorbidity with substance use, conduct, psychotic, neurodevelopmental, and neurocogni-\ntive disorders is less common.\nSubstance/Medication-Induced\n Anxiety Disorder\nDiagnostic Criteria\nA. Panic attacks or anxiety is predominant in the clinical picture.\nB. There is evidence from the history, physical examination, or laboratory findings of both\n(1) and (2):\n1. The symptoms in Criterion A developed during or soon after substance intoxication\nor withdrawal or after exposure to a medication.\n2. The involved substance/medication is capable of producing the symptoms in Crite-\nrion A.\nC. The disturbance is not better explained by an anxiety disorder that is not substance/\nmedication-induced. Such evidence of an independent anxiety disorder could include\nthe following:\nThe symptoms precede the onset of the substance/medication use; the symptoms\npersist for a substantial period of time (e.g., about 1 month) after the cessation of\nacute withdrawal or severe intoxication; or there is other evidence suggesting the\nexistence of an independent non-substance/medication-induced anxiety disorder\n(e.g., a history of recurrent non-substance/medication-related episodes).\nD. The disturbance does not occur exclusively during the course of a delirium.", "source": "dsm5.pdf"} {"id": "6e22897dbcbe-1", "page_content": "D. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning. \nNote: This diagnosis should be made instead of a diagnosis of substance intoxication or\nsubstance withdrawal only when the symptoms in Criterion A predominate in the clinical\npicture and they are sufficiently severe to warrant clinical attention. \nCoding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-\ntion]-induced anxiety disorders are indicated in the table below. Note that the ICD-10-CM\ncode depends on whether or not there is a comorbid substance use disorder present for\nthe same class of substance. If a mild substance use disorder is comorbid with the sub-\nstance-induced anxiety disorder, the 4th positio n character is \u201c1,\u201d and the clinician should\nrecord \u201cmild [substance] use disorder\u201d bef ore the substance-induced anxiety disorder\n(e.g., \u201cmild cocaine use disorder with cocai ne-induced anxiety disorder\u201d). If a moderate or\nsevere substance use disorder is comorbid with the substance-induced anxiety disorder,\nthe 4th position character is \u201c2,\u201d and the clinician should record \u201cmoderate [substance] use\ndisorder\u201d or \u201csevere [substance] use disorder,\u201d depending on the severity of the comorbid\nsubstance use disorder. If there is no comorbid substance use disorder (e.g., after a one-", "source": "dsm5.pdf"} {"id": "d4959745d124-0", "page_content": "Substance/Medication-Induced Anxiety Disorder 227\ntime heavy use of the substance), then the 4th position character is \u201c9,\u201d and the clinician\nshould record only the substance-induced anxiety disorder.\nSpecify if (see Table 1 in the chapter \u201cSubstance-Related and Addictive Disorders\u201d for di-\nagnoses associated with substance class):\nWith onset during intoxication: This specifier applies if criteria are met for intoxica-\ntion with the substance and the symptoms develop during intoxication.\nWith onset during withdrawal: This specifier applies if criteria are met for withdrawal\nfrom the substance and the symptoms develop during, or shortly after, withdrawal.\nWith onset after medication use: Symptoms may appear either at initiation of medi-\ncation or after a modification or change in use.\nRecording Procedures\nICD-9-CM. The name of the substance/medicati on-induced anxiety disorder begins\nwith the specific substance (e.g ., cocaine, salbutamol) that is presumed to be causing the\nanxiety symptoms. The diagnostic code is sele cted from the table included in the criteria\nset, which is based on the drug class. For substa nces that do not fit into any of the classes\n(e.g., salbutamol), the code for \u201cother substance\u201d should be used; and in cases in which\na substance is judged to be an etiological fact or but the specific class of substance is un-\nknown, the category \u201cunknown substance\u201d should be used.\nThe name of the disorder is followed by the specification of onset (i.e., onset during in-\ntoxication, onset during withdr awal, with onset duri ng medication use). Unlike the record-\ning procedures for ICD-10-CM, which comb ine the substance-induced disorder and", "source": "dsm5.pdf"} {"id": "d4959745d124-1", "page_content": "ing procedures for ICD-10-CM, which comb ine the substance-induced disorder and\nsubstance use disorder in to a single code, for ICD-9-CM a se parate diagnostic code is given\nfor the substance use disorder. For example, in the case of anxiety symptoms occurring dur-\ning withdrawal in a man with a severe lorazepam use disorder, the diagnosis is 292.89 loraz-\nepam-induced anxiety disorder, with onset du ring withdrawal. An additional diagnosis of\n304.10 severe lorazepam use disorder is also given. When more than one substance is judged\nto play a significant role in the development of anxiety symptoms, each should be listed sep-ICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate \nor severeWithout \nuse \ndisorder\nAlcohol 291.89 F10.180 F10.280 F10.980\nCaffeine 292.89 F15.180 F15.280 F15.980\nCannabis 292.89 F12.180 F12.280 F12.980\nPhencyclidine 292.89 F16.180 F16.280 F16.980\nOther hallucinogen 292.89 F16.180 F16.280 F16.980\nInhalant 292.89 F18.180 F18.280 F18.980\nOpioid 292.89 F11.188 F11.288 F11.988\nSedative, hypnotic, or anxiolytic 292.89 F13.180 F13.280 F13.980\nAmphetamine (or other \nstimulant)292.89 F15.180 F15.280 F15.980", "source": "dsm5.pdf"} {"id": "d4959745d124-2", "page_content": "stimulant)292.89 F15.180 F15.280 F15.980\nCocaine 292.89 F14.180 F14.280 F14.980\nOther (or unknown) substance 292.89 F19.180 F19.280 F19.980", "source": "dsm5.pdf"} {"id": "1b4e600c4cff-0", "page_content": "228 Anxiety Disorders\narately (e.g., 292.89 methylphenidate-induced an xiety disorder, with on set during intoxica-\ntion; 292.89 salbutamol-induced anxiety di sorder, with onset after medication use).\nICD-10-CM. The name of the substance/medication-induced anxiety disorder begins\nwith the specific substance (e.g ., cocaine, salbutamol) that is presumed to be causing the\nanxiety symptoms. The di agnostic code is selected from the table included in the criteria\nset, which is based on the drug class and presence or absence of a comorbid substance use\ndisorder. For substances that do not fit into any of the classes (e.g., salbutamol), the code\nfor \u201cother substance\u201d should be used; and in cases in which a substance is judged to be an\netiological factor but the specific class of substance is unknown, the category \u201cunknown\nsubstance\u201d should be used.\nWhen recording the name of the disorder, th e comorbid substance use disorder (if any)\nis listed first, followed by the word \u201cwith,\u201d followed by the name of the substance-induced\nanxiety disorder, followed by the specification of onset (i.e., onset during intoxication,\nonset during withdrawal, with onset during medication use). For example, in the case of\nanxiety symptoms occurring during withdrawal in a man with a severe lorazepam use dis-\norder, the diagnosis is F13.280 severe lor azepam use disorder with lorazepam-induced\nanxiety disorder, with onset du ring withdrawal. A separate diagnosis of the comorbid se-\nvere lorazepam use disorder is not given. If the substance-induced anxiety disorder occurs\nwithout a comorbid substance use disorder (e.g., after a one-time heavy use of the substance),", "source": "dsm5.pdf"} {"id": "1b4e600c4cff-1", "page_content": "no accompanying substance use disorder is no ted (e.g., F16.980 psilocybin-induced anxi-\nety disorder, with onset during intoxication). When more than one substance is judged to\nplay a significant role in the development of anxiety symptoms, each should be listed sep-\narately (e.g., F15.280 severe methylphenidate use disorder with methylphenidate-induced\nanxiety disorder, with onset during intoxica tion; F19.980 salbutamol-induced anxiety dis-\norder, with onset after medication use).\nDiagnostic Features\nThe essential features of substance/medicati on-induced anxiety di sorder are prominent\nsymptoms of panic or anxiety (Criterion A) that are judged to be due to the effects of a sub-\nstance (e.g., a drug of abuse, a medication, or a toxin exposure). The panic or anxiety symp-\ntoms must have developed duri ng or soon after substance in toxication or withdrawal or\nafter exposure to a medication, and the substa nces or medications must be capable of pro-\nducing the symptoms (Criteri on B2). Substance/medication-induced anxiety disorder\ndue to a prescribed treatment for a mental disorder or another medical condition must\nhave its onset while the individual is receivin g the medication (or during withdrawal, if a\nwithdrawal is associated with the medication ). Once the treatment is discontinued, the\npanic or anxiety symptoms will usually improv e or remit within days to several weeks to\na month (depending on the half-life of the su bstance/medication and the presence of with-\ndrawal). The diagnosis of substance/medicati on-induced anxiety disorder should not be\ngiven if the onset of the panic or anxiety symptoms precedes the substance/medication in-", "source": "dsm5.pdf"} {"id": "1b4e600c4cff-2", "page_content": "given if the onset of the panic or anxiety symptoms precedes the substance/medication in-\ntoxication or withdrawal, or if the symptoms persist for a subs tantial period of time (i.e.,\nusually longer than 1 month) from the time of severe intoxication or withdrawal. If the\npanic or anxiety symptoms persist for substantial periods of time, other causes for the\nsymptoms should be considered.\nThe substance/medication-ind uced anxiety disorder diagnosis should be made in-\nstead of a diagnosis of substance intoxication or substance withdrawal only when the\nsymptoms in Criterion A are predominant in th e clinical picture and are sufficiently severe\nto warrant independent clinical attention.\nAssociated Features Supporting Diagnosis", "source": "dsm5.pdf"} {"id": "de3c40d4d90e-0", "page_content": "symptoms in Criterion A are predominant in th e clinical picture and are sufficiently severe\nto warrant independent clinical attention.\nAssociated Features Supporting Diagnosis\nPanic or anxiety can occur in association with intoxication with the following classes of sub-\nstances: alcohol, caffeine, cannabis, phencyc lidine, other hallucinogens, inhalants, stimu-", "source": "dsm5.pdf"} {"id": "0dd51beecb0a-0", "page_content": "Substance/Medication-Induced Anxiety Disorder 229\nlants (including cocaine), and other (or unknown) substances. Panic or anxiety can occur in\nassociation with withdrawal from the following classes of substances: alcohol; opioids; sed-\natives, hypnotics, and anxiolytics; stimulants (including cocaine); and other (or unknown)\nsubstances. Some medications that evoke anxi ety symptoms include anesthetics and anal-\ngesics, sympathomimetics or other bronchodilato rs, anticholiner gics, insulin, thyroid prep-\narations, oral contraceptives, antihistamines, antiparkinsonian medica tions, corticosteroids,\nantihypertensive and ca rdiovascular medications, anticon vulsants, lithium carbonate, an-\ntipsychotic medications, and antidepressant medications. Heavy metals and toxins (e.g.,\norganophosphate insecticide, nerve gases, ca rbon monoxide, carbon dioxide, volatile sub-\nstances such as gasoline and paint) may also cause panic or anxiety symptoms.\nPrevalence\nThe prevalence of substance/me dication-induced anxiety disorder is not clear. General\npopulation data suggest that it may be rare, with a 12-month prevalence of approximately\n0.002%. However, in clinical populations, the prevalence is likely to be higher. \nDiagnostic Markers\nLaboratory assessments (e.g., urine toxicology) may be useful to measure substance intox-\nication as part of an assessment for subs tance/medication-induced anxiety disorder.\nDifferential Diagnosis\nSubstance intoxication and substance withdrawal. Anxiety symptoms commonly oc-\ncur in substance intoxi cation and substance withdrawal. The diagnosis of the substance-\nspecific intoxication or substance-specific wi thdrawal will usually suffice to categorize the", "source": "dsm5.pdf"} {"id": "0dd51beecb0a-1", "page_content": "specific intoxication or substance-specific wi thdrawal will usually suffice to categorize the\nsymptom presentation. A diag nosis of substance/medication-induced anxiety disorder\nshould be made in addition to substance intoxication or su bstance withdrawal when the\npanic or anxiety symptoms are predominant in the clinical picture and are sufficiently se-\nvere to warrant independent c linical attention. For example, panic or anxiety symptoms\nare characteristic of alcohol withdrawal. \nAnxiety disorder (i.e., not indu ced by a substance/medication). Substance/medication-\ninduced anxiety disorder is judged to be etio logically related to the substance/medication.\nSubstance/medication-induced anxiety disord er is distinguished from a primary anxiety\ndisorder based on the onset, course, and othe r factors with respect to substances/medica-\ntions. For drugs of abuse, there must be eviden ce from the history, physical examination, or\nlaboratory findings for use, intoxication, or withdrawal . Substance/medication-induced\nanxiety disorders arise only in association with intoxication or with drawal states, whereas\nprimary anxiety disorders may precede the onse t of substance/medication use. The pres-\nence of features that are atypical of a primary anxiety disorder, such as atypical age at onset\n(e.g., onset of panic disorder after age 45 year s) or symptoms (e.g., atypical panic attack\nsymptoms such as true vertigo, loss of balanc e, loss of consciousness , loss of bladder con-\ntrol, headaches, slurred speech) may suggest a substance/medication -induced etiology. A\nprimary anxiety disorder diagnosis is warranted if the panic or anxiety symptoms persist\nfor a substantial period of time (about 1 mont h or longer) after the end of the substance in-", "source": "dsm5.pdf"} {"id": "0dd51beecb0a-2", "page_content": "toxication or acute withdr awal or there is a histor y of an anxiety disorder.\nDelirium. If panic or anxiety symptoms occur exclusively during the course of delirium,\nthey are considered to be an associated feature of the de lirium and are not diagnosed sep-\narately. \nAnxiety disorder due to another medical condition. If the panic or anxiety symptoms\nare attributed to the physiological consequenc es of another medical condition (i.e., rather\nthan to the medication taken for the medical condition), anxi ety disorder due to another", "source": "dsm5.pdf"} {"id": "cc4147059e9a-0", "page_content": "230 Anxiety Disorders\nmedical condition should be diagnosed. The history often provides the basis for such a\njudgment. At times, a change in the treatment for the other medical condition (e.g., med-\nication substitution or discontinuation) may be needed to determine whether the medica-\ntion is the causative agent (in which case the symptoms may be better explained by\nsubstance/medication-induced anxiety disorder). If the disturbance is attributable to both\nanother medical condition and substance use, bo th diagnoses (i.e., anxiety disorder due to\nanother medical condition and substance/me dication-induced anxi ety disorder) may be\ngiven. When there is insufficie nt evidence to determine whether the panic or anxiety symp-\ntoms are attributable to a subs tance/medication or to anothe r medical condition or are pri-\nmary (i.e., not attributable to either a subs tance or another medical condition), a diagnosis\nof other specified or unspecified an xiety disorder wo uld be indicated.\nAnxiety Disorder Due to\nAnother Medical Condition\nDiagnostic Criteria 293.84 (F06.4)\nA. Panic attacks or anxiety is predominant in the clinical picture. \nB. There is evidence from the history, physical examination, or laboratory findings that the dis-\nturbance is the direct pathophysiological consequence of another medical condition. \nC. The disturbance is not better explained by another mental disorder. \nD. The disturbance does not occur exclusively during the course of a delirium. \nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nCoding note: Include the name of the other medical condition within the name of the men-", "source": "dsm5.pdf"} {"id": "cc4147059e9a-1", "page_content": "Coding note: Include the name of the other medical condition within the name of the men-\ntal disorder (e.g., 293.84 [F06.4] anxiety disorder due to pheochromocytoma). The other\nmedical condition should be coded and listed separately immediately before the anxiety\ndisorder due to the medical condition (e.g., 227.0 [D35.00] pheochromocytoma; 293.84\n[F06.4] anxiety disorder due to pheochromocytoma.\nDiagnostic Features\nThe essential feature of anxiety disorder due to another medical condition is clinically signifi-\ncant anxiety that is judged to be best explaine d as a physiological effect of another medical con-\ndition. Symptoms can include pr ominent anxiety symptoms or panic attacks (Criterion A).\nThe judgment that the symptoms are best explai ned by the associated physical condition must\nbe based on evidence from the history, physical examination, or laboratory findings (Criterion\nB). Additionally, it must be judged that the sy mptoms are not better accounted for by another\nmental disorder, in particular, adjustment disorder, with anxiety, in which the stressor is the\nmedical condition (Criterion C). In this case, an individual with adjustment disorder is espe-\ncially distressed about the mean ing or the consequences of th e associated medical condition.\nBy contrast, there is often a prominent physical component to the anxiety (e.g., shortness of\nbreath) when the anxiety is due to another medica l condition. The diagnosis is not made if the\nanxiety symptoms occur only during the course of a delirium (Criterion D). The anxiety symp-\ntoms must cause clinically significant distress or impairment in social, occupational, or other\nimportant areas of functioning (Criterion E).", "source": "dsm5.pdf"} {"id": "cc4147059e9a-2", "page_content": "important areas of functioning (Criterion E).\nIn determining whether the anxiety symptoms are attributable to another medical con-\ndition, the clinician must first establish the presence of the medica l condition. Further-\nmore, it must be established that anxiety symptoms can be etiologically related to the\nmedical condition through a physiological mech anism before making a judgment that this\nis the best explanation for the symptoms in a specific individual. A careful and compre-", "source": "dsm5.pdf"} {"id": "1edc1e907854-0", "page_content": "Anxiety Disorder Due to Another Medical Condition 231\nhensive assessment of multiple factors is ne cessary to make this judgment. Several aspects\nof the clinical presentation should be consider ed: 1) the presence of a clear temporal asso-\nciation between the onset, exacerbation, or re mission of the medical condition and the anx-\niety symptoms; 2) the presence of features th at are atypical of a primary anxiety disorder\n(e.g., atypical age at onset or course); and 3) evidence in the literature that a known phys-\niological mechanism (e.g., hyperthyroidism) ca uses anxiety. In addi tion, the disturbance\nmust not be better explained by a primar y anxiety disorder, a substance/medication-\ninduced anxiety disorder, or an other primary mental disorder (e.g., adjustment disorder). \nAssociated Features Supporting Diagnosis\nA number of medical conditions are known to include anxiety as a symptomatic manifes-\ntation. Examples include endocrine disease (e.g., hyperthyroidis m, pheochromocytoma,\nhypoglycemia, hyperadrenocortisolism), cardiovascular disorders (e.g., congestive heart\nfailure, pulmonary embolism, arrhythmia such as atrial fibrillation), respiratory illness\n(e.g., chronic obstructive pulmonary diseas e, asthma, pneumonia), metabolic distur-\nbances (e.g., vitamin B12 deficiency, porphyria), and neurological illness (e.g., neoplasms,\nvestibular dysfunction, encephalitis, seizure disorders). Anxiety due to another medical\ncondition is diagnosed when the medical cond ition is known to induce anxiety and when\nthe medical condition preceded the onset of the anxiety.\nPrevalence\nThe prevalence of anxiety disorder due to an other medical condition is unclear. There ap-", "source": "dsm5.pdf"} {"id": "1edc1e907854-1", "page_content": "The prevalence of anxiety disorder due to an other medical condition is unclear. There ap-\npears to be an elevated prevalence of anxi ety disorders among individuals with a variety\nof medical conditions, including asthma, hypert ension, ulcers, and arthritis. However, this\nincreased prevalence may be due to reasons ot her than the anxiety disorder directly caus-\ning the medical condition. \nDevelopment and Course\nThe development and course of anxiety diso rder due to another medical condition gen-\nerally follows the course of the underlying illness. This diagnosis is not meant to include\nprimary anxiety disorders that arise in the co ntext of chronic medical illness. This is im-\nportant to consider with older adults, who may experience chronic medical illness and\nthen develop independent anxiety disorder s secondary to the chronic medical illness.\nDiagnostic Markers\nLaboratory assessments and/or medical examin ations are necessary to confirm the diag-\nnosis of the associated medical condition. \nDifferential Diagnosis\nDelirium. A separate diagnosis of anxiety disord er due to another medical condition is\nnot given if the anxiety disturbance occurs exclusively during the course of a delirium.\nHowever, a diagnosis of anxiety disorder du e to another medical condition may be given\nin addition to a diagnosis of major neurocognitive disorder (dementia) if the etiology of\nanxiety is judged to be a physiological consequence of the pathological process causing the\nneurocognitive disorder and if anxiety is a prominent part of the clinical presentation. \nMixed presentation of symptoms (e.g., mood and anxiety). If the presentation includes\na mix of different types of symptoms, the spec ific mental disorder due to another medical\ncondition depends on which symptoms predominate in the clinical picture.\nSubstance/medication-induced anxiety disorder. If there is evidence of recent or pro-", "source": "dsm5.pdf"} {"id": "1edc1e907854-2", "page_content": "Substance/medication-induced anxiety disorder. If there is evidence of recent or pro-\nlonged substance use (including medications with psychoactive effects), withdrawal from", "source": "dsm5.pdf"} {"id": "6e98eb092daa-0", "page_content": "232 Anxiety Disorders\na substance, or exposure to a toxin, a su bstance/medication-induced anxiety disorder\nshould be considered. Certain medications are known to increase anxiety (e.g., corticoste-\nroids, estrogens, metoclopramide), and when this is the case, the medication may be the\nmost likely etiology, although it may be difficult to distinguish whether the anxiety is at-\ntributable to the medications or to the medica l illness itself. When a diagnosis of substance-\ninduced anxiety is being made in relation to recreational or nonprescribed drugs, it may be\nuseful to obtain a urine or blood drug screen or other appropriate laboratory evaluation.\nSymptoms that occur during or shortly after (i.e., within 4 weeks of) substance intoxication\nor withdrawal or after medication use may be especially indicative of a substance/medi-\ncation-induced anxiety disorder, depending on the type, duration, or amount of the sub-\nstance used. If the disturbance is associate d with both another medical condition and\nsubstance use, both diagnoses (i.e., anxiety disorder due to anothe r medical condition and\nsubstance/medication-induced an xiety disorder) can be given. Features such as onset af-\nter age 45 years or the presence of atypical symptoms during a panic attack (e.g., vertigo,\nloss of consciousness, loss of bladder or bowe l control, slurred speech, amnesia) suggest\nthe possibility that another medical condition or a substance may be causing the panic at-\ntack symptoms.\nAnxiety disorder (not due to a known medical condition). Anxiety disorder due to an-\nother medical condition should be distinguis hed from other anxiety disorders (especially\npanic disorder and generalized anxiety disorder). In other anxiety disorders, no specific\nand direct causative physiological mechanisms associated with anot her medical condition", "source": "dsm5.pdf"} {"id": "6e98eb092daa-1", "page_content": "and direct causative physiological mechanisms associated with anot her medical condition\ncan be demonstrated. Late age at onset, atyp ical symptoms, and the absence of a personal\nor family history of anxiety disorders suggest the need for a thorough assessment to rule\nout the diagnosis of anxiety diso rder due to another medical condition. Anxiety disorders\ncan exacerbate or pose increased risk for me dical conditions such as cardiovascular events\nand myocardial infarction and should not be diagnosed as anxiety disorder due to another\nmedical condition in these cases.\nIllness anxiety disorder. Anxiety disorder due to anothe r medical condition should be\ndistinguished from illness anxiety disorder. Illness anxiety disorder is characterized by\nworry about illness, concern about pain, and bod ily preoccupations. In the case of illness\nanxiety disorder, individuals may or may not have diagnosed medical conditions. Al-\nthough an individual with illness anxiety di sorder and a diagnose d medical condition is\nlikely to experience anxiety about the medical condition, the medical condition is not\nphysiologically related to the anxiety symptoms. \nAdjustment disorders. Anxiety disorder due to another medical condition should be\ndistinguished from adjustment disorders, with anxiety, or with anxiety and depressed\nmood. Adjustment diso rder is warranted when individual s experience a maladaptive re-\nsponse to the stress of having another medical condition. The reaction to stress usually\nconcerns the meaning or consequences of the stress, as compared with the experience of\nanxiety or mood symptoms that occur as a phy siological consequence of the other medical\ncondition. In adjustment disorder, the anxi ety symptoms are typically related to coping\nwith the stress of having a general medical condition, whereas in anxiety disorder due to\nanother medical condition, individuals are more likely to have prominent physical symp-\ntoms and to be focused on issues other than the stress of the illness itself.", "source": "dsm5.pdf"} {"id": "6e98eb092daa-2", "page_content": "toms and to be focused on issues other than the stress of the illness itself. \nAssociated feature of another mental disorder. Anxiety symptoms may be an associ-\nated feature of another ment al disorder (e.g., schizo phrenia, anorexia nervosa).", "source": "dsm5.pdf"} {"id": "375be34d1c68-0", "page_content": "Associated feature of another mental disorder. Anxiety symptoms may be an associ-\nated feature of another ment al disorder (e.g., schizo phrenia, anorexia nervosa). \nOther specified or unspeci fied anxiety disorder. This diagnosis is given if it cannot be\ndetermined whether the anxiety symptoms are primary, substance-induced, or associated\nwith another medical condition.", "source": "dsm5.pdf"} {"id": "9997e9a8b478-0", "page_content": "Other Specified Anxiety Disorder 233\nOther Specified Anxiety Disorder\n300.09 (F41.8)\nThis category applies to presentations in which symptoms characteristic of an anxiety dis-\norder that cause clinically significant distre ss or impairment in social, occupational, or oth-\ner important areas of functioning predominate but do not meet the full criteria for any of the\ndisorders in the anxiety disorders diagnostic class. The other specified anxiety disorder\ncategory is used in situations in which the clinician chooses to communicate the specific\nreason that the presentation does not meet the criteria for any specific anxiety disorder.\nThis is done by recording \u201cother specified anxiety disorder\u201d followed by the specific reason\n(e.g., \u201cgeneralized anxiety not occurring more days than not\u201d).\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Limited-symptom attacks.\n2.Generalized anxiety not occurring more days than not.\n3.Khy\u00e2l cap (wind attacks): See \u201cGlossary of Cultural Concepts of Distress\u201d in the Ap-\npendix.\n4.Ataque de nervios (attack of nerves): See \u201cGlossary of Cultural Concepts of Distress\u201d\nin the Appendix.\nUnspecified Anxiety Disorder\n300.00 (F41.9)\nThis category applies to presentations in which symptoms characteristic of an anxiety dis-\norder that cause clinically significant distre ss or impairment in social, occupational, or oth-\ner important areas of functioning predominate but do not meet the full criteria for any of the\ndisorders in the anxiety disorders diagnostic cl ass. The unspecified anxiety disorder cate-\ngory is used in situations in which the clinician chooses not to specify the reason that the\ncriteria are not met for a specific anxiety disorder, and includes presentations in which", "source": "dsm5.pdf"} {"id": "9997e9a8b478-1", "page_content": "criteria are not met for a specific anxiety disorder, and includes presentations in which\nthere is insufficient information to make a more specific diagnosis (e.g., in emergency room\nsettings).", "source": "dsm5.pdf"} {"id": "ecb9aba714cf-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "5c07888431e6-0", "page_content": "235 Obsessive-Compulsive and\nRelated Disorders\nObsessive-compulsive and related disorders in clude obsessive-compulsive\ndisorder (OCD), body dysmor phic disorder, hoarding diso rder, trichotillomania (hair-\npulling disorder), excoriation (skin-picking) disorder, substance/medication-induced ob-\nsessive-compulsive and related disorder, obsessive-compulsive and related disorder due\nto another medical condition, and other spec ified obsessive-compulsive and related dis-\norder and unspecified obsessive-compulsive and related disorder (e.g ., body-focused re-\npetitive behavior disorder, obsessional jealousy).\nOCD is characterized by the presence of obsessions and/or compulsions. Obsessions\nare recurrent and persistent th oughts, urges, or images that are experienced as intrusive\nand unwanted, whereas compulsions are repetitive behaviors or mental acts that an indi-\nvidual feels driven to perform in response to an obsession or according to rules that must\nbe applied rigidly. Some other obsessive-comp ulsive and related disorders are also char-\nacterized by preoccupations and by repetitive behaviors or mental acts in response to the\npreoccupations. Other obsessive-compulsive and related disorders are characterized pri-\nmarily by recurrent body -focused repetitive behaviors (e.g., hair pulling, sk in picking) and\nrepeated attempts to decrease or stop the behaviors.\nThe inclusion of a chapter on obsessive-compulsive and rela ted disorders in DSM-5 re-\nflects the increasing evidence of these disorders\u2019 relatedness to one an other in terms of a\nrange of diagnostic validators as well as the c linical utility of grouping these disorders in\nthe same chapter. Clinicians are encouraged to screen for these cond itions in individuals", "source": "dsm5.pdf"} {"id": "5c07888431e6-1", "page_content": "the same chapter. Clinicians are encouraged to screen for these cond itions in individuals\nwho present with one of them and be aware of overlaps between these conditions. At the\nsame time, there are important differences in diagnostic validators and treatment ap-\nproaches across these disorders. Moreover, there are close relationships between the anx-\niety disorders and some of the obsessive-compulsive and related disorders (e.g., OCD),\nwhich is reflected in the sequence of DSM-5 chapters, with obsessive-compulsive and re-\nlated disorders following anxiety disorders. \nThe obsessive-compulsive and related diso rders differ from developmentally norma-\ntive preoccupations and rituals by being exce ssive or persisting beyond developmentally\nappropriate periods. The distinction between the presence of subclinical symptoms and a\nclinical disorder requires assessment of a nu mber of factors, including the individual\u2019s\nlevel of distress and impa irment in functioning. \nThe chapter begins with OCD. It then co vers body dysmorphic disorder and hoarding\ndisorder, which are characterized by cognit ive symptoms such as perceived defects or\nflaws in physical appearance or the perceived need to save possessions, respectively. The\nchapter then covers trichotillomania (hair-pulling disorder) and excoriation (skin-picking)\ndisorder, which are characterized by recurrent body-focused repetitive behaviors. Finally,\nit covers substance/medication-induced obsessive-compulsive an d related disorder,\nobsessive-compulsive and relate d disorder due to another me dical condition, and other\nspecified obsessive-compulsive and related disorder and unspecified obsessive-compul-\nsive and related disorder.\nWhile the specific content of obsessions and compulsions varies among individuals,\ncertain symptom dimensions are common in OCD, including th ose of cleaning (contami-", "source": "dsm5.pdf"} {"id": "5c07888431e6-2", "page_content": "certain symptom dimensions are common in OCD, including th ose of cleaning (contami-\nnation obsessions and cleaning compulsions); symmetry (symmetry obsessions and repeat-", "source": "dsm5.pdf"} {"id": "53cff0365c63-0", "page_content": "236 Obsessive-Compulsive and Related Disorders\ning, ordering, and counting compulsions); fo rbidden or taboo thoug hts (e.g., aggressive,\nsexual, and religious obsessions and related co mpulsions); and harm (e .g., fears of harm to\noneself or others and related checking comp ulsions). The tic-related specifier of OCD is\nused when an individual has a curren t or past history of a tic disorder.\nBody dysmorphic disorder is characterize d by preoccupation with one or more per-\nceived defects or flaws in physical appearance that are not observable or appear only slight\nto others, and by repetitive behaviors (e.g., mirror checking, excessive grooming, skin\npicking, or reassurance seeking) or mental acts (e.g., comparing one\u2019s appearance with that\nof other people) in response to the appear ance concerns. The appearance preoccupations\nare not better explained by concerns with body fat or weight in an individual with an eat-\ning disorder. Muscle dysmorphia is a form of body dysmorphic disord er that is character-\nized by the belief that one\u2019s body build is too small or is insu fficiently muscular.\nHoarding disorder is characterized by persis tent difficulty discarding or parting with\npossessions, regardless of their actual value, as a result of a strong perceived need to save\nthe items and to distress associated with disc arding them. Hoarding disorder differs from\nnormal collecting. For example, symptoms of hoarding disorder result in the accumula-\ntion of a large number of possessions that co ngest and clutter active living areas to the ex-\ntent that their intended use is substantially compromised. The excessive acquisition form\nof hoarding disorder, which characterizes most but not all individuals with hoarding dis-", "source": "dsm5.pdf"} {"id": "53cff0365c63-1", "page_content": "of hoarding disorder, which characterizes most but not all individuals with hoarding dis-\norder, consists of excessive collecting, buying , or stealing of items that are not needed or\nfor which there is no available space.\nTrichotillomania (hair-pulling disorder) is characterized by recurrent pulling out of\none's hair resulting in hair loss, and repeated attempts to decrease or stop hair pulling.\nExcoriation (skin-picking) disord er is characterized by recurrent picking of one\u2019s skin re-\nsulting in skin lesions and repeated attempts to decrease or stop skin picking. The body-\nfocused repetitive behaviors that characterize these two disorders are not triggered by ob-\nsessions or preoccupations; however, they ma y be preceded or accompanied by various\nemotional states, such as feelin gs of anxiety or boredom. They may also be preceded by an\nincreasing sense of tension or may lead to gr atification, pleasure, or a sense of relief when\nthe hair is pulled out or the skin is picked. In dividuals with these disorders may have vary-\ning degrees of conscious awareness of the beha vior while engaging in it, with some indi-\nviduals displaying more focused attention on the behavior (with preceding tension and\nsubsequent relief) and other individuals displaying more automatic behavior (with the be-\nhaviors seeming to occur without full awareness).\nSubstance/medication-i nduced obsessive-compulsive an d related disorder consists of\nsymptoms that are due to substance intoxicati on or withdrawal or to a medication. Obses-\nsive-compulsive and related disorder due to another medica l condition involves symptoms\ncharacteristic of obsessive-comp ulsive and related disorders th at are the direct pathophysio-\nlogical consequence of a medical disorder. Othe r specified obsessive-compulsive and related", "source": "dsm5.pdf"} {"id": "53cff0365c63-2", "page_content": "logical consequence of a medical disorder. Othe r specified obsessive-compulsive and related\ndisorder and unspecified obsessive-compulsive and related disorder consist of symptoms\nthat do not meet criteria for a specific obse ssive-compulsive and related disorder because of\natypical presentation or uncertain etiology; th ese categories are also used for other specific\nsyndromes that are not listed in Section II and when insufficient information is available to di-\nagnose the presentation as another obsessive -compulsive and related disorder. Examples of", "source": "dsm5.pdf"} {"id": "4d129aa7d1b2-0", "page_content": "syndromes that are not listed in Section II and when insufficient information is available to di-\nagnose the presentation as another obsessive -compulsive and related disorder. Examples of\nspecific syndromes not listed in Section II, an d therefore diagnosed as other specified obses-\nsive-compulsive and related disorder or as unspecified obsessive-co mpulsive and related\ndisorder include body-focused repetitiv e behavior disord er and obsessional jealousy.\nObsessive-compulsive and relate d disorders that have a cognitive component have in-\nsight as the basis for specifiers; in each of th ese disorders, insight ranges from \u201cgood or fair\ninsight\u201d to \u201cpoor insight\u201d to \u201cabsent insight/ delusional beliefs\u201d with respect to disorder-\nrelated beliefs. For individuals whose obsess ive-compulsive and related disorder symp-\ntoms warrant the \u201cwith absent insight/delu sional beliefs\u201d specifier, these symptoms\nshould not be diagnosed as a psychotic disorder.", "source": "dsm5.pdf"} {"id": "28572a66c888-0", "page_content": "Obsessive-Compulsive Disorder 237\nObsessive-Compulsive Disorder\nDiagnostic Criteria 300.3 (F42)\nA. Presence of obsessions, compulsions, or both: \nObsessions are defined by (1) and (2): \n1. Recurrent and persistent thoughts, urges, or images that are experienced, at some\ntime during the disturbance, as intrusive and unwanted, and that in most individuals\ncause marked anxiety or distress.\n2. The individual attempts to ignore or suppres s such thoughts, urges, or images, or to\nneutralize them with some other thought or action (i.e., by performing a compulsion). \nCompulsions are defined by (1) and (2): \n1. Repetitive behaviors (e.g., hand washing, ordering, checking) or mental acts (e.g.,\npraying, counting, repeating words silently ) that the individual feels driven to per-\nform in response to an obsession or according to rules that must be applied rigidly.\n2. The behaviors or mental acts are aimed at preventing or reducing anxiety or dis-\ntress, or preventing some dreaded event or situation; however, these behaviors or\nmental acts are not connected in a realistic way with what they are designed to neu-\ntralize or prevent, or are clearly excessive.\nNote: Young children may not be able to articulate the aims of these behaviors or\nmental acts.\nB. The obsessions or compulsions are time-consuming (e.g., take more than 1 hour per\nday) or cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning. \nC. The obsessive-compulsive symptoms are not attributable to the physiological effects\nof a substance (e.g., a drug of abuse, a medication) or another medical condition.", "source": "dsm5.pdf"} {"id": "28572a66c888-1", "page_content": "D. The disturbance is not better explained by the symptoms of another mental disorder\n(e.g., excessive worries, as in generalized anxiety disorder; preoccupation with ap-\npearance, as in body dysmorphic disorder; difficulty discarding or parting with posses-\nsions, as in hoarding disorder; hair pulling, as in trichotillomania [hair-pulling disorder];\nskin picking, as in excoriation [skin-picking] disorder; stereotypies, as in stereotypic\nmovement disorder; ritualized eating behavior, as in eating disorders; preoccupation\nwith substances or gambling, as in substance-related and addictive disorders; preoc-\ncupation with having an illness, as in illness anxiety disorder; sexual urges or fantasies,\nas in paraphilic disorders; impulses, as in disruptive, impulse-control, and conduct dis-\norders; guilty ruminations, as in major depressive disorder; thought insertion or delu-\nsional preoccupations, as in schizophrenia spectrum and other psychotic disorders; or\nrepetitive patterns of behavior, as in autism spectrum disorder). \nSpecify if: \nWith good or fair insight: The individual recognizes that obsessive-compulsive dis-\norder beliefs are definitely or probably not true or that they may or may not be true.\nWith poor insight: The individual thinks obsessive-compulsive disorder beliefs are\nprobably true.\nWith absent insight/delusional beliefs: The individual is completely convinced that\nobsessive-compulsive disorder beliefs are true.\nSpecify if: \nTic-related: The individual has a current or past history of a tic disorder.", "source": "dsm5.pdf"} {"id": "bf5fb3edbd01-0", "page_content": "238 Obsessive-Compulsive and Related Disorders\nSpecifiers\nMany individuals with obsessive-compulsive disorder (OCD) have dysfunctional beliefs.\nThese beliefs can include an inflated sense of responsibility and the tendency to overesti-\nmate threat; perfectionism and intolerance of uncertainty; an d over-importance of thoughts\n(e.g., believing that having a fo rbidden thought is as bad as acting on it) and the need to\ncontrol thoughts. \nIndividuals with OCD vary in the degree of insight they have about the accuracy of the\nbeliefs that underlie their obsessive-compulsive symptoms. Many individuals have good or\nfair insight (e.g., the individual believes that the house definitely will not, probably will not,\nor may or may not burn down if the stove is not checked 30 times). Some have poor insight\n(e.g., the individual believes that the house w ill probably burn down if the stove is not\nchecked 30 times), and a few (4% or less) have absent insight/delu sional beliefs (e.g., the in-\ndividual is convinced that the house will burn down if the stove is not checked 30 times).\nInsight can vary within an individual over the course of the illness. Poorer insight has been\nlinked to worse long-term outcome.\nUp to 30% of individuals with OCD have a lifetime tic disorder. This is most common\nin males with onset of OCD in childhood. Thes e individuals tend to differ from those with-\nout a history of tic disorders in the themes of their OCD sy mptoms, comorbidity, course,\nand pattern of fam ilial transmission. \nDiagnostic Features\nThe characteristic symptoms of OCD are the pr esence of obsessions and compulsions (Cri-\nterion A). Obsessions are repetitive and persistent thoughts (e.g., of contamination), images", "source": "dsm5.pdf"} {"id": "bf5fb3edbd01-1", "page_content": "(e.g., of violent or horrific scenes), or urges (e.g., to stab someone) . Importantly, obsessions\nare not pleasurable or experi enced as voluntary: they ar e intrusive and unwanted and\ncause marked distress or anxiety in most indi viduals. The individual attempts to ignore or\nsuppress these obsessions (e.g., avoiding tri ggers or using thought suppression) or to neu-\ntralize them with another thought or ac tion (e.g., performing a compulsion). Compulsions\n(or rituals) are repetitive behaviors (e.g., washing, checking) or mental acts (e.g., counting,\nrepeating words silently) that the individual feels driven to perform in response to an\nobsession or according to rules that must be applied rigidly. Most individuals with OCD\nhave both obsessions and compulsions. Comp ulsions are typically performed in response\nto an obsession (e.g., thoughts of contaminatio n leading to washing rituals or that some-\nthing is incorrect leading to repeating rituals unt il it feels \u201cjust right\u201d). The aim is to reduce\nthe distress triggered by obsessions or to pr event a feared event (e.g., becoming ill). How-\never, these compulsions either are not connected in a realistic way to the feared event (e.g.,\narranging items symmetrically to prevent harm to a loved one) or are clearly excessive\n(e.g., showering for hours each day). Compulsions are not done for pleasure, although some\nindividuals experience relief from anxiety or distress. \nCriterion B emphasizes that obsessions and compulsions must be time-consuming (e.g.,\nmore than 1 hour per day) or cause clinically significant distress or impairment to warrant\na diagnosis of OCD. This criterion helps to distinguish the disorder from the occasional in-\ntrusive thoughts or repetitive behaviors that are common in the general population (e.g.,", "source": "dsm5.pdf"} {"id": "bf5fb3edbd01-2", "page_content": "trusive thoughts or repetitive behaviors that are common in the general population (e.g.,\ndouble-checking that a door is locked). The frequency and severity of obsessions and com-\npulsions vary across individuals with OCD (e.g., some have mild to moderate symptoms,\nspending 1\u20133 hours per day obsessing or doin g compulsions, where as others have nearly\nconstant intrusive thoughts or comp ulsions that can be incapacitating).\nAssociated Features Supporting Diagnosis\nThe specific content of obsessions and comp ulsions varies between individuals. However,", "source": "dsm5.pdf"} {"id": "303a497137ca-0", "page_content": "Associated Features Supporting Diagnosis\nThe specific content of obsessions and comp ulsions varies between individuals. However,\ncertain themes, or dimensions, are common, including those of cleaning (contamination\nobsessions and cleaning compulsions); sy mmetry (symmetry obsess ions and repeating,", "source": "dsm5.pdf"} {"id": "abfff7efd100-0", "page_content": "Obsessive-Compulsive Disorder 239\nordering, and counting compulsions); forbidden or taboo th oughts (e.g., aggressive, sexual,\nor religious obsessions and related compulsions) ; and harm (e.g., fears of harm to oneself\nor others and checking compulsions). Some individuals also have difficulties discarding\nand accumulate (hoard) object s as a consequence of typical obsessions and compulsions,\nsuch as fears of harming othe rs. These themes occur across different cultures, are rela-\ntively consistent over time in adults with th e disorder, and may be as sociated with differ-\nent neural substrates. Importantly, individu als often have symptoms in more than one\ndimension. \nIndividuals with OCD experience a range of affective responses when confronted with\nsituations that trigger obsessions and compul sions. For example, many individuals expe-\nrience marked anxiety that can include recurren t panic attacks. Others report strong feel-\nings of disgust. While perfor ming compulsions, some individuals report a distressing\nsense of \u201cincompleteness\u201d or uneasiness unt il things look, feel, or sound \u201cjust right.\u201d \nIt is common for individuals with the disorder to avoid people, places, and things that\ntrigger obsessions and compulsions. For example, individuals with contamination con-\ncerns might avoid public situat ions (e.g., restaurants, public restrooms) to reduce ex-\nposure to feared contaminants; individuals with intrusive thoughts about causing harm\nmight avoid social interactions. \nPrevalence\nThe 12-month prevalence of OCD in the United St ates is 1.2%, with a similar prevalence in-\nternationally (1.1%\u20131.8%). Females are affected at a slightly higher rate than males in", "source": "dsm5.pdf"} {"id": "abfff7efd100-1", "page_content": "adulthood, although males are more commonly affected in childhood. \nDevelopment and Course\nIn the United States, the mean age at onset of OCD is 19.5 years, and 25% of cases start by\nage 14 years. Onset after age 35 years is unusual but does occur. Males have an earlier age\nat onset than females: nearly 25% of males have onset before age 10 years. The onset of\nsymptoms is typically gradual; however, acute onset has also been reported.\nIf OCD is untreated, the cour se is usually chronic, often with waxing and waning symp-\ntoms. Some individuals have an episodic course, and a minority have a deteriorating\ncourse. Without treatment, remission rates in adults are low (e.g., 20% for those reevalu-\nated 40 years later). Onset in childhood or adolescence can le ad to a lifetim e of OCD. How-\never, 40% of individuals with onset of OCD in childhood or adolescence may experience\nremission by early adulthood. The course of OCD is often complicated by the co-occurrence\nof other disorders (see section \u201cC omorbidity\u201d for this disorder).\nCompulsions are more easily diagnosed in children than obsessions are because com-\npulsions are observable. However, most childr en have both obsessions and compulsions\n(as do most adults). The pattern of symptoms in adults can be stable over time, but it is\nmore variable in children. Some differences in the content of obsessions and compulsions\nhave been reported when children and adol escent samples have been compared with\nadult samples. These differences likely refl ect content appropriate to different develop-\nmental stages (e.g., higher rates of sexual an d religious obsessions in adolescents than in", "source": "dsm5.pdf"} {"id": "abfff7efd100-2", "page_content": "mental stages (e.g., higher rates of sexual an d religious obsessions in adolescents than in\nchildren; higher rates of harm obsessions [e.g ., fears of catastrophic events, such as death\nor illness to self or loved ones] in ch ildren and adolescents than in adults). \nRisk and Prognostic Factors\nTemperamental. Greater internalizing symptoms, hi gher negative emotionality, and\nbehavioral inhibition in childhood are possible temperamental risk factors. \nEnvironmental. Physical and sexual abuse in childho od and other stressful or traumatic\nevents have been associated with an increased risk for de veloping OCD. Some children", "source": "dsm5.pdf"} {"id": "87239e9d1a23-0", "page_content": "240 Obsessive-Compulsive and Related Disorders\nmay develop the sudden onset of obsessive- compulsive symptoms, which has been asso-\nciated with different environmental factors, including various infectious agents and a\npost-infectious auto immune syndrome.\nGenetic and physiological. The rate of OCD among first-degree relatives of adults with\nOCD is approximately two times that among fi rst-degree relatives of those without the\ndisorder; however, among first-degree relatives of individuals with onset of OCD in child-\nhood or adolescence, the rate is increased 10-fold. Familial transmission is due in part to\ngenetic factors (e.g., a concordance rate of 0.57 for monozygotic vs. 0.22 for dizygotic twins).\nDysfunction in the orbitofrontal cortex, anteri or cingulate cortex, and striatum have been\nmost strongly implicated.\nCulture-Related Diagnostic Issues \nOCD occurs across the world. There is substant ial similarity across cultures in the gender\ndistribution, age at onset, and comorbidity of OCD. Moreover, around the globe, there is a\nsimilar symptom structure in volving cleaning, symmetry, hoarding, taboo thoughts, or\nfear of harm. However, regional variation in symptom expression exists, and cultural\nfactors may shape the content of obsessions and compulsions.\nGender-Related Diagnostic Issues\nMales have an earlier age at onset of OCD than females and are more likely to have co-\nmorbid tic disorders. Gender differences in the pattern of symptom dimensions have been\nreported, with, for example, females more likel y to have symptoms in the cleaning dimen-\nsion and males more likely to have symptoms in the forbidden thoughts and symmetry di-\nmensions. Onset or exacerbation of OCD, as well as symptoms that can interfere with the", "source": "dsm5.pdf"} {"id": "87239e9d1a23-1", "page_content": "mother-infant relationship (e.g., aggressive ob sessions leading to avoidance of the infant),\nhave been reported in the peripartum period. \nSuicide Risk\nSuicidal thoughts occur at some point in as many as about half of individuals with OCD.\nSuicide attempts are also report ed in up to one-quarter of individuals with OCD; the pres-\nence of comorbid major depressiv e disorder increases the risk. \nFunctional Consequences of \nObsessive-Compu lsive Disorder\nOCD is associated with reduced quality of life as well as high levels of social and occupa-\ntional impairment. Impairment occurs across many different domains of life and is asso-\nciated with symptom severity. Impairment can be caused by the time spent obsessing and\ndoing compulsions. Avoi dance of situations that can tr igger obsessions or compulsions\ncan also severely restrict functioning. In addition, specific sympto ms can create specific\nobstacles. For example, obsessions about harm can make relationships with family and\nfriends feel hazardous; the result can be av oidance of these rela tionships. Obsessions\nabout symmetry can derail the timely completion of school or work projects because the\nproject never feels \u201cjust right,\u201d potentially resulting in school failure or job loss. Health\nconsequences can also occur. For example, individuals with contamination concerns may\navoid doctors\u2019 offices and hospit als (e.g., because of fears of exposure to germs) or develop\ndermatological problems (e.g., skin lesion s due to excessive washing). Sometimes the\nsymptoms of the disorder inte rfere with its own treatment (e .g., when medications are con-\nsidered contaminated). When th e disorder starts in childhood or adolescence, individuals\nmay experience developmental difficulties. Fo r example, adolescents may avoid socializ-", "source": "dsm5.pdf"} {"id": "87239e9d1a23-2", "page_content": "may experience developmental difficulties. Fo r example, adolescents may avoid socializ-\ning with peers; young adults may struggle when they leave home to live independently.", "source": "dsm5.pdf"} {"id": "64e7560d7e5d-0", "page_content": "Obsessive-Compulsive Disorder 241\nThe result can be few significant relationship s outside the family and a lack of autonomy\nand financial independence from their family of origin. In addition, some individuals with\nOCD try to impose rules and prohibitions on family members beca use of their disorder\n(e.g., no one in the family can have visitors to the house for fear of contamination), and this\ncan lead to family dysfunction. \nDifferential Diagnosis\nAnxiety disorders. Recurrent thoughts, avoidant behavi ors, and repetitive requests for\nreassurance can also occur in anxiety disorders. Ho wever, the recurrent thoughts that are\npresent in generalized anxiety disorder (i.e., worries) are usually ab out real-life concerns,\nwhereas the obsessions of OCD usually do no t involve real-life concerns and can include\ncontent that is odd, irrational, or of a se emingly magical nature; moreover, compulsions\nare often present and usually linked to the obsessions. Like individuals with OCD, indi-\nviduals with specific phobia can have a fear re action to specific objects or situations; how-\never, in specific phobia the feared object is usually much more circ umscribed, and rituals\nare not present. In social anxiety disorder (social phobia), the feared objects or situations\nare limited to social interactions, and avoida nce or reassurance seeking is focused on re-\nducing this social fear.\nMajor depressive disorder. OCD can be distinguished from the rumination of major\ndepressive disorder, in whic h thoughts are usually mood-c ongruent and not necessarily\nexperienced as intrusive or distressing; mo reover, ruminations are not linked to compul-\nsions, as is typical in OCD. \nOther obsessive-compulsive and related disorders. In body dysmorphic disorder, the", "source": "dsm5.pdf"} {"id": "64e7560d7e5d-1", "page_content": "Other obsessive-compulsive and related disorders. In body dysmorphic disorder, the\nobsessions and compulsions are limited to concerns about physical appearance; and in\ntrichotillomania (hair-pulling diso rder), the compulsive behavior is limited to hair pulling\nin the absence of obsessions. Hoarding diso rder symptoms focus exclusively on the per-\nsistent difficulty discarding or parting with possessions, marked distress associated with\ndiscarding items, and excessive accumulation of objects. However, if an individual has ob-\nsessions that are typical of OCD (e.g., concer ns about incompleteness or harm), and these\nobsessions lead to compulsive hoarding behaviors (e.g., acquirin g all objects in a set to at-\ntain a sense of completeness or not discarding old newspape rs because they may contain\ninformation that could prevent harm), a di agnosis of OCD should be given instead. \nEating disorders. OCD can be distinguished from anorexia nervosa in that in OCD the\nobsessions and compulsions are not limite d to concerns about weight and food.\nTics (in tic disorder) and stereotyped movements. A tic is a sudden, rapid, recurrent,\nnonrhythmic motor movement or vocalization (e.g., eye blinking, th roat clearing). A ste-\nreotyped movement is a repetitive, seemingly driven, nonfunctional motor behavior (e.g.,\nhead banging, body rocking, self-biting). Tics and ster eotyped movements are typically\nless complex than compulsions and are not aimed at neutralizing obsessions. However,\ndistinguishing between complex tics and comp ulsions can be difficult. Whereas compul-\nsions are usually preceded by obsessions, tics are often preceded by premonitory sensory", "source": "dsm5.pdf"} {"id": "64e7560d7e5d-2", "page_content": "urges. Some individuals have symptoms of both OCD and a tic disorder, in which case\nboth diagnoses may be warranted. \nPsychotic disorders. Some individuals with OCD have poor insight or even delusional\nOCD beliefs. However, they have obsessions and compulsions (disting uishing their\ncondition from delusional diso rder) and do not have other features of schizophrenia or\nschizoaffective disorder (e.g., hallucinations or formal thought disorder). \nOther compulsive-like behaviors. Certain behaviors are sometimes described as \u201ccom-\npulsive,\u201d including sexual behavior (in the ca se of paraphilias), ga mbling (i.e., gambling", "source": "dsm5.pdf"} {"id": "240703c216f5-0", "page_content": "242 Obsessive-Compulsive and Related Disorders\ndisorder), and substance use (e.g., alcohol us e disorder). However, these behaviors differ\nfrom the compulsions of OCD in that the pers on usually derives pleasure from the activity\nand may wish to resist it only beca use of its deleterious consequences.\nObsessive-compulsive personality disorder. Although obsessive-compulsive person-\nality disorder and OCD have similar names, the clinical manifestations of these disorders\nare quite different. Obsessive- compulsive personality disorder is not characterized by in-\ntrusive thoughts, images, or ur ges or by repetitive behavior s that are performed in re-\nsponse to these intrusions; instead, it in volves an enduring and pervasive maladaptive\npattern of excessive perfectionism and rigid co ntrol. If an individual manifests symptoms\nof both OCD and obsessive-compulsive persona lity disorder, both diagnoses can be given.\nComorbidity \nIndividuals with OCD often have other psycho pathology. Many adults with the disorder\nhave a lifetime diagnosis of an anxiety disord er (76%; e.g., panic disorder, social anxiety\ndisorder, generalized anxiety disorder, specific phobia) or a depressive or bipolar disorder\n(63% for any depressive or bipolar disorder, with the most common being major depres-\nsive disorder [41%]). Onset of OCD is usually later than for most co morbid anxiety disor-\nders (with the exception of separation anxiet y disorder) and PTSD bu t often precedes that\nof depressive disorders. Comorbid obsessi ve-compulsive personality disorder is also\ncommon in individuals with OCD (e.g., ranging from 23% to 32%). \nUp to 30% of individuals with OCD also have a lifetime tic disorder. A comorbid tic\ndisorder is most common in males with onset of OCD in childhood. These individuals", "source": "dsm5.pdf"} {"id": "240703c216f5-1", "page_content": "disorder is most common in males with onset of OCD in childhood. These individuals\ntend to differ from those without a history of tic disorders in the themes of their OCD\nsymptoms, comorbidity, course, and pattern of familial transmission. A triad of OCD, tic\ndisorder, and attention-deficit/hyperactivit y disorder can also be seen in children.\nDisorders that occur more frequently in individuals with OCD than in those without\nthe disorder include several obsessive-compulsive and related disorders such as body\ndysmorphic disorder, trichotillomania (hair-pulling disorder), and excoriation (skin-pick-\ning) disorder. Finally, an association betw een OCD and some disorders characterized by\nimpulsivity, such as oppositional de fiant disorder, has been reported. \nOCD is also much more common in individuals with certain other disorders than\nwould be expected based on its prevalence in the general population ; when one of those\nother disorders is diagnosed, the individual should be assessed for OCD as well. For ex-\nample, in individuals with schizophrenia or schizoaffective disorder, the prevalence of\nOCD is approximately 12%. Rates of OCD are also elevated in bipolar disorder; eating dis-\norders, such as anorexia nervosa and bu limia nervosa; and Tourette\u2019s disorder.\nBody Dysmorphic Disorder\nDiagnostic Criteria 300.7 (F45.22)\nA. Preoccupation with one or more perceived defects or flaws in physical appearance that\nare not observable or appear slight to others.\u00a0 \nB. At some point during the course of the disorder, the individual has performed repetitive\nbehaviors (e.g., mirror checking, excessive grooming, skin picking, reassurance seek-\ning) or mental acts (e.g., comparing his or her appearance with that of others) in re-", "source": "dsm5.pdf"} {"id": "240703c216f5-2", "page_content": "sponse to the appearance concerns.\nC. The preoccupation causes clinically significant distress or impairment in social, occu-\npational, or other important areas of functioning. \nD. The appearance preoccupation is not better explained by concerns with body fat or\nweight in an individual whose symptoms meet diagnostic criteria for an eating disorder.", "source": "dsm5.pdf"} {"id": "9a03d96b01f3-0", "page_content": "Body Dysmorphic Disorder 243\nSpecify if:\nWith muscle dysmorphia: The individual is preoccupied with the idea that his or her\nbody build is too small or insufficiently muscular. This specifier is used even if the indi-\nvidual is preoccupied with other body areas, which is often the case. \nSpecify if: \nIndicate degree of insight regarding body dysmorphic disorder beliefs (e.g., \u201cI look ugly\u201d or\n\u201cI look deformed\u201d).\nWith good or fair insight: The individual recognizes that\u00a0the body dysmorphic disor-\nder beliefs are definitely or probably not true or that they may or may not be true.\nWith poor insight: The individual thinks\u00a0that the body dysmorphic disorder beliefs are\nprobably true.\nWith absent insight/delusional beliefs: The individual is completely convinced that\nthe body dysmorphic disorder beliefs are true.\nDiagnostic Features \nIndividuals with body dysmorphic disorder (formerly known as dysmorphophobia ) are pre-\noccupied with one or more perceived defects or flaws in their physical appearance, which\nthey believe look ugly, unattractive, abnormal , or deformed (Criterion A). The perceived\nflaws are not observable or appear only slig ht to other individuals. Concerns range from\nlooking \u201cunattractive\u201d or \u201cnot right\u201d to looking \u201chideous\u201d or \u201clike a monster.\u201d Preoccu-\npations can focus on one or many body are as, most commonly the skin (e.g., perceived\nacne, scars, lines, wrinkles, paleness), hair (e.g., \u201cthinning\u201d hair or \u201ce xcessive\u201d body or fa-\ncial hair), or nose (e.g., size or shape). Howe ver, any body area can be the focus of concern", "source": "dsm5.pdf"} {"id": "9a03d96b01f3-1", "page_content": "(e.g., eyes, teeth, weight, stomach, breasts, le gs, face size or shape, lips, chin, eyebrows,\ngenitals). Some individuals are concerned abou t perceived asymmetry of body areas. The\npreoccupations are intrusive, unwanted, time-consuming (occurring, on average, 3\u20138\nhours per day), and usually diff icult to resist or control. \nExcessive repetitive behaviors or mental ac ts (e.g., comparing) are performed in re-\nsponse to the preoccupation (Criterion B). The individual feels driven to perform these be-\nhaviors, which are not pleasurable and may increase anxiety and dysphoria. They are\ntypically time-consuming and difficult to re sist or control. Common behaviors are com-\nparing one\u2019s appearance with that of other individuals; repeatedly checking perceived\ndefects in mirrors or other reflecting surf aces or examining them directly; excessively\ngrooming (e.g., combing, stylin g, shaving, plucking, or pull ing hair); camouflaging (e.g.,\nrepeatedly applying makeup or covering dislik ed areas with such things as a hat, clothing,\nmakeup, or hair); seeking reassurance about how the perceived flaws look; touching dis-\nliked areas to check them; excessively exerci sing or weight lifting; and seeking cosmetic\nprocedures. Some individuals exce ssively tan (e.g., to darken \u201cpale\u201d skin or diminish per-\nceived acne), repeatedly change their clothe s (e.g., to camouflage perceived defects), or\ncompulsively shop (e.g., for beauty produc ts). Compulsive skin picking intended to\nimprove perceived skin defects is common and can cause skin damage, infections, or\nruptured blood vessels. The preoccupation must cause clinically significant distress or im-", "source": "dsm5.pdf"} {"id": "9a03d96b01f3-2", "page_content": "ruptured blood vessels. The preoccupation must cause clinically significant distress or im-\npairment in social, occupational, or other important areas of functioning (Criterion C);\nusually both are present. Body dysmorphic diso rder must be differentiated from an eating\ndisorder.\nMuscle dysmorphia, a form of body dysmorphic disorder occurring almost exclusively\nin males, consists of preoccup ation with the idea that one\u2019s body is too small or insuffi-\nciently lean or muscular. Individuals with this form of the disorder actually have a nor-\nmal-looking body or are even very muscular . They may also be preoccupied with other\nbody areas, such as skin or hair. A majority (b ut not all) diet, exerc ise, and/or lift weights\nexcessively, sometimes causing bodily damage . Some use potentially dangerous anabolic-", "source": "dsm5.pdf"} {"id": "550b5c72923c-0", "page_content": "244 Obsessive-Compulsive and Related Disorders\nandrogenic steroids and other substances to try to make their body bigger and more mus-\ncular. Body dysmorphic disorder by proxy is a form of body dy smorphic disorder in\nwhich individuals are preoccupied with defects they perceive in another person\u2019s appear-\nance.\nInsight regarding body dysmorphic disorder beliefs can range from good to absent/\ndelusional (i.e., delusional beliefs consisting of complete conviction that the individual\u2019s\nview of their appearance is accurate and un distorted). On average, insight is poor; one-\nthird or more of individuals currently have delusional body dysmorphic disorder beliefs.\nIndividuals with delusional body dysmorphic di sorder tend to have greater morbidity in\nsome areas (e.g., suicidality), but this appears accounted fo r by their tendency to have\nmore severe body dysmorphic disorder symptoms. \nAssociated Features Supporting Diagnosis \nMany individuals with body dysmorphic disord er have ideas or delusions of reference,\nbelieving that other people take special notice of them or mock them because of how they\nlook. Body dysmorphic disorder is associated with high levels of anxiety, social anxiety,\nsocial avoidance, depressed mood, neuroticism, and perfectionism as well as low extro-\nversion and low self-esteem. Many individuals are ashamed of their appearance and their\nexcessive focus on how they look, and are relu ctant to reveal their concerns to others. A\nmajority of individuals receiv e cosmetic treatment to try to improve their perceived de-\nfects. Dermatological treatment and surgery ar e most common, but any type (e.g., dental,\nelectrolysis) may be received . Occasionally, individuals may perform surgery on them-\nselves. Body dysmorphic disorder appears to respond poorly to such treatments and", "source": "dsm5.pdf"} {"id": "550b5c72923c-1", "page_content": "selves. Body dysmorphic disorder appears to respond poorly to such treatments and\nsometimes becomes worse. Some individuals ta ke legal action or are violent toward the\nclinician because they are dissat isfied with the cosmetic outcome.\nBody dysmorphic disorder has been associat ed with executive dysfunction and visual\nprocessing abnormalities, with a bias for an alyzing and encoding details rather than ho-\nlistic or configural aspects of vi sual stimuli. Individuals with this disorder tend to have a\nbias for negative and threatening interpretati ons of facial expressions and ambiguous sce-\nnarios. \nPrevalence \nThe point prevalence among U.S. adults is 2.4% (2.5% in females and 2.2% in males). Out-\nside the United States (i.e., Germany), cu rrent prevalence is approximately 1.7%\u20131.8%,\nwith a gender distribution similar to that in the United States. The current prevalence is\n9%\u201315% among dermatology patients, 7%\u20138% am ong U.S. cosmetic surgery patients, 3%\u2013\n16% among international cosmetic surgery patients (most studies), 8% among adult orth-\nodontia patients, and 10% among patients presenting for oral or maxillofacial surgery.\nDevelopment and Course \nThe mean age at disorder onset is 16\u201317 years, the median age at onset is 15 years, and the\nmost common age at onset is 12\u201313 years. Two-thirds of individuals have disorder onset\nbefore age 18. Subclinical body dysmorphic diso rder symptoms begin, on average, at age\n12 or 13 years. Subclinical concerns usually ev olve gradually to the full disorder, although\nsome individuals experience abrupt onset of body dysmorphic disorder. The disorder", "source": "dsm5.pdf"} {"id": "550b5c72923c-2", "page_content": "some individuals experience abrupt onset of body dysmorphic disorder. The disorder\nappears to usually be chronic, although improvement is likely when evidence-based\ntreatment is received. The disorder\u2019s clinical features appear largely similar in children/\nadolescents and adults. Body dysm orphic disorder occurs in th e elderly, but little is known\nabout the disorder in this age group. Individu als with disorder onset before age 18 years\nare more likely to attempt suicide, have more comorbidity, and have gradual (rather than\nacute) disorder onset than those with adult-onset body dysmorphic disorder.", "source": "dsm5.pdf"} {"id": "65608a101fb3-0", "page_content": "Body Dysmorphic Disorder 245\nRisk and Prognostic Factors \nEnvironmental. Body dysmorphic disorder has been as sociated with high rates of child-\nhood neglect and abuse. \nGenetic and physiological. The prevalence of body dysmor phic disorder is elevated in\nfirst-degree relatives of individuals with obsessive-compulsi ve disorder (OCD).\nCulture-Related Diagnostic Issues \nBody dysmorphic disorder has be en reported internationally. It appears that the disorder\nmay have more similarities th an differences across races and cultures but that cultural\nvalues and preferences may influence symptom content to some degree. Taijin kyofusho,\nincluded in the traditional Japanese diagnost ic system, has a subtype similar to body dys-\nmorphic disorder: shubo-kyofu (\u201cthe phobia of a deformed body\u201d). \nGender-Related Diagnostic Issues \nFemales and males appear to have more similariti es than differences in terms of most clin-\nical features\u2014 for example, di sliked body areas, types of repetitive behaviors, symptom\nseverity, suicidality, comorbidity, illness course, and receipt of cosmetic procedures for\nbody dysmorphic disorder. However, males ar e more likely to have genital preoccupa-\ntions, and females are more likely to have a comorbid eating disord er. Muscle dysmorphia\noccurs almost exclusively in males. \nSuicide Risk\nRates of suicidal ideation and suicide attemp ts are high in both adults and children/ado-\nlescents with body dysmorphic disorder. Furthe rmore, risk for suicide appears high in ad-\nolescents. A substantial proportion of individuals attribute suicidal ideation or suicide\nattempts primarily to their appearance concerns. Individuals with body dysmorphic dis-\norder have many risk factors for completed suic ide, such as high rates of suicidal ideation", "source": "dsm5.pdf"} {"id": "65608a101fb3-1", "page_content": "order have many risk factors for completed suic ide, such as high rates of suicidal ideation\nand suicide attempts, demographic characterist ics associated with suicide, and high rates\nof comorbid major depressive disorder. \nFunctional Consequences of \nBody Dysmorphic Disorder\nNearly all individuals with body dysmorphic disorder experience impaired psychosocial\nfunctioning because of their appearance concerns. Impairment can range from moderate\n(e.g., avoidance of some social situations) to extreme and incapacitating (e.g., being com-\npletely housebound). On average, psychosocial functioning and quality of life are mark-\nedly poor. More severe body dysmorphic diso rder symptoms are associated with poorer\nfunctioning and quality of life. Most individu als experience impairment in their job, aca-\ndemic, or role function ing (e.g., as a parent or caregive r), which is often severe (e.g., per-\nforming poorly, missing school or work, not working). About 20% of youths with body\ndysmorphic disorder report dropping out of school primarily because of their body dys-\nmorphic disorder symptoms. Impair ment in social functioning (e.g., social activities, rela-\ntionships, intimacy), includ ing avoidance, is common. In dividuals may be housebound\nbecause of their body dysmor phic disorder symptoms, some times for years. A high pro-\nportion of adults and adolescents have been psychiatrically hospitalized.\nDifferential Diagnosis\nNormal appearance concerns and cl early noticeable physical defects. Body dysmor-\nphic disorder differs from normal appearance concerns in being characterized by exces-", "source": "dsm5.pdf"} {"id": "d55e7a5bc02d-0", "page_content": "246 Obsessive-Compulsive and Related Disorders\nsive appearance-related preoccupations and re petitive behaviors that are time-consuming,\nare usually difficult to resist or control, and ca use clinically significant distress or impair-\nment in functioning. Physical defects that ar e clearly noticeable (i.e., not slight) are not\ndiagnosed as body dysmorphic disorder. Ho wever, skin picking as a symptom of body\ndysmorphic disorder can cause noticeable skin lesions and scarring; in such cases, body dys-\nmorphic disorder should be diagnosed.\nEating disorders. In an individual with an eating di sorder, concerns ab out being fat are\nconsidered a symptom of the eating disorder rather than body dysmorphic disorder.\nHowever, weight concerns may occur in body dysmorphic disorder. Eating disorders and\nbody dysmorphic disorder can be comorbid, in which case both should be diagnosed. \nOther obsessive-compulsive and related disorders. The preoccupations and repetitive\nbehaviors of body dysmorphic disorder differ from obsessions and compulsions in OCD\nin that the former focus only on appearance. These disorders have other differences, such\nas poorer insight in body dysmorphic disorder. When sk in picking is intended to improve\nthe appearance of perceived skin defects, bo dy dysmorphic disorder, rather than excoria-\ntion (skin-picking) disorder, is diagnosed. Wh en hair removal (plucking, pulling, or other\ntypes of removal) is intended to improve pe rceived defects in the appearance of facial\nor body hair, body dysmorphic disorder is diagnosed rather than trichotillomania (hair-\npulling disorder).\nIllness anxiety disorder. Individuals with body dysmor phic disorder are not preoccu-\npied with having or acquiring a serious illness and do not have particularly elevated levels", "source": "dsm5.pdf"} {"id": "d55e7a5bc02d-1", "page_content": "pied with having or acquiring a serious illness and do not have particularly elevated levels\nof somatization. \nMajor depressive disorder. The prominent preoccupation with appearance and exces-\nsive repetitive behaviors in body dysmorphi c disorder differentiate it from major de-\npressive disorder. However, major depressi ve disorder and depressive symptoms are\ncommon in individuals with body dysmorphic disorder, often appearing to be secondary\nto the distress and impairment that body dysmorphic disorder causes. Body dysmorphic\ndisorder should be diagnosed in depressed individuals if diag nostic criteria for body dys-\nmorphic disorder are met. \nAnxiety disorders. Social anxiety and avoidance are common in body dysmorphic dis-\norder. However, unlike social anxiety disorder (social phobia), agoraphobia, and avoidant\npersonality disorder, body dy smorphic disorder includes prominent appearance-related\npreoccupation, which may be delusional, and repetitive behaviors, and the social anxiety\nand avoidance are due to concerns about perceived appearance defects and the belief or\nfear that other people will consider these indivi duals ugly, ridicule them, or reject them be-\ncause of their physical features. Unlike gene ralized anxiety disorder, anxiety and worry in\nbody dysmorphic disorder focus on perceived appearance flaws. \nPsychotic disorders. Many individuals with body dy smorphic disorder have delu-\nsional appearance beliefs (i.e., complete convic tion that their view of their perceived de-\nfects is accurate), which is diagnosed as body dysmorphic disorder, with absent insight/\ndelusional beliefs, not as delusional disorder. Appearance-related ideas or delusions of\nreference are common in body dysmorphic di sorder; however, unlike schizophrenia or\nschizoaffective disorder, body dysmorphic disorder involves prominent appearance pre-", "source": "dsm5.pdf"} {"id": "d55e7a5bc02d-2", "page_content": "schizoaffective disorder, body dysmorphic disorder involves prominent appearance pre-\noccupations and related repetitive behaviors, and disorganized behavior and other psy-\nchotic symptoms are absent (except for appearance beliefs , which may be delusional). \nOther disorders and symptoms. Body dysmorphic disorder should not be diagnosed if\nthe preoccupation is limited to discomfort with or a desire to be rid of one\u2019s primary and/", "source": "dsm5.pdf"} {"id": "adf5fc8ca0f2-0", "page_content": "Other disorders and symptoms. Body dysmorphic disorder should not be diagnosed if\nthe preoccupation is limited to discomfort with or a desire to be rid of one\u2019s primary and/\nor secondary sex characteristics in an individu al with g ender dysphoria or if the preoccu-\npation focuses on the belief th at one emits a foul or offens ive body odor as in olfactory\nreference syndrome (which is not a DSM-5 di sorder). Body identity integrity disorder", "source": "dsm5.pdf"} {"id": "2e0876d3a047-0", "page_content": "Hoarding Disorder 247\n(apotemnophilia) (which is not a DSM-5 disord er) involves a desire to have a limb ampu-\ntated to correct an experience of mismatch be tween a person\u2019s sense of body identity and\nhis or her actual anatomy. However, the conc ern does not focus on the limb\u2019s appearance,\nas it would in body dysmorphic disorder. Koro, a culturally related disorder that usually\noccurs in epidemics in Southeastern Asia, consists of a fear that the penis (labia, nipples, or\nbreasts in females) is shrink ing or retracting and will disa ppear into the abdomen, often\naccompanied by a belief that death will result . Koro differs from body dysmorphic disor-\nder in several ways, including a focus on death rather than preoccupation with perceived\nugliness. Dysmorphic concern (which is not a DSM-5 disorder) is a much broader construct\nthan, and is not equivalent to, body dysmorphi c disorder. It involves symptoms reflecting\nan overconcern with slight or imagined flaws in appearance.\nComorbidity \nMajor depressive disorder is the most commo n comorbid disorder, with onset usually af-\nter that of body dysmorphic disorder. Comorb id social anxiety disorder (social phobia),\nOCD, and substance-related disorders are also common.\nHoarding Disorder\nDiagnostic Criteria 300.3 (F42)\nA. Persistent difficulty discarding or parting with possessions, regardless of their actual value.\nB. This difficulty is due to a perceived need to save the items and to distress associated\nwith discarding them.\nC. The difficulty discarding possessions results in the accumulation of possessions that\ncongest and clutter active living areas and substantially compromises their intended", "source": "dsm5.pdf"} {"id": "2e0876d3a047-1", "page_content": "congest and clutter active living areas and substantially compromises their intended\nuse. If living areas are uncluttered, it is only because of the interventions of third parties\n(e.g., family members, cleaners, authorities).\nD. The hoarding causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning (including maintaining a safe environ-\nment for self and others).\nE. The hoarding is not attributable to another medical condition (e.g., brain injury, cere-\nbrovascular disease, Prader-Willi syndrome).\nF. The hoarding is not better explained by the symptoms of another mental disorder (e.g.,\nobsessions in obsessive-compulsive disorder, decreased energy in major depressive\ndisorder, delusions in schizophrenia or another psychotic disorder, cognitive deficits in\nmajor neurocognitive disorder, restricted interests in autism spectrum disorder). \nSpecify if:\nWith excessive acquisition: If difficulty discarding possessions is accompanied by ex-\ncessive acquisition of items that are not needed or for which there is no available space.\nSpecify if:\nWith good or fair insight: The individual recognizes that hoarding-related beliefs and\nbehaviors (pertaining to difficulty discarding items, clutter, or excessive acquisition) are\nproblematic.\nWith poor insight : The individual is mostly convinced that hoarding-related beliefs\nand behaviors (pertaining to difficulty discarding items, clutter, or excessive acquisi-\ntion) are not problematic despite evidence to the contrary.\nWith absent insight/delusional beliefs: The individual is completely convinced that\nhoarding-related beliefs and behaviors (pertaini ng to difficulty discarding items, clutter,\nor excessive acquisition) are not problematic despite evidence to the contrary.", "source": "dsm5.pdf"} {"id": "9c37f1ed9c63-0", "page_content": "248 Obsessive-Compulsive and Related Disorders\nSpecifiers\nWith excessive acquisition. Approximately 80%\u201390% of individuals with hoarding\ndisorder display excessive acquisition. The most frequent form of acqu isition is excessive\nbuying, followed by acquisition of free item s (e.g., leaflets, items discarded by others).\nStealing is less common. Some individuals may deny excessive acquisition when first as-\nsessed, yet it may appear later during the co urse of treatment. Individuals with hoarding\ndisorder typically experience distress if they are unable to or are prevented from acquiring\nitems.\nDiagnostic Features\nThe essential feature of hoarding disorder is persistent difficulties discarding or parting\nwith possessions, regardless of their actual value (Criterion A). The term persistent indi-\ncates a long-standing difficulty rather than more transient life circumstances that may lead\nto excessive clutter, such as inheriting prop erty. The difficulty in discarding possessions\nnoted in Criterion A refers to any form of discarding, including throwing away, selling,\ngiving away, or recycling. The main reasons given for these difficult ies are the perceived\nutility or aesthetic value of the items or stro ng sentimental attachment to the possessions.\nSome individuals feel responsi ble for the fate of their possessions and often go to great\nlengths to avoid being wasteful. Fears of lo sing important information are also common.\nThe most commonly saved item s are newspapers, magazines, old clothing, bags, books,\nmail, and paperwork, but virtually any item can be saved. The nature of items is not lim-\nited to possessions that most other people would define as useles s or of limited value.\nMany individuals collect and save large numbers of valuable things as well, which are of-\nten found in piles mixed with other less valuable items.", "source": "dsm5.pdf"} {"id": "9c37f1ed9c63-1", "page_content": "ten found in piles mixed with other less valuable items. \nIndividuals with hoarding disorder purpos efully save possessions and experience dis-\ntress when facing the prospect of discarding them (Criterion B). This criterion emphasizes\nthat the saving of possessions is intentional, which discriminates hoarding disorder from\nother forms of psychopathology that are ch aracterized by the pa ssive accumulation of\nitems or the absence of distress when possessions are removed. \nIndividuals accumulate large numbers of items that fill up and clutter active living ar-\neas to the extent that their intended use is no longer possible (Criterion C). For example,\nthe individual may not be able to cook in the kitchen, sleep in his or her bed, or sit in a\nchair. If the space can be used, it is only with great difficulty. Clutter is defined as a large\ngroup of usually unrelated or marginally rela ted objects piled together in a disorganized\nfashion in spaces designed for ot her purposes (e.g., tabletops, floor, hallway). Criterion C\nemphasizes the \u201cactive\u201d living areas of the ho me, rather than more peripheral areas, such\nas garages, attics, or basements, that are so metimes cluttered in homes of individuals with-\nout hoarding disorder. However, individuals with hoarding disorder often have posses-\nsions that spill beyond the active living areas and can occupy and impair the use of other\nspaces, such as vehicles, yards, the workplace, and friends\u2019 and relatives\u2019 houses. In some\ncases, living areas may be uncluttered because of the intervention of third parties\u00a0(e.g.,\nfamily members, cleaners, loca l authorities). Individuals who have been forced to clear\ntheir homes still have a symptom picture that meets criteria fo r hoarding disorder because", "source": "dsm5.pdf"} {"id": "9c37f1ed9c63-2", "page_content": "their homes still have a symptom picture that meets criteria fo r hoarding disorder because\nthe lack of clutter is due to a third-party intervention. Hoarding disorder contrasts with\nnormative collecting beha vior, which is organized and systematic, even if in some cases\nthe actual amount of possessions may be similar to the amount accumulated by an indi-\nvidual with hoarding disord er. Normative collecting does not produce the clutter, dis-\ntress, or impairment typi cal of hoarding disorder.", "source": "dsm5.pdf"} {"id": "3fde3c7e0fb2-0", "page_content": "vidual with hoarding disord er. Normative collecting does not produce the clutter, dis-\ntress, or impairment typi cal of hoarding disorder. \nSymptoms (i.e., difficulties discarding and/or clutter) must cause clinically significant\ndistress or impairment in social, occupational , or other important area s of functioning, in-\ncluding maintaining a safe environment for self and others (Criterion D). In some cases,", "source": "dsm5.pdf"} {"id": "6baa5ae711a9-0", "page_content": "Hoarding Disorder 249\nparticularly when there is poor insight, the individual may not report distress, and the im-\npairment may be apparent only to those arou nd the individual. However, any attempts to\ndiscard or clear the possessions by third pa rties result in high levels of distress. \nAssociated Features Supporting Diagnosis\nOther common features of hoarding disorder include indecisiveness, perfectionism,\navoidance, procrastination, di fficulty planning and organizing tasks, and distractibility.\nSome individuals with hoarding disorder live in unsanitary conditions that may be a log-\nical consequence of severely cluttered spaces and/or that are related to planning and or-\nganizing difficulties. Animal hoarding can be defined as the accumulation of a large number\nof animals and a failure to provide minimal st andards of nutrition, sanitation, and veter-\ninary care and to act on the de teriorating condition of the an imals (including disease, star-\nvation, or death) and the en vironment (e.g., severe overcrowding, extremely unsanitary\nconditions). Animal hoarding may be a spec ial manifestation of ho arding disorder. Most\nindividuals who hoard animals also hoard inan imate objects. The mo st prominent differ-\nences between animal and object hoarding are the extent of unsanitary conditions and the\npoorer insight in animal hoarding. \nPrevalence\nNationally representative prevalence studies of hoarding disorder are not available. Com-\nmunity surveys estimate the point prevalence of clinically significant hoarding in the\nUnited States and Europe to be approximately 2%\u20136%. Hoarding disorder affects both\nmales and females, but some epidemiological studies have reported a significantly greater\nprevalence among males. This contrasts with clinical samples, which are predominantly\nfemale. Hoarding symptoms appear to be almost three times more prevalent in older", "source": "dsm5.pdf"} {"id": "6baa5ae711a9-1", "page_content": "female. Hoarding symptoms appear to be almost three times more prevalent in older\nadults (ages 55\u201394 years) compared with younger adults (ages 34\u201344 years). \nDevelopment and Course\nHoarding appears to begin early in life and spans well into the late stages. Hoarding symp-\ntoms may first emerge around ages 11\u201315 years, start interfering with the individual\u2019s ev-\neryday functioning by the mid-20s, and cause clinically significant impairment by the\nmid-30s. Participants in clinical research stud ies are usually in their 50s. Thus, the severity\nof hoarding increases with each decade of lif e. Once symptoms begin, the course of hoard-\ning is often chronic, with few individuals reporting a waxing and waning course.\nPathological hoarding in children appears to be easily distin guished from develop-\nmentally adaptive saving and collecting behaviors. Because children and adolescents\ntypically do not control their living environm ent and discarding behaviors, the possible\nintervention of third parties (e.g., parents ke eping the spaces usable and thus reducing in-\nterference) should be considered when making the diagnosis. \nRisk and Prognostic Factors \nTemperamental. Indecisiveness is a prominent featur e of individuals wi th hoarding dis-\norder and their first-degree relatives.\nEnvironmental. Individuals with hoarding disorder often retrospectively report stressful\nand traumatic life events preceding the onset of the disorder or causing an exacerbation. \nGenetic and physiological. Hoarding behavior is familial, with about 50% of individu-\nals who hoard reporting having a relative who also hoards. Twin studies indicate that ap-\nproximately 50% of the variability in hoarding behavior is attr ibutable to additive genetic\nfactors.", "source": "dsm5.pdf"} {"id": "60fad56208e8-0", "page_content": "250 Obsessive-Compulsive and Related Disorders\nCulture-Related Diagnostic Issues\nWhile most of the research has been done in Western, industrialized countries and urban\ncommunities, the available data from non-Western and developing countries suggest that\nhoarding is a universal phenomenon wi th consistent clinical features. \nGender-Related Diagnostic Issues\nThe key features of hoarding disorder (i.e., difficulties discarding, excessive amount of\nclutter) are generally comparable in males an d females, but females tend to display more\nexcessive acquisition, particularly excessive buying, than do males. \nFunctional Consequences of Hoarding Disorder\nClutter impairs basic activities, such as moving through the house, cooking, cleaning, per-\nsonal hygiene, and even sleepin g. Appliances may be broken, and utilities such as water\nand electricity may be disconnected, as access for repair work may be difficult. Quality of\nlife is often considerably impaired. In severe cases, hoarding can put in dividuals at risk for\nfire, falling (especially elderly individuals), po or sanitation, and other health risks. Hoard-\ning disorder is associated with occupational impairment, poor physical health, and high\nsocial service utilization. Family relationsh ips are frequently under great strain. Conflict\nwith neighbors and local author ities is common, and a substa ntial proportion of individ-\nuals with severe hoarding disorder have been involved in legal eviction proceedings, and\nsome have a history of eviction. \nDifferential Diagnosis\nOther medical conditions. Hoarding disorder is not di agnosed if the symptoms are\njudged to be a direct conseque nce of another medical condition (Criterion E), such as trau-\nmatic brain injury, surgical resection for trea tment of a tumor or seizure control, cerebro-", "source": "dsm5.pdf"} {"id": "60fad56208e8-1", "page_content": "vascular disease, infections of the central ne rvous system (e.g., herpes simplex encephalitis),\nor neurogenetic conditions such as Prader -Willi syndrome. Damage to the anterior ven-\ntromedial prefrontal and cingulate cortices ha s been particularly associated with the ex-\ncessive accumulation of objects. In these individuals, the hoarding behavior is not present\nprior to the onset of the brain damage and a ppears shortly after the brain damage occurs.\nSome of these individuals appear to have li ttle interest in the accumulated items and are\nable to discard them easily or do not care if others discard them, whereas others appear to\nbe very reluctant to discard anything. \nNeurodevelopmental disorders. Hoarding disorder is not diagnosed if the accumula-\ntion of objects is judged to be a direct co nsequence of a neurodevel opmental disorder, such\nas autism spectrum disorder or intellectual disability (intellectual developmental disorder).\nSchizophrenia spectrum and other psychotic disorders. Hoarding disorder is not di-\nagnosed if the accumulation of objects is judged to be a direct consequence of delusions or\nnegative symptoms in schizophrenia sp ectrum and other psychotic disorders.\nMajor depressive episode. Hoarding disorder is not diagnosed if the accumulation of\nobjects is judged to be a dire ct consequence of ps ychomotor retardation, fatigue, or loss of\nenergy during a major depressive episode. \nObsessive-compulsive disorder. Hoarding disorder is not diagnosed if the symptoms\nare judged to be a direct consequence of typical obsessions or compulsions, such as fears\nof contamination, harm, or feelings of inco mpleteness in obsessive-compulsive disorder\n(OCD). Feelings of incomplete ness (e.g., losing one\u2019s identity , or having to document and\npreserve all life experiences) are the most frequent OCD symptoms associated with this", "source": "dsm5.pdf"} {"id": "60fad56208e8-2", "page_content": "preserve all life experiences) are the most frequent OCD symptoms associated with this\nform of hoarding. The accumulation of objects can also be the result of persistently avoid-", "source": "dsm5.pdf"} {"id": "a4618437d64e-0", "page_content": "Trichotillomania (Hair-Pulling Disorder) 251\ning onerous rituals (e.g., not discarding object s in order to avoid endless washing or check-\ning rituals).\nIn OCD, the behavior is gene rally unwanted and highly distressing, and the individual ex-\nperiences no pleasure or reward from it. Excessive acquisition is usually not present; if exces-\nsive acquisition is present, items are acquired because of a specific obsession (e.g., the need to\nbuy items that have been accidentally touched in order to avoid cont aminating other people),\nnot because of a genuine desire to possess the items. Individuals who hoard in the context of\nOCD are also more likely to accumulate bizarre it ems, such as trash, feces, urine, nails, hair,\nused diapers, or rotten food. Accumulation of su ch items is very unusual in hoarding disorder.\nWhen severe hoarding appears concurrently with other typical symptoms of OCD but\nis judged to be independent from these symptoms, both hoarding disorder and OCD may\nbe diagnosed. \nNeurocognitive disorders. Hoarding disorder is not diagnosed if the accumulation of\nobjects is judged to be a direct consequence of a degenerati ve disorder, such as neurocog-\nnitive disorder associated wi th frontotemporal lobar degeneration or Alzheimer\u2019s disease.\nTypically, onset of the accumu lating behavior is gradual and follows onset of the neuro-\ncognitive disorder. The accumulating behavior may be accompanied by self-neglect and\nsevere domestic squalor, alongside other neuropsychiatric symptoms, such as disinhibi-\ntion, gambling, rituals/stereotypies, tics, and self-injurious behaviors. \nComorbidity\nApproximately 75% of individuals with hoardi ng disorder have a comorbid mood or anx-", "source": "dsm5.pdf"} {"id": "a4618437d64e-1", "page_content": "iety disorder. The most common comorbid conditions are major depressive disorder (up\nto 50% of cases), social anxi ety disorder (social phobia), an d generalized anxiety disorder.\nApproximately 20% of individuals with hoardi ng disorder also have symptoms that meet\ndiagnostic criteria for OCD. These comorbidit ies may often be the main reason for consul-\ntation, because individuals are unlikely to spontaneously report hoarding symptoms, and\nthese symptoms are often not asked ab out in routine clinical interviews.\nTrichotillomania (Hair-Pulling Disorder)\nDiagnostic Criteria 312.39 (F63.3)\nA. Recurrent pulling out of one\u2019s hair, resulting in hair loss.\nB. Repeated attempts to decrease or stop hair pulling. \nC. The hair pulling causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning. \nD. The hair pulling or hair loss is not attri butable to another medical condition (e.g., a der-\nmatological condition). \nE. The hair pulling is not better explained by the symptoms of another mental disorder\n(e.g., attempts to improve a perceived defect or flaw in appearance in body dysmorphic\ndisorder).\nDiagnostic Features\nThe essential feature of trichotillomania (hai r-pulling disorder) is the recurrent pulling out\nof one\u2019s own hair (Criterion A). Hair pullin g may occur from any region of the body in\nwhich hair grows; the most co mmon sites are the scalp, eyebrows, and eyelids, while less\ncommon sites are axillary, facial, pubic, and peri-rectal regions. Hair-pulling sites may\nvary over time. Hair pulling may occur in brief episodes sc attered throughout the day or", "source": "dsm5.pdf"} {"id": "a4618437d64e-2", "page_content": "vary over time. Hair pulling may occur in brief episodes sc attered throughout the day or\nduring less frequent bu t more sustained periods that can continue for hours, and such hair", "source": "dsm5.pdf"} {"id": "f79d24941e23-0", "page_content": "252 Obsessive-Compulsive and Related Disorders\npulling may endure for months or years. Criterion A requires th at hair pulling lead to hair\nloss, although individuals with this disorder may pull hair in a widely distributed pattern\n(i.e., pulling single hairs from all over a site) such that hair loss may not be clearly visible.\nAlternatively, individuals may attempt to conceal or camouflage hair loss (e.g., by using\nmakeup, scarves, or wigs). Individuals with trichotillomania have made repeated at-\ntempts to decrease or stop hair pulling (Crite rion B). Criterion C indicates that hair pulling\ncauses clinically significant distress or impa irment in social, occupational, or other impor-\ntant areas of functioning. The term distress includes negative affects that may be experi-\nenced by individuals with hair pulling, such as feeling a lo ss of control, embarrassment,\nand shame. Significant impairment may occur in several different areas of functioning\n(e.g., social, occupational, academic, and leisure), in part because of avoidance of work,\nschool, or other public situations. \nAssociated Features Supporting Diagnosis\nHair pulling may be accompanied by a range of behaviors or rituals involving hair. Thus,\nindividuals may search for a particular kind of hair to pull (e.g., hairs with a specific tex-\nture or color), may try to pull out hair in a spec ific way (e.g., so that the root comes out in-\ntact), or may visually examine or tactilely or orally manipulate the hair after it has been\npulled (e.g., rolling the hair between the fingers, pulling the strand between the teeth, bit-\ning the hair into pieces, or swallowing the hair). \nHair pulling may also be preceded or acco mpanied by various emot ional states; it may", "source": "dsm5.pdf"} {"id": "f79d24941e23-1", "page_content": "be triggered by feelings of anxiety or boredo m, may be preceded by an increasing sense of\ntension (either immediately before pulling out the hair or when attempting to resist the\nurge to pull), or may lead to gratification, pleasure, or a sense of relief when the hair is\npulled out. Hair-pulling behavior may involv e varying degrees of conscious awareness,\nwith some individuals displaying more focused attention on the hair pulling (with pre-\nceding tension and subsequent relief), and other individuals displaying more automatic\nbehavior (in which the hair pulling seems to occur without full awareness). Many individ-\nuals report a mix of both behavioral styles. Some individuals experience an \u201citch-like\u201d or\ntingling sensation in the scalp that is alleviated by the act of pulling hair. Pain does not\nusually accompany hair pulling.\nPatterns of hair loss are highly variable. Ar eas of complete alopecia, as well as areas of\nthinned hair density, are common. When the sc alp is involved, there may be a predilection\nfor pulling out hair in the crown or parietal regions. There may be a pattern of nearly com-\nplete baldness except for a narrow perimeter around the outer margins of the scalp, par-\nticularly at the nape of the neck (\u201ctonsure trichotillomania\u201d). Eyebrows and eyelashes may\nbe completely absent. \nHair pulling does not usually occur in the pr esence of other individuals, except imme-\ndiate family members. Some in dividuals have urges to pull hair from other individuals\nand may sometimes try to find opportunities to do so surreptitiously. Some individuals\nmay pull hairs from pets, dolls, and other fi brous materials (e.g., sw eaters or carpets).\nSome individuals may deny their hair pulling to others. The majority of individuals with", "source": "dsm5.pdf"} {"id": "f79d24941e23-2", "page_content": "Some individuals may deny their hair pulling to others. The majority of individuals with\ntrichotillomania also have one or more other body-focused repetitive behaviors, including\nskin picking, nail biting, and lip chewing.\nPrevalence\nIn the general population, the 12-month preval ence estimate for trichotillomania in adults\nand adolescents is 1%\u20132%. Females are more frequently affected than males, at a ratio of\napproximately 10:1. This estimate likely reflects the true gender ratio of the condition, al-", "source": "dsm5.pdf"} {"id": "e6492e745660-0", "page_content": "and adolescents is 1%\u20132%. Females are more frequently affected than males, at a ratio of\napproximately 10:1. This estimate likely reflects the true gender ratio of the condition, al-\nthough it may also reflect differential treatment seeking based on ge nder or cultural at-\ntitudes regarding appearance (e.g., acceptan ce of normative hair loss among males).\nAmong children with trichotillo mania, males and females are more equally represented.", "source": "dsm5.pdf"} {"id": "2dde2fadb36c-0", "page_content": "Trichotillomania (Hair-Pulling Disorder) 253\nDevelopment and Course\nHair pulling may be seen in infants, and this behavior typically resolves during early devel-\nopment. Onset of hair pulling in trichotilloman ia most commonly coincides with, or follows\nthe onset of, puberty. Sites of hair pulling may vary over time. The usual course of trichotillo-\nmania is chronic, with some waxing and waning if the disorder is untreated. Symptoms may\npossibly worsen in females accompanying horm onal changes (e.g., menstruation, perimeno-\npause). For some individuals, the disorder may come and go for weeks, months, or years at a\ntime. A minority of individuals remit without su bsequent relapse within a few years of onset. \nRisk and Prognostic Factors\nGenetic and physiological. There is evidence for a genetic vulnerability to trichotillo-\nmania. The disorder is more common in in dividuals with obsessi ve-compulsive disorder\n(OCD) and their first-degree relative s than in the general population. \nCulture-Related Diagnostic Issues \nTrichotillomania appears to manifest similarly across cultures, although there is a paucity\nof data from non-Western regions.\nDiagnostic Markers\nMost individuals with trichotillomania admit to hair pulling; thus, dermatopathological\ndiagnosis is rarely required. Skin biopsy an d dermoscopy (or trichoscopy) of trichotillo-\nmania are able to differentiat e the disorder from other causes of alopecia. In trichotil-\nlomania, dermoscopy shows a range of charac teristic features, in cluding decreased hair\ndensity, short vellus hair, and broken hairs with different shaft lengths. \nFunctional Consequences of", "source": "dsm5.pdf"} {"id": "2dde2fadb36c-1", "page_content": "Functional Consequences of \nTrichotillomania (Hair-Pulling Disorder)\nTrichotillomania is associated with distress as well as with social and occupational impair-\nment. There may be irreversible damage to hair growth and hair quality. Infrequent med-\nical consequences of trichotillomania includ e digit purpura, muscul oskeletal injury (e.g.,\ncarpal tunnel syndrome; back, shoulder and neck pain), blepharitis, and dental damage\n(e.g., worn or broken teeth due to hair biting). Swallowing of hair (trichophagia) may lead\nto trichobezoars, with subs equent anemia, abdominal pain , hematemesis, nausea and\nvomiting, bowel obstruction, and even perforation. \nDifferential Diagnosis\nNormative hair re moval/manipulation. Trichotillomania should not be diagnosed when\nhair removal is performed solely for cosmetic reasons (i.e., to improve one\u2019s physical ap-\npearance). Many individuals twist and play with their hair, but this behavior does not usu-\nally qualify for a diagnosis of trichotillomania . Some individuals may bite rather than pull\nhair; again, this does not qualify for a diagnosis of trichotillomania.\nOther obsessive-compulsive and related disorders. Individuals with OCD and sym-\nmetry concerns may pull out hairs as part of their symmetry rituals, and individuals with\nbody dysmorphic disorder may remove body ha ir that they perceive as ugly, asymmetri-\ncal, or abnormal; in such cases a diagnosis of trichotillomania is not given. The description\nof body-focused repetitive behavior disorder in other specified ob sessive-compulsive and\nrelated disorder excludes individuals who meet diagnostic criteria for trichotillomania.", "source": "dsm5.pdf"} {"id": "cd865c4670b3-0", "page_content": "254 Obsessive-Compulsive and Related Disorders\nNeurodevelopmental disorders. In neurodevelopmental di sorders, hair pulling may\nmeet the definition of stereotypies (e.g., in stereotypic movement disorder). Tics (in tic dis-\norders) rarely lead to hair pulling.\nPsychotic disorder. Individuals with a psychotic disord er may remove hair in response\nto a delusion or hallucinati on. Trichotillomania is not diagnosed in such cases.\nAnother medical condition. Trichotillomania is not diagnosed if the hair pulling or hair\nloss is attributable to another medical conditio n (e.g., inflammation of the skin or other der-\nmatological conditions). Other causes of scarri ng alopecia (e.g., alop ecia areata, androgenic\nalopecia, telogen effluvium) or nonscarring al opecia (e.g., chronic discoid lupus erythema-\ntosus, lichen planopilaris, central centrifugal cicatricial alopecia, pseudopelade, folliculitis\ndecalvans, dissecting folliculitis, acne keloidalis nuchae) should be considered in individu-\nals with hair loss who deny hair pulling. Skin biopsy or dermoscopy ca n be used to differ-\nentiate individuals with tric hotillomania from those with dermatological disorders.\nSubstance-related disorders. Hair-pulling symptoms may be exacerbated by certain\nsubstances\u2014for example, stimulants\u2014but it is less likely that substances are the primary\ncause of persistent hair pulling. \nComorbidity\nTrichotillomania is often accompanied by ot her mental disorders, most commonly major\ndepressive disorder and excoriation (skin- picking) disorder. Repetitive body-focused", "source": "dsm5.pdf"} {"id": "cd865c4670b3-1", "page_content": "depressive disorder and excoriation (skin- picking) disorder. Repetitive body-focused\nsymptoms other than hair pulling or skin picking (e.g. nail biting) occur in the majority of\nindividuals with trichotillomania and may dese rve an additional diagnosis of other spec-\nified obsessive-compulsive and related disorder (i.e., body-focused repetitive behavior\ndisorder).\nExcoriation (Skin-Picking) Disorder\nDiagnostic Criteria 698.4 (L98.1)\nA. Recurrent skin picking resulting in skin lesions.\nB. Repeated attempts to decrease or stop skin picking.\nC. The skin picking causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning. \nD. The skin picking is not attributable to the physiological effects of a substance (e.g., co-\ncaine) or another medical condition (e.g., scabies). \nE. The skin picking is not better explained by symptoms of another mental disorder (e.g.,\ndelusions or tactile hallucinations in a psychotic disorder, attempts to improve a per-\nceived defect or flaw in appearance in body dysmorphic disorder, stereotypies in ste-\nreotypic movement disorder, or intention to harm oneself in nonsuicidal self-injury).\nDiagnostic Features\nThe essential feature of excori ation (skin-picking) disorder is recurrent picking at one\u2019s\nown skin (Criterion A). The mo st commonly picked sites are the face, arms, and hands, but\nmany individuals pick from multiple body sit es. Individuals may pick at healthy skin, at\nminor skin irregularities, at le sions such as pimples or calluse s, or at scabs from previous\npicking. Most individuals pick with their fi ngernails, although many use tweezers, pins,", "source": "dsm5.pdf"} {"id": "cd865c4670b3-2", "page_content": "or other objects. In addition to skin picking, there may be skin rubbing, squeezing, lancing,\nand biting. Individuals with excoriation diso rder often spend signif icant amounts of time\non their picking behavior, sometimes several hours per day, and such skin picking may", "source": "dsm5.pdf"} {"id": "acfc4e1e9b4a-0", "page_content": "Excoriation (Skin-Picking) Disorder 255\nendure for months or years. Cr iterion A requires that skin picking lead to skin lesions, al-\nthough individuals with this disorder often at tempt to conceal or camouflage such lesions\n(e.g., with makeup or clothing). Individuals with excoriation disorder have made repeated\nattempts to decrease or stop skin picking (Criterion B).\nCriterion C indicates that skin picking causes clinically significant distress or impair-\nment in social, occupational, or other im portant areas of func tioning. The term distress in-\ncludes negative affects that may be experience d by individuals with skin picking, such as\nfeeling a loss of control, em barrassment, and shame. Significant impairment may occur in\nseveral different areas of functioning (e.g., so cial, occupational, academic, and leisure), in\npart because of avoidance of social situations. \nAssociated Features Supporting Diagnosis\nSkin picking may be accompanied by a range of behaviors or rituals involving skin or scabs.\nThus, individuals may search for a particular kind of scab to pull, and they may examine,\nplay with, or mouth or swallow th e skin after it has be en pulled. Skin picking may also be pre-\nceded or accompanied by various emotional stat es. Skin picking may be triggered by feelings\nof anxiety or boredom, may be preceded by an increasing sense of tension (either immedi-\nately before picking the skin or when attempting to resist the urge to pick), and may lead to\ngratification, pleasure, or a sense of relief when the skin or scab has been picked. Some indi-\nviduals report picking in response to a minor skin irregularity or to relieve an uncomfortable\nbodily sensation. Pain is not routinely reported to accompany skin picking. Some individuals", "source": "dsm5.pdf"} {"id": "acfc4e1e9b4a-1", "page_content": "bodily sensation. Pain is not routinely reported to accompany skin picking. Some individuals\nengage in skin picking that is more focused (i .e., with preceding tens ion and subsequent re-\nlief), whereas others engage in more automatic picking (i.e., when skin picking occurs with-\nout preceding tension and without full awarene ss), and many have a mix of both behavioral\nstyles. Skin picking does not usually occur in the presence of other individuals, except im-\nmediate family members. Some individual s report picking the skin of others.\nPrevalence\nIn the general population, the lifetime prevalence for excoriation disorder in adults is 1.4%\nor somewhat higher. Three-quarters or more of individuals with the disorder are female.\nThis likely reflects the true gender ratio of the condition, although it may also reflect dif-\nferential treatment seeking based on gender or cultural attitudes regarding appearance.\nDevelopment and Course\nAlthough individuals with excoriation disorder may present at various ages, the skin pick-\ning most often has onset during adolescence, commonly coinciding wi th or following the\nonset of puberty. The disorder frequently begins with a dermatological condition, such\nas acne. Sites of skin picking may vary over time. The usual course is chronic, with some\nwaxing and waning if untreated. For some in dividuals, the disorder may come and go for\nweeks, months, or years at a time.\nRisk and Prognostic Factors\nGenetic and physiological. Excoriation disorder is more common in individuals with\nobsessive-compulsive disorder (OCD) and thei r first-degree family members than in the\ngeneral population.\nDiagnostic Markers\nMost individuals with excoriation disorder admit to skin picking; therefore, dermato-\npathological diagnosis is rarely required. Ho wever, the disorder ma y have characteristic", "source": "dsm5.pdf"} {"id": "acfc4e1e9b4a-2", "page_content": "pathological diagnosis is rarely required. Ho wever, the disorder ma y have characteristic\nfeatures on histopathology.", "source": "dsm5.pdf"} {"id": "7f1bcb6a2716-0", "page_content": "256 Obsessive-Compulsive and Related Disorders\nFunctional Consequences of \nExcoriation (Skin-Picking) Disorder \nExcoriation disorder is associated with distress as well as with social and occupational im-\npairment. The majority of indi viduals with this condition spend at least 1 hour per day\npicking, thinking about picking, and resist ing urges to pick. Many individuals report\navoiding social or entertainment events as well as going out in public. A majority of indi-\nviduals with the disorder also report experien cing work interference from skin picking on\nat least a daily or weekly basi s. A significant proportion of students with excoriation disor-\nder report having missed school, having expe rienced difficulties managing responsibilities\nat school, or having had diffi culties studying because of skin picking. Medical complica-\ntions of skin picking include ti ssue damage, scarring, and infe ction and can be life-threaten-\ning. Rarely, synovitis of the wrists due to ch ronic picking has been reported. Skin picking\noften results in significant tissue damage and sc arring. It frequently requires antibiotic treat-\nment for infection, and on o ccasion it may require surgery.\nDifferential Diagnosis\nPsychotic disorder. Skin picking may occur in response to a delusion (i.e., parasitosis)\nor tactile hallucination (i.e., fo rmication) in a psychotic disorder. In such cases, excoriation\ndisorder should not be diagnosed. \nOther obsessive-compulsive and related disorders. Excessive washing compulsions\nin response to contamination obsessions in in dividuals with OCD may lead to skin lesions,\nand skin picking may occur in individuals with body dysmorphic disorder who pick their", "source": "dsm5.pdf"} {"id": "7f1bcb6a2716-1", "page_content": "and skin picking may occur in individuals with body dysmorphic disorder who pick their\nskin solely because of appearance concerns; in such cases, excoriatio n disorder should not\nbe diagnosed. The description of body-focused repetitive behavior disorder in other spec-\nified obsessive-compulsive and related diso rder excludes individuals whose symptoms\nmeet diagnostic criteria for excoriation disorder.\nNeurodevelopmental disorders. While stereotypic movement disorder may be charac-\nterized by repetitive self-injurious behavior , onset is in the early developmental period.\nFor example, individuals with the neurogenetic condition Prader-Willi syndrome may\nhave early onset of skin picking, and their symptoms may meet criteria for stereotypic\nmovement disorder. While tics in individuals with Tourette\u2019s disorder may lead to self-\ninjury, the behavior is not ti c-like in excoriation disorder. \nSomatic symptom and related disorders. Excoriation disorder is not diagnosed if the\nskin lesion is primarily attributable to de ceptive behaviors in factitious disorder.\nOther disorders. Excoriation disorder is not diagnosed if the skin picking is primarily\nattributable to the intention to harm oneself th at is characteristic of nonsuicidal self-injury.\nOther medical conditions. Excoriation disorder is not di agnosed if the skin picking is\nprimarily attributable to another medical condition. For example, scabies is a dermatolog-\nical condition invariably associated with seve re itching and scratching. However, excori-\nation disorder may be precipitated or ex acerbated by an unde rlying dermatological\ncondition. For example, acne may lead to so me scratching and picking, which may also be\nassociated with comorbid excoriation diso rder. The differentiation between these two\nclinical situations (acne with some scratching and picking vs. acne with comorbid excori-", "source": "dsm5.pdf"} {"id": "7f1bcb6a2716-2", "page_content": "ation disorder) requires an assessment of the extent to which the individual\u2019s skin picking\nhas become independent of the unde rlying dermatological condition. \nSubstance/medication-induced disorders. Skin-picking symptoms may also be induced\nby certain substances (e.g., cocaine), in whic h case excoriation disorder should not be di-\nagnosed. If such skin picking is clinically significant, then a diagnosis of substance/med-\nication-induced obsessive-compulsive and re lated disorder should be considered.", "source": "dsm5.pdf"} {"id": "21ea0d9a4f8a-0", "page_content": "Substance/Medication-Induced Obsessive-Compulsive and Related Disorder 257\nComorbidity\nExcoriation disorder is often accompanied by other mental disorders. Such disorders in-\nclude OCD and trichotillomania (hair-pulling disorder), as well as major depressive dis-\norder. Repetitive body-focused symptoms othe r than skin picking an d hair pulling (e.g.,\nnail biting) occur in many individuals with excoriation disorder and may deserve an ad-\nditional diagnosis of other specified obsessive-compulsive and related disorder (i.e.,\nbody-focused repetitive behavior disorder).\nSubstance/Medication-Induced\n Obsessive-Compulsive and Related Disorder\nDiagnostic Criteria \nA. Obsessions, compulsions, skin picking, hair pulling, other body-focused repetitive be-\nhaviors, or other symptoms characteristic of the obsessive-compulsive and related dis-\norders predominate in the clinical picture. \nB. There is evidence from the history, physical examination, or laboratory findings of both\n(1) and (2):\n1. The symptoms in Criterion A developed during or soon after substance intoxication\nor withdrawal or after exposure to a medication.\n2. The involved substance/medication is capable of producing the symptoms in Crite-\nrion A.\nC. The disturbance is not better explained by an obsessive-compulsive and related disor-\nder that is not substance/medication-induced. Such evidence of an independent ob-\nsessive-compulsive and related disorder could include the following:\nThe symptoms precede the onset of the substance/medication use; the symptoms\npersist for a substantial period of time (e.g., about 1 month) after the cessation of acute\nwithdrawal or severe intoxication; or there is other evidence suggesting the exis-", "source": "dsm5.pdf"} {"id": "21ea0d9a4f8a-1", "page_content": "withdrawal or severe intoxication; or there is other evidence suggesting the exis-\ntence of an independent non-substance/medication-induced obsessive-compul-\nsive and related disorder (e.g., a history of recurrent non-substance/medication-\nrelated episodes). \nD. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nNote: This diagnosis should be made in addition to a diagnosis of substance intoxication\nor substance withdrawal only when the symptom s in Criterion A predominate in the clinical\npicture and are sufficiently severe to warrant clinical attention. \nCoding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-\ntion]-induced obsessive-compulsive and related disorders are indicated in the table below.\nNote that the ICD-10-CM code depends on whether or not there is a comorbid substance\nuse disorder present for the same class of substance. If a mild substance use disorder is\ncomorbid with the substance-induced obsessive-compulsive and related disorder, the 4th\nposition character is \u201c1,\u201d and the clinician should record \u201cmild [substance] use disorder\u201d\nbefore the substance-induced obsessive-compulsive and related disorder (e.g., \u201cmild co-\ncaine use disorder with cocaine-induced obs essive-compulsive and related disorder\u201d). If\na moderate or severe substance use disorder is comorbid with the substance-induced ob-\nsessive-compulsive and related disorder, the 4th position character is \u201c2,\u201d and the clinician\nshould record \u201cmoderate [substance] use disorder\u201d or \u201csevere [substance] use disorder,\u201d", "source": "dsm5.pdf"} {"id": "21ea0d9a4f8a-2", "page_content": "depending on the severity of the comorbid substance use disorder. If there is no comorbid", "source": "dsm5.pdf"} {"id": "ee2a016cee8d-0", "page_content": "258 Obsessive-Compulsive and Related Disorders\nsubstance use disorder (e.g., after a one-time heavy use of the substance), then the 4th\nposition character is \u201c9,\u201d and the clinician should record only the substance-induced ob-\nsessive-compulsive and related disorder.\nSpecify if (see Table 1 in the chapter \u201cSubstance-Related and Addictive Disorders\u201d for di-\nagnoses associated with substance class):\nWith onset during intoxication: If the criteria are met for intoxication with the sub-\nstance and the symptoms develop during intoxication.\nWith onset during withdrawal: If criteria are met for withdrawal from the substance\nand the symptoms develop during, or shortly after, withdrawal.\nWith onset after medication use: Symptoms may appear either at initiation of medi-\ncation or after a modification or change in use.\nRecording Procedures\nICD-9-CM. The name of the substanc e/medication-induced ob sessive-compulsive and\nrelated disorder begins with the specific subs tance (e.g., cocaine) that is presumed to be\ncausing the obsessive-compulsive and related symptoms. The diagnostic code is selected\nfrom the table included in the criteria set, wh ich is based on the drug class. For substances\nthat do not fit into any of the classes, the co de for \u201cother substance\u201d should be used; and in\ncases in which a substance is judged to be an etiological factor but the specific class of sub-\nstance is unknown, the category \u201cu nknown substance\u201d should be used.\nThe name of the disorder is followed by the sp ecification of onset (i.e., onset during in-\ntoxication, onset during withdrawal, with onse t after medication use). Unlike the record-\ning procedures for ICD-10-CM, which combine the substance-induced disorder and", "source": "dsm5.pdf"} {"id": "ee2a016cee8d-1", "page_content": "ing procedures for ICD-10-CM, which combine the substance-induced disorder and\nsubstance use disorder into a single code, for ICD-9-CM a separate diagnostic code is\ngiven for the substance use disorder. For exampl e, in the case of re petitive behaviors oc-\ncurring during intoxica tion in a man with a severe coca ine use disorder, the diagnosis is\n292.89 cocaine-induced obsessive-compulsive and related disorder, with onset during in-\ntoxication. An additional diagnosis of 304.20 severe cocaine use disorder is also given.\nWhen more than one substance is judged to play a significant role in the development of\nthe obsessive-compulsive and related disord er, each should be listed separately.\nICD-10-CM. The name of the substance/medication-induced obsessive-compulsive and re-\nlated disorder begins with the specific substance (e.g., cocaine) that is presumed to be causing\nthe obsessive-compulsive and related symptoms. Th e diagnostic code is selected from the ta-\nble included in the criteria set, which is based on the drug clas s and presence or absence of a\ncomorbid substance use disorder . For substances that do no t fit into any of the classes,\nthe code for \u201cother substance\u201d with no comorb id substance use should be used; and in cases in\nwhich a substance is judged to be an etiological fa ctor but the specific class of substance is un-\nknown, the category \u201cunknown substance\u201d with no comorbid substance use should be used.ICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate \nor severeWithout \nuse \ndisorder\nAmphetamine (or other", "source": "dsm5.pdf"} {"id": "ee2a016cee8d-2", "page_content": "or severeWithout \nuse \ndisorder\nAmphetamine (or other \nstimulant)292.89 F15.188 F15.288 F15.988\nCocaine 292.89 F14.188 F14.288 F14.988\nOther (or unknown) substance 292.89 F19.188 F19.288 F19.988", "source": "dsm5.pdf"} {"id": "db0e85921811-0", "page_content": "Substance/Medication-Induced Obsessive-Compulsive and Related Disorder 259\nWhen recording the name of the disorder, the comorbid substance use disorder (if any) is\nlisted first, followed by the wo rd \u201cwith,\u201d followed by the name of the substance-induced ob-\nsessive-compulsive and related diso rder, followed by the specification of onset (i.e., onset dur-\ning intoxication, onset during withdrawal, with onset after medication use). For example, in\nthe case of repetitive behaviors occurring during intoxication in a man with a severe cocaine\nuse disorder, the diagnosis is F14.288 severe co caine use disorder with cocaine-induced obses-\nsive-compulsive and related disorder, with onse t during intoxication. A separate diagnosis of\nthe comorbid severe cocaine use disorder is not given. If the substance-induced obsessive-\ncompulsive and related disorder occurs without a comorbid substance use disorder (e.g., after\na one-time heavy use of the substance), no accompanying substance use disorder is noted (e.g.,\nF15.988 amphetamine-induced obsessive-compulsive and related disorder, with onset during\nintoxication). When more than on e substance is judged to play a significant role in the devel-\nopment of the obsessive-compulsive and relate d disorder, each should be listed separately.\nDiagnostic Features\nThe essential features of substance/medicati on-induced obsessive-co mpulsive and related\ndisorder are prominent symptoms of an obsessive-compulsive and related disorder (Criterion\nA) that are judged to be attributable to the e ffects of a substance (e.g., drug of abuse, medica-\ntion). The obsessive-compulsive and related disorder symptoms must have developed during\nor soon after substance intoxication or withdraw al or after exposure to a medication or toxin,", "source": "dsm5.pdf"} {"id": "db0e85921811-1", "page_content": "or soon after substance intoxication or withdraw al or after exposure to a medication or toxin,\nand the substance/medication must be capable of producing the symptoms (Criterion B). Sub-\nstance/medication-induced obsessive-compulsive and related disorder due to a prescribed\ntreatment for a mental disorder or general medi cal condition must have its onset while the in-\ndividual is receiving the medi cation. Once the treatment is discontinued, the obsessive-com-\npulsive and related disorder symp toms will usually improve or remit within days to several\nweeks to 1 month (depending on the half-life of the substance/medica tion). The diagnosis of\nsubstance/medication-induced obsessive-comp ulsive and related disorder should not be\ngiven if onset of the obsessive-compulsive an d related disorder symp toms precedes the sub-\nstance intoxicati on or medication use, or if the symp toms persist for a substantial period of\ntime, usually longer than 1 month, from the time of severe into xication or with drawal. If the\nobsessive-compulsive and related disorder symptoms persist for a substantial period of time,\nother causes for the symptoms should be cons idered. The substance/medication-induced ob-\nsessive-compulsive and related disorder diagnosis should be made in addition to a diagnosis\nof substance intoxication only when the sympto ms in Criterion A pred ominate in the clinical\npicture and are sufficiently severe to warrant independent clinical attention\nAssociated Features Supporting Diagnosis\nObsessions, compulsions, hair pulling, skin pick ing, or other body-focused repetitive be-\nhaviors can occur in association with intoxication with the following classes of substances:\nstimulants (including cocaine) and other (o r unknown) substances. Heavy metals and tox-\nins may also cause obsessive-compulsive and related disorder symptoms. Laboratory as-", "source": "dsm5.pdf"} {"id": "db0e85921811-2", "page_content": "ins may also cause obsessive-compulsive and related disorder symptoms. Laboratory as-\nsessments (e.g., urine toxicology) may be usef ul to measure substance intoxication as part\nof an assessment for obsessive-co mpulsive and related disorders.\nPrevalence\nIn the general population, the very limited data that are available indicate that substance-\ninduced obsessive-compulsive and related disorder is very rare. \nDifferential Diagnosis\nSubstance intoxication. Obsessive-compulsive and relate d disorder symptoms may oc-", "source": "dsm5.pdf"} {"id": "3062d30d5a10-0", "page_content": "induced obsessive-compulsive and related disorder is very rare. \nDifferential Diagnosis\nSubstance intoxication. Obsessive-compulsive and relate d disorder symptoms may oc-\ncur in substance intoxication. The diagnosis of the substance-specific intoxication will usu-", "source": "dsm5.pdf"} {"id": "cfea8f18b238-0", "page_content": "260 Obsessive-Compulsive and Related Disorders\nally suffice to categorize the symptom presentation. A diagnosis of an obsessive-compulsive\nand related disorder should be made in additi on to substance intoxication when the symp-\ntoms are judged to be in exce ss of those usually associated with intoxication and are suf-\nficiently severe to warrant independent clinical attention.\nObsessive-compulsive and related disorder (i.e., not induced by a substance). Sub-\nstance/medication-induced obsessive-compulsive and related disorder is judged to be\netiologically related to the substance/medi cation. Substance/medi cation-induced obses-\nsive-compulsive and related disorder is dist inguished from a prim ary obsessive-compul-\nsive and related disorder by considering the onset, course, and other factors with respect\nto substances/medications. For drugs of abuse, there must be evidence from the history,\nphysical examination, or laboratory findings for use or intoxication. Substance/medica-\ntion-induced obsessive-compulsiv e and related disorder arises only in association with in-\ntoxication, whereas a primary obsessive-compulsive and relate d disorder may precede the\nonset of substance/medication use. The presence of features that are atypical of a primary\nobsessive-compulsive and relate d disorder, such as atypical age at onset of symptoms,\nmay suggest a substance-induced etiology. A primary obsessive-compulsive and related\ndisorder diagnosis is warranted if the sympto ms persist for a substa ntial period of time\n(about 1 month or longer) after the end of the substance intoxication or the individual has\na history of an obsessive-co mpulsive and related disorder.\nObsessive-compulsive and related disorder due to another medical condition. If the", "source": "dsm5.pdf"} {"id": "cfea8f18b238-1", "page_content": "Obsessive-compulsive and related disorder due to another medical condition. If the\nobsessive-compulsive and relate d disorder symptoms are attr ibutable to another medical\ncondition (i.e., rather than to the medication taken for the other me dical condition), obses-\nsive-compulsive and related di sorder due to another medical condition should be diag-\nnosed. The history often provides the basis for judgment. At times, a change in the\ntreatment for the other medical condition (e.g ., medication substitu tion or discontinua-\ntion) may be needed to determine whether or not the medication is the causative agent (in\nwhich case the symptoms may be better expl ained by substance/medication-induced ob-\nsessive-compulsive and related diso rder). If the disturbance is attributable to both another\nmedical condition and substance use, both diagnoses (i.e., obsessive-compulsive and related\ndisorder due to another medical condition and substance/medicati on-induced obsessive-\ncompulsive and related disorder) may be given. When there is insufficie nt evidence to de-\ntermine whether the symptoms are attributable to either a substanc e/medication or an-\nother medical condition or are primary (i.e., a ttributable to neither a substance/medication\nnor another medical condition), a diagnosis of other specified or unspecified obsessive-\ncompulsive and related disorder would be indicated.\nDelirium. If obsessive-compulsive and related disorder symptoms occur exclusively\nduring the course of delirium, they are consid ered to be an associated feature of the delir-\nium and are not diagnosed separately. \nObsessive-Compulsive and Related Disorder\nDue to Another Medical Condition\nDiagnostic Criteria 294.8 (F06.8)", "source": "dsm5.pdf"} {"id": "cfea8f18b238-2", "page_content": "Due to Another Medical Condition\nDiagnostic Criteria 294.8 (F06.8)\nA. Obsessions, compulsions, preoccupations with appearance, hoarding, skin picking,\nhair pulling, other body-focused repetitive beha viors, or other symptoms characteristic\nof obsessive-compulsive and related disorder predominate in the clinical picture. \nB. There is evidence from the history, physical examination, or laboratory findings that the\ndisturbance is the direct pathophysiological consequence of another medical condition. \nC. The disturbance is not better explained by another mental disorder.", "source": "dsm5.pdf"} {"id": "8b55b3fa25a9-0", "page_content": "Obsessive-Compulsive and Related Disorder Due to Another Medical Condition 261\nD. The disturbance does not occur exclusively during the course of a delirium. \nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nSpecify if:\nWith obsessive-compulsive disorder\u2013like symptoms: If obsessive-compulsive dis-\norder\u2013like symptoms predominate in the clinical presentation.\nWith appearance preoccupations: If preoccupation with perceived appearance de-\nfects or flaws predominates in the clinical presentation.\nWith hoarding symptoms: If hoarding predominates in the clinical presentation.\nWith hair-pulling symptoms: If hair pulling predominates in the clinical presentation.\nWith skin-picking symptoms: If skin picking predominates in the clinical presenta-\ntion.\nCoding note: Include the name of the other medical condition in the name of the mental\ndisorder (e.g., 294.8 [F06.8] obsessive-compulsive and related disorder due to\u00a0cerebral\ninfarction). The other medical condition should be coded and listed separately immediately\nbefore the obsessive-compulsive and related disorder due to the medical condition (e.g.,\n438.89 [I69.398] cerebral infarction; 294.8 [F06.8] obsessive-compulsive and related dis-\norder due to\u00a0cerebral infarction).\nDiagnostic Features\nThe essential feature of obsessive-compulsive an d related disorder due to another medical\ncondition is clinically significant obsessiv e-compulsive and related symptoms that are\njudged to be best explained as the direct pathophysiological consequence of another med-\nical condition. Symptoms can include pr ominent obsessions, compulsions, preoccu-\npations with appearance, hoarding, hair pull ing, skin picking, or other body-focused", "source": "dsm5.pdf"} {"id": "8b55b3fa25a9-1", "page_content": "pations with appearance, hoarding, hair pull ing, skin picking, or other body-focused\nrepetitive behaviors (Criterion A). The judgme nt that the symptoms are best explained by\nthe associated medical condition must be based on evidence from the history, physical ex-\namination, or laboratory findings (Criterion B). Additionally, it must be judged that the\nsymptoms are not better explained by another mental disorder (Criterion C). The diagno-\nsis is not made if the obsessive-compulsive and related symptoms o ccur only during the\ncourse of a delirium (Criterion D). The obsessive-compulsive and related symptoms must\ncause clinically significant distress or impairment in social, occupa tional, or other impor-\ntant areas of functioning (Criterion E).\nIn determining whether the ob sessive-compulsive and rela ted symptoms are attribut-\nable to another medical condit ion, a relevant medical condition must be present. Further-\nmore, it must be established that obsessive-compulsive and related symptoms can be\netiologically related to the medical condit ion through a pathophysiological mechanism\nand that this best explains the symptoms in the individual. Although there are no infallible\nguidelines for determining whether the relationship between the obsessive-compulsive\nand related symptoms and the medical conditio n is etiological, considerations that may\nprovide some guidance in making this diagno sis include the presence of a clear temporal\nassociation between the onset, exacerbation, or remission of the medical condition and the\nobsessive-compulsive and related symptoms; the presence of features that are atypical of\na primary obsessive-compulsive and related disord er (e.g., atypical age at onset or course);\nand evidence in the literature that a known physiological mechanism (e.g., striatal dam-\nage) causes obsessive-compulsive and rela ted symptoms. In addi tion, the disturbance", "source": "dsm5.pdf"} {"id": "8b55b3fa25a9-2", "page_content": "age) causes obsessive-compulsive and rela ted symptoms. In addi tion, the disturbance\ncannot be better explained by a primary obse ssive-compulsive and related disorder, a sub-\nstance/medication-induced obsessive-compul sive and related disorder, or another men-\ntal disorder.\nThere is some controversy about whether ob sessive-compulsive and related disorders\ncan be attributed to Group A streptococcal infection. Sydenham\u2019s chorea is the neurolog-", "source": "dsm5.pdf"} {"id": "af3e1fd796c3-0", "page_content": "262 Obsessive-Compulsive and Related Disorders\nical manifestation of rheumatic fever, which is in turn due to Group A streptococcal in-\nfection. Sydenham\u2019s chorea is characterized by a combination of motor and nonmotor\nfeatures. Nonmotor feat ures include obsessions, compulsi ons, attention deficit, and emo-\ntional lability. Although indi viduals with Sydenh am\u2019s chorea may present with non-\nneuropsychiatric features of acute rheumatic fe ver, such as carditis and arthritis, they may\npresent with obsessive-compu lsive disorder\u2013like symptoms; such individuals should\nbe diagnosed with obsessive-compulsive and related disorder due to another medical\ncondition. \nPediatric autoimmune neuropsychiatric diso rders associated with streptococcal infec-\ntions (PANDAS) has been identified as an other post-infectious autoimmune disorder\ncharacterized by the sudden onset of obsessions, compulsions, and/or tics accompanied\nby a variety of acute neuropsychiatric symptoms in the absence of chorea, carditis, or ar-\nthritis, after Group A streptoc occal infection. Although there is a body of evidence that\nsupports the existence of PANDAS, it remains a controversial diagnosis. Given this ongo-\ning controversy, the description of PANDAS ha s been modified to eliminate etiological\nfactors and to designate an expanded clinical entity: pediatric acute-onset neuropsychiat-\nric syndrome (PANS) or idiopathic childhood acute neuropsychiatric symptoms (CANS),\nwhich deserves further study.\nAssociated Features Supporting Diagnosis\nA number of other medical disorders are know n to include obsessive-compulsive and re-\nlated symptoms as a manifestation. Examples include disorders leading to striatal dam-\nage, such as cerebral infarction.", "source": "dsm5.pdf"} {"id": "af3e1fd796c3-1", "page_content": "age, such as cerebral infarction.\nDevelopment and Course\nThe development and course of obsessive-compulsive and rela ted disorder due to another\nmedical condition generally follows the course of the underlying illness. \nDiagnostic Markers\nLaboratory assessments and/or medical examinations are necessary to confirm the diag-\nnosis of another medical condition.\nDifferential Diagnosis\nDelirium. A separate diagnosis of obsessive-compul sive and related disorder due to an-\nother medical condition is not given if the disturbance occurs exclusively during the\ncourse of a delirium. Howeve r, a diagnosis of obsessive-compulsive and related disorder\ndue to another medical condition may be given in addition to a diagnosis of major neuro-\ncognitive disorder (dementia) if the etiolo gy of the obsessive-compulsive symptoms is\njudged to be a physiological consequence of the pathological process causing the dementia\nand if obsessive-compulsive symptoms are a pr ominent part of the clinical presentation. \nMixed presentation of symptoms (e.g., mood and obsessive-compulsive and related\ndisorder symptoms). If the presentation includes a mix of different types of symptoms,\nthe specific mental disorder due to another medical condition depends on which symp-\ntoms predominate in the clinical picture.\nSubstance/medication-induced obsessive-compulsive and related disorders. If there\nis evidence of recent or pr olonged substance use (including medications with psychoac-\ntive effects), withdrawal from a substance, or exposure to a toxin, a substance/medication-\ninduced obsessive-compulsive and related diso rder should be considered. When a sub-\nstance/medication-induced ob sessive-compulsive and related disorder is being diag-\nnosed in relation to drugs of abuse, it may be useful to obtain a urine or blood drug screen", "source": "dsm5.pdf"} {"id": "0b0bba9ee61b-0", "page_content": "Other Specified Obsessive-Compulsive and Related Disorder 263\nor other appropriate laboratory evaluation. Symptoms that o ccur during or shortly after\n(i.e., within 4 weeks of) substance intoxication or withdrawal or after medication use may\nbe especially indicative of a substance/medi cation-induced obsessive-compulsive and re-\nlated disorder, depending on the type, duration, or amount of the substance used.\nObsessive-compulsive and re lated disorders (primary). Obsessive-compulsive and re-\nlated disorder due to another medical condition should be distinguished fr om a primary\nobsessive-compulsive and related disorder. In primary mental disorders, no specific and\ndirect causative physiological mechanisms associated with a\u00a0medical condition can be\ndemonstrated. Late age at onse t or atypical symptoms suggest the need for a thorough as-\nsessment to rule out the diagnosis of obsessive-compulsive and related disorder due to an-\nother medical condition. \nIllness anxiety disorder. Illness anxiety disorder is charac terized by a preoccupation with\nhaving or acquiring a serious illness. In the case of illness anxiety disorder, individuals\nmay or may not have diagnosed medical conditions.\nAssociated feature of another mental disorder. Obsessive-compulsive and related symp-\ntoms may be an associated feature of another mental disorder (e.g., schizophrenia, an-\norexia nervosa). \nOther specified obsessive-compulsive and related disorder or unspecified obsessive-\ncompulsive and related disorder. These diagnoses are given if it is unclear whether the\nobsessive-compulsive and rela ted symptoms are primary, substance-induced, or due to\nanother medical condition.\nOther Specified Obsessive-Compulsive\nand Related Disorder\n300.3 (F42)\nThis category applies to presentations in which symptoms characteristic of an obsessive-", "source": "dsm5.pdf"} {"id": "0b0bba9ee61b-1", "page_content": "This category applies to presentations in which symptoms characteristic of an obsessive-\ncompulsive and related disorder that cause clinically significant distress or impairment in\nsocial, occupational, or other important areas of functioning predominate but do not meet\nthe full criteria for any of the disorders in the obsessive-compulsive and related disorders\ndiagnostic class. The other specified obsessive -compulsive and related disorder category\nis used in situations in which the clinician chooses to communicate the specific reason that\nthe presentation does not meet the criteria for any specific obsessive-compulsive and re-\nlated disorder. This is done by recording \u201cother specified obsessive-compulsive and relat-\ned disorder\u201d followed by the specific reason (e.g., \u201cbody-focused repetitive behavior\ndisorder\u201d).\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Body dysmorphic\u2013like disorder with actual flaws: This is similar to body dysmor-\nphic disorder except that the defects or flaws in physical appearance are clearly ob-\nservable by others (i.e., they are more noticeable than \u201cslight\u201d). In such cases, the\npreoccupation with these flaws is clearly excessive and causes significant impairment\nor distress.\n2.Body dysmorphic\u2013like disorder without repetitive behaviors: Presentations that\nmeet body dysmorphic disorder except that the individual has not performed repetitive\nbehaviors or mental acts in response to the appearance concerns. \n3.Body-focused repetitive behavior disorder: This is characterized by recurrent body-\nfocused repetitive behaviors (e.g., nail biting, lip biting, cheek chewing) and repeated\nattempts to decrease or stop the behaviors. These symptoms cause clinically significant", "source": "dsm5.pdf"} {"id": "65e22ae6e422-0", "page_content": "264 Obsessive-Compulsive and Related Disorders\ndistress or impairment in social, occupational , or other important areas of functioning\nand are not better explained by trichotillomania (hair-pulling disorder), excoriation (skin-\npicking) disorder, stereotypic movement disorder, or nonsuicidal self-injury. \n4.Obsessional jealousy: This is characterized by nondelusional preoccupation with a\npartner\u2019s perceived infidelity. The preoccupations may lead to repetitive behaviors or\nmental acts in response to the infidelity concerns; they cause clinically significant dis-\ntress or impairment in social, occupational, or other important areas of functioning; and\nthey are not better explained by another mental disorder such as delusional disorder,\njealous type, or paranoid personality disorder. \n5.Shubo-kyofu: A variant of taijin kyofusho (see \u201cGlossary of Cultural Concepts of Dis-\ntress\u201d in the Appendix) that is similar to body dysmorphic disorder and is characterized\nby excessive fear of having a bodily deformity.\n6.Koro: Related to dhat syndrome (see \u201cGlossary of Cultural Concepts of Distress\u201d in\nthe Appendix), an episode of sudden and intense anxiety that the penis (or the vulva\nand nipples in females) will recede into the body, possibly leading to death.\n7.Jikoshu-kyofu: A variant of taijin kyofusho (see \u201cGlossary of Cultural Concepts of Dis-\ntress\u201d in the Appendix) characterized by fear of having an offensive body odor (also\ntermed olfactory reference syndrome).\nUnspecified Obsessive-Compulsive\nand Related Disorder\n300.3 (F42)\nThis category applies to presentations in which symptoms characteristic of an obsessive-", "source": "dsm5.pdf"} {"id": "65e22ae6e422-1", "page_content": "This category applies to presentations in which symptoms characteristic of an obsessive-\ncompulsive and related disorder that cause clinically significant distress or impairment in\nsocial, occupational, or other important ar eas of functioning predominate but do not meet\nthe full criteria for any of the disorders in the obsessive-compulsive and related disorders\ndiagnostic class. The unspecified obsessive-co mpulsive and related disorder category is\nused in situations in which the clinician chooses not to specify the reason that the criteria\nare not met for a specific obsessive-compul sive and related disorder, and includes presen-\ntations in which there is insufficient information to make a more specific diagnosis (e.g., in\nemergency room settings).", "source": "dsm5.pdf"} {"id": "b40f2cafec9a-0", "page_content": "265Trauma- and\n Stressor-Related Disorders\nTrauma- and stressor-related disorders include disorders in which exposure to\na traumatic or stressful event is listed explicitly as a diagnostic criterion. These include reactive\nattachment disorder, disinhibit ed social engagement disorder , posttraumatic stress disor-\nder (PTSD), acute stress disorder, and adjustment disorders. Placement of this chapter reflects\nthe close relationship between these diagnoses and disorders in the surrounding chapters on\nanxiety disorders, obsessive-c ompulsive and related disorder s, and dissociative disorders.\nPsychological distress following exposure to a traumatic or stressful event is quite vari-\nable. In some cases, symptoms can be well understood with in an anxiety- or fear-based\ncontext. It is clear, however, that many in dividuals who have been exposed to a traumatic\nor stressful event exhibit a phenotype in which, rather than anxiety- or fear-based symp-\ntoms, the most prominent clin ical characteristics are anhedonic and dysphoric symptoms,\nexternalizing angry and aggressive symptoms, or dissociative symptoms. Because of these\nvariable expressions of clinic al distress following exposure to catastrophic or aversive\nevents, the aforementioned di sorders have been grouped under a separate category:\ntrauma- and stressor-related disorders. Furthermore, it is not uncommon for the clinical pic-\nture to include some combination of the ab ove symptoms (with or without anxiety- or\nfear-based symptoms). Such a heterogeneous picture has long been recognized in adjust-\nment disorders, as well. Social neglect\u2014that is, the absence of adequate caregiving during\nchildhood\u2014is a diagnostic requirement of both reactive attachment disorder and disin-\nhibited social engagement diso rder. Although the two disord ers share a common etiology,\nthe former is expressed as an internalizing di sorder with depressive symptoms and with-", "source": "dsm5.pdf"} {"id": "b40f2cafec9a-1", "page_content": "the former is expressed as an internalizing di sorder with depressive symptoms and with-\ndrawn behavior, while the latter is marked by disinhibition and externalizing behavior.\nReactive Attachment Disorder\nDiagnostic Criteria 313.89 (F94.1)\nA. A consistent pattern of inhibited, emotionally withdrawn behavior toward adult caregiv-\ners, manifested by both of the following:\n1. The child rarely or minimally seeks comfort when distressed.\n2. The child rarely or minimally responds to comfort when distressed.\nB. A persistent social and emotional disturbance c haracterized by at least two of the following:\n1. Minimal social and emotional responsiveness to others.\n2. Limited positive affect.\n3. Episodes of unexplained irritability, sadness, or fearfulness that are evident even\nduring nonthreatening interactions with adult caregivers.\nC. The child has experienced a pattern of extremes of insufficient care as evidenced by\nat least one of the following:\n1. Social neglect or deprivation in the form of persistent lack of having basic emotional\nneeds for comfort, stimulation, and affection met by caregiving adults.", "source": "dsm5.pdf"} {"id": "52ca76fdd30f-0", "page_content": "266 Trauma- and Stressor-Related Disorders\n2. Repeated changes of primary caregivers that limit opportunities to form stable at-\ntachments (e.g., frequent changes in foster care).\n3. Rearing in unusual settings that severely limit opportunities to form selective at-\ntachments (e.g., institutions with high child-to-caregiver ratios).\nD. The care in Criterion\u00a0C is presumed to be responsible for the disturbed behavior in Cri-\nterion A (e.g., the disturbances in Criterion A began following the lack of adequate care\nin Criterion C).\nE. The criteria are not met for autism spectrum disorder.\nF. The disturbance is evident before age 5 years.\nG. The child has a developmental age of at least 9 months.\nSpecify if:\nPersistent: The disorder has been present for more than 12 months.\nSpecify current severity: \nReactive attachment disorder is specified as severe when a child exhibits all symp-\ntoms of the disorder, with each symptom manifesting at relatively high levels.\nDiagnostic Features\nReactive attachment disorder of infancy or early childhood is characterized by a pattern of\nmarkedly disturbed and develo pmentally inappropriate attachment behaviors, in which a\nchild rarely or minimally turns preferentially to an attachment figure for comfort, support,\nprotection, and nurturance. The essential featur e is absent or grossly underdeveloped at-\ntachment between the child and putative caregiving adults. Children with reactive attach-\nment disorder are believed to have the capa city to form selective attachments. However,\nbecause of limited opportunitie s during early development, they fail to show the behavioral\nmanifestations of select ive attachments. That is, when di stressed, they show no consistent\neffort to obtain comfort, support, nurturance, or protection from caregivers. Furthermore,", "source": "dsm5.pdf"} {"id": "52ca76fdd30f-1", "page_content": "effort to obtain comfort, support, nurturance, or protection from caregivers. Furthermore,\nwhen distressed, children with this disorder do not respond more than minimally to com-\nforting efforts of caregivers. Thus, the disord er is associated with th e absence of expected\ncomfort seeking and response to comforting behaviors. As such, children with reactive\nattachment disorder show dimi nished or absent expression of positive emotions during\nroutine interactions with caregivers. In addi tion, their emotion regulation capacity is com-\npromised, and they displa y episodes of negative emotions of fear, sadness, or irritability\nthat are not readily explained. A diagnosis of reactive attachment disorder should not be\nmade in children who are developmentally unab le to form se lective attachments. For this\nreason, the child must have a develo pmental age of at least 9 months.\nAssociated Features Supporting Diagnosis\nBecause of the shared etiologica l association with social negl ect, reactive attachment dis-\norder often co-occurs with developmental dela ys, especially in delays in cognition and\nlanguage. Other associated features include stereotypies and other signs of severe neglect\n(e.g., malnutrition or signs of poor care). \nPrevalence\nThe prevalence of reactive atta chment disorder is unknown, bu t the disorder is seen rela-\ntively rarely in clinical settings. The disorder has been found in young children exposed to\nsevere neglect before being placed in foster care or raised in institutions. However, even in\npopulations of seve rely neglected children, the disord er is uncommon, occurring in less\nthan 10% of such children.", "source": "dsm5.pdf"} {"id": "572e4b453528-0", "page_content": "Reactive Attachment Disorder 267\nDevelopment and Course\nConditions of social neglect are often present in the first months of life in children diag-\nnosed with reactive attachment disorder, even before the disorder is diagnosed. The clin-\nical features of the disorder manifest in a similar fashion between the ages of 9 months and\n5 years. That is, signs of absent-to-minima l attachment behaviors and associated emotion-\nally aberrant behaviors are evident in childre n throughout this age range, although differ-\ning cognitive and motor abilities may affect how these behaviors ar e expressed. Without\nremediation and recovery through normative care giving environments, it appears that signs\nof the disorder may persist, at least for several years.\nIt is unclear whether reactive attachment disorder occurs in older children and, if so, how\nit differs from its presentation in young ch ildren. Because of this, the diagnosis should be\nmade with caution in children older than 5 years.\nRisk and Prognostic Factors \nEnvironmental. Serious social neglect is a diagnost ic requirement for reactive attach-\nment disorder and is also the only known risk factor for the disorder. However, the ma-\njority of severely neglecte d children do not develop the disorder. Prognosis appears to\ndepend on the quality of the caregiving environment following serious neglect. \nCulture-Related Diagnostic Issues\nSimilar attachment behaviors have been described in young children in many different\ncultures around the world. Ho wever, caution should be exercised in making the diagnosis\nof reactive attachment disorder in cultures in which attachment has not been studied.\nFunctional Consequences of \nReactive Attachment Disorder\nReactive attachment disorder significantly impairs young children\u2019s abilities to relate in-\nterpersonally to adults or peer s and is associated with functional impairment across many\ndomains of early childhood.\nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "572e4b453528-1", "page_content": "domains of early childhood.\nDifferential Diagnosis\nAutism spectrum disorder. Aberrant social behaviors mani fest in young children with\nreactive attachment disorder, but they also ar e key features of auti sm spectrum disorder.\nSpecifically, young children with either co ndition can manifest dampened expression of\npositive emotions, cognitive and language delays, and impairments in social reciprocity.\nAs a result, reactive attachment disorder must be differentiated from autism spectrum dis-\norder. These two disorders can be distinguished based on differential histories of neglect\nand on the presence of restricted interests or ritualized behaviors, specific deficit in social\ncommunication, and selective attachment beha viors. Children with reactive attachment\ndisorder have experienced a history of severe so cial neglect, although it is not always pos-\nsible to obtain detailed historie s about the precise nature of th eir experiences, especially in\ninitial evaluations. Children with autistic spec trum disorder will only rarely have a history\nof social neglect. The restricted interests an d repetitive behaviors ch aracteristic of autism\nspectrum disorder are not a feature of reactive attachment disorder. These clinical features\nmanifest as excessive adherenc e to rituals and routines; restricted, fixated interests; and\nunusual sensory reactions. However, it is important to note that children with either con-\ndition can exhibit stereotypic behaviors such as rocking or flapping. Children with either\ndisorder also may exhibit a range of intellectual functioning, but only children with autis-", "source": "dsm5.pdf"} {"id": "50f180297e39-0", "page_content": "268 Trauma- and Stressor-Related Disorders\ntic spectrum disorder exhibit selective impa irments in social communicative behaviors,\nsuch as intentional communication (i.e., im pairment in communication that is deliberate,\ngoal-directed, and aimed at influencing the be havior of the recipient). Children with reac-\ntive attachment disorder show social commu nicative functioning comparable to their\noverall level of intellectual functioning. Fina lly, children with autistic spectrum disorder\nregularly show attachment behavior typical for their develo pmental level. In contrast,\nchildren with reactive attachment disorder do so only rarely or inconsistently, if at all.\nIntellectual disability (intell ectual developmental disorder). Developmental delays of-\nten accompany reactive attachment disorder, but they should not be confused with the\ndisorder. Children with intellectual disability should exhibit social and emotional skills\ncomparable to their cognitive skills and do not demonstrate the profound reduction in\npositive affect and emotion regula tion difficulties evident in children with reactive attach-\nment disorder. In addition, developmentall y delayed children who have reached a cogni-\ntive age of 7\u20139 months should demonstrate selective attachments regardless of their\nchronological age. In contrast , children with reactive attach ment disorder show lack of\npreferred attachment despite ha ving attained a developmental age of at least 9 months.\nDepressive disorders. Depression in young children is also associated with reductions\nin positive affect. There is limited evidence, ho wever, to suggest that children with depres-\nsive disorders have impairments in attachment . That is, young children who have been di-\nagnosed with depressive disord ers still should seek and resp ond to comforting efforts by\ncaregivers.\nComorbidity\nConditions associated with neglect, includin g cognitive delays, language delays, and ste-", "source": "dsm5.pdf"} {"id": "50f180297e39-1", "page_content": "Conditions associated with neglect, includin g cognitive delays, language delays, and ste-\nreotypies, often co-occur with reactive atta chment disorder. Medical conditions, such as\nsevere malnutrition, may accompany signs of the disorder. Depressive symptoms also\nmay co-occur with reactive attachment disorder. \nDisinhibited Social Engagement Disorder\nDiagnostic Criteria 313.89 (F94.2)\nA. A pattern of behavior in which a child actively approaches and interacts with unfamiliar\nadults and exhibits at least two of the following:\n1. Reduced or absent reticence in approaching and interacting with unfamiliar adults.\n2. Overly familiar verbal or physical behavior (that is not consistent with culturally\nsanctioned and with age-appropriate social boundaries).\n3. Diminished or absent checking back with adult caregiver after venturing away, even\nin unfamiliar settings.\n4. Willingness to go off with an unfamiliar adult with minimal or no hesitation.\nB. The behaviors in Criterion A are not limited to impulsivity (as in attention-deficit/hyper-\nactivity disorder) but include socially disinhibited behavior. \nC. The child has experienced a pattern of extremes of insufficient care as evidenced by\nat least one of the following:\n1. Social neglect or deprivation in the form of persistent lack of having basic emotional\nneeds for comfort, stimulation, and affection met by caregiving adults.\n2. Repeated changes of primary caregivers that limit opportunities to form stable at-\ntachments (e.g., frequent changes in foster care).\n3. Rearing in unusual settings that severely limit opportunities to form selective at-\ntachments (e.g., institutions with high child-to-caregiver ratios).", "source": "dsm5.pdf"} {"id": "0150900b3db6-0", "page_content": "Disinhibited Social Engagement Disorder 269\nD. The care in Criterion C is presumed to be responsible for the disturbed behavior in Cri-\nterion A (e.g., the disturbances in Criterion A began following the pathogenic care in\nCriterion C).\nE. The child has a developmental age of at least 9 months.\nSpecify if:\nPersistent: The disorder has been present for more than 12 months.\nSpecify current severity:\nDisinhibited social engagement disorder is specified as severe when the child exhibits\nall symptoms of the disorder, with each symptom manifesting at relatively high levels.\nDiagnostic Features\nThe essential feature of disinhibited social en gagement disorder is a pattern of behavior\nthat involves culturally inappropriate, overl y familiar behavior with relative strangers\n(Criterion A). This overly familiar behavior violat es the social boundaries of the culture. A\ndiagnosis of disinhibited social engagement d isorder should not be made before children\nare developmentally able to form selective attachments. For this reason, the child must\nhave a developmental age of at least 9 months.\nAssociated Features Supporting Diagnosis\nBecause of the shared etiological association with social neglect, disinhibited social en-\ngagement disorder may co-occu r with developmental delays, especially cognitive and lan-\nguage delays, stereotypies, and other signs of severe neglect, such as malnutrition or poor\ncare. However, signs of the disorder often per sist even after these other signs of neglect are\nno longer present. Therefore, it is not uncomm on for children with the disorder to present\nwith no current signs of neglect. Moreover , the condition can present in children who\nshow no signs of disordered attachment. Th us, disinhibited social engagement disorder\nmay be seen in children with a history of neglect who lack attach ments or whose attach-\nments to their caregivers range from disturbed to secure. \nPrevalence", "source": "dsm5.pdf"} {"id": "0150900b3db6-1", "page_content": "ments to their caregivers range from disturbed to secure. \nPrevalence\nThe prevalence of disinhibited social attachment disorder is unknown. Nevertheless, the\ndisorder appears to be rare, occurring in a mi nority of children, even those who have been\nseverely neglected and subsequently placed in fo ster care or raised in institutions. In such\nhigh-risk populations, the condition occurs in only about 20% of ch ildren. The condition is\nseen rarely in other clinical settings. \nDevelopment and Course\nConditions of social neglect are often present in the first months of life in children diag-\nnosed with disinhibited social engagement di sorder, even before the disorder is diag-\nnosed. However, there is no evidence that ne glect beginning after age 2 years is associated\nwith manifestations of the disorder. If ne glect occurs early and signs of the disorder\nappear, clinical features of the disorder are moderately stable over time, particularly if\nconditions of neglect pe rsist. Indiscriminate social behavior and lack of reticence with un-\nfamiliar adults in toddlerhood are accompan ied by attention-seeking behaviors in pre-\nschoolers. When the disorder persists into middle childhood, clinical features manifest as\nverbal and physical overfamiliarity as well as inauthentic expression of emotions. These\nsigns appear particularly apparent when the child interacts with adults. Peer relationships\nare most affected in adolescence, with both indiscriminate behavior and conflicts appar-\nent. The disorder has not been described in adults.", "source": "dsm5.pdf"} {"id": "e8e4e1eea88d-0", "page_content": "270 Trauma- and Stressor-Related Disorders\nDisinhibited social engagement disorder ha s been described from the second year of\nlife through adolescence. There are some differences in manifestations of the disorder\nfrom early childhood through adolescence. At the youngest ages, across many cultures,\nchildren show reticenc e when interacting with strangers. Young children with the disorder\nfail to show reticence to approach, engage with, and even accompany adults. In preschool\nchildren, verbal and social intrusiveness appear most prominent, often accompanied by\nattention-seeking behavior. Ve rbal and physical overfamiliarity continue through middle\nchildhood, accomp anied by inauthentic expressions of emotion. In adolescence, indis-\ncriminate behavior extends to peers. Relative to healthy adolescents, adolescents with the\ndisorder have more \u201csuperficial\u201d peer relationships and more peer conflicts. Adult man-\nifestations of the disorder are unknown.\nRisk and Prognostic Factors \nEnvironmental. Serious social neglect is a diagnost ic requirement for disinhibited social\nengagement disorder and is also the only know n risk factor for the disorder. However, the\nmajority of severely neglected children do not develop the disorder . Neurobiological vul-\nnerability may differentiate neglected childr en who do and do not develop the disorder.\nHowever, no clear link with any specific neur obiological factors has been established. The\ndisorder has not been identified in children who experience social neglect only after age\n2 years. Prognosis is only mode stly associated with quality of the caregiving environment\nfollowing serious neglect. In many cases, th e disorder persists, even in children whose\ncaregiving environment be comes markedly improved.\nCourse modifiers. Caregiving quality seems to moderate the course of disinhibited so-\ncial engagement disorder. Nevertheless, ev en after placement in normative caregiving", "source": "dsm5.pdf"} {"id": "e8e4e1eea88d-1", "page_content": "cial engagement disorder. Nevertheless, ev en after placement in normative caregiving\nenvironments, some children show persistent signs of the disorder, at least through ado-\nlescence. \nFunctional Consequences of \nDisinhibited Social Engagement Disorder\nDisinhibited social engagement disorder significantly impairs young children\u2019s abilities to\nrelate interpersonally to adults and peers.\nDifferential Diagnosis\nAttention-deficit/hyperactivity disorder. Because of social impulsivity that sometimes\naccompanies attention-deficit/hyperactivity di sorder (ADHD), it is necessary to differ-\nentiate the two disorders. Children with disi nhibited social engagement disorder may be\ndistinguished from those with ADHD because th e former do not show difficulties with at-\ntention or hyperactivity. \nComorbidity\nLimited research has examined the issue of disorders comorbid with disinhibited social\nengagement disorder. Conditions associated with neglect, including cognitive delays,\nlanguage delays, and stereotypies, may co-occu r with disinhibited social engagement dis-\norder. In addition, children may be diagnosed with ADHD and disinhibited social engage-\nment disorder concurrently.", "source": "dsm5.pdf"} {"id": "56cac05e9954-0", "page_content": "Posttraumatic Stress Disorder 271\nPosttraumatic Stress Disorder\nDiagnostic Criteria 309.81 (F43.10)\nPosttraumatic Stress Disorder \nNote: The following criteria apply to adults, adolescents, and children older than 6 years.\nFor children 6 years and younger, see corresponding criteria below.\nA. Exposure to actual or threatened death, serious injury, or sexual violence in one (or\nmore) of the following ways:\n1. Directly experiencing the traumatic event(s).\n2. Witnessing, in person, the event(s) as it occurred to others.\n3. Learning that the traumatic event(s) occurre d to a close family member or close\nfriend. In cases of actual or threatened death of a family member or friend, the\nevent(s) must have been violent or accidental.\n4. Experiencing repeated or extreme exposure to aversive details of the traumatic\nevent(s) (e.g., first responders collecting human remains; police officers repeatedly\nexposed to details of child abuse).\nNote: Criterion A4 does not apply to exposur e through electronic media, television,\nmovies, or pictures, unless this exposure is work related.\nB. Presence of one (or more) of the following intrusion symptoms associated with the\ntraumatic event(s), beginning after the traumatic event(s) occurred:\n1. Recurrent, involuntary, and intrusive dist ressing memories of the traumatic event(s).\nNote: In children older than 6 years, repetitive play may occur in which themes or\naspects of the traumatic event(s) are expressed.\n2. Recurrent distressing dreams in which the content and/or affect of the dream are\nrelated to the traumatic event(s).\nNote: In children, there may be frightening dreams without recognizable content.", "source": "dsm5.pdf"} {"id": "56cac05e9954-1", "page_content": "Note: In children, there may be frightening dreams without recognizable content.\n3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if\nthe traumatic event(s) were recurring. (Such reactions may occur on a continuum,\nwith the most extreme expression being a complete loss of awareness of present\nsurroundings.)\nNote: In children, trauma-specific reenactment may occur in play.\n4. Intense or prolonged psychological distress at exposure to internal or external cues\nthat symbolize or resemble an aspect of the traumatic event(s).\n5. Marked physiological reactions to internal or external cues that symbolize or re-\nsemble an aspect of the traumatic event(s).\nC. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after\nthe traumatic event(s) occurred, as evidenced by one or both of the following:\n1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about\nor closely associated with the traumatic event(s).\n2. Avoidance of or efforts to avoid external reminders (people, places, conversations,\nactivities, objects, situations) that arouse distressing memories, thoughts, or feel-\nings about or closely associated with the traumatic event(s).\nD. Negative alterations in cognitions and mood associated with the traumatic event(s),\nbeginning or worsening after the traumatic event(s) occurred, as evidenced by two (or\nmore) of the following:\n1. Inability to remember an important aspect of the trauma tic event(s) (typically due to dis-\nsociative amnesia and not to other factors such as head injury, alcohol, or drugs).", "source": "dsm5.pdf"} {"id": "78b0e56ec306-0", "page_content": "272 Trauma- and Stressor-Related Disorders\n2. Persistent and exaggerated negative beliefs or expectations about oneself, others,\nor the world (e.g., \u201cI am bad,\u201d \u201cNo one can be trusted,\u201d \u201cThe world is completely\ndangerous,\u201d \u201cMy whole nervous system is permanently ruined\u201d).\n3. Persistent, distorted cognitions about the cause or consequences of the traumatic\nevent(s) that lead the individual to blame himself/herself or others.\n4. Persistent negative emotional state (e.g., fear, horror, anger, guilt, or shame).\n5. Markedly diminished interest or participation in significant activities.\n6. Feelings of detachment or estrangement from others.\n7. Persistent inability to experience positive emotions (e.g., inability to experience\nhappiness, satisfaction, or loving feelings).\nE. Marked alterations in arousal and reactivity associated with the traumatic event(s), be-\nginning or worsening after the traumatic event(s) occurred, as evidenced by two (or\nmore) of the following:\n1. Irritable behavior and angry outbursts (with little or no provocation) typically ex-\npressed as verbal or physical aggression toward people or objects.\n2. Reckless or self-destructive behavior.\n3. Hypervigilance.\n4. Exaggerated startle response.\n5. Problems with concentration.\n6. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).\nF. Duration of the disturbance (Criteria B, C, D, and E) is more than 1 month.\nG. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nH. The disturbance is not attributable to the physiological effects of a substance (e.g.,\nmedication, alcohol) or another medical condition.\nSpecify whether:", "source": "dsm5.pdf"} {"id": "78b0e56ec306-1", "page_content": "medication, alcohol) or another medical condition.\nSpecify whether:\nWith dissociative symptoms: The individual\u2019s symptoms meet the criteria for post-\ntraumatic stress disorder, and in addition, in response to the stressor, the individual ex-\nperiences persistent or recurrent symptoms of either of the following:\n1.Depersonalization: Persistent or recurrent experiences of feeling detached from,\nand as if one were an outside observer of, one\u2019s mental processes or body (e.g.,\nfeeling as though one were in a dream; feeling a sense of unreality of self or body\nor of time moving slowly).\n2.Derealization: Persistent or recurrent experiences of unreality of surroundings\n(e.g., the world around the individual is experienced as unreal, dreamlike, distant,\nor distorted).\nNote: To use this subtype, the dissociative symptoms must not be attributable to the\nphysiological effects of a substance (e.g., blackouts, behavior during alcohol intoxica-\ntion) or another medical condition (e.g., complex partial seizures).\nSpecify if:\nWith delayed expression: If the full diagnostic criteria are not met until at least 6 months\nafter the event (although the onset and expression of some symptoms may be immediate).\nPosttraumatic Stress Disorder for Children 6 Years and Younger\nA. In children 6 years and younger, exposure to actual or threatened death, serious injury,\nor sexual violence in one (or more) of the following ways:\n1. Directly experiencing the traumatic event(s).\n2. Witnessing, in person, the event(s) as it occurred to others, especially primary care-\ngivers.", "source": "dsm5.pdf"} {"id": "386f3144ad7b-0", "page_content": "Posttraumatic Stress Disorder 273\nNote: Witnessing does not include events that are witnessed only in electronic me-\ndia, television, movies, or pictures.\n3. Learning that the traumatic event(s) o ccurred to a parent or caregiving figure.\nB. Presence of one (or more) of the following intrusion symptoms associated with the\ntraumatic event(s), beginning after the traumatic event(s) occurred:\n1. Recurrent, involuntary, and intrusive distressing memories of the traumatic\nevent(s).\nNote: Spontaneous and intrusive memories may not necessarily appear distress-\ning and may be expressed as play reenactment.\n2. Recurrent distressing dreams in which the content and/or affect of the dream are\nrelated to the traumatic event(s).\nNote: It may not be possible to ascertain that the frightening content is related to\nthe traumatic event.\n3. Dissociative reactions (e.g., flashbacks) in which the child feels or acts as if the\ntraumatic event(s) were recurring. (Such reactions may occur on a continuum, with\nthe most extreme expression being a complete loss of awareness of present sur-\nroundings.) Such trauma-specific reenactment may occur in play.\n4. Intense or prolonged psychological distress at exposure to internal or external cues\nthat symbolize or resemble an aspect of the traumatic event(s).\n5. Marked physiological reactions to reminders of the traumatic event(s).\nC. One (or more) of the following symptoms, representing either persistent avoidance of\nstimuli associated with the traumatic event(s) or negative alterations in cognitions and\nmood associated with the traumatic event(s), must be present, beginning after the\nevent(s) or worsening after the event(s):\nPersistent Avoidance of Stimuli\n1. Avoidance of or efforts to avoid activities, places, or physical reminders that arouse", "source": "dsm5.pdf"} {"id": "386f3144ad7b-1", "page_content": "1. Avoidance of or efforts to avoid activities, places, or physical reminders that arouse\nrecollections of the traumatic event(s).\n2. Avoidance of or efforts to avoid people, conversations, or interpersonal situations\nthat arouse recollections of the traumatic event(s).\nNegative Alterations in Cognitions\n3. Substantially increased frequency of negative emotional states (e.g., fear, guilt,\nsadness, shame, confusion).\n4. Markedly diminished interest or participation in significant activities, including con-\nstriction of play.\n5. Socially withdrawn behavior.\n6. Persistent reduction in expression of positive emotions.\nD. Alterations in arousal and reactivity associated with the traumatic event(s), beginning\nor worsening after the traumatic event(s) occurred, as evidenced by two (or more) of\nthe following:\n1. Irritable behavior and angry outbursts (with little or no provocation) typically ex-\npressed as verbal or physical aggression toward people or objects (including ex-\ntreme temper tantrums).\n2. Hypervigilance.\n3. Exaggerated startle response.\n4. Problems with concentration.\n5. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).\nE. The duration of the disturbance is more than 1 month.", "source": "dsm5.pdf"} {"id": "83e5b6e115b3-0", "page_content": "274 Trauma- and Stressor-Related Disorders\nF. The disturbance causes clinically significant distress or impairment in relationships\nwith parents, siblings, peers, or other caregivers or with school behavior.\nG. The disturbance is not attributable to the physiological effects of a substance (e.g.,\nmedication or alcohol) or another medical condition.\nSpecify whether:\nWith dissociative symptoms: The individual\u2019s symptoms meet the criteria for post-\ntraumatic stress disorder, and the individual experiences persistent or recurrent symp-\ntoms of either of the following:\n1.Depersonalization: Persistent or recurrent experiences of feeling detached from,\nand as if one were an outside observer of, one\u2019s mental processes or body (e.g.,\nfeeling as though one were in a dream; feeling a sense of unreality of self or body\nor of time moving slowly).\n2.Derealization: Persistent or recurrent experiences of unreality of surroundings\n(e.g., the world around the individual is experienced as unreal, dreamlike, distant,\nor distorted).\nNote: To use this subtype, the dissociative symptoms must not be attributable to the\nphysiological effects of a substance (e.g., blackouts) or another medical condition\n(e.g., complex partial seizures).\nSpecify if:\nWith delayed expression: If the full diagnostic criteria are not met until at least\n6 months after the event (although the onset and expression of some symptoms may\nbe immediate).\nDiagnostic Features\nThe essential feature of posttraumatic stress disorder (PTSD) is the development of char-\nacteristic symptoms following exposure to one or more tr aumatic events. Emotional re-\nactions to the traumatic event (e.g., fear, he lplessness, horror) are no longer a part of\nCriterion A. The clinical presentation of PTSD varies. In some individuals, fear-based re-", "source": "dsm5.pdf"} {"id": "83e5b6e115b3-1", "page_content": "Criterion A. The clinical presentation of PTSD varies. In some individuals, fear-based re-\nexperiencing, emotional, and behavioral sy mptoms may predominate. In others, anhe-\ndonic or dysphoric mood states and negative cognitions may be most distressing. In some\nother individuals, arousal an d reactive-externalizing symptoms are prominent, while in\nothers, dissociative symptoms predominate. Finally, some individuals exhibit combina-\ntions of these symptom patterns. \nThe directly experienced traumatic events in Criterion A include, but are not limited\nto, exposure to war as a combatant or civilian, threatened or actual physical assault (e.g.,\nphysical attack, robbery, mugging, childhood phy sical abuse), threatened or actual sexual\nviolence (e.g., forced sexual penetration, al cohol/drug-facilitated se xual penetration, abu-\nsive sexual contact, noncontact sexual abuse, sexual trafficking), being kidnapped, being\ntaken hostage, terrorist attack, torture, incarc eration as a prisoner of war, natural or hu-\nman-made disasters, and severe motor vehicle accidents. For children, sexually violent\nevents may include developmentally inapprop riate sexual experiences without physical\nviolence or injury. A life-threatening illness or debilitating medical condition is not neces-\nsarily considered a traumatic event. Medical in cidents that qualify as traumatic events in-\nvolve sudden, catastrophic ev ents (e.g., waking during su rgery, anaphylactic shock).\nWitnessed events include, but are not limited to, observing threatened or serious injury,\nunnatural death, physical or sexual abuse of another person due to violent assault, domes-\ntic violence, accident, war or di saster, or a medical catastrophe in one\u2019s child (e.g., a life-", "source": "dsm5.pdf"} {"id": "83e5b6e115b3-2", "page_content": "threatening hemorrhage). Indirect exposure th rough learning about an event is limited to\nexperiences affecting close relatives or friend s and experiences that are violent or acciden-\ntal (e.g., death due to natural causes does no t qualify). Such events include violent per-", "source": "dsm5.pdf"} {"id": "e7b848fa1f82-0", "page_content": "Posttraumatic Stress Disorder 275\nsonal assault, suicide, serious accident, and se rious injury. The disorder may be especially\nsevere or long-lasting when the stressor is interpersonal and intentiona l (e.g., torture, sex-\nual violence). \nThe traumatic event can be reexperienced in various ways. Commonly, the individual\nhas recurrent, involuntary, and intrusive recollect ions of the event (Criterion B1). Intrusive\nrecollections in PTSD are distinguished from depressive rumination in that they apply\nonly to involuntary and intrusive distressing memories. The emphasis is on recurrent\nmemories of the event that us ually include sensory, emotiona l, or physiological behavioral\ncomponents. A common reexperiencing symptom is distressing dreams that replay the\nevent itself or that are representative or th ematically related to th e major threats involved\nin the traumatic event (Criterion B2). The in dividual may experience dissociative states\nthat last from a few seconds to several hours or even days , during which components of\nthe event are relived and the individual behaves as if the event were occurring at that mo-\nment (Criterion B3). Such events occur on a continuum from brief vi sual or other sensory\nintrusions about part of the traumatic event wi thout loss of reality or ientation, to complete\nloss of awareness of present surroundings. These episodes, often re ferred to as \u201cflash-\nbacks,\u201d are typically brief but can be associ ated with prolonged distress and heightened\narousal. For young children, reenactment of events related to trauma may appear in play\nor in dissociative states. Intense psychological distress (Criterion B4) or physiological re-\nactivity (Criterion B5) often occurs when the individual is exposed to triggering events that", "source": "dsm5.pdf"} {"id": "e7b848fa1f82-1", "page_content": "activity (Criterion B5) often occurs when the individual is exposed to triggering events that\nresemble or symbolize an aspect of the trauma tic event (e.g., windy days after a hurricane;\nseeing someone who resembles one\u2019s perpetrator). The trigge ring cue could be a physical\nsensation (e.g., dizziness for survivors of head trauma; rapid heartbeat for a previously\ntraumatized child), particularly for indivi duals with highly somatic presentations.\nStimuli associated with the trauma are pers istently (e.g., always or almost always)\navoided. The individual commonly makes delib erate efforts to avoid thoughts, memories,\nfeelings, or talking about the traumatic event (e .g., utilizing distraction techniques to avoid\ninternal reminders) (Criterion C1) and to av oid activities, objects, situations, or people\nwho arouse recollections of it (Criterion C2).\nNegative alterations in cognitions or mood associated with the event begin or worsen\nafter exposure to the event. These negative al terations can take various forms, including an\ninability to remember an important aspect of the traumatic event; such amnesia is typically\ndue to dissociative amnesia and is not due to he ad injury, alcohol, or drugs (Criterion D1).\nAnother form is persistent (i.e., always or almost always) and exaggerated negative ex-\npectations regarding important aspects of life a pplied to oneself, others, or the future (e.g.,\n\u201cI have always had bad judgment\u201d; \u201cPeople in authority can\u2019t be trusted\u201d) that may man-\nifest as a negative change in perceived identi ty since the trauma (e.g., \u201cI can\u2019t trust anyone\never again\u201d; Criterion D2). Individuals with PTSD may have persistent erroneous cogni-\ntions about the causes of the traumatic event that lead them to blame themselves or others", "source": "dsm5.pdf"} {"id": "e7b848fa1f82-2", "page_content": "tions about the causes of the traumatic event that lead them to blame themselves or others\n(e.g., \u201cIt\u2019s all my fault that my uncle abused me\u201d) (Criterion D3). A persistent negative\nmood state (e.g., fear, horror, anger, guilt, shame) either began or worsened after exposure\nto the event (Criterion D4). The individual may experience markedly diminished interest\nor participation in previously enjoyed activities (C riterion D5), feeling detached or es-\ntranged from other people (Criterion D6), or a persiste nt inability to feel positive emotions\n(especially happiness, joy, satisfaction, or em otions associated with intimacy, tenderness,", "source": "dsm5.pdf"} {"id": "48b39a9432d6-0", "page_content": "tranged from other people (Criterion D6), or a persiste nt inability to feel positive emotions\n(especially happiness, joy, satisfaction, or em otions associated with intimacy, tenderness,\nand sexuality) (Criterion D7).\nIndividuals with PTSD may be quick temp ered and may even engage in aggressive\nverbal and/or physical behavior with little or no provocation (e.g., yelling at people, get-\nting into fights, destroying objects) (Criterion E1). They may also engage in reckless or self-\ndestructive behavior such as dangerous drivin g, excessive alcohol or drug use, or self-\ninjurious or suicidal behavior (Criterion E2). \u00a0 PTSD is often characterized by a heightened\nsensitivity to potential threats, including t hose that are related to the traumatic experience\n(e.g., following a motor vehicle accident, being especially sensitive to the threat potentially", "source": "dsm5.pdf"} {"id": "f3584cd338dc-0", "page_content": "276 Trauma- and Stressor-Related Disorders\ncaused by cars or trucks) and those not relate d to the traumatic event (e.g., being fearful of\nsuffering a heart attack) (Criterion E3). Individuals with PTSD may be very reactive to un-\nexpected stimuli, displaying a heightened startle response, or jumpiness, to loud noises or\nunexpected movements (e.g., jumping markedly in response to a telephone ringing) (Cri-\nterion E4).\u00a0Concentration difficulties, includ ing difficulty remembering daily events (e.g.,\nforgetting one\u2019s telephone numb er) or attending to focused t asks (e.g., following a conver-\nsation for a sustained period of time), are commonly reported (Criterion E5). Problems\nwith sleep onset and maintenance are commo n and may be associated with nightmares\nand safety concerns or with generalized elevated arousal that interferes with adequate sleep\n(Criterion E6). Some in dividuals also experien ce persistent dissociative symptoms of de-\ntachment from their bodies (depersonalization) or the world around them (derealization);\nthis is reflected in the \u201cwith di ssociative symptoms\u201d specifier.\nAssociated Features Supporting Diagnosis\nDevelopmental regression, such as loss of la nguage in young children, may occur. Audi-\ntory pseudo-hallucinations, such as having the sensory experience of hearing one\u2019s\nthoughts spoken in one or more different voic es, as well as paranoid ideation, can be pres-\nent. Following prolonged, repeated, and seve re traumatic events (e.g., childhood abuse,\ntorture), the individual may additionally experi ence difficulties in regulating emotions or\nmaintaining stable interpersonal relationship s, or dissociative symptoms. When the trau-\nmatic event produces violent death, symptoms of both problematic bereavement and PTSD\nmay be present.", "source": "dsm5.pdf"} {"id": "f3584cd338dc-1", "page_content": "may be present. \nPrevalence\nIn the United States, projected lifetime risk for PTSD using DS M-IV criteria at age 75 years\nis 8.7%. Twelve-month prevalence among U.S. adults is about 3.5%. Lower estimates are\nseen in Europe and most Asian, African, an d Latin American countries, clustering around\n0.5%\u20131.0%. Although different groups have di fferent levels of exposure to traumatic\nevents, the conditional probability of developi ng PTSD following a similar level of expo-\nsure may also vary across cultural groups. Rates of PTSD are higher among veterans and\nothers whose vocation increases the risk of tr aumatic exposure (e.g., police, firefighters,\nemergency medical personnel). Highest rates (r anging from one-third to more than one-\nhalf of those exposed) are found among surv ivors of rape, military combat and captivity,\nand ethnically or politically motivated intern ment and genocide. The prevalence of PTSD\nmay vary across development; children and adolescents, including preschool children,\ngenerally have displayed lower prevalence following exposure to serious traumatic\nevents; however, this may be because previo us criteria were insufficiently developmen-\ntally informed. The prevalence of full-thresh old PTSD also appears to be lower among\nolder adults compared with the general popu lation; there is eviden ce that subthreshold\npresentations are more common th an full PTSD in later life and that these symptoms are\nassociated with substantial clinical impairme nt. Compared with U.S. non-Latino whites,\nhigher rates of PTSD have been reported among U.S. Latinos, African Americans, and\nAmerican Indians, and lower rates have been reported among Asian Americans, after ad-\njustment for traumatic exposu re and demographic variables.\nDevelopment and Course", "source": "dsm5.pdf"} {"id": "f3584cd338dc-2", "page_content": "justment for traumatic exposu re and demographic variables.\nDevelopment and Course\nPTSD can occur at any age, beginning after th e first year of life. Symptoms usually begin\nwithin the first 3 months after the trauma, although there may be a delay of months, or\neven years, before criteria for the diagnosis are met. There is abundant evidence for what\nDSM-IV called \u201cdelayed onset\u201d but is now call ed \u201cdelayed expression,\u201d with the recogni-\ntion that some symptoms typically appear immediately and that the delay is in meeting", "source": "dsm5.pdf"} {"id": "fb0d04dd09e8-0", "page_content": "DSM-IV called \u201cdelayed onset\u201d but is now call ed \u201cdelayed expression,\u201d with the recogni-\ntion that some symptoms typically appear immediately and that the delay is in meeting\nfull criteria.", "source": "dsm5.pdf"} {"id": "18f81ffdb474-0", "page_content": "Posttraumatic Stress Disorder 277\nFrequently, an individual\u2019s reaction to a tr auma initially meets cr iteria for acute stress\ndisorder in the immediate aftermath of the trauma. The symptoms of PTSD and the rela-\ntive predominance of different symptoms may vary over time. Duration of the symptoms\nalso varies, with complete recovery within 3 months occurring in approximately one-half\nof adults, while some individuals remain symptomatic for longer than 12 months and\nsometimes for more than 50 years. Symptom recurrence and intens ification may occur in\nresponse to reminders of the original trauma, ongoing life stressors, or newly experienced\ntraumatic events. For older individuals, dec lining health, worsening cognitive function-\ning, and social isolation ma y exacerbate PTSD symptoms.\nThe clinical expression of reexperiencing can vary across development. Young children\nmay report new onset of frightening dreams wi thout content specific to the traumatic event.\nBefore age 6 years (see criteria for preschool su btype), young children are more likely to ex-\npress reexperiencing symptoms through play th at refers directly or symbolically to the\ntrauma. They may not manifest fe arful reactions at the time of the exposure or during reex-\nperiencing. Parents may report a wide range of emotional or behavioral changes in young\nchildren. Children may focus on imagined interventions in their play or storytelling. In ad-\ndition to avoidance, children may become preoccupied with reminders. Because of young\nchildren\u2019s limitations in expressing thoughts or labeling emotions, negative alterations in\nmood or cognition tend to involve primarily mood changes. Children may experience co-\noccurring traumas (e.g., physical abuse, witnes sing domestic violence) and in chronic cir-\ncumstances may not be able to identify onset of symptomatology. Avoidant behavior may", "source": "dsm5.pdf"} {"id": "18f81ffdb474-1", "page_content": "cumstances may not be able to identify onset of symptomatology. Avoidant behavior may\nbe associated with restricted play or explor atory behavior in youn g children; reduced par-\nticipation in new activities in school-age children; or reluctance to pursue developmental op-\nportunities in adolescents (e.g ., dating, driving). Older children and adolescents may judge\nthemselves as cowardly. Adolescents may harb or beliefs of being changed in ways that\nmake them socially undesirable and estrange them from peers (e.g., \u201cNow I\u2019ll never fit in\u201d)\nand lose aspirations for the future. Irritable or aggressive behavior in children and adoles-\ncents can interfere with peer relationships and sch ool behavior. Reckless behavior may lead\nto accidental injury to self or others, thrill-seeking, or high-risk behaviors. Individuals who\ncontinue to experience PTSD into older ad ulthood may express fe wer symptoms of hy-\nperarousal, avoidance, and ne gative cognitions and mood compared with younger adults\nwith PTSD, although adults ex posed to traumatic events duri ng later life may display more\navoidance, hyperarousal, sleep problems, and crying spells than do younger adults exposed\nto the same traumatic events. In older individu als, the disorder is associated with negative\nhealth perceptions, primary care ut ilization, and suicidal ideation.\nRisk and Prognostic Factors\nRisk (and protective) factors are generally divided into pretraumatic , peritraumatic, and\nposttraumatic factors. \nPretraumatic factors\nTemperamental. These include childhood emotional prob lems by age 6 years (e.g., prior\ntraumatic exposure, externalizing or anxiety problems) and prior me ntal disorders (e.g.,\npanic disorder, depressive disorder, PTSD, or obsessive-compulsive disorder [OCD]).", "source": "dsm5.pdf"} {"id": "18f81ffdb474-2", "page_content": "panic disorder, depressive disorder, PTSD, or obsessive-compulsive disorder [OCD]).\nEnvironmental. These include lower socioeconomic st atus; lower education; exposure to\nprior trauma (especially during childhood); childhood adversity (e.g., economic depriva-\ntion, family dysfunction, parental separation or death); cultural charac teristics (e.g., fatal-\nistic or self-blaming coping strategies); lower intelligence; minority racial/ethnic status;", "source": "dsm5.pdf"} {"id": "6b7b90f32f74-0", "page_content": "tion, family dysfunction, parental separation or death); cultural charac teristics (e.g., fatal-\nistic or self-blaming coping strategies); lower intelligence; minority racial/ethnic status;\nand a family psychiatric history. Social suppo rt prior to event exposure is protective.\nGenetic and physiological. These include female gender and younger age at the time of\ntrauma exposure (for adults). Certain genotypes may either be protective or increase risk\nof PTSD after exposure to traumatic events.", "source": "dsm5.pdf"} {"id": "193a000b8fdd-0", "page_content": "278 Trauma- and Stressor-Related Disorders\nPeritraumatic factors\nEnvironmental. These include severity (dose) of th e trauma (the greater the magnitude\nof trauma, the greater the likelihood of PTSD), perceived life threat, personal injury, in-\nterpersonal violence (particularly trauma pe rpetrated by a caregiver or involving a wit-\nnessed threat to a caregiver in children), and, for military personnel, being a perpetrator,\nwitnessing atrocities, or killing the enemy. Fina lly, dissociation that occurs during the trauma\nand persists afterward is a risk factor.\nPosttraumatic factors\nTemperamental. These include negative appraisals, inappropriate coping strategies,\nand development of ac ute stress disorder.\nEnvironmental. These include subsequent exposure to repeated upsetting reminders, subse-\nquent adverse life events, and financial or other trauma-related losses. Social support (includ-\ning family stability, for children) is a protecti ve factor that moderate s outcome after trauma. \nCulture-Related Diagnostic Issues\nThe risk of onset and severity of PTSD may differ across cultural groups as a result of vari-\nation in the type of traumatic exposure (e.g., genocide), the impact on disorder severity of\nthe meaning attributed to the tr aumatic event (e.g., inability to perform funerary rites after\na mass killing), the ongoing so ciocultural context (e.g., re siding among unpunished per-\npetrators in postconflict settings), and other cultural factors (e.g., acculturative stress in\nimmigrants). The relative risk for PTSD of particular exposures (e .g., religious persecu-\ntion) may vary across cultural groups. The clin ical expression of the symptoms or symp-\ntom clusters of PTSD may vary culturally, particularly with respect to avoidance and", "source": "dsm5.pdf"} {"id": "193a000b8fdd-1", "page_content": "tom clusters of PTSD may vary culturally, particularly with respect to avoidance and\nnumbing symptoms, distressing dreams, and somatic symptoms (e.g., dizziness, short-\nness of breath, heat sensations).\nCultural syndromes and idioms of distress influence the expression of PTSD and the\nrange of comorbid disorders in different cultures by providi ng behavioral and cognitive\ntemplates that link traumatic exposures to specific symptoms. For example, panic attack\nsymptoms may be salient in PTSD among Cambodians and Latin Americans because of\nthe association of traumatic exposure with panic-like khy\u00e2l attacks and ataque de nervios.\nComprehensive evaluation of local expression s of PTSD should include assessment of cul-\ntural concepts of distress (see the chapter \u201cCultural Formulation\u201d in Section III).\nGender-Related Diagnostic Issues\nPTSD is more prevalent among females than among males across the lifespan. Females in\nthe general population experience PTSD for a longer duration than do males. At least some\nof the increased risk for PTSD in females appe ars to be attributable to a greater likelihood\nof exposure to traumatic events, such as rape, and other forms of interpersonal violence.\nWithin populations exposed specifically to such stressors, gender differences in risk for\nPTSD are attenuated or nonsignificant.\nSuicide Risk\nTraumatic events such as childhood abuse increa se a person\u2019s suicide risk. PTSD is associated\nwith suicidal ideation and suicide attempts, an d presence of the disorder may indicate which\nindividuals with ideation even tually make a suicide plan or actually attempt suicide.\nFunctional Consequences of \nPosttraumatic Stress Disorder\nPTSD is associated with high levels of social , occupational, and physical disability, as well\nas considerable economic costs and high leve ls of medical utilization. Impaired function-", "source": "dsm5.pdf"} {"id": "81fe5d0bd6b4-0", "page_content": "Posttraumatic Stress Disorder 279\ning is exhibited across social, interpersonal, develo pmental, educational, physical health,\nand occupational domains. In community and veteran samples, PTSD is associated with\npoor social and family relationships, absent eeism from work, lower income, and lower ed-\nucational and occupational success.\nDifferential Diagnosis\nAdjustment disorders. In adjustment disorders, the st ressor can be of any severity or\ntype rather than that required by PTSD Crit erion A. The diagnosis of an adjustment dis-\norder is used when the response to a stressor that meets PTSD Criterion A does not meet\nall other PTSD criteria (or criteria for another mental disorder). An adjustment disorder is\nalso diagnosed when the symptom pattern of PTSD occurs in response to a stressor that\ndoes not meet PTSD Criterion A (e .g., spouse leaving, being fired).\nOther posttraumatic diso rders and conditions. Not all psychopathology that occurs in\nindividuals exposed to an extreme stressor sh ould necessarily be attributed to PTSD. The\ndiagnosis requires that trauma exposure prec ede the onset or exacer bation of pertinent\nsymptoms. Moreover, if the symptom response pattern to the extreme stressor meets cri-\nteria for another mental disorder, these diagnoses should be given instead of, or in addi-\ntion to, PTSD. Other diagnoses and conditions are excluded if they are better explained by\nPTSD (e.g., symptoms of panic disorder that occur only after exposure to traumatic re-\nminders). If severe, symptom response patter ns to the extreme stressor may warrant a sep-\narate diagnosis (e.g., dissociative amnesia). \nAcute stress disorder. Acute stress disorder is distin guished from PTSD because the\nsymptom pattern in acute stress disorder is restricted to a duration of 3 days to 1 month", "source": "dsm5.pdf"} {"id": "81fe5d0bd6b4-1", "page_content": "following exposure to the traumatic event.\nAnxiety disorders and obsessive-compulsive disorder. In OCD, there are recurrent\nintrusive thoughts, but these meet the definition of an obsession. In addition, the intrusive\nthoughts are not related to an experienced traumatic event, compulsions are usually pres-\nent, and other symptoms of PTSD or acute stre ss disorder are typically absent. Neither the\narousal and dissociative symptoms of panic di sorder nor the avoidance, irritability, and\nanxiety of generalized anxiety disorder are associated with a specific traumatic event. The\nsymptoms of separation anxiety disorder are clearly related to separation from home or\nfamily, rather than to a traumatic event.\nMajor depressive disorder. Major depression may or may not be preceded by a trau-\nmatic event and should be diagnosed if othe r PTSD symptoms are absent. Specifically, ma-\njor depressive disorder does not include any PTSD Criterion B or C symptoms. Nor does it\ninclude a number of symptoms from PTSD Criterion D or E.\nPersonality disorders. Interpersonal difficulties that had their onset, or were greatly ex-\nacerbated, after exposure to a traumatic event may be an indica tion of PTSD, rather than a\npersonality disorder, in which such difficulties would be expected independently of any\ntraumatic exposure.\nDissociative disorders. Dissociative amnesia, dissociative identity disorder, and de-\npersonalization-derealization disorder may or may not be preceded by exposure to a trau-\nmatic event or may or may not have co-occurri ng PTSD symptoms. When full PTSD criteria\nare also met, however, the PTSD \u201cwith dissoci ative symptoms\u201d subtype should be considered.\nConversion disorder (functional neurological symptom disorder). New onset of somatic\nsymptoms within the context of posttraumati c distress might be an indication of PTSD", "source": "dsm5.pdf"} {"id": "81fe5d0bd6b4-2", "page_content": "symptoms within the context of posttraumati c distress might be an indication of PTSD\nrather than conversion disorder (functional neurological symptom disorder).\nPsychotic disorders. Flashbacks in PTSD must be di stinguished from illusions, halluci-\nnations, and other perceptual disturbances that may occur in schizophrenia, brief psy-\nchotic disorder, and other psychotic disord ers; depressive and bipolar disorders with", "source": "dsm5.pdf"} {"id": "ac976e3a3ea2-0", "page_content": "280 Trauma- and Stressor-Related Disorders\npsychotic features; delirium; substance/medication-induced disorders; and psychotic dis-\norders due to another medical condition. \nTraumatic brain injury. When a brain injury occurs in the context of a traumatic event (e.g.,\ntraumatic accident, bomb blast, acceleration/d eceleration trauma), symptoms of PTSD may\nappear. An event causing head trauma may also constitute a psychological traumatic event,\nand tramautic brain injury (TBI)\u2013related neurocognitive symptoms are not mutually exclusive\nand may occur concurrently. Sy mptoms previously termed postconcussive (e.g., headaches,\ndizziness, sensitivity to light or sound, irritability, concentration deficits) can occur in brain-\ninjured and non-brain-injured populations, in cluding individuals with PTSD. Because symp-\ntoms of PTSD and TBI-related neurocognitive symptoms can overlap, a differential diagnosis\nbetween PTSD and neurocognitive disorder sy mptoms attributable to TBI\u00a0may be possible\nbased on the presence of symptoms that are di stinctive to each presentation.\u00a0Whereas reexpe-\nriencing and avoidance are characteristic of PTSD and not the effects of TBI, persistent disori-\nentation and confusion are more specific to TBI (neurocognitive effects) than to PTSD.\nComorbidity\nIndividuals with PTSD are 80% more likely than those without PTSD to have symptoms\nthat meet diagnostic criteria for at least one other mental disorder (e.g., depressive, bipo-\nlar, anxiety, or substance use disorders). Comorbid substance use disorder and conduct\ndisorder are more common among males than among females. Among U.S. military per-\nsonnel and combat veterans who have been de ployed to recent wars in Afghanistan and", "source": "dsm5.pdf"} {"id": "ac976e3a3ea2-1", "page_content": "sonnel and combat veterans who have been de ployed to recent wars in Afghanistan and\nIraq, co-occurrence of PTSD and mild TBI is 48%. Although most young children with\nPTSD also have at least one other diagnosis, the patterns of comorbidity are different than\nin adults, with oppositional defiant disorder and separation anxiety disorder predominat-\ning. Finally, there is considerable comorb idity between PTSD and major neurocognitive\ndisorder and some overlapping sy mptoms between these disorders.\nAcute Stress Disorder\nDiagnostic Criteria 308.3 (F43.0)\nA. Exposure to actual or threatened death, serious injury, or sexual violation in one (or\nmore) of the following ways: \n1. Directly experiencing the traumatic event(s).\n2. Witnessing, in person, the event(s) as it occurred to others.\n3. Learning that the event(s) occurred to a close family member or close friend. Note:\nIn cases of actual or threatened death of a family member or friend, the event(s)\nmust have been violent or accidental.\n4. Experiencing repeated or extreme exposure to aversive details of the traumatic\nevent(s) (e.g., first responders collecting human remains, police officers repeatedly\nexposed to details of child abuse).\nNote: This does not apply to exposure through electronic media, television, mov-\nies, or pictures, unless this exposure is work related.\nB. Presence of nine (or more) of the following symptoms from any of the five categories\nof intrusion, negative mood, dissociation, avoidance, and arousal, beginning or wors-\nening after the traumatic event(s) occurred:\nIntrusion Symptoms\n1. Recurrent, involuntary, and intrusive distressing memories of the traumatic", "source": "dsm5.pdf"} {"id": "ac976e3a3ea2-2", "page_content": "1. Recurrent, involuntary, and intrusive distressing memories of the traumatic\nevent(s). Note: In children, repetitive play may occur in which themes or aspects of\nthe traumatic event(s) are expressed.", "source": "dsm5.pdf"} {"id": "ff88a20fccd8-0", "page_content": "Acute Stress Disorder 281\n2. Recurrent distressing dreams in which the content and/or affect of the dream are\nrelated to the event(s). Note: In children, there may be frightening dreams without\nrecognizable content.\n3. Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if\nthe traumatic event(s) were recurring. (Such reactions may occur on a continuum,\nwith the most extreme expression being a complete loss of awareness of present\nsurroundings.) Note: In children, trauma-specific reenactment may occur in play.\n4. Intense or prolonged psychological distress or marked physiological reactions in re-\nsponse to internal or external cues that symbolize or resemble an aspect of the\ntraumatic event(s).\nNegative Mood\n5. Persistent inability to experience positive emotions (e.g., inability to experience\nhappiness, satisfaction, or loving feelings).\nDissociative Symptoms\n6. An altered sense of the reality of one\u2019s surroundings or oneself (e.g., seeing oneself\nfrom another\u2019s perspective, bein g in a daze, time slowing).\n7. Inability to remember an important aspect of the traumatic event(s) (typically due to\ndissociative amnesia and not to other factors such as head injury, alcohol, or\ndrugs).\nAvoidance Symptoms\n8. Efforts to avoid distressing memories, thoughts, or feelings about or closely asso-\nciated with the traumatic event(s).\n9. Efforts to avoid external reminders (peopl e, places, conversations, activities, ob-\njects, situations) that arouse distressing memories, thoughts, or feelings about or\nclosely associated with the traumatic event(s).\nArousal Symptoms\n10. Sleep disturbance (e.g., difficulty falling or staying asleep, restless sleep).", "source": "dsm5.pdf"} {"id": "ff88a20fccd8-1", "page_content": "10. Sleep disturbance (e.g., difficulty falling or staying asleep, restless sleep).\n11. Irritable behavior and angry outbursts (with little or no provocation), typically ex-\npressed as verbal or physical aggression toward people or objects.\n12. Hypervigilance.\n13. Problems with concentration.\n14. Exaggerated startle response.\nC. Duration of the disturbance (symptoms in Criterion B) is 3 days to 1 month after trauma\nexposure.\nNote: Symptoms typically begin immediately after the trauma, but persistence for at\nleast 3 days and up to a month is needed to meet disorder criteria.\nD. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nE. The disturbance is not attributable to the physiological effects of a substance (e.g.,\nmedication or alcohol) or another medical c ondition (e.g., mild traumatic brain injury)\nand is not better explained by brief psychotic disorder.\nDiagnostic Features\nThe essential feature of acute stress disorder is the development of characteristic symp-\ntoms lasting from 3 days to 1 month following exposure to one or more traumatic events.\nTraumatic events that are expe rienced directly include, but are not limited to, exposure\nto war as a combatant or civilia n, threatened or actual violen t personal assault (e.g., sexual", "source": "dsm5.pdf"} {"id": "a46379b41c21-0", "page_content": "282 Trauma- and Stressor-Related Disorders\nviolence, physical attack, active combat, mugging, childhood physical and/or sexual vio-\nlence, being kidnapped, being taken hostage, terrorist attack, tortur e), natural or human-\nmade disasters (e.g., earthquake, hurricane, airplane crash), and severe accident (e.g.,\nsevere motor vehicle, industrial accident). For children, sexually traumatic events may\ninclude inappropriate sexual experiences with out violence or injury. A life-threatening\nillness or debilitating medical condition is no t necessarily consider ed a traumatic event.\nMedical incidents that qualify as traumatic even ts involve sudden, cata strophic events (e.g.,\nwaking during surgery, anaphylactic shock). St ressful events that do not possess the severe\nand traumatic components of ev ents encompassed by Criterion A may lead to an adjust-\nment disorder but not to acute stress disorder.\nThe clinical presentation of acute stress disorder may vary by individual but typically\ninvolves an anxiety response that includes some form of reexperiencing of or reactivity to\nthe traumatic event. In some individuals, a dissociative or detached presentation can pre-\ndominate, although these individuals typically will also display strong emotional or phys-\niological reactivity in response to trauma re minders. In other individuals, there can be a\nstrong anger response in which reactivity is characterized by irritable or possibly aggres-\nsive responses. The full symptom picture must be present for at least 3 days after the trau-\nmatic event and can be diagnosed only up to 1 month after the event. Symptoms that occur\nimmediately after the event but resolve in less than 3 days would not meet criteria for\nacute stress disorder.\nWitnessed events include, but are not limited to, observing threatened or serious in-", "source": "dsm5.pdf"} {"id": "a46379b41c21-1", "page_content": "Witnessed events include, but are not limited to, observing threatened or serious in-\njury, unnatural death, physical or sexual violence inflicted on another individual as a re-\nsult of violent assault, severe domestic violen ce, severe accident, war, and disaster; it may\nalso include witnessing a medical catastrophe (e.g., a life-threatening hemorrhage) involv-\ning one\u2019s child. Events experienced indirectly through learning about the event are limited\nto close relatives or close friends. Such even ts must have been violent or accidental\u2014death\ndue to natural causes does not qualify\u2014and in clude violent personal assault, suicide, se-\nrious accident, or serious injury. The disorder may be especially severe when the stressor\nis interpersonal and intentional (e .g., torture, rape). The like lihood of developing this dis-\norder may increase as the intensity of and physical proximity to the stressor increase.\nThe traumatic event can be reexperienced in various wa ys. Commonly, the individual\nhas recurrent and intrusive recollections of the event (Criterion B1). The recollections are\nspontaneous or triggered recurrent memories of the event that usua lly occur in response\nto a stimulus that is reminiscent of the traumatic experience (e.g., the sound of a backfiring\ncar triggering memories of gunshots). Thes e intrusive memories often include sensory\n(e.g., sensing the intense heat that was percei ved in a house fire), emotional (e.g., experi-\nencing the fear of believing that one was about to be stabbed), or physiological (e.g., expe-\nriencing the shortness of breath that one su ffered during a near-drowning) components.\nDistressing dreams may contain themes that are representative of or thematically re-\nlated to the major threats involved in the trau matic event. (For example, in the case of a", "source": "dsm5.pdf"} {"id": "a46379b41c21-2", "page_content": "motor vehicle accident surviv or, the distressing dreams may involve crashing cars gener-\nally; in the case of a combat soldier, the distressing dreams may involve being harmed in\nways other than combat.)\nDissociative states may last from a few seco nds to several hours, or even days, during\nwhich components of the event are relived an d the individual behaves as though experi-", "source": "dsm5.pdf"} {"id": "51099fdeb69e-0", "page_content": "Dissociative states may last from a few seco nds to several hours, or even days, during\nwhich components of the event are relived an d the individual behaves as though experi-\nencing the event at that moment. While disso ciative responses are common during a trau-\nmatic event, only dissociative responses that persist beyond 3 days after trauma exposure\nare considered for the diagnosis of acute st ress d isord er. For youn g children, reenactment\nof events related to trauma may appear in play and may include dissociative moments\n(e.g., a child who survives a motor vehicle accident may repe atedly crash toy cars during\nplay in a focused and distressing manner). These episodes, often referred to as flashbacks,\nare typically brief but involve a sense that th e traumatic event is oc curring in the present\nrather than being remembered in the past and are associated with significant distress.", "source": "dsm5.pdf"} {"id": "366448b8fc79-0", "page_content": "Acute Stress Disorder 283\nSome individuals with the disorder do not ha ve intrusive memories of the event itself,\nbut instead experience intense psychological distress or physiological reactivity when\nthey are exposed to triggering events that re semble or symbolize an aspect of the traumatic\nevent (e.g., windy days for child ren after a hurricane, entering an elevator for a male or fe-\nmale who was raped in an elevator, seeing someone who resembles one\u2019s perpetrator).\nThe triggering cue could be a physical sensation (e.g., a sense of heat for a burn victim, diz-\nziness for survivors of head tr auma), particularly for individuals with highly somatic pre-\nsentations. The individual may have a persistent inability to feel positive emotions (e.g.,\nhappiness, joy, satisfaction, or emotions asso ciated with intimacy, tenderness, or sexual-\nity) but can experience negative emotions su ch as fear, sadness, anger, guilt, or shame.\nAlterations in awareness can include depersonalization, a detached sense of oneself (e.g.,\nseeing oneself from the other side of the room), or derealization, having a distorted view of\none\u2019s surroundings (e.g., perceiving that thin gs are moving in slow motion, seeing things\nin a daze, not being aware of events that on e would normally encode ). Some individuals\nalso report an inability to remember an impo rtant aspect of the tr aumatic event that was\npresumably encoded. This symp tom is attributable to dissoc iative amnesia and is not at-\ntributable to head inju ry, alcohol, or drugs.\nStimuli associated with the trauma are persistently avoided. The individual may refuse\nto discuss the traumatic experience or may engage in avoidance strategies to minimize\nawareness of emotional reactions (e.g., excessive alcohol use when reminded of the ex-", "source": "dsm5.pdf"} {"id": "366448b8fc79-1", "page_content": "awareness of emotional reactions (e.g., excessive alcohol use when reminded of the ex-\nperience). This behavioral avoidance may include avoiding watching news coverage of\nthe traumatic experience, refusing to return to a workplace where the trauma occurred, or\navoiding interacting with others who shared the same traumatic experience.\nIt is very common for indivi duals with acute stress disorder to experience problems\nwith sleep onset and maintenance, which may be associated with nightmares or with gen-\neralized elevated arou sal that prevents adequate sleep. Individuals with acute stress dis-\norder may be quick tempered and may even en gage in aggressive verbal and/or physical\nbehavior with little provocation. Acute stress disorder is often characterized by a height-\nened sensitivity to potential th reats, including those that are related to the traumatic ex-\nperience (e.g., a motor vehicle accident vict im may be especially sensitive to the threat\npotentially caused by any cars or trucks) or those not related to the traumatic event (e.g.,\nfear of having a heart attack). Concentration difficulties, including difficulty remembering\ndaily events (e.g., forg etting one\u2019s telephone number) or attending to focused tasks (e.g.,\nfollowing a conversation for a sustained period of time), are commonly reported. Individ-\nuals with acute stress disorder may be very re active to unexpected stimuli, displaying a\nheightened startle response or jumpiness to loud noises or unexpe cted movements (e.g.,\nthe individual may jump markedly in the response to a telephone ringing). \nAssociated Features Supporting Diagnosis\nIndividuals with acute stress disorder common ly engage in catastrophic or extremely neg-\native thoughts about thei r role in the traumatic event, th eir response to the traumatic ex-\nperience, or the likelihood of future harm. For example, an individual with acute stress\ndisorder may feel excessively guilty about not having prevented the traumatic event or", "source": "dsm5.pdf"} {"id": "366448b8fc79-2", "page_content": "disorder may feel excessively guilty about not having prevented the traumatic event or\nabout not adapting to the experience more su ccessfully. Individuals with acute stress dis-\norder may also interpret their symptoms in a catastrophic manner, such that flashback\nmemories or emotional numbing may be interpreted as a sign of diminished mental ca-", "source": "dsm5.pdf"} {"id": "3948bfe87243-0", "page_content": "order may also interpret their symptoms in a catastrophic manner, such that flashback\nmemories or emotional numbing may be interpreted as a sign of diminished mental ca-\npacity. It is common for individuals with acute stress disorder to experience panic attacks\nin the initial month after trauma exposure th at may be triggered by trauma reminders or\nmay apparently occur spontaneously. Addition ally, individuals with acute stress disorder\nmay display chaotic or impulsive behavior. For example, individuals may drive reck-\nlessly, make irrational decisions, or gamble excessively. In children, there may be sig-\nnificant separation anxiety, possibly mani fested by excessive needs for attention from", "source": "dsm5.pdf"} {"id": "f5de72a0025a-0", "page_content": "284 Trauma- and Stressor-Related Disorders\ncaregivers. In the case of be reavement following a death that occurred in traumatic cir-\ncumstances, the symptoms of acute stress di sorder can involve acute grief reactions. In\nsuch cases, reexperiencing, dissociative, an d arousal symptoms ma y involve reactions to\nthe loss, such as intrusive memories of the ci rcumstances of the individual\u2019s death, disbe-\nlief that the individual has died, and ange r about the death. Po stconcussive symptoms\n(e.g., headaches, dizziness, sensitivity to light or sound, irritability, concentration deficits),\nwhich occur frequently following mild traumatic brain injury, are also frequently seen in\nindividuals with acute stress disorder. Po stconcussive symptoms are equally common in\nbrain-injured and non\u2013brain-injured populations, and the frequent occurrence of postcon-\ncussive symptoms could be attributable to acute stress disorder symptoms. \nPrevalence\nThe prevalence of acute stress disorder in recently trauma-exposed populations (i.e.,\nwithin 1 month of trauma exposure) varies ac cording to the nature of the event and the\ncontext in which it is assessed. In both U.S. and non-U.S. population s, acute stress disorder\ntends to be identified in less than 20% of ca ses following traumatic events that do not in-\nvolve interpersonal assault; 13%\u201321% of motor vehicle accidents, 14% of mild traumatic\nbrain injury, 19% of assault, 10% of severe burns, and 6%\u201312% of industrial accidents.\nHigher rates (i.e., 20%\u201350%) are reported following interpersonal traumatic events, in-\ncluding assault, rape, and witnessing a mass shooting. \nDevelopment and Course", "source": "dsm5.pdf"} {"id": "f5de72a0025a-1", "page_content": "cluding assault, rape, and witnessing a mass shooting. \nDevelopment and Course\nAcute stress disorder cannot be diagnosed un til 3 days after a traumatic event. Although\nacute stress disorder may prog ress to posttraumatic stress di sorder (PTSD) after 1 month,\nit may also be a transient stress response th at remits within 1 month of trauma exposure\nand does not result in PTSD. Approximately half of individuals who eventually develop\nPTSD initially present with acute stress diso rder. Symptom worsenin g during the initial\nmonth can occur, often as a result of ongoin g life stressors or further traumatic events. \nThe forms of reexperiencing can vary acro ss development. Unlike adults or adoles-\ncents, young children may report frightening dreams without content that clearly reflects\naspects of the trauma (e.g., waki ng in fright in the aftermath of the trauma but being unable\nto relate the content of the dream to the traumatic event). Ch ildren age 6 years and younger\nare more likely than older children to expres s reexperiencing symptoms through play that\nrefers directly or symbolically to the trauma. For example, a very young child who sur-\nvived a fire may draw pictures of flames. Yo ung children also do not necessarily manifest\nfearful reactions at the time of the exposure or even during reexperiencing. Parents typi-\ncally report a range of emotional expressions, such as anger, shame, or withdrawal, and\neven excessively bright positiv e affect, in young children who are traumatized. Although\nchildren may avoid reminders of the trauma, they sometimes become preoccupied with\nreminders (e.g., a young child bitten by a dog may talk about dogs constantly yet avoid go-\ning outside because of fear of coming into contact with a dog).", "source": "dsm5.pdf"} {"id": "f5de72a0025a-2", "page_content": "ing outside because of fear of coming into contact with a dog). \nRisk and Prognostic Factors\nTemperamental. Risk factors include prior mental diso rder, high levels of negative af-\nfectivity (neuroticism), greater perceived seve rity of the traumatic event, and an avoidant\ncoping style. Catastrophic appraisals of th e traumatic experience, often characterized by\nexaggerated appraisals of future harm, guilt, or hopelessness, are strongly predictive of\nacute stress disorder. \nEnvironmental. First and foremost, an individual must be exposed to a traumatic event to\nbe at risk for acute stress disorder. Risk fact ors for the disorder include a history of prior\ntrauma.", "source": "dsm5.pdf"} {"id": "bcc6fcbd2956-0", "page_content": "Acute Stress Disorder 285\nGenetic and physiological. Females are at greater risk for developing acute stress dis-\norder.\nElevated reactivity, as reflected by acousti c startle response, prior to trauma exposure\nincreases the risk for developing acute stress disorder. \nCulture-Related Diagnostic Issues\nThe profile of symptoms of acute stress disorder may vary cross-culturally, particularly\nwith respect to dissociative symptoms, ni ghtmares, avoidance, and somatic symptoms\n(e.g., dizziness, shortness of breath, heat se nsations). Cultural sy ndromes and idioms of\ndistress shape the local symptom profiles of acute stress disorder. Some cultural groups\nmay display variants of dissociative response s, such as possession or trancelike behaviors\nin the initial month after trauma exposure. Pa nic symptoms may be salient in acute stress\ndisorder among Cambodians because of the as sociation of traumatic exposure with panic-\nlike khy\u00e2l attacks, and ataque de nervios among Latin Americans may also follow a traumatic\nexposure. \nGender-Related Diagnostic Issues\nAcute stress disorder is more prevalent am ong females than among males. Sex-linked neu-\nrobiological differences in stre ss response may contribute to females\u2019 increased risk for\nacute stress disorder. The increased risk for the disorder in females may be attributable in\npart to a greater likelihood of exposure to th e types of traumatic events with a high con-\nditional risk for acute stress disorder, such as rape and other interpersonal violence. \nFunctional Consequences of Acute Stress Disorder\nImpaired functioning in social, interpersona l, or occupational domains has been shown\nacross survivors of accidents, assault, and rape who develop acute stress disorder. The ex-\ntreme levels of anxiety that may be associa ted with acute stress disorder may interfere", "source": "dsm5.pdf"} {"id": "bcc6fcbd2956-1", "page_content": "treme levels of anxiety that may be associa ted with acute stress disorder may interfere\nwith sleep, energy levels, and capacity to a ttend to tasks. Avoidance in acute stress dis-\norder can result in generalized withdrawal from many situations that are perceived as\npotentially threatening, which can lead to nonattendance of medical appointments, avoid-\nance of driving to important appointments, and absenteeism from work. \nDifferential Diagnosis\nAdjustment disorders. In acute stress disorder, the stress or can be of any severity rather\nthan of the severity and type required by Criterion A of acute stress di sorder. The diagnosis of\nan adjustment disorder is used when the response to a Criterion A event does not meet the cri-\nteria for acute stress disorder (o r another specific mental diso rder) and when the symptom pat-\ntern of acute stress disorder occurs in response to a stressor that does not meet Criterion A for\nexposure to actual or threatened death, serious injury, or sexual violence (e.g., spouse leaving,\nbeing fired). For example, severe stress reactions to life-threate ning illnesses that may include\nsome acute stress disorder symptoms may be more appropriately desc ribed as an adjustment\ndisorder. Some forms of acute stress response do not include acute stress disorder symptoms\nand may be characterized by anger, depression, or guilt. These responses are more appro-\npriately described as primarily an adjustment disorder. Depressive or anger responses in an\nadjustment disorder may involve rumination ab out the traumatic event, as opposed to invol-\nuntary and intrusive distressing memories in acute stress disorder.\nPanic disorder. Spontaneous panic attacks are very common in acute stress disorder.\nHowever, panic disorder is diagnosed only if panic attacks are unexpected and there is\nanxiety about future attacks or maladaptive changes in behavior associated with fear of\ndire consequences of the attacks.", "source": "dsm5.pdf"} {"id": "3a90204c1a7a-0", "page_content": "286 Trauma- and Stressor-Related Disorders\nDissociative disorders. Severe dissociative responses (i n the absence of characteristic\nacute stress disorder symptoms) may be di agnosed as derealization/depersonalization\ndisorder. If severe amnesia of the trauma persists in the ab sence of characteristic acute\nstress disorder symptoms, the diagnosis of dissociative amnesia may be indicated.\nPosttraumatic stress disorder. Acute stress disorder is dist inguished from PTSD because\nthe symptom pattern in acute stre ss disorder must occur within 1 month of the traumatic event\nand resolve within that 1-month period. If th e symptoms persist for more than 1 month and\nmeet criteria for PTSD, the diagnosis is ch anged from acute stre ss disorder to PTSD.\nObsessive-compulsive disorder. In obsessive-compulsive diso rder, there are recurrent\nintrusive thoughts, but these meet the definition of an obsession. In addition, the intrusive\nthoughts are not related to an experienced traumatic event, compulsions are usually pres-\nent, and other symptoms of acute st ress disorder are typically absent.\nPsychotic disorders. Flashbacks in acute stress disorder must be distinguished from il-\nlusions, hallucinations, and other perceptual disturbances that may occur in schizophre-\nnia, other psychotic disorders, depressive or bipolar disorder with psychotic features, a\ndelirium, substance/medication -induced disorders, and psychotic disorders due to an-\nother medical condition. Acut e stress disorder flashbacks ar e distinguished from these\nother perceptual disturbances by being direct ly related to the traumatic experience and by\noccurring in the absence of other psychotic or substance-induced features.\nTraumatic brain injury. When a brain injury occurs in the context of a traumatic event\n(e.g., traumatic accident, bomb blast, acceleration/deceleration trauma), symptoms of", "source": "dsm5.pdf"} {"id": "3a90204c1a7a-1", "page_content": "(e.g., traumatic accident, bomb blast, acceleration/deceleration trauma), symptoms of\nacute stress disorder may appear. An event causing head trauma may also constitute a\npsychological trau matic event, and tramautic brain injury (TBI)\u2013related neurocognitive\nsymptoms are not mutually exclusive and ma y occur concurrently. Symptoms previously\ntermed postconcussive (e.g., headaches, dizziness, sensitiv ity to light or sound, irritability,\nconcentration deficits) can occur in brain-injured and non\u2013brain injured populations, in-\ncluding individuals with acute stress disorder . Because symptoms of acute stress disorder\nand TBI-related neurocognitive symptoms can overlap, a differential diagnosis between\nacute stress disorder and neurocognitive di sorder symptoms attributable to TBI\u00a0may be\npossible based on the presence of symptoms that are distinctive to each presenta-\ntion.\u00a0Whereas reexperiencing and avoidance are characteristic of acut e stress disorder and\nnot the effects of TBI, persistent disorientation and confusion are more specific to TBI (neu-\nrocognitive effects) than to acute stress disord er. Furthermore, differential is aided by the\nfact that symptoms of acute stress disorder persist for up to only 1 month following trauma\nexposure.\nAdjustment Disorders\nDiagnostic Criteria\nA. The development of emotional or behavioral symptoms in response to an identifiable\nstressor(s) occurring within 3 months of the onset of the stressor(s).\nB. These symptoms or behaviors are clinically significant, as evidenced by one or both of\nthe following:\n1. Marked distress that is out of proportion to the severity or intensity of the stressor,\ntaking into account the external context and the cultural factors that might influence\nsymptom severity and presentation.\n2. Significant impairment in social, occupational, or other important areas of functioning.", "source": "dsm5.pdf"} {"id": "3a90204c1a7a-2", "page_content": "2. Significant impairment in social, occupational, or other important areas of functioning.\nC. The stress-related disturbance does not meet the criteria for another mental disorder\nand is not merely an exacerbation of a preexisting mental disorder.", "source": "dsm5.pdf"} {"id": "216738cedf4a-0", "page_content": "Adjustment Disorders 287\nD. The symptoms do not represent normal bereavement.\nE. Once the stressor or its consequences have terminated, the symptoms do not persist\nfor more than an additional 6 months.\nSpecify whether:\n309.0 (F43.21) With depressed mood: Low mood, tearfulness, or feelings of hope-\nlessness are predominant.\n309.24 (F43.22) With anxiety: Nervousness, worry, jitteriness, or separation anxiety\nis predominant.\n309.28 (F43.23) With mixed anxiety and depressed mood: A combination of de-\npression and anxiety is predominant.\n309.3 (F43.24) With disturbance of conduct: Disturbance of conduct is predominant.\n309.4 (F43.25) With mixed disturba nce of emotions and conduct: Both emotional\nsymptoms (e.g., depression, anxiety) and a disturbance of conduct are predominant.\n309.9 (F43.20) Unspecified: For maladaptive reactions that are not classifiable as one\nof the specific subtypes of adjustment disorder.\nDiagnostic Features\nThe presence of emotional or behavioral sympto ms in response to an identifiable stressor\nis the essential feature of adju stment disorders (Criterion A) . The stressor may be a single\nevent (e.g., a termination of a romantic relati onship), or there may be multiple stressors\n(e.g., marked business difficulties and marita l problems). Stressors may be recurrent (e.g.,\nassociated with seasonal busi ness crises, unfulfilling sexual relationships) or continuous\n(e.g., a persistent painful illness with increasi ng disability, living in a crime-ridden neigh-\nborhood). Stressors may affect a single individual, an entire family, or a larger group or", "source": "dsm5.pdf"} {"id": "216738cedf4a-1", "page_content": "community (e.g., a natural disaster). Some st ressors may accompany specific developmen-\ntal events (e.g., going to school, leaving a parental home, reentering a parental home, get-\nting married, becoming a parent, failing to attain occupational goals, retirement). \nAdjustment disorders may be diagnosed follo wing the death of a loved one when the\nintensity, quality, or persis tence of grief reactions exceeds what normally might be ex-\npected, when cultural, religious, or age-appr opriate norms are taken into account. A more\nspecific set of bereavement-relate d symptoms has been designated persistent complex be-\nreavement disorder.\nAdjustment disorders are associated with an increased risk of suicide attempts and\ncompleted suicide.\nPrevalence\nAdjustment disorders ar e common, although prevalence may vary widely as a function of\nthe population studied and the assessment me thods used. The percentage of individuals\nin outpatient mental health treatment with a principal diagnosis of an adjustment disorder\nranges from approximately 5% to 20%. In a hospital psychiatric consultation setting, it is\noften the most common diagno sis, frequently reaching 50%. \nDevelopment and Course\nBy definition, the disturbance in adjustment disorders begins within 3 months of onset of\na stressor and lasts no longer than 6 months after the stressor or its consequences have\nceased. If the stressor is an acute event (e.g., being fired from a job), the onset of the dis-\nturbance is usually immediate (i.e., within a few days) and the durati on is relatively brief\n(i.e., no more than a few mont hs). If the stressor or its co nsequences persist, the adjustment\ndisorder may also continue to be pr esent and become the persistent form.", "source": "dsm5.pdf"} {"id": "ca622c9454b4-0", "page_content": "288 Trauma- and Stressor-Related Disorders\nRisk and Prognostic Factors\nEnvironmental. Individuals from disadvantaged lif e circumstances experience a high\nrate of stressors and may be at increased risk for adjustment disorders.\nCulture-Related Diagnostic Issues\nThe context of the individual\u2019s cultural setting should be taken into account in making the\nclinical judgment of whether the individual\u2019s response to the stressor is maladaptive or\nwhether the associated distress is in excess of what would be expected. The nature, mean-\ning, and experience of the stressors and the ev aluation of the response to the stressors may\nvary across cultures. \nFunctional Consequences of Adjustment Disorders\nThe subjective distress or impa irment in functioning associat ed with adjustment disorders\nis frequently manifested as decreased perf ormance at work or school and temporary\nchanges in social relationships. An adjustment disorder may complicate the course of ill-\nness in individuals who have a general medica l condition (e.g., decreased compliance with\nthe recommended medical regimen; incr eased length of hospital stay). \nDifferential Diagnosis\nMajor depressive disorder. If an individual has symptoms that meet criteria for a major\ndepressive disorder in response to a stressor, the diagnosis of an adjustment disorder is\nnot applicable. The symptom profile of major depressive disorder differentiates it from ad-\njustment disorders.\nPosttraumatic stress disorder and acute stress disorder. In adjustment disorders, the\nstressor can be of any severity rather than of the severity and type required by Criterion A\nof acute stress disorder and posttraumatic st ress disorder (PTSD). In distinguishing ad-\njustment disorders from thes e two posttraumatic diagnoses, there are both timing and\nsymptom profile considerations. Adjustment disorders can be diagnosed immediately\nand persist up to 6 months afte r exposure to the traumatic event, whereas acute stress dis-", "source": "dsm5.pdf"} {"id": "ca622c9454b4-1", "page_content": "order can only occur between 3 days and 1 month of exposure to the stressor, and PTSD\ncannot be diagnosed until at least 1 month has passed since the occurrence of the traumatic\nstressor. The required symptom profile for PT SD and acute stress disorder differentiates\nthem from the adjustment disorders. With re gard to symptom profiles, an adjustment dis-\norder may be diagnosed following a traumatic event when an individu al exhibits symptoms\nof either acute stress disorder or PTSD that do not meet or exceed the diagnostic threshold\nfor either disorder. An adjustment disorder should also be diagno sed for individuals who\nhave not been exposed to a tr aumatic event but who otherwise exhibit the full symptom pro-\nfile of either acute st ress disorder or PTSD.\nPersonality disorders. With regard to personality disorders, some personality features\nmay be associated with a vulnerability to situat ional distress that may resemble an adjust-\nment disorder. The lifetime hist ory of personality functionin g will help inform the in-\nterpretation of distressed behaviors to aid in distinguishing a long-standing personality\ndisorder from an adjustment d isorder. In addition to some personality disorders incurring\nvulnerability to distress, stre ssors may also exacerbate pers onality disorder symptoms. In\nthe presence of a personality disorder, if the symptom criteria for an adjustment disorder\nare met, and the stress-related disturbance exceeds what may be attributable to maladap-\ntive personality disorder symptoms (i.e., Crit erion C is met), then the diagnosis of an ad-\njustment disorder should be made.", "source": "dsm5.pdf"} {"id": "13abc876bfdd-0", "page_content": "Other Specified Trauma- and Stressor-Related Disorder 289\nPsychological factors affecting other medical conditions. In psychological factors af-\nfecting other medical conditions, specific psychological entities (e.g., psychological symp-\ntoms, behaviors, other factors) exacerbate a medical condition. These psychological\nfactors can precipitate, exacerbate, or put an individual at risk for medical illness, or they\ncan worsen an existing condition. In contrast, an adjustment disorder is a reaction to the\nstressor (e.g., having a medical illness).\nNormative stress reactions. When bad things happen, most people get upset. This is\nnot an adjustment disorder. The diagnosis should only be made when the magnitude of\nthe distress (e.g., alterations in mood, anxiet y, or conduct) exceed s what would normally\nbe expected (which may vary in different cu ltures) or when the adverse event precipitates\nfunctional impairment.\nComorbidity\nAdjustment disorders can accompany most mental disorders and an y medical disorder.\nAdjustment disorders can be diagnosed in additi on to another mental disorder only if the\nlatter does not explain the partic ular symptoms that occur in reaction to the stressor. For\nexample, an individual may develop an adjustment disorder, with depressed mood, after\nlosing a job and at the same time have a di agnosis of obsessive-co mpulsive disorder. Or,\nan individual may have a depressive or bipo lar disorder and an adjustment disorder as\nlong as the criteria for both are met. Adju stment disorders are common accompaniments\nof medical illness and may be the major psychological response to a medical disorder.\nOther Specified Trauma- and\nStressor-Related Disorder\n309.89 (F43.8)\nThis category applies to presentations in which symptoms characteristic of a trauma- and", "source": "dsm5.pdf"} {"id": "13abc876bfdd-1", "page_content": "This category applies to presentations in which symptoms characteristic of a trauma- and\nstressor-related disorder that cause clinically significant distress or impairment in social,\noccupational, or other important areas of functioning predominate but do not meet the full\ncriteria for any of the disorders in the trauma- and stressor-related disorders diagnostic\nclass. The other specified trauma- and stressor- related disorder category is used in situa-\ntions in which the clinician chooses to communicate the specific reason that the presenta-\ntion does not meet the criteria for any specific trauma- and stressor-related disorder. This\nis done by recording \u201cother specified trauma- and stressor-related disorder\u201d followed by\nthe specific reason (e.g., \u201cpersistent complex bereavement disorder\u201d).\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Adjustment-like disorders with delayed on set of symptoms that occur more than\n3 months after the stressor.\n2.Adjustment-like disorders with prolonged duration of more than 6 months with-\nout prolonged duration of stressor.\n3.Ataque de nervios: See \u201cGlossary of Cultural Concepts of Distress\u201d in the Appendix.\n4.Other cultural syndromes: See \u201cGlossary of Cultural Concepts of Distress\u201d in the Ap-\npendix.\n5.Persistent complex bereavement disorder: This disorder is characterized by severe\nand persistent grief and mourning reactions (see the chapter \u201cConditions for Further\nStudy\u201d).", "source": "dsm5.pdf"} {"id": "b03c5f4e06cf-0", "page_content": "290 Trauma- and Stressor-Related Disorders\nUnspecified Trauma- and\nStressor-Related Disorder\n309.9 (F43.9)\nThis category applies to presentations in which symptoms characteristic of a trauma- and\nstressor-related disorder that cause clinically significant distress or impairment in social, oc-\ncupational, or other important areas of functioning predominate but do not meet the full cri-\nteria for any of the disorders in the trauma- and stressor-related disorders diagnostic class.\nThe unspecified trauma- or stressor-related disord er category is used in situations in which\nthe clinician chooses not to specify the reason that the criteria are not met for a specific\ntrauma- and stressor-related disorder, and includes presentations in which there is insuffi-\ncient information to make a more specific diagnosis (e.g., in emergency room settings).", "source": "dsm5.pdf"} {"id": "53e8e2f2eea8-0", "page_content": "291Dissociative\n Disorders\nDissociative disorders are characterized by a disrup tion of and/or discontinuity\nin the normal integration of consciousness, memory, identity, emotion, perception, body\nrepresentation, motor control, and behavior. Dissociative symptoms can potentially dis-\nrupt every area of psychological functioning. This chapter includes dissociative identity\ndisorder, dissociative amnesia, depersonalization/derealization disorder, other specified\ndissociative disorder, and unspecified dissociative disorder.\nDissociative symptoms are experienced as a) unbidden intrusions into awareness and\nbehavior, with accompanying losses of continuity in subjective experience (i.e., \u2018\u2018positive\u2019\u2019\ndissociative symptoms such as fragmentation of identity, depersonalization, and dereal-\nization) and/or b) inability to access inform ation or to control ment al functions that nor-\nmally are readily amenable to access or contro l (i.e., \u201cnegative\u2019\u2019 dissociative symptoms such\nas amnesia).\nThe dissociative disorders are frequently found in the af termath of trauma, and many\nof the symptoms, including embarrassment an d confusion about the symptoms or a desire\nto hide them, are influenced by the proximity to trauma. In DSM-5, the dissociative disor-\nders are placed next to, but are not part of, the trauma- and stressor-r elated disorders, re-\nflecting the close relationship between these di agnostic classes. Both acute stress disorder\nand posttraumatic stress disorder contain di ssociative symptoms, such as amnesia, flash-\nbacks, numbing, and depersonalization/derealization.\nDepersonalization/derealization disorder is characterized by clinically significant persis-\ntent or recurrent depersonalizat ion (i.e., experiences of unreality or detachment from one\u2019s", "source": "dsm5.pdf"} {"id": "53e8e2f2eea8-1", "page_content": "mind, self, or body) and/or derealization (i.e ., experiences of unreality or detachment from\none\u2019s surroundings). These alte rations of experience are accompanied by intact reality\ntesting. There is no evidence of any distin ction between individuals with predominantly\ndepersonalization versus derealization sympto ms. Therefore, individuals with this disor-\nder can have depersonalizatio n, derealization, or both.\nDissociative amnesia is characterized by an inability to recall autobiographical informa-\ntion. This amnesia may be localized (i.e., an even t or period of time), selective (i.e., a specific\naspect of an event), or generali zed (i.e., identity and life history). Dissociative amnesia is fun-\ndamentally an inability to recall autobiographic al information that is inconsistent with nor-\nmal forgetting. It may or may not involve purp oseful travel or bewildered wandering (i.e.,\nfugue). Although some individual s with amnesia promptly notice that they have \u201clost time\u201d\nor that they have a gap in their memory, most individuals with dissocia tive disorders are ini-\ntially unaware of their amnesias. For them, aw areness of amnesia occu rs only when personal\nidentity is lost or when circumstances make these individuals awar e that autobiographical\ninformation is missing (e.g., wh en they discover evidence of events they cannot recall or\nwhen others tell them or ask th em about events they cannot reca ll). Until and unless this hap-\npens, these individuals have \u201camnesia for their amnesia.\u201d Amnesia is experienced as an es-\nsential feature of dissociative amnesia; individuals may experience localized or selective", "source": "dsm5.pdf"} {"id": "53e8e2f2eea8-2", "page_content": "sential feature of dissociative amnesia; individuals may experience localized or selective\namnesia most commonly, or generalized amnesia rarely. Dissociative fugue is rare in per-\nsons with dissociative am nesia but common in dissoc iative identity disorder.\nDissociative identity disorder is characterized by a) the presence of two or more distinct\npersonality states or an experi ence of possession and b) recurrent episodes of amnesia. The", "source": "dsm5.pdf"} {"id": "90c3248e86fa-0", "page_content": "292 Dissociative Disorders\nfragmentation of identity may vary with culture (e.g., possession-form presentations) and cir-\ncumstance. Thus, individuals ma y experience discontinuities in identity and memory that\nmay not be immediately evident to others or are obscured by attempts to hide dysfunction. In-\ndividuals with dissociative identity disorder experience a) recurrent, inexplicable intrusions\ninto their conscious functioning and sense of se lf (e.g., voices; dissociated actions and speech;\nintrusive thoughts, emotions, and im pulses), b) alterations of sense of self (e.g., attitudes, pref-\nerences, and feeling like one\u2019s body or actions are not one\u2019s own), c) odd changes of perception\n(e.g., depersonalization or derealization, such as feeling deta ched from one\u2019s body while cut-\nting), and d) intermittent functional neurolog ical symptoms. Stress often produces transient\nexacerbation of dissociative symptoms that makes them more evident.\nThe residual category of other specified disso ciative disorder has seven examples: chronic\nor recurrent mixed dissociative symptoms that approach, but fall short of, the diagnostic cri-\nteria for dissociative identity disorder; dissociative states secondary to brainwashing or\nthought reform; two acute presentations, of less than 1 month\u2019s duration, of mixed dissociative\nsymptoms, one of which is also marked by the presence of psychotic symptoms; and three sin-\ngle-symptom dissociative presentations\u2014dissociat ive trance, dissociative stupor or coma, and\nGanser\u2019s syndrome (the giving of approximate and vague answers). \nDissociative Identity Disorder\nDiagnostic Criteria 300.14 (F44.81)\nA. Disruption of identity characterized by two or more distinct personality states, which", "source": "dsm5.pdf"} {"id": "90c3248e86fa-1", "page_content": "A. Disruption of identity characterized by two or more distinct personality states, which\nmay be described in some cultures as an experience of possession. The disruption in\nidentity involves marked discontinuity in sense of self and sense of agency, accompa-\nnied by related alterations in affect, behavior, consciousness, memory, perception,\ncognition, and/or sensory-motor functioning. These signs and symptoms may be ob-\nserved by others or reported by the individual. \nB. Recurrent gaps in the recall of everyday events, important personal information, and/\nor traumatic events that are inconsistent with ordinary forgetting.\nC. The symptoms cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning. \nD. The disturbance is not a normal part of a broadl y accepted cultural or religious practice.\nNote: In children, the symptoms are not better explained by imaginary playmates or\nother fantasy play.\nE. The symptoms are not attributable to the physiological effects of a substance (e.g.,\nblackouts or chaotic behavior during alcohol intoxication) or anot her medical condition\n(e.g., complex partial seizures).\nDiagnostic Features \nThe defining feature of dissocia tive identity disorder is the presence of two or more dis-\ntinct personality states or an experience of possession (Criterion A). The overtness or\ncovertness of these personality states, howeve r, varies as a function of psychological\nmotivation, current level of st ress, culture, internal conflicts and dynamics, and emotional\nresilience. Sustained periods of identity di sruption may occur when psychosocial pres-\nsures are severe and/or prolonged. In many possession-form cases of dissociative identity\ndisorder, and in a small proportion of non-po ssession-form cases, manifestations of alter-", "source": "dsm5.pdf"} {"id": "90c3248e86fa-2", "page_content": "nate identities are highly ove rt. Most individuals with non-possession-for m dissociative\nidentity disorder do not overtly display their discontinuity of identity for long periods of\ntime; only a small minority present to clinical attention wi th observable alternation of", "source": "dsm5.pdf"} {"id": "23a792105fa6-0", "page_content": "Dissociative Identity Disorder 293\nidentities. When alternate personality states are not directly observ ed, the disorder can be\nidentified by two clusters of symptoms: 1) sudden alterations or discontinuities in sense of\nself and sense of agency (Criterion A), and 2) recurrent dissociative amnesias (Criterion B).\nCriterion A symptoms are related to disconti nuities of experience that can affect any\naspect of an individual\u2019s functioning. Indivi duals with dissociative identity disorder may\nreport the feeling that they have suddenly become depersonalized observers of their\n\u201cown\u201d speech and actions, which they may feel po werless to stop (sense of self). Such in-\ndividuals may also report perceptions of voices (e.g., a child\u2019s voice; crying; the voice of a\nspiritual being). In some case s, voices are experienced as multiple, perplexing, indepen-\ndent thought streams over which the individual experiences no contro l. Strong emotions,\nimpulses, and even speech or other actions ma y suddenly emerge, without a sense of per-\nsonal ownership or control (sense of agency). These emotions and impulses are frequently\nreported as ego-dystonic and puzzling. Atti tudes, outlooks, and personal preferences\n(e.g., about food, activities, dress) may sudde nly shift and then shift back. Individuals may\nreport that their bodies feel different (e.g., like a small child, like the opposite gender, huge\nand muscular). Alterations in sense of self and loss of personal agency may be accompa-\nnied by a feeling th at these attitudes, emotions, an d behaviors\u2014even one\u2019s body\u2014are\n\u201cnot mine\u201d and/or are \u201cnot under my control.\u201d Although most Criterion A symptoms are", "source": "dsm5.pdf"} {"id": "23a792105fa6-1", "page_content": "\u201cnot mine\u201d and/or are \u201cnot under my control.\u201d Although most Criterion A symptoms are\nsubjective, many of these sudden discontinuitie s in speech, affect, and behavior can be wit-\nnessed by family, friends, or the clinician. Non-epileptic seizures and other conversion\nsymptoms are prominent in some presentation s of dissociative identity disorder, espe-\ncially in some non-Western settings.\nThe dissociative amnesia of in dividuals with dissociative id entity disorder manifests in\nthree primary ways: as 1) gaps in remote me mory of personal life events (e.g., periods of\nchildhood or adolescence; some important lif e events, such as the death of a grandparent,\ngetting married, giving birth); 2) lapses in dependable memory (e.g., of what happened\ntoday, of well-learned skills such as how to do their job, use a computer, read, drive); and\n3) discovery of evidence of their everyday ac tions and tasks that they do not recollect do-\ning (e.g., finding unexplained objects in thei r shopping bags or am ong their possessions;\nfinding perplexing writings or drawings that they must have created; discovering injuries;\n\u201ccoming to\u201d in the midst of doing something). Dissociative fugues, wherein the person\ndiscovers dissociated travel, are common. Thus, individuals with dissociative identity dis-\norder may report that they have suddenly found themselves at the beach, at work, in a night-\nclub, or somewhere at home (e.g., in the clos et, on a bed or sofa, in the corner) with no\nmemory of how they came to be there. Amnesia in individuals with dissociative identity dis-\norder is not limited to stressful or traumati c events; these individuals often cannot recall", "source": "dsm5.pdf"} {"id": "23a792105fa6-2", "page_content": "order is not limited to stressful or traumati c events; these individuals often cannot recall\neveryday events as well.\nIndividuals with dissociative identity disorder vary in their awareness and attitude to-\nward their amnesias. It is common for these in dividuals to minimize their amnestic symp-\ntoms. Some of their amnestic behaviors may be apparent to others\u2014as when these persons\ndo not recall somethin g they were witnessed to have done or said, when they cannot\nremember their own name, or when they do no t recognize their spouse, children, or close\nfriends.\nPossession-form identities in dissociative identity disorder typically manifest as be-\nhaviors that appear as if a \u201cspirit,\u201d supernatur al being, or outside person has taken control,", "source": "dsm5.pdf"} {"id": "18ea8dfca660-0", "page_content": "friends.\nPossession-form identities in dissociative identity disorder typically manifest as be-\nhaviors that appear as if a \u201cspirit,\u201d supernatur al being, or outside person has taken control,\nsuch that the individual begins speaking or acting in a distinctly different manner. For ex-\nample, an individual\u2019s beha vior may give the appearance that her identity has been\nreplaced by the \u201cghost\u201d of a girl who co mmitted suicide in the same community years\nbefore, speaking and acting as though she were still alive. Or an individual may be \u201ctaken\nover\u201d by a demon or deity, re sulting in profound impairment , and demanding that the in-\ndividual or a relative be punished for a past act, followed by more su btle periods of iden-\ntity alteration. However, the majority of possession states around the world are normal,\nusually part of spiritual practice, and do not meet criteria for dissociative identity disor-", "source": "dsm5.pdf"} {"id": "86dde35f3757-0", "page_content": "294 Dissociative Disorders\nder. The identities that arise during possessio n-form dissociative identity disorder present\nrecurrently, are unwanted and involuntary, cause clinically significant distress or impair-\nment (Criterion C), and are not a normal part of a broadly accepted cultural or religious\npractice (Criterion D).\nAssociated Features Supporting Diagnosis \nIndividuals with di ssociative identity disorder typically present with comorbid depression,\nanxiety, substance abuse, self-injury, non-epileptic seizures, or another common symp-\ntom. They often conceal, or are not fully aw are of, disruptions in consciousness, amnesia,\nor other dissociative symptoms. Many individu als with dissociative identity disorder re-\nport dissociative flashbacks during which they undergo a sensory reliving of a previous\nevent as though it were occurring in the presen t, often with a change of identity, a partial\nor complete loss of contact wi th or disorientation to current reality during the flashback,\nand a subsequent amnesia for the content of the flashback. Individuals with the disorder\ntypically report multiple types of interpersonal maltreatment during childhood and adult-\nhood. Nonmaltreatment forms of overwhelming early life events, such as multiple long,\npainful, early-life medical pr ocedures, also may be reported. Self-mutilation and suicidal\nbehavior are frequent. On standardized meas ures, these individuals report higher levels\nof hypnotizability and dissociativity compared with other clinical groups and healthy con-\ntrol subjects. Some individuals experience transient psychotic phenomena or episodes.\nSeveral brain regions have been implicated in the pathophysiology of dissociative identity\ndisorder, including the orbito frontal cortex, hippocampus, parahippocampal gyrus, and\namygdala.\nPrevalence\nThe 12-month preval ence of dissociative id entity disorder among adults in a small U.S.", "source": "dsm5.pdf"} {"id": "86dde35f3757-1", "page_content": "community study was 1.5%. The prevalence ac ross genders in that study was 1.6% for\nmales and 1.4% for females. \nDevelopment and Course\nDissociative identity disorder is associated with overwhelming experiences, traumatic\nevents, and/or abuse oc curring in childhood. The full disorder may first manifest at al-\nmost any age (from earliest childhood to late life). Dissociation in children may generate\nproblems with memory, concentration, attach ment, and traumatic play . Nevertheless, chil-\ndren usually do not present with identity changes; instead they present primarily with over-\nlap and interference among mental states (Cri terion A phenomena), with symptoms related\nto discontinuities of experience. Sudden changes in identity during adolescence may ap-\npear to be just adolescent turmoil or the ea rly stages of another mental disorder. Older\nindividuals may present to treatment with what appear to be late-life mood disorders, ob-\nsessive-compulsive disorder, paranoia, psycho tic mood disorders, or even cognitive dis-\norders due to dissociative amnesia. In some cases, disruptive affects and memories may\nincreasingly intrude into aw areness with advancing age. \nPsychological decompensation and overt change s in identity may be triggered by 1) re-\nmoval from the traumatizing situation (e.g., through leaving home); 2) the individual\u2019s\nchildren reaching the same age at which the in dividual was originally abused or trauma-\ntized; 3) later traumatic experiences, even seemingly inconsequential ones, like a minor\nmotor vehicle accident; or 4) th e death of, or the onset of a fatal illness in, their abuser(s).\nRisk and Prognostic Factors \nEnvironmental. Interpersonal physical and sexual abus e is associated with an increased", "source": "dsm5.pdf"} {"id": "86dde35f3757-2", "page_content": "Environmental. Interpersonal physical and sexual abus e is associated with an increased\nrisk of dissociative identity disorder. Prev alence of childhood abuse and neglect in the", "source": "dsm5.pdf"} {"id": "a4f3ea8dd64c-0", "page_content": "Dissociative Identity Disorder 295\nUnited States, Canada, and Europe among th ose with the disorder is about 90%. Other\nforms of traumatizing experiences, includin g childhood medical and surgical procedures,\nwar, childhood prostitution, and terrorism, have been reported.\nCourse modifiers. Ongoing abuse, later-life retrauma tization, comorbid ity with mental\ndisorders, severe medical illness, and delay in appropriate treatment are associated with\npoorer prognosis.\nCulture-Related Diagnostic Issues \nMany features of dissociative identity disord er can be influenced by the individual\u2019s cul-\ntural background. Individuals with this disorder may pres ent with prominent medically\nunexplained neurological symptoms, such as no n-epileptic seizures, paralyses, or sensory\nloss, in cultural settings where such symptoms are common. Similarly, in settings where\nnormative possession is common (e.g., rural areas in the developing world, among certain\nreligious groups in the United States and Euro pe), the fragmented identities may take the\nform of possessing spirits, de ities, demons, animals, or myth ical figures. Acculturation or\nprolonged intercultural contact may shape the characteristics of the other identities (e.g.,\nidentities in India may speak English exclu sively and wear Western clothes). Possession-\nform dissociative identity diso rder can be distinguished from culturally accepted posses-\nsion states in that the former is involunta ry, distressing, uncontro llable, and often recur-\nrent or persistent; involves conflict between the individual and his or her surrounding\nfamily, social, or work milieu; and is manifest ed at times and in places that violate the\nnorms of the culture or religion. \nGender-Related Diagnostic Issues\nFemales with dissociative identity disorder pr edominate in adult clinical settings but not", "source": "dsm5.pdf"} {"id": "a4f3ea8dd64c-1", "page_content": "Females with dissociative identity disorder pr edominate in adult clinical settings but not\nin child clinical settings. Adult males with dissociative identity disorder may deny their\nsymptoms and trauma histories, and this can lead to el evated rates of false negative di-\nagnosis. Females with dissociative identity di sorder present more frequently with acute\ndissociative states (e.g., flashb acks, amnesia, fugue, function al neurological [conversion]\nsymptoms, hallucinations, self-mutilation). Ma les commonly exhibit more criminal or vi-\nolent behavior than females; among males, comm on triggers of acute dissociative states in-\nclude combat, prison conditions, and physical or sexual assaults.\nSuicide Risk\nOver 70% of outpatients with dissociative id entity disorder have attempted suicide; mul-\ntiple attempts are common, and other self-inj urious behavior is frequent. Assessment of\nsuicide risk may be complicated when there is amnesia for past suicid al behavior or when\nthe presenting identity does no t feel suicidal and is unaware that other dissociated iden-\ntities do. \nFunctional Consequences of \nDissociative Identity Disorder\nImpairment varies widely, from apparently minimal (e.g., in high-functioning profession-\nals) to profound. Regardless of level of disability, individuals with dissociative identity\ndisorder commonly minimize the impact of their dissociative an d posttraumatic symp-\ntoms. The symptoms of higher-functioning in dividuals may impair their relational, mar-\nital, family, and parenting functions more th an their occupational and professional life\n(although the latter also may be affected). With appropriate treatment, many impaired in-\ndividuals show marked improvement in occupational and personal functioning. How-\never, some remain highly impaired in most ac tivities of living. These individuals may only", "source": "dsm5.pdf"} {"id": "a4f3ea8dd64c-2", "page_content": "ever, some remain highly impaired in most ac tivities of living. These individuals may only\nrespond to treatment very slowly, with gr adual reduction in or improved tolerance of", "source": "dsm5.pdf"} {"id": "43d9ae0f5ec7-0", "page_content": "296 Dissociative Disorders\ntheir dissociative and posttraumatic sympto ms. Long-term supportive treatment may\nslowly increase these individuals\u2019 ability to manage their symptoms and decrease use of\nmore restrictive levels of care. \nDifferential Diagnosis \nOther specified dissociative disorder. The core of dissociative identity disorder is the\ndivision of identity, with recurrent disruption of conscious functioning and sense of self.\nThis central feature is sh ared with one form of other specified dissociative disorder, which\nmay be distinguished from dissociative identity disorder by the presence of chronic or re-\ncurrent mixed dissociative symptoms that do not meet Criterion A for dissociative identity\ndisorder or are not accomp anied by recurrent amnesia.\nMajor depressive disorder. Individuals with dissociative identity disorder are often de-\npressed, and their symptoms may appear to m eet the criteria for a major depressive episode.\nRigorous assessment indicates that this depression in some cases does not meet full criteria for\nmajor depressive disorder. Othe r specified depressive disorder in individual s with dissocia-\ntive identity disorder often has an importan t feature: the depressed mood and cognitions fluc-\ntuate because they are experienced in some identity states but not others. \nBipolar disorders. Individuals with dissociative iden tity disorder are often misdiag-\nnosed with a bipolar disorder, mo st often bipolar II disorder. The relatively rapid shifts in\nmood in individuals with this disorder\u2014typica lly within minutes or hours, in contrast to\nthe slower mood changes typically seen in individuals with bipolar disorders\u2014are due to\nthe rapid, subjective shifts in mood commonly reported acro ss dissociative states, some-\ntimes accompanied by fluctuation in levels of activation. Furtherm ore, in dissociative\nidentity disorder, elevated or depressed mood may be displayed in conjunction with overt", "source": "dsm5.pdf"} {"id": "43d9ae0f5ec7-1", "page_content": "identity disorder, elevated or depressed mood may be displayed in conjunction with overt\nidentities, so one or the other mood may pred ominate for a relatively long period of time\n(often for days) or may shift within minutes.\nPosttraumatic stress disorder. Some traumatized individua ls have both posttraumatic\nstress disorder (PTSD) and dissociative identity disorder. Accordingly, it is crucial to dis-\ntinguish between individuals with PTSD only an d individuals who have both PTSD and\ndissociative identity disorder. This different ial diagnosis requires that the clinician estab-\nlish the presence or absence of dissociative sy mptoms that are not characteristic of acute\nstress disorder or PTSD. Some individuals wi th PTSD manifest diss ociative symptoms that\nalso occur in dissociative identity disorder: 1) amnesia for some aspe cts of trauma, 2) dis-\nsociative flashbacks (i.e., reliving of the trauma, with reduced awareness of one\u2019s current\norientation), and 3) symptoms of intrusion an d avoidance, negative alterations in cogni-\ntion and mood, and hyperarousal that are focu sed around the traumatic event. On the other\nhand, individuals with dissociative identity disorder manifest dissociative symptoms that\nare not a manifestation of PTSD: 1) amnesias for many everyday (i.e., nontraumatic) events,\n2) dissociative flashbacks that may be followe d by amnesia for the content of the flashback,\n3) disruptive intrusions (unrelated to trau matic material) by dissociated identity states\ninto the individual\u2019s sense of self and agency, and 4) infrequent, full-blown changes\namong different identity states.\nPsychotic disorders. Dissociative identity disorder may be confused with schizophre-", "source": "dsm5.pdf"} {"id": "43d9ae0f5ec7-2", "page_content": "Psychotic disorders. Dissociative identity disorder may be confused with schizophre-\nnia or other psychotic disorders. The personified, internally communicative inner voices\nof dissociative identity di sorder, especially of a child (e.g., \u201cI hear a little girl crying in a\ncloset and an angry man yelling at her\u201d), may be mistaken for psychotic hallucinations.\nDissociative experiences of identity fragmentat ion or possession, and of perceived loss of", "source": "dsm5.pdf"} {"id": "eaec0d5512d4-0", "page_content": "closet and an angry man yelling at her\u201d), may be mistaken for psychotic hallucinations.\nDissociative experiences of identity fragmentat ion or possession, and of perceived loss of\ncontrol over thoughts, feelings, impulses, and acts, may be confused with signs of formal\nthought disorder, such as thought insertion or withdrawal. Individu als with dissociative\nidentity disorder may also report visual, tact ile, olfactory, gustatory, and somatic halluci-\nnations, which are usually related to posttrau matic an d dissociative factors, such as partial", "source": "dsm5.pdf"} {"id": "f374808321d0-0", "page_content": "Dissociative Identity Disorder 297\nflashbacks. Individuals with dissociative iden tity disorder experience these symptoms as\ncaused by alternate identities, do not have delusional explanations for the phenomena,\nand often describe the symptoms in a personified way (e.g., \u201cI feel like someone else wants\nto cry with my eyes\u201d). Persecutory and derogato ry internal voices in dissociative identity\ndisorder associated with depressive symptoms may be misdiagnosed as major depression\nwith psychotic features. Chaotic identity change and acute intrusions that disrupt thought\nprocesses may be distinguished from brief psychotic disorder by the predominance of dis-\nsociative symptoms and amnesia for the episode, and diagnostic evaluation after cessation\nof the crisis can help confirm the diagnosis. \nSubstance/medication-induced disorders. Symptoms associated with the physiological\neffects of a substance can be distinguished from dissociative identity disorder if the sub-\nstance in question is judged to be et iologically related to the disturbance.\nPersonality disorders. Individuals with dissociative identity disorder often present identi-\nties that appear to encapsulat e a variety of severe personality disorder features, suggesting a\ndifferential diagnosis of personality disorder, especially of the borderline type. Importantly,\nhowever, the individual\u2019s longitudinal variabi lity in personality style (due to inconsistency\namong identities) differs from the pervasive an d persistent dysfunctio n in affect management\nand interpersonal relationships typical of those with personality disorders.\nConversion disorder (functional neurological symptom disorder). This disorder may be\ndistinguished from dissociative identity disord er by the absence of an identity disruption\ncharacterized by two or more distinct personality states or an experience of possession.\nDissociative amnesia in conver sion disorder is more limited and circumscribed (e.g., am-\nnesia for a non-epileptic seizure).", "source": "dsm5.pdf"} {"id": "f374808321d0-1", "page_content": "nesia for a non-epileptic seizure).\nSeizure disorders. Individuals with dissociative identity disorder may present with sei-\nzurelike symptoms and behaviors that resemb le complex partial seizures with temporal\nlobe foci. These include d\u00e9j\u00e0 vu, jamais vu, de personalization, derea lization, out-of-body\nexperiences, amnesia, disruptions of consci ousness, hallucinations, and other intrusion\nphenomena of sensation, affect, and thought . Normal electroencep halographic findings,\nincluding telemetry, differenti ate non-epileptic seiz ures from the seizurelike symptoms of\ndissociative identity disorder. Also, individua ls with dissociative identity disorder obtain\nvery high dissociation scores, whereas indivi duals with complex partial seizures do not.\nFactitious disorder and malingering. Individuals who feign dissociative identity disor-\nder do not report the subtle symptoms of intr usion characteristic of the disorder; instead\nthey tend to overreport well-publicized symp toms of the disorder, such as dissociative\namnesia, while underreporting less-publicized comorbid symptoms, such as depression.\nIndividuals who feign dissociative identity d isorder tend to be relatively undisturbed by\nor may even seem to enjoy \u201chaving\u201d the diso rder. In contrast, individuals with genuine\ndissociative identity disorder tend to be ashamed of and overwhelmed by their symptoms\nand to underreport their symptoms or deny th eir condition. Sequential observation, cor-\nroborating history, and intensive psycho metric and psychological assessment may be\nhelpful in assessment.\nIndividuals who malinger dissociative identity disorder usually create limited, stereo-\ntyped alternate identities, with feigned amnesia, related to the events for which gain is", "source": "dsm5.pdf"} {"id": "f374808321d0-2", "page_content": "typed alternate identities, with feigned amnesia, related to the events for which gain is\nsought. For example, they may present an \u201call-good\u201d identity and an \u201call-bad\u201d identity in\nhopes of gaining exculpation for a crime.\nComorbidity\nMany individuals with dissociative identity disorder present with a comorbid disorder. If", "source": "dsm5.pdf"} {"id": "cc4a74297ec6-0", "page_content": "hopes of gaining exculpation for a crime.\nComorbidity\nMany individuals with dissociative identity disorder present with a comorbid disorder. If\nnot assessed and treated specifically for the dissociative disorder, these individuals often\nreceive prolonged treatment for the comorbid diagnosis only, with limited overall treat-\nment response and resultant demoralization, and disability.", "source": "dsm5.pdf"} {"id": "55dabb4189c3-0", "page_content": "298 Dissociative Disorders\nIndividuals with dissociative identity disorder usually ex hibit a large number of co-\nmorbid disorders. In particular, most develo p PTSD. Other disorders that are highly co-\nmorbid with dissociative identity disorder include depressive di sorders, trauma- and\nstressor-related disorders, personality diso rders (especially avoidant and borderline per-\nsonality disorders), conversion disorder (functional neurological symptom disorder),\nsomatic symptom disorder, eating disorders, substance-related disorders, obsessive-\ncompulsive disorder, and sleep disorders. Dissociative alterations in identity, memory,\nand consciousness may affect the sympto m presentation of comorbid disorders.\nDissociative Amnesia\nDiagnostic Criteria 300.12 (F44.0)\nA. An inability to recall important autobiographical information, usually of a traumatic or\nstressful nature, that is inconsistent with ordinary forgetting.\nNote: Dissociative amnesia most often consists of localized or selective amnesia for a\nspecific event or events; or generalized amnesia for identity and life history.\nB. The symptoms cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nC. The disturbance is not attributable to the physiological effects of a substance (e.g., al-\ncohol or other drug of abuse, a medication) or a neurological or other medical condition\n(e.g., partial complex seizures, transient global amnesia, sequelae of a closed head in-\njury/traumatic brain injury, other neurological condition).\nD. The disturbance is not better explained by dissociative identity disorder, posttraumatic\nstress disorder, acute stress disorder, somatic symptom disorder, or major or mild neu-\nrocognitive disorder.\nCoding note: The code for dissociative amnesia without dissociative fugue is 300.12", "source": "dsm5.pdf"} {"id": "55dabb4189c3-1", "page_content": "(F44.0). The code for dissociative amnesia with dissociative fugue is 300.13 (F44.1).\nSpecify if:\n300.13 (F44.1) With dissociative fugue: Apparently purposeful travel or bewildered\nwandering that is associated with amnesia for identity or for other important autobio-\ngraphical information.\nDiagnostic Features\nThe defining characteristic of dissociative amnesia is an inability to recall important auto-\nbiographical information that 1) should be su ccessfully stored in me mory and 2) ordinar-\nily would be readily remembered (Criterion A). Dissociative amnesia differs from the\npermanent amnesias due to neurob iological damage or toxicity that prevent memory stor-\nage or retrieval in that it is always potentially reversible because the memory has been suc-\ncessfully stored. \nLocalized amnesia, a failure to recall events during a circumscribed period of time, is the\nmost common form of dissocia tive amnesia. Localized amnesi a may be broader than am-\nnesia for a single traumatic event (e.g., months or years associated with child abuse or in-\ntense combat). In selective amnesia, the individual can recall some , but not all, of the events\nduring a circumscribed period of time. Thus, the individual may remember part of a trau-\nmatic event but not other parts. Some individu als report both localized and selective am-\nnesias. \nGeneralized amnesia, a complete loss of memory for one\u2019 s life history, is rare. Individuals\nwith generalized amnesia may forget personal identity. Some lose previous knowledge\nabout the world (i.e., semantic knowledge) and can no longer access well-learned skills", "source": "dsm5.pdf"} {"id": "c35682d3f5a6-0", "page_content": "Dissociative Amnesia 299\n(i.e., procedural knowledge). Generalized amnesia has an acute onset; the perplexity, dis-\norientation, and purposeless wandering of individuals with generalized amnesia usually\nbring them to the attention of the police or psychiatric emergency services. Generalized\namnesia may be more common among combat veterans, sexual assault victims, and indi-\nviduals experiencing extreme emotional stress or conflict. \nIndividuals with dissociative amnesia are fr equently unaware (or only partially aware)\nof their memory problems. Many, especially those with localized am nesia, minimize the\nimportance of their memory loss and may be come uncomfortable when prompted to ad-\ndress it. In systematized amnesia, the individual loses memory for a specific category of in-\nformation (e.g., all memories relating to on e\u2019s family, a particular person, or childhood\nsexual abuse). In continuous amnesia, an individual forgets each new event as it occurs.\nAssociated Features Supporting Diagnosis\nMany individuals with dissociative amnesia are chronically impaired in their ability to\nform and sustain satisfactory relationships. Histories of trauma, child abuse, and victim-\nization are common. Some indivi duals with dissociative amnesia report dissociative flash-\nbacks (i.e., behavioral reexperiencing of trau matic events). Many have a history of self-\nmutilation, suicide attempts, and other high -risk behaviors. Depressive and functional\nneurological symptoms are common, as are depersonalization, auto-hypnotic symptoms,\nand high hypnotizability. Sexual dysfunctions are common. Mild traumatic brain injury\nmay precede dissociative amnesia. \nPrevalence\nThe 12-month prevalence for dissociative amnesia among ad ults in a small U.S. commu-", "source": "dsm5.pdf"} {"id": "c35682d3f5a6-1", "page_content": "nity study was 1.8% (1.0% fo r males; 2.6% for females). \nDevelopment and Course\nOnset of generalized amnesia is usually sudden . Less is known about the onset of localized\nand selective amnesias because these amnesias ar e seldom evident, even to the individual.\nAlthough overwhelming or intolerable events typically precede localized amnesia, its on-\nset may be delayed for ho urs, days, or longer. \nIndividuals may report multiple episodes of dissociative amnesia. A single episode\nmay predispose to future episodes. In between episodes of amnesia, the individual may or\nmay not appear to be acutely symptomatic. Th e duration of the forgotten events can range\nfrom minutes to decades. Some episodes of dissociative amnesia resolve rapidly (e.g.,\nwhen the person is removed from combat or some other stressful situation), whereas other\nepisodes persist for long periods of time. So me individuals may grad ually recall the dis-\nsociated memories years later. Dissociative capacities may decline with age, but not al-\nways. As the amnesia remits, there may be considerable distress, su icidal behavior, and\nsymptoms of posttraumatic stress disorder (PTSD). \nDissociative amnesia has been observed in young children, adolescents, and adults.\nChildren may be the most difficult to evaluate because they often have difficulty under-\nstanding questions about amnesia, and interviewers may find it difficult to formulate child-\nfriendly questions about memory and amnesia. Observations of apparent dissociative am-\nnesia are often difficult to differentiate from inattention, absorption , anxiety, oppositional\nbehavior, and learning disorders. Reports fr om several different sources (e.g., teacher,\ntherapist, case worker) may be needed to diagnose amnesia in children.", "source": "dsm5.pdf"} {"id": "c35682d3f5a6-2", "page_content": "therapist, case worker) may be needed to diagnose amnesia in children. \nRisk and Prognostic Factors \nEnvironmental. Single or repeated traumatic experiences (e.g., war, childhood maltreat-\nment, natural disaster, internment in conc entration camps, genocide) are common ante-", "source": "dsm5.pdf"} {"id": "bb37797d12fc-0", "page_content": "300 Dissociative Disorders\ncedents. Dissociative amnesia is more likely to occur with 1) a greater number of adverse\nchildhood experiences, particularly physical and/or sexual abuse, 2) interpersonal vio-\nlence; and 3) increased severity, frequency, and violence of the trauma. \nGenetic and physiological. There are no genetic studies of dissociative amnesia. Stud-\nies of dissociation report significant genetic an d environmental factors in both clinical and\nnonclinical samples. \nCourse modifiers. Removal from the traumatic circumstances underlying the dissociative\namnesia (e.g., combat) may bring about a rapid re turn of memory. The memory loss of indi-\nviduals with dissociative fugue may be particularly refractory. Onset of PTSD symptoms may\ndecrease localized, selective, or systematized amnesia. The returning memory, however, may\nbe experienced as flashbacks that alternate wi th amnesia for the content of the flashbacks. \nCulture-Related Diagnostic Issues\nIn Asia, the Middle East, and Latin America, non-epileptic seizures and other functional\nneurological symptoms may accompany dissociat ive amnesia. In cultur es with highly re-\nstrictive social traditions, th e precipitants of dissociative amnesia often do not involve\nfrank trauma. Instead, the amnesia is preceded by severe psychological stresses or con-\nflicts (e.g., marital conflict, other family d isturbances, attachment problems, conflicts due\nto restriction or oppression). \nSuicide Risk\nSuicidal and other self-destructive behavior s are common in individuals with dissociative\namnesia. Suicidal behavior may be a particular risk when the amnesia remits suddenly\nand overwhelms the individual with intolerable memories.\nFunctional Consequences of Dissociative Amnesia", "source": "dsm5.pdf"} {"id": "bb37797d12fc-1", "page_content": "Functional Consequences of Dissociative Amnesia \nThe impairment of individuals with localized, selective, or systemat ized dissociative am-\nnesia ranges from limited to severe. Individu als with chronic generalized dissociative am-\nnesia usually have impairment in all aspects of functioning. Even when these individuals\n\u201cre-learn\u201d aspects of their life history, au tobiographical memory remains very impaired.\nMost become vocationally an d interpersonally disabled. \nDifferential Diagnosis\nDissociative identity disorder. Individuals with dissociati ve amnesia may report de-\npersonalization and auto-hypnotic symptoms. In dividuals with dissociative identity dis-\norder report pervasive disconti nuities in sense of self and agency, accompanied by many\nother dissociative symptoms. The amnesias of individuals with localized, selective, and/\nor systematized dissociative amnesias are relatively stable. Amnesias in dissociative iden-\ntity disorder include amnesia for everyday events, finding of unexplained possessions,\nsudden fluctuations in skills and knowledge, ma jor gaps in recall of life history, and brief\namnesic gaps in interpersonal interactions.\nPosttraumatic stress disorder. Some individuals with PTSD cannot recall part or all of\na specific traumatic event (e.g., a rape victim with depersonalization and/or derealization\nsymptoms who cannot recall most events for the entire day of the rape). When that amne-\nsia extends beyond the immediat e time of the trauma, a comorbid diagnosis of dissociative\namnesia is warranted. \nNeurocognitive disorders. In neurocognitive disorders, memory loss for personal infor-\nmation is usually embedded in cognitive, lingu istic, affective, atte ntional, and behavioral", "source": "dsm5.pdf"} {"id": "97a14479287f-0", "page_content": "Dissociative Amnesia 301\ndisturbances. In dissociative amnesia, memory deficits are primarily for autobiographical\ninformation; intellectual and co gnitive abilities are preserved. \nSubstance-related disorders. In the context of repeated intoxication with alcohol or\nother substances/medications, there may be episod es of \u201cblack outs\u201d or periods for which the\nindividual has no memory. To aid in distingu ishing these episodes from dissociative am-\nnesia, a longitudinal history noting that the amnestic episodes occur only in the context of\nintoxication and do no t occur in other situations would help identify the source as sub-\nstance-induced; however the distinction may be difficult when the individual with dis-\nsociative amnesia may also misuse alcohol or other substances in the context of stressful\nsituations that may also exac erbate dissociative symptoms. Some individuals with comor-\nbid dissociative amnesia and substance use disorders will at tribute their memory prob-\nlems solely to the substance use. Prolonged us e of alcohol or other substances may result in\na substance-induced neurocognitive disorder that may be associated with impaired cog-\nnitive function, but in this co ntext the protracted history of substance use and the persis-\ntent deficits associated with the neurocognitive disorder would serve to distinguish it\nfrom dissociative amnesia, wher e there is typically no evidence of persistent impairment in\nintellectual functioning.\nPosttraumatic amnesia due to brain injury. Amnesia may occur in th e context of a trau-\nmatic brain injury (TBI) when th ere has been an impact to th e head or other mechanisms of\nrapid movement or displacement of the brain within the skull TBI. Other characteristics of\nTBI include loss of consciousness, disorientati on and confusion, or, in more severe cases,", "source": "dsm5.pdf"} {"id": "97a14479287f-1", "page_content": "neurological signs (e.g., abnormalities on neuroimaging, a new onset of seizures or a marked\nworsening of a preexisting seizure disorder, visual field cuts, anos mia). A neurocognitive\ndisorder attributable to TBI must present either immediately after brain injury occurs or im-\nmediately after the individual recovers consciousness after th e injury, and persist past the\nacute post-injury period. The cognitive presenta tion of a neurocognitive disorder following\nTBI is variable and includes difficulties in the domains of complex attention, executive func-\ntion, learning and memory as well as slowed speed of information processing and distur-\nbances in social cognition. Th ese additional features help di stinguish it from dissociative\namnesia. \nSeizure disorders. Individuals with seizure disorders may exhibit complex behavior dur-\ning seizures or post-ictally wi th subsequent amnesia. Some individuals with a seizure disorder\nengage in nonpurposive wandering that is lim ited to the period of seizure activity. Con-\nversely, behavior during a di ssociative fugue is usually purposeful, complex, and goal-\ndirected and may last for days, weeks, or long er. Occasionally, individuals with a seizure dis-\norder will report that earlier autobiographical me mories have been \u201cwiped out\u201d as the seizure\ndisorder progresses. Such memory loss is not associated with traumatic circumstances and ap-\npears to occur randomly. Serial electroencepha lograms usually show abnormalities. Telemet-\nric electroencephalographic monitoring usually shows an association between the episodes of\namnesia and seizure activity. Dissociativ e and epileptic amnesias may coexist.\nCatatonic stupor. Mutism in catatonic stupor may sugg est dissociative amnesia, but fail-", "source": "dsm5.pdf"} {"id": "97a14479287f-2", "page_content": "ure of recall is absent. Other catatonic symptoms (e.g., rigidity, post uring, negativism) are\nusually present.\nFactitious disorder and malingering. There is no test, battery of tests, or set of procedures\nthat invariably distinguishes dissociative am nesia from feigned amnesia. Individuals with\nfactitious disorder or malingering have been noted to continue their deception even during", "source": "dsm5.pdf"} {"id": "b24600f24386-0", "page_content": "that invariably distinguishes dissociative am nesia from feigned amnesia. Individuals with\nfactitious disorder or malingering have been noted to continue their deception even during\nhypnotic or barbiturate-facilitated interviews. Feigned amnesia is more common in individ-\nuals with 1) acute, florid dissociative amnesia; 2) financial, sexual, or legal problems; or 3) a\nwish to escape stressful circumstances. True amnesia can be associated with those same cir-\ncumstances. Many individuals who malinger confess spontane ously or when confronted.", "source": "dsm5.pdf"} {"id": "e7c242697deb-0", "page_content": "302 Dissociative Disorders\nNormal and age-related changes in memory. Memory decrements in major and mild\nneurocognitive disorders differ from those of dissociative amnesia, which are usually as-\nsociated with stressful events and are more specific, extensive, and/or complex.\nComorbidity\nAs dissociative amnesia begins to remit, a wide variety of affective phenomena may sur-\nface: dysphoria, grief, rage, shame, guilt, psychological conf lict and turmoil, and suicidal\nand homicidal ideation, impulses, and acts. These individuals may have symptoms that\nthen meet diagnostic criteria for persistent depressive disorder (dysthymia); major de-\npressive disorder; other specified or unspec ified depressive disord er; adjustment disor-\nder, with depressed mood; or adjustment disorder, with mixed disturbance of emotions\nand conduct. Many individuals with dissociative amnesia develop PTSD at some point\nduring their life, especially when the traumatic antecedent s of their amnesia are brought\ninto conscious awareness. \nMany individuals with dissociative amnesia have symptoms that meet diagnostic cri-\nteria for a comorbid somatic symptom or related disorder (and vice versa), including so-\nmatic symptom disorder and conversion di sorder (functional neurological symptom\ndisorder). Many individuals with dissociative amnesia have symptoms that meet diagnos-\ntic criteria for a personality disorder, especially dependent, avoidant, and borderline. \nDepersonalization/Derealization Disorder\nDiagnostic Criteria 300.6 (F48.1)\nA. The presence of persistent or recurrent experiences of depersonalization, derealiza-\ntion, or both:\n1.Depersonalization: Experiences of unreality, detachment, or being an outside ob-", "source": "dsm5.pdf"} {"id": "e7c242697deb-1", "page_content": "server with respect to one\u2019s thoughts, feelings, sensations, body, or actions (e.g.,\nperceptual alterations, distorted sense of time, unreal or absent self, emotional and/\nor physical numbing).\n2.Derealization: Experiences of unreality or detachment with respect to surround-\nings (e.g., individuals or objects are ex perienced as unreal, dreamlike, foggy, life-\nless, or visually distorted).\nB. During the depersonalization or derealization experiences, reality testing remains intact.\nC. The symptoms cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nD. The disturbance is not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, medication) or another medical condition (e.g., seizures).\nE. The disturbance is not better explained by another mental disorder, such as schizo-\nphrenia, panic disorder, major depressive di sorder, acute stress disorder, posttrau-\nmatic stress disorder, or another dissociative disorder.\nDiagnostic Features\nThe essential features of depe rsonalization/derealization diso rder are persistent or recur-\nrent episodes of depersonalization, derealization, or both. Episodes of depersonalization\nare characterized by a feeling of unreality or detachment from, or unfamiliarity with, one\u2019s\nwhole self or from aspects of the self (Cri terion A1). The indivi dual may feel detached\nfrom his or her entire being (e.g., \u201cI am no on e,\u201d \u201cI have no self\u201d). He or she may also feel\nsubjectively detached from aspects of the self , including feelings (e.g., hypoemotionality:", "source": "dsm5.pdf"} {"id": "ad9da6c352d9-0", "page_content": "Depersonalization/Derealization Disorder 303\n\u201cI know I have feelings but I don\u2019t feel them\u201d), thoughts (e.g., \u201cMy thoughts don\u2019t feel like\nmy own,\u201d \u201chead filled with cotton \u201d), whole body or body parts, or sensations (e.g., touch,\nproprioception, hunger, thirst, libido). There may also be a diminished sense of agency\n(e.g., feeling robotic, like an automaton; lacking control of one\u2019s speech or movements).\nThe depersonalization experience can sometimes be one of a split self, with one part ob-\nserving and one participating, known as an \u201co ut-of-body experience\u201d in its most extreme\nform. The unitary symptom of \u201cdepersonalization\u201d consists of several symptom factors:\nanomalous body experiences (i.e., unreality of the self and perceptual alterations); emo-\ntional or physical numbing; an d temporal distortions with anomalous subjective recall. \nEpisodes of derealization are characterize d by a feeling of unreality or detachment\nfrom, or unfamiliarity with, the world, be it individuals, inanimate objects, or all surround-\nings (Criterion A2). The individual may feel as if he or she were in a fog, dream, or bubble, or\nas if there were a veil or a glass wall between the individual and world around. Surround-\nings may be experienced as artificial, colorles s, or lifeless. Derealization is commonly ac-\ncompanied by subjective visual distortions, su ch as blurriness, heig htened acuity, widened\nor narrowed visual field, two-dimensionalit y or flatness, exaggerated three-dimensional-\nity, or altered distance or size of objects (i.e ., macropsia or micropsia). Auditory distortions", "source": "dsm5.pdf"} {"id": "ad9da6c352d9-1", "page_content": "can also occur, whereby voices or sounds ar e muted or heightened. In addition, Criterion\nC requires the presence of clinically signific ant distress or impairment in social, occupa-\ntional, or other important areas of functionin g, and Criteria D and E describe exclusionary\ndiagnoses. \nAssociated Features Supporting Diagnosis\nIndividuals with depersonalization/derealizat ion disorder may have difficulty describ-\ning their symptoms and may think they are \u201ccrazy\u201d or \u201cgoing crazy\u201d. Another common\nexperience is the fear of irreversible brai n damage. A commonly associated symptom is a\nsubjectively altered sense of time (i.e., too fast or too slow), as well as a subjective difficulty\nin vividly recalling past memories and owning them as personal and emotional. Vague so-\nmatic symptoms, such as head fullness, ting ling, or lightheadedne ss, are not uncommon.\nIndividuals may suffer extreme rumination or obsessional preoccupation (e.g., constantly\nobsessing about whether they really exist, or checking their perc eptions to determine\nwhether they appear real). Varying degrees of anxiety and depression are also common as-\nsociated features. Individuals with the disord er have been found to have physiological\nhyporeactivity to emotional stimuli. Neural substrates of interest include the hypotha-\nlamic-pituitary-adrenocortical ax is, inferior parietal lobule, and prefrontal cortical-limbic\ncircuits.\nPrevalence\nTransient depersonalization/derealization sy mptoms lasting hours to days are common\nin the general population. The 12-month prev alence of depersonalization/derealization\ndisorder is thought to be markedly less than for transient symptoms, although precise es-", "source": "dsm5.pdf"} {"id": "ad9da6c352d9-2", "page_content": "disorder is thought to be markedly less than for transient symptoms, although precise es-\ntimates for the disorder are unavailable. In general, approximately one-half of all adults\nhave experienced at least one lifetime episode of depersonalization/derealization. How-\never, symptomatology that meets full criter ia for depersonalization/derealization disor-\nder is markedly less common than transient sy mptoms. Lifetime prevalence in U.S. and\nnon-U.S. countries is approximat ely 2% (range of 0.8% to 2. 8%). The gender ratio for the\ndisorder is 1:1.\nDevelopment and Course\nThe mean age at onset of depersonalization/derealization disorder is 16 years, although the\ndisorder can start in early or middle childhood; a minority cannot recall ever not having had", "source": "dsm5.pdf"} {"id": "d0ce34bf5e40-0", "page_content": "304 Dissociative Disorders\nthe symptoms. Less than 20% of individuals experience onset after age 20 years and only\n5% after age 25 years. Onset in the fourth decade of life or later is highly unusual. Onset can\nrange from extremely sudden to gradual. Du ration of depersonalization/derealization\ndisorder episodes can vary greatly, from brief (hours or days) to prolonged (weeks,\nmonths, or years). Given the rari ty of disorder onset after age 40 years, in such cases the in-\ndividual should be examined more closely fo r underlying medical conditions (e.g., brain\nlesions, seizure disorders, sl eep apnea). The course of the disorder is often persistent.\nAbout one-third of cases involve discrete episodes; another third, continuous symptoms\nfrom the start; and still another third, an initially episodic co urse that even tually becomes\ncontinuous. \nWhile in some individuals the intensity of symptoms can wax and wane considerably,\nothers report an unwavering level of intensity that in extreme cases can be constantly pres-\nent for years or decades. Internal and extern al factors that affect symptom intensity vary\nbetween individuals, yet some typical pattern s are reported. Exacerbations can be trig-\ngered by stress, worsening mood or anxiety symptoms, novel or over stimulating settings,\nand physical factors such as lighting or lack of sleep. \nRisk and Prognostic Factors \nTemperamental. Individuals with depersonalization/ derealization disorder are charac-\nterized by harm-avoidant temperament, imma ture defenses, and both disconnection and\noverconnection schemata. Imma ture defenses such as idea lization/devaluation, projec-\ntion and acting out result in deni al of reality and poor adaptation. Cognitive disconnection", "source": "dsm5.pdf"} {"id": "d0ce34bf5e40-1", "page_content": "tion and acting out result in deni al of reality and poor adaptation. Cognitive disconnection\nschemata reflect defectiveness and emotional inhibi tion and subsume themes of abuse, ne-\nglect, and deprivation. Overconnection schemata involve impaired autonomy with themes\nof dependency, vulnerability, and incompetence.\nEnvironmental. There is a clear association between the disorder and childhood interper-\nsonal traumas in a substantial portion of individu als, although this association is not as prev-\nalent or as extreme in the nature of the trau mas as in other dissociative disorders, such as\ndissociative identity disorder. In particular, emotional abuse and emotional neglect have been\nmost strongly and consistently associated with the disorder. Other st ressors can include phys-\nical abuse; witnessing domestic violence; growing up with a se riously impaired, mentally ill\nparent; or unexpected de ath or suicide of a family member or close friend. Sexual abuse is a\nmuch less common antecedent but can be encountered. The most common proximal precipi-\ntants of the disorder are severe stress (interpersonal, financ ial, occupational), depression, anx-\niety (particularly panic attacks), and illicit drug use. Symptoms may be specifically induced by\nsubstances such as tetrahydrocannabinol, ha llucinogens, ketamine, MDMA (3,4-methylene-\ndioxymethamphetamine; \u201cecstasy \u201d) and salvia. Marijuana use may precipitate new-onset\npanic attacks and depersonalization/derealization symptoms simultaneously.\nCulture-Related Diagnostic Issues\nVolitionally induced experiences of depersonalization/dereali zation can be a part of med-\nitative practices that are prevalent in many religions and cult ures and should not be diag-", "source": "dsm5.pdf"} {"id": "d0ce34bf5e40-2", "page_content": "itative practices that are prevalent in many religions and cult ures and should not be diag-\nnosed as a disorder. However, there are in dividuals who initially induce these states\nintentionally but over time lose control over them and may develop a fear and aversion for\nrelated practices. \nFunctional Consequences of \nDepersonalization/De realization Disorder\nSymptoms of depersonalization/derealization disorder are highly distressing and are as-\nsociated with major morbidity. The affectivel y flattened and robotic demeanor that these", "source": "dsm5.pdf"} {"id": "b603a5e64d05-0", "page_content": "Depersonalization/Derealization Disorder 305\nindividuals often demonstrate may appear incongruent with the extreme emotional pain\nreported by those with the disorder. Impairment is often experienced in both interpersonal\nand occupational spheres, largel y due to the hypoemotionality with others, subjective diffi-\nculty in focusing and retaining information, and a general sense of disconnectedness from\nlife. \nDifferential Diagnosis\nIllness anxiety disorder. Although individuals with depersonalization/derealization dis-\norder can present with vague somatic complaints as well as fears of permanent brain dam-\nage, the diagnosis of depersonalization/derealization disorder is characterized by the\npresence of a constellation of typical depersonalization/derealization symptoms and the ab-\nsence of other manifestations of illness anxiety disorder. \nMajor depressive disorder. Feelings of numbness, deadne ss, apathy, and being in a\ndream are not uncommon in major depressive episodes. However, in depersonalization/\nderealization disorder, such symptoms are a ssociated with further symptoms of the dis-\norder. If the depersonalization/derealization clearly precedes the onset of a major depres-\nsive episode or clearly continues after its resolution, the diagnosis of depersonalization/\nderealization disorder applies. \nObsessive-compulsive disorder. Some individuals with depersonalization/dereal-\nization disorder can become obsessively preo ccupied with their subjective experience or\ndevelop rituals checking on the status of their symptoms. However, other symptoms of\nobsessive-compulsive disorder unrelated to depersonali zation/derealization are not\npresent. \nOther dissociative disorders. In order to diagnose depersonalization/derealization\ndisorder, the symptoms should not occur in th e context of another dissociative disorder,", "source": "dsm5.pdf"} {"id": "b603a5e64d05-1", "page_content": "disorder, the symptoms should not occur in th e context of another dissociative disorder,\nsuch as dissociative identity disorder. Differentiation from dissociative amnesia and con-\nversion disorder (functional neurological sy mptom disorder) is simpler, as the symptoms\nof these disorders do not overlap with those of depersonalization/derealization disorder. \nAnxiety disorders. Depersonalization/derealization is one of the symptoms of panic at-\ntacks, increasingly common as panic attack severity increases. Therefore, depersonal-\nization/derealization disorder should not be diagnosed when the symptoms occur only\nduring panic attacks that are part of panic disorder, social anxiety disorder, or specific\nphobia. In addition, it is not uncommon for depersonalization/derealization symptoms\nto first begin in the context of new-onset pani c attacks or as panic disorder progresses and\nworsens. In such presentations, the diagno sis of depersonalization/ derealization disorder\ncan be made if 1) the depersonalization/de realization component of the presentation is\nvery prominent from the start, clearly exceed ing in duration and intensity the occurrence\nof actual panic attacks; or 2) the depersona lization/derealization continues after panic dis-\norder has remitted or has be en successfully treated. \nPsychotic disorders. The presence of intact reality testing specifically regarding the\ndepersonalization/derealization symptoms is essential to differentiating depersonal-\nization/derealization disord er from psychotic disorder s. Rarely, positive-symptom\nschizophrenia can pose a diagnostic challenge when nihilistic delusions are present. For\nexample, an individual may complain that he or she is dead or the world is not real; this\ncould be either a subjective experience that the individual knows is not true or a delusional\nconviction.", "source": "dsm5.pdf"} {"id": "b603a5e64d05-2", "page_content": "conviction.\nSubstance/medication-induced disorders. Depersonalization/dere alization associated\nwith the physiological effects of substances duri ng acute intoxication or withdrawal is not\ndiagnosed as depersonalization/derealizatio n disorder. The most common precipitating\nsubstances are the illicit drugs marijuana, hallucinogens, ketamine, ecstasy, and salvia. In", "source": "dsm5.pdf"} {"id": "483f2a4c0bab-0", "page_content": "306 Dissociative Disorders\nabout 15% of all cases of depersonalization/derealization disorder, the symptoms are pre-\ncipitated by ingestion of such substances. If the symptoms persist for some time in the ab-\nsence of any further substance or medication use, the diagnosis of depersonalization/\nderealization disorder applies. This diagnosis is usually easy to establish since the vast ma-\njority of individuals with this presentation become highly phobic and aversive to the trig-\ngering substance and do not use it again.\nMental disorders due to another medical condition. Features such as onset after age\n40 years or the presence of atypical symptoms and course in any individual suggest the\npossibility of an underlying medical condition. In such cases, it is essential to conduct a\nthorough medical and neurological evaluation, which may include standard laboratory\nstudies, viral titers, an electroencephalogram, ve stibular testing, visual testing, sleep stud-\nies, and/or brain imaging. When the suspicion of an underlying seizure disorder proves\ndifficult to confirm, an ambulatory electr oencephalogram may be indicated; although\ntemporal lobe epilepsy is most commonly implicated, pariet al and frontal lobe epilepsy\nmay also be associated.\nComorbidity\nIn a convenience sample of adults recruite d for a number of depersonalization research\nstudies, lifetime comorbidities were high for unipolar depressive disorder and for any\nanxiety disorder, with a signific ant proportion of the sample having both disorders. Comor-\nbidity with posttraumatic stress disorder was low. The three most commonly co-occurring\npersonality disorders were avoidant, borderline, and ob sessive-compulsive.\nOther Specified Dissociative Disorder\n300.15 (F44.89)", "source": "dsm5.pdf"} {"id": "483f2a4c0bab-1", "page_content": "Other Specified Dissociative Disorder\n300.15 (F44.89)\nThis category applies to presentations in which symptoms characteristic of a dissociative\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the dissociative disorders diagnostic class. The other specified dissocia-\ntive disorder category is used in situations in which the clinician chooses to communicate\nthe specific reason that the presentation does not meet the criteria for any specific disso-\nciative disorder. This is done by recording \u201cother specified dissociative disorder\u201d followed\nby the specific reason (e.g., \u201cdissociative trance\u201d).\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Chronic and recurrent syndromes of mixed dissociative symptoms: This cate-\ngory includes identity disturbance associated with less-than-marked discontinuities in\nsense of self and agency, or alterations of identity or episodes of possession in an in-\ndividual who reports no dissociative amnesia. \n2.Identity disturbance due to prolong ed and intense coercive persuasion: Individ-\nuals who have been subjected to intense coercive persuasion (e.g., brainwashing,\nthought reform, indoctrination while captive, torture, long-term political imprisonment,\nrecruitment by sects/cults or by terror organizations) may present with prolonged\nchanges in, or conscious questioning of, their identity.\n3.Acute dissociative reactions to stressful events: This category is for acute, tran-\nsient conditions that typically last less than 1 month, and sometimes only a few hours\nor days. These conditions are characterized by constriction of consciousness; deper-", "source": "dsm5.pdf"} {"id": "483f2a4c0bab-2", "page_content": "or days. These conditions are characterized by constriction of consciousness; deper-\nsonalization; derealization; perceptual disturbances (e.g., time slowing, macropsia);", "source": "dsm5.pdf"} {"id": "f6cc518bdfb1-0", "page_content": "Unspecified Dissociative Disorder 307\nmicro-amnesias; transient stupor; and/or altera tions in sensory-motor functioning (e.g.,\nanalgesia, paralysis).\n4.Dissociative trance: This condition is characterized by an acute narrowing or com-\nplete loss of awareness of immediate surroundings that manifests as profound unre-\nsponsiveness or insensitivity to environmental stimuli. The unresponsiveness may be\naccompanied by minor stereotyped behaviors (e.g., finger movements) of which the in-\ndividual is unaware and/or that he or she cannot control, as well as transient paralysis\nor loss of consciousness. The dissociative trance is not a normal part of a broadly ac-\ncepted collective cultural or religious practice.\nUnspecified Dissociative Disorder\n300.15 (F44.9)\nThis category applies to presentations in which symptoms characteristic of a dissociative\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the dissociative disorders diagnostic class. The unspecified dissociative\ndisorder category is used in situations in which the clinician chooses not to specify the rea-\nson that the criteria are not met for a specific dissociative disorder, and includes presen-\ntations for which there is insufficient information to make a more specific diagnosis (e.g.,\nin emergency room settings).", "source": "dsm5.pdf"} {"id": "3b1e3c95d7b3-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "3bed04e2e120-0", "page_content": "309Somatic Symptom and\nRelated Disorders\nSomatic symptom disorder and other disorders with prominent somatic symp-\ntoms constitute a new ca tegory in DSM-5 called somatic symptom an d related disorders. This\nchapter includes the diagnoses of somatic sy mptom disorder, illness anxiety disorder, con-\nversion disorder (functional neurological symptom disorder), psychological factors affect-\ning other medical conditions, factitious disorder, other specified somatic symptom and\nrelated disorder, and unspecified somatic symp tom and related disorder. All of the disor-\nders in this chapter share a common feature: the prominence of soma tic symptoms associ-\nated with significant distress and impairment . Individuals with diso rders with prominent\nsomatic symptoms are commonly encountered in primary care and other medical settings\nbut are less commonly encountered in psychiatric and other mental health settings. These\nreconceptualized diagnoses, based on a reorga nization of DSM-IV somatoform disorder di-\nagnoses, are more useful for primary care and other medical (nonpsychiatric) clinicians.\nThe major diagnosis in this diagnostic cl ass, somatic symptom disorder, emphasizes\ndiagnosis made on the basis of positive sy mptoms and signs (distressing somatic symp-\ntoms plus abnormal thoughts, feelings, and behaviors in response to these symptoms)\nrather than the absence of a medical explanat ion for somatic symptoms. A distinctive char-\nacteristic of many individuals with somati c symptom disorder is not the somatic symp-\ntoms per se, but instead the way they present and interpret them. Incorporating affective,\ncognitive, and behavioral components into th e criteria for somatic symptom disorder pro-\nvides a more comprehensive and accurate reflecti on of the true clinical picture than can be\nachieved by assessing the somatic complaints alone.", "source": "dsm5.pdf"} {"id": "3bed04e2e120-1", "page_content": "achieved by assessing the somatic complaints alone.\nThe principles behind the changes in the somatic symptom and related diagnoses from\nDSM-IV are crucial in understanding th e DSM-5 diagnoses. The DSM-IV term somatoform\ndisorders was confusing and is replaced by somatic symptom and related disorders . In DSM-IV\nthere was a great deal of over lap across the somatoform disorders and a lack of clarity\nabout the boundaries of diag noses. Although individuals wi th these disorders primarily\npresent in medical rather than mental health settings, nonpsychiatric physicians found the\nDSM-IV somatoform diagnoses difficult to understand and use. The current DSM-5 clas-\nsification recognizes this overlap by reducing the total number of disorders as well as their\nsubcategories.\nThe previous criteria overemphasized the cent rality of medically unexplained symptoms.\nSuch symptoms are present to various degrees, particularly in conver sion disorder, but so-\nmatic symptom disorders can also accompany diagnosed medical disorders. The reli-\nability of determining that a somatic sympto m is medically unexplai ned is limited, and\ngrounding a diagnosis on the absence of an explanation is problematic and reinforces\nmind-body dualism. It is not appropriate to give an individual a mental disorder diagnosis\nsolely because a medical cause cannot be demo nstrated. Furthermore, the presence of a\nmedical diagnosis does not exclude the possibility of a comorbid ment al disorder, includ-\ning a somatic symptom and related disorder. Perhaps because of the predominant focus\non lack of medical explanation, individuals re garded these diagnoses as pejorative and de-\nmeaning, implying that their physical symp toms were not \u201creal.\u201d The new classification\ndefines the major diagnosis, somatic symptom d isorder, on the basis of positive symptoms", "source": "dsm5.pdf"} {"id": "3bed04e2e120-2", "page_content": "defines the major diagnosis, somatic symptom d isorder, on the basis of positive symptoms\n(distressing somatic symptoms plus abnormal thoughts, feelings, and behaviors in response", "source": "dsm5.pdf"} {"id": "fa6cfafbc7db-0", "page_content": "310 Somatic Symptom and Related Disorders\nto these symptoms). However, medically unexplained symptoms remain a key feature in\nconversion disorder and pseu docyesis (other specified somatic symptom and related dis-\norder) because it is possible to demonstrate de finitively in such disorders that the symp-\ntoms are not consistent with medical pathophysiology.\nIt is important to note that some other ment al disorders may initially manifest with pri-\nmarily somatic symptoms (e.g., major depressi ve disorder, panic disorder). Such diagno-\nses may account for the somatic symptoms, or they may occur alongside one of the somatic\nsymptom and related diso rders in this chapter. There is also considerable medical comor-\nbidity among somatizing individuals. Althou gh somatic symptoms are frequently associ-\nated with psychological distress and psyc hopathology, some somatic symptom and\nrelated disorders can arise spontaneously, and their causes can remain obscure. Anxiety\ndisorders and depressive disorders may acco mpany somatic symptom and related disor-\nders. The somatic component adds severity an d complexity to depressive and anxiety dis-\norders and results in higher severity, functi onal impairment, and ev en refractoriness to\ntraditional treatments. In rare instances, the degree of preoccupation may be so severe as\nto warrant consideration of a delusional disorder diagnosis.\nA number of factors may contribute to so matic symptom and related disorders. These\ninclude genetic and biological vulnerability (e.g., increased sensitivity to pain), early trau-\nmatic experiences (e.g., violence, abuse, deprivation), and learning (e.g., attention ob-\ntained from illness, lack of reinforcement of nonsomatic expressions of distress), as well as\ncultural/social norms that devalue and stig matize psychological suffering as compared", "source": "dsm5.pdf"} {"id": "fa6cfafbc7db-1", "page_content": "cultural/social norms that devalue and stig matize psychological suffering as compared\nwith physical suffering. Differences in medical care across cultures affect the presentation,\nrecognition, and management of these somatic presentations. Variations in symptom pre-\nsentation are likely the result of the interact ion of multiple factors within cultural con-\ntexts that affect how individuals identify and classify bodily sensations, perceive illness,\nand seek medical attention for them. Thus, somatic presentations can be viewed as expres-\nsions of personal suffering inserted in a cultural and social context.\nAll of these disorders are characterized by the prominent focus on somatic concerns\nand their initial presentation mainly in medical rather than mental health care settings. So-\nmatic symptom disorder offers a more clinica lly useful method of characterizing individ-\nuals who may have been considered in the pa st for a diagnosis of somatization disorder.\nFurthermore, approximately 75% of individuals previously diagnosed with hypochon-\ndriasis are subsumed under the diagnosis of somatic symptom diso rder. Howe ver, about\n25% of individuals with hypoch ondriasis have high health anxiety in the absence of so-\nmatic symptoms, and many such individuals\u2019 symptoms would not qualify for an anxiety\ndisorder diagnosis. The DSM-5 diagnosis of illness anxiety disorder is for this latter group\nof individuals. Illness anxiety disorder can be considered eith er in this diagnostic section\nor as an anxiety disorder. Because of the st rong focus on somatic concerns, and because ill-\nness anxiety disorder is most often encountere d in medical settings, for utility it is listed\nwith the somatic symptom and re lated disorders. In conversion disorder, the essential fea-\nture is neurological symptoms that are foun d, after appropriate neurological assessment,\nto be incompatible with neurological pathophysiology. Psychological factors affecting", "source": "dsm5.pdf"} {"id": "fa6cfafbc7db-2", "page_content": "to be incompatible with neurological pathophysiology. Psychological factors affecting\nother medical conditions is also included in th is chapter. Its essential feature is the pres-\nence of one or more clinically significant psyc hological or behavioral factors that adversely", "source": "dsm5.pdf"} {"id": "6e1015bd0a12-0", "page_content": "other medical conditions is also included in th is chapter. Its essential feature is the pres-\nence of one or more clinically significant psyc hological or behavioral factors that adversely\naffect a medical condition by increasing the risk for suffering, death, or disability. Like the\nother somatic symptom and related disorders, factitious disorder embodies persistent\nproblems related to illness percep tion and identity. In the great majority of reported cases\nof factitious disorder, both imposed on self and imposed on another, individuals present\nwith somatic symptoms and medical disease convi ction. C onsequently, DSM-5 factitious\ndisorder is included among the somatic symp tom and related disorders. Other specified\nsomatic symptom and related disorder and un specified somatic symptom and related dis-\norder include conditions for which some, but no t all, of the criteria for somatic symptom\ndisorder or illness anxiety disord er are met, as well as pseudocyesis.", "source": "dsm5.pdf"} {"id": "1354bc2dd1bf-0", "page_content": "Somatic Symptom Disorder 311\nSomatic Symptom Disorder\nDiagnostic Criteria 300.82 (F45.1)\nA. One or more somatic symptoms that are distressing or result in significant disruption\nof daily life. \nB. Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associ-\nated health concerns as manifested by at least one of the following: \n1. Disproportionate and persistent thoughts about the seriousness of one\u2019s symptoms.\n2. Persistently high level of anxiety about health or symptoms.\n3. Excessive time and energy devoted to these symptoms or health concerns.\nC. Although any one somatic symptom may not be continuously present, the state of be-\ning symptomatic is persistent (typically more than 6 months). \nSpecify if:\nWith predominant pain (previously pain disorder): This specifier is for individuals\nwhose somatic symptoms predominantly involve pain.\nSpecify if:\nPersistent: A persistent course is characterized by severe symptoms, marked impair-\nment, and long duration (more than 6 months).\nSpecify current severity: \nMild: Only one of the symptoms specified in Criterion B is fulfilled.\nModerate: Two or more of the symptoms specified in Criterion B are fulfilled.\nSevere: Two or more of the symptoms specified in Criterion B are fulfilled, plus there\nare multiple somatic complaints (or one very severe somatic symptom).\nDiagnostic Features\nIndividuals with somatic symptom disorder ty pically have multiple, current, somatic symp-\ntoms that are distressing or result in signific ant disruption of daily life (Criterion A), al-\nthough sometimes only one severe symptom, most commonly pain, is present. Symptoms\nmay be specific (e.g., localized pain) or rela tively nonspecific (e.g., fatigue). The symptoms", "source": "dsm5.pdf"} {"id": "1354bc2dd1bf-1", "page_content": "sometimes represent normal bodi ly sensations or discomfort that does not generally sig-\nnify serious disease. Somatic symptoms with out an evident medical explanation are not\nsufficient to make this diagnosis. The individu al\u2019s suffering is authen tic, whether or not it\nis medically explained.\nThe symptoms may or may not be associated with another medical condition. The di-\nagnoses of somatic symptom disorder and a concurrent medical illness are not mutually\nexclusive, and these frequently occur together . For example, an indi vidual may become se-\nriously disabled by symptoms of somatic sy mptom disorder after an uncomplicated myo-\ncardial infarction even if the myocardial infarc tion itself did not result in any disability. If\nanother medical condition or high risk for de veloping one is present (e.g., strong family\nhistory), the thoughts, feelings, and behavior s associated with this condition are excessive\n(Criterion B).\nIndividuals with somatic symptom disorder tend to have very high levels of worry\nabout illness (Criterion B). They appraise th eir bodily symptoms as unduly threatening,\nharmful, or troublesome and often think the worst about their health. Even when there is\nevidence to the contrary, some patients sti ll fear the medical seriousness of their symp-\ntoms. In severe somatic symptom disorder, he alth concerns may assume a central role in\nthe individual\u2019s life, becoming a feature of his or her identity and dominating interper-\nsonal relationships.", "source": "dsm5.pdf"} {"id": "adf090c901f7-0", "page_content": "312 Somatic Symptom and Related Disorders\nIndividuals typically experience distress that is principally focused on somatic symp-\ntoms and their significance. When asked direct ly about their distress, some individuals de-\nscribe it in relation to other aspects of thei r lives, while others deny any source of distress\nother than the somatic symptoms. Health-relat ed quality of life is often impaired, both\nphysically and mentally. In severe somatic symptom disorder, the impairment is marked,\nand when persistent, the diso rder can lead to invalidism.\nThere is often a high level of medical care utilization, which rarely alleviates the individ-\nual\u2019s concerns. Consequently, the patient may se ek care from multiple doctors for the same\nsymptoms. These individuals often seem unre sponsive to medical interventions, and new\ninterventions may only exacerbate the presenting symptoms . Some individuals with the dis-\norder seem unusually sensitive to medication si de effects. Some feel that their medical as-\nsessment and treatment have been inadequate. \nAssociated Features Supporting Diagnosis\nCognitive features include at tention focused on somatic symptoms, attribution of normal\nbodily sensations to physical illness (possibly with catastrophic interpretations), worry\nabout illness, and fear that any physical activity may damage the body. The relevant as-\nsociated behavioral features may include repe ated bodily checking for abnormalities, re-\npeated seeking of medical help and reassurance, and avoidance of physical activity. These\nbehavioral features are most pronounced in severe, persistent somatic symptom disorder.\nThese features are usually associated with freq uent requests for medical help for different\nsomatic symptoms. This may lead to medical consultations in which individuals are so fo-\ncused on their concerns about somatic symptom( s) that they cannot be redirected to other\nmatters. Any reassurance by the doctor that the symptoms are not indicative of serious", "source": "dsm5.pdf"} {"id": "adf090c901f7-1", "page_content": "matters. Any reassurance by the doctor that the symptoms are not indicative of serious\nphysical illness tends to be short-lived and/ or is experienced by the individuals as the\ndoctor not taking their sympto ms with due seriousness. As the focus on somatic symp-\ntoms is a primary feature of the disorder, in dividuals with somatic symptom disorder typ-\nically present to general medical health servic es rather than mental health services. The\nsuggestion of referral to a mental health spec ialist may be met with surprise or even frank\nrefusal by individuals with somatic symptom disorder.\nSince somatic symptom disorder is associated with depressive disorders, there is an in-\ncreased suicide risk. It is not known whethe r somatic symptom disorder is associated with\nsuicide risk independent of its asso ciation with depressive disorders.\nPrevalence \nThe prevalence of somatic symptom disorder is not known. However, the prevalence of\nsomatic symptom disorder is expected to be higher than that of the more restrictive DSM-\nIV somatization disorder (<1%) but lower than that of undifferentiated somatoform dis-\norder (approximately 19%). The prevalence of somatic symptom disorder in the general\nadult population may be around 5%\u20137%. Fema les tend to report more somatic symptoms\nthan do males, and the preval ence of somatic symptom diso rder is consequently likely to\nbe higher in females.\nDevelopment and Course\nIn older individuals, somatic symptoms and concurrent medical illnesses are common,\nand a focus on Criterion B is crucial for making the diagnosis.\u00a0Somatic symptom disorder\nmay be underdiagnosed in older adults either because certain somatic symptoms (e.g.,\npain, fatigue) are considered part of normal aging or because illness worry is considered", "source": "dsm5.pdf"} {"id": "adf090c901f7-2", "page_content": "pain, fatigue) are considered part of normal aging or because illness worry is considered\n\u201cunderstandable\u201d in older adults who have more general medical illnesses and medica-\ntions than do younger people. Concurrent de pressive disorder is common in older people\nwho present with numerous somatic symptoms.", "source": "dsm5.pdf"} {"id": "1b93f9d6b8ee-0", "page_content": "Somatic Symptom Disorder 313\nIn children, the most common symptoms are recurrent abdominal pain, headache, fa-\ntigue, and nausea. A single prominent symptom is more common in children than in\nadults. While young children may have somatic complaints, they rarely worry about \u201cill-\nness\u201d per se prior to adolescence. The parents\u2019 response to the sy mptom is important, as\nthis may determine the level of associated dist ress. It is the parent who may determine the\ninterpretation of symptoms and the associated time off school and medical help seeking. \nRisk and Prognostic Factors\nTemperamental. The personality trait of negative affe ctivity (neuroticism ) has been identi-\nfied as an independent correlate/risk factor of a high number of somatic symptoms. Comorbid\nanxiety or depression is common and ma y exacerbate symptoms and impairment.\nEnvironmental. Somatic symptom disorder is more freq uent in individuals with few years\nof education and low socioeconomic status, an d in those who have recently experienced\nstressful life events. \nCourse modifiers. Persistent somatic symptoms are associated with demographic fea-\ntures (female sex, older age, fewer years of education, lo wer socioeconomic status, un-\nemployment), a reported history of sexual ab use or other childhood adversity, concurrent\nchronic physical illness or psychiatric disorder (depression, anxiety, persistent depressive\ndisorder [dysthymia], panic), social stress, and reinforcing social factors such as illness\nbenefits. Cognitive factors that affect clinical course include sensitization to pain, height-\nened attention to bodily sen sations, and attribution of bod ily symptoms to a possible med-\nical illness rather than recognizing them as a normal phenomenon or psychological stress. \nCulture-Related Diagnostic Issues", "source": "dsm5.pdf"} {"id": "1b93f9d6b8ee-1", "page_content": "Culture-Related Diagnostic Issues\nSomatic symptoms are prominent in various \u201cculture-bound syndromes.\u201d High numbers\nof somatic symptoms are found in population -based and primary care studies around the\nworld, with a similar pattern of the most commonly reported soma tic symptoms, impair-\nment, and treatment seeking. The relationship between number of somatic symptoms and\nillness worry is similar in different cultures, and marked illness worry is associated with\nimpairment and greater treatment seeking across cultures. The relationship between nu-\nmerous somatic symptoms and depression a ppears to be very similar around the world\nand between different cult ures within one country.\nDespite these similarities, th ere are differences in somatic symptoms among cultures\nand ethnic groups. The description of somatic symptoms varies with linguistic and other\nlocal cultural factors. These somatic presenta tions have been described as \u201cidioms of dis-\ntress\u201d because somatic symptoms may have special meanings and shape patient-clinician\ninteractions in the particular cultural cont exts. \u201cBurnout,\u201d the sensation of heaviness or\nthe complaints of \u201cgas\u201d; too much heat in the body; or burning in the head are examples of\nsymptoms that are common in some cultures or ethnic groups but rare in others. Explan-\natory models also vary, and somatic symptoms may be attributed variously to particular\nfamily, work, or environmental stresses; general medical illness; the suppression of feel-\nings of anger and resentment; or certain culture-specific ph enomena, such as semen loss.\nThere may also be differences in medical trea tment seeking among cultural groups, in ad-\ndition to differences due to variable access to medical care services. Seeking treatment for\nmultiple somatic symptoms in general medical clinics is a worldwide phenomenon and\noccurs at similar rates among ethnic groups in the same country.", "source": "dsm5.pdf"} {"id": "1b93f9d6b8ee-2", "page_content": "occurs at similar rates among ethnic groups in the same country.\nFunctional Consequences of Somatic Symptom Disorder\nThe disorder is associated with marked impa irment of health status. Many individuals\nwith severe somatic symptom disorder are lik ely to have impaired health status scores\nmore than 2 standard deviatio ns below population norms.", "source": "dsm5.pdf"} {"id": "42c649b7fb81-0", "page_content": "314 Somatic Symptom and Related Disorders\nDifferential Diagnosis\nIf the somatic symptoms are consistent with an other mental disorder (e.g., panic disorder),\nand the diagnostic criteria for that disorder are fulfilled, then that mental disorder should\nbe considered as an alternative or additional diagnosis. A separate diagnosis of somatic\nsymptom disorder is not made if the somatic symptoms and related thoughts, feelings, or\nbehaviors occur only during major depressive episodes. If, as commonly occurs, the crite-\nria for both somatic symptom disorder and another mental disorder diagnosis are ful-\nfilled, then both should be coded, as both may require treatment. \nOther medical conditions. The presence of somatic symptoms of unclear etiology is not\nin itself sufficient to make the diagnosis of somatic symptom disorder. The symptoms of\nmany individuals with disorders like irritabl e bowel syndrome or fibromyalgia would not\nsatisfy the criterion necessary to diagnose somatic symptom disorder (Criterion B). Con-\nversely, the presence of somatic symptoms of an established medical disorder (e.g., diabe-\ntes or heart disease) does not exclude the di agnosis of somatic symptom disorder if the\ncriteria are otherwise met.\nPanic disorder. In panic disorder, somatic symptoms and anxiety about health tend to\noccur in acute episodes, wher eas in somatic symptom disorder, anxiety and somatic symp-\ntoms are more persistent.\nGeneralized anxiety disorder. Individuals with generalized anxiety disorder worry about\nmultiple events, situations, or activities, only one of whic h may involve their health. The\nmain focus is not usually somatic symptoms or fear of illness as it is in somatic symptom\ndisorder.\nDepressive disorders. Depressive disorders are comm only accompanied by somatic\nsymptoms. However, depressive disorders ar e differentiated from somatic symptom dis-", "source": "dsm5.pdf"} {"id": "42c649b7fb81-1", "page_content": "symptoms. However, depressive disorders ar e differentiated from somatic symptom dis-\norder by the core depressive symptoms of low (dysphoric) mo od and anhedonia. \nIllness anxiety disorder. If the individual has extensive worries about health but no or\nminimal somatic symptoms, it ma y be more appropriate to consider illness anxiety disorder.\nConversion disorder (functional neurological symptom disorder). In conversion disor-\nder, the presenting symptom is loss of function (e.g., of a limb), whereas in somatic symp-\ntom disorder, the focus is on the distress th at particular symptoms cause. The features\nlisted under Criterion B of somatic symptom diso rder may be helpful in differentiating the\ntwo disorders.\nDelusional disorder. In somatic symptom disorder, the in dividual\u2019s beliefs that somatic\nsymptoms might reflect serious underlying phy sical illness are not held with delusional\nintensity. Nonetheless, the in dividual\u2019s beliefs concerning the somatic symptoms can be\nfirmly held. In contrast, in delusional disorder, somatic subtype, the somatic symptom be-\nliefs and behavior are stronger than th ose found in somatic symptom disorder. \nBody dysmorphic disorder. In body dysmorphic disorder, the individual is excessively\nconcerned about, and preoccupied by, a perceived defect in his or her physical features. In\ncontrast, in somatic symptom disorder, the co ncern about somatic symptoms reflects fear\nof underlying illness, not of a defect in appearance.\nObsessive-compulsive disorder. In somatic symptom disorder , the recurrent ideas about\nsomatic symptoms or illness are less intrusive, and individuals with this disorder do not\nexhibit the associated repetiti ve behaviors aimed at reducing anxiety that occur in obses-\nsive-compulsive disorder.\nComorbidity", "source": "dsm5.pdf"} {"id": "42c649b7fb81-2", "page_content": "sive-compulsive disorder.\nComorbidity\nSomatic symptom disorder is associated with hi gh rates of comorbidity with medical dis-\norders as well as anxiety and depressive di sorders. When a concurrent medical illness is", "source": "dsm5.pdf"} {"id": "1dea90a401c3-0", "page_content": "Illness Anxiety Disorder 315\npresent, the degree of impairment is more ma rked than would be expected from the phys-\nical illness alone. When an individual\u2019s sy mptoms meet diagnostic criteria for somatic\nsymptom disorder, the disorder sh ould be diagnosed; however, in view of the frequent co-\nmorbidity, especially with anxiety and depre ssive disorders, evidence for these concur-\nrent diagnoses should be sought.\nIllness Anxiety Disorder\nDiagnostic Criteria 300.7 (F45.21)\nA. Preoccupation with having or acquiring a serious illness. \nB. Somatic symptoms are not present or, if pr esent, are only mild in intensity. If another\nmedical condition is present or there is a high risk for developing a medical condition\n(e.g., strong family history is present), the preoccupation is clearly excessive or dispro-\nportionate. \nC. There is a high level of anxiety about health, and the individual is easily alarmed about\npersonal health status.\nD. The individual performs excessive health-related behaviors (e.g., repeatedly checks\nhis or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doc-\ntor appointments and hospitals).\nE. Illness preoccupation has been present for at least 6 months, but the specific illness\nthat is feared may change over that period of time.\nF. The illness-related preoccupation is not better explained by another mental disorder, such\nas somatic symptom disorder, panic disorder, generalized anxiety disorder, body dysmor-\nphic disorder, obsessive-compulsive disor der, or delusional disorder, somatic type.\nSpecify whether:\nCare-seeking type: Medical care, including physician visits or undergoing tests and\nprocedures, is frequently used.\nCare-avoidant type: Medical care is rarely used.\nDiagnostic Features", "source": "dsm5.pdf"} {"id": "1dea90a401c3-1", "page_content": "Care-avoidant type: Medical care is rarely used.\nDiagnostic Features\nMost individuals with hypochondriasis are now classified as having somatic symptom\ndisorder; however, in a minority of cases, th e diagnosis of illness anxiety disorder applies\ninstead. Illness anxiety disorder entails a pr eoccupation with having or acquiring a seri-\nous, undiagnosed medical illness (Criterion A) . Somatic symptoms are not present or, if\npresent, are only mild in intensity (Criterion B). A thorough evaluation fails to identify a\nserious medical condition that accounts for the individual\u2019s concer ns. While the concern\nmay be derived from a nonpathological physica l sign or sensation, the individual\u2019s dis-\ntress emanates not primar ily from the physical complaint it self but rather from his or her\nanxiety about the meaning, significance, or ca use of the complaint (i.e., the suspected med-\nical diagnosis). If a physical sign or symptom is present, it is often a normal physiological\nsensation (e.g., orthostatic dizziness), a benign and self-limited dysf unction (e.g., transient\ntinnitus), or a bodily discomfo rt not generally considered indicative of disease (e.g., belch-\ning). If a diagnosable medical condition is present, the individual\u2019s anxiety and preoccu-\npation are clearly excessive and disproportionate to the severity of the condition (Criterion\nB). Empirical evidence and existing literatur e pertain to previously defined DSM hypo-\nchondriasis, and it is unclear to what extent and how precisely they apply to the descrip-\ntion of this new diagnosis.\nThe preoccupation with the idea that one is sick is accompanied by substantial anxiety\nabout health and disease (Criterion C). Indivi duals with illness anxiety disorder are easily", "source": "dsm5.pdf"} {"id": "17d8ac82f363-0", "page_content": "316 Somatic Symptom and Related Disorders\nalarmed about illness, such as by hearing abou t someone else falling ill or reading a health-\nrelated news story. Their concerns about undiagnosed disease do not respond to appro-\npriate medical reassurance, negative diagnostic tests, or benign course. The physician\u2019s at-\ntempts at reassurance and symptom palliation generally do not alleviate the individual\u2019s\nconcerns and may heighten them . Illness concerns assume a prominent place in the indi-\nvidual\u2019s life, affecting daily activities, and may even result in inva lidism. Illness becomes\na central feature of the individual\u2019s identity and self-image, a frequent topic of social dis-\ncourse, and a characteristic response to stressful life events. Individuals with the disorder\noften examine themselves repeatedly (e.g., ex amining one\u2019s throat in the mirror) (Crite-\nrion D). They research their suspected disease excessively (e.g., on the Internet) and re-\npeatedly seek reassurance from family, friends, or physicians. This incessant worrying often\nbecomes frustrating for others and may result in considerable strain within the family. In\nsome cases, the anxiety leads to maladaptive avoidance of situations (e.g., visiting sick\nfamily members) or activities (e.g., exercise ) that these individuals fear might jeopardize\ntheir health.\nAssociated Features Supporting Diagnosis\nBecause they believe they are medically ill, individuals with illness anxiety disorder are\nencountered far more frequently in medical than in mental health settings. The majority of\nindividuals with illness anxiety disorder have extensive yet unsatisfactory medical care,\nthough some may be too anxious to seek medi cal attention. They generally have elevated\nrates of medical utilization but do not utilize me ntal health services more than the general", "source": "dsm5.pdf"} {"id": "17d8ac82f363-1", "page_content": "rates of medical utilization but do not utilize me ntal health services more than the general\npopulation. They often consult multiple physi cians for the same problem and obtain re-\npeatedly negative diagnostic te st results. At times, medical attention leads to a paradoxical\nexacerbation of anxiety or to iatrogenic complications from diagnostic tests and proce-\ndures. Individuals with the disorder are genera lly dissatisfied with their medical care and\nfind it unhelpful, often feelin g they are not being taken seriously by physicians. At times,\nthese concerns may be justif ied, since physicians sometimes are dismissive or respond\nwith frustration or hostility. Th is response can occasionally result in a failure to diagnose\na medical condition that is present.\nPrevalence\nPrevalence estimates of illness anxiety disorder are based on estimates of the DSM-III and\nDSM-IV diagnosis hypochondriasis. The 1- to 2-year prevalen ce of health anxiety and/or\ndisease conviction in community surveys and population-based samp les ranges from 1.3%\nto 10%. In ambulatory medica l populations, the 6-month/1-ye ar prevalence rates are be-\ntween 3% and 8%. The prevalence of the disorder is similar in males and females.\nDevelopment and Course \nThe development and course of illness anxiety disorder are unclear. Illness anxiety disor-\nder is generally thought to be a chronic and relapsing condition with an age at onset in\nearly and middle adulthood. In population-b ased samples, health -related anxiety in-\ncreases with age, but the ages of individuals with high health anxi ety in medical settings\ndo not appear to differ from those of other patients in those settings. In older individuals,", "source": "dsm5.pdf"} {"id": "17d8ac82f363-2", "page_content": "do not appear to differ from those of other patients in those settings. In older individuals,\nhealth-related anxiety often focuses on memory loss; the disorder is thought to be rare in\nchildren.\nRisk and Prognostic Factors\nEnvironmental. Illness anxiety disorder may sometimes be precipitated by a major life\nstress or a serious but ultimately benign threat to the individu al\u2019s health. A history of child-", "source": "dsm5.pdf"} {"id": "26d68f2f7cf1-0", "page_content": "Illness Anxiety Disorder 317\nhood abuse or of a serious childhood illness may predispose to deve lopment of the disor-\nder in adulthood. \nCourse modifiers. Approximately one-third to one-half of individuals with illness anx-\niety disorder have a transient form, which is associated with less psychiatric comorbidity,\nmore medical comorbidity, and less severe illness anxiety disorder. \nCulture-Related Diagnostic Issues \nThe diagnosis should be made with caution in individuals whose ideas about disease are\ncongruent with widely held, culturally sanctioned beliefs. Little is known about the phe-\nnomenology of the disorder acro ss cultures, although the prevalence appears to be similar\nacross different countries with diverse cultures.\nFunctional Consequences of Illness Anxiety Disorder\nIllness anxiety disorder causes substantial role impairment and decrements in physical\nfunction and health-related quality of life. He alth concerns often interfere with interper-\nsonal relationships, disrupt family life, and damage occupational performance. \nDifferential Diagnosis\nOther medical conditions. The first differential diagnostic consideration is an underly-\ning medical condition, includin g neurological or endocrine conditions, occult malignan-\ncies, and other diseases that affect multiple body systems. The presence of a medical\ncondition does not rule out the possibility of coexisting illness anxiety disorder. If a med-\nical condition is present, the health-related anxiety and disease concerns are clearly dis-\nproportionate to its seriousnes s. Transient preoccupations related to a medical condition\ndo not constitute illn ess anxiety disorder. \nAdjustment disorders. Health-related anxiety is a norm al response to serious illness\nand is not a mental disorder. Such nonpathologic al health anxiety is clearly related to the\nmedical condition and is typica lly time-limited. If the health anxiety is severe enough, an", "source": "dsm5.pdf"} {"id": "26d68f2f7cf1-1", "page_content": "adjustment disorder may be diagnosed. Howeve r, only when the health anxiety is of suf-\nficient duration, severity, and distress can illnes s anxiety disorder be diagnosed. Thus, the\ndiagnosis requires the continuous persistence of disproportio nate health-related anxiety\nfor at least 6 months. \nSomatic symptom disorder. Somatic symptom disorder is diagnosed when significant\nsomatic symptoms are present. In contrast, individuals with illness anxiety disorder have\nminimal somatic symptoms and are primarily concerned with the idea they are ill. \nAnxiety disorders. In generalized anxiety disorder, individuals worry about multiple\nevents, situations, or activiti es, only one of which may invol ve health. In panic disorder,\nthe individual may be concerned that the pani c attacks reflect the presence of a medical ill-\nness; however, although these individuals may have health an xiety, their anxiety is typi-\ncally very acute and episodic. In illness anxi ety disorder, the health anxiety and fears are\nmore persistent and enduring. Individuals wi th illness anxiety disorder may experience\npanic attacks that are triggere d by their illness concerns. \nObsessive-compulsive and related disorders. Individuals with illness anxiety disor-\nder may have intrusive though ts about having a disease and also may have associated\ncompulsive behaviors (e.g., seeking reassurance) . However, in illness anxiety disorder, the\npreoccupations are usually focused on having a disease, whereas in obsessive-compulsive\ndisorder (OCD), the thoughts are intrusive an d are usually focused on fears of getting a\ndisease in the future. Most individuals with OCD have obsessions or compulsions involv-\ning other concerns in addition to fears about contracting disease. In body dysmorphic dis-", "source": "dsm5.pdf"} {"id": "3408170c152a-0", "page_content": "318 Somatic Symptom and Related Disorders\norder, concerns are limited to the individual\u2019s physical appearance, which is viewed as\ndefective or flawed.\nMajor depressive disorder. Some individuals with a major depressive episode rumi-\nnate about their health and worry excessively about illness. A separate diagnosis of illness\nanxiety disorder is not made if these concer ns occur only during major depressive epi-\nsodes. However, if excessive illness worry persists after remi ssion of an episode of major\ndepressive disorder, the diagnosis of illness anxiety disorder should be considered. \nPsychotic disorders. Individuals with illness anxiety disorder are not delusional and\ncan acknowledge the possibility that the feared disease is no t present. Their ideas do not\nattain the rigidity and intens ity seen in the somatic delusions occurring in psychotic dis-\norders (e.g., schizophrenia; delusional disord er, somatic type; major depressive disorder,\nwith psychotic features). True somatic delusions are generall y more bizarre (e.g., that an\norgan is rotting or dead) than the concerns seen in illness anxiety disorder. The concerns\nseen in illness anxiety disorder, though not founded in reality, are plausible. \nComorbidity\nBecause illness anxiety disorder is a new di sorder, exact co morbidities are unknown. Hy-\npochondriasis co-occurs with anxiety disorders (in particular, generalized anxiety disor-\nder, panic disorder, and OCD) and depressive disorders. Approximately two-thirds of\nindividuals with illness anxiety disorder are lik ely to have at least one other comorbid ma-\njor mental disorder. Individuals with illness anxiety disorder may have an elevated risk\nfor somatic symptom disorder and personality disorders.\nConversion Disorder\n(Functional Neurological Symptom Disorder)\nDiagnostic Criteria", "source": "dsm5.pdf"} {"id": "3408170c152a-1", "page_content": "Conversion Disorder\n(Functional Neurological Symptom Disorder)\nDiagnostic Criteria\nA. One or more symptoms of altered voluntary motor or sensory function.\nB. Clinical findings provide evidence of incompatibility between the symptom and recog-\nnized neurological or medical conditions.\nC. The symptom or deficit is not better explained by another medical or mental disorder.\nD. The symptom or deficit causes clinically significant distress or impairment in social, oc-\ncupational, or other important areas of functioning or warrants medical evaluation.\nCoding note: The ICD-9-CM code for conversion disorder is 300.11, which is assigned\nregardless of the symptom type. The ICD-10-CM code depends on the symptom type (see\nbelow).\nSpecify symptom type:\n(F44.4) With weakness or paralysis\n(F44.4) With abnormal movement (e.g., tremor, dystonic movement, myoclonus, gait\ndisorder)\n(F44.4) With swallowing symptoms\n(F44.4) With speech symptom (e.g., dysphonia, slurred speech)\n(F44.5) With attacks or seizures\n(F44.6) With anesthesia or sensory loss\n(F44.6) With special sensory symptom (e.g., visual, olfactory, or hearing distur-\nbance)\n(F44.7) With mixed symptoms", "source": "dsm5.pdf"} {"id": "35bef80a517f-0", "page_content": "Conversion Disorder (Functional Neurological Symptom Disorder) 319\nSpecify if:\nAcute episode: Symptoms present for less than 6 months.\nPersistent: Symptoms occurring for 6 months or more.\nSpecify if:\nWith psychological stressor (specify stressor)\nWithout psychological stressor\nDiagnostic Features\nMany clinicians use the alternative names of \u201cfunctional\u201d (referring to abnormal central\nnervous system functioning) or \u201cpsychogenic\u201d (referring to an assumed etiology) to de-\nscribe the symptoms of conversion disord er (functional neurol ogical symptom disor-\nder). In conversion disorder, there may be on e or more symptoms of various types. Motor\nsymptoms include weakness or paralysis; abno rmal movements, such as tremor or dys-\ntonic movements; gait abnormalities; and abnormal limb posturing. Sensory symptoms\ninclude altered, reduced, or absent skin sens ation, vision, or hearing. Episodes of abnor-\nmal generalized limb shaking with apparent im paired or loss of consciousness may resem-\nble epileptic seizures (also called psychogenic or non-epileptic seizures ). There may be\nepisodes of unresponsiveness resembling syncope or coma. Other symptoms include re-\nduced or absent speech volume (dysphonia/apho nia), altered articulation (dysarthria), a\nsensation of a lump in the th roat (globus), and diplopia. \nAlthough the diagnosis requires that the symptom is not explained by neurological\ndisease, it should not be ma de simply because results from investigations are normal or\nbecause the symptom is \u201cbizarre.\u201d There must be clinical findings that show clear evidence\nof incompatibility with neurological disease. Internal inconsistency at examination is one\nway to demonstrate incompatibility (i.e., demonstrating that physical signs elicited", "source": "dsm5.pdf"} {"id": "35bef80a517f-1", "page_content": "way to demonstrate incompatibility (i.e., demonstrating that physical signs elicited\nthrough one examination method are no longer positive when tested a different way). Ex-\namples of such examination findings include\n\u2022 Hoover\u2019s sign, in which weakness of hip exte nsion returns to normal strength with con-\ntralateral hip flexio n against resistance.\n\u2022 Marked weakness of ankle plantar-flexion when tested on the bed in an individual who\nis able to walk on tiptoes;\n\u2022 Positive findings on the tremor entrainmen t test. On this test, a unilateral tremor may\nbe identified as functional if the tremor ch anges when the individual is distracted away\nfrom it. This may be observed if the individual is asked to copy the examiner in making\na rhythmical movement with their unaffected hand and this causes the functional\ntremor to change such that it copies or \u201centrains\u201d to the rhythm of the unaffected hand\nor the functional tremor is suppressed, or no longer makes a simple rhythmical move-\nment.\n\u2022 In attacks resembling epilepsy or syncope (\u201c psychogenic\u201d non-epileptic attacks), the\noccurrence of closed eyes with resistance to opening or a normal simultaneous electro-\nencephalogram (although this alone does not exclude all forms of epilepsy or syncope).\n\u2022 For visual symptoms, a tubular visual field (i.e., tunnel vision).\nIt is important to note that the diagnosis of conversion disorder should be based on the\noverall clinical picture and not on a single clinical finding.\nAssociated Features Supporting Diagnosis\nA number of associated featur es can support the diagnosis of conversion disorder. There\nmay be a history of multiple similar somatic symptoms. Onset may be associated with\nstress or trauma, either psychological or physi cal in nature. The potential etiological rele-", "source": "dsm5.pdf"} {"id": "7bdffb3ac272-0", "page_content": "320 Somatic Symptom and Related Disorders\nvance of this stress or trauma may be sugges ted by a close temporal relationship. However,\nwhile assessment for stress and trauma is im portant, the diagnosis should not be withheld\nif none is found.\nConversion disorder is often associated wi th dissociative symptoms, such as deperson-\nalization, derealization, and dissociative amne sia, particularly at symptom onset or during\nattacks.\nThe diagnosis of conversion disorder does not require the judgment that the symptoms\nare not intentionally produced (i.e., not feigne d), as the definite ab sence of feigning may\nnot be reliably discerned. The phenomenon of la belle indiff\u00e9rence (i.e., lack of concern about\nthe nature or implications of the symptom) has been associated wi th conversion disorder\nbut it is not specific for conver sion disorder and should not be used to make the diagnosis.\nSimilarly the concept of secondary gain (i.e., when individuals derive external benefits such\nas money or release from respon sibilities) is also not specific to conversion disorder and\nparticularly in the context of definite evid ence for feigning, the diagnoses that should be\nconsidered instead would include factitious disorder or malingering (see the section \u201cDif-\nferential Diagnosis\u201d for this disorder).\nPrevalence\nTransient conversion symptoms are common, but the precise prevalence of the disorder is\nunknown. This is partly because the diagnosis usually requires assessment in secondary\ncare, where it is found in approximately 5% of referrals to neurology clinics. The incidence\nof individual persistent conversion sympto ms is estimated to be 2\u20135/100,000 per year.\nDevelopment and Course\nOnset has been reported throughout the life course. The on set of non-epileptic attacks", "source": "dsm5.pdf"} {"id": "7bdffb3ac272-1", "page_content": "peaks in the third decade, and motor symptoms have their peak onset in the fourth decade.\nThe symptoms can be transient or persistent. The prognosis may be better in younger chil-\ndren than in adolescents and adults.\nRisk and Prognostic Factors \nTemperamental. Maladaptive personality traits ar e commonly associated with conver-\nsion disorder.\nEnvironmental. There may be a history of childhood abuse and neglect. Stressful life\nevents are often, but not always, present. \nGenetic and physiological. The presence of neurological disease that causes similar symp-\ntoms is a risk factor (e.g., non-epileptic se izures are more common in patients who also\nhave epilepsy).\nCourse modifiers. Short duration of symptoms and acceptance of the diagnosis are pos-\nitive prognostic factors. Mala daptive personality traits, the presence of comorbid physical\ndisease, and the receipt of disability bene fits may be negative prognostic factors.\nCulture-Related Diagnostic Issues\nChanges resembling conversion (and dissoci ative) symptoms are common in certain\nculturally sanctioned rituals. If the sympto ms are fully explained within the particular\ncultural context and do not result in clinically significant distress or disability, then the di-\nagnosis of conversion di sorder is not made. \nGender-Related Diagnostic Issues\nConversion disorder is two to thre e times more common in females.", "source": "dsm5.pdf"} {"id": "2c8f37df5cd1-0", "page_content": "Conversion Disorder (Functional Neurological Symptom Disorder) 321\nFunctional Consequences of Conversion Disorder\nIndividuals with conversion symptoms may have substantial disability. The severity of dis-\nability can be similar to that experienced by individuals with comparable medical diseases. \nDifferential Diagnosis\nIf another mental disorder be tter explains the symptoms, th at diagnosis should be made.\nHowever the diagnosis of conversion disorder may be made in the presence of another\nmental disorder. \nNeurological disease. The main differential diagnosis is neurological disease that might\nbetter explain the symptoms. After a thorough neurological assessment, an unexpected\nneurological disease cause for the symptoms is rarely found at follow up. However, reas-\nsessment may be required if the symptoms appe ar to be progressive. Conversion disorder\nmay coexist with neurological disease.\nSomatic symptom disorder. Conversion disorder may be diagnosed in addition to so-\nmatic symptom disorder. Most of the somati c symptoms encountered in somatic symptom\ndisorder cannot be demonstrated to be clea rly incompatible with pathophysiology (e.g.,\npain, fatigue), whereas in conversion disorder , such incompatibility is required for the di-\nagnosis. The excessive thoughts, feelings, and behaviors characterizing somatic symptom\ndisorder are often absent in conversion disorder.\nFactitious disorder and malingering. The diagnosis of conversion disorder does not re-\nquire the judgment that the symptoms are not intentionally produced (i.e., not feigned),\nbecause assessment of conscious intention is unreliable. However definite evidence of\nfeigning (e.g., clear evidence that loss of fu nction is present during the examination but not\nat home) would suggest a diagno sis of factitious disorder if the individual\u2019s apparent aim\nis to assume the sick role or malingering if the aim is to obtain an incentive such as money.", "source": "dsm5.pdf"} {"id": "2c8f37df5cd1-1", "page_content": "Dissociative disorders. Dissociative symptoms are co mmon in individuals with con-\nversion disorder. If both conversion disorder and a dissociati ve disorder are present, both\ndiagnoses should be made. \nBody dysmorphic disorder. Individuals with body dysmorphic disorder are exces-\nsively concerned about a perceived defect in th eir physical features bu t do not complain of\nsymptoms of sensory or motor functi oning in the affected body part. \nDepressive disorders. In depressive disorders, individuals may report general heavi-\nness of their limbs, whereas the weakness of co nversion disorder is more focal and prom-\ninent. Depressive disorders ar e also differentiated by the presence of core depressive\nsymptoms. \nPanic disorder. Episodic neurological symptoms (e.g., tremors and paresthesias) can\noccur in both conversion disorder and panic attacks. In panic attacks, the neurological\nsymptoms are typically transient and acutely episodic with characteristic cardiorespira-\ntory symptoms. Loss of awareness with amne sia for the attack and violent limb move-\nments occur in non-epileptic atta cks, but not in panic attacks. \nComorbidity\nAnxiety disorders, especially panic disorder, and depressive disorders commonly co-occur\nwith conversion disorder. Somatic symptom diso rder may co-occur as well. Psychosis, sub-\nstance use disorder, and alcohol misuse ar e uncommon. Personalit y disorders are more\ncommon in individuals with conversion disorder than in the general population. Neuro-\nlogical or other medical cond itions commonly coexist with conversion disorder as well.", "source": "dsm5.pdf"} {"id": "c68fc1f54488-0", "page_content": "322 Somatic Symptom and Related Disorders\nPsychological Factors Affecting\n Other Medical Conditions\nDiagnostic Criteria 316 (F54)\nA. A medical symptom or condition (other than a mental disorder) is present. \nB. Psychological or behavioral factors adversely affect the medical condition in one of the\nfollowing ways: \n1. The factors have influenced the course of the medical condition as shown by a\nclose temporal association between the psychological factors and the development\nor exacerbation of, or delayed recovery from, the medical condition.\n2. The factors interfere with the treatment of the medical condition (e.g., poor adher-\nence).\n3. The factors constitute additional\u00a0well-established health risks for the individual.\n4. The factors influence the underlying pathophysiology, precipitating or exacerbating\nsymptoms\u00a0or necessitating medical attention.\nC. The psychological and behavioral factors in Criterion B are not better explained by an-\nother mental disorder (e.g., panic disorder , major depressive disorder, posttraumatic\nstress disorder).\nSpecify current severity:\nMild: Increases medical risk (e.g., inconsistent adherence with antihypertension treat-\nment). \nModerate: Aggravates underlying medical condition (e.g., anxiety aggravating\nasthma).\nSevere: Results in medical hospitalization or emergency room visit.\nExtreme: Results in severe, life-threatening risk (e.g., ignoring heart attack symp-\ntoms).\nDiagnostic Features\nThe essential feature of psychological factors affecting other medical conditions is the\npresence of one or more clinically significant psychological or behavi oral factors that ad-\nversely affect a medical condition by increasi ng the risk for suffering, death, or disability\n(Criterion B). These factors can adversely affe ct the medical condition by influencing its", "source": "dsm5.pdf"} {"id": "c68fc1f54488-1", "page_content": "(Criterion B). These factors can adversely affe ct the medical condition by influencing its\ncourse or treatment, by constituting an additi onal well-established health risk factor, or by\ninfluencing the underlying pathophysiology to precipitate or exac erbate symptoms\u00a0or to\nnecessitate medical attention. \nPsychological or behavioral factors include ps ychological distress, patterns of interper-\nsonal interaction, coping styles, and maladaptiv e health behaviors, such as denial of symp-\ntoms or poor adherence to medical reco mmendations. Common clin ical examples are\nanxiety-exacerbating asthma, denial of need for treatment for acute chest pain, and manip-\nulation of insulin by an individual with diab etes wishing to lose weight. Many different\npsychological factors have been demonstrated to adversely influence medical conditions\u2014\nfor example, symptoms of depression or anxi ety, stressful life events, relationship style,\npersonality traits, and coping styles. The adverse effects can range from acute, with imme-\ndiate medical consequences (e.g., Takotsubo cardiomyopathy) to chronic, occurring over a\nlong period of time (e.g., chronic occupational stress increasing risk for hypertension). Af-\nfected medical conditions can be those with clear pathophysiology (e.g., diabetes, cancer,\ncoronary disease), functional syndromes (e.g ., migraine, irritable bowel syndrome, fibro-\nmyalgia), or idiopathic medical sympto ms (e.g., pain, fatigue, dizziness).", "source": "dsm5.pdf"} {"id": "8274032ed8f7-0", "page_content": "Psychological Factors Affecting Other Medical Conditions 323\nThis diagnosis should be reserved for situations in which the effect of the psychological\nfactor on the medical condition is evident and the psychological factor has clinically sig-\nnificant effects on the course or outcome of the medical condition. Abnormal psychologi-\ncal or behavioral symptoms that develop in response to a medical condition are more\nproperly coded as an adjustme nt disorder (a clinically significant psychological response\nto an identifiable stressor). Th ere must be reasonable eviden ce to suggest an association\nbetween the psychological factors and the medical condition, although it may often not be\npossible to demonstrate direct causality or the mechanisms underlying the relationship.\nPrevalence\nThe prevalence of psychological factors affect ing other medical conditions is unclear. In\nU.S. private insurance billing data, it is a more common diagnosis than somatic symptom\ndisorders.\nDevelopment and Course\nPsychological factors affecting other medical conditions can occur across the lifespan. Par-\nticularly with young children, corroborative history from parents or school can assist the di-\nagnostic evaluation. Some conditions are characteri stic of particular life stages (e.g., in older\nindividuals, the stress associated with acting as a caregiver for an ill spouse or partner).\nCulture-Related Diagnostic Issues\nMany differences between cult ures may influence psychologi cal factors and their effects\non medical conditions, such as those in la nguage and communication style, explanatory\nmodels of illness, patterns of seeking health care, service availability and organization,\ndoctor-patient relationships and other healing practices, family and gender roles, and at-\ntitudes toward pain and death. Psychologica l factors affecting other medical conditions\nmust be differentiated from culturally specific behaviors such as using faith or spiritual\nhealers or other variations in illness manageme nt that are acceptable within a culture and", "source": "dsm5.pdf"} {"id": "8274032ed8f7-1", "page_content": "healers or other variations in illness manageme nt that are acceptable within a culture and\nrepresent an attempt to help the medical condition rather than interfere with it. These local\npractices may complement rather than obstruct evidence-based interventions. If they do\nnot adversely affect out comes, they should not be pathol ogized as psychological factors\naffecting other medical conditions.\nFunctional Consequences of Psychological Factors \nAffecting Other Medical Conditions\nPsychological and behavioral factors have been demonstrated to affect the course of many\nmedical diseases.\nDifferential Diagnosis\nMental disorder due to another medical condition. A temporal association between\nsymptoms of a mental disorder and those of a medical condition is also characteristic of a\nmental disorder due to another medical condition, but the presumed causality is in the op-\nposite direction. In a mental disorder du e to another medical condition, the medical\ncondition is judged to be caus ing the mental disorder through a direct physiological mech-\nanism. In psychological factors affecting other medical conditions, the psychological or be-\nhavioral factors are judged to affect the course of the medical condition.\nAdjustment disorders. Abnormal psychological or behavioral symptoms that develop in\nresponse to a medical condition are more proper ly coded as an adjustment disorder (a clin-\nically significant psychological response to an identifiable stressor). For example, an indi-", "source": "dsm5.pdf"} {"id": "63bac5dd8603-0", "page_content": "324 Somatic Symptom and Related Disorders\nvidual with angina that is precipitated when ever he becomes enraged would be diagnosed\nas having psychological factors affecting ot her medical conditions, whereas an individual\nwith angina who developed maladaptive anticipatory anxiety would be diagnosed as hav-\ning an adjustment disorder with anxiety. In clinical practice, however, psychological fac-\ntors and a medical condition are often mutua lly exacerbating (e.g., anxiety as both a\nprecipitant and a consequence of angina), in which case the distinction is arbitrary. Other\nmental disorders frequently result in medica l complications, most notably substance use\ndisorders (e.g., alcohol use disorder, tobacco use disorder). If an indi vidual has a coexisting\nmajor mental disorder that adversely affects or causes another medical condition, diagno-\nses of the mental disorder and the medical co ndition are usually sufficient. Psychological\nfactors affecting other medical conditions is diagnosed when the psychological traits or\nbehaviors do not meet criteria for a mental diagnosis. \nSomatic symptom disorder. Somatic symptom disorder is characterized by a combina-\ntion of distressing somatic symptoms and ex cessive or maladaptive thoughts, feelings,\nand behavior in response to these symptoms or associated health co ncerns. The individual\nmay or may not have a diagnosable medical cond ition. In contrast, in psychological factors\naffecting other medical conditions, the psycho logical factors advers ely affect a medical\ncondition; the individual\u2019s th oughts, feelings, and behavior are not necessarily excessive.\nThe difference is one of emphasis, rather than a clear-cut distinction. In psychological fac-\ntors affecting other medical conditions, the emphasis is on the exacerbation of the medical\ncondition (e.g., an individual with angina th at is precipitated whenever he becomes anx-", "source": "dsm5.pdf"} {"id": "63bac5dd8603-1", "page_content": "ious). In somatic symptom disorder, the empha sis is on maladaptive thoughts, feelings,\nand behavior (e.g., an individual with angina who worries constantly that she will have a\nheart attack, takes her blood pressure multiple times per day, and restricts her activities).\nIllness anxiety disorder. Illness anxiety disorder is charac terized by high illness anxiety\nthat is distressing and/or disruptive to daily life with minimal somatic symptoms. The fo-\ncus of clinical concern is the individual\u2019s wo rry about having a disease; in most cases, no\nserious disease is present. In psychological factors affecting other medical conditions, anx-\niety may be a relevant psychological factor affecting a medical condition, but the clinical\nconcern is the adverse effects on the medical condition.\nComorbidity\nBy definition, the diagnosis of psychological fa ctors affecting other medi cal conditions entails\na relevant psychological or behavioral syndro me or trait and a comorbid medical condition.\nFactitious Disorder\nDiagnostic Criteria 300.19 (F68.10)\nFactitious Disorder Imposed on Self \nA. Falsification of physical or psychological signs or symptoms, or induction of injury or\ndisease, associated with identified deception.\nB. The individual presents himself or herself to others as ill, impaired, or injured.\nC. The deceptive behavior is evident even in the absence of obvious external rewards.\nD. The behavior is not better explained by another mental disorder, such as delusional\ndisorder or another psychotic disorder.\nSpecify:\nSingle episode\nRecurrent episodes (two or more events of falsification of illness and/or induction of\ninjury)", "source": "dsm5.pdf"} {"id": "a463964d10ef-0", "page_content": "Factitious Disorder 325\nFactitious Disorder Imposed on Another \n(Previously Factitious Disorder by Proxy) \nA. Falsification of physical or psychological signs or symptoms, or induction of injury or\ndisease, in another, associated with identified deception.\nB. The individual presents another individual (vic tim) to others as ill, impaired, or injured.\nC. The deceptive behavior is evident even in the absence of obvious external rewards.\nD. The behavior is not better explained by another mental disorder, such as delusional\ndisorder or another psychotic disorder.\nNote: The perpetrator, not the victim, receives this diagnosis.\nSpecify:\nSingle episode\nRecurrent episodes (two or more events of falsification of illness and/or induction of\ninjury)\nRecording Procedures\nWhen an individual falsifies illness in another (e .g., children, adults, pets), the diagnosis is\nfactitious disorder imposed on another. The pe rpetrator, not the victim, is given the diag-\nnosis. The victim may be given an abuse di agnosis (e.g., 995.54 [T74.12X]; see the chapter\n\u201cOther Conditions That May Be a Focus of Clinical Attention\u201d). \nDiagnostic Features\nThe essential feature of factitious disorder is th e falsification of medical or psychological signs\nand symptoms in oneself or others that are as sociated with the identified deception. Indi-\nviduals with factitious disorder can also seek treatment for themselves or another following\ninduction of injury or disease. The diagnosis requires demonstrating that the individual is\ntaking surreptitious actions to misrepresent, simulate, or ca use signs or symptoms of ill-\nness or injury in the absence of obvious exte rnal rewards. Methods of illness falsification\ncan include exaggeration, fabrication, simula tion, and induction. While a preexisting med-", "source": "dsm5.pdf"} {"id": "a463964d10ef-1", "page_content": "ical condition may be present, the deceptive behavior or induction of injury associated\nwith deception causes others to view such in dividuals (or another) as more ill or impaired,\nand this can lead to excessive clinical intervention. Individuals with factitious disorder\nmight, for example, report feelings of depres sion and suicidality following the death of a\nspouse despite the death not being true or the individual\u2019s not ha ving a spouse; decep-\ntively report episodes of neurological symptoms (e.g., seizures, dizzine ss, or blacking out);\nmanipulate a laboratory test (e .g., by adding blood to urine) to falsely indicate an abnor-\nmality; falsify medical records to indicate an illness; ingest a substance (e.g., insulin or\nwarfarin) to induce an abnormal laboratory result or illness; or physically injure them-\nselves or induce illness in themselves or anot her (e.g., by injecting fecal material to produce\nan abscess or to induce sepsis).\nAssociated Features Supporting Diagnosis\nIndividuals with factitious disorder imposed on self or factitious disorder imposed on an-\nother are at risk for experiencing great psyc hological distress or functional impairment by\ncausing harm to themselves and others. Family , friends, and health care professionals are\nalso often adversely affected by their behavi or. Factitious disorders have similarities to\nsubstance use disorders, eating disorders, im pulse-control disorders, pedophilic disorder,\nand some other established disorders related to both the persistence of the behavior and\nthe intentional efforts to conceal the disord ered behavior through deception. Whereas\nsome aspects of factitious disorders might represent criminal behavior (e.g., factitious dis-", "source": "dsm5.pdf"} {"id": "24cb6600b13d-0", "page_content": "326 Somatic Symptom and Related Disorders\norder imposed on another, in which the parent\u2019s actions represent abuse and maltreat-\nment of a child), such criminal behavior and mental illness are not mutually exclusive. The\ndiagnosis of factitious disorder emphasizes the objective identification of falsification of\nsigns and symptoms of illness, rather than an inference abou t intent or possible underly-\ning motivation. Moreover, such behaviors, incl uding the induction of injury or disease, are\nassociated with deception. \nPrevalence\nThe prevalence of factitious disorder is unknow n, likely because of the role of deception in\nthis population. Among patients in hospital sett ings, it is estimated that about 1% of indi-\nviduals have presentations that meet the criteria for factitious disorder.\nDevelopment and Course\nThe course of factitious disorder is usually one of intermittent episodes. Single episodes\nand episodes that are characterized as pers istent and unremitting are both less common.\nOnset is usually in early adulthood, often after hospitalization for a medical condition or a\nmental disorder. When imposed on another, the disorder may begin after hospitalization\nof the individual\u2019s child or other dependent. In individuals with recu rrent episodes of fal-\nsification of signs and symptoms of illness and/ or induction of injury, this pattern of suc-\ncessive deceptive contact with medical personnel, including hospitalizations, may become\nlifelong. \nDifferential Diagnosis\nCaregivers who lie about abuse injuries in depe ndents solely to protect themselves from lia-\nbility are not diagnosed with factitious disord er imposed on another because protection from\nliability is an external reward (Criterion C, th e deceptive behavior is evident even in the ab-\nsence of obvious external rewards). Such caregi vers who, upon observation, analysis of med-", "source": "dsm5.pdf"} {"id": "24cb6600b13d-1", "page_content": "ical records, and/or interviews with others, are found to lie more extensively than needed for\nimmediate self-protect ion are diagnosed with factitious disorder imposed on another.\nSomatic symptom disorder. In somatic symptom disorder, there may be excessive at-\ntention and treatment seeking for perceived medical concerns, but there is no evidence that\nthe individual is providing false info rmation or behaving deceptively. \nMalingering. Malingering is differentiated from fact itious disorder by the intentional re-\nporting of symptoms for personal gain (e.g., money, time off work). In contrast, the diag-\nnosis of factitious disorder requires the absence of obvious rewards.\u00a0\nConversion disorder (functional neurological symptom disorder). Conversion disorder\nis characterized by neurological symptoms that are inconsistent with neurological patho-\nphysiology. Factitious disorder with neurological symptoms is distinguished from con-\nversion disorder by evidence of de ceptive falsification of symptoms. \nBorderline personality disorder. Deliberate physical self-harm in the absence of suicidal\nintent can also occur in association with other mental disorders su ch as borderline person-\nality disorder. Factitious disord er requires that the induction of injury occur in association\nwith deception. \nMedical condition or mental disorder not associated with intentional symptom falsifi-\ncation. Presentation of signs and sy mptoms of illness that do not conform to an identi-\nfiable medical condition or mental disorder increases the likelihood of the presence of a\nfactitious disorder. However, the diagnosis of factitious disorder does not exclude the\npresence of true medical cond ition or mental disorder, as comorbid illness often occurs in\nthe individual along with factitious disord er. For example, individuals who might manip-\nulate blood sugar levels to produce symptoms may also have diabetes.", "source": "dsm5.pdf"} {"id": "edcc5f1548b9-0", "page_content": "Other Specified Somatic Symptom and Related Disorder 327\nOther Specified Somatic Symptom and\nRelated Disorder\n300.89 (F45.8)\nThis category applies to presentations in which symptoms characteristic of a somatic\nsymptom and related disorder that cause clinically significant distress or impairment in so-\ncial, occupational, or other important areas of functioning predominate but do not meet the\nfull criteria for any of the disorders in the somatic symptom and related disorders diagnos-\ntic class.\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Brief somatic symptom disorder: Duration of symptoms is less than 6 months.\n2.Brief illness anxiety disorder: Duration of symptoms is less than 6 months.\n3.Illness anxiety disorder without excessive health-related behaviors: Criterion D\nfor illness anxiety disorder is not met.\n4.Pseudocyesis: A false belief of being pregnant that is associated with objective signs\nand reported symptoms of pregnancy.\nUnspecified Somatic Symptom and\nRelated Disorder\n300.82 (F45.9)\nThis category applies to presentations in which symptoms characteristic of a somatic\nsymptom and related disorder that cause clinically significant distress or impairment in so-\ncial, occupational, or other important areas of functioning predominate but do not meet the\nfull criteria for any of the disorders in the somatic symptom and related disorders diagnos-\ntic class. The unspecified somatic symptom and related disorder category should not be\nused unless there are decidedly unusual situations where there is insufficient information\nto make a more specific diagnosis.", "source": "dsm5.pdf"} {"id": "3bcc6ef48406-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "9e43f6e5a844-0", "page_content": "329Feeding and\nEating Disorders\nFeeding and eating disorders are characterized by a persistent disturbance of eat-\ning or eating-related behavior that results in the altered consumption or absorption of\nfood and that significantly impairs physical he alth or psychosocial functioning. Diagnos-\ntic criteria are provid ed for pica, rumination disorder, avoidant/restrictive food intake\ndisorder, anorexia nervosa, bulimia nervosa, and binge-eating disorder. \nThe diagnostic criteria for rumination diso rder, avoidant/restrictive food intake dis-\norder, anorexia nervosa, bulimia nervosa, and binge-eating disorder result in a classifica-\ntion scheme that is mutually ex clusive, so that during a sing le episode, only one of these\ndiagnoses can be assigned. The rationale for this approach is that, despite a number of\ncommon psychological and behavioral features , the disorders differ substantially in clin-\nical course, outcome, and treatment needs. A diagnosis of pica, however, may be assigned\nin the presence of any other feeding and eating disorder.\nSome individuals with disorders described in this chapter report eating-related symp-\ntoms resembling those typically endorsed by individuals with substance use disorders,\nsuch as craving and patterns of compulsive use. This resemblance may reflect the involve-\nment of the same neural systems, including th ose implicated in regulatory self-control and\nreward, in both groups of disorders. Howeve r, the relative contributions of shared and\ndistinct factors in the development and perp etuation of eating an d substance use disor-\nders remain insuffic iently understood.\nFinally, obesity is not included in DSM-5 as a mental disorder. Obesity (excess body fat)\nresults from the long-term excess of energy in take relative to energy expenditure. A range", "source": "dsm5.pdf"} {"id": "9e43f6e5a844-1", "page_content": "results from the long-term excess of energy in take relative to energy expenditure. A range\nof genetic, physiological, behavioral, and en vironmental factors that vary across individ-\nuals contributes to the development of obesit y; thus, obesity is not considered a mental\ndisorder. However, there are ro bust associations between ob esity and a number of mental\ndisorders (e.g., binge-eating disorder, depre ssive and bipolar disorders, schizophrenia).\nThe side effects of some psychotropic medica tions contribute importantly to the develop-\nment of obesity, and obesity may be a risk fa ctor for the development of some mental dis-\norders (e.g., depr essive disorders).\nPica\nDiagnostic Criteria\nA. Persistent eating of nonnutritive, nonfood substances over a period of at least 1 month.\nB. The eating of nonnutritive, nonfood substances is inappropriate to the developmental\nlevel of the individual. \nC. The eating behavior is not part of a culturally supported or socially normative practice.\nD. If the eating behavior occurs in the context of another mental disorder (e.g., intellectual\ndisability [intellectual developmental disorder], autism spectrum disorder, schizophre-\nnia) or medical condition (including pregnancy), it is sufficiently severe to warrant ad-\nditional clinical attention.", "source": "dsm5.pdf"} {"id": "4e0f66729e2e-0", "page_content": "330 Feeding and Eating Disorders\nCoding note: The ICD-9-CM code for pica is 307.52 and is used for children or adults.\nThe ICD-10-CM codes for pica are (F98.3) in children and (F50.8) in adults.\nSpecify if:\nIn remission: After full criteria for pica were previously met, the criteria have not been\nmet for a sustained period of time.\nDiagnostic Features\nThe essential feature of pica is the eating of on e or more nonnutritive, nonfood substances on a\npersistent basis over a period of at least 1 month (Criterion A) that is severe enough to warrant\nclinical attention. Typical substances ingested te nd to vary with age and availability and might\ninclude paper, soap, cloth, hair , string, wool, soil, chalk, talc um powder, paint, gum, metal,\npebbles, charcoal or coal, ash, clay, starch, or ice. The term nonfood is included because the di-\nagnosis of pica does not apply to ingestion of diet products that have minimal nutritional con-\ntent. There is typically no aversion to food in general. The eating of nonnutritive, nonfood\nsubstances must be developmentally inappropriate (Criterion B) and not part of a culturally\nsupported or socially normativ e practice (Criterion C). A minimum age of 2 years is suggested\nfor a pica diagnosis to exclude developmentally normal mouthing of objects by infants that re-\nsults in ingestion. The eating of nonnutritive, nonfood substances can be an associated feature\nof other mental disorders (e.g., intellectual disability [intellectual developmental disorder],\nautism spectrum disorder, schizo phrenia). If the eating behavior occurs exclusively in the con-", "source": "dsm5.pdf"} {"id": "4e0f66729e2e-1", "page_content": "text of another mental disorder, a separate diagnosis of pica should be made only if the eating\nbehavior is sufficiently severe to warrant additional clinical attention (Criterion D).\nAssociated Features Supporting Diagnosis\nAlthough deficiencies in vitamins or minerals (e .g., zinc, iron) have been reported in some\ninstances, often no specific biological abnorm alities are found. In some cases, pica comes\nto clinical attention only following general medical complications (e.g., mechanical bowel\nproblems; intestinal obstruction, such as that resulting from a bezoar; intestinal perfora-\ntion; infections such as toxoplasmosis and toxoca riasis as a result of ingesting feces or dirt;\npoisoning, such as by ingestion of lead-based paint).\nPrevalence\nThe prevalence of pica is unclear. Among in dividuals with intellectual disability, the prev-\nalence of pica appears to increase with the severity of the condition.\nDevelopment and Course\nOnset of pica can occur in childhood, adolesce nce, or adulthood, although childhood onset\nis most commonly reported. Pi ca can occur in otherwise normally developing children,\nwhereas in adults, it appears more likely to o ccur in the context of intellectual disability or\nother mental disorders. The ea ting of nonnutritive, nonfood substances may also manifest\nin pregnancy, when specific cravings (e.g., chalk or ice) might occur. The diagnosis of pica\nduring pregnancy is only appropriate if such cravings lead to the ingestion of nonnutri-\ntive, nonfood substances to the extent that th e eating of these substances poses potential\nmedical risks. The course of th e disorder can be protracted an d can result in medical emer-\ngencies (e.g., intestinal obstruction, acute weight loss, poisoning). The disorder can poten-", "source": "dsm5.pdf"} {"id": "4e0f66729e2e-2", "page_content": "tially be fatal depending on substances ingested.\nRisk and Prognostic Factors\nEnvironmental. Neglect, lack of supervision, and de velopmental delay can increase the\nrisk for this condition.", "source": "dsm5.pdf"} {"id": "b06001a8fff9-0", "page_content": "Pica 331\nCulture-Related Diagnostic Issues\nIn some populations, the eating of earth or other seemingly nonn utritive substances is believed\nto be of spiritual, medicinal, or other social value, or may be a culturally supported or socially\nnormative practice. Such behavior does not warrant a di agnosis of pica (Criterion C).\nGender-Related Diagnostic Issues\nPica occurs in both males and females. It ca n occur in females during pregnancy; however,\nlittle is known about the course of pica in the postpartum period. \nDiagnostic Markers\nAbdominal flat plate radiography, ultrasound, and other scanning methods may reveal\nobstructions related to pica. Blood tests and other laboratory tests can be used to ascertain\nlevels of poisoning or the nature of infection. \nFunctional Consequences of Pica\nPica can significantly impair physical functioning, but it is rarely the sole cause of impair-\nment in social functioning. Pica often occu rs with other disorders associated with im-\npaired social functioning.\nDifferential Diagnosis\nEating of nonnutritive, nonfood substances may occur during the course of other mental\ndisorders (e.g., autism spectr um disorder, schizophrenia) an d in Kleine-Levin syndrome.\nIn any such instance, an additional diagnosis of pica should be given only if the eating be-\nhavior is sufficiently persistent and severe to warrant additional clinical attention.\nAnorexia nervosa. Pica can usually be distinguished from the other feeding and eating\ndisorders by the consumption of nonnutritive, nonfoo d substances. It is important to note,\nhowever, that some presentations of anorexia nervosa include ingestion of nonnutritive,\nnonfood substances, such as paper tissues, as a means of attempting to control appetite. In", "source": "dsm5.pdf"} {"id": "b06001a8fff9-1", "page_content": "nonfood substances, such as paper tissues, as a means of attempting to control appetite. In\nsuch cases, when the eating of nonnutritive, nonfood substances is primarily used as a\nmeans of weight control, anorexia ne rvosa should be the primary diagnosis. \nFactitious disorder. Some individuals with factitious disorder may intentionally ingest\nforeign objects as part of the pattern of fals ification of physical symptoms. In such in-\nstances, there is an element of deception that is consistent with deliberate induction of in-\njury or disease. \nNonsuicidal self-injury and nonsuicidal self -injury behaviors in personality disorders.\nSome individuals may swallow potentially harm ful items (e.g., pins, needles, knives) in\nthe context of maladaptive be havior patterns associated with personality disorders or\nnonsuicidal self-injury. \nComorbidity\nDisorders most commonly comorb id with pica are autism spectrum disorder and intellec-\ntual disability (intellectual deve lopmental disorder), and, to a lesser degree, schizophrenia\nand obsessive-compulsive disorder. Pica can be associated with trichotillomania (hair-\npulling disorder) and exco riation (skin-picking) disorder. In comorbid presentations, the\nhair or skin is typically ingested. Pica can al so be associated with av oidant/restrictive food\nintake disorder, particularly in individuals with a strong sensory component to their pre-\nsentation. When an individual is known to have pica, assessment should include con-\nsideration of the possibility of gastrointestinal complications, poisoning, infection, and\nnutritional deficiency.", "source": "dsm5.pdf"} {"id": "8449876e89e0-0", "page_content": "332 Feeding and Eating Disorders\nRumination Disorder\nDiagnostic Criteria 307.53 (F98.21)\nA. Repeated regurgitation of food over a period of at least 1 month. Regurgitated food\nmay be re-chewed, re-swallowed, or spit out.\nB. The repeated regurgitation is not attributable to an associated gastrointestinal or other\nmedical condition (e.g., gastroesophageal reflux, pyloric stenosis).\nC. The eating disturbance does not occur exclusively during the course of anorexia nervosa,\nbulimia nervosa, binge-eating disorder, or\u00a0avoidant/restrictive food intake disorder.\u00a0\nD. If the symptoms occur in the context of another mental disorder (e.g., intellectual dis-\nability [intellectual developmental disorder ] or another neurodevelopmental disorder),\nthey are sufficiently severe to warrant additional clinical attention. \nSpecify if:\nIn remission: After full criteria for rumination disorder were previously met, the criteria\nhave not been met for a sustained period of time.\nDiagnostic Features\nThe essential feature of rumina tion disorder is the repeated regurgitation of food occur-\nring after feeding or eating over a period of at least 1 month (Criterion A). Previously swal-\nlowed food that may be partially digested is brought up into the mouth without apparent\nnausea, involuntary retching, or disgust. The food may be re-chewed and then ejected\nfrom the mouth or re-swallow ed. Regurgitation in ruminati on disorder should be fre-\nquent, occurring at least several times per we ek, typically daily. The behavior is not better\nexplained by an associated gastrointestinal or other medical condition (e.g., gastroesoph-\nageal reflux, pyloric stenosis) (Criterion B) and does not occur exclusively during the", "source": "dsm5.pdf"} {"id": "8449876e89e0-1", "page_content": "course of anorexia nervosa, bulimia nervosa, binge-eating disorder, or avoidant/restric-\ntive food intake disorder (Criterion C). If the symptoms occur in the context of another\nmental disorder (e.g., intellectual disability [intellectual developmen tal disorder], neuro-\ndevelopmental disorder), they must be suffici ently severe to warrant additional clinical\nattention (Criterion D) and should represent a primary aspect of the individual\u2019s presen-\ntation requiring intervention. The disorder may be diagnosed across the life span, par-\nticularly in individuals who also have in tellectual disability. Many individuals with\nrumination disorder can be dire ctly observed engaging in the behavior by the clinician. In\nother instances diagnosis can be made on the basis of self-report or corroborative informa-\ntion from parents or caregivers. Individuals may describe the behavior as habitual or out-\nside of their control.\nAssociated Features Supporting Diagnosis\nInfants with rumination disorder display a characteristic position of straining and arching\nthe back with the head held back, making sucking movements with their tongue. They\nmay give the impression of gaining satisfaction from the ac tivity. They ma y be irritable\nand hungry between episodes of regurgitation. Weight loss and failu re to make expected\nweight gains are common features in infants with rumination disorder. Malnutrition may\noccur despite the infant\u2019s appa rent hunger and the ingestion of relatively large amounts of\nfood, particularly in severe cases, when regurgitation imme diately follows each feeding\nepisode and regurgitated food is expelled. Malnutrition might also occur in older children\nand adults, particularly when the regurgitation is accompanied by restriction of intake.\nAdolescents and adults may attempt to disgui se the regurgitation behavior by placing a", "source": "dsm5.pdf"} {"id": "cccf2d1bd20d-0", "page_content": "Rumination Disorder 333\nhand over the mouth or coughing. Some will a void eating with others because of the ac-\nknowledged social undesirability of the behavi or. This may extend to an avoidance of eat-\ning prior to social situations, such as work or school (e.g., avoidi ng breakfast because it\nmay be followed by regurgitation).\nPrevalence\nPrevalence data for rumination disorder ar e inconclusive, but the disorder is commonly\nreported to be higher in certain groups, such as individuals with intellectual disability.\nDevelopment and Course\nOnset of rumination disorder can occur in in fancy, childhood, adolescence, or adulthood.\nThe age at onset in infants is usually between ag es 3 and 12 months. In infants, the disorder\nfrequently remits spontaneously, but its course can be protract ed and can result in medical\nemergencies (e.g., severe malnutrition). It can potentially be fatal, particularly in infancy.\nRumination disorder can have an episodic course or occur continuously until treated. In\ninfants, as well as in older individuals with intellectual disability (intellectual developmen-\ntal disorder) or other neurodevelopmental diso rders, the regurgitation and rumination be-\nhavior appears to have a self-soothing or self-stimulating func tion, similar to that of other\nrepetitive motor behaviors such as head banging. \nRisk and Prognostic Factors \nEnvironmental. Psychosocial problems such as lack of stimulation, neglect, stressful life\nsituations, and problems in the parent-child relationship may be predisposing factors in\ninfants and young children.\nFunctional Consequences of Rumination Disorder\nMalnutrition secondary to repeated regurgit ation may be associated with growth delay\nand have a negative effect on development an d learning potential. Some older individuals", "source": "dsm5.pdf"} {"id": "cccf2d1bd20d-1", "page_content": "and have a negative effect on development an d learning potential. Some older individuals\nwith rumination disorder deliberately restrict their food intake because of the social un-\ndesirability of regurgitation. They may therefore present with weight loss or low weight.\nIn older children, adolescents, and adults, soci al functioning is more likely to be adversely\naffected. \nDifferential Diagnosis\nGastrointestinal conditions. It is important to differentiate regurgitation in rumination\ndisorder from other conditions characterized by gastroesophageal re flux or vomiting. Con-\nditions such as gastroparesis, pyloric stenosis, hiatal hernia, and Sandifer syndrome in in-\nfants should be ruled out by appropriate physical examinations and laboratory tests.\nAnorexia nervosa and bulimia nervosa. Individuals with anorexia nervosa and bulimia\nnervosa may also engage in regurgitation with subsequent spitting ou t of food as a means\nof disposing of ingested calories be cause of concerns about weight gain. \nComorbidity\nRegurgitation with associated rumination can occur in the context of a concurrent medical\ncondition or another mental disorder (e.g., ge neralized anxiety disorder). When the regur-\ngitation occurs in this context, a diagnosis of ruminati on disorder is appropriate only when\nthe severity of the disturbance exceeds that routinely associated with such conditions or\ndisorders and warrants additional clinical attention.", "source": "dsm5.pdf"} {"id": "1a3531c298b6-0", "page_content": "334 Feeding and Eating Disorders\nAvoidant/Restrictive Food Intake Disorder\nDiagnostic Criteria 307.59 (F50.8)\nA. An eating or feeding disturbance (e.g., apparent lack of interest in eating or food; avoid-\nance based on the sensory characteristics of food; concern about aversive conse-\nquences of eating) as manifested by persistent failure to meet appropriate nutritional\nand/or energy needs\u00a0associated with\u00a0one (or more) of the following:\n1. Significant weight loss (or failure to achieve expected weight gain or faltering\ngrowth in children).\n2. Significant nutritional deficiency.\n3. Dependence on enteral feeding or oral nutritional supplements.\n4. Marked interference with psychosocial functioning.\nB. The disturbance is not better explained by lack of available food or by an associated\nculturally sanctioned practice.\nC. The eating disturbance does not occur exclusively during the course of anorexia ner-\nvosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which\none\u2019s body weight or shape is experienced.\nD. The eating disturbance is not attributable to a concurrent medical condition or not bet-\nter explained by another mental disorder. When the eating disturbance occurs in the\ncontext of another condition or disorder, t he severity of the eating disturbance exceeds\nthat routinely associated with the condition or disorder and warrants additional clinical\nattention.\nSpecify if:\nIn remission: After full criteria for avoidant/restrictive food intake disorder were previ-\nously met, the criteria have not been met for a sustained period of time.\nDiagnostic Features\nAvoidant/restrictive food intake disorder replaces and extends the DSM-IV diagnosis of\nfeeding disorder of infancy or early childhood. The main diagnostic feature of avoidant/\nrestrictive food intake disorder is avoidance or restriction of food intake (Criterion A)", "source": "dsm5.pdf"} {"id": "1a3531c298b6-1", "page_content": "restrictive food intake disorder is avoidance or restriction of food intake (Criterion A)\nmanifested by clinically significant failure to meet requirements for nutrition or insuffi-\ncient energy intake through oral intake of food. One or more of the following key features\nmust be present: significant weight loss, si gnificant nutritional deficiency (or related\nhealth impact), dependence on enteral feedin g or oral nutritional supplements, or marked\ninterference with psychosocial functioning. The determination of whether weight loss is\nsignificant (Criterion A1) is a clinical judgme nt; instead of losing weight, children and ad-\nolescents who have not completed growth may not maintain weight or height increases\nalong their developmental trajectory.\nDetermination of significant nu tritional deficiency (Criterion A2) is also based on clin-\nical assessment (e.g., assessment of dietary intake, physical examination, and laboratory\ntesting), and related impact on physical health can be of a similar seve rity to that seen in\nanorexia nervosa (e.g., hypother mia, bradycardia, anemia). In severe cases, particularly in\ninfants, malnutrition can be life threatening. \u201cDependence\u201d on enteral feeding or oral nu-\ntritional supplements (Criterion A3) means that supplementary feeding is required to sus-\ntain adequate intake. Examples of individu als requiring supplementary feeding include\ninfants with failure to thrive who require na sogastric tube feeding, children with neuro-\ndevelopmental disorders who are dependent on nutritionally complete supplements, and\nindividuals who rely on gastrostomy tube feeding or complete oral nutrition supplements\nin the absence of an underlying medical condit ion. Inability to participate in normal social", "source": "dsm5.pdf"} {"id": "23364751610b-0", "page_content": "Avoidant/Restrictive Food Intake Disorder 335\nactivities, such as eating with others, or to sustain relationsh ips as a result of the distur-\nbance would indicate marked interference wi th psychosocial functioning (Criterion A4).\nAvoidant/restrictive food intake disorder does not include avoidance or restriction of\nfood intake related to lack of availability of food or to cultural practices (e.g., religious fast-\ning or normal dieting) (Criterion B), nor does it include developmentally normal behaviors\n(e.g., picky eating in toddlers, reduced intake in older adults). The disturbance is not better\nexplained by excessive concern about body weight or shape (Criterion C) or by concurrent\nmedical factors or mental disorders (Criterion D). \nIn some individuals, food av oidance or restriction may be based on the sensory char-\nacteristics of qualities of fo od, such as extreme sensitivity to appearance, color, smell,\ntexture, temperature, or taste. Such behavior has been described as \u201crestrictive eating,\u201d\n\u201cselective eating,\u201d \u201cchoosy eating,\u201d \u201cperseverant eating,\u201d \u201cchronic food refusal,\u201d and\n\u201cfood neophobia\u201d and may manifest as refusal to eat particular brands of foods or to tol-\nerate the smell of food being eaten by others . Individuals with heightened sensory sensi-\ntivities associated with autism may show similar behaviors. \nFood avoidance or restriction may also repr esent a conditioned negative response as-\nsociated with food intake following, or in an ticipation of, an aversive experience, such as\nchoking; a traumatic investigation, usually invo lving the gastrointestinal tract (e.g., esoph-\nagoscopy); or repeated vomiting. The terms functional dysphagia and globus hystericus have\nalso been used for such conditions. \nAssociated Features Supporting Diagnosis", "source": "dsm5.pdf"} {"id": "23364751610b-1", "page_content": "also been used for such conditions. \nAssociated Features Supporting Diagnosis \nSeveral features may be associated with food avoidance or reduced food intake, including\na lack of interest in eating or food, leading to weight loss or faltering growth. Very young\ninfants may present as being too sleepy, distre ssed, or agitated to feed. Infants and young\nchildren may not engage with the primary ca regiver during feeding or communicate hun-\nger in favor of other activities. In older child ren and adolescents, food avoidance or restric-\ntion may be associated with more generali zed emotional difficulties that do not meet\ndiagnostic criteria for an an xiety, depressive, or bipolar disorder, sometimes called \u201cfood\navoidance emotional disorder.\u201d \nDevelopment and Course\nFood avoidance or restriction associated with in sufficient intake or lack of interest in eat-\ning most commonly develops in infancy or early childhood and may persist in adulthood.\nLikewise, avoidance based on sensory characterist ics of food tends to arise in the first de-\ncade of life but may persist into adulthood. Avoidance related to aversive consequences\ncan arise at any age. The scant literature re garding long-term outcomes suggests that food\navoidance or restriction based on sensory aspects is relatively stable and long-standing,\nbut when persisting into adulthood, such avoidance/restriction can be associated with rel-\natively normal functioning. There is currently insufficient evidence directly linking avoid-\nant/restrictive food intake disorder and subsequent onset of an eating disorder. \nInfants with avoidant/restrictive food intake disorder may be irritable and difficult to\nconsole during feeding, or ma y appear apathetic and withdrawn. In some instances, par-\nent-child interaction may contri bute to the infant\u2019s feeding problem (e.g., presenting food", "source": "dsm5.pdf"} {"id": "23364751610b-2", "page_content": "inappropriately, or interpreting the infant\u2019s be havior as an act of aggression or rejection).\nInadequate nutritional intake may exacerbate the associated fe atures (e.g., irritability, de-\nvelopmental lags) and further contribute to f eeding difficulties. Associated factors include\ninfant temperament or developm ental impairments that reduce an infant\u2019s responsiveness", "source": "dsm5.pdf"} {"id": "16fb421d0f5b-0", "page_content": "velopmental lags) and further contribute to f eeding difficulties. Associated factors include\ninfant temperament or developm ental impairments that reduce an infant\u2019s responsiveness\nto feeding. Coexisting parental psychopathology, or child abus e or neglect, is suggested if\nfeeding and weight improve in response to ch anging caregivers. In infants, children, and\nprepubertal adolescents, avoidant/restrictive food intake di sorder may be associated with\ngrowth delay, and the resulting malnutrition negatively affects development and learning", "source": "dsm5.pdf"} {"id": "f5b05865b915-0", "page_content": "336 Feeding and Eating Disorders\npotential. In older children, adolescents, an d adults, social functioning tends to be ad-\nversely affected. Regardless of the age, fami ly function may be affected, with heightened\nstress at mealtimes and in other feeding or ea ting contexts involving friends and relatives.\nAvoidant/restrictive food intake disorder manifests more commonly in children than\nin adults, and there may be a long delay betw een onset and clinical presentation. Triggers\nfor presentation vary considerably and includ e physical, social, and emotional difficulties.\nRisk and Prognostic Factors\nTemperamental. Anxiety disorders, autism spectrum disorder, obsessive-compulsive\ndisorder, and attention-deficit/ hyperactivity disorder may in crease risk for avoidant or\nrestrictive feeding or eating behavi or characteristic of the disorder. \nEnvironmental. Environmental risk factors for avoida nt/restrictive f ood intake disor-\nder include familial anxiety. Higher rates of feeding disturbances may occur in children of\nmothers with eating disorders. \nGenetic and physiological. History of gastrointestinal co nditions, gastroesophageal re-\nflux disease, vomiting, and a range of othe r medical problems has been associated with\nfeeding and eating behaviors characteristic of avoidant/restrictive food intake disorder.\nCulture-Related Diagnostic Issues\nPresentations similar to avoidant/restrictive fo od intake disorder occur in various popu-\nlations, including in the United States, Cana da, Australia, and Euro pe. Avoidant/restrictive\nfood intake disorder should not be diagnosed when avoidance of food intake is solely re-\nlated to specific religious or cultural practices.\nGender-Related Diagnostic Issues\nAvoidant/restrictive food intake disorder is equally common in males and females in in-", "source": "dsm5.pdf"} {"id": "f5b05865b915-1", "page_content": "Avoidant/restrictive food intake disorder is equally common in males and females in in-\nfancy and early childhood, but avoidant/restric tive food intake di sorder comorbid with\nautism spectrum disorder has a male predominance. Food avoidance or restriction related\nto altered sensory sensitivities can occur in some physiological conditions, most notably\npregnancy, but is not usually extreme and does not meet full criter ia for the disorder.\nDiagnostic Markers\nDiagnostic markers include malnutrition, low weight, growth delay, and the need for ar-\ntificial nutrition in the absence of any clear medical condition other than poor intake.\nFunctional Consequences of Avoidant/Restrictive \nFood Intake Disorder\nAssociated developmental and fu nctional limitations include impairment of physical de-\nvelopment and social difficulties that can have a significant negative impact on family\nfunction. \nDifferential Diagnosis\nAppetite loss preceding restricted intake is a nonspecific symptom that can accompany a\nnumber of mental diagnoses. Avoidant/restrictive food intake disorder can be diagnosed\nconcurrently with the disorders below if all criteria are met, and the eating disturbance re-\nquires specific clinical attention. \nOther medical conditions (e.g., gastrointest inal disease, food allergies and intoler-\nances, occult malignancies). Restriction of food intake ma y occur in other medical condi-", "source": "dsm5.pdf"} {"id": "3eac465a1b36-0", "page_content": "Avoidant/Restrictive Food Intake Disorder 337\ntions, especially those with on going symptoms such as vomiting, loss of appetite, nausea, ab-\ndominal pain, or diarrhea. A diag nosis of avoidant/restrictive food intake disorder requires\nthat the disturbance of intake is beyond that directly accounted for by physical symptoms con-\nsistent with a medical condition; the eating d isturbance may also persis t after being triggered\nby a medical condition and following resolution of the medical condition. \nUnderlying medical or comorbid mental cond itions may complicate feeding and eating.\nBecause older individuals, postsurgical pati ents, and individuals receiving chemotherapy\noften lose their appetite, an additional diagno sis of avoidant/restric tive food intake dis-\norder requires that the eating disturbance is a primary focus for intervention. \nSpecific neurological/neuromuscular, structural, or congenital disorders and condi-\ntions associated with feeding difficulties. Feeding difficulties are common in a number\nof congenital and neurological conditions often related to problems with oral/esophageal/\npharyngeal structure and function, such as hy potonia of musculature, tongue protrusion,\nand unsafe swallowing. Avoidant/restrictive food intake disorder can be diagnosed in in-\ndividuals with such presentations as long as all diagnostic criteria are met.\nReactive attachment disorder. Some degree of withdrawal is characteristic of reactive\nattachment disorder and can lead to a distur bance in the caregiver-child relationship that\ncan affect feeding and the child\u2019s intake. Avoi dant/restrictive food intake disorder should\nbe diagnosed concurrently only if all criter ia are met for both di sorders and the feeding\ndisturbance is a primary focus for intervention.\nAutism spectrum disorder. Individuals with autism spectr um disorder often present with", "source": "dsm5.pdf"} {"id": "3eac465a1b36-1", "page_content": "Autism spectrum disorder. Individuals with autism spectr um disorder often present with\nrigid eating behaviors and heightened sensor y sensitivities. However, these features do\nnot always result in the level of impairment that would be required for a diagnosis of\navoidant/restrictive food intake disorder. Avoidant/restrictive food intake disorder should\nbe diagnosed concurrently only if all criteria are met for both disorders and when the eat-\ning disturbance requires specific treatment.\nSpecific phobia, social anxiety disorder (social phobia), and other anxiety disorders.\nSpecific phobia, other type, specifies \u201csituation s that may lead to choking or vomiting\u201d and\ncan represent the primary trigge r for the fear, anxiety, or avoidance required for diagnosis.\nDistinguishing specific phobia from avoidant/res trictive food intake disorder can be dif-\nficult when a fear of choking or vomiting h as resulted in food avoidance. Although avoid-\nance or restriction of food intake secondar y to a pronounced fear of choking or vomiting\ncan be conceptualized as specific phobia, in situations when the eating problem becomes\nthe primary focus of clinical attention, avoidant/restrictive food intake disorder becomes\nthe appropriate diagnosis. In social anxiety disorder, the individual may present with a\nfear of being observed by others while eating , which can also occur in avoidant/restrictive\nfood intake disorder. \nAnorexia nervosa. Restriction of energy intake relati ve to requirements leading to sig-\nnificantly low body weight is a core featur e of anorexia nervosa. However, individuals\nwith anorexia nervosa also display a fear of ga ining weight or of becoming fat, or persis-\ntent behavior that interferes with weight gain , as well as specific disturbances in relation to", "source": "dsm5.pdf"} {"id": "3eac465a1b36-2", "page_content": "tent behavior that interferes with weight gain , as well as specific disturbances in relation to\nperception and experience of their own body weight and shape. These features are not\npresent in avoidant/restrictive food intake disorder, and the two disorders should not be\ndiagnosed concurrently. Differential diagnosis between avoidant/restrictive food intake\ndisorder and anorexia nervosa may be difficult, especially in late childhood and early ad-", "source": "dsm5.pdf"} {"id": "f98300b65cd9-0", "page_content": "diagnosed concurrently. Differential diagnosis between avoidant/restrictive food intake\ndisorder and anorexia nervosa may be difficult, especially in late childhood and early ad-\nolescence, because these disorders may share a number of common symptoms (e.g., food\navoidance, low weight). Differential diagnosis is also potentially difficult in individuals\nwith anorex ia nervosa who deny any fear of fatness but nonetheless engage in persistent\nbehaviors that prevent weight gain and who do not recognize the medical seriousness of\ntheir low weight\u2014a presentation sometimes termed \u201cnon-fat phobic anorexia nervosa.\u201d\nFull consideration of symptoms, course, and fa mily history is advised, and diagnosis may", "source": "dsm5.pdf"} {"id": "dec6a2601a61-0", "page_content": "338 Feeding and Eating Disorders\nbe best made in the context of a clinical rela tionship over time. In some individuals, avoid-\nant/restrictive food intake disorder might precede the onset of anorexia nervosa.\nObsessive-compulsive disorder. Individuals with obsessive-compulsive disorder may\npresent with avoidance or restri ction of intake in relation to preoccupations with food or\nritualized eating behavior. Avoidant/restrictive food intake disorder should be diagnosed\nconcurrently only if all criteria are met for both disorders and when the aberrant eating is\na major aspect of the clinical presenta tion requiring specific intervention.\nMajor depressive disorder. In major depressive disorder, a ppetite might be affected to\nsuch an extent that individuals present with significantly restricted food intake, usually in\nrelation to overall energy intake and often a ssociated with weight loss. Usually appetite\nloss and related reduction of intake abate wi th resolution of mood problems. Avoidant/\nrestrictive food intake disorder should only be used concurrently if fu ll criteria are met for\nboth disorders and when the eating d isturbance requires specific treatment.\nSchizophrenia spectrum disorders. Individuals with schizophrenia, delusional disor-\nder, or other psychotic disorders may exhibit odd eating behaviors, avoidance of specific\nfoods because of delusional beliefs, or other ma nifestations of avoidant or restrictive in-\ntake. In some cases, delusional beliefs may contribute to a concern about negative conse-\nquences of ingesting certain foods. Avoidant/r estrictive food intake disorder should be\nused concurrently only if all criteria are me t for both disorders and when the eating dis-\nturbance requires specific treatment.\nFactitious disorder or factitious disorder imposed on another. Avoidant/restrictive\nfood intake disorder should be differentiated fr om factitious disorder or factitious disor-", "source": "dsm5.pdf"} {"id": "dec6a2601a61-1", "page_content": "food intake disorder should be differentiated fr om factitious disorder or factitious disor-\nder imposed on another. In orde r to assume the sick role, so me individuals with factitious\ndisorder may intentionally describe diets that are much more restrictive than those they\nare actually able to consume, as well as comp lications of such behavior, such as a need for\nenteral feedings or nutritional supplements, an inability to tolera te a normal range of\nfoods, and/or an inability to participate normally in age-a ppropriate situations involving\nfood. The presentation may be impressively dramatic and engaging, and the symptoms re-\nported inconsistently. In factitious disorder imposed on another, the caregive r describes\nsymptoms consistent with avoidant/restric tive food intake di sorder and may induce\nphysical symptoms such as failure to gain weig ht. As with any diagno sis of factitious dis-\norder imposed on another, the caregiver receives the diagnosis rather than the affected in-\ndividual, and diagnosis should be made only on the basis of a careful, comprehensive\nassessment of the affected individual, the caregiver, and their interaction. \nComorbidity\nThe most commonly observed disorders comorb id with avoidant/restrictive food intake\ndisorder are anxiety disorders, obsessive- compulsive disorder, and neurodevelopmental\ndisorders (specifically autism spectrum disorder, attention-deficit/hyperactivity disor-\nder, and intellectual disability [int ellectual developm ental disorder]).\nAnorexia Nervosa\nDiagnostic Criteria\nA. Restriction of energy intake relative to requirements, leading to\u00a0a\u00a0significantly low\u00a0body\nweight in the context of age, sex, developmental trajectory, and physical health.\u00a0 Sig-\nnificantly low weight is defined as a weight that is\u00a0less than minimally normal or, for", "source": "dsm5.pdf"} {"id": "dec6a2601a61-2", "page_content": "children and adolescents, less than that minimally expected.\nB. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes\nwith\u00a0weight gain, even though\u00a0at a significantly\u00a0low weight.", "source": "dsm5.pdf"} {"id": "22d80b8ef811-0", "page_content": "Anorexia Nervosa 339\nC. Disturbance in the way in which one\u2019s body weight or shape is experienced, undue in-\nfluence of body weight or shape on self-eval uation, or persistent lack of recognition of\nthe seriousness of the current low body weight.\nCoding note: The ICD-9-CM code for anorexia nervosa is 307.1, which is assigned re-\ngardless of the subtype. The ICD-10-CM code depends on the subtype (see below).\nSpecify whether:\n(F50.01) Restricting type: During the last 3 months, the individual has not engaged in re-\ncurrent episodes of binge eating or purging behavior (i.e., self-induced vomiting or the mis-\nuse of laxatives, diuretics, or enemas). This subtype describes presentations in which\nweight loss is accomplished primarily through dieting, fasting, and/or excessive exercise.\n(F50.02) Binge-eating/purging type: During the last 3 months, the individual has en-\ngaged in\u00a0recurrent episodes of binge eat ing or purging behavior (i.e., self-induced\nvomiting or the misuse of laxatives, diuretics, or enemas).\nSpecify if:\nIn partial remission: After full criteria for anorexia ne rvosa were previously met, Cri-\nterion A (low body weight) has not been met for a sustained period, but either Criterion\nB (intense fear of gaining weight or becoming fat or behavior that interferes with weight\ngain) or Criterion C (disturbances in self-perception of weight and shape) is still met.\nIn full remission: After full criteria for anorexia ner vosa were previously met, none of\nthe criteria have been met for a sustained period of time.", "source": "dsm5.pdf"} {"id": "22d80b8ef811-1", "page_content": "the criteria have been met for a sustained period of time.\nSpecify current severity:\nThe minimum level of severity is based, for adults, on current body mass index (BMI) (see\nbelow) or, for children and adolescents, on BMI percentile. The ranges below are derived\nfrom World Health Organization categories for thinness in adults; for children and adoles-\ncents, corresponding BMI percentiles should be used. The level of severity may be in-\ncreased to reflect clinical symptoms, the degree of functional disability, and the need for\nsupervision.\nMild: BMI \u2265 17 kg/m2 \nModerate: BMI 16\u201316.99 kg/m2 \nSevere: BMI 15\u201315.99 kg/m2 \nExtreme: BMI < 15 kg/m2\nSubtypes\nMost individuals with the binge-eating/purging type of anorexia nervosa who binge eat\nalso purge through self-induced vomiting or th e misuse of laxatives, diuretics, or enemas.\nSome individuals with this subtype of anorexia nervosa do not binge eat but do regularly\npurge after the consumption of small amounts of food. \nCrossover between the subtypes over the c ourse of the disorder is not uncommon;\ntherefore, subtype description should be used to describe current symptoms rather than\nlongitudinal course.\nDiagnostic Features\nThere are three essential features of anorexia nervosa: persistent en ergy intake restriction;\nintense fear of gaining weight or of becoming fat, or persistent behavior that interferes\nwith\u00a0weight gain; and a disturbance in self-perceived weight or shape. The individual main-\ntains a body weight that is below a minimally normal level for age, sex, developmental tra-\njectory, and physical health (Criterion A). In dividuals\u2019 body weights frequently meet this", "source": "dsm5.pdf"} {"id": "22d80b8ef811-2", "page_content": "jectory, and physical health (Criterion A). In dividuals\u2019 body weights frequently meet this\ncriterion following a significant weight loss, but among children and adolescents, there\nmay alternatively be failure to make expected weight gain or to maintain a normal devel-\nopmental trajectory (i.e., while grow ing in height) instead of weight loss.", "source": "dsm5.pdf"} {"id": "42fe2aeb505e-0", "page_content": "340 Feeding and Eating Disorders\nCriterion A requires that the individual\u2019s weight be significantly low (i.e., less than\nminimally normal or, for children and adoles cents, less than that minimally expected).\nWeight assessment can be challenging because normal weight range differs among indi-\nviduals, and different thresholds have been published defining thinness or underweight\nstatus. Body mass index (BMI; calculated as weight in kilograms/height in meters2) is a\nuseful measure to assess body weight for height. For adults, a BMI of 18.5 kg/m2 has been\nemployed by the Centers for Disease Control and Prevention (CDC) and the World Health\nOrganization (WHO) as the lower limit of normal body we ight. Therefore, most adults with\na BMI greater than or equal to 18.5\u00a0kg/m2 would not be considered to have a significantly\nlow body weight. On the other ha nd, a BMI of lower than 17.0\u00a0kg/m2 has been considered\nby the WHO to indicate moderate or severe thinness; therefore, an individual with a BMI\nless than 17.0\u00a0kg/m2 would likely be considered to have a significantly low weight. An\nadult with a BMI between 17.0 and 18.5\u00a0kg/m2, or even above 18.5\u00a0kg/m2, might be consid-\nered to have a significantly low weight if clinical history or other physiological informa-\ntion supports this judgment.\nFor children and adolescents, de termining a BMI-for-age percentile is useful (see, e.g.,\nthe CDC BMI percentile calculator for children and teenagers. As for adults, it is not pos-\nsible to provide definitive standards for judgin g whether a child\u2019s or an adolescent\u2019s weight\nis significantly low, and variations in deve lopmental trajectories among youth limit the", "source": "dsm5.pdf"} {"id": "42fe2aeb505e-1", "page_content": "is significantly low, and variations in deve lopmental trajectories among youth limit the\nutility of simple numerical guidelines. The CD C has used a BMI-for-age below the 5th per-\ncentile as suggesting underweight; however, children and adolesce nts with a BMI above\nthis benchmark may be judged to be significantly underweight in light of failure to main-\ntain their expected growth trajectory. In su mmary, in determining whether Criterion A is\nmet, the clinician should consider available numerical guidelines, as well as the individual\u2019s\nbody build, weight history, an d any physiological disturbances.\nIndividuals with this disorder typically display an intense fear of gaining weight or of\nbecoming fat (Criterion B). This intense fear of becoming fat is usually not alleviated by\nweight loss. In fact, concern about weight gain may increase even as weight falls. Younger\nindividuals with anorexia nervosa, as well as some adults, may not recognize or acknowl-\nedge a fear of weight gain. In the absence of another explanation for the significantly low\nweight, clinician inference drawn from collateral history, observatio nal data, physical and\nlaboratory findings, or longitudinal course eith er indicating a fear of weight gain or sup-\nporting persistent behaviors that prevent it may be used to es tablish Criterion B. \nThe experience and significance of body weight and shape are distorted in these indi-\nviduals (Criterion C). Some individuals feel globally overweight. Others realize that they\nare thin but are still concerned th at certain body parts, partic ularly the abdomen, buttocks,\nand thighs, are \u201ctoo fat.\u201d They may employ a variety of techniques to evaluate their body\nsize or weight, including frequent weighing, obsessive measuring of body parts, and per-", "source": "dsm5.pdf"} {"id": "42fe2aeb505e-2", "page_content": "size or weight, including frequent weighing, obsessive measuring of body parts, and per-\nsistent use of a mirror to check for perceived areas of \u201cfat.\u201d The self-esteem of individuals\nwith anorexia nervosa is highly dependent on their perceptions of body shape and weight.\nWeight loss is often viewed as an impressive ac hievement and a sign of extraordinary self-\ndiscipline, whereas weight gain is perceived as an unacceptable failure of self-control. Al-\nthough some individuals with this disorder may acknowledge being thin, they often do\nnot recognize the serious medical implic ations of their malnourished state. \nOften, the individual is brought to professional attention by family members after marked", "source": "dsm5.pdf"} {"id": "92bad521506a-0", "page_content": "not recognize the serious medical implic ations of their malnourished state. \nOften, the individual is brought to professional attention by family members after marked\nweight loss (or failure to make expected weight gains) has occurred. If individuals seek help\non their own, it is usually because of dist ress over the somatic and psychological sequelae\nof starvation. It is rare for an individual with anorexia nervosa to complain of weight loss\nper se. In fact, individuals with anorexia nervos a frequently either lack insight into or deny\nthe problem. It is therefore often important to obtain information from family members or\nother sources to evaluate the history of weight loss and other features of the illness.", "source": "dsm5.pdf"} {"id": "f27696263265-0", "page_content": "Anorexia Nervosa 341\nAssociated Features Supporting Diagnosis\nThe semi-starvation of anorex ia nervosa, and the purging behaviors sometimes associated\nwith it, can result in significant and potentially life-threatening medical conditions. The\nnutritional compromise associated with this disorder affects most major organ systems\nand can produce a variety of disturbances. Ph ysiological disturbances, including amenor-\nrhea and vital sign abnormalities, are comm on. While most of the physiological distur-\nbances associated with malnutrition are reversible with nutritiona l rehabilitation, some,\nincluding loss of bone mineral density, are often not completely re versible. Behaviors such\nas self-induced vomiting and misuse of laxa tives, diuretics, and enemas may cause a num-\nber of disturbances that lead to abnormal la boratory findings; howe ver, some individuals\nwith anorexia nervosa exhibit no laboratory abnormalities. \nWhen seriously underweight, ma ny individuals with anorex ia nervosa have depressive\nsigns and symptoms such as depressed mood, so cial withdrawal, irrita bility, insomnia, and\ndiminished interest in sex. Because these feat ures are also observed in individuals without\nanorexia nervosa who are significantly undern ourished, many of the depressive features\nmay be secondary to the physiological sequelae of semi-starvation, although they may also\nbe sufficiently severe to warr ant an additional diagnosis of major depressive disorder. \nObsessive-compulsive features, both related and unrelated to food, are often prominent.\nMost individuals with anorexia nervosa are pr eoccupied with thoughts of food. Some col-\nlect recipes or hoard food. Ob servations of behaviors associated with other forms of star-\nvation suggest that obsessions and compulsi ons related to food may be exacerbated by", "source": "dsm5.pdf"} {"id": "f27696263265-1", "page_content": "vation suggest that obsessions and compulsi ons related to food may be exacerbated by\nundernutrition. When individuals with anorexia nervosa exhibit obsessions and compul-\nsions that are not related to food, body shape, or weight, an additional diagnosis of obses-\nsive-compulsive disorder (OCD) may be warranted.\nOther features sometimes associated with anorexia nervosa incl ude concerns about\neating in public, feelings of ineffectiveness, a strong desire to control one\u2019s environment,\ninflexible thinking, limited social spontaneity, and overly restrained emotional ex-\npression. Compared with indivi duals with anorexia nervosa, restricting type, those with\nbinge-eating/purging type have higher rates of impulsivity and are more likely to abuse\nalcohol and other drugs. \nA subgroup of individuals with anorexia ne rvosa show excessive levels of physical ac-\ntivity. Increases in physical activity often precede onset of the disorder, and over the\ncourse of the disorder increased activity ac celerates weight loss. During treatment, exces-\nsive activity may be difficult to control, thereby jeopardizing weight recovery.\nIndividuals with anorexia nervosa may misu se medications, such as by manipulating\ndosage, in order to achieve we ight loss or avoid weight ga in. Individuals with diabetes\nmellitus may omit or reduce insulin doses in order to minimi ze carbohydrate metabolism. \nPrevalence\nThe 12-month prevalence of anorexia nervosa among youn g females is approximately\n0.4%. Less is known about prevalence among ma les, but anorexia nerv osa is far less com-\nmon in males than in females, with clinical populations generally reflecting approximately\na 10:1 female-to-male ratio. \nDevelopment and Course", "source": "dsm5.pdf"} {"id": "f27696263265-2", "page_content": "a 10:1 female-to-male ratio. \nDevelopment and Course\nAnorexia nervosa commonly begins during adolescence or young adulthood. It rarely be-\ngins before puberty or after age 40, but cases of both early and late onset have been de-\nscribed. The onset of this disorder is often a ssociated with a stressful life event, such as\nleaving home for college. The course and outcom e of anorexia nervosa are highly variable.\nYounger individuals may manifest atypical features, including denying \u201cfear of fat.\u201d Older", "source": "dsm5.pdf"} {"id": "e22288f4cbc8-0", "page_content": "342 Feeding and Eating Disorders\nindividuals more likely have a longer duration of illness, and their clinical presentation may\ninclude more signs and symptoms of long-stand ing disorder. Clinicians should not exclude\nanorexia nervosa from the differential diag nosis solely on the basis of older age.\nMany individuals have a period of changed ea ting behavior prior to full criteria for the\ndisorder being met. Some individuals with anorexia nervosa recover fully after a single\nepisode, with some ex hibiting a fluctuating pattern of weight gain followed by relapse,\nand others experiencing a chronic course over many years. Hospitalization may be re-\nquired to restore weight and to address medical complications. Most individuals with an-\norexia nervosa experience remission within 5 years of presentation. Among individuals\nadmitted to hospitals, overall remission rates may be lower. The crude mortality rate (CMR)\nfor anorexia nervosa is approximately 5% pe r decade. Death most commonly results from\nmedical complications associated with the disorder itself or from suicide.\nRisk and Prognostic Factors \nTemperamental. Individuals who develop anxiety disorders or display obsessional\ntraits in childhood are at increased risk of developing anorexia nervosa.\nEnvironmental. Historical and cross-cultural variab ility in the prevalence of anorexia\nnervosa supports its association with cultures and settings in which thinness is valued. Oc-\ncupations and avocations that encourage thinness, such as modeling and elite athletics, are\nalso associated with increased risk. \nGenetic and physiological. There is an increased risk of anorexia nervosa and bulimia\nnervosa among first-degree biolog ical relatives of individuals with the disorder. An in-\ncreased risk of bipolar and depressive diso rders has also been found among first-degree", "source": "dsm5.pdf"} {"id": "e22288f4cbc8-1", "page_content": "creased risk of bipolar and depressive diso rders has also been found among first-degree\nrelatives of individuals with anorexia nervos a, particularly relati ves of individuals with\nthe binge-eating/purging type. Concordance rates for anorexia nervosa in monozygotic\ntwins are significantly higher than those for dizygotic twins. A range of brain abnormali-\nties has been described in an orexia nervosa using functional imaging technologies (func-\ntional magnetic resonance imaging, positro n emission tomography). The degree to which\nthese findings reflect changes associated with malnutrition versus primary abnormalities\nassociated with the disorder is unclear.\nCulture-Related Diagnostic Issues\nAnorexia nervosa occurs across culturally and so cially diverse populations, although available\nevidence suggests cross-cultural variation in its occurrence and pres entation. Anorexia ner-\nvosa is probably most prevalent in post-industr ialized, high-income coun tries such as in the\nUnited States, many European c ountries, Australia, New Zealand, and Japan, but its incidence\nin most low- and middle-income countries is uncertain. Whereas the prevalence of anorexia\nnervosa appears comparatively low among Latino s, African Americans, and Asians in the\nUnited States, clinicians should be aware that mental health service utilization among individ-\nuals with an eating disorder is significantly lo wer in these ethnic groups and that the low rates\nmay reflect an ascertainment bias. The presenta tion of weight concer ns among individuals\nwith eating and feeding disorders varies substa ntially across cultural contexts. The absence of\nan expressed intense fear of we ight gain, sometimes referred to as \u201cfat phobia,\u201d appears to be\nrelatively more common in popu lations in Asia, where the rati onale for dietary restriction is", "source": "dsm5.pdf"} {"id": "e22288f4cbc8-2", "page_content": "commonly related to a more culturally sanction ed complaint such as gastrointestinal discom-\nfort. Within the United States, presentations with out a stated intense fear of weight gain may\nbe comparatively more common among Latino groups.\nDiagnostic Markers\nThe following laboratory abnorm alities may be observed in anorexia nervosa; their pres-\nence may serve to increase diagnostic confidence.", "source": "dsm5.pdf"} {"id": "27ad603b8ac1-0", "page_content": "Anorexia Nervosa 343\nHematology. Leukopenia is common, with the loss of all cell types but usually with ap-\nparent lymphocytosis. Mild anemia can occur, as well as thrombocytopenia and, rarely,\nbleeding problems. \nSerum chemistry. Dehydration may be reflected by an elevated blood urea nitrogen\nlevel. Hypercholesterolemia is common. Hepa tic enzyme levels may be elevated. Hypo-\nmagnesemia, hypozincemia, hypophosphatemia, and hyperamylasemia are occasionally\nobserved. Self-induced vomiting may lead to metabolic alkalosis (elevated serum bicarbon-\nate), hypochloremia, and hypokalemia; laxative abuse may cause a mild metabolic acidosis. \nEndocrine. Serum thyroxine (T4) levels are usually in the low-normal rang e; triiodothy-\nronine (T3) levels are decreased, while reverse T3 levels are elevated. Females have low se-\nrum estrogen levels, whereas males have low levels of se rum testosterone.\nElectrocardiography. Sinus bradycardia is common, and, rarely, arrhythmias are noted.\nSignificant prolongation of the QTc interv al is observed in some individuals. \nBone mass. Low bone mineral density, with specific areas of osteopenia or osteoporo-\nsis, is often seen. The risk of fr acture is significantly elevated.\nElectroencephalography. Diffuse abnormalities, reflecting a metabolic encephalopa-\nthy, may result from significant fluid and electrolyte disturbances. \nResting energy expenditure. There is often a significant redu ction in resting energy ex-\npenditure.", "source": "dsm5.pdf"} {"id": "27ad603b8ac1-1", "page_content": "penditure.\nPhysical signs and symptoms. Many of the physical sign s and symptoms of anorexia\nnervosa are attributable to starvation. Amen orrhea is commonly present and appears to\nbe an indicator of physiological dysfunction. If present, amenorrhea is usually a conse-\nquence of the weight loss, but in a minority of individuals it may actually precede the\nweight loss. In prepubertal females, menarche may be delayed. In addition to amenorrhea,\nthere may be complaints of constipation, abdo minal pain, cold intole rance, lethargy, and\nexcess energy.\nThe most remarkable finding on physical ex amination is emaciation. Commonly, there\nis also significant hypotension, hypothermia, and bradycardia. Some individuals develop\nlanugo, a fine downy body hair. Some de velop peripheral edema, especially during\nweight restoration or upon cessation of laxa tive and diuretic abuse. Rarely, petechiae or\necchymoses, usually on the extremities, may indicate a bleeding diathesis. Some individ-\nuals evidence a yellowing of the skin associat ed with hypercarotenemia. As may be seen in\nindividuals with bulimia nervosa, individu als with anorexia ne rvosa who self-induce\nvomiting may have hypertrophy of the salivary glands, particularly the parotid glands, as\nwell as dental enamel erosion. Some individu als may have scars or calluses on the dorsal\nsurface of the hand from repeated contac t with the teeth while inducing vomiting.\nSuicide Risk\nSuicide risk is elevated in anorexia nervosa, with rates reported as 12 per 100,000 per year.", "source": "dsm5.pdf"} {"id": "27ad603b8ac1-2", "page_content": "Comprehensive evaluation of individuals wi th anorexia nervosa should include assess-\nment of suicide-related ideation and behavior s as well as other risk factors for suicide, in-\ncluding a history of suicide attempt(s). \nFunctional Consequences of Anorexia Nervosa\nIndividuals with anorexia nervosa may exhibit a range of functional limitations associated\nwith the disorder. While some individuals rema in active in social and professional func-\ntioning, others demonstrate significant social isolation and/or failure to fulfill academic or\ncareer potential.", "source": "dsm5.pdf"} {"id": "191e429f0e88-0", "page_content": "344 Feeding and Eating Disorders\nDifferential Diagnosis\nOther possible causes of either significantly low body weight or significant weight loss\nshould be considered in the differential diagno sis of anorexia nervosa, especially when the\npresenting features are atypical (e.g., onset after age 40 years). \nMedical conditions (e.g., gastrointestinal disease, hyperthyroidism, occult malignan-\ncies, and acquired immunodeficiency syndrome [AIDS]). Serious weight loss may oc-\ncur in medical conditions, but individuals with these disorders usually do not also mani-\nfest a disturbance in the way their body weig ht or shape is experienced or an intense fear\nof weight gain or persist in behaviors that interfere with appropriate weight gain. Acute\nweight loss associated with a medical condition can occasionally be followed by the onset\nor recurrence of anorexia nervosa, which can initially be masked by the comorbid medical\ncondition. Rarely, anorexia nervosa develo ps after bariatric surgery for obesity. \nMajor depressive disorder. In major depressive disorder, severe weight loss may occur,\nbut most individuals with major depressive diso rder do not have either a desire for exces-\nsive weight loss or an inte nse fear of gaining weight. \nSchizophrenia. Individuals with schizophrenia may exhibit odd eating behavior and oc-\ncasionally experience significant weight loss, but they rarely show the fear of gaining\nweight and the body image disturbance requir ed for a diagnosis of anorexia nervosa. \nSubstance use disorders. Individuals with subs tance use disorders may experience low\nweight due to poor nutritional intake but gene rally do not fear gaining weight and do not\nmanifest body image di sturbance. Individuals who abuse substances that reduce appetite\n(e.g., cocaine, stimulan ts) and who also endorse fear of weight gain should be carefully", "source": "dsm5.pdf"} {"id": "191e429f0e88-1", "page_content": "evaluated for the possibility of comorbid anorexia nervosa, given that the substance use\nmay represent a persistent behavior that inte rferes with weight gain (Criterion B).\nSocial anxiety disorder (social phobia), ob sessive-compulsive disorder, and body dys-\nmorphic disorder. Some of the features of anorexia ne rvosa overlap with the criteria for\nsocial phobia, OCD, and body dysmorphic diso rder. Specifically, individuals may feel hu-\nmiliated or embarrassed to be seen eating in public, as in social phobia; may exhibit obses-\nsions and compulsions related to food, as in OCD; or may be preoccupied with an imagined\ndefect in bodily appearance, as in body dysmor phic disorder. If the in dividual with anorexia\nnervosa has social fears that are limited to eating behavior alone, the diagnosis of social pho-\nbia should not be made, but social fears unrelate d to eating behavior (e.g., excessive fear of\nspeaking in public) may warrant an additional diagnosis of social phobia. Similarly, an ad-\nditional diagnosis of OCD should be considered only if the individu al exhibits obsessions\nand compulsions unrelated to food (e.g., an ex cessive fear of contamination), and an addi-\ntional diagnosis of body dysmorphic disorder sh ould be considered only if the distortion is\nunrelated to body shape and size (e.g., preoccupation th at one\u2019s nose is too big).\nBulimia nervosa. Individuals with bulimia nervosa ex hibit recurrent ep isodes of binge\neating, engage in inappropriat e behavior to avoid weight ga in (e.g., self-induced vomit-\ning), and are overly concerned with body sh ape and weight. However, unlike individuals", "source": "dsm5.pdf"} {"id": "191e429f0e88-2", "page_content": "ing), and are overly concerned with body sh ape and weight. However, unlike individuals\nwith anorexia nervosa, binge-eating/purging type, individuals with bulimia nervosa main-\ntain body weight at or ab ove a minimally normal level.\nAvoidant/restrictive food intake disorder. Individuals with this disorder may exhibit\nsignificant weight loss or significant nutritiona l deficiency, but they do not have a fear of\ngaining weight or of becoming fat, nor do th ey have a disturbance in the way they expe-\nrience their body shape and weight. \nComorbidity", "source": "dsm5.pdf"} {"id": "4228cd0a6431-0", "page_content": "gaining weight or of becoming fat, nor do th ey have a disturbance in the way they expe-\nrience their body shape and weight. \nComorbidity\nBipolar, depressive, and anxiety disorders commonly co-occur with anorexia nervosa.\nMany individuals with anorexia nervosa report the presence of either an anxiety disorder", "source": "dsm5.pdf"} {"id": "f707d82d72d2-0", "page_content": "Bulimia Nervosa 345\nor symptoms prior to onset of their eating d isorder. OCD is described in some individuals\nwith anorexia nervosa, especially those with the restricting type. Alcohol use disorder and\nother substance use disorders may also be co morbid with anorexia nervosa, especially\namong those with the binge-eating/purging type.\nBulimia Nervosa\nDiagnostic Criteria 307.51 (F50.2)\nA. Recurrent episodes of binge eating. An episode of binge eating is characterized by\nboth of the following:\n1. Eating, in a discrete period of time (e.g.,\u00a0within any 2-hour period), an amount of\nfood that is definitely larger than what most individuals would eat in a similar period\nof time under similar circumstances.\n2. A sense of lack of control over eating during the episode (e.g., a feeling that one\ncannot stop eating or control what or how much one is eating).\nB. Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such\nas self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting;\nor excessive exercise.\nC. The binge eating and inappropriate compensatory behaviors both occur, on average,\nat least once\u00a0a week for 3 months.\nD. Self-evaluation is unduly influenced by body shape and weight.\nE. The disturbance does not occur exclusively during episodes of anorexia nervosa.\nSpecify if:\nIn partial remission: After full criteria for bulimia nervosa were previously met, some,\nbut not all, of the criteria have been met for a sustained period of time.\nIn full remission: After full criteria for bulimia nervosa were previously met, none of\nthe criteria have been met for a sustained period of time.\nSpecify current severity:", "source": "dsm5.pdf"} {"id": "f707d82d72d2-1", "page_content": "the criteria have been met for a sustained period of time.\nSpecify current severity:\nThe minimum level of severity is based on the frequency of inappropriate compensatory\nbehaviors (see below). The level of severity may be increased to reflect other symptoms\nand the degree of functional disability.\nMild: An average of 1\u20133 episodes of inappropriate compensatory behaviors per week.\nModerate: An average of 4\u20137 episodes of inappropriate compensatory behaviors per\nweek.\nSevere: An average of 8\u201313 episodes of inappropriate compensatory behaviors per\nweek.\nExtreme: An average of 14 or more episodes of inappropriate compensatory behav-\niors per week.\nDiagnostic Features\nThere are three essential features of bulimia nervosa: recurrent episodes of binge eating\n(Criterion A), recurrent inappropriate comp ensatory behaviors to prevent weight gain\n(Criterion B), and self-evaluat ion that is unduly influenced by body shape and weight\n(Criterion D). To qualify for the diagnosis, the binge eating and inappropriate compensa-\ntory behaviors must occur, on average, at least once per week for 3 months (Criterion C).\nAn \u201cepisode of binge eating\u201d is defined as eating, in a discrete period of time, an\namount of food that is definitely larger than most individuals would eat in a similar period\nof time under similar circumstances (Criterion A1). The context in which the eating occurs", "source": "dsm5.pdf"} {"id": "b4d2dca84a7a-0", "page_content": "346 Feeding and Eating Disorders\nmay affect the clinician\u2019s esti mation of whether the intake is excessive. For example, a\nquantity of food that might be regarded as excessive for a typical meal might be consid-\nered normal during a celebration or holiday me al. A \u201cdiscrete period of time\u201d refers to a\nlimited period, usually less than 2 hours. A single episode of binge eating need not be re-\nstricted to one setting. For example, an individual may begin a binge in a restaurant and\nthen continue to eat on re turning home. Continual snacki ng on small amounts of food\nthroughout the day would not be considered an eating binge. \nAn occurrence of excessive food consumptio n must be accompanied by a sense of lack\nof control (Criterion A2) to be considered an episode of binge eating. An indicator of loss\nof control is the inability to refrain from eating or to stop eating once started. Some indi-\nviduals describe a dissociative quality during , or following, the bing e-eating episodes. The\nimpairment in control associated with binge eating may not be abso lute; for example, an\nindividual may continue binge eating while the telephone is ringing but will cease if a\nroommate or spouse unexpected ly enters the room. Some in dividuals report that their\nbinge-eating episodes are no longer characterize d by an acute feeling of loss of control but\nrather by a more generalized pattern of uncont rolled eating. If individuals report that they\nhave abandoned efforts to control their eati ng, loss of control should be considered as\npresent. Binge eating can also be planned in some instances.\nThe type of food co nsumed during binges varies both across individuals and for a\ngiven individual. Binge eating appears to be characterized more by an abnormality in the", "source": "dsm5.pdf"} {"id": "b4d2dca84a7a-1", "page_content": "given individual. Binge eating appears to be characterized more by an abnormality in the\namount of food consumed than by a craving for a specific nutrient. However, during binges,\nindividuals tend to eat foods they would otherwise avoid. \nIndividuals with bulimia nervosa are typica lly ashamed of their eating problems and\nattempt to conceal their symptoms. Binge eating usually occurs in secrecy or as inconspic-\nuously as possible. The binge eating often cont inues until the individual is uncomfortably,\nor even painfully, full. The most common antecedent of binge eating is negative affect.\nOther triggers include interpersonal stressors; dietary restraint; negative feelings related\nto body weight, body shape, and food; and boredom. Binge eating may minimize or mit-\nigate factors that precipitated the episode in the short-term, but negative self-evaluation\nand dysphoria often are the delayed consequences.\nAnother essential feature of bulimia nervosa is the recurrent use of inappropriate com-\npensatory behaviors to prevent weight gain, collectively referred to as purge behaviors or\npurging (Criterion B). Many individuals with bulimia nervosa employ several methods to\ncompensate for binge eating. Vomiting is the most common inappropriate compensatory\nbehavior. The immediate effects of vomiting include relief from physical discomfort and re-\nduction of fear of gaining weight. In some cases, vomiting becomes a goal in itself, and the\nindividual will binge eat in orde r to vomit or will vomit after eating a small amount of food.\nIndividuals with bulimia nervosa may use a vari ety of methods to induce vomiting, includ-\ning the use of fingers or instruments to stimulate the gag reflex. Individuals generally\nbecome adept at inducing vomit ing and are eventually able to vomit at will. Rarely, indi-", "source": "dsm5.pdf"} {"id": "b4d2dca84a7a-2", "page_content": "viduals consume syrup of ipecac to induce vomiting. Other purging behaviors include the\nmisuse of laxatives and diuretics. A number of other compensatory methods may also be\nused in rare cases. Individuals with bulim ia nervosa may misuse enemas following epi-\nsodes of binge eating, but this is seldom th e sole compensatory method employed. Individ-\nuals with this disorder may take thyroid ho rmone in an attempt to avoid weight gain.", "source": "dsm5.pdf"} {"id": "dd9f8235e899-0", "page_content": "sodes of binge eating, but this is seldom th e sole compensatory method employed. Individ-\nuals with this disorder may take thyroid ho rmone in an attempt to avoid weight gain.\nIndividuals with diabetes mellitus and bulimia nervosa may omit or reduce insulin doses in\norder to reduce the metabolism of food cons umed during eating bi nges. Individuals with\nbulimia nervosa may fast for a da y or more or exercise excessive ly in an attempt to prevent\nweight gain. Exercise may be considered excessi ve when it significantly interferes with im-\nportant activities, when it occurs at inappr opria te times or in i nappropriate settings, or\nwhen the individual continues to exercise despite injury or other medical complications.\nIndividuals with bulimia nervosa place an ex cessive emphasis on body shape or weight\nin their self-evaluation, and these factors ar e typically extremely important in determining", "source": "dsm5.pdf"} {"id": "9078eaafc90a-0", "page_content": "Bulimia Nervosa 347\nself-esteem (Criterion D). Individuals with this disorder may closely resemble those with\nanorexia nervosa in their fear of gaining weight, in their desire to lose weight, and in the\nlevel of dissatisfaction with their bodies. Ho wever, a diagnosis of bulimia nervosa should\nnot be given when the disturbance occurs only during episodes of anorexia nervosa (Cri-\nterion E).\nAssociated Features Supporting Diagnosis\nIndividuals with bulimia nervosa typically ar e within the normal weight or overweight\nrange (body mass index [BMI] \u2265 18.5 and < 30 in adults). The disorder occurs but is un-\ncommon among obese individuals. Between eati ng binges, individuals with bulimia ner-\nvosa typically restrict their to tal caloric consumption and preferentially select low-calorie\n(\u201cdiet\u201d) foods while avoiding foods that they pe rceive to be fattening or likely to trigger a\nbinge.\nMenstrual irregularity or amenorrhea ofte n occurs among females with bulimia ner-\nvosa; it is uncertain whether su ch disturbances are related to weight fluctuations, to nu-\ntritional deficiencies, or to emotional dist ress. The fluid and electrolyte disturbances\nresulting from the purging behavior are some times sufficiently severe to constitute med-\nically serious problems. Rare but potentially fatal complications include esophageal tears,\ngastric rupture, and cardiac arrhythmias. Serious cardiac and skeletal myopathies have\nbeen reported among individual s following repeated use of syrup of ipecac to induce vom-\niting. Individuals who chronically abuse laxatives may become dependent on their use to\nstimulate bowel movements. Gastrointestin al symptoms are commonly associated with\nbulimia nervosa, and rectal prolapse has also been reported among individuals with this", "source": "dsm5.pdf"} {"id": "9078eaafc90a-1", "page_content": "disorder.\nPrevalence\nTwelve-month prevalence of bulimia ner vosa among young female s is 1%\u20131.5%. Point\nprevalence is highest among young adults si nce the disorder peaks in older adolescence\nand young adulthood. Less is known about th e point prevalence of bulimia nervosa in\nmales, but bulimia nervosa is far less common in males than it is in females, with an ap-\nproximately 10:1 female-to-male ratio. \nDevelopment and Course\nBulimia nervosa commonly begins in adolesce nce or young adulthood. Onset before pu-\nberty or after age 40 is uncommon. The binge eating frequently begins during or after an\nepisode of dieting to lose weight. Experiencing multiple stressful lif e events also can pre-\ncipitate onset of bulimia nervosa.\nDisturbed eating behavior persists for at least several years in a high percentage of\nclinic samples. The course may be chronic or intermittent, with periods of remission\nalternating with recurrences of binge eating. However, over longer -term follow-up, the\nsymptoms of many individuals appear to diminish with or without treatment, although\ntreatment clearly impacts outcome. Periods of remission longer than 1 year are associated\nwith better long-term outcome.\nSignificantly elevated risk fo r mortality (all-cause and suic ide) has been reported for\nindividuals with bulimia nervosa. The CMR (c rude mortality rate) for bulimia nervosa is\nnearly 2% per decade. \nDiagnostic cross-over from initial bulimia ne rvosa to anorexia nervosa occurs in a mi-\nnority of cases (10%\u201315%). Individuals who do experience cross-over to anorexia nervosa", "source": "dsm5.pdf"} {"id": "9078eaafc90a-2", "page_content": "commonly will revert back to bulimia nervosa or have multiple occurrences of cross-overs\nbetween these disorders. A subset of individu als with bulimia nervosa continue to binge\neat but no longer engage in inappropriate compensatory behaviors, and therefore their", "source": "dsm5.pdf"} {"id": "c332a027d6c5-0", "page_content": "348 Feeding and Eating Disorders\nsymptoms meet criteria for binge-eating disord er or other specified eating disorder. Diag-\nnosis should be based on the current (i.e., past 3 months) clinical presentation.\nRisk and Prognostic Factors \nTemperamental. Weight concerns, low self-esteem, de pressive symptoms, social anxi-\nety disorder, and overanxious d isorder of childhood are associated with increased risk for\nthe development of bulimia nervosa. \nEnvironmental. Internalization of a thin body ideal has been found to increase risk for\ndeveloping weight concerns, which in turn increase risk for the development of bulimia\nnervosa. Individuals who experienced childhood sexual or physical abuse are at increased\nrisk for developing bulimia nervosa. \nGenetic and physiological. Childhood obesity and early pubertal maturation increase\nrisk for bulimia nervosa. Familial transmission of bulimia ne rvosa may be present, as well\nas genetic vulnerabilities for the disorder.\nCourse modifiers. Severity of psychiatric comorbidity predicts worse long-term outcome\nof bulimia nervosa.\nCulture-Related Diagnostic Issues\nBulimia nervosa has been reported to occur wi th roughly similar frequencies in most in-\ndustrialized countries, including the United States, Canada, many European countries,\nAustralia, Japan, New Zealand, and South Afri ca. In clinical studies of bulimia nervosa in\nthe United States, individuals presenting with this disorder are pr imarily white. However,\nthe disorder also occurs in ot her ethnic groups and with prevalence comparable to esti-\nmated prevalences observed in white samples.\nGender-Related Diagnostic Issues\nBulimia nervosa is far more common in females than in males. Males are especially under-", "source": "dsm5.pdf"} {"id": "c332a027d6c5-1", "page_content": "represented in treatment-seeking samples, for reasons that have not yet been systemati-\ncally examined.\nDiagnostic Markers\nNo specific diagnostic test for bulimia nerv osa currently exists. However, several labora-\ntory abnormalities may occur as a conseque nce of purging and may increase diagnostic\ncertainty. These include fluid and electrolyte abnormalities, such as hypokalemia (which\ncan provoke cardiac arrhythmias), hypochloremia, and hyponatremia. The loss of gastric\nacid through vomiting may prod uce a metabolic alkalosis (elevated serum bicarbonate),\nand the frequent induction of diarrhea or de hydration through laxative and diuretic abuse\ncan cause metabolic acidosis. Some individual s with bulimia nervosa exhibit mildly ele-\nvated levels of serum amylase, pr obably reflecting an increase in the salivary isoenzyme.\nPhysical examination usually yields no physical findings. However, inspection of the\nmouth may reveal significant and permanent loss of dental enamel, especially from lin-\ngual surfaces of the front teeth due to recurrent vomiting. These teeth may become\nchipped and appear ragged and \u201cmoth-eaten.\u201d There may also be an increased frequency\nof dental caries. In some individuals, the salivary glands, particularly the parotid glands,\nmay become notably enlarged. Individuals who induce vomiting by manually stimulating\nthe gag reflex may develop calluses or scars on the dorsal surface of the hand from re-\npeated contact with the teeth. Serious cardia c and skeletal myopathies have been reported\namong individuals following repeated use of syrup of ipecac to induce vomiting.", "source": "dsm5.pdf"} {"id": "832184a7e67f-0", "page_content": "Bulimia Nervosa 349\nSuicide Risk\nSuicide risk is elevated in bu limia nervosa. Comprehensive ev aluation of individuals with\nthis disorder should include assessment of su icide-related ideation and behaviors as well\nas other risk factors for suicide, including a history of suicide attempts.\nFunctional Consequences of Bulimia Nervosa\nIndividuals with bulimia nervosa may exhibit a range of functional limitations associated\nwith the disorder. A minority of individuals report severe role impairment, with the so-\ncial-life domain most likely to be ad versely affected by bulimia nervosa. \nDifferential Diagnosis\nAnorexia nervosa, binge-eating/purging type. Individuals whose bi nge-eating behav-\nior occurs only during episodes of anorexia nervosa are given the diagnosis anorexia ner-\nvosa, binge-eating/purging type, and should not be given the additional diagnosis of\nbulimia nervosa. For individuals with an init ial diagnosis of anorexia nervosa who binge\nand purge but whose presentation no longer meets the full criteria for anorexia nervosa,\nbinge-eating/purging type (e.g., when weight is normal), a diagnosis of bulimia ner-\nvosa should be given only when all criteria for bulimia nervosa have been met for at least\n3m o n t h s . \nBinge-eating disorder. Some individuals binge eat but do not engage in regular inap-\npropriate compensatory behaviors. In these ca ses, the diagnosis of binge-eating disorder\nshould be considered.\nKleine-Levin syndrome. In certain neurological or other medical conditions, such as\nKleine-Levin syndrome, there is disturbed eating behavior, but the characteristic psycho-", "source": "dsm5.pdf"} {"id": "832184a7e67f-1", "page_content": "Kleine-Levin syndrome, there is disturbed eating behavior, but the characteristic psycho-\nlogical features of bulimia nervosa, such as overconcern with body shape and weight, are\nnot present. \nMajor depressive disorder, with atypical features. Overeating is common in major de-\npressive disorder, with atypical features, but individuals with this disorder do not engage\nin inappropriate compensatory behaviors an d do not exhibit the excessive concern with\nbody shape and weight characteristic of bulimia nervosa. If criteria for both disorders are\nmet, both diagnoses should be given. \nBorderline personality disorder. Binge-eating behavior is included in the impulsive be-\nhavior criterion that is part of the definition of borderline personality disorder. If the cri-\nteria for both borderline personality disorder and bulimia nervosa are met, both diagnoses\nshould be given.\nComorbidity \nComorbidity with mental diso rders is common in individuals with bulimia nervosa, with\nmost experiencing at least on e other mental disorder and many experiencing multiple co-\nmorbidities. Comorbidity is not limited to any particular su bset but rather occurs across a\nwide range of mental disorders. There is an increased frequency of depressive symptoms\n(e.g., low self-esteem) and bipo lar and depressive disorders (particularly depressive dis-\norders) in individuals with bu limia nervosa. In many indivi duals, the mood disturbance\nbegins at the same time as or following th e development of bulimia nervosa, and individ-\nuals often ascribe their mood disturbances to the bulimia nervosa. However, in some in-\ndividuals, the mood disturbance clearly precedes the development of bulimia nervosa.\nThere may also be an increased frequency of anxiety symptoms (e.g., fear of social situa-", "source": "dsm5.pdf"} {"id": "832184a7e67f-2", "page_content": "tions) or anxiety disorders. These mood and anxiety disturbances fr equently remit follow-", "source": "dsm5.pdf"} {"id": "18867adeda2e-0", "page_content": "350 Feeding and Eating Disorders\ning effective treatment of the bulimia nervosa. The lifetime prevalence of substance use,\nparticularly alcohol or stimulant use, is at least 30% among individuals with bulimia ner-\nvosa. Stimulant use often begins in an attempt to control appetite and weight. A substan-\ntial percentage of individuals with bulimia nervosa also have personality features that\nmeet criteria for one or more personality diso rders, most frequently borderline personality\ndisorder.\nBinge-Eating Disorder\nDiagnostic Criteria 307.51 (F50.8)\nA. Recurrent episodes of binge eating. An episode of binge eating is characterized\nby\u00a0both of the following:\n1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of\nfood that is definitely larger than what most people would eat in a similar period of\ntime under similar circumstances.\n2. A sense of lack of control over eating during the episode (e.g., a feeling that one\ncannot stop eating or control what or how much one is eating).\nB. The binge-eating episodes are associated with three (or more) of the following:\n1. Eating much more rapidly than normal.\n2. Eating until feeling uncomfortably full.\n3. Eating large amounts of food when not feeling physically hungry.\n4. Eating alone because of\u00a0feeling embarrassed by how much one is eating.\n5. Feeling disgusted with oneself, depressed, or very guilty afterward.\nC. Marked distress regarding binge eating is present.\nD. The binge eating occurs, on average, at least once a week for 3 months.\nE. The binge eating is not associated with the recurrent use of inappropriate compensa-\ntory behavior as in bulimia nervosa and does not occur exclusively during the course", "source": "dsm5.pdf"} {"id": "18867adeda2e-1", "page_content": "tory behavior as in bulimia nervosa and does not occur exclusively during the course\nof bulimia nervosa or anorexia nervosa.\nSpecify if:\nIn partial remission: After full criteria for binge-eating disorder were previously met,\nbinge eating occurs at an average frequency of less than one episode per week for a\nsustained period of time. \nIn full remission: After full criteria for binge-eating disorder were previously met, none\nof the criteria have been met for a sustained period of time.\nSpecify current severity:\nThe minimum level of severity is based on the frequency of episodes of binge eating (see\nbelow). The level of severity may be increased to reflect other symptoms and the degree\nof functional disability.\nMild: 1\u20133 binge-eating episodes per week.\nModerate: 4\u20137 binge-eating episodes per week.\nSevere: 8\u201313 binge-eating episodes per week.\nExtreme: 14 or more binge-eating episodes per week.\nDiagnostic Features\nThe essential feature of binge-eating disorder is recurrent episodes of binge eating that\nmust occur, on average, at le ast once per week for 3 months (Criterion D). An \u201cepisode of\nbinge eating\u201d is defined as eating, in a discrete pe riod of time, an amount of food that is defi-", "source": "dsm5.pdf"} {"id": "36a5f66f1c72-0", "page_content": "Binge-Eating Disorder 351\nnitely larger than most people would eat in a similar period of time under similar circum-\nstances (Criterion A1). The context in which the eating occurs may affect the clinician\u2019s\nestimation of whether the intake is excessive. For example, a quantity of food that might be\nregarded as excessive for a typical meal migh t be considered normal during a celebration\nor holiday meal. A \u201cdiscrete period of time\u201d refers to a limited pe riod, usually less than\n2 hours. A single episode of binge eating need not be restricted to one setting. For example,\nan individual may begin a binge in a restaurant and then continue to eat on returning\nhome. Continual snacking on small amounts of food throughout the day would not be con-\nsidered an eating binge. \nAn occurrence of excessive food consumptio n must be accompanie d by a sense of lack\nof control (Criterion A2) to be considered an episode of binge eating. An indicator of loss\nof control is the inability to refrain from eating or to stop eating once started. Some indi-\nviduals describe a dissociative quality during , or following, the bing e-eating episodes. The\nimpairment in control associated with binge eating may not be abso lute; for example, an\nindividual may continue binge eating while the telephone is ringing but will cease if a\nroommate or spouse unexpected ly enters the room. Some in dividuals report that their\nbinge-eating episodes are no longer characterize d by an acute feeling of loss of control but\nrather by a more generalized pattern of uncont rolled eating. If individuals report that they\nhave abandoned efforts to control their eating , loss of control may still be considered as\npresent. Binge eating can also be planned in some instances.", "source": "dsm5.pdf"} {"id": "36a5f66f1c72-1", "page_content": "present. Binge eating can also be planned in some instances.\nThe type of food consumed during binges varies both across individuals and for a given\nindividual. Binge eating appears to be characterized more by an abnormality in the amount\nof food consumed than by a cr aving for a specific nutrient.\nBinge eating must be characterized by marked distress (Criterion C) and at least three\nof the following features: eating much more rapidly than normal; eating until feeling un-\ncomfortably full; eating large amounts of food when not feeling physically hungry; eating\nalone because of\u00a0feeling embarrassed by how much one is eating; and feeling disgusted\nwith oneself, depressed, or very guilty afterward (Criterion B).\nIndividuals with binge-eating disorder are typically ashamed of their eating problems\nand attempt to conceal their symptoms. Binge ea ting usually occurs in secrecy or as incon-\nspicuously as possible. The most common antece dent of binge eating is negative affect.\nOther triggers include interpersonal stressors; dietary restraint; negative feelings related\nto body weight, body shape, and food; and boredom. Binge eating may minimize or mit-\nigate factors that precipitated the episode in the short-term, but negative self-evaluation\nand dysphoria often are the delayed consequences.\nAssociated Features Supporting Diagnosis\nBinge-eating disorder occurs in normal-weight/ overweight and obese individuals. It is re-\nliably associated with overweight and obes ity in treatment-seekin g individuals. Never-\ntheless, binge-eating disorder is distinct from obesity. Most obese individuals do not\nengage in recurrent binge eating. In addition, compared with weight-matched obese indi-\nviduals without binge-eating disorder, those with the disorder consume more calories in\nlaboratory studies of eating behavior and ha ve greater functional impairment, lower qual-", "source": "dsm5.pdf"} {"id": "36a5f66f1c72-2", "page_content": "laboratory studies of eating behavior and ha ve greater functional impairment, lower qual-\nity of life, more subjective distress, and greater psychiatric comorbidity.\nPrevalence\nTwelve-month prevalence of binge-eating disorder among U.S. adult (age 18 or older) fe-\nmales and males is 1.6% and 0.8%, respectively. The gender ratio is far less skewed in binge-\neating disorder than in bulimia nervosa. Bing e-eating disorder is as prevalent among fe-", "source": "dsm5.pdf"} {"id": "aa2521dcfe9f-0", "page_content": "males and males is 1.6% and 0.8%, respectively. The gender ratio is far less skewed in binge-\neating disorder than in bulimia nervosa. Bing e-eating disorder is as prevalent among fe-\nmales from racial or ethnic minority groups as has been reported for white females. The\ndisorder is more prevalent among individual s seeking weight-loss treatment than in the\ngeneral population.", "source": "dsm5.pdf"} {"id": "0bc1b5eca31b-0", "page_content": "352 Feeding and Eating Disorders\nDevelopment and Course\nLittle is known about the deve lopment of binge-eating disorder. Both binge eating and\nloss-of-control eating without objectively ex cessive consumption occur in children and are\nassociated with increased body fat, weight gain, and increases in psychological symptoms.\nBinge eating is common in adolescent and college-age samples. Loss -of-control eating or\nepisodic binge eating may represent a prodroma l phase of eating disorders for some indi-\nviduals. \nDieting follows the development of binge eating in many indi viduals with binge-\neating disorder. (This is in contrast to bu limia nervosa, in which dysfunctional dieting\nusually precedes the onset of binge eating.) Binge-eating disorder typically begins in ad-\nolescence or young adulthood but can begin in later adulthood. In dividuals with binge-\neating disorder who seek treatment usually ar e older than individuals with either bulimia\nnervosa or anorexia nerv osa who seek treatment.\nRemission rates in both natural course an d treatment outcome studies are higher for\nbinge-eating disorder than fo r bulimia nervosa or anorexia nervosa. Binge-eating disorder\nappears to be relatively persistent, and the cour se is comparable to that of bulimia nervosa\nin terms of severity and duration. Crossover from binge-eating diso rder to other eating\ndisorders is uncommon.\nRisk and Prognostic Factors \nGenetic and physiological. Binge-eating disorder appears to run in families, which may\nreflect additive genetic influences. \nCulture-Related Diagnostic Issues\nBinge-eating disorder occurs with roughly similar frequencies in most industrialized\ncountries, including the United States, Cana da, many European countries, Australia, and", "source": "dsm5.pdf"} {"id": "0bc1b5eca31b-1", "page_content": "countries, including the United States, Cana da, many European countries, Australia, and\nNew Zealand. In the United States, the prevalence of binge-eating disorder appears com-\nparable among non-Latino whites, Latinos, Asians, and African Americans.\nFunctional Consequences of Binge-Eating Disorder\nBinge-eating disorder is associated with a ra nge of functional consequences, including so-\ncial role adjustment problems, impaired health-related quality of life and life satisfaction,\nincreased medical morbidity and mortality, an d associated increased health care utiliza-\ntion compared with body mass index (BMI)\u2013ma tched control subjects. It may also be as-\nsociated with an increased risk for weig ht gain and the development of obesity.\nDifferential Diagnosis\nBulimia nervosa. Binge-eating disorder has recurrent binge eating in common with bu-\nlimia nervosa but differs from the latter disord er in some fundamental respects. In terms of\nclinical presentation, the recurrent inapprop riate compensatory behavior (e.g., purging,\ndriven exercise) seen in bulim ia nervosa is absent in binge-eating disorder. Unlike in-\ndividuals with bulimia nervosa, individuals wi th binge-eating disorder typically do not\nshow marked or sustained dietary restriction designed to influence body weight and\nshape between binge-eating episodes. They may, however, report frequent attempts at\ndieting. Binge-eating disorder al so differs from bulimia nervosa in terms of response to treat-\nment. Rates of improvement ar e consistently higher among individuals with binge-eating\ndisorder than among those with bulimia nervosa.\nObesity. Binge-eating disorder is associated with overweight and obesity but has\nseveral key features that are distinct from ob esity. First, levels of overvaluation of body", "source": "dsm5.pdf"} {"id": "5bc2af34dab4-0", "page_content": "Other Specified Feeding or Eating Disorder 353\nweight and shape are higher in obese individuals with the disorder than in those without\nthe disorder. Second, rates of psychiatric comorbidity are significantly higher among\nobese individuals with the disorder compared with those without the disorder. Third, the\nlong-term successful outcome of evidence-based psychological treatments for binge-\neating disorder can be contrasted with the absence of effective long-term treatments for\nobesity.\nBipolar and depressive disorders. Increases in appetite and weight gain are included\nin the criteria for major depressive episode an d in the atypical features specifiers for de-\npressive and bipolar disorders. Increased eati ng in the context of a major depressive epi-\nsode may or may not be associated with loss of control. If the full crit eria for both disorders\nare met, both diagnoses can be given. Binge eating and other symptoms of disordered eat-\ning are seen in association with bipolar disorder . If the full criteria for both disorders are\nmet, both diagnoses should be given.\nBorderline personality disorder. Binge eating is included in the impulsive behavior cri-\nterion that is part of the definition of border line personality disorder. If the full criteria for\nboth disorders are met, both diagnoses should be given.\nComorbidity \nBinge-eating disorder is associated with si gnificant psychiatric comorbidity that is com-\nparable to that of bulimia ne rvosa and anorexia nervosa. Th e most common comorbid dis-\norders are bipolar disorders, depressive disorders, anxiety disorders, and, to a lesser\ndegree, substance use disorders. The psychiat ric comorbidity is linked to the severity of\nbinge eating and not to the degree of obesity.\nOther Specified Feeding or Eating Disorder\n307.59 (F50.8)", "source": "dsm5.pdf"} {"id": "5bc2af34dab4-1", "page_content": "Other Specified Feeding or Eating Disorder\n307.59 (F50.8)\nThis category applies to presentations in wh ich symptoms characteristic of a feeding and\neating disorder that cause clinically significant distress or impairment in social, occupation-\nal, or other important areas of functioning predominate but do not meet the full criteria for\nany of the disorders in the feeding and eating disorders diagnostic class. The other spec-\nified feeding or eating disorder category is used in situations in which the clinician chooses\nto communicate the specific reason that the presentation does not meet the criteria for any\nspecific feeding and eating disorder. This is done by recording \u201cother specified feeding or\neating disorder\u201d followed by the specific reason (e.g., \u201cbulimia nervosa of low frequency\u201d).\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Atypical anorexia nervosa: All of the criteria for anorexia nervosa are met, except\nthat despite significant weight loss, the indi vidual\u2019s weight is within or above the normal\nrange.\n2.Bulimia nervosa (of low freque ncy and/or limited duration): All of the criteria for\nbulimia nervosa are met, except that the binge eating and inappropriate compensatory\nbehaviors occur, on average, less than once a week and/or for less than 3 months.\n3.Binge-eating disorder (of low frequency and/ or limited duration): All of the criteria\nfor binge-eating disorder are met, except that the binge eating occurs, on average, less\nthan once a week and/or for less than 3 months.\n4.Purging disorder: Recurrent purging behavior to influence weight or shape (e.g., self-\ninduced vomiting; misuse of laxatives, diur etics, or other medications) in the absence", "source": "dsm5.pdf"} {"id": "5bc2af34dab4-2", "page_content": "of binge eating.", "source": "dsm5.pdf"} {"id": "b03670a3652a-0", "page_content": "354 Feeding and Eating Disorders\n5.Night eating syndrome: Recurrent episodes of night eating, as manifested by eating\nafter awakening from sleep or by excessive food consumption after the evening meal.\nThere is awareness and recall of the eating. The night eating is not better explained by\nexternal influences such as changes in the individual\u2019s sleep-wake cycle or by local so-\ncial norms. The night eating causes significant distress and/or impairment in function-\ning. The disordered pattern of eating is not better explained by binge-eating disorder\nor another mental disorder, including substance use, and is not attributable to another\nmedical disorder or to an effect of medication.\nUnspecified Feeding or Eating Disorder\n307.50 (F50.9)\nThis category applies to presentations in which symptoms characteristic of a feeding and\neating disorder that cause clinically significant distress or impairment in social, occupation-\nal, or other important areas of functioning predominate but do not meet the full criteria for\nany of the disorders in the feeding and eating disorders diagnostic class. The unspecified\nfeeding or eating disorder category is used in situations in which the clinician chooses not\nto specify the reason that the criteria are not met for a specific feeding and eating disorder,\nand includes presentations in which there is insufficient information to make a more spe-\ncific diagnosis (e.g., in emergency room settings).", "source": "dsm5.pdf"} {"id": "5b68674020cd-0", "page_content": "355Elimination\n Disorders\nElimination disorders all involve the inappropriate elimination of urine or feces\nand are usually first diagnosed in childhood or adolescence. This group of disorders in-\ncludes enuresis, the repeated voiding of urine into inappropriate places, and encopresis, the\nrepeated passage of feces into inappropriate places. Subtypes are provided to differentiate\nnocturnal from diurnal (i.e., during waking hours) voiding for enuresis and the presence or\nabsence of constipation and ove rflow incontinence for encopresis. Although there are min-\nimum age requirements for diagnosis of both disorders, these are based on developmental\nage and not solely on chronological age. Both disorders may be volun tary or involuntary.\nAlthough these disorder s typically occur separa tely, co-occurrence may also be observed. \nEnuresis\nDiagnostic Criteria 307.6 (F98.0)\nA. Repeated voiding of urine into bed or clothes, whether involuntary or intentional.\nB. The behavior is clinically significant as manifested by either a frequency of at least twice a\nweek for at least 3 consecutive months or the presence of clinically significant distress or\nimpairment in social, academic (occupational), or other important areas of functioning.\nC. Chronological age is at least 5 years (or equivalent developmental level).\nD. The behavior is not attributable to the physiological effects of a substance (e.g., a di-\nuretic, an antipsychotic medication) or another medical condition (e.g., diabetes, spina\nbifida, a seizure disorder).\nSpecify whether:\nNocturnal only: Passage of urine only during nighttime sleep.\nDiurnal only: Passage of urine during waking hours.\nNocturnal and diurnal: A combination of the two subtypes above.\nSubtypes", "source": "dsm5.pdf"} {"id": "5b68674020cd-1", "page_content": "Subtypes\nThe nocturnal-only subtype of enuresis, sometimes referred to as monosymptomatic enure-\nsis, is the most common subtype and involves incontinence only during nighttime sleep,\ntypically during the fi rst one-third of the night. The di urnal-only subtype occurs in the\nabsence of nocturnal enuresis and may be referred to simply as urinary incontinence. Indi-\nviduals with this subtype can be divided in to two groups. Individu als with \u201curge incon-\ntinence\u201d have sudden urge symptoms and de trusor instability, whereas individuals with\n\u201cvoiding postponement\u201d consciously defer micturition urges until incontinence results.\nThe nocturnal-and-diurnal subtype is also known as nonmonosymptomatic enuresis.\nDiagnostic Features\nThe essential feature of enuresis is repeated voiding of urine during the day or at night into\nbed or clothes (Criterion A). Most often the voiding is involuntary, bu t occasionally it may", "source": "dsm5.pdf"} {"id": "e42df137b3b6-0", "page_content": "356 Elimination Disorders\nbe intentional. To qualify for a diagnosis of enuresis, the voiding of urine must occur at\nleast twice a week for at least 3 consecutive months or must cause clinically significant dis-\ntress or impairment in social, academic (occu pational), or other im portant areas of func-\ntioning (Criterion B). The indi vidual must have reached an age at which continence is\nexpected (i.e., a chronological age of at leas t 5 years or, for childre n with developmental\ndelays, a mental age of at least 5 years) (Cri terion C). The urinary incontinence is not at-\ntributable to the physiological effects of a substance (e.g., a diuretic, an antipsychotic med-\nication) or another medical co ndition (e.g., diabetes, spina bifida, a seizure disorder)\n(Criterion D).\nAssociated Features Supporting Diagnosis\nDuring nocturnal enuresis, occasionally the voiding takes place during rapid eye movement\n(REM) sleep, and the child may recall a dream that involved the act of urinating. During day-\ntime (diurnal) enuresis, the child defers voiding until incontinence occurs, sometimes because\nof a reluctance to use the toilet as a result of social anxiety or a preoccupation with school or\nplay activity. The enuretic event most commonly occurs in the early afternoon on school days\nand may be associated with symptoms of disr uptive behavior. The enuresis commonly per-\nsists after appropriate treatment of an associat ed infection. \nPrevalence\nThe prevalence of enuresis is 5%\u201310% am ong 5-year-olds, 3%\u20135% among 10-year-olds,", "source": "dsm5.pdf"} {"id": "e42df137b3b6-1", "page_content": "and around 1% among individuals 15 years or older.\nDevelopment and Course\nTwo types of course of enuresis have been de scribed: a \u201cprimary\u201d type, in which the indi-\nvidual has never established urinary continence, and a \u201csecondary\u201d type, in which the dis-\nturbance develops after a period of establis hed urinary continence. There are no differences\nin prevalence of comorbid me ntal disorders between the two types. By definition, primary\nenuresis begins at age 5 years. The most co mmon time for the onset of secondary enuresis\nis between ages 5 and 8 years, but it may occur at any time. After age 5 years, the rate of spon-\ntaneous remission is 5%\u201310% per year. Most ch ildren with the disord er become continent\nby adolescence, but in approximately 1% of cases the disorder continues into adulthood.\nDiurnal enuresis is uncommon after age 9 year s. While occasional diurnal incontinence is\nnot uncommon in middle childhood, it is substantially more common in those who also\nhave persistent nocturnal enures is. When enuresis persists in to late childhood or adoles-\ncence, the frequency of incontinence may in crease, whereas continence in early childhood\nis usually associated with a dec lining frequency of wet nights.\nRisk and Prognostic Factors\nEnvironmental. A number of predisposing factors for enuresis have been suggested, in-\ncluding delayed or lax toilet training and psychosocial stress.\nGenetic and physiological. Enuresis has been associated with delays in the develop-\nment of normal circadian rhyt hms of urine production, with resulting nocturnal polyuria\nor abnormalities of central v asopressin receptor sensitivity, and reduced functional blad-", "source": "dsm5.pdf"} {"id": "e42df137b3b6-2", "page_content": "or abnormalities of central v asopressin receptor sensitivity, and reduced functional blad-\nder capacities with bladder hyperreactivity (unstable bladder syndrome). Nocturnal en-\nuresis is a genetically heterogeneous disorder. Heritability has been shown in family, twin,\nand segregation analyses. Risk for childhood nocturnal enuresis is approximately 3.6 times\nhigher in offspring of enuretic mothers and 10.1 times higher in the presence of paternal\nurinary incontinence. The risk magnitudes fo r nocturnal enuresis and diurnal incontinence\nare similar.", "source": "dsm5.pdf"} {"id": "7bca22a7b524-0", "page_content": "Encopresis 357\nCulture-Related Diagnostic Issues \nEnuresis has been reported in a variety of Eu ropean, African, and Asian countries as well\nas in the United States. At a national level, prevalence rates are remarkably similar, and\nthere is great similarity in the developmenta l trajectories found in different countries.\nThere are very high rates of enuresis in orphanages and other residential institutions,\nlikely related to the mode and environment in which toilet training occurs. \nGender-Related Diagnostic Issues\nNocturnal enuresis is more common in males. Diurnal incontinence is more common in fe-\nmales. The relative risk of having a child who develops enuresis is greater for previously\nenuretic fathers than for pr eviously enuretic mothers. \nFunctional Consequences of Enuresis\nThe amount of impairment associated with enur esis is a function of the limitation on the\nchild\u2019s social activities (e.g., ineligibility fo r sleep-away camp) or its effect on the child\u2019s\nself-esteem, the degree of social ostracism by peers, and the anger, punishment, and rejec-\ntion on the part of caregivers.\nDifferential Diagnosis\nNeurogenic bladder or another medical condition. The diagnosis of enuresis is not made\nin the presence of a neurogenic bladder or an other medical condition that causes polyuria or\nurgency (e.g., untreated diabetes mellitus or diabetes insipidus) or during an acute urinary\ntract infection. However, a diagnosis is compat ible with such conditions if urinary inconti-\nnence was regularly present prior to the development of another me dical condition or if it per-\nsists after the institution of appropriate treatment of the medical condition.\nMedication side effects. Enuresis may occur during treatment with antipsychotic med-", "source": "dsm5.pdf"} {"id": "7bca22a7b524-1", "page_content": "Medication side effects. Enuresis may occur during treatment with antipsychotic med-\nications, diuretics, or other medications that may induce incontinence. In this case, the di-\nagnosis should not be made in isolation but may be noted as a medication side effect.\nHowever, a diagnosis of enuresis may be made if urinary incontinence was regularly pres-\nent prior to treatment with the medication.\nComorbidity\nAlthough most children with enuresis do not have a comorbid mental disorder, the prevalence\nof comorbid behavioral symptoms is higher in children with enuresis than in children without\nenuresis. Developmental delays, including speech, language, learning, and motor skills\ndelays, are also present in a portion of childr en with enuresis. Encopresis, sleepwalking, and\nsleep terror disorder may be present. Urinar y tract infections are more common in children\nwith enuresis, especially the diurnal subtype, than in those who are continent.\nEncopresis\nDiagnostic Criteria 307.7 (F98.1)\nA. Repeated passage of feces into inappropriate places (e.g., clothing, floor), whether in-\nvoluntary or intentional.\nB. At least one such event occurs each month for at least 3 months.\nC. Chronological age is at least 4 years (or equivalent developmental level).\nD. The behavior is not attributable to the physiological effects of a substance (e.g., laxa-\ntives) or another medical condition except through a mechanism involving constipation.", "source": "dsm5.pdf"} {"id": "85f82dd39354-0", "page_content": "358 Elimination Disorders\nSpecify whether:\nWith constipation and overflow incontinence: There is evidence of constipation on\nphysical examination or by history.\nWithout constipation and overflow incontinence: There is no evidence of constipa-\ntion on physical examination or by history.\nSubtypes\nFeces in the with constipation and overflow incontinence subtype are characteristically\n(but not invariably) poorly fo rmed, and leakage can be infr equent to cont inuous, occur-\nring mostly during the day and rarely during sleep. Only part of the feces is passed during\ntoileting, and the incontinence resolves after treatment of the constipation.\nIn the without constipation and overflow inco ntinence subtype, feces are likely to be of\nnormal form and consistency, and soiling is intermittent. Feces may be deposited in a\nprominent location. This is usually associated with the presence of oppositional defiant\ndisorder or conduct disorder or may be th e consequence of anal masturbation. Soiling\nwithout constipation appears to be less common than soiling with constipation.\nDiagnostic Features\nThe essential feature of encopresis is repeated passage of feces into in appropriate places (e.g.,\nclothing or floor) (Criterion A). Most often the passage is involuntary but occasionally may be\nintentional. The event must occur at least once a month for at least 3\u00a0months (Criterion B), and\nthe chronological age of the child must be at least 4 years (or for children with developmental\ndelays, the mental age must be at least 4 years) (Criterion C). The fecal incontinence must not\nbe exclusively attributable to the physiological ef fects of a substance (e.g., laxatives) or another\nmedical condition except thr ough a mechanism involving constipation (Criterion D).", "source": "dsm5.pdf"} {"id": "85f82dd39354-1", "page_content": "medical condition except thr ough a mechanism involving constipation (Criterion D).\nWhen the passage of feces is involuntary rath er than intentional, it is often related to\nconstipation, impaction, and retention with subsequent overflow. The constipation may\ndevelop for psychological reasons (e.g., anxiet y about defecating in a particular place, a\nmore general pattern of anxious or oppositional behavior), leading to avoidance of defeca-\ntion. Physiological predispositi ons to constipation include ineffectual straining or paradox-\nical defecation dynamics, with contraction rath er than relaxation of the external sphincter\nor pelvic floor during straining for defecati on. Dehydration associated with a febrile ill-\nness, hypothyroidism, or a medication side ef fect can also induce constipation. Once con-\nstipation has developed, it may be complicated by an anal fissure, painful defecation, and\nfurther fecal retention. The con sistency of the stool may vary. In some individuals the stool\nmay be of normal or near-normal consistency. In other individuals\u2014such as those with\noverflow incontinence secondary to fecal retention\u2014it may be liquid.\nAssociated Features Supporting Diagnosis\nThe child with encopresis often feels ashame d and may wish to avoid situations (e.g.,\ncamp, school) that might lead to embarrassment. The amount of impairment is a function\nof the effect on the child's self-esteem, the degree of social ostracism by peers, and the an-\nger, punishment, and rejection on the part of caregivers. Smearing feces may be deliberate\nor accidental, resulting from the child\u2019s attempt to clean or hide feces that were passed in-\nvoluntarily. When the incontinence is clearly deliberate, features of oppositional defiant", "source": "dsm5.pdf"} {"id": "85f82dd39354-2", "page_content": "voluntarily. When the incontinence is clearly deliberate, features of oppositional defiant\ndisorder or conduct disorder may also be present. Many children with encopresis and\nchronic constipation also have enuresis symp toms and may have associated urinary reflux\nin the bladder or ureters that may lead to chronic urinary infections, the symptoms of\nwhich may remit with treatment of the constipation.", "source": "dsm5.pdf"} {"id": "58b662064b21-0", "page_content": "Other Specified Elimination Disorder 359\nPrevalence\nIt is estimated that approximately 1% of 5-year-olds have encopresis, and the disorder is\nmore common in males than in females.\nDevelopment and Course\nEncopresis is not diagnosed until a child has re ached a chronological ag e of at least 4\u00a0years\n(or for children with developmental delays, a mental age of at least 4 years). Inadequate,\ninconsistent toilet training and psychosocial st ress (e.g., entering school, the birth of a sib-\nling) may be predisposing factors. Two types of course have been described: a \u201cprimary\u201d\ntype, in which the individual has never established fecal continence, and a \u201csecondary\u201d\ntype, in which the disturbance develops after a period of established fecal continence. En-\ncopresis can persist, with interm ittent exacerbations, for years.\nRisk and Prognostic Factors\nGenetic and physiological. Painful defecation can lead to co nstipation and a cycle of with-\nholding behaviors that make encopresis more likely. Use of some medications (e.g., anti-\nconvulsants, cough suppressants) may increase constipation and make encopresis more\nlikely.\nDiagnostic Markers\nIn addition to physical examination, gastrointestinal imaging (e.g., abdominal radiograph)\nmay be informative to assess retained stool an d gas in the colon. Additional tests, such as\nbarium enema and anorectal ma nography, may be used to help exclude other medical\nconditions, such as Hirschsprung\u2019s disease.\nDifferential Diagnosis\nA diagnosis of encopresis in the presence of another medical condition is appropriate only\nif the mechanism involves constipation that cannot be explained by other medical condi-", "source": "dsm5.pdf"} {"id": "58b662064b21-1", "page_content": "if the mechanism involves constipation that cannot be explained by other medical condi-\ntions. Fecal incontinence related to other me dical conditions (e.g., chronic diarrhea, spina\nbifida, anal stenosis) would not warrant a DSM-5 diagnosis of encopresis.\nComorbidity\nUrinary tract infections can be comorbid with encopresis and are more common in females.\nOther Specified Elimination Disorder\n \nThis category applies to presentations in which symptoms characteristic of an elimination\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the elimination disorders di agnostic class. The other specified elimination\ndisorder category is used in situations in which the clinician chooses to communicate the\nspecific reason that the presentation does not meet the criteria for any specific elimination\ndisorder. This is done by recording \u201cother s pecified elimination disorder\u201d followed by the\nspecific reason (e.g., \u201clow-frequency enuresis\u201d).\nCoding note: Code 788.39 (N39.498) for other specified elimi nation disorder with urinary\nsymptoms; 787.60 (R15.9) for other specified elimination disorder with fecal symptoms.", "source": "dsm5.pdf"} {"id": "a82e2cbdfc5a-0", "page_content": "360 Elimination Disorders\nUnspecified Elimination Disorder\n \nThis category applies to presentations in which symptoms characteristic of an elimination\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the elimination disorders di agnostic class. The unspecified elimination dis-\norder category is used in situations in which the clinician chooses not to specify the reason\nthat the criteria are not met for a specific elimination disorder, and includes presentations\nin which there is insufficient information to make a more specific diagnosis (e.g., in emer-\ngency room settings).\nCoding note: Code 788.30 (R32) for unspecified elimination disorder with urinary symp-\ntoms; 787.60 (R15.9) for unspecified elimination disorder with fecal symptoms.", "source": "dsm5.pdf"} {"id": "93742c44df3b-0", "page_content": "361Sleep-Wake\n Disorders\nThe DSM-5 classification of sleep-wake disorders is intended for use by general\nmental health and medical clinicians (those caring for adult, geriatric, and pediatric pa-\ntients). Sleep-wake disorders encompass 10 d isorders or disorder groups: insomnia disor-\nder, hypersomnolence disorder, narcolepsy, br eathing-related sleep disorders, circadian\nrhythm sleep-wake disorders, non\u2013rapid eye movement (NRE M) sleep arousal disorders,\nnightmare disorder, rapid eye movement (REM) sleep behavior disorder, restless legs syn-\ndrome, and substance/medication-induced sleep disorder. Individuals with these disor-\nders typically present with sleep-wake complain ts of dissatisfaction regarding the quality,\ntiming, and amount of sleep. Resulting dayt ime distress and impairme nt are core features\nshared by all of these sleep-wake disorders.\nThe organization of this chapter is designed to facilitate differential diagnosis of sleep-\nwake complaints and to clarify when referral to a sleep specialist is appropriate for further\nassessment and treatment planning. The DSM-5 sleep disorders nosology uses a simple,\nclinically useful approach, while also reflecti ng scientific advances in epidemiology, ge-\nnetics, pathophysiology, assessment, and in terventions research since DSM-IV. In some\ncases (e.g., insomnia disorder ), a \u201clumping\u201d approach has been adopted, whereas in oth-\ners (e.g., narcolepsy), a \u201cspli tting\u201d approach has been taken, reflecting the availability of\nvalidators derived from epidem iological, neurobiological, and interventions research. \nSleep disorders are often accompanied by de pression, anxiety, an d cognitive changes\nthat must be addressed in treatment planni ng and management. Fu rthermore, persistent", "source": "dsm5.pdf"} {"id": "93742c44df3b-1", "page_content": "that must be addressed in treatment planni ng and management. Fu rthermore, persistent\nsleep disturbances (both insomn ia and excessive sleepiness) ar e established risk factors for\nthe subsequent development of mental illne sses and substance use disorders. They may\nalso represent a prodromal expression of an episode of mental illness, allowing the possi-\nbility of early intervention to preemp t or to attenuate a full-blown episode.\nThe differential diagnosis of sleep-wake co mplaints necessitates a multidimensional\napproach, with consideration of possibly coexisting medical and neurological conditions.\nCoexisting clinical conditions are the rule, no t the exception. Sleep disturbances furnish a\nclinically useful indicator of medical and ne urological conditions that often coexist with\ndepression and other common mental disord ers. Prominent among these comorbidities\nare breathing-related sleep disorders, disord ers of the heart and lungs (e.g., congestive\nheart failure, chronic obstructive pulmonary disease), neurodegenerative disorders (e.g.,\nAlzheimer\u2019s disease), and disorders of the musculoskeletal system (e.g., osteoarthritis).\nThese disorders not only may disturb sleep but also may th emselves be worsened during\nsleep (e.g., prolonged apneas or electrocardi ographic arrhythmias during REM sleep; con-\nfusional arousals in patients with dementing illness; seizures in persons with complex\npartial seizures). REM sleep behavior disorder is often an early indicator of neurodegen-\nerative disorders (alpha synucleinopathies) li ke Parkinson\u2019s disease. For all of these rea-\nsons\u2014related to differential diagnosis, clinic al comorbidity, and fa cilitation of treatment\nplanning\u2014sleep disorders are included in DSM-5.", "source": "dsm5.pdf"} {"id": "93742c44df3b-2", "page_content": "planning\u2014sleep disorders are included in DSM-5.\nThe approach taken to the clas sification of sleep-wake disorders in DSM-5 can be under-\nstood within the context of \u201clumping versus splitting.\u201d DSM-IV represented an effort to\nsimplify sleep-wake disorders cl assification and thus aggregated diagnoses under broader,\nless differentiated labels. At the other pole, the International Classification of Sleep Disorders,", "source": "dsm5.pdf"} {"id": "a860251340e7-0", "page_content": "362 Sleep-Wake Disorders\n2nd Edition (ICSD-2) elaborated numerous diagnostic subtypes. DSM-IV was prepared for\nuse by mental health and general medical clinicians who are not experts in sleep medicine.\nICSD-2 reflected the science and opinions of the sleep specialist community and was pre-\npared for use by specialists. \nThe weight of available evidence supports the superior performance characteristics\n(interrater reliability, as well as convergent, discriminant, and face validity) of simpler, less-\ndifferentiated approaches to diagnosis of sleep-wake disord ers. The text accompanying\neach set of diagnostic criteria provides linka ges to the corresponding disorders included in\nICSD-2. The DSM-5 sleep-wake disorders classif ication also specifies corresponding non-\npsychiatric listings (e.g., ne urology codes) from the International Classification of Diseases\n(ICD).\nThe field of sleep disorders medicine has progressed in this direction since the publi-\ncation of DSM-IV. The use of biological validators is now embodied in the DSM-5 classi-\nfication of sleep-wake disorder s, particularly for disorders of excessive sleepiness, such as\nnarcolepsy; for breathing-rela ted sleep disorders, for whic h formal sleep studies (i.e.,\npolysomnography) are indicated; and for rest less legs syndrome, which can often coexist\nwith periodic limb movements during sleep, detectable via polysomnography.\nInsomnia Disorder\nDiagnostic Criteria 307.42 (F51.01)\nA. A predominant complaint of dissatisfaction with sleep quantity or quality, associated\nwith one (or more) of the following symptoms:\n1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep\nwithout caregiver intervention.)\n2. Difficulty maintaining sleep, characterized by frequent awakenings or problems re-", "source": "dsm5.pdf"} {"id": "a860251340e7-1", "page_content": "2. Difficulty maintaining sleep, characterized by frequent awakenings or problems re-\nturning to sleep after awakenings. (In children, this may manifest as difficulty return-\ning to sleep without caregiver intervention.)\n3. Early-morning awakening with inability to return to sleep.\nB. The sleep disturbance causes clinically significant distress or impairment in social, oc-\ncupational, educational, academic, behavioral, or other important areas of functioning.\nC. The sleep difficulty occurs at least 3 nights per week.\nD. The sleep difficulty is present for at least 3 months.\nE. The sleep difficulty occurs despite adequate opportunity for sleep.\nF. The insomnia is not better explained by and does not occur exclusively during the\ncourse of another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep dis-\norder, a circadian rhythm sleep-wake disorder, a parasomnia).\nG. The insomnia is not attributable to the physiological effects of a substance (e.g., a drug\nof abuse, a medication).\nH. Coexisting mental disorders and medical conditions do not adequately explain the pre-\ndominant complaint of insomnia.\nSpecify if:\nWith non\u2013sleep disorder mental comorbidity, including substance use disorders\nWith other medical comorbidity\nWith other sleep disorder\nCoding note: The code 307.42 (F51.01) applies to all three specifiers. Code also the\nrelevant associated mental disorder, medica l condition, or other sleep disorder imme-\ndiately after the code for insomnia disorder in order to indicate the association.", "source": "dsm5.pdf"} {"id": "367ad79fb3bd-0", "page_content": "Insomnia Disorder 363\nSpecify if:\nEpisodic: Symptoms last at least 1 month but less than 3 months.\nPersistent: Symptoms last 3 months or longer.\nRecurrent: Two (or more) episodes within the space of 1 year.\nNote: Acute and short-term insomnia (i.e., symptoms lasting less than 3 months but oth-\nerwise meeting all criteria with regard to frequency, intensity, distress, and/or impairment)\nshould be coded as an other specified insomnia disorder.\nNote. The diagnosis of insomnia disorder is given whether it occurs as an independent\ncondition or is comorbid with another mental disorder (e.g., major depressive disorder),\nmedical condition (e.g., pain), or another sleep disorder (e.g., a breathing-related sleep dis-\norder). For instance, insomnia may develop it s own course with some anxiety and depres-\nsive features but in the absenc e of criteria being met for an y one mental disorder. Insomnia\nmay also manifest as a clinical feature of a more predominant ment al disorder . Persistent\ninsomnia may even be a risk factor for depression and is a common residual symptom af-\nter treatment for this condition. With comorb id insomnia and a mental disorder, treatment\nmay also need to target both conditions. Give n these different courses, it is often impossi-\nble to establish the precise nature of the rela tionship between these clinical entities, and\nthis relationship may change over time. Therefore, in th e presence of insomnia and a co-\nmorbid disorder, it is not ne cessary to make a causal attribution between the two condi-\ntions. Rather, the diagnosis of insomnia disord er is made with concurrent specification of\nthe clinically comorbid conditions. A concurre nt insomnia diagnosis should only be con-", "source": "dsm5.pdf"} {"id": "367ad79fb3bd-1", "page_content": "the clinically comorbid conditions. A concurre nt insomnia diagnosis should only be con-\nsidered when the insomnia is sufficiently severe to warrant independent clinical attention;\notherwise, no separate diagnosis is necessary.\nDiagnostic Features\nThe essential feature of insomnia disorder is dissatisfaction with sleep quantity or quality\nwith complaints of difficulty initiating or maintaining sleep. The sleep complaints are ac-\ncompanied by clinically significant distress or impairment in social, occupational, or other\nimportant areas of functioning. The sleep dist urbance may occur during the course of an-\nother mental disorder or medical condition, or it may occur independently.\nDifferent manifestations of insomnia can oc cur at different times of the sleep period. Sleep-\nonset insomnia (or initial insomnia ) involves difficulty initia ting sleep at bedtime. Sleep mainte-\nnance insomnia (or middle insomnia ) involves frequent or prol onged awakenings throughout\nthe night. Late insomnia involves early-morning awakening with an inability to return to sleep.\nDifficulty maintaining sleep is the most co mmon single symptom of insomnia, followed by\ndifficulty falling asleep, while a combination of these symptoms is th e most common presen-\ntation overall. The specific type of sleep comp laint often varies over time. Individuals who\ncomplain of difficulty falling asleep at one time may later complain of difficulty maintaining\nsleep, and vice versa. Symptoms of difficulty falling asleep and difficulty maintaining sleep\ncan be quantified by the individual\u2019s retrospect ive self-report, sleep di aries, or other methods,\nsuch as actigraphy or polysomnography, but th e diagnosis of insomnia disorder is based on\nthe individual\u2019s subjecti ve perception of sleep or a caretaker\u2019s report. \nNonrestorative sleep, a complaint of poor sleep quality that does not leave the individual\nrested upon awakening despite adequate du ration, is a common sleep complaint usually", "source": "dsm5.pdf"} {"id": "367ad79fb3bd-2", "page_content": "rested upon awakening despite adequate du ration, is a common sleep complaint usually\noccurring in association with difficulty initiating or maintaining sleep, or less frequently in\nisolation. This complaint can also be reported in association with other sleep disorders\n(e.g., breathing-related sleep disorder). When a complaint of nonres torative sleep occurs\nin isolation (i.e., in the absence of difficulty initiating and/or maintaining sleep) but all di-", "source": "dsm5.pdf"} {"id": "fb4bed39333e-0", "page_content": "(e.g., breathing-related sleep disorder). When a complaint of nonres torative sleep occurs\nin isolation (i.e., in the absence of difficulty initiating and/or maintaining sleep) but all di-\nagnostic criteria with regard to frequency, duration, and daytime distress and impairments\nare otherwise met, a diagnosis of other specif ied insomnia disorder or unspecified insom-\nnia disorder is made.", "source": "dsm5.pdf"} {"id": "b6e75e316028-0", "page_content": "364 Sleep-Wake Disorders\nAside from the frequency and du ration criteria required to make the diagnosis, addi-\ntional criteria are useful to quantify insomnia severity. These quantitative criteria, while\narbitrary, are provided for illustrative purpose only. For instance, difficulty initiating sleep\nis defined by a subjective sleep latency greater than 20\u201330 minutes, and difficulty maintain-\ning sleep is defined by a subjective time awake after sleep onset greater than 20\u201330 min-\nutes. Although there is no standard definition of early-morning awakening, this symptom\ninvolves awakening at least 30 minutes before the scheduled time and before total sleep\ntime reaches 6\u00bd hours. It is essential to take into account no t only the final awakening time\nbut also the bedtime on the previ ous evening. Awakening at 4:00 A.M. does not have the\nsame clinical significance in those who go to bed at 9:00 P.M. as in those who go to bed at\n11:00 P.M. Such a symptom may also reflect an age- dependent decrease in the ability to sus-\ntain sleep or an age-dependent shift in the timing of the main sleep period. \nInsomnia disorder involves daytime impairments as well as nighttime sleep difficulties.\nThese include fatigue or, less commonly, dayt ime sleepiness; the latter is more common\namong older individuals and wh en insomnia is comorbid with another medical condition\n(e.g., chronic pain) or sleep disorder (e.g., sl eep apnea). Impairment in cognitive performance\nmay include difficulties with attention, concentration and memory, and even with performing\nsimple manual skills. Associated mood disturba nces are typically described as irritability or\nmood lability and less commonly as depressive or anxiety symptoms. Not all individuals with\nnighttime sleep disturbances are distressed or have functional impairment. For example, sleep", "source": "dsm5.pdf"} {"id": "b6e75e316028-1", "page_content": "nighttime sleep disturbances are distressed or have functional impairment. For example, sleep\ncontinuity is often interrupted in healthy olde r adults who nevertheless identify themselves\nas good sleepers. A diagnosis of insomnia disorder should be reserved for those individuals\nwith significant daytime distress or impairment related to their nighttime sleep difficulties.\nAssociated Features Supporting Diagnosis \nInsomnia is often associated with physiological and cognitive arousal and conditioning\nfactors that interfere with sleep. A preoccupati on with sleep and distress due to the inabil-\nity to sleep may lead to a vicious cycle: the more the individual strives to sleep, the more\nfrustration builds and further im pairs sleep. Thus, excessive attention and efforts to sleep,\nwhich override normal sleep-onset mechanisms, may contribute to the development of in-\nsomnia. Individuals with persistent insomnia may also acquire maladapt ive sleep habits\n(e.g., spending excessive time in bed; following an erratic sleep schedule; napping) and\ncognitions (e.g., fear of sleeplessness; apprehensions of daytime impairments; clock mon-\nitoring) during the course of the disorder. Engaging in such activities in an environment in\nwhich the individual has frequently spent sleepless nights may further compound the con-\nditioned arousal and perpetuate sleep difficulties. Conversely, the individual may fall asleep\nmore easily when not trying to do so. Some individuals also report better sleep when away\nfrom their own bedrooms and their usual routines. \nInsomnia may be accompanied by a variety of daytime complaints and symptoms, in-\ncluding fatigue, decreased en ergy, and mood disturbances. Symptoms of anxiety or de-\npression that do not meet criteria for a specif ic mental disorder may be present, as well as\nan excessive focus on the perceived effect s of sleep loss on daytime functioning. \nIndividuals with inso mnia may have elevated scores on self-report psychological or", "source": "dsm5.pdf"} {"id": "b6e75e316028-2", "page_content": "Individuals with inso mnia may have elevated scores on self-report psychological or\npersonality inventories with profiles indicati ng mild depression and anxiety, a worrisome\ncognitive style, an emotion-focused and intern alizing style of conflict resolution, and a so-", "source": "dsm5.pdf"} {"id": "e0e5dd91a2fd-0", "page_content": "personality inventories with profiles indicati ng mild depression and anxiety, a worrisome\ncognitive style, an emotion-focused and intern alizing style of conflict resolution, and a so-\nmatic focus. Patterns of neurocognitive impairment among individuals with insomnia dis-\norder are inconsistent, although there may be impairments in performing tasks of higher\ncomplexity and those requiring frequent ch anges in performance strategy. Individuals\nwith insomnia often require more effo rt to maintain cognitive performance.\nPrevalence\nPopulation-based estimates indicate that about one-third of adults report insomnia symp-\ntoms, 10%\u201315% experience associated daytime impairments, and 6%\u201310% have symptoms", "source": "dsm5.pdf"} {"id": "00813b1f1c66-0", "page_content": "Insomnia Disorder 365\nthat meet criteria for insomnia disorder. Insomnia disorder is the most prevalent of all\nsleep disorders. In primary care settings, approximately 10%\u201320% of individuals complain\nof significant insomnia symp toms. Insomnia is a more prevalent complaint among fe-\nmales than among males, with a gender ratio of about 1.44:1. Although insomnia can be a\nsymptom or an independent disorder, it is mo st frequently observed as a comorbid con-\ndition with another medical condition or ment al disorder. For instance, 40%\u201350% of indi-\nviduals with insomnia also present with a comorbid mental disorder. \nDevelopment and Course\nThe onset of insomnia symptoms can occur at any time during life, but the first episode is\nmore common in young adulthood. Less frequently, insomnia begins in childhood or ad-\nolescence. In women, new-onset insomnia may occur during menopause and persist even\nafter other symptoms (e.g., hot flashes) have resolved. Insomnia may have a late-life onset,\nwhich is often associated with the onse t of other health-related conditions. \nInsomnia can be situational, persistent, or recurrent. Situational or acute insomnia usu-\nally lasts a few days or a few weeks and is often associated with life events or rapid changes\nin sleep schedules or environment. It usually resolves once the initial precipitating event\nsubsides. For some individuals, perhaps those more vulnerable to sl eep disturbances, in-\nsomnia may persist long after the initial trigge ring event, possibly because of conditioning\nfactors and heightened arousal. The factors that precipitate insomnia may differ from\nthose that perpetuate it. For example, an in dividual who is bedridden with a painful injury\nand has difficulty sleeping may then develop negative associations for sleep. Conditioned", "source": "dsm5.pdf"} {"id": "00813b1f1c66-1", "page_content": "and has difficulty sleeping may then develop negative associations for sleep. Conditioned\narousal may then persist and lead to persiste nt insomnia. A similar course may develop in\nthe context of an acute psychological stress or a mental disorder. For instance, insomnia that\noccurs during an episode of major depressive disorder can become a focus of attention,\nwith consequent negative conditioning, and pe rsist even after resolution of the depressive\nepisode. In some cases, insomnia may also have an insidious onse t without any identifi-\nable precipitating factor. \nThe course of insomnia may also be episodic, with recurrent episodes of sleep difficul-\nties associated with the occurrence of stress ful events. Chronicity rates range from 45%\nto 75% for follow-ups of 1\u20137 years. Even wh en the course of the insomnia has become\nchronic, there is night-to -night variability in sleep patterns, with an occasional restful night\u2019s\nsleep interspersed with several nights of poor sleep. The characteristics of insomnia may\nalso change over time. Many individuals with insomnia have a history of \u201clight\u201d or easily\ndisturbed sleep prior to onset of more persistent sleep problems.\nInsomnia complaints are mo re prevalent among middle-age and older adults. The type\nof insomnia symptom changes as a function of age, with difficulties initiating sleep being\nmore common among young adults and proble ms maintaining sleep occurring more fre-\nquently among middle-age and older individuals. \nDifficulties initiating and maintaining sleep can also occur in children and adolescents,\nbut there are more limited data on prevalence, risk factors, and comorbidity during these\ndevelopmental phases of the lifespan. Sleep diff iculties in childhood can result from con-\nditioning factors (e.g., a child who does not lear n to fall asleep or return to sleep without", "source": "dsm5.pdf"} {"id": "00813b1f1c66-2", "page_content": "the presence of a parent) or from the absence of consistent sleep schedules and bedtime\nroutines. Insomnia in adolescenc e is often triggered or exacer bated by irregular sleep sched-\nules (e.g., phase delay). In both children an d adolescents, psycholo gical and medical fac-\ntors can contribute to insomnia.\nThe increased prevalence of insomnia in olde r adults is partly explained by the higher", "source": "dsm5.pdf"} {"id": "27d76ccd0f4f-0", "page_content": "tors can contribute to insomnia.\nThe increased prevalence of insomnia in olde r adults is partly explained by the higher\nincidence of physical health problems with aging. Changes in sleep patterns associated with\nthe normal developmental process must be diff erentiated from those exceeding age-related\nchanges. Although polysomnography is of limit ed value in the routine evaluation of in-\nsomnia, it may be more useful in the differen tial diagnosis among older adults because the\netiologies of insomnia (e.g., sleep apnea) are more often identifiable in older individuals.", "source": "dsm5.pdf"} {"id": "fd5a79147a5b-0", "page_content": "366 Sleep-Wake Disorders\nRisk and Prognostic Factors \nWhile the risk and prognostic factors discussed in this section increase vulnerability to in-\nsomnia, sleep disturbances are more likely to occur when predisposed individuals are ex-\nposed to precipitating events, such as major lif e events (e.g., illness, separation) or less\nsevere but more chronic daily stress. Most individuals resume normal sleep patterns after\nthe initial triggering event ha s disappeared, but others\u2014perha ps those more vulnerable to\ninsomnia\u2014continue experiencing persistent sleep difficulties. Perpetuating factors such as\npoor sleep habits, irregular sleep scheduling, an d the fear of not sleeping feed into the in-\nsomnia problem and may contribute to a vicious cycle that may induce persistent insomnia.\nTemperamental. Anxiety or worry-prone personality or cognitive styles, increased arousal\npredisposition, and tendency to repress emot ions can increase vulne rability to insomnia.\nEnvironmental. Noise, light, uncomfortably high or low temperature, and high altitude\nmay also increase vulnerability to insomnia.\nGenetic and physiological. Female gender and advancing age are associated with in-\ncreased vulnerability to insomn ia. Disrupted sleep and insomnia display a familial dispo-\nsition. The prevalence of insomnia is hi gher among monozygoti c twins relative to\ndizygotic twins; it is also higher in first-degree family members comp ared with the general\npopulation. The extent to which this link is inherited through a genetic predisposition,\nlearned by observations of pare ntal models, or established as a by-product of another psy-\nchopathology remains undetermined.\nCourse modifiers. Deleterious course modifiers incl ude poor sleep hygiene practices\n(e.g., excessive caffeine use, irregular sleep schedules).\nGender-Related Diagnostic Issues", "source": "dsm5.pdf"} {"id": "fd5a79147a5b-1", "page_content": "(e.g., excessive caffeine use, irregular sleep schedules).\nGender-Related Diagnostic Issues\nInsomnia is a more prevalent complaint among females than among males, with first onset\noften associated with the birth of a new child or with menopause. Despite higher preva-\nlence among older females, polysomnographic studies su ggest better preservation of\nsleep continuity and slow-wave sleep in older females than in older males.\nDiagnostic Markers\nPolysomnography usually shows impairments of sleep continuity (e.g., increased sleep la-\ntency and time awake after sleep onset and de creased sleep efficiency [percentage of time\nin bed asleep] and may show increased stage 1 sleep and decreased stages 3 and 4 sleep.\nThe severity of these sleep im pairments does not always ma tch the individual\u2019s clinical\npresentation or subjective complaint of poor sleep, as individuals with insomnia often un-\nderestimate sleep duration and overestimate wakefulness relative to polysomnography.\nQuantitative electroencephalographic analyses may indicate that individuals with insom-\nnia have greater high-frequency electroencepha lography power relative to good sleepers\nboth around the sleep onset period and duri ng non\u2013rapid eye movement sleep, a feature\nsuggestive of increased cortical arousal. Individual s with insomnia disorder may have a\nlower sleep propensity and typically do not show increased daytime sleepiness on objec-\ntive sleep laboratory measures compared wi th individuals without sleep disorders. \nOther laboratory measures show evidence, although not consistently, of increased\narousal and a generalized activation of the hypothalamic-pituitary-adrenal axis (e.g., in-\ncreased cortisol levels, heart rate variability, reactivity to stre ss, metabolic rate). In general,\nfindings are consistent with the hypothesis that increased physiological and cognitive\narousal plays a significant role in insomnia disorder.", "source": "dsm5.pdf"} {"id": "fd5a79147a5b-2", "page_content": "arousal plays a significant role in insomnia disorder.\nIndividuals with insomnia di sorder may appear either fatigued or haggard or, con-\nversely, overaroused and \u201cwired.\u201d However, there are no consistent or characteristic\nabnormalities on physical examination. Ther e may be an increased incidence of stress-", "source": "dsm5.pdf"} {"id": "b090afd45084-0", "page_content": "Insomnia Disorder 367\nrelated psychophysiological symptoms (e.g., tension headache, muscle tension or pain,\ngastrointestinal symptoms).\nFunctional Consequences of Insomnia Disorder\nInterpersonal, social, and occupational problems may develop as a result of insomnia or\nexcessive concern with sleep, increased daytim e irritability, and poor concentration. De-\ncreased attention and concentrat ion are common and may be related to higher rates of ac-\ncidents observed in insomnia. Persistent in somnia is also associated with long-term\nconsequences, including increased risks of ma jor depressive disorder, hypertension, and\nmyocardial infarction; increased absenteeism and reduced productivity at work; reduced\nquality of life; and increased economic burden. \nDifferential Diagnosis\nNormal sleep variations. Normal sleep duration varies considerably across individuals.\nSome individuals who require little sleep (\u201cshort sleepers\u201d) may be concerned about their\nsleep duration. Short sl eepers differ from individuals with insomnia disorder by the lack of\ndifficulty falling or staying asleep and by the absence of characteristic daytime symptoms\n(e.g., fatigue, concentration pr oblems, irritability). However, some short sleepers may desire\nor attempt to sleep for a longer period of time and, by prolonging time in bed, may create an\ninsomnia-like sleep pattern. Clinical insomnia also should be distinguished from normal,\nage-related sleep changes. Insomnia must also be distinguished from sleep deprivation due\nto inadequate opportunity or circumstance for sleep resulting, for example, from an emer-\ngency or from professional or family obligations forcing th e individual to stay awake. \nSituational/acute insomnia. Situational/acute insomnia is a condition lasting a few days\nto a few weeks, often associated with life events or with changes in sleep schedules. These\nacute or short-term insomnia symptoms may also produce si gnificant distress and inter-", "source": "dsm5.pdf"} {"id": "b090afd45084-1", "page_content": "acute or short-term insomnia symptoms may also produce si gnificant distress and inter-\nfere with social, personal, and occupational functioning. When such symptoms are fre-\nquent enough and meet all other criteria exce pt for the 3-month duration, a diagnosis of\nother specified insomnia disorder or unspecified insomnia disorder is made.\nDelayed sleep phase and shift work types of circadian rhythm sleep-wake disorder.\nIndividuals with the delayed sleep phase type of circadian rhythm sl eep-wake disorder re-\nport sleep-onset insomnia only when they try to sleep at socially normal times, but they do\nnot report difficulty falling asleep or stayin g asleep when their bed and rising times are\ndelayed and coincide with thei r endogenous circadian rhythm. Shift work type differs from\ninsomnia disorder by the history of recent shift work. \nRestless legs syndrome. Restless legs syndrome often produces difficulties initiating\nand maintaining sleep. However, an urge to move the legs and any accompanying unpleas-\nant leg sensations are features that differentiate this disorder fr om insomnia disorder. \nBreathing-related sleep disorders. Most individuals with a breathing-related sleep dis-\norder have a history of loud snoring, breath ing pauses during sleep, and excessive daytime\nsleepiness. Nonetheless, as many as 50% of individuals with sleep apnea may also report\ninsomnia symptoms, a feature that is more common among females and older adults.\nNarcolepsy. Narcolepsy may cause insomnia complaints but is distinguished from in-\nsomnia disorder by the predominance of sy mptoms of excessive daytime sleepiness, cat-\naplexy, sleep paralysis, and sleep-related hallucinations.\nParasomnias. Parasomnias are characterized by a comp laint of unusual behavior or events\nduring sleep that may lead to intermittent awakenings and difficulty resuming sleep.", "source": "dsm5.pdf"} {"id": "b090afd45084-2", "page_content": "during sleep that may lead to intermittent awakenings and difficulty resuming sleep.\nHowever, it is these behavioral events, rather than the insomnia per se, that dominate the\nclinical picture.", "source": "dsm5.pdf"} {"id": "a1cbd36079b5-0", "page_content": "368 Sleep-Wake Disorders\nSubstance/medication-induced sl eep disorder, insomnia type. Substance/medication-\ninduced sleep disorder, insomnia type, is distinguished from insomnia disorder by the fact\nthat a substance (i.e., a drug of abuse, a medica tion, or exposure to a toxin) is judged to be\netiologically related to the insomnia (see \u201cSubstance/Medicatio n-Induced Sleep Disor-\nder\u201d later in this chapter). Fo r example, insomnia occurring only in the context of heavy\ncoffee consumption would be diagnosed as caffeine-induced sleep disorder, insomnia\ntype, with onset during intoxication.\nComorbidity\nInsomnia is a common comorbidity of many medical conditions, including diabetes, cor-\nonary heart disease, chronic obstructive pulm onary disease, arthritis, fibromyalgia, and\nother chronic pain conditions. The risk relati onship appears to be bidirectional: insomnia\nincreases the risk of medical conditions, and medical problems increase the risk of insom-\nnia. The direction of the relationship is not always clear and may change over time; for this\nreason, comorbid insomnia is the preferred terminology in th e presence of coexisting in-\nsomnia with another medical co ndition (or mental disorder).\nIndividuals with insomnia disorder frequent ly have a comorbid mental disorder, par-\nticularly bipolar, depressive, and anxiety diso rders. Persistent insomnia represents a risk\nfactor or an early symptom of subsequent bi polar, depressive, anxi ety, and substance use\ndisorders. Individuals with insomnia may misuse medicati ons or alcohol to help with\nnighttime sleep, anxiolytics to combat tension or anxiety, and caffeine or other stimulants\nto combat excessive fatigue. In addition to worsening the insomnia, this type of substance", "source": "dsm5.pdf"} {"id": "a1cbd36079b5-1", "page_content": "to combat excessive fatigue. In addition to worsening the insomnia, this type of substance\nuse may in some cases progress to a substance use disorder.\nRelationship to Internat ional Classification of \nSleep Disorders\nThere are several distinct inso mnia phenotypes relating to the perceived source of the in-\nsomnia that are recognized by the International Classifica tion of Sleep Disorders, 2nd Edition\n(ICSD-2). These include psychophysiological insomnia, idiopathic insomnia, sleep-state mispercep-\ntion, and inadequate sleep hygiene. Despite their clinical appeal and heuristic value, there is\nlimited evidence to support these distinct phenotypes.\nHypersomnolence Disorder\nDiagnostic Criteria 307.44 (F51.11)\nA. Self-reported excessive sleepiness (hypersomnolence) despite a main sleep period\nlasting at least 7 hours, with at least one of the following symptoms: \n1. Recurrent periods of sleep or lapses into sleep within the same day.\n2. A prolonged main sleep episode of more than 9 hours per day that is nonrestorative\n(i.e., unrefreshing).\n3. Difficulty being fully awake after abrupt awakening.\nB. The hypersomnolence occurs at least three times per week, for at least 3 months.\nC. The hypersomnolence is accompanied by si gnificant distress or impairment in cogni-\ntive, social, occupational, or other important areas of functioning. \nD. The hypersomnolence is not better explai ned by and does not occur exclusively during\nthe course of another sleep disorder (e.g., narcolepsy, breathing-related sleep disor-\nder, circadian rhythm sleep-wake disorder, or a parasomnia).\nE. The hypersomnolence is not attributable to the physiological effects of a substance", "source": "dsm5.pdf"} {"id": "a1cbd36079b5-2", "page_content": "E. The hypersomnolence is not attributable to the physiological effects of a substance\n(e.g., a drug of abuse, a medication).", "source": "dsm5.pdf"} {"id": "87cb8d4c2f9f-0", "page_content": "Hypersomnolence Disorder 369\nF. Coexisting mental and medical disorders do not adequately explain the predominant\ncomplaint of hypersomnolence.\nSpecify if:\nWith mental disorder , including substance use disorders\nWith medical condition\nWith another sleep disorder\nCoding note: The code 307.44 (F51.11) applies to all three specifiers. Code also the\nrelevant associated mental disorder, medi cal condition, or other sleep disorder im-\nmediately after the code for hypersomnolence disorder in order to indicate the associ-\nation.\nSpecify if:\nAcute: Duration of less than 1 month.\nSubacute: Duration of 1\u20133 months.\nPersistent: Duration of more than 3 months.\nSpecify current severity:\nSpecify severity based on degree of difficulty maintaining daytime alertness as manifested\nby the occurrence of multiple attacks of irresistible sleepiness within any given day occur-\nring, for example, while sedentary, driving, visiting with friends, or working. \nMild: Difficulty maintaining daytime alertness 1\u20132 days/week.\nModerate: Difficulty maintaining daytime alertness 3\u20134 days/week.\nSevere: Difficulty maintaining daytime alertness 5\u20137 days/week.\nDiagnostic Features\nHypersomnolence is a broad diagnostic term and incl udes symptoms of excessive quantity\nof sleep (e.g., extended nocturnal sleep or involuntary daytime sleep), deteriorated quality\nof wakefulness (i.e., sleep propensity duri ng wakefulness as shown by difficulty awaken-\ning or inability to remain awake when required ), and sleep inertia (i.e., a period of im-\npaired performance and reduced vigilance following awakening from the regular sleep\nepisode or from a nap) (Criterion A). Indivi duals with this disorder fall asleep quickly and", "source": "dsm5.pdf"} {"id": "87cb8d4c2f9f-1", "page_content": "have a good sleep efficiency (>90%). They may have difficulty waking up in the morning,\nsometimes appearing confused, co mbative, or ataxic. This pr olonged impairment of alert-\nness at the sleep-wake transition is often referred to as sleep inertia (i.e., sleep drunkenness).\nIt can also occur upon awaken ing from a daytime nap. During that period, the individual\nappears awake, but there is a decline in moto r dexterity, behavior may be very inappro-\npriate, and memory deficits, di sorientation in time and spac e, and feelings of grogginess\nmay occur. This period may last some minutes to hours. \nThe persistent need for sleep can lead to auto matic behavior (usually of a very routine,\nlow-complexity type) that the individual carrie s out with little or no subsequent recall. For\nexample, individuals may find themselves having driven several miles from where they\nthought they were, unaware of the \u201cautomatic\u201d driving they did in the preceding minutes.\nFor some individuals with hypersomnolence disorder, the major sleep episode (for most\nindividuals, nocturnal sleep) has a duration of 9 hours or more. However, the sleep is often\nnonrestorative and is followed by difficulty awakening in the morning. For other individ-\nuals with hypersomnolence disorder, the majo r sleep episode is of normal nocturnal sleep\nduration (6\u20139 hours). In these cases, the excessive sleepiness is characterized by several un-\nintentional daytime naps. These daytime naps tend to be relatively long (often lasting 1 hour\nor more), are experienced as no nrestorative (i.e., unrefreshing), and do not lead to improved\nalertness. Individuals with hypersomnolence have daytime naps near ly everyday regard-", "source": "dsm5.pdf"} {"id": "87cb8d4c2f9f-2", "page_content": "alertness. Individuals with hypersomnolence have daytime naps near ly everyday regard-\nless of the nocturnal sleep duration. Subjective sleep quality may or may not be reported as\ngood. Individuals typically feel sleepiness developing over a period of time, rather than", "source": "dsm5.pdf"} {"id": "0387e27b524d-0", "page_content": "370 Sleep-Wake Disorders\nexperiencing a sudden sleep \u201cattack.\u201d Unintent ional sleep episodes typically occur in low-\nstimulation and low-activity situations (e.g ., while attending lectures, reading, watching\ntelevision, or driving long dist ances), but in more severe cases they can manifest in high-\nattention situations such as at work, in meetings, or at social gatherings.\nAssociated Features Supporting Diagnosis\nNonrestorative sleep, automatic behavior, di fficulties awakening in the morning, and\nsleep inertia, although common in hypersomnolence disorder, may also be seen in a variety\nof conditions, including narcolepsy. Appr oximately 80% of indi viduals with hyper-\nsomnolence report that their sleep is nonres torative, and as many have difficulties awak-\nening in the morning. Sleep inertia, thou gh less common (i.e., observed in 36%\u201350% of\nindividuals with hypersomnolence disorder), is highly specific to hypersomnolence. Short\nnaps (i.e., duration of less than 30 minutes) are often unrefreshing. Individuals with hy-\npersomnolence often appear sleepy and may even fall asleep in the clinician\u2019s waiting\narea. \nA subset of individuals with hypersomnolenc e disorder have a family history of hy-\npersomnolence and also have symptoms of autonomic nervous system dysfunction, in-\ncluding recurrent vascular-type headaches, reactivity of the peripheral vascular system\n(Raynaud\u2019s phenomenon), and fainting.\nPrevalence\nApproximately 5%\u201310% of individuals who cons ult in sleep disorders clinics with com-\nplaints of daytime sleepiness are diagnosed as having hypersomnolence disorder. It is es-", "source": "dsm5.pdf"} {"id": "0387e27b524d-1", "page_content": "timated that about 1% of the European and U.S. general population has episodes of sleep\ninertia. Hypersomnolence occurs with relati vely equal frequency in males and females.\nDevelopment and Course\nHypersomnolence disorder has a persistent course, with a prog ressive evolution in the se-\nverity of symptoms. In most extreme cases, sl eep episodes can last up to 20 hours. How-\never, the average nighttime sleep duration is around 9\u00bd hours. While many individuals\nwith hypersomnolence are able to reduce their sleep time during working days, weekend\nand holiday sleep is greatly increased (by up to 3 hours). Awakenings are very difficult\nand accompanied by sleep inertia episodes in nearly 40% of cases. Hypersomnolence fully\nmanifests in most cases in late adolescence or early adulthood, with a mean age at onset of\n17\u201324 years. Individuals with hypersomnolence disorder are diagnosed, on average, 10\u201315\nyears after the appearance of the firs t symptoms. Pediatric cases are rare. \nHypersomnolence has a progressive onset, wi th symptoms beginning between ages 15\nand 25 years, with a gradual progression over weeks to months. For most individuals, the\ncourse is then persistent and stable, unless tr eatment is initiated. The development of other\nsleep disorders (e.g., breathing-related sleep disorder) may worsen the degree of sleepi-\nness. Although hyperactivity may be one of th e presenting signs of daytime sleepiness in\nchildren, voluntary napping increases with ag e. This normal phenomenon is distinct from\nhypersomnolence.\nRisk and Prognostic Factors\nEnvironmental. Hypersomnolence can be increased te mporarily by psychological stress", "source": "dsm5.pdf"} {"id": "0387e27b524d-2", "page_content": "Environmental. Hypersomnolence can be increased te mporarily by psychological stress\nand alcohol use, but they have not been documented as environmental precipitating\nfactors. Viral infections have been report ed to have preceded or accompanied hyper-\nsomnolence in about 10% of cases. Viral infections, such as HIV pneumonia, infectious\nmononucleosis, and Guillain-Barr\u00e9 syndrome, can also evolve into hypersomnolence within", "source": "dsm5.pdf"} {"id": "c3cd75b89055-0", "page_content": "Hypersomnolence Disorder 371\nmonths after the infection. Hypersomnolenc e can also appear within 6\u201318 months follow-\ning a head trauma. \nGenetic and physiological. Hypersomnolence may be fami lial, with an autosomal-\ndominant mode of inheritance. \nDiagnostic Markers\nNocturnal polysomnography demonstrates a no rmal to prolonged sleep duration, short\nsleep latency, and normal to increased slee p continuity. The distribution of rapid eye\nmovement (REM) sleep is also normal. Sleep e fficiency is mostly greater than 90%. Some\nindividuals with hypersomnolence disorder have increased amounts of slow-wave sleep.\nThe multiple sleep latency te st documents sleep tendency, typically indicated by mean\nsleep latency values of less than 8 minutes. In hypersomnolence disorder, the mean sleep\nlatency is typically less than 10 minutes and fr equently 8 minutes or less. Sleep-onset REM\nperiods (SOREMPs; i.e., the occurrence of REM sleep within 20 minutes of sleep onset)\nmay be present but occur less than two time s in four to five nap opportunities. \nFunctional Consequences of Hypersomnolence Disorder\nThe low level of alertness that occurs while an individual fights the need for sleep can lead\nto reduced efficiency, diminished concentration, and poor memory during daytime activ-\nities. Hypersomnolence can lead to significan t distress and dysfunction in work and social\nrelationships. Prolonged nocturnal sleep and difficulty awakening can result in difficulty\nin meeting morning obligations, such as arrivi ng at work on time. Unintentional daytime\nsleep episodes can be embarrassing and even dangerous, if, for instance, the individual is\ndriving or operating machinery when the episode occurs. \nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "c3cd75b89055-1", "page_content": "driving or operating machinery when the episode occurs. \nDifferential Diagnosis\nNormative variation in sleep. \u201cNormal\u201d sleep duration varies considerably in the general\npopulation. \u201cLong sleepers\u201d (i.e., individuals who require a greater than average amount\nof sleep) do not have excessive sleepiness, sleep inertia, or automatic behavior when they\nobtain their required amount of nocturnal sleep . Sleep is reported to be refreshing. If social\nor occupational demands lead to shorter nocturnal sleep, daytime symptoms may appear.\nIn hypersomnolence disorder, by contrast, symp toms of excessive sleepiness occur regard-\nless of nocturnal sleep duration. An inad equate amount of no cturnal sleep, or behaviorally\ninduced insufficient sleep syndrome, can produce symptoms of daytime sleepiness very similar\nto those of hypersomnolence. An average slee p duration of fewer than 7 hours per night\nstrongly suggests inadequate nocturnal sleep , and an average of more than 9\u201310 hours of\nsleep per 24-hour period suggests hypersomnole nce. Individuals with inadequate noctur-\nnal sleep typically \u201ccatch up\u201d with longer sleep durations on days when they are free from\nsocial or occupational demands or on vaca tions. Unlike hypersom nolence, insufficient\nnocturnal sleep is unlikely to persist unabat ed for decades. A diagnosis of hypersomno-\nlence disorder should not be made if there is a question regarding the adequacy of noctur-\nnal sleep duration. A diagnostic and therapeutic trial of sleep extension for 10\u201314 days can\noften clarify the diagnosis.\nPoor sleep quality and fatigue. Hypersomnolence disorder should be distinguished\nfrom excessive sleepiness related to insufficient sleep quantity or quality and fatigue (i.e.,\ntiredness not necessarily relieved by increase d sleep and unrelated to sleep quantity or", "source": "dsm5.pdf"} {"id": "c3cd75b89055-2", "page_content": "tiredness not necessarily relieved by increase d sleep and unrelated to sleep quantity or\nquality). Excessive sleepiness and fatigue ar e difficult to differentiate and may overlap\nconsiderably. \nBreathing-related sleep disorders. Individuals with hypersomnolence and breathing-\nrelated sleep disorders may have similar patterns of excessive sleepiness. Breathing-", "source": "dsm5.pdf"} {"id": "075fe4ce9934-0", "page_content": "372 Sleep-Wake Disorders\nrelated sleep disorders are suggested by a hist ory of loud snoring, pauses in breathing\nduring sleep, brain injury, or cardiovascular disease and by the presence of obesity, oro-\npharyngeal anatomical abnormalities, hyperten sion, or heart failure on physical examina-\ntion. Polysomnographic studies can confirm the presence of apneic events in breathing-\nrelated sleep disorder (and their ab sence in hypersomnolence disorder).\nCircadian rhythm sleep-wake disorders. Circadian rhythm sleep-wake disorders are\noften characterized by daytime sleepiness. A\u00a0 history of an abnormal sleep-wake schedule\n(with shifted or irregular hours) is present in individuals with a circadian rhythm sleep-\nwake disorder. \nParasomnias. Parasomnias rarely produce the prol onged, undisturbed nocturnal sleep\nor daytime sleepiness characterist ic of hypersomnolence disorder.\nOther mental disorders. Hypersomnolence disorder must be distinguished from mental\ndisorders that include hypersomnolence as an essential or associated fe ature. In particular,\ncomplaints of daytime sleepiness may occur in a major depressive episode, with atypical fea-\ntures, and in the depressed phase of bipolar di sorder. Assessment for ot her mental disorders is\nessential before a diagnosis of hypersomnolence disorder is co nsidered. A diagnosis of hyper-\nsomnolence disorder can be made in the presence of another current or past mental disorder. \nComorbidity\nHypersomnolence can be associated with depressive disorders, bipolar disorders (during a\ndepressive episode), and major depressive disorder, with seas onal pattern. Many individu-\nals with hypersomnolence disorder have symptoms of depression that may meet criteria for", "source": "dsm5.pdf"} {"id": "075fe4ce9934-1", "page_content": "als with hypersomnolence disorder have symptoms of depression that may meet criteria for\na depressive disorder. This presentation may be related to the psycho social consequences of\npersistent increased sleep need. Individuals with hypersomnolence disorder are also at\nrisk\u00a0for substance-related disord ers, particularly related to self-medication with stimulants.\nThis general lack of specificity may contribu te to very heterogeneous profiles among indi-\nviduals whose symptoms meet the same diagnostic criteria for hypersomnolence disorder.\nNeurodegenerative conditions, such as Alzhei mer\u2019s disease, Parkinson\u2019s disease, and mul-\ntiple system atrophy, may also be associated with hypersomnolence. \nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates nine\nsubtypes of \u201chypersomnias of central origin ,\u201d including recurrent hypersomnia (Kleine-\nLevin syndrome).\nNarcolepsy\nDiagnostic Criteria\nA. Recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping oc-\ncurring within the same day. These must have been occurring at least three times per\nweek over the past 3 months. \nB. The presence of at least one of the following:\n1. Episodes of cataplexy, defined as either (a) or (b), occurring at least a few times\nper month: \na. In individuals with long-standing disease, brief (seconds to minutes) episodes\nof sudden bilateral loss of muscle tone with maintained consciousness that are\nprecipitated by laughter or joking.", "source": "dsm5.pdf"} {"id": "f34fa341c338-0", "page_content": "Narcolepsy 373\nb. In children or in individuals within 6 months of onset, spontaneous grimaces or\njaw-opening episodes with tongue thrusting or a global hypotonia, without any\nobvious emotional triggers.\n2. Hypocretin deficiency, as measured usi ng cerebrospinal fluid (CSF) hypocretin-1\nimmunoreactivity values (less than or equal to one-third of values obtained in\nhealthy subjects tested using the same assay, or less than or equal to 110 pg/mL).\nLow CSF levels of hypocretin-1 must not be observed in the context of acute brain\ninjury, inflammation, or infection.\n3. Nocturnal sleep polysomnography showing rapid eye movement (REM) sleep la-\ntency less than or equal to 15 minutes, or a multiple sleep latency test showing a\nmean sleep latency less than or equal to 8 minutes and two or more sleep-onset\nREM periods.\nSpecify whether:\n347.00 (G47.419) Na rcolepsy without cataplexy but with hypocretin deficiency: Cri-\nterion B requirements of low CSF hypocretin-1 levels and positive polysomnography/\nmultiple sleep latency test are met, but no cataplexy is present (Criterion B1 not met).\n347.01 (G47.411) Narcolepsy with cataplexy but without hypocretin deficiency:\nIn this rare subtype (less than 5% of narcolepsy cases), Criterion B requirements of\ncataplexy and positive polysomnography/multiple sleep latency test are met, but CSF\nhypocretin-1 levels are normal (Criterion B2 not met).\n347.00 (G47.419) Autosomal dominant cereb ellar ataxia, deafness, and narco-", "source": "dsm5.pdf"} {"id": "f34fa341c338-1", "page_content": "lepsy: This subtype is caused by exon 21 DNA (cytosine-5)-methyltransferase-1 mu-\ntations and is characterized by late-onset (age 30\u201340 years) narcolepsy (with low or\nintermediate CSF hypocretin-1 levels), deafness, cerebellar ataxia, and eventually de-\nmentia. \n347.00 (G47.419) Autosomal dominant narcolepsy, obesity, and type 2 diabetes:\nNarcolepsy, obesity, and type 2 diabetes and low CSF hypocretin-1 levels have been\ndescribed in rare cases and are associated with a mutation in the myelin oligodendro-\ncyte glycoprotein gene.\n347.10 (G47.429) Narcolepsy secondary to a nother medical condition: This sub-\ntype is for narcolepsy that develops secondary to medical conditions that cause infec-\ntious (e.g., Whipple\u2019s disease, sarcoidosis), traumatic, or tumoral destruction of\nhypocretin neurons.\nCoding note (for ICD-9-CM code 347.10 only): Code first the underlying medical con-\ndition (e.g., 040.2 Whipple\u2019s disease; 347.10 narcolepsy secondary to Whipple\u2019s dis-\nease).\nSpecify current severity:\nMild: Infrequent cataplexy (less than once per week), need for naps only once or twice\nper day, and less disturbed nocturnal sleep.\nModerate: Cataplexy once daily or every few days, disturbed nocturnal sleep, and\nneed for multiple naps daily.\nSevere: Drug-resistant cataplexy with multiple attacks daily, nearly constant sleepi-", "source": "dsm5.pdf"} {"id": "f34fa341c338-2", "page_content": "ness, and disturbed nocturnal sleep (i.e., movements, insomnia, and vivid dreaming).\nSubtypes\nIn narcolepsy without cataplexy but with hypocretin deficiency, unclear \u201ccataplexy-like\u201d\nsymptoms may be reported (e.g., the symptoms are not triggered by emotions and are un-\nusually long lasting). In extremely rare cases, cerebrospinal fluid (CSF) levels of hypocre-\ntin-1 are low, and polysomnographic/multiple sleep latency test (MSLT) results are\nnegative: repeating the test is advised before establishing the subtype diagnosis. In narco-", "source": "dsm5.pdf"} {"id": "b67b78ce3afe-0", "page_content": "374 Sleep-Wake Disorders\nlepsy with cataplexy but withou t hypocretin deficiency, test results for human leukocyte\nantigen (HLA) DQB1*06:02 may be negative. Seiz ures, falls of other origin, and conversion\ndisorder (functional neurological symptom disorder) should be excluded. In narcolepsy\nsecondary to infectious (e.g., Whipple\u2019s dise ase, sarcoidosis), traumatic, or tumoral de-\nstruction of hypocretin neuron s, test results for HLA DQB1* 06:02 may be positive and may\nresult from the insult triggeri ng the autoimmune process. In other cases, the destruction of\nhypocretin neurons may be secondary to trau ma or hypothalamic surgery. Head trauma\nor infections of the central nervous system can, however, produce tran sitory decreases in\nCSF hypocretin-1 levels without hypocret in cell loss, complicating the diagnosis.\nDiagnostic Features\nThe essential features of sleepiness in narcolep sy are recurrent daytime naps or lapses into\nsleep. Sleepiness typica lly occurs daily but must occur at a minimum three times a week\nfor at least 3 months (Criterion A). Narcolep sy generally produces cataplexy, which most\ncommonly presents as brief episodes (seconds to minutes) of sudden, bilateral loss of mus-\ncle tone precipitated by emotions, typically laughing and joking. Muscles affected may\ninclude those of the neck, jaw, arms, legs, or whole body, resulting in head bobbing, jaw\ndropping, or complete falls. Individuals are awake and aware during cataplexy. To meet\nCriterion B1(a), cataplexy must be triggered by laughter or joking and must occur at least\na few times per month when the condition is untreated or in the past.", "source": "dsm5.pdf"} {"id": "b67b78ce3afe-1", "page_content": "a few times per month when the condition is untreated or in the past.\nCataplexy should not be confused with \u201cwea kness\u201d occurring in the context of athletic\nactivities (physiological) or ex clusively after unusual emotiona l triggers such as stress or\nanxiety (suggesting possible psychopathology). Episodes lasting hours or days, or those not\ntriggered by emotions, are unlikely to be cata plexy, nor is rolling on the floor while laugh-\ning hysterically.\nIn children close to onset, genuine cataplexy can be atypical, affecting primarily the\nface, causing grimaces or jaw opening with tongue thrusting (\u201ccataplectic faces\u201d). Alter-\nnatively, cataplexy may present as low-grad e continuous hypotonia, yielding a wobbling\nwalk. In these cases, Criterion B1(b) can be met in children or in individuals within 6 months\nof a rapid onset.\nNarcolepsy-cataplexy nearly always results from the loss of hypothalamic hypocretin\n(orexin)\u2013producing cells, causin g hypocretin deficiency (less than or equal to one-third of\ncontrol values, or 110 pg/mL in most laboratori es). Cell loss is likely autoimmune, and ap-\nproximately 99% of affected individuals carry HLA-DQB1*06:02 (vs. 12%\u201338% of control\nsubjects). Thus, checking for the presence of DQB1*06:02 pr ior to a lumbar puncture for eval-\nuation of CSF hypocretin-1 immu noreactivity may be useful. Ra rely, low CSF levels of hypo-\ncretin-1 occur without cataplexy, notably in youths who may develop cataplexy later. CSF", "source": "dsm5.pdf"} {"id": "b67b78ce3afe-2", "page_content": "hypocretin-1 measurement represents the gold standard, excepting associated severe con-\nditions (neurological, inflammatory, infectious , trauma) that can inte rfere with the assay.\nA nocturnal polysomnographic sleep study followed by an MSLT can also be used to\nconfirm the diagnosis (Criterion B3). These tests must be performed after the individual\nhas stopped all psychotropic medications, fo llowing 2 weeks of adequate sleep time (as\ndocumented with sleep diaries, actigraphy). Short rapid eye movement (REM) latency\n(sleep-onset REM period, REM latency less than or equal to 15 minutes) during polysom-\nnography is sufficient to confirm the diagnosi s and meets Criterion B3. Alternatively, the\nMSLT result must be positive, showing a mean sleep latency of less than or equal to 8 min-\nutes and two or more sleep-onset REM periods in four to five naps.\nAssociated Features Supporting Diagnosis", "source": "dsm5.pdf"} {"id": "0ec681541d2a-0", "page_content": "MSLT result must be positive, showing a mean sleep latency of less than or equal to 8 min-\nutes and two or more sleep-onset REM periods in four to five naps.\nAssociated Features Supporting Diagnosis \nWhen sleepiness is severe, automatic behavior s may occur, with the individual continuing\nhis or her activities in a semi-automatic, ha zelike fashion without memory or conscious-\nness. Approximately 20%\u201360% of individuals experience vivid hypnagogic hallucinations", "source": "dsm5.pdf"} {"id": "a9aa2189803d-0", "page_content": "Narcolepsy 375\nbefore or upon falling asleep or hypnopompic hallucinations just after awakening. These\nhallucinations are distinct from the less vivid, nonhallucinatory dreamlike mentation at\nsleep onset that occurs in normal sleepers. Nightmares and vivid dreaming are also fre-\nquent in narcolepsy, as is REM sleep behavior disorder. Approximately 20%\u201360% of indi-\nviduals experience sleep paralysis upon falling asleep or awakening, leaving them awake\nbut unable to move or speak. However, many normal sleepers also report sleep paralysis,\nespecially with stress or slee p deprivation. Nocturnal eating may occur. Obesity is com-\nmon. Nocturnal sleep disruption with freque nt long or short awakenings is common and\ncan be disabling.\nIndividuals may appear sleepy or fall asleep in the waiting area or during clinical ex-\namination. During cataplexy, individuals may slump in a chair and have slurred speech or\ndrooping eyelids. If the clinician has time to check reflexes during cataplexy (most attacks\nare less than 10 seconds), reflexes are abo lished\u2014an important finding distinguishing gen-\nuine cataplexy from conversion disorder. \nPrevalence\nNarcolepsy-cataplexy affects 0.02%\u20130.04% of the general population in most countries.\nNarcolepsy affects both genders, with possibly a slight male preponderance. \nDevelopment and Course \nOnset is typically in children and adolescents/young adults but rarely in older adults.\nTwo peaks of onset are suggested, at ages 15\u201325 years and ages 30\u201335 years. Onset can be\nabrupt or progressive (over years). Severity is highest when onset is abrupt in children,", "source": "dsm5.pdf"} {"id": "a9aa2189803d-1", "page_content": "abrupt or progressive (over years). Severity is highest when onset is abrupt in children,\nand then decreases with age or with treatment, so that symptoms such as cataplexy can oc-\ncasionally disappear. Abrupt onset in young, prepubescent children can be associated\nwith obesity and premature puberty, a phenotype more frequently observed since 2009. In\nadolescents, onset is more difficu lt to pinpoint. Onset in adults is often unclear, with some\nindividuals reporting having ha d excessive sleepiness since bi rth. Once the disorder has\nmanifested, the course is persistent and lifelong.\nIn 90% of cases, the first symptom to manife st is sleepiness or in creased sleep, followed\nby cataplexy (within 1 year in 50% of cases, within 3 years in 85%). Sleepiness, hypnagogic\nhallucinations, vivid dreaming , and REM sleep behavior disorder (excessive movements\nduring REM sleep) are early symptoms. Excessiv e sleep rapidly progresses to an inability\nto stay awake during the day, and to maintain good sleep at night, without a clear increase\nin total 24-hour sleep needs. In the first months, cataplexy may be atypical, especially in\nchildren. Sleep paralysis usually develops ar ound puberty in child ren with prepubertal\nonset. Exacerbations of symptoms suggest la ck of compliance with medications or devel-\nopment of a concurrent sleep disorder, notably sleep apnea.\nYoung children and adolescents with narcolepsy often develop a ggression or behav-\nioral problems secondary to sleepiness and/ or nighttime sleep disruption. Workload and\nsocial pressure increase thro ugh high school and college, reducing available sleep time at\nnight. Pregnancy does not seem to modify symptoms consisten tly. After retirement, indi-", "source": "dsm5.pdf"} {"id": "a9aa2189803d-2", "page_content": "viduals typically have more opportunity for napping, reducing the need for stimulants.\nMaintaining a regular schedule benefits individuals at all ages. \nRisk and Prognostic Factors\nTemperamental. Parasomnias, such as sleepwalking, bruxism, REM sleep behavior dis-\norder, and enuresis, may be more common in individuals who deve lop narcolepsy. Indi-\nviduals commonly report that they need more sleep than other family members. \nEnvironmental. Group A streptococcal throat infect ion, influenza (notably pandemic\nH1N1 2009), or other winter infections are lik ely triggers of the autoimmune process, pro-", "source": "dsm5.pdf"} {"id": "af6167433076-0", "page_content": "376 Sleep-Wake Disorders\nducing narcolepsy a few months later. Head trauma and abrupt changes in sleep-wake\npatterns (e.g., job changes, stress) may be additional triggers. \nGenetic and physiological. Monozygotic twins are 25%\u201332% concordant for narcolepsy.\nThe prevalence of narcolepsy is 1%\u20132% in firs t-degree relatives (a 10- to 40-fold increase\noverall). Narcolepsy is strongly associated with DQB1*06:02 (99% vs. 12%\u201338% in control\nsubjects of various ethnic gr oups; 25% in the general U.S. population). DQB1*03:01 in-\ncreases, while DQB1*05:01, DQB1*06:01, and DQB1*06:03 reduce risk in the presence of\nDQB1*06:02, but the effect is small. Polymorphisms within the T-cell receptor alpha gene\nand other immune modulating gene s also modulate risk slightly.\nCulture-Related Diagnostic Issues\nNarcolepsy has been described in all ethnic groups and in many cultures. Among African\nAmericans, more cases present without cataplexy or with atypical cataplexy, complicating\ndiagnosis, especially in the presence of obesity and obstructive sleep apnea.\nDiagnostic Markers\nFunctional imaging suggests impaired hypo thalamic responses to humorous stimuli.\nNocturnal polysomnography followed by an MS LT is used to confirm the diagnosis of\nnarcolepsy, especially when the disorder is first being diagnosed and before treatment has\nbegun, and if hypocretin deficiency has not been documented biochemically. The poly-\nsomnography/MSLT should be performed after the individual is no longer taking any", "source": "dsm5.pdf"} {"id": "af6167433076-1", "page_content": "somnography/MSLT should be performed after the individual is no longer taking any\npsychotropic drugs and after re gular sleep-wake patterns, with out shift work or sleep de-\nprivation, have been documented.\nA sleep-onset REM period during the poly somnography (REM sleep latency less than\nor equal to 15 minutes) is highly specific (a pproximately 1% positive in control subjects)\nbut moderately sensitive (approximately 50%). A positive MSLT result displays an aver-\nage sleep latency of less than or equal to 8 minutes, and sleep-onset REM periods in two or\nmore naps on a four- or five-nap test. The MS LT result is positive in 90%\u201395% of individ-\nuals with narcolepsy versus 2%\u20134% of control subjects or individuals with other sleep dis-\norders. Additional polysomnographic findings often include frequent arousals, decreased\nsleep efficiency, and increased stage 1 sleep. Periodic limb moveme nts (found in about\n40% of individuals with narcolepsy) and sleep apnea are often noted.\nHypocretin deficiency is demonstrated by measuring CSF hypocretin-1 immunoreac-\ntivity. The test is particular ly useful in individuals with suspected conversion disorder\nand those without typical cataplexy, or in treatment-refractory cases. The diagnostic value\nof the test is not affected by medications, sleep deprivation, or circadian time, but the find-\nings are uninterpretable when the individual is severely ill with a concurrent infection or\nhead trauma or is comatose. CSF cytology, protein, and glucose are within normal range\neven when sampled within weeks of rapid onse t. CSF hypocretin-1 in these incipient cases", "source": "dsm5.pdf"} {"id": "af6167433076-2", "page_content": "is typically already very diminished or undetectable.\nFunctional Consequenc es of Narcolepsy \nDriving and working are impaired, and indivi duals with narcolepsy should avoid jobs\nthat place themselves (e.g., working with mach inery) or others (e.g., bus driver, pilot) in\ndanger. Once the narcolepsy is controlled wi th therapy, patients can usually drive, al-\nthough rarely long distances alone. Untreated individuals are also at risk for social isola-\ntion and accidental injury to themselves or others. Social relations may suffer as these\nindividuals strive to avert cataplexy by exerting control over emotions. \nDifferential Diagnosis \nOther hypersomnias. Hypersomnolence and narcolepsy are similar with respect to the\ndegree of daytime sleepiness, age at onset, an d stable course over time but can be distin-", "source": "dsm5.pdf"} {"id": "2e4888d17e38-0", "page_content": "Narcolepsy 377\nguished based on distinctive clinical and labo ratory features. Individuals with hypersom-\nnolence typically have longer and less disrupted nocturnal sleep, greater difficulty\nawakening, more persistent daytime sleepine ss (as opposed to more discrete \u201csleep at-\ntacks\u201d in narcolepsy), longer and less refreshing daytime sleep episodes, and little or no\ndreaming during daytime naps. By contrast, individuals with narcolepsy have cataplexy\nand recurrent intrusions of elements of REM sleep into the transition between sleep and\nwakefulness (e.g., sleep-related hallucination s and sleep paralysis). The MSLT typically\ndemonstrates shorter sleep latenc ies (i.e., greater physiological sleepiness) as well as the\npresence of multiple sleep-onset REM periods in individuals with narcolepsy.\nSleep deprivation and insufficient nocturnal sleep. Sleep deprivation and insufficient\nnocturnal sleep are common in adolescents and shift workers. In adolescents, difficulties\nfalling asleep at night are common, causing sleep deprivation. The MSLT result may be\npositive if conducted while the individual is sleep deprived or while his or her sleep is\nphase delayed. \nSleep apnea syndromes. Sleep apneas are especially likely in the presence of obesity.\nBecause obstructive sleep apnea is more freque nt than narcolepsy, ca taplexy may be over-\nlooked (or absent), and the individual is as sumed to have obstructive sleep apnea unre-\nsponsive to usual therapies. \nMajor depressive disorder. Narcolepsy or hypersomnia may be associated or confused\nwith depression. Cataplexy is not present in depression. The MSLT re sults are most often\nnormal, and there is dissociation between subj ective and objective sleepiness, as measured", "source": "dsm5.pdf"} {"id": "2e4888d17e38-1", "page_content": "normal, and there is dissociation between subj ective and objective sleepiness, as measured\nby the mean sleep latency during the MSLT.\nConversion disorder (functional neurological symptom disorder). Atypical features,\nsuch as long-lasting cataplexy or unusual tr iggers, may be present in conversion disorder\n(functional neurological symptom disorder). Individuals may report sleeping and dream-\ning, yet the MSLT does not show the characteristic sleep-onset REM period. Full-blown,\nlong-lasting pseudocataplexy may occur during consultation, allowing the examining\nphysician enough time to verify reflexes, which remain intact. \nAttention-deficit/hyperactivity disord er or other behavioral problems. In children and\nadolescents, sleepiness can ca use behavioral problems, including aggressiveness and in-\nattention, leading to a misdiagnosis of attention-deficit/hype ractivity disorder.\nSeizures. In young children, cataplexy can be misd iagnosed as seizures. Seizures are not\ncommonly triggered by emotions, and when they are, the trigger is not usually laughing or\njoking. During a seizure, individuals are more likely to hurt themselves when falling. Sei-\nzures characterized by isolated atonia are rare ly seen in isolation of other seizures, and\nthey also have signatures on the electroencephalogram. \nChorea and movement disorders. In young children, cataplexy can be misdiagnosed as\nchorea or pediatric autoimmune neuropsychiatric disorders associated with streptococcal\ninfections, especially in the co ntext of a strep throat infectio n and high antistreptolysin O\nantibody levels. Some children may have an overlapping movement d isorder close to on-\nset of the cataplexy.", "source": "dsm5.pdf"} {"id": "2e4888d17e38-2", "page_content": "set of the cataplexy.\nSchizophrenia. In the presence of florid and vivid hypnagogic hallucinations, individuals\nmay think these experiences are real\u2014a feature that suggests schizophrenia. Similarly,\nwith stimulant treatment, pers ecutory delusions may develop. If cataplexy is present, the\nclinician should first assume that these sympto ms are secondary to narcolepsy before con-\nsidering a co-occurring diagnosis of schizophrenia. \nComorbidity\nNarcolepsy can co-occur with bipolar, depressi ve, and anxiety disorders, and in rare cases\nwith schizophrenia. Narcolepsy is also associ ated with increased body mass index or obe-", "source": "dsm5.pdf"} {"id": "659a7952d99a-0", "page_content": "378 Sleep-Wake Disorders\nsity, especially when the narcolepsy is untreated. Rapid weight gain is common in young\nchildren with a sudden disease onset. Comorbid sleep apnea sh ould be considered if there\nis a sudden aggravation of preexisting narcolepsy.\nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classificat ion of Sleep Disorders, 2nd Edition (ICSD-2), differentiates five\nsubtypes of narcolepsy.\nBreathing-Related Sleep Disorders\nThe breathing-related sleep disorders category encompasses three relatively distinct dis-\norders: obstructive sleep apnea hypopnea, ce ntral sleep apnea, an d sleep-related hypo-\nventilation. \nObstructive Sleep Apnea Hypopnea\nDiagnostic Criteria 327.23 (G47.33)\nA. Either (1) or (2): \n1. Evidence by polysomnography of at least five obstructive apneas or hypopneas per\nhour of sleep and either of the following sleep symptoms:\na. Nocturnal breathing disturbances: snor ing, snorting/gasping, or breathing\npauses during sleep.\nb. Daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportuni-\nties to sleep that is not better explained by another mental disorder (including a\nsleep disorder) and is not attribut able to another medical condition.\n2. Evidence by polysomnography of 15 or more obstructive apneas and/or hypopneas\nper hour of sleep regardless of accompanying symptoms.\nSpecify current severity:\nMild: Apnea hypopnea index is less than 15.\nModerate: Apnea hypopnea index is 15\u201330.\nSevere: Apnea hypopnea index is greater than 30.\nSpecifiers", "source": "dsm5.pdf"} {"id": "659a7952d99a-1", "page_content": "Severe: Apnea hypopnea index is greater than 30.\nSpecifiers\nDisease severity is measured by a count of the number of apneas plus hypopneas per hour\nof sleep (apnea hypopnea index) using polysomnography or other ov ernight monitoring.\nOverall severity is also informed by levels of nocturnal desaturation and sleep fragmen-\ntation (measured by brain cortical arousal frequency and sleep stages) and degree of as-\nsociated symptoms and daytime impairment. However, the exact number and thresholds\nmay vary according to the specific measureme nt techniques used, and these numbers may\nchange over time. Regardless of the apnea hy popnea index (count) pe r se, the disorder is\nconsidered to be more severe when apneas and hypopneas are accompanied by significant\noxygen hemoglobin desaturation (e.g., when more than 10% of the sleep time is spent at\ndesaturation levels of less than 90%) or wh en sleep is severely fragmented as shown by an", "source": "dsm5.pdf"} {"id": "4500b2f508d3-0", "page_content": "Obstructive Sleep Apnea Hypopnea 379\nelevated arousal index (arousal index greater th an 30) or reduced stages in deep sleep (e.g.,\npercentage stage N3 [slow-wave sleep] less than 5%).\nDiagnostic Features\nObstructive sleep apnea hypopnea is the most common breathing-related sleep disorder.\nIt is characterized by repeated episodes of upper (pharyngeal) airw ay obstruction (apneas\nand hypopneas) during sleep. Apnea refers to the total absence of airflow, and hypopnea re-\nfers to a reduction in airflow. Each apnea or hypopnea represents a reduction in breathing\nof at least 10 seconds in duration in adults or two missed breaths in children and is typi-\ncally associated with drops in oxygen saturation of 3% or greater and/or an electroenceph-\nalographic arousal. Both sleep-related (nocturnal) and wake-time symptoms are common.\nThe cardinal symptoms of obstructive sleep apnea hypopnea are snoring and daytime\nsleepiness. \nObstructive sleep apnea hypopnea in adults is diagnosed on the basis of polysom-\nnographic findings and symptoms. The diagnosis is based on symptoms of 1) nocturnal\nbreathing disturbances (i.e., snoring, snorti ng/gasping, breathing pauses during sleep), or\n2) daytime sleepiness, fatigue, or unrefreshi ng sleep despite suffic ient opportunities to\nsleep that are not better explained by another mental disorder and not attributable to an-\nother medical condition, along with 3) eviden ce by polysomnography of five or more ob-\nstructive apneas or hypopneas per hour of sleep (Criterion A1). Diagnosis can be made in", "source": "dsm5.pdf"} {"id": "4500b2f508d3-1", "page_content": "the absence of these symptoms if there is evidence by polysomnography of 15 or more ob-\nstructive apneas and/or hypopneas pe r hour of sleep (Criterion A2). \nSpecific attention to disturbe d sleep occurring in association with snoring or breathing\npauses and physical findings that increase ri sk of obstructive sleep apnea hypopnea (e.g.,\ncentral obesity, crowded pharyngeal airway, el evated blood pressure) is needed to reduce\nthe chance of misdiagnosing this treatable condition.\nAssociated Features Supporting Diagnosis\nBecause of the frequency of nocturnal awakenin gs that occur with obstructive sleep apnea\nhypopnea, individuals may report symptoms of insomnia. Other common, though non-\nspecific, symptoms of obstructive sleep apne a hypopnea are heartbur n, nocturia, morning\nheadaches, dry mouth, erectile dysfunction, and reduced li bido. Rarely, individuals may\ncomplain of difficulty breathing while lying supine or sleeping. Hypertension may occur\nin more than 60% of individuals with obstructive sleep apnea hypopnea.\nPrevalence\nObstructive sleep apnea hypopnea is a very common disorder, affecting at least 1%\u20132% of\nchildren, 2%\u201315% of middle-age adults, and mo re than 20% of older individuals. In the\ngeneral community, prevalence rates of undiagnosed obst ructive sleep apnea hypopnea\nmay be very high in elderly individuals. Sinc e the disorder is strongly associated with obe-\nsity, increases in obesity rates are likely to be accompanied by an increased prevalence of\nthis disorder. Prevalen ce may be particularly high amon g males, older adults, and certain", "source": "dsm5.pdf"} {"id": "4500b2f508d3-2", "page_content": "racial/ethnic groups. In adults, the male-to-female ratio of obstructive sleep apnea hypop-\nnea ranges from 2:1 to 4:1. Ge nder differences decline in olde r age, possibly because of an\nincreased prevalence in females after menopause. There is no gender difference among\nprepubertal children.\nDevelopment and Course\nThe age distribution of obstructive sleep apnea hypopnea likely follows a J-shaped distri-\nbution. There is a peak in children ages 3\u20138 years when the nasopharynx may be compro-\nmised by a relatively large mass of tonsillar tissue compared with the size of the upper", "source": "dsm5.pdf"} {"id": "8beb9a95a094-0", "page_content": "380 Sleep-Wake Disorders\nairway. With growth of the airway and regression of lymphoid tissue during later child-\nhood, there is reduction in prevalence. Then, as obesity prevalence increases in midlife and\nfemales enter menopause, obstructive sleep apnea hypopnea again increases. The course\nin older age is unclear; the disorder may level off after age 65 years, but in other individ-\nuals, prevalence may increase with aging. Beca use there is some age dependency of the oc-\ncurrence of apneas and hypopneas, polysomnog raphic results must be interpreted in light\nof other clinical data. In particular, signific ant clinical symptoms of insomnia or hyper-\nsomnia should be investigated re gardless of the individual\u2019s age.\nObstructive sleep apnea hypopnea usually ha s an insidious onset, gradual progression,\nand persistent course. Typically the loud snorin g has been present for many years, often since\nchildhood, but an increase in its severity may lead the individual to seek evaluation. Weight\ngain may precipitate an increase in sympto ms. Although obstructive sleep apnea hypopnea\ncan occur at any age, it most commonly mani fests among individuals ages 40\u201360 years. Over\n4\u20135 years, the average apnea hypo pnea index increases in adults and older individuals by ap-\nproximately two apneas/hypopneas per hour. Th e apnea hypopnea index is increased and in-\ncident obstructive sleep apnea hypopnea is greater among indivi duals who are older, who are\nmale, or who have a higher baseline body mass index (BMI) or increa se their BMI over time.\nSpontaneous resolution of obstructive sleep ap nea hypopnea has been reported with weight", "source": "dsm5.pdf"} {"id": "8beb9a95a094-1", "page_content": "Spontaneous resolution of obstructive sleep ap nea hypopnea has been reported with weight\nloss, particularly after bariatric surgery. In children, seasonal va riation in obstructive sleep ap-\nnea hypopnea has been observed, as has improvement with overall growth.\nIn young children, the signs and symptoms of obstructive sleep apnea hypopnea may be\nmore subtle than in adults, making diagnosis more difficult to establish. Polysomnography is\nuseful in confirming diagnosis. Evidence of fragmentation of sleep on the polysomnogram\nmay not be as apparent as in studies of older individuals, possibly because of the high homeo-\nstatic drive in young individuals. Symptoms su ch as snoring are usually parent-reported and\nthus have reduced sensitivity. Agitated arousals and unusual sleep postures, such as sleeping\non the hands and knees, may oc cur. Nocturnal enuresis also may occur and should raise the\nsuspicion of obstructive sleep apnea hypopnea if it recurs in a child who was previously dry at\nnight. Children may also manife st excessive daytime sleepiness, although this is not as com-\nmon or pronounced as in adults. Daytime mouth breathing, difficulty in swallowing, and poor\nspeech articulation are also common features in children. Children younger than 5 years more\noften present with nighttime symptoms, such as observed apneas or labored breathing, than\nwith behavioral symptoms (i.e., the nighttime symptoms are more noticeable and more often\nbring the child to clinical attention). In childre n older than 5 years, daytime symptoms such as\nsleepiness and behavioral problems (e.g., impulsivity and hyperactivity), attention-deficit/\nhyperactivity disorder, learning difficulties, and morning head aches are more often the focus\nof concern. Children with obstructive sleep apnea hypopnea also may present with failure to", "source": "dsm5.pdf"} {"id": "8beb9a95a094-2", "page_content": "of concern. Children with obstructive sleep apnea hypopnea also may present with failure to\nthrive and developmental delays. In young children, obesity is a less common risk factor,\nwhile delayed growth and \u201cfailure to thrive\u201d may be present.\nRisk and Prognostic Factors\nGenetic and physiological. The major risk factors for ob structive sleep apnea hypopnea\nare obesity and male gender. Others include maxillary-mandi bular retrognathia or micro-\ngnathia, positive family history of sleep apnea, genetic syndromes that reduce upper\nairway patency (e.g., Down\u2019s syndrome, Trea cher Collin\u2019s syndrome), adenotonsillar hy-", "source": "dsm5.pdf"} {"id": "e3cc1721b74f-0", "page_content": "gnathia, positive family history of sleep apnea, genetic syndromes that reduce upper\nairway patency (e.g., Down\u2019s syndrome, Trea cher Collin\u2019s syndrome), adenotonsillar hy-\npertrophy (especially in youn g children), menopause (in fema les), and various endocrine\nsyndromes (e.g., acromegaly). Compared with premenopausal females, males are at in-\ncreased risk for obstruct ive sleep apnea hypopnea, possibly reflecting the influences of sex\nhormones on ventilatory control and body fat distribution, as well as because of gender\ndifferences in airway structure. Medication s for mental disorders and medical conditions\nthat tend to induce somnolence may worsen the course of apnea symptoms if these med-\nications are not managed carefully.", "source": "dsm5.pdf"} {"id": "b8127e62f516-0", "page_content": "Obstructive Sleep Apnea Hypopnea 381\nObstructive sleep apnea hypopnea has a strong genetic basis, as evidenced by the sig-\nnificant familial aggregation of the apnea hy popnea index. The prevalence of obstructive\nsleep apnea hypopnea is approximately twice as high among the first-degree relatives of\nprobands with obstructive sleep apnea hypopn ea as compared with members of control\nfamilies. One-third of the variance in the apnea hypopnea index is explained by shared fa-\nmilial factors. Although genetic markers with diagnostic or prognostic value are not yet\navailable for use, eliciting a family history of obstructive sleep apnea hypopnea should in-\ncrease the clinical suspicion for the disorder.\nCulture-Related Diagnostic Issues\nThere is a potential for sleepiness and fatigue to be reported differently across cultures. In\nsome groups, snoring may be considered a si gn of health and thus may not trigger con-\ncerns. Individuals of Asian ancestry may be at increased risk for obstructive sleep apnea\nhypopnea despite relatively low BMI, possibly reflecting the influence of craniofacial risk\nfactors that narrow the nasopharynx.\nGender-Related Issues \nFemales may more commonly report fatigue rather than sleepiness and may underreport\nsnoring. \nDiagnostic Markers\nPolysomnography provides quan titative data on frequency of sleep-related respiratory\ndisturbances and associated changes in oxygen saturation and sleep continuity. Polysom-\nnographic findings in children differ from th ose in adults in that children demonstrate\nlabored breathing, partial obst ructive hypoventilation with cyclical desaturations, hyper-\ncapnia and paradoxical movements. Apnea hy popnea index levels as low as 2 are used to\ndefine thresholds of abnormality in children.", "source": "dsm5.pdf"} {"id": "b8127e62f516-1", "page_content": "define thresholds of abnormality in children.\nArterial blood gas measurements while the in dividual is awake are usually normal, but\nsome individuals can have waking hypoxemia or hypercapnia. This pattern should alert the\nclinician to the possibility of coexisting lung disease or hypoventilation. Imaging procedures\nmay reveal narrowing of the u pper airway. Cardiac testing ma y show evidence of impaired\nventricular function. Individuals with severe no cturnal oxygen desaturation may also have el-\nevated hemoglobin or hematocrit values. Vali dated sleep measures (e.g., multiple sleep la-\ntency test [MSLT], maintenance of wake fulness test) may identify sleepiness.\nFunctional Consequences of \nObstructive Sleep Apnea Hypopnea\nMore than 50% of individuals with moderate to severe obstructive sleep apnea hypopnea\nreport symptoms of daytime sleepiness. A twof old increased risk of occupational accidents\nhas been reported in association with sympto ms of snoring and slee piness. Motor vehicle\ncrashes also have been reported to be as mu ch as sevenfold higher among individuals with\nelevated apnea hypopnea index values. Clinicians should be cognizant of state govern-\nment requirements for reporting this disorder , especially in relati onship to commercial\ndrivers. Reduced scores on measures of health -related quality of life are common in individ-\nuals with obstructive sleep apnea hypopnea, wi th the largest decrements observed in the\nphysical and vitality subscales.\nDifferential Diagnosis\nPrimary snoring and other sleep disorders. Individuals with obstructive sleep apnea\nhypopnea must be differentiat ed from individuals with primary snoring (i.e., otherwise", "source": "dsm5.pdf"} {"id": "b17702a8a81b-0", "page_content": "382 Sleep-Wake Disorders\nasymptomatic individuals who snore and do not have abnorm alities on overnight polysom-\nnography). Individuals with obstructive sl eep apnea hypopnea may additionally report\nnocturnal gasping and choking. The presence of sleepiness or other daytime symptoms\nnot explained by other etiolo gies suggests the diagnosis of obstructive sleep apnea hypop-\nnea, but this differentiation requires polysomnography. Defi nitive differential diagnosis\nbetween hypersomnia, central sleep apnea, sleep-related hypoventilation, and obstructive\nsleep apnea hypopnea also requ ires polysomnographic studies.\nObstructive sleep apnea hypopnea must be diff erentiated from other causes of sleepi-\nness, such as narcolepsy, hypersomnia, and ci rcadian rhythm sleep d isorders. Obstructive\nsleep apnea hypopnea can be differentiated from narcolepsy by the absence of cataplexy,\nsleep-related hallucinations, and sleep paraly sis and by the presence of loud snoring,\ngasping during sleep, or observed apneas in sleep. Daytime sleep episodes in narcolepsy\nare characteristically shorter, more refreshing, and more of ten associated with dreaming.\nObstructive sleep apnea hypopnea shows characteristic apneas and hypopneas and oxy-\ngen desaturation during nocturnal polysomnog raphic studies. Narcolepsy results in mul-\ntiple sleep-onset rapid eye movement (REM) periods during the MS LT. Narcolepsy, like\nobstructive sleep apnea hypopnea, may be asso ciated with obesity, and some individuals\nhave concurrent narcolepsy and obstructive sleep apnea hypopnea. A diagnosis of narco-", "source": "dsm5.pdf"} {"id": "b17702a8a81b-1", "page_content": "lepsy does not exclude the di agnosis of obstructive sleep apnea hypopnea, as the two con-\nditions may co-occur.\nInsomnia disorder. For individuals complaining of difficulty initiating or maintaining\nsleep or early-morning awakenings, insomnia disorder can be differen tiated from obstruc-\ntive sleep apnea hypopnea by the absence of sn oring and the absence of the history, signs,\nand symptoms characteri stic of the latter disorder. However, insomnia and obstructive\nsleep apnea hypopnea may coexist, and if so , both disorders may need to be addressed\nconcurrently to improve sleep.\nPanic attacks. Nocturnal panic attacks may include symptoms of gasping or choking\nduring sleep that may be difficult to distinguish clinically from obst ructive sleep apnea hy-\npopnea. However, the lower frequency of episo des, intense autonomic arousal, and lack of\nexcessive sleepiness differentiate nocturnal pa nic attacks from obstructive sleep apnea hy-\npopnea. Polysomnography in individuals with nocturnal panic attacks does not reveal the\ntypical pattern of apneas or oxygen desaturation characteristic of obstructive sleep apnea\nhypopnea. Individuals with obstructive slee p apnea hypopnea do not provide a history of\ndaytime panic attacks. \nAttention-deficit/hyperactivity disorder. Attention-deficit/hyperact ivity disorder in chil-\ndren may include symptoms of inattention, academic impairment, hyperactivity, and in-\nternalizing behaviors, all of which may also be symptoms of chil dhood obstructive sleep\napnea hypopnea. The presence of other symptoms and signs of childhood obstructive\nsleep apnea hypopnea (e.g., labored breathing or snoring during sleep and adenotonsillar", "source": "dsm5.pdf"} {"id": "b17702a8a81b-2", "page_content": "hypertrophy) would suggest the presence of obstructive sl eep apnea hypopnea. Obstruc-\ntive sleep apnea hypopnea and attention-de ficit/hyperactivity disorder may commonly\nco-occur, and there may be causal links between them; therefore, risk factors such as en-\nlarged tonsils, obesity, or a family history of sleep apnea may help alert the clinician to\ntheir co-occurrence.\nSubstance/medication-induced insomnia or hypersomnia. Substance use and substance\nwithdrawal (including medications) can prod uce insomnia or hypersomnia. A careful his-\ntory is usually sufficient to identify the relevant substa nce/medication, and follow-up\nshows improvement of the sleep distur bance after discontinuation of the substance/med-", "source": "dsm5.pdf"} {"id": "c5ebe016eb2d-0", "page_content": "tory is usually sufficient to identify the relevant substa nce/medication, and follow-up\nshows improvement of the sleep distur bance after discontinuation of the substance/med-\nication. In other cases, the use of a substanc e/medication (e.g., alcohol, barbiturates, ben-\nzodiazepines, tobacco) has been shown to exacerbate obst ructive sleep apnea hypopnea.\nAn individual with sy mptoms and signs cons istent with obstructive sleep apnea hypop-", "source": "dsm5.pdf"} {"id": "f9a468c8d709-0", "page_content": "Central Sleep Apnea 383\nnea should receive that diagnosis, even in th e presence of concurrent substance use that is\nexacerbating the condition.\nComorbidity\nSystemic hypertension, coronary artery disease, heart failure, stroke, diabetes, and increased\nmortality are consistently asso ciated with obstructive slee p apnea hypopnea. Risk esti-\nmates vary from 30% to as much as 300% for moderate to severe obstructive sleep apnea\nhypopnea. Evidence of pulmonary hypertensi on and right heart fa ilure (e.g., cor pulmo-\nnale, ankle edema, hepatic congestion) are ra re in obstructive sleep apnea hypopnea and\nwhen present indicate either very severe di sease or associated hypoventilation or cardio-\npulmonary comorbidities. Obstructive sleep apnea hypopnea also may occur with in-\ncreased frequency in association with a number of medical or neurological conditions (e.g.,\ncerebrovascular disease, Parkinson\u2019s disease). Physical findings refl ect the co-occurrence of\nthese conditions.\nAs many as one-third of individuals referred for evaluation of obstructive sleep apnea\nhypopnea report symptoms of depression, with as many of 10% having depression scores\nconsistent with moderate to severe depressi on. Severity of obstructive sleep apnea hypop-\nnea, as measured by the apnea hypopnea index, has been found to be correlated with se-\nverity of symptoms of depression. This a ssociation may be stronger in males than in\nfemales.\nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates 11 sub-\ntypes of \u201csleep-related breath ing disorders,\u201d including primary central sleep apnea, ob-", "source": "dsm5.pdf"} {"id": "f9a468c8d709-1", "page_content": "types of \u201csleep-related breath ing disorders,\u201d including primary central sleep apnea, ob-\nstructive sleep apnea, and sle ep-related hypoventilation.\nCentral Sleep Apnea\nDiagnostic Criteria\nA. Evidence by polysomnography of five or more central apneas per hour of sleep.\nB. The disorder is not better explained by another current sleep disorder.\nSpecify whether:\n327.21 (G47.31) Idiopathic central sleep apnea: Characterized by repeated epi-\nsodes of apneas and hypopneas during sleep caused by variability in respiratory effort\nbut without evidence of airway obstruction.\n786.04 (R06.3) Cheyne-Stokes breathing: A pattern of periodic crescendo-\ndecrescendo variation in tidal volume that results in central apneas and hypopneas at\na frequency of at least five events per hour, accompanied by frequent arousal.\n780.57 (G47.37) Central sleep apnea comorbid with opioid use: The pathogenesis\nof this subtype is attributed to the effects of opioids on the respiratory rhythm genera-\ntors in the medulla as well as the differential effects on hypoxic versus hypercapnic re-\nspiratory drive.\nCoding note (for 780.57 [G47.37] code only): When an op ioid use disorder is present, first\ncode the opioid use disorder: 305.50 (F11.10) m ild opioid use disorder or 304.00 (F11.20)\nmoderate or severe opioid use disorder; then code 780.57 (G47.37) central sleep apnea\ncomorbid with opioid use. When an opioid use disorder is not present (e.g., after a one-", "source": "dsm5.pdf"} {"id": "f9a468c8d709-2", "page_content": "time heavy use of the substance), code only 780.57 (G47.37) central sleep apnea comor-\nbid with opioid use.", "source": "dsm5.pdf"} {"id": "910ad5b41fc6-0", "page_content": "384 Sleep-Wake Disorders\nNote: See the section \u201cDiagnostic Features\u201d in text.\nSpecify current severity:\nSeverity of central sleep apnea is graded according to the frequency of the breathing\ndisturbances as well as the extent of associated oxygen desaturation and sleep frag-\nmentation that occur as a consequence of repetitive respiratory disturbances.\nSubtypes\nIdiopathic central sleep apnea and Cheyne-Stokes breathing are characterized by increased\ngain of the ventilatory contro l system, also referred to as high loop gain, which leads to in-\nstability in ventilation and PaCO2 levels. This instability is termed periodic breathing and\ncan be recognized by hyperventilation alternating with hypoventilation. Individuals with\nthese disorders typically have pCO2 levels while awake that are slightly hypocapneic or\nnormocapneic. Central sleep apnea may also mani fest during initiation of treatment of ob-\nstructive sleep apnea hypopnea or may occur in association with obstructive sleep apnea\nhypopnea syndrome (termed complex sleep apnea ). The occurrence of central sleep apnea in\nassociation with obstructive slee p apnea is also considered to be due to high loop gain. In\ncontrast, the pathogenesis of central sleep apnea comorbid wi th opioid use has been at-\ntributed to the effects of opioids on the re spiratory rhythm generators in the medulla as\nwell as to its differential effects on hypoxic versus hypercapneic respiratory drive. These\nindividuals may have elevated pCO2 levels while awake. Individuals receiving chronic\nmethadone maintenance therapy have been no ted to have increased somnolence and de-\npression, although the ro le of breathing disorders associated with opioid medication in caus-\ning these problems has not been studied. \nSpecifiers", "source": "dsm5.pdf"} {"id": "910ad5b41fc6-1", "page_content": "ing these problems has not been studied. \nSpecifiers\nAn increase in the central apnea index (i.e., number of central apneas per hour of sleep) re-\nflects an increase in severity of central sleep apnea. Sleep continuity and quality may be\nmarkedly impaired with reductions in restor ative stages of non\u2013rapid eye movement (REM)\nsleep (i.e., decreased slow-wav e sleep [stage N3]). In indi viduals with severe Cheyne-\nStokes breathing, the pattern can also be ob served during resting wakefulness, a finding\nthat is thought to be a poor prognostic marker for mortality. \nDiagnostic Features\nCentral sleep apnea disorders ar e characterized by repeated episodes of apneas and hy-\npopneas during sleep caused by variability in respiratory effort. These are disorders of\nventilatory control in which resp iratory events occur in a peri odic or intermittent pattern.\nIdiopathic central sleep apnea is characterized by sleepiness, insomnia, and awakenings due\nto dyspnea in association with five or more central apneas per hour of sleep. Central sleep\napnea occurring in individuals with heart failu re, stroke, or renal failure typically have a\nbreathing pattern called Cheyne-Stok es breathing, which is characterized by a pattern of\nperiodic crescendo-decrescendo variation in tidal volume that results in central apneas\nand hypopneas occurring at a frequency of at least five events per hour that are accompa-\nnied by frequent arousals. Central and obstru ctive sleep apneas may coexist; the ratio of\ncentral to obstructive apneas/hypopneas may be used to identify which condition is pre-\ndominant.\nAlterations in neuromuscular control of br eathing can occur in association with med-", "source": "dsm5.pdf"} {"id": "910ad5b41fc6-2", "page_content": "Alterations in neuromuscular control of br eathing can occur in association with med-\nications or substances used in individuals with mental health conditions, which can cause\nor exacerbate impairme nts of respiratory rhythm and ventilation. Individuals taking these\nmedications have a sleep-related breathing diso rder that could contribute to sleep distur-\nbances and symptoms such as sleepiness, confusion, and depression. Specifically, chronic", "source": "dsm5.pdf"} {"id": "683810da764d-0", "page_content": "Central Sleep Apnea 385\nuse of long-acting opioid medications is often associated with im pairment of respiratory con-\ntrol leading to central sleep apnea.\nAssociated Features Supporting Diagnosis\nIndividuals with central sleep apnea hypopneas can manifest with sleepiness or insomnia.\nThere can be complaints of sleep fragment ation, including awakening with dyspnea.\nSome individuals are asymptomatic. Obstruct ive sleep apnea hypopnea can coexist with\nCheyne-Stokes breathing, and thus snoring and abruptly terminating apneas may be ob-\nserved during sleep. \nPrevalence\nThe prevalence of idiopathic central sleep apnea is unknown but thought to be rare. The\nprevalence of Cheyne-Stokes breathing is high in individuals with depressed cardiac ven-\ntricular ejection fraction. In individuals with an ejection fraction of less than 45%, the prev-\nalence has been reported to be 20% or high er. The male-to-female ratio for prevalence is\neven more highly skewed toward males than for obstructive sleep apnea hypopnea. Prev-\nalence increases with age, and most patients are older than 60 years. Cheyne-Stokes breath-\ning occurs in approximately 20% of individu als with acute stroke. Central sleep apnea\ncomorbid with opioid use occurs in approxim ately 30% of individuals taking chronic opi-\noids for nonmalignant pain and similarly in individuals receiving methadone mainte-\nnance therapy. \nDevelopment and Course\nThe onset of Cheyne-Stokes breathing appears tied to the deve lopment of heart failure. The\nCheyne-Stokes breathing pattern is associated with oscillations in heart rate, blood pres-\nsure and oxygen desaturation, and elevated sy mpathetic nervous system activity that can", "source": "dsm5.pdf"} {"id": "683810da764d-1", "page_content": "sure and oxygen desaturation, and elevated sy mpathetic nervous system activity that can\npromote progression of heart failure. The clinic al significance of Cheyne-Stokes breathing\nin the setting of stroke is no t known, but Cheyne-Stokes breathing may be a transient find-\ning that resolves with time after acute stro ke. Central sleep apnea comorbid with opioid\nuse has been documented with chro nic use (i.e., several months). \nRisk and Prognostic Factors\nGenetic and physiological. Cheyne-Stokes breathing is freq uently present in individu-\nals with heart failure. The coexistence of atrial fibrillation further increases risk, as do older\nage and male gender. Cheyne-Stokes breathing is also seen in association with acute stroke\nand possibly renal failure. The underlying ventila tory instability in the setting of heart fail-\nure has been attributed to increased ventilatory chemos ensitivity and hyperventilation\ndue to pulmonary vascular congestion and ci rculatory delay. Central sleep apnea is seen\nin individuals taking long-acting opioids.\nDiagnostic Markers\nPhysical findings seen in individuals with a Cheyne-Stokes breathing pattern relate to its\nrisk factors. Findings consiste nt with heart failure, such as jugular venous distension, S3\nheart sound, lung crackles, and lower extremity edema, may be present. Polysomnogra-\nphy is used to characterize the breathing characteristics of each breathing-related sleep\ndisorder subtype. Central sl eep apneas are recorded when periods of breathing cessation\nfor longer than 10 seconds occur. Cheyne-Sto kes breathing is characterized by a pattern of\nperiodic crescendo-decrescend o variation in tidal volume that results in central apneas\nand hypopneas occurring at a frequency of at least five events per hour that are accompa-", "source": "dsm5.pdf"} {"id": "683810da764d-2", "page_content": "nied by frequent arousals. The cycle length of Cheyne-Stokes breathing (or time from end\nof one central apnea to the end of the next apnea) is about 60 seconds.", "source": "dsm5.pdf"} {"id": "aa226ac33825-0", "page_content": "386 Sleep-Wake Disorders\nFunctional Consequences of Central Sleep Apnea\nIdiopathic central sleep apnea has been report ed to cause symptoms of disrupted sleep, in-\ncluding insomnia and sleepines s. Cheyne-Stokes breathing with comorbid heart failure\nhas been associated with excessive sleepine ss, fatigue, and insomnia, although many in-\ndividuals may be asymptomatic. Coexistence of heart failure and Cheyne-Stokes breath-\ning may be associated with increased card iac arrhythmias and increased mortality or\ncardiac transplantation. Individuals with central sleep apnea comorbid with opioid use\nmay present with symptoms of sleepiness or insomnia.\nDifferential Diagnosis\nIdiopathic central sleep apnea must be distinguished from other breathing-related sleep\ndisorders, other sleep disorders, and medical conditions and mental disorders that cause\nsleep fragmentation, sleepiness, and fatigue. This is achieved using polysomnography.\nOther breathing-related sleep disorders and sleep disorders. Central sleep apnea can\nbe distinguished from obstructive sleep apne a hypopnea by the presen ce of at least five\ncentral apneas per hour of sleep. These condit ions may co-occur, but central sleep apnea is\nconsidered to predominate when the ratio of central to obstructive respiratory events ex-\nceeds 50%.\nCheyne-Stokes breathing can be distinguishe d from other mental disorders, including\nother sleep disorders, and othe r medical conditions that caus e sleep fragmentation, sleep-\niness, and fatigue based on the presence of a predisposing condition (e.g., heart failure or\nstroke) and signs and polysomnographic evidence of the characteristic breathing pattern.\nPolysomnographic respiratory findings can help distinguish Cheyne-Stokes breathing\nfrom insomnia due to other medical conditio ns. High-altitude periodic breathing has a", "source": "dsm5.pdf"} {"id": "aa226ac33825-1", "page_content": "from insomnia due to other medical conditio ns. High-altitude periodic breathing has a\npattern that resembles Cheyne-Stokes breathin g but has a shorter cycle time, occurs only\nat high altitude, and is not associated with heart failure. \nCentral sleep apnea comorbid with opioid us e can be differentiated from other types of\nbreathing-related sleep disorders based on the use of long-acting opioid medications in\nconjunction with polysomnographic evidence of central apneas and periodic or ataxic\nbreathing. It can be distinguished from inso mnia due to drug or substance use based on\npolysomnographic evidence of central sleep apnea.\nComorbidity\nCentral sleep apnea disorders are frequently pr esent in users of long-acting opioids, such\nas methadone. Individuals taking these medi cations have a sleep-related breathing disor-\nder that could contribute to sleep disturbances and symptoms such as sleepiness, confu-\nsion, and depression. While the individual is asleep, breathing patterns such as central\napneas, periodic apneas, and ataxic breathing may be observed. Obstructive sleep apnea\nhypopnea may coexist with central sleep apnea, and features consiste nt with this condi-\ntion can also be present (see \u201cObstructive Sleep Apnea Hypopnea\u201d earlier in this chapter).\nCheyne-Stokes breathing is more commonly obse rved in association with conditions that\ninclude heart failure, stroke, and renal failure and is seen more frequently in individuals\nwith atrial fibrillation. Individuals with Ch eyne-Stokes breathing are more likely to be\nolder, to be male, and to have lower weight than individual s with obstructive sleep apnea\nhypopnea.", "source": "dsm5.pdf"} {"id": "499a31d2c748-0", "page_content": "Sleep-Related Hypoventilation 387\nSleep-Related Hypoventilation\nDiagnostic Criteria\nA. Polysomnograpy demonstrates episodes of decreased respiration associated with el-\nevated CO2 levels. ( Note: In the absence of objective measurement of CO2, persistent\nlow levels of hemoglobin oxygen saturation unassociated with apneic/hypopneic\nevents may indicate hypoventilation.)\nB. The disturbance is not better explained by another current sleep disorder.\nSpecify whether:\n327.24 (G47.34) Idiopathic hypoventilation: This subtype is not attributable to any\nreadily identified condition.\n327.25 (G47.35) Congenital centr al alveolar hypoventilation: This subtype is a rare\ncongenital disorder in which the individual typically presents in the perinatal period with\nshallow breathing, or cyanosis and apnea during sleep.\n327.26 (G47.36) Comorbid sleep -related hypoventilation: This subtype occurs as a\nconsequence of a medical condition, such as a pulmonary disorder (e.g., interstitial\nlung disease, chronic obstructive pulmonary disease) or a neuromuscular or chest wall\ndisorder (e.g., muscular dystrophies, postpolio syndrome, cervical spinal cord injury,\nkyphoscoliosis), or medications (e.g., benzodiazepines, opiates). It also occurs with\nobesity (obesity hypoventilation disorder), where it reflects a combination of increased\nwork of breathing due to reduced chest wall compliance and ventilation-perfusion mis-\nmatch and variably reduced ventilatory drive. Such individuals usually are character-\nized by body mass index of greater than 30 and hypercapnia during wakefulness (with\na pCO2 of greater than 45), without other evidence of hypoventilation.", "source": "dsm5.pdf"} {"id": "499a31d2c748-1", "page_content": "Specify current severity:\nSeverity is graded according to the degree of hypoxemia and hypercarbia present dur-\ning sleep and evidence of end organ impairment due to these abnormalities (e.g., right-\nsided heart failure). The presence of blood gas abnormalities during wakefulness is an\nindicator of greater severity.\nSubtypes\nRegarding obesity hypoventilati on disorder, the prevalence of obesity hypoventilation in\nthe general population is not known but is thought to be increasing in association with the\nincreased prevalence of obesity and extreme obesity.\nDiagnostic Features\nSleep-related hypoventilation can occur in dependently or, more frequently, comorbid\nwith medical or neurological disorders, medi cation use, or substa nce use disorder. Al-\nthough symptoms are not mandatory to make this diagnosis, individuals often report\nexcessive daytime sleepiness, frequent arou sals and awakenings during sleep, morning\nheadaches, and insomnia complaints. \nAssociated Features Supporting Diagnosis\nIndividuals with sleep-related hypoventilation can present with sl eep-related complaints\nof insomnia or sleepiness. Episodes of orth opnea can occur in individuals with diaphragm\nweakness. Headaches upon awakening may be pr esent. During sleep, episodes of shallow\nbreathing may be observed, an d obstructive sleep apnea hypo pnea or central sleep apnea\nmay coexist. Consequences of ventilatory in sufficiency, includin g pulmonary hyperten-\nsion, cor pulmonale (right heart failure), polycythemia, and neurocognitive dysfunction,", "source": "dsm5.pdf"} {"id": "f0434e26566a-0", "page_content": "388 Sleep-Wake Disorders\ncan be present. With progression of ventilato ry insufficiency, bloo d gas abnormalities ex-\ntend into wakefulness. Features of the me dical condition causing sleep-related hypoven-\ntilation can also be present. Episodes of hy poventilation may be as sociated with frequent\narousals or bradytachycardia. Individuals ma y complain of excessive sleepiness and in-\nsomnia or morning headaches or may present wi th findings of neuroc ognitive dysfunction\nor depression. Hypoventilation may not be present during wakefulness.\nPrevalence\nIdiopathic sleep-related hypoventilation in adults is very uncommon. The prevalence of\ncongenital central alveolar hy poventilation is unknown, but the disorder is rare. Comor-\nbid sleep-related hypoventilation (i.e., hypo ventilation comorbid with other conditions,\nsuch as chronic obstructive pulmonary diseas e [COPD], neuromuscular disorders, or obe-\nsity) is more common.\nDevelopment and Course\nIdiopathic sleep-related hypove ntilation is thought to be a slowly progressive disorder of\nrespiratory impairment. When th is disorder occurs comorbidly with other disorders (e.g.,\nCOPD, neuromuscular disorders, obesity), diseas e severity reflects the severity of the un-\nderlying condition, and the disorder progre sses as the condition worsens. Complications\nsuch as pulmonary hypertension, cor pulmon ale, cardiac dysrhythmias, polycythemia,\nneurocognitive dysfunction, and worsening re spiratory failure can develop with increas-\ning severity of blood gas abnormalities. \nCongenital central alveolar hypoventilation usually manifests at birth with shallow,", "source": "dsm5.pdf"} {"id": "f0434e26566a-1", "page_content": "Congenital central alveolar hypoventilation usually manifests at birth with shallow,\nerratic, or absent breathing. This disorder can also manifest during infancy, childhood,\nand adulthood because of va riable penetrance of the PHOX2B mutation. Children with\ncongenital central alveolar hypo ventilation are more likely to have disorders of the auto-\nnomic nervous system, Hirschsprung\u2019s disease, neural crest tumors, and characteristic box-\nshaped face (i.e., the face is short relative to its width).\nRisk and Prognostic Factors\nEnvironmental. Ventilatory drive can be reduced in individuals using central nervous\nsystem depressants, including benzod iazepines, opiates, and alcohol. \nGenetic and physiological. Idiopathic sleep-related hypoventilation is associated with\nreduced ventilatory drive due to a blunted chemoresponsiveness to CO2 (reduced respi-\nratory drive; i.e., \u201cwon\u2019t brea the\u201d), reflecting underlying neurological deficits in centers\ngoverning the control of ventilation. More co mmonly, sleep-related hypoventilation is co-\nmorbid with another medical condition, su ch as a pulmonary diso rder, a neuromuscular\nor chest wall disorder, or hypothyroidism, or with use of medications (e.g., benzodiaze-\npines, opiates). In these conditions, the hy poventilation may be a consequence of in-\ncreased work of breathing and/or impairment of respiratory muscle function (i.e., \u201ccan\u2019t\nbreathe\u201d) or reduced respiratory drive (i.e., \u201cwon\u2019t breathe\u201d).\nNeuromuscular disorders influence breathin g through impairment of respiratory mo-\ntor innervation or respiratory muscle function. They include conditions such as amyo-", "source": "dsm5.pdf"} {"id": "f0434e26566a-2", "page_content": "tor innervation or respiratory muscle function. They include conditions such as amyo-\ntrophic lateral sclerosis, spinal cord injury , diaphragmatic paralysis, myasthenia gravis,\nLambert-Eaton syndrome, toxic or metabolic myopathies, postpolio syndrome, and Char-\ncot-Marie-Tooth syndrome. \nCongenital central alveolar hypoventilation is a genetic disorder at tributable to muta-\ntions of PHOX2B, a gene that is crucial for the de velopment of the embryonic autonomic\nnervous system and neural crest derivatives. Children with congenital central alveolar hy-\npoventilation show blunted vent ilatory responses to hypercapnia, especially in non\u2013rapid\neye movement sleep.", "source": "dsm5.pdf"} {"id": "c898c0c59f81-0", "page_content": "Sleep-Related Hypoventilation 389\nGender-Related Diagnostic Issues\nGender distributions for sleep-related hypove ntilation occurring in association with co-\nmorbid conditions reflect the gender distributions of the co morbid conditions. For exam-\nple, COPD is more frequently present in males and with increasing age. \nDiagnostic Markers \nSleep-related hypoventilation is diagnosed using polysomnography showing sleep-related\nhypoxemia and hypercapnia that is not better explained by another breathing-related sleep\ndisorder. The documentation of increased arterial pCO2 levels to greater than 55 mmHg\nduring sleep or a 10 mmHg or greater increase in pCO2 levels (to a level that also exceeds\n50 mmHg) during sleep in comparison to awake supine values, for 10 minutes or longer, is\nthe gold standard for diagnosis. However, obtaining arterial blood gas determinations dur-\ning sleep is impractical, and non-invasive measures of pCO2 have not been adequately val-\nidated during sleep and are not widely used during polysomnography in adults. Prolonged\nand sustained decreases in oxyg en saturation (oxygen saturation of less than 90% for more\nthan 5 minutes with a nadir of at least 85%, or oxygen saturation of less than 90% for at least\n30% of sleep time) in the absence of evidence of upper airway obstruction are often used as\nan indication of sleep- related hypoventilation; however, this finding is not sp ecific, as there\nare other potential causes of hypoxemia, such as that due to lung disease.\nFunctional Consequences of \nSleep-Related Hypoventilation\nThe consequences of sleep-related hypoventilati on are related to the effects of chronic ex-", "source": "dsm5.pdf"} {"id": "c898c0c59f81-1", "page_content": "The consequences of sleep-related hypoventilati on are related to the effects of chronic ex-\nposure to hypercapnia and hypoxemia. Th ese blood gas derangements cause vasocon-\nstriction of the pulmonary va sculature leading to pulmon ary hypertension, which, if\nsevere, can result in right-sided heart failure (cor pulmonale). Hypo xemia can lead to dys-\nfunction of organs such as the brain, blood, and heart, leading to outcomes such as cog-\nnitive dysfunction, polycythemia, and cardiac arrhythmias. Hypercapnia can depress\nventilatory drive, leading to pr ogressive respiratory failure. \nDifferential Diagnosis\nOther medical conditions affecting ventilation. In adults, the idiopathic variety of sleep-\nrelated hypoventilation is very uncommon and is determined by excluding the presence of\nlung diseases, skeletal malformations, neuromuscular disorders, and other medical and\nneurological disorders or medications that affect ventilation. Sleep-related hypoventila-\ntion must be distinguished from other causes of sleep-related hypoxemia, such as that due\nto lung disease.\nOther breathing-related sleep disorders. Sleep-related hypoventilation can be distin-\nguished from obstructive sleep apnea hypopnea and central sleep apnea based on clinical\nfeatures and findings on polysomnography. Sl eep-related hypoventilation typically shows\nmore sustained periods of oxygen desaturation rather that the periodic episodes seen in\nobstructive sleep apnea hypopnea and central sleep apnea. Obstructive sleep apnea hy-\npopnea and central sleep apnea also show a pa ttern of discrete epis odes of re peated air-\nflow decreases that can be absent in sleep-related hypoventilation.\nComorbidity", "source": "dsm5.pdf"} {"id": "c898c0c59f81-2", "page_content": "flow decreases that can be absent in sleep-related hypoventilation.\nComorbidity \nSleep-related hypoventilation often occurs in a ssociation with a pulmonary disorder (e.g., in-\nterstitial lung disease, COPD), with a neurom uscular or chest wall disorder (e.g., muscular\ndystrophies, post-polio syndrome, cervical spinal cord in jury, obesity, kyphoscoliosis), or,", "source": "dsm5.pdf"} {"id": "39f8696626b3-0", "page_content": "390 Sleep-Wake Disorders\nmost relevant to the mental he alth provider, with medication use (e.g., benzodiazepines, opi-\nates). Congenital central alveol ar hypoventilation often occurs in association with autonomic\ndysfunction and may occur in association with Hirschsprung\u2019s disease. COPD, a disorder of\nlower airway obstruction usually associated with cigarette sm oking, can result in sleep-\nrelated hypoventilation and hypoxemia. The pres ence of coexisting obstructive sleep apnea\nhypopnea is thought to exacerbate hypoxemia and hypercapnia during sleep and wakeful-\nness. The relationship between congenital central alveolar hypoventilation and idiopathic\nsleep-related hypoventilation is unclear; in some individuals, idiopathic sleep-related hy-\npoventilation may represent cases of late-onset congenital central alveolar hypoventilation.\nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classificat ion of Sleep Disorders, 2nd Edition (ICSD-2), combines sleep-\nrelated hypoventilation and sleep-related hypo xemia under the category of sleep-related\nhypoventilation/hypoxemic syndromes. This ap proach to classificati on reflects the fre-\nquent co-occurrence of disorder s that lead to hypoventilation and hypoxemia. In contrast,\nthe classification used in DS M-5 reflects evidence that th ere are distinct sleep-related\npathogenetic processes le ading to hypoventilation.\nCircadian Rhythm Sleep-Wake Disorders\nDiagnostic Criteria\nA. A persistent or recurrent pattern of sleep disruption that is primarily due to an alteration\nof the circadian system or to a misalignment between the endogenous circadian\nrhythm and the sleep\u2013wake schedule required by an individual\u2019s physical environment", "source": "dsm5.pdf"} {"id": "39f8696626b3-1", "page_content": "rhythm and the sleep\u2013wake schedule required by an individual\u2019s physical environment\nor social or professional schedule. \nB. The sleep disruption leads to excessive sleepiness or insomnia, or both.\nC. The sleep disturbance causes clinically significant distress or impairment in social, oc-\ncupational, and other important areas of functioning.\nCoding note: For ICD-9-CM, code 307.45 for all subtypes. For ICD-10-CM, code is based\non subtype.\nSpecify whether:\n307.45 (G47.21) Delayed sleep phase type: A pattern of delayed sleep onset and\nawakening times, with an inability to fall asleep and awaken at a desired or convention-\nally acceptable earlier time.\nSpecify if:\nFamilial: A family history of delayed sleep phase is present.\nSpecify if:\nOverlapping with non-24-hour sleep-wake type: Delayed sleep phase type\nmay overlap with another circadian rhythm sleep-wake disorder, non-24-hour\nsleep-wake type. \n307.45 (G47.22) Advanced sleep phase type: A pattern of advanced sleep onset and\nawakening times, with an inability to remain awake or asleep until the desired or con-\nventionally acceptable later sleep or wake times.\nSpecify if:\nFamilial: A family history of advanced sleep phase is present. \n307.45 (G47.23) Irregular sleep-wake type: A temporally disorganized sleep-wake\npattern, such that the timing of sleep and wake periods is variable throughout the 24-\nhour period.", "source": "dsm5.pdf"} {"id": "1071011f5e14-0", "page_content": "Circadian Rhythm Sleep-Wake Disorders 391\n307.45 (G47.24) Non-24-hour sleep-wake type: A pattern of sleep-wake cycles that\nis not synchronized to the 24-hour environment, with a consistent daily drift (usually to\nlater and later times) of sleep onset and wake times.\n307.45 (G47.26) Shift work type: Insomnia during the major sleep period and/or ex-\ncessive sleepiness (including inadvertent sleep) during the major awake period asso-\nciated with a shift work schedule (i.e., requiring unconventional work hours).\n307.45 (G47.20) Unspecified type\nSpecify if:\nEpisodic: Symptoms last at least 1 month but less than 3 months.\nPersistent: Symptoms last 3 months or longer.\nRecurrent: Two or more episodes occur within the space of 1 year.\nDelayed Sleep Phase Type\nDiagnostic Features\nThe delayed sleep phase type is based primarily on a history of a delay in the timing of the\nmajor sleep period (usually more than 2 hours) in relation to the desired sleep and wake-\nup time, resulting in symptoms of insomnia and excessive sleepiness. When allowed to set\ntheir own schedule, individuals with delayed sleep phase type exhibit normal sleep qual-\nity and duration for age. Symptoms of slee p-onset insomnia, diffic ulty waking in the\nmorning, and excessive early day sleepiness are prominent.\nAssociated Features Supporting Diagnosis\nCommon associated features of delayed sleep phase type include a hi story of mental dis-\norders or a concurrent mental disorder. Ex treme and prolonged difficulty awakening with\nmorning confusion is also common. Psychophy siological insomnia may develop as a re-\nsult of maladaptive behaviors that impair sleep and increase arousal because of repeated", "source": "dsm5.pdf"} {"id": "1071011f5e14-1", "page_content": "sult of maladaptive behaviors that impair sleep and increase arousal because of repeated\nattempts to fall asleep at an earlier time.\nPrevalence\nPrevalence of delayed sleep phase type in the general population is approximately 0.17%\nbut appears to be greater than 7% in adolescents. Although the prevalence of familial de-\nlayed sleep phase type has not been established , a family history of delayed sleep phase is\npresent in individuals with delayed sleep phase type. \nDevelopment and Course\nCourse is persistent, lasting longer than 3 mo nths, with intermittent exacerbations through-\nout adulthood. Although age at onset is variable, symptoms begin typically in adolescence\nand early adulthood and persist for several mo nths to years before diagnosis is estab-\nlished. Severity may decrease with ag e. Relapse of symptoms is common.\nClinical expression may vary across the lif espan depending on social, school, and work\nobligations. Exacerbation is usua lly triggered by a change in work or school schedule that\nrequires an early rise time. Individuals wh o can alter their work schedules to accommo-\ndate the delayed circadian sleep and wake timing can experience remission of symptoms. \nIncreased prevalence in adolescence may be a consequence of both physiological and be-\nhavioral factors. Hormonal changes may be involved specifically, as delayed sleep phase is as-\nsociated with the onset of puberty. Thus, de layed sleep phase type in adolescents should be\ndifferentiated from the common delay in the timi ng of circadian rhythms in this age group. In\nthe familial form, the course is persistent and may not improve significantly with age.", "source": "dsm5.pdf"} {"id": "6195edf2bffe-0", "page_content": "392 Sleep-Wake Disorders\nRisk and Prognostic Factors\nGenetic and physiological. Predisposing factors may include a longer than average cir-\ncadian period, changes in light sensitivity, an d impaired homeostatic sleep drive. Some in-\ndividuals with delayed sleep phase type may be hypersensi tive to evening light, which\ncan serve as a delay signal to the circadian cloc k, or they may be hy posensitive to morning\nlight such that its phase-advancing effects ar e reduced. Genetic factors may play a role in\nthe pathogenesis of familial and sporadic forms of delayed sleep phase type, including\nmutations in circadian genes (e.g., PER3 , CKIe ).\nDiagnostic Markers\nConfirmation of the diagnosis includes a complete history and use of a sleep diary or actigra-\nphy (i.e., a wrist-worn motion detector that mo nitors motor activity for prolonged periods and\ncan be used as a proxy for sleep-wake patterns for at least 7 days). Th e period covered should\ninclude weekends, when social an d occupational obligations are le ss strict, to ensure that the\nindividual exhibits a consistently delayed slee p-wake pattern. Biomarkers such as salivary\ndim light melatonin onset should be obtain ed only when the diagnosis is unclear.\nFunctional Consequences of Delayed Sleep Phase Type\nExcessive early day sleepiness is prominent. Ex treme and prolonged difficulty awakening\nwith morning confusion (i.e., sleep inertia) is also common. The severity of insomnia and\nexcessive sleepiness symptoms varies substa ntially among individuals and largely de-\npends on the occupational and social demands on the individual. \nDifferential Diagnosis\nNormative variations in sleep. Delayed sleep phase type must be distinguished from\n\u201cnormal\u201d sleep patterns in which an individual has a late schedule that does not cause", "source": "dsm5.pdf"} {"id": "6195edf2bffe-1", "page_content": "\u201cnormal\u201d sleep patterns in which an individual has a late schedule that does not cause\npersonal, social, or occupational distress (m ost commonly seen in adolescents and young\nadults).\nOther sleep disorders. Insomnia disorder and other circadian rhythm sleep-wake dis-\norders should be included in the differenti al. Excessive sleepiness may also be caused by\nother sleep disturbances, such as breathing- related sleep disorders, insomnias, sleep-\nrelated movement disorders, and medical, ne urological, and mental disorders. Overnight\npolysomnography may help in evaluating for other comorbid sleep disorders, such as\nsleep apnea. The circadian nature of delaye d sleep phase type, howe ver, should differen-\ntiate it from other disorders with similar complaints.\nComorbidity\nDelayed sleep phase type is strongly associated with depression, personality disorder, and\nsomatic symptom disorder or illness anxiety d isorder. In addition, comorbid sleep disor-\nders, such as insomnia disorder, restless legs syndrome, and sleep apnea, as well as depres-\nsive and bipolar disorders and anxiety disord ers, can exacerbate symptoms of insomnia\nand excessive sleepiness. Delayed sleep phase type may overlap with another circadian\nrhythm sleep-wake diso rder, non-24-ho ur sleep-wake type. Sighted individuals with non-\n24-hour sleep-wake type disorder commonly also have a history of delayed circadian sleep\nphase.", "source": "dsm5.pdf"} {"id": "6061d43f9662-0", "page_content": "Circadian Rhythm Sleep-Wake Disorders 393\nAdvanced Sleep Phase Type\nSpecifiers \nAdvanced sleep phase type may be document ed with the specified \u201cfamilial.\u201d Although\nthe prevalence of familial adva nced sleep phase type has no t been established, a family\nhistory of advanced sleep phase is present in individuals with advanced sleep phase type.\nIn this type, specific mutations demonstrate an autosomal dominant mode of inheritance.\nIn the familial form, onset of symptoms ma y occur earlier (during childhood and early\nadulthood), the course is persistent, and the se verity of symptoms may increase with age.\nDiagnostic Features\nAdvanced sleep phase type is characterized by sleep-wake times that are several hours\nearlier than desired or conventional times. Di agnosis is based primarily on a history of an\nadvance in the timing of the major sleep period (usually more than 2 hours) in relation to\nthe desired sleep and wake-up time, with sy mptoms of early morning insomnia and ex-\ncessive daytime sleepiness. When allowed to set their schedule, individuals with ad-\nvanced sleep phase type will exhibit norm al sleep quality and duration for age. \nAssociated Features Supporting Diagnosis\nIndividuals with advanced sleep phase type are \u201cmorning types,\u201d having earlier sleep-\nwake times, with the timing of circadian biom arkers such as melatonin and core body tem-\nperature rhythms occurring 2\u20134 hours earlier th an normal. When required to keep a con-\nventional schedule requiring a delay of bedtim e, these individuals will continue to have an\nearly rise time, leading to persistent sleep de privation and daytime sleepiness. Use of hyp-\nnotics or alcohol to combat sleep-maintenance insomnia and stimulants to reduce daytime\nsleepiness may lead to substance abuse in these individuals. \nPrevalence", "source": "dsm5.pdf"} {"id": "6061d43f9662-1", "page_content": "sleepiness may lead to substance abuse in these individuals. \nPrevalence\nThe estimated prevalence of advanced sleep phase type is approximately 1% in middle-\nage adults. Sleep-wake times and circadian pha se advance in older individuals, probably\naccounting for increased prevalence in this population.\nDevelopment and Course\nOnset is usually in late adulthood. In the familial form, onset can be earlier. The course is typ-\nically persistent, lasting more than 3 months, but the severity may increase depending on work\nand social schedules. The advanced sleep pha se type is more common in older adults. \nClinical expression may vary across the lif espan depending on social, school, and work\nobligations. Individuals who can alter their work schedules to ac commodate the advanced\ncircadian sleep and wake timing can experience remission of symptoms. Increasing age\ntends to advance the sleep phase, however, it is unclear whether the common age-associ-\nated advanced sleep phase type is due solely to a change in circadian timing (as seen in the\nfamilial form) or also to age-related changes in the homeostatic regulation of sleep, result-\ning in earlier awakening. Severi ty, remission, and relapse of symptoms suggest lack of ad-\nherence to behavioral and environmental trea tments designed to control sleep and wake\nstructure and lig ht exposure.", "source": "dsm5.pdf"} {"id": "10c8fd79f2da-0", "page_content": "394 Sleep-Wake Disorders\nRisk and Prognostic Factors\nEnvironmental. Decreased late afternoon/early evening exposure to light and/or expo-\nsure to early morning light du e to early morning awakening can increase the risk of ad-\nvanced sleep phase type by advancing circadian rhythms. By going to bed early, these\nindividuals are not exposed to light in the phase delay region of the curve, resulting in per-\npetuation of advanced phase. In familial adva nced sleep phase type, a shortening of the\nendogenous circadian period can result in an advanced sleep phase, although circadian pe-\nriod does not appear to system atically decrease with age. \nGenetic and physiological. Advanced sleep phase type ha s demonstrated an autoso-\nmal dominant mode of inheritance, including a PER2 gene mutation causing hypophos-\nphorylation of the PER2 protein and a missense mutation in CKI.\nCulture-Related Diagnostic Issues\nAfrican Americans may have a shorter circad ian period and larger magnitude phase ad-\nvances to light than do Caucasians, possibly increasing the risk for development of ad-\nvanced sleep phase type in this population.\nDiagnostic Markers\nA sleep diary and actigraphy may be used as diagnostic markers, as described earlier for\ndelayed sleep phase type. \nFunctional Consequences of Advanced Sleep Phase Type\nExcessive sleepiness associated with advanced sleep phase can have a negative effect on\ncognitive performance, social interaction, and safety. Use of wake-promoting agents to\ncombat sleepiness or sedatives for early mo rning awakening may increase potential for\nsubstance abuse.\nDifferential Diagnosis\nOther sleep disorders. Behavioral factors such as irre gular sleep schedules, voluntary\nearly awakening, and exposure to light in th e early morning should be considered, partic-", "source": "dsm5.pdf"} {"id": "10c8fd79f2da-1", "page_content": "early awakening, and exposure to light in th e early morning should be considered, partic-\nularly in older adults . Careful attention should be paid to rule out other sleep-wake dis-\norders, such as insomnia disorder, and other mental disorders and medical conditions that\ncan cause early morning awakening. \nDepressive and bipolar disorders. Because early morning awaken ing, fatigue, and sleep-\niness are prominent features of major depres sive disorder, depressive and bipolar disor-\nders must also be considered. \nComorbidity\nMedical conditions and mental disorders wi th the symptom of early morning awakening,\nsuch as insomnia, can co-occur with the advance sleep phase type. \nIrregular Sleep-Wake Type\nDiagnostic Features\nThe diagnosis of irregular sleep-wake type is based primarily on a history of symptoms of\ninsomnia at night (during the usual sleep pe riod) and excessive sleepiness (napping) dur-\ning the day. Irregular sleep-wake type is char acterized by a lack of discernable sleep-wake", "source": "dsm5.pdf"} {"id": "f0d721742ed4-0", "page_content": "Circadian Rhythm Sleep-Wake Disorders 395\ncircadian rhythm. There is no major sleep period, and sleep is fragmented into at least\nthree periods during the 24-hour day. \nAssociated Features Supporting Diagnosis\nIndividuals with irregular slee p-wake type typically present with insomnia or excessive\nsleepiness, depending on the time of day. Sleep and wake periods across 24 hours are frag-\nmented, although the longest sleep period tends to occur between 2:00 A.M. and 6:00 A.M.\nand is usually less than 4 hours. A history of isolation or reclusion may occur in association\nwith the disorder and contribute to the symptoms via a lack of external stimuli to help en-\ntrain a normal pattern. Individuals or their ca regivers report frequent naps throughout the\nday. Irregular sleep-wake type is most comm only associated with neurodegenerative dis-\norders, such as major neurocognitive disorder, and many neurodevelopmental disorders\nin children. \nPrevalence\nPrevalence of irregular sleep-wake type in the general population is unknown. \nDevelopment and Course\nThe course of irregular sleep-wak e type is persistent. Age at onset is variable, but the dis-\norder is more common in older adults. \nRisk and Prognostic Factors\nTemperamental. Neurodegenerative disorders, such as Alzheimer\u2019s disease, Parkinson\u2019s\ndisease, and Huntington\u2019s disease, and neur odevelopmental disorders in children in-\ncrease the risk for irregular sleep-wake type. \nEnvironmental. Decreased exposure to environmenta l light and structured daytime ac-\ntivity can be associated with a low-amplitud e circadian rhythm. Hospitalized individuals\nare especially prone to such weak external en training stimuli, and even outside the hospi-", "source": "dsm5.pdf"} {"id": "f0d721742ed4-1", "page_content": "are especially prone to such weak external en training stimuli, and even outside the hospi-\ntal setting, individuals with major neurocogni tive disorder (i.e., dementia) are exposed to\nsignificantly less bright light. \nDiagnostic Markers\nA detailed sleep history and a sleep diary (by a caregiver) or actigraphy help confirm the\nirregular sleep-wake pattern.\nFunctional Consequences of \nIrregular Sleep-Wake Type\nLack of a clearly discernible major sleep and wake period in irregular sleep-wake type re-\nsults in insomnia or excessive sleepiness, depending on the time of day. Disruption of the\ncaregiver\u2019s sleep also often occurs and is an important consideration.\nDifferential Diagnosis\nNormative variations in sleep. Irregular sleep-wake type sh ould be distinguished from\na voluntary irregular sleep-wake schedule and po or sleep hygiene, which can result in in-\nsomnia and excessive sleepiness. \nOther medical conditions and mental disorders. Other causes of insomnia and daytime\nsleepiness, including comorbid medical condit ions and mental disorders or medication,\nshould be considered.", "source": "dsm5.pdf"} {"id": "061d56cffb46-0", "page_content": "396 Sleep-Wake Disorders\nComorbidity\nIrregular sleep-wake type is often comorbid with neurodegenerat ive and neurodevelop-\nmental disorders, such as major neurocognitive disorder, inte llectual disability (intellec-\ntual developmental disorder), and traumatic br ain injury. It is also comorbid with other\nmedical conditions and mental disorders in wh ich there is social isolation and/or lack of\nlight and structured activities. \nNon-24-Hour Sleep-Wake Type\nDiagnostic Features\nThe diagnosis of non-24-hour sleep-wake type is based primarily on a history of symp-\ntoms of insomnia or excessive sleepiness related to abnormal synchronization between the\n24-hour light-dark cycle and the endogenous circadian rhythm. Individuals typically pre-\nsent with periods of insomnia, excessive sleepiness, or both, which alternate with short\nasymptomatic periods. Starting with the asymptomatic period, when the individual\u2019s\nsleep phase is aligned to the external envi ronment, sleep latency will gradually increase\nand the individual will complain of sleep-onset insomnia. As the sleep phase continues to\ndrift so that sleep time is no w in the daytime, the individu al will have trouble staying\nawake during the day and will complain of sleepiness. Because the circadian period is not\naligned to the external 24-hour environment, symptoms will depend on when an individ-\nual tries to sleep in relation to the circadian rhythm of sleep propensity. \nAssociated Features Supporting Diagnosis\nNon-24-hour sleep-wake type is most common among blind or visually impaired individ-\nuals who have decreased light perception. In si ghted individuals, there is often a history of\ndelayed sleep phase and of decreased exposure to light and structured social and physical\nactivity. Sighted individuals with non-24-h our sleep-wake type also demonstrate in-", "source": "dsm5.pdf"} {"id": "061d56cffb46-1", "page_content": "activity. Sighted individuals with non-24-h our sleep-wake type also demonstrate in-\ncreased sleep duration.\nPrevalence\nPrevalence of non-24-hour sleep-wake type in the general population is unclear, but the\ndisorder appears rare in sighte d individuals. The prevalence in blind individuals is esti-\nmated to be 50%.\nDevelopment and Course\nCourse of non-24-hour sleep-wake type is per sistent, with intermittent remission and ex-\nacerbations due to changes in work and social schedules throughout the lifespan. Age at\nonset is variable, depending on the onset of visual impairment. In sighted individuals, be-\ncause of the overlap with delayed sleep phase type, non-24-hour sleep-wake type may de-\nvelop in adolescence or early adulthood. Remi ssion and relapse of symptoms in blind and\nsighted individuals largely depend on adhere nce to treatments designed to control sleep\nand wake structure and light exposure.\nClinical expression may vary across the lif espan depending on social, school, and work\nobligations. In adolescents and adults, irre gular sleep-wake schedules and exposure to\nlight or lack of light at critical times of the day can exacerbate the effects of sleep loss and\ndisrupt circadian entrainment. Consequently , symptoms of insomnia, daytime sleepiness,\nand school, professional, and interpersonal functioning may worsen.\nRisk and Prognostic Factors\nEnvironmental. In sighted individuals, decreased expo sure or sensitivit y to light and so-\ncial and physical activity cues may contribute to a free-running circadian rhythm. With the", "source": "dsm5.pdf"} {"id": "df4e06b31af4-0", "page_content": "Circadian Rhythm Sleep-Wake Disorders 397\nhigh frequency of mental disorders involving social isol ation and cases of non-24-hour\nsleep-wake type developing after a change in sl eep habits (e.g., night shift work, job loss),\nbehavioral factors in combination with physi ological tendency may precipitate and per-\npetuate this disorder in sighte d individuals. Hospitalized indi viduals with neurological and\npsychiatric disorders can become insensitive to social cues, predisposing them to the de-\nvelopment of non-24-hour sleep-wake type.\nGenetic and physiological. Blindness is a risk factor for non-24-hour sleep-wake type.\nNon-24-hour sleep-wake type has been as sociated with traumatic brain injury.\nDiagnostic Markers\nDiagnosis is confirmed by history and sleep di ary or actigraphy for an extended period.\nSequential measurement of phase markers (e.g ., melatonin) can help determine circadian\nphase in both sighted and blind individuals.\nFunctional Consequences of \nNon-24-Hour Sleep-Wake Type\nComplaints of insomnia (sleep onset and sleep maintenance), excessive sleepiness, or both\nare prominent. The unpredictability of sleep an d wake times (typically a daily delay drift)\nresults in an inability to attend school or maintain a steady job and may increase potential\nfor social isolation. \nDifferential Diagnosis\nCircadian rhythm sleep-wake disorders. In sighted individuals, non-24-hour sleep-wake\ntype should be differentiated from delayed sl eep phase type, as individuals with delayed\nsleep phase type may display a similar progressive delay in sleep period for several days. \nDepressive disorders. Depressive symptoms and depressive disorders may result in\nsimilar circadian dysregulation and symptoms. \nComorbidity", "source": "dsm5.pdf"} {"id": "df4e06b31af4-1", "page_content": "similar circadian dysregulation and symptoms. \nComorbidity\nBlindness is often comorbid with non-24-hour sleep-wake type, as are depressive and bi-\npolar disorders with social isolation.\nShift Work Type\nDiagnostic Features\nDiagnosis is primarily based on a history of th e individual working outside of the normal\n8:00 A.M. to 6:00 P.M. daytime window (particularly at ni ght) on a regularly scheduled (i.e.,\nnon-overtime) basis. Symptoms of excessive sleepiness at work, and impaired sleep at\nhome, on a persistent basis are prominent. Pres ence of both sets of symptoms are usually\nrequired for a diagnosis of shift work type. Ty pically, when the individual reverts to a day-\nwork routine, symptoms resolve. Although the etiology is slightly different, individuals\nwho travel across many time zones on a very frequent basis may experience effects similar\nto those experienced by individuals with shift work type who work rotating shifts. \nPrevalence\nThe prevalence of shift work ty pe is unclear, but the disorder is estimated to affect 5%\u201310%\nof the night worker population (16%\u201320% of the workforce). Prevalence rises with advance-\nment into middle-age and beyond (Drake et al. 2004).", "source": "dsm5.pdf"} {"id": "bb26def4e27f-0", "page_content": "398 Sleep-Wake Disorders\nDevelopment and Course\nShift work type can appear in individuals of any age but is more prevalent in individuals\nolder than 50 years and typically worsens with the passage of time if the disruptive work\nhours persist. Although older adults may sh ow similar rates of circadian phase adjust-\nment to a change in routine as do younger adults, they appear to experience significantly\nmore sleep disruption as a consequence of the circadian phase shift.\nRisk and Prognostic Factors\nTemperamental. Predisposing factors include a morn ing-type disposition, a need for\nlong (i.e., more than 8 hours) sleep duration s in order to feel well rested, and strong com-\npeting social and domestic needs (e.g., parents of young children). Individuals who are able\nto commit to a nocturnal lifestyle, with fe w competing day-oriented demands, appear at\nlower risk for shift work type. \nGenetic and physiological. Because shift workers are more likely than day workers to\nbe obese, obstructive sleep apnea may be present and may exacerbate the symptoms.\nDiagnostic Markers\nA history and sleep diary or actigraphy may be useful in diagnosis, as discussed earlier for\ndelayed sleep phase type. \nFunctional Consequences of Shift Work Type \nIndividuals with shift work type not only ma y perform poorly at work but also appear to\nbe at risk for accidents both at work and on the drive home. They may also be at risk for\npoor mental health (e.g., alcohol use diso rder, substance use diso rder, depression) and\nphysical health (e.g., gastrointestinal disorder s, cardiovascular dise ase, diabetes, cancer).\nIndividuals with a history of bipolar disorder are particularly vulnerable to shift work\ntype\u2013related episodes of mania resulting from missed nights of sleep. Shift work type of-", "source": "dsm5.pdf"} {"id": "bb26def4e27f-1", "page_content": "type\u2013related episodes of mania resulting from missed nights of sleep. Shift work type of-\nten results in interpersonal problems. \nDifferential Diagnosis\nNormative variations in sleep with shift work. The diagnosis of shift work type, as op-\nposed to the \u201cnormal\u201d difficulties of shift wo rk, must depend to some extent on the sever-\nity of symptoms and/or level of distress experienced by the individual. Presence of shift\nwork type symptoms even when the individual is able to live on a da y-oriented routine for\nseveral weeks at a time may suggest the presence of other sleep disord ers, such as sleep ap-\nnea, insomnia, and narcolepsy, which should be ruled out. \nComorbidity\nShift work type has been associated with in creased alcohol use disorder, other substance\nuse disorders, and depression. A variety of physical health disorders (e.g., gastrointestinal\ndisorders, cardiovascular disease, diabetes, ca ncer) have been found to be associated with\nprolonged exposure to shift work.\nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates nine\ncircadian rhythm sleep disord ers, including jet lag type.", "source": "dsm5.pdf"} {"id": "8c5bfa65374c-0", "page_content": "Non\u2013Rapid Eye Movement Sleep Arousal Disorders 399\nParasomnias \nParasomnias are disorders characterized by abnormal behavioral, experiential, or physio-\nlogical events occurring in association with sleep, specific sleep stages, or sleep-wake tran-\nsitions. The most common parasomnia s\u2014non\u2013rapid eye movement (NREM) sleep\narousal disorders and rapid eye movement (REM) sleep behavi or disorder\u2014represent ad-\nmixtures of wakefulness and NREM sleep an d wakefulness and REM sleep, respectively.\nThese conditions serve as a reminder that sleep and wakefulness are not mutually exclu-\nsive and that sleep is not necessarily a global, whole-brain phenomenon. \nNon\u2013Rapid Eye Movement\nSleep Arousal Disorders\nDiagnostic Criteria\nA. Recurrent episodes of incomplete awakeni ng from sleep, usually occurring during the\nfirst third of the major sleep episode, accompanied by either one of the following:\n1.Sleepwalking: Repeated episodes of rising from bed during sleep and walking\nabout. While sleepwalking, the individual has a blank, staring face; is relatively un-\nresponsive to the efforts of others to communicate with him or her; and can be\nawakened only with great difficulty.\n2.Sleep terrors: Recurrent episodes of abrupt terror arousals from sleep, usually be-\nginning with a panicky scream. There is intense fear and signs of autonomic\narousal, such as mydriasis, tachycardia, rapid breathing, and sweating, during\neach episode. There is relative unresponsiveness to efforts of others to comfort the\nindividual during the episodes.\nB. No or little (e.g., only a single visual scene) dream imagery is recalled.\nC. Amnesia for the episodes is present.", "source": "dsm5.pdf"} {"id": "8c5bfa65374c-1", "page_content": "C. Amnesia for the episodes is present.\nD. The episodes cause clinically significant di stress or impairment in social, occupational,\nor other important areas of functioning.\nE. The disturbance is not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication).\nF. Coexisting mental and medical disorders do not explain the episodes of sleepwalking\nor sleep terrors.\nCoding note: For ICD-9-CM, code 307.46 for all subtypes. For ICD-10-CM, code is based\non subtype.\nSpecify whether:\n307.46 (F51.3) Sleepwalking type\nSpecify if:\nWith sleep-related eating\nWith sleep-related sexual behavior (sexsomnia)\n307.46 (F51.4) Sleep terror type", "source": "dsm5.pdf"} {"id": "a10bbcf0f82f-0", "page_content": "400 Sleep-Wake Disorders\nDiagnostic Features \nThe essential feature of non\u2013 rapid eye movement (NREM) sleep arousal disorders is the\nrepeated occurrence of incomple te arousals, usually beginning during the first third of the\nmajor sleep episode (Criterion A), that typica lly are brief, lasting 1\u201310 minutes, but may be\nprotracted, lasting up to 1 hour. The maximum duration of an event is unknown. The eyes\nare typically open during these events. Many individuals exhibit both subtypes of arousals\non different occasions, which underscores the unitary underlying pathophysiology. The\nsubtypes reflect varying degrees of simult aneous occurrence of wakefulness and NREM\nsleep, resulting in complex behaviors arising from sleep with varying degrees of conscious\nawareness, motor activity, and autonomic activation.\nThe essential feature of sleepwalking is repeated episodes of complex motor behavior\ninitiated during sleep, including rising from bed and walking about (Criterion A1). Sleep-\nwalking episodes begin during any stage of NREM sleep, most commonly during slow-\nwave sleep and therefore most often occurring during the firs t third of the night. During\nepisodes, the individual has reduced alertness and responsiveness, a blank stare, and rel-\native unresponsiveness to communication with others or effo rts by others to awaken the\nindividual. If awakened during the episode (or on awakening the following morning), the\nindividual has limited recall for the episode. Af ter the episode, there may initially be a brief\nperiod of confusion or difficult y orienting, followed by full recovery of cognitive function\nand appropriate behavior. \nThe essential feature of sleep terrors is the repeated occurrenc e of precipitous awaken-\nings from sleep, usually beginning with a pani cky scream or cry (Criterion A2). Sleep ter-", "source": "dsm5.pdf"} {"id": "a10bbcf0f82f-1", "page_content": "rors usually begin during the first third of the major sleep episode and last 1\u201310 minutes,\nbut they may last considerably longer, partic ularly in children. The episodes are accom-\npanied by impressive autonomic arousal and behavioral manifestations of intense fear.\nDuring an episode, the individual is difficult to awaken or comfort. If the individual awak-\nens after the sleep terror, little or none of th e dream, or only fragmentary, single images,\nare recalled. During a typical episode of sleep terrors, the individual abruptly sits up in\nbed screaming or crying, with a frightened ex pression and autonomic signs of intense anx-\niety (e.g., tachycardia, rapid breathing, sweating, dilati on of the pupils). The individual\nmay be inconsolable and is usually unresponsive to the efforts of others to awaken or com-\nfort him or her. Slee p terrors are also called \u201cnight terrors\u201d or \u201cpavor nocturnus.\u201d\nAssociated Features Supporting Diagnosis\nSleepwalking episodes can include a wide va riety of behaviors. Episodes may begin with\nconfusion: the individual may simply sit up in bed, look about, or pick at the blanket or\nsheet. This behavior then becomes progress ively complex. The in dividual may actually\nleave the bed and walk into closets, out of th e room, and even out of buildings. Individuals\nmay use the bathroom, eat, talk, or engage in more complex behaviors. Running and fran-\ntic attempts to escape some apparent threat can also occur. Most behaviors during sleep-\nwalking episodes are routine and of low complexity. However, cases of unlocking doors\nand even operating machinery (driving an au tomobile) have been reported. Sleepwalking\ncan also include inappropriate behavior (e.g., commonly, urinating in a\u00a0closet or waste-", "source": "dsm5.pdf"} {"id": "a10bbcf0f82f-2", "page_content": "basket). Most episodes l ast for several minutes to a half hour but may be more protracted.\nInasmuch as sleep is a state of relative analgesia, painful injuries sustained during sleep-\nwalking may not be appreciated until awakening after the fact.\nThere are two \u201cspecialized\u201d fo rms of sleepwalking: sleep-related eating behavior and", "source": "dsm5.pdf"} {"id": "d347aa735a14-0", "page_content": "walking may not be appreciated until awakening after the fact.\nThere are two \u201cspecialized\u201d fo rms of sleepwalking: sleep-related eating behavior and\nsleep-related sexual behavior (sexsomn ia or sleep sex). Individuals with sleep-related eating\nexperience unwanted recurrent episodes of eating with varying degrees of amnesia, rang-\ning from no awareness to full awareness with out the ability to not eat. During these epi-\nsodes, inappropriate foods may be ingested. In dividuals with sleep-re lated eating disorder\nmay find evidence of their eating only the next morning. In sexsomnia, varying degrees of", "source": "dsm5.pdf"} {"id": "2dd3486dcb01-0", "page_content": "Non\u2013Rapid Eye Movement Sleep Arousal Disorders 401\nsexual activity (e.g., masturbation, fondling, groping, sexual intercourse) occur as complex\nbehaviors arising from sleep wi thout conscious awareness. Th is condition is more common\nin males and may result in serious interper sonal relationship problems or medicolegal\nconsequences.\nDuring a typical episode of sleep terrors, th ere is often a sense of overwhelming dread,\nwith a compulsion to escape. Although fragmentary vivid dream images may occur, a story-\nlike dream sequence (as in nightmares) is not reported. Most commonly, the individual does\nnot awaken fully, but returns to sleep and has amnesia for the episode on awakening the next\nmorning. Usually only one episode will occur on any one night. Occasionally several episodes\nmay occur at intervals throughout the night. Th ese events rarely arise during daytime naps. \nPrevalence\nIsolated or infrequent NREM sleep arousal disorders are ve ry common in the general pop-\nulation. From 10% to 30% of children have had at least one episode of sleepwalking, and\n2%\u20133% sleepwalk often. The prevalence of slee pwalking disorder, marked by repeated ep-\nisodes and impairment or dist ress, is much lower, probably in the range of 1%\u20135%. The\nprevalence of sleepwalking episodes (not sleepwalking disorder) is 1.0%\u20137.0% among\nadults, with weekly to monthly episodes o ccurring in 0.5%\u20130.7%. The lifetime prevalence\nof sleepwalking in adults is 29.2%, with a p ast-year prevalence of sleepwalking of 3.6%.\nThe prevalence of sleep terrors in the general population is unknown. The prevalence", "source": "dsm5.pdf"} {"id": "2dd3486dcb01-1", "page_content": "The prevalence of sleep terrors in the general population is unknown. The prevalence\nof sleep terror episodes (as op posed to sleep terror disorder, in which there is recurrence\nand distress or impairment) is approximately 36.9 % at 18 months of age, 19.7% at 30 months\nof age, and 2.2% in adults. \nDevelopment and Course\nNREM sleep arousal disorders occur most co mmonly in childhood and diminish in fre-\nquency with increasing age. The onset of sl eepwalking in adults with no prior history of\nsleepwalking as children should prompt a search for specific etiologies, such as obstruc-\ntive sleep apnea, nocturnal seiz ures, or effect of medication. \nRisk and Prognostic Factors \nEnvironmental. Sedative use, sleep deprivation, sl eep-wake schedule disruptions, fa-\ntigue, and physical or emotional stress increa se the likelihood of ep isodes. Fever and sleep\ndeprivation can produce an increased freq uency of NREM sleep arousal disorders. \nGenetic and physiological. A family history for sleepwalking or sleep terrors may oc-\ncur in up to 80% of individuals who sleepwal k. The risk for sleepwalking is further in-\ncreased (to as much as 60% of offspring) when both parents have a history of the disorder.\nIndividuals with sleep terrors frequently ha ve a positive family history of either sleep\nterrors or sleepwalking, with as high as a 10-fo ld increase in the prevalence of the disorder\namong first-degree biological relatives. Slee p terrors are much more common in monozy-\ngotic twins as compared with dizygotic twins. The exact mode of inheritance is unknown.\nGender-Related Diagnostic Issues", "source": "dsm5.pdf"} {"id": "2dd3486dcb01-2", "page_content": "Gender-Related Diagnostic Issues\nViolent or sexual activity during sleepwalking episodes is more likely to occur in adults.\nEating during sleepwalking epis odes is more commonly seen in females. Sleepwalking oc-\ncurs more often in females during childhood but more often in males during adulthood. \nOlder children and adults provide a more de tailed recollection of fearful images asso-\nciated with sleep terrors than do younger ch ildren, who are more likely to have complete\namnesia or report only a vague sense of fear. Among children, sleep terrors are more com-\nmon in males than in females. Among adults, the sex ratio is even.", "source": "dsm5.pdf"} {"id": "033995875931-0", "page_content": "402 Sleep-Wake Disorders\nDiagnostic Markers\nNREM sleep arousal disorders arise from an y stage of NREM sleep but most commonly\nfrom deep NREM sleep (slow-wave sleep). They are most likely to appear in the first third\nof the night and do not commonly occur duri ng daytime naps. During the episode, the\npolysomnogram may be obscured with movement artifact. In the absence of such artifact,\nthe electroencephalogram typically shows theta or alpha frequency activity during the ep-\nisode, indicating partial or incomplete arousal. \nPolysomnography in conjunctio n with audiovisual monitoring can be used to document\nepisodes of sleepwalking. In the absence of ac tually capturing an event during a polysomno-\ngraphic recording, there are no polysomnogra phic features that can serve as a marker for\nsleepwalking. Sleep deprivation may increase the likelihood of capturing an event. As a group,\nindividuals who sleepwalk show instability of de ep NREM sleep, but th e overlap in findings\nwith individuals who do not sleepwalk is great en ough to preclude use of this indicator in es-\ntablishing a diagnosis. Unlike arousals from RE M sleep associated with nightmares, in which\nthere is an increase in heart rate and respiratio n prior to the arousal, the NREM sleep arousals\nof sleep terrors begin precipitou sly from sleep, without anticipatory autonomic changes. The\narousals are associated with impressive autono mic activity, with doubling or tripling of\nthe heart rate. The pathophysiology is poorly unde rstood, but there appears to be instability in\nthe deeper stages of NREM sleep. Absent capturing an event during a formal sleep study,\nthere are no reliable polysomnographic indicators of the tendency to experience sleep terrors.\nFunctional Consequences of", "source": "dsm5.pdf"} {"id": "033995875931-1", "page_content": "Functional Consequences of \nNon-REM Sleep Arousal Disorders\nFor the diagnosis of a NREM sl eep arousal disorder to be ma de, the individual or house-\nhold members must experience clinically signi ficant distress or impairment, although pa-\nrasomnia symptoms may occur occasionally in nonclinical populations and would be\nsubthreshold for the diagnosis. Embarrassment concerning the episodes can impair social\nrelationships. Social isolation or occupational difficulties ca n result. The determination of a\n\u201cdisorder\u201d depends on a number of factors, which may vary on an individual basis and\nwill depend on the frequency of events, potential for violence or injurious behaviors, em-\nbarrassment, or disruption/distr ess of other household member s. Severity determination\nis best made based on the nature or consequenc e of the behaviors rather than simply on fre-\nquency. Uncommonly, NREM sleep arousal disorders may result in serious injury to the\nindividual or to someone trying to console the individual. Inju ries to others are confined to\nthose in close proximity; individuals are not \u201csought out.\u201d Typically, sleepwalking in both\nchildren and adults is not associated with si gnificant mental disorders. For individuals\nwith sleep-related eating behaviors, unknowingly preparing or eati ng food during the\nsleep period may create problems such as poor diabetes control, weight gain, injury (cuts\nand burns), or consequences of eating dangerous or toxic in edibles. NREM sleep arousal\ndisorders may rarely result in violent or injurious behaviors with forensic implications.\nDifferential Diagnosis\nNightmare disorder. In contrast to individuals with NREM sleep arousal disorders, in-\ndividuals with nightmar e disorder typically awaken eas ily and completely, report vivid\nstorylike dreams accompanying the episodes, and tend to have episodes later in the night.", "source": "dsm5.pdf"} {"id": "033995875931-2", "page_content": "storylike dreams accompanying the episodes, and tend to have episodes later in the night.\nNREM sleep arousal disorders occur during NREM sleep, whereas nightmares usually oc-\ncur during REM sleep. Parents of children with NREM sleep arousal disorders may mis-\ninterpret reports of fragme ntary imagery as nightmares.\nBreathing-related sleep disorders. Breathing disorders during sleep can also produce", "source": "dsm5.pdf"} {"id": "a073d0bc8359-0", "page_content": "interpret reports of fragme ntary imagery as nightmares.\nBreathing-related sleep disorders. Breathing disorders during sleep can also produce\nconfusional arousals with subsequent amnesi a. However, breathin g-related sleep disor-\nders are also characterized by characteristic symptoms of snoring, breathing pauses, and", "source": "dsm5.pdf"} {"id": "5f7458615094-0", "page_content": "Non\u2013Rapid Eye Movement Sleep Arousal Disorders 403\ndaytime sleepiness. In some individuals, a breathing-related sleep disorder may precipi-\ntate episodes of sleepwalking.\nREM sleep behavior disorder. REM sleep behavior disorder may be difficult to distin-\nguish from NREM sleep arousal disorders. REM sleep behavior disorder is characterized\nby episodes of prominent, co mplex movements, often involving personal injury arising\nfrom sleep. In contrast to NR EM sleep arousal disorders, REM sleep behavior disorder oc-\ncurs during REM sleep. Individuals with REM sleep behavior disorder awaken easily and\nreport more detailed and vivid dream content than do individuals wi th NREM sleep arousal\ndisorders. They often report that they \u201cact out dreams.\u201d \nParasomnia overlap syndrome. Parasomnia overlap syndrome consists of clinical and\npolysomnographic features of both sleepwa lking and REM sleep behavior disorder.\nSleep-related seizures. Some types of seizures can prod uce episodes of very unusual\nbehaviors that occur predominantly or exclu sively during sleep. Nocturnal seizures may\nclosely mimic NREM sleep arousal disorders but tend to be more stereotypic in nature, oc-\ncur multiple times nightly, and be more likel y to occur from daytime naps. The presence of\nsleep-related seizures does not preclude the presence of NREM sleep arousal disorders.\nSleep-related seizures should be classified as a form of epilepsy.\nAlcohol-induced blackouts. Alcohol-induced blackouts may be associated with extremely\ncomplex behaviors in the absence of other suggestions of intoxication. They do not involve\nthe loss of consciousness but rather reflect an isolated di sruption of memory for events\nduring a drinking episode. By history, these behaviors may be indistinguishable from those\nseen in NREM sleep arousal disorders.", "source": "dsm5.pdf"} {"id": "5f7458615094-1", "page_content": "seen in NREM sleep arousal disorders.\nDissociative amnesia, with dissociative fugue. Dissociative fugue may be extremely\ndifficult to distinguish from sleepwalking. Unlike all other parasomnias, nocturnal disso-\nciative fugue arises from a period of wakefu lness during sleep, rather than precipitously\nfrom sleep without intervening wakefulness. A history of recurrent childhood physical or\nsexual abuse is usually present (b ut may be difficult to obtain).\nMalingering or other voluntary behavior occurring during wakefulness. As with disso-\nciative fugue, malingering or other voluntary behavior o ccurring during wakefulness\narises from wakefulness.\nPanic disorder. Panic attacks may also cause abrupt awakenings from deep NREM sleep\naccompanied by fearfulness, but these episode s produce rapid and complete awakening with-\nout the confusion, amnesia, or motor activity typical of NREM sleep arousal disorders. \nMedication-induced complex behaviors. Behaviors similar to those in NREM sleep\narousal disorders can be induced by use of, or withdrawal from, substances or medica-\ntions (e.g., benzodiazepines, nonbenzodiazepine sedative-hypnotics, opiates, cocaine, nic-\notine, antipsychotics, tricyclic antidepressant s, chloral hydrate). Such behaviors may arise\nfrom the sleep period and may be extremel y complex. The underlying pathophysiology\nappears to be a relatively isolated amnesia. In such cases, substance/medication-induced\nsleep disorder, parasomnia type, should be diagnosed (see \u201cSubstance/Medication-\nInduced Sleep Disorder\u201d la ter in this chapter).\nNight eating syndrome. The sleep-related eating disorder form of sleepwalking is to be", "source": "dsm5.pdf"} {"id": "5f7458615094-2", "page_content": "Night eating syndrome. The sleep-related eating disorder form of sleepwalking is to be\ndifferentiated from night eating syndrome, in which there is a delay in the circadian rhythm\nof food ingestion and an association with insomnia and/or depression. \nComorbidity\nIn adults, there is an association between sleepwalking and major depressive episodes and\nobsessive-compulsive disorder. Children or ad ults with sleep terro rs may have elevated\nscores for depression and anxiet y on personality inventories.", "source": "dsm5.pdf"} {"id": "b27e3fbfa22d-0", "page_content": "404 Sleep-Wake Disorders\nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classificat ion of Sleep Disorders, 2nd Edition, includes \u201cconfusional\narousal\u201d as a NREM sleep arousal disorder.\nNightmare Disorder\nDiagnostic Criteria 307.47 (F51.5)\nA. Repeated occurrences of extended, extremely dysphoric, and well-remembered\ndreams that usually involve efforts to avoid threats to survival, security, or physical in-\ntegrity and that generally occur during the second half of the major sleep episode.\nB. On awakening from the dysphoric dreams, the individual rapidly becomes oriented and\nalert.\nC. The sleep disturbance causes clinically significant distress or impairment in social, oc-\ncupational, or other important areas of functioning.\nD. The nightmare symptoms are not attributable to the physiological effects of a sub-\nstance (e.g., a drug of abuse, a medication).\nE. Coexisting mental and medical disorders do not adequately explain the predominant\ncomplaint of dysphoric dreams.\nSpecify if:\nDuring sleep onset\nSpecify if:\nWith associated non\u2013sleep disorder, including substance use disorders\nWith associated othe r medical condition\nWith associated ot her sleep disorder\nCoding note: The code 307.47 (F51.5) applies to all three specifiers. Code also the\nrelevant associated mental disorder, medical condition, or other sleep disorder imme-\ndiately after the code for nightmare disorder in order to indicate the association.\nSpecify if:\nAcute: Duration of period of nightmares is 1 month or less.\nSubacute: Duration of period of nightmares is greater than 1 month but less than\n6 months.\nPersistent: Duration of period of nightmares is 6 months or greater.\nSpecify current severity:", "source": "dsm5.pdf"} {"id": "b27e3fbfa22d-1", "page_content": "Specify current severity: \nSeverity can be rated by the frequency with which the nightmares occur:\nMild: Less than one episode per week on average.\nModerate: One or more episodes per week but less than nightly.\nSevere: Episodes nightly.\nDiagnostic Features\nNightmares are typically lengthy, elaborate, st orylike sequences of dream imagery that\nseem real and that incite anxiety, fear, or other dysphoric emotio ns. Nightmare content\ntypically focuses on attempts to avoid or cope with immi nent danger but may involve\nthemes that evoke other negative emotions. Nightmares occurring after traumatic experi-\nences may replicate the threatening situation (\u201creplicative nightmares\u201d), but most do not.\nOn awakening, nightmares are well remembered and can be described in detail. They arise", "source": "dsm5.pdf"} {"id": "240c4f130162-0", "page_content": "Nightmare Disorder 405\nalmost exclusively during rapid eye moveme nt (REM) sleep and can thus occur through-\nout sleep but are more likely in the second half of the major sleep episode when dreaming\nis longer and more intense. Factors that incr ease early-night REM intensity, such as sleep\nfragmentation or deprivation, jet lag, and REM-sensitive medications, might facilitate\nnightmares earlier in the night, including at sleep onset.\nNightmares usually terminate with awakening and rapid return of full alertness. How-\never, the dysphoric emotions may persist into wakefulness and contribute to difficulty re-\nturning to sleep and lasting daytime distress . Some nightmares, known as \u201cbad dreams,\u201d\nmay not induce awakening and are recalled only later. If nightmare s occur during sleep-\nonset REM periods ( hypnagogic ), the dysphoric emotion is frequently accompanied by a\nsense of being both awake and unable to move voluntarily ( isolated sleep paralysis ). \nAssociated Features Supporting Diagnosis\nMild autonomic arousal, including sweating, tachycardia, and tachypnea, may character-\nize nightmares. Body movements and vocalizations are not characteristic because of REM\nsleep\u2013related loss of skeletal muscle tone, but such behavi ors may occur under situations\nof emotional stress or sleep fragmentation and in posttraumatic stress disorder (PTSD).\nWhen talking or emoting occurs, it is typica lly a brief event terminating the nightmare. \nIndividuals with frequent nightmares are at substantially greater r isk for suicidal ide-\nation and suicide attempts, even when gender and mental illness are taken into account. \nPrevalence\nPrevalence of nightmares in creases through childhood into adolescence. From 1.3% to\n3.9% of parents report that their preschool children have nightmares \u201coften\u201d or \u201calways\u201d.", "source": "dsm5.pdf"} {"id": "240c4f130162-1", "page_content": "Prevalence increases from ages 10 to 13 for both males and females but continues to in-\ncrease to ages 20\u201329 for females (while decreasing for males), when it can be twice as high\nfor females as for males. Prevalen ce decreases steadily with age for both sexes, but the gen-\nder difference remains. Among adults, prevalen ce of nightmares at least monthly is 6%,\nwhereas prevalence for frequent nightmare s is 1%\u20132%. Estimates often combine idio-\npathic and posttraumatic nightmares indiscriminately.\nDevelopment and Course\nNightmares often begin between ages 3 and 6 years but reach a peak prevalence and se-\nverity in late adolescence or early adulthood. Nigh tmares most likely appear in children\nexposed to acute or chronic psychosocial stressors and thus may not resolve spontane-\nously. In a minority, frequent nightmares pers ist into adulthood, becoming virtually a life-\nlong disturbance. Although specific nightm are content may reflect the individual\u2019s age,\nthe essential features of the diso rder are the same across age groups. \nRisk and Prognostic Factors \nTemperamental. Individuals who experience nightmares report more frequent past ad-\nverse events, but not necessarily trauma, an d often display personality disturbances or\npsychiatric diagnosis. \nEnvironmental. Sleep deprivation or fragmentation, and irregular sleep-wake schedules\nthat alter the timing, intensity, or quantity of REM sleep, can put individuals at risk for\nnightmares.\nGenetic and physiological. Twin studies have identified genetic effects on the disposi-\ntion to nightmares and their co-occurrence with other parasomnias (e.g., sleeptalking). \nCourse modifiers. Adaptive parental bedside behaviors, such as soothing the child fol-\nlowing nightmares, may protect agai nst developing chronic nightmares.", "source": "dsm5.pdf"} {"id": "a9104b3aa461-0", "page_content": "406 Sleep-Wake Disorders\nCulture-Related Diagnostic Issues\nThe significance attributed to nightmares may va ry by culture, and sensitivity to such be-\nliefs may facilitate disclosure.\nGender-Related Diagnostic Issues\nAdult females report having ni ghtmares more frequently th an do adult males. Nightmare\ncontent differs by sex, with adult females tend ing to report themes of sexual harassment or\nof loved ones disappearing/dying, and adult males tending to report themes of physical\naggression or war/terror. \nDiagnostic Markers\nPolysomnographic studies demonstrate abrupt awakenings from REM sleep, usually during\nthe second half of the night, prior to report of a nightmare. Heart, respiratory, and eye move-\nment rates may quicken or increase in variab ility before awakening. Nightmares following\ntraumatic events may also arise during non-REM (NREM), particularly stage 2, sleep. The typ-\nical sleep of individuals with nightmares is mild ly impaired (e.g., redu ced efficiency, less slow-\nwave sleep, more awakenings), with more frequent periodic leg movements in sleep and rel-\native sympathetic nervous system activation after REM sleep deprivation. \nFunctional Consequences of Nightmare Disorder\nNightmares cause more significant subjective distress than demonstrable social or occu-\npational impairment. However, if awakenings are frequent or result in sleep avoidance,\nindividuals may experience excessive daytime sleepiness, poor concentration, depression,\nanxiety, or irritability. Freque nt childhood nightmares (e.g., several per week), may cause\nsignificant distress to parents and child.\nDifferential Diagnosis\nSleep terror disorder. Both nightmare disorder and sleep terror disorder include awak-\nenings or partial awakenings with fearfuln ess and autonomic activation, but the two dis-\norders are differentiable. Nightmares typically occur later in the night, during REM sleep,", "source": "dsm5.pdf"} {"id": "a9104b3aa461-1", "page_content": "orders are differentiable. Nightmares typically occur later in the night, during REM sleep,\nand produce vivid, storylike, and clearly re called dreams; mild autonomic arousal; and\ncomplete awakenings. Sleep terrors typically arise in the first third of the night during\nstage 3 or 4 NREM sleep and produce either no dream recall or images without an elabo-\nrate storylike quality. The terr ors lead to partial awakenings that leave the individual con-\nfused, disoriented, and only partially resp onsive and with substantial autonomic arousal.\nThere is usually amnesia for the event in the morning. \nREM sleep behavior disorder. The presence of complex motor activity during fright-\nening dreams should prompt further evaluation for REM sleep behavior disorder, which\noccurs more typically among late middle-age males and, unlike nightmare disorder, is as-\nsociated with often violent dream enactment s and a history of nocturnal injuries. The\ndream disturbance of REM sleep behavior diso rder is described by patients as nightmares\nbut is controlled by appropriate medication. \nBereavement. Dysphoric dreams may occur during bereavement but typically involve\nloss and sadness and are followed by self-refle ction and insight, rather than distress, on\nawakening. \nNarcolepsy. Nightmares are a frequent complaint in narcolepsy, but the presence of ex-\ncessive sleepiness and cataplexy differentiates this condition from nightmare disorder. \nNocturnal seizures. Seizures may rarely manifest as nightmares and should be evalu-\nated with polysomnography and continuous video electroencephalography. Nocturnal\nseizures usually involve stereotypical motor activity. Associated nightmares, if recalled,", "source": "dsm5.pdf"} {"id": "7be2d87f73ae-0", "page_content": "Rapid Eye Movement Sleep Behavior Disorder 407\nare often repetitive in nature or reflect epilept ogenic features such as the content of diurnal\nauras (e.g., unmotivated dread), phosphenes, or ictal imagery. Disord ers of arousal, espe-\ncially confusional arousals, may also be present.\nBreathing-related sleep disorders. Breathing-related sleep disorders can lead to awaken-\nings with autonomic arousal, but these are not usually accompanied by recall of nightmares. \nPanic disorder. Attacks arising during sleep can produce abrupt awakenings with au-\ntonomic arousal and fearfulness, but nightmares are typically not reported and symptoms\nare similar to panic attacks arising during wakefulness. \nSleep-related dissociative disorders. Individuals may recall actual physical or emo-\ntional trauma as a \u201cdream\u201d during elec troencephalography-documented awakenings.\nMedication or substance use. Numerous substances/medicat ions can precipitate night-\nmares, including dopaminergics; beta-adrener gic antagonists and other antihypertensives;\namphetamine, cocaine, and other stimulants; antidepressants; smoking cessation aids;\nand melatonin. Withdrawal of REM sleep\u2013su ppressant medications (e.g., antidepressants)\nand alcohol can produce REM sleep rebound accompanied by nightmares. If nightmares\nare sufficiently severe to warrant independent clinical attention, a diagnosis of substance/\nmedication-induced sleep disorder should be considered. \nComorbidity\nNightmares may be comorbid with several medical conditions, including coronary heart\ndisease, cancer, parkinsonism, and pain, and ca n accompany medical treatments, such as he-\nmodialysis, or withdrawal from medications or substances of abuse. Nightmares frequently", "source": "dsm5.pdf"} {"id": "7be2d87f73ae-1", "page_content": "modialysis, or withdrawal from medications or substances of abuse. Nightmares frequently\nare comorbid with other mental disorders, in cluding PTSD; insomnia disorder; schizophrenia;\npsychosis; mood, anxiety, adjustment, and personality disorders; and grief during be-\nreavement. A concurrent nightmare disorder diagnosis should only be considered when in-\ndependent clinical attention is warranted (i.e., Criteria A\u2013C are met). Otherwise, no separate\ndiagnosis is necessary. These conditions should be listed under the appropriate comorbid\ncategory specifier. However, nightmare disorder may be diagnosed as a separate disorder in\nindividuals with PTSD if the nightmares are temporally unrelated to PTSD (i.e., preceding\nother PTSD symptoms or persisting after other PTSD symptoms have resolved).\nNightmares are normally characteristic of REM sleep behavior disorder, PTSD, and acute\nstress disorder, but nightmare di sorder may be independently coded if nightmares preceded\nthe condition and their frequency or severity necessitates independent clinical attention. The\nlatter may be determined by asking whether ni ghtmares were a proble m before onset of the\nother disorder and whether they continued after other symptoms had remitted. \nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classification of Sleep Disorders, 2nd Edition (ICSD-2), presents similar di-\nagnostic criteria fo r nightmare disorder.\nRapid Eye Movement Sleep Behavior Disorder\nDiagnostic Criteria 327.42 (G47.52)\nA. Repeated episodes of arousal during sleep associated with vocalization and/or com-\nplex motor behaviors. \nB. These behaviors arise during rapid eye movement (REM) sleep and therefore usually\noccur more than 90 minutes after sleep onset, are more frequent during the later por-\ntions of the sleep period, and uncommonly occur during daytime naps.", "source": "dsm5.pdf"} {"id": "d2b5123bb7c6-0", "page_content": "408 Sleep-Wake Disorders\nC. Upon awakening from these episodes, the individual is completely awake, alert, and\nnot confused or disoriented.\nD. Either of the following: \n1. REM sleep without atonia on polysomnographic recording.\n2. A history suggestive of REM sleep behavior disorder and an established synuclein-\nopathy diagnosis (e.g., Parkinson\u2019s disease, multiple system atrophy).\nE. The behaviors cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning (which may include injury to self or the\nbed partner).\nF. The disturbance is not attributable to the physiological effects of a substance (e.g., a\ndrug of abuse, a medication) or another medical condition.\nG. Coexisting mental and medical disorders do not explain the episodes.\nDiagnostic Features\nThe essential feature of rapid eye movement (REM) sleep behavior disorder is repeated\nepisodes of arousal, often associated with vo calizations and/or complex motor behaviors\narising from REM sleep (Criterion A). These be haviors often reflect motor responses to the\ncontent of action-filled or violent dreams of being attacked or trying to escape from a\nthreatening situation, which may be termed dream enacting behaviors. The vocalizations are\noften loud, emotion-fill ed, and profane. These behaviors may be very bothersome to the\nindividual and the bed partner and may result in significant injury (e.g., falling, jumping,\nor flying out of bed; running, punching, thru sting, hitting, or kicking). Upon awakening,\nthe individual is immediately awake, alert, and oriented (Criterion C) and is often able to\nrecall dream mentation, which closely correlates with the observed behavior. The eyes\ntypically remain closed during these events. The diagnosis of REM sleep behavior disor-\nder requires clinically significant distress or impairment (Criterion E); this determination", "source": "dsm5.pdf"} {"id": "d2b5123bb7c6-1", "page_content": "der requires clinically significant distress or impairment (Criterion E); this determination\nwill depend on a number of factors, including the frequency of events, the potential for vi-\nolence or injurious behaviors, embarrassment , and distress in othe r household members. \nAssociated Features Supporting Diagnosis\nSeverity determination is best made based on the nature or conseq uence of the behavior\nrather than simply on frequency. Although the behaviors are typically prominent and vi-\nolent, lesser behaviors may also occur. \nPrevalence\nThe prevalence of REM sleep behavior disord er is approximately 0.38%\u20130.5% in the gen-\neral population. Prevalence in patients with psychiatric disorders may be greater, possibly\nrelated to medications prescribed for the psychiatric disorder.\nDevelopment and Course\nThe onset of REM sleep behavior disorder may be gradual or rapid, and the course is usu-\nally progressive. REM sleep behavior disorder associated with neurodegenerative disor-\nders may improve as the unde rlying neurodegenerative disorder progresses. Because of\nthe very high association with the later appe arance of an underlyi ng neurodegenerative\ndisorder, most notably one of the synucleino pathies (Parkinson\u2019s disease, multiple system\natrophy, or major or mild neurocognitive di sorder with Lewy bodies), the neurological\nstatus of individuals with REM sleep behavior disorder should be closely monitored.\nREM sleep behavior disorder overwhelmingly affects males older than 50 years, but in-\ncreasingly this disorder is being identified in females and in younger individuals. Symp-", "source": "dsm5.pdf"} {"id": "54b8dd66884a-0", "page_content": "Rapid Eye Movement Sleep Behavior Disorder 409\ntoms in young individuals, particularly young females, should raise the possibility of\nnarcolepsy or medication-induced REM sleep behavior disorder. \nRisk and Prognostic Factors \nGenetic and physiological. Many widely prescribed medications, including tricyclic\nantidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reup-\ntake inhibitors, and beta-blockers, may resu lt in polysomnographic evidence of REM sleep\nwithout atonia and in frank REM sleep behavior disorder. It is not known whether the\nmedications per se result in REM sleep behavi or disorder or they unmask an underlying\npredisposition.\nDiagnostic Markers\nAssociated laboratory findin gs from polysomnography indicate increased tonic and/or\nphasic electromyographic activi ty during REM sleep that is normally associated with mus-\ncle atonia. The increased muscle activity variably affects different muscle groups, mandating\nmore extensive electromyographi c monitoring than is employed in conventional sleep stud-\nies. For this reason, it is su ggested that electrom yographic monitoring include the submen-\ntalis, bilateral extensor digito rum, and bilateral anterior tibi alis muscle groups. Continuous\nvideo monitoring is mandator y. Other polysomnographic findings may include very fre-\nquent periodic and aperiodic extremity el ectromyography acti vity during non-REM\n(NREM) sleep. This polysomnography observation, termed REM sleep without atonia, is pres-\nent in virtually all cases of REM sleep behavi or disorder but may also be an asymptomatic\npolysomnographic finding. Clinical dream-enacting behaviors coupled with the polysom-\nnographic finding of REM without atonia is necessary for the diagnosis of REM sleep behav-", "source": "dsm5.pdf"} {"id": "54b8dd66884a-1", "page_content": "nographic finding of REM without atonia is necessary for the diagnosis of REM sleep behav-\nior disorder. REM sleep without atonia with out a clinical history of dream-enacting\nbehaviors is simply an asymptomatic polyso mnographic observation. It is not known\nwhether isolated REM sleep without atonia is a precursor to REM sleep behavior disorder.\nFunctional Consequences of \nRapid Eye Movement Sl eep Behavior Disorder\nREM sleep behavior disorder may occur in isol ated occasions in otherwise unaffected in-\ndividuals. Embarrassment concer ning the episodes can impair social relationships. Indi-\nviduals may avoid situations in which others might become aware of the disturbance,\nvisiting friends overnight, or sleeping with be d partners. Social isolation or occupational\ndifficulties can result. Uncommonly, REM sleep behavior disorder may result in serious\ninjury to the victim or to the bed partner.\nDifferential Diagnosis\nOther parasomnias. Confusional arousals, sleepwalking, and sleep terrors can easily be\nconfused with REM sleep behavior disorder. In general, these disorders occur in younger\nindividuals. Unlike REM sleep behavior disorder, they arise from deep NREM sleep and\ntherefore tend to occur in the early portion of the sleep period. Awakening from a confu-\nsional arousal is associated with confusion, disorientation, and incomplete recall of dream\nmentation accompanying the behavior. Polysomnographic monitoring in the disorders of\narousal reveals normal REM atonia.\nNocturnal seizures. Nocturnal seizures may perfectly mimic REM sleep behavior disor-\nder, but the behaviors are generally more st ereotyped. Polysomnographic monitoring em-\nploying a full electroencephalographic seiz ure montage may differentiate the two. REM\nsleep without atonia is not present on polysomnographic monitoring.", "source": "dsm5.pdf"} {"id": "dfe075e09066-0", "page_content": "410 Sleep-Wake Disorders\nObstructive sleep apnea. Obstructive sleep apnea may result in behaviors indistin-\nguishable from REM sleep behavior disorder . Polysomnographic monitoring is necessary\nto differentiate between the two. In this ca se, the symptoms resolv e following effective\ntreatment of the obstructive sleep apnea, and REM sleep without atonia is not present on\npolysomnography monitoring.\nOther specified dissociative disorder (sleep-related psychogenic dissociative disorder).\nUnlike virtually all other parasomnias, which arise precipitously from NREM or REM\nsleep, psychogenic dissociative behaviors aris e from a period of well-defined wakefulness\nduring the sleep period. Unlike REM sleep behavi or disorder, this condition is more prev-\nalent in young females.\nMalingering. Many cases of malingering in which the individual reports problematic\nsleep movements perfectly mimic the clinical features of REM sleep behavior disorder,\nand polysomnographic documentation is mandatory.\nComorbidity\nREM sleep behavior diso rder is present concurrently in approximately 30% of patients\nwith narcolepsy. When it occurs in narcolep sy, the demographics reflect the younger age\nrange of narcolepsy, with equal frequency in males and females. Based on findings from\nindividuals presenting to sleep clinics, most individuals (>50%) with initially \u201cidiopathic\u201d\nREM sleep behavior disorder will eventually develop a neurodegenerative disease\u2014most\nnotably, one of the synucleinopathies (Parkins on\u2019s disease, multiple system atrophy, or\nmajor or mild neurocognitive disorder with Lewy bodies). REM sleep behavior disorder\noften predates any other sign of these disorder s by many years (often more than a decade).\nRelationship to Internat ional Classification of \nSleep Disorders", "source": "dsm5.pdf"} {"id": "dfe075e09066-1", "page_content": "Relationship to Internat ional Classification of \nSleep Disorders\nREM sleep behavior disorder is virtually identical to REM sleep beha vior disorder in the\nInternational Classification of Sleep Disorders, 2nd Edition (ICSD-2).\nRestless Legs Syndrome\nDiagnostic Criteria 333.94 (G25.81)\nA. An urge to move the legs, usually accompanied by or in response to uncomfortable and\nunpleasant sensations in the legs, characterized by all of the following:\n1. The urge to move the legs begins or wors ens during periods of rest or inactivity.\n2. The urge to move the legs is partial ly or totally relieved by movement.\n3. The urge to move the legs is worse in the evening or at night than during the day,\nor occurs only in the evening or at night. \nB. The symptoms in Criterion A occur at least three times per week and have persisted\nfor at least 3 months.\nC. The symptoms in Criterion A are accompanied by significant distress or impairment in\nsocial, occupational, educational, academic, behavioral, or other important areas of\nfunctioning. \nD. The symptoms in Criterion A are not attributable to another mental disorder or medical\ncondition (e.g., arthritis, l eg edema, peripheral ischemia, leg cramps) and are not better\nexplained by a behavioral condition (e.g., positional discomfort, h abitual foot tapping).\nE. The symptoms are not attributable to the physiological effects of a drug of abuse or\nmedication (e.g., akathisia).", "source": "dsm5.pdf"} {"id": "bdf6d2ae9ddf-0", "page_content": "Restless Legs Syndrome 411\nDiagnostic Features\nRestless legs syndrome (RLS) is a sensorimotor, neurological sleep disorder characterized\nby a desire to move the legs or arms, usua lly associated with uncomfortable sensations\ntypically described as creeping, crawling, tingling, burning, or itch ing (Criterion A). The\ndiagnosis of RLS is based primarily on patient self-report and history. Symptoms are\nworse when the individual is at rest, and freq uent movements of the legs occur in an effort\nto relieve the uncomfortable sensations. Sympto ms are worse in the evening or night, and\nin some individuals they occur only in the ev ening or night. Evening worsening occurs in-\ndependently of any differences in activity. It is important to differentiate RLS from other\nconditions such as positional discom fort and leg cramps (Criterion D).\nThe symptoms of RLS can delay sleep onset and awaken the individual from sleep and\nare associated with significant sleep fragmentation. The relief obtained from moving the\nlegs may no longer be apparent in severe ca ses. RLS is associated with daytime sleepiness\nand is frequently accompanied by significant clinical distress or functional impairment.\nAssociated Features Supporting Diagnosis\nPeriodic leg movements in sleep (PLMS) can serve as corroborating ev idence for RLS, with\nup to 90% of individuals di agnosed with RLS demonstratin g PLMS when recordings are\ntaken over multiple nights. Periodic leg mo vements during wakefulness are supportive of\nan RLS diagnosis. Reports of difficulty initiating and maintaining sleep and of excessive\ndaytime sleepiness may also support the diagnosis of RLS. Additional supportive features\ninclude a family history of RLS among first- degree relatives and a reduction in symptoms,\nat least initially, with dopaminergic treatment. \nPrevalence", "source": "dsm5.pdf"} {"id": "bdf6d2ae9ddf-1", "page_content": "at least initially, with dopaminergic treatment. \nPrevalence \nPrevalence rates of RLS vary widely when br oad criteria are utilized but range from 2% to\n7.2% when more defined criteria are employed . When frequency of symptoms is at least\nthree times per week with moderate or severe distress, the prevalence rate is 1.6%; when\nfrequency of symptoms is a minimum of one ti me per week, the prevalence rate is 4.5%.\nFemales are 1.5\u20132 times more likely than males to have RLS. RLS also increases with age.\nThe prevalence of RLS may be lower in Asian populations. \nDevelopment and Course\nThe onset of RLS typically occurs in the seco nd or third decade. Approximately 40% of in-\ndividuals diagnosed with RLS during adul thood report having experienced symptoms\nbefore age 20 years, and 20% report having experienced symptoms before age 10 years.\nPrevalence rates of RLS increase steadily with age until about age 60 years, with symptoms\nremaining stable or decreasing slightly in older age groups. Compared with nonfamilial\ncases, familial RLS usually has a younger age at onset and a slower pr ogressive course. The\nclinical course of RLS differs by age at onset. When onset occurs before age 45, there is of-\nten a slow progression of symptoms. In late-onset RLS, rapid progression is typical, and\naggravating factors are common. Symptoms of RLS appear similar acro ss the lifespan, re-\nmaining stable or decreasing slightly in older age groups.\nDiagnosis of RLS in children can be diff icult because of the self-report component.\nWhile Criterion A for adults assumes that the description of \u201curge to move\u201d is by the pa-", "source": "dsm5.pdf"} {"id": "bdf6d2ae9ddf-2", "page_content": "tient, pediatric diagnosis requir es a description in the child\u2019s own words rather than by a\nparent or caretaker. Typically children age 6 years or older are able to provide detailed, ad-\nequate descriptors of RLS. However, children rarely use or understand the word \u201curge,\u201d\nreporting instead that their legs \u201chave to\u201d or \u201cgot to\u201d move. Also, potentially related to\nprolonged periods of sitting during class, tw o-thirds of children and adolescents report\ndaytime leg sensations. Thus, fo r diagnostic Criterion A3, it is important to compare equal", "source": "dsm5.pdf"} {"id": "b2d51cd58470-0", "page_content": "412 Sleep-Wake Disorders\nduration of sitting or lying down in the day to sitting or lying down in the evening or night.\nNocturnal worsening tends to persist even in the context of pediatric RLS. As with RLS in\nadults, there is a significant negative impact on sleep, mood, cognition, and function. Im-\npairment in children and adolescents is mani fested more often in behavioral and educa-\ntional domains. \nRisk and Prognostic Factors \nGenetic and physiological. Predisposing factors includ e female gender, advancing\nage, genetic risk variants, an d family history of RLS. Precipitating factors are often time-\nlimited, such as iron defici ency, with most individuals resuming normal sleep patterns\nafter the initial triggering even t has disappeared. Genetic risk variants also play a role in\nRLS secondary to such disorder s as uremia, suggesting that individuals with a genetic sus-\nceptibility develop RLS in the presence of further risk factors. RLS has a strong familial\ncomponent. \nThere are defined pathophysi ological pathways subserving RLS. Genome-wide asso-\nciation studies have found that RLS is significantly associated with common genetic vari-\nants in intronic or intergenic regions in MEIS1 , BTBD9 , and MAP2K5 on chromosomes 2p,\n6p, and 15q, respectively. The ass ociation of these three varian ts with RLS has been inde-\npendently replicated. BTBD9 confers a very large (80%) exce ssive risk when even a single\nallele is present. Because of the high frequenc y of this variant in individuals of European\ndescent, the population attributable risk (P AR) approximates 50%. At-risk alleles associ-", "source": "dsm5.pdf"} {"id": "b2d51cd58470-1", "page_content": "ated with MEIS1 and BTBD9 are less common in individuals of African or Asian descent,\nperhaps suggesting lower risk fo r RLS in these populations. \nPathophysiological mechanisms in RLS also in clude disturbances in the central dopa-\nminergic system and disturbances in iron metabolism. The endo genous opiate system\nmay also be involved. Treatment effect s of dopaminergic drugs (primarily D2 and D3 non-\nergot agonists) provide further support that RLS is grounded in dysfunctional central\ndopaminergic pathways. While the effective treatment of RLS has also been shown to sig-\nnificantly reduce depressive symptoms, seroto nergic antidepressants can induce or aggra-\nvate RLS in some individuals. \nGender-Related Diagnostic Issues\nAlthough RLS is more prevalent in females than in males, there are no diagnostic differ-\nences according to gender. However, the prev alence of RLS during pregnancy is two to\nthree times greater than in the general population. RLS associated with pregnancy peaks\nduring the third trimester and improves or reso lves in most cases soon after delivery. The\ngender difference in prevalence of RLS is explai ned at least in part by parity, with nullipa-\nrous females being at the same r isk of RLS as age-matched males.\nDiagnostic Markers\nPolysomnography demonstrates significant abnormalities in RLS, commonly increased\nlatency to sleep, and higher arousal index. Polysomnography with a preceding immobili-\nzation test may provide an indicator of the motor sign of RLS, periodic limb movements,\nunder standard conditions of sleep and during quiet resting, both of which can provoke RLS\nsymptoms.\nFunctional Consequences of Restless Legs Syndrome", "source": "dsm5.pdf"} {"id": "b2d51cd58470-2", "page_content": "symptoms.\nFunctional Consequences of Restless Legs Syndrome\nForms of RLS severe enough to si gnificantly impair functioning or associated with mental dis-\norders, including depression an d anxiety, occur in approximately 2%\u20133% of the population. \nAlthough the impact of milder symptoms is less well ch aracterized, in dividuals with\nRLS complain of disruption in at least one activity of daily li ving, with up to 50% reporting", "source": "dsm5.pdf"} {"id": "14cfeaad4948-0", "page_content": "Substance/Medication-Induced Sleep Disorder 413\na negative impact on mood, and 47.6% reporting a lack of energy. The most common conse-\nquences of RLS are sleep disturbance, includ ing reduced sleep time , sleep fragmentation,\nand overall disturbance; depression, generalize d anxiety disorder, panic disorder, and post-\ntraumatic stress disorder; and quality-of-life impairments. RLS can result in daytime sleep-\niness or fatigue and is frequently accompanied by significant distress or impairment in\naffective, social, occupational, educational, academic, behavioral, or cognitive functioning. \nDifferential Diagnosis \nThe most important conditions in the differential diagnosis of RLS are leg cramps, posi-\ntional discomfort, arthralgias/arthritis, myalgias, positional ischemia (numbness), leg\nedema, peripheral neuropathy, radiculopathy, and habitual foot tapping. \u201cKnotting\u201d of\nthe muscle (cramps), relief with a single postural shift, limitation to joints, soreness to pal-\npation (myalgias), and other abnormalities on physical exam ination are not characteristic\nof RLS. Unlike RLS, nocturnal leg cramps do not typically present with the desire to move\nthe limbs nor are there frequent limb movements. Less common conditions to be differen-\ntiated from RLS include neuroleptic-induced akathisia, myelopathy, symptomatic venous\ninsufficiency, peripheral artery disease, ec zema, other orthopedic problems, and anxiety-\ninduced restlessness. Worsening at night an d periodic limb movements are more common\nin RLS than in medication-induced akathisia or peripheral neuropathy. \nWhile is it important that RLS symptoms not be solely accounted for by another medical", "source": "dsm5.pdf"} {"id": "14cfeaad4948-1", "page_content": "While is it important that RLS symptoms not be solely accounted for by another medical\nor behavioral condition, it should also be appreciated that any of thes e similar conditions can\noccur in an individual with RLS. This necessi tates a separate focus on each possible condi-\ntion in the diagnostic process and when assessing impact. For cases in which the diagnosis of\nRLS is not certain, evaluation for the supportive features of RLS, particularly PLMS or a fam-\nily history of RLS, may be helpful. Clinical features, such as response to a dopaminergic\nagent and positive family history for RLS, can help with the differential diagnosis.\nComorbidity\nDepressive disorders, anxiety disorders, an d attentional disorder s are commonly comor-\nbid with RLS and are discussed in the sectio n \u201cFunctional Consequences of Restless Legs\nSyndrome.\u201d The main medical disorder comorbid with RLS is cardiovascular disease.\nThere may be an association with numerous other medical disorders, including hyperten-\nsion, narcolepsy, migraine, Parkinson\u2019s disease, multiple sclerosis, peripheral neuropathy,\nobstructive sleep apnea, diabetes mellitus, fibromyalgia, osteoporosis, obesity, thyroid\ndisease, and cancer. Iron defi ciency, pregnancy, and chronic renal failure are also comor-\nbid with RLS.\nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classifica tion of Sleep Disorders, 2nd Edition (ICSD-2), presents similar diag-\nnostic criteria for RLS but does not contain a criterion specifying fr equency or duration of\nsymptoms.\nSubstance/Medication-Induced Sleep Disorder\nDiagnostic Criteria \nA. A prominent and severe disturbance in sleep.\nB. There is evidence from the history, physical examination, or laboratory findings of both", "source": "dsm5.pdf"} {"id": "14cfeaad4948-2", "page_content": "B. There is evidence from the history, physical examination, or laboratory findings of both\n(1) and (2):", "source": "dsm5.pdf"} {"id": "2d7ee498ee1e-0", "page_content": "414 Sleep-Wake Disorders\n1. The symptoms in Criterion A developed during or soon after substance intoxication\nor after withdrawal from or exposure to a medication.\n2. The involved substance/medication is capable of producing the symptoms in Crite-\nrion A.\nC. The disturbance is not better explained by a sleep disorder that is not substance/\nmedication-induced. Such evidence of an independent sleep disorder could include\nthe following:\nThe symptoms precede the onset of the substance/medication use; the symptoms\npersist for a substantial period of time (e.g., about 1 month) after the cessation of\nacute withdrawal or severe intoxication; or there is other evidence suggesting the\nexistence of an independent non-substance/medication-induced sleep disorder\n(e.g., a history of recurrent non-substance/medication-related episodes).\nD. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nNote: This diagnosis should be made instead of a diagnosis of substance intoxication or\nsubstance withdrawal only when the symptoms in Criterion A predominate in the clinical\npicture and when they are sufficiently severe to warrant clinical attention.\nCoding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-\ntion]-induced sleep disorders are indicated in the table below. Note that the ICD-10-CM\ncode depends on whether or not there is a comorbid substance use disorder present for\nthe same class of substance. If a mild substance use disorder is comorbid with the sub-\nstance-induced sleep disorder, the 4th position character is \u201c1,\u201d and the clinician should", "source": "dsm5.pdf"} {"id": "2d7ee498ee1e-1", "page_content": "record \u201cmild [substance] use disorder\u201d before the substance-induced sleep disorder (e.g.,\n\u201cmild cocaine use disorder with cocaine-induc ed sleep disorder\u201d). If a moderate or severe\nsubstance use disorder is comorbid with the substance-induced sleep disorder, the 4th po-\nsition character is \u201c2,\u201d and the clinician shoul d record \u201cmoderate [substance] use disorder\u201d\nor \u201csevere [substance] use disorder,\u201d depending on the severity of the comorbid substance\nuse disorder. If there is no comorbid substance use disorder (e.g., after a one-time heavy\nuse of the substance), then the 4th position character is \u201c9,\u201d and the clinician should record\nonly the substance-induced sleep disorder. A m oderate or severe tobacco use disorder is\nrequired in order to code a tobacco-induced sleep disorder; it is not permissible to code a\ncomorbid mild tobacco use disorder or no tobacco use disorder with a tobacco-induced\nsleep disorder.\nSpecify whether:\nInsomnia type: Characterized by difficulty falling asleep or maintaining sleep, frequent\nnocturnal awakenings, or nonrestorative sleep.\nDaytime sleepiness type: Characterized by predominant complaint of excessive\nsleepiness/fatigue during waking hours or, less commonly, a long sleep period.\nParasomnia type: Characterized by abnormal behavioral events during sleep.\nMixed type: Characterized by a substance/m edication-induced sleep problem charac-\nterized by multiple types of sleep symptoms, but no symptom clearly predominates.\nSpecify if (see Table 1 in the chapter \u201cSubstance-Related and Addictive Disorders\u201d for di-\nagnoses associated with substance class):\nWith onset during intoxication: This specifier should be used if criteria are met for", "source": "dsm5.pdf"} {"id": "2d7ee498ee1e-2", "page_content": "With onset during intoxication: This specifier should be used if criteria are met for\nintoxication with the substance/medication and symptoms developed during the intox-\nication period.\nWith onset during disco ntinuation/withdrawal: This specifier should be used if cri-\nteria are met for discontinuation/withdrawal from the substance/medication and symp-\ntoms developed during, or shortly after, discontinuation of the substance/medication.", "source": "dsm5.pdf"} {"id": "6f187f82920c-0", "page_content": "Substance/Medication-Induced Sleep Disorder 415\nRecording Procedures\nICD-9-CM. The name of the substance/medication-induced sleep disorder begins with\nthe specific substance (e.g., cocaine, bupropion) that is presumed to be causing the sleep\ndisturbance. The diagnostic code is selected from the table included in the criteria set,\nwhich is based on the drug class. For substances that do not fit into any of the classes (e.g.,\nbupropion), the code for \u201cother substance\u201d should be used; and in cases in which a sub-\nstance is judged to be an etiological factor but the specific class of substance is unknown,\nthe category \u201cunknown substance\u201d should be used.\nThe name of the disorder is followed by the sp ecification of onset (i.e., onset during in-\ntoxication, onset during discontinuation/withdrawal), followed by the subtype designa-\ntion (i.e., insomnia type, daytime sleepine ss type, parasomnia type, mixed type). Unlike\nthe recording procedures for ICD-10-CM, wh ich combine the substance-induced disorder\nand substance use disorder into a single code, for ICD-9-CM a separate diagnostic code\nis given for the substance use disorder. For ex ample, in the case of insomnia occurring\nduring withdrawal in a man with a severe lorazepam use disorder, the diagnosis is 292.85\nlorazepam-induced sleep disorder, with onset during withdrawal, insomnia type. An ad-\nditional diagnosis of 304.10 severe lorazepam us e disorder is also given. When more than\none substance is judged to play a significant role in the developmen t of the sleep distur-\nbance, each should be listed separately (e.g., 292.85 alcohol-induced sleep disorder, with", "source": "dsm5.pdf"} {"id": "6f187f82920c-1", "page_content": "onset during intoxication, insomnia type; 292. 85 cocaine-induced sleep disorder, with on-\nset during intoxication, insomnia type). \nICD-10-CM. The name of the substance/medication-induced sleep disorder begins with the\nspecific substance (e.g., cocaine, bupropion) that is presumed to be causing the sleep distur-\nbance. The diagnostic code is selected from the ta ble included in the criteria set, which is based\non the drug class and presence or absence of a comorbid substance use disorder. For sub-\nstances that do not fit into any of the classes (e.g., bupropion), the code for \u201cother substance\u201d\nshould be used; and in cases in which a substance is judged to be an etiological factor but the\nspecific class of substance is unknown, the category \u201cunknown substance\u201d should be used.\nWhen recording the name of the disorder, th e comorbid substance use disorder (if any)\nis listed first, followed by the word \u201cwith,\u201d followed by the name of the substance-induced\nsleep disorder, followed by the specification of onset (i.e., onset during intoxication, onsetICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate \nor severeWithout \nuse \ndisorder\nAlcohol 291.82 F10.182 F10.282 F10.982\nCaffeine 292.85 F15.182 F15.282 F15.982\nCannabis 292.85 F12.188 F12.288 F12.988\nOpioid 292.85 F11.182 F11.282 F11.982", "source": "dsm5.pdf"} {"id": "6f187f82920c-2", "page_content": "Opioid 292.85 F11.182 F11.282 F11.982\nSedative, hypnotic, or anxiolytic 292.85 F13.182 F13.282 F13.982\nAmphetamine (or other \nstimulant)292.85 F15.182 F15.282 F15.982\nCocaine 292.85 F14.182 F14.282 F14.982\nTobacco 292.85 NA F17.208 NA\nOther (or unknown) substance 292.85 F19.182 F19.282 F19.982", "source": "dsm5.pdf"} {"id": "cabffd88697b-0", "page_content": "416 Sleep-Wake Disorders\nduring discontinuation/withdrawal), followed by the subtype designation (i.e., insomnia\ntype, daytime sleepiness type, parasomnia type , mixed type). For example, in the case of\ninsomnia occurring during withdrawal in a ma n with a severe lorazepam use disorder, the\ndiagnosis is F13.282 severe lorazepam use disorder with lorazepam-induced sleep disor-\nder, with onset during withdrawal, insomnia type. A separate diagnosis of the comorbid\nsevere lorazepam use disorder is not given. If the substance-induced sleep disorder occurs\nwithout a comorbid substance use disorder (e.g., with medication use), no accompanying\nsubstance use disorder is noted (e.g., F19.98 2 bupropion-induced sleep disorder, with on-\nset during medication use, insomnia type). When more than one substance is judged to\nplay a significant role in the development of the sleep disturbance, each should be listed\nseparately (e.g., F10.282 severe alcohol use disorder with alcohol-induced sleep disorder,\nwith onset during intoxication, insomnia ty pe; F14.282 severe cocaine use disorder with\ncocaine-induced sleep disord er, with onset during into xication, insomnia type).\nDiagnostic Features\nThe essential feature of substance/medication -induced sleep disorder is a prominent sleep\ndisturbance that is suffi ciently severe to warrant independen t clinical attent ion (Criterion A)\nand that is judged to be primarily associated with the pharmacological effects of a substance\n(i.e., a drug of abuse, a medication, toxin ex posure) (Criterion B). Depending on the sub-\nstance involved, one of four types of sleep di sturbances is reported. Insomnia type and day-", "source": "dsm5.pdf"} {"id": "cabffd88697b-1", "page_content": "time sleepiness type are most common, while parasomnia type is seen less often. The mixed\ntype is noted when more than one type of sl eep disturbance\u2013related symptom is present and\nnone predominates. The disturbance must not be better explained by another sleep disorder\n(Criterion C). A substance/medication-induced sleep disorder is distinguished from insom-\nnia disorder or a disorder associated with excessive daytime sleepines s by considering onset\nand course. For drugs of abuse, there must be evidence of intoxication or withdrawal from\nthe history, physical examination, or laboratory findings. Substance/medication-induced\nsleep disorder arises only in association wi th intoxication or di scontinuation/withdrawal\nstates, whereas other sleep disorders may preced e the onset of substance use or occur during\ntimes of sustained abstinence. As discontinuation/withdrawal states for some substances\ncan be protracted, onset of th e sleep disturbance can occur 4 weeks after cessation of sub-\nstance use, and the disturbance may have feat ures atypical of other sleep disorders (e.g.,\natypical age at onset or course). The diagnosi s is not made if the sleep disturbance occurs\nonly during a delirium (Criterion D). The symptoms must cause clinically significant dis-\ntress or impairment in social, occupational, or other important areas of functioning (Crite-\nrion E). This diagnosis should be made instea d of a diagnosis of substance intoxication or\nsubstance withdrawal only when the symptoms in Criterion A predominate in the clinical\npicture and when the symptoms warrant independent clinical attention. \nAssociated Features Supporting Diagnosis\nDuring periods of substance/medication use, intoxication, or withdrawal, individuals fre-\nquently complain of dysphoric mood, includin g depression and anxiety, irritability, cog-\nnitive impairment, inability to concentrate, and fatigue.", "source": "dsm5.pdf"} {"id": "cabffd88697b-2", "page_content": "nitive impairment, inability to concentrate, and fatigue. \nProminent and severe sleep disturbances can occur in association with intoxication\nwith the following classes of substances: alco hol; caffeine; cannabis; opioids; sedatives,\nhypnotics, or anxiolytics; st imulants (including cocaine); and other (or unknown) sub-\nstances. Prominent and severe sleep disturbances can occur in association with withdrawal", "source": "dsm5.pdf"} {"id": "e83914094106-0", "page_content": "hypnotics, or anxiolytics; st imulants (including cocaine); and other (or unknown) sub-\nstances. Prominent and severe sleep disturbances can occur in association with withdrawal\nfrom the following classes of substances: alcohol; caffeine; cannabis; opioids; sedatives,\nhypnotics, or anxiolytics; stimulant (includi ng cocaine); tobacco; and other (or unknown)\nsubstances. Some medications that invoke sl eep disturbances include adrenergic agonists\nand antagonists, dopamine agonists and antagonists, cholinergic agonists and antagonists,\nserotonergic agonists and antagonists, antihistamines, and corticosteroids.", "source": "dsm5.pdf"} {"id": "346c17c7d02b-0", "page_content": "Substance/Medication-Induced Sleep Disorder 417\nAlcohol. Alcohol-induced sleep disorder typica lly occurs as insomnia type. During\nacute intoxication, alcohol produces an immedi ate sedative effect depending on dose, ac-\ncompanied by increased stages 3 and 4 non\u2013 rapid eye movement (NREM) sleep and re-\nduced rapid eye movement (REM) sleep. Following these initial e ffects, there may be\nincreased wakefulness, restless sleep, and vivid and anxiety-laden dreams for the remain-\ning sleep period. In parallel, stages 3 and 4 sleep are reduced, and wakefulness and REM\nsleep are increased. Alcohol can aggravate br eathing-related sleep disorder. With habitual\nuse, alcohol continues to show a short-lived sedati ve effect in the first half of the night, fol-\nlowed by sleep continuity disruption in the second half. During alcohol withdrawal, there\nis extremely disrupted sleep continuity, and an increased amount and intensity of REM\nsleep, associated frequently with vivid drea ming, which in extreme form, constitutes part\nof alcohol withdrawal delirium. After acut e withdrawal, chronic alcohol users may con-\ntinue to complain of light, fragmented sleep for weeks to years associated with a persistent\ndeficit in slow-wave sleep.\nCaffeine. Caffeine-induced sleep disorder produces insomnia in a dose-dependent man-\nner, with some individuals presenting with daytime sleepiness related to withdrawal. \nCannabis. Acute administration of cannabis may shorten sleep latency, though arous-\ning effects with increments in sleep latenc y also occur. Cannabis enhances slow-wave\nsleep and suppresses REM sleep after acute administration. In chronic users, tolerance to\nthe sleep-inducing and slow-wave sleep\u2013enha ncing effects develops. Upon withdrawal,\nsleep difficulties and unpleasant dreams have been reported lasting for several weeks.", "source": "dsm5.pdf"} {"id": "346c17c7d02b-1", "page_content": "sleep difficulties and unpleasant dreams have been reported lasting for several weeks.\nPolysomnography studies demonstrate reduced slow-wave sleep and increased REM sleep\nduring this phase.\nOpioids. Opioids may produce an increase in sleepiness and in subjective depth of sleep,\nand reduced REM sleep, during acute short-te rm use. With continued administration, tol-\nerance to the sedative effects of opioids de velops and there are co mplaints of insomnia.\nConsistent with their respiratory depressant effects, opioids exacerbate sleep apnea.\nSedative, hypnotic, or anxiolytic substances. Sedatives, hypnotics, and anxiolytics (e.g.,\nbarbiturates, benzodiazepines receptor agon ists, meprobamate, glutethimide, methypry-\nlon) have similar effects as opioids on sleep. During acute intoxication, sedative-hypnotic\ndrugs produce the expected incr ease in sleepiness and decrea se in wakefulness. Chronic\nuse (particularly of barbiturates and the ol der nonbarbiturate, no nbenzodiazepine drugs)\nmay cause tolerance with subsequent return of insomnia. Daytime sleepiness may occur.\nSedative-hypnotic drugs can increase the frequency and severity of obstructive sleep ap-\nnea events. Parasomnias are associated with us e of benzodiazepine receptor agonists, es-\npecially when these medications are taken at higher doses and when they are combined\nwith other sedative drugs. Ab rupt discontinuation of chronic sedative, hypnotic, or anx-\niolytic use can lead to withdrawal but mo re commonly rebound insomnia, a condition of\nan exacerbation of insomnia upon drug disc ontinuation for 1\u20132 days reported to occur", "source": "dsm5.pdf"} {"id": "346c17c7d02b-2", "page_content": "even with short-term use. Sedative, hypnotic, or anxiolytic drugs with short durations of\naction are most likely to produce complain ts of rebound insomnia, whereas those with\nlonger durations of action are more often asso ciated with daytime sl eepiness. Any sedative,\nhypnotic, or anxiolytic drug can potentiall y cause daytime sedation, withdrawal, or re-\nbound insomnia. \nAmphetamines and related substances and other stimulants. Sleep disorders induced\nby amphetamine and related substances and other stimulants are characterized by insomnia", "source": "dsm5.pdf"} {"id": "9d8348b52863-0", "page_content": "bound insomnia. \nAmphetamines and related substances and other stimulants. Sleep disorders induced\nby amphetamine and related substances and other stimulants are characterized by insomnia\nduring intoxication and excessi ve sleepiness during withdrawal. During acute intoxication,\nstimulants reduce the total amount of sleep, incr ease sleep latency and sleep continuity distur-\nbances, and decrease REM sleep. Slow-wave slee p tends to be reduced. During withdrawal\nfrom chronic stimulant use, there is both pr olonged nocturnal sleep duration and excessive\ndaytime sleepiness. Multiple sleep latency te sts may show increased daytime sleepiness dur-", "source": "dsm5.pdf"} {"id": "5d87a0abc73e-0", "page_content": "418 Sleep-Wake Disorders\ning the withdrawal phase. Drugs like 3,4- methylenedioxymethamphetamine (MDMA; \u201cec-\nstasy\u201d) and related substances lead to restless and disturbed sleep with in 48 hours of intake;\nfrequent use of these compounds is associated with persisting symptoms of anxiety, depres-\nsion, and sleep disturbances, even during longer-term abstinence.\nTobacco. Chronic tobacco consumption is associat ed primarily with symptoms of insom-\nnia, decreased slow-wave sleep with a reductio n of sleep efficiency, and increased daytime\nsleepiness. Withdrawal from tobacco can lead to impaired sleep. Individuals who smoke\nheavily may experience regular nocturnal awakenings caused by tobacco craving.\nOther or unknown substances/medications. Other substances/medications may pro-\nduce sleep disturbances, particularly medications that affect the central or autonomic\nnervous systems (e.g., adrenergic agonists an d antagonists, dopamine agonists and antag-\nonists, cholinergic agonists an d antagonists, serotonergic agonists and antagonists, anti-\nhistamines, corticosteroids). \nDevelopment and Course\nInsomnia in children can be identified by eith er a parent or the child. Often the child has a\nclear sleep disturbance associated with initiation of a medication but may not report\nsymptoms, although parents observe the slee p disturbances. The use of some illicit sub-\nstances (e.g., cannabis, ecstasy) is prevalen t in adolescence and early adulthood. Insomnia\nor any other sleep disturbance encountered in this age group should prompt careful con-\nsideration of whether the sleep disturbance is due to consumption of these substances.\nHelp-seeking behavior for the sleep disturbance in these age groups is limited, and thus", "source": "dsm5.pdf"} {"id": "5d87a0abc73e-1", "page_content": "Help-seeking behavior for the sleep disturbance in these age groups is limited, and thus\ncorroborative report may be elic ited from a parent, caregiver, or teacher. Older individuals\ntake more medications and are at increased risk for developing a substance/medication-\ninduced sleep disorder. They may interpret sleep disturbance as part of normal aging and\nfail to report symptoms. Individuals with ma jor neurocognitive disorder (e.g., dementia)\nare at risk for substance/me dication-induced sleep disord ers but may not report symp-\ntoms, making corroborative report from caregiver(s) particularly important.\nRisk and Prognostic Factors\nRisk and prognostic factors involved in subs tance abuse/dependence or medication use\nare normative for certain age groups. They are relevant for, and likely applicable to, the\ntype of sleep disturbance encountered (see th e chapter \u201cSubstance-Related and Addictive\nDisorders\u201d for descriptions of resp ective substance use disorders).\nTemperamental. Substance use generally precipitates or accompanies insomnia in vul-\nnerable individuals. Thus, presence of insomnia in response to stress or change in sleep en-\nvironment or timing can represent a risk for developing substance/medication-induced\nsleep disorder. A similar risk may be present for individuals with other sleep disorders\n(e.g., individuals with hypersomnia who use stimulants).\nCulture-Related Diagnostic Issues\nThe consumption of substances, including pres cribed medications, may depend in part on\ncultural background and specif ic local drug regulations. \nGender-Related Diagnostic Issues\nGender-specific prevalences (i.e., females affected more than males at a ratio of about 2:1) exist\nfor patterns of consumption of some substances (e.g., alcohol). The same amount and duration\nof consumption of a given substance may lead to highly different sleep-related outcomes in", "source": "dsm5.pdf"} {"id": "5d87a0abc73e-2", "page_content": "of consumption of a given substance may lead to highly different sleep-related outcomes in\nmales and females based on, for example, gender -specific differences in hepatic functioning.", "source": "dsm5.pdf"} {"id": "62cd79944e01-0", "page_content": "Substance/Medication-Induced Sleep Disorder 419\nDiagnostic Markers\nEach of the substance/medica tion-induced sleep disorders produces electroencephalo-\ngraphic sleep patterns that are as sociated with, but cannot be considered diagnostic of, other\ndisorders. The electroencephalo graphic sleep profile for each substance is related to the\nstage of use, whether intake/intoxication, chronic use, or wi thdrawal following discontinu-\nation of the substance. All-night polysomnography can help define the severity of insomnia\ncomplaints, while the multiple sleep latency test provides information about the severity of\ndaytime sleepiness. Monitoring of nocturnal respiration and periodic limb movements with\npolysomnography may verify a substance\u2019s im pact on nocturnal breathing and motor be-\nhavior. Sleep diaries for 2 weeks and actigraphy are considered helpful in confirming the\npresence of substance/medication-induced sleep disorder. Dr ug screening ca n be of use\nwhen the individual is not aware or unwilling to relate information about substance intake.\nFunctional Consequences of \nSubstance/Medication-I nduced Sleep Disorder\nWhile there are many functional consequences associated with sleep disorders, the only\nunique consequence for substa nce/medication-induced sleep disorder is increased risk\nfor relapse. The degree of sleep disturbance during alcohol withdrawal (e.g., REM sleep\nrebound predicts risk of relapse of drinking ). Monitoring of sleep quality and daytime\nsleepiness during and after withdrawal may provide clinically meaningful information on\nwhether an individual is at increased risk for relapse.\nDifferential Diagnosis\nSubstance intoxication or substance withdrawal. Sleep disturbances are commonly en-\ncountered in the context of substance intoxi cation or substance discontinuation/with-\ndrawal. A diagnosis of substance/medication-induced sleep disorder should be made", "source": "dsm5.pdf"} {"id": "62cd79944e01-1", "page_content": "drawal. A diagnosis of substance/medication-induced sleep disorder should be made\ninstead of a diagnosis of substance intoxicati on or substance withdrawal only when the\nsleep disturbance is predominant in the clinic al picture and is suffi ciently severe to war-\nrant independent clinical attention. \nDelirium. If the substance/medication-induced sl eep disturbance occurs exclusively dur-\ning the course of a delirium, it is not diagnosed separately. \nOther sleep disorders. A substance/medication-induced sl eep disorder is distinguished\nfrom another sleep disorder if a substance/medication is judged to be etiologically related to\nthe symptoms. A su bstance/medication-induc ed sleep disorder attributed to a prescribed\nmedication for a mental disorder or medical co ndition must have its onset while the individual\nis receiving the medication or during disconti nuation, if there is a discontinuation/with-\ndrawal syndrome associated with the medication. Once treatment is discontinued, the sleep\ndisturbance will usually remit within days to several weeks. If symptoms persist beyond\n4 weeks, other causes for the sleep disturbanc e\u2013related symptoms should be considered. Not\ninfrequently, individuals with another sleep di sorder use medications or drugs of abuse to\nself-medicate their symptoms (e.g., alcohol fo r management of insomn ia). If the substance/\nmedication is judged to play a significant role in the exacerbation of the sleep disturbance, an\nadditional diagnosis of a substance/medicati on-induced sleep disorder may be warranted. \nSleep disorder due to an other medical condition. Substance/medication-induced sleep\ndisorder and sleep disorder associated with another medical condition may produce sim-\nilar symptoms of insomnia, daytime sleepiness, or a parasomnia. Many individuals with\nother medical conditions that cause sleep disturbance are treated with medications that", "source": "dsm5.pdf"} {"id": "62cd79944e01-2", "page_content": "other medical conditions that cause sleep disturbance are treated with medications that\nmay also cause sleep disturbances. The chrono logy of symptoms is the most important fac-\ntor in distinguishing between th ese two sources of sleep symptoms. Difficulties with sleep\nthat clearly preceded the use of any medication for treatment of a medical condition would", "source": "dsm5.pdf"} {"id": "aab38fc2d6af-0", "page_content": "420 Sleep-Wake Disorders\nsuggest a diagnosis of sleep disorder associated with another medical condition. Con-\nversely, sleep symptoms that appear only afte r the initiation of a particular medication/\nsubstance suggest a substance/medication-ind uced sleep disorder. If the disturbance is\ncomorbid with another medical condition and is also exacerbated by substance use, both\ndiagnoses (i.e., sleep disorder associated with another medical condition and substance/\nmedication-induced sleep disorder) are given. When there is insuffici ent evidence to de-\ntermine whether the sleep distur bance is attributable to a substance/medication or to an-\nother medical condition or is primary (i.e., not due to either a substance/medication or\nanother medical condition), a diagnosis of ot her specified sleep-wake disorder or unspec-\nified sleep-wake disorder is indicated.\nComorbidity\nSee the \u201cComorbidity\u201d sections for other sleep disorders in this chapter, including insom-\nnia, hypersomnolence, centra l sleep apnea, sleep-related hypoventilation, and circadian\nrhythm sleep-wake disorders, shift work type.\nRelationship to Internat ional Classification of \nSleep Disorders\nThe International Classifica tion of Sleep Disorders, 2nd Edition (ICSD-2), lists sleep disorders\n\u201cdue to drug or substance\u201d under their respective phenotypes (e.g., insomnia, hypersomnia).\nOther Specified Insomnia Disorder\n780.52 (G47.09)\nThis category applies to presentations in which symptoms characteristic of insomnia disorder\nthat cause clinically significant distress or impairment in social, occupational, or other important\nareas of functioning predominate but do not meet th e full criteria for insomnia disorder or any\nof the disorders in the sleep-wake disorders diagnostic class. The other specified insomnia dis-", "source": "dsm5.pdf"} {"id": "aab38fc2d6af-1", "page_content": "of the disorders in the sleep-wake disorders diagnostic class. The other specified insomnia dis-\norder category is used in situations in which the clinician chooses to communicate the specific\nreason that the presentation does not meet the criteria for insomnia disorder or any specific\nsleep-wake disorder. This is done by recording \u201cother specified insomnia disorder\u201d followed by\nthe specific reason (e.g., \u201cbrief insomnia disorder\u201d).\nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude the following:\n1.Brief insomnia disorder: Duration is less than 3 months.\n2.Restricted to no nrestorative sleep: Predominant complaint is nonrestorative sleep\nunaccompanied by other sleep symptoms such as difficulty falling asleep or remaining\nasleep.\nUnspecified Insomnia Disorder\n780.52 (G47.00)\nThis category applies to presentations in which symptoms characteristic of insomnia disor-\nder that cause clinically significant distress or impairment in social, occupational, or other\nimportant areas of functioning predominate but do not meet the full criteria for insomnia dis-\norder or any of the disorders in the sleep-wake disorders diagnostic class. The unspecified", "source": "dsm5.pdf"} {"id": "3b63fcba8eca-0", "page_content": "Other Specified Hypersomnolence Disorder 421\ninsomnia disorder category is used in situations in which the clinician chooses not to specify\nthe reason that the criteria are not met for insomnia disorder or a specific sleep-wake dis-\norder, and includes presentations in which there is insufficient information to make a more\nspecific diagnosis.\nOther Specified Hypersomnolence Disorder\n780.54 (G47.19)\nThis category applies to presentations in which symptoms characteristic of hypersomno-\nlence disorder that cause clinically signific ant distress or impairment in social, occupation-\nal, or other important areas of functioning predominate but do not meet the full criteria for\nhypersomnolence disorder or any of the disorders in the sleep-wake disorders diagnostic\nclass. The other specified hypersomnolence disorder category is used in situations in\nwhich the clinician chooses to communicate the specific reason that the presentation does\nnot meet the criteria for hypersomnolence diso rder or any specific sleep-wake disorder.\nThis is done by recording \u201cother specified hypersomnolence disorder\u201d followed by the spe-\ncific reason (e.g., \u201cbrief-duration hyperso mnolence,\u201d as in Kleine-Levin syndrome).\nUnspecified Hypersomnolence Disorder\n780.54 (G47.10)\nThis category applies to presentations in which symptoms characteristic of hypersomno-\nlence disorder that cause clinically signific ant distress or impairment in social, occupation-\nal, or other important areas of functioning predominate but do not meet the full criteria for\nhypersomnolence disorder or any of the disorders in the sleep-wake disorders diagnostic\nclass. The unspecified hypersomnolence disorder category is used in situations in which\nthe clinician chooses not to specify the reason that the criteria are not met for hypersom-", "source": "dsm5.pdf"} {"id": "3b63fcba8eca-1", "page_content": "the clinician chooses not to specify the reason that the criteria are not met for hypersom-\nnolence disorder or a specific sleep-wake disorder, and includes presentations in which\nthere is insufficient information to make a more specific diagnosis.\nOther Specified Sleep-Wake Disorder\n780.59 (G47.8)\nThis category applies to presentations in which symptoms characteristic of a sleep-wake\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the sleep-wake disorders diagnostic class and do not qualify for a diagno-\nsis of other specified insomnia disorder or other specified hypersomnolence disorder. The\nother specified sleep-wake disorder category is used in situations in which the clinician\nchooses to communicate the specific reason that the presentation does not meet the\ncriteria for any specific sleep-wake disorder . This is done by recording \u201cother specified\nsleep-wake disorder\u201d followed by the specific reason (e.g., \u201crepeated arousals during rapid\neye movement sleep without polysomnography or history of Parkinson\u2019s disease or other\nsynucleinopathy\u201d).", "source": "dsm5.pdf"} {"id": "30d55d25fb8e-0", "page_content": "422 Sleep-Wake Disorders\nUnspecified Sleep-Wake Disorder\n780.59 (G47.9)\nThis category applies to presentations in which symptoms characteristic of a sleep-wake\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the sleep-wake disorders di agnostic class and do not qualify for a diagno-\nsis of unspecified insomnia disorder or unspecified hypersomnolence disorder. The un-\nspecified sleep-wake disorder category is used in situations in which the clinician chooses\nnot to specify the reason that the criteria are not met for a specific sleep-wake disorder,\nand includes presentations in which there is insufficient information to make a more spe-\ncific diagnosis.", "source": "dsm5.pdf"} {"id": "931a5cddf0a9-0", "page_content": "423Sexual\n Dysfunctions\nSexual dysfunctions include delayed ejaculation, er ectile disorder, female orgasmic\ndisorder, female sexual intere st/arousal disorder, genito-pelvic pain/penetration disorder,\nmale hypoactive sexual desire disorder, premature (early) ejac ulation, substance/medication-\ninduced sexual dysfunction, other specified se xual dysfunction, and unspecified sexual dys-\nfunction. Sexual dysfunctions ar e a heterogeneous group of disorders that are typically char-\nacterized by a clinically significant disturbance in a person\u2019s ability to respond sexually or to\nexperience sexual pleasure. An individual may have several sexual dysfunctions at the same\ntime. In such cases, all of the dysfunctions should be diagnosed. \nClinical judgment should be used to determin e if the sexual difficulties are the result of\ninadequate sexual stimulation; in these cases, there may still be a need for care, but a di-\nagnosis of a sexual dysfunctio n would not be made. These cases may include, but are not\nlimited to, conditions in which lack of know ledge about effective stimulation prevents the\nexperience of arousal or orgasm.\nSubtypes are used to designate the onset of the difficulty. In many individuals with\nsexual dysfunctions, the time of onset may in dicate different etiolo gies and interventions.\nLifelong refers to a sexual problem that has been present from first sexu al experiences, and\nacquired applies to sexual disorders that develop after a period of relatively normal sexual\nfunction. Generalized refers to sexual difficulties that are not limited to certain types of\nstimulation, situatio ns, or partners, and situational refers to sexual difficulties that only oc-\ncur with certain types of stimul ation, situations, or partners.\nIn addition to the lifelong/ acquired and generalized/situational subtypes, a number", "source": "dsm5.pdf"} {"id": "931a5cddf0a9-1", "page_content": "In addition to the lifelong/ acquired and generalized/situational subtypes, a number\nof factors must be considered during the asse ssment of sexual dysfunction, given that they\nmay be relevant to etiology and/or treatment, and that may contribute, to varying degrees,\nacross individuals: 1) partner factors (e.g., pa rtner\u2019s sexual problems; partner\u2019s health sta-\ntus); 2) relationship factors (e.g., poor communication; disc repancies in desire for sexual\nactivity); 3) individual vulnerability factors (e .g., poor body image; history of sexual or emo-\ntional abuse), psychiatric comorbidity (e.g., depr ession, anxiety), or stre ssors (e.g., job loss,\nbereavement); 4) cultural or religious factors (e.g., inhibitions re lated to prohibitions against\nsexual activity or pleasure; attitudes toward sexuality); and 5) medical factors relevant to\nprognosis, course, or treatment.\nClinical judgment about the di agnosis of sexual dysfunction should take into consideration\ncultural factors that may influe nce expectations or engender pr ohibitions about the experience\nof sexual pleasure. Aging may be associated wi th a normative decrease in sexual response. \nSexual response has a requisite biological underpinning, yet is usually experienced in\nan intrapersonal, interpersonal, and cultural context. Thus, sexual fu nction involves a com-\nplex interaction among biological, sociocultural, and psychological factors. In many clinical\ncontexts, a precise understanding of the etiolo gy of a sexual problem is unknown. Nonethe-\nless, a sexual dysfunction diagnosis requires ruling out problems that are better explained\nby a nonsexual mental disorder, by the effects of a substance (e.g., drug or medication), by", "source": "dsm5.pdf"} {"id": "931a5cddf0a9-2", "page_content": "a medical condition (e.g., due to pelvic nerve damage), or by severe relationship distress,\npartner violence, or other stressors. \nIf the sexual dysfunction is mostly explainabl e by another nonsexual mental disorder (e.g.,\ndepressive or bipolar disorder, anxiety disord er, posttraumatic stress disorder, psychotic dis-", "source": "dsm5.pdf"} {"id": "f8a728ab8389-0", "page_content": "424 Sexual Dysfunctions\norder), then only the other mental disorder diagnosis should be made. If the problem is\nthought to be better explained by the use/misuse or discontinuation of a drug or substance, it\nshould be diagnosed accordingly as a substance/medication-induced sexual dysfunction. If\nthe sexual dysfunction is attributable to anot her medical condition (e.g., peripheral neuropa-\nthy), the individual would not receive a psychiatric diagnosis. If severe relationship distress,\npartner violence, or significant stressors better ex plain the sexual difficulties, then a sexual dys-\nfunction diagnosis is not made, but an appropriat e V or Z code for the relationship problem or\nstressor may be listed. In many cases, a precise etiological relationship between another con-\ndition (e.g., a medical condition) and a sexual dysfunction cannot be established. \nDelayed Ejaculation\nDiagnostic Criteria 302.74 (F52.32)\nA. Either of the following symptoms must be experienced on almost all or all occasions\n(approximately 75%\u2013100%) of partnered sexual activity (in identified situational con-\ntexts or, if generalized, in all contexts), and without the individual desiring delay:\n1. Marked delay in ejaculation.\n2. Marked infrequency or absence of ejaculation.\nB. The symptoms in Criterion A have persist ed for a minimum duration of approximately\n6 months.\nC. The symptoms in Criterion A cause clinically significant distress in the individual.\nD. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a\nconsequence of severe relationship distress or other significant stressors and is not at-\ntributable to the effects of a substance/medication or another medical condition.\nSpecify whether:\nLifelong: The disturbance has been present since the individual became sexually active.", "source": "dsm5.pdf"} {"id": "f8a728ab8389-1", "page_content": "Lifelong: The disturbance has been present since the individual became sexually active.\nAcquired: The disturbance began after a period of relatively normal sexual function.\nSpecify whether:\nGeneralized: Not limited to certain types of stimulation, situations, or partners.\nSituational: Only occurs with certain types of stimulation, situations, or partners.\nSpecify current severity:\nMild: Evidence of mild distress over the symptoms in Criterion A.\nModerate: Evidence of moderate distress ov er the symptoms in Criterion A.\nSevere: Evidence of severe or extreme distress over the symptoms in Criterion A.\nDiagnostic Features\nThe distinguishing feature of delayed ejaculation is a marked delay in or inability to\nachieve ejaculation (Cri terion A). The man reports difficulty or inability to ejaculate de-\nspite the presence of adequate sexual stimul ation and the desire to ejaculate. The present-\ning complaint usually involves partnered sexual activity. In most cases, the diagnosis will\nbe made by self-report of the individual. The defini tion of \u201cdelay\u201d does not have precise\nboundaries, as there is noconsensus as to what constitutes a reasonable time to reach or-\ngasm or what is unacceptably long fo r most men and their sexual partners.\nAssociated Features Supporting Diagnosis\nThe man and his partner may report prolonged thrusting to achieve or gasm to the point of\nexhaustion or genital discomfo rt and then ceasing efforts. Some men may report avoiding", "source": "dsm5.pdf"} {"id": "cb4c8d2f27b3-0", "page_content": "Delayed Ejaculation 425\nsexual activity because of a re petitive pattern of difficulty ejaculating. Some sexual partners\nmay report feeling less sexually attractive because their partner ca nnot ejaculate easily.\nIn addition to the subtypes \u201clifelong/acqu ired\u201d and \u201cgeneralized/situational,\u201d the fol-\nlowing five factors must be considered during assessment and diagnosis of delayed ejacu-\nlation, given that they may be relevant to etiology and/or treatment: 1) partner factors (e.g.,\npartner\u2019s sexual pr oblems, partner\u2019s health status); 2) relationship factors (e.g., poor com-\nmunication, discrepancies in desire for sexual activity); 3) individual vulnerability factors\n(e.g., poor body image; history of sexual or emotional abuse), psychiatric comorbidity (e.g.,\ndepression, anxiety), or stressor s (e.g., job loss, bereavement); 4) cultural/religious factors\n(e.g., inhibitions related to prohibitions agains t sexual activity; attitudes toward sexuality);\nand 5) medical factors relevant to prognosis, course, or treatment. Each of these factors may\ncontribute differently to the presenting symptoms of different men with this disorder.\nPrevalence\nPrevalence is unclear because of the lack of a precise definition of this syndrome. It is the\nleast common male sexual complaint. Only 75% of men report always ejaculating during\nsexual activity, and less than 1% of men will complain of problems with reaching ejacula-\ntion that last more than 6 months.\nDevelopment and Course\nLifelong delayed ejaculation begins with ea rly sexual experiences and continues through-\nout life. By definition, acquired delayed ejaculation begins after a period of normal sexual\nfunction. There is minimal evidence concerni ng the course of acquired delayed ejacula-", "source": "dsm5.pdf"} {"id": "cb4c8d2f27b3-1", "page_content": "function. There is minimal evidence concerni ng the course of acquired delayed ejacula-\ntion. The prevalence of delaye d ejaculation appears to remain relatively constant until\naround age 50 years, when the incidence begins to increase significantly. Men in their 80s\nreport twice as much difficulty ejac ulating as men younger than 59 years.\nRisk and Prognostic Factors\nGenetic and physiological. Age-related loss of the fast-conducting peripheral sensory\nnerves and age-related decreased sex steroid secretion may be associated with the increase\nin delayed ejaculation in men older than 50 years.\nCulture-Related Diagnostic Issues\nComplaints of ejaculatory delay vary across countries and cultures. Such complaints are\nmore common among men in Asian population s than in men living in Europe, Australia,\nor the United States. This variation may be attributable to cultural or genetic differences\nbetween cultures.\nFunctional Consequences of Delayed Ejaculation\nDifficulty with ejaculation may contribute to difficulties in conception. Delayed ejacula-\ntion is often associated with considerable psychological distre ss in one or both partners.\nDifferential Diagnosis\nAnother medical condition. The major differential diagnosis is between delayed ejacu-\nlation fully explained by another medical illness or injury and delayed ejaculation with a\npsychogenic, idiopathic, or combined psycho logical and medical etiology. A situational\naspect to the complaint is suggestive of a psychological basis for the problem (e.g., men\nwho can ejaculate during sexual activity with one sex but not the other; men who can ejac-\nulate with one partner but not another of the same sex; men with paraphilic arousal pat-", "source": "dsm5.pdf"} {"id": "102beb683e01-0", "page_content": "426 Sexual Dysfunctions\nterns; men who require highly ritualized ac tivity to ejaculate during partnered sexual\nactivity). Another medical illness or injury ma y produce delays in ejaculation independent\nof psychological issues. For example, inability to ejaculate can be caused by interruption of\nthe nerve supply to the genitals , such as can occur after traumatic surgical injury to the\nlumbar sympathetic ganglia, abdominoperitoneal surgery, or lumbar sympathectomy.\nEjaculation is thought to be under autonomic nervous system control involving the hypo-\ngastric (sympathetic) and pudendal (parasym pathetic) nerves. A number of neurodegen-\nerative diseases, such as multiple sclerosis and diabetic and alcoholic neuropathy, can\ncause inability to ejaculate. Delayed ejaculat ion should also be diffe rentiated from retro-\ngrade ejaculation (i.e., ejaculation into the bladder), which may follow transurethral pros-\ntatic resection.\nSubstance/medication use. A number of pharmacological agents, such as antidepres-\nsants, antipsychotics, alpha sympathetic drugs, and opioid drugs, can cause ejaculatory\nproblems.\nDysfunction with orgasm. It is important in the history to ascertain whether the com-\nplaint concerns delayed ejaculation or the sensation of orgasm, or both. Ejaculation occurs\nin the genitals, whereas the experience of orga sm is believed to be primarily subjective.\nEjaculation and orgasm usually occur together but not always. For example, a man with a\nnormal ejaculatory pattern may complain of decreased pleasure (i.e., anhedonic ejacula-\ntion). Such a complaint would not be coded as delayed ejaculation but could be coded as\nother specified sexual dysfunction or unspecified sexual dysfunction. \nComorbidity", "source": "dsm5.pdf"} {"id": "102beb683e01-1", "page_content": "other specified sexual dysfunction or unspecified sexual dysfunction. \nComorbidity \nThere is some evidence to sugge st that delayed ejaculation may be more common in severe\nforms of major de pressive disorder. \nErectile Disorder\nDiagnostic Criteria 302.72 (F52.21)\nA. At least one of the three following symptoms must be experienced on almost all or all\n(approximately 75%\u2013100%) occasions of sexual activity (in identified situational con-\ntexts or, if generalized, in all contexts):\n1. Marked difficulty in obtaining an erection during sexual activity.\n2. Marked difficulty in maintaining an erection until the completion of sexual activity.\n3. Marked decrease in erectile rigidity.\nB. The symptoms in Criterion A have persist ed for a minimum duration of approximately\n6 months.\nC. The symptoms in Criterion A cause clinically significant distress in the individual.\nD. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a\nconsequence of severe relationship distress or other significant stressors and is not at-\ntributable to the effects of a substance/medication or another medical condition.\nSpecify whether:\nLifelong: The disturbance has been present since the individual became sexually ac-\ntive.\nAcquired: The disturbance began after a period of relatively normal sexual function.\nSpecify whether:\nGeneralized: Not limited to certain types of stimulation, situations, or partners.\nSituational: Only occurs with certain types of stimulation, situations, or partners.", "source": "dsm5.pdf"} {"id": "92589cad5391-0", "page_content": "Erectile Disorder 427\nSpecify current severity:\nMild: Evidence of mild distress over the symptoms in Criterion A.\nModerate: Evidence of moderate distress ov er the symptoms in Criterion A.\nSevere: Evidence of severe or extreme distress over the symptoms in Criterion A.\nDiagnostic Features\nThe essential feature of erectile disorder is the repeated failure to obtain or maintain erec-\ntions during partnered sexual activities (Crite rion A). A careful sexual history is necessary\nto ascertain that the problem has been present for a significant duration of time (i.e., at least\napproximately 6 months) and occurs on the majo rity of sexual occasions (i.e., at least 75%\nof the time). Symptoms may occur only in sp ecific situations involving certain types of\nstimulation or partners, or they may occur in a generalized manner in all types of situa-\ntions, stimulatio n, or partners. \nAssociated Features Supporting Diagnosis\nMany men with erectile disorder may have lo w self-esteem, low self-c onfidence, and a de-\ncreased sense of masculinity, and may experience depressed affect. Fear and/or avoid-\nance of future sexual encounters may occu r. Decreased sexual satisfaction and reduced\nsexual desire in the individual\u2019s partner are common. \nIn addition to the subtypes \u201clifelong/acqu ired\u201d and \u201cgeneralized/situational,\u201d the fol-\nlowing five factors must be considered during assessment and diagnosis of erectile disorder\ngiven that they may be relevant to etiology and/or treatment: 1) partner factors (e.g., part-\nner\u2019s sexual problems, partner\u2019s health status); 2) relationship factors (e.g., poor communi-\ncation, discrepancies in desire for sexual activity); 3) in dividual vulnerability factors (e.g.,", "source": "dsm5.pdf"} {"id": "92589cad5391-1", "page_content": "poor body image, history of sexual or emotional abuse), psychiatric comorbidity (e.g., de-\npression, anxiety), or stressors (e.g., job loss, bereavement); 4) cultural/religious factors (e.g.,\ninhibitions related to prohibitions against sexual activity; attitudes toward sexuality); and\n5) medical factors relevant to prognosis, cour se, or treatment. Each of these factors may con-\ntribute differently to the pr esenting symptoms of differe nt men with this disorder. \nPrevalence\nThe prevalence of lifelong vers us acquired erectile disorder is unknown. There is a strong\nage-related increase in both prevalence and incidence of problems with erection, particu-\nlarly after age 50 years. Approximately 13%\u201321% of men ages 40\u201380 years complain of oc-\ncasional problems with erections. Approxim ately 2% of men younger than age 40\u201350 years\ncomplain of frequent problems with erecti ons, whereas 40%\u201350% of men older than 60\u201370\nyears may have significant problems with erec tions. About 20% of me n fear erectile prob-\nlems on their first sexual experience, wherea s approximately 8% experienced erectile prob-\nlems that hindered penetration duri ng their first sexual experience.\nDevelopment and Course \nErectile failure on first sexual attempt has been found to be related to having sex with a pre-\nviously unknown partner, concomit ant use of drugs or alcohol, not wanting to have sex, and\npeer pressure. There is minimal evidence rega rding the persistence of such problems after\nthe first attempt. It is assumed that most of these problems spontane ously remit without pro-\nfessional intervention, but some men may contin ue to have episodic problems. In contrast,", "source": "dsm5.pdf"} {"id": "92589cad5391-2", "page_content": "fessional intervention, but some men may contin ue to have episodic problems. In contrast,\nacquired erectile disorder is of ten associated with biological factors such as diabetes and car-\ndiovascular disease. Acquired er ectile disorder is likely to be persistent in most men.\nThe natural history of lifelong erectile disorder is unknown. Clinical observation sup-\nports the association of lifelong erectile diso rder with psychological factors that are self-", "source": "dsm5.pdf"} {"id": "c6a638180e11-0", "page_content": "428 Sexual Dysfunctions\nlimiting or responsive to ps ychological interventions, wher eas, as noted above, acquired\nerectile disorder is more likely to be related to biological factors and to be persistent. The\nincidence of erectile disorder increases with age. A minority of men diagnosed as having\nmoderate erectile failure ma y experience spontaneous remission of symptoms without\nmedical intervention. Distress as sociated with erectile disord er is lower in older men as\ncompared with younger men.\nRisk and Prognostic Factors\nTemperamental. Neurotic personality traits may be associated with erectile problems in col-\nlege students, and submissive personality traits may be associated with erectile problems in\nmen age 40 years and older. Alexithymia (i.e., deficits in cognitive processing of emotions) is\ncommon in men diagnosed with \u201cpsychogenic\u201d er ectile dysfunction. Erectile problems are\ncommon in men diagnosed with depression and posttraumatic stress disorder.\nCourse modifiers. Risk factors for acquired erectile disorder include age, smoking to-\nbacco, lack of physical exercise, diabetes, and decreased desire.\nCulture-Related Diagnostic Issues\nComplaints of erectile disorder have been foun d to vary across countries. It is unclear to\nwhat extent these differences represent differ ences in cultural expectations as opposed to\ngenuine differences in the fr equency of erectile failure.\nDiagnostic Markers\nNocturnal penile tumescence testing and meas ured erectile turgidity during sleep can be\nemployed to help differentiate organic from psychogenic erectile problems on the as-\nsumption that adequate erections during ra pid eye movement sleep indicate a psycholog-\nical etiology to the problem. A number of other diagnostic procedures may be employed\ndepending on the clinician\u2019s assessment of their relevance given the individual\u2019s age, co-", "source": "dsm5.pdf"} {"id": "c6a638180e11-1", "page_content": "depending on the clinician\u2019s assessment of their relevance given the individual\u2019s age, co-\nmorbid medical problems, and clinical pres entation. Doppler ultrasonography and intra-\nvascular injection of vasoactive drugs, as we ll as invasive diagnostic procedures such as\ndynamic infusion cavernosography, can be used to assess vascular integrity. Pudendal\nnerve conduction studies, including somato sensory evoked potentials, can be employed\nwhen a peripheral neuropathy is suspected. In men also complaining of decreased sexual\ndesire, serum bioavailable or free testosterone is frequently assessed to determine if the\ndifficulty is secondary to endocrinological factors. Thyroid function may also be assessed.\nDetermination of fasting serum glucose is useful to screen for the pres ence of diabetes mel-\nlitus. The assessment of serum lipids is important, as erectile disorder in men 40 years and\nolder is predictive of the future risk of coronary artery disease.\nFunctional Consequences of Erectile Disorder\nErectile disorder can interfere with fertility and produce both indivi dual and interpersonal\ndistress. Fear and/or avoidance of sexual en counters may interfere with the ability to de-\nvelop intimate relationships.\nDifferential Diagnosis\nNonsexual mental disorders. Major depressive disorder and erectile disorder are closely\nassociated, and erectile diso rder accompanying severe de pressive disorder may occur.\nNormal erectile function. The differential should include consideration of normal erec-\ntile function in men with excessive expectations.", "source": "dsm5.pdf"} {"id": "2c104f9515ba-0", "page_content": "Female Orgasmic Disorder 429\nSubstance/medication use. Another major differential diagnosis is whether the erectile\nproblem is secondary to substa nce/medication use. An onset that coincides with the be-\nginning of substance/medication use and that dissipates with discontinuation of the sub-\nstance/medication or dose reduction is su ggestive of a substance/medication-induced\nsexual dysfunction.\nAnother medical condition. The most difficult aspect of the differential diagnosis of erec-\ntile disorder is ruling out erec tile problems that are fully explained by medical factors. Such\ncases would not receive a diagnosis of a ment al disorder. The distinction between erectile\ndisorder as a mental disorder and erectile dy sfunction as the result of another medical con-\ndition is usually unclear, and many cases will have complex, interactive biological and psy-\nchiatric etiologies. If the individual is older than 40\u201350 years and/or has concomitant\nmedical problems, the differential diagnosis should include medical etiologies, especially\nvascular disease. The presence of an organic disease known to cause erectile problems does\nnot confirm a causal relationship. For exampl e, a man with diabetes mellitus can develop\nerectile disorder in response to psychological stress. In general, erectile dysfunction due to\norganic factors is generalized and gradual in onset. An exception would be erectile problems\nafter traumatic injury to the nervous innervation of the genital organs (e.g., spinal cord injury).\nErectile problems that are situational and inco nsistent and that have an acute onset after a\nstressful life event are most often due to psychological events. An age of less than 40 years is\nalso suggestive of a psychologi cal etiology to the difficulty.\nOther sexual dysfunctions. Erectile disorder may coexist with premature (early) ejacu-\nlation and male hypoactive sexual desire disorder.", "source": "dsm5.pdf"} {"id": "2c104f9515ba-1", "page_content": "lation and male hypoactive sexual desire disorder.\nComorbidity \nErectile disorder can be comorbid with other sexual diagnoses, such as premature (early)\nejaculation and male hypoactive sexual desire disorder, as well as with anxiety and de-\npressive disorders. Erectile disorder is co mmon in men with lowe r urinary tract symptoms\nrelated to prostatic hypertrophy. Erectile diso rder may be comorbid with dyslipidemia, car-\ndiovascular disease, hypogonadism, multiple sclerosis, diabetes mellitus, and other diseases\nthat interfere with the vascular, neurological , or endocrine function necessary for normal\nerectile function.\nRelationship to Internationa l Classification of Diseases\nErectile response is coded as failure of genital response in ICD-10 (F2.2).\nFemale Orgasmic Disorder\nDiagnostic Criteria 302.73 (F52.31)\nA. Presence of either of the following symptoms and experienced on almost all or all (ap-\nproximately 75%\u2013100%) occasions of sexual ac tivity (in identified situational contexts\nor, if generalized, in all contexts):\n1. Marked delay in, marked infrequency of, or absence of orgasm.\n2. Markedly reduced intensity of orgasmic sensations.\nB. The symptoms in Criterion A have persist ed for a minimum duration of approximately\n6 months.\nC. The symptoms in Criterion A cause clinically significant distress in the individual.\nD. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a\nconsequence of severe relationship distress (e.g., partner violence) or other significant", "source": "dsm5.pdf"} {"id": "13dd287ab742-0", "page_content": "430 Sexual Dysfunctions\nstressors and is not attributable to the effects of a substance/medication or another\nmedical condition.\nSpecify whether:\nLifelong: The disturbance has been present since the individual became sexually active.\nAcquired: The disturbance began after a period of relatively normal sexual function.\nSpecify whether:\nGeneralized: Not limited to certain types of stimulation, situations, or partners.\nSituational: Only occurs with certain types of stimulation, situations, or partners.\nSpecify if:\nNever experienced an orgasm under any situation.\nSpecify current severity:\nMild: Evidence of mild distress over the symptoms in Criterion A.\nModerate: Evidence of moderate distress ov er the symptoms in Criterion A.\nSevere: Evidence of severe or extreme distress over the symptoms in Criterion A. \nDiagnostic Features \nFemale orgasmic disorder is characterize d by difficulty experiencing orgasm and/or\nmarkedly reduced intensity of orgasmic sensat ions (Criterion A). Women show wide vari-\nability in the type or intensity of stimulation that elicits orgasm. Similarly, subjective descrip-\ntions of orgasm are extremely varied, suggesti ng that it is experienced in very different\nways, both across women and on different occasions by the same woman. For a diagnosis\nof female orgasmic disorder, symptoms must be experienced on almost all or all (approx-\nimately 75%\u2013100%) occasions of sexual activity (in identified situational contexts or, if\ngeneralized, in all contexts) and have a mi nimum duration of approximately 6 months.\nThe use of the minimum severity and duration criteria is intended to distinguish transient\norgasm difficulties from more persistent orgasmic dysfunction. The inclusion of \u201capprox-\nimately\u201d in Criterion B allows for clinician judgment in cases in which symptom duration\ndoes not meet the recommended 6-month threshold.", "source": "dsm5.pdf"} {"id": "13dd287ab742-1", "page_content": "does not meet the recommended 6-month threshold.\nFor a woman to have a diagnosis of female or gasmic disorder, clinically significant dis-\ntress must accompany the symptoms (Criterion C). In many cases of orgasm problems, the\ncauses are multifactorial or cannot be determined. If female org asmic disorder is deemed\nto be better explained by another mental diso rder, the effects of a substance/medication,\nor a medical condition, then a diagnosis of fe male orgasmic disorder would not be made.\nFinally, if interpersonal or significant contextual factors, such as severe relationship dis-\ntress, intimate partner violence, or other signi ficant stressors, are present, then a diagnosis\nof female orgasmic diso rder would not be made.\nMany women require clitoral stimulation to reach orgasm, and a relatively small pro-\nportion of women report that they always ex perience orgasm during penile-vaginal inter-\ncourse. Thus, a woman\u2019s experiencing orgasm through clitoral stim ulation but not during\nintercourse does not meet criteria for a clinic al diagnosis of female orgasmic disorder. It is\nalso important to consider whether orgasmic difficulties are the result of inadequate sex-\nual stimulation; in these cases, there may still be a need for care, but a diagnosis of female\norgasmic disorder would not be made.\nAssociated Features Supporting Diagnosis \nAssociations between specific patterns of personality traits or psychopathology and orgas-\nmic dysfunction have generally not been su pported. Compared with women without the\ndisorder, some women with female orgasmic disorder may have greater difficulty com-\nmunicating about sexual issues. Overall sexual satisfaction, however, is not strongly cor-\nrelated with orgasmic experien ce. Many women report high le vels of sexual satisfaction", "source": "dsm5.pdf"} {"id": "e85df0824f15-0", "page_content": "Female Orgasmic Disorder 431\ndespite rarely or never experiencing orgasm . Orgasmic difficulties in women often co-\noccur with problems related to sexual interest and arousal.\nIn addition to the subtypes \u201clifelong/acquired\u201d and \u201cgeneralized/situational,\u201d the fol-\nlowing five factors must be considered during assessment and diagnosis of female orgas-\nmic disorder given that they may be relevant to etiology and/or treatment: 1) partner\nfactors (e.g., partner\u2019s sexual problems, partner\u2019s health status); 2) relationship factors\n(e.g., poor communication, discre pancies in desire for sexual activity); 3) individual vul-\nnerability factors (e.g., poor body image, history of sexual or emotional abuse), psychiatric\ncomorbidity (e.g., depression, anxiety), or st ressors (e.g., job loss, bereavement); (4) cul-\ntural/religious factors (e.g., inhibitions relate d to prohibitions against sexual activity;\nattitudes toward sexuality); and 5) medical fact ors relevant to prognosis, course, or treat-\nment. Each of these factors may contribute differently to the presenting symptoms of dif-\nferent women with this disorder. \nPrevalence \nReported prevalence rates for female orgasmic problems in women vary widely, from 10%\nto 42%, depending on multiple factors (e.g., ag e, culture, duration, and severity of symp-\ntoms); however, these estimates do not take into account the presence of distress. Only a\nproportion of women experiencing orgasm di fficulties also report associated distress.\nVariation in how symptoms are assessed (e.g., the duration of symptoms and the recall pe-\nriod) also influence prevalence rates. Approx imately 10% of women do not experience or-", "source": "dsm5.pdf"} {"id": "e85df0824f15-1", "page_content": "gasm throughout their lifetime. \nDevelopment and Course \nBy definition, lifelong female orgasmic disorder indicates that the orgasmic difficulties have\nalways been present, whereas the acquired subtype would be assigned if the woman\u2019s or-\ngasmic difficulties developed after a pe riod of normal orgasmic functioning. \nA woman\u2019s first experience of orgasm can occur any time from the prepubertal period\nto well into adulthood. Women show a more variable pattern in age at first orgasm than do\nmen, and women\u2019s reports of having experien ced orgasm increase with age. Many women\nlearn to experience orgasm as they experien ce a wide variety of stimulation and acquire\nmore knowledge about their bodies. Women\u2019s rates of orgasm consistency (defined as\n\u201cusually or always\u201d experiencing orgasm) are higher during masturbation than during\nsexual activity with a partner. \nRisk and Prognostic Factors \nTemperamental. A wide range of psychological factors, such as anxiety and concerns\nabout pregnancy, can potentially interfere wi th a woman\u2019s ability to experience orgasm.\nEnvironmental. There is a strong association betw een relationship problems, physical\nhealth, and mental health and orgasm difficulties in women. Sociocultural factors (e.g.,\ngender role expectations and religious norms) are also important influences on the expe-\nrience of orgasmic difficulties.\nGenetic and physiological. Many physiological factors may influence a woman\u2019s expe-\nrience of orgasm, including medical conditio ns and medications. Conditions such as mul-\ntiple sclerosis, pelvic nerve da mage from radical hysterectomy, and spinal cord injury can\nall influence orgasmic functioning in women. Selective serotonin reuptake inhibitors are\nknown to delay or inhibit orgasm in women. Women with vulvovaginal atrophy (charac-\nterized by symptoms such as vaginal dryness, itching, and pain) are significantly more", "source": "dsm5.pdf"} {"id": "e85df0824f15-2", "page_content": "terized by symptoms such as vaginal dryness, itching, and pain) are significantly more\nlikely to report orgasm difficulties than are women without this condition. Menopausal\nstatus is not consistently associated with the likelihood of orgasm difficulties. There may\nbe a significant genetic contribution to vari ation in female orgasmic function. However,", "source": "dsm5.pdf"} {"id": "a8465d2febfd-0", "page_content": "432 Sexual Dysfunctions\npsychological, sociocultural, and physiological factors likely interact in complex ways to\ninfluence women\u2019s experience of orgasm and of orgasm difficulties. \nCulture-Related Diagnostic Issues \nThe degree to which lack of orgasm in women is regarded as a problem that requires treat-\nment may vary depending on cultural context. In addition, women differ in how important\norgasm is to their sexual satisfaction. Ther e may be marked sociocultural and generational\ndifferences in women\u2019s orgasmic ability. For example, the prevalence of inability to reach or-\ngasm has ranged from 17.7% (in Northern Europe) to 42.2% (i n Southeast Asia). \nDiagnostic Markers \nAlthough measurable physiological change s occur during female orgasm, including\nchanges in hormones, pelvic floor musculature, and brain activation, there is significant\nvariability in these indicators of orgasm across women. In clinical situations, the diagnosis\nof female orgasmic disorder is based on a woman\u2019s self-report.\nFunctional Consequences of Female Orgasmic Disorder \nThe functional consequences of female orgasmic disorder are unclear. Although there is a\nstrong association between relationship proble ms and orgasmic difficulties in women, it is\nunclear whether relationship factors are risk fa ctors for orgasmic difficulties or are conse-\nquences of those difficulties.\nDifferential Diagnosis\nNonsexual mental disorders. Nonsexual mental disorders, such as major depressive\ndisorder, which is characterized by markedly dimi nished interest or pleasure in all, or al-\nmost all, activities, may explain female orgasm ic disorder. If the orgasmic difficulties are\nbetter explained by another me ntal disorder, then a diagnosis of female orgasmic disorder\nwould not be made. \nSubstance/medication-induced sexual dysfunction. Substance/medication use may\nexplain the orgasmic difficulties.", "source": "dsm5.pdf"} {"id": "a8465d2febfd-1", "page_content": "explain the orgasmic difficulties.\nAnother medical condition. If the disorder is due to an other medical condition (e.g.,\nmultiple sclerosis, spinal cord injury), then a diagnosis of female orgasmic disorder would\nnot be made. \nInterpersonal factors. If interpersonal or significant co ntextual factors, such as severe\nrelationship distress, intimate partner violen ce, or other significant stressors, are associ-\nated with the orgasmic difficulties, then a diagnosis of female orgasmic disorder would\nnot be made.\nOther sexual dysfunctions. Female orgasmic disorder may occur in association with other\nsexual dysfunctions (e.g., female sexual intere st/arousal disorder). Th e presence of another\nsexual dysfunction does not rule out a diagnosi s of female orgasmic disorder. Occasional or-\ngasmic difficulties that are short-term or infreq uent and are not accompanied by clinically sig-\nnificant distress or impairment are not diagno sed as female orgasmic disorder. A diagnosis is\nalso not appropriate if the problems are the result of inadequate sexual stimulation. \nComorbidity\nWomen with female orgasmic disorder may have co-occurring sexu al interest/arousal\ndifficulties. Women with diagnoses of other no nsexual mental disorder s, such as major de-\npressive disorder, may experience lower sexu al interest/arousal, and this may indirectly\nincrease the likelihood of orgasmic difficulties.", "source": "dsm5.pdf"} {"id": "40c6c3d3644b-0", "page_content": "Female Sexual Interest/Arousal Disorder 433\nFemale Sexual Interest/Arousal Disorder\nDiagnostic Criteria 302.72 (F52.22)\nA. Lack of, or significantly reduced, sexual interest/arousal, as manifested by at least\nthree of the following:\n1. Absent/reduced interest in sexual activity.\n2. Absent/reduced sexual/erotic thoughts or fantasies. \n3. No/reduced initiation of sexual activity, and typically unreceptive to a partner\u2019s at-\ntempts to initiate. \n4. Absent/reduced sexual excitement/pleasure during sexual activity in\u00a0almost all or\nall (approximately 75%\u2013100%)\u00a0sexual encounters (in identified situational contexts\nor, if generalized, in all contexts).\n5. Absent/reduced sexual interest/arousal in response to any internal or external sex-\nual/erotic cues (e.g., written, verbal, visual).\n6. Absent/reduced genital or nongenital sensations during sexual activity in\u00a0almost all\nor all (approximately 75%\u2013100%)\u00a0sexual encounters (in identified situational con-\ntexts or, if generalized, in all contexts).\nB. The symptoms in Criterion A have persist ed for a minimum duration of approximately\n6 months.\nC. The symptoms in Criterion A cause clinically significant distress in the individual.\nD. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a\nconsequence of severe relationship distress (e.g., partner violence) or other significant\nstressors and is not attributable to the effects of a substance/medication or another\nmedical condition.\nSpecify whether:\nLifelong: The disturbance has been present since the individual became sexually\nactive.\nAcquired: The disturbance began after a period of relatively normal sexual function.\nSpecify whether:", "source": "dsm5.pdf"} {"id": "40c6c3d3644b-1", "page_content": "Specify whether:\nGeneralized: Not limited to certain types of stimulation, situations, or partners.\nSituational: Only occurs with certain types of stimulation, situations, or partners.\nSpecify current severity:\nMild: Evidence of mild distress over the symptoms in Criterion A.\nModerate: Evidence of moderate distress ov er the symptoms in Criterion A.\nSevere: Evidence of severe or extreme distress over the symptoms in Criterion A.\nDiagnostic Features \nIn assessing female sexual interest/arousal di sorder, interpersonal co ntext must be taken\ninto account. A \u201cdesire discrepancy,\u201d in whic h a woman has lower desire for sexual activ-\nity than her partner, is not suff icient to diagnose female sexu al interest/arousal disorder.\nIn order for the criteria for the disorder to be met, there must be absence or reduced fre-\nquency or intensity of at least three of six indicators (Criterion A) for a minimum duration\nof approximately 6 months (Criterion B). Th ere may be different symptom profiles across\nwomen, as well as variability in how sexual in terest and arousal are expressed. For exam-\nple, in one woman, sexual interest/arousal di sorder may be expressed as a lack of interest\nin sexual activity, an absence of erotic or se xual thoughts, and reluct ance to initiate sexual\nactivity and respond to a partner\u2019s sexual invi tations. In another woman, an inability to be-\ncome sexually excited, to resp ond to sexual stimuli with se xual desire, and a correspond-", "source": "dsm5.pdf"} {"id": "8c3b66d14027-0", "page_content": "434 Sexual Dysfunctions\ning lack of signs of physical sexual arousa l may be the primary features. Because sexual\ndesire and arousal frequently coex ist and are elicited in respon se to adequate sexual cues,\nthe criteria for female sexual in terest/arousal disorder take into account that difficulties in\ndesire and arousal often simult aneously characterize the co mplaints of women with this\ndisorder. Short-term changes in sexual interest or arousal are common and may be adaptive\nresponses to events in a woma n\u2019s life and do not represent a sexual dysfunction. Diagnosis\nof female sexual interest/arousal disorder requires a minimum duration of symptoms of\napproximately 6 months as a reflection that the symptoms must be a persistent problem.\nThe estimation of persistence may be determin ed by clinical judgment when a duration of\n6 months cannot be ascertained precisely.\nThere may be absent or reduced frequency or inte nsity of interest in se xual activity (Crite-\nrion A1), which was previously termed hypoactive sexual desire disorder. The frequency or inten-\nsity of sexual and erotic thoughts or fantasie s may be absent or reduced (Criterion A2). The\nexpression of fantasies varies widely across women and may include memories of past sexual\nexperiences. The normative decline in sexual thoughts with age should be taken into account\nwhen this criterion is being assessed. Absence or reduced frequency of initiating sexual activ-\nity and of receptivity to a partner\u2019s sexual invitations (Criterion A3) is a behaviorally focused\ncriterion. A couple\u2019s beliefs and preferences for sexual initiation patterns are highly relevant to\nthe assessment of this criterion. There may be ab sent or reduced sexual excitement or pleasure\nduring sexual activity in\u00a0almos t all or all (approximately 75%\u2013 100%) sexual encounters (Cri-", "source": "dsm5.pdf"} {"id": "8c3b66d14027-1", "page_content": "terion A4). Lack of pleasure is a common presenting clinical complaint in women with low de-\nsire. Among women who report low sexual desire , there are fewer sexual or erotic cues that\nelicit sexual interest or arousal (i.e., there is a lack of \u201cresponsive desire\u201d). Assessment of the\nadequacy of sexual stimuli will assist in determining if there is a difficulty with responsive sex-\nual desire (Criterion A5). Freque ncy or intensity of genital or nongenital sensations during sex-\nual activity may be reduced or absent (Crite rion A6). This may include reduced vaginal\nlubrication/vasocongestion, but because physiological measures of genital sexual response do\nnot differentiate women who report sexual arousal concerns from those who do not, the self-\nreport of reduced or absent genital or nongenital sensations is sufficient. \nFor a diagnosis of female sexual interest/arousal disorder to be made, clinically signif-\nicant distress must accompany the symptoms in Criterion A. Distress may be experienced\nas a result of the lack of sexual interest/arousal or as a result of significant interference in\na woman\u2019s life and well-being. If a lifelong lack of sexual desire is better explained by one\u2019s\nself-identification as \u201casexual,\u201d then a diagnosis of female sexual interest/arousal disor-\nder would not be made.\nAssociated Features Supporting Diagnosis \nFemale sexual interest/arousal disorder is fr equently associated with problems in experi-\nencing orgasm, pain experienced during sexual activity, infrequent sexual activity, and\ncouple-level discrepancies in desire. Relationship difficulties and mood disorders are also\nfrequently associated features of female sexual interest/arousal disorder. Unrealistic ex-\npectations and norms regarding the \u201cappropriate\u201d level of sexual intere st or arousal, along", "source": "dsm5.pdf"} {"id": "8c3b66d14027-2", "page_content": "pectations and norms regarding the \u201cappropriate\u201d level of sexual intere st or arousal, along\nwith poor sexual techniques and lack of info rmation about sexuality, may also be evident\nin women diagnosed with female sexual interest/arousal disorder. The latter, as well as\nnormative beliefs about gender roles, are importan t factors to consider.", "source": "dsm5.pdf"} {"id": "993ed7f16962-0", "page_content": "in women diagnosed with female sexual interest/arousal disorder. The latter, as well as\nnormative beliefs about gender roles, are importan t factors to consider.\nIn addition to the subtypes \u201clifelong/acquired\u201d and \u201cgeneralized/situational,\u201d the follow-\ning five factors must be considered during asse ssment and diagnosis of female sexual interest/\narousal disorder given that they may be relevant to etiology and/or treatment: 1) partner fac-\ntors (e.g., partner\u2019s sexual prob lems, partner\u2019s health status); 2) relationship factors (e.g., poor\ncommunication, discrepancies in de sire for sexual activity); 3) individual vulnerability factors\n(e.g., poor body image, history of sexual or emotional abuse), ps ychiatric comorbidity (e.g., de-\npression, anxiety), or stressors (e.g., job loss, bereavement); 4) cultural/religious factors (e.g.,\ninhibitions related to prohibitions against sexu al activity; attitudes toward sexuality); and", "source": "dsm5.pdf"} {"id": "706f68f43ef3-0", "page_content": "Female Sexual Interest/Arousal Disorder 435\n5) medical factors relevant to pr ognosis, course, or treatment. Note that each of these factors\nmay contribute differently to the presenting sy mptoms of different women with this disorder.\nPrevalence \nThe prevalence of female sexual interest/arousal disorder, as defined in this manual, is\nunknown. The prevalence of low sexual desire and of problems with sexual arousal (with\nand without associated distress), as defined by DSM-IV or ICD-10, may vary markedly in\nrelation to age, cultural setting, duration of symptoms, and presence of distress. Regard-\ning duration of symptoms, there are striking differences in prevalence estimates between\nshort-term and persistent problems related to lack of sexual intere st. When distress about\nsexual functioning is requir ed, prevalence estimates are markedly lower. Some older\nwomen report less distress ab out low sexual desire than y ounger women, although sexual\ndesire may decrease with age. \nDevelopment and Course \nBy definition, lifelong female sexual interest /arousal disorder suggests that the lack of\nsexual interest or arousal has been present fo r the woman\u2019s entire sexual life. For Criteria\nA3, A4, and A6, which assess functioning duri ng sexual activity, a subtype of lifelong\nwould mean presence of symptoms since the in dividual\u2019s first sexual experiences. The ac-\nquired subtype would be assigned if the difficu lties with sexual interest or arousal de-\nveloped after a period of nonproblematic se xual functioning. Adaptive and normative\nchanges in sexual functioning may result from partner-related, interpersonal, or personal\nevents and may be transient in nature. Howe ver, persistence of symptoms for approxi-\nmately 6 months or more would constitute a sexual dysfunction.\nThere are normative changes in sexual interest and arousal across the life span. Fur-", "source": "dsm5.pdf"} {"id": "706f68f43ef3-1", "page_content": "There are normative changes in sexual interest and arousal across the life span. Fur-\nthermore, women in relationships of longer du ration are more likely to report engaging in\nsex despite no obvious feelings of sexual desi re at the outset of a sexual encounter com-\npared with women in shorter-duration relationships. Vaginal dryness in older women is\nrelated to age and menopausal status. \nRisk and Prognostic Factors \nTemperamental. Temperamental factors include negati ve cognitions and attitudes about\nsexuality and past history of mental disorders. Differences in propensity for sexual excitation\nand sexual inhibition may also predict the likelihood of developi ng sexual problems.\nEnvironmental. Environmental factors include relationship difficulties, partner sexual\nfunctioning, and developmental history, such as early relationships with caregivers and\nchildhood stressors. \nGenetic and physiological. Some medical conditions (e.g., diabetes mellitus, thyroid\ndysfunction) can be risk factors for female se xual interest/arousal disorder. There appears\nto be a strong influence of genetic factors on vulnerability to sexual problems in women.\nPsychophysiological research using vaginal photoplethysmography has not found differ-\nences between women with and without perceived lack of genital arousal.\nCulture-Related Diagnostic Issues \nThere is marked variability in prevalence rates of low desire across cultures. Lower rates of\nsexual desire may be more common among East Asian women compared with Euro-\nCanadian women. Although the lower levels of sexual desire and arousal found in men\nand women from East Asian countries compared with Euro-American groups may reflect\nless interest in sex in those cultures, the possibility remains that such group differences are\nan artifact of the measures used to quanti fy desire. A judgment about whether low sexual", "source": "dsm5.pdf"} {"id": "dab1beee4e45-0", "page_content": "436 Sexual Dysfunctions\ndesire reported by a woman from a certain ethnocultural group meets criteria for female\nsexual interest/arousal disorder must take into account the fact that different cultures may\npathologize some behaviors and not others.\nGender-Related Diagnostic Issues\nBy definition, the diagnosis of female sexual interest/arousal disorder is only given to\nwomen. Distressing difficulties with sexual desire in men would be considered under\nmale hypoactive sexual desire disorder.\nFunctional Consequences of \nFemale Sexual Intere st/Arousal Disorder \nDifficulties in sexual interest/a rousal are often associated with decreased relationship sat-\nisfaction.\nDifferential Diagnosis \nNonsexual mental disorders. Nonsexual mental disorders, such as major depressive\ndisorder, in which there is \u201cmarkedly diminished interest or pleasure in all, or almost all,\nactivities most of the day, nearly every day,\u201d may explain the lack of sexual interest/\narousal. If the lack of interest or arousal is completely attributable to another mental dis-\norder, then a diagnosis of female sexual in terest/arousal disorder would not be made.\nSubstance/medication use. Substance or medication use may explain the lack of inter-\nest/arousal.\nAnother medical condition. If the sexual symptoms are co nsidered to be almost exclu-\nsively associated with the effe cts of another medical conditio n (e.g., diabetes mellitus, en-\ndothelial disease, thyroid dysfunction, centra l nervous system diseas e), then a diagnosis\nof female sexual inte rest/arousal disorder would not be made. \nInterpersonal factors. If interpersonal or significant co ntextual factors, such as severe\nrelationship distress, intimate partner violence , or other significant stressors, explain the", "source": "dsm5.pdf"} {"id": "dab1beee4e45-1", "page_content": "relationship distress, intimate partner violence , or other significant stressors, explain the\nsexual interest/arousal symptoms, then a diag nosis of female sexual interest/arousal dis-\norder would not be made.\nOther sexual dysfunctions. The presence of another sexu al dysfunction does not rule\nout a diagnosis of female sexual interest/arousal disorder. It is common for women to ex-\nperience more than one sexual dysfunction. For example, the presence of chronic genital\npain may lead to a lack of desire for the (p ainful) sexual activity. Lack of interest and\narousal during sexual activity may impair or gasmic ability. For some women, all aspects\nof the sexual response may be unsatisfying and distressing.\nInadequate or absent sexual stimuli. When differential diagnoses are being considered,\nit is important to assess the adequacy of se xual stimuli within the woman\u2019s sexual experi-\nence. In cases where inadequate or absent sexual stimuli are co ntributing to the clinical pic-\nture, there may be evidence for clinical care , but a sexual dysfunction diagnosis would not\nbe made. Similarly, transient and adaptive alte rations in sexual functioning that are second-\nary to a significant life or personal event must be considered in the differential diagnosis.\nComorbidity\nComorbidity between sexual interest/arousal problems and other sexual difficulties is\nextremely common. Sexual distress and dissatis faction with sex life are also highly cor-\nrelated in women with low sexual desire. Dist ressing low desire is associated with depres-\nsion, thyroid problems, anxiety, urinary incontinence, and other medical factors. Arthritis\nand inflammatory or i rritable bowel disease are also associated with sexual arousal prob-", "source": "dsm5.pdf"} {"id": "75e8bce31cc4-0", "page_content": "Genito-Pelvic Pain/Penetration Disorder 437\nlems. Low desire appears to be comorbid wi th depression, sexual and physical abuse in\nadulthood, global mental functioning, and use of alcohol. \nGenito-Pelvic Pain/Penetration Disorder\nDiagnostic Criteria 302.76 (F52.6)\nA. Persistent or recurrent difficulties with one (or more) of the following:\n1. Vaginal penetration during intercourse.\n2. Marked vulvovaginal or pelvic pain during vaginal intercourse or penetration attempts. \n3. Marked fear or anxiety about vulvovaginal or pelvic pain in anticipation of, during,\nor as a result of vaginal penetration.\n4. Marked tensing or tightening of the pelvic floor muscles during attempted vaginal\npenetration.\nB. The symptoms in Criterion A have persist ed for a minimum duration of approximately\n6 months.\nC. The symptoms in Criterion A cause clinically significant distress in the individual.\nD. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a\nconsequence of a severe relationship distress (e.g., partner violence) or other signifi-\ncant stressors and is not attributable to the effects of a substance/medication or an-\nother medical condition.\nSpecify whether:\nLifelong: The disturbance has been present since the individual became sexually active.\nAcquired: The disturbance began after a period of relatively normal sexual function.\nSpecify current severity:\nMild: Evidence of mild distress over the symptoms in Criterion A.\nModerate: Evidence of moderate distress ov er the symptoms in Criterion A.\nSevere: Evidence of severe or extreme distress over the symptoms in Criterion A.\nDiagnostic Features \nGenito-pelvic pain/penetration disorder refe rs to four commonly comorbid symptom di-", "source": "dsm5.pdf"} {"id": "75e8bce31cc4-1", "page_content": "mensions: 1) difficulty having in tercourse, 2) genito-pelvic pain , 3) fear of pain or vaginal\npenetration, and 4) tension of the pelvic fl oor muscles (Criterion A). Because major diffi-\nculty in any one of these symptom dimensions is often sufficient to cause clinically sig-\nnificant distress, a diagnosis can be made on the basis of marked difficulty in only one\nsymptom dimension. However, a ll four symptom dimensions should be assessed even if a\ndiagnosis can be made on the basis of only one symptom dimension. \nMarked difficulty having vaginal intercourse/penetration (Criterion A1) can vary from a total in-\nability to experience vaginal penetration in an y situation (e.g., interc ourse, gynecological ex-\naminations, tampon insertion) to the ability to easily experience penetration in one situation\nand but not in another. Although the most comm on clinical situation is when a woman is un-\nable to experience intercourse or penetration with a partner, difficult ies in undergoing re-\nquired gynecological examinat ions may also be present. Marked vulvovaginal or pelvic pain\nduring vaginal intercourse or penetration attempts (Criterion A2) refers to pain occurring in differ-\nent locations in the genito-pelvic area. Location of pain as well as intensity should be assessed.\nTypically, pain can be characterized as superf icial (vulvovaginal or occurring during penetra-\ntion) or deep (pelvic; i.e., not felt until deeper penetrat ion). The intensity of the pain is often not\nlinearly related to distress or interference with sexual intercourse or other sexual activities.\nSome genito-pelvic pain only occurs when provoked (i.e., by intercourse or mechanical stim-", "source": "dsm5.pdf"} {"id": "62233565208f-0", "page_content": "438 Sexual Dysfunctions\nulation); other genito-pelvic pa in may be spontaneous as well as provoked. Genito-pelvic pain\ncan also be usefully characterized qualitatively (e.g., \u201cburning,\u201d \u201ccutting,\u201d \u201cshooting,\u201d \u201cthrob-\nbing\u201d). The pain may persist for a period afte r intercourse is completed and may also occur\nduring urination. Typically, the pain experience d during sexual intercourse can be reproduced\nduring a gynecological examination.\nMarked fear or anxiety about vulvov aginal or pelvic pain either in anticipation of, or during, or\nas a result of vaginal penetration (Criterion A3) is commonly reported by women who have\nregularly experienced pain during sexual inte rcourse. This \u201cnormal\u201d reaction may lead to\navoidance of sexual/intimate situations. In ot her cases, this marked fear does not appear\nto be closely related to the experience of pa in but nonetheless leads to avoidance of inter-\ncourse and vaginal penetration situations. Some have describe d this as similar to a phobic\nreaction except that the phobic object may be vaginal penetration or the fear of pain.\nMarked tensing or tightening of the pelvic floor muscles during attempted vaginal penetration\n(Criterion A4) can vary from reflexive-like spasm of the pelvic floor in response to at-\ntempted vaginal entry to \u201cnormal/voluntary\u201d muscle guarding in response to the antici-\npated or the repeated experience of pain or to fear or anxiety. In the case of \u201cnormal/\nguarding\u201d reactions, penetratio n may be possible under circumstances of relaxation. The\ncharacterization and assessment of pelvic floo r dysfunction is often best undertaken by a\nspecialist gynecologist or by a pelvic floor physical therapist. \nAssociated Features Supporting Diagnosis", "source": "dsm5.pdf"} {"id": "62233565208f-1", "page_content": "Associated Features Supporting Diagnosis \nGenito-pelvic pain/penetration di sorder is frequently associated with other sexual dysfunc-\ntions, particularly reduced sexual desire and interest (female sexual interest/arousal disor-\nder). Sometimes desire and interest are preserved in sexual situations that are not painful or\ndo not require penetration. Even when indivi duals with geni to-pelvic pain/p enetration dis-\norder report sexual interest/mot ivation, there is of ten behavioral avoidance of sexual situ-\nations and opportunities. Avoidance of gynecological examinations despite medical\nrecommendations is also frequen t. The pattern of avoidance is si milar to that seen in phobic\ndisorders. It is common for women who have no t succeeded in having sexual intercourse to\ncome for treatment only when they wish to conceive. Many women wi th genito-pelvic pain/\npenetration disorder will experience associated relationship/marital problems; they also of-\nten report that the symptoms significantly diminish their fee lings of femininity. \nIn addition to the subtype \u201clifelong/acquired,\u201d five factors should be considered dur-\ning assessment and diagnosis of genito-pelvi c pain/penetration di sorder because they\nmay be relevant to etiology and/or treatmen t: 1) partner factors (e.g., partner\u2019s sexual\nproblems, partner\u2019s health status); 2) relationship factors (e.g., poor communication, dis-\ncrepancies in desire for sexual activity); 3) individual vulnerability factors (e.g., poor body\nimage, history of sexual or emotional abuse), psychiatric comorbidity (e.g., depression,\nanxiety), or stressors (e.g., job loss, bereavemen t); 4) cultural/religious factors (e.g., inhi-", "source": "dsm5.pdf"} {"id": "62233565208f-2", "page_content": "bitions related to prohibitions against sexual activity; attitudes toward sexuality); and\n5) medical factors relevant to prognosis, cour se, or treatment. Each of these factors may\ncontribute differently to the presenting symp toms of different women with this disorder.\nThere are no valid physiological measures of any of the component symptom dimen-\nsions of genito-pelvic pain/penetration diso rder. Validated psychome tric inventories may\nbe used to formally assess the pain and anxiety components related to genito-pelvic pain/\npenetration disorder.\nPrevalence", "source": "dsm5.pdf"} {"id": "bb9418393cf5-0", "page_content": "be used to formally assess the pain and anxiety components related to genito-pelvic pain/\npenetration disorder.\nPrevalence \nThe prevalence of genito-pelvic pain/penetration disorder is unknown. Howe ver, approx-\nimately 15% of women in North America report recurrent pain during intercourse. Diffi-\nculties having intercourse appear to be a freque nt referral to sexual dysfunction clinics and\nto specialist clinicians.", "source": "dsm5.pdf"} {"id": "640e04d1ce20-0", "page_content": "Genito-Pelvic Pain/Penetration Disorder 439\nDevelopment and Course \nThe development and course of genito-pelvic pa in/penetration disorder is unclear. Because\nwomen generally do not seek treatment until they experience problems in sexual functioning,\nit can, in general, be difficult to characterize genito-pelvic pain/penetration disorder as life-\nlong (primary) or acquired (secondary). Alth ough women typically come to clinical atten-\ntion after the initiation of sexual activity, there are often earlier clinical signs. For example,\ndifficulty with or the avoidanc e of use of tampons is an important predictor of later problems.\nDifficulties with vaginal penetration (inability or fear or pain) may not be obvious until sex-\nual intercourse is attempted. Ev en once intercourse is attemp ted, the frequency of attempts\nmay not be significant or regular. In cases where it is difficult to establish whether symptom-\natology is lifelong or acquired, it is useful to determine the presence of any consistent period\nof successful pain-, fear-, and tension-free intercourse. If the ex perience of such a period can\nbe established, then genito-pelvic pain/penet ration disorder can be characterized as ac-\nquired. Once symptomatology is well establishe d for a period of approximately 6 months,\nthe probability of spontaneous and significan t symptomatic remission appears to diminish.\nComplaints related to genito-pelvic pain pe ak during early adulthood and in the peri-\nand postmenopausal period. Women with compla ints about difficulty having intercourse\nappear to be primarily premenopausal. There may also be an increa se in genito-pelvic\npain\u2013related symptoms in the postpartum period.\nRisk and Prognostic Factors", "source": "dsm5.pdf"} {"id": "640e04d1ce20-1", "page_content": "Risk and Prognostic Factors \nEnvironmental. Sexual and/or physical abuse have often been cited as predictors of the\nDSM-IV-defined sexual pain di sorders dyspareunia and vaginismus. This is a matter of con-\ntroversy in the current literature.\nGenetic and physiological. Women experiencing superficial pain during sexual inter-\ncourse often report the onset of the pain after a history of vaginal infections. Even after the in-\nfections have resolved and there are no known residual physical findings, the pain persists.\nPain during tampon insertion or the inability to insert tampons before any sexual contact has\nbeen attempted is an importan t risk factor for genito-pelvic pain/penetration disorder.\nCulture-Related Diagnostic Issues \nIn the past, inadequate sexual education and religious orthodoxy have often been consid-\nered to be culturally related predisposing fa ctors to the DSM-IV diagnosis of vaginismus.\nThis perception appears to be confirmed by recent reports from Turkey, a primarily Mus-\nlim country, indicating a strikingly high prev alence for the disorder. However, most avail-\nable research, although limited in scope, does not support this notion (Lahaie et al. 2010). \nGender-Related Diagnostic Issues\nBy definition, the diagnosis of genito-pelvic pain/penetration disorder is only given to\nwomen. There is relatively new research concerning urological chronic pelvic pain syn-\ndrome in men, suggesting that men may expe rience some similar problems. The research\nand clinical experience are not sufficiently de veloped yet to justify the application of this\ndiagnosis to men. Other specified sexual dy sfunction or unspecified sexual dysfunction\nmay be diagnosed in men appearing to fit this pattern.\nFunctional Consequences of \nGenito-Pelvic Pain/Penetration Disorder", "source": "dsm5.pdf"} {"id": "640e04d1ce20-2", "page_content": "Functional Consequences of \nGenito-Pelvic Pain/Penetration Disorder\nFunctional difficulties in ge nito-pelvic pain/pen etration disorder are often associated\nwith interference in relationship satisfacti on and sometimes with the ability to conceive\nvia penile/vaginal intercourse.", "source": "dsm5.pdf"} {"id": "2d07e16668f2-0", "page_content": "440 Sexual Dysfunctions\nDifferential Diagnosis\nAnother medical condition. In many instances, women with genito-pelvic pain/pene-\ntration disorder will also be diagnosed with another medical condition (e.g., lichen scle-\nrosus, endometriosis, pelvic inflammatory disease, vulvovaginal atrophy). In some cases,\ntreating the medical condition may alleviate the genito-pelvic pain/penetration disorder.\nMuch of the time, this is not the case. There are no reliable tools or diagnostic methods to\nallow clinicians to know whether the medica l condition or genito-pelvic pain/penetration\ndisorder is primary. Often, the associated medi cal conditions are difficult to diagnose and\ntreat. For example, the increased incidence of postmenopausal pain during intercourse\nmay sometimes be attributable to vaginal dr yness or vulvova ginal atrophy as sociated with\ndeclining estrogen levels. The relationship, however, between vulv ovaginal atrophy/dry-\nness, estrogen, and pain is not well understood. \nSomatic symptom and related disorders. Some women with genito-pelvic pain/pene-\ntration disorder may also be diagnosable with somatic symptom disorder. Since both\ngenito-pelvic pain/penetration disorder and the somatic symptom and related disorders\nare new diagnoses, it is not yet clear whet her they can be reliably differentiated. Some\nwomen diagnosed with genito-pelvic pain/penetration disorder will also be diagnosed\nwith a specific phobia. \nInadequate sexual stimuli. It is important that the clinician, in considering differential diag-\nnoses, assess the adequacy of se xual stimuli within the woman\u2019s sexual experience. Sexual sit-\nuations in which there is inadequate foreplay or arousal may lead to difficulties in penetration,", "source": "dsm5.pdf"} {"id": "2d07e16668f2-1", "page_content": "uations in which there is inadequate foreplay or arousal may lead to difficulties in penetration,\npain, or avoidance. Erectile dysfunction or premature ejacul ation in the male partner may\nresult in difficulties with penetration. These conditions should be carefully assessed. In some\nsituations, a diagnosis of genito-pelvic pain/p enetration disorder may not be appropriate. \nComorbidity\nComorbidity between genito-pel vic pain/penetration disorder and other sexual difficul-\nties appears to be common. Comorbidity with relationship distress is also common. This is\nnot surprising, since in Western cultures the inability to have (pain-free) intercourse with\na desired partner and the avoidance of sexual opportunities may be either a contributing\nfactor to or the result of other sexual or re lationship problems. Because pelvic floor symp-\ntoms are implicated in the diagnosis of geni to-pelvic pain/penetrati on disorder, there is\nlikely to be a higher prevalence of other diso rders related to the pelvic floor or reproduc-\ntive organs (e.g., interstitial cystitis, constipation, vaginal infection, endometriosis, irrita-\nble bowel syndrome).\nMale Hypoactive Sexual Desire Disorder\nDiagnostic Criteria 302.71 (F52.0)\nA. Persistently or recurrently deficient (or absent) sexual/erotic thoughts or fantasies and\ndesire for sexual activity. The judgment of deficiency is made by the clinician, taking\ninto account factors that affect sexual functioning, such as age and general and socio-\ncultural contexts of the individual\u2019s life.\nB. The symptoms in Criterion A have persist ed for a minimum duration of approximately\n6 months.\nC. The symptoms in Criterion A cause clinically significant distress in the individual.\nD. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a", "source": "dsm5.pdf"} {"id": "2d07e16668f2-2", "page_content": "D. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a\nconsequence of severe relationship distress or other significant stressors and is not at-\ntributable to thes effects of a substance/medication or another medical condition.", "source": "dsm5.pdf"} {"id": "06e74122664b-0", "page_content": "Male Hypoactive Sexual Desire Disorder 441\nSpecify whether:\nLifelong: The disturbance has been present since the individual became sexually\nactive.\nAcquired: The disturbance began after a period of relatively normal sexual function.\nSpecify whether:\nGeneralized: Not limited to certain types of stimulation, situations, or partners.\nSituational: Only occurs with certain types of stimulation, situations, or partners.\nSpecify current severity:\nMild: Evidence of mild distress over the symptoms in Criterion A.\nModerate: Evidence of moderate distress ov er the symptoms in Criterion A.\nSevere: Evidence of severe or extreme distress over the symptoms in Criterion A.\nDiagnostic Features \nWhen an assessment for male hypoactive sexu al desire disorder is being made, inter-\npersonal context must be take n into account. A \u201cdesire discrepancy,\u201d in which a man has\nlower desire for sexual activity than his partne r, is not sufficient to diagnose male hypo-\nactive sexual desire d isorder. Both low/absent desire fo r sex and deficient/absent sexual\nthoughts or fantasies are required for a diag nosis of the disorder. There may be variation\nacross men in how sexual desire is expressed. \nThe lack of desire for sex and deficient/absent erotic though ts or fantasies must be per-\nsistent or recurrent and must occur for a mi nimum duration of approximately 6 months.\nThe inclusion of this duration criterion is me ant to safeguard against making a diagnosis in\ncases in which a man\u2019s low sexual desire may represent an adaptive response to adverse\nlife conditions (e.g., concern about a partner\u2019s pregnancy when the man is considering ter-\nminating the relationship). The introduction of \u201capproximately\u201d in Criterion B allows for\nclinician judgment in cases in which sympto m duration does not meet the recommended\n6-month threshold.", "source": "dsm5.pdf"} {"id": "06e74122664b-1", "page_content": "6-month threshold.\nAssociated Features Supporting Diagnosis \nMale hypoactive sexual desire disorder is some times associated with erectile and/or ejac-\nulatory concerns. For example, persistent difficulties obtaining an erection may lead a man\nto lose interest in sexual activity. Men with hypoactive sexual desire disorder often report\nthat they no longer initiate sexual activity and that they are minima lly receptive to a part-\nner\u2019s attempt to initiate. Sexual activities (e.g ., masturbation or part nered sexual activity)\nmay sometimes occur even in the presence of low sexual desire. Relationship-specific pref-\nerences regarding patterns of sexual initiation must be taken into account when making a\ndiagnosis of male hypoactive sexual desire di sorder. Although men are more likely to ini-\ntiate sexual activity, and thus low desire may be characterized by a pattern of non-initiation,\nmany men may prefer to have their partner init iate sexual activity. In such situations, the\nman\u2019s lack of receptivity to a partner\u2019s initiati on should be considered when evaluating low\ndesire.\nIn addition to the subtypes \u201clifelong/acquired\u201d and \u201cgeneralized/situational,\u201d the fol-\nlowing five factors must be considered duri ng assessment and diagnosis of male hypo-\nactive sexual desire disorder given that they may be relevant to et iology and/or treatment:\n1) partner factors (e.g., partne r\u2019s sexual problems, partner\u2019s health status); 2) relationship\nfactors (e.g., poor communication , discrepancies in desire for sexual activity); 3) individ-\nual vulnerability factors (e.g., po or body image, history of se xual or emotional abuse), psy-\nchiatric comorbidity (e.g., depression, anxiety), or stressors (e.g., job loss, bereavement);", "source": "dsm5.pdf"} {"id": "06e74122664b-2", "page_content": "4) cultural/religious factors (e.g., inhibitions related to prohibitions against sexual activity;\nattitudes toward sexuality); and 5) medical fact ors relevant to prognosis, course, or treat-", "source": "dsm5.pdf"} {"id": "a67436aa370e-0", "page_content": "442 Sexual Dysfunctions\nment. Each of these factors may contribute differently to the presenting symptoms of dif-\nferent men with this disorder. \nPrevalence \nThe prevalence of male hypoactive sexual de sire disorder varies depending on country of\norigin and method of assess ment. Approximately 6% of younger men (ages 18\u201324 years)\nand 41% of older men (ages 66\u201374 years) have problems with sexual desire. However, a\npersistent lack of interest in sex, lasting 6 months or more, affects only a small proportion\nof men ages 16\u201344 (1.8%). \nDevelopment and Course \nBy definition, lifelong male hypoactive sexual desire disorder indicates that low or no sex-\nual desire has always been present, whereas th e acquired subtype would be assigned if the\nman\u2019s low desire developed afte r a period of normal sexual desire. There is a requirement\nthat low desire persist for approximately 6 months or more; thus, short-term changes in\nsexual desire should not be diagnosed as male hypoactive se xual desire disorder. \nThere is a normative age-related decline in se xual desire. Like women, men identify a\nvariety of triggers for their sexual desire, and they describe a wide range of reasons that\nthey choose to engage in sexual activity. Although erotic visual cues may be more potent\nelicitors of desire in younger men, the potenc y of sexual cues may decrease with age and\nmust be considered when evaluating men for hypoactive sexual desire disorder. \nRisk and Prognostic Factors \nTemperamental. Mood and anxiety symptoms appear to be strong predictors of low de-\nsire in men. Up to half of men with a past history of psychiatric symptoms may have mod-\nerate or severe loss of desire, compared with only 15% of those without such a history. A", "source": "dsm5.pdf"} {"id": "a67436aa370e-1", "page_content": "man\u2019s feelings about himself, his perception of his partner\u2019s sexual desire toward him,\nfeelings of being emotionally connected, and contextual vari ables may all negatively (as\nwell as positively) affect sexual desire.\nEnvironmental. Alcohol use may increase the occurr ence of low desire. Among gay men,\nself-directed homophobia, interp ersonal problems, attitudes, lack of adequate sex educa-\ntion, and trauma resulting from early life ex periences must be taken into account in ex-\nplaining the low desire. Social and cultural co ntextual factors should also be considered.\nGenetic and physiological. Endocrine disorders such as hyperprolactinemia signifi-\ncantly affect sexual desire in me n. Age is a significant risk fact or for low desire in men. It is\nunclear whether or not men with low desire a lso have abnormally low levels of testoster-\none; however, among hypogonadal men, low desire is common. There also may be a crit-\nical threshold below which testosterone will af fect sexual desire in men and above which\nthere is little effect of test osterone on men\u2019s desire. \nCulture-Related Diagnostic Issues \nThere is marked variability in prevalence rate s of low desire across cultures, ranging from\n12.5% in Northern European me n to 28% in Southeast Asian men ages 40\u201380 years. Just as\nthere are higher rates of low desire among East Asian subgroups of women, men of East\nAsian ancestry also have higher rates of lo w desire. Guilt about se x may mediate this as-\nsociation between East Asian ethnicity and sexual desire in men.\nGender-Related Diagnostic Issues\nIn contrast to the classification of sexual d isorders in women, desire and arousal disorders", "source": "dsm5.pdf"} {"id": "a67436aa370e-2", "page_content": "In contrast to the classification of sexual d isorders in women, desire and arousal disorders\nhave been retained as separate constructs in men. Despite some similarities in the experi-", "source": "dsm5.pdf"} {"id": "58e6419bf655-0", "page_content": "Premature (Early) Ejaculation 443\nence of desire across men and women, and the fact that desire fluctuates over time and is\ndependent on contextual factors, men do repo rt a significantly higher intensity and fre-\nquency of sexual desire compared with women.\nDifferential Diagnosis\nNonsexual mental disorders. Nonsexual mental disorders, such as major depressive\ndisorder, which is characterized by \u201cmarkedly dimi nished interest or pleasure in all, or al-\nmost all, activities,\u201d may explai n the lack of sexual desire. If the lack of desire is better\nexplained by another mental disorder, then a diagnosis of male hypoactive sexual desire\ndisorder would not be made. \nSubstance/medication use. Substance/medication use may explain the lack of sexual\ndesire.\nAnother medical condition. If the low/absent desire and de ficient/absent erotic thoughts\nor fantasies are better explained by the effect s of another medical co ndition (e.g., hypogo-\nnadism, diabetes mellitus, thyroid dysfunction, central nervous system disease), then a di-\nagnosis of male hypoactive sexual desire disorder w ould not be made. \nInterpersonal factors. If interpersonal or significant co ntextual factors, such as severe\nrelationship distress or other sig nificant stressors, are associated with the loss of desire in\nthe man, then a diagnosis of male hypoactive sexual desire disorder would not be made.\nOther sexual dysfunctions. The presence of another sexual dysfunction does not rule out a\ndiagnosis of male hypoactive sexu al desire disorder; there is some evidence that up to one-half\nof men with low sexual desire also have erecti le difficulties, and slightly fewer may also have\nearly ejaculation difficulties. If the man\u2019s low desire is explained by self-identification as an", "source": "dsm5.pdf"} {"id": "58e6419bf655-1", "page_content": "early ejaculation difficulties. If the man\u2019s low desire is explained by self-identification as an\nasexual, then a diagnosis of male hypoac tive sexual desire disorder is not made. \nComorbidity\nDepression and other ment al disorders, as well as endocr inological factors, are often co-\nmorbid with male hypoacti ve sexual desire disorder.\nPremature (Early) Ejaculation\nDiagnostic Criteria 302.75 (F52.4)\nA. A persistent or recurrent pattern of ejacul ation occurring during partnered sexual activ-\nity within approximately 1 minute following vaginal penetration and before the individ-\nual wishes it.\nNote: Although the diagnosis of premature (early ) ejaculation may be applied to indi-\nviduals engaged in nonvaginal sexual activities, specific duration criteria have not been\nestablished for these activities.\nB. The symptom in Criterion A must have been present for at least 6 months and must be\nexperienced on almost all or all (approximately 75%\u2013100%) occasions of sexual activ-\nity (in identified situational contexts or, if generalized, in all contexts).\nC. The symptom in Criterion A causes clinically significant distress in the individual.\nD. The sexual dysfunction is not better explained by a nonsexual mental disorder or as a\nconsequence of severe relationship distress or other significant stressors and is not at-\ntributable to the effects of a substance/medication or another medical condition.\nSpecify whether:\nLifelong: The disturbance has been present since the individual became sexually active.\nAcquired: The disturbance began after a period of relatively normal sexual function.", "source": "dsm5.pdf"} {"id": "d4e26bf6a7ce-0", "page_content": "444 Sexual Dysfunctions\nSpecify whether:\nGeneralized: Not limited to certain types of stimulation, situations, or partners.\nSituational: Only occurs with certain types of stimulation, situations, or partners.\nSpecify current severity:\nMild: Ejaculation occurring within approximately 30 seconds to 1 minute of vaginal\npenetration.\nModerate: Ejaculation occurring within approximately 15\u201330 seconds of vaginal pen-\netration.\nSevere: Ejaculation occurring prior to sexual activity, at the start of sexual activity, or\nwithin approximately 15 seconds of vaginal penetration.\nDiagnostic Features\nPremature (early) ejaculation is manifested by ej aculation that occurs prior to or shortly af-\nter vaginal penetration, operationalized by an individual\u2019s estimate of ejaculatory latency\n(i.e., elapsed time before ej aculation) after vaginal penetr ation. Estimated and measured\nintravaginal ejaculatory latencies are highly co rrelated as long as the ejaculatory latency is\nof short duration; therefore, self-reported esti mates of ejaculatory latency are sufficient for\ndiagnostic purposes. A 60-second intravaginal ejaculatory latency time is an appropriate\ncutoff for the diagnosis of lifelong prematur e (early) ejaculation in heterosexual men.\nThere are insufficient data to determine if th is duration criterion can be applied to ac-\nquired premature (early) ejaculation. The du rational definition may apply to males of\nvarying sexual orientations, since ejaculatory latencies appear to be similar across men of\ndifferent sexual orientations and ac ross different sexual activities. \nAssociated Features Supporting Diagnosis\nMany males with premature (early) ejaculation complain of a sense of lack of control over\nejaculation and report apprehension about thei r anticipated inability to delay ejaculation\non future sexual encounters.\nThe following factors may be relevant in the evaluation of any sexual dysfunction:", "source": "dsm5.pdf"} {"id": "d4e26bf6a7ce-1", "page_content": "The following factors may be relevant in the evaluation of any sexual dysfunction:\n1) partner factors (e.g., partner\u2019s sexual problems, partner\u2019s health status); 2) relationship fac-\ntors (e.g., poor communication, discrepancies in desire for sexual activity); 3) individual\nvulnerability factors (e.g., poor body image, history of sexual or emotional abuse), psychiatric\ncomorbidity (e.g., depression, anxiety), and stressors (e.g., job loss, bereavement); 4) cultural/\nreligious factors (e.g., inhibitions related to prohibitions against sexual activity; attitudes\ntoward sexuality); and 5) medical factors relevant to prognosis, course, or treatment.\nPrevalence\nEstimates of the prevalence of premature (ear ly) ejaculation vary widely depending on the\ndefinition utilized. Internationally, more than 20%\u201330% of men ages 18\u201370 years report\nconcern about how rapidly they ejaculate. Wi th the new definition of premature (early)\nejaculation (i.e., ejaculation occurring within approximately 1 minute of vaginal penetra-\ntion), only 1%\u20133% of men woul d be diagnosed with the disorder. Prevalence of premature\n(early) ejaculation may increase with age.\nDevelopment and Course\nBy definition, lifelong premature (early) ejaculat ion starts during a male\u2019s initial sexual ex-\nperiences and persists thereafter. Some men may experience prematur e (early) ejaculation\nduring their initial sexual encoun ters but gain ejaculatory contro l over time. It is the persis-\ntence of ejaculatory problems fo r longer than 6 months that determines the diagnosis of pre-\nmature (early) ejaculation. In contrast, some men develop the disorder after a period of", "source": "dsm5.pdf"} {"id": "60d111dd19a7-0", "page_content": "Premature (Early) Ejaculation 445\nhaving a normal ejaculat ory latency, known as acquired premature (early) ejaculation. There is\nfar less known about acquired premature (early) ejaculation than about lifelong premature\n(early) ejaculation. The acquired form likely has a later onset, usually appearing during or af-\nter the fourth decade of life. Lifelong is relative ly stable throughout life. Little is known about\nthe course of acquired prematur e (early) ejaculation. Reversal of medical conditions such as\nhyperthyroidism and prostatitis appears to rest ore ejaculatory latencies to baseline values.\nLifelong premature (early) ejac ulation begins with early sexual experiences and persists\nthroughout an individual\u2019s life. In approxim ately 20% of men with premature (early) ejacu-\nlation, ejaculatory latencies decrease further wi th age. Age and relationship length have been\nfound to be negatively associated with pr evalence of prematur e (early) ejaculation.\nRisk and Prognostic Factors\nTemperamental. Premature (early) ejaculation may be more common in men with anx-\niety disorders, especially social anxiety disorder (social phobia).\nGenetic and physiological. There is a moderate genetic contribution to lifelong prema-\nture (early) ejaculation. Premature (early) ejaculation may be associated with dopamine\ntransporter gene polymorphism or serotonin transporter gene polymorphism. Thyroid\ndisease, prostatitis, and drug withdrawal are associated with acquired premature (early)\nejaculation. Positron emission tomography measu res of regional cerebral blood flow dur-\ning ejaculation have shown primary activation in the mesocephalic tr ansition zone, includ-\ning the ventral tegmental area.\nCulture-Related Diagnostic Issues", "source": "dsm5.pdf"} {"id": "60d111dd19a7-1", "page_content": "ing the ventral tegmental area.\nCulture-Related Diagnostic Issues\nPerception of what constitutes a normal ejac ulatory latency is different in many cultures.\nMeasured ejaculatory latencies may differ in so me countries. Such differences may be ex-\nplained by cultural or religious factors as well as genetic differences between populations.\nGender-Related Diagnostic Issues\nPremature (early) ejaculation is a sexual disorder in males. Males and their sexual partners\nmay differ in their perception of what consti tutes an acceptable ejaculatory latency. There\nmay be increasing concerns in females about early ejaculation in their sexual partners,\nwhich may be a reflection of changing societal attitudes concerning female sexual activity. \nDiagnostic Markers\nEjaculatory latency is usually mo nitored in research settings by the sexual partner utilizing\na timing device (e.g., stopwatch), though this is not ideal in real-life sexual situations. For\nvaginal intercourse, the time between intravag inal penetration and ejaculation is measured. \nFunctional Consequences of \nPremature (Early) Ejaculation\nA pattern of premature (early) ejaculation may be associated with decreased self-esteem, a\nsense of lack of control, and adverse conseq uences for partner relationships. It may also\ncause personal distress in the sexual partner and decreased sexual satisfaction in the sexual\npartner. Ejaculation prior to penetration may be associated with diffi culties in conception.\nDifferential Diagnosis\nSubstance/medication-induced sexual dysfunction. When problems with premature\nejaculation are due exclusively to substance use, intoxicati on, or withdrawal, substance/\nmedication-induced sexual dysfunction should be diagnosed.", "source": "dsm5.pdf"} {"id": "09e5f2b255a1-0", "page_content": "446 Sexual Dysfunctions\nEjaculatory concerns that do not meet diagnostic criteria. It is necessary to identify\nmales with normal ejaculatory latencies who de sire longer ejaculatory latencies and males\nwho have episodic premature (early) ejaculat ion (e.g., during the fi rst sexual encounter\nwith a new partner when a short ejaculatory la tency may be common or normative). Neither\nof these situations would lead to a diagnosis of premature (early) ejaculation, even though\nthese situations may be d istressing to some males.\nComorbidity \nPremature (early) ejaculation may be associated with erectile problems. In many cases, it\nmay be difficult to determin e which difficulty preceded the other. Lifelong premature\n(early) ejaculation may be associated with ce rtain anxiety disorders. Acquired premature\n(early) ejaculation may be associated with pros tatitis, thyroid disease, or drug withdrawal\n(e.g., during opioid withdrawal).\nSubstance/Medication-Induced\n Sexual Dysfunction\nDiagnostic Criteria\nA. A clinically significant disturbance in sexual function is predominant in the clinical picture.\nB. There is evidence from the history, physical examination, or laboratory findings of both\n(1) and (2):\n1. The symptoms in Criterion A developed during or soon after substance intoxication\nor withdrawal or after exposure to a medication.\n2. The involved substance/medication is capable of producing the symptoms in Crite-\nrion A.\nC. The disturbance is not better explained by a sexual dysfunction that is not substance/\nmedication-induced. Such evidence of an independent sexual dysfunction could in-\nclude the following:\nThe symptoms precede the onset of the substance/medication use; the symptoms\npersist for a substantial period of time (e.g., about 1 month) after the cessation of\nacute withdrawal or severe intoxication; or there is other evidence suggesting the", "source": "dsm5.pdf"} {"id": "09e5f2b255a1-1", "page_content": "acute withdrawal or severe intoxication; or there is other evidence suggesting the\nexistence of an independent non-substance/medication-induced sexual dysfunc-\ntion (e.g., a history of recurrent non-substance/medication-related episodes). \nD. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress in the individual.\nNote: This diagnosis should be made instead of a diagnosis of substance intoxication or\nsubstance withdrawal only when the symptoms in Criterion A predominate in the clinical\npicture and are sufficiently severe to warrant clinical attention.\nCoding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-\ntion]-induced sexual dysfunctions are indicated in the table below. Note that the ICD-10-CM\ncode depends on whether or not there is a comorbid substance use disorder present for the\nsame class of substance. If a mild substance use disorder is comorbid with the substance-\ninduced sexual dysfunction, the 4th position character is \u201c1,\u201d and the clinician should record\n\u201cmild [substance] use disorder\u201d before the substance-induced sexual dysfunction (e.g., \u201cmild\ncocaine use disorder with cocaine-induced sexual dysfunction\u201d). If a moderate or severe\nsubstance use disorder is comorbid with the substance-induced sexual dysfunction, the 4th\nposition character is \u201c2,\u201d and the clinician sh ould record \u201cmoderate [substance] use disorder\u201d\nor \u201csevere [substance] use disorder,\u201d depending on the severity of the comorbid substance", "source": "dsm5.pdf"} {"id": "80cfebf21b6d-0", "page_content": "Substance/Medication-Induced Sexual Dysfunction 447\nuse disorder. If there is no comorbid substance use disorder (e.g., after a one-time heavy\nuse of the substance), then the 4th position character is \u201c9,\u201d and the clinician should record\nonly the substance-induced sexual dysfunction.\nSpecify if (see Table 1 in the chapter \u201cSubstance-Related and Addictive Disorders\u201d for di-\nagnoses associated with substance class):\nWith onset during intoxication: If the criteria are met for intoxication with the sub-\nstance and the symptoms develop during intoxication.\nWith onset during withdrawal: If criteria are met for withdrawal from the substance\nand the symptoms develop during, or shortly after, withdrawal.\nWith onset after medication use: Symptoms may appear either at initiation of medi-\ncation or after a modification or change in use.\nSpecify current severity:\nMild: Occurs on 25%\u201350% of occasions of sexual activity.\nModerate: Occurs on 50%\u201375% of occasions of sexual activity.\nSevere: Occurs on 75% or more of occasions of sexual activity.\nRecording Procedures\nICD-9-CM. The name of the substance/medication-induced sexual dysfunction begins\nwith the specific substance (e.g., alcohol, fluoxetine) that is presumed to be causing the\nsexual dysfunction. The diagnost ic code is selected from the table included in the criteria\nset, which is based on the drug class. For substa nces that do not fit into any of the classes\n(e.g., fluoxetine), the code for \u201cother substa nce\u201d should be used; and in cases in which a\nsubstance is judged to be an etiological factor but the specific class of substance is un-\nknown, the category \u201cunknown substance\u201d should be used.", "source": "dsm5.pdf"} {"id": "80cfebf21b6d-1", "page_content": "known, the category \u201cunknown substance\u201d should be used.\nThe name of the disorder is followed by the sp ecification of onset (i.e., onset during in-\ntoxication, onset during withdrawal, with onse t after medication use), followed by the se-\nverity specifier (e.g., mild, moderate, severe ). Unlike the recording procedures for ICD-10-\nCM, which combine the substance-induced disord er and substance use disorder into a sin-\ngle code, for ICD-9-CM a separate diagnostic code is given for the su bstance use disorder.\nFor example, in the case of erectile dysfun ction occurring during intoxication in a man\nwith a severe alcohol use diso rder, the diagnosis is 291.89 al cohol-induced sexual dysfunc-\ntion, with onset during intoxication, modera te. An additional diagnosis of 303.90 severe\nalcohol use disorder is also given. When more than one substance is judged to play a sig-ICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate \nor severeWithout \nuse \ndisorder\nAlcohol 291.89 F10.181 F10.281 F10.981\nOpioid 292.89 F11.181 F11.281 F11.981\nSedative, hypnotic, or \nanxiolytic292.89 F13.181 F13.281 F13.981\nAmphetamine (or other \nstimulant)292.89 F15.181 F15.281 F15.981\nCocaine 292.89 F14.181 F14.281 F14.981\nOther (or unknown) substance 292.89 F19.181 F19.281 F19.981", "source": "dsm5.pdf"} {"id": "d7cdfdca7826-0", "page_content": "448 Sexual Dysfunctions\nnificant role in the development of the sexual dysfunction, each should be listed separately\n(e.g., 292.89 cocaine-induced sexual dysfunctio n with onset during intoxication, moderate;\n292.89 fluoxetine-induced sexu al dysfunction, with onset after medication use). \nICD-10-CM. The name of the substance/medication-induced sexual dysfunction begins\nwith the specific substance (e.g., alcohol, fluoxetine) that is presumed to be causing the\nsexual dysfunction. The diagnost ic code is selected from the table included in the criteria\nset, which is based on the drug class and presence or absence of a comorbid substance use\ndisorder. For substances that do not fit into any of the classes (e.g., fluoxetine), the code for\n\u201cother substance\u201d should be used; and in cases in which a substance is judged to be an eti-\nological factor but the specific class of subs tance is unknown, the category \u201cunknown sub-\nstance\u201d should be used.\nWhen recording the name of the disorder, th e comorbid substance use disorder (if any)\nis listed first, followed by the word \u201cwith,\u201d followed by the name of the substance-induced\nsexual dysfunction, followed by the specification of onset (i.e., onset during intoxication,\nonset during withdrawal, with onset after medi cation use), followed by the severity spec-\nifier (e.g., mild, moderate, severe). For example, in the case of erectile dysfunction occur-\nring during intoxication in a man with a severe alcohol use disorder, the diagnosis is\nF10.281 moderate alcohol use disorder with alcohol-induced se xual dysfunction, with on-\nset during intoxication, moderate. A separate diagnosis of the comorbid severe alcohol use\ndisorder is not given. If the substance-induced sexual dysfunction occurs without a co-", "source": "dsm5.pdf"} {"id": "d7cdfdca7826-1", "page_content": "disorder is not given. If the substance-induced sexual dysfunction occurs without a co-\nmorbid substance use disorder (e.g., after a one-time heavy use of the substance), no ac-\ncompanying substance use disorder is note d (e.g., F15.981 amphetamine-induced sexual\ndysfunction, with onset during intoxication). When more than one substance is judged to\nplay a significant role in the development of the sexual dysfunction, each should be listed\nseparately (e.g., F14.181 mild cocaine use di sorder with cocaine-induced sexual dysfunc-\ntion, with onset during intoxication, mode rate; F19.981 fluoxetine-induced sexual dys-\nfunction, with onset after medication use, moderate). \nDiagnostic Features\nThe major feature is a disturbance in sexual function that has a temporal relationship with\nsubstance/medication initiation, dose increa se, or substance/medication discontinuation.\nAssociated Features Supporting Diagnosis\nSexual dysfunctions can occur in association wi th intoxication with the following classes of\nsubstances: alcohol; opioids; sedatives, hypnotic s, or anxiolytics; stimulants (including co-\ncaine); and other (or unknown) substances. Sexual dysfunctions can occur in association\nwith withdrawal from the following classes of substances: alcohol; opioids; sedatives, hyp-\nnotics, or anxiolytics; and other (or unknown) substances. Medications that can induce sex-\nual dysfunctions include antidepressants, an tipsychotics, and horm onal contraceptives.\nThe most commonly reported side effect of antidepressant drugs is difficulty with or-\ngasm or ejaculation. Problems with desire and erection are less frequent. Approximately\n30% of sexual complaints are clinically sign ificant. Certain agents, such as bupropion and", "source": "dsm5.pdf"} {"id": "d7cdfdca7826-2", "page_content": "mirtazapine, appear not to be associated with sexual side effects. \nThe sexual problems associated with anti psychotic drugs, including problems with\nsexual desire, erection, lubrication, ejaculation, or orgasm, have occurred with typical as\nwell as atypical agents. However, problems are less common with prolactin-sparing anti-\npsychotics than with agents that cause significant prolactin elevation.\nAlthough the effects of mood stabilizers on se xual function are unclear, it is possible\nthat lithium and anticonvulsants, with the poss ible exception of lamotrigine, have adverse", "source": "dsm5.pdf"} {"id": "e48821031038-0", "page_content": "Although the effects of mood stabilizers on se xual function are unclear, it is possible\nthat lithium and anticonvulsants, with the poss ible exception of lamotrigine, have adverse\neffects on sexual desire. Problems with orgasm may occur with gabape ntin. Similarly, there\nmay be a higher prevalence of erectile and orgasmic problems associ ated with benzodiaz-\nepines. There have not been such reports with buspirone.", "source": "dsm5.pdf"} {"id": "20125d22f9ea-0", "page_content": "Substance/Medication-Induced Sexual Dysfunction 449\nMany nonpsychiatric medications, such as ca rdiovascular, cytotoxic, gastrointestinal,\nand hormonal agents, are associated with distur bances in sexual function. Illicit substance\nuse is associated with decreased sexual desire, erectile dysfunction, and difficulty reach-\ning orgasm. Sexual dysfunctions are also seen in individuals receiving methadone but are\nseldom reported by patients receiving buprenorphine. Chro nic alcohol abuse and chronic\nnicotine abuse are associated with erectile problems.\nPrevalence\nThe prevalence and the incidence of substa nce/medication-induced sexual dysfunction\nare unclear, likely because of underreporting of treatment-em ergent sexual side effects.\nData on substance/medication-induced sexual dysfunction typically concern the effects of\nantidepressant drugs. The prevalence of an tidepressant-induced sexual dysfunction var-\nies in part depending on the specific agent. Approximately 25%\u201380% of individuals taking\nmonoamine oxidase inhibitors, tricyclic anti depressants, serotone rgic antidepressants,\nand combined serotonergic-adrenergic antidepr essants report sexual side effects. There\nare differences in the incidence of sexual si de effects between some serotonergic and com-\nbined adrenergic-serotonergic antidepressants, although it is unclear if these differences\nare clinically significant.\nApproximately 50% of individuals taking antipsychotic medications will experience\nadverse sexual side e ffects, including problems with se xual desire, erection, lubrication,\nejaculation, or orgasm. The incidence of thes e side effects among different antipsychotic\nagents is unclear.\nExact prevalence and incidence of sexual dysfunctions among users of nonpsychiatric\nmedications such as cardiovascular, cytotoxic, gastrointestinal, and hormonal agents are", "source": "dsm5.pdf"} {"id": "20125d22f9ea-1", "page_content": "medications such as cardiovascular, cytotoxic, gastrointestinal, and hormonal agents are\nunknown. Elevated rates of sexual dysfunction have been reported with methadone or\nhigh-dose opioid drugs for pain. There are incr eased rates of decrease d sexual desire, erec-\ntile dysfunction, and difficulty reaching org asm associated with illicit substance use. The\nprevalence of sexual problems appears related to chronic drug abuse and appears higher\nin individuals who abuse heroin (approximately 60%\u201370%) than in individuals who abuse\namphetamines or 3,4-methylenedioxymethamphe tamine (i.e., MDMA, ecstasy). Elevated\nrates of sexual dysfunction are also seen in individuals receiving methadone but are sel-\ndom reported by patients receiving bupren orphine. Chronic alcohol abuse and chronic\nnicotine abuse are related to higher rates of erectile problems.\nDevelopment and Course\nThe onset of antidepressant-induced sexual dy sfunction may be as early as 8 days after the\nagent is first taken. Approximately 30% of indi viduals with mild to moderate orgasm de-\nlay will experience spontaneous remission of the dysfunction within 6 months. In some\ncases, serotonin reuptake inhibitor\u2013induce d sexual dysfunction may persist after the\nagent is discontinued. The time to onset of sexual dysfunctio n after initiation of antipsy-\nchotic drugs or drugs of abuse is unknown. It is probable that the adverse effects of nico-\ntine and alcohol may not appear until after ye ars of use. Premature (early) ejaculation can\nsometimes occur after cessation of opioid use. There is some evidence that disturbances in\nsexual function related to substance/medication use increase with age. \nCulture-Related Diagnostic Issues\nThere may be an interaction among cultural fa ctors, the influence of medications on sexual", "source": "dsm5.pdf"} {"id": "20125d22f9ea-2", "page_content": "There may be an interaction among cultural fa ctors, the influence of medications on sexual\nfunctioning, and the response of the individual to those changes.\nGender-Related Diagnostic Issues\nSome gender differences in sexual side effects may exist.", "source": "dsm5.pdf"} {"id": "f7c5da0fb15f-0", "page_content": "450 Sexual Dysfunctions\nFunctional Consequences of \nSubstance/Medication-Indu ced Sexual Dysfunction\nMedication-induced sexual dysfunction ma y result in medication noncompliance.\nDifferential Diagnosis\nNon-substance/medication-induced sexual dysfunctions. Many mental conditions, such\nas depressive, bipolar, anxiet y, and psychotic disorders, ar e associated with disturbances\nof sexual function. Thus, differentiating a substance/medication-induced sexual dys-\nfunction from a manifestation of the underlying mental disorder can be quite difficult. The\ndiagnosis is usually established if a close re lationship between substance/medication ini-\ntiation or discontinuation is observed. A clear diagnosis can be established if the problem\noccurs after substance/medication initiation, dissipates with substance/medication dis-\ncontinuation, and recurs with introduction of the same agent. Most substance/medication-in-\nduced side effects occur shortly after initiation or discontinuation. Sexual side effects that\nonly occur after chronic use of a substance/medication may be extremely difficult to di-\nagnose with certainty. \nOther Specified Sexual Dysfunction\n302.79 (F52.8)\nThis category applies to presentations in which symptoms characteristic of a sexual dys-\nfunction that cause clinically significant di stress in the individual predominate but do not\nmeet the full criteria for any of the disorders in the sexual dysfunctions diagnostic class.\nThe other specified sexual dysfunction category is used in situations in which the clinician\nchooses to communicate the specific reason that the presentation does not meet the cri-\nteria for any specific sexual dysfunction. This is done by recording \u201cother specified sexual\ndysfunction\u201d followed by the specific reason (e.g., \u201csexual aversion\u201d).\nUnspecified Sexual Dysfunction\n302.70 (F52.9)\nThis category applies to presentations in which symptoms characteristic of a sexual dys-", "source": "dsm5.pdf"} {"id": "f7c5da0fb15f-1", "page_content": "This category applies to presentations in which symptoms characteristic of a sexual dys-\nfunction that cause clinically significant di stress in the individual predominate but do not\nmeet the full criteria for any of the disorders in the sexual dysfunctions diagnostic class.\nThe unspecified sexual dysfunction category is used in situations in which the clinician\nchooses not to specify the reason that the criteria are not met for a specific sexual dys-\nfunction, and includes presentations for which there is insufficient information to make a\nmore specific diagnosis.", "source": "dsm5.pdf"} {"id": "b87337576ebf-0", "page_content": "451 Gender\n Dysphoria\nIn this chapter, there is one overarching diagnosis of gender dysphoria, with sepa-\nrate developmentally appropriate criteria sets for children and for adolescents and adults.\nThe area of sex and gender is highly controve rsial and has led to a proliferation of terms\nwhose meanings vary over time and within and between disciplines. An additional source\nof confusion is that in English \u201csex\u201d connotes both male/female and se xuality. This chapter\nemploys constructs and terms as they are wide ly used by clinicians from various disci-\nplines with specialization in this area. In this chapter, sex and sexual refer to the biological\nindicators of male and female (understood in the context of reproductive capacity), such\nas in sex chromosomes, gonads, sex hormon es, and nonambiguous internal and external\ngenitalia. Disorders of sex deve lopment denote condit ions of inborn somatic deviations of\nthe reproductive tract from the norm and/or discrepancies among the biological indica-\ntors of male and female. Cross-sex hormone treatment denotes the use of feminizing hor-\nmones in an individual assigned male at birth based on traditional biological indicators or\nthe use of masculinizing hormones in an individual assigned female at birth.\nThe need to introduce the term gender arose with the realization that for individuals\nwith conflicting or ambiguous biological indicato rs of sex (i.e., \u201cintersex\u201d), the lived role in\nsociety and/or the identification as male or female could not be uniformly associated with\nor predicted from the biological indicators and, later, that some individuals develop an\nidentity as female or male at variance with their uniform set of classical biological indica-\ntors. Thus, gender is used to denote the public (and usually legally recognized) lived role as", "source": "dsm5.pdf"} {"id": "b87337576ebf-1", "page_content": "boy or girl, man or woman, but, in contrast to certain social construc tionist theories, biolog-\nical factors are seen as contributing, in intera ction with social and psychological factors, to\ngender development. Gender assignment refers to the initial assignment as male or female.\nThis occurs usually at birth and, thereby, yields the \u201cnatal gender.\u201d Gender-atypical refers to\nsomatic features or behaviors th at are not typical (in a statisti cal sense) of individuals with\nthe same assigned gender in a given so ciety and historical era; for behavior, gender-noncon-\nforming is an alternative descriptive term. Gender reassignment denotes an official (and usu-\nally legal) change of gender. Gender identity is a category of social identity and refers to an\nindividual\u2019s identification as male, female, or, occasionally, some ca tegory other than male\nor female. Gender dysphoria as a general descriptive term refers to an individual\u2019s affective/\ncognitive discontent with the assigned gender but is more specific ally defined when used\nas a diagnostic category. Transgender refers to the broad spectrum of individuals who tran-\nsiently or persistently identify with a gender different from their natal gender. Transsexual\ndenotes an individual who seeks, or has undergone, a social transition from male to female\nor female to male, which in many, but not all, cases also involves a somatic transition by\ncross-sex hormone treatment and genital surgery ( sex reassignment surgery). \nGender dysphoria refers to the distress that ma y accompany the incongruence between\none\u2019s experienced or expressed gender and one\u2019s assigned gender. Although not all indi-\nviduals will experience distress as a result of such incongruence , many are distressed if the", "source": "dsm5.pdf"} {"id": "b87337576ebf-2", "page_content": "desired physical interventions by means of hormones and/or surg ery are not avail able.\nThe cu rrent term is more descriptive than the previous DSM-IV term gender identity disor-\nder and focuses on dysphoria as the clin ical problem, not identity per se.", "source": "dsm5.pdf"} {"id": "e907ecd30a12-0", "page_content": "452 Gender Dysphoria\nGender Dysphoria\nDiagnostic Criteria \nGender Dysphoria in Children 302.6 (F64.2)\nA. A marked incongruence between one\u2019s experienced/expressed gender and assigned\ngender, of at least 6 months\u2019 duration, as manifested by at least six of the following\n(one of which must be Criterion A1):\n1. A strong desire to be of the other gender or an insistence that one is the other gen-\nder (or some alternative gender different from one\u2019s assigned gender).\n2. In boys (assigned gender), a strong preference for cross-dressing or simulating fe-\nmale attire; or in girls (assigned gender), a strong preference for wearing only typ-\nical masculine clothing and a strong resistance to the wearing of typical feminine\nclothing.\n3. A strong preference for cross-gender roles in make-believe play or fantasy play.\n4. A strong preference for the toys, games, or activities stereotypically used or en-\ngaged in by the other gender.\n5. A strong preference for playmates of the other gender.\n6. In boys (assigned gender), a strong rejection of typically masculine toys, games,\nand activities and a strong avoidance of rough-and-tumble play; or in girls (as-\nsigned gender), a strong rejection of typically feminine toys, games, and activities.\n7. A strong dislike of one\u2019s sexual anatomy.\n8. A strong desire for the primary and/or secondary sex characteristics that match\none\u2019s experienced gender.\nB. The condition is associated with clinically significant distress or impairment in social,\nschool, or other important areas of functioning.\nSpecify if:\nWith a disorder of sex development (e.g., a congenital adrenogenital disorder such", "source": "dsm5.pdf"} {"id": "e907ecd30a12-1", "page_content": "as 255.2 [E25.0] congenital adrenal hyperplasia or 259.50 [E34.50] androgen insensi-\ntivity syndrome).\nCoding note: Code the disorder of sex development as well as gender dysphoria.\nGender Dysphoria in Adolescents and Adults 302.85 (F64.1)\nA. A marked incongruence between one\u2019s experienced/expressed gender and assigned\ngender, of at least 6 months\u2019 duration, as manifested by at least two of the following:\n1. A marked incongruence between one\u2019s experienced/expressed gender and pri-\nmary and/or secondary sex characteristics (or in young adolescents, the antici-\npated secondary sex characteristics).\n2. A strong desire to be rid of one\u2019s primary and/or secondary sex characteristics be-\ncause of a marked incongruence with one\u2019s experienced/expressed gender (or in\nyoung adolescents, a desire to prevent the development of the anticipated second-\nary sex characteristics).\n3. A strong desire for the primary and/or secondary sex characteristics of the other\ngender.\n4. A strong desire to be of the other gender (or some alternative gender different from\none\u2019s assigned gender).\n5. A strong desire to be treated as the ot her gender (or some alternative gender dif-\nferent from one\u2019s assigned gender).\n6. A strong conviction that one has the typical feelings and reactions of the other gen-\nder (or some alternative gender different from one\u2019s assigned gender).", "source": "dsm5.pdf"} {"id": "f6a9bd4b799c-0", "page_content": "Gender Dysphoria 453\nB. The condition is associated with clinically significant distress or impairment in social,\noccupational, or other important areas of functioning.\nSpecify if:\nWith a disorder of sex development (e.g., a congenital adrenogenital disorder such\nas 255.2 [E25.0] congenital adrenal hyperplasia or 259.50 [E34.50] androgen insensi-\ntivity syndrome).\nCoding note: Code the disorder of sex development as well as gender dysphoria.\nSpecify if:\nPosttransition: The individual has transitioned to full-time living in the desired gender\n(with or without legalization of gender change) and has undergone (or is preparing to\nhave) at least one cross-sex medical proc edure or treatment regimen\u2014namely, regu-\nlar cross-sex hormone treatment or gender reassignment surgery confirming the desired\ngender (e.g., penectomy, vaginoplasty in a natal male; mastectomy or phalloplasty in\na natal female).\nSpecifiers \nThe posttransition specifier may be used in th e context of continuing treatment procedures\nthat serve to support the new gender assignment. \nDiagnostic Features \nIndividuals with gender dysphoria have a ma rked incongruence between the gender they\nhave been assigned to (usually at birth, referred to as natal gender) and their experienced/\nexpressed gender. This discrepancy is the core componen t of the diagnosis. There must\nalso be evidence of distress about this inco ngruence. Experienced gender may include al-\nternative gender identities beyond binary stereotypes. Consequently, the distress is not\nlimited to a desire to simply be of the other gender, but may incl ude a desire to be of an al-", "source": "dsm5.pdf"} {"id": "f6a9bd4b799c-1", "page_content": "ternative gender, provided that it differs from the individual\u2019s assigned gender. \nGender dysphoria manifests itself differently in different age groups. Prepubertal natal\ngirls with gender dysphoria may express the wish to be a boy, assert they are a boy, or as-\nsert they will grow up to be a man. They prefer boys\u2019 clothing and hairstyles, are often\nperceived by strangers as boys, and may ask to be called by a boy\u2019s na me. Usually, they dis-\nplay intense negative reactions to parental attempts to have them wear dresses or other\nfeminine attire. Some may refuse to attend sc hool or social events where such clothes are\nrequired. These girls may demonstrate marked cr oss-gender identification in role-playing,\ndreams, and fantasies. Contac t sports, rough-and-tumble pl ay, traditional boyhood games,\nand boys as playmates are most often preferred. They show lit tle interest in stereotypically\nfeminine toys (e.g., dolls) or activities (e.g., feminine dress-up or role-play). Occasionally,\nthey refuse to urinate in a sitting position. Some natal girls may express a desire to have a\npenis or claim to have a penis or that they will grow one when older. They may also state that\nthey do not want to deve lop breasts or menstruate.\nPrepubertal natal boys with gender dysphoria may express the wish to be a girl or as-\nsert they are a girl or that they will grow up to be a woman. They have a preference for\ndressing in girls\u2019 or women\u2019s clothes or ma y improvise clothing from available materials\n(e.g., using towels, aprons, and scarves for lo ng hair or skirts). These children may role-", "source": "dsm5.pdf"} {"id": "f6a9bd4b799c-2", "page_content": "play female figures (e.g., play ing \u201cmother\u201d) and often are intensely interested in female\nfantasy figures. Traditional feminine activities, stereotypical games, and pastimes (e.g.,\n\u201cplaying house\u201d; drawing feminine pictures; watc hing television or videos of favorite fe-\nmale characters) are most often preferred. Stereotypical female-type dolls (e.g., Barbie) are\noften favorite toys, and girls are their prefer red playmates. They avoid rough-and-tumble\nplay and competitive sports and have little inte rest in stereotypically masculine toys (e.g.,\ncars, trucks). Some may pretend not to have a penis and insist on sitting to urinate. More", "source": "dsm5.pdf"} {"id": "86a5207be0eb-0", "page_content": "454 Gender Dysphoria\nrarely, they may state that they find their penis or testes disgusting, that they wish them re-\nmoved, or that they have, or wish to have, a vagina.\nIn young adolescents with gender dysphoria, clinical features may resemble those of\nchildren or adults with the co ndition, depending on develo pmental level. As secondary\nsex characteristics of young adolescents are no t yet fully developed, these individuals may\nnot state dislike of them, but they are co ncerned about imminent physical changes. \nIn adults with gender dysphoria, the di screpancy between experienced gender and\nphysical sex characteristics is often, but not always, accompanied by a desire to be rid of\nprimary and/or secondary sex ch aracteristics and/or a strong desire to acquire some pri-\nmary and/or secondary sex characteristics of the other gender. To varying degrees, adults\nwith gender dysphoria may ad opt the behavior, clothing, and mannerisms of the experi-\nenced gender. They feel uncomfortable being re garded by others, or functioning in soci-\nety, as members of their assigned gender. Some adults may have a strong desire to be of a\ndifferent gender and treated as such, and they may have an inner certainty to feel and re-\nspond as the experienced gender without seek ing medical treatment to alter body char-\nacteristics. They may find other ways to resolve the incongruence between experienced/\nexpressed and assigned gender by partially livin g in the desired role or by adopting a gen-\nder role neither conventionally male nor conventionally female.\nAssociated Features Supporting Diagnosis\nWhen visible signs of puberty develop, natal bo ys may shave their legs at the first signs of\nhair growth. They sometimes bind their genitals to make erections less visible. Girls may", "source": "dsm5.pdf"} {"id": "86a5207be0eb-1", "page_content": "hair growth. They sometimes bind their genitals to make erections less visible. Girls may\nbind their breasts, walk with a stoop, or use lo ose sweaters to make breasts less visible. In-\ncreasingly, adolescents request, or may obta in without medical prescription and supervi-\nsion, hormonal suppressors (\u201cblockers\u201d) of gonadal steroids (e.g., gonadotropin-releasing\nhormone [GnRH] analog, spironolactone). Clinically refe rred adolescents often want hor-\nmone treatment and many also wish for gender reassignment surgery. Adolescents living in\nan accepting environment may open ly express the desire to be and be treated as the experi-\nenced gender and dress partly or completely as the experienced gender, have a hairstyle typ-\nical of the experienced gender, preferentially s eek friendships with peer s of the other gender,\nand/or adopt a new first name consistent with the experienced gender. Older adolescents,\nwhen sexually active, usually do not show or allow partners to touch their sexual organs. For\nadults with an aversion toward their genitals, sexual activity is constrained by the preference\nthat their genitals not be seen or touched by their partners. Some adults may seek hormone\ntreatment (sometimes without medical prescrip tion and supervision) and gender reassign-\nment surgery. Others are satisfied with either hormone treatment or surgery alone.\nAdolescents and adults with gender dysphoria before gender reassignment are at in-\ncreased risk for suicidal ideation, suicide a ttempts, and suicides. After gender reassign-\nment, adjustment may vary, an d suicide risk may persist.\nPrevalence \nFor natal adult males, prevalence ranges from 0.005% to 0.014%, and for natal females,", "source": "dsm5.pdf"} {"id": "86a5207be0eb-2", "page_content": "from 0.002% to 0.003%. Since not all adults seeking hormone treatment and surgical reas-\nsignment attend specialty clinics, these rate s are likely modest underestimates. Sex differ-\nences in rate of referrals to specialty clinics vary by age group. In children, sex ratios of\nnatal boys to girls range from 2:1 to 4.5:1. In adolescents, the sex ratio is close to parity; in\nadults, the sex ratio favors natal males, with ratios ranging from 1:1 to 6.1:1. In two coun-\ntries, the sex ratio appears to favor nata l females (Japan: 2.2:1; Poland: 3.4:1). \nDevelopment and Course", "source": "dsm5.pdf"} {"id": "b9863a0db760-0", "page_content": "tries, the sex ratio appears to favor nata l females (Japan: 2.2:1; Poland: 3.4:1). \nDevelopment and Course \nBecause expression of gender dysphoria varies wi th age, there are separate criteria sets for\nchildren versus adolescents and adults. Criter ia for children are defined in a more con-", "source": "dsm5.pdf"} {"id": "066728e1758f-0", "page_content": "Gender Dysphoria 455\ncrete, behavioral manner than those for adolescents and adults. Many of the core criteria\ndraw on well-documented behavioral gender differences between typically developing\nboys and girls. Young children are less likely than older children, ad olescents, and adults\nto express extreme and persistent anatomic dysphoria. In adolescents and adults, incon-\ngruence between experienced gender and somati c sex is a central feature of the diagnosis.\nFactors related to distress and impairment al so vary with age. A very young child may\nshow signs of distress (e.g., intense crying) on ly when parents tell the child that he or she\nis \u201creally\u201d not a member of the other gender but only \u201cdesires\u201d to be. Distress may not be\nmanifest in social environments supportive of the child\u2019s desire to live in the role of the\nother gender and may emerge only if the desi re is interfered with. In adolescents and\nadults, distress may manifest because of stro ng incongruence between experienced gender\nand somatic sex. Such distress may, however, be mitigated by supportive environments and\nknowledge that biomedical treatments exist to reduce incongruence. Impairment (e.g.,\nschool refusal, development of depression, anxiety, and substance abuse) may be a conse-\nquence of gender dysphoria.\nGender dysphoria without a disorder of sex development. For clinic-referred children,\nonset of cross-gender behaviors is usually betw een ages 2 and 4 years. This corresponds to\nthe developmental time period in which most typically developing children begin ex-\npressing gendered behaviors and interests. For some preschool-age children, both perva-\nsive cross-gender behaviors and the expressed desire to be the other gender may be\npresent, or, more rarely, labeling oneself as a member of the other gender may occur. In", "source": "dsm5.pdf"} {"id": "066728e1758f-1", "page_content": "some cases, the expressed desire to be the othe r gender appears later, usually at entry into\nelementary school. A small minority of childre n express discomfort wi th their sexual anat-\nomy or will state the desire to have a sexual anatomy correspondin g to the experienced\ngender (\u201canatomic dysphoria\u201d). Expressions of anatomic dysphoria become more com-\nmon as children with ge nder dysphoria approach and anticipate puberty. \nRates of persistence of gender dysphoria fr om childhood into adolescence or adulthood\nvary. In natal males, persistence has ranged fr om 2.2% to 30%. In natal females, persistence\nhas ranged from 12% to 50%. Persistence of gender dysphoria is mo destly correlated with\ndimensional measures of severity ascertaine d at the time of a childhood baseline assess-\nment. In one sample of natal males, lower socioeconomic background was also modestly\ncorrelated with persistence. It is unclear if particular therapeutic approaches to gender\ndysphoria in children are related to rates of long-term persistence. Extant follow-up sam-\nples consisted of children receiving no formal therapeutic interventi on or receiving ther-\napeutic interventions of various types, ranging from ac tive efforts to reduce gender\ndysphoria to a more neutral, \u201cwatchful waiting\u201d approach. It is unclear if children \u201cen-\ncouraged\u201d or supported to live socially in the desired gender will show higher rates of per-\nsistence, since such children have not yet b een followed longitudinally in a systematic\nmanner. For both natal male and female ch ildren showing persistence, almost all are\nsexually attracted to individuals of their na tal sex. For natal male children whose gender", "source": "dsm5.pdf"} {"id": "066728e1758f-2", "page_content": "sexually attracted to individuals of their na tal sex. For natal male children whose gender\ndysphoria does not per sist, the majority are androphilic (sexually attracted to males) and of-\nten self-identify as gay or homosexual (rangi ng from 63% to 100%). In natal female chil-\ndren whose gender dysphoria does no t persist, the percentage who are gynephilic (sexually\nattracted to females) and sel f-identify as lesbian is lower (ranging from 32% to 50%).\nIn both adolescent and adult natal males, there are t wo broad trajectories for develop-", "source": "dsm5.pdf"} {"id": "0becad1d34a8-0", "page_content": "attracted to females) and sel f-identify as lesbian is lower (ranging from 32% to 50%).\nIn both adolescent and adult natal males, there are t wo broad trajectories for develop-\nment of gender dysphoria: early onset and late onset. Early-onset gender dysphoria starts in\nchildhood and continues into adolescence and adulthood; or, there is an intermittent pe-\nriod in which the gender dysphoria desists and these individuals self-i dentify as gay or ho-\nmosexual, followed by recurren ce of gender dysphoria. Late-onset gender dysphoria occurs\naround puberty or much later in life. Some of these individuals report having had a desire\nto be of the other gender in childhood that was not expressed verbally to others. Others do\nnot recall any signs of childhood gender dysp horia. For adolescent males with late-onset\ngender dysphoria, parents often report surpri se because they did not see signs of gender", "source": "dsm5.pdf"} {"id": "a16ccb105764-0", "page_content": "456 Gender Dysphoria\ndysphoria during childhood. Expressions of anatomic dysphoria are more common and\nsalient in adolescents and adults once seco ndary sex characterist ics have developed. \nAdolescent and adult natal males with earl y-onset gender dysphoria are almost al-\nways sexually attracted to men (androphilic). Adolescents and adults with late-onset gen-\nder dysphoria frequently engage in transves tic behavior with sexual excitement. The\nmajority of these individuals are gynephilic or sexually attracted to other posttransition\nnatal males with late-onset ge nder dysphoria. A substantia l percentage of adult males\nwith late-onset gender dyspho ria cohabit with or are marrie d to natal females. After gen-\nder transition, many self-identify as lesbian. Among adult natal males with gender dyspho-\nria, the early-onset group seeks out clinical care for hormone treatment and reassignment\nsurgery at an earlier age than does the late-onset group. The late-onset group may have more\nfluctuations in the degree of gender dyspho ria and be more ambivalent about and less\nlikely satisfied after gender reassignment surgery. \nIn both adolescent and adult natal females, the most common course is the early-onset\nform of gender dysphoria. The late-onset fo rm is much less common in natal females com-\npared with natal males. As in natal males with gender dysphoria, there may have been a\nperiod in which the gender dysphoria desisted and these individuals self-identified as les-\nbian; however, with recurrence of gender dysphoria, clinical consultation is sought, often\nwith the desire for hormone treatment and reas signment surgery. Parents of natal adoles-", "source": "dsm5.pdf"} {"id": "a16ccb105764-1", "page_content": "with the desire for hormone treatment and reas signment surgery. Parents of natal adoles-\ncent females with the late-onset form also report surprise, as no signs of childhood gender\ndysphoria were evident. Expressions of anat omic dysphoria are mu ch more common and\nsalient in adolescents and adults than in children.\nAdolescent and adult natal females with early-onset gender dysphoria are almost\nalways gynephilic. Adolescents and adults with the late-onset form of gender dysphoria\nare usually androphilic and after gender transit ion self-identify as gay men. Natal females\nwith the late-onset form do not have co-occu rring transvestic behavi or with sexual ex-\ncitement. \nGender dysphoria in association with a disorder of sex development. Most individuals\nwith a disorder of sex development who develop gender dysphoria have already come to\nmedical attention at an early age. For many, st arting at birth, issues of gender assignment\nwere raised by physicians and parents. More over, as infertility is quite common for this\ngroup, physicians are more willing to perfor m cross-sex hormone treatments and genital\nsurgery before adulthood.\nDisorders of sex development in general are frequently as sociated with gender-atypi-\ncal behavior starting in early childhood. Howeve r, in the majority of cases, this does not\nlead to gender dysphoria. As individuals with a disorder of sex development become\naware of their medical history and condition, many experience uncertainty about their\ngender, as opposed to developing a firm co nviction that they are another gender. How-\never, most do not progress to gender transit ion. Gender dysphoria and gender transition\nmay vary considerably as a function of a disord er of sex development, its severity, and as-\nsigned gender.", "source": "dsm5.pdf"} {"id": "a16ccb105764-2", "page_content": "signed gender. \nRisk and Prognostic Factors\nTemperamental. For individuals with gender dyspho ria without a disorder of sex de-\nvelopment, atypical gender behavior among individuals with early-onset gender dyspho-\nria develops in early preschool age, and it is possible that a high degree of atypicality\nmakes the development of gender dysphoria and its persistence into adolescence and\nadulthood more likely.\nEnvironmental. Among individuals with gender dysphoria without a disorder of sex de-\nvelopment, males with gender dysphoria (in both childhood and adolescence) more com-", "source": "dsm5.pdf"} {"id": "020dee77a5b3-0", "page_content": "adulthood more likely.\nEnvironmental. Among individuals with gender dysphoria without a disorder of sex de-\nvelopment, males with gender dysphoria (in both childhood and adolescence) more com-\nmonly have older brothers than do males without the condition. Additional predisposing", "source": "dsm5.pdf"} {"id": "de069a3697c9-0", "page_content": "Gender Dysphoria 457\nfactors under consideration, especially in indi viduals with late-onset gender dysphoria (ad-\nolescence, adulthood), include habitual fetishistic transvesti sm developing into autogyne-\nphilia (i.e., sexual arousal asso ciated with the thought or imag e of oneself as a woman) and\nother forms of more general social, psychological, or developmental problems.\nGenetic and physiological. For individuals with gender dy sphoria without a disorder of\nsex development, some genetic contribution is suggested by evidence for (weak) familial-\nity of transsexualism among nontwin siblings, increased concordance for transsexualism\nin monozygotic compared with dizygotic same -sex twins, and some degree of heritability\nof gender dysphoria. As to endocrine findin gs, no endogenous systemic abnormalities in\nsex-hormone levels have been found in 46,XY individuals, whereas there appear to be in-\ncreased androgen levels (in the range found in hirsute women but far below normal male\nlevels) in 46,XX individuals. Overall, current evidence is insufficient to label gender dys-\nphoria without a disorder of sex development as a form of intersexuality limited to the cen-\ntral nervous system.\nIn gender dysphoria associated with a disorder of sex development, the likelihood of\nlater gender dysphoria is increased if pren atal production and utilization (via receptor\nsensitivity) of androgens are grossly atypical re lative to what is usually seen in individuals\nwith the same assigned gender. Examples incl ude 46,XY individuals with a history of nor-\nmal male prenatal hormone milieu but inborn nonhormonal genital defects (as in cloacal", "source": "dsm5.pdf"} {"id": "de069a3697c9-1", "page_content": "bladder exstrophy or penile agenesis) and who have been assigned to the female gender.\nThe likelihood of gender dysphoria is furthe r enhanced by additional, prolonged, highly\ngender-atypical postnatal androgen exposure with somatic virilization as may occur in fe-\nmale-raised and noncastrated 46,XY individu als with 5-alpha reductase-2 deficiency or\n17-beta-hydroxysteroid dehydrog enase-3 deficiency or in female-raised 46,XX individuals\nwith classical congenital adrenal hyperplasi a with prolonged periods of non-adherence to\nglucocorticoid replacement therapy. Howeve r, the prenatal androgen milieu is more\nclosely related to gendered behavior than to gender identity. Many individuals with dis-\norders of sex development and markedly gend er-atypical behavior do not develop gender\ndysphoria. Thus, gender-atypical behavior by itself should not be interpreted as an indi-\ncator of current or future gend er dysphoria. There appears to be a higher rate of gender\ndysphoria and patient-initiated gender change from assigned female to male than from as-\nsigned male to female in 46,XY individu als with a disorder of sex development.\nCulture-Related Diagnostic Issues\nIndividuals with gender dysphoria have be en reported across many countries and cul-\ntures. The equivalent of gender dysphoria ha s also been reported in individuals living in\ncultures with institutionalized gender categories other than ma le or female. It is unclear\nwhether with these individuals the diagnostic criteria for gender dysphoria would be met.\nDiagnostic Markers \nIndividuals with a somatic disorder of sex development show some correlation of final\ngender identity outcome with the degree of prenatal androgen production and utilization.", "source": "dsm5.pdf"} {"id": "de069a3697c9-2", "page_content": "gender identity outcome with the degree of prenatal androgen production and utilization.\nHowever, the correlation is not robust enough for the biological factor, where ascertain-\nable, to replace a detailed an d comprehensive diagnostic in terview evaluation for gender\ndysphoria. \nFunctional Consequences of Gender Dysphoria\nPreoccupation with cross-gender wishes may de velop at all ages after the first 2\u20133 years of\nchildhood and often interfere with daily activities. In older children, failure to develop\nage-typical same-sex peer relationships and skills may lead to isolation from peer groups\nand to distress. Some children may refuse to attend school because of teasing and harass-", "source": "dsm5.pdf"} {"id": "7ad2ab5633ed-0", "page_content": "458 Gender Dysphoria\nment or pressure to dress in attire associated with their assigned sex. Also in adolescents\nand adults, preoccupation with cross-gender w ishes often interferes with daily activities.\nRelationship difficulties, including sexual relationship problems, are common, and func-\ntioning at school or at work may be impa ired. Gender dysphoria, along with atypical\ngender expression, is associated with high le vels of stigmatization , discrimination, and\nvictimization, leading to nega tive self-concept, increased ra tes of mental disorder comor-\nbidity, school dropout, and economic marginalization, including unemployment, with at-\ntendant social and mental health risks, especially in individuals from resource-poor family\nbackgrounds. In addition, these individuals\u2019 access to health services and mental health\nservices may be impeded by structural barriers, such as institutional discomfort or inex-\nperience in working with this patient population.\nDifferential Diagnosis\nNonconformity to gender roles. Gender dysphoria should be distinguished from sim-\nple nonconformity to stereotypical gender role behavior by the strong desire to be of an-\nother gender than the assigned one and by th e extent and pervasivene ss of gender-variant\nactivities and interests. The diagnosis is not meant to mere ly describe nonconformity to\nstereotypical gender role behavior (e.g., \u201ct omboyism\u201d in girls, \u201cgirly-boy\u201d behavior in\nboys, occasional cross-dressing in adult men). Given the increased openness of atypical\ngender expressions by individuals across the entire range of the transgender spectrum, it\nis important that the clinical diagnosis be lim ited to those individuals whose distress and\nimpairment meet the specified criteria.\nTransvestic disorder. Transvestic disorder occurs in he terosexual (or bisexual) adoles-", "source": "dsm5.pdf"} {"id": "7ad2ab5633ed-1", "page_content": "cent and adult males (rarely in females) fo r whom cross-dressing behavior generates sex-\nual excitement and causes distress and/or impairment without drawing their primary\ngender into question. It is occasionally ac companied by gender dysphoria. An individual\nwith transvestic disorder who also has clinica lly significant gender dysphoria can be given\nboth diagnoses. In many cases of late-onset gender dysphoria in gynephilic natal males,\ntransvestic behavior with sexu al excitement is a precursor.\nBody dysmorphic disorder. An individual with body dy smorphic disorder focuses on\nthe alteration or removal of a sp ecific body part because it is perceived as abnormally formed,\nnot because it represents a repudiated assign ed gender. When an individual\u2019s presenta-\ntion meets criteria for both gender dysphori a and body dysmorphic disorder, both diag-\nnoses can be given. Individuals wishing to have a healthy limb amputated (termed by\nsome body integrity identity disorder) because it makes them feel more \u201ccomplete\u201d usually\ndo not wish to change gender, but rather desi re to live as an amput ee or a disabled person.\nSchizophrenia and other psychotic disorders. In schizophrenia, there may rarely be\ndelusions of belonging to some other gender. In the absence of psychotic symptoms, in-\nsistence by an individual with gender dysphori a that he or she is of some other gender is\nnot considered a delusion. Schizophrenia (or other psychotic disorders) and gender dys-\nphoria may co-occur.\nOther clinical presentations. Some individuals with an emasculinization desire who\ndevelop an alternative, nonmale/nonfemale ge nder identity do have a presentation that", "source": "dsm5.pdf"} {"id": "7ad2ab5633ed-2", "page_content": "develop an alternative, nonmale/nonfemale ge nder identity do have a presentation that\nmeets criteria for gender dys phoria. However, some males seek castration and/or penec-\ntomy for aesthetic reasons or to remove psychological effects of androgens without chang-\ning male identity; in these cases, the cr iteria for gender dysphoria are not met. \nComorbidity \nClinically referred children with gender dysphoria show elevated le vels of emotional and\nbehavioral problems\u2014most commonly, anxiety, disruptive and impulse-control, and de-", "source": "dsm5.pdf"} {"id": "814e4a1db13e-0", "page_content": "Other Specified Gender Dysphoria 459\npressive disorders. In prepub ertal children, increasing age is associated with having more\nbehavioral or emotional problems; this is rela ted to the increasing non-acceptance of gen-\nder-variant behavior by others. In older chil dren, gender-variant behavior often leads to\npeer ostracism, which may lead to more be havioral problems. The prevalence of mental\nhealth problems differs among cultures; these differences may also be related to differences\nin attitudes toward gender variance in child ren. However, also in some non-Western cul-\ntures, anxiety has been found to be relatively common in individuals with gender dysphoria,\neven in cultures with accepting attitudes to ward gender-variant be havior. Autism spec-\ntrum disorder is more prevalent in clinica lly referred children with gender dysphoria than\nin the general population. Clinically referred adolescents with gender dysphoria appear to\nhave comorbid mental disorders, with anxi ety and depressive disorders being the most\ncommon. As in children, autism spectrum disorder is more pr evalent in clinically referred\nadolescents with gender dysphoria than in the general population. Clinically referred\nadults with gender dysphoria may have coexisting mental he alth problems, most commonly\nanxiety and depres sive disorders.\nOther Specified Gender Dysphoria\n302.6 (F64.8)\nThis category applies to presentations in which symptoms characteristic of gender dys-\nphoria that cause clinically significant distress or impairment in social, occupational, or other\nimportant areas of functioning predominate but do not meet the full criteria for gender dys-\nphoria. The other specified gender dysphoria category is used in situations in which the\nclinician chooses to communicate the specific reason that the presentation does not meet", "source": "dsm5.pdf"} {"id": "814e4a1db13e-1", "page_content": "clinician chooses to communicate the specific reason that the presentation does not meet\nthe criteria for gender dysphoria. This is done by recording \u201cother specified gender dys-\nphoria\u201d followed by the specific r eason (e.g., \u201cbrief gender dysphoria\u201d).\nAn example of a presentation that can be specified using the \u201cother specified\u201d desig-\nnation is the following:\nThe current disturbance meets symptom cr iteria for gender dysphoria, but the\nduration is less than 6 months.\nUnspecified Gender Dysphoria\n302.6 (F64.9)\nThis category applies to presentations in which symptoms characteristic of gender dys-\nphoria that cause clinically significant distress or impairment in social, occupational, or oth-\ner important areas of functioning predominate but do not meet the full criteria for gender\ndysphoria. The unspecified gender dysphoria category is used in situations in which the\nclinician chooses not to specify the reason that the criteria are not met for gender dyspho-\nria, and includes presentations in which there is insufficient information to make a more\nspecific diagnosis.", "source": "dsm5.pdf"} {"id": "56522a32a695-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "ef093cb4cf28-0", "page_content": "461Disruptive, Impulse-Control,\nand Conduct Disorders\nDisruptive, impulse-control, and conduct disorders include conditions involv-\ning problems in the self-control of emotions and behaviors. While other disorders in DSM-\n5 may also involve problems in emotional and/or behavioral regulation, the disorders in\nthis chapter are unique in that these problems are manifested in behaviors that violate the\nrights of others (e.g., aggression, destructio n of property) and/or that bring the individual\ninto significant conflict with societal norms or authority figures. The underlying causes of\nthe problems in the self-control of emotions and behaviors can vary greatly across the dis-\norders in this chapter and among individu als within a given diagnostic category. \nThe chapter includes opposition al defiant disorder, intermi ttent explosive disorder, con-\nduct disorder, antisocial person ality disorder (which is described in the chapter \u201cPersonality\nDisorders\u201d), pyromania, kleptomania, and ot her specified and unspecified disruptive, im-\npulse-control, and conduct disorders. Althou gh all the disorders in the chapter involve\nproblems in both emotional and behavioral re gulation, the source of variation among the\ndisorders is the relative emphas is on problems in the two types of self-control. For example,\nthe criteria for conduct disorder focus largely on poorly controlled behaviors that violate the\nrights of others or that violat e major societal norms. Many of the behavioral symptoms (e.g.,\naggression) can be a result of poorly controlled emotions such as anger. At the other extreme,\nthe criteria for intermittent explosive disorder focus largely on such poorly controlled emo-\ntion, outbursts of anger that are disproportionate to the interpersonal or other provocation\nor to other psychosocial stressors. Intermediate in impact to these two disorders is opposi-", "source": "dsm5.pdf"} {"id": "ef093cb4cf28-1", "page_content": "tional defiant disorder, in which the criteria are more evenly distributed between emotions\n(anger and irritation) and be haviors (argumentati veness and defiance). Pyromania and\nkleptomania are less commonly used diagnoses characterized by poor impulse control re-\nlated to specific behaviors (fire setting or stealing) that reliev e internal tension. Other speci-\nfied disruptive, impulse-control, and conduct disorder is a category for conditions in which\nthere are symptoms of conduct disorder, oppositional defiant disorder, or other disruptive,\nimpulse-control, and conduct disorders, but th e number of symptoms does not meet the di-\nagnostic threshold for any of th e disorders in this chapter, even though there is evidence of\nclinically significant impairment associated with the symptoms. \nThe disruptive, impulse-control, and conduct disorders all tend to be more common in\nmales than in females, although the relative degree of male predominance may differ both\nacross disorders and within a disorder at differe nt ages. The disorders in this chapter tend to\nhave first onset in childhood or adolescence. In fact, it is very rare for ei ther conduct disorder or\noppositional defiant disorder to first emerge in adulthood. There is a developmental relation-\nship between oppositional defiant disorder and conduct disorder, in th at most cases of con-\nduct disorder previously would have met criteria for opposition al defiant disorder, at least in\nthose cases in which conduct disorder emerges prior to adolescence. However, most children\nwith oppositional defiant disorder do not ev entually develop conduct disorder. Furthermore,\nchildren with opposition al defiant disorder are at risk fo r eventually developing other prob-\nlems besides conduct disorder, includ ing anxiety and depr essive disorders.\nMany of the symptoms that define the disruptive, impulse-control, and conduct disor-\nders are behaviors that can occur to some degree in typically developing individuals.", "source": "dsm5.pdf"} {"id": "ef093cb4cf28-2", "page_content": "ders are behaviors that can occur to some degree in typically developing individuals.\nThus, it is critical that the frequency, persistence , pervasiveness across situations, and im-", "source": "dsm5.pdf"} {"id": "23d54d1db1d6-0", "page_content": "462 Disruptive, Impulse-Control, and Conduct Disorders\npairment associated with the behaviors indica tive of the diagnosis be considered relative\nto what is normative for a person\u2019s age, gend er, and culture when determining if they are\nsymptomatic of a disorder. \nThe disruptive, impulse-control, and conduc t disorders have been linked to a common\nexternalizing spectrum associated with the personality dimensions labeled as disinhibition\nand (inversely) constraint and, to a lesser extent, negative emotionality. These shared per-\nsonality dimensions could acco unt for the high level of como rbidity among these disorders\nand their frequent comorbidity with substanc e use disorders and antisocial personality\ndisorder. However, the specific nature of th e shared diathesis that constitutes the exter-\nnalizing spectrum remains unknown. \nOppositional Defiant Disorder\nDiagnostic Criteria 313.81 (F91.3)\nA. A pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness lasting\nat least 6 months as evidenced by at least four symptoms from any of the following cate-\ngories, and exhibited during interaction with at least one individual who is not a sibling.\nAngry/Irritable Mood\n1. Often loses temper.\n2. Is often touchy or easily annoyed.\n3. Is often angry and resentful.\nArgumentative/Defiant Behavior\n4. Often argues with authority figures or, for children and adolescents, with adults.\n5. Often actively defies or refuses to comply with requests from authority figures or\nwith rules.\n6. Often deliberately annoys others.\n7. Often blames others for his or her mistakes or misbehavior.\nVindictiveness\n8. Has been spiteful or vindictive at least twice within the past 6 months.", "source": "dsm5.pdf"} {"id": "23d54d1db1d6-1", "page_content": "Note: The persistence and frequency of these behaviors should be used to distinguish\na behavior that is within normal limits from a behavior that is symptomatic. For children\nyounger than 5 years, the behavior should occur on most days for a period of at least\n6 months unless otherwise noted (Criterion A8). For individuals 5 years or older, the\nbehavior should occur at least once per week for at least 6 months, unless otherwise\nnoted (Criterion A8). While these frequency criteria provide guidance on a minimal lev-\nel of frequency to define symptoms, other factors should also be considered, such as\nwhether the frequency and intensity of the behaviors are outside a range that is nor-\nmative for the individual\u2019s developmental level, gender, and culture.\nB. The disturbance in behavior is associated with distress in the individual or others in his or\nher immediate social context (e.g., family, peer group, work colleagues), or it impacts neg-\natively on social, educational, occupational, or other important areas of functioning. \nC. The behaviors do not occur exclusively during the course of a psychotic, substance\nuse, depressive, or bipolar disorder. Also, the criteria are not met for disruptive mood\ndysregulation disorder.\nSpecify current severity:\nMild: Symptoms are confined to only one setting (e.g., at home, at school, at work, with\npeers).", "source": "dsm5.pdf"} {"id": "a457eebee5bd-0", "page_content": "Oppositional Defiant Disorder 463\nModerate: Some symptoms are present in at least two settings.\nSevere: Some symptoms are present in three or more settings.\nSpecifiers\nIt is not uncommon for individuals with oppositional defiant disorder to show symptoms\nonly at home and only with family member s. However, the pervasiveness of the symp-\ntoms is an indicator of the severity of the disorder.\nDiagnostic Features\nThe essential feature of oppositional defiant disorder is a frequent and persistent pattern\nof angry/irritable mood, argumentative/defi ant behavior, or vindictiveness (Criterion\nA). It is not unusual for individuals with oppositional defiant disorder to show the behav-\nioral features of the disorder without proble ms of negative mood. However, individuals\nwith the disorder who show the angry/irrita ble mood symptoms typically show the be-\nhavioral features as well. \nThe symptoms of oppositional defiant disorder may be confined to only one setting,\nand this is most frequently the home. Indi viduals who show enough symptoms to meet\nthe diagnostic threshold, even if it is only at home, may be significantly impaired in their\nsocial functioning. However, in more severe cases, the symptoms of the disorder are pres-\nent in multiple settings. Given that the pervas iveness of symptoms is an indicator of the\nseverity of the disorder, it is critical that the individual\u2019s behavior be assessed across mul-\ntiple settings and relationships. Because these behaviors are common among siblings, they\nmust be observed during interactions with persons other than siblings. Also, because\nsymptoms of the disorder are ty pically more evident in intera ctions with adults or peers\nwhom the individual knows well, they may not be apparent during a clinical examination. \nThe symptoms of oppositional defiant disord er can occur to some degree in individu-", "source": "dsm5.pdf"} {"id": "a457eebee5bd-1", "page_content": "The symptoms of oppositional defiant disord er can occur to some degree in individu-\nals without this disorder. There are several ke y considerations for de termining if the be-\nhaviors are symptomatic of oppo sitional defiant disorder. First, the diagnostic threshold\nof four or more symptoms within the preceding 6 months must be met. Second, the per-\nsistence and frequency of the symptoms should exceed what is normative for an individ-\nual\u2019s age, gender, and culture. For example, it is not unusual for preschool children to\nshow temper tantrums on a weekly basis. Te mper outbursts for a preschool child would be\nconsidered a symptom of oppositional defiant d isorder only if they occurred on most days\nfor the preceding 6 months, if they occurred with at least three other symptoms of the dis-\norder, and if the temper outbursts contribu ted to the significant impairment associated\nwith the disorder (e.g., led to destruction of property during outbursts, resulted in the\nchild being asked to leave a preschool). \nThe symptoms of the disorder often are part of a pattern of pr oblematic interactions\nwith others. Furthermore, individuals with this disorder typically do not regard themselves\nas angry, oppositional, or defian t. Instead, they often justify their behavior as a response to\nunreasonable demands or circumstances. Thus, it can be difficult to disentangle the rela-\ntive contribution of the individual with the disorder to the problematic interactions he or\nshe experiences. For example, children with oppositional defiant disorder may have ex-\nperienced a history of hostile parenting, and it is often impossible to determine if the\nchild\u2019s behavior caused the parents to act in a more hostile manner toward the child, if the", "source": "dsm5.pdf"} {"id": "a457eebee5bd-2", "page_content": "child\u2019s behavior caused the parents to act in a more hostile manner toward the child, if the\nparents\u2019 hostility led to the ch ild\u2019s problematic behavior, or if there was so me combination\nof both. Whether or not the clinician can sepa rate the relative contributions of potential\ncausal factors should not influence whether or not the diagnosis is made. In the event that\nthe child may be living in particularly poor conditions where neglect or mistreatment may\noccur (e.g., in institutional settings), clinical attention to reducing the contribution of the", "source": "dsm5.pdf"} {"id": "a6ddaa79aec9-0", "page_content": "the child may be living in particularly poor conditions where neglect or mistreatment may\noccur (e.g., in institutional settings), clinical attention to reducing the contribution of the\nenvironment may be helpful.", "source": "dsm5.pdf"} {"id": "3bc8ee4d4add-0", "page_content": "464 Disruptive, Impulse-Control, and Conduct Disorders\nAssociated Features Supporting Diagnosis\nIn children and adolescents, oppositional defian t disorder is more prevalent in families in\nwhich child care is disrupted by a succession of different caregivers or in families in which\nharsh, inconsistent, or negl ectful child-rearing practice s are common. Two of the most\ncommon co-occurring conditions with oppositi onal defiant disorder are attention-deficit/\nhyperactivity disorder (ADHD) and conduct disorder (see the section \u201cComorbidity\u201d for\nthis disorder). Oppositional defiant disorder has been associated with increased risk for\nsuicide attempts, even after comorb id disorders are controlled for. \nPrevalence\nThe prevalence of oppositional defiant disord er ranges from 1% to 11%, with an average\nprevalence estimate of around 3.3%. The rate of oppositional defiant disorder may vary\ndepending on the age and gender of the child . The disorder appears to be somewhat more\nprevalent in males than in females (1.4:1) pr ior to adolescence. This male predominance is\nnot consistently found in samples of adolescents or adults. \nDevelopment and Course\nThe first symptoms of oppositional defiant di sorder usually appear during the preschool\nyears and rarely later than early adolescence. Oppositional defiant disorder often precedes\nthe development of conduct disorder, especial ly for those with the childhood-onset type\nof conduct disorder. However, many children and adolescents with oppositional defiant\ndisorder do not subsequently develop cond uct disorder. Oppositional defiant disorder\nalso conveys risk for the development of anxi ety disorders and major depressive disorder,\neven in the absence of conduct disorder. The defiant, argumentative, and vindictive symp-\ntoms carry most of the risk for conduct disorder, whereas the angry-irritable mood symp-", "source": "dsm5.pdf"} {"id": "3bc8ee4d4add-1", "page_content": "toms carry most of the risk for emotional disorders. \nManifestations of the disorder across de velopment appear consistent. Children and\nadolescents with oppositional defiant disorder are at increase d risk for a number of prob-\nlems in adjustment as adults, including anti social behavior, impu lse-control problems,\nsubstance abuse, anxiety, and depression.\nMany of the behaviors associated with oppositional defiant disorder increase in fre-\nquency during the preschool period and in adol escence. Thus, it is especially critical dur-\ning these development periods that the freq uency and intensity of these behaviors be\nevaluated against normative leve ls before it is decided that they are symptoms of opposi-\ntional defiant disorder.\nRisk and Prognostic Features\nTemperamental. Temperamental factors related to problems in emotional regulation\n(e.g., high levels of emotiona l reactivity, poor frustration to lerance) have been predictive\nof the disorder.\nEnvironmental. Harsh, inconsistent, or neglectful child-rearing practices are common in\nfamilies of children and adolescents with oppo sitional defiant disorder, and these parent-\ning practices play an important role in many causal theories of the disorder. \nGenetic and physiological. A number of neurobiological markers (e.g., lower heart rate\nand skin conductance reactivity; reduced basal cortisol reactivity; abnormalities in the pre-\nfrontal cortex and amygdala) have been associated with oppositional defiant disorder.\nHowever, the vast majority of studies have not separated children with oppositional de-\nfiant disorder from those with conduct diso rder. Thus, it is unclear whether there are\nmarkers specific to oppositional defiant disorder.", "source": "dsm5.pdf"} {"id": "c4ada1dcc1c0-0", "page_content": "Oppositional Defiant Disorder 465\nCulture-Related Diagnostic Issues\nThe prevalence of the disorder in children an d adolescents is relatively consistent across\ncountries that differ in race and ethnicity.\nFunctional Consequences of \nOppositional Defiant Disorder\nWhen oppositional defiant disorder is pers istent throughout deve lopment, individuals\nwith the disorder experience frequent conflic ts with parents, teachers, supervisors, peers,\nand romantic partners. Such problems often re sult in significant impairments in the indi-\nvidual\u2019s emotional, social, academ ic, and occupational adjustment. \nDifferential Diagnosis\nConduct disorder. Conduct disorder and oppositional defiant disorder are both related\nto conduct problems that bring the individual in conflict with adults and other authority\nfigures (e.g., teachers, work supervisors). Th e behaviors of oppositional defiant disorder\nare typically of a less severe nature than those of conduct disorder and do not include ag-\ngression toward people or anima ls, destruction of property, or a pattern of theft or deceit.\nFurthermore, oppositional defian t disorder includes problems of emotional dysregulation\n(i.e., angry and irritable mood) that are not in cluded in the definition of conduct disorder. \nAttention-deficit/hyperactivity disorder. ADHD is often comorbid with oppositional de-\nfiant disorder. To make the additional diagnosis of oppositional defiant disorder, it is impor-\ntant to determine that the indivi dual\u2019s failure to conform to requ ests of others is not solely in\nsituations that demand sustained effort and attention or demand that the individual sit still. \nDepressive and bipolar disorders. Depressive and bipolar di sorders often involve neg-\native affect and irritability. As a result, a di agnosis of oppositional defiant disorder should", "source": "dsm5.pdf"} {"id": "c4ada1dcc1c0-1", "page_content": "not be made if the symptoms occur exclusiv ely during the course of a mood disorder. \nDisruptive mood dysregulation disorder. Oppositional defiant disorder shares with dis-\nruptive mood dysregulation disorder the symp toms of chronic negative mood and temper\noutbursts. However, the severity, frequency, and chronicity of temp er outbursts are more\nsevere in individuals with di sruptive mood dysregulation disorder than in those with\noppositional defiant disorder. Thus, only a minority of ch ildren and adolescents whose\nsymptoms meet criteria for oppo sitional defiant disorder woul d also be diagnosed with dis-\nruptive mood dysregulation disorder. When the mood disturbance is severe enough to meet\ncriteria for disruptive mood dysregulation disorder, a diagnosis of oppositional defiant dis-\norder is not given, even if all criteria for oppositional defiant disorder are met.\nIntermittent explosive disorder. Intermittent explosive disorder also involves high\nrates of anger. However, indi viduals with this disorder sh ow serious aggr ession toward\nothers that is not part of the defini tion of oppositional defiant disorder. \nIntellectual disability (intell ectual developmental disorder). In individuals with intel-\nlectual disability, a diagnosis of oppositional defiant disorder is gi ven only if the opposi-\ntional behavior is markedly greater than is commonly observed among individuals of\ncomparable mental age and with comparab le severity of intellectual disability. \nLanguage disorder. Oppositional defiant disorder must also be distinguished from a\nfailure to follow directions that is the resu lt of impaired language comprehension (e.g.,\nhearing loss). \nSocial anxiety disorder (social phobia). Oppositional defiant disord er must also be dis-\ntinguished from defiance due to fear of negative evaluation associated with social anxiety\ndisorder.", "source": "dsm5.pdf"} {"id": "77437b7cc78d-0", "page_content": "466 Disruptive, Impulse-Control, and Conduct Disorders\nComorbidity \nRates of oppositional defiant disorder are mu ch higher in samples of children, adoles-\ncents, and adults with ADHD, and this may be the result of shared temperamental risk fac-\ntors. Also, oppositional defiant disorder of ten precedes conduct di sorder, although this\nappears to be most common in children wi th the childhood-onset subtype. Individuals\nwith oppositional defiant disorder are also at increased risk for anxiety disorders and ma-\njor depressive disorder, and this seems largel y attributable to the presence of the angry-\nirritable mood symptoms. Adolescents and adul ts with oppositional defiant disorder also\nshow a higher rate of substance use disorders, al though it is unclear if this association is in-\ndependent of the comorbidity with conduct disorder. \nIntermittent Explosive Disorder\nDiagnostic Criteria 312.34 (F63.81)\nA. Recurrent behavioral outbursts representing a failure to control aggressive impulses\nas manifested by either of the following:\n1. Verbal aggression (e.g., temper tantrums, tirades, verbal arguments or fights) or\nphysical aggression toward property, animals, or other individuals, occurring twice\nweekly, on average, for a period of 3 months. The physical aggression does not re-\nsult in damage or destruction of property and does not result in physical injury to\nanimals or other individuals. \n2. Three behavioral outbursts involving damage or destruction of property and/or\nphysical assault involving physical injury against animals or other individuals occur-\nring within a 12-month period. \nB. The magnitude of aggressiveness expressed during the recurrent outbursts is grossly\nout of proportion to the provocation or to any precipitating psychosocial stressors.", "source": "dsm5.pdf"} {"id": "77437b7cc78d-1", "page_content": "out of proportion to the provocation or to any precipitating psychosocial stressors. \nC. The recurrent aggressive outbursts are not premeditated (i.e., they are impulsive and/\nor anger-based) and are not committed to achieve some tangible objective (e.g.,\nmoney, power, intimidation).\nD. The recurrent aggressive outbursts cause either marked distress in the individual or\nimpairment in occupational or interpersonal functioning, or are associated with finan-\ncial or legal consequences. \nE. Chronological age is at least 6 years (or equivalent developmental level).\nF. The recurrent aggressive outbursts are not better explained by another mental disor-\nder (e.g., major depressive disorder, bipolar disorder, disruptive mood dysregulation\ndisorder, a psychotic disorder, antisocial personality disorder, borderline personality\ndisorder) and are not attributable to another medical condition (e.g., head trauma, Alz-\nheimer\u2019s disease) or to the physiological effects of a substance (e.g., a drug of abuse,\na medication). For children ages 6\u201318 years, aggressive behavior that occurs as part\nof an adjustment disorder should not be considered for this diagnosis. \nNote: This diagnosis can be made in addition to the diagnosis of attention-deficit/hyper-\nactivity disorder, conduct disorder, oppositional defiant disorder, or autism spectrum dis-\norder when recurrent impulsive aggressive outbursts are in excess of those usually seen\nin these disorders and warrant independent clinical attention.\nDiagnostic Features\nThe impulsive (or anger-based) aggressive outb ursts in intermittent explosive disorder have\na rapid onset and, typically, li ttle or no prodromal period. Ou tbursts typically last for less", "source": "dsm5.pdf"} {"id": "8aed63087f5c-0", "page_content": "Intermittent Explosive Disorder 467\nthan 30 minutes and commonly occur in respon se to a minor provocation by a close intimate\nor associate. Individuals with intermittent ex plosive disorder often have less severe epi-\nsodes of verbal and/or nondamaging, nondestruc tive, or noninjurious physical assault (Cri-\nterion A1) in between more severe destructive/ assaultive episodes (Cri terion A2). Criterion\nA1 defines frequent (i.e., twice weekly, on aver age, for a period of 3 months) aggressive out-\nbursts characterized by temper tantrums, tirades, verbal arguments or fights, or assault\nwithout damage to objects or without injury to animals or other individuals. Criterion A2\ndefines infrequent (i.e., three in a 1-year pe riod) impulsive aggressi ve outbursts character-\nized by damaging or destroying an object, regardless of its tangible value, or by assaulting/\nstriking or otherwise causing physical injury to an animal or to another individual. Regard-\nless of the nature of the impulsive aggressive outburst, the core feature of intermittent\nexplosive disorder is failure to control impulsiv e aggressive behavior in response to subjec-\ntively experienced provocation (i.e., psychosocial stressor) that would not typically result in\nan aggressive outburst (Criterion B). The aggressive outbursts are generally impulsive and/\nor anger-based, rather than premeditated or instrumental (Criterion C) and are associated\nwith significant distress or impairment in psyc hosocial function (Cri terion D). A diagnosis\nof intermittent explosive disorder should not be given to individuals younger than 6 years,\nor the equivalent developmental level (Criterion E), or to individual s whose aggressive out-", "source": "dsm5.pdf"} {"id": "8aed63087f5c-1", "page_content": "or the equivalent developmental level (Criterion E), or to individual s whose aggressive out-\nbursts are better explained by another mental di sorder (Criterion F). A diagnosis of intermit-\ntent explosive disorder should not be gi ven to individuals with disruptive mood\ndysregulation disorder or to individuals whose impulsive aggressive outbursts are attribut-\nable to another medical condition or to the phys iological effects of a substance (Criterion F).\nIn addition, children ages 6\u201318 years should not receive this diagnosis when impulsive ag-\ngressive outbursts occur in the context of an adjustment disorder (Criterion F). \nAssociated Features Supporting Diagnosis \nMood disorders (unipolar), anxiety disorders, and substance use disorders are associated\nwith intermittent explosive di sorder, although onset of thes e disorders is typically later\nthan that of intermitte nt explosive disorder. \nPrevalence\nOne-year prevalence data for intermittent expl osive disorder in the United States is about\n2.7% (narrow definition). Intermittent explosive disorder is more prevalent among\nyounger individuals (e.g., youn ger than 35\u201340 years), compared with older individuals\n(older than 50 years), and in individuals with a high school education or less. \nDevelopment and Course\nThe onset of recurrent, problematic, impulsive aggressive beha vior is most common in late\nchildhood or adolescence and ra rely begins for the first time after age 40 years. The core\nfeatures of intermitte nt explosive disorder, typically, ar e persistent and continue for many\nyears.\nThe course of the disorder may be episodic, with recurrent periods of impulsive ag-\ngressive outbursts. Intermittent explosive disorder appears to follow a chronic and persis-\ntent course over many years. It also appears to be quite common regardless of the presence", "source": "dsm5.pdf"} {"id": "8aed63087f5c-2", "page_content": "tent course over many years. It also appears to be quite common regardless of the presence\nor absence of attentio n-deficit/hyperactivity disorder (ADHD) or disruptive, impulse-\ncontrol, and conduct disorders (e.g., conduct disorder, oppo sitional defiant disorder). \nRisk and Prognostic Factors \nEnvironmental. Individuals with a history of physica l and emotional trauma during the\nfirst two decades of life are at increased risk for intermittent explosive disorder.", "source": "dsm5.pdf"} {"id": "a7020899682e-0", "page_content": "468 Disruptive, Impulse-Control, and Conduct Disorders\nGenetic and physiological. First-degree relatives of individuals with intermittent ex-\nplosive disorder are at increase d risk for intermittent explos ive disorder, and twin studies\nhave demonstrated a substantial geneti c influence for impulsive aggression. \nResearch provides neurobiolo gical support for the presence of serotonergic abnormal-\nities, globally and in the brain, specifically in areas of the limbic sy stem (anterior cingulate)\nand orbitofrontal cortex in individuals with intermittent explos ive disorder. Amygdala\nresponses to anger stimuli, during function al magnetic resonance imaging scanning, are\ngreater in individuals with intermittent expl osive disorder compared with healthy indi-\nviduals.\nCulture-Related Diagnostic Issues \nThe lower prevalence of intermittent explosive disorder in some regions (Asia, Middle\nEast) or countries (Romania, Nigeria), compared with the United States, suggests that in-\nformation about recurrent, prob lematic, impulsive aggressive behaviors either is not elic-\nited on questioning or is less likely to be present, because of cultural factors.\nGender-Related Diagnostic Issues\nIn some studies the prevalence of intermittent explosive diso rder is greater in males than\nin females (odds ratio = 1.4\u20132.3); other st udies have found no gender difference. \nFunctional Consequences of \nIntermittent Explosive Disorder\nSocial (e.g., loss of friends, relatives, marita l instability), occupational (e.g., demotion, loss\nof employment), financial (e.g., due to value of objects destroyed), and legal (e.g., civil\nsuits as a result of aggressive behavior against person or prop erty; criminal charges for as-\nsault) problems often develop as a result of intermit tent explosive disorder. \nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "a7020899682e-1", "page_content": "Differential Diagnosis\nA diagnosis of intermittent ex plosive disorder shou ld not be made when Criteria A1 and/\nor A2 are only met during an episode of another mental disorder (e.g., major depressive\ndisorder, bipolar disorder, psychotic disorder ), or when impulsive aggressive outbursts\nare attributable to another me dical condition or to the physio logical effects of a substance\nor medication. This diagnosis also should not be made, particularly in children and ado-\nlescents ages 6\u201318 years, when the impulsive aggressive outbursts occur in the context of\nan adjustment disorder. Other examples in which recurrent, proble matic, impulsive ag-\ngressive outbursts may, or may not, be diag nosed as intermittent explosive disorder in-\nclude the following. \nDisruptive mood dysregulation disorder. In contrast to intermittent explosive disorder,\ndisruptive mood dysregulation disorder is charac terized by a persistently negative mood state\n(i.e., irritability, anger) most of the day, nearly every day, between impulsive aggressive out-\nbursts. A diagnosis of disruptive mood dysregul ation disorder can only be given when the on-\nset of recurrent, problematic, impulsive aggressive outbursts is before age 10 years. Finally, a\ndiagnosis of disruptive mood dysregulation di sorder should not be made for the first time\nafter age 18 years. Otherwise, these diagnoses are mutually exclusive. \nAntisocial personality disorder or borderline personality disorder. Individuals with an-\ntisocial personality disorder or borderline personality disorder often display recurrent,\nproblematic impulsive aggressive outbursts. However, the level of impulsive aggression\nin individuals with antisocial personality di sorder or borderline personality disorder is\nlower than that in individuals with intermittent explosive disorder.", "source": "dsm5.pdf"} {"id": "6f07f8cee167-0", "page_content": "Conduct Disorder 469\nDelirium, major neurocognitive disorder, an d personality change due to another med-\nical condition, aggressive type. A diagnosis of intermittent ex plosive disorder should not\nbe made when aggressive outbur sts are judged to result from the physiological effects of an-\nother diagnosable medical condition (e.g., brain in jury associated with a change in personality\ncharacterized by aggressive outbursts; comple x partial epilepsy). Nonspecific abnormalities\non neurological examination (e.g., \u201csoft signs\u201d) and nonspecific electroencephalographic\nchanges are compatible with a diagnosis of interm ittent explosive disorder unless there is a di-\nagnosable medical condition that better expl ains the impulsive aggressive outbursts. \nSubstance intoxication or substance withdrawal. A diagnosis of inte rmittent explosive\ndisorder should not be made when impulsive aggressive outbursts are nearly always as-\nsociated with intoxicati on with or withdrawal from substa nces (e.g., alcohol, phencyclidine,\ncocaine and other stimulants, barbiturates, inhalants). However, when a sufficient number\nof impulsive aggressive outbur sts also occur in the absence of substance intoxication or\nwithdrawal, and these warrant in dependent clinical attention, a diagnosis of intermittent\nexplosive disorder may be given. \nAttention-deficit/hyperactivity disorder, conduct disorder, oppositional defiant disor-\nder, or autism spectrum disorder. Individuals with any of these childhood-onset dis-\norders may exhibit impulsive aggressive outbursts. Individu als with ADHD are typically\nimpulsive and, as a result, may also exhibit impulsive aggressive outbursts. While indi-\nviduals with conduct disorder can exhibit impulsive aggressive outbur sts, the form of ag-", "source": "dsm5.pdf"} {"id": "6f07f8cee167-1", "page_content": "gression characterized by the diagnostic criter ia is proactive and predatory. Aggression in\noppositional defiant disorder is typically char acterized by temper ta ntrums and verbal ar-\nguments with authority figures, whereas impu lsive aggressive outbursts in intermittent\nexplosive disorder are in response to a broader array of provocation and include physical\nassault. The level of impulsive aggression in individuals with a history of one or more of\nthese disorders has been reported as lower than that in comparab le individuals whose\nsymptoms also meet intermitte nt explosive disorder Criteria A through E. Accordingly, if\nCriteria A through E are also met, and the impulsive aggressive out bursts warrant inde-\npendent clinical attention, a diagnosis of intermittent expl osive disorder may be given. \nComorbidity\nDepressive disorders, anxiet y disorders, and substance us e disorders are most commonly\ncomorbid with intermittent explosive disord er. In addition, individuals with antisocial\npersonality disorder or borderline personality disorder, and individuals with a history of\ndisorders with disruptive beha viors (e.g., ADHD, conduct di sorder, oppositional defiant\ndisorder), are at greater risk for como rbid intermittent explosive disorder.\nConduct Disorder\nDiagnostic Criteria\nA. A repetitive and persistent pattern of behavior in which the basic rights of others or ma-\njor age-appropriate societal norms or rules ar e violated, as manifested by the presence\nof at least three of the following 15 criteria in the past 12 months from any of the cate-\ngories below, with at least one criter ion present in the past 6 months:\nAggression to People and Animals\n1. Often bullies, threatens, or intimidates others.\n2. Often initiates physical fights.", "source": "dsm5.pdf"} {"id": "6f07f8cee167-2", "page_content": "2. Often initiates physical fights.\n3. Has used a weapon that can cause serious physical harm to others (e.g., a bat,\nbrick, broken bottle, knife, gun).", "source": "dsm5.pdf"} {"id": "032dc74d619d-0", "page_content": "470 Disruptive, Impulse-Control, and Conduct Disorders\n4. Has been physically cruel to people.\n5. Has been physically cruel to animals.\n6. Has stolen while confronting a victim (e.g., mugging, purse snatching, extortion,\narmed robbery).\n7. Has forced someone into sexual activity.\nDestruction of Property\n8. Has deliberately engaged in fire setting with the intention of causing serious damage.\n9. Has deliberately destroyed others\u2019 property (other than by fire setting).\nDeceitfulness or Theft\n10. Has broken into someone else\u2019s house, building, or car.\n11. Often lies to obtain goods or favors or to avoid obligations (i.e., \u201ccons\u201d others).\n12. Has stolen items of nontrivial value without confronting a victim (e.g., shoplifting,\nbut without breaking and entering; forgery).\nSerious Violations of Rules\n13. Often stays out at night despite parental prohibitions, beginning before age 13 years.\n14. Has run away from home overnight at least twice while living in the parental or pa-\nrental surrogate home, or once without returning for a lengthy period.\n15. Is often truant from school, beginning before age 13 years.\nB. The disturbance in behavior causes clinically significant impairment in social, aca-\ndemic, or occupational functioning.\nC. If the individual is age 18 years or older, criteria are not met for antisocial personality\ndisorder.\nSpecify whether:\n312.81 (F91.1) Childhood-onset type: Individuals show at least one symptom char-\nacteristic of conduct disorder prior to age 10 years.\n312.82 (F91.2) Adolescent-onset type: Individuals show no symptom characteristic\nof conduct disorder prior to age 10 years.", "source": "dsm5.pdf"} {"id": "032dc74d619d-1", "page_content": "of conduct disorder prior to age 10 years. \n312.89 (F91.9) Unspecified onset: Criteria for a diagnosis of conduct disorder are\nmet, but there is not enough information available to determine whether the onset of\nthe first symptom was before or after age 10 years. \nSpecify if:\nWith limited prosocial emotions: To qualify for this specifier, an individual must have dis-\nplayed at least two of the following characteristics persistently over at least 12 months and\nin multiple relationships and settings. These characteristics reflect the individual\u2019s typical\npattern of interpersonal and emotional functioning over this period and not just occasional\noccurrences in some situations. Thus, to assess the criteria for the specifier, multiple infor-\nmation sources are necessary. In addition to the individual\u2019s self-report, it is necessary to\nconsider reports by others who have know n the individual for extended periods of time\n(e.g., parents, teachers, co-workers, extended family members, peers).\nLack of remorse or guilt: Does not feel bad or guilty when he or she does some-\nthing wrong (exclude remorse when expre ssed only when caught and/or facing\npunishment). The individual shows a general lack of concern about the negative\nconsequences of his or her actions. For ex ample, the individual is not remorseful\nafter hurting someone or does not care about the consequences of breaking rules.\nCallous\u2014lack of empathy: Disregards and is unconcerned about the feelings of\nothers. The individual is described as cold and uncaring. The person appears more\nconcerned about the effects of his or her actions on himself or herself, rather than\ntheir effects on others, even when they result in substantial harm to others.", "source": "dsm5.pdf"} {"id": "3a2912a03708-0", "page_content": "Conduct Disorder 471\nUnconcerned about performance: Does not show concern about poor/problem-\natic performance at school, at work, or in other important activities. The individual\ndoes not put forth the effort necessary to perform well, even when expectations are\nclear, and typically blames other s for his or her poor performance.\nShallow or deficient affect: Does not express feelings or show emotions to others,\nexcept in ways that seem shallow, insincere, or superficial (e.g., actions contradict the\nemotion displayed; can turn emotions \u201con\u201d or \u201coff\u201d quickly) or when emotional expres-\nsions are used for gain (e.g., emotions displayed to manipulate or intimidate others).\nSpecify current severity:\nMild: Few if any conduct problems in excess of those required to make the diagnosis\nare present, and conduct problems cause relatively minor harm to others (e.g., lying,\ntruancy, staying out after dark without permission, other rule breaking).\nModerate: The number of conduct problems and the effect on others are intermediate\nbetween those specified in \u201cmild\u201d and those in \u201csevere\u201d (e.g., stealing without confront-\ning a victim, vandalism).\nSevere: Many conduct problems in excess of those required to make the diagnosis are\npresent, or conduct problems cause considerable harm to others (e.g., forced sex, physical\ncruelty, use of a weapon, stealing while c onfronting a victim, breaking and entering).\nSubtypes\nThree subtypes of conduct disorder are provided based on the age at onset of the disorder.\nOnset is most accurately estimated with information from both the youth and the care-\ngiver; estimates are often 2 years later than actu al onset. Both subtypes can occur in a mild,\nmoderate, or severe form. An unspecified-onse t subtype is designated when there is in-", "source": "dsm5.pdf"} {"id": "3a2912a03708-1", "page_content": "sufficient information to determine age at onset.\nIn childhood-onset conduct disorder, indivi duals are usually male, frequently display\nphysical aggression toward others, have disturbed peer rela tionships, may have had op-\npositional defiant disorder during early ch ildhood, and usually have symptoms that meet\nfull criteria for conduct disord er prior to puberty. Many children with this subtype also\nhave concurrent attention-deficit/hyperactiv ity disorder (ADHD) or other neurodevel-\nopmental difficulties. Individuals with childho od-onset type are more likely to have per-\nsistent conduct disorder into adulthood than are those with adolescent-onset type. As\ncompared with individuals with childhood-ons et type, individuals with adolescent-onset\nconduct disorder are less likely to display a ggressive behaviors and tend to have more\nnormative peer relationships (although they often display conduct problems in the com-\npany of others). These individuals are less lik ely to have conduct disorder that persists into\nadulthood. The ratio of males to females with conduct disorder is more balanced for the\nadolescent-onset type than for the childhood-onset type.\nSpecifiers\nA minority of individuals with conduct disorder exhibit characteristics that qualify for the\n\u201cwith limited prosocial emotions\u201d specifier. The indicators of this specifier are those that\nhave often been labeled as callous and unemot ional traits in research. Other personality\nfeatures, such as thrill seeking, fearlessness,\u00a0and insensitivity to punishment, may also dis-\ntinguish those with characteri stics described in the specifier. Individuals with character-\nistics described in this specifier may be mo re likely than other individuals with conduct\ndisorder to engage in aggression that is planned for instrumental gain. Individuals with\nconduct disorder of any subtype or any level of severity can have characteristics that qual-", "source": "dsm5.pdf"} {"id": "3a2912a03708-2", "page_content": "conduct disorder of any subtype or any level of severity can have characteristics that qual-\nify for the specifier \u201cwith limited prosocial em otions,\u201d although individuals with the spec-\nifier are more likely to have childhood-onset ty pe and a severity specifier rating of severe.", "source": "dsm5.pdf"} {"id": "d7c0927da89a-0", "page_content": "472 Disruptive, Impulse-Control, and Conduct Disorders\nAlthough the validity of self-report to assess the presence of the specifier has been sup-\nported in some research contexts, individual s with conduct disorder with this specifier\nmay not readily admit to the traits in a clinical interview. Thus, to assess the criteria for the\nspecifier, multiple information sources are ne cessary. Also, because the indicators of the\nspecifier are characteristics that reflect the in dividual\u2019s typical pattern of interpersonal and\nemotional functioning, it is important to co nsider reports by others who have known the\nindividual for extended periods of time an d across relationships and settings (e.g., par-\nents, teachers, co-workers, extended family members, peers).\nDiagnostic Features\nThe essential feature of conduct disorder is a repetitive and persistent pattern of behavior\nin which the basic rights of others or major age-appropriate societal norms or rules are vi-\nolated (Criterion A). These be haviors fall into four main groupings: aggressive conduct\nthat causes or threatens physical harm to other people or animals (Criteria A1\u2013A7); non-\naggressive conduct that causes property loss or damage (Criteria A8\u2013A9); deceitfulness or\ntheft (Criteria A10\u2013A12); and serious violations of rules (Criteria A13\u2013A15). Three or more\ncharacteristic behaviors must ha ve been present during the pa st 12 months, with at least\none behavior present in the past 6 months. The disturbance in behavior causes clinically\nsignificant impairment in social, academic, or occupational functioning (Criterion B). The\nbehavior pattern is usually pres ent in a variety of settings, su ch as home, at school, or in\nthe community. Because individu als with conduct disorder ar e likely to minimize their\nconduct problems, the clinician often must rely on additional informants. However, infor-", "source": "dsm5.pdf"} {"id": "d7c0927da89a-1", "page_content": "conduct problems, the clinician often must rely on additional informants. However, infor-\nmants\u2019 knowledge of the individual\u2019s conduct problems may be limited if they have inad-\nequately supervised the individual or the individual has concealed symptom behaviors.\nIndividuals with conduct disorder often initiate aggressive behavior and react aggres-\nsively to others. They may display bullying, th reatening, or intimidating behavior (includ-\ning bullying via messaging on Web-based social media) (Criterion A1); initiate frequent\nphysical fights (Criteri on A2); use a weapon that can caus e serious physical harm (e.g., a bat,\nbrick, broken bottle, knife, gun) (Criterion A3); be physically cruel to people (Criterion A4)\nor animals (Criterion A5); steal while confronting a victim (e.g., mugging, purse snatching,\nextortion, armed robbery) (Criterion A6); or force someone into sexual activity (Criterion A7).\nPhysical violence may take the form of rape, assault, or, in rare cases, homicide. Deliberate\ndestruction of others\u2019 property may include delibe rate fire setting with the intention of caus-\ning serious damage (Criterion A8) or deliberate destroying of other people\u2019s property in\nother ways (e.g., smashing car windows, vandal izing school property) (C riterion A9). Acts of\ndeceitfulness or theft may include breaking into someone else\u2019s house, building, or car (Crite-\nrion A10); frequently lying or breaking promises to obtain goods or favors or to avoid debts\nor obligations (e.g., \u201cconning\u201d other individual s) (Criterion A11); or stealing items of non-\ntrivial value without confronting the victim (e.g., shoplifting, forgery, fraud) (Criterion A12).", "source": "dsm5.pdf"} {"id": "d7c0927da89a-2", "page_content": "Individuals with conduct diso rder may also frequently commit serious violations of\nrules (e.g., school, parental, workplace). Children with cond uct disorder often have a pat-\ntern, beginning before age 13 years, of stay ing out late at night despite parental prohi-\nbitions (Criterion A13). Children may also show a pattern of running away from home\novernight (Criterion A14). To be considered a symptom of conduct disorder, the running\naway must have occurred at le ast twice (or only once if the individual did not return for a", "source": "dsm5.pdf"} {"id": "c0d19c1fa0ad-0", "page_content": "overnight (Criterion A14). To be considered a symptom of conduct disorder, the running\naway must have occurred at le ast twice (or only once if the individual did not return for a\nlengthy period). Runaway episodes that occur as a direct consequence of physical or sex-\nual abuse do not typically qualify for this criterion. Children with conduct disorder may\noften be truant from school, beginning prior to age 13 years (Criterion A15).\nAssociated Features Supporting Diagnosis\nEspecially in ambiguous situ ations, aggressive individual s with conduct disorder fre-\nquently misperceive the intentio ns of others as more hostile and threatening than is the", "source": "dsm5.pdf"} {"id": "fee43fa5c762-0", "page_content": "Conduct Disorder 473\ncase and respond with aggression that they th en feel is reasonable and justified. Person-\nality features of trait negative emotionality and poor self-control, including poor frustra-\ntion tolerance, irritability, temper outbursts, suspiciousness, insens itivity to punishment,\nthrill seeking, and recklessnes s, frequently co-occur with conduct disorder. Substance\nmisuse is often an associated fe ature, particularly in adolescent females. Suicidal ideation,\nsuicide attempts, and completed suicide occur at a higher-than-expected rate in individu-\nals with conduct disorder. \nPrevalence\nOne-year population prevalence estimates range from 2% to more than 10%, with a median\nof 4%. The prevalence of conduct disorder a ppears to be fairly consistent across various\ncountries that differ in race and ethnicity. Pr evalence rates rise from childhood to adoles-\ncence and are higher among males than amon g females. Few children with impairing con-\nduct disorder receive treatment.\nDevelopment and Course\nThe onset of conduct disorder may occur as ea rly as the preschool years, but the first sig-\nnificant symptoms usually emerge during the period from middle childhood through\nmiddle adolescence. Oppositi onal defiant disorder is a common precursor to the child-\nhood-onset type of conduct disorder. Conduct disorder may be diagnosed in adults, how-\never, symptoms of conduct di sorder usually emerge in ch ildhood or adol escence, and\nonset is rare after age 16 years. The course of conduct disorder after onset is variable. In a\nmajority of individuals, the disorder remits by adulthood. Many individuals with conduct\ndisorder\u2014particularly those with adolescent-onset type and those with few and milder", "source": "dsm5.pdf"} {"id": "fee43fa5c762-1", "page_content": "disorder\u2014particularly those with adolescent-onset type and those with few and milder\nsymptoms\u2014achieve adequate social and occupa tional adjustment as adults. However, the\nearly-onset type predicts a worse prognosis and an increased risk of criminal behavior,\nconduct disorder, and substance-related disord ers in adulthood. Individuals with conduct\ndisorder are at risk for later mood disorders, anxiety disorders, posttraumatic stress dis-\norder, impulse-control disord ers, psychotic disorders, so matic symptom disorders, and\nsubstance-related disorders as adults. \nSymptoms of the disorder vary with age as the individual develops increased physical\nstrength, cognitive abilities, and sexual ma turity. Symptom behaviors that emerge first\ntend to be less serious (e.g., lying, shoplifti ng), whereas conduct problems that emerge last\ntend to be more severe (e.g., rape, theft wh ile confronting a victim ). However, there are\nwide differences among individuals, with some enga ging in the more damaging behaviors\nat an early age (which is predictive of a worse prognosis). When individuals with conduct\ndisorder reach adulthood, symptoms of aggres sion, property destruction, deceitfulness,\nand rule violation, including violence against co-workers, partners, and children, may be ex-\nhibited in the workplace and the home, such that antisocial personality disorder may be\nconsidered. \nRisk and Prognostic Factors\nTemperamental. Temperamental risk factors include a difficult undercontrolled infant\ntemperament and lower-than-average intelligence , particularly with regard to verbal IQ.\nEnvironmental. Family-level risk factors include parental rejection and neglect, inconsis-\ntent child-rearing practices, harsh discipline, physical or sexual abuse, lack of supervision,\nearly institutional living, freque nt changes of caregivers, large family size, parental criminal-", "source": "dsm5.pdf"} {"id": "fee43fa5c762-2", "page_content": "early institutional living, freque nt changes of caregivers, large family size, parental criminal-\nity, and certain kinds of familial psychopath ology (e.g., substance-related disorders). Com-\nmunity-level risk factors include peer rejection, association with a delinquent peer group,\nand neighborhood exposure to violence. Both types of risk factors te nd to be more common\nand severe among individuals with the child hood-onset su btype of conduct disorder.", "source": "dsm5.pdf"} {"id": "74696c8bf732-0", "page_content": "474 Disruptive, Impulse-Control, and Conduct Disorders\nGenetic and physiological. Conduct disorder is influenced by both genetic and envi-\nronmental factors. The risk is increased in child ren with a biological or adoptive parent or\na sibling with conduct disorder. The disorder also appears to be more common in children\nof biological parents with severe alcohol us e disorder, depressive and bipolar disorders, or\nschizophrenia or biological parents who have a history of ADHD or conduct disorder.\nFamily history particularly characterizes in dividuals with the childhood-onset subtype of\nconduct disorder. Slower resting heart rate has been reliably noted in individuals with\nconduct disorder compared with those without the disorder, and this marker is not char-\nacteristic of any other mental disorder. Reduced autonomic fe ar conditioning, particularly\nlow skin conductance, is also well documented. However, these psychophysiological find-\nings are not diagnostic of the disorder. Structural and functional differences in brain areas\nassociated with affect regulation and affect processing, particularly frontotemporal-limbic\nconnections involving the brain\u2019s ventral pref rontal cortex and amygdala, have been con-\nsistently noted in individuals with conduct d isorder compared with those without the dis-\norder. However, neuroimaging findings are not diagnostic of the disorder.\nCourse modifiers. Persistence is more likely for indi viduals with behaviors that meet\ncriteria for the childhood-onset subtype and qualify for the specifier \u201cwith limited pro-\nsocial emotions\u201d. The risk that conduct disorder will persist is also increased by co-occurring\nADHD and by substance abuse. \nCulture-Related Diagnostic Issues\nConduct disorder diagnosis may at times be potentially misapplied to individuals in set-\ntings where patterns of disruptive behavior are viewed as near-normative (e.g., in very", "source": "dsm5.pdf"} {"id": "74696c8bf732-1", "page_content": "tings where patterns of disruptive behavior are viewed as near-normative (e.g., in very\nthreatening, high-crime areas or war zones). Therefore, the context in which the undesir-\nable behaviors have occurr ed should be considered.\nGender-Related Diagnostic Issues\nMales with a diagnosis of conduct disorder frequently exhibit fighting, stealing, vandalism,\nand school discipline problems. Females with a diagnosis of conduct disorder are more likely\nto exhibit lying, truancy, running away, subs tance use, and prostitution. Whereas males tend\nto exhibit both physical aggression and relation al aggression (behavior that harms social re-\nlationships of others), females tend to exhibit relatively more relational aggression.\nFunctional Consequences of Conduct Disorder \nConduct disorder behaviors may lead to sch ool suspension or expulsion, problems in\nwork adjustment, legal difficulties, sexually transmitted diseases, unplanned pregnancy,\nand physical injury from accidents or fights . These problems may preclude attendance in\nordinary schools or living in a parental or foster home. Conduct disorder is often associ-\nated with an early onset of sexual behavior, alcohol use, to bacco smoking, use of illegal\nsubstances, and reckless and risk-taking acts. Ac cident rates appear to be higher among in-\ndividuals with conduct disord er compared with those without the disorder. These func-\ntional consequences of conduct disorder may predict health difficulties when individuals\nreach midlife. It is not uncommon for individu als with conduct disorder to come into con-\ntact with the criminal justice system for engaging in illegal behavior. Conduct disorder is\na common reason for treatment referral and is frequently diagnosed in mental health fa-\ncilities for children, especially in forensic practice. It is associated with impairment that is\nmore severe and chronic than that expe rienced by other clinic-referred children.\nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "74696c8bf732-2", "page_content": "Differential Diagnosis\nOppositional defiant disorder. Conduct disorder and oppositi onal defiant disorder are\nboth related to symptoms that bring the indi vidual in conflict with adults and other au-", "source": "dsm5.pdf"} {"id": "8b24a243d1f7-0", "page_content": "Conduct Disorder 475\nthority figures (e.g., parents, teachers, work supervisors). The behaviors of oppositional\ndefiant disorder are typically of a less severe nature than those of individuals with conduct\ndisorder and do not include aggression towa rd individuals or animals, destruction of\nproperty, or a pattern of theft or deceit. Fu rthermore, oppositional defiant disorder in-\ncludes problems of emotional dysregulation (i.e ., angry and irritable mood) that are not in-\ncluded in the definition of conduct disorder. When criteria are met for both oppositional\ndefiant disorder and conduct disord er, both diagnoses can be given.\nAttention-deficit/hyperactivity disorder. Although children with ADHD often exhibit\nhyperactive and impulsive behavior that may be disruptive, this behavior does not by it-\nself violate societal norms or the rights of others and therefore does not usually meet cri-\nteria for conduct disorder. When criteria are met for both ADHD and conduct disorder, both\ndiagnoses should be given.\nDepressive and bipolar disorders. Irritability, aggression, and conduct problems can\noccur in children or adolescents with a majo r depressive disorder, a bipolar disorder, or\ndisruptive mood dysregulation disorder. The behaviorial problems associated with these\nmood disorders can usually be distinguished from the pattern of conduct problems seen in\nconduct disorder based on their course. Spec ifically, persons with conduct disorder will\ndisplay substantial levels of aggressive or non-aggressive conduct problems during peri-\nods in which there is no mood disturbance, ei ther historically (i.e., a history of conduct\nproblems predating the onset of the mood disturbance) or concurrently (i.e., display of\nsome conduct problems that ar e premeditated and do not occur during periods of intense", "source": "dsm5.pdf"} {"id": "8b24a243d1f7-1", "page_content": "some conduct problems that ar e premeditated and do not occur during periods of intense\nemotional arousal). In those cases in which cr iteria for conduct disorder and a mood dis-\norder are met, both diagnoses can be given. \nIntermittent explosive disorder. Both conduct disorder and intermittent explosive dis-\norder involve high rates of aggression. However, the aggression in individuals with inter-\nmittent explosive disorder is limited to impu lsive aggression and is not premeditated, and\nit is not committed in order to achieve some tangible objectiv e (e.g., money, power, intim-\nidation). Also, the definition of intermittent explosive disorder does not include the non-\naggressive symptoms of conduct disorder. If criteria for both disorders are met, the diag-\nnosis of intermittent explosive disorder sh ould be given only when the recurrent impul-\nsive aggressive outbursts warrant in dependent clinical attention. \nAdjustment disorders. The diagnosis of an adjustment di sorder (with disturbance of con-\nduct or with mixed disturbance of emotions an d conduct) should be co nsidered if clinically\nsignificant conduct problems that do not meet the criteria for another specific disorder de-\nvelop in clear association with the onset of a psychosocial stressor and do not resolve within\n6 months of the termination of the stressor (o r its consequences). Cond uct disorder is diag-\nnosed only when the conduct problems represen t a repetitive and pers istent pattern that is\nassociated with impairment in social, academic, or occupational functioning.\nComorbidity\nADHD and oppositional defiant disorder are both common in individuals with conduct\ndisorder, and this comorbid presentation pr edicts worse outcomes. Individuals who show\nthe personality features associated with anti social personality disorder often violate the", "source": "dsm5.pdf"} {"id": "8b24a243d1f7-2", "page_content": "the personality features associated with anti social personality disorder often violate the\nbasic rights of others or violate major age-appr opriate societal norms, and as a result their\npattern of behavior often meets criteria fo r conduct disorder. Conduct disorder may also\nco-occur with one or more of the following me ntal disorders: specif ic learning disorder,\nanxiety disorders, depressive or bipolar diso rders, and substance-related disorders. Aca-", "source": "dsm5.pdf"} {"id": "ce75b0f34688-0", "page_content": "co-occur with one or more of the following me ntal disorders: specif ic learning disorder,\nanxiety disorders, depressive or bipolar diso rders, and substance-related disorders. Aca-\ndemic achievement, particularly in reading an d other verbal skills, is often below the level\nexpected on the basis of age and intelligence and may justify the additional diagnosis of\nspecific learning disorder or a communication disorder.", "source": "dsm5.pdf"} {"id": "d68ab5d8f5a6-0", "page_content": "476 Disruptive, Impulse-Control, and Conduct Disorders\nAntisocial Personality Disorder\nCriteria and text for antisocial personality disorder can be found in the chapter \u201cPerson-\nality Disorders.\u201d Because this disorder is closely connected to the spectrum of \u201cexternal-\nizing\u201d conduct disorders in this chapter, as we ll as to the disorders in the adjoining chapter\n\u201cSubstance-Related and Addictiv e Disorders,\u201d it is dual code d here as well as in the chap-\nter \u201cPersonality Disorders.\u201d\nPyromania\nDiagnostic Criteria 312.33 (F63.1)\nA. Deliberate and purposeful fire setting on more than one occasion.\nB. Tension or affective arousal before the act.\nC. Fascination with, interest in, curiosity about, or attraction to fire and its situational con-\ntexts (e.g., paraphernalia, uses, consequences).\nD. Pleasure, gratification, or relief when setting fires or when witnessing or participating\nin their aftermath.\nE. The fire setting is not done for monetary gain, as an expression of sociopolitical ideol-\nogy, to conceal criminal activity, to express anger or vengeance, to improve one\u2019s living\ncircumstances, in response to a delusion or hallucination, or as a result of impaired\njudgment (e.g., in major neurocognitive disorder, intellectual disability [intellectual de-\nvelopmental disorder], substance intoxication).\nF. The fire setting is not better explained by conduct disorder, a manic episode, or anti-\nsocial personality disorder.\nDiagnostic Features\nThe essential feature of pyromania is the pres ence of multiple episodes of deliberate and\npurposeful fire setting (Criterion A). Individuals with this disorder experience tension or af-\nfective arousal before setting a fi re (Criterion B). There is a f ascination with, interest in, cu-", "source": "dsm5.pdf"} {"id": "d68ab5d8f5a6-1", "page_content": "riosity about, or attraction to fire and its situational contexts (e.g., paraphernalia, uses,\nconsequences) (Criterion C). Individuals with this disorder are often regular \u201cwatchers\u201d at\nfires in their neig hborhoods, may set off false alarms, and derive pleasure from institutions,\nequipment, and personnel associat ed with fire. They may spend time at the local fire depart-\nment, set fires to be affiliated with the fire department, or even beco me firefighters. Individ-\nuals with this disorder experi ence pleasure, gratification, or relief when setting the fire,\nwitnessing its effects, or participating in its aftermath (Criterion D). The fire setting is not\ndone for monetary gain, as an expression of so ciopolitical ideology, to conceal criminal ac-\ntivity, to express anger or vengeance, to impr ove one\u2019s living circumstances, or in response\nto a delusion or a hallucination (Criterion E). The fire setting does not result from impaired\njudgment (e.g., in major neurocog nitive disorder or intellectual disability [intellectual devel-\nopmental disorder]). The diagnosis is not made if the fire setting is better explained by con-\nduct disorder, a manic episode, or antiso cial personality disorder (Criterion F).\nAssociated Features Supporting Diagnosis\nIndividuals with pyromania may make considerable advance preparation for starting a\nfire. They may be indifferent to the consequences to life or property caused by the fire, or", "source": "dsm5.pdf"} {"id": "fed490a4568c-0", "page_content": "Pyromania 477\nthey may derive satisfaction from the resulting property destruction. The behaviors may\nlead to property damage, legal co nsequences, or injury or loss of life to the fire setter or to\nothers. Individuals who impulsively set fires (who may or may not have pyromania) often\nhave a current or past history of alcohol use disorder.\nPrevalence\nThe population prevalence of pyromania is no t known. The lifetime prevalence of fire set-\nting, which is just one component of pyromania and not sufficient for a diagnosis by itself,\nwas reported as 1.13% in a population sample, but the mo st common como rbidities were\nantisocial personality disorder, substance use disorder, bipolar disorder, and pathological\ngambling (gambling disorder). In contrast, pyromania as a primary diagnosis appears to\nbe very rare. Among a sample of persons reachi ng the criminal system with repeated fire\nsetting, only 3.3% had symptoms th at met full criteria for pyromania. \nDevelopment and Course\nThere are insufficient data to establish a typi cal age at onset of pyromania. The relation-\nship between fire setting in childhood and pyromania in adulthood has not been docu-\nmented. In individuals with pyromania, fire -setting incidents are episodic and may wax\nand wane in frequency. Longitudinal course is unknown. Although fire setting is a major\nproblem in children and adolescents (over 40% of those arrested for arson offenses in the\nUnited States are younger than 18 years), pyromania in childhood appears to be rare. Ju-\nvenile fire setting is usually associated with conduct disorder, attention-deficit/hyperac-\ntivity disorder, or an adjustment disorder.\nGender-Related Diagnostic Issues", "source": "dsm5.pdf"} {"id": "fed490a4568c-1", "page_content": "tivity disorder, or an adjustment disorder.\nGender-Related Diagnostic Issues\nPyromania occurs much more often in males, es pecially those with poorer social skills and\nlearning difficulties.\nDifferential Diagnosis\nOther causes of intentional fire setting. It is important to rule out other causes of fire\nsetting before giving the diagnosis of pyroma nia. Intentional fire setting may occur for\nprofit, sabotage, or revenge; to conceal a crime; to make a po litical statement (e.g., an act of\nterrorism or protest); or to attract attention or recognition (e.g., setting a fire in order to dis-\ncover it and save the day). Fire setting may also occur as part of developmental experi-\nmentation in childhood (e.g., playing with matches, lighters, or fire). \nOther mental disorders. A separate diagnosis of pyromania is not given when fire set-\nting occurs as part of conduct disorder, a mani c episode, or antisocial personality disorder,\nor if it occurs in response to a delusion or a hallucination (e.g., in schizophrenia) or is at-\ntributable to the physiological effects of anot her medical condition (e.g., epilepsy). The di-\nagnosis of pyromania should also not be gi ven when fire setting results from impaired\njudgment associated with major neurocognitive disorder, intellectual disability, or sub-\nstance intoxication.\nComorbidity\nThere appears to be a high co-occurrence of substance use disorders, gambling disorder,\ndepressive and bipolar disorder s, and other disruptive, impu lse-control, and conduct dis-\norders with pyromania.", "source": "dsm5.pdf"} {"id": "82a8422ebc55-0", "page_content": "478 Disruptive, Impulse-Control, and Conduct Disorders\nKleptomania\nDiagnostic Criteria 312.32 (F63.2)\nA. Recurrent failure to resist impulses to steal objects that are not needed for personal\nuse or for their monetary value.\nB. Increasing sense of tension immediately before committing the theft.\nC. Pleasure, gratification, or relief at the time of committing the theft.\nD. The stealing is not committed to express anger or vengeance and is not in response\nto a delusion or a hallucination.\nE. The stealing is not better explained by conduct disorder, a manic episode, or antisocial\npersonality disorder.\nDiagnostic Features\nThe essential feature of kleptomania is the recurrent failure to resist impulses to steal items\neven though the items are not ne eded for personal use or for their monetary value (Criterion\nA). The individual experiences a rising subjective sense of tension before the theft (Criterion B)\nand feels pleasure, gratification, or relief when committing the theft (Criterion C). The stealing\nis not committed to express anger or vengeance, is not done in response to a delusion or hal-\nlucination (Criterion D), and is not better explained by conduc t disorder, a manic episode, or\nantisocial personality disorder (Criterion E). The objects are stolen despite the fact that they are\ntypically of little value to the individual, who could have afforded to pay for them and often\ngives them away or discards them. Occasionally the individual may hoard the stolen objects or\nsurreptitiously return them. Al though individuals with this disorder will generally avoid\nstealing when immediate arrest is probable (e.g., in full view of a po lice officer), they usually\ndo not preplan the thefts or fully take into ac count the chances of apprehension. The stealing is", "source": "dsm5.pdf"} {"id": "82a8422ebc55-1", "page_content": "done without assistance from, or collaboration with, others.\nAssociated Features Supporting Diagnosis\nIndividuals with kleptomania typically attempt to resist the impulse to steal, and they are\naware that the act is wrong and senseless. The individual frequently fears being appre-\nhended and often feels depressed or guilty about the thefts. Neurotransmitter pathways\nassociated with behavioral addictions, includ ing those associated with the serotonin, do-\npamine, and opioid systems, appear to play a role in kleptomania as well.\nPrevalence\nKleptomania occurs in about 4%\u201324% of indivi duals arrested for shoplifting. Its preva-\nlence in the general population is very rare, at approximately 0.3%\u20130.6%. Females outnum-\nber males at a ratio of 3:1.\nDevelopment and Course\nAge at onset of kleptomania is variable, but th e disorder often begins in adolescence. How-\never, the disorder may begin in childhood, adolescence, or adulthood, and in rare cases\nin late adulthood. There is little systematic information on the course of kleptomania, but\nthree typical courses have been described: sp oradic with brief episodes and long periods\nof remission; episodic with protracted peri ods of stealing and periods of remission; and\nchronic with some degree of fluctuation. Th e disorder may continue for years, despite\nmultiple convictions for shoplifting.", "source": "dsm5.pdf"} {"id": "752c0bcb8d6e-0", "page_content": "Other Specified Disruptive, Impulse-Control, and Conduct Disorder 479\nRisk and Prognostic Factors\nGenetic and physiological. There are no controlled family history studies of kleptoma-\nnia. However, first-degree relatives of in dividuals with klepto mania may have higher\nrates of obsessive-compulsive disorder than the general population. There also appears to\nbe a higher rate of substance use disorders, including alcohol use disorder, in relatives of\nindividuals with kleptomania than in the general population. \nFunctional Consequenc es of Kleptomania\nThe disorder may cause legal, family , career, and personal difficulties.\nDifferential Diagnosis\nOrdinary theft. Kleptomania should be distinguishe d from ordinary acts of theft or\nshoplifting. Ordinary theft (whether planned or impulsive) is deliberate and is motivated\nby the usefulness of the object or its monetary worth. Some individuals, especially adoles-\ncents, may also steal on a dare, as an act of re bellion, or as a rite of passage. The diagnosis\nis not made unless other characteristic featur es of kleptomania are also present. Klepto-\nmania is exceedingly rare, whereas sh oplifting is relatively common. \nMalingering. In malingering, individuals may simulate the symptoms of kleptomania to\navoid criminal prosecution. \nAntisocial personality disorder and conduct disorder. Antisocial personality disorder\nand conduct disorder are distinguished from kleptomania by a general pattern of antiso-\ncial behavior. \nManic episodes, psychotic episodes, and major neurocognitive disorder. Kleptomania\nshould be distinguished from intentional or inadvertent stealing that may occur during a\nmanic episode, in response to delusions or ha llucinations (as in, e.g. , schizophrenia), or as", "source": "dsm5.pdf"} {"id": "752c0bcb8d6e-1", "page_content": "a result of a major neurocognitive disorder.\nComorbidity\nKleptomania may be associated with compulsive buying as well as with depressive and\nbipolar disorders (especially major depressive disorder), anxiety disorders, eating disor-\nders (particularly bulimia ner vosa), personality disorders, substance use disorders (espe-\ncially alcohol use disorder), and other disruptive, impulse-control, and conduct disorders. \nOther Specified Disruptive, Impulse-Control,\nand Conduct Disorder\n312.89 (F91.8)\nThis category applies to presentations in which symptoms characteristic of a disruptive,\nimpulse-control, and conduct disorder that cause clinically significant distress or impair-\nment in social, occupational, or other impor tant areas of functioning predominate but do\nnot meet the full criteria for any of the disor ders in the disruptive, impulse-control, and con-\nduct disorders diagnostic class. The other specified disruptive, impulse-control, and con-\nduct disorder category is used in situations in which the clinician chooses to communicate\nthe specific reason that the presentation does not meet the criteria for any specific disrup-\ntive, impulse-control, and conduct disorder. This is done by recording \u201cother specified dis-\nruptive, impulse-control, and conduct disorder\u201d followed by the specific reason (e.g.,\n\u201crecurrent behavioral outbursts of insufficient frequency\u201d).", "source": "dsm5.pdf"} {"id": "4454b054a705-0", "page_content": "480 Disruptive, Impulse-Control, and Conduct Disorders\nUnspecified Disruptive, Impulse-Control,\n and Conduct Disorder\n312.9 (F91.9)\nThis category applies to presentations in which symptoms characteristic of a disruptive,\nimpulse-control, and conduct disorder that cause clinically significant distress or impair-\nment in social, occupational, or other impor tant areas of functioning predominate but do\nnot meet the full criteria for any of the disorders in the disruptive, impulse-control, and con-\nduct disorders diagnostic class. The unspecif ied disruptive, impulse-control, and conduct\ndisorder category is used in situations in which the clinician chooses not to specify the rea-\nson that the criteria are not met for a specific disruptive, impulse-control, and conduct dis-\norder, and includes presentations in which there is insufficient information to make a more\nspecific diagnosis (e.g., in emergency room settings).", "source": "dsm5.pdf"} {"id": "f2e7f06c46c0-0", "page_content": "481Substance-Related and\nAddictive Disorders\nThe substance-related disorders encompass 10 separate classes of drugs: alco-\nhol; caffeine; cannabis; hallucinogens (with separate categories for phencyclidine [or sim-\nilarly acting arylcyclohexylamines] and ot her hallucinogens); inhalants; opioids;\nsedatives, hypnotics, and anxiolytics; stimul ants (amphetamine-type substances, cocaine,\nand other stimulants); tobacco ; and other (or unknown) subs tances. These 10 classes are\nnot fully distinct. All drugs that are taken in excess have in common direct activation of\nthe brain reward system, which is involved in the reinforcement of behaviors and the pro-\nduction of memories. They produce such an in tense activation of the reward system that\nnormal activities may be neglected. Inst ead of achieving reward system activation\nthrough adaptive behaviors, drugs of abuse directly activate the reward pathways. The\npharmacological mechanisms by which each class of drugs produces reward are different,\nbut the drugs typically activate the system and produce feelings of pleasure, often re-\nferred to as a \u201chigh.\u201d Furthe rmore, individuals with lower levels of self-control, which\nmay reflect impairments of brain inhibitory mechanisms, may be particularly predisposed\nto develop substance use disord ers, suggesting that the root s of substance use disorders\nfor some persons can be seen in behaviors long before the onset of actual substance use\nitself.\nIn addition to the substance-related disorders, this chapter also includes gambling dis-\norder, reflecting evidence that gambling be haviors activate reward systems similar to\nthose activated by drugs of abuse and produce some behavi oral symptoms that appear\ncomparable to those produced by the substa nce use disorders. Other excessive behavioral", "source": "dsm5.pdf"} {"id": "f2e7f06c46c0-1", "page_content": "comparable to those produced by the substa nce use disorders. Other excessive behavioral\npatterns, such as Internet gaming, have also been described, but the research on these and\nother behavioral syndromes is less clear. Thus, groups of repetitive behaviors, which some\nterm behavioral addictions, with such subcategories as \u201csex addiction,\u201d \u201cexercise addiction,\u201d\nor \u201cshopping addiction,\u201d are not included becaus e at this time there is insufficient peer-re-\nviewed evidence to establish the diagnostic criteria and co urse descriptions needed to\nidentify these behaviors as mental disorders. \nThe substance-related disorder s are divided into two groups: substance use disorders\nand substance-induced disorders. The followi ng conditions may be classified as sub-\nstance-induced: intoxication, withdrawal, an d other substance/medication-induced men-\ntal disorders (psychotic disord ers, bipolar and related disorders, depressive disorders,\nanxiety disorders, obsessive-compulsive and re lated disorders, sleep disorders, sexual dys-\nfunctions, delirium, and neurocognitive disorders). \nThe current section begins with a general di scussion of criteria sets for a substance\nuse disorder, substance intoxication and withdrawal, and other substance/medication-\ninduced mental disorders, at least some of which are a pplicable across classes of sub-\nstances. Reflecting some unique aspects of the 10 substance classes relevant to this chapter,\nthe remainder of the chapter is organized by the class of substance and describes their\nunique aspects. To facilitate differential diagnosis, the text and criteria for the remaining\nsubstance/medication-induced mental disorder s are included with disorders with which\nthey share phenomenology (e.g ., substance/medication-induced depressive disorder is in\nthe chapter \u201cDepressive Disorder s\u201d). The broad diagnostic cate gories associated with each\nspecific group of substances are shown in Table 1.", "source": "dsm5.pdf"} {"id": "1ccb7175d70e-0", "page_content": "482 Substance-Related and Addictive DisordersTABLE 1 Diagnoses associated with substance class\n\u00a0Psychotic \ndisordersBipolar \ndisordersDepres-\nsive \ndisordersAnxiety \ndisordersObsessive-\ncompulsive \nand related \ndisordersSleep \ndisordersSexual \ndysfunc-\ntions DeliriumNeuro-\ncognitive \ndisordersSubstance \nuse \ndisordersSub-\nstance \nintoxi-\ncationSub-\nstance \nwith-\ndrawal\nAlcohol I/W I/W I/W I/W I/W I/W I/W I/W/P X X X\nCaffeine \u00a0 \u00a0 I \u00a0 I/W \u00a0 \u00a0 \u00a0 X X\nCannabis I \u00a0 I \u00a0 I/W \u00a0 I X X X\nHallucinogens\nPhencyclidine I I I I \u00a0 \u00a0 I X X \u00a0\nOther hallucino-\ngensI* I I I \u00a0 \u00a0 I X X \u00a0\nInhalants I I\u00a0 I\u00a0 \u00a0 \u00a0 \u00a0 I I/P X X \u00a0\nOpioids I/W W \u00a0 I/W I/W I/W X X X\nSedatives, \nhypnotics, or \nanxiolyticsI/W I/W I/W W I/W I/W I/W I/W/P X X X\nStimulants** I I/W I/W I/W I/W I/W I I X X X\nTobacco \u00a0 \u00a0 \u00a0 \u00a0 W \u00a0 \u00a0 X \u00a0 X\nOther (or \nunknown)I/W I/W I/W I/W I/W I/W I/W I/W I/W/P X X X\nNote. X = The category is recognized in DSM-5.\nI = The specifier \u201cwith onset during intoxication\u201d may be noted for the category.\nW = The specifier \u201cwith onset during with drawal\u201d may be noted for the category.", "source": "dsm5.pdf"} {"id": "1ccb7175d70e-1", "page_content": "W = The specifier \u201cwith onset during with drawal\u201d may be noted for the category.\nI/W = Either \u201cwith onset during intoxication\u201d or \u201cwith onset during withdrawal\u201d may be noted for the category.\nP = The disorder is persisting.\n*Also hallucinogen persisting perception disorder (flashbacks).\n**Includes amphetamine-type substances, coca ine, and other or unspecified stimulants.", "source": "dsm5.pdf"} {"id": "96e94eb61be8-0", "page_content": "Substance Use Disorders 483\nSubstance-Related Disorders\nSubstance Use Disorders\nFeatures\nThe essential feature of a substance use disorder is a cluster of cognitive, behavioral, and\nphysiological symptoms indicating that the individual continues using the substance de-\nspite significant substance-related problems. As seen in Table 1, the diagnosis of a sub-\nstance use disorder can be applied to all 10 cl asses included in this chapter except caffeine.\nFor certain classes some symptoms are less sa lient, and in a few instances not all symptoms\napply (e.g., withdrawal symptoms are not sp ecified for phencyclidin e use disorder, other\nhallucinogen use disorder, or inhalant use disorder). \nAn important characteristic of substance use disorders is an underlying change in brain cir-\ncuits that may persist beyond detoxification, part icularly in individuals with severe disorders.\nThe behavioral effect s of these brain changes may be exhibited in the repeated relapses and in-\ntense drug craving when the individuals are exposed to drug-related stimuli. These persistent\ndrug effects may benefit from long-term approaches to treatment.\nOverall, the diagnosis of a su bstance use disorder is based on a pathological pattern of\nbehaviors related to use of the substance. To as sist with organization, Criterion A criteria can\nbe considered to fit within overall groupings of impaired control, social impairment, risky use,\nand pharmacological criteria. Impaired control over substance use is the first criteria grouping\n(Criteria 1\u20134). The individual may take the substance in larger amounts or over a longer pe-\nriod than was originally intended (Criterion 1). The individual may express a persistent de-\nsire to cut down or regulate substance use and may report multiple unsuccessful efforts to", "source": "dsm5.pdf"} {"id": "96e94eb61be8-1", "page_content": "sire to cut down or regulate substance use and may report multiple unsuccessful efforts to\ndecrease or discontinue use (Cri terion 2). The individual may sp end a great deal of time ob-\ntaining the substance, using the substance, or recovering from its effects (Criterion 3). In\nsome instances of more severe substance use disorders, virtually all of the individual\u2019s daily\nactivities revolve around the substance. Craving (Criterion 4) is manifested by an intense de-\nsire or urge for the drug that may occur at an y time but is more likely when in an environ-\nment where the drug previous ly was obtained or used. Cr aving has also been shown to\ninvolve classical conditioning and is associated with activation of specific reward structures\nin the brain. Craving is queried by asking if there has ever been a time when they had such\nstrong urges to take the drug th at they could not think of anythi ng else. Current craving is of-\nten used as a treatment outcome measure becaus e it may be a signal of impending relapse.\nSocial impairment is the second grouping of criteria (Criteria 5\u20137) . Recurrent substance\nuse may result in a failure to fulfill major role obligations at work, sc hool, or home (Crite-\nrion 5). The individual may continue substanc e use despite having persistent or recurrent\nsocial or interpersonal problems caused or ex acerbated by the effects of the substance (Cri-\nterion 6). Important social, occupational, or re creational activities ma y be given up or re-\nduced because of substance us e (Criterion 7). The individual may withdraw from family\nactivities and hobbies in order to use the substance. \nRisky use of the substance is the third grouping of criteria (Criteria 8\u20139). This may take", "source": "dsm5.pdf"} {"id": "96e94eb61be8-2", "page_content": "the form of recurrent substanc e use in situations in which it is physically hazardous (Cri-\nterion 8). The individual may continue substance use despite knowledge of having a per-\nsistent or recurrent physical or psychological problem that is likely to have been caused or\nexacerbated by the substance (Criterion 9). The key issue in evaluating this criterion is not\nthe existence of the problem, but rather the in dividual\u2019s failure to abstain from using the\nsubstance despite the difficulty it is causing.", "source": "dsm5.pdf"} {"id": "16579293b264-0", "page_content": "484 Substance-Related and Addictive Disorders\nPharmacological criteria are the final grouping (Criteria 10 and 11). Tolerance (Crite-\nrion 10) is signaled by requiring a markedly in creased dose of the substance to achieve the\ndesired effect or a markedly reduced effect when the usual dose is consumed. The degree\nto which tolerance develops varies greatly across different individuals as well as across\nsubstances and may involve a va riety of central nervous system effects. For example, tol-\nerance to respiratory depression and tolerance to sedating and motor coordination may\ndevelop at different rates, depending on the substance. Tolerance ma y be difficult to de-\ntermine by history alone, and la boratory tests may be helpful (e .g., high blood levels of the\nsubstance coupled with little evidence of into xication suggest that tolerance is likely). Tol-\nerance must also be distinguished from indi vidual variability in the initial sensitivity to\nthe effects of particular substances. For exam ple, some first-time alcohol drinkers show\nvery little evidence of intoxication with thre e or four drinks, whereas others of similar\nweight and drinking histories have slurred speech and incoordination. \nWithdrawal (Criterion 11) is a syndrome th at occurs when blood or tissue concentra-\ntions of a substance decline in an individual who had maintained prolonged heavy use of\nthe substance. After developi ng withdrawal symptoms, the individual is likely to con-\nsume the substance to relieve the symptoms . Withdrawal symptoms vary greatly across\nthe classes of substances, and separate criter ia sets for withdrawal are provided for the\ndrug classes. Marked and generally easily me asured physiological signs of withdrawal are\ncommon with alcohol, opioids, and sedatives, hypnotics, and anxiolytics. Withdrawal", "source": "dsm5.pdf"} {"id": "16579293b264-1", "page_content": "signs and symptoms with stimulants (amphetamines and cocaine), as well as tobacco and\ncannabis, are often present but may be le ss apparent. Significant withdrawal has not been\ndocumented in humans after repeated use of phencyclidine, other hallucinogens, and in-\nhalants; therefore, this criterion is not incl uded for these substances. Neither tolerance nor\nwithdrawal is necessary for a diagnosis of a substance use disorder. However, for most\nclasses of substances, a past history of withdraw al is associated with a more severe clinical\ncourse (i.e., an earlier onset of a substance us e disorder, higher levels of substance intake,\nand a greater number of substance-related problems).\nSymptoms of tolerance and withdrawal occurring during appropriate medical treat-\nment with prescribed medications (e.g., opio id analgesics, sedatives, stimulants) are spe-\ncifically not counted when diagnosing a substance use disorder. The appearance of normal,\nexpected pharmacological tolerance and withdrawal during the course of medical treat-\nment has been known to lead to an erroneou s diagnosis of \u201caddiction\u201d even when these\nwere the only symptoms pr esent. Indivi duals whose only symptoms are those that occur\nas a result of medical treatment (i.e., tolera nce and withdrawal as part of medical care\nwhen the medications are taken as prescribed) sh ould not receive a diagnosis solely on the\nbasis of these symptoms. However, prescripti on medications can be used inappropriately,\nand a substance use disorder can be correc tly diagnosed when there are other symptoms\nof compulsive, drug-seeking behavior.\nSeverity and Specifiers\nSubstance use disorders occur in a broad range of severity, from mild to severe, with se-\nverity based on the number of symptom criteria endorsed. As a general estimate of sever-", "source": "dsm5.pdf"} {"id": "16579293b264-2", "page_content": "verity based on the number of symptom criteria endorsed. As a general estimate of sever-\nity, a mild substance use disorder is suggested by the presence of two to three symptoms,\nmoderate by four to five symptoms, and severe by six or more symptoms. Changing severity\nacross time is also reflected by reductions or increases in the fr equency and/or dose of\nsubstance use, as assessed by the individual\u2019s own report, report of knowledgeable others,", "source": "dsm5.pdf"} {"id": "24110c724397-0", "page_content": "across time is also reflected by reductions or increases in the fr equency and/or dose of\nsubstance use, as assessed by the individual\u2019s own report, report of knowledgeable others,\nclinician\u2019s observations, and biological testing. The following course specifiers and descrip-\ntive features specifiers are a lso available for substance use di sorders: \u201cin early remission,\u201d\n\u201cin sustained remission,\u201d \u201con maintenance th erapy,\u201d and \u201cin a cont rolled environment.\u201d\nDefinitions of each are provided within respective criteria sets.", "source": "dsm5.pdf"} {"id": "9c297ac34fec-0", "page_content": "Substance Use Disorders 485\nRecording Procedures for Substance Use Disorders\nThe clinician should use the code that applies to the class of substances but record the\nname of the specific substance. For example, the clinician should record 304.10 (F13.20)\nmoderate alprazolam use disorder (rather than moderate seda tive, hypnotic, or anxiolytic\nuse disorder) or 305.70 (F15.10) mild methamphetamine use disorder (rather than mild\nstimulant use disorder). For substances that do not fit into any of the classes (e.g., anabolic\nsteroids), the appropriate code for \u201cother su bstance use disorder\u201d should be used and the\nspecific substance indicated (e.g., 305.90 [F19.10] mild anabolic steroid use disorder). If the\nsubstance taken by the individual is unknown, the code for the class \u201cother (or unknown)\u201d\nshould be used (e.g., 304.90 [F 19.20] severe unknown substance use disorder). If criteria\nare met for more than one substance use diso rder, all should be diagnosed (e.g., 304.00\n[F11.20] severe heroin use disorder; 304.20 [F14.20] moderate cocaine use disorder).\nThe appropriate ICD-10-CM code for a subs tance use disorder depends on whether\nthere is a comorbid substance-induced disorder (including intoxication and withdrawal). In\nthe above example, the diagnostic code for moderate alprazolam use disorder, F13.20, re-\nflects the absence of a comorbid alprazolam -induced mental disorder. Because ICD-10-CM\ncodes for substance-induced disorders indicate both the presence (or absence) and severity", "source": "dsm5.pdf"} {"id": "9c297ac34fec-1", "page_content": "codes for substance-induced disorders indicate both the presence (or absence) and severity\nof the substance use disorder, ICD-10-CM co des for substance use disorders can be used\nonly in the absence of a substance-induced di sorder. See the individu al substance-specific\nsections for additional coding information.\nNote that the word addiction is not applied as a diagnostic term in this classification,\nalthough it is in common usage in many countr ies to describe severe problems related to\ncompulsive and habitual use of substances. The more neutral term substance use disorder is\nused to describe the wide range of the disorder , from a mild form to a severe state of chron-\nically relapsing, compulsive drug taking. So me clinicians will choose to use the word ad-\ndiction to describe more extreme presentations, but the word is omitted from the official\nDSM-5 substance use disorder diagnostic term inology because of its uncertain definition\nand its potentially negative connotation. \nSubstance-Induced Disorders\nThe overall category of subs tance-induced disorders includ es intoxication, withdrawal,\nand other substance/medication-induced ment al disorders (e.g., substance-induced psy-\nchotic disorder, substance-in duced depressive disorder).\nSubstance Intoxication and Withdrawal\nCriteria for substance intoxica tion are included within the substance-specific sections of\nthis chapter. The essential fe ature is the development of a reversible substance-specific\nsyndrome due to the recent ingestion of a subs tance (Criterion A). The clinically significant\nproblematic behavioral or psychological changes associated with intoxication (e.g., bellig-\nerence, mood lability, impaired judgment) are attributable to the phy siological effects of\nthe substance on the central nervous system and develop during or shortly after use of the\nsubstance (Criterion B). The symptoms are not attributable to another medical condition", "source": "dsm5.pdf"} {"id": "9c297ac34fec-2", "page_content": "substance (Criterion B). The symptoms are not attributable to another medical condition\nand are not better explained by another mental disorder (Criterion D). Substance intoxi-\ncation is common among those with a substance use disorder but also occurs frequently in\nindividuals without a substance use disorder. This category does not apply to tobacco. \nThe most common changes in intoxication involve disturba nces of perception, wake-\nfulness, attention, thinking, judgment, psychomotor behavi or, and interpersonal behav-\nior. Short-term, or \u201cacute,\u201d intoxications may have different signs and symptoms than", "source": "dsm5.pdf"} {"id": "363727bf4474-0", "page_content": "486 Substance-Related and Addictive Disorders\nsustained, or \u201cchronic,\u201d intoxications. For example, moderate cocaine doses may initially\nproduce gregariousness, but social withdrawal may develop if such doses are frequently\nrepeated over days or weeks.\nWhen used in the physiological sense, the term intoxication is broader than substance\nintoxication as defined here. Many substances may produce physiological or psychologi-\ncal changes that are not necessarily problematic. For example, an individual with tachy-\ncardia from substance use has a physiological effe ct, but if this is the only symptom in the\nabsence of problematic behavior, the diagnosis of intoxication would not apply. Intoxica-\ntion may sometimes persist beyond the time when the substance is detectable in the body.\nThis may be due to enduring central nervous system effects, the recovery of which takes\nlonger than the time for elimination of the su bstance. These longer-term effects of intoxi-\ncation must be distinguished from withdraw al (i.e., symptoms initiated by a decline in\nblood or tissue concentrat ions of a substance).\nCriteria for substance withdrawal are included within the su bstance-specific sections of\nthis chapter. The essential feat ure is the development of a subs tance-specific problematic be-\nhavioral change, with physiologic al and cognitive concomitants, that is due to the cessation of,\nor reduction in, heavy and prolonged substance use (Criterion A). The substance-specific syn-\ndrome causes clinically significant distress or impairment in social, oc cupational, or other im-\nportant areas of functioning (Criterion C). The symptoms are not due to another medical\ncondition and are not better explained by anot her mental disorder (Criterion D). Withdrawal\nis usually, but not always, as sociated with a substance use disorder. Most individuals with", "source": "dsm5.pdf"} {"id": "363727bf4474-1", "page_content": "is usually, but not always, as sociated with a substance use disorder. Most individuals with\nwithdrawal have an urge to re-administe r the substance to reduce the symptoms. \nRoute of Administration and Speed of Substance Effects\nRoutes of administration that produce more rapid and efficient absorption into the blood-\nstream (e.g., intravenous, smoking, intranasal \u201csnorting\u201d) te nd to result in a more intense\nintoxication and an increased likelihood of an escalating pattern of substance use leading\nto withdrawal. Similarly, rapi dly acting substances are more likely than slower-acting\nsubstances to produce immediate intoxication. \nDuration of Effects\nWithin the same drug category, relatively sh ort-acting substances tend to have a higher\npotential for the development of withdrawal th an do those with a longer duration of ac-\ntion. However, longer-acting substances tend to have longer withdrawal duration. The\nhalf-life of the substance parallels aspects of wi thdrawal: the longer the duration of action,\nthe longer the time between cessation and th e onset of withdrawal symptoms and the lon-\nger the withdrawal duration. In general, the longer the acute withdrawal period, the less\nintense the syndrome tends to be.\nUse of Multiple Substances\nSubstance intoxication and withdrawal often involve several substances used simultane-\nously or sequentially. In these cases, each diagnosis should be recorded separately.\nAssociated Laboratory Findings\nLaboratory analyses of blood and urine samples can help determine recent use and the specific\nsubstances involved. However, a positive laboratory test result do es not by itself indicate that\nthe individual has a pattern of substance use that meets criteria for a substance-induced or sub-\nstance use disorder, and a negative test result does not by itself rule out a diagnosis.\nLaboratory tests can be useful in identify ing withdrawal. If the individual presents", "source": "dsm5.pdf"} {"id": "363727bf4474-2", "page_content": "Laboratory tests can be useful in identify ing withdrawal. If the individual presents\nwith withdrawal from an unknown substance, laboratory tests may help identify the sub-\nstance and may also be helpful in differentiating withdrawal from other mental disorders.", "source": "dsm5.pdf"} {"id": "cb38f94683f0-0", "page_content": "Substance-Induced Disorders 487\nIn addition, normal functionin g in the presence of high bl ood levels of a substance sug-\ngests considerable tolerance.\nDevelopment and Course\nIndividuals ages 18\u201324 years have relatively hi gh prevalence rates for the use of virtually\nevery substance. Intoxication is usually the initial substance-related disorder and often be-\ngins in the teens. Withdrawal can occur at any age as long as the relevant drug has been\ntaken in sufficient doses over an extended period of time. \nRecording Procedures for Intoxication and Withdrawal\nThe clinician should use the code that applies to the class of substances but record the\nname of the specific substance. For example, the clinician sh ould record 292. 0 (F13.239) seco-\nbarbital withdrawal (rather than sedative, hypnotic, or anxiolytic withdrawal) or 292.89\n(F15.129) methamphetamine intoxication (rathe r than stimulant intoxication). Note that\nthe appropriate ICD-10-CM diagnostic code fo r intoxication depends on whether there is\na comorbid substance use diso rder. In this case, the F15.129 code for methamphetamine in-\ndicates the presence of a comorbid mild methamphetamine use disorder. If there had been\nno comorbid methamphetamine use disorder , the diagnostic code would have been\nF15.929. ICD-10-CM coding rules require th at all withdrawal codes imply a comorbid\nmoderate to severe substance use disorder fo r that substance. In the above case, the code\nfor secobarbital withdrawal (F13.239) indicates the comorbid presence of a moderate to se-\nvere secobarbital use disorder . See the coding note for the substance-specific intoxication", "source": "dsm5.pdf"} {"id": "cb38f94683f0-1", "page_content": "vere secobarbital use disorder . See the coding note for the substance-specific intoxication\nand withdrawal syndromes for the actual coding options.\nFor substances that do not fit into any of the cl asses (e.g., anabolic steroids), the appropriate\ncode for \u201cother substance intoxication\u201d should be used and the specific substance indicated\n(e.g., 292.89 [F19.929] anabolic steroid intoxication). If the substance taken by the individual is\nunknown, the code for the class \u201cother (or unknown)\u201d should be used (e.g., 292.89 [F19.929]\nunknown substance intoxication). If there are sy mptoms or problems associated with a partic-\nular substance but criteria are not met for any of the substance-specific disorders, the unspec-\nified category can be used (e.g., 292.9 [F12.99] unspecified cannabis-related disorder).\nAs noted above, the substance-related codes in ICD-10-CM combine the substance use dis-\norder aspect of the clinical picture and the su bstance-induced aspect into a single combined\ncode. Thus, if both heroin withdrawal and modera te heroin use disorder are present, the single\ncode F11.23 is given to cover both presentati ons. In ICD-9-CM, separate diagnostic codes\n(292.0 and 304.00) are given to indicate withdr awal and a moderate heroin use disorder, re-\nspectively. See the individual substance-specific sections for additional coding information. \nSubstance/Medication-Induced Mental Disorders\nThe substance/medication-induced mental di sorders are potentially severe, usually tem-\nporary, but sometimes persisti ng central nervous system (C NS) syndromes that develop\nin the context of the effects of substances of abuse, medications, or several toxins. They are", "source": "dsm5.pdf"} {"id": "cb38f94683f0-2", "page_content": "in the context of the effects of substances of abuse, medications, or several toxins. They are\ndistinguished from the substance use disorder s, in which a cluster of cognitive, behav-\nioral, and physiological symptoms contribute to the continued use of a substance despite\nsignificant substance-related problems. The substance/medication-induced mental disor-\nders may be induced by the 10 classes of subs tances that produce su bstance use disorders,\nor by a great variety of other medications used in medical treatment. Each substance-\ninduced mental disorder is desc ribed in the relevant chapter (e.g., \u201cDepressive Disorders,\u201d\n\u201cNeurocognitive Disorders\u201d), an d therefore, only a brief description is offered here. All\nsubstance/medication-induced disorders share common characte ristics. It is important to", "source": "dsm5.pdf"} {"id": "f71e8a4a28a4-0", "page_content": "\u201cNeurocognitive Disorders\u201d), an d therefore, only a brief description is offered here. All\nsubstance/medication-induced disorders share common characte ristics. It is important to\nrecognize these common features to aid in th e detection of these disorders. These features\nare described as follows:", "source": "dsm5.pdf"} {"id": "ea452adf7c90-0", "page_content": "488 Substance-Related and Addictive Disorders\nA. The disorder represents a clinically signif icant symptomatic presentation of a relevant\nmental disorder.\nB. There is evidence from the history, physical examination, or laboratory findings of\nboth of the following:\n1. The disorder developed during or within 1 month of a substance intoxication or\nwithdrawal or taking a medication; and\n2. The involved substance/medication is ca pable of producing th e mental disorder.\nC. The disorder is not better explained by an in dependent mental disorder (i.e., one that is\nnot substance- or medication-induced). Such evidence of an independent mental dis-\norder could include the following:\n1. The disorder preceded the onset of severe intoxication or withdrawal or exposure\nto the medication; or\n2. The full mental disorder persisted for a substa ntial period of time (e.g., at least 1 month)\nafter the cessation of acute withdrawal or severe intoxication or taking the medica-\ntion. This criterion does not apply to su bstance-induced neurocognitive disorders\nor hallucinogen persisting perception disorder, which persist beyond the cessation\nof acute intoxication or withdrawal.\nD. The disorder does not occur exclusiv ely during the course of a delirium.\nE. The disorder causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nFeatures\nSome generalizations can be made regarding the categories of substances capable of produc-\ning clinically relevant substance-induced mental disorders. In general, the more sedating\ndrugs (sedative, hypnotics, or anxiolytics, and alcohol) can produce prominent and clini-\ncally significant depressive disorders during in toxication, while anxiet y conditions are likely", "source": "dsm5.pdf"} {"id": "ea452adf7c90-1", "page_content": "cally significant depressive disorders during in toxication, while anxiet y conditions are likely\nto be observed during withdrawal syndromes from these substances. Also, during intoxica-\ntion, the more stimulating substances (e.g., am phetamines and cocaine) are likely to be as-\nsociated with substance-induced psychoti c disorders and substance-induced anxiety\ndisorders, with substance-indu ced major depressive episodes observed during withdrawal.\nBoth the more sedating and mo re stimulating drugs are likely to produce significant but\ntemporary sleep and sexual dist urbances. An overview of the relationship between specific\ncategories of substanc es and specific psychiatric syndromes is presented in Table 1.\nThe medication-induced conditions includ e what are often idiosyncratic CNS reac-\ntions or relatively extreme examples of side effects for a wide range of medications taken\nfor a variety of medical concerns. These includ e neurocognitive complications of anesthet-\nics, antihistamines, antihypertensives, and a variety of other medications and toxins (e.g.,\norganophosphates, insecticides, carbon monoxi de), as described in the chapter on neuro-\ncognitive disorders. Psychotic syndromes may be temporarily experienced in the context\nof anticholinergic, cardiovascul ar, and steroid drugs, as well as during use of stimulant-\nlike and depressant-like prescription or over-the-counter drugs. Temporary but severe\nmood disturbances can be observed with a wi de range of medications, including steroids,\nantihypertensives, disulfiram, and any prescription or over-the- counter depressant or\nstimulant-like substances. A similar range of medications can be associated with tempo-\nrary anxiety syndromes, sexual dysfunct ions, and conditions of disturbed sleep.", "source": "dsm5.pdf"} {"id": "ea452adf7c90-2", "page_content": "rary anxiety syndromes, sexual dysfunct ions, and conditions of disturbed sleep.\nIn general, to be considered a substance/ medication-induced mental disorder, there\nmust be evidence that the diso rder being observed is not likely to be better explained by an\nindependent mental condition. The latter are most likely to be seen if the mental disorder\nwas present before the severe intoxication or withdrawal or medication administration, or,\nwith the exception of several substance-induced persisting disorders listed in Table 1, con-\ntinued more than 1 month after cessation of acute withdrawal, severe intoxication, or use", "source": "dsm5.pdf"} {"id": "6b2a97b96d33-0", "page_content": "Substance-Induced Disorders 489\nof the medications. When symptoms are only observed during a delirium (e.g., alcohol\nwithdrawal delirium), the mental disorder sh ould be diagnosed as a delirium, and the\npsychiatric syndrome occurring during the delirium should not also be diagnosed sepa-\nrately, as many symptoms (including disturba nces in mood, anxiety, and reality testing)\nare commonly seen during agitated, confused states. The features associated with each rel-\nevant major mental disorder are similar whether observed with independent or sub-\nstance/medication-induced mental disorders. However, individuals with substance/\nmedication-induced mental disorders are lik ely to also demonstrate the associated fea-\ntures seen with the specific category of subs tance or medication, as listed in other subsec-\ntions of this chapter. \nDevelopment and Course\nSubstance-induced mental disord ers develop in the context of intoxication or withdrawal\nfrom substances of abuse, and medication-i nduced mental disorders are seen with pre-\nscribed or over-the-counter medications that are taken at the suggest ed doses. Both condi-\ntions are usually temporary and li kely to disappear with in 1 month or so of cessation of acute\nwithdrawal, severe intoxication, or use of th e medication. Exceptions to these generaliza-\ntions occur for certain long-d uration substance-in duced disorders: substance-associated\nneurocognitive disorders that relate to conditions such as alcohol- induced neurocognitive\ndisorder, inhalant-induced neurocognitive disord er, and sedative-, hypnotic-, or anxiolytic-\ninduced neurocognitive disorder; and hallucinogen persisting perception disorder (\u201cflash-\nbacks\u201d; see the section \u201cHallucinogen-Related Disorders\u201d later in this chapter). However,", "source": "dsm5.pdf"} {"id": "6b2a97b96d33-1", "page_content": "most other substance/medication -induced mental disorders, re gardless of the severity of\nthe symptoms, are likely to impr ove relatively quickly with ab stinence and unlikely to re-\nmain clinically relevant for more than 1 month after complete cessation of use.\nAs is true of many consequences of heavy substance use, some individuals are more\nand others less prone toward specific substance-induced disorders. Similar types of pre-\ndispositions may make some individuals more likely to develop psychiatric side effects of\nsome types of medications, but not others. However, it is unclear whether individuals\nwith family histories or personal prior hist ories with independent psychiatric syndromes\nare more likely to develop the induced synd rome once the consideration is made as to\nwhether the quantity and frequency of the substance was sufficient to lead to the devel-\nopment of a substanc e-induced syndrome.\nThere are indications that the intake of su bstances of abuse or some medications with\npsychiatric side effects in the context of a pree xisting mental disorder is likely to result in\nan intensification of the preexisting indepe ndent syndrome. The risk for substance/med-\nication-induced mental disorders is likely to increase with both the quantity and the fre-\nquency of consumption of the relevant substance.\nThe symptom profiles for the substance/medication-induced mental disorders resem-\nble independent mental disorders. While the symptoms of substance/medication-in-\nduced mental disorders can be identical to those of independent mental disorders (e.g.,\ndelusions, hallucinations, psychoses, major de pressive episodes, anxiety syndromes), and\nalthough they can have the same severe conseq uences (e.g., suicide) , most induced mental\ndisorders are likely to improve in a matt er of days to weeks of abstinence.", "source": "dsm5.pdf"} {"id": "6b2a97b96d33-2", "page_content": "disorders are likely to improve in a matt er of days to weeks of abstinence.\nThe substance/medication-induced mental di sorders are an important part of the dif-\nferential diagnoses for the independent psychiatric conditions. The importance of recog-\nnizing an induced mental disorder is similar to the relevance of identifying the possible\nrole of some medical conditions and medication reaction s before diagnosing an indepen-", "source": "dsm5.pdf"} {"id": "1c58e457e731-0", "page_content": "nizing an induced mental disorder is similar to the relevance of identifying the possible\nrole of some medical conditions and medication reaction s before diagnosing an indepen-\ndent mental disorder. Symptoms of substanc e- and medication-induced mental disorders\nmay be identical cross-sectionally to those of independent mental disorders but have dif-\nferent treatments and prognoses from the independent condition.", "source": "dsm5.pdf"} {"id": "1e8037b48f7d-0", "page_content": "490 Substance-Related and Addictive Disorders\nFunctional Consequences of Substance/Medication-\nInduced Mental Disorders\nThe same consequences related to the relevant independent mental disorder (e.g., suicide\nattempts) are likely to apply to the substance/medi cation-induced mental disorders, but\nthese are likely to disappear within 1 month after abstinence. Similarly, the same func-\ntional consequences associated with the relevant substance use disorder are likely to be seen\nfor the substance-indu ced mental disorders.\nRecording Procedures fo r Substance/Medication-\nInduced Mental Disorders\nCoding notes and separate recording procedures for ICD-9-CM and ICD-10-CM codes for\nother specific substance/medi cation-induced mental diso rders are provided in other\nchapters of the manual with disorders with which they share phenomenology (see the sub-\nstance/medication-indu ced mental disorders in these chapters: \u201cSchizophrenia Spectrum\nand Other Psychotic Disorders,\u201d \u201cBipolar and Related Disorders,\u201d \u201cDepressive Disor-\nders,\u201d \u201cAnxiety Disorders,\u201d \u201cObsessive-Compulsive and Related Disorders,\u201d \u201cSleep-\nWake Disorders,\u201d \u201cSexual Dysfunctions,\u201d and \u201cNeurocognitive Disorders\u201d). Generally,\nfor ICD-9-CM, if a mental disorder is induced by a substance use disorder, a separate di-\nagnostic code is given for the specific substance use disorder, in addition to the code for the\nsubstance/medication-induced mental disord er. For ICD-10-CM, a single code combines\nthe substance-induced mental disorder with the substance use disorder. A separate diag-\nnosis of the comorbid substance use disorder is not given, although the name and severity\nof the specific substance use disorder (whe n present) are used when recording the sub-", "source": "dsm5.pdf"} {"id": "1e8037b48f7d-1", "page_content": "of the specific substance use disorder (whe n present) are used when recording the sub-\nstance/medication-induced mental disorder. ICD-10-CM codes are also provided for sit-\nuations in which the substance/ medication-induced mental di sorder is not induced by a\nsubstance use disorder (e.g., when a disorder is induced by one-time use of a substance or\nmedication). Additional information needed to record the diagnostic name of the sub-\nstance/medication-induce d mental disorder is provided in the sect ion \u201cRecording Proce-\ndures\u201d for each substance/medication-induced mental disorder in its respective chapter.\nAlcohol-Related Disorders\nAlcohol Use Disorder\nAlcohol Intoxication\nAlcohol Withdrawal\nOther Alcohol-Induced Disorders\nUnspecified Alcohol-Related Disorder\nAlcohol Use Disorder\nDiagnostic Criteria \nA. A problematic pattern of alcohol use leading to clinically significant impairment or dis-\ntress, as manifested by at least two of the following, occurring within a 12-month period:\n1. Alcohol is often taken in larger amounts or over a longer period than was intended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control alcohol use.", "source": "dsm5.pdf"} {"id": "812206b63b32-0", "page_content": "Alcohol Use Disorder 491\n3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol,\nor recover from its effects.\n4. Craving, or a strong desire or urge to use alcohol.\n5. Recurrent alcohol use resulting in a failure to fulfill major role obligations at work,\nschool, or home.\n6. Continued alcohol use despite having persist ent or recurrent social or interpersonal\nproblems caused or exacerbated by the effects of alcohol.\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of alcohol use.\n8. Recurrent alcohol use in situations in which it is physically hazardous.\n9. Alcohol use is continued despite knowledge of having a persistent or recurrent\nphysical or psychological problem that is likely to have been caused or exacerbated\nby alcohol.\n10. Tolerance, as defined by either of the following:\na. A need for markedly increased amounts of alcohol to achieve intoxication or de-\nsired effect.\nb. A markedly diminished effect with continued use of the same amount of alcohol.\n11. Withdrawal, as manifested by either of the following:\na. The characteristic withdrawal syndrome fo r alcohol (refer to Criteria A and B of\nthe criteria set for alcohol withdrawal, pp. 499\u2013500).\nb. Alcohol (or a closely related substance, such as a benzodiazepine) is taken to\nrelieve or avoid withdrawal symptoms.\nSpecify if:\nIn early remission: After full criteria for alcohol us e disorder were previously met,\nnone of the criteria for alcohol use disorder have been met for at least 3 months but for\nless than 12 months (with the exception that Criterion A4, \u201cCraving, or a strong desire\nor urge to use alcohol,\u201d may be met).", "source": "dsm5.pdf"} {"id": "812206b63b32-1", "page_content": "or urge to use alcohol,\u201d may be met).\nIn sustained remission: After full criteria for alcohol use disorder were previously\nmet, none of the criteria for alcohol use disorder have been met at any time during a\nperiod of 12 months or longer (with the exception that Criterion A4, \u201cCraving, or a\nstrong desire or urge to use alcohol,\u201d may be met). \nSpecify if:\nIn a controlle d environment: This additional specifier is used if the individual is in an\nenvironment where access to alcohol is restricted. \nCode based on current severity: Note for ICD-10-CM codes: If an alcohol intoxication,\nalcohol withdrawal, or another alcohol-induced m ental disorder is also present, do not use\nthe codes below for alcohol use disorder. Instead, the comorbid alcohol use disorder is\nindicated in the 4th character of the alco hol-induced disorder code (see the coding note\nfor alcohol intoxication, alcohol withdrawal, or a specific alcohol-induced mental disorder).\nFor example, if there is comorbid alcohol intoxication and alcohol use disorder, only the\nalcohol intoxication code is given, with the 4th character indicating whether the comorbid\nalcohol use disorder is mild, moderate, or severe: F10.129 for mild alcohol use disorder\nwith alcohol intoxication or F10.229 for a moderat e or severe alcohol use disorder with al-\ncohol intoxication.\nSpecify current severity:\n305.00 (F10.10) Mild: Presence of 2\u20133 symptoms.\n303.90 (F10.20) Moderate: Presence of 4\u20135 symptoms.\n303.90 (F10.20) Severe: Presence of 6 or more symptoms.", "source": "dsm5.pdf"} {"id": "e2d5a53bc425-0", "page_content": "492 Substance-Related and Addictive Disorders\nSpecifiers\n\u201cIn a controlled environment\u201d app lies as a further specifier of remission if the individual is\nboth in remission and in a controlled environm ent (i.e., in early remission in a controlled\nenvironment or in sustained remission in a controlled environmen t). Examples of these\nenvironments are closely supe rvised and substanc e-free jails, therapeutic communities,\nand locked hospital units. \nSeverity of the disorder is based on the number of diagno stic criteria endorsed.\u00a0For a\ngiven individual, changes in severity of alcoho l use disorder across ti me are also reflected\nby reductions in the frequency (e.g., days of use per month) and/or dose (e.g., number of\nstandard drinks consumed per day) of alcohol used, as assessed by the individual\u2019s self-\nreport, report of knowledgeabl e others, clinician observations, and, when practical, bio-\nlogical testing (e.g., elevations in blood test s as described in the section \u201cDiagnostic Mark-\ners\u201d for this disorder).\nDiagnostic Features\nAlcohol use disorder is defined by a cluste r of behavioral and physical symptoms, which\ncan include withdrawal, tolerance, and cravin g. Alcohol withdrawal is characterized by\nwithdrawal symptoms that de velop approximately 4\u201312 hours after the reduction of in-\ntake following prolonged, heavy alcohol inge stion. Because withdrawal from alcohol can\nbe unpleasant and intense, individuals may continue to consume alcohol despite adverse\nconsequences, often to avoid or to relieve withdrawal symptoms. Some withdrawal symp-\ntoms (e.g., sleep problems) can persist at lower intensities for months and can contribute to\nrelapse. Once a pattern of re petitive and intense use develo ps, individuals with alcohol\nuse disorder may devote substantial periods of time to obtaining and consuming alcoholic", "source": "dsm5.pdf"} {"id": "e2d5a53bc425-1", "page_content": "use disorder may devote substantial periods of time to obtaining and consuming alcoholic\nbeverages. \nCraving for alcohol is indicated by a strong desire to drink that makes it difficult to\nthink of anything else and that often results in the onset of drinking. School and job per-\nformance may also suffer either from the aftereffects of drinking or from actual intoxica-\ntion at school or on the job; child care or household responsibilities may be neglected; and\nalcohol-related absences may o ccur from school or work. The individual may use alcohol\nin physically hazardous circumstances (e.g., driving an automobile, swimming, operating\nmachinery while intoxicated). Finally, individu als with an alcohol use disorder may con-\ntinue to consume alco hol despite the knowledge that continued consumption poses sig-\nnificant physical (e.g., blackouts, liver disease ), psychological (e.g., depression), social, or\ninterpersonal problems (e.g., violent argume nts with spouse while intoxicated, child\nabuse).\nAssociated Features Supporting Diagnosis\nAlcohol use disorder is often associated wi th problems similar to those associated with\nother substances (e.g., cannabis ; cocaine; heroin; amphetamin es; sedatives, hypnotics, or\nanxiolytics). Alcohol may be used to alleviate the unwanted effects of these other\nsubstances or to substitute for them when they are not av ailable. Symptoms of conduct\nproblems, depression, anxiety, and insomnia frequently accompany heavy drinking and\nsometimes precede it. \nRepeated intake of high doses of alcohol can affect nearly every organ system, espe-\ncially the gastrointestinal tract, cardiovasc ular system, and the central and peripheral ner-\nvous systems. Gastrointestinal effects includ e gastritis, stomach or duodenal ulcers, and,", "source": "dsm5.pdf"} {"id": "e2d5a53bc425-2", "page_content": "in about 15% of individuals who use alcohol he avily, liver cirrhosis and/or pancreatitis.\nThere is also an increased rate of cancer of the esophagus, stomach, and other parts of the\ngastrointestinal tract. One of the most comm only associated conditions is low-grade hy-\npertension. Cardiomyopathy and other myopat hies are less common but occur at an in-", "source": "dsm5.pdf"} {"id": "fa041c1b425f-0", "page_content": "Alcohol Use Disorder 493\ncreased rate among those who drink very he avily. These factors, along with marked\nincreases in levels of triglycerides and low- density lipoprotein cholesterol, contribute to\nan elevated risk of heart disease. Periphe ral neuropathy may be evidenced by muscular\nweakness, paresthesias, and decreased peripher al sensation. More persistent central ner-\nvous system effects include cognitive deficits, severe memory impairment, and degener-\native changes in the cerebellum. These effects are related to the direct effects of alcohol or\nof trauma and to vitamin deficiencies (parti cularly of the B vitamins, including thiamine).\nOne devastating central nervous system e ffect is the relatively rare alcohol-induced per-\nsisting amnestic disorder, or Wernicke-Korsakoff syndrome, in which the ability to encode\nnew memory is severely impaired. This condition would now be described within the chap-\nter \u201cNeurocognitive Disorder s\u201d and would be termed a substance/medicati on-induced neuro-\ncognitive disorder.\nAlcohol use disorder is an important contribu tor to suicide risk du ring severe intoxi-\ncation and in the context of a temporary alco hol-induced depressive and bipolar disorder.\nThere is an increased rate of suicidal behavior as well as of completed suicide among in-\ndividuals with the disorder.\nPrevalence \nAlcohol use disorder is a common disorder. In the United States, the 12-month prevalence\nof alcohol use disorder is estimated to be 4.6% among 12- to 17-year-olds and 8.5% among\nadults age 18 years and older in the United St ates. Rates of the disorder are greater among\nadult men (12.4%) than among adult women (4 .9%). Twelve-month prevalence of alcohol", "source": "dsm5.pdf"} {"id": "fa041c1b425f-1", "page_content": "use disorder among adults decreases in midd le age, being greatest among individuals 18-\nto 29-years-old (16.2%) and lowest among individuals age 65 years and older (1.5%).\nTwelve-month prevalence varies markedly across race/ethnic subgroups of the U.S.\npopulation. For 12- to 17-year-olds, rates ar e greatest among Hispanics (6.0%) and Native\nAmericans and Alaska Natives (5.7%) relative to whites (5.0%), Afri can Americans (1.8%),\nand Asian Americans and Pacific Islanders (1.6 %). In contrast, amon g adults, the 12-month\nprevalence of alcohol use di sorder is clearly greater among Native Americans and Alaska\nNatives (12.1%) than among whites (8.9%), Hispanics (7.9%), African Americans (6.9%),\nand Asian Americans and Pacific Islanders (4.5%).\nDevelopment and Course\nThe first episode of alcohol into xication is likely to occur during the mid-teens. Alcohol-\nrelated problems that do not m eet full criteria for a use disord er or isolated problems may\noccur prior to age 20 years, but the age at onse t of an alcohol use disorder with two or more\nof the criteria clustered together peaks in th e late teens or early to mid 20s. The large ma-\njority of individuals who develop alcohol-relate d disorders do so by their late 30s. The first\nevidence of withdrawal is not likely to appear until after many other aspects of an alcohol\nuse disorder have developed. An earlier onset of alcohol use disorder is observed in ado-\nlescents with preexisting conduct problems and those with an earlier onset of intoxication.\nAlcohol use disorder has a variable course th at is characterized by periods of remission", "source": "dsm5.pdf"} {"id": "fa041c1b425f-2", "page_content": "Alcohol use disorder has a variable course th at is characterized by periods of remission\nand relapse. A decision to stop drinking, often in response to a crisis, is likely to be followed\nby a period of weeks or more of abstinence , which is often followed by limited periods of\ncontrolled or nonproblematic drinking. However, once alcohol intake resumes, it is highly\nlikely that consumption will rapidly escalate and that severe problems will once again\ndevelop.\nAlcohol use disorder is often erroneously pe rceived as an intractable condition, per-\nhaps based on the fact that individuals who present for treatment typically have a\u00a0history\nof many years of severe alco hol-related problems. However, these most severe cases rep-", "source": "dsm5.pdf"} {"id": "973624fc8990-0", "page_content": "haps based on the fact that individuals who present for treatment typically have a\u00a0history\nof many years of severe alco hol-related problems. However, these most severe cases rep-\nresent only a small proportion of individuals with this disorder, and the typical individual\nwith the disorder has a much more promising prognosis.", "source": "dsm5.pdf"} {"id": "644c05504cfb-0", "page_content": "494 Substance-Related and Addictive Disorders\nAmong adolescents, conduct disorder and repeated antisocial behavior often co-occur\nwith alcohol- and with other substance-relate d disorders. While most individuals with al-\ncohol use disorder develop the condition be fore age 40 years, perhaps 10% have later\nonset. Age-related physical changes in older individuals result in increased brain suscep-\ntibility to the depressant effect s of alcohol; decreased rates of liver metabolism of a variety\nof substances, including alcohol; and decrease d percentages of body water. These changes\ncan cause older people to develop more seve re intoxication and su bsequent problems at\nlower levels of consumption. Al cohol-related problems in older people are also especially\nlikely to be associated with other medical complications.\nRisk and Prognostic Factors\nEnvironmental. Environmental risk and prognostic factors may include cultural atti-\ntudes toward drinking and intoxication, the availability of alcohol (including price),\nacquired personal experiences with alcohol, and stress levels. Additional potential medi-\nators of how alcohol problems develop in predisposed individuals include heavier peer\nsubstance use, exaggerated positive expectations of the effects of alcohol, and suboptimal\nways of coping with stress. \nGenetic and physiological. Alcohol use disorder runs in families, with 40%\u201360% of the\nvariance of risk explained by genetic influenc es. The rate of this condition is three to four\ntimes higher in close relatives of individuals with alcohol use disorder, with values highest\nfor individuals with a greater nu mber of affected relatives, closer genetic relationships to\nthe affected person, and higher severity of the alcohol-related problems in those relatives.\nA significantly higher rate of alcohol use disorders exists in the monozygotic twin than in\nthe dizygotic twin of an individual with the condition. A three- to fourfold increase in risk", "source": "dsm5.pdf"} {"id": "644c05504cfb-1", "page_content": "has been observed in children of individuals with alcohol use disorder, even when these\nchildren were given up for adoption at birth and raised by adoptive parents who did not\nhave the disorder.\nRecent advances in our understanding of genes that operate through intermediate\ncharacteristics (or phe notypes) to affect the risk of alco hol use disorder can help to identify\nindividuals who might be at pa rticularly low or high risk for alcohol use disorder. Among\nthe low-risk phenotypes are the acute alcohol-related skin flush (seen most prominently in\nAsians). High vulnerability is associated with preexisting schizophrenia or bipolar disor-\nder, as well as impulsivity (producing enha nced rates of all substance use disorders and\ngambling disorder), and a high risk specifically for alcohol use disorder is associated with\na low level of response (low sensitivity) to alcohol. A number of gene variations may ac-\ncount for low response to alcohol or modulate the dopamine reward systems; it is impor-\ntant to note, however, that any one gene variat ion is likely to explain only 1%\u20132% of the risk\nfor these disorders.\nCourse modifiers. In general, high levels of impulsivity are associated with an earlier\nonset and more severe alcohol use disorder. \nCulture-Related Diagnostic Issues\nIn most cultures, alcohol is the most frequently used intoxicating substance and contrib-\nutes to considerable morbidity and mortality. An estimate d 3.8% of all global deaths and\n4.6% of global disability-adjusted life-years are attribut able to alcohol. In the United States,\n80% of adults (age 18 years and older) have co nsumed alcohol at some time in their lives,\nand 65% are current drinkers (last 12 months). An estimated 3.6% of the world population", "source": "dsm5.pdf"} {"id": "644c05504cfb-2", "page_content": "(15\u201364 years old) has a current (12-month) alcohol use disorder, with a lower prevalence\n(1.1%) found in the Afri can region, a higher rate (5.2%) found in the Am erican region (North,\nSouth, and Central America and the Caribbean) , and the highest rate (10.9%) found in the", "source": "dsm5.pdf"} {"id": "b65f96284e10-0", "page_content": "(1.1%) found in the Afri can region, a higher rate (5.2%) found in the Am erican region (North,\nSouth, and Central America and the Caribbean) , and the highest rate (10.9%) found in the\nEastern Europe region.", "source": "dsm5.pdf"} {"id": "4006202247dc-0", "page_content": "Alcohol Use Disorder 495\nPolymorphisms of genes for the alcohol- metabolizing enzymes alcohol dehydroge-\nnase and aldehyde dehydrogenase are most ofte n seen in Asians and affect the response to\nalcohol. When consuming alcoho l, individuals with these gene variations can experience a\nflushed face and palpitations, reactions that ca n be so severe as to lim it or preclude future\nalcohol consumption and diminish the risk fo r alcohol use disorder. These gene variations\nare seen in as many as 40% of Japanese, Chinese, Korean, and related groups worldwide\nand are related to lower risks for the disorder.\nDespite small variations regarding individual criterion items, the diagnostic criteria\nperform equally well across mo st race/ethnicity groups.\nGender-Related Diagnostic Issues\nMales have higher rates of drinking and rela ted disorders than fema les. However, because\nfemales generally weigh less than males, have more fat and less water in their bodies, and\nmetabolize less alcohol in their esophagus and stomach, they are likely to develop higher\nblood alcohol levels per drink than males. Females who drink heavily may also be more\nvulnerable than males to some of the physical consequences associated with alcohol, in-\ncluding liver disease.\nDiagnostic Markers\nIndividuals whose heavier drinking places them at elevated risk for alcohol use disorder\ncan be identified both through standardized qu estionnaires and by elevations in blood test\nresults likely to be seen with regular heavie r drinking. These measures do not establish a\ndiagnosis of an alcohol-related disorder but can be useful in highlighting individuals for\nwhom more information should be gathered. Th e most direct test available to measure al-\ncohol consumption cross-sectionally is blood alcohol concentration, which can also be used to", "source": "dsm5.pdf"} {"id": "4006202247dc-1", "page_content": "cohol consumption cross-sectionally is blood alcohol concentration, which can also be used to\njudge tolerance to alcohol. For example, an individual with a conc entration of 150 mg of\nethanol per deciliter (dL) of blood who does not show signs of intoxication can be pre-\nsumed to have acquired at le ast some degree of tolerance to alcohol. At 200 mg/dL, most\nnontolerant individuals demons trate severe intoxication. \nRegarding laboratory tests, one sensitive la boratory indicator of heavy drinking is a\nmodest elevation or high-normal levels (>35 units) of gamma-glutamyltransferase (GGT).\nThis may be the only laboratory finding. At least 70% of indi viduals with a high GGT level\nare persistent heavy drinkers (i.e., consuming ei ght or more drinks daily on a regular basis).\nA second test with comparable or even higher levels of sensitivity and specificity is carbo-\nhydrate-deficient transferrin (CDT), with levels of 20 units or higher us eful in identifying in-\ndividuals who regularly consum e eight or more drinks daily. Since both GGT and CDT\nlevels return toward normal within days to weeks of stopping drinking, both state markers\nmay be useful in monitoring abstinence, espe cially when the clinician observes increases,\nrather than decreases, in thes e values over time\u2014a finding indicating that the person is\nlikely to have returned to heavy drinking. The combination of tests for CDT and GGT may\nhave even higher levels of sens itivity and specificity than eith er test used alone. Additional\nuseful tests include the mean corpuscular volume (MCV), whic h may be elevated to high-\nnormal values in individuals who drink heavily\u2014 a change that is due to the direct toxic ef-", "source": "dsm5.pdf"} {"id": "4006202247dc-2", "page_content": "normal values in individuals who drink heavily\u2014 a change that is due to the direct toxic ef-\nfects of alcohol on erythropoiesis. Although the MCV can be used to help identify those who\ndrink heavily, it is a poor method of monitori ng abstinence because of the long half-life of\nred blood cells. Liver function tests (e.g., alanine aminotransfe rase [ALT] and alkaline phos-\nphatase) can reveal liver injury that is a co nsequence of heavy drinking. Other potential\nmarkers of heavy drinking that are more nons pecific for alcohol but can help the clinician\nthink of the possible effects of alcohol include elevations in blood levels or lipids (e.g., tri-", "source": "dsm5.pdf"} {"id": "6be45f17556a-0", "page_content": "markers of heavy drinking that are more nons pecific for alcohol but can help the clinician\nthink of the possible effects of alcohol include elevations in blood levels or lipids (e.g., tri-\nglycerides and high-density li poprotein cholesterol) and high -normal levels of uric acid.\nAdditional diagnostic markers relate to sign s and symptoms that reflect the consequences\noften associated with persistent heavy drinki ng. For example, dyspepsia, nausea, and bloat-", "source": "dsm5.pdf"} {"id": "850d42cbe677-0", "page_content": "496 Substance-Related and Addictive Disorders\ning can accompany gastritis, and hepatomegaly, esophageal varices, and hemorrhoids may\nreflect alcohol-induced changes in the liver. Other physical signs of heavy drinking include\ntremor, unsteady gait, insomnia, and erectile dy sfunction. Males with chronic alcohol use dis-\norder may exhibit decreased testicular size and feminizing effects associated with reduced\ntestosterone levels. Repeated he avy drinking in females is associated with menstrual irregu-\nlarities and, during pregnancy, spontaneous abortion and fetal alcohol syndrome. Individu-\nals with preexisting histories of epilepsy or se vere head trauma are more likely to develop\nalcohol-related seizures. Alcohol withdrawal ma y be associated with nausea, vomiting, gas-\ntritis, hematemesis, dry mouth, puffy blot chy complexion, and mild peripheral edema.\nFunctional Consequences of Alcohol Use Disorder\nThe diagnostic features of alcohol use disord er highlight major area s of life functioning\nlikely to be impaired. These include driving and operating machinery, school and work,\ninterpersonal relationships and communication, and health. Alcoho l-related disorders\ncontribute to absenteeism from work, job-re lated accidents, and low employee productiv-\nity. Rates are elevated in homeless individual s, perhaps reflecting a downward spiral in\nsocial and occupational functioning, although most individuals with alcohol use disorder\ncontinue to live with their families and function within their jobs.\nAlcohol use disorder is associated with a significant increase in the risk of accidents, vi-\nolence, and suicide. It is estimated that one in five intensive care un it admissions in some\nurban hospitals is related to al cohol and that 40% of individu als in the United States ex-\nperience an alcohol-related adverse event at so me time in their lives, with alcohol account-", "source": "dsm5.pdf"} {"id": "850d42cbe677-1", "page_content": "perience an alcohol-related adverse event at so me time in their lives, with alcohol account-\ning for up to 55% of fatal driving events. Severe alcohol use disorder, especially in\nindividuals with antisocial personality disorder, is associated with the commission of\ncriminal acts, including homicide. Severe problematic alcohol use also contributes to dis-\ninhibition and feelings of sadness and irritab ility, which contribute to suicide attempts and\ncompleted suicides.\nUnanticipated alcohol withdrawal in hospitalized individuals for whom a diagnosis of\nalcohol use disorder has been overlooked can a dd to the risks and costs of hospitalization\nand to time spent in the hospital.\nDifferential Diagnosis\nNonpathological use of alcohol. The key element of alcohol use disorder is the use of\nheavy doses of alcohol with resulting repeated and significant distress or impaired func-\ntioning. While most drinkers sometimes consume enough alcohol to feel intoxicated, only\na minority (less than 20%) ever develop al cohol use disorder. Therefore, drinking, even\ndaily, in low doses and occasional intoxication do not by themselves make this diagnosis.\nSedative, hypnotic, or anxiolytic use disorder. The signs and symptoms of alcohol use\ndisorder are similar to those seen in sedative, hypnotic, or anxiolytic use disorder. The two\nmust be distinguished, however, because the c ourse may be different, especially in rela-\ntion to medical problems.\nConduct disorder in childhood and adult antisocial personality disorder. Alcohol use\ndisorder, along with other substa nce use disorders, is seen in the majority of individuals\nwith antisocial personality and preexisting conduct disorder. Because these diagnoses are\nassociated with an early onset of alcohol use disorder as well as a worse prognosis, it is im-\nportant to establish both conditions.\nComorbidity", "source": "dsm5.pdf"} {"id": "850d42cbe677-2", "page_content": "portant to establish both conditions.\nComorbidity\nBipolar disorders, schizophrenia, and antisocial personality disorder are associated with a\nmarkedly increased rate of alcohol use disorder , and several anxiety and depressive disorders", "source": "dsm5.pdf"} {"id": "719af157229e-0", "page_content": "Alcohol Intoxication 497\nmay relate to alcohol use disorder as well. At least a part of the reported association between\ndepression and moderate to severe alcohol use disorder may be attributable to temporary, al-\ncohol-induced comorbid depressive symptoms re sulting from the acute effects of intoxication\nor withdrawal. Severe, repeated alcohol intoxication may also suppress immune mechanisms\nand predispose individuals to infections and increase the risk for cancers.\nAlcohol Intoxication\nDiagnostic Criteria\nA. Recent ingestion of alcohol.\nB. Clinically significant problematic behavioral or psychological changes (e.g., inappropri-\nate sexual or aggressive behavior, mood lability, impaired judgment) that developed\nduring, or shortly after, alcohol ingestion.\nC. One (or more) of the following signs or symptoms developing during, or shortly after,\nalcohol use:\n1. Slurred speech.\n2. Incoordination.\n3. Unsteady gait.\n4. Nystagmus.\n5. Impairment in attention or memory.\n6. Stupor or coma.\nD. The signs or symptoms are not attributable to another medical condition and are not better\nexplained by another mental disorder, in cluding intoxication with another substance.\nCoding note: The ICD-9-CM code is 303.00. The ICD-10-CM code depends on whether\nthere is a comorbid alcohol use disorder. If a mild alcohol use disorder is comorbid, the\nICD-10-CM code is F10.129, and if a moderate or severe alcohol use disorder is comorbid,\nthe ICD-10-CM code is F10.229. If there is no comorbid alcohol use disorder, then the\nICD-10-CM code is F10.929.\nDiagnostic Features", "source": "dsm5.pdf"} {"id": "719af157229e-1", "page_content": "ICD-10-CM code is F10.929.\nDiagnostic Features\nThe essential feature of alcohol intoxication is the presence of clinically significant problematic\nbehavioral or psychological chan ges (e.g., inappropriate sexual or aggressive behavior, mood\nlability, impaired judgment, impaired social or occupational functioning) that develop during,\nor shortly after, alcohol ingestion (Criterion B). These changes are accompanied by evidence of\nimpaired functioning and ju dgment and, if intoxication is inte nse, can result in a life-threaten-\ning coma. The symptoms must not be attributable to another medical co ndition (e.g., diabetic\nketoacidosis), are not a reflection of conditions such as delirium, and are not related to intoxi-\ncation with other depressant drugs (e.g., benzodiazepines) (Crite rion D). The levels of incoor-\ndination can interfere with driving abilities and performance of usual activities to the point of\ncausing accidents. Evidence of alcohol use can be obtained by smelling alcohol on the individ-\nual\u2019s breath, eliciting a history from the indivi dual or another observer, and, when needed,\nhaving the individual provide breath, blood , or urine samples for toxicology analyses.\nAssociated Features Supporting Diagnosis\nAlcohol intoxication is sometimes associated with amnesia for the events that occurred\nduring the course of the intoxication (\u201cbl ackouts\u201d). This phenomenon may be related to\nthe presence of a high blood alcohol level an d, perhaps, to the rapidity with which this\nlevel is reached. During even mild alcohol in toxication, different symptoms are likely to be", "source": "dsm5.pdf"} {"id": "1dd283340456-0", "page_content": "498 Substance-Related and Addictive Disorders\nobserved at different time points. Evidence of mild intoxication with alcohol can be seen in\nmost individuals after approximately two drin ks (each standard drink is approximately\n10\u201312 grams of ethanol and raises the blood alcohol concentration approximately 20 mg/\ndL). Early in the drinking period, when blood alcohol levels are rising, symptoms often\ninclude talkativeness, a sensation of well-being, and a\u00a0bright, expansive mood. Later, es-\npecially when blood alcohol levels are falling, the individual is likely to become progres-\nsively more depressed, withdrawn, and cognitively impair ed. At very high blood alcohol\nlevels (e.g., 200\u2013300 mg/dL), an individual who has not developed tolerance for alcohol is\nlikely to fall asleep and enter a first stage of anesthesia. Higher blood alcohol levels (e.g., in\nexcess of 300\u2013400 mg/dL) can cause inhibition of respiration and pulse and even death in\nnontolerant individuals. The duration of in toxication depends on how much alcohol was\nconsumed over what period of time. In general, the body is able to metabolize approxi-\nmately one drink per hour, so that the blood alcohol level generally decreases at a rate of\n15\u201320 mg/dL per hour. Signs and symptoms of in toxication are likely to be more intense\nwhen the blood alcohol level is rising than when it is falling.\nAlcohol intoxication is an important contri butor to suicidal behavior. There appears to\nbe an increased rate of suic idal behavior, as well as of co mpleted suicide, among persons\nintoxicated by alcohol. \nPrevalence \nThe large majority of alcohol consumers are likely to have been intoxicated to some degree at", "source": "dsm5.pdf"} {"id": "1dd283340456-1", "page_content": "The large majority of alcohol consumers are likely to have been intoxicated to some degree at\nsome point in their lives. For ex ample, in 2010, 44% of 12th-grad e students admitted to having\nbeen \u201cdrunk in the past year,\u201d with more than 70% of college students reporting the same.\nDevelopment and Course\nIntoxication usually occurs as an episode usua lly developing over minutes to hours and typi-\ncally lasting several hours. In th e United States, the average age at first intoxication is approx-\nimately 15 years, with the highest prevalence at approximately 18\u201325 years. Frequency and\nintensity usually decrease with further advancin g age. The earlier the onset of regular intoxi-\ncation, the greater the likelihood the individual will go on to develop alcohol use disorder.\nRisk and Prognostic Factors\nTemperamental. Episodes of alcohol intoxication increase with personality characteris-\ntics of sensation seeking and impulsivity.\nEnvironmental. Episodes of alcohol intoxication increase with a heavy drinking envi-\nronment.\nCulture-Related Diagnostic Issues\nThe major issues parallel the cultural differ ences regarding the use of alcohol overall.\nThus, college fraternities and sororities ma y encourage alcohol intoxication. This condi-\ntion is also frequent on certain dates of cultur al significance (e.g., New Year\u2019s Eve) and, for\nsome subgroups, during specif ic events (e.g., wakes following funerals). Other subgroups\nencourage drinking at religious celebrations (e.g., Jewish and Catholic holidays), while\nstill others strongly discourage all drinking or intoxication (e.g., some religious groups,\nsuch as Mormons, fundamenta list Christians, and Muslims).\nGender-Related Diagnostic Issues\nHistorically, in many Western societies, ac ceptance of drinking and drunkenness is more", "source": "dsm5.pdf"} {"id": "1dd283340456-2", "page_content": "Historically, in many Western societies, ac ceptance of drinking and drunkenness is more\ntolerated for males, but such gender differences may be much less prominent in recent\nyears, especially during adolescence and young adulthood.", "source": "dsm5.pdf"} {"id": "2442a869cc41-0", "page_content": "Alcohol Withdrawal 499\nDiagnostic Markers\nIntoxication is usually established by observing an individual\u2019s behavior and smelling alcohol\non the breath. The degree of into xication increases with an individual\u2019s blood or breath alcohol\nlevel and with the ingestion of other substanc es, especially those with sedating effects.\nFunctional Consequences of Alcohol Intoxication\nAlcohol intoxication contributes to the more than 30,000 alcohol-related drinking deaths in\nthe United States each year. In addition, intoxication with this drug contributes to huge\ncosts associated with drunk driving, lost time from school or work, as well as interpersonal\narguments and physical fights.\nDifferential Diagnosis\nOther medical conditions. Several medical (e.g., diabetic acidosis) and neurological condi-\ntions (e.g., cerebellar ataxia, multiple sclerosis) can temporarily resemble alcohol intoxication. \nSedative, hypnotic, or anxiolytic intoxication. Intoxication with se dative, hypnotic, or\nanxiolytic drugs or with other sedating subs tances (e.g., antihistam ines, anticholinergic\ndrugs) can be mistaken for alcohol intoxicati on. The differential requires observing alco-\nhol on the breath, measuring blood or breath alcohol levels , ordering a medical workup,\nand gathering a good history. The signs and symptoms of sedative-hypnotic intoxication\nare very similar to those observed with alco hol and include similar problematic behavioral\nor psychological changes. These changes are accompanied by evidence of impaired func-\ntioning and judgment\u2014which, if intense, can result in a life-threat ening coma\u2014and levels\nof incoordination that can interfere with driving abilities and with performing usual\nactivities. However, there is no smell as there is with alcohol, but there is likely to be evi-", "source": "dsm5.pdf"} {"id": "2442a869cc41-1", "page_content": "dence of misuse of the depressant drug in the blood or urine toxicology analyses.\nComorbidity\nAlcohol intoxication may occu r comorbidly with other subs tance intoxication, especially\nin individuals with conduct disorder or antisocial personality disorder.\nAlcohol Withdrawal\nDiagnostic Criteria\nA. Cessation of (or reduction in) alcohol use that has been heavy and prolonged.\nB. Two (or more) of the following, developing within several hours to a few days after the\ncessation of (or reduction in) alcohol use described in Criterion A:\n1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).\n2. Increased hand tremor.\n3. Insomnia.\n4. Nausea or vomiting.\n5. Transient visual, tactile, or auditory hallucinations or illusions.\n6. Psychomotor agitation.\n7. Anxiety.\n8. Generalized tonic-clonic seizures.\nC. The signs or symptoms in Criterion B cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning.", "source": "dsm5.pdf"} {"id": "987a7225aaf6-0", "page_content": "500 Substance-Related and Addictive Disorders\nD. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication or withdrawal from\nanother substance.\nSpecify if:\nWith perceptual disturbances: This specifier applies in the rare instance when hal-\nlucinations (usually visual or tactile) occur with intact reality testing, or auditory, visual,\nor tactile illusions occur in the absence of a delirium.\nCoding note: The ICD-9-CM code is 291.81. The ICD-10-CM code for alcohol withdrawal\nwithout perceptual disturbances is F10.239, and the ICD-10-CM code for alcohol withdrawal\nwith perceptual disturbances is F10.232. Note that the ICD-10-CM code indicates the comor-\nbid presence of a moderate or severe alcohol use disorder, reflecting the fact that alcohol with-\ndrawal can only occur in the presence of a moderate or severe alcohol use disorder. It is not\npermissible to code a comorbid mild alcohol use disorder with alcohol withdrawal.\nSpecifiers\nWhen hallucinations occur in the absence of delirium (i.e., in a clea r sensorium), a diagno-\nsis of substance/medication-induced ps ychotic disorder should be considered.\nDiagnostic Features\nThe essential feature of alcoho l withdrawal is the presence of a characteristic withdrawal\nsyndrome that develops within several hours to a few days after the cessation of (or re-\nduction in) heavy and prolon ged alcohol use (Criteria A and B). The withdrawal syn-\ndrome includes two or more of the sympto ms reflecting autonomic hyperactivity and\nanxiety listed in Criterion B, along with gastrointestinal symptoms.\nWithdrawal symptoms cause clinically signific ant distress or impairment in social, oc-", "source": "dsm5.pdf"} {"id": "987a7225aaf6-1", "page_content": "Withdrawal symptoms cause clinically signific ant distress or impairment in social, oc-\ncupational, or other important areas of functi oning (Criterion C). The symptoms must not\nbe attributable to another me dical condition and are not be tter explained by another men-\ntal disorder (e.g., generalized anxiety diso rder), including intoxication or withdrawal\nfrom another substance (e.g., sedative, hypnotic, or anxiolytic withdrawal) (Criterion D).\nSymptoms can be relieved by administering alcohol or benzodiazepines (e.g., diazepam).\nThe withdrawal symptoms typically begin when blood concentrations of alcohol decline\nsharply (i.e., within 4\u201312 hours) after alcohol us e has been stopped or re duced. Reflecting the\nrelatively fast metabolism of alcohol, symptoms of alcohol withdrawal usually peak in inten-\nsity during the second day of abstinence and ar e likely to improve markedly by the fourth or\nfifth day. Following acute withdrawal, however, symptoms of anxiety, insomnia, and auto-\nnomic dysfunction may persist for up to 3\u20136 months at lower levels of intensity.\nFewer than 10% of individuals who develop alcohol withdrawal will ever develop dra-\nmatic symptoms (e.g., severe autonomic hypera ctivity, tremors, alcohol withdrawal delir-\nium). Tonic-clonic seizures occur in fewer than 3% of individuals.\nAssociated Features Supporting Diagnosis\nAlthough confusion and changes in consciousness are not core criteria for alcohol with-\ndrawal, alcohol withdrawal delirium (see \u201cDe lirium\u201d in the chapte r \u201cNeurocognitive Dis-\norders\u201d) may occur in the context of withdrawal . As is true for any agitated, confused state,\nregardless of the cause, in addition to a disturbance of cons ciousness and cognition, with-", "source": "dsm5.pdf"} {"id": "987a7225aaf6-2", "page_content": "drawal delirium can include visual, tactile, or (rarely) auditory hallucinations (delirium tre-\nmens). When alcohol withdrawal delirium develo ps, it is likely that a clinically relevant\nmedical condition may be present (e.g., liver fa ilure, pneumonia, gastrointestinal bleeding,\nsequelae of head trauma, hypoglycemia, an electrolyte imbalance, postoperative status).", "source": "dsm5.pdf"} {"id": "e8b9c43a5959-0", "page_content": "Alcohol Withdrawal 501\nPrevalence\nIt is estimated that approximately 50% of mi ddle-class, highly functional individuals with\nalcohol use disorder have ev er experienced a full alcohol withdrawal syndrome. Among\nindividuals with alcohol use disorder who are hospitalized or homeless, the rate of al-\ncohol withdrawal may be greater than 80%. Less than 10% of individuals in withdrawal\never demonstrate alcoho l withdrawal delirium or withdrawal seizures. \nDevelopment and Course\nAcute alcohol withdrawal occurs as an episode usually lasting 4\u20135 days and only after\nextended periods of heavy drinking. Withdrawal is relatively rare in individuals younger\nthan 30 years, and the risk and seve rity increase with increasing age.\nRisk and Prognostic Factors\nEnvironmental. The probability of developing alco hol withdrawal increases with the\nquantity and frequency of alcohol consumptio n. Most individuals with this condition are\ndrinking daily, consuming large amounts (appr oximately more than eight drinks per day)\nfor multiple days. However, there are large inter-individual differences, with enhanced\nrisks for individuals with concurrent medical conditions, those with family histories of al-\ncohol withdrawal (i.e., a gene tic component), those with pr ior withdrawals, and individ-\nuals who consume sedative, hy pnotic, or anxiolytic drugs.\nDiagnostic Markers\nAutonomic hyperactivity in the context of moderately high but falling blood alcohol levels\nand a history of prolonged heavy drinking in dicate a likelihood of alcohol withdrawal.\nFunctional Consequences of Alcohol Withdrawal\nSymptoms of withdrawal may serve to perpet uate drinking behaviors and contribute to\nrelapse, resulting in persistently impaired so cial and occupational functioning. Symptoms\nrequiring medically supervised detoxification result in hospital utilization and loss of\nwork productivity. Overall, the presence of withdrawal is associated with greater func-", "source": "dsm5.pdf"} {"id": "e8b9c43a5959-1", "page_content": "work productivity. Overall, the presence of withdrawal is associated with greater func-\ntional impairment and poor prognosis. \nDifferential Diagnosis\nOther medical conditions. The symptoms of alcohol withdrawal can also be mimicked\nby some medical conditions (e.g., hypoglycemia and diabetic ketoacidosis). Essential\ntremor, a disorder that frequently runs in families, may erroneou sly suggest the tremu-\nlousness associated with alcohol withdrawal. \nSedative, hypnotic, or anxiolytic withdrawal. Sedative, hypnotic, or anxiolytic with-\ndrawal produces a syndrome very sim ilar to that of alcohol withdrawal.\nComorbidity\nWithdrawal is more likely to occur with heavie r alcohol intake, and that might be most of-\nten observed in individuals with conduct di sorder and antisocial personality disorder.\nWithdrawal states are also more severe in ol der individuals, individuals who are also de-\npendent on other depressant drugs (sedativ e-hypnotics), and individuals who have had\nmore alcohol withdrawal experiences in the past.", "source": "dsm5.pdf"} {"id": "6a37ceb7be22-0", "page_content": "502 Substance-Related and Addictive Disorders\nOther Alcohol-Induced Disorders\nThe following alcohol-induced disorders are desc ribed in other chapters of the manual with\ndisorders with which they share phenomenol ogy (see the substance/medication-induced\nmental disorders in these chapters): alcohol-induced psychotic disorder (\u201cSchizophrenia Spec-\ntrum and Other Psychotic Disorders\u201d); alcoho l-induced bipolar diso rder (\u201cBipolar and\nRelated Disorders\u201d); alcohol-induced depressive disorder (\u201cDepressive Disorders\u201d); alcohol-\ninduced anxiety disorder (\u201cAnxiety Disorders\u201d); alcohol-induced sl eep disorder (\u201cSleep-\nWake Disorders\u201d); alcohol-induced sexual dysfunction (\u201cSexual Dysfunctions\u201d); and alcohol-\ninduced major or mild neurocognitive disorder (\u201cNeurocognitive Disorders\u201d). For alcohol\nintoxication delirium an d alcohol withdrawal delirium, see th e criteria and discussion of de-\nlirium in the chapter \u201cNeurocognitive Disorder s.\u201d These alcohol-induced disorders are diag-\nnosed instead of alcohol intoxication or alcohol withdrawal only when the symptoms are\nsufficiently severe to warrant independent clinical attention.\nFeatures\nThe symptom profiles for an al cohol-induced condition resemble independent mental disor-\nders as described elsewhere in DSM-5. However, the alcohol- induced disorder is temporary\nand observed after severe intoxication with an d/or withdrawal from alcohol. While the symp-\ntoms can be identical to those of independent mental disorders (e.g., psychoses, major depres-\nsive disorder), and while they can have the same severe consequences (e.g., suicide attempts),\nalcohol-induced conditions are li kely to improve without formal treatment in a matter of days\nto weeks after cessation of severe intoxication and/or withdrawal. \nEach alcohol-induced mental disorder is listed in the relevant diagnostic section and there-", "source": "dsm5.pdf"} {"id": "6a37ceb7be22-1", "page_content": "Each alcohol-induced mental disorder is listed in the relevant diagnostic section and there-\nfore only a brief description is offered here. Alcohol-induced disorder s must have developed\nin the context of severe intoxication and/or wi thdrawal from the substance capable of produc-\ning the mental disorder. In addition, there must be evidence that the disorder being observed\nis not likely to be better expl ained by another non-alcohol-indu ced mental disorder. The latter\nis likely to occur if the mental disorder was present before the severe intoxication or with-\ndrawal, or continued more than 1 month after the cessation of severe intoxication and/or with-\ndrawal. When symptoms are observed only during a delirium, they should be considered part\nof the delirium and not diagnosed separately, as many symptoms (including disturbances in\nmood, anxiety, and reality testin g) are commonly seen during ag itated, confused states. The al-\ncohol-induced disorder must be clinically relevant, causing significant levels of distress or sig-\nnificant functional impairment. Finally, there are indications that the intake of substances of\nabuse in the context of a preexisting mental disorder are likely to result in an intensification of\nthe preexisting independent syndrome. \nThe features associated with each relevant major mental disorder (e.g., psychotic epi-\nsodes, major depressive disorder) are similar whether observed with an independent or an\nalcohol-induced condition. However, indivi duals with alcohol-induced disorders are\nlikely to also demonstrate the associated feat ures seen with an alcohol use disorder, as\nlisted in the subsections of this chapter.\nRates of alcohol-induced diso rders vary somewhat by diag nostic category. For exam-\nple, the lifetime risk for major depressive epis odes in individuals with alcohol use disorder", "source": "dsm5.pdf"} {"id": "6a37ceb7be22-2", "page_content": "ple, the lifetime risk for major depressive epis odes in individuals with alcohol use disorder\nis approximately 40%, but only about one-third to one-half of these represent independent\nmajor depressive syndromes observed outside the context of intoxication. Similar rates of\nalcohol-induced sleep and anxiet y conditions are likely, but alcohol-induced psychotic ep-\nisodes are fairly rare. \nDevelopment and Course", "source": "dsm5.pdf"} {"id": "c049f92ab95a-0", "page_content": "alcohol-induced sleep and anxiet y conditions are likely, but alcohol-induced psychotic ep-\nisodes are fairly rare. \nDevelopment and Course\nOnce present, the symptoms of an alcohol-in duced condition are likely to remain clinically\nrelevant as long as the individual continues to experience severe intoxication and/or with-", "source": "dsm5.pdf"} {"id": "d4bc91b94ba2-0", "page_content": "Unspecified Alcohol-Related Disorder 503\ndrawal. While the symptoms are identical to those of independent mental disorders (e.g.,\npsychoses, major depressive disorder), and while they can have the same severe conse-\nquences (e.g., suicide attempts), all alcohol-induced syndromes other than alcohol-\ninduced neurocognitive disord er, amnestic confabulatory ty pe (alcohol-induced persist-\ning amnestic disorder), regardless of the se verity of the symptoms, are likely to improve\nrelatively quickly and unlikely to remain clin ically relevant for more than 1 month after\ncessation of severe intoxication and/or withdrawal. \nThe alcohol-induced disorders are an important part of the differential diagnoses for\nthe independent mental conditions. Independ ent schizophrenia, major depressive disor-\nder, bipolar disorder, and anxiety disorders, su ch as panic disorder, are likely to be asso-\nciated with much longer-lasting periods of symptoms and often require longer-term\nmedications to optimize the probability of improvement or recovery . The alcohol-induced\nconditions, on the other hand, are likely to be much shorter in duration and disappear\nwithin several days to 1 month after cessatio n of severe intoxication and/or withdrawal,\neven without psychotropic medications. \nThe importance of recognizing an alcohol- induced disorder is similar to the relevance\nof identifying the possible role of some endo crine conditions and medication reactions be-\nfore diagnosing an independent mental disorder. In light of the high prevalence of alcohol\nuse disorders worldwide, it is important that these alcohol- induced diagnoses be consid-\nered before independent ment al disorders are diagnosed.\nUnspecified Alcohol-Related Disorder\n291.9 (F10.99)\nThis category applies to presentations in which symptoms characteristic of an alcohol-\nrelated disorder that cause clinically significant distress or impairment in social, occupa-", "source": "dsm5.pdf"} {"id": "d4bc91b94ba2-1", "page_content": "related disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any specific alcohol-related disorder or any of the disorders in the substance-related\nand addictive disorders diagnostic class.\nCaffeine-Related Disorders\nCaffeine Intoxication\nCaffeine Withdrawal\nOther Caffeine-Induced Disorders\nUnspecified Caffeine-Related Disorder\nCaffeine Intoxication\nDiagnostic Criteria 305.90 (F15.929)\nA. Recent consumption of caffeine (typically a high dose well in excess of 250 mg).\nB. Five (or more) of the following signs or symptoms developing during, or shortly after,\ncaffeine use:\n1. Restlessness.\n2. Nervousness.", "source": "dsm5.pdf"} {"id": "7fcb79462704-0", "page_content": "504 Substance-Related and Addictive Disorders\n3. Excitement.\n4. Insomnia.\n5. Flushed face.\n6. Diuresis.\n7. Gastrointestinal disturbance.\n8. Muscle twitching.\n9. Rambling flow of thought and speech.\n10. Tachycardia or cardiac arrhythmia.\n11. Periods of inexhaustibility.\n12. Psychomotor agitation.\nC. The signs or symptoms in Criterion B cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning.\nD. The signs or symptoms are not attributable to another medical condition and are not bet-\nter explained by another mental disorder, including intoxication with another substance.\nDiagnostic Features\nCaffeine can be consumed from a number of di fferent sources, including coffee, tea, caf-\nfeinated soda, \u201cenergy\u201d drinks, over-the-cou nter analgesics and cold remedies, energy\naids (e.g., drinks), weight-loss aids, and chocol ate. Caffeine is also increasingly being used\nas an additive to vitamins and to food prod ucts. More than 85% of children and adults con-\nsume caffeine regularly. Some caffeine user s display symptoms consistent with problem-\natic use, including tolerance and withdrawal (see \u201cCaffeine Withdrawal\u201d later in this\nchapter); the data are not available at this time to determine the clinical significance of a\ncaffeine use disorder and its pr evalence. In contrast, there is evidence that caffeine with-\ndrawal and caffeine intoxication are clinically significant and sufficiently prevalent.\nThe essential feature of caffein e intoxication is recent cons umption of caffeine and five\nor more signs or symptoms th at develop during or shortly after caffeine use (Criteria A", "source": "dsm5.pdf"} {"id": "7fcb79462704-1", "page_content": "or more signs or symptoms th at develop during or shortly after caffeine use (Criteria A\nand B). Symptoms include restlessness, nervousness, excitement, insomnia, flushed face,\ndiuresis, and gastrointestinal complaints, which can occur with low doses (e.g., 200 mg) in\nvulnerable individuals such as children, the el derly, or individuals who have not been ex-\nposed to caffeine previously. Symptoms that ge nerally appear at levels of more than 1 g/\nday include muscle twitching, rambling flow of thought and speech, tachycardia or car-\ndiac arrhythmia, periods of inexhaustibility, and psychomotor agitation. Caffeine intoxi-\ncation may not occur despite high caffeine inta ke because of the development of tolerance.\nThe signs or symptoms must cause clinically significant distress or impairment in social,\noccupational, or other importan t areas of functioning (Criterion C). The signs or symp-\ntoms must not be attr ibutable to another medical condit ion and are not better explained by\nanother mental disorder (e.g., an anxiety disorder) or intoxi cation with another substance\n(Criterion D).\nAssociated Features Supporting Diagnosis\nMild sensory disturbances (e.g., ringing in the ears and flashes of light) may occur with high\ndoses of caffeine. Although large doses of caffeine can increase heart rate, smaller doses can\nslow heart rate. Whether excess caffeine intake can cause headaches is unclear. On physical\nexamination, agitation, restlessness, sweati ng, tachycardia, flushed face, and increased\nbowel motility may be seen. Caffeine blood levels may provide important information for\ndiagnosis, particularly when the individual is a poor historian, although these levels are not\ndiagnostic by themselves in view of the individual variation in response to caffeine.", "source": "dsm5.pdf"} {"id": "1d92a839f354-0", "page_content": "Caffeine Intoxication 505\nPrevalence\nThe prevalence of caffeine intoxication in the gene ral population is un clear. In the United\nStates, approximately 7% of individuals in the population may experience five or more symp-\ntoms along with functional impairment consiste nt with a diagnosis of caffeine intoxication.\nDevelopment and Course \nConsistent with a half-life of caffeine of approximately 4\u20136 hours, caffeine intoxication\nsymptoms usually remit within the first day or so and do not have any known long-lasting\nconsequences. However, individuals who consum e very high doses of caffeine (i.e., 5\u201310\ng) may require immediate medical attent ion, as such doses can be lethal.\nWith advancing age, individuals are likely to demonstrate increasingly intense reac-\ntions to caffeine, with greater complaints of interference with sleep or feelings of hyper-\narousal. Caffeine intoxicati on among young individuals after consumption of highly\ncaffeinated products, includin g energy drinks, has been observed. Children and adoles-\ncents may be at increased risk for caffeine into xication because of low body weight, lack of\ntolerance, and lack of kn owledge about the pharmacolog ical effects of caffeine.\nRisk and Prognostic Factors\nEnvironmental. Caffeine intoxication is often seen among individuals who use caffeine\nless frequently or in those who have recently increased their caffeine intake by a substan-\ntial amount. Furthermore, oral contraceptives significantly de crease the elimination of caf-\nfeine and consequently may incre ase the risk of intoxication. \nGenetic and physiological. Genetic factors may affect risk of caffeine intoxication.\nFunctional Consequences of Caffeine Intoxication\nImpairment from caffeine intoxication may have serious consequences, including dys-", "source": "dsm5.pdf"} {"id": "1d92a839f354-1", "page_content": "Impairment from caffeine intoxication may have serious consequences, including dys-\nfunction at work or school, social indiscretions, or failure to fulfill role obligations. More-\nover, extremely high doses of caffeine can be fa tal. In some cases, caffeine intoxication may\nprecipitate a caffeine-induced disorder. \nDifferential Diagnosis\nOther mental disorders. Caffeine intoxication may be characterized by symptoms (e.g.,\npanic attacks) that resemble primary mental diso rders. To meet criteria for caffeine intoxica-\ntion, the symptoms must not be associated with another medical condition or another mental\ndisorder, such as an anxiety di sorder, that could better expl ain them. Manic episodes; panic\ndisorder; generalized anxiety disorder; amphetami ne intoxication; sedative, hypnotic, or anx-\niolytic withdrawal or tobacco withdrawal; slee p disorders; and medication-induced side ef-\nfects (e.g., akathisia) can cause a clinical picture that is similar to that of caffeine intoxication. \nOther caffeine-induced disorders. The temporal relationship of the symptoms to increased\ncaffeine use or to abstinence from caffeine help s to establish the diagno sis. Caffeine intoxica-\ntion is differentiated from caffeine-induced anxiety disorder, with onset during intoxication\n(see \u201cSubstance/Medicat ion-Induced Anxiety Disorder\u201d in the chapter \u201cAnxiety Disorders\u201d),\nand caffeine-induced sleep disorder, with onse t during intoxication (see \u201cSubstance/Medica-\ntion-Induced Sleep Disorder\u201d in the chapter \u201cS leep-Wake Disorders\u201d), by the fact that the\nsymptoms in these latter disorders are in excess of those usually associ ated with caffeine in-\ntoxication and are severe enough to wa rrant independent clinical attention.", "source": "dsm5.pdf"} {"id": "8b2534bd44b1-0", "page_content": "506 Substance-Related and Addictive Disorders\nComorbidity\nTypical dietary doses of caffeine have not been consistently associated with medical prob-\nlems. However, heavy use (e.g., >400 mg) can cause or exacerbate anxiety and somatic\nsymptoms and gastrointestinal distress. With acute, extremely high doses of caffeine,\ngrand mal seizures and respiratory failure may re sult in death. Excessive caffeine use is as-\nsociated with depressive diso rders, bipolar disorders, eati ng disorders, psychotic disor-\nders, sleep disorders, and subs tance-related disorders, wher eas individuals with anxiety\ndisorders are more likely to avoid caffeine.\nCaffeine Withdrawal\nDiagnostic Criteria 292.0 (F15.93)\nA. Prolonged daily use of caffeine.\nB. Abrupt cessation of or reduction in caffeine use, followed within 24 hours by three (or\nmore) of the following signs or symptoms: \n1. Headache.\n2. Marked fatigue or drowsiness.\n3. Dysphoric mood, depressed mood, or irritability.\n4. Difficulty concentrating.\n5. Flu-like symptoms (nausea, vomiting, or muscle pain/stiffness).\nC. The signs or symptoms in Criterion B cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning.\nD. The signs or symptoms are not associated with the physiological effects of another\nmedical condition (e.g., migraine, viral illness) and are not better explained by another\nmental disorder, including intoxication or withdrawal from another substance.\nDiagnostic Features\nThe essential feature of caffeine withdrawal is the presence of a characteristic withdrawal\nsyndrome that develops after the abrupt cessation of (or substantial reduction in) pro-\nlonged daily caffeine ingestion (Criterion B) . The caffeine withdrawal syndrome is indi-", "source": "dsm5.pdf"} {"id": "8b2534bd44b1-1", "page_content": "longed daily caffeine ingestion (Criterion B) . The caffeine withdrawal syndrome is indi-\ncated by three or more of the following (Criterion B): headache; marked fatigue or\ndrowsiness; dysphoric mood, depressed mood, or irritability; difficulty concentrating;\nand flu-like symptoms (nausea, vomiting, or muscle pain/stiffness). The withdrawal syn-\ndrome causes clinical significant distress or impairment in social, occupational, or other\nimportant areas of functioning (Criterion C) . The symptoms must not be associated with\nthe physiological effects of another medical co ndition and are not better explained by an-\nother mental disorder (Criterion D). \nHeadache is the hallmark feature of caffeine withdrawal and may be diffuse, gradual\nin development, throbbing, severe, and sensitive to move ment. However, other symptoms\nof caffeine withdrawal can occur in the abse nce of headache. Caffeine is the most widely\nused behaviorally active drug in the world and is present in many different types of bev-\nerages (e.g., coffee, tea, mat\u00e9, soft drinks, energy drinks), foods, energy aids, medications,\nand dietary supplements. Because caffeine ingestion is often integrated into social customs\nand daily rituals (e.g., coffee break, tea time ), some caffeine consumers may be unaware of\ntheir physical dependence on caffeine. Thus, caffeine withdrawal symptoms could be un-\nexpected and misattributed to other causes (e.g ., the flu, migraine). Furthermore, caffeine\nwithdrawal symptoms may occur when indivi duals are required to abstain from foods\nand beverages prior to medical procedures or when a usual caffeine dose is missed be-\ncause of a change in routine (e.g., during travel, weekends).", "source": "dsm5.pdf"} {"id": "41680c833a20-0", "page_content": "Caffeine Withdrawal 507\nThe probability and severity of caffeine with drawal generally increase as a function of\nusual daily caffeine dose. However, there is large variability among individuals and\nwithin individuals across different episodes in the incidence, severity, and time course of\nwithdrawal symptoms. Caffeine withdrawal sy mptoms may occur after abrupt cessation\nof relatively low chronic daily doses of caffeine (i.e., 100 mg).\nAssociated Features Supporting Diagnosis\nCaffeine abstinence has been shown to be as sociated with impaired behavioral and cogni-\ntive performance (e.g., sustai ned attention). Electroencepha lographic studies have shown\nthat caffeine withdrawal symptoms are significantly associated with increases in theta\npower and decreases in beta-2 power. Decre ased motivation to work and decreased socia-\nbility have also been reported during caffe ine withdrawal. Increased analgesic use during\ncaffeine withdrawal has been documented.\nPrevalence\nMore than 85% of adults and children in th e United States regularly consume caffeine,\nwith adult caffeine consumers ingesting abou t 280 mg/day on average. The incidence and\nprevalence of the caffeine withdrawal syndro me in the general population are unclear. In\nthe United States, headache may occur in a pproximately 50% of cases of caffeine absti-\nnence. In attempts to permanently stop caffein e use, more than 70% of individuals may ex-\nperience at least one caffeine withdrawal sy mptom (47% may experience headache), and\n24% may experience headache plus one or more other symptoms as well as functional\nimpairment due to withdrawal. Among individu als who abstain from caffeine for at least\n24 hours but are not trying to permanently stop caffeine use, 11% may experience head-\nache plus one or more other symptoms as well as functional impairment. Caffeine con-", "source": "dsm5.pdf"} {"id": "41680c833a20-1", "page_content": "ache plus one or more other symptoms as well as functional impairment. Caffeine con-\nsumers can decrease the incidence of caffeine withdrawal by using ca ffeine daily or only\ninfrequently (e.g., no more than 2 consecutive days). Gradual reductio n in caffeine over a\nperiod of days or weeks may decrease the incidence and severity of caffeine withdrawal. \nDevelopment and Course\nSymptoms usually begin 12\u201324 hours after the last caffeine dose and peak after 1\u20132 days\nof abstinence. Caffeine withdrawal symptoms last for 2\u20139 days, with the possibility of\nwithdrawal headaches occurring for up to 21 days. Symptoms usually remit rapidly\n(within 30\u201360 minutes) after re-ingestion of caffeine. \nCaffeine is unique in that it is a behavioral ly active drug that is consumed by individ-\nuals of nearly all ages. Rates of caffeine consumption and overall level of caffeine con-\nsumption increase with age until the early to mid-30s and then level off. Although caffeine\nwithdrawal among children and adolescents has been documented, relatively little is\nknown about risk factors for caffeine withdrawal among this age group. The use of highly\ncaffeinated energy drinks is increasing with in young individuals, which could increase\nthe risk for caffeine withdrawal. \nRisk and Prognostic Factors \nTemperamental. Heavy caffeine use has been observ ed among individuals with mental\ndisorders, including eating disorders; smoker s; prisoners; and drug and alcohol abusers.\nThus, these individuals could be at higher risk for caffeine withdrawal upon acute caffeine\nabstinence.\nEnvironmental. The unavailability of caffeine is an environmental risk factor for incipi-\nent withdrawal symptoms. While caffeine is le gal and usually widely available, there are\nconditions in which caffeine use may be restricted, such as during medical procedures,", "source": "dsm5.pdf"} {"id": "41680c833a20-2", "page_content": "conditions in which caffeine use may be restricted, such as during medical procedures,\npregnancy, hospitalizations, religious observances, wartime, travel, and research partici-", "source": "dsm5.pdf"} {"id": "a6bad50fc8bc-0", "page_content": "508 Substance-Related and Addictive Disorders\npation. These external enviro nmental circumstances may precipitate a withdrawal syn-\ndrome in vulnerable individuals. \nGenetic and physiological factors. Genetic factors appear to increase vulnerability to\ncaffeine withdrawal, but no specific genes have been identified. \nCourse modifiers. Caffeine withdrawal symptoms usua lly remit within 30\u201360 minutes\nof reexposure to caffeine. Doses of caffeine significantly less than one\u2019s usual daily dose\nmay be sufficient to prevent or attenuate caffeine withdrawal sy mptoms (e.g., consump-\ntion of 25 mg by an individual who typically consumes 300 mg).\nCulture-Related Diagnostic Issues\nHabitual caffeine consumers who fast for religio us reasons may be at increased r isk for caf-\nfeine withdrawal. \nFunctional Consequences of \nCaffeine Withdrawal Disorder\nCaffeine withdrawal symptoms can vary from mild to extreme, at times causing functional\nimpairment in normal daily activities. Rates of functional impairment range from 10% to\n55% (median 13%), with rates as high as 73% found among individuals who also show\nother problematic features of caffeine use. Ex amples of functional impairment include be-\ning unable to work, exercise, or care for child ren; staying in bed all day; missing religious\nservices; ending a vacation early; and cancelling a social gathering. Caffeine withdrawal\nheadaches may be described by individuals as \u201cthe worst headaches\u201d ever experienced.\nDecrements in cognitive and motor pe rformance have also been observed. \nDifferential Diagnosis\nOther medical disorders an d medical side effects. Several disorders should be consid-\nered in the differential diagnosis of caffeine withdrawal. Caffeine withdrawal can mimic\nmigraine and other headache di sorders, viral illnesses, sinu s conditions, tension, other", "source": "dsm5.pdf"} {"id": "a6bad50fc8bc-1", "page_content": "drug withdrawal states (e.g., from amphetami nes, cocaine), and medication side effects.\nThe final determination of caffeine withdrawal should rest on a determination of the pat-\ntern and amount consumed, the time interval between caffeine ab stinence and onset of\nsymptoms, and the particular clinical features presented by the individual. A challenge\ndose of caffeine followed by symptom remis sion may be used to confirm the diagnosis.\nComorbidity\nCaffeine withdrawal may be associated with major depressive disorder, generalized anx-\niety disorder, panic disorder, antisocial person ality disorder in adul ts, moderate to severe\nalcohol use disorder, and cannabis and cocaine use. \nOther Caffeine-Induced Disorders\nThe following caffeine-induced disorders are described in other chapters of the manual\nwith disorders with which they share phenomenology (see the substance/medication-\ninduced mental disorders in these chapters): caffeine-induced anxiety disorder (\u201cAnxiety\nDisorders\u201d) and caffeine-indu ced sleep disorder (\u201cSleep-W ake Disorders\u201d). These caf-\nfeine-induced disorders are diagnosed instead of caffeine intoxicati on or caffeine with-\ndrawal only when the symptoms are sufficie ntly severe to warrant independent clinical\nattention.", "source": "dsm5.pdf"} {"id": "af072a6663e8-0", "page_content": "Unspecified Caffeine-Related Disorder 509\nUnspecified Caffeine-Related Disorder\n292.9 (F15.99)\nThis category applies to presentations in which symptoms characteristic of a caffeine-\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any specific caffeine-related disorder or any of the disorders in the substance-related\nand addictive disorders diagnostic class.\nCannabis-Related Disorders\nCannabis Use Disorder\nCannabis Intoxication\nCannabis Withdrawal\nOther Cannabis-Induced Disorders\nUnspecified Cannabis-Related Disorder\nCannabis Use Disorder\nDiagnostic Criteria \nA. A problematic pattern of cannabis use leading to clinically significant impairment or dis-\ntress, as manifested by at least two of the following, occurring within a 12-month period:\n1. Cannabis is often taken in larger amounts or over a longer period than was intended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control cannabis use.\n3. A great deal of time is spent in activities necessary to obtain cannabis, use canna-\nbis, or recover from its effects.\n4. Craving, or a strong desire or urge to use cannabis.\n5. Recurrent cannabis use resulting in a failure to fulfill major role obligations at work,\nschool, or home.\n6. Continued cannabis use despite having persist ent or recurrent social or interper-\nsonal problems caused or exacerbated by the effects of cannabis.\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of cannabis use.\n8. Recurrent cannabis use in situations in which it is physically hazardous.\n9. Cannabis use is continued despite knowledge of having a persistent or recurrent", "source": "dsm5.pdf"} {"id": "af072a6663e8-1", "page_content": "9. Cannabis use is continued despite knowledge of having a persistent or recurrent\nphysical or psychological problem that is likely to have been caused or exacerbated\nby cannabis.\n10. Tolerance, as defined by either of the following:\na. A need for markedly increased amounts of cannabis to achieve intoxication or\ndesired effect.\nb. Markedly diminished effect with continued use of the same amount of cannabis.\n11. Withdrawal, as manifested by either of the following: \na. The characteristic withdrawal syndrome for cannabis (refer to Criteria A and B\nof the criteria set for cannabis withdrawal, pp. 517\u2013518).", "source": "dsm5.pdf"} {"id": "2903920f10be-0", "page_content": "510 Substance-Related and Addictive Disorders\nb. Cannabis (or a closely related substance) is taken to relieve or avoid withdrawal\nsymptoms.\nSpecify if:\nIn early remission: After full criteria for cannabis us e disorder were previously met,\nnone of the criteria for cannabis use disorder have been met for at least 3 months but\nfor less than 12 months (with the exception that Criterion A4, \u201cCraving, or a strong de-\nsire or urge to use cannabis,\u201d may be met).\nIn sustained remission: After full criteria for cannabis use disorder were previously\nmet, none of the criteria for cannabis use disorder have been met at any time during a\nperiod of 12 months or longer (with the exception that Criterion A4, \u201cCraving, or a\nstrong desire or urge to use cannabis,\u201d may be present).\nSpecify if:\nIn a controlled environment: This additional specifier is used if the individual is in an\nenvironment where access to cannabis is restricted. \nCode based on current severity: Note for ICD-10-CM codes: If a cannabis intoxication,\ncannabis withdrawal, or another cannabis-induced mental disorder is also present, do not\nuse the codes below for cannabis use disorder. Instead, the comorbid cannabis use disorder\nis indicated in the 4th character of the cannabis-induced disorder code (see the coding note\nfor cannabis intoxication, cannabis withdrawal, or a specific cannabis-induced mental disor-\nder). For example, if there is comorbid cannabis-induced anxiety disorder and cannabis use\ndisorder, only the cannabis-induced anxiety disorder code is given, with the 4th character\nindicating whether the comorbid cannabis use disorder is mild, moderate, or severe:\nF12.180 for mild cannabis use disorder with cannabis-induced anxiety disorder or F12.280", "source": "dsm5.pdf"} {"id": "2903920f10be-1", "page_content": "F12.180 for mild cannabis use disorder with cannabis-induced anxiety disorder or F12.280\nfor a moderate or severe cannabis use diso rder with cannabis-induced anxiety disorder.\nSpecify current severity:\n305.20 (F12.10) Mild: Presence of 2\u20133 symptoms.\n304.30 (F12.20) Moderate: Presence of 4\u20135 symptoms.\n304.30 (F12.20) Severe: Presence of 6 or more symptoms.\nSpecifiers\n\u201cIn a controlled environment\u201d app lies as a further specifier of remission if the individual is\nboth in remission and in a controlled environm ent (i.e., in early remission in a controlled\nenvironment or in sustained remission in a controlled environmen t). Examples of these\nenvironments are closely supe rvised and substanc e-free jails, therapeutic communities,\nand locked hospital units. \nChanging severity across time in an individual may also be reflected by changes in the\nfrequency (e.g., days of use per month or ti mes used per day) and/or dose (e.g., amount\nused per episode) of cannabis, as assessed by in dividual self-report, report of knowledge-\nable others, clinician\u2019s observ ations, and biological testing.\nDiagnostic Features\nCannabis use disorder and the other cannabis-re lated disorders include problems that are\nassociated with substances derived from the cannabis plant and chemically similar syn-\nthetic compounds. Over time, this plant material has accumulated many names (e.g.,\nweed, pot, herb, grass, reefer, mary jane, da gga, dope, bhang, skunk, boom, gangster, kif,\nand ganja). A concentrated extraction of the cannabis plant that is also commonly used is\nhashish. Cannabis is the generic and perhaps the most appropriate scientific term for the", "source": "dsm5.pdf"} {"id": "2903920f10be-2", "page_content": "hashish. Cannabis is the generic and perhaps the most appropriate scientific term for the\npsychoactive substance(s) derived from the pl ant, and as such it is used in this manual\nto refer to all forms of cannabis-like substances, including synthetic cannabinoid com-\npounds.", "source": "dsm5.pdf"} {"id": "3b7051e52671-0", "page_content": "Cannabis Use Disorder 511\nSynthetic oral formulations (pill/capsules) of delta-9-tetrahydrocannabinol (delta-9-\nTHC) are available by prescripti on for a number of approved medical indications (e.g., for\nnausea and vomiting caused by chemotherapy; for anorexia and weight loss in individuals\nwith AIDS). Other synthetic cannabinoid co mpounds have been manufactured and dis-\ntributed for nonmedical use in the form of plant material that has been sprayed with a can-\nnabinoid formulation (e.g., K2, Spice, JWH-018, JWH-073). \nThe cannabinoids have diverse effects in the brain, prominent among which are actions\non CB1 and CB2 cannabinoid receptors that ar e found throughout the central nervous sys-\ntem. Endogenous ligands for these receptor s behave essentially like neurotransmitters.\nThe potency of cannabis (delta-9-THC concentration) that is generally available varies\ngreatly, ranging from 1% to approximately 15% in typical cannabis plant material and\n10%\u201320% in hashish. During the past two de cades, a steady increase in the potency of\nseized cannabis has been observed. \nCannabis is most commonly smoked via a variety of methods: pipes, water pipes\n(bongs or hookahs), cigarettes (joints or reefer s), or, most recently, in the paper from hol-\nlowed out cigars (blunts). Cannabis is also sometimes ingested orally, typically by mixing\nit into food. More recently, devices have be en developed in which cannabis is \u201cvapor-\nized.\u201d Vaporization involves heating the plant material to release psychoactive cannabi-\nnoids for inhalation. As with other psychoactive substances, smoking (and vaporization)", "source": "dsm5.pdf"} {"id": "3b7051e52671-1", "page_content": "noids for inhalation. As with other psychoactive substances, smoking (and vaporization)\ntypically produces more rapid onset and more intense experiences of the desired effects. \nIndividuals who regularly use cannabis can develop all the genera l diagnostic features\nof a substance use disorder. Cannabis use diso rder is commonly observed as the only sub-\nstance use disorder experienced by the individu al; however, it also frequently occurs con-\ncurrently with other types of substance use di sorders (i.e., alcohol, cocaine, opioid). In\ncases for which multiple types of substances are used, many times the individual may\nminimize the symptoms related to cannabis, as the symptoms may be less severe or cause\nless harm than those directly related to the use of the other substances. Pharmacological\nand behavioral tolerance to most of the effect s of cannabis has been reported in individuals\nwho use cannabis persistently. Generally, tolerance is lost when cannabis use is discontin-\nued for a significant period of time (i.e., for at least several months). \nNew to DSM-5 is the recognition that abrupt cessation of daily or near-daily cannabis\nuse often results in the onset of a cannabis withdrawal syndrome. Common symptoms of\nwithdrawal include irritability, anger or ag gression, anxiety, depressed mood, restless-\nness, sleep difficulty, and decreased appetite or weight loss. Although typically not as\nsevere as alcohol or opiate withdrawal, the cannabis withdrawal syndrome can cause sig-\nnificant distress and contribute to difficulty quitting or relapse among those trying to\nabstain. \nIndividuals with cannabis use disorder may use cannabis throughout the day over a\nperiod of months or years, and thus may spend many hours a da y under the influence.\nOthers may use less frequently, but their use causes recurrent problems related to family,", "source": "dsm5.pdf"} {"id": "3b7051e52671-2", "page_content": "Others may use less frequently, but their use causes recurrent problems related to family,\nschool, work, or other important activities (e.g ., repeated absences at work; neglect of fam-\nily obligations). Periodic cannabis use and intoxication can negatively affect behavioral\nand cognitive functioning and thus interfere with optimal performance at work or school,\nor place the individual at increased physical risk when performing activities that could be\nphysically hazardous (e.g., driving a car; playing certain sports; performing manual work\nactivities, including operating machinery). Ar guments with spouses or parents over the", "source": "dsm5.pdf"} {"id": "72c13218ace1-0", "page_content": "physically hazardous (e.g., driving a car; playing certain sports; performing manual work\nactivities, including operating machinery). Ar guments with spouses or parents over the\nuse of cannabis in the home, or its use in th e presence of children, can adversely impact\nfamily functioning and are common features of those with cannabis use disorder. Last, in-\ndividuals with cannabis use disorder may continue using despite knowledge of physical\nproblems (e.g., chronic cough related to smoking) or psychological problems (e.g., exces-\nsive sedation or exacerbation of other ment al health problems) associated with its use.\nWhether or not cannabis is being used for legitimate medical reasons may also affect\ndiagnosis. When a substance is taken as indicated for a medical condition, symptoms of", "source": "dsm5.pdf"} {"id": "ac0b8eb356f3-0", "page_content": "512 Substance-Related and Addictive Disorders\ntolerance and withdrawal will naturally occur and should not be used as the primary cri-\nteria for determining a diagnosis of a substance use disorder. Although medical uses of\ncannabis remain controversial and equivocal, use for medical circumstances should be\nconsidered when a diagnosis is being made. \nAssociated Features Supporting Diagnosis\nIndividuals who regularly use cannabis often report that it is being used to cope with\nmood, sleep, pain, or other physiological or psychological problems, and those diagnosed\nwith cannabis use disorder frequently do have concurrent other mental disorders. Careful\nassessment typically reveals reports of cannabis use contributing to exacerbation of these\nsame symptoms, as well as other reasons for freq uent use (e.g., to experience euphoria, to\nforget about problems, in respon se to anger, as an enjoyable social activity). Related to this\nissue, some individuals who use cannabis mult iple times per day for the aforementioned\nreasons do not perceive themselves as (and thus do not report) spending an excessive\namount of time under the influence or recovering from the effects of cannabis, despite be-\ning intoxicated on cannabis or coming down from it effects for the majority of most days.\nAn important marker of a substance use disorder diagnosis, particularly in milder cases, is\ncontinued use despite a clear risk of negative co nsequences to other valued activities or re-\nlationships (e.g., school, work, sport activity, partner or parent relationship). \nBecause some cannabis users are motivated to minimize their amount or frequency of\nuse, it is important to be aware of common signs and symptoms of cannabis use and intox-\nication so as to better assess the extent of us e. As with other substances, experienced users\nof cannabis develop behavioral and pharmacolo gical tolerance such that it can be difficult", "source": "dsm5.pdf"} {"id": "ac0b8eb356f3-1", "page_content": "of cannabis develop behavioral and pharmacolo gical tolerance such that it can be difficult\nto detect when they are under the influence. Signs of acute and chro nic use include red eyes\n(conjunctival injection), cannabis odor on clot hing, yellowing of finger tips (from smoking\njoints), chronic cough, burning of incense (to hide the odor), and exaggerated craving and\nimpulse for specific foods, sometimes at unusual times of the day or night. \nPrevalence \nCannabinoids, especially cann abis, are the most widely us ed illicit psychoactive sub-\nstances in the United States. The 12-month prevalence of ca nnabis use disorder (DSM-IV\nabuse and dependence rates combined) is appr oximately 3.4% among 12- to 17-year-olds\nand 1.5% among adults age 18 years and older. Rates of cannabis use disorder are greater\namong adult males (2.2%) than among adult females (0.8%) and among 12- to 17-year-old\nmales (3.8%) than among 12- to 17-year-old females (3.0%). Twelve-month prevalence\nrates of cannabis use disorder among adults decrease with age, with rates highest among\n18- to 29-year-olds (4.4%) and lowest amon g individuals age 65 years and older (0.01%).\nThe high prevalence of cannabis use disord er likely reflects the much more widespread\nuse of cannabis relative to other illicit drug s rather than greater addictive potential. \nEthnic and racial differences in prevalence are moderate. Twelve-month prevalences\nof cannabis use disorder vary markedly across racial-ethnic subgroups in the United\nStates. For 12- to 17-year-olds, rates are hi ghest among Native American and Alaska Na-", "source": "dsm5.pdf"} {"id": "ac0b8eb356f3-2", "page_content": "tives (7.1%) compared with Hispanics (4.1%) , whites (3.4%), African Americans (2.7%),\nand Asian Americans and Pacific Islanders (0.9%). Among adults, the prevalence of can-\nnabis use disorder is also highest among Nati ve Americans and Alaska Natives (3.4%) rel-\native to rates among African Americans (1.8%) , whites (1.4%), Hispanics (1.2%), and Asian\nand Pacific Islanders (1.2%). During the past decade the prevalence of cannabis use disor-\nder has increased among adults and adolescent s. Gender differences in cannabis use dis-", "source": "dsm5.pdf"} {"id": "43b2d1dd9dac-0", "page_content": "and Pacific Islanders (1.2%). During the past decade the prevalence of cannabis use disor-\nder has increased among adults and adolescent s. Gender differences in cannabis use dis-\norder generally are concordant with those in other substance use disorders. Cannabis use\ndisorder is more commonly observed in males, although the magnitude of this difference\nis less among adolescents.", "source": "dsm5.pdf"} {"id": "9a84fbcb3a97-0", "page_content": "Cannabis Use Disorder 513\nDevelopment and Course\nThe onset of cannabis use disorder can occur at any time during or following adolescence,\nbut onset is most commonly during adolescenc e or young adulthood. Although much less\nfrequent, onset of cannabis use disorder in the preteen years or in the late 20s or older can\noccur. Recent acceptance by some of the us e and availability of \u201cmedical marijuana\u201d may\nincrease the rate of onset of cannabis use disorder among older adults.\nGenerally, cannabis use disorder develops over an extended period of time, although\nthe progression appears to be more rapid in ad olescents, particularly those with pervasive\nconduct problems. Most people who develop a cannabis use disorder typically establish a\npattern of cannabis use that gradually increases in both frequency and amount. Cannabis,\nalong with tobacco and alcohol, is traditiona lly the first substance that adolescents try.\nMany perceive cannabis use as less harmful than alcohol or tobacco use, and this percep-\ntion likely contributes to increased use. Moreover, cannabis intoxication does not typically\nresult in as severe behavioral and cognitive dysfunction as does sig nificant alcohol intox-\nication, which may increase the probability of more frequent use in more diverse situa-\ntions than with alcohol. These factors likely contribute to the potential rapid transition\nfrom cannabis use to a cannabis use disord er among some adolescents and the common\npattern of using throughout the day that is commonly ob served among those with more\nsevere cannabis use disorder.\nCannabis use disorder among preteens, adoles cents, and young adults is typically ex-\npressed as excessive use with peers that is a component of a pattern of other delinquent\nbehaviors usually associated with conduct pr oblems. Milder cases primarily reflect con-\ntinued use despite clear problems related to di sapproval of use by other peers, school ad-", "source": "dsm5.pdf"} {"id": "9a84fbcb3a97-1", "page_content": "ministration, or family, which also places the youth at risk for physical or behavioral\nconsequences. In more severe cases, there is a progression to using alone or using through-\nout the day such that use interferes with da ily functioning and takes the place of previ-\nously established, prosocial activities.\nWith adolescent users, changes in mood stab ility, energy level, and eating patterns are\ncommonly observed. These signs and symptoms ar e likely due to the direct effects of can-\nnabis use (intoxication) and the subsequent effects following acute intoxication (coming\ndown), as well as attempts to conceal use from others. Sc hool-related problems are com-\nmonly associated with cannabis use disorder in adolescents, particularly a dramatic drop\nin grades, truancy, and reduced interest in general school activities and outcomes.\nCannabis use disorder among adults typically involves well-establish ed patterns of daily\ncannabis use that continue despite clear psycho social or medical problems. Many adults have\nexperienced repeated desire to st op or have failed at repeated cessation attempts. Milder adult\ncases may resemble the more common adolescent cases in that cannabis use is not as frequent\nor heavy but continues despite po tential significant consequences of sustained use. The rate of\nuse among middle-age and older adults appears to be increasing, likely because of a cohort ef-\nfect resulting from high prevalence of use in the late 1960s and the 1970s.\nEarly onset of cannabis use (e.g., prior to ag e 15 years) is a robust predictor of the de-\nvelopment of cannabis use disorder and other types of substance use disorders and mental\ndisorders during young adulthood. Such early onset is likely related to concurrent other\nexternalizing problems, most notably conduc t disorder symptoms. However, early onset", "source": "dsm5.pdf"} {"id": "9a84fbcb3a97-2", "page_content": "externalizing problems, most notably conduc t disorder symptoms. However, early onset\nis also a predictor of internalizing problems and as such probably reflects a general risk\nfactor for the development of mental health disorders.\nRisk and Prognostic Factors", "source": "dsm5.pdf"} {"id": "522f0fdde213-0", "page_content": "is also a predictor of internalizing problems and as such probably reflects a general risk\nfactor for the development of mental health disorders.\nRisk and Prognostic Factors\nTemperamental. A history of conduct disorder in ch ildhood or adolescence and antiso-\ncial personality disorder are risk factors for the developmen t of many substance-related\ndisorders, including cannabis-related disorders. Other risk factors include externalizing", "source": "dsm5.pdf"} {"id": "26ff7d1188e8-0", "page_content": "514 Substance-Related and Addictive Disorders\nor internalizing disorders during childhood or adolescence. Youths with high behavioral\ndisinhibition scores show early-onset substance use disorders, including cannabis use dis-\norder, multiple substance involvem ent, and early conduct problems.\nEnvironmental. Risk factors include academic failure , tobacco smoking, unstable or abu-\nsive family situation, use of cannabis among immediate family members, a family history\nof a substance use disorder, and low socioecono mic status. As with all substances of abuse,\nthe ease of availability of the substance is a ri sk factor; cannabis is relatively easy to obtain\nin most cultures, which increases the risk of developing a cannabis use disorder.\nGenetic and physiological. Genetic influences contribute to the development of canna-\nbis use disorders. Heritable factors contribute between 30% and 80% of the total variance\nin risk of cannabis use disorders. It should be noted that common genetic and shared en-\nvironmental influences between cannabis and other types of substance use disorders sug-\ngest a common genetic basis for adolesce nt substance use and conduct problems. \nCulture-Related Diagnostic Issues\nCannabis is probably the world\u2019s most commo nly used illicit substance. Occurrence of\ncannabis use disorder across countries is unkn own, but the prevalence rates are likely sim-\nilar among developed countries. It is frequently among the fi rst drugs of experimentation\n(often in the teens) of all cultur al groups in the United States. \nAcceptance of cannabis for medical purposes varies widely across and within cultures.\nCultural factors (acceptability and legal status ) that might impact diagnosis relate to dif-\nferential consequences across cultures for dete ction of use (i.e., arrest, school suspensions,\nor employment suspension). The general change in substance use disorder diagnostic cri-", "source": "dsm5.pdf"} {"id": "26ff7d1188e8-1", "page_content": "or employment suspension). The general change in substance use disorder diagnostic cri-\nteria from DSM-IV to DSM-5 (i.e., removal of the recurrent substance-related legal prob-\nlems criterion) mitigates this concern to some degree.\nDiagnostic Markers\nBiological tests for cannabinoid metabolites are useful for determining if an individual has\nrecently used cannabis. Such testing is help ful in making a diagnosis, particularly in\nmilder cases if an individual denies using while others (family, work, school) purport con-\ncern about a substance use problem. Because cannabinoids are fat soluble, they persist in\nbodily fluids for extended periods of time an d are excreted slowly. Expertise in urine test-\ning methods is needed to reliably interpret results. \nFunctional Consequences of Cannabis Use Disorder\nFunctional consequences of cannabis use disord er are part of the di agnostic criteria. Many\nareas of psychosocial, cognitive, and health functioning may be co mpromised in relation\nto cannabis use disorder. Cognitive function, particularly higher executive function, ap-\npears to be compromised in cannabis users, an d this relationship appears to be dose de-\npendent (both acutely and chronically). This may contribute to increased difficulty at\nschool or work. Cannabis use has been related to a reduction in prosocial goal-directed ac-\ntivity, which some have labeled an amotivational syndrome, that manifests itself in poor\nschool performance and employ ment problems. These problems may be related to perva-\nsive intoxication or recovery from the effects of intoxication . Similarly, cannabis-associated\nproblems with social relationships are common ly reported in those with cannabis use dis-\norder. Accidents due to engagement in pote ntially dangerous behaviors while under the", "source": "dsm5.pdf"} {"id": "26ff7d1188e8-2", "page_content": "order. Accidents due to engagement in pote ntially dangerous behaviors while under the\ninfluence (e.g., driving, sport, recreational or employment ac tivities) are also of concern.\nCannabis smoke contains high levels of carc inogenic compounds that place chronic users\nat risk for respiratory illnesses similar to those experienced by to bacco smokers. Chronic\ncannabis use may contribute to the onset or exacerbation of many ot her mental disorders.", "source": "dsm5.pdf"} {"id": "df69d082d098-0", "page_content": "at risk for respiratory illnesses similar to those experienced by to bacco smokers. Chronic\ncannabis use may contribute to the onset or exacerbation of many ot her mental disorders.\nIn particular, concern has been raised about cannabis use as a causal factor in schizophrenia\nand other psychotic disorders. Cannabis use ca n contribute to the onset of an acute psy-", "source": "dsm5.pdf"} {"id": "9ba577c4d177-0", "page_content": "Cannabis Use Disorder 515\nchotic episode, can exacerbate some sympto ms, and can adversely affect treatment of a\nmajor psychotic illness.\nDifferential Diagnosis\nNonproblematic use of cannabis. The distinction between nonproblematic use of can-\nnabis and cannabis use disorder can be difficult to make because social, behavioral, or psy-\nchological problems may be difficult to attribut e to the substance, especially in the context\nof use of other substances. Also, denial of heavy cannabis use and the attribution that can-\nnabis is related to or causing substantial problems are common among individuals who\nare referred to treatment by others (i.e., sch ool, family, employer, criminal justice system).\nOther mental disorders. Cannabis-induced disorder may be characterized by symp-\ntoms (e.g., anxiety) that resemble primary mental disorders (e.g., gene ralized anxiety dis-\norder vs. cannabis-induced anxiety disorder, with generalized anxiety, with onset during\nintoxication). Chronic intake of cannabis can produce a lack of motivation that resembles\npersistent depressive disorder (dysthymia). Acute adverse reactions to cannabis should be\ndifferentiated from the symptoms of panic di sorder, major depressive disorder, delusional\ndisorder, bipolar disorder, or schizophrenia , paranoid type. Physical examination will\nusually show an increased pulse and conjunctiv al injection. Urine toxicological testing can\nbe helpful in making a diagnosis.\nComorbidity\nCannabis has been commonly thought of as a \u201cgateway\u201d drug because individuals who\nfrequently use cannabis have a much greater lifetime probabili ty than nonusers of using\nwhat are commonly considered more dangerou s substances, like opioids or cocaine. Can-\nnabis use and cannabis use disorder are highly comorbid with other substance use disor-", "source": "dsm5.pdf"} {"id": "9ba577c4d177-1", "page_content": "nabis use and cannabis use disorder are highly comorbid with other substance use disor-\nders. Co-occurring mental co nditions are common in canna bis use disorder. Cannabis use\nhas been associated with poor er life satisfaction; increased mental health treatment and\nhospitalization; and higher rates of depressi on, anxiety disorders, suicide attempts, and\nconduct disorder. Individuals with past-year or lifetime cannabis use disorder have high\nrates of alcohol use disorder (greater than 50%) and tobacco use disorder (53%). Rates of\nother substance use disorders are also likely to be high among individuals with cannabis\nuse disorder. Among those seeking treatmen t for a cannabis use disorder, 74% report\nproblematic use of a secondary or tertiary su bstance: alcohol (40%), cocaine (12%), meth-\namphetamine (6%), and heroin or other opia tes (2%). Among those younger than 18 years,\n61% reported problematic use of a secondary su bstance: alcohol (48%), cocaine (4%), meth-\namphetamine (2%), and heroin or other opiates (2%). Cannabis use disorder is also often\nobserved as a secondary problem among those with a primary diagnosis of other substance\nuse disorders, with approximately 25%\u201380% of those in treatment for another substance\nuse disorder reporting use of cannabis.\nIndividuals with past-year or lifetime diag noses of cannabis use disorder also have\nhigh rates of concurrent ment al disorders other than substa nce use disorders. Major de-\npressive disorder (11%), any anxiety disorder (24%), and bipolar I disorder (13%) are quite\ncommon among individuals with a past-year di agnosis of a cannabis use disorder, as are\nantisocial (30%), obsessive-co mpulsive, (19%), and paranoid (18%) personality disorders.\nApproximately 33% of adolescents with canna bis use disorder have internalizing disor-", "source": "dsm5.pdf"} {"id": "9ba577c4d177-2", "page_content": "Approximately 33% of adolescents with canna bis use disorder have internalizing disor-\nders (e.g., anxiety, depressio n, posttraumatic stre ss disorder), and 60% have externalizing\ndisorders (e.g., conduct disorder, atte ntion-deficit/hyperactivity disorder).\nAlthough cannabis use can impact multiple asp ects of normal human functioning, in-\ncluding the cardiovascular, immune, neuromuscular, ocular, reproductive, and respira-\ntory systems, as well as appetite and cognit ion/perception, there are few clear medical", "source": "dsm5.pdf"} {"id": "a2fef782bff1-0", "page_content": "cluding the cardiovascular, immune, neuromuscular, ocular, reproductive, and respira-\ntory systems, as well as appetite and cognit ion/perception, there are few clear medical\nconditions that commonly co-occur with cannab is use disorder. The most significant health", "source": "dsm5.pdf"} {"id": "64dbe42afa19-0", "page_content": "516 Substance-Related and Addictive Disorders\neffects of cannabis involve the respiratory system, and chronic cannabis smokers exhibit\nhigh rates of respiratory symptoms of bronch itis, sputum production, shortness of breath,\nand wheezing.\nCannabis Intoxication\nDiagnostic Criteria\nA. Recent use of cannabis.\nB. Clinically significant problematic behavio ral or psychological changes (e.g., impaired\nmotor coordination, euphoria, anxiety, sensat ion of slowed time, impaired judgment,\nsocial withdrawal) that developed during, or shortly after, cannabis use.\nC. Two (or more) of the following signs or symptoms developing within 2 hours of canna-\nbis use:\n1. Conjunctival injection.\n2. Increased appetite.\n3. Dry mouth.\n4. Tachycardia.\nD. The signs or symptoms are not attributable to another medical condition and are not better\nexplained by another mental disorder, including intoxication with another substance.\nSpecify if:\nWith perceptual disturbances: Hallucinations with intact reality testing or auditory, vi-\nsual, or tactile illusions occur in the absence of a delirium.\nCoding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether\nor not there is a comorbid cannabis use diso rder and whether or not there are perceptual\ndisturbances. \nFor cannabis intoxication, with out perceptual disturbances: If a mild cannabis use\ndisorder is comorbid, the ICD-10-CM code is F12.129, and if a moderate or severe\ncannabis use disorder is comorbid, the ICD-10-CM code is F12.229. If there is no co-", "source": "dsm5.pdf"} {"id": "64dbe42afa19-1", "page_content": "morbid cannabis use disorder, then the ICD-10-CM code is F12.929.\nFor cannabis intoxication, wit h perceptual disturbances: If a mild cannabis use\ndisorder is comorbid, the ICD-10-CM code is F12.122, and if a moderate or severe\ncannabis use disorder is comorbid, the ICD-10-CM code is F12.222. If there is no co-\nmorbid cannabis use disorder, then the ICD-10-CM code is F12.922.\nSpecifiers\nWhen hallucinations occur in the absence of inta ct reality testing, a diagnosis of substance/\nmedication-induced psychotic di sorder should be considered.\nDiagnostic Features \nThe essential feature of cannabis intoxication is the presence of clinically significant prob-\nlematic behavioral or psychological changes th at develop during, or shortly after, canna-\nbis use (Criterion B). Intoxication typically begins with a \u201chigh\u201d feeling followed by\nsymptoms that include euphoria with inapprop riate laughter and grandiosity, sedation,\nlethargy, impairment in short- term memory, difficulty carrying out complex mental pro-\ncesses, impaired judgment, distorted sensory perceptions, impaired motor performance,\nand the sensation that time is passing slowly. Occasionally, anxiety (which can be severe),", "source": "dsm5.pdf"} {"id": "c1686cc48fbe-0", "page_content": "Cannabis Withdrawal 517\ndysphoria, or social withdrawal occurs. These psychoactive effects are accompanied by\ntwo or more of the following signs, developi ng within 2 hours of cannabis use: conjuncti-\nval injection, increased appetite, dry mouth, and tachycardia (Criterion C). \nIntoxication develops within minutes if the cannabis is smoked but may take a few\nhours to develop if the cannabis is ingested orally. The effects usually last 3\u20134 hours, with\nthe duration being somewhat lo nger when the substance is in gested orally. The magnitude\nof the behavioral and physiological changes depends on the dose, the method of adminis-\ntration, and the characteristics of the individual using the substance, such as rate of absorp-\ntion, tolerance, and sensitivity to the effects of the substance. Because most cannabinoids,\nincluding delta-9-tetrahydrocannabinol (delta-9-T HC), are fat soluble, the effects of canna-\nbis or hashish may occasionally persist or re occur for 12\u201324 hours because of the slow re-\nlease of psychoactive substances from fa tty tissue or to ente rohepatic circulation.\nPrevalence\nThe prevalence of actual episodes of cannabis intoxication in the general population is un-\nknown. However, it is probable that most ca nnabis users would at some time meet criteria\nfor cannabis intoxication. Given this, the prev alence of cannabis users and the prevalence\nof individuals experiencing canna bis intoxication are likely similar.\nFunctional Consequences of Cannabis Intoxication\nImpairment from cannabis intoxication ma y have serious consequences, including dys-\nfunction at work or school, social indiscretion s, failure to fulfill role obligations, traffic ac-\ncidents, and having unprotected sex. In rare cases, cannabis intoxication may precipitate a", "source": "dsm5.pdf"} {"id": "c1686cc48fbe-1", "page_content": "cidents, and having unprotected sex. In rare cases, cannabis intoxication may precipitate a\npsychosis that may vary in duration. \nDifferential Diagnosis\nNote that if the clinical presentation includes hallucinations in the absence of intact reality\ntesting, a diagnosis of subs tance/medication-induced psyc hotic disorder should be con-\nsidered.\nOther substance intoxication. Cannabis intoxicati on may resemble intoxication with\nother types of substances. However, in contrast to cannabis intoxication, alcohol intoxica-\ntion and sedative, hypnotic, or anxiolytic in toxication frequently decrease appetite, in-\ncrease aggressive behavior, and produce nyst agmus or ataxia. Hallucinogens in low doses\nmay cause a clinical picture that resembles cannabis intoxication. Phencyclidine, like can-\nnabis, can be smoked and also causes perceptual changes, but phencyclidine intoxication\nis much more likely to cause ataxia and aggressive behavior. \nOther cannabis-induced disorders. Cannabis intoxication is distinguished from the other\ncannabis-induced disorders (e.g., cannabis-in duced anxiety disorder, with onset during\nintoxication) because the symptoms in these latter disorders predomin ate the clinical pre-\nsentation and are severe enough to wa rrant independent clinical attention. \nCannabis Withdrawal\nDiagnostic Criteria 292.0 (F12.288)\nA. Cessation of cannabis use that has been heavy and prolonged (i.e., usually daily or\nalmost daily use over a period of at least a few months).\nB. Three (or more) of the following signs and symptoms develop within approximately 1 week\nafter Criterion A:", "source": "dsm5.pdf"} {"id": "790b41f6b08a-0", "page_content": "518 Substance-Related and Addictive Disorders\n1. Irritability, anger, or aggression.\n2. Nervousness or anxiety.\n3. Sleep difficulty (e.g., insomnia, disturbing dreams).\n4. Decreased appetite or weight loss.\n5. Restlessness.\n6. Depressed mood.\n7. At least one of the following physical symptoms causing significant discomfort: ab-\ndominal pain, shakiness/tremors, sweating, fever, chills, or headache.\nC. The signs or symptoms in Criterion B cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning.\nD. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication or withdrawal from\nanother substance.\nCoding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for cannabis withdrawal\nis F12.288. Note that the ICD-10-CM code indicates the comorbid presence of a moderate\nor severe cannabis use disorder, reflecting the fact that cannabis withdrawal can only oc-\ncur in the presence of a moderate or severe cannabis use disorder. It is not permissible to\ncode a comorbid mild cannabis use disorder with cannabis withdrawal.\nDiagnostic Features\nThe essential feature of cannabis withdrawal is the presence of a characteristic withdrawal\nsyndrome that develops after the cessation of or substantial reduction in heavy and pro-\nlonged cannabis use. In addition to the sympto ms in Criterion B, the following may also be\nobserved postabstinence: fatigu e, yawning, difficulty concentrating, and rebound periods\nof increased appetite and hypersomnia that follo w initial periods of loss of appetite and in-\nsomnia. For the diagnosis, withdrawal symptoms must cause clinically significant distress", "source": "dsm5.pdf"} {"id": "790b41f6b08a-1", "page_content": "somnia. For the diagnosis, withdrawal symptoms must cause clinically significant distress\nor impairment in social, occu pational, or other important ar eas of functioning (Criterion\nC). Many cannabis users report smoking cannabi s or taking other substances to help re-\nlieve withdrawal symptoms, and many report that withdrawal symptoms make quitting\ndifficult or have contributed to relapse. Th e symptoms typically ar e not of sufficient se-\nverity to require medical attention, but medica tion or behavioral strategies may help alle-\nviate symptoms and improve prognosis in those trying to quit using cannabis.\nCannabis withdrawal is commonly observed in individuals seeking treatment for can-\nnabis use as well as in heavy cannabis users who are not seeking treatment. Among indi-\nviduals who have used cannabis regularly during some period of their lifetime, up to one-\nthird report having experienced cannabis wi thdrawal. Among adults and adolescents en-\nrolled in treatment or heavy cannabis users, 50%\u201395% report cannabis withdrawal. These\nfindings indicate that cannabis withdrawal occurs am ong a substantial subset of regular\ncannabis users who try to quit. \nDevelopment and Course\nThe amount, duration, and frequency of canna bis smoking that is required to produce an\nassociated withdrawal disorder during a quit attempt are unknown. Most symptoms have\ntheir onset within the first 24\u201372 hours of ce ssation, peak within the first week, and last\napproximately 1\u20132 weeks. Sleep difficulties may last more than 30 days. Cannabis with-\ndrawal has been documented among adolescents and adults. Withdrawal tends to be more\ncommon and severe among adults, most likely related to the more persistent and greater\nfrequency and quantity of use among adults.", "source": "dsm5.pdf"} {"id": "273eb788c643-0", "page_content": "Unspecified Cannabis-Related Disorder 519\nRisk and Prognostic Factors\nEnvironmental. Most likely, the prevalence and severity of cannabis withdrawal are\ngreater among heavier cannabis users, and part icularly among those seeking treatment for\ncannabis use disorders. Withdrawal severity also appears to be positiv ely related to the se-\nverity of comorbid sympto ms of mental disorders. \nFunctional Consequences of Cannabis Withdrawal\nCannabis users report using cannabis to re lieve withdrawal symp toms, suggesting that\nwithdrawal might contribute to ongoing expr ession of cannabis use disorder. Worse out-\ncomes may be associated with greater withdraw al. A substantial proportion of adults and\nadolescents in treatment for moderate to se vere cannabis use disorder acknowledge mod-\nerate to severe withdrawal symptoms, and ma ny complain that these symptoms make ces-\nsation more difficult. Cannabis users report having relapsed to cannabis use or initiating\nuse of other drugs (e.g., tranquilizers) to pr ovide relief from cannabis withdrawal symp-\ntoms. Last, individuals living with cannabis us ers observe significant withdrawal effects,\nsuggesting that such symptoms ar e disruptive to daily living. \nDifferential Diagnosis\nBecause many of the symptoms of cannabis wi thdrawal are also symptoms of other sub-\nstance withdrawal syndromes or of depressi ve or bipolar disorder s, careful evaluation\nshould focus on ensuring that the symptoms ar e not better explained by cessation from an-\nother substance (e.g., tobacco or alcohol with drawal), another mental disorder (general-\nized anxiety disorder, major depressive disorder), or another medical condition.\nOther Cannabis-Induced Disorders\nThe following cannabis-induced disorders are desc ribed in other chapters of the manual with\ndisorders with which they share phenomenology (see the substance/medication-induced", "source": "dsm5.pdf"} {"id": "273eb788c643-1", "page_content": "disorders with which they share phenomenology (see the substance/medication-induced\nmental disorders in these chapters): cannab is-induced psychotic disorder (\u201cSchizophrenia\nSpectrum and Other Psychotic Disorders\u201d); cannabis-induced anxiet y disorder (\u201cAnxiety\nDisorders\u201d); and cannabis-induced sleep diso rder (\u201cSleep-Wake Disorders\u201d). For cannabis\nintoxication delirium, see the criteria and disc ussion of delirium in the chapter \u201cNeurocog-\nnitive Disorders.\u201d These cannabis-induced diso rders are diagnosed instead of cannabis in-\ntoxication or cannabis withdrawal when the symptoms are sufficiently severe to warrant\nindependent clinical attention. \nUnspecified Cannabis-Related Disorder\n292.9 (F12.99)\nThis category applies to presentations in which symptoms characteristic of a cannabis-\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any specific cannabis-related disorder or any of the disorders in the substance-related\nand addictive disorders diagnostic class.", "source": "dsm5.pdf"} {"id": "84545818c4b2-0", "page_content": "520 Substance-Related and Addictive Disorders\nHallucinogen-Related Disorders\nPhencyclidine Use Disorder\nOther Hallucinogen Use Disorder\nPhencyclidine Intoxication\nOther Hallucinogen Intoxication\nHallucinogen Persisting Perception Disorder\nOther Phencyclidine-Induced Disorders\nOther Hallucinogen-Induced Disorders\nUnspecified Phencyclidine-Related Disorder\nUnspecified Hallucino gen-Related Disorder\nPhencyclidine Use Disorder\nDiagnostic Criteria \nA. A pattern of phencyclidine (or a pharmacologically similar substance) use leading to\nclinically significant impairment or distress, as manifested by at least two of the follow-\ning, occurring within a 12-month period:\n1. Phencyclidine is often taken in larger amounts or over a longer period than was in-\ntended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control phency-\nclidine use.\n3. A great deal of time is spent in activities necessary to obtain phencyclidine, use the\nphencyclidine, or recover from its effects.\n4. Craving, or a strong desire or urge to use phencyclidine.\n5. Recurrent phencyclidine use resulting in a failure to fulfill major role obligations at\nwork, school, or home (e.g., repeated absences from work or poor work performance\nrelated to phencyclidine use; phencyclidine-related absences, suspensions, or ex-\npulsions from school; neglec t of children or household).\n6. Continued phencyclidine use despite having persistent or recurrent social or inter-\npersonal problems caused or exacerbated by the effects of the phencyclidine (e.g.,\narguments with a spouse about consequences of intoxication; physical fights).", "source": "dsm5.pdf"} {"id": "84545818c4b2-1", "page_content": "arguments with a spouse about consequences of intoxication; physical fights).\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of phencyclidine use.\n8. Recurrent phencyclidine use in situations in which it is physically hazardous (e.g.,\ndriving an automobile or operating a machine when impaired by a phencyclidine).\u00a0\n9. Phencyclidine use is continued despite knowledge of having a persistent or recur-\nrent physical or psychological problem that is likely to have been caused or exac-\nerbated by the phencyclidine.\n10. Tolerance, as defined by either of the following: \na. A need for markedly increased amounts of the phencyclidine to achieve intoxi-\ncation or desired effect.\nb. A markedly diminished effect with continued use of the same amount of the\nphencyclidine.", "source": "dsm5.pdf"} {"id": "a1d0aeb2d4cf-0", "page_content": "Phencyclidine Use Disorder 521\nNote: Withdrawal symptoms and signs are not established for phencyclidines, and so this\ncriterion does not apply. (Withdrawal from phencyclidines has been reported in animals\nbut not documented in human users.)\nSpecify if:\nIn early remission: After full criteria for phencyclidine use disorder were previously\nmet, none of the criteria for phencyclidine use disorder have been met for at least\n3 months but for less than 12 months (with the exception that Criterion A4, \u201cCraving,\nor a strong desire or urge to use the phencyclidine,\u201d may be met).\nIn sustained remission: After full criteria for phencyclidine use disorder were previ-\nously met, none of the criteria for phencyclidine use disorder have been met at any time\nduring a period of 12 months or longer (wit h the exception that Criterion A4, \u201cCraving,\nor a strong desire or urge to use the phencyclidine,\u201d may be met).\nSpecify if:\nIn a controlle d environment: This additional specifier is used if the individual is in an\nenvironment where access to phencyclidines is restricted.\nCoding based on current severity: Note for ICD-10-CM codes: If a phencyclidine intoxica-\ntion or another phencyclidine-induced mental disorder is also present, do not use the codes\nbelow for phencyclidine use disorder. Instead, the comorbid phencyclidine use disorder is in-\ndicated in the 4th character of the phencyclidine-induced disorder code (see the coding note\nfor phencyclidine intoxication or a specific phencyclidine-induced mental disorder). For ex-", "source": "dsm5.pdf"} {"id": "a1d0aeb2d4cf-1", "page_content": "ample, if there is comorbid phencyclidine-induced psychotic disorder, only the phencyclidine-\ninduced psychotic disorder code is given, with the 4th character indicating whether the co-\nmorbid phencyclidine use disorder is mild, moderate, or severe: F16.159 for mild phencycli-\ndine use disorder with phencyclidine-induced psyc hotic disorder or F16.259 for a moderate\nor severe phencyclidine use disorder with phencyclidine-induced psychotic disorder.\nSpecify current severity:\n305.90 (F16.10) Mild: Presence of 2\u20133 symptoms.\n304.60 (F16.20) Moderate: Presence of 4\u20135 symptoms.\n304.60 (F16.20) Severe: Presence of 6 or more symptoms.\nSpecifiers\n\u201cIn a controlled environment\u201d app lies as a further specifier of remission if the individual is\nboth in remission and in a controlled environm ent (i.e., in early remission in a controlled\nenvironment or in sustained remission in a controlled environment). Examples of these\nenvironments are closely supe rvised and substanc e-free jails, therapeutic communities,\nand locked hospital units. \nDiagnostic Features\nThe phencyclidines (or phencyclidine-like substances) include phencyclidine (e.g., PCP,\n\u201cangel dust\u201d) and less potent but similarly ac ting compounds such as ketamine, cyclohex-\namine, and dizocilpine. These substances were first developed as dissociative anesthetics\nin the 1950s and became street drugs in the 1960s. They produce feelings of separation\nfrom mind and body (hence \u201cd issociative\u201d) in low doses, an d at high doses, stupor and", "source": "dsm5.pdf"} {"id": "a1d0aeb2d4cf-2", "page_content": "coma can result. These substances are most commonly smoked or taken orally, but they\nmay also be snorted or injected. Although the primary psychoactive ef fects of PCP last for\na few hours, the total elimination rate of this drug from the body typically extends 8 days\nor longer. The hallucinogenic effects in vulne rable individuals may last for weeks and may\nprecipitate a persistent psychotic episode resembling schizophrenia. Ketamine has been\nobserved to have utility in the treatment of major depressive disorder. Withdrawal symp-", "source": "dsm5.pdf"} {"id": "9b3d172f8f3c-0", "page_content": "522 Substance-Related and Addictive Disorders\ntoms have not been clearly established in hu mans, and therefore the withdrawal criterion\nis not included in the diagnosis of phencyclidine use disorder. \nAssociated Features Supporting Diagnosis\nPhencyclidine may be detected in urine for up to 8 days or even longer at very high doses. In\naddition to laboratory tests to detect its presence, characteristic symptoms resulting from\nintoxication with phencyclidine or related su bstances may aid in its diagnosis. Phencycli-\ndine is likely to produce dissociative sympto ms, analgesia, nystagmus, and hypertension,\nwith risk of hypotension and shock. Violen t behavior can also occur with phencyclidine\nuse, as intoxicated persons may believe that they are being attacked. Residual symptoms\nfollowing use may resemble schizophrenia. \nPrevalence\nThe prevalence of phen cyclidine use disorder is unknown. Approximately 2.5% of the pop-\nulation reports having ever used phencyclidine. The proportion of users increases with\nage, from 0.3% of 12- to 17-year-olds, to 1.3% of 18- to 25-year -olds, to 2.9% of those age 26\nyears and older reporting ever using phencyclid ine. There appears to have been an in-\ncrease among 12th graders in both ever used (to 2.3% from 1.8%) and past-year use (to 1.3%\nfrom 1.0%) of phencyclidine. Past-year use of ketamine appears relatively stable among\n12th graders (1.6%\u20131.7% over the past 3 years).\nRisk and Prognostic Factors", "source": "dsm5.pdf"} {"id": "9b3d172f8f3c-1", "page_content": "Risk and Prognostic Factors \nThere is little information about risk factor s for phencyclidine use disorder. Among indi-\nviduals admitted to substanc e abuse treatment, those for whom phencyclidine was the\nprimary substance were younger than those admitted for other substance use, had lower\neducational levels, and were more likely to be located in the West and Northeast regions of\nthe United States, compared with other admissions. \nCulture-Related Diagnostic Issues\nKetamine use in youths ages 16\u201323 years ha s been reported to be more common among\nwhites (0.5%) than among other ethnic gr oups (range 0%\u20130.3%). Among individuals ad-\nmitted to substance abuse treatment, those for whom phencyclidine was the primary sub-\nstance were predominantly black (49%) or Hispanic (29%).\nGender-Related Diagnostic Issues\nMales make up about three-quarters of those with phencyclidine-related emergency room\nvisits.\nDiagnostic Markers\nLaboratory testing may be useful, as phencyclidin e is present in the urine in intoxicated in-\ndividuals up to 8 days after ingestion. The in dividual\u2019s history, along with certain physical\nsigns, such as nystagmus, analgesia and pr ominent hypertension, may aid in distinguish-\ning the phencyclidine clinical picture from that of other hallucinogens. \nFunctional Consequences of Phencyclidine Use Disorder\nIn individuals with phencyclidine use disorder, there may be physical evidence of injuries\nfrom accidents, fights, and falls. Chronic use of phencyclidine may lead to deficits in mem-\nory, speech, and cognition that may last for months. Cardiovascular and neurological tox-", "source": "dsm5.pdf"} {"id": "9b3d172f8f3c-2", "page_content": "ory, speech, and cognition that may last for months. Cardiovascular and neurological tox-\nicities (e.g., seizures, dystonias, dyskinesia s, catalepsy, hypothermia or hyperthermia)\nmay result from intoxication with phencyclid ine. Other consequences include intracranial\nhemorrhage, rhabdomyolysis, respiratory problems, and (occasionally) cardiac arrest.", "source": "dsm5.pdf"} {"id": "d059e72b3ec8-0", "page_content": "Other Hallucinogen Use Disorder 523\nDifferential Diagnosis \nOther substance use disorders. Distinguishing the effects of phencyclidine from those\nof other substances is import ant, since it may be a common additive to other substances\n(e.g., cannabis, cocaine).\nSchizophrenia and other mental disorders. Some of the effects of phencyclidine and\nrelated substance use may resemble symptoms of other psychiatric disorders, such as psy-\nchosis (schizophrenia), low mood (major de pressive disorder), vi olent aggressive be-\nhaviors (conduct disorder, antisocial person ality disorder). Discerning whether these\nbehaviors occurred before the intake of the dr ug is important in the differentiation of acute\ndrug effects from preexisting mental disord er. Phencyclidine-induced psychotic disorder\nshould be considered when there is impaired reality testing in individuals experiencing\ndisturbances in perception result ing from ingestion of phencyclidine.\nOther Hallucinogen Use Disorder\nDiagnostic Criteria \nA. A problematic pattern of hallucinogen (other than phencyclidine) use leading to clini-\ncally significant impairment or distress, as manifested by at least two of the following,\noccurring within a 12-month period: \n1. The hallucinogen is often taken in larger amounts or over a longer period than was\nintended.\n2. There is a persistent desire or unsuccessfu l efforts to cut down or control halluci-\nnogen use.\n3. A great deal of time is spent in activities necessary to obtain the hallucinogen, use\nthe hallucinogen, or recover from its effects.\n4. Craving, or a strong desire or urge to use the hallucinogen.\n5. Recurrent hallucinogen use resulting in a failure to fulfill major role obligations at", "source": "dsm5.pdf"} {"id": "d059e72b3ec8-1", "page_content": "5. Recurrent hallucinogen use resulting in a failure to fulfill major role obligations at\nwork, school, or home (e.g., repeated absences from work or poor work perfor-\nmance related to hallucinogen use; hallucinogen-related absences, suspensions,\nor expulsions from school; neglect of children or household).\n6. Continued hallucinogen use despite having persistent or recurrent social or inter-\npersonal problems caused or exacerbated by the effects of the hallucinogen (e.g.,\narguments with a spouse about consequences of intoxication; physical fights).\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of hallucinogen use.\n8. Recurrent hallucinogen use in situations in which it is physically hazardous\u00a0(e.g.,\ndriving an automobile or operating a mach ine when impaired by the hallucinogen).\n9. Hallucinogen use is continued despite knowledge of having a persistent or recur-\nrent physical or psychological problem t hat is likely to have been caused or exac-\nerbated by the hallucinogen.\n10. Tolerance, as defined by either of the following: \na. A need for markedly increased amounts of the hallucinogen to achieve intoxi-\ncation or desired effect.\nb. A markedly diminished effect with continued use of the same amount of the hal-\nlucinogen.\nNote: Withdrawal symptoms and signs are not established for hallucinogens, and so this\ncriterion does not apply.", "source": "dsm5.pdf"} {"id": "69a5b15dea7b-0", "page_content": "524 Substance-Related and Addictive Disorders\nSpecify the particular hallucinogen.\nSpecify if:\nIn early remission: After full criteria for other hallucinogen use disorder were previ-\nously met, none of the criteria for other hallucinogen use disorder have been met for\nat least 3 months but for less than 12 months (with the exception that Criterion A4,\n\u201cCraving, or a strong desire or urge to use the hallucinogen,\u201d may be met).\nIn sustained remission: After full criteria for other hallucinogen use disorder were\npreviously met, none of the criteria for other hallucinogen use disorder have been met\nat any time during a period of 12 months or longer (with the exception that Criterion A4,\n\u201cCraving, or a strong desire or urge to use the hallucinogen,\u201d may be met).\nSpecify if:\nIn a controlled environment: This additional specifier is used if the individual is in an\nenvironment where access to hallucinogens is restricted.\nCoding based on current severity: Note for ICD-10-CM codes: If a hallucinogen intoxication\nor another hallucinogen-induced mental disorder is also present, do not use the codes below\nfor hallucinogen use disorder. Instead, the comorb id hallucinogen use disorder is indicated in\nthe 4th character of the hallucinogen-induced disorder code (see the coding note for halluci-\nnogen intoxication or specific hallucinogen-induced mental disorder). For example, if there is\ncomorbid hallucinogen-induced psychotic disorder and hallucinogen use disorder, only the\nhallucinogen-induced psychotic disorder code is given, with the 4th character indicating wheth-\ner the comorbid hallucinogen use disorder is mild, moderate, or severe: F16.159 for mild hal-", "source": "dsm5.pdf"} {"id": "69a5b15dea7b-1", "page_content": "lucinogen use disorder with hallucinogen-induced psychotic disorder or F16.259 for a\nmoderate or severe hallucinogen use disorder with hallucinogen-induced psychotic disorder.\nSpecify current severity:\n305.30 (F16.10) Mild: Presence of 2\u20133 symptoms.\n304.50 (F16.20) Moderate: Presence of 4\u20135 symptoms.\n304.50 (F16.20) Severe: Presence of 6 or more symptoms.\nSpecifiers\n\u201cIn a controlled environment\u201d app lies as a further specifier of remission if the individual is\nboth in remission and in a controlled environm ent (i.e., in early remission in a controlled\nenvironment or in sustained remission in a controlled environmen t). Examples of these\nenvironments are closely supe rvised and substanc e-free jails, therapeutic communities,\nand locked hospital units. \nDiagnostic Features \nHallucinogens comprise a diverse group of subs tances that, despite ha ving different chem-\nical structures and possibly involving diffe rent molecular mechan isms, produce similar\nalterations of percepti on, mood, and cognition in users. Hallucinogens included are phenyl-\nalkylamines (e.g., mescaline, DOM [2,5-d imethoxy-4-methylam phetamine], and MDMA\n[3,4-methylenedioxymethamphetamine; also called \u201cecstasy \u201d]); the indoleamines, includ-\ning psilocybin (i.e., psilocin) and dimethyltryptamine (DMT); an d the ergolines, such as LSD\n(lysergic acid diethylamide) and morning glory seeds. In addition, miscellaneous other", "source": "dsm5.pdf"} {"id": "69a5b15dea7b-2", "page_content": "ethnobotanical compounds are classifi ed as \u201challucinogens,\u201d of which Salvia divinorum and\njimsonweed are two examples. Excluded from the hallucinogen group are cannabis and its\nactive compound, delta-9-tetrahydrocannabino l (THC) (see the section \u201cCannabis-Related\nDisorders\u201d). These substances can have hallucinogenic effects but are diagnosed separately\nbecause of significant differences in their psychological and behavioral effects.\nHallucinogens are usually taken orally, al though some forms are smoked (e.g., DMT,\nsalvia) or (rarely) taken intranasally or by in jection (e.g., ecstasy). Duration of effects varies", "source": "dsm5.pdf"} {"id": "8834df5efc70-0", "page_content": "Other Hallucinogen Use Disorder 525\nacross types of hallucinogens. Some of th ese substances (i.e., LS D, MDMA) have a long\nhalf-life and extended duration such that us ers may spend hours to days using and/or re-\ncovering from the effects of these drugs. Ho wever, other hallucinogenic drugs (e.g., DMT,\nsalvia) are short acting. Tolerance to hallucinogens develops with repeated use and has\nbeen reported to have both autonomic and psyc hological effects. Cros s-tolerance exists be-\ntween LSD and other hallucinogens (e.g., psil ocybin, mescaline) but does not extend to\nother drug categories such as amphetamines and cannabis.\nMDMA/ecstasy as a hallucinogen may have distin ctive effects attributable to both its hal-\nlucinogenic and its stimulant properties. Amon g heavy ecstasy users, continued use despite\nphysical or psychological problems, tolerance, hazardous use, and sp ending a great deal of\ntime obtaining the substance are the most commonly reported criteria\u2014over 50% in adults\nand over 30% in a younger sample , while legal problems related to substance use and persis-\ntent desire/inability to quit are rarely reported. As found for other substances, diagnostic cri-\nteria for other hallucinogen use disorder are arrayed along a single continuum of severity. \nOne of the generic criteria for substance us e disorders, a clinically significant with-\ndrawal syndrome, has not been consistently documented in humans, and therefore the di-\nagnosis of hallucinogen withdrawal syndrome is not included in DSM-5. However, there\nis evidence of withdrawal from MDMA, wi th endorsement of two or more withdrawal\nsymptoms observed in 59%\u201398% in selected samples of ecstasy users. Both psychological", "source": "dsm5.pdf"} {"id": "8834df5efc70-1", "page_content": "symptoms observed in 59%\u201398% in selected samples of ecstasy users. Both psychological\nand physical problems have been common ly reported as withdrawal problems. \nAssociated Features Supporting Diagnosis \nThe characteristic symptom feat ures of some of the hallucinogens can aid in diagnosis if\nurine or blood toxicology result s are not available. For exam ple, individuals who use LSD\ntend to experience visual hallucinations that can be frightening. Individuals intoxicated\nwith hallucinogens may exhibit a temporary increase in suicidality. \nPrevalence\nOf all substance use disorders, other hallucinogen use disorder is one of the rarest. The\n12-month prevalence is estimated to be 0.5% among 12- to 17-year-olds and 0.1% among\nadults age 18 and older in the United States. Rates are higher in adult males (0.2%) compared\nwith females (0.1%), but the oppo site is observed in adolescent samples ages 12\u201317, in which\nthe 12-month rate is slightly higher in females (0 .6%) than in males (0.4%). Rates are highest in\nindividuals younger than 30 years, with the peak occurring in individuals ages 18\u201329 years\n(0.6%) and decreasing to virtually 0.0% among individuals age 45 and older. \nThere are marked ethnic differences in 12-mo nth prevalence of ot her hallucinogen use\ndisorder. Among youths ages 12\u201317 years, 12-month prevalence is higher among Native\nAmericans and Alaska Natives (1.2%) than am ong Hispanics (0.6%), whites (0.6%), Afri-\ncan Americans (0.2%), and Asian Americans and Pacific Islanders (0.2%). Among adults,\n12-month prevalence of other hallucinogen use disorder is similar for Native Americans", "source": "dsm5.pdf"} {"id": "8834df5efc70-2", "page_content": "12-month prevalence of other hallucinogen use disorder is similar for Native Americans\nand Alaska Natives, whites, and Hispanics (a ll 0.2%) but somewhat lower for Asian Amer-\nicans and Pacific Islanders (0.07%) and Africa n Americans (0.03%). Past-year prevalence is\nhigher in clinical samples (e.g., 19% in ad olescents in treatment) . Among individuals cur-\nrently using hallucinogens in the general popu lation, 7.8% (adult) to 17% (adolescent) had\na problematic pattern of use that met criteria for past-year other hallucinogen use disorder.\nAmong select groups of individuals who use hallucinogens (e.g., recent heavy ecstasy\nuse), 73.5% of adults and 77% of adolescents have a problematic pattern of use that may\nmeet other hallucinogen use disorder criteria.\nDevelopment and Course", "source": "dsm5.pdf"} {"id": "c4aacd31b497-0", "page_content": "use), 73.5% of adults and 77% of adolescents have a problematic pattern of use that may\nmeet other hallucinogen use disorder criteria.\nDevelopment and Course\nUnlike most substances where an early age at on set is associated with elevations in risk for\nthe corresponding use disorder, it is unclear wh ether there is an association of an early age", "source": "dsm5.pdf"} {"id": "eb5ca428a430-0", "page_content": "526 Substance-Related and Addictive Disorders\nat onset with elevations in risk for other hallucinogen use disorder. However, patterns of\ndrug consumption have been found to differ by age at onset, with early-onset ecstasy users\nmore likely to be polydrug users than their later-onset counterpar ts. There may be a dis-\nproportionate influence of use of specific hallu cinogens on risk of developing other hallu-\ncinogen use disorder, with use of ecstasy/MDMA increasing the risk of the disorder\nrelative to use of other hallucinogens.\nLittle is known regarding the co urse of other hallucinogen use disorder, but it is generally\nthought to have low incidence, low persistence, and high rates of recovery. Adolescents are es-\npecially at risk for using these drugs, and it is estimated that 2.7% of youths ages 12\u201317 years\nhave used one or more of these drugs in the past 12 months, with 44 % having used ecstasy/\nMDMA. Other hallucinogen use disorder is a disorder observed primarily in individuals\nyounger than 30 years, with rates vanishingly rare among older adults.\nRisk and Prognostic Factors \nTemperamental. In adolescents but not consistently in adults, MDMA use is associated with\nan elevated rate of other hallucinogen use di sorder. Other substance use disorders, particu-\nlarly alcohol, tobacco, and cannabis, and major depressive disorder are associated with ele-\nvated rates of other hallucino gen use disorder. Antisocial personality disorder may be\nelevated among individuals who use more than two other drugs in addition to hallucinogens,\ncompared with their counterparts with less exte nsive use history. The influence of adult anti-\nsocial behaviors\u2014but not conduct disorder or antisocial personality disorder\u2014on other hal-", "source": "dsm5.pdf"} {"id": "eb5ca428a430-1", "page_content": "social behaviors\u2014but not conduct disorder or antisocial personality disorder\u2014on other hal-\nlucinogen use disorder may be stronger in female s than in males. Use of specific hallucinogens\n(e.g., salvia) is prominent am ong individuals ages 18\u201325 years with other risk-taking behaviors\nand illegal activities. Cannabis use has also been implicated as a precursor to initiation of use of\nhallucinogens (e.g., ecstasy), along with early use of alcohol and tobacco. Higher drug use by\npeers and high sensation seeking have also been associated with elevated rates of ecstasy use.\nMDMA/ecstasy use appears to signify a more severe group of hallucinogen users.\nGenetic and physiological. Among male twins, total varian ce due to additive genetics\nhas been estimated to range from 26% to 79%, with inconsistent evidence for shared envi-\nronmental influences. \nCulture-Related Diagnostic Issues \nHistorically, hallucinogens have been used as part of established re ligious practices, such\nas the use of peyote in the Native American Church and in Mexico. Ritual use by indige-\nnous populations of psilocybin obtained from certain types of mushrooms has occurred in\nSouth America, Mexico, and some areas in the United States, or of ayahuasca in the Santo\nDaime and Uni\u00e3o de Vegetal sects. Regular use of peyote as part of religious rituals is not\nlinked to neuropsychological or psychological de ficits. For adults, no race or ethnicity dif-\nferences for the full criteria or for any indi vidual criterion are apparent at this time. \nGender-Related Diagnostic Issues \nIn adolescents, females may be less likely th an males to endorse \u201chazardous use,\u201d and fe-\nmale gender may be associated with increase d odds of other hallucinogen use disorder.", "source": "dsm5.pdf"} {"id": "eb5ca428a430-2", "page_content": "male gender may be associated with increase d odds of other hallucinogen use disorder. \nDiagnostic Markers \nLaboratory testing can be useful in distin guishing among the different hallucinogens.\nHowever, because some agents (e.g., LSD) are so potent that as little as 75 micrograms can\nproduce severe reactions, typical toxicologi cal examination will not always reveal which\nsubstance has been used.", "source": "dsm5.pdf"} {"id": "74eb5b4519e5-0", "page_content": "Phencyclidine Intoxication 527\nFunctional Consequences of \nOther Hallucinogen Use Disorder\nThere is evidence for long-term neurotoxic effects of MDMA/ecstasy use, including im-\npairments in memory, psychological function , and neuroendocrine function; serotonin\nsystem dysfunction; and sleep disturbance; as well as adverse effects on brain microvas-\nculature, white matter maturation, and damage to axons. Use of MDMA/ecstasy may di-\nminish functional connectiv ity among brain regions. \nDifferential Diagnosis\nOther substance use disorders. The effects of hallucinogens must be distinguished from\nthose of other substances (e.g., amphetamines ), especially because contamination of the\nhallucinogens with other dr ugs is relatively common. \nSchizophrenia. Schizophrenia also must be ruled out, as some affected individuals (e.g.,\nindividuals with schizophrenia who exhibit paranoia) may falsely attribute their symp-\ntoms to use of hallucinogens. \nOther mental disorders or medical conditions. Other potential disorders or conditions\nto consider include panic disorder, depressive and bipolar disorders, alcohol or sedative\nwithdrawal, hypoglycemia and other metabolic conditions, seizure disorder, stroke, oph-\nthalmological disorder, and central nervous sy stem tumors. Careful history of drug tak-\ning, collateral reports from family and friends (if possible), age, clin ical history, physical\nexamination, and toxicology reports should be useful in arriving at the final diagnostic de-\ncision. \nComorbidity\nAdolescents who use MDMA/ecstasy and other ha llucinogens, as well as adults who have\nrecently used ecstasy, have a higher preval ence of other substance use disorders compared\nwith nonhallucinogen substance users. Individuals who use halluc inogens exhibit eleva-", "source": "dsm5.pdf"} {"id": "74eb5b4519e5-1", "page_content": "with nonhallucinogen substance users. Individuals who use halluc inogens exhibit eleva-\ntions of nonsubstance mental disorders (espec ially anxiety, depressi ve, and bipolar disor-\nders), particularly with use of ecstasy and salvia. Rates of antisocial personality disorder (but\nnot conduct disorder) are significantly elevated among individuals with other hallucinogen\nuse disorder, as are rates of adult antisocial behavior. However, it is unclear whether the\nmental illnesses may be precursors to rather than consequences of other hallucinogen use\ndisorder (see the section \u201cRisk and Prognostic Factors\u201d for this disorder). Both adults and\nadolescents who use ecstasy are mo re likely than other drug us ers to be polydrug users and\nto have other drug use disorders. \nPhencyclidine Intoxication\nDiagnostic Criteria\nA. Recent use of phencyclidine (or a pharmacologically similar substance).\nB. Clinically significant problematic behavioral changes (e.g., belligerence, assaultive-\nness, impulsiveness, unpredictability, psychomotor agitation, impaired judgment) that\ndeveloped during, or shortly after, phencyclidine use.\nC. Within 1 hour, two (or more) of the following signs or symptoms:\nNote: When the drug is smoked, \u201csnorted,\u201d or used intravenously, the onset may be\nparticularly rapid.\n1. Vertical or horizontal nystagmus.\n2. Hypertension or tachycardia.", "source": "dsm5.pdf"} {"id": "06edb0ff22c2-0", "page_content": "528 Substance-Related and Addictive Disorders\n3. Numbness or diminished responsiveness to pain.\n4. Ataxia.\n5. Dysarthria.\n6. Muscle rigidity.\n7. Seizures or coma.\n8. Hyperacusis.\nD. The signs or symptoms are not attributable to another medical condition and are not better\nexplained by another mental disorder, including intoxication with another substance.\nCoding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether\nthere is a comorbid phencyclidine use disorder. If a mild phencyclidine use disorder is co-\nmorbid, the ICD-10-CM code is F16.129, and if a moderate or severe phencyclidine use\ndisorder is comorbid, the ICD-10-CM code is F16.229. If there is no comorbid phencycli-\ndine use disorder, then the ICD-10-CM code is F16.929.\nNote: In addition to the section \u201cFunctional Co nsequences of Phencyclidine Intoxication,\u201d\nsee the corresponding section in phencyclidine use disorder.\nDiagnostic Features\nPhencyclidine intoxication reflects the clinica lly significant behavioral changes that occur\nshortly after ingestion of this substance (or a pharmacologically similar substance). The\nmost common clinical presentations of phencyclidine intoxication include disorientation,\nconfusion without hallucinations, hallucination s or delusions, a catatonic-like syndrome,\nand coma of varying severity. The intoxication typically last s for several hours but, de-\npending on the type of clinic al presentation and whether other drugs besides phencycli-\ndine were consumed, may last for several days or longer.\nPrevalence", "source": "dsm5.pdf"} {"id": "06edb0ff22c2-1", "page_content": "dine were consumed, may last for several days or longer.\nPrevalence\nUse of phencyclidine or related substances ma y be taken as an estimate of the prevalence\nof intoxication. Approximately 2.5% of the po pulation reports having ever used phency-\nclidine. Among high school students, 2.3% of 12th graders report ever using phencycli-\ndine, with 57% having used in the past 12 months. This represents an increase from prior\nto 2011. Past-year use of ketamine, which is assessed separately from other substances, has\nremained stable over time, with about 1.7% of 12th graders reporting use.\nDiagnostic Markers \nLaboratory testing may be useful, as phencycl idine is detectable in urine for up to 8 days\nfollowing use, although the levels are only weakly associated with an individual\u2019s clinical\npresentation and may therefore not be useful for case management. Creatine phosphoki-\nnase and aspartate aminotransfe rase levels may be elevated.\nFunctional Consequences of Phencyclidine Intoxication\nPhencyclidine intoxication produces extensiv e cardiovascular and neurological (e.g., sei-\nzures, dystonias, dyskinesias, catalepsy, hypothermia or hyperthermia) toxicity.\nDifferential Diagnosis\nIn particular, in the absence of intact realit y testing (i.e., without in sight into any percep-\ntual abnormalities), an additional diagno sis of phencyclidine-induced psychotic disorder\nshould be considered.\nOther substance intoxication. Phencyclidine intoxication should be differentiated from\nintoxication due to other su bstances, including other hallucinogens; amphetamine, co-", "source": "dsm5.pdf"} {"id": "8fcc74f9437e-0", "page_content": "Other Hallucinogen Intoxication 529\ncaine, or other stimulants; an d anticholinergics, as well as withdrawal from benzodiaze-\npines. Nystagmus and bizarre and violent be havior may distinguish intoxication due to\nphencyclidine from that due to other substances . Toxicological tests may be useful in mak-\ning this distinction, since phencyclidine is detectable in urine for up to 8 days after use.\nHowever, there is a weak correlation between quantitative toxicology levels of phencycli-\ndine and clinical presentation that diminishes the utility of the laboratory findings for pa-\ntient management. \nOther conditions. Other conditions to be considered include schizophrenia, depression,\nwithdrawal from other drugs (e .g., sedatives, alcohol), cert ain metabolic disorders like hy-\npoglycemia and hyponatremia, central nervous system tumors, seizur e disorders, sepsis,\nneuroleptic malignant syndro me, and vascular insults.\nOther Hallucinogen Intoxication\nDiagnostic Criteria\nA. Recent use of a hallucinogen (other than phencyclidine). \nB. Clinically significant problematic behavioral or psychological changes (e.g., marked\nanxiety or depression, ideas of reference, fear of \u201closing one\u2019s mind,\u201d paranoid ide-\nation, impaired judgment) that developed during, or shortly after, hallucinogen use. \nC. Perceptual changes occurring in a state of full wakefulness and alertness (e.g., sub-\njective intensification of perceptions, depersonalization, derealization, illusions, hallu-\ncinations, synesthesias) that developed during, or shortly after, hallucinogen use.", "source": "dsm5.pdf"} {"id": "8fcc74f9437e-1", "page_content": "D. Two (or more) of the following signs developing during, or shortly after, hallucinogen\nuse: \n1. Pupillary dilation.\n2. Tachycardia.\n3. Sweating.\n4. Palpitations.\n5. Blurring of vision.\n6. Tremors.\n7. Incoordination.\nE. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication with another sub-\nstance.\nCoding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether\nthere is a comorbid hallucinogen use disorder. If a mild hallucinogen use disorder is co-\nmorbid, the ICD-10-CM code is F16.129, and if a moderate or severe hallucinogen use\ndisorder is comorbid, the ICD-10-CM code is F16.229. If there is no comorbid hallucinogen\nuse disorder, then the ICD-10-CM code is F16.929.\nNote: For information on Associated Features Supporting Diagnosis and Culture-Related\nDiagnostic Issues, see the corresponding sections in other hallucinogen use disorder.\nDiagnostic Features\nOther hallucinogen intoxication reflects the c linically significant behavioral or psycholog-\nical changes that occur shortly after ingestio n of a hallucinogen. Depending on the specific\nhallucinogen, the intoxication may last only minutes (e.g., for salvia) or several hours or\nlonger (e.g., for LSD [lysergic acid diethy lamide] or MDMA [3,4-methylenedioxymetham-\nphetamine]).", "source": "dsm5.pdf"} {"id": "07561e7d2b9f-0", "page_content": "530 Substance-Related and Addictive Disorders\nPrevalence\nThe prevalence of other hallucinogen intoxica tion may be estimated by use of those sub-\nstances. In the United States, 1.8% of individuals age 12 years or older report using hallu-\ncinogens in the past year. Use is more preval ent among younger individuals, with 3.1% of\n12- to 17-year-olds and 7.1% of 18- to 25-year-olds using hallucinogens in the past year,\ncompared with only 0.7% of individuals ag e 26 years or older. Twelve-month prevalence\nfor hallucinogen use is more common in ma les (2.4%) than in fe males (1.2%), and even\nmore so among 18- to 25-year-olds (9.2% for males vs. 5.0% for females). In contrast,\namong individuals ages 12\u201317 years, there are no gender differences (3.1% for both gen-\nders). These figures may be used as proxy es timates for gender-related differences in the\nprevalence of other ha llucinogen intoxication. \nSuicide Risk\nOther hallucinogen intoxication may lead to in creased suicidality, al though suicide is rare\namong users of hallucinogens.\nFunctional Consequences of \nOther Hallucinogen Intoxication \nOther hallucinogen intoxication can have serious consequences. The perceptual distur-\nbances and impaired judgment associated wi th other hallucinogen intoxication can result\nin injuries or fatalities from automobile crashes, physical fi ghts, or unintentional self-\ninjury (e.g., attempts to \u201cfly\u201d from high plac es). Environmental factors and the personality", "source": "dsm5.pdf"} {"id": "07561e7d2b9f-1", "page_content": "and expectations of the individual using the hallucinogen may contribute to the nature of\nand severity of halluc inogen intoxication. Continued use of hallucinogens, particularly\nMDMA, has also been linked with neurotoxic effects.\nDifferential Diagnosis\nOther substance intoxication. Other hallucinogen intoxication should be differentiated\nfrom intoxication with amphetamines, cocaine, or other stimulants; anticholinergics; in-\nhalants; and phencyclidine. Toxicological tests are useful in making this distinction, and\ndetermining the route of administration may also be useful.\nOther conditions. Other disorders and conditions to be considered include schizophre-\nnia, depression, withdrawal from other drugs (e.g., sedatives, alcohol), certain metabolic\ndisorders (e.g., hypoglycemia), seizure disorders, tumors of the central nervous system,\nand vascular insults.\nHallucinogen persisting perception disorder. Other hallucinogen intoxication is dis-\ntinguished from hallucinogen persisting percep tion disorder because the symptoms in the\nlatter continue episodically or continuously for weeks (or long er) after the most recent in-\ntoxication.\nOther hallucinogen-induced disorders. Other hallucinogen intoxication is distinguished\nfrom the other hallucinogen-induced disorder s (e.g., hallucinogen- induced anxiety disor-\nder, with onset during intoxication) because the symptoms in these latter disorders pre-\ndominate the clinical presentation and are severe enough to warrant independent clinical\nattention.", "source": "dsm5.pdf"} {"id": "5eb3c4154b55-0", "page_content": "Hallucinogen Persisting Perception Disorder 531\nHallucinogen Persisting Perception Disorder\nDiagnostic Criteria 292.89 (F16.983)\nA. Following cessation of use of a hallucinogen, the reexperiencing of one or more of the\nperceptual symptoms that were experienced while intoxicated with the hallucinogen\n(e.g., geometric hallucinations, false perceptions of movement in the peripheral visual\nfields, flashes of color, intensified colors, trails of images of moving objects, positive\nafterimages, halos around objects, macropsia and micropsia).\nB. The symptoms in Criterion A cause clinically significant distress or impairment in so-\ncial, occupational, or other important areas of functioning. \nC. The symptoms are not attributable to another medical condition (e.g., anatomical le-\nsions and infections of the brain, visual epilepsies) and are not better explained by an-\nother mental disorder (e.g., delirium, ma jor neurocognitive disorder, schizophrenia) or\nhypnopompic hallucinations.\nDiagnostic Features\nThe hallmark of hallucinogen persisting percep tion disorder is the reexperiencing, when the\nindividual is sober, of the pe rceptual disturbances that were experienced while the individ-\nual was intoxicated with the hallucinogen (C riterion A). The symptoms may include any\nperceptual perturbations, but visual disturbanc es tend to be predomin ant. Typical of the ab-\nnormal visual perceptions are geometric hallucinations, false percep tions of movement in\nthe peripheral visual fields, flashes of color, in tensified colors, trails of images of moving ob-\njects (i.e., images left suspended in the path of a moving object as seen in stroboscopic pho-", "source": "dsm5.pdf"} {"id": "5eb3c4154b55-1", "page_content": "tography), perceptions of entire objects, po sitive afterimages (i.e., a same-colored or\ncomplementary-colored \u201cshadow\u201d of an object remaining after removal of the object), halos\naround objects, or misperception of images as too large (macropsia) or too small (micropsia).\nDuration of the visual disturbances may be ep isodic or nearly continuous and must cause\nclinically significant distress or impairment in social, occupational, or other important areas\nof functioning (Criterion B). The disturbances may last for weeks, months, or years. Other\nexplanations for the disturbances (e.g., brain lesions, preexisting psychosis, seizure disor-\nders, migraine aura without headaches) must be ruled out (Criterion C).\nHallucinogen persisting perception disorder occurs primarily after LSD (lysergic acid\ndiethylamide) use, but not exclusively. There does not appear to be a strong correlation be-\ntween hallucinogen persisting perception disord er and number of occasions of hallucino-\ngen use, with some instances of hallucinogen persisting perception disorder occurring in\nindividuals with minimal exposure to hallucinogens. Some instances of hallucinogen per-\nsisting perception disorder may be triggered by use of other substa nces (e.g., cannabis or\nalcohol) or in adaptation to dark environments.\nAssociated Features Supporting Diagnosis\nReality testing remains intact in individuals with hallucinogen persisting perception dis-\norder (i.e., the individual is aware that the disturbance is linked to the effect of the drug).\nIf this is not the case, another disorder might better explain the abnormal perceptions.\nPrevalence\nPrevalence estimates of hallucinogen persisting perception disorder are unknown. Initial\nprevalence estimates of the disorder among individuals who use hallucinogens is approx-\nimately 4.2%.", "source": "dsm5.pdf"} {"id": "2420523000d7-0", "page_content": "532 Substance-Related and Addictive Disorders\nDevelopment and Course\nLittle is known about the development of hallucinogen persisting perception disorder. Its\ncourse, as suggested by its name, is persistent, lasting for weeks, months, or even years in\ncertain individuals. \nRisk and Prognostic Factors\nThere is little evidence regarding risk factor s for hallucinogen persisting perception dis-\norder, although genetic factors have been suggested as a possible explanation underlying\nthe susceptibility to LSD effects in this condition. \nFunctional Consequences of \nHallucinogen Persisting Perception Disorder\nAlthough hallucinogen persisting perception disorder remains a chronic condition in\nsome cases, many individuals with the disord er are able to suppres s the disturbances and\ncontinue to function normally. \nDifferential Diagnosis\nConditions to be ruled out include schizophrenia, other drug effects, neurodegenerative\ndisorders, stroke, brain tumors, infections, an d head trauma. Neuroimaging results in hal-\nlucinogen persisting perception disorder cases are typically negative. As noted earlier, re-\nality testing remains intact (i.e., the individual is aware that the disturbance is linked to the\neffect of the drug); if this is not the case, another disorder (e.g., psychotic disorder, another\nmedical condition) might better ex plain the abnormal perceptions. \nComorbidity\nCommon comorbid mental disorders accomp anying hallucinogen persisting perception\ndisorder are panic disorder , alcohol use disorder, and major depressive disorder. \nOther Phencyclidine-Induced Disorders\nOther phencyclidine-induced diso rders are described in other chapters of the manual with\ndisorders with which they share phenomeno logy (see the substance/medication-induced\nmental disorders in these chap ters): phencyclidine-induced psychotic disorder (\u201cSchizo-", "source": "dsm5.pdf"} {"id": "2420523000d7-1", "page_content": "mental disorders in these chap ters): phencyclidine-induced psychotic disorder (\u201cSchizo-\nphrenia Spectrum and Other Psychotic Disord ers\u201d); phencyclidine-induced bipolar dis-\norder (\u201cBipolar and Related Disorders\u201d); phencyclidine-induced depressive disorder\n(\u201cDepressive Disorders\u201d); and phencyclidin e-induced anxiety disorder (\u201cAnxiety Disor-\nders\u201d). For phencyclidine-induced intoxication delirium, see the criteria and discussion of\ndelirium in the chapter \u201cNeurocognitive Di sorders.\u201d These phencyclidine-induced disor-\nders are diagnosed instead of phencyclidine in toxication only when the symptoms are suf-\nficiently severe to warrant in dependent clinical attention. \nOther Hallucinogen-Induced Disorders\nThe following other hallucinogen- induced disorders are describe d in other chapters of the\nmanual with disorder s with which they share phenome nology (see the substance/medi-\ncation-induced mental disorders in these chapters): other hallucinogen\u2013induced psychotic\ndisorder (\u201cSchizophrenia Spect rum and Other Psychotic Diso rders\u201d); other hallucinogen\u2013\ninduced bipolar disorder (\u201cBi polar and Related Disorders\u201d); other hallucinogen\u2013induced", "source": "dsm5.pdf"} {"id": "457dd12b7a99-0", "page_content": "Unspecified Phencyclidine-Related Disorder 533\ndepressive disorder (\u201cDepressive Disorders\u201d ); and other hallucinogen\u2013induced anxiety\ndisorder (\u201cAnxiety Disorders\u201d). For other hallu cinogen intoxication delirium, see the cri-\nteria and discussion of delirium in the chapter \u201cNeurocognitive Di sorders.\u201d These hallu-\ncinogen-induced disorders are diagnosed inst ead of other hallucinogen intoxication only\nwhen the symptoms are sufficiently severe to warrant independent clinical attention. \nUnspecified Phencyclidine-Related Disorder\n292.9 (F16.99)\nThis category applies to presentations in which symptoms characteristic of a phencycli-\ndine-related disorder that cause clinically significant distress or impairment in social, oc-\ncupational, or other important areas of functioning predominate but do not meet the full\ncriteria for any specific phencyclidine-related disorder or any of the disorders in the sub-\nstance-related and addictive disorders diagnostic class.\nUnspecified Hallucinogen-Related Disorder\n292.9 (F16.99)\nThis category applies to presentations in which symptoms characteristic of a hallucinogen-\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any specific hallucinogen-related disorder or any of the disorders in the substance-\nrelated and addictive disorders diagnostic class.\nInhalant-Related Disorders\nInhalant Use Disorder\nInhalant Intoxication\nOther Inhalant-Induced Disorders\nUnspecified Inhalant-Related Disorder\nInhalant Use Disorder\nDiagnostic Criteria \nA. A problematic pattern of use of a hydrocarbon-based inhalant substance leading to\nclinically significant impairment or distress, as manifested by at least two of the follow-", "source": "dsm5.pdf"} {"id": "457dd12b7a99-1", "page_content": "clinically significant impairment or distress, as manifested by at least two of the follow-\ning, occurring within a 12-month period:\n1. The inhalant substance is often taken in larger amounts or over a longer period than\nwas intended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control use of the\ninhalant substance.", "source": "dsm5.pdf"} {"id": "5c16a6a7229a-0", "page_content": "534 Substance-Related and Addictive Disorders\n3. A great deal of time is spent in activities necessary to obtain the inhalant substance,\nuse it, or recover from its effects.\n4. Craving, or a strong desire or urge to use the inhalant substance.\n5. Recurrent use of the inhalant substance resulting in a failure to fulfill major role ob-\nligations at work, school, or home.\n6. Continued use of the inhalant substance des pite having persistent or recurrent so-\ncial or interpersonal problems caused or exacerbated by the effects of its use.\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of use of the inhalant substance.\n8. Recurrent use of the inhalant substance in situations in which it is physically haz-\nardous.\n9. Use of the inhalant substance is continued despite knowledge of having a persis-\ntent or recurrent physical or psychological problem that is likely to have been\ncaused or exacerbated by the substance.\n10. Tolerance, as defined by either of the following: \na. A need for markedly increased amounts of the inhalant substance to achieve\nintoxication or desired effect.\nb. A markedly diminished effect with continued use of the same amount of the in-\nhalant substance.\nSpecify the particular inhalant: When possible, the particular substance involved should\nbe named (e.g., \u201csolvent use disorder\u201d).\nSpecify if:\nIn early remission: After full criteria for inhalant use disorder were previously met,\nnone of the criteria for inhalant use disor der have been met for at least 3 months but\nfor less than 12 months (with the exception that Criterion A4, \u201cCraving, or a strong de-\nsire or urge to use the inhalant substance,\u201d may be met).", "source": "dsm5.pdf"} {"id": "5c16a6a7229a-1", "page_content": "sire or urge to use the inhalant substance,\u201d may be met).\nIn sustained remission: After full criteria for inhalant use disorder were previously\nmet, none of the criteria for inhalant use disorder have been met at any time during a\nperiod of 12 months or longer (with the exception that Criterion A4, \u201cCraving, or a\nstrong desire or urge to use the inhalant substance,\u201d may be met).\nSpecify if:\nIn a controlled environment: This additional specifier is used if the individual is in an\nenvironment where access to inhalant substances is restricted. \nCoding based on current severity: Note for ICD-10-CM codes: If an inhalant intoxication\nor another inhalant-induced mental disorder is also present, do not use the codes below\nfor inhalant use disorder. Instead, the comorbid inhalant use disorder is indicated in the\n4th character of the inhalant-induced disorder code (see the coding note for inhalant intox-\nication or a specific inhalant-induced mental di sorder). For example, if there is comorbid\ninhalant-induced depressive disorder and i nhalant use disorder, only the inhalant-induced\ndepressive disorder code is given, with the 4th character indicating whether the comorbid\ninhalant use disorder is mild, moderate, or severe: F18.14 for mild inhalant use disorder\nwith inhalant-induced depressive disorder or F 18.24 for a moderate or severe inhalant use\ndisorder with inhalant-induced depressive disorder.\nSpecify current severity:\n305.90 (F18.10) Mild: Presence of 2\u20133 symptoms.\n304.60 (F18.20) Moderate: Presence of 4\u20135 symptoms.\n304.60 (F18.20) Severe: Presence of 6 or more symptoms.", "source": "dsm5.pdf"} {"id": "a5ec6a5b784d-0", "page_content": "Inhalant Use Disorder 535\nSpecifiers\nThis manual recognizes volatile hydrocarbon use meeting the above diagnostic criteria as\ninhalant use disorder. Volatile hydrocarbons are toxic gases from glues, fuels, paints, and\nother volatile compounds. When possible, th e particular substance involved should be\nnamed (e.g., \u201ctoluene use disorder\u201d). However, most compounds that are inhaled are a\nmixture of several substances that can produce psychoactive effects, and it is often difficult\nto ascertain the exact substance responsible fo r the disorder. Unless there is clear evidence\nthat a single, unmixed substance has been used , the general term inhalant should be used\nin recording the diagnosis. Disorders arising from inhalation of nitrous oxide or of amyl-,\nbutyl-, or isobutylnitrite are considered as other (or unkn own) substance use disorder. \n\u201cIn a controlled environment\u201d applies as a fu rther specifier of remission if the individ-\nual is both in remission and in a controlled en vironment (i.e., in early remission in a con-\ntrolled environment or in su stained remission in a contro lled environment). Examples of\nthese environments are closely supervised and substance-free jails, therapeutic communi-\nties, and locked hospital units. \nThe severity of individuals\u2019 inhalant use di sorder is assessed by the number of diag-\nnostic criteria endorsed. Changing severity of individuals\u2019 inhalant use disorder across\ntime is reflected by reductions in the frequency (e.g., days used per month) and/or dose\n(e.g., tubes of glue per day) used, as assessed by the individual\u2019s self-report, report of oth-\ners, clinician\u2019s observations, and bi ological testing (when practical).\nDiagnostic Features\nFeatures of inhalant use disorder include repe ated use of an inhalant substance despite the", "source": "dsm5.pdf"} {"id": "a5ec6a5b784d-1", "page_content": "Features of inhalant use disorder include repe ated use of an inhalant substance despite the\nindividual\u2019s knowing that the substance is causing serious problems for the individual\n(Criterion A9). Those problems are re flected in the diagnostic criteria. \nMissing work or school or inability to perform typical responsibilities at work or school\n(Criterion A5), and continued us e of the inhalant substance even though it causes arguments\nwith family or friends, fights, and other social or interpersonal proble ms (Criterion A6), may\nbe seen in inhalant use disorder. Limiting family contact, work or school obligations, or rec-\nreational activities (e.g., sports , games, hobbies) may also occu r (Criterion A7). Use of inhal-\nants when driving or operating dangerous equipment (Criterion A8) is also seen.\nTolerance (Criterion A10) and mild withdraw al are each reported by about 10% of in-\ndividuals who use inhalants, and a few individuals use inhalants to avoid withdrawal.\nHowever, because the withdrawal symptoms ar e mild, this manual neither recognizes a\ndiagnosis of inhalant withdrawal nor counts withdrawal complaints as a diagnostic crite-\nrion for inhalant use disorder. \nAssociated Features Supporting Diagnosis\nA diagnosis of inhalant use disorder is suppo rted by recurring epis odes of intoxication\nwith negative results in standard drug screens (which do not detect inhalants); possession,\nor lingering odors, of inhalant substances; peri-oral or peri-nasal \u201cglue-sniffer\u2019s rash\u201d; as-\nsociation with other individuals known to use inhalants; membership in groups with prev-\nalent inhalant use (e.g., some native or abor iginal communities, ho meless children in street\ngangs); easy access to certain inhalant substances; paraphernalia possession; presence of", "source": "dsm5.pdf"} {"id": "a5ec6a5b784d-2", "page_content": "gangs); easy access to certain inhalant substances; paraphernalia possession; presence of\nthe disorder\u2019s characteristic medical compli cations (e.g., brain white matter pathology,\nrhabdomyolysis); and the presence of multiple substance use disorders. Inhalant use and\ninhalant use disorder are asso ciated with past suicide atte mpts, especially among adults\nreporting previous episodes of low mood or anhedonia.\nPrevalence\nAbout 0.4% of Americans ages 12\u201317 years have a pattern of use that me ets criteria for in-\nhalant use disorder in the past 12 months. Among those youths, the prevalence is highest", "source": "dsm5.pdf"} {"id": "50bf431766d0-0", "page_content": "536 Substance-Related and Addictive Disorders\nin Native Americans and lowest in African Americans. Prevalence falls to about 0.1% among\nAmericans ages 18\u201329 years, and only 0.02% when all Americans 18 years or older are con-\nsidered, with almost no females and a prepon derance of European Am ericans. Of course,\nin isolated subgroups, prevalence may di ffer considerably from these overall rates. \nDevelopment and Course\nAbout 10% of 13-year-old American children re port having used inhalants at least once;\nthat percentage remains stable through age 17 years. Among those 12- to 17-year-olds who\nuse inhalants, the more-used substances includ e glue, shoe polish, or toluene; gasoline or\nlighter fluid; or spray paints. \nOnly 0.4% of 12- to 17-year-olds progress to inhalant use disorder; those youths tend to\nexhibit multiple other problems. The declining prevalence of inhalant use disorder after\nadolescence indicates that this disorder usually remits in early adulthood.\nVolatile hydrocarbon use disorder is rare in prepubertal children, most common in ad-\nolescents and young adults, and uncommon in older persons. Calls to poison-control cen-\nters for \u201cintentional abuse\u201d of inhalants peak with calls involving individuals at age 14 years.\nOf adolescents who use inhalants, perhaps on e-fifth develop inhalant use disorder; a few\ndie from inhalant-related accide nts, or \u201csudden sniffing death\u201d. But the disorder apparently\nremits in many individuals after adolescence. Prevalence declines dramatically among in-\ndividuals in their 20s. Those with inhalant use disorder extending into adulthood often", "source": "dsm5.pdf"} {"id": "50bf431766d0-1", "page_content": "dividuals in their 20s. Those with inhalant use disorder extending into adulthood often\nhave severe problems: substance use disorder s, antisocial personality disorder, and sui-\ncidal ideation with attempts. \nRisk and Prognostic Factors \nTemperamental. Predictors of progression from nonuse of inhalant s, to use, to inhalant\nuse disorder include comorbid non-inhalant substance use disorders and either conduct\ndisorder or antisocial personality disorder. Other predictors are ea rlier onset of inhalant\nuse and prior use of mental health services. \nEnvironmental. Inhalant gases are widely and legally available, increasing the risk of mis-\nuse. Childhood maltreatment or trauma also is associated with youthful progression from\ninhalant non-use to inhalant use disorder. \nGenetic and physiological. Behavioral disinhibition is a highly heritable general propensity\nto not constrain behavior in socially acceptable ways, to break social norms and rules, and to\ntake dangerous risks, pursuing rewards excessi vely despite dangers of adverse consequences.\nYouths with strong behavioral disinhibition show risk factors for inhala nt use disorder: early-\nonset substance use disorder, multiple substa nce involvement, and ea rly conduct problems.\nBecause behavioral disinhibition is under stro ng genetic influence, youths in families with\nsubstance and antisocial problems are at elevated risk for i nhalant use disorder.\nCulture-Related Diagnostic Issues\nCertain native or aboriginal communities have experienced a high prevalence of inhalant\nproblems. Also, in some countr ies, groups of homeless children in street gangs have ex-\ntensive inhalant use problems.\nGender-Related Diagnostic Issues\nAlthough the prevalence of inhalant use disord er is almost identical in adolescent males\nand females, the disorder is very rare among adult females.\nDiagnostic Markers", "source": "dsm5.pdf"} {"id": "50bf431766d0-2", "page_content": "and females, the disorder is very rare among adult females.\nDiagnostic Markers\nUrine, breath, or saliva tests may be valuable for assessing concurrent use of non-inhalant\nsubstances by individuals with inhalant us e disorder. However, technical problems and", "source": "dsm5.pdf"} {"id": "54b29e23a5be-0", "page_content": "Inhalant Use Disorder 537\nthe considerable expense of analyses make fr equent biological testing for inhalants them-\nselves impractical.\nFunctional Consequences of Inhalant Use Disorder \nBecause of inherent toxicity, use of butane or propane is not infrequently fatal. Moreover,\nany inhaled volatile hydrocarbons may produc e \u201csudden sniffing death\u201d from cardiac ar-\nrhythmia. Fatalities may occur even on the first inhalant exposure and are not thought to\nbe dose-related. Volatile hydrocarbon use impairs neurobehavioral function and causes\nvarious neurological, gastrointestinal, cardiovascular, and pulmonary problems. \nLong-term inhalant users are at increased risk for tuberculosis, HIV/AIDS, sexually\ntransmitted diseases, depression , anxiety, bronchitis, asthma , and sinusitis. Deaths may\noccur from respiratory depression, arrhythmia s, asphyxiation, aspiration of vomitus, or\naccident and injury.\nDifferential Diagnosis\nInhalant exposure (unintentional) from industrial or other accidents. This designation\nis used when findings suggest repeated or continuous inhalant exposure but the involved\nindividual and other informants deny an y history of purposeful inhalant use.\nInhalant use (intentional), without meeting criteria for inhalant use disorder. Inhalant use\nis common among adolescents, but for most of th ose individuals, the inhalant use does not\nmeet the diagnostic standard of two or more Criterion A items for i nhalant use disorder in\nthe past year.\nInhalant intoxication, without meeting criteria for inhalant use disorder. Inhalant intox-\nication occurs frequently duri ng inhalant use disorder but also may occur among individ-\nuals whose use does not meet criteria for inha lant use disorder, which requires at least two\nof the 10 diagnostic criteria in the past year.", "source": "dsm5.pdf"} {"id": "54b29e23a5be-1", "page_content": "of the 10 diagnostic criteria in the past year.\nInhalant-induced disorders (i .e., inhalant-induced psychotic disorder, depressive dis-\norder, anxiety disorder, neurocognitive disorder, other inhalant-induced disorders)\nwithout meeting criteria for inhalant use disorder. Criteria are met for a psychotic, de-\npressive, anxiety, or major neurocognitive disorder, and there is evidence from history,\nphysical examination, or laboratory findings that the deficits are etiologically related to\nthe effects of inhalant substances. Yet, criter ia for inhalant use disorder may not be met\n(i.e., fewer than 2 of the 10 criteria were present).\nOther substance use disorders, especially those involving sedating substances (e.g.,\nalcohol, benzodiazepines, barbiturates). Inhalant use disorder commonly co-occurs\nwith other substance use disorders, and the sy mptoms of the disorders may be similar and\noverlapping. To disentangle symptom patterns, it is helpful to inquire about which symp-\ntoms persisted during periods when some of the substances were not being used.\nOther toxic, metabolic, traumatic, neoplastic, or infectious disorders impairing central or\nperipheral nervous system function. Individuals with inhalant use disorder may pre-\nsent with symptoms of pernicious anemia, su bacute combined degeneration of the spinal\ncord, psychosis, major or minor cognitive d isorder, brain atrophy, leukoencephalopathy,\nand many other nervous system disorders. Of co urse, these disorder s also may occur in\nthe absence of inhalant use disorder. A history of little or no inhalant use helps to exclude\ninhalant use disorder as the source of these problems.\nDisorders of other organ systems. Individuals with inhalant use disorder may present", "source": "dsm5.pdf"} {"id": "54b29e23a5be-2", "page_content": "Disorders of other organ systems. Individuals with inhalant use disorder may present\nwith symptoms of hepatic or renal damage, rhabdomyolysis, methemoglobinemia, or symp-\ntoms of other gastrointestinal, cardiovascular, or pulmonary diseases. A history of little or no\ninhalant use helps to exclude inhalant use diso rder as the source of such medical problems.", "source": "dsm5.pdf"} {"id": "43cd741d07a5-0", "page_content": "538 Substance-Related and Addictive Disorders\nComorbidity\nIndividuals with inhalant use disorder receiv ing clinical care often have numerous other\nsubstance use disorders. Inhalant use disord er commonly co-occurs with adolescent con-\nduct disorder and adult antisocial personality disorder. Adult inhalant use and inhalant\nuse disorder also are strongly associated wi th suicidal ideation and suicide attempts.\nInhalant Intoxication\nDiagnostic Criteria\nA. Recent intended or unintended short-term, high-dose exposure to inhalant sub-\nstances, including volatile hydrocarbons such as toluene or gasoline.\nB. Clinically significant problematic behavioral or psychological changes (e.g., belliger-\nence, assaultiveness, apathy, impaired judgment ) that developed during, or shortly af-\nter, exposure to inhalants.\nC. Two (or more) of the following signs or symptoms developing during, or shortly after,\ninhalant use or exposure:\n1. Dizziness.\n2. Nystagmus.\n3. Incoordination.\n4. Slurred speech.\n5. Unsteady gait.\n6. Lethargy.\n7. Depressed reflexes.\n8. Psychomotor retardation.\n9. Tremor.\n10. Generalized muscle weakness.\n11. Blurred vision or diplopia.\n12. Stupor or coma.\n13. Euphoria.\nD. The signs or symptoms are not attributable to another medical condition and are not bet-\nter explained by another mental disorder, including intoxication with another substance.\nCoding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether\nthere is a comorbid inhalant use disorder. If a mild inhalant use disorder is comorbid, the", "source": "dsm5.pdf"} {"id": "43cd741d07a5-1", "page_content": "ICD-10-CM code is F18.129, and if a moderate or severe inhalant use disorder is comor-\nbid, the ICD-10-CM code is F18.229. If there is no comorbid inhalant use disorder, then\nthe ICD-10-CM code is F18.929.\nNote: For information on Developm ent and Course, Risk and Prognostic Factors, Culture-\nRelated Diagnostic Issues, and Diagnostic Markers, see the co rresponding sections in in-\nhalant use disorder.\nDiagnostic Features\nInhalant intoxication is an inhalant-related, cl inically significant mental disorder that de-\nvelops during, or immediately after, intended or unintended inhalation of a volatile hy-\ndrocarbon substance. Volatile hydrocarbons are toxic gases fr om glues, fuels, paints, and\nother volatile compounds. When it is possible to do so, the particular substance involved\nshould be named (e.g., toluene intoxication). Among those who do, the intoxication clears\nwithin a few minutes to a few hours after th e exposure ends. Thus, inhalant intoxication\nusually occurs in brief episodes that may recur.", "source": "dsm5.pdf"} {"id": "589ad44217cc-0", "page_content": "Inhalant Intoxication 539\nAssociated Features Supporting Diagnosis\nInhalant intoxication may be indicated by eviden ce of possession, or lingering odors, of in-\nhalant substances (e.g., glue, paint thinner, gasoline, butane lighters); apparent intoxica-\ntion occurring in the age range with the highest prevalence of inhalant use (12\u201317 years);\nand apparent intoxication with negative results from the standard drug screens that usu-\nally fail to identify inhalants.\nPrevalence\nThe prevalence of actual episode s of inhalant intoxication in the general population is un-\nknown, but it is probable that most inhalant users would at some time exhibit use that\nwould meet criteria for inhalant intoxication disorder. Therefore, the prevalence of inhal-\nant use and the prevalence of inhalant intoxi cation disorder are likely similar. In 2009 and\n2010, inhalant use in the past year was reported by 0.8% of all Americans older than 12 years;\nthe prevalence was highest in younger age groups (3.6% for individuals 12 to 17 years old,\nand 1.7% for individuals 18 to 25 years old).\nGender-Related Diagnostic Issues\nGender differences in the prevalence of inhalant intoxication in the general population are\nunknown. However, if it is assumed that most inhalant users eventually experience inhal-\nant intoxication, gender differences in the prevalence of inhalant users likely approximate\nthose in the proportions of males and females experiencing inhalant intoxication. Regard-\ning gender differences in the pr evalence of inhalant users in the United States, 1% of males\nolder than 12 years and 0.7% of females older than 12 years have used inhalants in the pre-", "source": "dsm5.pdf"} {"id": "589ad44217cc-1", "page_content": "vious year, but in the younger age groups more females than males have used inhalants\n(e.g., among 12- to 17-year-olds, 3. 6% of males and 4.2% of females).\nFunctional Consequences of Inhalant Intoxication\nUse of inhaled substances in a closed container, such as a plastic bag over the head, may\nlead to unconsciousness, anoxia, and death. Separately, \u201csudden sniffing death,\u201d likely\nfrom cardiac arrhythmia or arrest, may occu r with various volatile inhalants. The en-\nhanced toxicity of certain vola tile inhalants, such as butane or propane, also causes fatal-\nities. Although inhalant intoxication itself is of short duration, it may produce persisting\nmedical and neurological problems, especi ally if the intoxications are frequent. \nDifferential Diagnosis\nInhalant exposure, without meeting the criteria for inhalant intoxication disorder.\nThe individual intentionally or unintentionally inhaled substances, but the dose was in-\nsufficient for the diagnostic criteria for inhalant use disorder to be met.\nIntoxication and other substance/medica tion-induced disorders from other sub-\nstances, especially from sedating substances (e.g., alcohol, benzodiazepines, barbi-\nturates). These disorders may have similar signs and symptoms, but the intoxication is\nattributable to other intoxicants that may be identified via a toxicology sc reen. Differenti-\nating the source of the intoxication may invo lve discerning evidence of inhalant exposure\nas described for inhalant use disorder. A diag nosis of inhalant intoxication may be sug-\ngested by possession, or linger ing odors, of inhalant substances (e.g., glue, paint thinner,", "source": "dsm5.pdf"} {"id": "589ad44217cc-2", "page_content": "gasoline, butane lighters,); paraphernalia poss ession (e.g., rags or bags for concentrating\nglue fumes); perioral or perinasal \u201cglue-sniffe r\u2019s rash\u201d; reports from family or friends that\nthe intoxicated individual possesses or uses inhalants; apparent intoxication despite neg-\native results on standard drug screens (which usually fail to identify inhalants); apparent\nintoxication occurring in that age range with the highest prevalence of inhalant use (12\u201317", "source": "dsm5.pdf"} {"id": "5af3b3c396ce-0", "page_content": "540 Substance-Related and Addictive Disorders\nyears); association with others known to use inhalants; membership in certain small com-\nmunities with prevalent inhalant use (e.g., so me native or aborigin al communities, home-\nless street children and adoles cents); or unusual access to certain inhalant substances.\nOther inhalant-related disorders. Episodes of inhalant intoxication do occur during,\nbut are not identical with, other inhalant-related disorders. Those inha lant-related disorders\nare recognized by their respective diagnostic criteria: inhalant use disorder, inhalant-\ninduced neurocognitive disorder, inhalant-i nduced psychotic disorder, inhalant-induced\ndepressive disorder, inhalant-induced anxiet y disorder, and other inhalant-induced dis-\norders.\nOther toxic, metabolic, traumatic, neoplastic, or infectious disorders that impair brain\nfunction and cognition. Numerous neurological and other medical conditions may pro-\nduce the clinically significant behavioral or psychological changes (e.g., belligerence, as-\nsaultiveness, apathy, impaired judgment) that also characterize inhalant intoxication. \nOther Inhalant-Induced Disorders\nThe following inhalant-induced disorders are described in other chapters of the manual\nwith disorders with which they share ph enomenology (see the substance/medication-\ninduced mental disorders in these chapters): inhalant-induced psychotic disorder (\u201cSchizo-\nphrenia Spectrum and Other Psychotic Disord ers\u201d); inhalant-induced depressive disorder\n(\u201cDepressive Disorders\u201d); inhalant-induced an xiety disorder (\u201cAnxiet y Disorders\u201d); and in-\nhalant-induced major or mild neurocognitive disorder (\u201cNeur ocognitive Disorders\u201d). For\ninhalant intoxication delirium, see the criteria and discussion of de lirium in the chapter", "source": "dsm5.pdf"} {"id": "5af3b3c396ce-1", "page_content": "\u201cNeurocognitive Disorders.\u201d Thes e inhalant-induced disorders are diagnosed instead of in-\nhalant intoxication only when symptoms are sufficiently severe to warrant independent\nclinical attention. \nUnspecified Inhalant-Related Disorder\n292.9 (F18.99)\nThis category applies to presentations in which symptoms characteristic of an inhalant-\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any specific inhalant-related disorder or any of the disorders in the substance-related\nand addictive disorders diagnostic class.\nOpioid-Related Disorders\nOpioid Use Disorder\nOpioid Intoxication\nOpioid Withdrawal\nOther Opioid-Induced Disorders\nUnspecified Opioid -Related Disorder", "source": "dsm5.pdf"} {"id": "74d0bb1953c3-0", "page_content": "Opioid Use Disorder 541\nOpioid Use Disorder\nDiagnostic Criteria\nA. A problematic pattern of opioid use leading to clinically significant impairment or distress,\nas manifested by at least two of the fo llowing, occurring within a 12-month period:\n1. Opioids are often taken in larger amounts or over a longer period than was in-\ntended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control opioid use.\n3. A great deal of time is spent in activities necessary to obtain the opioid, use the opi-\noid, or recover from its effects.\n4. Craving, or a strong desire or urge to use opioids.\n5. Recurrent opioid use resulting in a failure to fulfill major role obligations at work,\nschool, or home.\n6. Continued opioid use despite having persisten t or recurrent social or interpersonal\nproblems caused or exacerbated by the effects of opioids.\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of opioid use.\n8. Recurrent opioid use in situations in which it is physically hazardous.\n9. Continued opioid use despite knowledge of having a persistent or recurrent physi-\ncal or psychological problem that is likely to have been caused or exacerbated by\nthe substance.\n10. Tolerance, as defined by either of the following: \na. A need for markedly increased amounts of opioids to achieve intoxication or de-\nsired effect.\nb. A markedly diminished effect with continued use of the same amount of an opioid.\nNote: This criterion is not considered to be met for those taking opioids solely under\nappropriate medical supervision.\n11. Withdrawal, as manifested by either of the following:\na. The characteristic opioid withdrawal syndr ome (refer to Criteria A and B of the", "source": "dsm5.pdf"} {"id": "74d0bb1953c3-1", "page_content": "a. The characteristic opioid withdrawal syndr ome (refer to Criteria A and B of the\ncriteria set for opioid withdrawal, pp. 547\u2013548).\nb. Opioids (or a closely related substance) are taken to relieve or avoid withdrawal\nsymptoms.\nNote: This criterion is not considered to be met for those individuals taking opioids\nsolely under appropriate medical supervision.\nSpecify if:\nIn early remission: After full criteria for opioid use disorder were previously met, none\nof the criteria for opioid use disorder have been met for at least 3 months but for less\nthan 12 months (with the exception that Criterion A4, \u201cCraving, or a strong desire or\nurge to use opioids,\u201d may be met).\nIn sustained remission: After full criteria for opioid us e disorder were previously met,\nnone of the criteria for opioid use disorder have been met at any time during a period\nof 12 months or longer (with the exception that Criterion A4, \u201cCraving, or a strong de-\nsire or urge to use opioids,\u201d may be met). \nSpecify if:\nOn maintenance therapy: This additional specifier is used if the individual is taking a\nprescribed agonist medication such as methadone or buprenorphine and none of the\ncriteria for opioid use disorder have been met for that class of medication (except tol-\nerance to, or withdrawal from, the agonist). This category also applies to those individ-", "source": "dsm5.pdf"} {"id": "717d5da0c07e-0", "page_content": "542 Substance-Related and Addictive Disorders\nuals being maintained on a partial agonist, an agonist/antagonist, or a full antagonist\nsuch as oral naltrexone or depot naltrexone. \nIn a controlled environment: This additional specifier is used if the individual is in an\nenvironment where access to opioids is restricted.\nCoding based on current severity: Note for ICD-10-CM codes: If an opioid intoxication,\nopioid withdrawal, or another opioid-induced ment al disorder is also present, do not use\nthe codes below for opioid use disorder. Instead, the comorbid opioid use disorder is indi-\ncated in the 4th character of the opioid-indu ced disorder code (see the coding note for opi-\noid intoxication, opioid withdrawal, or a spec ific opioid-induced mental disorder). For\nexample, if there is comorbid opioid-induc ed depressive disorder and opioid use disorder,\nonly the opioid-induced depressive disorder code is given, with the 4th character indicating\nwhether the comorbid opioid use disorder is mi ld, moderate, or severe: F11.14 for mild opi-\noid use disorder with opioid-induced depressive disorder or F11.24 for a moderate or se-\nvere opioid use disorder with opi oid-induced depressive disorder.\nSpecify current severity:\n305.50 (F11.10) Mild: Presence of 2\u20133 symptoms.\n304.00 (F11.20) Moderate: Presence of 4\u20135 symptoms.\n304.00 (F11.20) Severe: Presence of 6 or more symptoms.\nSpecifiers\nThe \u201con maintenance therapy\u201d specifier applies as a further specifier of remission if the in-\ndividual is both in remission and receiving maintenance therapy. \u201cIn a controlled environ-", "source": "dsm5.pdf"} {"id": "717d5da0c07e-1", "page_content": "dividual is both in remission and receiving maintenance therapy. \u201cIn a controlled environ-\nment\u201d applies as a further specifier of remission if the individual is both in remission and in\na controlled environment (i.e., in early remission in a controlled environment or in sustained\nremission in a controlled envi ronment). Examples of these en vironments are closely super-\nvised and substance-free jail s, therapeutic communities, an d locked hospital units. \nChanging severity across time in an individual is also reflected by reductions in the fre-\nquency (e.g., days of use per month) and/or dose (e.g., injections or number of pills) of an\nopioid, as assessed by the individual\u2019s self-r eport, report of knowledgeable others, clini-\ncian\u2019s observations, and biological testing.\nDiagnostic Features\nOpioid use disorder includes signs and sympto ms that reflect compulsive, prolonged self-\nadministration of opioid substances that are used for no legitimate medical purpose or, if\nanother medical condition is pres ent that requires opioid treatment, that are used in doses\ngreatly in excess of the amount needed for th at medical condition. (F or example, an indi-\nvidual prescribed analgesic opioids for pain re lief at adequate dosing will use significantly\nmore than prescribed and not only because of persistent pain.) Individuals with opioid use\ndisorder tend to develop such regular patterns of compulsive drug use that daily activities\nare planned around obtaining and administer ing opioids. Opioids are usually purchased\non the illegal market but may also be obtained from physicians by falsifying or exagger-\nating general medical problems or by receiv ing simultaneous prescr iptions from several\nphysicians. Health care professionals with op ioid use disorder will often obtain opioids by\nwriting prescriptions for themselves or by dive rting opioids that have been prescribed for", "source": "dsm5.pdf"} {"id": "717d5da0c07e-2", "page_content": "writing prescriptions for themselves or by dive rting opioids that have been prescribed for\npatients or from pharmacy supplies. Most individuals with opioid use disorder have\nsignificant levels of tolerance and will experience withdrawal on abrupt discontinuation\nof opioid substances. Individuals with opio id use disorder ofte n develop conditioned\nresponses to drug-related stimuli (e.g., cr aving on seeing any he roin powder\u2013like sub-\nstance)\u2014a phenomenon that occu rs with most drugs that cause intense psychological\nchanges. These responses probably contribute to relapse, are difficult to extinguish, and typ-\nically persist long after detoxification is completed.", "source": "dsm5.pdf"} {"id": "153bd6176760-0", "page_content": "Opioid Use Disorder 543\nAssociated Features Supporting Diagnosis\nOpioid use disorder can be asso ciated with a history of drug-r elated crimes (e.g., posses-\nsion or distribution of drugs, forgery, burglary, robbery, larc eny, receiving stolen goods).\nAmong health care professionals and individuals who have ready access to controlled\nsubstances, there is often a different pattern of illegal activities involving problems with\nstate licensing boards, professional staffs of hospitals, or other administrative agencies.\nMarital difficulties (including divorce), un employment, and irregular employment are of-\nten associated with opioid use diso rder at all socioeconomic levels.\nPrevalence\nThe 12-month prevalence of opioid use disord er is approximately 0. 37% among adults age\n18 years and older in the community population. This may be an underestimate because of\nthe large number of incarcerated individuals wi th opioid use disorders. Rates are higher in\nmales than in females (0.49% vs. 0.26%), with the male-to-female ratio typically being 1.5:1\nfor opioids other than heroin (i.e., available by prescription) and 3:1 for heroin. Female ad-\nolescents may have a higher likelihood of developing opioid use disorders. The preva-\nlence decreases with age, with the prevalence highest (0.82%) among adults age 29 years or\nyounger, and decreasing to 0.09% among adul ts age 65 years and older. Among adults, the\nprevalence of opioid use di sorder is lower among African Americans at 0.18% and over-\nrepresented among Native Americans at 1.25%. It is close to average among whites (0.38%),\nAsian or Pacific Islanders (0.35%), and Hispanics (0.39%).", "source": "dsm5.pdf"} {"id": "153bd6176760-1", "page_content": "Asian or Pacific Islanders (0.35%), and Hispanics (0.39%).\nAmong individuals in the United States ages 12\u201317 years, the overall 12-month prev-\nalence of opioid use disorder in the community population is approximately 1.0%, but the\nprevalence of heroin use disorder is less than 0.1%. By contrast, analgesic use disorder is\nprevalent in about 1.0% of those ages 12\u201317 years, speaking to the importance of opioid an-\nalgesics as a group of substances with significant health consequences.\nThe 12-month prevalence of problem opioid use in European countries in the commu-\nnity population ages 15\u201364 years is betwee n 0.1% and 0.8%. The average prevalence of\nproblem opioid use in the European Unio n and Norway is between 0.36% and 0.44%.\nDevelopment and Course\nOpioid use disorder can begin at any age, bu t problems associated with opioid use are\nmost commonly first observed in the late teens or early 20s. Once opioid use disorder\ndevelops, it usually continues over a period of many years, even though brief periods of\nabstinence are frequent. In treated populati ons, relapse following abstinence is common.\nEven though relapses do occur, and while so me long-term mortality rates may be as high\nas 2% per year, about 20%\u201330% of individuals with opioid use disorder achieve long-term\nabstinence. An exception concerns that of military service perso nnel who became depen-\ndent on opioids in Vietnam; over 90% of this population who had been dependent on opi-\noids during deployment in Vietnam achieved abstinence after they returned, but they\nexperienced increased rates of alcohol or amph etamine use disorder as well as increased", "source": "dsm5.pdf"} {"id": "153bd6176760-2", "page_content": "experienced increased rates of alcohol or amph etamine use disorder as well as increased\nsuicidality.\nIncreasing age is associated with a decrease in prevalence as a result of early mortality\nand the remission of sy mptoms after age 40 years (i.e., \u201cmaturing out\u201d). However, many\nindividuals continue have presentations that m eet opioid use disorder criteria for decades.\nRisk and Prognostic Factors\nGenetic and physiological. The risk for opiate use disorder can be related to individual,\nfamily, peer, and social environmental factors, but within these domains, genetic factors\nplay a particularly important role both dire ctly and indirectly. For instance, impulsivity\nand novelty seeking are individu al temperaments that relate to the propensity to develop", "source": "dsm5.pdf"} {"id": "2d78e6703bb9-0", "page_content": "544 Substance-Related and Addictive Disorders\na substance use disorder but may themselves be genetically determined. Peer factors may\nrelate to genetic predisposition in terms of how an individual selects his or her environ-\nment. \nCulture-Related Diagnostic Issues\nDespite small variations regarding individual criterion items, opioid use disorder diag-\nnostic criteria perform equally well across most race/ethnicity groups. Individuals from\nethnic minority populations living in econom ically deprived area s have been overrep-\nresented among individuals with opioid use disorder. However, over time, opioid use\ndisorder is seen more often among white middle-class individuals, especially females,\nsuggesting that differences in use reflect the availability of opioid drugs and that other so-\ncial factors may impact prevalence. Medical personnel who have ready access to opioids\nmay be at increased risk for opioid use disorder. \nDiagnostic Markers\nRoutine urine toxicology test re sults are often positive for opioid drugs in individuals with\nopioid use disorder. Urine test results remain positive for most opioids (e.g., heroin, mor-\nphine, codeine, oxycodone, propoxyphene) for 12\u201336 hours after administration. Fentanyl\nis not detected by standard urine tests but can be identified by more specialized proce-\ndures for several days. Methadone, buprenorphine (or buprenorphine/naloxone combi-\nnation), and LAAM ( L-alpha-acetylmethadol) have to be specifically tested for and will not\ncause a positive result on routine tests for opiates. They can be detected for several days up\nto more than 1 week. Laboratory evidence of the presence of other substances (e.g., co-\ncaine, marijuana, alcohol, amphetamines, benzodiazepines) is common . Screening test re-", "source": "dsm5.pdf"} {"id": "2d78e6703bb9-1", "page_content": "sults for hepatitis A, B, and C virus are positive in as many as 80%\u201390% of injection opioid\nusers, either for hepatitis antigen (signifying ac tive infection) or for hepatitis antibody (sig-\nnifying past infection). HIV is prevalent in injection opioid users as well. Mildly elevated\nliver function test results are common, either as a result of re solving hepatitis or from toxic\ninjury to the liver due to contaminants that have been mixed with the injected opioid. Sub-\ntle changes in cortisol secretion patterns and body temperature regulation have been ob-\nserved for up to 6 months following opioid detoxification.\nSuicide Risk\nSimilar to the risk generally observed for a ll substance use disorders, opioid use disorder\nis associated with a heightened risk for suicide attempts and completed suicides. Particu-\nlarly notable are both accidental and deliberate opioid overdose s. Some suicide risk factors\noverlap with risk factors for an opioid use di sorder. In addition, repeated opioid intoxica-\ntion or withdrawal may be associated with severe depressions that, although temporary,\ncan be intense enough to lead to suicide attempts and completed su icides. Available data\nsuggest that nonfatal accidental opioid ov erdose (which is common) and attempted sui-\ncide are distinct clinically significant proble ms that should not be mistaken for each other.\nFunctional Consequences of Opioid Use Disorder\nOpioid use is associated with a lack of mu cous membrane secretions, causing dry mouth\nand nose. Slowing of gastrointestinal activity and a decrease in gut motility can produce\nsevere constipation. Visual acuity may be im paired as a result of pupillary constriction\nwith acute administration. In individuals who inject opioids, sclerosed veins (\u201ctracks\u201d)\nand puncture marks on the lower portions of the upper extremities are common. Veins", "source": "dsm5.pdf"} {"id": "2d78e6703bb9-2", "page_content": "and puncture marks on the lower portions of the upper extremities are common. Veins\nsometimes become so severely sclerosed that peripheral edema develops, and individuals\nswitch to injecting in veins in the legs, neck , or groin. When these veins become unusable,\nindividuals often inject directly into their su bcutaneous tissue (\u201csk in-popping\u201d), resulting", "source": "dsm5.pdf"} {"id": "d9549a007679-0", "page_content": "Opioid Use Disorder 545\nin cellulitis, abscesses, and circ ular-appearing scars from healed skin lesions. Tetanus and\nClostridium botulinum infections are relatively rare bu t extremely serious consequences of\ninjecting opioids, especially with contaminated needles. Infections may also occur in\u00a0other\norgans and include bacterial endocarditis, hepa titis, and HIV infection. Hepatitis C infec-\ntions, for example, may occur in up to 90% of persons who inject opioids. In addition, the\nprevalence of HIV infection ca n be high among individuals who inject drugs, a large pro-\nportion of whom are individuals with opioid use disorder. HIV infection rates have been\nreported to be as high as 60% among heroin users with opioid use disorder in some areas\nof the United States or the Russian Federati on. However, the incidence may also be 10% or\nless in other areas, especially those where a ccess to clean injection material and parapher-\nnalia is facilitated.\nTuberculosis is a particularly serious problem among individuals who use drugs in-\ntravenously, especially those who are dependen t on heroin; infection is usually asymptom-\natic and evident only by the presence of a posi tive tuberculin skin test. However, many cases\nof active tuberculosis have been found, espe cially among those who are infected with HIV.\nThese individuals often have a newly acquired infection but also are likely to experience\nreactivation of a prior infection be cause of impaired immune function. \nIndividuals who sniff heroin or other opioid s into the nose (\u201csnorting\u201d) often develop\nirritation of the nasal mucosa, sometimes acco mpanied by perforation of the nasal septum.\nDifficulties in sexual functioning are common. Males often experience erectile dysfunction", "source": "dsm5.pdf"} {"id": "d9549a007679-1", "page_content": "Difficulties in sexual functioning are common. Males often experience erectile dysfunction\nduring intoxication or chronic use. Female s commonly have disturbances of reproductive\nfunction and irregular menses.\nIn relation to infections such as cellulitis, hepatitis, HIV infection, tuberculosis, and en-\ndocarditis, opioid use d isorder is associated with a mort ality rate as high as 1.5%\u20132% per\nyear. Death most often results from overdose, accidents, injuries, AIDS, or other general\nmedical complications. Accidents and injuries due to violence that is associated with buy-\ning or selling drugs are common. In some areas, violence accounts for more opioid-related\ndeaths than overdose or HIV infection. Phy siological dependence on opioids may occur in\nabout half of the infants born to females with opioid use disorder; this can produce a se-\nvere withdrawal syndrome requiring medical treatment. Although low birth weight is\nalso seen in children of mothers with opioid use disorder, it is usually not marked and is\ngenerally not associated with serious adverse consequences.\nDifferential Diagnosis\nOpioid-induced mental disorders. Opioid-induced disorders o ccur frequently in individ-\nuals with opioid use disorder. Opioid-induced disorders may be characterized by symptoms\n(e.g., depressed mood) that rese mble primary mental disorders (e.g., persistent depressive dis-\norder [dysthymia] vs. opioid-induced depressive disorder, with depressive features, with on-\nset during intoxication). Opioids are less likel y to produce symptoms of mental disturbance\nthan are most other drug s of abuse. Opioid intoxication and opioid withdrawal are distin-\nguished from the other opioid-induced disorder s (e.g., opioid-induced depressive disorder,\nwith onset during intoxication ) because the symptoms in thes e latter disorders predominate", "source": "dsm5.pdf"} {"id": "d9549a007679-2", "page_content": "with onset during intoxication ) because the symptoms in thes e latter disorders predominate\nthe clinical presentation and are severe enou gh to warrant independent clinical attention.\nOther substance intoxication. Alcohol intoxication and seda tive, hypnotic, or anxiolytic\nintoxication can cause a clinical picture that resembles that for opioid intoxication. A diag-\nnosis of alcohol or sedative, hypnotic, or anxiol ytic intoxication can usually be made based\non the absence of pupillary constriction or the lack of a response to naloxone challenge. In", "source": "dsm5.pdf"} {"id": "9044b246c9a4-0", "page_content": "nosis of alcohol or sedative, hypnotic, or anxiol ytic intoxication can usually be made based\non the absence of pupillary constriction or the lack of a response to naloxone challenge. In\nsome cases, intoxication may be due both to opioids and to alcohol or other sedatives. In\nthese cases, the naloxone challenge will no t reverse all of the sedative effects. \nOther withdrawal disorders. The anxiety and restlessness associated with opioid with-\ndrawal resemble symptoms seen in sedative-hypnotic withdrawal. However, opioid\nwithdrawal is also accompanied by rhinorrhea , lacrimation, and pupillary dilation, which", "source": "dsm5.pdf"} {"id": "ef9de64711e2-0", "page_content": "546 Substance-Related and Addictive Disorders\nare not seen in sedative-type withdrawal. Dilated pupils ar e also seen in hallucinogen\nintoxication and stimulant in toxication. However, other si gns or symptoms of opioid\nwithdrawal, such as nausea, vomiting, diarrhea, abdominal cramps, rhinorrhea, or lacri-\nmation, are not present. \nComorbidity \nThe most common medical conditions associated with opioid use disorder are viral (e.g.,\nHIV, hepatitis C virus) and bact erial infections, particularly among users of opioids by in-\njection. These infections are less common in opioid use disorder with prescription opioids.\nOpioid use disorder is often associated with other substance use disord ers, especially those\ninvolving tobacco, alcohol, cannabis, stimulants, and benzodiazepines, which are often\ntaken to reduce symptoms of op ioid withdrawal or craving for opioids, or to enhance the ef-\nfects of administered opioids. Individuals with opioid use disorder are at risk for the devel-\nopment of mild to moderate depression that meets symptomatic and duration criteria for\npersistent depressive disorder (dysthymia) or, in some cases, for major depressive disorder.\nThese symptoms may represent an opioid-induc ed depressive disorder or an exacerbation\nof a preexisting primary depres sive disorder. Periods of depression are especially common\nduring chronic intoxication or in association with physical or psychosocial stressors that are\nrelated to the opioid use disorder. Insomnia is common, especially during withdrawal. An-\ntisocial personality disorder is much more common in individuals with opioid use disorder\nthan in the general population. Posttraumatic stress disorder is also seen with increased fre-\nquency. A history of conduct disorder in childh ood or adolescence has been identified as a", "source": "dsm5.pdf"} {"id": "ef9de64711e2-1", "page_content": "significant risk factor for substance-related disorders, especially opioid use disorder.\nOpioid Intoxication\nDiagnostic Criteria\nA. Recent use of an opioid.\nB. Clinically significant problematic behavioral or psychological changes (e.g., initial eu-\nphoria followed by apathy, dysphoria, psychomotor agitation or retardation, impaired\njudgment) that developed during, or shortly after, opioid use.\nC. Pupillary constriction (or pupillary dilation due to anoxia from severe overdose) and\none (or more) of the following signs or symptoms developing during, or shortly after,\nopioid use:\n1. Drowsiness or coma.\n2. Slurred speech.\n3. Impairment in attention or memory.\nD. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication with another sub-\nstance.\nSpecify if:\nWith perceptual disturbances: This specifier may be noted in the rare instance in\nwhich hallucinations with intact reality testing or auditory, visual, or tactile illusions oc-\ncur in the absence of a delirium.\nCoding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether\nor not there is a comorbid opioid use disorder and whether or not there are perceptual dis-\nturbances. \nFor opioid intoxication without perceptual disturbances: If a mild opioid use dis-\norder is comorbid, the ICD-10-CM code is F11.129, and if a moderate or severe opioid", "source": "dsm5.pdf"} {"id": "2207e2f41c60-0", "page_content": "Opioid Withdrawal 547\nuse disorder is comorbid, the ICD-10-CM code is F11.229. If there is no comorbid opi-\noid use disorder, then the ICD-10-CM code is F11.929.\nFor opioid intoxication wit h perceptual disturbances: If a mild opioid use disorder\nis comorbid, the ICD-10-CM code is F11.122, and if a moderate or severe opioid use\ndisorder is comorbid, the ICD-10-CM code is F11.222. If there is no comorbid opioid\nuse disorder, then the ICD-10-CM code is F11.922.\nDiagnostic Features\nThe essential feature of opioid intoxication is the presence of clinically significant prob-\nlematic behavioral or psychological changes (e .g., initial euphoria followed by apathy,\ndysphoria, psychomotor agitation or retardat ion, impaired judgment) that develop dur-\ning, or shortly after, opioid use (Criteria A and B). Intoxication is accompanied by pupil-\nlary constriction (unless ther e has been a severe overdose with consequent anoxia and\npupillary dilation) and one or more of the fo llowing signs: drowsiness (described as be-\ning \u201con the nod\u201d), slurred speech, and impairme nt in attention or memory (Criterion C);\ndrowsiness may progress to co ma. Individuals with opioid intoxication may demonstrate\ninattention to the environment, even to the point of ignoring potentially harmful events.\nThe signs or symptoms must not be attributab le to another medical condition and are not\nbetter explained by another me ntal disorder (Criterion D).\nDifferential Diagnosis\nOther substance intoxication. Alcohol intoxication and se dative-hypnotic intoxication", "source": "dsm5.pdf"} {"id": "2207e2f41c60-1", "page_content": "Other substance intoxication. Alcohol intoxication and se dative-hypnotic intoxication\ncan cause a clinical picture that resembles op ioid intoxication. A diagnosis of alcohol or\nsedative-hypnotic intoxication can usually be made based on the absence of pupillary con-\nstriction or the lack of a response to a naloxo ne challenge. In some cases, intoxication may\nbe due both to opioids and to alcohol or other sedatives. In these cases, the naloxone chal-\nlenge will not reverse all of the sedative effects. \nOther opioid-related disorders. Opioid intoxication is distinguished from the other\nopioid-induced disorders (e.g., opioid-induced depressive disorder, with onset during in-\ntoxication) because the symptoms in the latter disorders predominate in the clinical pre-\nsentation and meet full criteria for the relevant disorder.\nOpioid Withdrawal\nDiagnostic Criteria 292.0 (F11.23)\nA. Presence of either of the following:\n1. Cessation of (or reduction in) opioid use that has been heavy and prolonged (i.e.,\nseveral weeks or longer).\n2. Administration of an opioid antagonist after a period of opioid use.\nB. Three (or more) of the following developing within minutes to several days after Criterion A:\n1. Dysphoric mood.\n2. Nausea or vomiting.\n3. Muscle aches.\n4. Lacrimation or rhinorrhea.\n5. Pupillary dilation, piloerection, or sweating.", "source": "dsm5.pdf"} {"id": "3f170d2b599d-0", "page_content": "548 Substance-Related and Addictive Disorders\n6. Diarrhea.\n7. Yawning.\n8. Fever.\n9. Insomnia.\nC. The signs or symptoms in Criterion B cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning.\nD. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication or withdrawal from\nanother substance.\nCoding note: The ICD-9-CM code is 292.0. The IC D-10-CM code for opioid withdrawal is\nF11.23. Note that the ICD-10-CM code indicates the comorbid presence of a moderate or\nsevere opioid use disorder, reflecting the fact that opioid withdrawal can only occur in the\npresence of a moderate or severe opioid use disorder. It is not permissible to code a co-\nmorbid mild opioid use disorder with opioid withdrawal.\nDiagnostic Features\nThe essential feature of opioid withdrawal is the presence of a characteristic withdrawal\nsyndrome that develops after the cessation of (or reduction in) opioid use that has been\nheavy and prolonged (Cri terion A1). The withdrawal synd rome can also be precipitated\nby administration of an opioid antagonist (e.g., naloxone or naltrexone) after a period of\nopioid use (Criterion A2). This may also occur after administration of an opioid partial ag-\nonist such as buprenorphine to a person currently using a full opioid agonist.\nOpioid withdrawal is characte rized by a\u00a0pattern of signs and symptoms that are oppo-\nsite to the acute agonist effects. The first of these are subjective and consist of complaints of\nanxiety, restlessness, and an \u201cachy feeling\u201d that is often located in the back and legs, along", "source": "dsm5.pdf"} {"id": "3f170d2b599d-1", "page_content": "with irritability and increased sensitivity to pain. Three or more of the following must be\npresent to make a diagnosis of opioid with drawal: dysphoric mood; nausea or vomiting;\nmuscle aches; lacrimation or rhinorrhea; pu pillary dilation, piloerection, or increased\nsweating; diarrhea; yawning; fever; and insomn ia (Criterion B). Piloerection and fever are\nassociated with more severe withdrawal and are not often seen in routine clinical practice\nbecause individuals with opioid use disorder usually obtain substances before with-\ndrawal becomes that far advanced. These sy mptoms of opioid withdrawal must cause\nclinically significant distress or impairment in social, occupational, or other important ar-\neas of functioning (Criterion C). The symptoms must not be attributable to another med-\nical condition and are not better explained by another mental diso rder (Criterion D).\nMeeting diagnostic criteria for opioid withdr awal alone is not sufficient for a diagnosis of\nopioid use disorder, but concurrent symptoms of craving and drug-seeking behavior are\nsuggestive of comorbid opioid use disorder. ICD-10-CM codes only allow a diagnosis of\nopioid withdrawal in the presence of comorb id moderate to severe opioid use disorder.\nThe speed and severity of withdrawal associat ed with opioids depend on the half-life of\nthe opioid used. Most individuals who are physiologically dependent on short-acting drugs\nsuch as heroin begin to have withdrawal symptoms within 6\u201312 hours after the last dose.\nSymptoms may take 2\u20134 days to emerge in th e case of longer-acting drugs such as metha-\ndone, LAAM ( L-alpha-acetylmethadol), or buprenorph ine. Acute withdrawal symptoms for", "source": "dsm5.pdf"} {"id": "3f170d2b599d-2", "page_content": "a short-acting opioid such as heroin usuall y peak within 1\u20133 days and gradually subside\nover a period of 5\u20137 days. Less acute withdrawal symptoms can last for weeks to months.\nThese more chronic symptoms include anxiety, dysphoria, anhedonia, and insomnia.", "source": "dsm5.pdf"} {"id": "533e5168b852-0", "page_content": "Opioid Withdrawal 549\nAssociated Features Supporting Diagnosis\nMales with opioid withdrawal may experien ce piloerection, sweating, and spontaneous\nejaculations while awake. Opioid withdrawal is distinct from opioid use disorder and\ndoes not necessarily occur in the presence of the drug-seeking behavior associated with\nopioid use disorder. Opioid withdrawal may o ccur in any individual after cessation of re-\npeated use of an opioid, whether in the se tting of medical management of pain, during\nopioid agonist therapy fo r opioid use disorder, in the contex t of private recreational use, or\nfollowing attempts to self-treat sympto ms of mental disorders with opioids.\nPrevalence\nAmong individuals from various clinical settings, opioid withdrawal occurred in 60% of\nindividuals who had used heroin at least once in the prior 12 months. \nDevelopment and Course\nOpioid withdrawal is typical in the course of an opioid use disorder. It can be part of an es-\ncalating pattern in which an opioid is used to reduce withdrawal symptoms, in turn lead-\ning to more withdrawal at a later time. Fo r persons with an established opioid use\ndisorder, withdrawal and attempts to relieve withdrawal are typical. \nDifferential Diagnosis\nOther withdrawal disorders. The anxiety and restlessness associated with opioid with-\ndrawal resemble symptoms seen in sedative-hypnotic withdrawal. However, opioid with-\ndrawal is also accompanied by rhinorrhea, la crimation, and pupillary dilation, which are\nnot seen in sedative-type withdrawal. \nOther substance intoxication. Dilated pupils are also seen in hallucinogen intoxication\nand stimulant intoxication. However, other signs or symptoms of opioid withdrawal, such\nas nausea, vomiting, diarrhea, abdominal cram ps, rhinorrhea, and lacrimation, are not", "source": "dsm5.pdf"} {"id": "533e5168b852-1", "page_content": "present. \nOther opioid-ind uced disorders. Opioid withdrawal is distinguished from the other\nopioid-induced disorders (e.g., opioid-induced depressive disorder, with onset during\nwithdrawal) because the symptoms in these latt er disorders are in ex cess of those usually\nassociated with opioid withdrawal and meet full criteria for th e relevant disorder.\nOther Opioid-Induced Disorders\nThe following opioid-induced di sorders are described in other chapters of the manual with\ndisorders with which they share phenomenology (see the substance/medication-induced\nmental disorders in these chapters): opioid-i nduced depressive diso rder (\u201cDepressive Dis-\norders\u201d); opioid-induced anxi ety disorder (\u201cAnxiety Disord ers\u201d); opioid-induced sleep\ndisorder (\u201cSleep-Wake Disord ers\u201d); and opioid-induced sexual dysfunction (\u201cSexual Dys-\nfunctions\u201d). For opioid intoxica tion delirium and opioid with drawal delirium, see the crite-\nria and discussion of delirium in the chapter \u201cNeurocognitive Disorders.\u201d These opioid-\ninduced disorders are diagnosed instead of opio id intoxication or opioid withdrawal only\nwhen the symptoms are suffici ently severe to warrant inde pendent clinical attention.", "source": "dsm5.pdf"} {"id": "6dc043c0ca89-0", "page_content": "550 Substance-Related and Addictive Disorders\nUnspecified Opioid-Related Disorder\n292.9 (F11.99)\nThis category applies to presentations in which symptoms characteristic of an opioid-\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any specific opioid-related disorder or any of the disorders in the substance-related and\naddictive disorders diagnostic class.\nSedative-, Hypnotic-, \nor Anxiolytic-Related Disorders\nSedative, Hypnotic, or Anxiolytic Use Disorder\nSedative, Hypnotic, or Anxiolytic Intoxication\nSedative, Hypnotic, or Anxiolytic Withdrawal\nOther Sedative-, Hypnotic-, or Anxiolytic-Induced Disorders\nUnspecified Sedative-, Hypnotic-, or Anxiolytic-R elated Disorder\nSedative, Hypnotic, or Anxiolytic Use Disorder\nDiagnostic Criteria\nA. A problematic pattern of sedative, hypnotic, or anxiolytic use leading to clinically signif-\nicant impairment or distress, as manifested by at least two of the following, occurring\nwithin a 12-month period: \n1. Sedatives, hypnotics, or anxiolytics are often taken in larger amounts or over a lon-\nger period than was intended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control sedative,\nhypnotic, or anxiolytic use.\n3. A great deal of time is spent in activities necessary to obtain the sedative, hypnotic,\nor anxiolytic; use the sedative, hypnotic, or anxiolytic; or recover from its effects.", "source": "dsm5.pdf"} {"id": "6dc043c0ca89-1", "page_content": "4. Craving, or a strong desire or urge to use the sedative, hypnotic, or anxiolytic.\n5. Recurrent sedative, hypnotic, or anxiolytic use resulting in a failure to fulfill major\nrole obligations at work, school, or home (e.g., repeated absences from work or\npoor work performance related to sedative, hypnotic, or anxiolytic use; sedative-,\nhypnotic-, or anxiolytic-related absences, suspensions, or expulsions from school;\nneglect of children or household).\n6. Continued sedative, hypnotic, or anxiolytic use despite having persistent or re-\ncurrent social or interpersonal problem s caused or exacerbated by the effects of\nsedatives, hypnotics, or anxiolytics (e.g., arguments with a spouse about conse-\nquences of intoxication; physical fights).\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of sedative, hypnotic, or anxiolytic use.", "source": "dsm5.pdf"} {"id": "dcbe2aaa1870-0", "page_content": "Sedative, Hypnotic, or Anxiolytic Use Disorder 551\n8. Recurrent sedative, hypnotic, or anxiolytic use in situations in which it is physically\nhazardous (e.g., driving an automobile or operating a machine when impaired by\nsedative, hypnotic, or anxiolytic use).\n9. Sedative, hypnotic, or anxiolytic use is continued despite knowledge of having a\npersistent or recurrent physical or psychological problem that is likely to have been\ncaused or exacerbated by the sedative, hypnotic, or anxiolytic.\n10. Tolerance, as defined by either of the following: \na. A need for markedly increased amounts of the sedative, hypnotic, or anxiolytic\nto achieve intoxication or desired effect.\nb. A markedly diminished effect with continued use of the same amount of the sed-\native, hypnotic, or anxiolytic.\nNote: This criterion is not considered to be met for individuals taking sedatives,\nhypnotics, or anxiolytics under medical supervision.\n11. Withdrawal, as manifested by either of the following:\na. The characteristic withdrawal syndrome for sedatives, hypnotics, or anxiolytics\n(refer to Criteria A and B of the criteria set for sedative, hypnotic, or anxiolytic\nwithdrawal, pp. 557\u2013558).\nb. Sedatives, hypnotics, or anxiolytics (or a closely related substance, such as al-\ncohol) are taken to relieve or avoid withdrawal symptoms.\nNote: This criterion is not considered to be met for individuals taking sedatives,\nhypnotics, or anxiolytics under medical supervision.\nSpecify if:", "source": "dsm5.pdf"} {"id": "dcbe2aaa1870-1", "page_content": "hypnotics, or anxiolytics under medical supervision.\nSpecify if:\nIn early remission: After full criteria for sedative, hypnotic, or anxiolytic use disorder\nwere previously met, none of the criteria for sedative, hypnotic, or anxiolytic use disor-\nder have been met for at least 3 months but for less than 12 months (with the exception\nthat Criterion A4, \u201cCraving, or a strong desire or urge to use the sedative, hypnotic, or\nanxiolytic,\u201d may be met).\nIn sustained remission: After full criteria for sedative, hypnotic, or anxiolytic use dis-\norder were previously met, none of the criteria for sedative, hypnotic, or anxiolytic use\ndisorder have been met at any time during a period of 12 months or longer (with the\nexception that Criterion A4, \u201cCraving, or a strong desire or urge to use the sedative,\nhypnotic, or anxiolytic,\u201d may be met).\nSpecify if:\nIn a controlle d environment: This additional specifier is used if the individual is in an\nenvironment where access to sedatives, hypnotics, or anxiolytics is restricted.\nCoding based on current severity: Note for ICD-10-CM codes: If a sedative, hypnotic, or\nanxiolytic intoxication; sedative, hypnotic, or anxiolytic withdrawal; or another sedative-,\nhypnotic-, or anxiolytic-induced mental disor der is also present, do not use the codes be-\nlow for sedative, hypnotic, or anxiolytic use disorder. Instead the comorbid sedative, hyp-", "source": "dsm5.pdf"} {"id": "dcbe2aaa1870-2", "page_content": "notic, or anxiolytic use disorder is indicated in the 4th character of the sedative-, hypnotic-,\nor anxiolytic-induced disorder (see the coding no te for sedative, hypnotic, or anxiolytic in-\ntoxication; sedative, hypnotic, or anxiolytic withdrawal; or specific sedative-, hypnotic-, or\nanxiolytic-induced mental disorder). For example, if there is comorbid sedative-, hypnotic-,\nor anxiolytic-induced depressive disorder and sedative, hypnotic, or anxiolytic use disor-\nder, only the sedative-, hypnotic-, or anxiolyti c-induced depressive disorder code is given\nwith the 4th character indicating whether the comorbid sedative, hypnotic, or anxiolytic use\ndisorder is mild, moderate, or severe: F13.14 for mild sedative, hypnotic, or anxiolytic use\ndisorder with sedative-, hypnotic-, or anxiolytic-induced depressive disorder or F13.24 for\na moderate or severe sedative, hypnotic, or anxiolytic use disorder with sedative-, hypnotic-,\nor anxiolytic-induced depressive disorder.", "source": "dsm5.pdf"} {"id": "781530c90e5e-0", "page_content": "552 Substance-Related and Addictive Disorders\nSpecify current severity:\n305.40 (F13.10) Mild: Presence of 2\u20133 symptoms.\n304.10 (F13.20) Moderate: Presence of 4\u20135 symptoms.\n304.10 (F13.20) Severe: Presence of 6 or more symptoms.\nSpecifiers\n\u201cIn a controlled environment\u201d app lies as a further specifier of remission if the individual is\nboth in remission and in a controlled environm ent (i.e., in early remission in a controlled\nenvironment or in sustained remission in a controlled environmen t). Examples of these\nenvironments are closely supe rvised and substanc e-free jails, therapeutic communities,\nand locked hospital units. \nDiagnostic Features\nSedative, hypnotic, or anxiolytic substances include benzodiazepines, benzodiazepine-\nlike drugs (e.g., zolpidem, zaleplon), carb amates (e.g., glutethimide, meprobamate),\nbarbiturates (e.g., secobarbital), and barbitur ate-like hypnotics (e.g ., glutethimide, meth-\naqualone). This class of substances includes all prescription slee ping medications and\nalmost all prescription antianxiety medica tions. Nonbenzodiazep ine antianxiety agents\n(e.g., buspirone, gepirone) are not included in this class because they do not appear to be\nassociated with significant misuse.\nLike alcohol, these agents are brain depressants and can produce similar substance/\nmedication-induced and substa nce use disorders. Sedative, hypnotic, or anxiolytic sub-\nstances are available both by prescription an d illegally. Some individuals who obtain these", "source": "dsm5.pdf"} {"id": "781530c90e5e-1", "page_content": "stances are available both by prescription an d illegally. Some individuals who obtain these\nsubstances by prescription will develop a seda tive, hypnotic, or anxi olytic use disorder,\nwhile others who misuse these substances or use them for intoxicati on will not develop a\nuse disorder. In particular, sedatives, hypnotics, or anxiolytics with rapid onset and/or\nshort to intermediate lengths of action may be taken for intoxicati on purposes, although\nlonger acting substances in this clas s may be taken for intoxication as well.\nCraving (Criterion A4), either while using or during a period of abstinence, is a typical\nfeature of sedative, hypnotic, or anxiolytic use disorder. Misuse of substances from this\nclass may occur on its own or in conjunction with use of other substances. For example, in-\ndividuals may use intoxicating doses of se datives or benzodiaze pines to \u201ccome down\u201d\nfrom cocaine or amphetamines or use high doses of benzodiazepines in combination with\nmethadone to \u201cboost\u201d its effects. \nRepeated absences or poor work performance, school absences, suspensions or expul-\nsions, and neglect of children or household (Criterion A5) may be related to sedative, hyp-\nnotic, or anxiolytic use disorder, as may the continued use of the substances despite\narguments with a spouse abou t consequences of intoxication or despite physical fights\n(Criterion A6). Limiting contact with family or friends, avoiding work or school, or stop-\nping participation in hobbies, sports, or games (Criterion A7) and recurrent sedative,\nhypnotic, or anxiolytic use when driving an automobile or operatin g a machine when im-", "source": "dsm5.pdf"} {"id": "781530c90e5e-2", "page_content": "paired by sedative, hypnotic, or anxiolytic us e (Criterion A8) are also seen in sedative,\nhypnotic, or anxiolytic use disorder.\nVery significant levels of tolerance and wi thdrawal can develop to the sedative, hyp-\nnotic, or anxiolytic. There may be evidence of tolerance and withdrawal in the absence of\na diagnosis of a sedative, hypnotic, or anxiolytic use disorder in an individual who has\nabruptly discontinued use of benzodiazepines that were taken for long periods of time at\nprescribed and therapeutic doses. In these case s, an additional diagnosis of sedative, hyp-\nnotic, or anxiolytic use disorder is made only if other criteria are met. That is, sedative,\nhypnotic, or anxiolytic medications may be prescribed for appropriate medical purposes,\nand depending on the dose regimen, these drugs may then produce tolerance and with-", "source": "dsm5.pdf"} {"id": "5d3c5dac9159-0", "page_content": "Sedative, Hypnotic, or Anxiolytic Use Disorder 553\ndrawal. If these drugs are prescribed or recommended for appropriate medical purposes,\nand if they are used as prescribed, the result ing tolerance or withdrawal does not meet the\ncriteria for diagnosing a substance use disord er. However, it is necessary to determine\nwhether the drugs were appropriately prescribed and used (e.g., falsifying medical symp-\ntoms to obtain the medication; using more medication than prescribed; obtaining the med-\nication from several doctors without info rming them of the others\u2019 involvement). \nGiven the unidimensional nature of the symp toms of sedative, hypnotic, or anxiolytic\nuse disorder, severity is based on the number of criteria endorsed.\nAssociated Features Supporting Diagnosis\nSedative, hypnotic, or anxiolytic use disorder is often associated with other substance use dis-\norders (e.g., alcohol, cannabis, opioid, stimulant use disorders). Sedatives are often used to al-\nleviate the unwanted effects of these other substances. With repeated use of the substance,\ntolerance develops to the sedative effects, an d a progressively higher dose is used. However,\ntolerance to brain stem depressa nt effects develops much more slowly, and as the individual\ntakes more substance to achieve euphoria or other desired effects, there may be a sudden onset\nof respiratory depression and hypotension, which may result in death. Intense or repeated\nsedative, hypnotic, or anxiolytic intoxication may be associated with severe de pression that,\nalthough temporary, can lead to suicide attempt and completed suicide. \nPrevalence\nThe 12-month prevalences of DS M-IV sedative, hypnotic, or an xiolytic use disorder are es-", "source": "dsm5.pdf"} {"id": "5d3c5dac9159-1", "page_content": "timated to be 0.3% among 12- to 17-year-ol ds and 0.2% among adults age 18 years and\nolder. Rates of DSM-IV sedative, hypnotic, or anxiolytic use disorder are slightly greater\namong adult males (0.3%) than among adult fe males, but for 12- to 17-year-olds, the rate\nfor females (0.4%) exceeds that for males (0.2%). The 12-month prevalence of DSM-IV\nsedative, hypnotic, or anxiolytic use disorder decreases as a function of age and is great-\nest among 18- to 29-year-olds (0.5%) and lo west among individuals 65 years and older\n(0.04%).\nTwelve-month prevalence of se dative, hypnotic, or anxiolytic use disorder varies across\nracial/ethnic subgroups of the U.S. population . For 12- to 17-year-olds, rates are greatest\namong whites (0.3%) relative to African Amer icans (0.2%), Hispanics (0.2%), Native Amer-\nicans (0.1%), and Asian Americans and Pacifi c Islanders (0.1%). Among adults, 12-month\nprevalence is greatest amon g Native Americans and Alaska Natives (0.8%), with rates of\napproximately 0.2% among African Americans, whites, and Hispanics and 0.1% among\nAsian Americans and Pacific Islanders.\nDevelopment and Course\nThe usual course of sedative, hypnotic, or anxiolytic use disorder involves individuals in\ntheir teens or 20s who escalate their occasional use of seda tive, hypnotic, or anxiolytic\nagents to the point at which they develop prob lems that meet criteria for a diagnosis. This", "source": "dsm5.pdf"} {"id": "5d3c5dac9159-2", "page_content": "pattern may be especially likely among indi viduals who have other substance use disor-\nders (e.g., alcohol, opioids, stimulants). An in itial pattern of intermit tent use socially (e.g.,\nat parties) can lead to daily use and high leve ls of tolerance. Once this occurs, an increasing\nlevel of interpersonal difficulties, as well as increasingly severe episodes of cognitive dys-\nfunction and physiological wi thdrawal, can be expected.\nThe second and less frequently observed clinical course begins with an individual who\noriginally obtained the medication by prescrip tion from a physician, usually for the treat-\nment of anxiety, insomnia, or somatic complain ts. As either tolerance or a need for higher\ndoses of the medication develops, there is a gr adual increase in the dose and frequency of", "source": "dsm5.pdf"} {"id": "374a746e3997-0", "page_content": "ment of anxiety, insomnia, or somatic complain ts. As either tolerance or a need for higher\ndoses of the medication develops, there is a gr adual increase in the dose and frequency of\nself-administration. The individu al is likely to continue to justify use on the basis of his or\nher original symptoms of anxiety or insomn ia, but substance-seeking behavior becomes", "source": "dsm5.pdf"} {"id": "5ecd762a4c4c-0", "page_content": "554 Substance-Related and Addictive Disorders\nmore prominent, and the individual may seek out multiple physicians to obtain sufficient\nsupplies of the medication. Tolerance can reach high levels, and withdrawal (including\nseizures and withdrawal delirium) may occur. \nAs with many substance use disorders, sedati ve, hypnotic, or anxiol ytic use disorder gen-\nerally has an onset during adolescence or early adult life. There is an increased risk for misuse\nand problems from many psychoactive substances as individuals age. In particular, cognitive\nimpairment increases as a side effect with ag e, and the metabolism of sedatives, hypnotics, or\nanxiolytics decreases with age among older indi viduals. Both acute and chronic toxic effects\nof these substances, especially effects on co gnition, memory, and motor coordination, are\nlikely to increase with age as a consequence of pharmacodynamic and pharmacokinetic age-\nrelated changes. Individuals with major neuroc ognitive disorder (dementia) are more likely\nto develop intoxication and impaired phy siological functioning at lower doses.\nDeliberate intoxication to achieve a \u201chigh\u201d is most likely to be observed in teenagers\nand individuals in their 20s. Problems associate d with sedatives, hypnotics, or anxiolytics\nare also seen in individuals in their 40s and older who escalate the dose of prescribed med-\nications. In older individuals, intoxicati on can resemble a progressive dementia.\nRisk and Prognostic Factors \nTemperamental. Impulsivity and novelty seeking are in dividual temperaments that re-\nlate to the propensity to develop a substanc e use disorder but may themselves be geneti-\ncally determined. \nEnvironmental. Since sedatives, hypnotics, or anxiolytics are all pharmaceuticals, a key", "source": "dsm5.pdf"} {"id": "5ecd762a4c4c-1", "page_content": "risk factor relates to availability of the substances. In the United States, the historical pat-\nterns of sedative, hypn otic, or anxiolytic misuse relate to the broad prescribing patterns.\nFor instance, a marked decrease in prescription of barbiturates was associated with an in-\ncrease in benzodiazepine pres cribing. Peer factors may rela te to genetic predisposition in\nterms of how individuals select their environment. Other individuals at heightened risk\nmight include those with alcohol use disorder who may receive repeated prescriptions in\nresponse to their complaints of al cohol-related anxiety or insomnia.\nGenetic and physiological. As for other substance use diso rders, the risk for sedative,\nhypnotic, or anxiolytic use disorder can be re lated to individual, family, peer, social, and\nenvironmental factors. Within these domains, genetic factors play a particularly important\nrole both directly and indirectly. Overall, ac ross development, genetic factors seem to play\na larger role in the onset of sedative, hypnotic, or anxiolytic use disorder as individuals age\nthrough puberty into adult life. \nCourse modifiers. Early onset of use is associated with greater likelihood for develop-\ning a sedative, hypnotic, or anxiolytic use disorder.\nCulture-Related Diagnostic Issues\nThere are marked variations in prescription patt erns (and availability) of this class of sub-\nstances in different countries, which may lead to variations in prevalence of sedative, hyp-\nnotic, or anxiolytic use disorders.\nGender-Related Diagnostic Issues\nFemales may be at higher risk than males for prescription drug mi suse of sedative, hyp-\nnotic, or anxiolytic substances.\nDiagnostic Markers", "source": "dsm5.pdf"} {"id": "5ecd762a4c4c-2", "page_content": "notic, or anxiolytic substances.\nDiagnostic Markers\nAlmost all sedative, hypnotic, or anxiolytic substances can be identified through labora-\ntory evaluations of urine or blood (the latter of which can quantify the amounts of these", "source": "dsm5.pdf"} {"id": "2b048318a8a9-0", "page_content": "Sedative, Hypnotic, or Anxiolytic Use Disorder 555\nagents in the body). Urine tests are likely to remain positive for up to approximately 1 week\nafter the use of long-acting substa nces, such as diazepam or flurazepam.\nFunctional Consequences of \nSedative, Hypnotic, or Anxiolytic Use Disorder\nThe social and interpersonal co nsequences of sedative, hypnot ic, or anxiolytic use disorder\nmimic those of alcohol in terms of the potentia l for disinhibited behavior. Accidents, interper-\nsonal difficulties (such as argume nts or fights), and interference with work or school perfor-\nmance are all common outcomes. Physical examinat ion is likely to reveal evidence of a mild\ndecrease in most aspects of autonomic nervous system functioning, including a slower pulse,\na slightly decreased respiratory rate, and a slight drop in blood pressure (most likely to occur\nwith postural changes). At high doses, sedative, hypnotic, or an xiolytic substances can be le-\nthal, particularly when mixed with alcohol, al though the lethal dosage varies considerably\namong the specific substances. Overdoses may be associated with a deterioration in vital signs\nthat signals an impending medical emergency (e .g., respiratory arrest from barbiturates).\nThere may be consequences of trauma (e.g., internal bleeding or a subdural hematoma) from\naccidents that occur while intoxicated. Intraven ous use of these substances can result in med-\nical complications related to the use of contaminated needles (e.g., hepatitis and HIV). \nAcute intoxication can result in accidental injuries and automobile accidents. For elderly\nindividuals, even short-term use of these sedati ng medications at prescr ibed doses can be as-", "source": "dsm5.pdf"} {"id": "2b048318a8a9-1", "page_content": "sociated with an increased risk for cognitive problems and falls. The disinhibiting effects of\nthese agents, like alcohol, may potentially cont ribute to overly aggressive behavior, with sub-\nsequent interpersonal and legal problems. Accide ntal or deliberate overdoses, similar to those\nobserved for alcohol use disorder or repeated alcohol intoxication, can occur. In contrast to\ntheir wide margin of safety when used alone, benzodiazepines taken in combination with al-\ncohol can be particularly dangerous, and accidental overdoses are reported commonly. Acci-\ndental overdoses have also been reported in individuals who deliberately misuse barbiturates\nand other nonbenzodiazepine sedatives (e.g., me thaqualone), but since these agents are much\nless available than the benzodiazepines, the freq uency of overdosing is low in most settings.\nDifferential Diagnosis\nOther mental disorders or medical conditions. Individuals with se dative-, hypnotic-,\nor anxiolytic-induced disorders may present with symptoms (e.g., anxiety) that resemble\nprimary mental disorders (e.g., generalized an xiety disorder vs. sedative-, hypnotic-, or\nanxiolytic-induced anxiety disorder, with on set during withdrawal). The slurred speech,\nincoordination, and other associa ted features characteristic of sedative, hypnotic, or anx-\niolytic intoxication could be the result of an other medical condition (e .g., multiple sclero-\nsis) or of a prior head trauma (e.g., a subdural hematoma).\nAlcohol use disorder. Sedative, hypnotic, or anxiolytic use disorder must be differenti-\nated from alcohol use disorder.\nClinically appropriate use of sedative, hypnotic, or anxiolytic medications. Individuals", "source": "dsm5.pdf"} {"id": "2b048318a8a9-2", "page_content": "Clinically appropriate use of sedative, hypnotic, or anxiolytic medications. Individuals\nmay continue to take benzodiazepine medication according to a physician\u2019s direction for a\nlegitimate medical indication over extended pe riods of time. Even if physiological signs of\ntolerance or withdrawal are manifested, many of these individuals do not develop symp-\ntoms that meet the criteria for sedative, hypnotic, or anxiolytic use disorder because they\nare not preoccupied with obtaining the substanc e and its use does not interfere with their\nperformance of usual social or occupational roles.\nComorbidity\nNonmedical use of sedative, hypnotic, or anxi olytic agents is associated with alcohol use", "source": "dsm5.pdf"} {"id": "5fdd81aef979-0", "page_content": "performance of usual social or occupational roles.\nComorbidity\nNonmedical use of sedative, hypnotic, or anxi olytic agents is associated with alcohol use\ndisorder, tobacco use disorder, and, generally, illicit drug use. There may also be an over-", "source": "dsm5.pdf"} {"id": "456d5af61c8f-0", "page_content": "556 Substance-Related and Addictive Disorders\nlap between sedative, hypnotic, or anxiolytic use disorder an d antisocial personality dis-\norder; depressive, bipolar, and anxiety disorders; and other substance use disorders, such\nas alcohol use disorder and illicit drug use disorders. Antisocial behavior and antisocial\npersonality disorder are especially associated with sedative, hypnotic, or anxiolytic use\ndisorder when the substances are obtained illegally.\nSedative, Hypnotic, or Anxiolytic Intoxication\nDiagnostic Criteria\nA. Recent use of a sedative, hypnotic, or anxiolytic.\nB. Clinically significant maladaptive behavioral or psychological changes (e.g., inappro-\npriate sexual or aggressive behavior, m ood lability, impaired judgment) that developed\nduring, or shortly after, sedative, hypnotic, or anxiolytic use. \nC. One (or more) of the following signs or symptoms developing during, or shortly after,\nsedative, hypnotic, or anxiolytic use: \n1. Slurred speech.\n2. Incoordination.\n3. Unsteady gait.\n4. Nystagmus.\n5. Impairment in cognition (e.g., attention, memory).\n6. Stupor or coma.\nD. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication with another sub-\nstance.\nCoding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether\nthere is a comorbid sedative, hypnotic, or anxiolytic use disorder. If a mild sedative, hyp-", "source": "dsm5.pdf"} {"id": "456d5af61c8f-1", "page_content": "notic, or anxiolytic use disorder is comorbid, the ICD-10-CM code is F13.129, and if a mod-\nerate or severe sedative, hypnotic, or anxio lytic use disorder is comorbid, the ICD-10-CM\ncode is F13.229. If there is no comorbid sedative, hypnotic, or anxiolytic use disorder, then\nthe ICD-10-CM code is F13.929.\nNote: For information on Developm ent and Course; Risk and Prognostic Factors; Culture-\nRelated Diagnostic Issues; Diagnostic Marker s; Functional Consequences of Sedative,\nHypnotic, or Anxiolytic Intoxication; and Co morbidity, see the corre sponding sections in\nsedative, hypnotic, or anxiolytic use disorder.\nDiagnostic Features\nThe essential feature of sedative, hypnotic, or anxiolytic intoxication is the presence of clini-\ncally significant maladaptive behavioral or ps ychological changes (e.g ., inappropriate sexual\nor aggressive behavior, mood lability, impair ed judgment, impaired social or occupational\nfunctioning) that develo p during, or shortly after, use of a sedative, hypnotic, or anxiolytic\n(Criteria A and B). As with other brain depressants, such as alcohol, these behaviors may be ac-\ncompanied by slurred speech, incoordination (at le vels that can interfere with driving abilities\nand with performing usual activities to the poin t of causing falls or automobile accidents), an\nunsteady gait, nystagmus, impairment in cogn ition (e.g., attentional or memory problems),", "source": "dsm5.pdf"} {"id": "456d5af61c8f-2", "page_content": "and stupor or coma (Criterion C). Memory impa irment is a prominent feature of sedative, hyp-\nnotic, or anxiolytic intoxication and is most often characterized by an anterograde amnesia that\nresembles \u201calcoholic blackouts,\u201d which can be disturbing to the individual. The symptoms\nmust not be attributable to another medical co ndition and are not better explained by another", "source": "dsm5.pdf"} {"id": "f5cc83286908-0", "page_content": "Sedative, Hypnotic, or Anxiolytic Withdrawal 557\nmental disorder (Criterion D). Intoxication ma y occur in individuals who are receiving these\nsubstances by prescription, are borrowing the medi cation from friends or relatives, or are de-\nliberately taking the substance to achieve intoxication.\nAssociated Features Supporting Diagnosis\nAssociated features include taking more medi cation than prescribed, taking multiple dif-\nferent medications, or mixing sedative, hypnotic, or anxiolytic agents with alcohol, which\ncan markedly increase the effects of these agents. \nPrevalence\nThe prevalence of sedative, hypnotic, or anxi olytic intoxication in the general population\nis unclear. However, it is probable that most nonmedical users of sedatives, hypnotics, or\nanxiolytics would at some time have signs or symptoms that meet criteria for sedative,\nhypnotic, or anxiolytic intoxication; if so, then the prevalence of nonmedical sedative,\nhypnotic, or anxiolytic use in the general po pulation may be simila r to the prevalence of\nsedative, hypnotic, or anxiolytic intoxicati on. For example, tranquilizers are used non-\nmedically by 2.2% of Amer icans older than 12 years. \nDifferential Diagnosis\nAlcohol use disorders. Since the clinical presentations may be identical, distinguishing sed-\native, hypnotic, or anxiolytic intoxication from alcohol use disorders requires evidence for re-\ncent ingestion of sedative, hypnot ic, or anxiolytic medications by self-report, informant report,\nor toxicological testing. Many individuals who misuse sedatives, hypnotics, or anxiolytics may", "source": "dsm5.pdf"} {"id": "f5cc83286908-1", "page_content": "also misuse alcohol and other su bstances, and so multiple intoxi cation diagnoses are possible. \nAlcohol intoxication. Alcohol intoxication may be distin guished from sedative, hypnotic,\nor anxiolytic intoxication by the smell of al cohol on the breath. Otherwise, the features of\nthe two disorders may be similar.\nOther sedative-, hypnotic-, or anxiolytic-induced disorders. Sedative, hypnotic, or anx-\niolytic intoxication is distin guished from the other sedative-, hypnotic-, or anxiolytic-\ninduced disorders (e.g., sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with\nonset during withdrawal) because the sympto ms in the latter disorders predominate in\nthe clinical presentation and are severe enough to warrant clinical attention.\nNeurocognitive disorders. In situations of cognitive im pairment, traumatic brain in-\njury, and delirium from other causes, sedative s, hypnotics, or anxiolytics may be intoxi-\ncating at quite low dosages. The differential diagnosis in these complex settings is based\non the predominant syndrome. An additional diagnosis of sedative, hypnotic, or anxio-\nlytic intoxication may be appropriate even if the substance has been ingested at a low dos-\nage in the setting of these other (o r similar) co-occu rring conditions. \nSedative, Hypnotic, or Anxiolytic Withdrawal\nDiagnostic Criteria\nA. Cessation of (or reduction in) sedative, hypnotic, or anxiolytic use that has been pro-\nlonged. \nB. Two (or more) of the following, developing within several hours to a few days after the ces-", "source": "dsm5.pdf"} {"id": "f5cc83286908-2", "page_content": "sation of (or reduction in) sedative, hypnotic, or anxiolytic use described in Criterion A: \n1. Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100 bpm).\n2. Hand tremor.", "source": "dsm5.pdf"} {"id": "632aa0fdeec7-0", "page_content": "558 Substance-Related and Addictive Disorders\n3. Insomnia.\n4. Nausea or vomiting.\n5. Transient visual, tactile, or auditory hallucinations or illusions.\n6. Psychomotor agitation.\n7. Anxiety.\n8. Grand mal seizures.\nC. The signs or symptoms in Criterion B cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning. \nD. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication or withdrawal from\nanother substance.\nSpecify if:\nWith perceptual disturbances: This specifier may be noted when hallucinations with in-\ntact reality testing or auditory, visual, or tactile illusions occur in the absence of a delirium.\nCoding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for sedative, hypnotic,\nor anxiolytic withdrawal depends on whether or not there is a comorbid moderate or se-\nvere sedative, hypnotic, or anxiolytic use di sorder and whether or not there are perceptual\ndisturbances. For sedative, hypnotic, or anxiolytic withdrawal without perceptual distur-\nbances, the ICD-10-CM code is F13.239. For sedative, hypnotic, or anxiolytic withdrawal\nwith perceptual disturbances, the ICD-10-CM code is F13.232. Note that the ICD-10-CM\ncodes indicate the comorbid presence of a moderate or severe sedative, hypnotic, or anx-\niolytic use disorder, reflecting the fact that sedative, hypnotic, or anxiolytic withdrawal can", "source": "dsm5.pdf"} {"id": "632aa0fdeec7-1", "page_content": "only occur in the presence of a moderate or severe sedative, hypnotic, or anxiolytic use\ndisorder. It is not permissible to code a comorbid mild sedative, hypnotic, or anxiolytic use\ndisorder with sedative, hypnotic, or anxiolytic withdrawal.\nNote: For information on Developm ent and Course; Risk and Prognostic Factors; Culture-\nRelated Diagnostic Issues; Functional Conseq uences of Sedative, Hypnotic, or Anxiolytic\nWithdrawal; and Comorbidity, see the corresp onding sections in sedative, hypnotic, or\nanxiolytic use disorder.\nDiagnostic Features\nThe essential feature of sedative, hypnotic, or anxiolytic withdrawal is the presence of a char-\nacteristic syndrome that develops after a marked decrease in or cessation of intake after several\nweeks or more of regular use (C riteria A and B). This withdrawal syndrome is characterized by\ntwo or more symptoms (similar to alcohol with drawal) that include au tonomic hyperactivity\n(e.g., increases in heart rate, respiratory rate, blood pressure, or body temperature, along with\nsweating); a tremor of the hands; insomnia ; nausea, sometimes accompanied by vomiting;\nanxiety; and psychomotor agitation. A grand mal seizure may occur in perhaps as many as\n20%\u201330% of individuals undergoing untreated withdrawal from these substances. In severe\nwithdrawal, visual, tactile, or auditory hallucinations or illus ions can occur but are usually in\nthe context of a delirium. If the individual\u2019s rea lity testing is intact (i.e., he or she knows the\nsubstance is causing the hallucinations) and the illusions occur in a clear sensorium, the spec-", "source": "dsm5.pdf"} {"id": "632aa0fdeec7-2", "page_content": "ifier \u201cwith perceptual disturbances\u201d can be note d. When hallucinations occur in the absence of\nintact reality testing, a diagnosis of substanc e/medication-induced ps ychotic disorder should\nbe considered. The symptoms cause clinically si gnificant distress or impairment in social, oc-\ncupational, or other important areas of functioning (Criterion C). The symptoms must not be\nattributable to anothe r medical condition and are not bette r explained by an other mental dis-\norder (e.g., alcohol withdrawal or generalized anxiety disorder) (Criterion D). Relief of with-\ndrawal symptoms with admini stration of any sedative-hypnotic agent would support a\ndiagnosis of sedative, hypnotic, or anxiolytic withdrawal.", "source": "dsm5.pdf"} {"id": "441bcce87705-0", "page_content": "Sedative, Hypnotic, or Anxiolytic Withdrawal 559\nAssociated Features Supporting Diagnosis\nThe timing and severity of the withdrawal sy ndrome will differ depending on the specific\nsubstance and its pharmacokinetics and ph armacodynamics. For example, withdrawal\nfrom shorter-acting substances that are rapidl y absorbed and that have no active metabo-\nlites (e.g., triazolam) can begi n within hours after the subs tance is stopped; withdrawal\nfrom substances with long-acting metabolites (e.g., diazepam) may not begin for 1\u20132 days\nor longer. The withdrawal syndrome produced by substances in this class may be charac-\nterized by the development of a delirium that can be life-threatening. There may be evi-\ndence of tolerance and withdr awal in the absence of a diagnosis of a substance use\ndisorder in an individual who has abruptly discontinued benzodiazepines that were taken\nfor long periods of time at prescribed and therapeutic doses. Howe ver, ICD-10-CM codes\nonly allow a diagnosis of seda tive, hypnotic, or anxiolytic withdrawal in the presence of\ncomorbid moderate to severe sedative, hypnotic, or anxiolytic use disorder.\nThe time course of the withdr awal syndrome is generally predicted by the half-life of\nthe substance. Medications whose actions typica lly last about 10\u00a0hours or less (e.g., loraz-\nepam, oxazepam, temazepam) produce withdr awal symptoms within 6\u20138 hours of de-\ncreasing blood levels that peak in intensity on the second day and improve markedly by\nthe fourth or fifth day. For substances with longer half-lives (e .g., diazepam), symptoms", "source": "dsm5.pdf"} {"id": "441bcce87705-1", "page_content": "may not develop for more than 1 week, peak in intensity during the second week, and de-\ncrease markedly during the third or fourth week. There may be additional longer-term\nsymptoms at a much lower level of inte nsity that persist for several months.\nThe longer the substance has been taken and the higher the dosages used, the more likely\nit is that there will be severe withdrawal. However, withdrawal has been reported with as little\nas 15 mg of diazepam (or its eq uivalent in other benzodiazepines) when taken daily for several\nmonths. Doses of approximately 40 mg of diazepa m (or its equivalent) daily are more likely to\nproduce clinically relevant withdrawal symptoms, and even higher doses (e.g., 100 mg of di-\nazepam) are more likely to be followed by withdrawal seizures or delirium. Sedative, hyp-\nnotic, or anxiolytic withdrawal delirium is ch aracterized by disturbances in consciousness and\ncognition, with visual, tactile, or auditory ha llucinations. When present, sedative, hypnotic, or\nanxiolytic withdrawal delirium should be diagnosed instead of withdrawal.\nPrevalence \nThe prevalence of sedative, hypnotic, or anxiolytic withdrawal is unclear. \nDiagnostic Markers\nSeizures and autonomic instability in the setting of a history of prolonged exposure to sed-\native, hypnotic, or anxiolytic medications su ggest a high likelihood of sedative, hypnotic,\nor anxiolytic withdrawal. \nDifferential Diagnosis\nOther medical disorders. The symptoms of sedative, hypnotic, or anxiolytic with-\ndrawal may be mimicked by other medical cond itions (e.g., hypoglyc emia, diabetic keto-", "source": "dsm5.pdf"} {"id": "441bcce87705-2", "page_content": "acidosis). If seizures are a feature of the seda tive, hypnotic, or anxi olytic withdrawal, the\ndifferential diagnosis includes the various causes of seizures (e.g., infections, head injury,\npoisonings). \nEssential tremor. Essential tremor, a disorder that frequently runs in families, may\nerroneously suggest the tremulousness associat ed with sedative, hypnotic, or anxiolytic\nwithdrawal. \nAlcohol withdrawal. Alcohol withdrawal produces a sy ndrome very similar to that of\nsedative, hypnotic, or anxiolytic withdrawal.", "source": "dsm5.pdf"} {"id": "65504de9d269-0", "page_content": "560 Substance-Related and Addictive Disorders\nOther sedative-, hypnotic-, or anxiolytic-induced disorders. Sedative, hypnotic, or anx-\niolytic withdrawal is distingu ished from the other sedative-, hypnotic-, or anxiolytic-\ninduced disorders (e.g., sedative-, hypnotic-, or anxiolytic-induced anxiety disorder, with\nonset during withdrawal) beca use the symptoms in the latter disorders predominate in\nthe clinical presentation and are severe enough to warrant clinical attention.\nAnxiety disorders. Recurrence or worsening of an underlying anxiety disorder pro-\nduces a syndrome similar to sedative, hypnotic, or anxiolytic withdrawal. Withdrawal\nwould be suspected with an abrupt reduction in the dosage of a sedative, hypnotic, or anx-\niolytic medication. When a taper is under wa y, distinguishing the withdrawal syndrome\nfrom the underlying anxiety disorder can be difficult. As with alco hol, lingering with-\ndrawal symptoms (e.g., anxiety, moodiness, and trouble sleeping) can be mistaken for\nnon-substance/medication-induc ed anxiety or depr essive disorders (e.g., generalized\nanxiety disorder).\nOther Sedative-, Hypnotic-, \nor Anxiolytic-Induced Disorders\nThe following sedative-, hypnotic-, or anxiolyt ic-induced disorders are described in other\nchapters of the manual with disorders with which they share phenomenology (see the sub-\nstance/medication-induced mental disorders in these chapters): sedative-, hypnotic-, or\nanxiolytic-induced psychotic disorder (\u201cSchizophrenia Spectrum and Other Psychotic\nDisorders\u201d); sedative-, hypnotic-, or anxiolytic -induced bipolar disord er (\u201cBipolar and Re-", "source": "dsm5.pdf"} {"id": "65504de9d269-1", "page_content": "lated Disorders\u201d); sedative-, hypnotic-, or anxiolytic-induced depressive disorder (\u201cDe-\npressive Disorders\u201d); sedative-, hypnotic-, or anxiolytic-induced anxiety disorder\n(\u201cAnxiety Disorders\u201d); sedative-, hypnotic-, or anxiolytic-induced sleep disorder (\u201cSleep-\nWake Disorders\u201d); sedative-, hypnotic-, or anxiolytic-induc ed sexual dysfunction (\u201cSex-\nual Dysfunctions\u201d); and sedative-, hypnotic-, or anxiolytic-induced major or mild neuro-\ncognitive disorder (\u201cNeurocog nitive Disorders\u201d). For seda tive, hypnotic, or anxiolytic\nintoxication delirium and sedative, hypnotic, or anxiolytic withdrawal delirium, see the\ncriteria and discussion of delirium in the chapter \u201cNeurocognitive Disorders.\u201d These sed-\native-, hypnotic-, or anxiolytic-induced disorders are diagnosed inst ead of sedative, hyp-\nnotic, or anxiolytic intoxication or sedative, hypnotic, or anxiolytic withdrawal only when\nthe symptoms are sufficiently severe to warrant independent clinical attention.\nUnspecified Sedative-, Hypnotic-,\nor Anxiolytic-Related Disorder\n292.9 (F13.99)\nThis category applies to presentations in which symptoms characteristic of a sedative-,\nhypnotic-, or anxiolytic-related disorder that cause clinically significant distress or impair-\nment in social, occupational, or other impor tant areas of functioning predominate but do\nnot meet the full criteria for any specific s edative-, hypnotic-, or anxiolytic-related disorder\nor any of the disorders in the substance-related and addictive disorders diagnostic class.", "source": "dsm5.pdf"} {"id": "87fcca424143-0", "page_content": "Stimulant Use Disorder 561\nStimulant-Related Disorders\nStimulant Use Disorder\nStimulant Intoxication\nStimulant Withdrawal\nOther Stimulant-Induced Disorders\nUnspecified Stimulant-Related Disorder\nStimulant Use Disorder\nDiagnostic Criteria \nA. A pattern of amphetamine-type substance, cocaine, or other stimulant use leading to\nclinically significant impairment or distress, as manifested by at least two of the follow-\ning, occurring within a 12-month period:\n1. The stimulant is often taken in larger amounts or over a longer period than was in-\ntended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control stimulant use.\n3. A great deal of time is spent in activities necessary to obtain the stimulant, use the\nstimulant, or recover from its effects.\n4. Craving, or a strong desire or urge to use the stimulant.\n5. Recurrent stimulant use resulting in a failure to fulfill major role obligations at work,\nschool, or home.\n6. Continued stimulant use despite having persi stent or recurrent social or interper-\nsonal problems caused or exacerbated by the effects of the stimulant.\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of stimulant use.\n8. Recurrent stimulant use in situations in which it is physically hazardous.\n9. Stimulant use is continued despite knowledge of having a persistent or recurrent\nphysical or psychological problem that is likely to have been caused or exacerbated\nby the stimulant.\n10. Tolerance, as defined by either of the following:\na. A need for markedly increased amounts of the stimulant to achieve intoxication\nor desired effect.\nb. A markedly diminished effect with continued use of the same amount of the", "source": "dsm5.pdf"} {"id": "87fcca424143-1", "page_content": "b. A markedly diminished effect with continued use of the same amount of the\nstimulant.\nNote: This criterion is not considered to be met for those taking stimulant medica-\ntions solely under appropriate medical supervision, such as medications for atten-\ntion-deficit/hyperactivity disorder or narcolepsy. \n11. Withdrawal, as manifested by either of the following: \na. The characteristic withdrawal syndrome fo r the stimulant (refer to Criteria A and\nB of the criteria set for stimulant withdrawal, p. 569).\nb. The stimulant (or a closely related substance) is taken to relieve or avoid with-\ndrawal symptoms.", "source": "dsm5.pdf"} {"id": "416e351c1bbf-0", "page_content": "562 Substance-Related and Addictive Disorders\nNote: This criterion is not considered to be met for those taking stimulant medica-\ntions solely under appropriate medical supervision, such as medications for atten-\ntion-deficit/hyperactivity disorder or narcolepsy.\nSpecify if:\nIn early remission: After full criteria for stimulant use disorder were previously met,\nnone of the criteria for stimulant use disorder have been met for at least 3 months but\nfor less than 12 months (with the exception that Criterion A4, \u201cCraving, or a strong de-\nsire or urge to use the stimulant,\u201d may be met).\nIn sustained remission: After full criteria for stimulant use disorder were previously\nmet, none of the criteria for stimulant use disorder have been met at any time during a\nperiod of 12 months or longer (with the exception that Criterion A4, \u201cCraving, or a\nstrong desire or urge to use the stimulant,\u201d may be met).\nSpecify if:\nIn a controlled environment: This additional specifier is used if the individual is in an\nenvironment where access to stimulants is restricted. \nCoding based on current severity: Note for ICD-10-CM codes: If an amphetamine in-\ntoxication, amphetamine withdrawal, or anot her amphetamine-induced mental disorder is\nalso present, do not use the codes below for amphetamine use disorder. Instead, the co-\nmorbid amphetamine use disorder is indicat ed in the 4th character of the amphetamine-\ninduced disorder code (see the coding note for amphetamine intoxication, amphetamine\nwithdrawal, or a specific amphetamine-induced m ental disorder). For example, if there is\ncomorbid amphetamine-type or other stimulant-induced depressive disorder and amphet-", "source": "dsm5.pdf"} {"id": "416e351c1bbf-1", "page_content": "comorbid amphetamine-type or other stimulant-induced depressive disorder and amphet-\namine-type or other stimulant use disorder, only the amphetamine-type or other stimulant-\ninduced depressive disorder code is given, with the 4th character indicating whether the\ncomorbid amphetamine-type or other stimulant use disorder is mild, moderate, or severe:\nF15.14 for mild amphetamine-type or other st imulant use disorder with amphetamine-type\nor other stimulant-induced depressive disorder or F15.24 for a moderate or severe am-\nphetamine-type or other stimulant use disorder with amphetamine-type or other stimulant-\ninduced depressive disorder. Similarly, if there is comorbid cocaine-induced depressive\ndisorder and cocaine use disorder, only the cocaine-induced depressive disorder code is\ngiven, with the 4th character indicating whether the comorbid cocaine use disorder is mild,\nmoderate, or severe: F14.14 for mild cocaine use disorder with cocaine-induced depressive\ndisorder or F14.24 for a moderate or severe cocaine use disorder with cocaine-induced\ndepressive disorder. \nSpecify current severity:\nMild: Presence of 2\u20133 symptoms.\n305.70 (F15.10) Amphetamine-type substance\n305.60 (F14.10) Cocaine\n305.70 (F15.10) Other or unspecified stimulant\nModerate: Presence of 4\u20135 symptoms.\n304.40 (F15.20) Amphetamine-type substance\n304.20 (F14.20) Cocaine\n304.40 (F15.20) Other or unspecified stimulant\nSevere: Presence of 6 or more symptoms.\n304.40 (F15.20) Amphetamine-type substance\n304.20 (F14.20) Cocaine", "source": "dsm5.pdf"} {"id": "416e351c1bbf-2", "page_content": "304.20 (F14.20) Cocaine\n304.40 (F15.20) Other or unspecified stimulant", "source": "dsm5.pdf"} {"id": "cd991c573a21-0", "page_content": "Stimulant Use Disorder 563\nSpecifiers\n\u201cIn a controlled environment\u201d app lies as a further specifier of remission if the individual is\nboth in remission and in a controlled environm ent (i.e., in early remission in a controlled\nenvironment or in sustained remission in a controlled environment). Examples of these\nenvironments are closely supe rvised and substanc e-free jails, therapeutic communities,\nand locked hospital units. \nDiagnostic Features\nThe amphetamine and amphetamine-type stimul ants include substances with a substi-\ntuted-phenylethylamine struct ure, such as amphetamine, dextroamphetamine, and meth-\namphetamine. Also included are those substanc es that are structura lly different but have\nsimilar effects, such as methylphenidate. These substances are usually taken orally or in-\ntravenously, although methamphetamine is also taken by the nasal route. In addition to\nthe synthetic amphetamine-type compounds, th ere are naturally occurring, plant-derived\nstimulants such as kh\u00e2t. Amphetamines and other stimulants may be obtained by prescrip-\ntion for the treatment of obesity, attention-deficit/hyperactivity disorder, and narcolepsy.\nConsequently, prescribed stimul ants may be diverted into the illegal market. The effects of\namphetamines and amphetamine-like drugs are sim ilar to those of cocaine, such that the\ncriteria for stimulant use disord er are presented here as a sing le disorder with the ability to\nspecify the particular stimulant used by the individual. Cocaine may be consumed in sev-\neral preparations (e.g., coca leaves, coca pa ste, cocaine hydrochloride, and cocaine alka-\nloids such as freebase and crack) that differ in potency because of varying levels of purity", "source": "dsm5.pdf"} {"id": "cd991c573a21-1", "page_content": "and speed of onset. However, in all forms of the substance, cocaine is the active ingredient.\nCocaine hydrochloride powder is usually \u201csnorted\u201d through the nostrils or dissolved in\nwater and injected intravenously.\nIndividuals exposed to amphetamine-type stimulants or cocaine can develop stimu-\nlant use disorder as rapidly as 1 week, although the onset is not always th is rapid. Re-\ngardless of the route of administration, tole rance occurs with repeated use. Withdrawal\nsymptoms, particularly hypersomnia, increa sed appetite, and dysphoria, can occur and\ncan enhance craving. Most individuals with stimulant use disorder have experienced tol-\nerance or withdrawal. \nUse patterns and course are similar for di sorders involving amphetamine-type stimu-\nlants and cocaine, as both substances are po tent central nervous system stimulants with\nsimilar psychoactive and sympathomimetic effects. Amphetamine-type stimulants are\nlonger acting than cocaine and thus are used fewer times per day. Usage may be chronic or\nepisodic, with binges punctuated by brief no n-use periods. Aggressive or violent behavior\nis common when high doses are smoked, ingested, or administered intravenously. Intense\ntemporary anxiety resembling panic disorder or generalized anxiety disorder, as well as\nparanoid ideation and psychotic episodes that resemble schizophrenia, is seen with high-\ndose use.\nWithdrawal states are associated with temporary but intense depressive symptoms that\ncan resemble a major depressive episode; the depressive symptoms usually resolve within\n1 week. Tolerance to amphetamine -type stimulants develops and leads to escalation of the\ndose. Conversely, some users of amphetami ne-type stimulants develop sensitization,\ncharacterized by enhanced effects.\nAssociated Features Supporting Diagnosis", "source": "dsm5.pdf"} {"id": "cd991c573a21-2", "page_content": "characterized by enhanced effects.\nAssociated Features Supporting Diagnosis\nWhen injected or smoked, stimulants typica lly produce an instant feeling of well-being,\nconfidence, and euphoria. Dramatic behavior al changes can rapidly develop with stimu-\nlant use disorder. Chaotic behavior, social is olation, aggressive behavior, and sexual dys-\nfunction can result from long -term stimulant use disorder.", "source": "dsm5.pdf"} {"id": "2255e87c1cc0-0", "page_content": "564 Substance-Related and Addictive Disorders\nIndividuals with acute intoxication may pr esent with rambling speech, headache, tran-\nsient ideas of reference, and tinnitus. There may be paranoid ideati on, auditory halluci-\nnations in a clear sensorium, and tactile hallucinations, which the individual usually\nrecognizes as drug effects. Thre ats or acting out of aggressive behavior may occur. Depres-\nsion, suicidal ideation, irritability, anhedonia, emotional lability, or disturbances in atten-\ntion and concentration commonly occur during withdrawal. Mental disturbances associated\nwith cocaine use usually resolve hours to days after cessation of use but can persist for\n1 month. Physiological changes during stimulant withdrawal ar e opposite to those of the\nintoxication phase, sometimes including bradycardia. Temporary depressive symptoms\nmay meet symptomatic and duration criteria for major depressive episode. Histories con-\nsistent with repeated panic attacks, social an xiety disorder (social phobia)\u2013like behavior,\nand generalized anxiety\u2013like syndromes are co mmon, as are eating disorders. One ex-\ntreme instance of stimulant toxicity is st imulant-induced psychotic disorder, a disorder\nthat resembles schizophrenia, with delusions and hallucinations. \nIndividuals with stimulant use disorder of ten develop conditioned responses to drug-\nrelated stimuli (e.g., craving on seeing an y white powderlike substance). These responses\ncontribute to relapse, are difficult to extinguish, and persist after detoxification.\nDepressive symptoms with su icidal ideation or behavior can occur and are generally\nthe most serious problems seen during stimulant withdrawal.\nPrevalence \nStimulant use disorder: amphetamine-type stimulants. Estimated 12-month prevalence", "source": "dsm5.pdf"} {"id": "2255e87c1cc0-1", "page_content": "Stimulant use disorder: amphetamine-type stimulants. Estimated 12-month prevalence\nof amphetamine-type stimulant use disorder in the United States is 0.2% among 12- to 17-\nyear-olds and 0.2% among individuals 18 year s and older. Rates are similar among adult\nmales and females (0.2%), but among 12- to 17- year-olds, the rate for females (0.3%) is\ngreater than that for males (0.1%). Intravenou s stimulant use has a male-to-female ratio of\n3:1 or 4:1, but rates are more balanced amon g non-injecting users, with males representing\n54% of primary treatment admissions. Twelve -month prevalence is greater among 18- to\n29-year-olds (0.4%) compared with 45- to 64-ye ar-olds (0.1%). For 12- to 17-year-olds, rates\nare highest among whites and African Americans (0.3%) compared with Hispanics (0.1%)\nand Asian Americans and Pacific Islanders (0.01%), with amphetamine-type stimulant use\ndisorder virtually absent among Native Americans. Among adults, rates are highest among\nNative Americans and Alaska Natives (0.6%) compared with whites (0.2%) and Hispanics\n(0.2%), with amphetamine-type stimulant use disorder virtually absent among African\nAmericans and Asian Americans and Pacific Islanders. Past-year nonprescribed use of\nprescription stimulants occu rred among 5%\u20139% of children through high school, with\n5%\u201335% of college-age persons reporting past-year use.\nStimulant use disorder: cocaine. Estimated 12-month prevalence of cocaine use disorder", "source": "dsm5.pdf"} {"id": "2255e87c1cc0-2", "page_content": "Stimulant use disorder: cocaine. Estimated 12-month prevalence of cocaine use disorder\nin the United States is 0.2% among 12- to 17- year-olds and 0.3% amon g individuals 18 years\nand older. Rates are higher among males (0 .4%) than among females (0.1%). Rates are\nhighest among 18- to 29-year-olds (0.6%) and lo west among 45- to 64-year-olds (0.1%). Among\nadults, rates are greater among Native Amer icans (0.8%) compared with African Ameri-\ncans (0.4%), Hispanics (0.3%), whites (0.2%) , and Asian Americans and Pacific Islanders\n(0.1%). In contrast, for 12- to 17-year-olds, rates are similar among Hispanics (0.2%), whites\n(0.2%), and Asian Americans and Pacific Islanders (0.2%); and lower among African Amer-\nicans (0.02%); with cocaine use disorder vi rtually absent among Native Americans and\nAlaska Natives.\nDevelopment and Course\nStimulant use disorders occur throughout all levels of society and are more common among", "source": "dsm5.pdf"} {"id": "d20ea3b23bf6-0", "page_content": "Alaska Natives.\nDevelopment and Course\nStimulant use disorders occur throughout all levels of society and are more common among\nindividuals ages 12\u201325 years compared with indi viduals 26 years and olde r. First regular use", "source": "dsm5.pdf"} {"id": "1e6813e80fe2-0", "page_content": "Stimulant Use Disorder 565\namong individuals in treatment occurs, on average, at approximately age 23 years. For pri-\nmary methamphetamine\u2013primary treatment admissions, the average age is 31 years.\nSome individuals begin stimulant use to control weight or to improve performance in\nschool, work, or athlet ics. This includes obtaining medications such as methylphenidate or\namphetamine salts prescribed to others for the treatment of attention-deficit/hyperac-\ntivity disorder. Stimulant use disorder can develop rapidly with intravenous or smoked\nadministration; among primary admissions fo r amphetamine-type stimulant use, 66% re-\nported smoking, 18% reported inje cting, and 10% reported snorting. \nPatterns of stimulant administration include episodic or daily (or almost daily) use.\nEpisodic use tends to be separated by 2 or more days of non-use (e.g., intense use over a\nweekend or on one or more weekdays). \u201cBin ges\u201d involve continuous high-dose use over\nhours or days and are often associated with physical dependence. Binges usually termi-\nnate only when stimulant supplies are deplet ed or exhaustion ensues. Chronic daily use\nmay involve high or low doses, often with an increase in dose over time.\nStimulant smoking and intravenous use are a ssociated with rapid progression to se-\nvere-level stimulant use disorder, often occu rring over weeks to months. Intranasal use of\ncocaine and oral use of amphetamine-type stim ulants result in more gradual progression\noccurring over months to years. With continui ng use, there is a diminution of pleasurable\neffects due to tolerance and an increase in dysphoric effects. \nRisk and Prognostic Factors", "source": "dsm5.pdf"} {"id": "1e6813e80fe2-1", "page_content": "Risk and Prognostic Factors \nTemperamental. Comorbid bipolar disorder, schizophrenia, antisocial personality disor-\nder, and other substance use disorders are risk factors for developing stimulant use disorder\nand for relapse to cocaine use in treatment samp les. Also, impulsivity and similar personality\ntraits may affect treatment outcomes. Childhood conduct disorder and adult antisocial per-\nsonality disorder are associated with the la ter development of stim ulant-related disorders.\nEnvironmental. Predictors of cocaine use among teenagers include prenatal cocaine ex-\nposure, postnatal cocaine use by parents, and exposure to community violence during\nchildhood. For youths, especially females, risk factors include living in an unstable home\nenvironment, having a psychiatric conditio n, and associating with dealers and users.\nCulture-Related Diagnostic Issues\nStimulant use\u2013attendant disorders affect all ra cial/ethnic, socioeconomic, age, and gender\ngroups. Diagnostic issues may be related to societal consequenc es (e.g., arrest, school sus-\npensions, employment suspension). Despite sm all variations, cocaine and other stimulant\nuse disorder diagnostic criteria perform eq ually across gender and race/ethnicity groups.\nChronic use of cocaine impairs cardiac left ventricular function in African Americans.\nApproximately 66% of individuals admitt ed for primary methamphetamine/amphet-\namine-related disorders are non-Hispanic whit e, followed by 21% of Hispanic origin, 3%\nAsian and Pacific Islander, and 3% non-Hispanic black.\nDiagnostic Markers\nBenzoylecgonine, a metabolite of cocaine, typi cally remains in the urine for 1\u20133 days after\na single dose and may be present for 7\u201312 days in individuals using repeated high doses.", "source": "dsm5.pdf"} {"id": "1e6813e80fe2-2", "page_content": "Mildly elevated liver function tests can be pr esent in cocaine injectors or users with con-\ncomitant alcohol use. There are no neurobiological markers of diagnostic utility. Discon-\ntinuation of chronic cocaine use may be asso ciated with electroencephalographic changes,\nsuggesting persistent abnormalit ies; alterations in secretion patterns of prolactin; and\ndownregulation of dopamine receptors.\nShort-half-life amphetamine-type stim ulants (MDMA [3,4-methylenedioxy- N-methyl-\namphetamine], methamphetamine) can be detected for 1\u20133 days, and possibly up to 4 days", "source": "dsm5.pdf"} {"id": "f6e98fbf0313-0", "page_content": "566 Substance-Related and Addictive Disorders\ndepending on dosage and metabolism. Hair sampl es can be used to detect presence of am-\nphetamine-type stimulants for up to 90 days. Other laboratory findings, as well as physical\nfindings and other medical conditions (e.g., weight loss, malnutrition; poor hygiene), are\nsimilar for both cocaine and amphet amine-type stimulant use disorder.\nFunctional Consequences of Stimulant Use Disorder \nVarious medical conditions may occur dependin g on the route of administration. Intrana-\nsal users often develop sinusitis, irritation, bl eeding of the nasal mucosa, and a perforated\nnasal septum. Individuals who smoke the drugs are at increased risk for respiratory prob-\nlems (e.g., coughing, bronchitis, and pneumonitis). Injectors have puncture marks and\n\u201ctracks,\u201d most commonly on their forearms. Ri sk of HIV infection increases with frequent\nintravenous injections and unsafe sexual acti vity. Other sexually transmitted diseases,\nhepatitis, and tuberculosis and other lung infections are also seen . Weight loss and mal-\nnutrition are common. \nChest pain may be a common symptom during stimulant intoxication. Myocardial in-\nfarction, palpitations and arrhythmias, sudden death from respiratory or cardiac arrest,\nand stroke have been associated with stimulant use among young and otherwise healthy\nindividuals. Seizures can occur with stimulant use. Pneumothorax can result from per-\nforming Valsalva-like maneuvers done to better absorb inhaled smoke. Traumatic injuries\ndue to violent behavior are common among in dividuals trafficking drugs. Cocaine use is\nassociated with irregularities in placental bl ood flow, abruptio placentae, premature labor\nand delivery, and an increased prevalence of infants with very low birth weights.", "source": "dsm5.pdf"} {"id": "f6e98fbf0313-1", "page_content": "and delivery, and an increased prevalence of infants with very low birth weights.\nIndividuals with stimulant use disorder may become involved in theft, prostitution, or\ndrug dealing in order to acquire drugs or money for drugs. \nNeurocognitive impairment is common am ong methamphetamine users. Oral health\nproblems include \u201cmeth mouth\u201d with gum dise ase, tooth decay, and mouth sores related\nto the toxic effects of smoking the drug and to bruxism while intoxicated. Adverse pulmo-\nnary effects appear to be le ss common for amphetamine-type stimulants because they are\nsmoked fewer times per day. Emergency department visits are common for stimulant-re-\nlated mental disorder symptoms, injury, skin infections, and dental pathology. \nDifferential Diagnosis\nPrimary mental disorders. Stimulant-induced disorders may resemble primary mental\ndisorders (e.g., major depressive disorder) (for discussion of th is differential diagnosis, see\n\u201cStimulant Withdrawal\u201d). The mental disturbanc es resulting from the effects of stimulants\nshould be distinguished from the symptoms of schizophrenia; depressive and bipolar dis-\norders; generalized anxiety disorder; and panic disorder.\nPhencyclidine intoxication. Intoxication with phencyclidine (\u201cPCP\u201d or \u201cangel dust\u201d) or\nsynthetic \u201cdesigner drugs\u201d such as mephedrone (known by different names, including\n\u201cbath salts\u201d) may cause a similar clinical pict ure and can only be di stinguished from stim-\nulant intoxication by the presence of coca ine or amphetamine-type substance metabolites\nin a urine or plasma sample. \nStimulant intoxication and withdrawal. Stimulant intoxication and withdrawal are dis-\ntinguished from the other stimulant-induced di sorders (e.g., anxiety disorder, with onset", "source": "dsm5.pdf"} {"id": "f6e98fbf0313-2", "page_content": "during intoxication) because the symptoms in the latter disorders predominate the clinical\npresentation and are severe enough to warrant independent clinical attention.\nComorbidity\nStimulant-related disorders often co-occur wi th other substance use disorders, especially\nthose involving substances with sedative properties, which are often taken to reduce in-", "source": "dsm5.pdf"} {"id": "ec63b2c8876f-0", "page_content": "Stimulant Intoxication 567\nsomnia, nervousness, and other unpleasant side effects. Cocaine users often use alcohol,\nwhile amphetamine-type stimulant users ofte n use cannabis. Stimulant use disorder may\nbe associated with posttraumatic stress diso rder, antisocial personality disorder, atten-\ntion-deficit/hyperacti vity disorder, and gambling di sorder. Cardiopulmonary problems\nare often present in individuals seeking treatm ent for cocaine-related problems, with chest\npain being the most common. Medical problems occur in response to adulterants used as\n\u201ccutting\u201d agents. Cocaine users who ingest co caine cut with levamisole, an antimicrobial\nand veterinary medication, may experience agranulocytosis and febrile neutropenia. \nStimulant Intoxication\nDiagnostic Criteria\nA. Recent use of an amphetamine-type substance, cocaine, or other stimulant.\nB. Clinically significant problematic behavioral or psychological changes (e.g., euphoria\nor affective blunting; changes in sociability; hypervigilance; interpersonal sensitivity;\nanxiety, tension, or anger; stereotyped behaviors; impaired judgment) that developed\nduring, or shortly after, use of a stimulant. \nC. Two (or more) of the following signs or symptoms, developing during, or shortly after,\nstimulant use: \n1. Tachycardia or bradycardia.\n2. Pupillary dilation.\n3. Elevated or lowered blood pressure.\n4. Perspiration or chills.\n5. Nausea or vomiting.\n6. Evidence of weight loss.\n7. Psychomotor agitation or retardation.\n8. Muscular weakness, respiratory depression , chest pain, or cardiac arrhythmias.", "source": "dsm5.pdf"} {"id": "ec63b2c8876f-1", "page_content": "8. Muscular weakness, respiratory depression , chest pain, or cardiac arrhythmias.\n9. Confusion, seizures, dyskinesias, dystonias, or coma.\nD. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication with another sub-\nstance.\nSpecify the specific intoxicant (i.e., amphetamine-type substance, cocaine, or other\nstimulant).\nSpecify if:\nWith perceptual disturbances: This specifier may be noted when hallucinations with\nintact reality testing or auditory, visual, or tactile illusions occur in the absence of a de-\nlirium.\nCoding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether\nthe stimulant is an amphetamine, cocaine, or other stimulant; whether there is a comorbid\namphetamine, cocaine, or other stimulant use disorder; and whether or not there are per-\nceptual disturbances.\nFor amphetamine, cocaine, or other stimulant intoxication, without perceptual dis-\nturbances: If a mild amphetamine or other stimulant use disorder is comorbid, the ICD-\n10-CM code is F15.129, and if a moderate or severe amphetamine or other stimulant use\ndisorder is comorbid, the ICD-10-CM code is F15.229. If there is no comorbid amphet-\namine or other stimulant use disorder, then the ICD-10-CM code is F15.929. Similarly, if\na mild cocaine use disorder is comorbid, the ICD-10-CM code is F14.129, and if a mod-", "source": "dsm5.pdf"} {"id": "ec63b2c8876f-2", "page_content": "erate or severe cocaine use disorder is comorbid, the ICD-10-CM code is F14.229. If\nthere is no comorbid cocaine use disorder, then the ICD-10-CM code is F14.929.", "source": "dsm5.pdf"} {"id": "bbba0afea597-0", "page_content": "568 Substance-Related and Addictive Disorders\nFor amphetamine, cocaine, or other stimulant intoxication, with perceptual distur-\nbances: If a mild amphetamine or other stimulant use disorder is comorbid, the ICD-10-\nCM code is F15.122, and if a moderate or severe amphetamine or other stimulant use\ndisorder is comorbid, the ICD-10-CM code is F15.222. If there is no comorbid amphet-\namine or other stimulant use disorder, then the ICD-10-CM code is F15.922. Similarly, if\na mild cocaine use disorder is comorbid, the ICD-10-CM code is F14.122, and if a mod-\nerate or severe cocaine use disorder is comorbid, the ICD-10-CM code is F14.222. If\nthere is no comorbid cocaine use disorder, then the ICD-10-CM code is F14.922.\nDiagnostic Features\nThe essential feature of stimulant intoxicati on, related to amphetamine-type stimulants\nand cocaine, is the presence of clinically significant behavioral or psychological changes\nthat develop during, or shortly after, use of stimulants (Criteria A and B). Auditory hallu-\ncinations may be prominent, as may paranoid ideation, and these symptoms must be dis-\ntinguished from an independent psychotic disorder such as schizophrenia. Stimulant\nintoxication usually begins with a \u201chigh\u201d f eeling and includes one or more of the follow-\ning: euphoria with enhanced vigor, gregarious ness, hyperactivity, restlessness, hypervig-\nilance, interpersonal sensitivity, talkativenes s, anxiety, tension, alertness, grandiosity,", "source": "dsm5.pdf"} {"id": "bbba0afea597-1", "page_content": "stereotyped and repetitive behavior, anger, impaired judgment, and, in the case of chronic\nintoxication, affective blunting with fatigue or sadness and social withdrawal. These be-\nhavioral and psychological changes are acco mpanied by two or more of the following\nsigns and symptoms that develop during or sh ortly after stimulant us e: tachycardia or bra-\ndycardia; pupillary dilation; el evated or lowered blood pressu re; perspiration or chills;\nnausea or vomiting; evidence of weight loss ; psychomotor agitation or retardation; mus-\ncular weakness, respiratory depression, chest pain, or card iac arrhythmias; and confu-\nsion, seizures, dyskinesias, dystonias, or coma (Criterion C). Intoxi cation, either acute or\nchronic, is often associated with impaired so cial or occupational functioning. Severe in-\ntoxication can lead to convulsions, cardiac arrhythmias, hyperpyrexia, and death. For the\ndiagnosis of stimulant intoxica tion to be made, the symptoms must not be attributable\nto another medical condition and not better explained by anot her mental disorder (Crite-\nrion D). While stimulant intoxica tion occurs in individuals with stimulant use disorders, in-\ntoxication is not a criterion for stimulant us e disorder, which is confirmed by the presence\nof two of the 11 diagnostic criteria for use disorder. \nAssociated Features Supporting Diagnosis\nThe magnitude and direction of the behavioral and physiological changes depend on many\nvariables, including the dose used and the ch aracteristics of the individual using the sub-\nstance or the context (e.g., tolerance, rate of absorption, chronicity of use, context in which", "source": "dsm5.pdf"} {"id": "bbba0afea597-2", "page_content": "it is taken). Stimulant effects such as eupho ria, increased pulse an d blood pressure, and\npsychomotor activity are most commonly seen . Depressant effects such as sadness, brady-\ncardia, decreased blood pressure, and decr eased psychomotor activity are less common\nand generally emerge only wi th chronic high-dose use. \nDifferential Diagnosis\nStimulant-induced disorders. Stimulant intoxication is distinguished from the other\nstimulant-induced disorders (e.g., stimulant- induced depressive di sorder, bipolar disor-\nder, psychotic disorder, anxiety disorder) because the severity of the intoxication symp-\ntoms exceeds that associated with the stim ulant-induced disorders, and the symptoms\nwarrant independent clinical attention. Stimulant intoxication delirium would be distin-\nguished by a disturbance in level of awareness and change in cognition.", "source": "dsm5.pdf"} {"id": "5ef83f118f9e-0", "page_content": "Stimulant Withdrawal 569\nOther mental disorders. Salient mental disturbances associated with stimulant intoxi-\ncation should be distinguished from the symptoms of schizophrenia, paranoid type; bi-\npolar and depressive disorders; generalized anxiety disorder; and panic disorder as\ndescribed in DSM-5.\nStimulant Withdrawal\nDiagnostic Criteria\nA. Cessation of (or reduction in) prolonged amphetamine-type substance, cocaine, or\nother stimulant use.\nB. Dysphoric mood and two (or more) of the following physiological changes, developing\nwithin a few hours to several days after Criterion A:\n1. Fatigue. \n2. Vivid, unpleasant dreams.\n3. Insomnia or hypersomnia.\n4. Increased appetite.\n5. Psychomotor retardation or agitation.\nC. The signs or symptoms in Criterion B cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning. \nD. The signs or symptoms are not attributable to another medical condition and are not\nbetter explained by another mental disorder, including intoxication or withdrawal from\nanother substance.\nSpecify the specific substance that causes the withdrawal syndrome (i.e., amphet-\namine-type substance, cocaine, or other stimulant).\nCoding note: The ICD-9-CM code is 292.0. The ICD-10-CM code depends on whether\nthe stimulant is an amphetamine, cocaine, or other stimulant. The ICD-10-CM code for\namphetamine or an other stimulant withdrawal is F15.23, and the ICD-10-CM for cocaine\nwithdrawal is F14.23. Note that the ICD-10-CM code indicates the comorbid presence of\na moderate or severe amphetamine, cocaine, or other stimulant use disorder, reflecting", "source": "dsm5.pdf"} {"id": "5ef83f118f9e-1", "page_content": "a moderate or severe amphetamine, cocaine, or other stimulant use disorder, reflecting\nthe fact that amphetamine, cocaine, or other stimulant withdrawal can only occur in the\npresence of a moderate or severe amphetamine, cocaine, or other stimulant use disorder.\nIt is not permissible to code a comorbid mild amphetamine, cocaine, or other stimulant use\ndisorder with amphetamine, cocaine, or other stimulant withdrawal.\nDiagnostic Features\nThe essential feature of stimulant withdrawal is the presence of a characteristic with-\ndrawal syndrome that develops within a few hours to several days after the cessation of\n(or marked reduction in) stimulant use (genera lly high dose) that has been prolonged (Cri-\nterion A). The withdrawal syndrome is char acterized by the development of dysphoric\nmood accompanied by two or more of the fo llowing physiological changes: fatigue, vivid\nand unpleasant dreams, insomnia or hypers omnia, increased appetite, and psychomotor\nretardation or agitation (Crite rion B). Bradycardia is often present and is a reliable mea-\nsure of stimulant withdrawal.\nAnhedonia and drug craving can often be pres ent but are not part of the diagnostic cri-\nteria. These symptoms cause clinically signif icant distress or impairment in social, occu-\npational, or other important areas of functioning (Criterion C). The symptoms must not be\nattributable to another medica l condition and are not better explained by another mental\ndisorder (Criterion D).", "source": "dsm5.pdf"} {"id": "fb0affb37449-0", "page_content": "570 Substance-Related and Addictive Disorders\nAssociated Features Supporting Diagnosis\nAcute withdrawal symptoms (\u201ca crash\u201d) are ofte n seen after periods of repetitive high-dose\nuse (\u201cruns\u201d or \u201cbinges\u201d). These periods are char acterized by intense and unpleasant feelings of\nlassitude and depression and increased appetite, generally requiring several days of rest and\nrecuperation. Depressive symptoms with suicidal ideation or behavior can occur and are gen-\nerally the most serious problems seen during \u201ccrashing\u201d or other forms of stimulant with-\ndrawal. The majority of individuals with st imulant use disorder experience a withdrawal\nsyndrome at some point, and virtually all in dividuals with the diso rder report tolerance.\nDifferential Diagnosis \nStimulant use disorder and other stimulant-induced disorders. Stimulant withdrawal\nis distinguished from stimulan t use disorder and from the other stimulant-induced disor-\nders (e.g., stimulant-induced intoxication delirium, depressi ve disorder, bipolar disorder,\npsychotic disorder, anxiety disorder, sexual dysfunction, sleep disorder) because the\nsymptoms of withdrawal predominate the clin ical presentation and are severe enough to\nwarrant independent clinical attention.\nOther Stimulant-Induced Disorders\nThe following stimulant-induced disorders (w hich include amphetamine-, cocaine-, and\nother stimulant\u2013induced disorder s) are described in other chapters of the manual with dis-\norders with which they share phenomenol ogy (see the substance/medication-induced\nmental disorders in these chapters): stimulan t-induced psychotic disorder (\u201cSchizophrenia\nSpectrum and Other Psychotic Disorders\u201d); st imulant-induced bipolar disorder (\u201cBipolar\nand Related Disorders\u201d); stimulant-induced de pressive disorder (\u201cDe pressive Disorders\u201d);", "source": "dsm5.pdf"} {"id": "fb0affb37449-1", "page_content": "and Related Disorders\u201d); stimulant-induced de pressive disorder (\u201cDe pressive Disorders\u201d);\nstimulant-induced anxiety disorder (\u201cAnxiet y Disorders\u201d); stimulant-induced obsessive-\ncompulsive disorder (\u201cObsessive-Compulsive and Related Disorders\u201d); stimulant-induced\nsleep disorder (\u201cSleep-Wake Disorders\u201d); and stimulant-induced sexual dysfunction (\u201cSex-\nual Dysfunctions\u201d). For stimulant intoxication delirium, see the criteria and discussion of\ndelirium in the chapter \u201cNeurocognitive Disorders.\u201d These stimulant-induced disorders\nare diagnosed instead of stimulant intoxication or stimulant withdrawal only when the\nsymptoms are sufficiently severe to wa rrant independent clinical attention. \nUnspecified Stimulant-Related Disorder\nThis category applies to presentations in which symptoms characteristic of a stimulant-\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any specific stimulant-related disorder or any of the disorders in the substance-related\nand addictive disorders diagnostic class.\nCoding note: The ICD-9-CM code is 292.9. The ICD-10-CM code depends on whether\nthe stimulant is an amphetamine, cocaine, or another stimulant. The ICD-10-CM code for\nan unspecified amphetamine- or other stimulant-related disorder is F15.99. The ICD-10-\nCM code for an unspecified cocaine-related disorder is F14.99.", "source": "dsm5.pdf"} {"id": "6966dc13fcb0-0", "page_content": "Tobacco Use Disorder 571\nTobacco-Related Disorders\nTobacco Use Disorder\nTobacco Withdrawal\nOther Tobacco-Ind uced Disorders\nUnspecified Tobacco-Related Disorder\nTobacco Use Disorder\nDiagnostic Criteria \nA. A problematic pattern of tobacco use leading to clinically significant impairment or dis-\ntress, as manifested by at least two of the following, occurring within a 12-month period:\n1. Tobacco is often taken in larger amounts or over a longer period than was intended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control tobacco use.\n3. A great deal of time is spent in activities necessary to obtain or use tobacco.\n4. Craving, or a strong desire or urge to use tobacco.\n5. Recurrent tobacco use resulting in a failure to fulfill major role obligations at work,\nschool, or home (e.g., interference with work).\n6. Continued tobacco use despite having persistent or recurrent social or interper-\nsonal problems caused or exacerbated by the effects of tobacco (e.g., arguments\nwith others about tobacco use).\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of tobacco use.\n8. Recurrent tobacco use in situations in which it is physically hazardous (e.g., smok-\ning in bed).\n9. Tobacco use is continued despite knowledge of having a persistent or recurrent\nphysical or psychological problem that is likely to have been caused or exacerbated\nby tobacco.\n10. Tolerance, as defined by either of the following:\na. A need for markedly increased amounts of tobacco to achieve the desired effect.\nb. A markedly diminished effect with conti nued use of the same amount of tobacco.\n11. Withdrawal, as manifested by either of the following:", "source": "dsm5.pdf"} {"id": "6966dc13fcb0-1", "page_content": "11. Withdrawal, as manifested by either of the following:\na. The characteristic withdraw al syndrome for tobacco (refer to Criteria A and B of\nthe criteria set for tobacco withdrawal).\nb. Tobacco (or a closely related substance, such as nicotine) is taken to relieve or\navoid withdrawal symptoms.\nSpecify if:\nIn early remission: After full criteria for tobacco use disorder were previously met,\nnone of the criteria for tobacco use disorder have been met for at least 3 months but\nfor less than 12 months (with the exception that Criterion A4, \u201cCraving, or a strong de-\nsire or urge to use tobacco,\u201d may be met).\nIn sustained remission: After full criteria for tobacco use disorder were previously\nmet, none of the criteria for tobacco use disorder have been met at any time during a\nperiod of 12 months or longer (with the exception that Criterion A4, \u201cCraving, or a\nstrong desire or urge to use tobacco,\u201d may be met).", "source": "dsm5.pdf"} {"id": "f5893c1a8e34-0", "page_content": "572 Substance-Related and Addictive Disorders\nSpecify if:\nOn maintenance therapy: The individual is taking a long-term maintenance medica-\ntion, such as nicotine replacement medication, and no criteria for tobacco use disorder\nhave been met for that class of medication (except tolerance to, or withdrawal from,\nthe nicotine replacement medication).\nIn a controlled environment: This additional specifier is used if the individual is in an\nenvironment where access to tobacco is restricted.\nCoding based on current severity: Note for ICD-10-CM codes: If a tobacco withdrawal or\ntobacco-induced sleep disorder is also present, do not use the codes below for tobacco use\ndisorder. Instead, the comorbid tobacco use disorder is indicated in the 4th character of the\ntobacco-induced disorder code (see the coding note for tobacco withdrawal or tobacco-\ninduced sleep disorder). For example, if ther e is comorbid tobacco-induced sleep disorder and\ntobacco use disorder, only the tobacco-induced sleep disorder code is given, with the 4th char-\nacter indicating whether the comorbid tobacco use disorder is moderate or severe: F17.208\nfor moderate or severe tobacco use disorder with tobacco-induced sleep disorder. It is not per-\nmissible to code a comorbid mild tobacco use disorder with a tobacco-induced sleep disorder.\nSpecify current severity:\n305.1 (Z72.0) Mild: Presence of 2\u20133 symptoms.\n305.1 (F17.200) Moderate: Presence of 4\u20135 symptoms.\n305.1 (F17.200) Severe: Presence of 6 or more symptoms.\nSpecifiers\n\u201cOn maintenance therapy\u201d applies as a further specifier to individuals being maintained on\nother tobacco cessation me dication (e.g., bupropio n, varenicline) and as a further specifier of", "source": "dsm5.pdf"} {"id": "f5893c1a8e34-1", "page_content": "remission if the individual is both in remissi on and on maintenance therapy. \u201cIn a controlled\nenvironment\u201d applies as a further specifier of re mission if the individual is both in remission\nand in a controlled environment (i.e., in early remission in a controlled environment or in sus-\ntained remission in a controlled environment). Examples of these environments are closely su-\npervised and substance-free jails, therapeutic communities, and locked hospital units. \nDiagnostic Features\nTobacco use disorder is common among individu als who use cigarettes and smokeless to-\nbacco daily and is uncommon among individuals who do not use tobacco daily or who use\nnicotine medications. Tolerance to tobacco is exemplified by the disappearance of nausea\nand dizziness after repeated intake and with a more intense effect of tobacco the first time\nit is used during the day. Cessation of to bacco use can produce a well-defined withdrawal\nsyndrome. Many individuals with tobacco use disorder use tobacco to relieve or to avoid\nwithdrawal symptoms (e.g., after being in a sit uation where use is restricted). Many indi-\nviduals who use tobacco have tobacco-relat ed physical symptoms or diseases and con-\ntinue to smoke. The large majority report crav ing when they do not smoke for several hours.\nSpending excessive time usin g tobacco can be exemplified by chain-smoking (i.e., smok-\ning one cigarette after another with no time between cigarettes). Because tobacco sources\nare readily and legally available, and because nicotine intoxication is very rare, spending a\ngreat deal of time attempting to procure toba cco or recovering from its effects is uncom-\nmon. Giving up important social, occupational , or recreational acti vities can occur when\nan individual forgoes an activity because it occurs in tobacco use\u2013restricted areas. Use of", "source": "dsm5.pdf"} {"id": "f5893c1a8e34-2", "page_content": "an individual forgoes an activity because it occurs in tobacco use\u2013restricted areas. Use of\ntobacco rarely results in failu re to fulfill major role obligat ions (e.g., in terference with\nwork, interference with home obligations), bu t persistent social or interpersonal problems\n(e.g., having arguments with others about to bacco use, avoiding social situations because\nof others\u2019 disapproval of tobacco use) or use that is physically hazardous (e.g., smoking in", "source": "dsm5.pdf"} {"id": "91613cc283f7-0", "page_content": "Tobacco Use Disorder 573\nbed, smoking around flammable chemicals) oc cur at an intermediate prevalence. Although\nthese criteria are less often endorsed by toba cco users, if endorsed, they can indicate a\nmore severe disorder.\nAssociated Features Supporting Diagnosis\nSmoking within 30 minutes of waking, smoking daily, smoking more cigarettes per day,\nand waking at night to smoke are associated with tobacco use di sorder. Environmental\ncues can evoke craving and withdrawal. Serious medical conditions, such as lung and\nother cancers, cardiac and pulmonary disease , perinatal problems, cough, shortness of\nbreath, and accelerated skin aging, often occur.\nPrevalence\nCigarettes are the most commonly used toba cco product, representing over 90% of to-\nbacco/nicotine use. In the United States, 57% of adults have never been smokers, 22% are\nformer smokers, and 21% are current smokers. Approximately 20% of current U.S. smok-\ners are nondaily smokers. The prevalence of sm okeless tobacco use is less than 5%, and the\nprevalence of tobacco use in pipes and cigars is less than 1%. \nDSM-IV nicotine dependence criteria can be used to estimate the prevalence of tobacco\nuse disorder, but since they are a subset of to bacco use disorder criteria, the prevalence of\ntobacco use disorder will be somewhat greater. The 12-month prevalence of DSM-IV nic-\notine dependence in the United States is 13% among adults age 18 years and older. Rates\nare similar among adult males (14%) and fe males (12%) and decline in age from 17%\namong 18- to 29-year-old s to 4% among individuals age 65 years and older. The prevalence", "source": "dsm5.pdf"} {"id": "91613cc283f7-1", "page_content": "of current nicotine dependence is greate r among Native American and Alaska Natives\n(23%) than among whites (14%) but is less am ong African Americans (10%), Asian Amer-\nicans and Pacific Islanders (6%), and Hispan ics (6%). The prevalence among current daily\nsmokers is approximately 50%.\nIn many developing nations, the prevalence of smoking is much greater in males than\nin females, but this is not the case in develope d nations. However, ther e often is a lag in the\ndemographic transition such that smoking increases in females at a later time. \nDevelopment and Course\nThe majority of U.S. adolescents experiment with tobacco use, and by age 18 years, about\n20% smoke at least monthly. Most of these in dividuals become daily tobacco users. Initi-\nation of smoking after age 21 years is rare. In general, some of the to bacco use disorder cri-\nteria symptoms occur soon after beginning to bacco use, and many individuals\u2019 pattern of\nuse meets current tobacco use diso rder criteria by late adolescence. More than 80% of in-\ndividuals who use tobacco atte mpt to quit at some time, but 60% relapse within 1 week\nand less than 5% remain abstinent for life . However, most indivi duals who use tobacco\nmake multiple attempts such that one-half of tobacco users eventually abstain. Individuals\nwho use tobacco who do quit usually do not do so until after age 30 years. Although non-\ndaily smoking in the United States was previ ously rare, it has beco me more prevalent in\nthe last decade, especially among younger individuals who use tobacco. \nRisk and Prognostic Factors \nTemperamental. Individuals with externalizing pers onality traits are more likely to", "source": "dsm5.pdf"} {"id": "91613cc283f7-2", "page_content": "Temperamental. Individuals with externalizing pers onality traits are more likely to\ninitiate tobacco use. Children with attentio n-deficit/hyperactivity disorder or conduct\ndisorder, and adults with depr essive, bipolar, anxiety, pers onality, psychotic, or other\nsubstance use disorders, are at higher risk of starting and continuing tobacco use and of to-\nbacco use disorder.", "source": "dsm5.pdf"} {"id": "1da9fb2422d1-0", "page_content": "574 Substance-Related and Addictive Disorders\nEnvironmental. Individuals with low incomes and low educational levels are more likely\nto initiate tobacco use an d are less likely to stop.\nGenetic and physiological. Genetic factors contribute to the onset of tobacco use, the\ncontinuation of tobacco use, and the developm ent of tobacco use disorder, with a degree of\nheritability equivalent to that observed with other substance use disorders (i.e., about\n50%). Some of this risk is specific to toba cco, and some is common with the vulnerability to\ndeveloping any substance use disorder. \nCulture-Related Diagnostic Issues \nCultures and subcultures vary widely in their acceptance of the use of tobacco. The prev-\nalence of tobacco use declined in the United States from the 1960s through the 1990s, but\nthis decrease has been less evident in Africa n American and Hispanic populations. Also,\nsmoking in developing countries is more prev alent than in developed nations. The degree\nto which these cultural differences are due to income, education, and tobacco control ac-\ntivities in a country is unclear. Non-Hispan ic white smokers appear to be more likely to\ndevelop tobacco use disorder than are smoker s. Some ethnic differences may be biologi-\ncally based. African American males tend to have higher nicotine blood levels for a given\nnumber of cigarettes, and this might contribute to greater difficulty in quitting. Also, the\nspeed of nicotine metabolism is significantly different for whites compared with African\nAmericans and can vary by genotypes associated with ethnicities.\nDiagnostic Markers\nCarbon monoxide in the breath, and nicotine and its metabolite cotinine in blood, saliva, or\nurine, can be used to measure the extent of cu rrent tobacco or nicotine use; however, these\nare only weakly related to tobacco use disorder.", "source": "dsm5.pdf"} {"id": "1da9fb2422d1-1", "page_content": "are only weakly related to tobacco use disorder. \nFunctional Consequences of Tobacco Use Disorder\nMedical consequences of tobacco use often be gin when tobacco users are in their 40s and\nusually become progressively more debilitat ing over time. One-half of smokers who do\nnot stop using tobacco will die early from a tobacco-related illness, and smoking-related\nmorbidity occurs in more than one-half of tobacco users. Most medical conditions result\nfrom exposure to carbon monoxide, tars, an d other non-nicotine components of tobacco.\nThe major predictor of reversibility is duration of smoking. Secondhand smoke increases\nthe risk of heart disease and cancer by 30%. Long-term use of nicotine medications does\nnot appear to cause medical harm. \nComorbidity\nThe most common medical diseases from smoking are cardiovascular illnesses, chronic\nobstructive pulmonary disease, and cancers. Smoking also increases perinatal problems,\nsuch as low birth weight and miscarriage. Th e most common psychiat ric comorbidities are\nalcohol/substance, depressive, bipolar, anxiet y, personality, and attention-deficit/hyper-\nactivity disorders. In individuals with curren t tobacco use disorder, the prevalence of cur-\nrent alcohol, drug, anxiety, depressive, bi polar, and personality disorders ranges from\n22% to 32%. Nicotine-dependent smokers are 2.7\u20138.1 times more likely to have these dis-\norders than nondependent smokers, never-smokers, or ex-smokers.", "source": "dsm5.pdf"} {"id": "527028b211c4-0", "page_content": "Tobacco Withdrawal 575\nTobacco Withdrawal\nDiagnostic Criteria 292.0 (F17.203)\nA. Daily use of tobacco for at least several weeks.\nB. Abrupt cessation of tobacco use, or reduction in the amount of tobacco used, followed\nwithin 24 hours by four (or more) of the following signs or symptoms:\n1. Irritability, frustration, or anger.\n2. Anxiety.\n3. Difficulty concentrating.\n4. Increased appetite.\n5. Restlessness.\n6. Depressed mood.\n7. Insomnia.\nC. The signs or symptoms in Criterion B cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning.\nD. The signs or symptoms are not attributed to another medical condition and are not bet-\nter explained by another mental disorder, including intoxication or withdrawal from an-\nother substance.\nCoding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for tobacco withdrawal\nis F17.203. Note that the ICD-10-CM code indicates the comorbid presence of a moderate\nor severe tobacco use disorder, reflecting the fact that tobacco withdrawal can only occur\nin the presence of a moderate or severe toba cco use disorder. It is not permissible to code\na comorbid mild tobacco use disorder with tobacco withdrawal.\nDiagnostic Features\nWithdrawal symptoms impair the ability to st op tobacco use. The symptoms after absti-\nnence from tobacco are in large part due to nicotine deprivation. Symptoms are much\nmore intense among individuals who smoke cigarettes or use smokeless tobacco than\namong those who use nicotine medications. This difference in symptom intensity is likely\ndue to the more rapid onset and higher levels of nicotine with cigarette smoking. Tobacco", "source": "dsm5.pdf"} {"id": "527028b211c4-1", "page_content": "due to the more rapid onset and higher levels of nicotine with cigarette smoking. Tobacco\nwithdrawal is common among daily tobacco users who stop or reduce but can also occur\namong nondaily users. Typically, heart rate decreases by 5\u201312 beats per minute in the first\nfew days after stopping smoking, and weight increases an average of 4\u20137 lb (2\u20133 kg) over\nthe first year after stopping smoking. Tobacco withdrawal can produce clinically signifi-\ncant mood changes and functional impairment. \nAssociated Features Supporting Diagnosis\nCraving for sweet or sugary foods and impaired performance on tasks requiring vigilance\nare associated with tobacco withdrawal. Abstinence can increase constipation, coughing,\ndizziness, dreaming/nightmare s, nausea, and sore throat. Smoking increases the metab-\nolism of many medications used to treat mental disorders; thus, cessation of smoking can\nincrease the blood levels of these medications, and this can produce clinically significant\noutcomes. This effect appears to be due not to nicotine but rather to other compounds in\ntobacco.", "source": "dsm5.pdf"} {"id": "8e09707e96cf-0", "page_content": "576 Substance-Related and Addictive Disorders\nPrevalence\nApproximately 50% of tobacco users who quit for 2 or more days will have symptoms that\nmeet criteria for tobacco withdrawal. The most commonly endorsed signs and symptoms\nare anxiety, irritability, and difficulty concentrating. The least commonly endorsed symp-\ntoms are depression and insomnia. \nDevelopment and Course\nTobacco withdrawal usually begins within 24 hours of stopping or cutting down on to-\nbacco use, peaks at 2\u20133 days after abstinence, and lasts 2\u20133 weeks. Tobacco withdrawal\nsymptoms can occur among adolescent tobacco users, even prior to daily tobacco use. Pro-\nlonged symptoms beyond 1 month are uncommon. \nRisk and Prognostic Factors \nTemperamental. Smokers with depressive disorders, bipolar disorders, anxiety disor-\nders, attention-deficit/hypera ctivity disorder, and other substance use disorders have\nmore severe withdrawal.\nGenetic and physiological. Genotype can influence the probability of withdrawal upon\nabstinence. \nDiagnostic Markers\nCarbon monoxide in the breath, and nicotine and its metabolite cotinine in blood, saliva, or\nurine, can be used to measure the extent of tobacco or nicotine use but are only weakly re-\nlated to tobacco withdrawal.\nFunctional Consequences of Tobacco Withdrawal\nAbstinence from cigarettes can cause clinically significant distress. Withdrawal impairs\nthe ability to stop or control tobacco use. Whether tobacco withdraw al can prompt a new\nmental disorder or recurrence of a mental disorder is debatable, but if this occurs, it would\nbe in a small minority of tobacco users. \nDifferential Diagnosis\nThe symptoms of tobacco with drawal overlap with those of other substance withdrawal", "source": "dsm5.pdf"} {"id": "8e09707e96cf-1", "page_content": "Differential Diagnosis\nThe symptoms of tobacco with drawal overlap with those of other substance withdrawal\nsyndromes (e.g., alcohol withdrawal; sedative, hypnotic, or anxiolytic withdrawal; stim-\nulant withdrawal; caffeine withdrawal; opioid withdrawal); caffeine intoxication; anxiety,\ndepressive, bipolar, and sleep disorders; an d medication-induced akathisia. Admission to\nsmoke-free inpatient units or voluntary smoking cessation ca n induce withdrawal symp-\ntoms that mimic, intensify, or disguise othe r disorders or adverse effects of medications\nused to treat mental disorders (e.g., irritabi lity thought to be du e to alcohol withdrawal\ncould be due to tobacco with drawal). Reduction in sympto ms with the use of nicotine\nmedications confirms the diagnosis. \nOther Tobacco-Induced Disorders\nTobacco-induced sleep disorder is discussed in the chapter \u201cSleep -Wake Disorders\u201d (see\n\u201cSubstance/Medication-In duced Sleep Disorder\u201d).", "source": "dsm5.pdf"} {"id": "b752852695aa-0", "page_content": "Unspecified Tobacco-Related Disorder 577\nUnspecified Tobacco-Related Disorder\n292.9 (F17.209)\nThis category applies to presentations in which symptoms characteristic of a tobacco-\nrelated disorder that cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning predominate but do not meet the full criteria\nfor any specific tobacco-related disorder or any of the disorders in the substance-related\nand addictive disorders diagnostic class.\nOther (or Unknown) \nSubstance\u2013Related Disorders\nOther (or Unknown) Su bstance Use Disorder\nOther (or Unknown) Substance Intoxication\nOther (or Unknown) Substance Withdrawal\nOther (or Unknown) Subs tance\u2013Induced Disorders\nUnspecified Other (or Unknown) Substance\u2013Related Disorder\nOther (or Unknown) Substance Use Disorder\nDiagnostic Criteria\nA. A problematic pattern of use of an intoxicating substance not able to be classified\nwithin the alcohol; caffeine; cannabis; hallucinogen (phencyclidine and others); inhal-\nant; opioid; sedative, hypnotic, or anxiolytic; stimulant; or tobacco categories and lead-\ning to clinically significant impairment or distress, as manifested by at least two of the\nfollowing, occurring within a 12-month period: \n1. The substance is often taken in larger amounts or over a longer period than was\nintended.\n2. There is a persistent desire or unsuccessful efforts to cut down or control use of the\nsubstance.\n3. A great deal of time is spent in activities necessary to obtain the substance, use the\nsubstance, or recover from its effects.\n4. Craving, or a strong desire or urge to use the substance.\n5. Recurrent use of the substance resulting in a failure to fulfill major role obligations\nat work, school, or home.", "source": "dsm5.pdf"} {"id": "b752852695aa-1", "page_content": "at work, school, or home.\n6. Continued use of the substance despite having persistent or recurrent social or in-\nterpersonal problems caused or exacerbated by the effects of its use.\n7. Important social, occupational, or recreat ional activities are given up or reduced be-\ncause of use of the substance.\n8. Recurrent use of the substance in situations in which it is physically hazardous.\n9. Use of the substance is continued despite knowledge of having a persistent or re-\ncurrent physical or psychological problem that is likely to have been caused or ex-\nacerbated by the substance.", "source": "dsm5.pdf"} {"id": "791eecf6e49a-0", "page_content": "578 Substance-Related and Addictive Disorders\n10. Tolerance, as defined by either of the following:\na. A need for markedly increased amounts of the substance to achieve intoxication\nor desired effect.\nb. A markedly diminished effect with continued use of the same amount of the sub-\nstance.\n11. Withdrawal, as manifested by either of the following: \na. The characteristic withdrawal syndrome fo r other (or unknown) substance (refer to\nCriteria A and B of the criteria sets fo r other [or unknown] substance withdrawal,\np. 583).\nb. The substance (or a closely related substance) is taken to relieve or avoid with-\ndrawal symptoms.\nSpecify if:\nIn early remission: After full criteria for other (or unknown) substance use disorder were\npreviously met, none of the criteria for other (or unknown) substance use disorder have\nbeen met for at least 3 months but for less than 12 months (with the exception that Cri-\nterion A4, \u201cCraving, or a strong desire or urge to use the substance,\u201d may be met).\nIn sustained remission: After full criteria for other (or unknown) substance use disor-\nder were previously met, none of the criteria for other (or unknown) substance use dis-\norder have been met at any time during a period of 12 months or longer (with the\nexception that Criterion A4, \u201cCraving, or a strong desire or urge to use the substance,\u201d\nmay be met).\nSpecify if:\nIn a controlled environment: This additional specifier is used if the individual is in an\nenvironment where access to the substance is restricted.\nCoding based on current severity: Note for ICD-10-CM codes: If an other (or unknown) sub-", "source": "dsm5.pdf"} {"id": "791eecf6e49a-1", "page_content": "stance intoxication, other (or unknown) substance withdrawal, or another other (or unknown)\nsubstance\u2013induced mental disorder is present, do not use the codes below for other (or un-\nknown) substance use disorder. Instead, the comorbid other (or unknown) substance use dis-\norder is indicated in the 4th character of the other (or unknown) substance\u2013induced disorder\ncode (see the coding note for other (or unknown) substance intoxication, other (or unknown)\nsubstance withdrawal, or specific other (or unknown) substance\u2013induced mental disorder).\nFor example, if there is comorbid other (or unknown) substance\u2013induced depressive disorder\nand other (or unknown) substance use disorder, only the other (or unknown) substance\u2013\ninduced depressive disorder code is given, with the 4th character indicating whether the co-\nmorbid other (or unknown) substance use disorder is mild, moderate, or severe: F19.14 for\nother (or unknown) substance use disorder with other (or unknown) substance\u2013induced de-\npressive disorder or F19.24 for a moderate or severe other (or unknown) substance use dis-\norder with other (or unknown) substance\u2013induced depressive disorder.\nSpecify current severity:\n305.90 (F19.10) Mild: Presence of 2\u20133 symptoms.\n304.90 (F19.20) Moderate: Presence of 4\u20135 symptoms.\n304.90 (F19.20) Severe: Presence of 6 or more symptoms.\nSpecifiers\n\u201cIn a controlled environment\u201d app lies as a further specifier of remission if the individual is\nboth in remission and in a controlled environm ent (i.e., in early remission in a controlled", "source": "dsm5.pdf"} {"id": "791eecf6e49a-2", "page_content": "environment or in sustained remission in a controlled environmen t). Examples of these\nenvironments are closely supe rvised and substanc e-free jails, therapeutic communities,\nand locked hospital units.", "source": "dsm5.pdf"} {"id": "03f5cda4e20b-0", "page_content": "Other (or Unknown) Substance Use Disorder 579\nDiagnostic Features\nThe diagnostic class other (or unknown) su bstance use and related disorders comprises\nsubstance-related disorders unrelated to alco hol; caffeine; cannabis; hallucinogens (phen-\ncyclidine and others); inhalants; opioids; sedative, hypnotics, or anxiolytics; stimulants\n(including amphetamine and cocaine); or tobacco. Such substances include anabolic ste-\nroids; nonsteroidal anti-inflammatory drugs; cortisol; antiparkinsoni an medications; an-\ntihistamines; nitrous oxide; amyl-, butyl-, or isobutyl-nitrites; betel nut, which is chewed\nin many cultures to produce mild euphoria an d a floating sensation; kava (from a South\nPacific pepper plant), which produces sedation , incoordination, weight loss, mild hepati-\ntis, and lung abnormalities; or cathinones (including kh\u00e2t plant agents and synthetic chem-\nical derivatives) that produce stimulant effe cts. Unknown substance- related disorders are\nassociated with unidentified substances, such as intoxications in which the individual can-\nnot identify the ingested drug, or substance use disorders involving either new, black mar-\nket drugs not yet identified or familia r drugs illegally sold under false names.\nOther (or unknown) substance use disorder is a mental disorder in which repeated use\nof an other or unknown substance typically continues, despite the individual\u2019s knowing\nthat the substance is causing serious problems for the individual. Th ose problems are re-\nflected in the diagnostic criteria . When the substance is known, it should be reflected in the\nname of the disorder upon coding (e.g., nitrous oxide use disorder).\nAssociated Features Supporting Diagnosis", "source": "dsm5.pdf"} {"id": "03f5cda4e20b-1", "page_content": "Associated Features Supporting Diagnosis\nA diagnosis of other (or unknown) substance us e disorder is supporte d by the individual\u2019s\nstatement that the substance involved is not among the nine classes listed in this chapter; by re-\ncurring episodes of intoxication with negative results in standard drug screens (which may not\ndetect new or rarely used substances); or by the presence of symptoms characteristic of an un-\nidentified substance that has newly appeared in the individual\u2019s community.\nBecause of increased access to nitrous oxide (\u201claughing ga s\u201d), membership in certain\npopulations is associated with diagnosis of ni trous oxide use disorder. The role of this gas\nas an anesthetic agent leads to misuse by so me medical and dental professionals. Its use as\na propellant for commercial products (e.g., whipped cream dispensers) contributes to\nmisuse by food service workers. With recent widespread availability of the substance in\n\u201cwhippet\u201d cartridges for use in home whipped cream dispensers, ni trous oxide misuse by\nadolescents and young adults is significant, especially among those who also inhale vola-\ntile hydrocarbons. Some continuously usin g individuals, inhaling from as many as 240\nwhippets per day, may present with serious medical complications and mental conditions,\nincluding myeloneuropathy, spinal cord su bacute combined degeneration, peripheral\nneuropathy, and psychosis. These conditions are also associated with a diagnosis of ni-\ntrous oxide use disorder. \nUse of amyl-, butyl-, and iso butyl nitrite gases has been observed among homosexual\nmen and some adolescents, especially those with conduct disorder. Membership in these\npopulations may be associated with a diagnosis of amyl-, butyl-, or is obutyl-nitrite use dis-\norder. However, it has not been determined that these substances produce a substance use", "source": "dsm5.pdf"} {"id": "03f5cda4e20b-2", "page_content": "order. However, it has not been determined that these substances produce a substance use\ndisorder. Despite tolerance, these gases may no t alter behavior through central effects, and\nthey may be used only for their peripheral effects.\nSubstance use disorders generall y are associated with elevated risks of suicide, but there\nis no evidence of unique risk factors for suicide with other (or unknown) substance use\ndisorder.\nPrevalence\nBased on extremely limited data, the prevalence of other (or unknown) substance use disorder", "source": "dsm5.pdf"} {"id": "d8e875f5a3ab-0", "page_content": "disorder.\nPrevalence\nBased on extremely limited data, the prevalence of other (or unknown) substance use disorder\nis likely lower than that of use disorders involv ing the nine substance classes in this chapter.", "source": "dsm5.pdf"} {"id": "1eeb74a18418-0", "page_content": "580 Substance-Related and Addictive Disorders\nDevelopment and Course\nNo single pattern of development or course characterizes the pharmacologically varied\nother (or unknown) substance use disorders. Often unknown substance use disorders will\nbe reclassified when the unknown substance eventually is identified. \nRisk and Prognostic Factors\nRisk and prognostic factors for other (or un known) substance use disorders are thought to\nbe similar to those for most substance use disorders and include the presence of any other\nsubstance use disorders, conduct disorder, or antisocial personality disorder in the indi-\nvidual or the individual\u2019s family; early onse t of substance problems ; easy availability of\nthe substance in the individual\u2019s environment; childhood maltreatment or trauma; and ev-\nidence of limited early self-control and behavioral disinhibition. \nCulture-Related Diagnostic Issues\nCertain cultures may be associated with ot her (or unknown) substance use disorders in-\nvolving specific indigenous substances with in the cultural region, such as betel nut.\nDiagnostic Markers\nUrine, breath, or saliva tests may correctly identify a commonly used substance falsely\nsold as a novel product. However, routine clin ical tests usually cannot identify truly un-\nusual or new substances, which may requir e testing in specialized laboratories. \nDifferential Diagnosis\nUse of other or unknown substances without meeting criteria for other (or unknown)\nsubstance use disorder. Use of unknown substances is not rare among adolescents, but\nmost use does not meet the diag nostic standard of two or mo re criteria for other (or un-\nknown) substance use disorder in the past year.\nSubstance use disorders. Other (or unknown) substanc e use disorder may co-occur\nwith various substance use diso rders, and the symptoms of the disorders may be similar", "source": "dsm5.pdf"} {"id": "1eeb74a18418-1", "page_content": "with various substance use diso rders, and the symptoms of the disorders may be similar\nand overlapping. To disentangle symptom pattern s, it is helpful to inquire about which\nsymptoms persisted during periods when some of the substances were not being used.\nOther (or unknown) substance/medication-induced disorder. This diagnosis should\nbe differentiated from instances when the indi vidual\u2019s symptoms meet full criteria for one\nof the following disorders, and that disorder is caused by an other or unknown substance:\ndelirium, major or mild neurocognitive disorder, psychoti c disorder, depressive disorder,\nanxiety disorder, sexual dysf unction, or sleep disorder.\nOther medical conditions. Individuals with substance us e disorders, including other\n(or unknown) substance use disorder, may present with symptoms of many medical dis-\norders. These disorders also may occur in the absence of other (or unknown) substance use\ndisorder. A history of little or no use of ot her or unknown substances helps to exclude\nother (or unknown) substance use disord er as the source of these problems.\nComorbidity\nSubstance use disorders, including other (o r unknown) substance use disorder, are com-\nmonly comorbid with one another, with adol escent conduct disorder and adult antisocial\npersonality disorder, and with suicid al ideation and suicide attempts.", "source": "dsm5.pdf"} {"id": "fc476ed28421-0", "page_content": "Other (or Unknown) Substance Intoxication 581\nOther (or Unknown) Substance Intoxication\nDiagnostic Criteria\nA. The development of a reversible substance-specific syndrome attributable to recent in-\ngestion of (or exposure to) a substance that is not listed elsewhere or is unknown.\nB. Clinically significant problematic behavioral or psychological changes that are attribut-\nable to the effect of the substance on the central nervous system (e.g., impaired motor\ncoordination, psychomotor agitation or retardation, euphoria, anxiety, belligerence,\nmood lability, cognitive impairment, impaired judgment, social withdrawal) and develop\nduring, or shortly after, use of the substance.\nC. The signs or symptoms are not attributable to another medical condition and are not bet-\nter explained by another mental disorder, in cluding intoxication with another substance.\nCoding note: The ICD-9-CM code is 292.89. The ICD-10-CM code depends on whether\nthere is a comorbid other (or unknown) substance use disorder involving the same sub-\nstance. If a mild other (or unknown) substance use disorder is comorbid, the ICD-10-CM\ncode is F19.129, and if a moderate or severe other (or unknown) substance use disorder is\ncomorbid, the ICD-10-CM code is F19.229. If there is no comorbid other (or unknown) sub-\nstance use disorder involving the same substance, then the ICD-10-CM code is F19.929.\nNote: For information on Risk and Prognostic Factors, Culture-Related Diagnostic Issues,\nand Diagnostic Markers, see the correspondin g sections in other (or unknown) substance\nuse disorder.\nDiagnostic Features", "source": "dsm5.pdf"} {"id": "fc476ed28421-1", "page_content": "use disorder.\nDiagnostic Features\nOther (or unknown) substance intoxication is a clinically significant mental disorder that\ndevelops during, or immediately after, use of either a) a substance not elsewhere ad-\ndressed in this chapter (i.e., alcohol; caff eine; cannabis; phencyclidine and other halluci-\nnogens; inhalants; opioids; sedatives, hypnotics , or anxiolytics; stimulants; or tobacco) or\nb) an unknown substance. If the substance is known, it should be reflected in the name of\nthe disorder upon coding.\nApplication of the diagnostic criteria for other (or unknow n) substance intoxication is\nvery challenging. Criterion A requires development of a reversible \u201csubstance-specific\nsyndrome,\u201d but if the substance is unknown, that syndrome usually will be unknown. To\nresolve this conflict, clinicians may ask the in dividual or obtain co llateral history as to\nwhether the individual has experienced a similar episode after using substances with the\nsame \u201cstreet\u201d name or from the same source . Similarly, hospital emergency departments\nsometimes recognize over a few days numerous presentations of a severe, unfamiliar in-\ntoxication syndrome from a newly available, previously unknown substance. Because of\nthe great variety of intoxicating substances, Criterion B can provide only broad examples\nof signs and symptoms from some intoxications, with no threshold for the number of\nsymptoms required for a diagnosis; clinical judgment guides those decisions. Criterion C\nrequires ruling out other medical conditio ns, mental disorders, or intoxications.\nPrevalence\nThe prevalence of other (or unknown) substance intoxication is unknown.\nDevelopment and Course\nIntoxications usually appear and then peak minu tes to hours after use of the substance, but\nthe onset and course vary with the substanc e and the route of administration. Generally,", "source": "dsm5.pdf"} {"id": "745a5c209b0f-0", "page_content": "582 Substance-Related and Addictive Disorders\nsubstances used by pulmonary inhalation and intravenous injection have the most rapid\nonset of action, while those ingested by mouth and requiring metabolism to an active\nproduct are much slower. (For example, after ingestion of certain mushrooms, the first\nsigns of an eventually fatal intoxication may not appear for a few days.) Intoxication ef-\nfects usually resolve within hours to a very few days. However, the body may completely\neliminate an anesthetic gas such as nitrous ox ide just minutes after use ends. At the other\nextreme, some \u201chit-and-run\u201d intoxicating su bstances poison systems, leaving permanent\nimpairments. For example, MPTP (1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine), a con-\ntaminating by-product in the synthesis of a certain opioid, kills dopaminergic cells and in-\nduces permanent parkinsonism in user s who sought opioid intoxication. \nFunctional Consequences of \nOther (or Unknown) Substance Intoxication\nImpairment from intoxication with any subs tance may have serious consequences, includ-\ning dysfunction at work, social indiscretions, problems in interpersonal relationships, fail-\nure to fulfill role obligations, traffic accide nts, fighting, high-risk behaviors (i.e., having\nunprotected sex), and substance or medication overdose. The pattern of consequences will\nvary with the particular substance.\nDifferential Diagnosis\nUse of other or unknown substance, without meeting criteria for other (or unknown)\nsubstance intoxication. The individual used an other or unknown substance(s), but the\ndose was insufficient to produce symptoms that meet the diag nostic criteria required for\nthe diagnosis.", "source": "dsm5.pdf"} {"id": "745a5c209b0f-1", "page_content": "the diagnosis.\nSubstance intoxication or other subs tance/medication-induced disorders. Familiar sub-\nstances may be sold in the black market as novel products, and individuals may experience\nintoxication from those substances. History, to xicology screens, or chemical testing of the\nsubstance itself may help to identify it.\nDifferent types of other (or unknown) substance\u2013related disorders. Episodes of other\n(or unknown) substance intoxication may occur during, but are distinct from, other (or un-\nknown) substance use disorder, unspecified other (or unknown) substance\u2013related disor-\nder, and other (or unknown) substance\u2013induced disorders. \nOther toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that impair\nbrain function and cognition. Numerous neurological and other medical conditions may\nproduce rapid onset of signs and symptoms mimi cking those of intoxica tions, including the\nexamples in Criterion B. Parado xically, drug withdrawals also must be ruled out, because, for\nexample, lethargy may indicate withdrawal from one drug or intoxication with another drug.\nComorbidity\nAs with all substance-related disorders, adolescent conduct disorder, adult antisocial per-\nsonality disorder, and other subs tance use disorders tend to co-occur with other (or un-\nknown) substance intoxication.", "source": "dsm5.pdf"} {"id": "2aacc0763f6d-0", "page_content": "Other (or Unknown) Substance Withdrawal 583\nOther (or Unknown) Substance Withdrawal\nDiagnostic Criteria 292.0 (F19.239)\nA. Cessation of (or reduction in) use of a substance that has been heavy and prolonged.\nB. The development of a substance-specific syndrome shortly after the cessation of (or\nreduction in) substance use.\nC. The substance-specific syndrome causes clinically significant distress or impairment\nin social, occupational, or other important areas of functioning.\nD. The symptoms are not attributable to anot her medical condition and are not better ex-\nplained by another mental disorder, including withdrawal from another substance.\nE. The substance involved cannot be classified under any of the other substance catego-\nries (alcohol; caffeine; cannabis; opioids; sedatives, hypnotics, or anxiolytics; stimu-\nlants; or tobacco) or is unknown.\nCoding note: The ICD-9-CM code is 292.0. The ICD-10-CM code for other (or unknown) sub-\nstance withdrawal is F19.239. Note that the ICD-10-CM code indicates the comorbid presence\nof a moderate or severe other (or unknown) substance use disorder. It is not permissible to\ncode a comorbid mild other (or unknown) substance use disorder with other (or unknown) sub-\nstance withdrawal.\nNote: For information on Risk and Prognostic Fa ctors and Diagnostic Markers, see the cor-\nresponding sections in other (or unknown) substance use disorder.\nDiagnostic Features\nOther (or unknown) substance withdrawal is a clinically significant mental disorder that\ndevelops during, or within a few hours to days after, reducing or terminating dosing with\na substance (Criteria A and B). Although recent dose reduction or termination usually is", "source": "dsm5.pdf"} {"id": "2aacc0763f6d-1", "page_content": "a substance (Criteria A and B). Although recent dose reduction or termination usually is\nclear in the history, other diagnostic procedur es are very challenging if the drug is un-\nknown. Criterion B requires development of a \u201csubstance-specific syndrome\u201d (i.e., the in-\ndividual\u2019s signs and sympto ms must correspond with th e known withdrawal syndrome\nfor the recently stopped drug)\u2014a requirement that rarely can be met with an unknown\nsubstance. Consequently, clinical judgment must guide such decisions when information\nis this limited. Criterion D requ ires ruling out other medical conditions, mental disorders,\nor withdrawals from familiar substances. When the substance is known, it should be re-\nflected in the name of the disorder upon coding (e.g., betel nut withdrawal).\nPrevalence\nThe prevalence of other (or unknown) substance withdrawal is unknown.\nDevelopment and Course\nWithdrawal signs commonly appe ar some hours after use of the substance is terminated,\nbut the onset and course vary greatly, depending on the dose typically used by the person\nand the rate of elimination of the specific su bstance from the body. At peak severity, with-\ndrawal symptoms from some substances involve only mode rate levels of discomfort,\nwhereas withdrawal from other substances may be fatal. Withdrawal-associated dyspho-\nria often motivates relapse to substance us e. Withdrawal symptoms slowly abate over\ndays, weeks, or months, depending on the particular drug and dose s to which the indi-\nvidual became tolerant.\nCulture-Related Diagnostic Issues\nCulture-related issues in diagnosis will vary with the particular substance.", "source": "dsm5.pdf"} {"id": "baf74c81d598-0", "page_content": "584 Substance-Related and Addictive Disorders\nFunctional Consequences of \nOther (or Unknown) Substance Withdrawal\nWithdrawal from any substance may have serious consequences, including physical signs\nand symptoms (e.g., malaise, vi tal sign changes, abdominal distress, headache), intense\ndrug craving, anxiety, depre ssion, agitation, psychotic symp toms, or cognitive impairments.\nThese consequences may lead to problems such as dysfunction at work, problems in in-\nterpersonal relationships, failure to fulfill role obligations, traffic accidents, fighting, high-\nrisk behavior (e.g., having unprotected sex), suicide attempts, and substance or medica-\ntion overdose. The pattern of consequences will vary with the particular substance.\nDifferential Diagnosis\nDose reduction after extended dosing, but no t meeting the criteria for other (or un-\nknown) substance withdrawal. The individual used other (or unknown) substances,\nbut the dose that was used was insufficient to produce symptoms that meet the criteria re-\nquired for the diagnosis.\nSubstance withdrawal or other substance/medication-induced disorders. Familiar\nsubstances may be sold in the black market as novel products, and individuals may expe-\nrience withdrawal when discontinuing those substances. History, toxicology screens, or\nchemical testing of the substance itself may help to identify it. \nDifferent types of other (or unknown) substance\u2013related disorders. Episodes of other\n(or unknown) substance withdrawal may occur during, but are distinct from, other (or un-\nknown) substance use disorder, unspecified other (or unknown) substance\u2013related disor-\nder, and unspecified other (or unkn own) substance\u2013induced disorders.\nOther toxic, metabolic, traumatic, neoplastic, vascular, or infectious disorders that im-\npair brain function and cognition. Numerous neurological and other medical condi-", "source": "dsm5.pdf"} {"id": "baf74c81d598-1", "page_content": "pair brain function and cognition. Numerous neurological and other medical condi-\ntions may produce rapid onset of signs and symptoms mimi cking those of withdrawals.\nParadoxically, drug intoxications also must be ruled out, because, for example, lethargy\nmay indicate withdrawal from one drug or intoxication with another drug.\nComorbidity\nAs with all substance-related disorders, adolescent conduct disorder, adult antisocial per-\nsonality disorder, and other substance use disorders likely co-occur with other (or un-\nknown) substance withdrawal.\nOther (or Unknown) \nSubstance\u2013Induced Disorders\nBecause the category of other or unknown subs tances is inherently ill-defined, the extent\nand range of induced disorders are uncertain. Nevertheless, othe r (or unknown) sub-\nstance\u2013induced disorders are possible and are described in other chapters of the manual\nwith disorders with which they share phenomenology (see the substance/medication-\ninduced mental disorders in these chapters): other (or unknown) substance\u2013induced psy-\nchotic disorder (\u201cSchizophren ia Spectrum and Other Psychotic Disorders\u201d); other (or un-\nknown substance\u2013induced bipolar disorder (\u201c Bipolar and Related Disorders\u201d); other (or\nunknown) substance\u2013induced depressive diso rder (\u201cDepressive Disorders\u201d); other (or\nunknown) substance\u2013induced anxiety disorders (\u201cAnxiety Disorders\u201d); other (or un-\nknown) substance\u2013induced obsessive-compu lsive disorder (\u201cObsessive-Compulsive and\nRelated Disorders\u201d); other (or unknown) substance\u2013indu ced sleep disorder (\u201cSleep-Wake", "source": "dsm5.pdf"} {"id": "a6c2b6b28fcf-0", "page_content": "Unspecified Other (or Unknown) Substance\u2013Related Disorder 585\nDisorders\u201d); other (or unknown) substance\u2013induced sexual dysfunction (\u201cSexual Dys-\nfunctions\u201d); and other (or un known) substance/me dication\u2013induced major or mild neu-\nrocognitive disorder (\u201cNeurocognitive Diso rders\u201d). For other (or unknown) substance\u2013\ninduced intoxication delirium and other (o r unknown) substance\u2013induced withdrawal\ndelirium, see the criteria and discussion of delirium in the chapter \u201cNeurocognitive Dis-\norders.\u201d These other (or unknown) substanc e\u2013induced disorders are diagnosed instead of\nother (or unknown) substance intoxication or other (or unknown) substance withdrawal\nonly when the symptoms are sufficiently seve re to warrant independent clinical attention.\nUnspecified Other (or Unknown)\nSubstance\u2013Related Disorder\n292.9 (F19.99)\nThis category applies to presentations in which symptoms characteristic of an other (or un-\nknown) substance\u2013related disorder that cause clinically significant distress or impairment\nin social, occupational, or other important areas of functioning predominate but do not\nmeet the full criteria for any specific other (or unknown) substance\u2013related disorder or any\nof the disorders in the substance-related disorders diagnostic class.\nNon-Substance-Related Disorders\nGambling Disorder\nDiagnostic Criteria 312.31 (F63.0)\nA. Persistent and recurrent problematic gambling behavior leading to clinically significant\nimpairment or distress, as indicated by the individual exhibiting four (or more) of the fol-\nlowing in a 12-month period:\n1. Needs to gamble with increasing amounts of money in order to achieve the desired\nexcitement.\n2. Is restless or irritable when attempting to cut down or stop gambling.", "source": "dsm5.pdf"} {"id": "a6c2b6b28fcf-1", "page_content": "2. Is restless or irritable when attempting to cut down or stop gambling.\n3. Has made repeated unsuccessful efforts to control, cut back, or stop gambling.\n4. Is often preoccupied with gambling (e.g., having persistent thoughts of reliving past\ngambling experiences, handicapping or planni ng the next venture, thinking of ways\nto get money with which to gamble).\n5. Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed).\n6. After losing money gambling, often returns another day to get even (\u201cchasing\u201d one\u2019s\nlosses).\n7. Lies to conceal the extent of involvement with gambling.\n8. Has jeopardized or lost a significant rela tionship, job, or educational or career op-\nportunity because of gambling.\n9. Relies on others to provide money to relieve desperate financial situations caused\nby gambling.\nB. The gambling behavior is not better explained by a manic episode.", "source": "dsm5.pdf"} {"id": "18b27b425ac5-0", "page_content": "586 Substance-Related and Addictive Disorders\nSpecify if:\nEpisodic: Meeting diagnostic criteria at more than one time point, with symptoms sub-\nsiding between periods of gambling disorder for at least several months.\nPersistent: Experiencing continuous symptoms, to meet diagnostic criteria for multiple\nyears.\nSpecify if:\nIn early remission: After full criteria for gambling disorder were previously met, none\nof the criteria for gambling disorder have been met for at least 3 months but for less\nthan 12 months.\nIn sustained remission: After full criteria for gambling disorder were previously met,\nnone of the criteria for gambling disorder have been met during a period of 12 months\nor longer.\nSpecify current severity:\nMild: 4\u20135 criteria met.\nModerate: 6\u20137 criteria met.\nSevere: 8\u20139 criteria met.\nNote: Although some behavioral conditions th at do not involve in gestion of substances\nhave similarities to substance-related disorders, only one disord er\u2014gambling disorder\u2014\nhas sufficient data to be included in this section.\nSpecifiers\nSeverity is based on the number of criteria endorsed. Individuals with mild gambling dis-\norder may exhibit only 4\u20135 of the criteria, with the most frequently endorsed criteria usu-\nally related to preoccupation with gamb ling and \u201cchasing\u201d losses. Individuals with\nmoderately severe gambli ng disorder exhibit more of the criteria (i.e., 6\u20137). Individuals\nwith the most severe form will exhibit all or mo st of the nine criteria (i.e., 8\u20139). Jeopardiz-\ning relationships or career o pportunities due to gambling and relying on others to provide\nmoney for gambling losses are typically the least often endorsed criteria and most often oc-", "source": "dsm5.pdf"} {"id": "18b27b425ac5-1", "page_content": "money for gambling losses are typically the least often endorsed criteria and most often oc-\ncur among those with more severe gambling disorder. Furthermore, individuals present-\ning for treatment of gambling disorder typically have moderate to severe forms of the\ndisorder.\nDiagnostic Features\nGambling involves risking something of value in the hopes of obtaining something of\ngreater value. In many cultur es, individuals gamble on game s and events, and most do so\nwithout experiencing problems. However, so me individuals develo p substantial impair-\nment related to their gambling behaviors. Th e essential feature of gambling disorder is\npersistent and recurrent maladaptive gambling behavior that disrupts personal, family,\nand/or vocational pursuits (Criterion A). Gamb ling disorder is defined as a cluster of four\nor more of the symptoms listed in Criterion A occurring at any time in the same 12-month\nperiod.\nA pattern of \u201cchasing one\u2019s losses\u201d may deve lop, with an urgent need to keep gam-\nbling (often with the placing of larger bets or the taking of greater risks) to undo a loss or\nseries of losses. The individual may abandon his or her gambling strategy and try to win\nback losses all at once. Although many gamblers may \u201cchase\u201d for short periods of time, it\nis the frequent, and often long-term, \u201cchase\u201d that is characteristic of gambling disorder\n(Criterion A6). Individuals may lie to family members, therapists, or others to conceal the\nextent of involvement with gambling; these instances of deceit may also include, but\nare not limited to, covering up illegal behaviors such as forgery, fraud, theft, or embez-\nzlement to obtain money with which to gamble (Criterion A7). Individuals may also en-", "source": "dsm5.pdf"} {"id": "bebf16bca4ae-0", "page_content": "Gambling Disorder 587\ngage in \u201cbailout\u201d behavior, turning to family or others for help with a desperate financial\nsituation that was caused by gambling (Criterion A9). \nAssociated Features Supporting Diagnosis \nDistortions in thinking (e.g., denial, superstitions, a sense of power and control over the\noutcome of chance events, overconfidence) ma y be present in individuals with gambling\ndisorder. Many individuals with gambling diso rder believe that money is both the cause\nof and the solution to their problems. Some individuals with gambling disorder are im-\npulsive, competitive, energetic, restless, an d easily bored; they may be overly concerned\nwith the approval of others and may be gene rous to the point of extravagance when win-\nning. Other individuals with gambling disord er are depressed and lonely, and they may\ngamble when feeling helpless, guilty, or depres sed. Up to half of individuals in treatment\nfor gambling disorder have suicidal ideati on, and about 17% have attempted suicide.\nPrevalence \nThe past-year prevalence rate of gambling di sorder is about 0.2%\u20130.3% in the general pop-\nulation. In the general population, the lifetim e prevalence rate is about 0.4%\u20131.0%. For fe-\nmales, the lifetime prevalence rate of gambling disorder is about 0.2%, and for males it is\nabout 0.6%. The lifetime prevalence of path ological gambling among African Americans is\nabout 0.9%, among whites about 0.4% , and among Hispanics about 0.3%. \nDevelopment and Course \nThe onset of gambling disorder can occur du ring adolescence or young adulthood, but in\nother individuals it manifests during middle or even older adulthood. Generally, gam-", "source": "dsm5.pdf"} {"id": "bebf16bca4ae-1", "page_content": "other individuals it manifests during middle or even older adulthood. Generally, gam-\nbling disorder develops over the course of years, although the progression appears to be\nmore rapid in females than in males. Most individuals who develop a gambling disorder\nevidence a pattern of gambling that gradually increases in both frequency and amount of\nwagering. Certainly, milder fo rms can develop into more severe cases. Most individuals\nwith gambling disorder report that one or tw o types of gambling are most problematic for\nthem, although some individuals participate in many forms of gambling. Individuals are\nlikely to engage in certain types of gambling (e.g., buying scratch tickets daily) more fre-\nquently than others (e.g., playing slot machin es or blackjack at the casino weekly). Fre-\nquency of gambling can be related more to the type of gambling than to the severity of the\noverall gambling disorder. For example, purcha sing a single scratch ticket each day may\nnot be problematic, while less frequent casino , sports, or card gambling may be part of a\ngambling disorder. Similarly, amounts of money spent wagering are not in themselves in-\ndicative of gambling disorder. Some individuals can wager thousands of dollars per\nmonth and not have a problem with gambling, while others may wager much smaller\namounts but experience substantia l gambling-related difficulties. \nGambling patterns may be regular or episod ic, and gambling disorder can be persis-\ntent or in remission. Gambling can increase during periods of stress or depression and\nduring periods of substance use or abstinen ce. There may be periods of heavy gambling\nand severe problems, times of total abstin ence, and periods of nonproblematic gambling.\nGambling disorder is some times associated with spontaneous, long-term remissions.\nNevertheless, some individual s underestimate their vulner ability to develop gambling", "source": "dsm5.pdf"} {"id": "bebf16bca4ae-2", "page_content": "Nevertheless, some individual s underestimate their vulner ability to develop gambling\ndisorder or to return to gamb ling disorder following remission. When in a period of re-\nmission, they may incorrectly assume that th ey will have no problem regulating gambling\nand that they may gamble on some forms no nproblematically, only to experience a return\nto gambling disorder. \nEarly expression of gambling disorder is mo re common among males than among fe-\nmales. Individuals who begin gambling in yo uth often do so with family members or", "source": "dsm5.pdf"} {"id": "9bd8ed7b5711-0", "page_content": "588 Substance-Related and Addictive Disorders\nfriends. Development of early-life gambling diso rder appears to be associated with impul-\nsivity and substance abuse. Many high scho ol and college students who develop gambling\ndisorder grow out of the disorder over time , although it remains a lifelong problem for\nsome. Mid- and later-life onse t of gambling disorder is more common among females than\namong males. \nThere are age and gender variations in the type of gambling activities and the preva-\nlence rates of gambling disorder. Gambling d isorder is more common among younger and\nmiddle-age persons than among older adults . Among adolescents and young adults, the\ndisorder is more prevalent in males than in females. Younger indivi duals prefer different\nforms of gambling (e.g., sports betting), while older adults are more likely to develop\nproblems with slot machine and bingo gamblin g. Although the proportions of individuals\nwho seek treatment for gambling disorder ar e low across all age groups, younger individ-\nuals are especially unlikely to present for treatment. \nMales are more likely to begin gambling earlie r in life and to have a younger age at on-\nset of gambling disorder than females, who ar e more likely to begin gambling later in life\nand to develop gambling disorder in a shorte r time frame. Females with gambling disor-\nder are more likely than males with gambling disorder to have depressive, bipolar, and\nanxiety disorders. Females also have a later age at onset of the disorder and seek treatment\nsooner, although rates of treatment seekin g are low (<10%) among individuals with gam-\nbling disorder regardless of gender. \nRisk and Prognostic Factors\nTemperamental. Gambling that begins in childhood or early adolescence is associated\nwith increased rates of gambling disorder. Gambling disorder also appears to aggregate", "source": "dsm5.pdf"} {"id": "9bd8ed7b5711-1", "page_content": "with increased rates of gambling disorder. Gambling disorder also appears to aggregate\nwith antisocial personality disorder, depre ssive and bipolar disorders, and other sub-\nstance use disorders, particul arly with alcohol disorders. \nGenetic and physiological. Gambling disorder can aggregate in families, and this effect\nappears to relate to both environmental and genetic factors. Gambling problems are more\nfrequent in monozygotic than in dizygotic twins. Gambling disorder is also more preva-\nlent among first-degree relati ves of individuals with modera te to severe alcohol use dis-\norder than among the general population.\nCourse modifiers. Many individuals, including adolesce nts and young adults, are likely to\nresolve their problems with gambling disorder over time, although a strong predictor of\nfuture gambling problems is prior gambling problems.\nCulture-Related Diagnostic Issues\nIndividuals from specific cultures and races/ethnicities are more likely to participate in\nsome types of gambling activities than others (e.g., pai gow, cockfights , blackjack, horse rac-\ning). Prevalence rates of gambling disorder are higher among African Americans than\namong European Americans, with rates for Hi spanic Americans similar to those of Euro-\npean Americans. Indigenous populations have high prevalence rates of gambling disorder. \nGender-Related Diagnostic Issues\nMales develop gambling disorder at higher rates than females, alth ough this gender gap\nmay be narrowing. Males tend to wager on di fferent forms of gambling than females, with\ncards, sports, and horse race gambling more prevalent among males, and slot machine and\nbingo gambling more common among females.", "source": "dsm5.pdf"} {"id": "c597cdce75e3-0", "page_content": "Gambling Disorder 589\nFunctional Consequences of Gambling Disorder\nAreas of psychosocial, health, and mental heal th functioning may be adversely affected by\ngambling disorder. Specifically, individuals with gambling disorder may, because of their\ninvolvement with gambling, jeopardize or lo se important relationships with family mem-\nbers or friends. Such problems may occur from repeatedly lying to others to cover up the\nextent of gambling or from requesting money that is used for gambling or to pay off gam-\nbling debts. Employment or educational activities may likewise be adversely impacted by\ngambling disorder; absenteeism or poor work or school performance can occur with gam-\nbling disorder, as individuals may gamble duri ng work or school h ours or be preoccupied\nwith gambling or its adverse co nsequence when they should be working or studying. In-\ndividuals with gambling disorder have poor general health and utilize medical services at\nhigh rates. \nDifferential Diagnosis\nNondisordered gambling. Gambling disorder must be distinguished from professional\nand social gambling. In professional gambling , risks are limited and discipline is central.\nSocial gambling typically occurs with friends or colleagues and lasts for a limited period of\ntime, with acceptable losses. Some individu als can experience problems associated with\ngambling (e.g., short-term chasin g behavior and loss of control) that do not meet the full\ncriteria for gambling disorder. \nManic episode. Loss of judgment and excessive gambling may occur during a manic ep-\nisode. An additional diagnosis of gambling d isorder should be given only if the gambling\nbehavior is not better explained by manic ep isodes (e.g., a histor y of maladaptive gam-\nbling behavior at times other than during a manic episode). Alternatively, an individual\nwith gambling disorder may, during a period of gambling, exhibit behavior that resembles", "source": "dsm5.pdf"} {"id": "c597cdce75e3-1", "page_content": "with gambling disorder may, during a period of gambling, exhibit behavior that resembles\na manic episode, but once the individual is away from the gambling, these manic-like fea-\ntures dissipate.\nPersonality disorders. Problems with gambling may occur in individuals with antisocial\npersonality disorder and other personality disorders. If the criteria are met for both disor-\nders, both can be diagnosed. \nOther medical conditions. Some patients taking dopaminergic medications (e.g., for\nParkinson\u2018s disease) may expe rience urges to gamble. If such symptoms dissipate when\ndopaminergic medications are reduced in dosag e or ceased, then a diagnosis of gambling\ndisorder would not be indicated. \nComorbidity\nGambling disorder is associated with poor general health. In addition, some specific med-\nical diagnoses, such as tachycardia and an gina, are more common among individuals with\ngambling disorder than in the general popula tion, even when other substance use disor-\nders, including tobacco use disorder, are cont rolled for. Individuals with gambling disor-\nder have high rates of comorbidity with ot her mental disorders, such as substance use\ndisorders, depressive d isorders, anxiety disorders, and personality disorders. In some in-\ndividuals, other mental disorders may preced e gambling disorder and be either absent or\npresent during the manifestat ion of gambling disorder. Gamb ling disorder may also occur\nprior to the onset of other ment al disorders, especially anxi ety disorders and substance use\ndisorders.", "source": "dsm5.pdf"} {"id": "e44a7d7977f4-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "bd4fffb98008-0", "page_content": "591Neurocognitive\n Disorders\nThe neurocognitive disorders (NCDs) (referred to in DSM-IV as \u201cDementia,\nDelirium, Amnestic, and Other Cognitive Di sorders\u201d) begin with delirium, followed by\nthe syndromes of major NCD, mild NCD, an d their etiological su btypes. The major or\nmild NCD subtypes are NCD due to Alzheimer\u2019s disease; vascular NCD; NCD with Lewy\nbodies; NCD due to Parkinso n\u2019s disease; frontotemporal NCD; NCD due to traumatic\nbrain injury; NCD due to HIV infection; su bstance/medication-induced NCD; NCD due\nto Huntington\u2019s disease; NC D due to prion disease; NCD du e to another medical condi-\ntion; NCD due to multiple etiologies; and unspecified NCD. The NCD category encom-\npasses the group of disorders in which the primar y clinical deficit is in cognitive function,\nand that are acquired rather than developmental. Although cognitive deficits are present\nin many if not all mental disorders (e.g., schizophrenia, bipolar diso rders), only disorders\nwhose core features are cognitive are includ ed in the NCD category. The NCDs are those\nin which impaired cognition has not been present since birth or very early life, and thus\nrepresents a decline from a previou sly attained level of functioning.\nThe NCDs are unique among DSM-5 categories in that these are syndromes for which\nthe underlying pathology, and frequently the etiology as well, can potentially be deter-\nmined. The various underlying disease entities have all been the subject of extensive re-\nsearch, clinical experience, and expert consen sus on diagnostic crit eria. The DSM-5 criteria", "source": "dsm5.pdf"} {"id": "bd4fffb98008-1", "page_content": "for these disorders have been developed in close consultation with the expert groups for\neach of the disease entities and align as closely as possible with the current consensus cri-\nteria for each of them. The potential utility of biomarkers is also discussed in relation to\ndiagnosis. Dementia is subsumed under the newly named entity major neurocognitive dis-\norder , although the term dementia is not precluded from use in the etiological subtypes in\nwhich that term is standard. Furthermore, DSM-5 recognizes a less severe level of cogni-\ntive impairment, mild neurocognitive disorder, which can also be a focus of care, and which\nin DSM-IV was subsumed under \u201cCognitive Disorder Not Otherwise Specified.\u201d Diagnos-\ntic criteria are provided for both these synd romic entities, followed by diagnostic criteria\nfor the different etiological subtypes. Several of the NCDs frequently coexist with one an-\nother, and their relationships may be multip ly characterized under different chapter sub-\nheadings, including \u201cDifferential Diagnosis\u201d (e.g., NCD due to Alzheimer\u2019s disease vs.\nvascular NCD), \u201cRisk and Prognostic Factors\u201d (e.g., vascular path ology increasing the\nclinical expression of Alzheimer\u2019s disease), and/or \u201cComorbidity\u201d (e.g., mixed Alzhei-\nmer\u2019s disease\u2013vascular pathology). \nThe term dementia is retained in DSM-5 for contin uity and may be used in settings\nwhere physicians and patients are accustomed to this term. Although dementia is the cus-\ntomary term for disorders like the degenerative dementias that usually affect older adults,\nthe term neurocognitive disorder is widely used and often preferred for conditions affect-\ning younger individuals, such as impairment secondary to traumatic brain injury or HIV", "source": "dsm5.pdf"} {"id": "bd4fffb98008-2", "page_content": "ing younger individuals, such as impairment secondary to traumatic brain injury or HIV\ninfection. Furthermore, the major NCD definition is some what broader than the term\ndementia, in that individuals with substantial decline in a single domain can receive this di-\nagnosis, most notably the DSM-IV category of \u201cAmnestic Disorder,\u201d which would now be\ndiagnosed as major NCD due to another medical condition and for which the term demen-\ntia would not be used.", "source": "dsm5.pdf"} {"id": "e3cbf4be0b5a-0", "page_content": "592 Neurocognitive Disorders\nNeurocognitive Domains\nThe criteria for the various NCDs are all base d on defined cognitive domains. Table 1 pro-\nvides for each of the key domains a working definition, examples of symptoms or obser-\nvations regarding impairments in everyday activities, and examples of assessments. The\ndomains thus defined, along with guidelines for clinical thresholds, form the basis on\nwhich the NCDs, their levels, and their subtypes may be diagnosed.", "source": "dsm5.pdf"} {"id": "d3cc162b5ffc-0", "page_content": "Neurocognitive Disorders 593TABLE 1 Neurocognitive domains\nCognitive domain Examples of symptoms or observations Examples of assessments \nComplex attention \n(sustained attention, \ndivided attention, \nselective attention, \nprocessing speed)Major: Has increased difficulty in environments with multiple \nstimuli (TV, radio, conversation); is easily distracted by compet-\ning events in the environment. Is unable to attend unless input is \nrestricted and simplified. Has difficulty holding new information \nin mind, such as recalling phone numbers or addresses just given, \nor reporting what was just said. Is unable to perform mental cal-\nculations. All thinking takes longer than usual, and components \nto be processed must be simplified to one or a few.\nMild: Normal tasks take longer than previously. Begins to find \nerrors in routine task s; finds work needs more double-checking \nthan previously. Thinking is ea sier when not competing with \nother things (radio, TV, other conversations, cell phone, driving).Sustained attention: Maintenance of attention over time (e.g., pressing \na button every time a tone is heard, and over a period of time). \nSelective attention: Maintenance of attention despite competing stim-\nuli and/or distractors: hearing nu mbers and letters read and asked \nto count only letters.\nDivided attention: Attending to two tasks within the same time \nperiod: rapidly tapping while lear ning a story being read. Process-\ning speed can be quantified on any task by timing it (e.g., time to \nput together a design of blocks; time to match symbols with num-\nbers; speed in responding, such as counting speed or serial 3 \nspeed). \nExecutive function \n(planning, decision \nmaking, working", "source": "dsm5.pdf"} {"id": "d3cc162b5ffc-1", "page_content": "speed). \nExecutive function \n(planning, decision \nmaking, working \nmemory, respond-\ning to feedback/\nerror correction, \noverriding habits/\ninhibition, mental \nflexibility)Major: Abandons complex projects. Needs to focus on one task \nat a time. Needs to rely on othe rs to plan instrumental activi-\nties of daily living or make decisions. \nMild: Increased effort required to complete multistage projects. \nHas increased difficulty multitasking or difficulty resuming a \ntask interrupted by a visitor or phone call. May complain of \nincreased fatigue from the extra effort required to organize, \nplan, and make decisions. May repo rt that large social gather-\nings are more taxing or less enjoyable because of increased \neffort required to follow shifting conversations.Planning: Ability to find the exit to a maze; interpret a sequential pic-\nture or object arrangement.\nDecision making: Performance of tasks that assess process of deciding \nin the face of competing alternat ives (e.g., simulated gambling).\nWorking memory: Ability to hold information for a brief period and to \nmanipulate it (e.g., adding up a lis t of numbers or repeating a series \nof numbers or words backward).\nFeedback/error utilization: Ability to benefit from feedback to infer the \nrules for solving a problem.\nOverriding habits/inhibition: Ability to choose a more complex and \neffortful solution to be correct (e.g., looking away from the direc-\ntion indicated by an arrow; naming the color of a word\u2019s font rather \nthan naming the word).\nMental/cognitive flexibility: Ability to shift between two concepts, \ntasks, or response rules (e.g., from number to letter, from verbal to", "source": "dsm5.pdf"} {"id": "d3cc162b5ffc-2", "page_content": "tasks, or response rules (e.g., from number to letter, from verbal to \nkey-press response, from adding numbers to ordering numbers, \nfrom ordering objects by si ze to ordering by color).", "source": "dsm5.pdf"} {"id": "8228e232adda-0", "page_content": "594 Neurocognitive DisordersLearning and mem-\nory (immediate \nmemory, recent \nmemory [including \nfree recall, cued \nrecall, and recogni-\ntion memory], \nvery-long-term \nmemory [semantic; \nautobiographical], \nimplicit learning) Major: Repeats self in conversation, often within the same con-\nversation. Cannot keep track of short list of items when shop-\nping or of plans for the day. Requires frequent reminders to \norient to task at hand.\nMild: Has difficulty recalling recent events, and relies increas-\ningly on list making or calendar. Needs occasional reminders \nor re-reading to keep track of characters in a movie or novel. \nOccasionally may repeat self over a few weeks to the same per-\nson. Loses track of whether bills have already been paid.\nNote: Except in severe forms of major neurocognitive disorder, \nsemantic, autobiographical, an d implicit memory are rela-\ntively preserved, compar ed with recent memory. Immediate memory span: Ability to repeat a list of words or digits. \nNote: Immediate memory sometimes subsumed under \u201cworking \nmemory\u201d (see \u201cExecutive Function\u201d).\nRecent memory: Assesses the process of encoding new information \n(e.g., word lists, a short story, or diagrams). The aspects of recent \nmemory that can be tested include 1) free recall (the person is asked \nto recall as many words, diagrams, or elements of a story as possi-\nble); 2) cued recall (examiner aids recall by providing semantic cues \nsuch as \u201cList all the food items on the list\u201d or \u201cName all of the chil-\ndren from the story\u201d); and 3) re cognition memory (examiner asks", "source": "dsm5.pdf"} {"id": "8228e232adda-1", "page_content": "dren from the story\u201d); and 3) re cognition memory (examiner asks \nabout specific items\u2014e.g., \u201cWas \u2019apple\u2019 on the list?\u201d\u00a0 or \u201cDid you \nsee this diagram or figure?\u201d). Othe r aspects of memory that can be \nassessed include semantic memory (memory for facts), autobio-\ngraphical memory (memory for pers onal events or people), and \nimplicit (procedural) learning (u nconscious learning of skills).\nLanguage (expres-\nsive language \n[including nam-\ning, word finding, \nfluency, and gram-\nmar, and syntax] \nand receptive \nlanguage)Major: Has significant difficulties with expressive or receptive \nlanguage. Often uses general-use phrases such as \u201cthat thing\u201d \nand \u201cyou know what I mean,\u201d and prefers general pronouns \nrather than names. With seve re impairment, may not even \nrecall names of closer friends and family. Idiosyncratic word \nusage, grammatical errors, and spontaneity of output and \neconomy of utterances occur. Stereotypy of speech occurs; \necholalia and automatic speec h typically precede mutism.\nMild: Has noticeable word-finding difficulty. May substitute \ngeneral for specific terms. May avoid use of specific names of \nacquaintances. Grammatical errors involve subtle omission or \nincorrect use of articles, prepos itions, auxiliary verbs, etc. Expressive language: Confrontational naming (identification of objects \nor pictures); fluency (e.g., name as many items as possible in a \nsemantic [e.g., animals] or phonemic [e.g., words starting with \u201cf\u201d] \ncategory in 1 minute).", "source": "dsm5.pdf"} {"id": "8228e232adda-2", "page_content": "category in 1 minute).\nGrammar and syntax (e.g., omission or incorrect use of articles, prep-\nositions, auxiliary verbs): Errors observed during naming and flu-\nency tests are compared with norm s to assess frequency of errors \nand compare with normal slips of the tongue.\nReceptive language: Comprehension (word definition and object-\npointing tasks involving animate and inanimate stimuli): perfor-\nmance of actions/activities according to verbal command.TABLE 1 Neurocognitive domains (continued)\nCognitive domain Examples of symptoms or observations Examples of assessments", "source": "dsm5.pdf"} {"id": "3310d5afb3c5-0", "page_content": "Neurocognitive Disorders 595Perceptual-motor \n(includes abilities \nsubsumed under \nthe terms visual \nperception, visuo-\nconstructional, \nperceptual-motor, \npraxis, and gnosis ) Major: Has significant difficulties with previously familiar activ-\nities (using tools, driving motor vehicle), navigating in familiar \nenvironments; is often more confused at dusk, when shadows \nand lowering levels of light change perceptions. \nMild: May need to rely more on maps or others for directions. \nUses notes and follows others to get to a new place. May find \nself lost or turned around when not concentrating on task.\u00a0Is \nless precise in parking. Needs to expend greater effort for spa-\ntial tasks such as carpentry, assembly, sewing, or knitting.Visual perception: Line bisection tasks can be used to detect basic \nvisual defect or attentional neglect. Motor-free perceptual tasks \n(including facial recognition) require the identification and/or \nmatching of figures\u2014best when task s cannot be verbally mediated \n(e.g., figures are not objects); some require the decision of whether \na figure can be \u201creal\u201d or no t based on dimensionality.\u00a0 \nVisuoconstructional: Assembly of items requiring hand-eye coordina-\ntion, such as drawing, copying, and block assembly. \nPerceptual-motor: Integrating perception with purposeful movement \n(e.g., inserting blocks into a form board without visual cues; rap-\nidly inserting pegs into a slotted board).\nPraxis: Integrity of learned movements, such as ability to imitate \ngestures (wave goodbye) or pant omime use of objects to command \n(\u201cShow me how you would use a hammer\u201d).", "source": "dsm5.pdf"} {"id": "3310d5afb3c5-1", "page_content": "(\u201cShow me how you would use a hammer\u201d).\nGnosis: Perceptual integrity of awaren ess and recognition, such as \nrecognition of faces and colors.\nSocial cognition \n(recognition of \nemotions, theory \nof mind)Major: Behavior clearly out of acceptable social range; shows \ninsensitivity to social standards of modesty in dress or of polit-\nical, religious, or sexual topics of conversation. Focuses exces-\nsively on a topic despite group\u2019s disinterest or direct feedback. \nBehavioral intention without regard to family or friends. \nMakes decisions without regard to safety (e.g., inappropriate \nclothing for weather or social setting). Typically, has little \ninsight into these changes.\nMild: Has subtle changes in behavior or attitude, often described \nas a change in personality, such as less ability to recognize \nsocial cues or read facial expressions, decreased empathy, \nincreased extraversion or introversion, decreased inhibition, \nor subtle or episodic apathy or restlessness.Recognition of emotions: Identification of emot ion in images of faces \nrepresenting a variety of both positive and negative emotions.\nTheory of mind: Ability to consider another person\u2019s mental state \n(thoughts, desires, intentions) or experience\u2014story cards with \nquestions to elicit information about the mental stat e of the individ-\nuals portrayed, such as \u201cWhere will the girl look for the lost bag?\u201d \nor \u201cWhy is the boy sad?\u201d\u00a0 TABLE 1 Neurocognitive domains (continued)\nCognitive domain Examples of symptoms or observations Examples of assessments", "source": "dsm5.pdf"} {"id": "93b6bf655355-0", "page_content": "596 Neurocognitive Disorders\nDelirium\nDiagnostic Criteria \nA. A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift atten-\ntion) and awareness (reduced orientation to the environment).\nB. The disturbance develops over a short period of time (usually hours to a few days), rep-\nresents a change from baseline attention and awareness, and tends to fluctuate in se-\nverity during the course of a day.\nC. An additional disturbance in cognition (e.g., memory deficit, disorientation, language,\nvisuospatial ability, or perception). \nD. The disturbances in Criteria A and C are not better explained by another preexisting,\nestablished, or evolving neurocognitive disorder and do not occur in the context of a\nseverely reduced level of arousal, such as coma.\nE. There is evidence from the history, physical examination, or laboratory findings that the\ndisturbance is a direct physiological consequence of another medical condition, sub-\nstance intoxication or withdrawal (i.e., due to a drug of abuse or to a medication), or\nexposure to a toxin, or is due to multiple etiologies.\nSpecify whether:\nSubstance intoxication delirium: This diagnosis should be made instead of sub-\nstance intoxication when the symptoms in Criteria A and C predominate in the clinical\npicture and when they are sufficiently severe to warrant clinical attention.\nCoding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance] in-\ntoxication delirium are indicated in the table below. Note that the ICD-10-CM code\ndepends on whether or not there is a comorbid substance use disorder present for\nthe same class of substance. If a mild substance use disorder is comorbid with the", "source": "dsm5.pdf"} {"id": "93b6bf655355-1", "page_content": "the same class of substance. If a mild substance use disorder is comorbid with the\nsubstance intoxication delirium, the 4th position character is \u201c1,\u201d and the clinician\nshould record \u201cmild [substance] use disorder\u201d before the substance intoxication de-\nlirium (e.g., \u201cmild cocaine use disorder with cocaine intoxication delirium\u201d). If a mod-\nerate or severe substance use disorder is comorbid with the substance intoxication\ndelirium, the 4th position character is \u201c2,\u201d and the clinician should record \u201cmoderate\n[substance] use disorder\u201d or \u201csevere [substance] use disorder,\u201d depending on the\nseverity of the comorbid substance use disorder. If there is no comorbid substance\nuse disorder (e.g., after a one-time heavy use of the substance), then the 4th posi-\ntion character is \u201c9,\u201d and the clinician should record only the substance intoxication\ndelirium.\nICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate or \nsevereWithout use \ndisorder\nAlcohol 291.0 F10.121 F10.221 F10.921\nCannabis 292.81 F12.121 F12.221 F12.921\nPhencyclidine 292.81 F16.121 F16.221 F16.921\nOther hallucinogen 292.81 F16.121 F16.221 F16.921\nInhalant 292.81 F18.121 F18.221 F18.921\nOpioid 292.81 F11.121 F11.221 F11.921", "source": "dsm5.pdf"} {"id": "a0f332bb7258-0", "page_content": "Delirium 597\nSubstance withdrawal delirium: This diagnosis should be made instead of sub-\nstance withdrawal when the symptoms in Criteria A and C predominate in the clinical\npicture and when they are sufficiently severe to warrant clinical attention.\nCode [specific substance] withdrawal delirium: 291.0 (F10.231) alcohol; 292.0\n(F11.23) opioid; 292.0 (F13.231) sedative, hypnotic, or anxiolytic; 292.0 (F19.231)\nother (or unknown) substance/medication.\nMedication-induced delirium: This diagnosis applies when the symptoms in Criteria\nA and C arise as a side effect of a medication taken as prescribed.\nCoding note: The ICD-9-CM code for [specific medication]-induced delirium is\n292.81. The ICD-10-CM code depends on the type of medication. If the medication\nis an opioid taken as prescribed, the code is F11.921. If the medication is a seda-\ntive, hypnotic, or anxiolytic taken as prescribed, the code is F13.921. If the medica-\ntion is an amphetamine-type or other stimulant taken as prescribed, the code is\nF15.921. For medications that do not fit into any of the classes (e.g., dexametha-\nsone) and in cases in which a substance is judged to be an etiological factor but the\nspecific class of substance is unknown, the code is F19.921.\n293.0 (F05) Delirium due to another medical condition: There is evidence from the\nhistory, physical examination, or laboratory findings that the disturbance is attributable\nto the physiological consequences of another medical condition.", "source": "dsm5.pdf"} {"id": "a0f332bb7258-1", "page_content": "to the physiological consequences of another medical condition.\nCoding note: Include the name of the other medical condition in the name of the\ndelirium (e.g., 293.0 [F05] delirium due to hepatic encephalopathy). The other med-\nical condition should also be coded and listed separately immediately before the\ndelirium due to another medical condition (e.g., 572.2 [K72.90] hepatic encepha-\nlopathy; 293.0 [F05] delirium due to hepatic encephalopathy).\n293.0 (F05) Delirium due to multiple etiologies: There is evidence from the history,\nphysical examination, or laboratory findings that the delirium has more than one etiol-\nogy (e.g., more than one etiological medical condition; another medical condition plus\nsubstance intoxication or medication side effect).\nCoding note: Use multiple separate codes reflecting specific delirium etiologies\n(e.g., 572.2 [K72.90] hepatic encephalopathy, 293.0 [F05] delirium due to hepatic\nfailure; 291.0 [F10.231] alcohol withdrawal de lirium). Note that the etiological med-\nical condition both appears as a separate code that precedes the delirium code and\nis substituted into the delirium due to another medical condition rubric. \nSpecify if:\nAcute: Lasting a few hours or days.\nPersistent: Lasting weeks or months.Sedative, hypnotic, or anxioly tic 292.81 F13.121 F13.221 F13.921\nAmphetamine (or other \nstimulant)292.81 F15.121 F15.221 F15.921", "source": "dsm5.pdf"} {"id": "a0f332bb7258-2", "page_content": "stimulant)292.81 F15.121 F15.221 F15.921\nCocaine 292.81 F14.121 F14.221 F14.921\nOther (or unknown) substance 292.81 F19.121 F19.221 F19.921ICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate or \nsevereWithout use \ndisorder", "source": "dsm5.pdf"} {"id": "82dff363697a-0", "page_content": "598 Neurocognitive Disorders\nSpecify if:\nHyperactive: The individual has a hyperactive level of psychomotor activity that may be\naccompanied by mood lability, agitation, and/or refusal to cooperate with medical care.\nHypoactive: The individual has a hypoactive level of psychomotor activity that may be\naccompanied by sluggishness and lethargy that approaches stupor.\nMixed level of activity: The individual has a normal level of psychomotor activity even\nthough attention and awareness are disturbed. Also includes individuals whose activity\nlevel rapidly fluctuates.\nRecording Procedures\nSubstance intoxication delirium\nICD-9-CM. The name of the substance/medication intoxication delirium begins with\nthe specific substance (e.g., co caine, dexamethasone) that is presumed to be causing the\ndelirium. The diagnostic code is selected from the table includ ed in the criteria set, which\nis based on the drug class. For substances that do not fit into any of the classes (e.g., dexa-\nmethasone), the code for \u201cother substance\u201d should be used; and in cases in which a sub-\nstance is judged to be an etiological factor but the specific class of substance is unknown,\nthe category \u201cunknown substance\u201d should be used.\nThe name of the disorder is followed by the course (i.e., acute, persistent), followed by\nthe specifier indicating level of psychomotor activity (i.e., hyperactive, hypoactive, mixed\nlevel of activity). Unlike the recording proc edures for ICD-10-CM, which combine the sub-\nstance/medication intoxication delirium and subs tance use disorder into a single code, for\nICD-9-CM a separate diagnostic code is give n for the substance use disorder. For example,", "source": "dsm5.pdf"} {"id": "82dff363697a-1", "page_content": "in the case of acute hyperactive intoxication delirium occurring in a man with a severe co-\ncaine use disorder, the diagnosis is 292.81 cocaine intoxication delirium, acute, hyperac-\ntive. An additional diagnosis of 304.20 severe cocaine use disorder is also given. If the\nintoxication delirium occurs without a comorbid substance use disorder (e.g., after a one-\ntime heavy use of the substance), no accompan ying substance use disorder is noted (e.g.,\n292.81 phencyclidine intoxication delirium, acute, hypoactive).\nICD-10-CM. The name of the substance/ medication intoxication de lirium begins with the\nspecific substance (e.g., cocaine, dexamethasone) that is presumed to be causing the delirium.\nThe diagnostic code is selected from the table in cluded in the criteria set, which is based on the\ndrug class and presence or absence of a comorbid substance use disorder. For substances that\ndo not fit into any of the classes (e.g., dexamethasone), the code for \u201cother substance\u201d should\nbe used; and in cases in which a substance is judg ed to be an etiological factor but the specific\nclass of substance is unknown, the category \u201cunknown substance\u201d should be used.\nWhen recording the name of the disorder, the comorbid substance use disorder (if any) is\nlisted first, followed by the word \u201cwith,\u201d foll owed by the name of th e substance intoxication\ndelirium, followed by the course (i.e., acute, persistent), follo wed by the specifier indicating\nlevel of psychomotor activity (i.e., hyperactive, hypoactive, mixed level of activity). For exam-", "source": "dsm5.pdf"} {"id": "82dff363697a-2", "page_content": "ple, in the case of acute hyperactive intoxication delirium occurring in a man with a severe co-\ncaine use disorder, the diagnosis is F14.221 severe cocaine use disorder with cocaine\nintoxication delirium, acute, hy peractive. A separate diagnosis of the comorbid severe cocaine\nuse disorder is not given. If the intoxication delirium occurs without a comorbid substance use\ndisorder (e.g., after a one-time heavy use of the substance), no accompanying substance use\ndisorder is noted (e.g., F16.921 phencyclidine intoxication delirium, acute, hypoactive). \nSubstance withdrawal delirium\nICD-9-CM. The name of the substance/medication withdrawal delirium begins with the\nspecific substance (e.g., alcohol) that is presumed to be causing the withdrawal delirium. The", "source": "dsm5.pdf"} {"id": "0af9659e3abd-0", "page_content": "ICD-9-CM. The name of the substance/medication withdrawal delirium begins with the\nspecific substance (e.g., alcohol) that is presumed to be causing the withdrawal delirium. The\ndiagnostic code is selected from substance-spec ific codes included in the coding note included", "source": "dsm5.pdf"} {"id": "e48c68f8ea3a-0", "page_content": "Delirium 599\nin the criteria set. The name of the disorder is fo llowed by the course (i.e., acute, persistent), fol-\nlowed by the specifier indicating level of psycho motor activity (i.e., hy peractive, hypoactive,\nmixed level of activity). Unlike the recording procedures for ICD-10-CM, which combine the\nsubstance/medication withdrawal delirium and su bstance use disorder into a single code, for\nICD-9-CM a separate diagnostic code is given for the substance use disorder. For example, in\nthe case of acute hyperactive withdrawal delirium occurring in a man with a severe alcohol use\ndisorder, the diagnosis is 291.0 alcohol withdrawal delirium, acute, hyperactive. An additional\ndiagnosis of 303.90 severe alcohol use disorder is also given.\nICD-10-CM. The name of the substa nce/medication withdrawal delirium begins with\nthe specific substance (e.g., al cohol) that is presumed to be causing the withdrawal delir-\nium. The diagnostic code is selected from su bstance-specific codes included in the coding\nnote included in the criteria set. When re cording the name of the disorder, the comorbid\nmoderate or severe substance use disorder (if any) is listed first, followed by the word\n\u201cwith,\u201d followed by the substance withdrawal delirium, followed by the course (i.e., acute,\npersistent), followed by the specifier indicating level of psychomotor activity (i.e., hyper-\nactive, hypoactive, mixed level of activity). Fo r example, in the case of acute hyperactive\nwithdrawal delirium occurring in a man with a severe alcohol use disorder, the diagnosis\nis F10.231 severe alcohol use disorder with alcohol withdrawal delirium, acute, hyperac-", "source": "dsm5.pdf"} {"id": "e48c68f8ea3a-1", "page_content": "tive. A separate diagnosis of the comorbid severe alcohol use disorder is not given. \nMedication-induced delirium. The name of the medication-induced delirium begins\nwith the specific substance (e.g., dexamethasone) that is presumed to be causing the de-\nlirium. The name of the disorder is followed by the course (i.e., acute, persistent), followed\nby the specifier indicating le vel of psychomotor activity (i.e., hyperactive, hypoactive,\nmixed level of activity). For example, in th e case of acute hyperactive medication-induced\ndelirium occurring in a man using dexamethasone as prescribed, the diagnosis is 292.81\n(F19.921) dexamethasone-induced delirium, acute, hyperactive.\nSpecifiers\nRegarding course, in hospital settings, delirium usually lasts about 1 week, but some\nsymptoms often persist even after indivi duals are discharged from the hospital. \nIndividuals with delirium may rapidly switch between hyperactive and hypoactive\nstates. The hyperactive state may be more common or more frequently recognized and\noften is associated with medication side effe cts and drug withdrawal . The hypoactive state\nmay be more frequent in older adults.\nDiagnostic Features\nThe essential feature of deliriu m is a disturbance of attention or awareness that is accom-\npanied by a change in baseline cognition that cannot be better explained by a preexisting\nor evolving neurocognitive disorder (NCD). The disturbance in attention (Criterion A) is\nmanifested by reduced ability to direct, focus, sustain, and shift attention. Questions must\nbe repeated because the individual\u2019s attentio n wanders, or the individual may perseverate\nwith an answer to a previous question rather than appropriately shift attention. The indi-", "source": "dsm5.pdf"} {"id": "e48c68f8ea3a-2", "page_content": "with an answer to a previous question rather than appropriately shift attention. The indi-\nvidual is easily distracted by irrelevant st imuli. The disturbance in awareness is mani-\nfested by a reduced orientation to the environment or at times even to oneself.\nThe disturbance develops over a short period of time, usually hours to a few days, and\ntends to fluctuate during the course of the day, often with worsen ing in the evening and\nnight when external orienting stimuli decrease (Criterion B). There is evidence from the\nhistory, physical examination, or laboratory findings that the disturbance is a physiologi-\ncal consequence of an underlying medical condition, substance intoxication or with-", "source": "dsm5.pdf"} {"id": "b921808313a4-0", "page_content": "history, physical examination, or laboratory findings that the disturbance is a physiologi-\ncal consequence of an underlying medical condition, substance intoxication or with-\ndrawal, use of a medication, or a toxin ex posure, or a combinat ion of these factors\n(Criterion E). The etiology should be coded a ccording to the etiologically appropriate sub-\ntype (i.e., substance or medication intoxica tion, substance withdr awal, another medical", "source": "dsm5.pdf"} {"id": "ae76c0e0f97a-0", "page_content": "600 Neurocognitive Disorders\ncondition, or multiple etiologi es). Delirium often occurs in the context of an underlying\nNCD. The impaired brain function of individuals with mild and major NCD renders them\nmore vulnerable to delirium.\nThere is an accompanying change in at le ast one other area that may include memory\nand learning (particularly recent memory), diso rientation (particularly to time and place),\nalteration in language, or perceptual distorti on or a perceptual-motor disturbance (Crite-\nrion C). The perceptual dist urbances accompanying delirium include misinterpretations,\nillusions, or hallucinations; these disturbances are typically visual, but may occur in other\nmodalities as well, and range from simple an d uniform to highly complex. Normal atten-\ntion/arousal, delirium, and coma lie on a cont inuum, with coma defined as the lack of any\nresponse to verbal stimuli. The ability to evaluate cognition to diagnose delirium depends\non there being a level of arousal sufficient for response to verbal stim ulation; hence, delir-\nium should not be diagnosed in the context of coma (Criterion D). Many noncomatose pa-\ntients have a reduced level of arousal. Those patients who show only minimal responses to\nverbal stimulation are incapable of engaging with attempts at standardized testing or even\ninterview. This inability to engage should be classified as severe inattention. Low-arousal\nstates (of acute onset) should be recognized as indicating severe inattention and cognitive\nchange, and hence delirium. They are clinically indistinguishable from delirium diag-\nnosed on the basis of inattentio n or cognitive change elicited through cognitive testing and\ninterview. \nAssociated Features Supporting Diagnosis", "source": "dsm5.pdf"} {"id": "ae76c0e0f97a-1", "page_content": "interview. \nAssociated Features Supporting Diagnosis\nDelirium is often associated with a disturbanc e in the sleep-wake cycl e. This disturbance\ncan include daytime sleepiness, nighttime ag itation, difficulty falling asleep, excessive\nsleepiness throughout the day, or wakefulnes s throughout the night. In some cases, com-\nplete reversal of the night-day sleep-wake cy cle can occur. Sleep-wake cycle disturbances\nare very common in delirium and have been proposed as a core criterion for the diagnosis.\nThe individual with deliri um may exhibit emotional di sturbances, such as anxiety,\nfear, depression, irritability, anger, euphori a, and apathy. There may be rapid and unpre-\ndictable shifts from one emot ional state to another. The di sturbed emotional state may also\nbe evident in calling out, screaming, cursin g, muttering, moaning, or making other\nsounds. These behaviors are especially prevalent at nigh t and under conditions in which\nstimulation and environmen tal cues are lacking. \nPrevalence\nThe prevalence of delirium is highest amon g hospitalized older individuals and varies\ndepending on the individuals\u2019 characteristics, setting of care, and se nsitivity of the detec-\ntion method. The prevalence of delirium in the community overall is low (1%\u20132%) but in-\ncreases with age, rising to 14% among individuals older than 85 years. The prevalence is\n10%\u201330% in older individuals presenting to emergency departments, where the delirium\noften indicates a medical illness. \nThe prevalence of delirium when individuals are admitted to the hospital ranges from\n14% to 24%, and estimates of the incidence of delirium arising du ring hospitalization", "source": "dsm5.pdf"} {"id": "ae76c0e0f97a-2", "page_content": "range from 6% to 56% in general hospital populations. Delirium occurs in 15%\u201353% of\nolder individuals postoperatively and in 70% \u201387% of those in intensive care. Delirium oc-\ncurs in up to 60% of individuals in nursing ho mes or post\u2013acute care settings and in up to\n83% of all individuals at the end of life.\nDevelopment and Course\nWhile the majority of individuals with deli rium have a full recovery with or without\ntreatment, early recognition and intervention usually shortens the duration of the delir-", "source": "dsm5.pdf"} {"id": "4c6b808f7df3-0", "page_content": "Delirium 601\nium. Delirium may progress to stupor, coma, seizures, or death, particularly if the under-\nlying cause remains untreated. Mortality amon g hospitalized individuals with delirium is\nhigh, and as many as 40% of individuals with delirium, particularly those with malignan-\ncies and other significant underlying medical illness, die within a year after diagnosis. \nRisk and Prognostic Factors \nEnvironmental. Delirium may be increased in the cont ext of functional impairment, im-\nmobility, a history of falls, low levels of activity, and use of drugs and medications with\npsychoactive properties (particularly alcohol and anticholinergics).\nGenetic and physiological. Both major and mild NCDs can increase the risk for delir-\nium and complicate the course. Older individu als are especially susceptible to delirium\ncompared with younger adults. Susceptibilit y to delirium in infancy and through child-\nhood may be greater than in early and mi ddle adulthood. In ch ildhood, delirium may be\nrelated to febrile illnesses and certain medications (e.g., anticholinergics).\nDiagnostic Markers\nIn addition to laboratory find ings characteristic of underlying medical conditions (or in-\ntoxication or withdrawal states), there is often generalized slowing on electroencephalog-\nraphy, and fast activity is oc casionally found (e.g., in some cases of alcohol withdrawal\ndelirium). However, electroence phalography is insufficiently sensitive and specific for di-\nagnostic use.\nFunctional Consequences of Delirium \nDelirium itself is associated with increased functional decline and risk of institutional\nplacement. Hospitalized individuals 65 years or older with delirium have three times the", "source": "dsm5.pdf"} {"id": "4c6b808f7df3-1", "page_content": "placement. Hospitalized individuals 65 years or older with delirium have three times the\nrisk of nursing home placemen t and about three times the func tional decline as hospital-\nized patients without delirium at both discharge and 3 months postdischarge. \nDifferential Diagnosis \nPsychotic disorders and bipolar and depre ssive disorders with psychotic features.\nDelirium that is characterized by vivid hallucinations, delusions, language disturbances,\nand agitation must be distinguished from br ief psychotic disorder, schizophrenia, schizo-\nphreniform disorder, and other psychotic disord ers, as well as from bipolar and depres-\nsive disorders with psychotic features.\nAcute stress disorder. Delirium associated with fear, an xiety, and dissociative symptoms,\nsuch as depersonalization, must be distingu ished from acute stress disorder, which is pre-\ncipitated by exposure to a severely traumatic event.\nMalingering and factitious disorder. Delirium can be distinguished from these disor-\nders on the basis of the often atypical presen tation in malingering and factitious disorder\nand the absence of another medical condition or substance that is etiologically related to\nthe apparent cognitive disturbance.\nOther neurocognitive disorders. The most common differential diagnostic issue when\nevaluating confusion in older adults is dise ntangling symptoms of delirium and dementia.\nThe clinician must determine whether the in dividual has delirium; a delirium superim-\nposed on a preexisting NCD, such as that due to Alzheimer\u2019s disease; or an NCD without\ndelirium. The traditional distinction between delirium and dementia according to acute-\nness of onset and temporal course is particularly difficult in those elderly individuals who\nhad a prior NCD that may not have been reco gnized, or who develop persistent cognitive", "source": "dsm5.pdf"} {"id": "4c6b808f7df3-2", "page_content": "had a prior NCD that may not have been reco gnized, or who develop persistent cognitive\nimpairment following an episode of delirium.", "source": "dsm5.pdf"} {"id": "132f4dcfd83a-0", "page_content": "602 Neurocognitive Disorders\nOther Specified Delirium\n780.09 (R41.0)\nThis category applies to presentations in which symptoms characteristic of delirium that\ncause clinically significant distress or impairm ent in social, occupational, or other impor-\ntant areas of functioning predominate but do not meet the full criteria for delirium or any of\nthe disorders in the neurocognitive disorders diagnostic class. The other specified delirium\ncategory is used in situations in which the clinician chooses to communicate the specific\nreason that the presentation does not meet the criteria for delirium or any specific neuro-\ncognitive disorder. This is done by recording \u201cother specified delirium\u201d followed by the spe-\ncific reason (e.g., \u201cattenuated delirium syndrome\u201d).\nAn example of a presentation that can be specified using the \u201cother specified\u201d desig-\nnation is the following:\nAttenuated delirium syndrome: This syndrome applies in cases of delirium in which\nthe severity of cognitive impairment falls short of that required for the diagnosis, or in\nwhich some, but not all, diagnostic criteria for delirium are met.\nUnspecified Delirium\n780.09 (R41.0)\nThis category applies to presentations in which symptoms characteristic of delirium that\ncause clinically significant distress or impairm ent in social, occupational, or other impor-\ntant areas of functioning predominate but do not meet the full criteria for delirium or any of\nthe disorders in the neurocognitive disorder s diagnostic class. The unspecified delirium\ncategory is used in situations in which the clinician chooses not to specify the reason that\nthe criteria are not met for delirium, and includes presentations for which there is insuffi-\ncient information to make a more specific diagnosis (e.g., in emergency room settings).", "source": "dsm5.pdf"} {"id": "132f4dcfd83a-1", "page_content": "cient information to make a more specific diagnosis (e.g., in emergency room settings).\nMajor and Mild Neurocognitive Disorders\nMajor Neurocognitive Disorder\nDiagnostic Criteria\nA. Evidence of significant cognitive decline from a previous level of performance in one\nor more cognitive domains (complex attent ion, executive function, learning and mem-\nory, language, perceptual-motor, or social cognition) based on:\n1. Concern of the individual, a knowledgeable informant, or the clinician that there has\nbeen a significant decline in cognitive function; and\n2. A substantial impairment in cognitive performance, preferably documented by stan-\ndardized neuropsychological testing or, in its absence, another quantified clinical\nassessment.\nB. The cognitive deficits interfere with independence in everyday activities (i.e., at a min-\nimum, requiring assistance with complex instrumental activities of daily living such as\npaying bills or managing medications).\nC. The cognitive deficits do not occur e xclusively in the context of a delirium.", "source": "dsm5.pdf"} {"id": "3e37ba963d43-0", "page_content": "Major and Mild Neurocognitive Disorders 603\nD. The cognitive deficits are not better explai ned by another mental disorder (e.g., major\ndepressive disorder, schizophrenia).\nSpecify whether due to:\nAlzheimer\u2019s disease (pp. 611\u2013614)\nFrontotemporal lobar degeneration (pp. 614\u2013618)\nLewy body disease (pp. 618\u2013621)\nVascular disease (pp. 621\u2013624)\nTraumatic brain injury (pp. 624\u2013627)\nSubstance/medication use (pp. 627\u2013632)\nHIV infection (pp. 632\u2013634)\nPrion disease (pp. 634\u2013636)\nParkinson\u2019s disease (pp. 636\u2013638)\nHuntington\u2019s disease (pp. 638\u2013641)\nAnother medical condition (pp. 641\u2013642)\nMultiple etiologies (pp. 642\u2013643)\nUnspecified (p. 643)\nCoding note: Code based on medical or substance etiology. In some cases, there is need\nfor an additional code for the etiological medi cal condition, which must immediately pre-\ncede the diagnostic code for major neurocognitive disorder, as follows: \nEtiological subtypeAssociated etiological \nmedical code for major \nneurocognitive disorderaMajor neurocogni-\ntive disorder codebMild neurocogni-\ntive disorder codec\nAlzheimer\u2019s \ndiseaseProbable: 331.0 (G30.9)\nPossible: no additional \nmedical codeProbable: 294.1x \n(F02.8x)\nPossible: 331.9 \n(G31.9)c331.83 (G31.84)\n(Do not use addi-", "source": "dsm5.pdf"} {"id": "3e37ba963d43-1", "page_content": "(Do not use addi-\ntional code for \nAlzheimer\u2019s \ndisease.)\nFrontotemporal \nlobar degeneration Probable: 331.19 \n(G31.09)\nPossible: no additional \nmedical codeProbable: 294.1x \n(F02.8x)\nPossible: 331.9 \n(G31.9)c331.83 (G31.84) \n(Do not use addi-\ntional code for \nfrontotemporal \ndisease.)\nLewy body disease Probable: 331.82 \n(G31.83)\nPossible: no additional \nmedical codeProbable: 294.1x \n(F02.8x)\nPossible: 331.9 \n(G31.9)c331.83 (G31.84) \n(Do not use addi-\ntional code for \nLewy body disease.)\nVascular disease No additional medical \ncodeProbable: 290.40 \n(F01.5x)\nPossible: 331.9 \n(G31.9)c331.83 (G31.84) \n(Do not use addi-\ntional code for the \nvascular disease.)\nTraumatic brain \ninjury907.0 (S06.2X9S) 294.1x (F02.8x) 331.83 (G31.84)\n(Do not use additional \ncode for the trau-\nmatic brain injury.)\nSubstance/\nmedication-\ninducedNo additional medical \ncodeCode based on the \ntype of substance \ncausing the major \nneurocognitive \ndisorderc, dCode based on the \ntype of substance", "source": "dsm5.pdf"} {"id": "3e37ba963d43-2", "page_content": "disorderc, dCode based on the \ntype of substance \ncausing the mild \nneurocognitive \ndisorderd", "source": "dsm5.pdf"} {"id": "5af21aea5c37-0", "page_content": "604 Neurocognitive Disorders\nHIV infection 042 (B20) 294.1x (F02.8x) 331.83 (G31.84) \n(Do not use addi-\ntional code for HIV \ninfection.)\nPrion disease 046.79 (A81.9) 294.1x (F02.8x) 331.83 (G31.84)\n(Do not use addi-\ntional code for \nprion disease.)\nParkinson\u2019s \ndiseaseProbable: 332.0 (G20)\nPossible: No additional \nmedical codeProbable: 294.1x \n(F02.8x)\nPossible: 331.9 \n(G31.9)c331.83 (G31.84) \n(Do not use addi-\ntional code for \nParkinson\u2019s \ndisease.)\nHuntington\u2019s \ndisease333.4 (G10) 294.1x (F02.8x) 331.83 (G31.84)\n(Do not use addi-\ntional code for \nHuntington\u2019s \ndisease.)\nDue to another \nmedical conditionCode the other medical \ncondition first \n(e.g., 340 [G35] \nmultiple sclerosis)294.1x (F02.8x) 331.83 (G31.84)\n(Do not use addi-\ntional codes for the \npresumed etiologi-\ncal medical condi-\ntions.)\nDue to multiple \netiologiesCode all of the etiological \nmedical conditions first \n(with the exception of \nvascular disease) 294.1x (F02.8x) \n(Plus the code for", "source": "dsm5.pdf"} {"id": "5af21aea5c37-1", "page_content": "(Plus the code for \nthe relevant sub-\nstance/medication-\ninduced major neu-\nrocognitive disor-\nders if substances \nor medications \nplay a role in the \netiology.)331.83 (G31.84) \n(Plus the code for \nthe relevant sub-\nstance/medication-\ninduced mild neuro-\ncognitive disor-\nders if substances \nor medications play \na role in the etiol-\nogy. Do not use ad-\nditional codes for \nthe presumed \netiological medical \nconditions.)\nUnspecified neuro-\ncognitive disorderNo additional medical \ncode799.59 (R41.9) 799.59 (R41.9)\naCode first, before code for major neurocognitive disorder.\nbCode fifth character based on symptom specifier: .x0 without behavioral disturbance; .x1 with be-\nhavioral disturbance (e.g., psychotic symptoms, mo od disturbance, agitatio n, apathy, or other be-\nhavioral symptoms).\ncNote: Behavioral disturbance specifier cannot be coded but should still be indicated in writing.\ndSee \u201cSubstance/Medication-Induced Majo r or Mild Neurocognitive Disorder.\u201dEtiological subtypeAssociated etiological \nmedical code for major \nneurocognitive disorderaMajor neurocogni-\ntive disorder codebMild neurocogni-\ntive disorder codec", "source": "dsm5.pdf"} {"id": "c4ec325f6ceb-0", "page_content": "Major and Mild Neurocognitive Disorders 605\nSpecify: \nWithout behavioral disturbance: If the cognitive disturbance is not accompanied by\nany clinically significant behavioral disturbance.\nWith behavioral disturbance (specify disturbance): If the cognitive disturbance is ac-\ncompanied by a clinically significant behavioral disturbance (e.g., psychotic symptoms,\nmood disturbance, agitation, apathy, or other behavioral symptoms).\nSpecify current severity:\nMild: Difficulties with instrumental activities of daily living (e.g., housework, managing\nmoney).\nModerate: Difficulties with basic activities of daily living (e.g., feeding, dressing).\nSevere: Fully dependent.\nMild Neurocognitive Disorder\nDiagnostic Criteria\nA. Evidence of modest cognitive decline from a previous level of performance in one or\nmore cognitive domains (complex attention, executive function, learning and memory,\nlanguage, perceptual-motor, or social cognition) based on:\n1. Concern of the individual, a knowledgeable informant, or the clinician that there has\nbeen a mild decline in cognitive function; and\n2. A modest impairment in cognitive per formance, preferably documented by stan-\ndardized neuropsychological testing or, in its absence, another quantified clinical\nassessment.\nB. The cognitive deficits do not interfere with capacity for independence in everyday\nactivities (i.e., complex instrumental activities of daily living such as paying bills or\nmanaging medications are preserved, but gr eater effort, compensatory strategies, or\naccommodation may be required).\nC. The cognitive deficits do not occur e xclusively in the context of a delirium.\nD. The cognitive deficits are not better explai ned by another mental disorder (e.g., major\ndepressive disorder, schizophrenia).\nSpecify whether due to:\nAlzheimer\u2019s disease (pp. 611\u2013614)", "source": "dsm5.pdf"} {"id": "c4ec325f6ceb-1", "page_content": "Specify whether due to:\nAlzheimer\u2019s disease (pp. 611\u2013614)\nFrontotemporal lobar degeneration (pp. 614\u2013618)\nLewy body disease (pp. 618\u2013621)\nVascular disease (pp. 621\u2013624)\nTraumatic brain injury (pp. 624\u2013627)\nSubstance/medication use (pp. 627\u2013632)\nHIV infection (pp. 632\u2013634)\nPrion disease (pp. 634\u2013636)\nParkinson\u2019s disease (pp. 636\u2013638)\nHuntington\u2019s disease (pp. 638\u2013641)\nAnother medical condition (pp. 641\u2013642)\nMultiple etiologies (pp. 642\u2013643)\nUnspecified (p. 643)\nCoding note: For mild neurocognitive disorder due to any of the medical etiologies listed\nabove, code 331.83 (G31.84). Do not use additional codes for the presumed etiological\nmedical conditions. For substance/medicati on-induced mild neurocognitive disorder, code\nbased on type of substance; see \u201cSubstance/ Medication-Induced Major or Mild Neurocog-\nnitive Disorder.\u201d For unspecified mild neurocognitive disorder, code 799.59 (R41.9).", "source": "dsm5.pdf"} {"id": "ddde3cde8f35-0", "page_content": "606 Neurocognitive Disorders\nSpecify: \nWithout behavioral disturbance: If the cognitive disturbance is not accompanied by\nany clinically significant behavioral disturbance.\nWith behavioral disturbance (specify disturbance): If the cognitive disturbance is ac-\ncompanied by a clinically significant behavioral disturbance (e.g., psychotic symptoms,\nmood disturbance, agitation, apathy, or other behavioral symptoms).\nSubtypes\nMajor and mild neurocognitive disorders (NCD s) are primarily subtyped according to the\nknown or presumed etiological/pa thological entity or entities underlying the cognitive de-\ncline. These subtypes are distin guished on the basis of a combin ation of time course, charac-\nteristic domains affected, and associated sy mptoms. For certain etio logical subtypes, the\ndiagnosis depends substantially on the presence of a potentially causative entity, such as Par-\nkinson\u2019s or Huntington\u2019s disease, or a traumati c brain injury or stroke in the appropriate time\nperiod. For other etiological subt ypes (generally the neurodegenerative diseases like Alzhei-\nmer\u2019s disease, frontotemporal lobar degenerati on, and Lewy body disease), the diagnosis is\nbased primarily on the cognitive, behavioral, an d functional symptoms. Typically, the differ-\nentiation among these syndromes that lack an independently recognized etiological entity is\nclearer at the level of major NCD than at the level of mild NCD, but sometimes characteristic\nsymptoms and associated features are present at the mild level as well. \nNCDs are frequently managed by clinicians in multiple disciplines. For many sub-\ntypes, multidisciplinary international expert groups have developed specialized consen-\nsus criteria based on clinicopathological corr elation with underlying brain pathology. The\nsubtype criteria here have been harm onized with those expert criteria.\nSpecifiers", "source": "dsm5.pdf"} {"id": "ddde3cde8f35-1", "page_content": "subtype criteria here have been harm onized with those expert criteria.\nSpecifiers\nEvidence for distinct be havioral features in NCDs has been recognized, particularly in the\nareas of psychotic symptoms and depression . Psychotic features are common in many\nNCDs, particularly at the mild-to-moderate stage of major NCDs due to Alzheimer\u2019s dis-\nease, Lewy body disease, an d frontotemporal lobar degene ration. Paranoia and other\ndelusions are common features, and often a persecutory theme may be a prominent aspect\nof delusional ideation. In contrast to psychotic disorders with onset in earlier life (e.g.,\nschizophrenia), disorganized speech and diso rganized behavior are not characteristic of\npsychosis in NCDs. Hallucinations may occur in any modality, although visual hallucina-\ntions are more common in NCDs than in de pressive, bipolar, or psychotic disorders.\nMood disturbances, including depression, anxiety, and elat ion, may occur. Depression\nis common early in the course (including at the mild NCD level) of NCD due to Alzhei-\nmer\u2019s disease and Parkinson\u2019s disease, while elation may occur more commonly in fron-\ntotemporal lobar degeneration. When a full a ffective syndrome meetin g diagnostic criteria\nfor a depressive or bipolar disorder is pres ent, that diagnosis should be coded as well.\nMood symptoms are increasingly recognized to be a significant feature in the earliest stages\nof mild NCDs such that clinical recogn ition and intervention may be important.\nAgitation is common in a wide variety of NCDs, particularly in major NCD of moder-\nate to severe severity, and often occurs in th e setting of confusion or frustration. It may", "source": "dsm5.pdf"} {"id": "ddde3cde8f35-2", "page_content": "ate to severe severity, and often occurs in th e setting of confusion or frustration. It may\narise as combative behaviors, particularly in the context of resisting caregiving duties such\nas bathing and dressing. Agitation is characte rized as disruptive motor or vocal activity\nand tends to occur with advanced stages of cognitive impairment across all of the NCDs.\nIndividuals with NCD can present with a wi de variety of behavioral symptoms that\nare the focus of treatment. Sleep disturbance is a common symptom that can create a need\nfor clinical attention and may include symptoms of insomnia, hypersomnia, and circadian", "source": "dsm5.pdf"} {"id": "47d105e1fe68-0", "page_content": "are the focus of treatment. Sleep disturbance is a common symptom that can create a need\nfor clinical attention and may include symptoms of insomnia, hypersomnia, and circadian\nrhythm disturbances.", "source": "dsm5.pdf"} {"id": "eec291eed380-0", "page_content": "Major and Mild Neurocognitive Disorders 607\nApathy is common in mild and mild major NCD. It is observed particularly in NCD due\nto Alzheimer\u2019s disease and ma y be a prominent feature of NCD due to frontotemporal\nlobar degeneration. Apathy is typically char acterized by diminished motivation and re-\nduced goal-directed behavior accompanied by decreased emotional responsiveness.\nSymptoms of apathy may manifest early in the course of NCDs when a loss of motivation\nto pursue daily activities or hobbies may be observed.\nOther important behavioral symptoms include wandering, disinhibition, hyperpha-\ngia, and hoarding. Some of these symptoms are characteristic of specific disorders, as dis-\ncussed in the relevant sections. When more th an one behavioral disturbance is observed,\neach type should be noted in writing with the specifier \u201cwith behavioral symptoms.\u201d \nDiagnostic Features\nMajor and mild NCDs exist on a spectrum of cognitive and functional impairment. Major\nNCD corresponds to the conditio n referred to in DSM-IV as dementia, retained as an alter-\nnative in this volume. The co re feature of NCDs is acquir ed cognitive decline in one or\nmore cognitive domains (Criterion A) based on both 1) a concern about cognition on the\npart of the individual, a knowledgeable informant, or the clinician, and 2) performance on\nan objective assessment that falls below the expected level or that has been observed to de-\ncline over time. Both a concer n and objective evidence are re quired because they are com-\nplementary. When there is an exclusive focus on objectiv e testing, a disorder may go\nundiagnosed in high-functioning individuals whose currently \u201cnormal\u201d performance ac-\ntually represents a substantial decline in abilities, or an illness may be incorrectly diag-", "source": "dsm5.pdf"} {"id": "eec291eed380-1", "page_content": "tually represents a substantial decline in abilities, or an illness may be incorrectly diag-\nnosed in individuals whose currently \u201clow\u201d performance does not represent a change\nfrom their own baseline or is a result of extraneous factors li ke test conditions or a passing\nillness. Alternatively, excessive focus on subj ective symptoms may fail to diagnose illness\nin individuals with poor insigh t, or whose informants deny or fail to notice their symptoms,\nor it may be overly sensitiv e in the so-called worried well.\nA cognitive concern differs from a complaint in that it may or may not be voiced spon-\ntaneously. Rather, it may need to be elicited by careful questioning about specific symp-\ntoms that commonly occur in individuals wi th cognitive deficits (see Table 1 in the\nintroduction to this chapter). For example, memory concerns include difficulty remember-\ning a short grocery list or keeping track of the plot of a television program; executive con-\ncerns include difficulty resuming a task wh en interrupted, organizing tax records, or\nplanning a holiday meal. At the mild NCD level, the individual is likely to describe these\ntasks as being more difficult or as requiring ex tra time or effort or compensatory strategies.\nAt the major NCD level, such tasks may on ly be completed with assistance or may be\nabandoned altogether. At the mild NCD level, individuals and their families may not no-\ntice such symptoms or may view them as norm al, particularly in the elderly; thus, careful\nhistory taking is of paramount importance. The difficulties must represent changes rather\nthan lifelong patterns: the individual or info rmant may clarify this i ssue, or the clinician\ncan infer change from prior experience with the patient or from occupational or other\nclues. It is also critical to determine that the difficulties are related to cognitive loss rather", "source": "dsm5.pdf"} {"id": "eec291eed380-2", "page_content": "clues. It is also critical to determine that the difficulties are related to cognitive loss rather\nthan to motor or sensory limitations. \nNeuropsychological testing, with performance compared with norms appropriate to\nthe patient\u2019s age, educational attainment, and cultural background, is part of the standard\nevaluation of NCDs and is part icularly critical in the evaluation of mild NCD. For major\nNCD, performance is typically 2 or more standard deviations below appropriate norms", "source": "dsm5.pdf"} {"id": "2b5b71fd39ac-0", "page_content": "evaluation of NCDs and is part icularly critical in the evaluation of mild NCD. For major\nNCD, performance is typically 2 or more standard deviations below appropriate norms\n(3rd percentile or below). For mild NCD, performance typically lies in the 1\u20132 standard de-\nviation range (between the 3rd and 16th perc entiles). However, neur opsychological test-\ning is not available in all settings, and neuropsychological thresholds are sensitive to the\nspecific test(s) and norms employed, as well as to test conditions, sensory limitations, and\nintercurrent illness. A variety of brief office-based or \u201cbedside\u201d asse ssments, as described", "source": "dsm5.pdf"} {"id": "0184da59cf14-0", "page_content": "608 Neurocognitive Disorders\nin Table 1, can also supply objective data in settings where such testing is unavailable or\ninfeasible. In any case, as with cognitive co ncerns, objective perfor mance must be inter-\npreted in light of the individual\u2019s prior pe rformance. Optimally, this information would\nbe available from a prior administration of the same test, but often it must be inferred\nbased on appropriate norms, along with the individual\u2019s educational history, occupation,\nand other factors. Norms are more challenging to interpret in individuals with very high\nor very low levels of education and in indivi duals being tested outside their own language\nor cultural background. \nCriterion B relates to the individual\u2019s leve l of independence in everyday functioning.\nIndividuals with major NCD will have impairment of sufficient severity so as to interfere\nwith independence, such that others will have to take over tasks that the individuals were\npreviously able to complete on their own. Individuals with mild NCD will have preserved\nindependence, although there may be subtle in terference with function or a report that\ntasks require more effort or take more time than previously. \nThe distinction between major and mild NCD is inherently arbitrary, and the disorders\nexist along a continuum. Precis e thresholds are therefore difficult to determine. Careful\nhistory taking, observation, and integration wi th other findings are required, and the im-\nplications of diagnosis should be considered when an individual\u2019s clinical manifestations\nlie at a boundary.\nAssociated Features Supporting Diagnosis\nTypically the associated features that suppo rt a diagnosis of major or mild NCD will be\nspecific to the etiological subtype (e.g., neur oleptic sensitivity and visual hallucinations in\nNCD due to Lewy body disease). Diagnostic features specific to each of the subtypes are\nfound in the relevant sections.\nPrevalence", "source": "dsm5.pdf"} {"id": "0184da59cf14-1", "page_content": "found in the relevant sections.\nPrevalence\nThe prevalence of NCD varies widely by ag e and by etiological su btype. Overall preva-\nlence estimates are generally only availabl e for older population s. Among individuals\nolder than 60 years, prevalence increases steep ly with age, so prev alence estimates are\nmore accurate for narrow age bands than for br oad categories such as \u201cover 65\u201d (where the\nmean age can vary greatly with the life expect ancy of the given population). For those eti-\nological subtypes occurring across the lifespa n, prevalence estimates for NCD are likely to\nbe available, if at all, only as the fraction of individuals who develop NCD among those\nwith the relevant condition (e.g., tr aumatic brain injury, HIV infection).\nOverall prevalence estimates for dementia (which is largely congruent with major\nNCD) are approximately 1%\u20132% at age 65 years and as high as 30% by age 85 years. The\nprevalence of mild NCD is very sensitive to th e definition of the di sorder, particularly in\ncommunity settings, where evaluations are less de tailed. In addition, in contrast with clin-\nical settings, where cognitive concern must be high to seek and locate care, there may be a\nless clear decline from baseline functioning. Es timates of the prevalence of mild cognitive\nimpairment (which is substantially congruent with mild NCD) among older individuals\nare fairly variable, ranging from 2% to 10% at age 65 and 5% to 25% by age 85.\nDevelopment and Course \nThe course of NCD varies acro ss etiological subtypes, and this variation can be useful in\ndifferential diagnosis. Some subtypes (e.g., those related to traumatic brain injury or", "source": "dsm5.pdf"} {"id": "0184da59cf14-2", "page_content": "differential diagnosis. Some subtypes (e.g., those related to traumatic brain injury or\nstroke) typically begin at a specific time and (at least after initial symptoms related to in-\nflammation or swelling subside) remain stat ic. Others may fluctuate over time (although\nif this occurs, the possibility of delirium superimposed on NCD should be considered).\nNCDs due to neurodegenerative diseases like Alzheimer\u2019s disease or frontotemporal\nlobar degeneration typically are marked by insidious onset and gradual progression, and", "source": "dsm5.pdf"} {"id": "9e7af252cf07-0", "page_content": "Major and Mild Neurocognitive Disorders 609\nthe pattern of onset of cognitive deficits and associated features helps to distinguish among\nthem. \nNCDs with onset in childhood and adolescence may have broad repercussions for so-\ncial and intellectual development, and in th is setting intellectual disability (intellectual\ndevelopmental disorder) and/or other neurod evelopmental disorders may also be diag-\nnosed to capture the full diagnostic picture and ensure the provision of a broad range of\nservices. In older individuals, NCDs often occu r in the setting of medical illnesses, frailty,\nand sensory loss, which complicate the clin ical picture for diagnosis and treatment. \nWhen cognitive loss occurs in youth to midlife, individuals and families are likely to\nseek care. NCDs are typically easiest to identify at younger ages, although in some settings\nmalingering or other factitious disorders may be a concern. Very late in life, cognitive\nsymptoms may not cause concern or may go unnoticed. In late life, mild NCD must also be\ndistinguished from the more mo dest deficits associated with \u201cnormal aging,\u201d although a\nsubstantial fraction of what has been ascribe d to normal aging likely represents prodromal\nphases of various NCDs. In addition, it beco mes harder to recognize mild NCD with age\nbecause of the increasing prevalence of me dical illness and sensory deficits. It becomes\nharder to differentiate among subtypes with ag e because there are multiple potential sources\nof neurocognitive decline.\nRisk and Prognostic Factors \nRisk factors vary not only by etiological subtype but also by age at onset within etiological\nsubtypes. Some subtypes are distributed thro ughout the lifespan, whereas others occur\nexclusively or primarily in late life. Even within the NCDs of aging, the relative prevalence", "source": "dsm5.pdf"} {"id": "9e7af252cf07-1", "page_content": "varies with age: Alzheimer\u2019s disease is unco mmon before age 60 years, and the prevalence\nincreases steeply thereafter, while the overa ll less common frontotemporal lobar degener-\nation has earlier onset and represents a progre ssively smaller fraction of NCDs with age. \nGenetic and physiological. The strongest risk factor for major and mild NCDs is age,\nprimarily because age increases the risk of neurodegenerative and cerebrovascular dis-\nease. Female gender is associat ed with higher prevalence of dementia overall, and especially\nAlzheimer\u2019s disease, but this difference is larg ely, if not wholly, attr ibutable to greater lon-\ngevity in females. \nCulture-Related Diagnostic Issues\nIndividuals\u2019 and families\u2019 level of awareness and concern about neurocognitive symp-\ntoms may vary across ethnic and occupational groups. Neurocognitive symptoms are\nmore likely to be noticed, particularly at the mild level, in individuals who engage in com-\nplex occupational, domestic, or recreational activities. In addition , norms for neuropsy-\nchological testing tend to be available only for broad populations, and thus they may not\nbe easily applicable to individuals with less than high school ed ucation or those being\nevaluated outside their primary language or culture. \nGender-Related Diagnostic Issues\nLike age, culture, and occupa tion, gender issues may affect the level of concern and aware-\nness of cognitive symptoms. In addition, for la te-life NCDs, females are likely to be older,\nto have more medical comorbidity, and to liv e alone, which can complicate evaluation and\ntreatment. In addition, there are gender differ ences in the frequency of some of the etio-\nlogical subtypes.\nDiagnostic Markers", "source": "dsm5.pdf"} {"id": "9e7af252cf07-2", "page_content": "logical subtypes.\nDiagnostic Markers\nIn addition to a careful history, neuropsych ological assessments are the key measures for\ndiagnosis of NCDs, particularly at the mild level, where functional changes are minimal", "source": "dsm5.pdf"} {"id": "c95d788e40f4-0", "page_content": "610 Neurocognitive Disorders\nand symptoms more subtle. Ideally, individu als will be referred for formal neuropsycho-\nlogical testing, which will provide a quantitative assessment of all relevant domains and\nthus help with diagnosis; provide guidance to the family on areas where the individual\nmay require more support; and serve as a be nchmark for further decline or response to\ntherapies. When such testing is unavailable or not feasible, the brief assessments in Table 1\ncan provide insight into each domain. More glob al brief mental status tests may be helpful\nbut may be insensitive, particul arly to modest changes in a single domain or in those with\nhigh premorbid abilities, and may be overly sensitive in those with low premorbid abilities.\nIn distinguishing among etiological subtypes, additional diagnostic markers may\ncome into play, particularly neuroimaging studies such as magnetic resonance imaging\nscans and positron emission tomography scans. In addition, specific markers may be in-\nvolved in the assessment of specific subtypes and may become more important as addi-\ntional research findings accumulate over time, as discussed in the relevant sections. \nFunctional Consequences of \nMajor and Mild Neurocognitive Disorders \nBy definition, major and mild NCDs affect func tioning, given the central role of cognition in\nhuman life. Thus, the criteria for the disorder s, and the threshold for differentiating mild\nfrom major NCD, are based in part on functi onal assessment. Within major NCD there is a\nbroad range of functional impairment, as implem ented in the severity specifiers. In addition,\nthe specific functions that are compromised can help identify the cognitive domains affected,\nparticularly when neuropsychological testing is not available or is difficult to interpret. \nDifferential Diagnosis\nNormal cognition. The differential diagnosis between normal cognition and mild NCD,", "source": "dsm5.pdf"} {"id": "c95d788e40f4-1", "page_content": "Differential Diagnosis\nNormal cognition. The differential diagnosis between normal cognition and mild NCD,\nas between mild and major NCD, is challenging because the boundaries are inherently ar-\nbitrary. Careful history taking and objective as sessment are critical to these distinctions. A\nlongitudinal evaluation using quantified a ssessments may be key in detecting mild NCD.\nDelirium. Both mild and major NCD may be difficult to distinguish from a persistent de-\nlirium, which can co-occur. Careful assessment of attention and arou sal will help to make\nthe distinction.\nMajor depressive disorder. The distinction between mild NCD and major depressive\ndisorder, which may co-occur with NCD, can also be challenging. Specific patterns of cog-\nnitive deficits may be helpfu l. For example, consistent memory and executive function\ndeficits are typical of Alzheimer\u2019s disease, whereas nonspecific or more variable perfor-\nmance is seen in major depression. Alternat ively, treatment of the depressive disorder\nwith repeated observation over time may be required to make the diagnosis.\nSpecific learning disorder and other neurodevelopmental disorders. A careful clari-\nfication of the individual\u2019s baseline status will help distinguish an NCD from a specific\nlearning disorder or other neurodevelopmental disorders. Additional issues may enter the\ndifferential for specific etiological subtypes, as described in the relevant sections.\nComorbidity \nNCDs are common in older individuals and thus often co-occur with a wide variety of age-\nrelated diseases that may co mplicate diagnosis or treatme nt. Most notable of these is\ndelirium, for which NCD increases the risk. In older individuals, a delirium during hos-", "source": "dsm5.pdf"} {"id": "c95d788e40f4-2", "page_content": "pitalization is, in many cases, the first time that an NCD is noticed, although a careful his-\ntory will often reveal evidence of earlier decline. Mixed NC Ds are also common in older\nindividuals, as many etiological entities incre ase in prevalence with age. In younger indi-\nviduals, NCD often co-occurs with neurodevelop mental disorders; for example, a head in-", "source": "dsm5.pdf"} {"id": "f51e91283e7c-0", "page_content": "Major or Mild Neurocognitive Disorder Due to Alzheimer\u2019s Disease 611\njury in a preschool child may also lead to significant developmental and learning issues.\nAdditional comorbidity of NCD is often relate d to the etiological subtype, as discussed in\nthe relevant sections. \nMajor or Mild Neurocognitive Disorder\n Due to Alzheimer\u2019s Disease\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. There is insidious onset and gradual progression of impairment in one or more cognitive\ndomains (for major neurocognitive disorder, at least two domains must be impaired).\nC. Criteria are met for either probable or possible Alzheimer\u2019s disease as follows:\nFor major neurocognitive disorder:\nProbable Alzheimer\u2019s disease is diagnosed if either of the following is present; oth-\nerwise, possible Alzheimer\u2019s disease should be diagnosed.\n1. Evidence of a causative Alzheimer\u2019s disease genetic mutation from family history\nor genetic testing. \n2. All three of the following are present:\na. Clear evidence of decline in memory and learning and at least one other cogni-\ntive domain (based on detailed history or serial neuropsychological testing).\nb. Steadily progressive, gradual decline in cognition, without extended plateaus.\nc. No evidence of mixed etiology (i.e., absence of other neurodegenerative or\ncerebrovascular disease, or another neurological, mental, or systemic disease\nor condition likely contributing to cognitive decline).\nFor mild neurocognitive disorder:\nProbable Alzheimer\u2019s disease is diagnosed if there is evidence of a causative Alz-\nheimer\u2019s disease genetic mutation from either genetic testing or family history.\nPossible Alzheimer\u2019s disease is diagnosed if there is no evidence of a causative Alz-\nheimer\u2019s disease genetic mutation from either genetic testing or family history, and all", "source": "dsm5.pdf"} {"id": "f51e91283e7c-1", "page_content": "heimer\u2019s disease genetic mutation from either genetic testing or family history, and all\nthree of the following are present:\n1. Clear evidence of decline in memory and learning.\n2. Steadily progressive, gradual decline in cognition, without extended plateaus.\n3. No evidence of mixed etiology (i.e., absence of other neurodegenerative or cere-\nbrovascular disease, or another neurologica l or systemic disease or condition likely\ncontributing to cognitive decline).\nD. The disturbance is not better explained by cerebrovascular disease, another neurode-\ngenerative disease, the effects of a substance, or another mental, neurological, or sys-\ntemic disorder.\nCoding note: For probable major neurocognitive disorder due to Alzheimer\u2019s disease,\nwith behavioral disturbance, code first 331.0 (G30.9) Alzheimer\u2019s disease, followed by\n294.11 (F02.81) major neurocognitive disorder due to Alzheimer\u2019s disease. For probable\nneurocognitive disorder due to Alzheimer\u2019s disease, without behavioral disturbance, code\nfirst 331.0 (G30.9) Alzheimer\u2019s disease, followed by 294.10 (F02.80) major neurocognitive\ndisorder due to Alzheimer\u2019s disease, without behavioral disturbance.\nFor possible major neurocognitive disor der due to Alzheimer\u2019s disease, code 331.9\n(G31.9) possible major neurocognitive disorder due to Alzheimer\u2019s disease. ( Note: Do not\nuse the additional code for Alzheimer\u2019s disease. Behavioral disturbance cannot be coded\nbut should still be indicated in writing.)", "source": "dsm5.pdf"} {"id": "b55b7c071645-0", "page_content": "612 Neurocognitive Disorders\nFor mild neurocognitive disorder due to Alzheimer\u2019s disease, code 331.83 (G31.84).\n(Note: Do not use the additional code for Alzheimer\u2019s disease. Behavioral disturbance\ncannot be coded but should still be indicated in writing.)\nDiagnostic Features \nBeyond the neurocognitive disorder (NCD) syndro me (Criterion A), the core features of ma-\njor or mild NCD due to Alzheimer\u2019s disease include an insidious onset and gradual pro-\ngression of cognitive and beha vioral symptoms (Criterion B) . The typical presentation is\namnestic (i.e., with impairment in memory and learning). Unusual nonamnestic presen-\ntations, particularly visuospa tial and logopenic aphasic vari ants, also exist. At the mild\nNCD phase, Alzheimer\u2019s disease manifests typically with impairment in memory and learn-\ning, sometimes accompanied by deficits in executive function. At the major NCD phase,\nvisuoconstructional/perceptual -motor ability and language w ill also be impaired, partic-\nularly when the NCD is moderate to severe. Social cognition tends to be preserved until\nlate in the course of the disease. \nA level of diagnostic certainty must be sp ecified denoting Alzheimer\u2019s disease as the\n\u201cprobable\u201d or \u201cpossible\u201d etiology (Criterion C). Probable Alzheimer\u2019s disease is diagnosed in\nboth major and mild NCD if there is evidence of a causative Alzheimer\u2019s disease gene, ei-\nther from genetic testing or from an autosomal dominant family history coupled with au-\ntopsy confirmation or a genetic test in an affected family member. For major NCD, a\ntypical clinical picture, without extended plat eaus or evidence of mixed etiology, can also", "source": "dsm5.pdf"} {"id": "b55b7c071645-1", "page_content": "typical clinical picture, without extended plat eaus or evidence of mixed etiology, can also\nbe diagnosed as due to probab le Alzheimer\u2019s disease. For mild NCD, given the lesser de-\ngree of certainty that the deficits will prog ress, these features are only sufficient for a\npossible Alzheimer\u2019s etiology. If the etiology appe ars mixed, mild NCD due to multiple eti-\nologies should be diagnosed. In any case, for both mild and major NCD due to Alzhei-\nmer\u2019s disease, the clinical features must no t suggest another primary etiology for the NCD\n(Criterion D). \nAssociated Features Supporting Diagnosis\nIn specialty clinical settings, approximately 80% of individuals with major NCD due to\nAlzheimer\u2019s disease have behavioral and psyc hological manifestations; these features are\nalso frequent at the mild NCD stage of impa irment. These symptoms are as or more dis-\ntressing than cognitive manifestations and ar e frequently the reason that health care is\nsought. At the mild NCD stage or the mildest level of majo r NCD, depression and/or ap-\nathy are often seen. With moderately severe major NCD, psychotic fe atures, irritability,\nagitation, combativeness, and wandering are common. Late in the illness, gait distur-\nbance, dysphagia, incontinence, myoc lonus, and seizures are observed.\nPrevalence\nThe prevalence of overall deme ntia (major NCD) rises steeply with age. In high-income\ncountries, it ranges from 5% to 10% in the seventh decade to at least 25% thereafter. U.S.\ncensus data estimates suggest that approxim ately 7% of individuals diagnosed with Alz-", "source": "dsm5.pdf"} {"id": "b55b7c071645-2", "page_content": "heimer\u2019s disease are between ages 65 and 74 years, 53% are between ages 75 and 84 years,\nand 40% are 85 years and older. The percentage of dementias attributable to Alzheimer\u2019s\ndisease ranges from about 60% to over 90%, depending on the setting and diagnostic cri-\nteria. Mild NCD due to Alzheimer\u2019s disease is likely to represent a substantial fraction of\nmild cognitive impairment (MCI) as well.\nDevelopment and Course\nMajor or mild NCD due to Alzheimer\u2019s disease progresses gradually, sometimes with\nbrief plateaus, through severe dementia to death. The mean duration of survival after di-", "source": "dsm5.pdf"} {"id": "2eac55f64161-0", "page_content": "Major or Mild Neurocognitive Disorder Due to Alzheimer\u2019s Disease 613\nagnosis is approximately 10 years, reflecting th e advanced age of the majority of individ-\nuals rather than the course of the disease; some individuals can live with the disease for as\nlong as 20 years. Late-stage individuals are eventually mute and bedbound. Death most\ncommonly results from aspiration in those who survive through the full course. In mild\nNCD due to Alzheimer\u2019s disease, impairments increase over time, and functional status\ngradually declines until symptoms reach the threshold for the diagnosis of major NCD. \nThe onset of symptoms is usually in the eighth and ninth decades; early-onset forms\nseen in the fifth and sixth decades are often related to known causative mutations. Symp-\ntoms and pathology do not differ markedly at different onset ages. However, younger in-\ndividuals are more likely to survive the full course of the disease, while older individuals\nare more likely to have numerous medical co morbidities that affect the course and man-\nagement of the illness. Diagnostic complexity is higher in older adults because of the in-\ncreased likelihood of comorbid me dical illness and mixed pathology.\nRisk and Prognostic Factors\nEnvironmental. Traumatic brain injury increases risk for major or mild NCD due to Alz-\nheimer\u2019s disease.\nGenetic and physiological. Age is the strongest risk factor for Alzheimer\u2019s disease. The\ngenetic susceptibility polymorphism apolipoprotein E4 increases risk and decreases age\nat onset, particularly in homozygous individu als. There are also extremely rare causative\nAlzheimer\u2019s disease genes. Individuals with Down\u2019s syndrome (trisomy 21) develop Alz-\nheimer\u2019s disease if they survive to midlife. Multiple vascular risk factors influence risk for", "source": "dsm5.pdf"} {"id": "2eac55f64161-1", "page_content": "heimer\u2019s disease if they survive to midlife. Multiple vascular risk factors influence risk for\nAlzheimer\u2019s disease and may act by increasing cerebrovascular pathology or also through\ndirect effects on Alzheimer pathology. \nCulture-Related Diagnostic Issues\nDetection of an NCD may be more difficult in cultural and socioeconomic settings where\nmemory loss is considered normal in old age, where older adults face fewer cognitive de-\nmands in everyday life, or where very low educational levels pose greater challenges to\nobjective cognitive assessment.\nDiagnostic Markers\nCortical atrophy, amyloid-predominant neuritic plaques, and tau-predominant neurofibril-\nlary tangles are hallmarks of the pathological diagnosis of Alzheimer\u2019s disease and may be\nconfirmed via postmortem histopathological examination. For early-onset cases with auto-\nsomal dominant inheritance, a mutation in on e of the known causative Alzheimer\u2019s disease\ngenes\u2014amyloid precursor protein (APP), presen ilin 1 (PSEN1), or presenilin 2 (PSEN2)\u2014\nmay be involved, and genetic testing for such mutations is commercially available, at least\nfor PSEN1. Apolipoprotein E4 cannot serve as a diagnostic marker because it is only a risk\nfactor and neither necessary nor sufficient for disease occurrence.\nSince amyloid beta-42 deposition in the br ain occurs early in the pathophysiological\ncascade, amyloid-based diagnostic tests such as amyloid imaging on brain positron emis-\nsion tomography (PET) scans and reduced leve ls of amyloid beta-42 in the cerebrospinal\nfluid (CSF) may have diagnostic value. Signs of neuronal injury, such as hippocampal and\ntemporoparietal cortical atrophy on a magnetic resonance image scan, temporoparietal", "source": "dsm5.pdf"} {"id": "2eac55f64161-2", "page_content": "temporoparietal cortical atrophy on a magnetic resonance image scan, temporoparietal\nhypometabolism on a fluorodeoxyglucose PET sc an, and evidence for elevated total tau\nand phospho-tau levels in CSF, provide evidence of neuronal damage but are less specific\nfor Alzheimer\u2019s disease. At present, these biomarkers are not fully validated, and many\nare available only in tertiary care settings. However, some of them, along with novel bio-\nmarkers, will likely move into wider clinical practice in the coming years.", "source": "dsm5.pdf"} {"id": "e6a3600e33dd-0", "page_content": "614 Neurocognitive Disorders\nFunctional Consequences of Major or Mild \nNeurocognitive Disorder Du e to Alzheimer\u2019s Disease\nThe prominence of memory loss can cause significant difficulties relatively early in the\ncourse. Social cognition (and thus social func tioning) and procedural memory (e.g., danc-\ning, playing musical instruments) may be relatively preserved for extended periods.\nDifferential Diagnosis\nOther neurocognitive disorders. Major and mild NCDs due to other neurodegenera-\ntive processes (e.g., Lewy body disease, fron totemporal lobar degene ration) share the in-\nsidious onset and gradual decline caused by Alzheimer\u2019s disease but have distinctive core\nfeatures of their own. In major or mild vascular NCD, th ere is typically history of stroke\ntemporally related to the onset of cognitive impairment, and infarcts or white matter hy-\nperintensities are judged sufficient to accoun t for the clinical picture. However, particu-\nlarly when there is no clear hi story of stepwise decline, ma jor or mild vascular NCD can\nshare many clinical features with Alzheimer\u2019s disease. \nOther concurrent, active neurological or systemic illness. Other neurological or sys-\ntemic illness should be considered if there is an appropriate temporal relationship and\nseverity to account for the clinical picture. At the mild NCD level, it may be difficult to dis-\ntinguish an Alzheimer\u2019s disease etiology from that of another medical condition (e.g., thy-\nroid disorders, vitamin B12 deficiency). \nMajor depressive disorder. Particularly at the mild NCD level, the differential diagnosis\nalso includes major depression. The presence of depression may be associated with re-\nduced daily functioning and poor concentration that may resemble an NCD, but improve-\nment with treatment of depression may be useful in making the distinction. \nComorbidity", "source": "dsm5.pdf"} {"id": "e6a3600e33dd-1", "page_content": "ment with treatment of depression may be useful in making the distinction. \nComorbidity\nMost individuals with Alzheimer\u2019s disease are elderly and have multiple medical conditions\nthat can complicate diagnosis and influence th e clinical course. Major or mild NCD due to\nAlzheimer\u2019s disease commonly co-occurs with cerebrovascular disease, which contributes\nto the clinical picture. When a comorbid condition contribute s to the NCD in an individual\nwith Alzheimer\u2019s disease, then NCD due to multiple etiologies should be diagnosed.\nMajor or Mild Frontotemporal\nNeurocognitive Disorder\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. The disturbance has insidious onset and gradual progression.\nC. Either (1) or (2):\n1. Behavioral variant:\na. Three or more of the following behavioral symptoms:\ni. Behavioral disinhibition.\nii. Apathy or inertia.\niii. Loss of sympathy or empathy.\niv. Perseverative, stereotyped or compulsive/ritualistic behavior.\nv. Hyperorality and dietary changes.\nb. Prominent decline in social cognition and/or executive abilities.", "source": "dsm5.pdf"} {"id": "258fe4e80718-0", "page_content": "Major or Mild Frontotemporal Neurocognitive Disorder 615\n2. Language variant:\na. Prominent decline in language ability, in the form of speech production, word\nfinding, object naming, grammar, or word comprehension.\nD. Relative sparing of learning and memory and perceptual-motor function.\nE. The disturbance is not better explained by cerebrovascular disease, another neurode-\ngenerative disease, the effects of a substance, or another mental, neurological, or sys-\ntemic disorder.\nProbable frontotemporal neurocognitive disorder is diagnosed if either of the following\nis present; otherwise, possible frontotemporal neurocognitive disorder should be di-\nagnosed: \n1. Evidence of a causative frontotemporal neur ocognitive disorder genetic mutation, from\neither family history or genetic testing.\n2. Evidence of disproportionate frontal and/or temporal lobe involvement from neuroim-\naging.\nPossible frontotemporal neurocognitive disorder is diagnosed if there is no evidence\nof a genetic mutation, and neuroimaging has not been performed.\nCoding note: For probable major neurocognitive disorder due to frontotemporal lobar de-\ngeneration, with behavioral disturbance, code first 331.19 (G31.09) frontotemporal dis-\nease, followed by 294.11 (F02.81) probable major neurocognitive disorder due to\nfrontotemporal lobar degeneration, with behavioral disturbance. For probable major neu-\nrocognitive disorder due to frontotemporal lobar degeneration, without behavioral distur-\nbance, code first 331.19 (G31.09) frontotemporal disease, followed by 294.10 (F02.80)\nprobable major neurocognitive disorder due to frontotemporal lobar degeneration, without", "source": "dsm5.pdf"} {"id": "258fe4e80718-1", "page_content": "probable major neurocognitive disorder due to frontotemporal lobar degeneration, without\nbehavioral disturbance.\nFor possible major neurocognitive disorder due to frontotemporal lobar degeneration, code\n331.9 (G31.9) possible major neurocognitive disorder due to frontotemporal lobar degen-\neration. ( Note: Do not use the additional code for frontote mporal disease. Behavioral distur-\nbance cannot be coded but should still be indicated in writing.)\nFor mild neurocognitive disorder due to frontotemporal lobar degeneration, code 331.83\n(G31.84). (Note: Do not use the additional code for frontotemporal disease. Behavioral\ndisturbance cannot be coded but should still be indicated in writing.)\nDiagnostic Features\nMajor or mild frontotemporal neurocognitive disorder (NCD) comprises a number of syn-\ndromic variants characterized by the progressi ve development of behavioral and personality\nchange and/or language impairment. The behavioral variant and three language variants (se-\nmantic, agrammatic/nonfluent, and logopenic) ex hibit distinct patterns of brain atrophy and\nsome distinctive neuropathology. The criteria must be met for either the behavioral or the lan-\nguage variant to make the diagnosis, but many individuals present with features of both.\nIndividuals with behavioral-variant major or mild frontotemporal NCD present with\nvarying degrees of apathy or disinhibition. They may lose interest in socialization, self-\ncare, and personal responsibilities, or displa y socially inappropriate behaviors. Insight is\nusually impaired, and this often delays medical consultation. The first referral is often to a\npsychiatrist. Individuals may develop changes in social style, and in religious and political", "source": "dsm5.pdf"} {"id": "258fe4e80718-2", "page_content": "psychiatrist. Individuals may develop changes in social style, and in religious and political\nbeliefs, with repetitive movements, hoarding, changes in ea ting behavior, and hyperoral-\nity. In later stages, loss of sphincter contro l may occur. Cognitive decline is less prominent,\nand formal testing may show relatively few deficits in the early stages. Common neuro-\ncognitive symptoms are lack of planning and organization, distractib ility, and poor judg-\nment. Deficits in executive function, such as poor performance on tests of mental", "source": "dsm5.pdf"} {"id": "0d579a69ebcf-0", "page_content": "616 Neurocognitive Disorders\nflexibility, abstract reasoning, and response inhibition, are present, but learning and mem-\nory are relatively spared, and perceptual-mot or abilities are almost always preserved in\nthe early stages. \nIndividuals with language-variant major or mild frontotemporal NCD present with pri-\nmary progressive aphasia with gradual onse t, with three subtypes commonly described:\nsemantic variant, agrammatic/n onfluent variant, and logopenic variant, and each variant\nhas distinctive features and corresponding neuropathology.\n\u201cProbable\u201d is distinguished from \u201cpossibl e\u201d frontotemporal NCD by the presence of\ncausative genetic factors (e.g., mutations in the gene coding for microtubule-associated pro-\ntein tau) or by the presence of distinctive at rophy or reduced activity in frontotemporal re-\ngions on structural or functional imaging. \nAssociated Features Supporting Diagnosis\nExtrapyramidal features may be prominent in some cases, with an overlap with syn-\ndromes such as progressive supranuclear pa lsy and corticobasal dege neration. Features of\nmotor neuron disease may be present in some cases (e.g., muscle atrophy, weakness). A\nsubset of individuals develop visual hallucinations.\nPrevalence\nMajor or mild frontotemporal NCD is a common cause of early-onset NCD in individuals\nyounger than 65 years. Population prevalen ce estimates are in th e range of 2\u201310 per\n100,000. Approximately 20%\u201325% of cases of frontotemporal NCD occur in individuals\nolder than 65 years. Frontotemporal NCD accoun ts for about 5% of all cases of dementia in", "source": "dsm5.pdf"} {"id": "0d579a69ebcf-1", "page_content": "unselected autopsy series. Prevalence estima tes of behavioral variant and semantic lan-\nguage variant are higher among males, and prevalence estimates of nonfluent language\nvariant are higher among females. \nDevelopment and Course\nIndividuals with major or m ild frontotemporal NCD commonly present in the sixth de-\ncade of life, although the age at onset varies from the third to the ninth decades. The dis-\nease is gradually progressive, with median survival being 6\u201311 years after symptom onset\nand 3\u20134 years after diagnosis. Survival is shorter and decline is faster in major or mild fron-\ntotemporal NCD than in typical Alzheimer\u2019s disease. \nRisk and Prognostic Factors\nGenetic and physiological. Approximately 40% of individuals with major or mild fron-\ntotemporal NCD have a family history of early-onset NCD, and approximately 10% show an\nautosomal dominant inheritance pattern. A number of genetic factors have been identified,\nsuch as mutations in the gene encoding the microtubule asso ciated protein tau (MAPT), the\ngranulin gene (GRN), and the C9ORF72 gene. A number of families with causative muta-\ntions have been identified (see the section \u201cD iagnostic Markers\u201d for th is disorder), but many\nindividuals with known familial transmission do not have a known mutation. The presence\nof motor neuron disease is associated with a more rapi d deterioration. \nDiagnostic Markers\nComputed tomography (CT) or structural magnetic resonance imaging (MRI) may show\ndistinct patterns of atrophy. In behavioral-variant major or mild frontotemporal NCD,\nboth frontal lobes (especially the medial frontal lobes) and the anterior temporal lobes are", "source": "dsm5.pdf"} {"id": "0d579a69ebcf-2", "page_content": "both frontal lobes (especially the medial frontal lobes) and the anterior temporal lobes are\natrophic. In semantic language\u2013variant majo r or mild frontotemporal NCD, the middle,\ninferior, and anterior temporal lobes are at rophic bilaterally but asymmetrically, with the", "source": "dsm5.pdf"} {"id": "e27a7bf27674-0", "page_content": "Major or Mild Frontotemporal Neurocognitive Disorder 617\nleft side usually being more affected. Nonfluent la nguage\u2013variant major or mild fronto-\ntemporal NCD is associated with predominantly left posterior fr ontal-insular atrophy.\nThe logopenic variant of major or mild fron totemporal NCD is associated with predomi-\nnantly left posterior perisylvian or parietal atrophy. Functional imaging demonstrates hy-\npoperfusion and/or cortical hypometabolism in the corresponding brain regions, which\nmay be present in the early stages in the abse nce of structural abno rmality. Emerging bio-\nmarkers for Alzheimer\u2019s disease (e.g., cerebrospinal fluid amyl oid-beta and tau levels, and\namyloid imaging) may help in the differential diagnosis, but the dist inction from Alzhei-\nmer\u2019s disease can remain difficult (the logopeni c variant is in fact often a manifestation of\nAlzheimer\u2019s disease).\nIn familial cases of frontotemporal NCD, the identification of genetic mutations may\nhelp confirm the diagnosis. Mutations associated with frontote mporal NCD include\nthe genes encoding microtubule-associated protein tau (MAPT) and granulin (GRN),\nC9ORF72, transactive response DNA-binding protein of 43 kDa (TDP-43, or TARDBP),\nvalosin-containing protein (V CP), chromatin modifying protein 2B (CHMP2B), and fused\nin sarcoma protein (FUS). \nFunctional Consequences of Major or Mild \nFrontotemporal Neurocognitive Disorder\nBecause of the relative early age at onset of the disorder, the disorder oftens affects work-\nplace and family life. Because of the involvem ent of language and/or behavior, function is", "source": "dsm5.pdf"} {"id": "e27a7bf27674-1", "page_content": "often more severely impaired relatively early in the course . For individuals with the be-\nhavioral variant, prior to diagnostic clarific ation there may be significant family disrup-\ntion, legal involvement, and problems in the workplace because of socially inappropriate\nbehaviors. The functional impairment due to behavioral change and language dysfunc-\ntion, which can include hyperorality, impuls ive wandering, and other dishinhibited be-\nhaviors, may far exceed that due to the co gnitive disturbance and may lead to nursing\nhome placement or institutionalization. Thes e behaviors can be severely disruptive, even\nin structured care settings, particularly wh en the individuals are otherwise healthy, non-\nfrail, and free of othe r medical comorbidities. \nDifferential Diagnosis\nOther neurocognitive disorders. Other neurodegenerative diseases may be distinguished\nfrom major or mild frontotemporal NCD by th eir characteristic features. In major or mild\nNCD due to Alzheimer\u2019s disease, decline in learning and memory is an early feature.\nHowever, 10%\u201330% of patients presenting with a syndrome suggestive of major or mild\nfrontotemporal NCD are found at autopsy to have Alzheimer\u2019s disease pathology. This oc-\ncurs more frequently in individuals who present with progressi ve dysexecutive syn-\ndromes in the absence of behavioral changes or movement disorder or in those with the\nlogopenic variant.\nIn major or mild NCD with Lewy bodies, co re and suggestive features of Lewy bodies\nmust be present. In major or mild NCD due to Parkinson\u2019s disease, spontaneous parkin-\nsonism emerges well befo re the cognitive decline. In majo r or mild vascular NCD, depend-\ning on affected brain regions, there may also be loss of executive ability and behavioral", "source": "dsm5.pdf"} {"id": "e27a7bf27674-2", "page_content": "ing on affected brain regions, there may also be loss of executive ability and behavioral\nchanges such as apathy, and this disorder should be considered in the differential diagno-\nsis. However, history of a cerebrovascular event is temporally related to the onset of cog-\nnitive impairment in major or mild vascular NCD, and neuroimaging reveals infarctions\nor white matter lesions sufficient to account for the clinical picture. \nOther neurological conditions. Major or mild frontotemporal NCD overlaps with pro-\ngressive supranuclear palsy, corticobasal degeneration, and motor neuron disease\nclinically as well as pathologically. Progressive supranuclear palsy is characterized by", "source": "dsm5.pdf"} {"id": "acd424b40587-0", "page_content": "618 Neurocognitive Disorders\nsupranuclear gaze palsies and axial-predominant parkinsoni sm. Pseudobulbar signs may\nbe present, and retropulsion is often prom inent. Neurocognitive assessment shows psy-\nchomotor slowing, poor working memory, and executive dysfunction. Corticobasal degen-\neration presents with asymmetr ic rigidity, limb apraxia, postural instability, myoclonus,\nalien limb phenomenon, and cortical sensory loss. Many individuals wi th behavioral-variant\nmajor or mild frontotemporal NCD show features of motor neuron disease, which tend to\nbe mixed upper and predominantly lower motor neuron disease. \nOther mental disorders and medical conditions. Behavioral-variant major or mild fron-\ntotemporal NCD may be mistaken for a primary mental disorder, such as major depression,\nbipolar disorders, or schizophrenia, and individuals with this variant often present initially\nto psychiatry. Over time, the development of progressive neurocognitive difficulties will\nhelp to make the distinction. A careful medi cal evaluation will help to exclude treatable\ncauses of NCDs, such as meta bolic disturbances, nutritional deficiencies, and infections. \nMajor or Mild Neurocognitive Disorder\nWith Lewy Bodies\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. The disorder has an insidious onset and gradual progression.\nC. The disorder meets a combination of core diagnostic features and suggestive diagnos-\ntic features for either probable or possibl e neurocognitive disorder with Lewy bodies.\nFor probable major or mild neurocognitive disorder with Lewy bodies, the indi-\nvidual has two core features, or one suggestive feature with one or more core features.", "source": "dsm5.pdf"} {"id": "acd424b40587-1", "page_content": "vidual has two core features, or one suggestive feature with one or more core features.\nFor possible major or mild neurocognitive disorder with Lewy bodies, the individ-\nual has only one core feature, or one or more suggestive features.\n1. Core diagnostic features: \na. Fluctuating cognition with pronounced variations in attention and alertness.\nb. Recurrent visual hallucinations that are well formed and detailed.\nc. Spontaneous features of parkinsonism, with onset subsequent to the develop-\nment of cognitive decline.\n2. Suggestive diagnostic features:\na. Meets criteria for rapid eye movement sleep behavior disorder.\nb. Severe neuroleptic sensitivity.\nD. The disturbance is not better explained by cerebrovascular disease, another neurode-\ngenerative disease, the effects of a substance, or another mental, neurological, or sys-\ntemic disorder.\nCoding note: For probable major neurocognitive disorder with Lewy bodies, with behav-\nioral disturbance, code first 331.82 (G31.83) Lewy body disease, followed by 294.11\n(F02.81) probable major neurocognitive disorder with Lewy bodies, with behavioral distur-\nbance. For probable major neurocognitive disorder with Lewy bodies, without behavioral\ndisturbance, code first 331.82 (G31.83) Lewy body disease, followed by 294.10 (F02.80)\nprobable major neurocognitive disorder with Lewy bodies, without behavioral disturbance.\nFor possible major neurocognitive disorder with Lewy bodies, code 331.9 (G31.9) possible\nmajor neurocognitive disorder with Lewy bodies. ( Note: Do not use the additional code for", "source": "dsm5.pdf"} {"id": "acd424b40587-2", "page_content": "Lewy body disease. Behavioral disturbance cannot be coded but should still be indicated\nin writing.)", "source": "dsm5.pdf"} {"id": "3d8530893195-0", "page_content": "Major or Mild Neurocognitive Disorder With Lewy Bodies 619\nFor mild neurocognitive disorder with Lewy bodies, code 331.83 (G31.84). ( Note: Do not\nuse the additional code for Lewy body disease. Behavioral disturbance cannot be coded\nbut should still be indicated in writing.)\nDiagnostic Features\nMajor or mild neurocognitive disorder with Lewy bodies (NCDLB), in the case of major\nneurocognitive disorder (NCD), corresponds to the condition known as dementia with\nLewy bodies (DLB). The disorder includes not only progressive cognitive impairment\n(with early changes in complex attention and ex ecutive function rather than learning and\nmemory) but also recurrent complex visual hallucinations; and concurrent symptoms of\nrapid eye movement (REM) sleep behavior diso rder (which can be a very early manifes-\ntation); as well as hallucinations in other sensory modalities, depression, and delusions.\nThe symptoms fluctuate in a pattern that can resemble a delirium, but no adequate under-\nlying cause can be found. The variable pres entation of NCDLB symptoms reduces the like-\nlihood of all symptoms being observed in a brief clinic visit and necessitates a thorough\nassessment of caregive r observations. The use of assessment scales specifically designed to\nassess fluctuation may aid in diagnosis. Anot her core feature is spontaneous parkinson-\nism, which must begin after the onset of cognit ive decline; by convention, major cognitive\ndeficits are observed at least 1 year befo re the motor symptoms. The parkinsonism must\nalso be distinguished from neuroleptic-induce d extrapyramidal signs. Accurate diagnosis\nis essential to safe treatment planning, as up to 50% of individuals with NCDLB have se-", "source": "dsm5.pdf"} {"id": "3d8530893195-1", "page_content": "vere sensitivity to neuroleptic drugs, and these medications should be used with extreme\ncaution in managing the psychotic manifestations.\nThe diagnosis of mild NCDLB is appropriate for individuals who present with the core\nor suggestive features at a stage when cognitive or functional impairments are not of suf-\nficient severity to fulfill criteria for major NC D. However, as for all mild NCDs, there will\noften be insufficient ev idence to justify any si ngle etiology, and use of the unspecified di-\nagnosis is most appropriate.\nAssociated Features Supporting Diagnosis\nIndividuals with NCDLB frequently experience repeated falls and syncope and transient\nepisodes of unexplained loss of consciousness. Autonomic dysfunction, such as ortho-\nstatic hypotension and urinary incontinen ce, may be observed. Auditory and other\nnonvisual hallucinations are common, as are sy stematized delusions, delusional misiden-\ntification, and depression.\nPrevalence\nThe few population-based prev alence estimates for NCDLB available range from 0.1% to\n5% of the general elderly popu lation, and from 1.7% to 30.5 % of all dementia cases. In\nbrain bank (autopsy) series, the pathological lesions known as Lewy bodies are present in\n20%\u201335% of cases of dementia. The male-to- female ratio is approximately 1.5:1. \nDevelopment and Course \nNCDLB is a gradually progressive disorder with insidious onset. However, there is often\na prodromal history of confusional episodes (delirium) of acute onset, often precipitated\nby illness or surgery. The distinction between NCDLB, in which Lewy bodies are primar-", "source": "dsm5.pdf"} {"id": "3d8530893195-2", "page_content": "ily cortical in location, and major or mild NC D due to Parkinson\u2019s disease, in which the pa-\nthology is primarily in the basal ganglia, is the order in which th e cognitive and motor\nsymptoms emerge. In NCDLB, th e cognitive decline is manifest ed early in the course of ill-\nness, at least a year before the onset of mo tor symptoms (see the section \u201cDifferential Di-", "source": "dsm5.pdf"} {"id": "51c1f56013e3-0", "page_content": "620 Neurocognitive Disorders\nagnosis\u201d for this disorder). Disease course may be characterized by occasional plateaus\nbut eventually progresses through severe deme ntia to death. Average duration of survival\nis 5\u20137 years in clinical series. Onset of symptoms is typically observed from the sixth\nthrough the ninth decades of life, with most cases having their onset when affected indi-\nviduals are in their mid-70s.\nRisk and Prognostic Factors \nGenetic and physiological. Familial aggregation may occur, and several risk genes have\nbeen identified, but in most cases of NCDLB, there is no family history.\nDiagnostic Markers\nThe underlying neurodegenerative disease is primarily a synucleinopathy due to alpha-\nsynuclein misfolding and aggregation. Cognitiv e testing beyond the use of a brief screen-\ning instrument may be necessary to define de ficits clearly. Assessment scales developed to\nmeasure fluctuation can be useful. The associated condition REM sl eep behavior disorder\nmay be diagnosed through a formal sleep study or identified by questioning the patient or\ninformant about relevant symptoms. Neurolep tic sensitivity (challenge) is not recom-\nmended as a diagnostic marker but raises suspicion of NCDLB if it occurs. A diagnosti-\ncally suggestive feature is low striatal dopa mine transporter uptake on single photon\nemission computed tomography (SPECT) or positron emission tomography (PET) scan.\nOther clinically useful markers potentially include relative preservation of medial tempo-\nral structures on computed tomography (C T)/magnetic resonance imaging (MRI) brain\nscan; reduced striatal dopamine transporter uptake on SPECT/PET scan; generalized low\nuptake on SPECT/PET perfusion scan with re duced occipital activity; abnormal (low up-", "source": "dsm5.pdf"} {"id": "51c1f56013e3-1", "page_content": "take) MIBG myocardial scintigraphy suggest ing sympathetic denervation; and prominent\nslow-wave activity on the electroencephalo gram with temporal lobe transient waves.\nFunctional Consequences of Major or Mild \nNeurocognitive Disord er With Lewy Bodies\nIndividuals with NCDLB are more functionally impaired than would be expected for their\ncognitive deficits when contrasted to individuals with other neurodegenerative diseases,\nsuch as Alzheimer\u2019s disease. This is largely a result of motor and autonomic impairments,\nwhich cause problems with toileting, transfer ring, and eating. Sleep disorders and prom-\ninent psychiatric symptoms may also add to functional di fficulties. Consequently, the qual-\nity of life of individuals with NCDLB is often significantly worse than that of individuals\nwith Alzheimer\u2019s disease.\nDifferential Diagnosis \nMajor or mild neurocognitive diso rder due to Parkinson\u2019s disease. A key differenti-\nating feature in clinical diagnosis is the tempor al sequence in which the parkinsonism and\nthe NCD appear. For NCD due to Parkinson\u2019s disease, the individual must develop cog-\nnitive decline in the context of established Parkinson\u2019s disease; by convention, the decline\nshould not reach the stage of major NCD until at least 1 year after Parkinson\u2019s is diagnosed.\nIf less than a year has passed since the onset of motor symptoms, the diagnosis is NCDLB.\nThis distinction is clearer at the major NCD level than at the mild NCD level. \nThe timing and sequence of parkinsonism an d mild NCD may be more difficult to de-\ntermine because the onset and clinical presentation can be ambiguous, and unspecified\nmild NCD should be diagnosed if the othe r core and suggestive features are absent.", "source": "dsm5.pdf"} {"id": "8c58997002e8-0", "page_content": "Major or Mild Vascular Neurocognitive Disorder 621\nComorbidity \nLewy body pathology frequent ly coexists with Alzheimer\u2019s disease and cerebrovascular\ndisease pathology, particularly among the olde st age groups. In Alzheimer\u2019s disease, there\nis concomitant synuclein pathology in 60% of cases (if amygdala-restricted cases are in-\ncluded). In general, there is a higher rate of Lewy body pathology in individuals with de-\nmentia than in older individuals without dementia. \nMajor or Mild Vascular Neurocognitive Disorder\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. The clinical features are consistent with a vascular etiology, as suggested by either of\nthe following: \n1. Onset of the cognitive deficits is temporally related to one or more cerebrovascular\nevents.\n2. Evidence for decline is prominent in complex attention (including processing\nspeed) and frontal-executive function.\nC. There is evidence of the presence of cere brovascular disease from history, physical\nexamination, and/or neuroimaging consider ed sufficient to account for the neurocog-\nnitive deficits. \nD. The symptoms are not better explained by another brain disease or systemic disorder.\nProbable vascular neurocognitive disorder is diagnosed if one of the following is pres-\nent; otherwise possible vascular neurocognitive disorder should be diagnosed:\n1. Clinical criteria are supported by neuroimaging evidence of significant parenchymal in-\njury attributed to cerebrovascula r disease (neuroimaging-supported).\n2. The neurocognitive syndrome is temporally related to one or more documented cere-\nbrovascular events.\n3. Both clinical and genetic (e.g., cerebral aut osomal dominant arteriopathy with subcortical", "source": "dsm5.pdf"} {"id": "8c58997002e8-1", "page_content": "infarcts and leukoencephalopathy) evidence of cerebrovascular disease is present.\nPossible vascular neuroc ognitive disorder is diagnosed if the clinical criteria are met\nbut neuroimaging is not available and the tem poral relationship of the neurocognitive syn-\ndrome with one or more cerebrovascular events is not established.\nCoding note: For probable major vascular neurocognitive disorder, with behavioral dis-\nturbance, code 290.40 (F01.51). For probable major vascular neurocognitive disorder,\nwithout behavioral disturbance, code 290.40 (F01.50). For possible major vascular neuro-\ncognitive disorder, with or without behavioral disturbance, code 331.9 (G31.9). An addi-\ntional medical code for the cerebrovascular disease is not needed.\nFor mild vascular neurocognitive disorder, code 331.83 (G31.84). ( Note: Do not use an\nadditional code for the vascular disease. Behavioral disturbance cannot be coded but\nshould still be indicated in writing.)\nDiagnostic Features\nThe diagnosis of major or mild vascular neurocognitive diso rder (NCD) requires the es-\ntablishment of an NCD (Criterion A) and the determination that cere brovascular disease is\nthe dominant if not exclusive pathology that accounts for the cognitive deficits (Criteria B\nand C). Vascular etiology may range from large vessel stroke to micr ovascular disease; the", "source": "dsm5.pdf"} {"id": "da59f1d82beb-0", "page_content": "622 Neurocognitive Disorders\npresentation is therefore very heterogeneous, stemming from the types of vascular lesions\nand their extent and location. The lesions may be focal, multifocal, or diffuse and occur in\nvarious combinations. \nMany individuals with major or mild vascul ar NCD present with multiple infarctions,\nwith an acute stepwise or fluctuating dec line in cognition, and intervening periods of\nstability and even some improvement. Others may have gradual onset with slow pro-\ngression, a rapid development of deficits follo wed by relative stabilit y, or another complex\npresentation. Major or mild vascular NCD wi th a gradual onset an d slow progression is\ngenerally due to small vessel disease leading to lesions in the white matter, basal ganglia,\nand/or thalamus. The gradual progression in these cases is often punctuated by acute\nevents that leave subtle neurological deficits. The cognitive deficits in these cases can be at-\ntributed to disruption of cortical-subcortical circuits, and complex attention, particularly\nspeed of information processing, and exec utive ability are likely to be affected.\nAssessing for the presence of sufficient cerebrovascular disease relies on history, phys-\nical examination, and neuroimaging (Criterion C). Etiological certainty requires the dem-\nonstration of abnormalities on neuroimaging. The lack of neuroimaging can result in\nsignificant diagnostic inaccuracy by overlooking \u201csilent\u201d brain infarction and white mat-\nter lesions. However, if the neurocognitive im pairment is temporally associated with one\nor more well-documented strokes, a probable diagnosis can be made in the absence of neu-\nroimaging. Clinical evidence of cerebrovascular disease includes documented history of\nstroke, with cognitive decline temporally assoc iated with the event, or physical signs con-", "source": "dsm5.pdf"} {"id": "da59f1d82beb-1", "page_content": "stroke, with cognitive decline temporally assoc iated with the event, or physical signs con-\nsistent with stroke (e.g., hemi paresis; pseudobulbar syndrome , visual field defect). Neuro-\nimaging (magnetic resonance imaging [MRI] or computed tomography [CT]) evidence of\ncerebrovascular disease comprises one or more of the following: one or more large vessel\ninfarcts or hemorrhages, a strategically placed single infarct or hemorrhage (e.g., in angu-\nlar gyrus, thalamus, basal forebrain), two or mo re lacunar infarcts outside the brain stem,\nor extensive and confluent white matter lesions. The latter is often termed small vessel dis-\nease or subcortical ischemic changes on clinical neuroimaging evaluations.\nFor mild vascular NCD, history of a single stroke or extensive white matter disease is gen-\nerally sufficient. For major vascular NCD, two or more strokes, a strate gically placed stroke,\nor a combination of white matter disease and one or more lacunes is generally necessary.\nThe disorder must not be better explained by another disorder. For example, promi-\nnent memory deficit early in the course mi ght suggest Alzheimer' s disease, early and\nprominent parkinsonian features would suggest Parkinson's disease, and a close associa-\ntion between onset and depression would suggest depression.\nAssociated Features Supporting Diagnosis\nA neurological assessmen t often reveals history of stroke and/or transient ischemic epi-\nsodes, and signs indicative of brain infarctions. Also commonly associated are personality\nand mood changes, abulia, depression, and emotional lability. The development of late-\nonset depressive symptoms accompanied by psychomotor slowing and executive dys-", "source": "dsm5.pdf"} {"id": "da59f1d82beb-2", "page_content": "onset depressive symptoms accompanied by psychomotor slowing and executive dys-\nfunction is a common presentation among olde r adults with progressive small vessel isch-\nemic disease (\u201cvascular depression\u201d).\nPrevalence\nMajor or mild vascular NCD is the second most common cause of NCD after Alzheimer\u2019s\ndisease. In the United States, population prevalence estimates for vascular dementia range\nfrom 0.2% in the 65\u201370 years age group to 16% in individuals 80 years and older. Within\n3 months following stroke, 20%\u201330% of individuals are diagnosed with dementia. In neu-", "source": "dsm5.pdf"} {"id": "17f6aabd9c7b-0", "page_content": "from 0.2% in the 65\u201370 years age group to 16% in individuals 80 years and older. Within\n3 months following stroke, 20%\u201330% of individuals are diagnosed with dementia. In neu-\nropathology series, the prevalence of vascular dementia increases from 13% at age 70 years\nto 44.6% at age 90 years or older, in comp arison with Alzheimer\u2019s disease (23.6%\u201351%) and\ncombined vascular dementia and Alzheimer\u2019s disease (2%\u201346.4%). Higher prevalence has", "source": "dsm5.pdf"} {"id": "aaeb490ce2bd-0", "page_content": "Major or Mild Vascular Neurocognitive Disorder 623\nbeen reported in African Americans compared with Caucasians, and in East Asian countries\n(e.g., Japan, China). Prevalence is higher in males than in females.\nDevelopment and Course\nMajor or mild vascular NCD can occur at an y age, although the prevalence increases ex-\nponentially after age 65 years. In older indivi duals, additional pathologies may partly ac-\ncount for the neurocognitive de ficits. The course may vary fr om acute onset with partial\nimprovement to stepwise decline to progressive decline, with fluctuations and plateaus of\nvarying durations. Pure subcortical major or mild vascular NCD can have a slowly pro-\ngressive course that simulates major or mild NCD due to Alzheimer\u2019s disease.\nRisk and Prognostic Factors\nEnvironmental. The neurocognitive outcomes of vascular brain injury are influenced by\nneuroplasticity factors such as education, physical exercise, and mental activity.\nGenetic and physiological. The major risk factors for major or mild vascular NCD are the\nsame as those for cerebrovascular disease, incl uding hypertension, diab etes, smoking, obesity,\nhigh cholesterol levels, high homocysteine levels, other risk factors for atherosclerosis and ar-\nteriolosclerosis, atrial fibrillati on, and other conditions increasing the risk of cerebral emboli.\nCerebral amyloid angiopathy is an important risk factor in which amyloid deposits occur\nwithin arterial vessels. Another key risk factor is the hereditary condition cerebral autosomal\ndominant arteriopathy with subcortical infarcts and leukoencephalopathy, or CADASIL.\nDiagnostic Markers\nStructural neuroimaging, using MRI or CT, ha s an important role in the diagnostic pro-", "source": "dsm5.pdf"} {"id": "aaeb490ce2bd-1", "page_content": "cess. There are no other established biomar kers of major or mild vascular NCD. \nFunctional Consequences of \nMajor or Mild Vascular Neurocognitive Disorder\nMajor or mild vascular NCD is commonly asso ciated with physical deficits that cause ad-\nditional disability. \nDifferential Diagnosis \nOther neurocognitive disorders. Since incidental brain infarctions and white matter le-\nsions are common in older individuals, it is important to consider other possible etiologies\nwhen an NCD is present. A history of memory deficit early in the course, and progressive\nworsening of memory, language, executive function, and perceptual-motor abilities in the\nabsence of corresponding focal lesions on br ain imaging, are suggestive of Alzheimer\u2019s\ndisease as the primary diagnosis. Potential bi omarkers currently being validated for Alz-\nheimer\u2019s disease, such as cerebrospinal fluid levels of beta-amyloid and phosphorylated\ntau, and amyloid imaging, may prove to be helpful in the differential diagnosis. NCD with\nLewy bodies is distinguished fr om major or mild vascular NCD by its core features of fluc-\ntuating cognition, visual hallu cinations, and spontaneous parkinsonism. While deficits in\nexecutive function and language occur in majo r or mild vascular NC D, the insidious onset\nand gradual progression of behavioral features or language impairment are characteristic\nof frontotemporal NCD and are no t typical of vascular etiology.\nOther medical conditions. A diagnosis of major or mild vascular NCD is not made if\nother diseases (e.g., brain tumor, multiple sc lerosis, encephalitis, toxic or metabolic disor-\nders) are present and are of su fficient severity to account for the cognitive impairment.", "source": "dsm5.pdf"} {"id": "542b5cb9ccd1-0", "page_content": "624 Neurocognitive Disorders\nOther mental disorders. A diagnosis of major or mild vascular NCD is inappropriate if\nthe symptoms can be entirely attributed to delirium, although delirium may sometimes be\nsuperimposed on a preexisting major or mild vascular NCD, in which case both diagnoses\ncan be made. If the criteria for major depressive disorder are met and the cognitive impair-\nment is temporally related to the likely onse t of the depression, major or mild vascular\nNCD should not be diagnosed. However, if the NCD preceded the development of the de-\npression, or the severity of the cognitive impairment is out of proportion to the severity of\nthe depression, both should be diagnosed. \nComorbidity\nMajor or mild NCD due to Alzheimer\u2019s dise ase commonly co-occurs with major or mild\nvascular NCD, in which case both diagnoses should be made. Major or mild vascular NCD\nand depression frequently co-occur. \nMajor or Mild Neurocognitive Disorder\nDue to Traumatic Brain Injury\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. There is evidence of a traumatic brain injury\u2014that is, an impact to the head or other\nmechanisms of rapid movement or displacement of the brain within the skull, with one\nor more of the following: \n1. Loss of consciousness.\n2. Posttraumatic amnesia.\n3. Disorientation and confusion.\n4. Neurological signs (e.g., neuroimaging demonstrating injury; a new onset of sei-\nzures; a marked worsening of a preexisting seizure disorder; visual field cuts; an-\nosmia; hemiparesis).\nC. The neurocognitive disorder presents imm ediately after the occurrence of the trau-\nmatic brain injury or immediately after recovery of consciousness and persists past the", "source": "dsm5.pdf"} {"id": "542b5cb9ccd1-1", "page_content": "matic brain injury or immediately after recovery of consciousness and persists past the\nacute post-injury period.\nCoding note: For major neurocognitive disorder due to traumatic brain injury, with behavioral\ndisturbance: For ICD-9-CM, first code 907.0 late effect of intracranial injury without skull frac-\nture, followed by 294.11 major neurocognitive disorder due to traumatic brain injury, with be-\nhavioral disturbance. For ICD-10-CM, first code S06.2X9S diffuse traumatic brain injury with\nloss of consciousness of unspecified duration, sequela; followed by F02.81 major neurocog-\nnitive disorder due to traumatic brain injury, with behavioral disturbance.\nFor major neurocognitive disorder due to traumatic brain injury, without behavioral distur-\nbance: For ICD-9-CM, first code 907.0 late effect of intracranial injury without skull fracture,\nfollowed by 294.10 major neurocognitive disorder due to traumatic brain injury, without be-\nhavioral disturbance. For ICD-10-CM, first code S06.2X9S diffuse traumatic brain injury with\nloss of consciousness of unspecified duration, sequela; followed by F02.80 major neurocog-\nnitive disorder due to traumatic brain injury, without behavioral disturbance.\nFor mild neurocognitive disorder due to traumatic brain injury, code 331.83 (G31.84).\n(Note: Do not use the additional code for traumatic brain injury. Behavioral disturbance\ncannot be coded but should still be indicated in writing.)", "source": "dsm5.pdf"} {"id": "26d4a670d6fc-0", "page_content": "Major or Mild Neurocognitive Disorder Due to Traumatic Brain Injury 625\nSpecifiers\nRate the severity of the neuroc ognitive disorder (NCD), not the underlying traumatic brain\ninjury (see the section \u201cDevelopment and Course\u201d for this disorder).\nDiagnostic Features\nMajor or mild NCD due to traumatic brain injury (TBI) is caused by an impact to the head,\nor other mechanisms of rapid movement or di splacement of the brain within the skull, as\ncan happen with blast injuries. Traumatic brain injury is defined as brain trauma with spe-\ncific characteristics that include at least one of the following: loss of consciousness, post-\ntraumatic amnesia, diso rientation and confusion, or, in more severe cases, neurological\nsigns (e.g., positive neuroimaging, a new onset of seizures or a marked worsening of a pre-\nexisting seizure disorder, visual field cuts, anosmia, hemiparesi s) (Criterion B). To be at-\ntributable to TBI, the NCD must present either immediately after the brain injury occurs or\nimmediately after the individu al recovers consciousness afte r the injury and persist past\nthe acute post-injury period (Criterion C). \nThe cognitive presentation is variable. Difficulties in the domains of complex attention,\nexecutive ability, learning, an d memory are common as well as slowing in speed of infor-\nmation processing and disturbances in social cognition. In more seve re TBI in which there\nis brain contusion, intracranial hemorrhage, or penetrating injury, there may be additional\nneurocognitive deficits, such as aphasia, neglect, and constructional dyspraxia.\nAssociated Features Supporting Diagnosis\nMajor or mild NCD due to TBI may be accompanied by disturbances in emotional function", "source": "dsm5.pdf"} {"id": "26d4a670d6fc-1", "page_content": "Major or mild NCD due to TBI may be accompanied by disturbances in emotional function\n(e.g., irritability, easy frus tration, tension and anxiety, affective lability); personality\nchanges (e.g., disinhibition, apathy, suspic iousness, aggression); physical disturbances\n(e.g., headache, fatigue, slee p disorders, vertigo or dizziness, tinnitus or hyperacusis, pho-\ntosensitivity, anosmia, reduced tolerance to psychotropic medication s); and, particularly\nin more severe TBI, neurolog ical symptoms and signs (e.g., seizures, hemiparesis, visual\ndisturbances, cranial nerve deficits) an d evidence of orthopedic injuries.\nPrevalence\nIn the United States, 1.7 million TBIs occur a nnually, resulting in 1.4 million emergency de-\npartment visits, 275,000 hospitalizations, and 52,000 deaths. About 2% of the population\nlives with TBI-associated disabi lity. Males account for 59% of TBIs in the United States.\nThe most common etiologies of TBI in the Unit ed States are falls, vehicular accidents, and\nbeing struck on the head. Collisions and blows to the head that occur in the course of con-\ntact sports are increasingly re cognized as sources of mild TB I, with a concern that repeated\nmild TBI may have cumulatively persisting sequelae.\nDevelopment and Course\nThe severity of a TBI is rated at the time of injury/initial assessment as mild, moderate, or\nsevere according to the thresholds in Table 2.\nThe severity rating of the TBI itself does not necessarily correspon d to the severity of\nthe resulting NCD. The course of recovery fr om TBI is variable, depending not only on the", "source": "dsm5.pdf"} {"id": "26d4a670d6fc-2", "page_content": "specifics of the injury but also on cofactors, such as age, prior history of brain damage, or\nsubstance abuse, that may favor or impede recovery.", "source": "dsm5.pdf"} {"id": "aa53889845a8-0", "page_content": "626 Neurocognitive Disorders\nNeurobehavioral symptoms tend to be most severe in the immediate aftermath of the\nTBI. Except in the case of severe TBI, the typi cal course is that of complete or substantial\nimprovement in associated neurocognitive, neurological, and psyc hiatric symptoms and\nsigns. Neurocognitive symptoms associated with mild TBI tend to resolve within days to\nweeks after the injury with complete resoluti on typical by 3 months. Other symptoms that\nmay potentially co-occur with the neurological symptoms (e.g., depression, irritability,\nfatigue, headache, photosensitivity, sleep dist urbance) also tend to resolve in the weeks\nfollowing mild TBI. Substantial subsequent deterioration in these areas should trigger con-\nsideration of additional diagnoses. However, repeated mild TBI may be associated with\npersisting neurocognitive disturbance. \nWith moderate and severe TBI, in addition to persistence of neurocognitive deficits,\nthere may be associated neurophysiological, emotional, and behavi oral complications.\nThese include seizures (particula rly in the first year), photosen sitivity, hyperacu sis, irritabil-\nity, aggression, depression, sl eep disturbance, fatigue, apat hy, inability to resume occu-\npational and social functioning at pre-injury level, and deterioration in interpersonal\nrelationships. Moderate and seve re TBI have been associated with increased risk of depres-\nsion, aggression, and possibly neurodegenerative diseases such as Alzheimer\u2019s disease.\nThe features of persisting majo r or mild NCD due to TBI will vary by age, specifics of\nthe injury, and cofactors. Persisting TBI-related impairment in an infant or child may be re-\nflected in delays in reaching developmental mi lestones (e.g., language acquisition), worse", "source": "dsm5.pdf"} {"id": "aa53889845a8-1", "page_content": "flected in delays in reaching developmental mi lestones (e.g., language acquisition), worse\nacademic performance, and possibly impaired social development. Among older teenag-\ners and adults, persisting symptoms may incl ude various neurocognitive deficits, irrita-\nbility, hypersensitivity to light and sound, e asy fatigability, and mood changes, including\ndepression, anxiety, hostility, or apathy. In older individuals with depleted cognitive re-\nserve, mild TBI is more likely to result in incomplete recoveries.\nRisk and Prognostic Factors \nRisk factors for traumatic brain injury. Traumatic brain injury rates vary by age, with\nthe highest prevalence among individuals younge r than 4 years, older adolescents, and in-\ndividuals older than 65 years. Falls are the mo st common cause of TBI, with motor vehicle\naccidents being second. Sports concussions are frequent causes of TBI in older children,\nteenagers, and young adults.\nRisk factors for neurocognitive disorder after traumatic brain injury. Repeated con-\ncussions can lead to persistent NCD and neur opathological evidence of traumatic enceph-\nalopathy. Co-occurring intoxication with a substance may incr ease the severity of a TBI\nfrom a motor vehicle accident, but whether into xication at the time of injury worsens neu-\nrocognitive outcome is unknown.\nCourse modifiers. Mild TBI generally resolves within a few weeks to months, although res-\nolution may be delayed or incomplete in the context of repeated TB I. Worse outcome fromTABLE 2 Severity ratings for tr aumatic brain injury\nInjury characteristic Mild TBI Moderate TBI Severe TBI\nLoss of consciousness <30 min 30 minutes\u201324 hours >24 hours\nPosttraumatic amnesia <24 ho urs 24 hours\u20137 days >7 days", "source": "dsm5.pdf"} {"id": "aa53889845a8-2", "page_content": "Posttraumatic amnesia <24 ho urs 24 hours\u20137 days >7 days\nDisorientation and confusion \nat initial assessment \n(Glasgow Coma Scale \nScore)13\u201315 (not below 13 \nat 30 minutes)9\u201312 3\u20138", "source": "dsm5.pdf"} {"id": "ef21048a1e93-0", "page_content": "Substance/Medication-Induced Major or Mild Neurocognitive Disorder 627\nmoderate to severe TBI is associated with older ag e (older than 40 years) and initial clinical pa-\nrameters, such as low Glasgow Coma Scale score; worse motor function; pupillary nonreac-\ntivity; and computed tomography (CT) evidence of brain injury (e.g., petechial hemorrhages,\nsubarachnoid hemorrhage, midline shift, obliteration of third ventricle).\nDiagnostic Markers\nBeyond neuropsycholog ical testing, CT scanning may reveal petechial hemorrhages,\nsubarachnoid hemorrhage, or evidence of contusion. Magn etic resonance image scanning\nmay also reveal hyperintensities suggestive of microhemorrhages. \nFunctional Consequences of Major or Mild \nNeurocognitive Disorder Due to Traumatic Brain Injury \nWith mild NCD due to TBI, individuals may re port reduced cognitive efficiency, difficulty\nconcentrating, and lessened abilit y to perform usual activities. With major NCD due to TBI, an\nindividual may have di fficulty in independent living an d self-care. Prominent neuromotor\nfeatures, such as severe incoordination, ataxia , and motor slowing, may be present in major\nNCD due to TBI and may add to functional diffi culties. Individuals with TBI histories report\nmore depressive symptoms, and these can amp lify cognitive complaints and worsen func-\ntional outcome. Additionally, loss of emotional control, including aggre ssive or inappropriate\naffect and apathy, may be present after more se vere TBI with greater neurocognitive impair-\nment. These features may compound difficulti es with independent living and self-care.\nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "ef21048a1e93-1", "page_content": "Differential Diagnosis\nIn some instances, severity of neurocognitive symptoms ma y appear to be inconsistent\nwith the severity of the TBI. After previously undetected neurologic al complications (e.g.,\nchronic hematoma) are excluded , the possibility of diagnoses such as somatic symptom\ndisorder or factitious disorder need to be considered. Posttraumatic stress disorder (PTSD)\ncan co-occur with the NCD and have overlappi ng symptoms (e.g., difficulty concentrat-\ning, depressed mood, aggressiv e behavioral disinhibition).\nComorbidity\nAmong individuals with substa nce use disorders, the neurocognitive effects of the sub-\nstance contribute to or compound the TBI-as sociated neurocognitive change. Some symp-\ntoms associated with TBI may overlap with sy mptoms found in cases of PTSD, and the two\ndisorders may co-occur, especia lly in military populations. \nSubstance/Medication-Induced\n Major or Mild Neurocognitive Disorder\nDiagnostic Criteria\nA. The criteria are met for major or mild neurocognitive disorder.\nB. The neurocognitive impairments do not occur exclusively during the course of a delir-\nium and persist beyond the usual duration of intoxication and acute withdrawal.\nC. The involved substance or medication and duration and extent of use are capable of\nproducing the neurocognitive impairment.\nD. The temporal course of the neurocognitive deficits is consistent with the timing of sub-\nstance or medication use and abstinence (e.g., the deficits remain stable or improve\nafter a period of abstinence).", "source": "dsm5.pdf"} {"id": "831acef0b754-0", "page_content": "628 Neurocognitive Disorders\nE. The neurocognitive disorder is not attributable to another medical condition or is not\nbetter explained by another mental disorder.\nCoding note: The ICD-9-CM and ICD-10-CM codes for the [specific substance/medica-\ntion]-induced neurocognitive disorders are indi cated in the table below. Note that the ICD-\n10-CM code depends on whether or not there is a comorbid substance use disorder present\nfor the same class of substance. If a mild substance use disorder is comorbid with the sub-\nstance-induced neurocognitive disorder, the 4th position character is \u201c1,\u201d and the clinician\nshould record \u201cmild [substance] use disorder\u201d before the substance-induced neurocognitive\ndisorder (e.g., \u201cmild inhalant use disorder wi th inhalant-induced major neurocognitive disor-\nder\u201d). If a moderate or severe substance use disorder is comorbid with the substance-\ninduced neurocognitive disorder, the 4th position character is \u201c2,\u201d and the clinician should\nrecord \u201cmoderate [substance] use disorder\u201d or \u201csevere [substance] use disorder,\u201d depending\non the severity of the comorbid substance use disorder. If there is no comorbid substance\nuse disorder, then the 4th position character is \u201c9,\u201d and the clinician should record only the\nsubstance-induced neurocognitive disorder. For some classes of substances (i.e., alcohol;\nsedatives, hypnotics, anxiolytics), it is not permissible to code a comorbid mild substance\nuse disorder with a substance-induced neurocog nitive disorder; only a comorbid moderate\nor severe substance use disorder, or no substance use disorder, can be diagnosed. Behav-", "source": "dsm5.pdf"} {"id": "831acef0b754-1", "page_content": "or severe substance use disorder, or no substance use disorder, can be diagnosed. Behav-\nioral disturbance cannot be coded but should still be indicated in writing.\nICD-10-CM\nICD-9-CMWith use \ndisorder, \nmildWith use \ndisorder, \nmoderate or \nsevereWithout use \ndisorder\nAlcohol (major neurocognitive \ndisorder), nonamnestic- \nconfabulatory type291.2 NA F10.27 F10.97\nAlcohol (major neurocognitive \ndisorder), amnestic- \nconfabulatory type291.1 NA F10.26 F10.96\nAlcohol (mild neurocognitive \ndisorder)291.89 NA F10.288 F10.988\nInhalant (major neurocognitive \ndisorder)292.82 F18.17 F18.27 F18.97\nInhalant (mild neurocognitive \ndisorder)292.89 F18.188 F18.288 F18.988\nSedative, hypnotic, or anxiolytic \n(major neurocognitive disorder)292.82 NA F13.27 F13.97\nSedative, hypnotic, or anxiolytic \n(mild neurocognitive disorder)292.89 NA F13.288 F13.988\nOther (or unknown) substance \n(major neurocognitive disorder)292.82 F19.17 F19.27 F19.97\nOther (or unknown) substance \n(mild neurocognitive disorder)292.89 F19.188 F19.288 F19.988", "source": "dsm5.pdf"} {"id": "27495aa63249-0", "page_content": "Substance/Medication-Induced Major or Mild Neurocognitive Disorder 629\nSpecify if: \nPersistent: Neurocognitive impairment continues to be significant after an extended\nperiod of abstinence.\nRecording Procedures\nICD-9-CM. The name of the substance/medication-i nduced neurocogniti ve disorder be-\ngins with the specific substance/medication (e.g ., alcohol) that is presumed to be causing\nthe neurocognitive symptoms. Th e diagnostic code is selected from the table included in\nthe criteria set, which is based on the drug clas s. For substances that do not fit into any of\nthe classes, the code for \u201cother substance\u201d should be used; and in cases in which a substance\nis judged to be an etiological factor but the sp ecific class of substance is unknown, the cat-\negory \u201cunknown substance\u201d should be used.\nThe name of the disorder (i.e., [specific su bstance]-induced major neurocognitive dis-\norder or [specific substance]-induced mild neurocognitive disorder) is followed by the\ntype in the case of alcohol (i.e., nonamnestic-confabulatory type, amnestic-confabulatory\ntype), followed by specification of duration (i .e., persistent). Unlike the recording procedures\nfor ICD-10-CM, which combine the substanc e/medication-induced disorder and sub-\nstance use disorder into a single code, for ICD-9-CM a separate diagnostic code is given for\nthe substance use disorder. For example, in th e case of persistent amnestic-confabulatory\nsymptoms in a man with a severe alcohol use disorder, the diagnosis is 291.1 alcohol-\ninduced major neurocognitive d isorder, amnestic-confabulatory type, persistent. An addi-", "source": "dsm5.pdf"} {"id": "27495aa63249-1", "page_content": "tional diagnosis of 303.90 severe alcohol use diso rder is also given. If the substance/medi-\ncation-induced neurocognitive disorder occurs without a comorbid substance use disorder\n(e.g., after a sporadic heavy use of inhalants) , no accompanying substance use disorder is\nnoted (e.g., 292.82 inhalant-induced mild neurocognitive disorder). \nICD-10-CM. The name of the substance/medicati on-induced neurocognitive disorder\nbegins with the specific substance (e.g., alcoho l) that is presumed to be causing the neuro-\ncognitive symptoms. The diagnostic code is sele cted from the table included in the criteria\nset, which is based on the drug class and pres ence or absence of a comorbid substance use\ndisorder. For substances that do not fit into any of the cla sses, the code for \u201cother sub-\nstance\u201d should be used; and in cases in which a substance is judged to be an etiological fac-\ntor but the specific class of substance is unknown, the category \u201cunknown substance\u201d\nshould be used.\nWhen recording the name of the disorder, the comorbid substa nce use disorder (if any) is\nlisted first, followed by the word \u201cwith,\u201d followe d by the name of the disorder (i.e., [specific\nsubstance]-induced major neurocognitive diso rder or [specific substance]-induced mild\nneurocognitive disorder), follow ed by the type in the case of alcohol (i.e., nonamnestic-con-\nfabulatory type, amnestic-confabulatory type), followed by specification of duration (i.e.,\npersistent). For example, in the case of pers istent amnestic-confabulatory symptoms in a", "source": "dsm5.pdf"} {"id": "27495aa63249-2", "page_content": "man with a severe alcohol use disorder, the di agnosis is F10.26 severe alcohol use disorder\nwith alcohol-induced major neur ocognitive disorder, amnestic -confabulatory type, persis-\ntent. A separate diagnosis of the comorbid severe alcohol use disorder is not given. If the\nsubstance-induced neurocognitive disorder occurs without a comorbid substance use dis-\norder (e.g., after a sporadic heavy use of inha lants), no accompanying substance use disor-\nder is noted (e.g., F18.98 8 inhalant-induced mild neurocognitive disorder).\nDiagnostic Features \nSubstance/medication-induced major or mild NCD is characterized by neurocognitive\nimpairments that persist beyond the usual du ration of intoxication and acute withdrawal\n(Criterion B). Initially, these manifestations can reflect slow recovery of brain functions", "source": "dsm5.pdf"} {"id": "77d3fdfaf3e6-0", "page_content": "impairments that persist beyond the usual du ration of intoxication and acute withdrawal\n(Criterion B). Initially, these manifestations can reflect slow recovery of brain functions\nfrom a period of prolonged su bstance use, and improvements in neurocognitive as well as", "source": "dsm5.pdf"} {"id": "a65e9bc57a9a-0", "page_content": "630 Neurocognitive Disorders\nbrain imaging indicators may be seen over ma ny months. If the diso rder continues for an\nextended period, persistent should be specified. The give n substance and its use must be\nknown to be capable of causing the observed impairments (Criterion C). While nonspecific\ndecrements in a range of cognitive abilities can occur with nearly any substance of abuse\nand a variety of medications, some patterns occur more frequently with selected drug\nclasses. For example, NCD due to sedative, hypno tic, or anxiolytic drugs (e.g., benzodiaz-\nepines, barbiturates) ma y show greater disturbances in memory than in other cognitive\nfunctions. NCD induced by alcohol frequently manifests with a co mbination of impair-\nments in executive-function and memory and learning domains. Th e temporal course of\nthe substance-induced NCD must be consistent with that of use of the given substance\n(Criterion D). In alcohol-induced amnestic confabulatory (Korsakoff \u2019s) NCD, the features\ninclude prominent amnesia (severe difficulty learning new information with rapid forget-\nting) and a tendency to confabulate. These ma nifestations may co-occur with signs of thi-\namine encephalopathy (Wernicke\u2019s encephalopathy) with associated features such as\nnystagmus and ataxia. Ophthalmoplegia of Wernicke\u2019s encephalopathy is typically charac-\nterized by a lateral gaze paralysis.\nIn addition to or independent of the mo re common neurocognitive symptoms related\nto methamphetamine use (e.g., difficulties wi th learning and memory; executive func-\ntion), methamphetamine use can also be associat ed with evidence of vascular injury (e.g.,", "source": "dsm5.pdf"} {"id": "a65e9bc57a9a-1", "page_content": "focal weakness, unilateral incoordination, as ymmetrical reflexes). The most common neu-\nrocognitive profile approximates that seen in vascular NCD. \nAssociated Features Supporting Diagnosis\nIntermediate-duration NC D induced by drugs with central nervous system depressant effects\nmay manifest with added symptoms of increased irritability, anxiety, sleep disturbance, and\ndysphoria. Intermediate-duration NCD induced by stimulant drugs may manifest with re-\nbound depression, hypersomnia, and apathy. In severe forms of substance/medication-\ninduced major NCD (e.g., associ ated with long-term alcohol use), there may be prominent\nneuromotor features, such as incoordination, ataxia, and motor slowing. There may also be\nloss of emotional control, including aggres sive or inappropriat e affect, or apathy.\nPrevalence\nThe prevalence of these conditions is not know n. Prevalence figures for substance abuse are\navailable, and substance/medica tion-induced major or mild NCDs are more likely in those\nwho are older, have longer use, and have other risk factors such as nutritional deficits.\nFor alcohol abuse, the rate of mild NCD of intermediate duration is approximately 30%\u2013\n40% in the first 2 months of abstinence. Mild NCD may persist, particularly in those who do\nnot achieve stable abstinence until after age 50 years. Major NCD is rare and may result from\nconcomitant nutritional deficits, as in al cohol-induced amnestic confabulatory NCD.\nFor individuals quitting cocaine, metham phetamine, opioids, phencyclidine, and sed-\native, hypnotics, or anxiolytics, substance/medication-induced mild NCD of intermediate\nduration may occur in one-third or more, and there is some evidence that these substances", "source": "dsm5.pdf"} {"id": "a65e9bc57a9a-2", "page_content": "duration may occur in one-third or more, and there is some evidence that these substances\nmay also be associated with persistent mild NCD. Major NCD associated with these sub-\nstances is rare, if it occurs at all. In the case of methamph etamine, cerebr ovascular disease\ncan also occur, resulting in diffuse or focal brain injury that can be of mild or major neu-\nrocognitive levels. Solvent expo sure has been linked to both major and mild NCD of both\nintermediate and persistent duration. \nThe presence of NCD induced by cannabis and various hallucinogens is controversial.\nWith cannabis, intoxication is accompanied by various neur ocognitive disturbances, but\nthese tend to clear with abstinence.", "source": "dsm5.pdf"} {"id": "74b236111e90-0", "page_content": "Substance/Medication-Induced Major or Mild Neurocognitive Disorder 631\nDevelopment and Course\nSubstance use disorders tend to commence du ring adolescence and peak in the 20s and\n30s. Although longer history of severe substa nce use disorder is associated with greater\nlikelihood of NCD, the relationships are not straightforward, with substantial and even\ncomplete recovery of neurocognitive func tions being common among individuals who\nachieve stable abstinence prior to age 50 ye ars. Substance/medication-induced major or\nmild NCD is most likely to become persistent in individuals who continue abuse of sub-\nstances past age 50 years, presumably becaus e of a combination of lessened neural plas-\nticity and beginnings of other age-related br ain changes. Earlier commencement of abuse,\nparticularly of alcohol, may lead to defects in later neural development (e.g., later stages of\nmaturation of frontal circuitries), which may have effects on social cognition as well as\nother neurocognitive abilities. For alcohol-induced NCD, there may be an additive effect\nof aging and alcohol-induced brain injury.\nRisk and Prognostic Factors\nRisk factors for substance/medication-induced NCDs include older age, longer use, and\npersistent use past age 50 years. In additi on, for alcohol-induced NCD, long-term nutri-\ntional deficiencies, liver disease, vascular r isk factors, and cardiovascular and cerebrovas-\ncular disease may contribute to risk. \nDiagnostic Markers\nMagnetic resonance imaging (MRI) of individuals with chronic alcohol abuse frequently\nreveals cortical thinning, white matter loss, and enlargement of sulci and ventricles. While\nneuroimaging abnormalities are more common in those with NCDs, it is possible to ob-", "source": "dsm5.pdf"} {"id": "74b236111e90-1", "page_content": "serve NCDs without neuroimaging abnormalitie s, and vice versa. Specialized techniques\n(e.g., diffusion tensor imaging) may reveal damage to specific white matter tracts. Mag-\nnetic resonance spectroscopy may reveal reduction in N-acetylaspartate, and increase in\nmarkers of inflammation (e.g., myoinositol) or white matter injury (e.g., choline). Many of\nthese brain imaging changes and neurocogniti ve manifestations reverse following suc-\ncessful abstinence. In individuals with meth amphetamine use disorder, MRI may also re-\nveal hyperintensities suggestive of microhem orrhages or larger areas of infarction.\nFunctional Consequences of Substance/Medication-\nInduced Major or Mild Neurocognitive Disorder\nThe functional consequences of substance/ medication-induced mild NCD are sometimes\naugmented by reduced cognitive efficiency an d difficulty concentrating beyond that seen\nin many other NCDs. In addition, at both major and mild levels, substance/medication-\ninduced NCDs may have associated motor syndro mes that increase the level of functional\nimpairment. \nDifferential Diagnosis\nIndividuals with substance use disorders, substance intoxica tion, and substance withdrawal\nare at increased risk for othe r conditions that may independently, or through a compounding\neffect, result in neurocognitive disturbance. These include hi story of traumatic brain injury\nand infections that can accompany substance use disorder (e.g., HIV, hepatitis C virus, syph-\nilis). Therefore, presence of substance/medi cation-induced major or mild NCD should be\ndifferentiated from NCDs arising outside the co ntext of substance use, intoxication, and with-\ndrawal, including these accompanying cond itions (e.g., traumatic brain injury).", "source": "dsm5.pdf"} {"id": "8989362f25bc-0", "page_content": "632 Neurocognitive Disorders\nComorbidity\nSubstance use disorders, substance intoxicati on, and substance withdrawal are highly co-\nmorbid with other mental disorders. Comorb id posttraumatic stre ss disorder, psychotic\ndisorders, depressive and bi polar disorders, and neurodev elopmental disorders can con-\ntribute to neurocognitive impairment in substance users. Traumatic brain injury occurs\nmore frequently with substance use, complicati ng efforts to determine the etiology of NCD\nin such cases. Severe, long-term alcohol use disorder can be associated with major organ\nsystem disease, including cerebrovascular disease and cirrhosis. Amphetamine-induced\nNCD may be accompanied by major or mild vascular NCD, also secondary to amphet-\namine use.\nMajor or Mild Neurocognitive Disorder\n Due to HIV Infection\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. There is documented infection with human immunodeficiency virus (HIV).\nC. The neurocognitive disorder is not bette r explained by non-HIV conditions, including\nsecondary brain diseases such as progre ssive multifocal leukoencephalopathy or\ncryptococcal meningitis.\nD. The neurocognitive disorder is not attribut able to another medical condition and is not\nbetter explained by a mental disorder.\nCoding note: For major neurocognitive disorder due to HIV infection, with behavioral dis-\nturbance, code first 042 (B20) HIV infection, followed by 294.11 (F02.81) major neurocog-\nnitive disorder due to HIV infection, with behavioral disturbance. For major neurocognitive\ndisorder due to HIV infection, without behavioral disturbance, code first 042 (B20) HIV in-", "source": "dsm5.pdf"} {"id": "8989362f25bc-1", "page_content": "fection, followed by 294.10 (F02.80) major neurocognitive disorder due to HIV infection,\nwithout behavioral disturbance.\nFor mild neurocognitive disorder due to HIV infection, code 331.83 (G31.84). (Note: Do\nnot use the additional code for HIV infection. Behavioral disturbance cannot be coded but\nshould still be indicated in writing.)\nDiagnostic Features \nHIV disease is caused by infection with hu man immunodeficiency virus type-1 (HIV-1),\nwhich is acquired through exposure to bodily fluids of an infected person through injection\ndrug use, unprotected sexual contact, or acci dental or iatrogenic exposure (e.g., contami-\nnated blood supply, needle puncture injury to medical personnel). HIV infects several types\nof cells, most particularly immune cells. Over time, the infection can cause severe depletion\nof \u201cT-helper\u201d (CD4) lymphocytes, resulting in severe immunocompromise, often leading to\nopportunistic infections and neoplasms. This advanced form of HIV infection is termed\nacquired immune deficiency syndrome (AIDS). Diagnosis of HIV is confirmed by established\nlaboratory methods such as enzyme-linked immunosorbent assay for HIV antibody with\nWestern blot confirmation and/or polymera se chain reaction\u2013based assays for HIV. \nSome individuals with HIV infection deve lop an NCD, which generally shows a \u201csub-\ncortical pattern\u201d with prominently impaired executive function, slowing of processing\nspeed, problems with more demanding attentio nal tasks, and difficulty in learning new\ninformation, but fewer problems with recall of learned information. In major NCD, slow-\ning may be prominent. Language difficulties , such as aphasia, are uncommon, although\nreductions in fluency may be observed. HIV pathogenic proc esses can affect any part of", "source": "dsm5.pdf"} {"id": "8989362f25bc-2", "page_content": "the brain; therefore, other patterns are possible.", "source": "dsm5.pdf"} {"id": "7c10c6082f59-0", "page_content": "Major or Mild Neurocognitive Disorder Due to HIV Infection 633\nAssociated Features Supporting Diagnosis\nMajor or mild NCD due to HIV infection is usually more prevalent in individuals with\nprior episodes of severe immunosuppression, high viral loads in the cerebrospinal fluid,\nand indicators of advanced HIV disease such as anemia and hypoalbuminemia. Individ-\nuals with advanced NCD may experience prom inent neuromotor features such as severe\nincoordination, ataxia, and moto r slowing. There may be loss of emotional control, includ-\ning aggressive or inappropriate affect or apathy. \nPrevalence\nDepending on stage of HIV disease, approx imately one-third to over one-half of HIV-\ninfected individuals have at least mild neuroc ognitive disturbance, but some of these dis-\nturbances may not meet the full criteria for mild NCD. An estimated 25% of individuals\nwith HIV will have signs and symptoms that meet criteria for mild NCD, and in fewer than\n5% would criteria for major NCD be met. \nDevelopment and Course \nAn NCD due to HIV infection can resolve, improve, slowly worsen, or have a fluctuating\ncourse. Rapid progression to profound neur ocognitive impairment is uncommon in the\ncontext of currently available combination antiviral treatment; co nsequently, an abrupt\nchange in mental status in an individual with HIV may prompt an evaluation of other\nmedical sources for the cognitive change, incl uding secondary infections. Because HIV in-\nfection preferentially affects subcortical regi ons over the course of illness, including deep\nwhite matter, the progression of the disorder follows a \u201csubcortical \u201d pattern. Since HIV\ncan affect a variety of brain regions, and the illness can take on many different trajectories", "source": "dsm5.pdf"} {"id": "7c10c6082f59-1", "page_content": "can affect a variety of brain regions, and the illness can take on many different trajectories\ndepending on associated comorbidities and cons equences of HIV, the overall course of an\nNCD due to HIV infection has considerable heterogeneity. A subc ortical neurocognitive\nprofile may interact with age over the life course, when psychomo tor slowing and motor\nimpairments such as slowed gait may occur as a consequence of other age-related condi-\ntions so that the overall progression ma y appear more pronounced in later life. \nIn developed countries, HIV disease is primar ily a condition of adults, with acquisition\nvia risky behaviors (e.g., unprotected sex, inje ction drug use) beginning in late adolescence\nand peaking during young and middle adulth ood. In developing countries, particularly\nsub-Saharan Africa, where HIV testing and an tiretroviral treatments for pregnant women\nare not readily available, perinatal transmis sion is common. The NCD in such infants and\nchildren may present primarily as neurodevelopment al delay. As individuals treated for\nHIV survive into older age, additive and in teractive neurocognitive effects of HIV and\naging, including other NCDs (e .g., due to Alzheimer\u2019s dise ase, due to Parkinson\u2019s dis-\nease), are possible. \nRisk and Prognostic Factors\nRisk and prognostic factors for HIV infection. Risk factors for HIV infection include injec-\ntion drug use, unprotected sex, and unprotecte d blood supply and othe r iatrogenic factors. \nRisk and prognostic factors for major or mild neurocognitive disorder due to HIV in-\nfection. Paradoxically, NCD due to HIV infection ha s not declined significantly with the\nadvent of combined antiretrov iral therapy, although the most severe presentations (con-", "source": "dsm5.pdf"} {"id": "7c10c6082f59-2", "page_content": "sistent with the diagnosis of major NCD) ha ve decreased sharply. Contributory factors\nmay include inadequate control of HIV in the central nervous system (CNS), the evolution\nof drug-resistant viral strains, the effects of chronic long-term systemic and brain inflam-\nmation, and the effects of comorb id factors such as aging, drug abuse, past history of CNS\ntrauma, and co-infections, such as with the hepatitis C virus. Chronic exposure to antiret-\nroviral drugs also raises the po ssibility of neurotoxicity, alth ough this has not been defin-\nitively established.", "source": "dsm5.pdf"} {"id": "7e4c5f7a5b5b-0", "page_content": "634 Neurocognitive Disorders\nDiagnostic Markers\nSerum HIV testing is required for the diagnosis. In addition, HIV charac terization of the cere-\nbrospinal fluid may be helpful if it reveals a disp roportionately high viral load in cerebrospinal\nfluid versus in the plasma. Neuroimaging (i.e., magnetic resonance im aging [MRI]) may reveal\nreduction in total brain volume, cortical thi nning, reduction in white matter volume, and\npatchy areas of abnormal white matter (hyper intensities). MRI or lumbar puncture may be\nhelpful to exclude a specific medical condition such as cryptococcus infection or herpes en-\ncephalitis that may contribute to CNS changes in the context of AIDS. Specialized techniques\nsuch as diffusion tensor imaging may reveal damage to specific white matter tracts. \nFunctional Consequences of Major or Mild \nNeurocognitive Disorder Due to HIV Infection\nFunctional consequences of ma jor or mild NCD due to HIV infection are variable across\nindividuals. Thus, impaired executive abiliti es and slowed information processing may\nsubstantially interfere with the complex dise ase management decisions required for ad-\nherence to the combined antire troviral therapy regimen. The likelihood of comorbid dis-\nease may further create functional challenges. \nDifferential Diagnosis\nIn the presence of comorbidities, such as other infections (e.g., hepati tis C virus, syphilis),\ndrug abuse (e.g., methamphetamine abuse), or prior head injury or neurodevelopmental\nconditions, major or mild NCD due to HIV infe ction can be diagnosed provided there is ev-\nidence that infection with HIV has worsened any NCDs due to such preexisting or comorbid\nconditions. Among older adults, onset of neur ocognitive decline rela ted to cerebrovascular", "source": "dsm5.pdf"} {"id": "7e4c5f7a5b5b-1", "page_content": "conditions. Among older adults, onset of neur ocognitive decline rela ted to cerebrovascular\ndisease or neurodegeneration (e.g., major or mild NCD due to Alzheimer\u2019s disease) may\nneed to be differentiated. In general, stable, fluctuating (without progression) or improving\nneurocognitive status would favor an HIV et iology, whereas steady or stepwise deter-\nioration would suggest neurodeg enerative or vascular etiolo gy. Because more severe im-\nmunodeficiency can result in opportunistic in fections of the brain (e.g., toxoplasmosis;\ncryptococcosis) and neoplasia (e.g., CNS lymphoma), sudden onset of an NCD or sudden\nworsening of that disorder demands acti ve investigation of non-HIV etiologies.\nComorbidity\nHIV disease is accompanied by chronic systemic and neuro-inflammation that can be as-\nsociated with cerebrovascular disease and metabolic syndrome. These complications can\nbe part of the pathogenesis of major or mild NCD due to HIV infectio n. HIV frequently co-\noccurs with conditions such as substance use disorders when the substance has been in-\njected and other sexually transmitted disorders. \nMajor or Mild Neurocognitive Disorder\n Due to Prion Disease\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. There is insidious onset, and rapid progression of impairment is common.\nC. There are motor features of prion disease, such as myoclonus or ataxia, or biomarker\nevidence.", "source": "dsm5.pdf"} {"id": "57ec07e67b54-0", "page_content": "Major or Mild Neurocognitive Disorder Due to Prion Disease 635\nD. The neurocognitive disorder is not attribut able to another medical condition and is not\nbetter explained by another mental disorder.\nCoding note: For major neurocognitive disorder due to prion disease, with behavioral dis-\nturbance, code first 046.79 (A81.9) prion disease, followed by 294.11 (F02.81) major\nneurocognitive disorder due to prion disease, with behavioral disturbance. For major neu-\nrocognitive disorder due to prion disease, without behavioral disturbance, code first\n046.79 (A81.9) prion disease, followed by 294.10 (F02.80) major neurocognitive disorder\ndue to prion disease, without behavioral disturbance.\nFor mild neurocognitive disorder due to prion disease, code 331.83 (G31.84). (Note: Do\nnot use the additional code for prion disease. Behavioral disturbance cannot be coded but\nshould still be indicated in writing.)\nDiagnostic Features\nThe classification of major or mild neurocogni tive disorder (NCD) due to prion disease in-\ncludes NCDs due to a group of subacute sp ongiform encephalopathies (including Creutz-\nfeldt-Jakob disease, variant Creutzfeldt-Jakob disease, kuru, Gerstmann-Str\u00e4ussler-\nScheinker syndrome, and fatal insomnia) ca used by transmissible agents known as prions.\nThe most common type is sporadic Creutzfeld t-Jakob disease, typically referred to as\nCreutzfeldt-Jakob disease (CJD). Variant CJD is much rarer and is associated with trans-", "source": "dsm5.pdf"} {"id": "57ec07e67b54-1", "page_content": "mission of bovine spongiform encephalopathy, also called \u201cmad cow disease.\u201d Typically,\nindividuals with CJD present with neurocognitive deficits , ataxia, and abnormal move-\nments such as myoclonus, chorea, or dystonia; a startle reflex is also common. Typically,\nthe history reveals rapid progression to major NCD over as little as 6 months, and thus the\ndisorder is typically seen only at the major le vel. However, many individuals with the dis-\norder may have atypical presentations, and the disease can be confirmed only by biopsy or\nat autopsy. Individuals with variant CJD may present with a greater preponderance of\npsychiatric symptoms, characterized a by lo w mood, withdrawal, and anxiety. Prion dis-\nease is typically not diagnosed without at le ast one of the characteristic biomarker fea-\ntures: recognized lesions on magnetic resonance imaging with DWI (diffusion-weighted\nimaging) or FLAIR (flu id-attenuated inversion recovery), tau or 14-3-3 protein in cerebro-\nspinal fluid, characteristic triphasic waves on electroencephalogram, or, for rare familial\nforms, family history or genetic testing. \nPrevalence\nThe annual incidence of sporadic CJD is a pproximately one or two cases per million peo-\nple. Prevalence is unknown but ve ry low given the short survival.\nDevelopment and Course\nPrion disease may develop at any age in adults\u2014the peak age for the sporadic CJD is ap-\nproximately 67 years\u2014although it has been report ed to occur in individuals spanning the\nteenage years to late life. Prodromal symptoms of prion disease may include fatigue, anx-\niety, problems with appetite or sleeping, or difficulties with concentration. After several", "source": "dsm5.pdf"} {"id": "57ec07e67b54-2", "page_content": "iety, problems with appetite or sleeping, or difficulties with concentration. After several\nweeks, these symptoms may be followed by incoordination, altered vision, or abnormal\ngait or other movements that may be myoclonic, choreoathetoid, or ballistic, along with a\nrapidly progressive dementia. The disease typi cally progresses very rapidly to the major\nlevel of impairment over several months. More rarely, it can progress over 2 years and ap-\npear similar in its course to other NCDs.", "source": "dsm5.pdf"} {"id": "4f65ee2c77dd-0", "page_content": "636 Neurocognitive Disorders\nRisk Factors and Prognosis\nEnvironmental. Cross-species transmission of prion infections, with agents that are\nclosely related to the human form, has been demonstrated (e.g., the outbreak of bovine\nspongiform encephalopathy inducing variant CJD in the United Kingdom during the mid-\n1990s). Transmission by corneal transplantation and by human growth factor injection has\nbeen documented, and anecdotal cases of tran smission to health care workers have been\nreported.\nGenetic and physiological. There is a genetic component in up to 15% of cases, associ-\nated with an autosoma l dominant mutation.\nDiagnostic Markers\nPrion disease can be definitively confirmed only by biopsy or at autopsy. Although there are\nno distinctive findings on cerebrospinal fluid analysis across the prion diseases, reliable bio-\nmarkers are being developed and include 14-3-3 protein (particularly for sporadic CJD) as\nwell as tau protein. Magnetic resonance brain imaging is currently considered the most sen-\nsitive diagnostic test when DWI is performed, with the most common finding being multi-\nfocal gray matter hyperintensities in subcortical and cortical regions. In some individuals,\nthe electroencephalogram reve als periodic sharp, often triphasic and synchronous dis-\ncharges at a rate of 0.5\u20132 Hz at some point during the course of the disorder. \nDifferential Diagnosis\nOther major neurocognitive disorders. Major NCD due to prion disease may appear\nsimilar in its course to other NCDs, but prio n diseases are typically distinguished by their\nrapid progression and prominent cerebellar and motor symptoms.\nMajor or Mild Neurocognitive Disorder\nDue to Parkinson\u2019s Disease\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.", "source": "dsm5.pdf"} {"id": "4f65ee2c77dd-1", "page_content": "Diagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. The disturbance occurs in the setting of established Parkinson\u2019s disease.\nC. There is insidious onset and gradual progression of impairment.\nD. The neurocognitive disorder is not attribut able to another medical condition and is not\nbetter explained by another mental disorder.\nMajor or mild neurocognitive disorder probably due to Parkinson\u2019s disease should\nbe diagnosed if 1 and 2 are both met. Major or mild neurocognitive disorder possibly\ndue to Parkinson\u2019s disease should be diagnosed if 1 or 2 is met:\n1. There is no evidence of mixed etiology (i.e., absence of other neurodegenerative or\ncerebrovascular disease or another neurological, mental, or systemic disease or con-\ndition likely contributing to cognitive decline).\n2. The Parkinson\u2019s disease clearly precedes the onset of the neurocognitive disorder.\nCoding note: For major neurocognitive disorder probably due to Parkinson\u2019s disease,\nwith behavioral disturbance, code first 332.0 (G20) Parkinson\u2019s disease, followed by\n294.11 (F02.81) major neurocognitive disorder probably due to Parkinson\u2019s disease, with\nbehavioral disturbance. For major neurocognitive disorder probably due to Parkinson\u2019s\ndisease, without behavioral disturbance, code first 332.0 (G20) Parkinson\u2019s disease, fol-", "source": "dsm5.pdf"} {"id": "f75099e5c10c-0", "page_content": "Major or Mild Neurocognitive Disorder Due to Parkinson\u2019s Disease 637\nlowed by 294.10 (F02.80) major neurocognitive disorder probably due to Parkinson\u2019s dis-\nease, without behavioral disturbance.\nFor major neurocognitive disorder possibly due to Parkinson\u2019s disease, code 331.9\n(G31.9) major neurocognitive disorder possibly due to Parkinson\u2019s disease. ( Note: Do not\nuse the additional code for Parkinson\u2019s disease. Behavioral disturbance cannot be coded\nbut should still be indicated in writing.)\nFor mild neurocognitive disorder due to Parkinson\u2019s disease, code 331.83 (G31.84).\n(Note: Do not use the additional code for Parkinson\u2019s disease. Behavioral disturbance\ncannot be coded but should still be indicated in writing.)\nDiagnostic Features\nThe essential feature of major or mild neurocognitive disorder (NCD) due to Parkinson\u2019s\ndisease is cognitive decline following the onset of Parkinson\u2019s disease. The disturbance\nmust occur in the setting of established Parkinson\u2019s disease (Criterion B), and deficits must\nhave developed gradually (Criterion C). The NCD is viewed as probably due to Parkinson\u2019s\ndisease when there is no evidence of another disorder that might be contributing to the\ncognitive decline and when the Parkinson\u2019s disease clearly precedes onset of the NCD. The\nNCD is considered possibly due to Parkinson\u2019s disease either when there is no evidence of\nanother disorder that might be contributing to the cognitive decline or when the Parkin-\nson\u2019s disease precedes onset of the NCD, but not both.\nAssociated Features Supporting Diagnosis\nFrequently present features include apathy , depressed mood, anxious mood, hallucina-\ntions, delusions, personality changes, rapid eye movement sleep behavior disorder, and\nexcessive daytime sleepiness. \nPrevalence", "source": "dsm5.pdf"} {"id": "f75099e5c10c-1", "page_content": "excessive daytime sleepiness. \nPrevalence \nThe prevalence of Parkinson\u2019s disease in the United States steadily increases with age from\napproximately 0.5% between ages 65 and 69 to 3% at age 85 years and older. Parkinson\u2019s\ndisease is more common in males than in females. Among individuals with Parkinson\u2019s\ndisease, as many as 75% will develop a major NC D sometime in the course of their disease.\nThe prevalence of mild NCD in Parkinso n\u2019s disease has been estimated at 27%. \nDevelopment and Course\nOnset of Parkinson\u2019s disease is typically betw een the sixth and ninth decades of life, with\nmost expression in the early 60s. Mild NCD ofte n develops relatively early in the course of\nParkinson\u2019s disease, whereas major impairme nt typically does not occur until late. \nRisk and Prognostic Factors\nEnvironmental. Risk factors for Parkinson\u2019s disease include exposure to herbicides and\npesticides.\nGenetic and physiological. Potential risk factors for NC D among individuals with Par-\nkinson\u2019s disease include older age at diseas e onset and increasing duration of disease. \nDiagnostic Markers\nNeuropsychological testing, with a focus on test s that do not rely on motor function, is crit-\nical in detecting the core cogn itive deficits, particularly at the mild NCD phase. Structural\nneuroimaging and dopamine transporter scans, such as DaT scans, may differentiate\nLewy body\u2013related dementias (Parkinson\u2019s and dementia wi th Lewy bodies) from non\u2013", "source": "dsm5.pdf"} {"id": "f3c139abc488-0", "page_content": "638 Neurocognitive Disorders\nLewy body\u2013related dementias (e.g., Alzheimer\u2019s disease) and can sometimes be helpful in\nthe evaluation of major or mild NCD due to Parkinson\u2019s disease.\nDifferential Diagnosis\nMajor or mild neurocognitive disorder with Lewy bodies. This distinction is based sub-\nstantially on the timing and sequence of mo tor and cognitive symptoms. For NCD to be at-\ntributed to Parkinson\u2019s diseas e, the motor and other symptoms of Parkinson\u2019s disease must\nbe present well before (by convention, at leas t 1 year prior) cognit ive decline has reached\nthe level of major NCD, whereas in major or mild NCD with Lewy bodies, cognitive symp-\ntoms begin shortly before, or concurrent wi th, motor symptoms. For mild NCD, the timing\nis harder to establish because the diagnosis itse lf is less clear and th e two disorders exist on\na continuum. Unless Parkinson\u2019s disease has been established for some time prior to the\nonset of cognitive decline, or typical features of major or mild NCD with Lewy bodies are\npresent, it is preferable to diagnose unspecified mild NCD.\nMajor or mild neurocognitive disorder due to Alzheimer\u2019s disease. The motor features\nare the key to distinguishing major or mild NCD due to Parkinson\u2019s disease from major or\nmild NCD due to Alzheimer\u2019s disease. However, the two disorders can co-occur.\nMajor or mild vascular neurocognitive disorder. Major or mild vascular NCD may pre-\nsent with parkinsonian features such as psychomotor slowing that may occur as a conse-\nquence of subcortical small vessel disease. However, the parkinsonian features typically\nare not sufficient for a diagnosis of Parkinson\u2019s disease, and the course of the NCD usually\nhas a clear association with cerebrovascular changes.", "source": "dsm5.pdf"} {"id": "f3c139abc488-1", "page_content": "has a clear association with cerebrovascular changes.\nNeurocognitive disorder due to another medical condition (e.g., neurodegenerative\ndisorders). When a diagnosis of major or mild NC D due to Parkinson\u2019s disease is being\nconsidered, the distinction must also be made from other brain diso rders, such as progres-\nsive supranuclear palsy, corticobasal degeneration, multiple system atrophy, tumors, and\nhydrocephalus. \nNeuroleptic-induced parkinsonism. Neuroleptic-induced parkinsonism can occur in\nindividuals with other NCDs, particularly when dopamine-blocking drugs are prescribed\nfor the behavioral manifest ations of such disorders\nOther medical conditions. Delirium and NCDs due to side effects of dopamine-blocking\ndrugs and other medical conditio ns (e.g., sedation or impair ed cognition, severe hypothy-\nroidism, B12 deficiency) must al so be ruled out. \nComorbidity \nParkinson\u2019s disease may coexist with Alzheimer\u2019 s disease and cerebrovascular disease, espe-\ncially in older individuals. The compounding of multiple pathological features may diminish\nthe functional abilities of individuals with Pa rkinson\u2019s disease. Moto r symptoms and frequent\nco-occurrence of depression or apathy can make functional impairment worse.\nMajor or Mild Neurocognitive Disorder\n Due to Huntington\u2019s Disease\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. There is insidious onset and gradual progression.\nC. There is clinically established Huntington\u2019 s disease, or risk for Huntington\u2019s disease\nbased on family history or genetic testing.", "source": "dsm5.pdf"} {"id": "f96228da4022-0", "page_content": "Major or Mild Neurocognitive Disorder Due to Huntington\u2019s Disease 639\nD. The neurocognitive disorder is not attribut able to another medical condition and is not\nbetter explained by another mental disorder.\nCoding note: For major neurocognitive disorder due to Huntington\u2019s disease, with behav-\nioral disturbance, code first 333.4 (G10) Huntington\u2019s disease, followed by 294.11\n(F02.81) major neurocognitive disorder due to Huntington\u2019s disease, with behavioral dis-\nturbance. For major neurocognitive disorder due to Huntington\u2019s disease, without behav-\nioral disturbance, code first 333.4 (G10) Huntington\u2019s disease, followed by 294.10 (F02.80)\nmajor neurocognitive disorder due to Huntington\u2019s disease, without behavioral disturbance.\nFor mild neurocognitive disorder due to Huntington\u2019s disease, code 331.83 (G31.84).\n(Note: Do not use the additional code for Huntington\u2019s disease. Behavioral disturbance\ncannot be coded but should still be indicated in writing.)\nDiagnostic Features\nProgressive cognitive impairment is a core feature of Huntington \u2019s disease, with early changes\nin executive function (i.e., processing speed, organization, and planni ng) rather than learn-\ning and memory. Cognitive and associated beha vioral changes often precede the emergence\nof the typical motor abnormalities of bradykinesia (i.e., slowing of voluntary movement)\nand chorea (i.e., involuntary jerking movements). A diagnosis of definite Huntington\u2019s dis-\nease is given in the presence of unequivocal, extrapyramidal motor ab normalities in an in-\ndividual with either a family history of Huntington\u2019s disease or genetic testing showing a\nCAG trinucleotide repeat expansion in the HTT gene, located on chromosome 4.", "source": "dsm5.pdf"} {"id": "f96228da4022-1", "page_content": "Associated Features Supporting Diagnosis\nDepression, irritability, anxiety, obsessive -compulsive symptoms, and apathy are fre-\nquently, and psychosis more rarely, associat ed with Huntington\u2019s disease and often pre-\ncede the onset of motor symptoms.\nPrevalence\nNeurocognitive deficits are an eventual ou tcome of Huntington\u2019s disease; the worldwide\nprevalence is estimated to be 2.7 per 100,000. The prevalence of Huntington\u2019s disease in\nNorth America, Europe, and Australia is 5.7 pe r 100,000, with a much lower prevalence of\n0.40 per 100,000 in Asia. \nDevelopment and Course\nThe average age at diagnosis of Huntington\u2019s disease is approximately 40 years, although\nthis varies widely. Age at onset is inversely correlated with CAG expansion length. Juve-\nnile Huntington\u2019s disease (ons et before age 20) may present more commonly with brady-\nkinesia, dystonia, and rigidity than with the choreic movements characteristic of the adult-\nonset disorder. The disease is gradually progre ssive, with median survival approximately\n15 years after motor symptom diagnosis.\nPhenotypic expression of Huntington\u2019s diseas e varies by presence of motor, cognitive,\nand psychiatric symptoms. Psychiatric and co gnitive abnormalities can predate the motor\nabnormality by at least 15 years. Initial symp toms requiring care often include irritabity,\nanxiety, or depressed mood. Other behavioral disturbances may include pronounced ap-\nathy, disinhibition, impulsivit y, and impaired insight, with apathy often becoming more\nprogressive over time. Early movement symptoms may involve the appearance of fidget-\niness of the extremitie s as well as mild apraxia (i.e., difficulty with purposeful movements),", "source": "dsm5.pdf"} {"id": "f96228da4022-2", "page_content": "particularly with fine motor tasks. As the disorder progre sses, other motor problems in-\nclude impaired gait (ataxia ) and postural instability. Motor impairment eventually affects\nspeech production ( dysarthria ) such that the speech becomes very difficult to understand,", "source": "dsm5.pdf"} {"id": "1a33b9f8496c-0", "page_content": "640 Neurocognitive Disorders\nwhich may result in significant distress resu lting from the communication barrier in the\ncontext of comparatively intact cognition. Advanced motor disease severely affects gait\nwith progressive ataxia. Eventually individuals become nonambulatory. End-stage motor\ndisease impairs motor control of eating and swallowing, typically a major contributor to\nthe death of the individual from aspiration pneumonia.\nRisk and Prognostic Factors \nGenetic and physiological. The genetic basis of Huntington\u2019s disease is a fully penetrant\nautosomal dominant expansion of th e CAG trincleotide, often called a CAG repeat in the\nhuntingtin gene. A repeat length of 36 or more is invariably associated with Huntington\u2019s\ndisease, with longer repeat lengths associated with early age at onset. A CAG repeat length\nof 36 or more is invariably asso ciated with Huntington\u2019s disease.\nDiagnostic Markers\nGenetic testing is the primary laboratory test for the determination of Huntington\u2019s dis-\nease, which is an autosomal dominant disord er with complete penetrance. The trinucleo-\ntide CAG is observed to have a repeat ex pansion in the gene that encodes huntingtin\nprotein on chromosome 4. A di agnosis of Huntington\u2019s disease is not made in the presence\nof the gene expansion alone, but the diagno sis is made only after symptoms become man-\nifest. Some individuals with a positive family history request genetic testing in a presymp-\ntomatic stage. Associat ed features may also include neur oimaging changes; volume loss in\nthe basal ganglia, particularly the caudate nu cleus and putamen, is well known to occur\nand progresses over the course of illness. Other structural and functional changes have\nbeen observed in brain imagin g but remain research measures.\nFunctional Consequences of Major or Mild", "source": "dsm5.pdf"} {"id": "1a33b9f8496c-1", "page_content": "Functional Consequences of Major or Mild \nNeurocognitive Disorder Du e to Huntington\u2019s Disease\nIn the prodromal phase of illness and at early diagnosis, occupational decline is most com-\nmon, with most individuals repo rting some loss of ability to engage in their typical work.\nThe emotional, behavioral, and cognitive aspects of Huntington\u2019s disease, such as disin-\nhibition and personality changes, are highly associated with functional decline. Cognitive\ndeficits that contribute most to functional decline may incl ude speed of processing, initi-\nation, and attention rather th an memory impairment. Given that Huntington\u2019s disease on-\nset occurs in productive years of life, it may have a very disruptive effect on performance\nin the work setting as well as social and fam ily life. As the disease progresses, disability\nfrom problems such as impair ed gait, dysarthria, and impulsive or irritable behaviors may\nsubstantially add to the level of impairment and daily care needs, over and above the care\nneeds attributable to the cognitive decline. Severe choreic moveme nts may substantially\ninterfere with provision of care such as bathing, dressing, and toileting.\nDifferential Diagnosis\nOther mental disorders. Early symptoms of Huntington\u2019s disease may include instabil-\nity of mood, irritability, or compulsive behaviors that may suggest another mental disor-\nder. However, genetic testing or the develo pment of motor symptoms will distinguish the\npresence of Huntington\u2019s disease.\nOther neurocognitive disorders. The early symptoms of Huntington\u2019s disease, particu-\nlarly symptoms of executive dysfunction an d impaired psychomotor speed, may resemble\nother neurocognitive disorders (NCDs), such as major or mild vascular NCD.", "source": "dsm5.pdf"} {"id": "a528aec0036a-0", "page_content": "Major or Mild Neurocognitive Disorder Due to Another Medical Condition 641\nOther movement disorders. Huntington\u2019s disease must also be differentiated from other\ndisorders or conditions associated with chorea, such as Wilson\u2019s disease, drug-induced\ntardive dyskinesia, Sydenham\u2019s chorea, systemic lupus erythematosus, or senile chorea.\nRarely, individuals may present with a course similar to that of Huntington\u2019s disease but\nwithout positive genetic testin g; this is considered to be a Huntington\u2019s disease pheno-\ncopy that results from a variet y of potential genetic factors.\nMajor or Mild Neurocognitive Disorder\n Due to Another Medical Condition\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. There is evidence from the history, physical examination, or laboratory findings that the\nneurocognitive disorder is the pathophysi ological consequence of another medical\ncondition. \nC. The cognitive deficits are not better explained by another mental disorder or another\nspecific neurocognitive disorder (e.g., Alzheimer\u2019s disease, HIV infection).\nCoding note: For major neurocognitive disorder due to another medical condition, with\nbehavioral disturbance, code first the other medical condition, followed by the major neu-\nrocognitive disorder due to another medical condition, with behavioral disturbance (e.g.,\n340 [G35] multiple sclerosis, 294.11 [F02.81] major neurocognitive disorder due to multi-\nple sclerosis, with behavioral disturbance). For major neurocognitive disorder due to an-\nother medical condition, without behavioral disturbance, code first the other medical\ncondition, followed by the major neurocognitive disorder due to another medical condition,\nwithout behavioral disturbance (e.g., 340 [G35] multiple sclerosis, 294.10 [F02.80] major", "source": "dsm5.pdf"} {"id": "a528aec0036a-1", "page_content": "neurocognitive disorder due to multiple sclerosis, without behavioral disturbance).\nFor mild neurocognitive disorder due to another medical condition, code 331.83 (G31.84).\n(Note: Do not use the additional code for the other medical condition. Behavioral distur-\nbance cannot be coded but should still be indicated in writing.)\nDiagnostic Features\nA number of other medical co nditions can cause neurocognitive disorders (NCDs). These\nconditions include structural lesions (e.g., primary or secondary brain tumors, subdural\nhematoma, slowly progressive or normal-press ure hydrocephalus), hypoxia related to hy-\npoperfusion from heart failure, endocrine co nditions (e.g., hypothyroidism, hypercalce-\nmia, hypoglycemia), nutritional conditions (e.g., deficiencies of thiamine or niacin), other\ninfectious conditions (e.g., neurosyphilis, cryptococcosis), im mune disorders (e.g., tempo-\nral arteritis, systemic lupus erythematosus), hepatic or rena l failure, metabolic conditions\n(e.g., Kufs\u2019 disease, adrenoleukodystrophy, metachromatic leukodystrophy, other storage\ndiseases of adulthood and childhood), and ot her neurological conditions (e.g., epilepsy,\nmultiple sclerosis). Unusual causes of central nervous system injury, such as electrical\nshock or intracranial radiation, are generally evident from the history. The temporal asso-\nciation between the onset or exacerbation of the medical condition and the development of\nthe cognitive deficit offers the greatest supp ort that the NCD is induced by the medical\ncondition. Diagnostic certainty regarding this relationship may be increased if the neuro-\ncognitive deficits ameliorate partially or stab ilize in the context of treatment of the medical", "source": "dsm5.pdf"} {"id": "a528aec0036a-2", "page_content": "condition.", "source": "dsm5.pdf"} {"id": "c985a6efd973-0", "page_content": "642 Neurocognitive Disorders\nDevelopment and Course\nTypically the course of the NCD progresses in a manner that is commensurate with progres-\nsion of the underlying medical disorder. In ci rcumstances where the medical disorder is treat-\nable (e.g., hypothyroidism), th e neurocognitive deficit may im prove or at least not progress.\nWhen the medical condition has a deteriorative course (e.g., secondary progressive multiple\nsclerosis), the neurocognitive deficits will progre ss along with the tempor al course of illness.\nDiagnostic Markers\nAssociated physical examinatio n and laboratory findings and other clinical features de-\npend on the nature and severity of the medical condition. \nDifferential Diagnosis\nOther major or mild neurocognitive disorder. The presence of an attributable medical\ncondition does not entirely exclude the possibility of another major or mild NCD. If cog-\nnitive deficits persist following successful treatment of an associated medical condition,\nthen another etiology may be responsible for the cognitive decline.\nMajor or Mild Neurocognitive Disorder\n Due to Multiple Etiologies\nDiagnostic Criteria \nA. The criteria are met for major or mild neurocognitive disorder.\nB. There is evidence from the history, physical examination, or laboratory findings that the\nneurocognitive disorder is the pathophysiological consequence of more than one etio-\nlogical process, excluding substances (e.g., neurocognitive disorder due to Alzhei-\nmer\u2019s disease with subsequent development of vascular neurocognitive disorder).\nNote: Please refer to the diagnostic criteria for the various neurocognitive disorders due\nto specific medical conditions for guidance on establishing the pa rticular etiologies. \nC. The cognitive deficits are not better ex plained by another mental disorder and do not\noccur exclusively during the course of a delirium.", "source": "dsm5.pdf"} {"id": "c985a6efd973-1", "page_content": "occur exclusively during the course of a delirium.\nCoding note: For major neurocognitive disorder due to multiple etiologies, with behavioral\ndisturbance, code 294.11 (F02.81) ; for major neurocognitive disorder due to multiple etiolo-\ngies, without behavioral disturbance, code 294.10 (F02.80). All of the etiological medical\nconditions (with the exception of vascular disease) should be coded and listed separately\nimmediately before major neurocognitive diso rder due to multiple etiologies (e.g., 331.0\n[G30.9] Alzheimer\u2019s disease; 331.82 [G31.83] Lewy body disease; 294.11 [F02.81] major\nneurocognitive disorder due to multiple etiologies, with behavioral disturbance).\nWhen a cerebrovascular etiology is contributin g to the neurocognitive disorder, the diagno-\nsis of vascular neurocognitive disorder should be listed in addition to major neurocognitive\ndisorder due to multiple etiologies. For example, for a presentation of major neurocognitive\ndisorder due to both Alzheimer\u2019s disease and va scular disease, with behavioral disturbance,\ncode the following: 331.0 (G30.9) Alzheimer\u2019s disease; 294.11 (F02.81) major neurocogni-\ntive disorder due to multiple etiologies, with behavioral disturbance; 290.40 (F01.51) major\nvascular neurocognitive disorder, with behavioral disturbance.\nFor mild neurocognitive disorder due to multiple etiologies, code 331.83 (G31.84). (Note:\nDo not use the additional codes for the etiologies. Behavioral disturbance cannot be coded\nbut should still be indicated in writing.)", "source": "dsm5.pdf"} {"id": "8e47094228ea-0", "page_content": "Unspecified Neurocognitive Disorder 643\nThis category is included to cover the clinical presentation of a neurocognitive disorder (NCD)\nfor which there is evidence that multiple medical conditions have played a probable role in the\ndevelopment of the NCD. In addition to evidence indicative of the presence of multiple med-\nical conditions that are known to cause NCD (i .e., findings from the hi story and physical ex-\namination, and laboratory findings), it may be he lpful to refer to the diag nostic criteria and text\nfor the various medical etiologies (e.g., NCD du e to Parkinson\u2019s disease) for more information\non establishing the etiological connection for that particular medical condition.\nUnspecified Neurocognitive Disorder\n799.59 (R41.9)\nThis category applies to presentations in which symptoms characteristic of a neurocogni-\ntive disorder that cause clinically significant distress or impairment in social, occupational,\nor other important areas of functioning predominate but do not meet the full criteria for any\nof the disorders in the neurocognitive diso rders diagnostic class. The unspecified neuro-\ncognitive disorder category is used in situations in which the precise etiology cannot be\ndetermined with sufficient certainty to make an etiological attribution.\nCoding note: For unspecified major or mild neurocognitive disorder, code 799.59 (R41.9).\n(Note: Do not use additional codes for any presumed etiological medical conditions. Be-\nhavioral disturbance cannot be coded but may be indicated in writing.)", "source": "dsm5.pdf"} {"id": "029e5ac1ce9a-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "936837fa2b94-0", "page_content": "645Personality\n Disorders\nThis chapter begins with a general definition of personality disorder that applies\nto each of the 10 specific personality disorders. A personality disorder is an enduring pattern\nof inner experience and behavior that deviates markedly from the expectations of the in-\ndividual\u2019s culture, is pervasive and inflexible , has an onset in adolescence or early adult-\nhood, is stable over time, and lead s to distress or impairment. \nWith any ongoing review process, especially one of this complexity, different view-\npoints emerge, and an effort was made to accommodate them. Thus, personality disorders\nare included in both Sections II and III. The material in Section II represents an update of\ntext associated with the same criteria foun d in DSM-IV-TR, whereas Section III includes\nthe proposed research model for personality disorder diagnosis and conceptualization de-\nveloped by the DSM-5 Personality and Persona lity Disorders Work Group. As this field\nevolves, it is hoped that both versions will serve clinical practice and research initiatives,\nrespectively.\nThe following personality disorders are included in this chapter.\n\u2022Paranoid personality disorder is a pattern of distrust and suspiciousness such that oth-\ners\u2019 motives are interp reted as malevolent.\n\u2022Schizoid personality disorder is a pattern of detachment fr om social relationships and\na restricted range of emotional expression.\n\u2022Schizotypal personality disorder is a pattern of acute discomfort in close relationships,\ncognitive or perceptual distortions, and eccentricities of behavior.\n\u2022Antisocial personality disorder is a pattern of disregard for, and violation of, the rights\nof others.\n\u2022Borderline personality disorder is a pattern of instability in interpersonal relation-\nships, self-image, and affects, and marked impulsivity.", "source": "dsm5.pdf"} {"id": "936837fa2b94-1", "page_content": "ships, self-image, and affects, and marked impulsivity.\n\u2022Histrionic personality disorder is a pattern of excessive emotionality and attention\nseeking.\n\u2022Narcissistic personality disorder is a pattern of grandiosity, need for admiration, and\nlack of empathy.\n\u2022Avoidant personality disorder is a pattern of social inhibition, feelings of inadequacy,\nand hypersensitivity to negative evaluation.\n\u2022Dependent personality disorder is a pattern of submissive and clinging behavior re-\nlated to an excessive need to be taken care of.\n\u2022Obsessive-compulsive personality disorder is a pattern of preoccupation with order-\nliness, perfectionism, and control.\n\u2022Personality change due to another medical condition is a persistent personality dis-\nturbance that is judged to be due to the direct physiological effects of a medical condi-\ntion (e.g., frontal lobe lesion).\n\u2022Other specified personality disorder and unspecified personality disorder is a cate-\ngory provided for two situations: 1) the individual\u2019s personality pattern meets the gen-\neral criteria for a personality disorder, an d traits of several different personality\ndisorders are present, but the criteria for any specific pers onality disorder are not met;", "source": "dsm5.pdf"} {"id": "3012ad54c992-0", "page_content": "646 Personality Disorders\nor 2) the individual\u2019s personality pattern m eets the general criteria for a personality dis-\norder, but the individual is considered to have a personality disorder that is not in-\ncluded in the DSM-5 classification (e.g., passive-aggressive personality disorder).\nThe personality disorders are grouped into thre e clusters based on descriptive similarities.\nCluster A includes paranoid, schizoid, and schi zotypal personality diso rders. Individuals with\nthese disorders often appear odd or eccentric. Cluster B includes antisocial, borderline, histri-\nonic, and narcissistic personality disorders. In dividuals with these disorders often appear dra-\nmatic, emotional, or erratic. Cluster C in cludes avoidant, dependent, and obsessive-\ncompulsive personality disorders. Individuals with these disorders often appear anxious or\nfearful. It should be noted that this clustering system, although useful in some research and ed-\nucational situations, has serious limitations and has not been consistently validated. \nMoreover, individuals freque ntly present with co-occu rring personality disorders\nfrom different clusters. Prevalence estimates fo r the different clusters suggest 5.7% for dis-\norders in Cluster A, 1.5% for disorders in Cl uster B, 6.0% for disorders in Cluster C, and\n9.1% for any personality disorder, indicating frequent co-occurrence of disorders from dif-\nferent clusters. Data from the 2001\u20132002 National Epidemiologic Survey on Alcohol and\nRelated Conditions suggest that approximately 15% of U.S. adults have at least one per-\nsonality disorder.\nDimensional Models for Personality Disorders\nThe diagnostic approach used in this manual represents the categorical perspective that\npersonality disorders are qualit atively distinct clinical synd romes. An alternative to the", "source": "dsm5.pdf"} {"id": "3012ad54c992-1", "page_content": "personality disorders are qualit atively distinct clinical synd romes. An alternative to the\ncategorical approach is the dimensional perspective that personality disorders represent\nmaladaptive variants of personality traits that merge imperceptibly into normality and\ninto one another. See Section III for a full description of a dimensional model for person-\nality disorders. The DSM-IV personality disord er clusters (i.e., odd-eccentric, dramatic-\nemotional, and anxious- fearful) may also be viewed as dimensions representing spectra of\npersonality dysfunction on a continuum with other mental disorders. The alternative di-\nmensional models have much in common and together appear to cover the important ar-\neas of personality dysfunction. Their integration, clinical utility, and relationship with the\npersonality disorder diagnostic categories and various aspects of personality dysfunction\nare under active investigation.\nGeneral Personality Disorder\nCriteria\nA. An enduring pattern of inner experience and behavior that deviates markedly from the\nexpectations of the individual\u2019s culture. This pattern is manifested in two (or more) of\nthe following areas:\n1. Cognition (i.e., ways of perceiving and interpreting self, other people, and events).\n2. Affectivity (i.e., the range, intensity, lability, and appropriateness of emotional re-\nsponse).\n3. Interpersonal functioning.\n4. Impulse control.\nB. The enduring pattern is inflexible and per vasive across a broad range of personal and\nsocial situations.\nC. The enduring pattern leads to clinically signi ficant distress or impairment in social, oc-\ncupational, or other important areas of functioning.", "source": "dsm5.pdf"} {"id": "1ead71772b03-0", "page_content": "General Personality Disorder 647\nD. The pattern is stable and of long duration, and its onset can be traced back at least to\nadolescence or early adulthood.\nE. The enduring pattern is not better explained as a manifestation or consequence of an-\nother mental disorder.\nF. The enduring pattern is not attributable to the physiological effects of a substance (e.g.,\na drug of abuse, a medication) or another medical condition (e.g., head trauma).\nDiagnostic Features\nPersonality traits are enduring patterns of perceiving, relating to, and thinking about the en-\nvironment and oneself that are exhibited in a wide range of social and personal contexts.\nOnly when personality traits are inflexible and maladaptive and cause significant func-\ntional impairment or subjective distress do th ey constitute personality disorders. The essen-\ntial feature of a personality disorder is an en during pattern of inner experience and behavior\nthat deviates markedly from the expectations of the individual\u2019s culture and is manifested\nin at least two of the following areas: cognition, affectivity, interpersonal functioning, or im-\npulse control (Criterion A). This enduring pattern is inflexib le and pervasive across a broad\nrange of personal and social sit uations (Criterion B) and leads to clinically significant dis-\ntress or impairment in social, occupational, or other important areas of functioning (Crite-\nrion C). The pattern is stable and of long duration, and its onset can be traced back at least\nto adolescence or early adulthood (Criterion D). The pattern is not better explained as a\nmanifestation or consequence of another mental disorder (Criterion E) and is not attribut-\nable to the physiological effects of a substanc e (e.g., a drug of abuse, a medication, exposure\nto a toxin) or another medical condition (e.g., head trauma) (Criterion F). Specific diagnostic", "source": "dsm5.pdf"} {"id": "1ead71772b03-1", "page_content": "criteria are also provided for each of the pe rsonality disorders included in this chapter. \nThe diagnosis of personality disorders requires an evaluation of the individual\u2019s long-\nterm patterns of functioning, and the partic ular personality features must be evident by\nearly adulthood. The personality traits that define these disorders must also be distin-\nguished from characteristics th at emerge in response to sp ecific situational stressors or\nmore transient mental states (e .g., bipolar, depressive, or an xiety disorders; substance in-\ntoxication). The clinician should assess the stability of pers onality traits over time and\nacross different situations. Although a single interview with the in dividual is sometimes\nsufficient for making the diagnosis, it is of ten necessary to conduct more than one inter-\nview and to space these over time. Assessment ca n also be complicated by the fact that the\ncharacteristics that define a personality di sorder may not be considered problematic by\nthe individual (i.e., the traits are often ego-sy ntonic). To help overcome this difficulty, sup-\nplementary information from other informants may be helpful.\nDevelopment and Course\nThe features of a personality disorder usually become recogn izable during adolescence or\nearly adult life. By definition, a personality disorder is an enduring pattern of thinking,\nfeeling, and behaving that is relatively stable over time. Some types of personality disorder\n(notably, antisocial and borderli ne personality disorders) tend to become less evident or to\nremit with age, whereas this appears to be less true for some other types (e.g., obsessive-\ncompulsive and schizotypal personality disorders).\nPersonality disorder categories may be app lied with children or adolescents in those\nrelatively unusual instances in which the individual\u2019s particular maladaptive personality\ntraits appear to be pervasive, persistent, an d unlikely to be limited to a particular devel-", "source": "dsm5.pdf"} {"id": "1ead71772b03-2", "page_content": "traits appear to be pervasive, persistent, an d unlikely to be limited to a particular devel-\nopmental stage or another mental disorder. It sh ould be recognized that the traits of a per-", "source": "dsm5.pdf"} {"id": "a2a45caebee6-0", "page_content": "traits appear to be pervasive, persistent, an d unlikely to be limited to a particular devel-\nopmental stage or another mental disorder. It sh ould be recognized that the traits of a per-\nsonality disorder that appear in childhood will often not persist unchanged into adult life.\nFor a personality disorder to be diagnosed in an individual younger than 18 years, the fea-\ntures must have been present fo r at least 1 year. The one exception to this is antisocial per-", "source": "dsm5.pdf"} {"id": "bc1dee4e3699-0", "page_content": "648 Personality Disorders\nsonality disorder, which cannot be diagnosed in individuals younger than 18 years. Al-\nthough, by definition, a personality disorder requires an onset no later than early\nadulthood, individuals may not come to clinical attention until relatively late in life. A per-\nsonality disorder may be exacer bated following the loss of significant supporting persons\n(e.g., a spouse) or previously stabilizing social situations (e.g ., a job). However, the devel-\nopment of a change in person ality in middle adulthood or later life warrants a thorough\nevaluation to determine the possible presence of a personality change due to another med-\nical condition or an unrecogn ized substance use disorder.\nCulture-Related Diagnostic Issues\nJudgments about personality functioning must take into account the in dividual\u2019s ethnic, cul-\ntural, and social background. Personality disord ers should not be confused with problems as-\nsociated with acculturation following immigratio n or with the expressi on of habits, customs,\nor religious and political values professed by the individual\u2019s culture of origin. It is useful for\nthe clinician, especially when evaluating some one from a different background, to obtain ad-\nditional information from informants who are fa miliar with the person\u2019s cultural background.\nGender-Related Diagnostic Issues\nCertain personality disorders (e.g., antisocial personality disorder) are diagnosed more\nfrequently in males. Others (e.g., borderline, histrionic, and dependent personality disor-\nders) are diagnosed more freque ntly in females. Although these differences in prevalence\nprobably reflect real gender differences in the presence of such patterns, clinicians must be\ncautious not to overdiagnose or underdiagnos e certain personality disorders in females or\nin males because of social stereotypes about typical gender roles and behaviors.\nDifferential Diagnosis", "source": "dsm5.pdf"} {"id": "bc1dee4e3699-1", "page_content": "in males because of social stereotypes about typical gender roles and behaviors.\nDifferential Diagnosis\nOther mental disorders and personality traits. Many of the specific criteria for the per-\nsonality disorders describe features (e.g., su spiciousness, dependency, insensitivity) that\nare also characteristic of episo des of other mental disorders. A personality disorder should\nbe diagnosed only when the defining characte ristics appeared before early adulthood, are\ntypical of the individual\u2019s long-term function ing, and do not occur exclusively during an\nepisode of another mental diso rder. It may be particularly difficult (and not particularly\nuseful) to distinguish personality disorders from persistent mental disorders such as per-\nsistent depressive disorder that have an ea rly onset and an enduring, relatively stable\ncourse. Some personality diso rders may have a \u201cspectrum\u201d relationship to other mental\ndisorders (e.g., schizotypal personality disord er with schizophrenia; avoidant personality\ndisorder with social anxiety disorder [social phobia]) based on phe nomenological or bio-\nlogical similarities or familial aggregation.\nPersonality disorders must be distinguished from personality traits that do not reach\nthe threshold for a personality disorder. Person ality traits are diagnosed as a personality\ndisorder only when they are inflexible, maladaptive, and persisting and cause significant\nfunctional impairment or subjective distress.\nPsychotic disorders. For the three personality disorders that may be related to the psy-\nchotic disorders (i.e., paranoid, schizoid, and schizotypal), there is an exclusion criterion\nstating that the pattern of behavior must no t have occurred exclusively during the course\nof schizophrenia, a bipolar or depressive disorder with psycho tic features, or another psy-\nchotic disorder. When an individual has a pers istent mental disorder (e.g., schizophrenia)", "source": "dsm5.pdf"} {"id": "bc1dee4e3699-2", "page_content": "that was preceded by a preexisting personalit y disorder, the personality disorder should\nalso be recorded, followed by \u201cpremorbid\u201d in parentheses.\nAnxiety and depressive disorders. The clinician must be cautious in diagnosing per-", "source": "dsm5.pdf"} {"id": "ebd30b31591e-0", "page_content": "also be recorded, followed by \u201cpremorbid\u201d in parentheses.\nAnxiety and depressive disorders. The clinician must be cautious in diagnosing per-\nsonality disorders during an episode of a depressive disorder or an anxiety disorder, be-", "source": "dsm5.pdf"} {"id": "f215466d316b-0", "page_content": "Paranoid Personality Disorder 649\ncause these conditions may have cross-sectio nal symptom features that mimic personality\ntraits and may make it more difficult to evaluate retrospectively the individual\u2019s long-term\npatterns of functioning. \nPosttraumatic stress disorder. When personality changes emerge and persist after an\nindividual has been exposed to extreme stress, a diagnosis of posttraumatic stress disorder\nshould be considered. \nSubstance use disorders. When an individual has a substance use disorder, it is impor-\ntant not to make a personality disorder diag nosis based solely on behaviors that are con-\nsequences of substance intoxication or withdraw al or that are associated with activities in\nthe service of sustaining substance use (e.g., antisocial behavior). \nPersonality change due to another medical condition. When enduring changes in per-\nsonality arise as a result of the physiological effects of another medical condition (e.g.,\nbrain tumor), a diagnosis of personality chan ge due to another medical condition should\nbe considered.\nCluster A Personality Disorders\nParanoid Personality Disorder\nDiagnostic Criteria 301.0 (F60.0)\nA. A pervasive distrust and suspiciousness of others such that their motives are inter-\npreted as malevolent, beginning by early adulthood and present in a variety of con-\ntexts, as indicated by four (or more) of the following:\n1. Suspects, without sufficient basis, that others are exploiting, harming, or deceiving\nhim or her.\n2. Is preoccupied with unjustified doubts about the loyalty or trustworthiness of friends\nor associates.\n3. Is reluctant to confide in others because of unwarranted fear that the information\nwill be used maliciously against him or her.\n4. Reads hidden demeaning or threatening meanings into benign remarks or events.", "source": "dsm5.pdf"} {"id": "f215466d316b-1", "page_content": "4. Reads hidden demeaning or threatening meanings into benign remarks or events.\n5. Persistently bears grudges (i.e., is unforgiving of insults, injuries, or slights).\n6. Perceives attacks on his or her character or reputation that are not apparent to oth-\ners and is quick to react angrily or to counterattack.\n7. Has recurrent suspicions, without justification, regarding fidelity of spouse or sexual\npartner.\nB. Does not occur exclusively during the course of schizophrenia, a bipolar disorder or\ndepressive disorder with psychotic features, or another psychotic disorder and is not\nattributable to the physiological effects of another medical condition.\nNote: If criteria are met prior to the onset of schizophrenia, add \u201cpremorbid,\u201d i.e., \u201cparanoid\npersonality disorder (premorbid).\u201d\nDiagnostic Features\nThe essential feature of parano id personality disorder is a pattern of pervasive distrust\nand suspiciousness of others such that their motives are interpreted as malevolent. This\npattern begins by early adulthood and is present in a variety of contexts.", "source": "dsm5.pdf"} {"id": "ec7ee21b86f6-0", "page_content": "650 Personality Disorders\nIndividuals with this disorder assume that other people will exploit, harm, or deceive\nthem, even if no evidence exists to support th is expectation (Criterion A1). They suspect on\nthe basis of little or no eviden ce that others are plotting against them and may attack them\nsuddenly, at any time and without reason. They often feel that they have been deeply and\nirreversibly injured by another person or persons even when there is no objective evidence\nfor this. They are preoccupied with unjustifie d doubts about the loyalty or trustworthiness\nof their friends and associates, whose actions are minutely scrutinize d for evidence of hos-\ntile intentions (Criterion A2). Any perceived deviation from trustworthiness or loyalty\nserves to support their underlying assumptions. They are so amazed when a friend or as-\nsociate shows loyalty that they cannot trust or believe it. If they get into trouble, they ex-\npect that friends and associates w ill either attack or ignore them.\nIndividuals with paranoid personality disord er are reluctant to confide in or become\nclose to others because they fear that the information they share will be used against them\n(Criterion A3). They may refuse to answer personal questions, saying that the information\nis \u201cnobody\u2019s business.\u201d They read hidden meanings that are demeaning and threatening\ninto benign remarks or events (Criterion A4). For example, an individual with this disor-\nder may misinterpret an honest mistake by a store clerk as a deliberate attempt to short-\nchange, or view a casual humorous remark by a co-worker as a seri ous character attack.\nCompliments are often misinterpreted (e.g., a compliment on a new acquisition is mis-\ninterpreted as a criticism for selfishness; a compliment on an accomplishment is misinter-", "source": "dsm5.pdf"} {"id": "ec7ee21b86f6-1", "page_content": "interpreted as a criticism for selfishness; a compliment on an accomplishment is misinter-\npreted as an attempt to coerce more and better performance). They may view an offer of\nhelp as a criticism that they ar e not doing well enough on their own.\nIndividuals with this disorder persistently bear grudges and are unwilling to forgive\nthe insults, injuries, or slights that they th ink they have received (Criterion A5). Minor\nslights arouse major hostility, and the hostile f eelings persist for a long time. Because they\nare constantly vigilant to the harmful intentions of others, they very often feel that their\ncharacter or reputation has been attacked or that they have been slighted in some other\nway. They are quick to counterattack and react with anger to perceived insults (Criterion\nA6). Individuals with this disorder may be pathologically jealous, often suspecting that\ntheir spouse or sexual partner is unfaithful without any adequate ju stification (Criterion\nA7). They may gather trivial and circumstantial \u201cevidence\u201d to support their jealous beliefs.\nThey want to maintain complete control of intimate relationships to avoid being betrayed\nand may constantly question and challenge th e whereabouts, actions, intentions, and fi-\ndelity of their spouse or partner.\nParanoid personality disorder should not be diagnosed if the pattern of behavior oc-\ncurs exclusively during the course of schizo phrenia, a bipolar disorder or depressive dis-\norder with psychotic features, or another psychoti c disorder, or if it is attributable to the\nphysiological effects of a neurological (e.g., temporal lobe epilepsy) or another medical\ncondition (Criterion B).\nAssociated Features Supporting Diagnosis\nIndividuals with paranoid personality disorder are generally difficult to get along with\nand often have problems with close relationsh ips. Their excessive suspiciousness and hos-", "source": "dsm5.pdf"} {"id": "ec7ee21b86f6-2", "page_content": "and often have problems with close relationsh ips. Their excessive suspiciousness and hos-\ntility may be expressed in over t argumentativeness, in recurr ent complaining, or by quiet,\napparently hostile aloofness. Because they ar e hypervigilant for potential threats, they\nmay act in a guarded, secretive, or devious manner and appear to be \u201ccold\u201d and lacking in\ntender feelings. Although they may appear to be objective, rational , and unemotional, they", "source": "dsm5.pdf"} {"id": "596dceeebe44-0", "page_content": "may act in a guarded, secretive, or devious manner and appear to be \u201ccold\u201d and lacking in\ntender feelings. Although they may appear to be objective, rational , and unemotional, they\nmore often display a labile range of affect, with hostile, stub born, and sarcastic expressions\npredominating. Their combative and suspicious nature may elicit a hostile response in\nothers, which then serves to conf irm their original expectations.\nBecause individuals with paranoid personality disorder lack trust in others, they have\nan excessive need to be self-sufficient and a strong sense of autonomy. They also need to", "source": "dsm5.pdf"} {"id": "bbb4a1c9205b-0", "page_content": "Paranoid Personality Disorder 651\nhave a high degree of control over those around them. They are often rigid, critical of oth-\ners, and unable to collaborate, although they have great difficulty accepting criticism them-\nselves. They may blame others for their own shortcomings. Because of their quickness to\ncounterattack in response to the threats they perceive around them, they may be litigious\nand frequently become involved in legal disputes. Individuals with this disorder seek to\nconfirm their preconceived nega tive notions regarding people or situations they encounter,\nattributing malevolent motivati ons to others that are projections of their own fears. They\nmay exhibit thinly hidden, unrealistic grandios e fantasies, are often attuned to issues of\npower and rank, and tend to develop negative stereotypes of others, particularly those\nfrom population groups distinct from their own. Attracted by simplistic formulations of the\nworld, they are often wary of ambiguous situations. They ma y be perceived as \u201cfanatics\u201d\nand form tightly knit \u201ccults\u201d or groups with others who share their paranoid belief systems.\nParticularly in response to stress, individu als with this disorder may experience very\nbrief psychotic episodes (lasting minutes to hour s). In some instances, paranoid personal-\nity disorder may appear as the premorbid ante cedent of delusional disorder or schizo-\nphrenia. Individuals with paranoid personal ity disorder may deve lop major depressive\ndisorder and may be at increased risk fo r agoraphobia and obsessive-compulsive dis-\norder. Alcohol and other substance use disord ers frequently occur. The most common co-\noccurring personality disorders appear to be schizotypal, schizoid, narcissistic, avoidant,\nand borderline.\nPrevalence\nA prevalence estimate for paranoid personality based on a probability subsample from", "source": "dsm5.pdf"} {"id": "bbb4a1c9205b-1", "page_content": "Prevalence\nA prevalence estimate for paranoid personality based on a probability subsample from\nPart II of the National Comorbidity Survey Replication suggests a prevalence of 2.3%,\nwhile the National Epidemiologic Survey on Alcohol and Related Conditions data suggest\na prevalence of paranoid personality disorder of 4.4%.\nDevelopment and Course \nParanoid personality disorder may be first apparent in childhood and adolescence with\nsolitariness, poor peer relationships, social anxiety, underachievement in school, hyper-\nsensitivity, peculiar thoughts and language, and idiosyncratic fantasies. These children\nmay appear to be \u201codd\u201d or \u201ceccentric\u201d and attr act teasing. In clinical samples, this disorder\nappears to be more commonly diagnosed in males.\nRisk and Prognostic Factors\nGenetic and physiological. There is some evidence for an increased prevalence of par-\nanoid personality disorder in relatives of probands with schizophrenia and for a more spe-\ncific familial relationship with delusional disorder, persecutory type.\nCulture-Related Diagnostic Issues\nSome behaviors that are influenced by sociocultural contexts or specific life circumstances\nmay be erroneously labeled paranoid and may ev en be reinforced by the process of clinical\nevaluation. Members of minority groups, immi grants, political and economic refugees, or\nindividuals of different ethnic backgrounds may display guarded or defensive behaviors\nbecause of unfamiliarity (e.g., language barriers or lack of knowledge of rules and regula-\ntions) or in response to the perceived neglect or indifference of the majority society. These\nbehaviors can, in turn, generate anger and fr ustration in those who deal with these indi-\nviduals, thus setting up a vicious cycle of mutual mistrust, which should not be confused\nwith paranoid personality diso rder. Some ethnic groups also display culturally related be-\nhaviors that can be misinterpreted as paranoid.", "source": "dsm5.pdf"} {"id": "2c09a54ae11b-0", "page_content": "652 Personality Disorders\nDifferential Diagnosis\nOther mental disorders with psychotic symptoms. Paranoid personality disorder can\nbe distinguished from delusional disorder, pe rsecutory type; schizophrenia; and a bipolar or\ndepressive disorder with psychotic features be cause these disorders are all characterized by a\nperiod of persistent psychotic symptoms (e.g., delusions and hallucinations). For an additional\ndiagnosis of paranoid personality disorder to be given, the personal ity disorder must have\nbeen present before the onset of psychotic sy mptoms and must persist when the psychotic\nsymptoms are in remission. When an individual has another persistent mental disorder (e.g.,\nschizophrenia) that was preceded by paranoid personality disorder, paranoid personality dis-\norder should also be recorded, follo wed by \u201cpremorbid\u201d in parentheses.\nPersonality change due to another medical condition. Paranoid personality disorder\nmust be distinguished from personality ch ange due to another medical condition, in\nwhich the traits that emerge ar e attributable to the direct effects of another medical condi-\ntion on the central nervous system. \nSubstance use disorders. Paranoid personality disorder must be distinguished from\nsymptoms that may develop in associat ion with persistent substance use. \nParanoid traits associated with physical handicaps. The disorder must also be distin-\nguished from paranoid traits associated with the development of physical handicaps (e.g.,\na hearing impairment).\nOther personality disorders and personality traits. Other personality disorders may be\nconfused with paranoid person ality disorder because they ha ve certain features in common.\nIt is therefore important to distinguish among these disorders based on differences in their\ncharacteristic features. However, if an individu al has personality features that meet criteria\nfor one or more personality disorders in additi on to paranoid personality disorder, all can be\ndiagnosed. Paranoid personality disorder an d schizotypal personality disorder share the", "source": "dsm5.pdf"} {"id": "2c09a54ae11b-1", "page_content": "diagnosed. Paranoid personality disorder an d schizotypal personality disorder share the\ntraits of suspiciousness, interpersonal aloofne ss, and paranoid ideati on, but schizotypal per-\nsonality disorder also includes symptoms such as magical thinking, unusual perceptual ex-\nperiences, and odd thinking and speech. Indivi duals with behaviors th at meet criteria for\nschizoid personality disorder ar e often perceived as strange, ec centric, cold, and aloof, but\nthey do not usually have prominent paranoid ideation. The tendency of individuals with\nparanoid personality disorder to react to minor stimuli with anger is also seen in borderline\nand histrionic personality disorders. However, these disord ers are not necessarily associ-\nated with pervasive suspiciousness. People with avoidant personality disorder may also be\nreluctant to confide in others, but more from fear of being embarrassed or found inadequate\nthan from fear of others\u2019 malicious intent. Although antisocial behavior may be present in\nsome individuals with paranoid personality diso rder, it is not usually motivated by a desire\nfor personal gain or to exploit others as in an tisocial personality diso rder, but rather is more\noften attributable to a desire for revenge. In dividuals with narcissistic personality disorder\nmay occasionally display suspiciousness, social withdrawal, or alienation, but this derives\nprimarily from fears of having thei r imperfections or flaws revealed. \nParanoid traits may be adaptive, particul arly in threatening environments. Paranoid\npersonality disorder should be diagnosed only when these tr aits are inflexible, maladap-\ntive, and persisting and cause significant functional impairment or subjective distress.\nSchizoid Personality Disorder\nDiagnostic Criteria 301.20 (F60.1)\nA. A pervasive pattern of detachment from social relationships and a restricted range of", "source": "dsm5.pdf"} {"id": "2c09a54ae11b-2", "page_content": "A. A pervasive pattern of detachment from social relationships and a restricted range of\nexpression of emotions in interpers onal settings, beginning by early adulthood and", "source": "dsm5.pdf"} {"id": "1cf44b33d756-0", "page_content": "A. A pervasive pattern of detachment from social relationships and a restricted range of\nexpression of emotions in interpers onal settings, beginning by early adulthood and\npresent in a variety of contexts, as indicated by four (or more) of the following:", "source": "dsm5.pdf"} {"id": "153e39019b77-0", "page_content": "Schizoid Personality Disorder 653\n1. Neither desires nor enjoys close relationships, including being part of a family.\n2. Almost always chooses solitary activities.\n3. Has little, if any, interest in having sexual experiences with another person.\n4. Takes pleasure in few, if any, activities.\n5. Lacks close friends or confidants other than first-degree relatives.\n6. Appears indifferent to the praise or criticism of others.\n7. Shows emotional coldness, detachment, or flattened affectivity.\nB. Does not occur exclusively during the course of schizophrenia, a bipolar disorder or\ndepressive disorder with psychotic features, another psychotic disorder, or autism\nspectrum disorder and is not attributable to the physiological effects of another medical\ncondition.\nNote: If criteria are met prior to the onset of schizophrenia, add \u201cpremorbid,\u201d i.e., \u201cschiz-\noid personality disorder (premorbid).\u201d\nDiagnostic Features\nThe essential feature of schizo id personality disorder is a pe rvasive pattern of detachment\nfrom social relationships and a restricted range of expression of emotions in interpersonal\nsettings. This pattern begins by early adulth ood and is present in a variety of contexts.\nIndividuals with schizoid personality disord er appear to lack a desire for intimacy,\nseem indifferent to opportunities to develop close relationships, and do not seem to derive\nmuch satisfaction from being part of a family or other social group (Criterion A1). They\nprefer spending time by themselves, rather than being with other people. They often ap-\npear to be socially isolated or \u201cloners\u201d and al most always choose solitary activities or hob-\nbies that do not include interaction with others (Criterion A2). They prefer mechanical or\nabstract tasks, such as computer or mathemat ical games. They may have very little interest", "source": "dsm5.pdf"} {"id": "153e39019b77-1", "page_content": "abstract tasks, such as computer or mathemat ical games. They may have very little interest\nin having sexual experiences with another person (Criterion A3) and take pleasure in few,\nif any, activities (Criterion A4). There is usually a reduced experience of pleasure from sen-\nsory, bodily, or interpersonal ex periences, such as walking on a beach at sunset or having\nsex. These individuals have no close friends or confidants, except possibly a first-degree\nrelative (Criterion A5).\nIndividuals with schizoid personality disord er often seem indifferent to the approval\nor criticism of others and do not appear to be bothered by what others may think of them\n(Criterion A6). They may be oblivious to the no rmal subtleties of social interaction and of-\nten do not respond appropriately to social cues so that they seem socially inept or super-\nficial and self-absorbed. They usually displa y a \u201cbland\u201d exterior without visible emotional\nreactivity and rarely reciprocate gestures or facial expressions, such as smiles or nods (Cri-\nterion A7). They claim that they rarely expe rience strong emotions such as anger and joy.\nThey often display a constricted affect and ap pear cold and aloof. However, in those very\nunusual circumstances in which these indivi duals become at least temporarily comfort-\nable in revealing themselves, they may ackn owledge having painful feelings, particularly\nrelated to social interactions.\nSchizoid personality disorder should not be diagnosed if th e pattern of behavior occurs\nexclusively during the course of schizophrenia , a bipolar or depressive disorder with psy-\nchotic features, another psychotic disorder, or au tism spectrum disorder, or if it is attrib-\nutable to the physiological effects of a neurological (e.g., temporal lobe epilepsy) or another\nmedical condition (Criterion B).", "source": "dsm5.pdf"} {"id": "153e39019b77-2", "page_content": "medical condition (Criterion B).\nAssociated Features Supporting Diagnosis\nIndividuals with schizoid personality disord er may have particular difficulty expressing\nanger, even in response to direct provocation, which contributes to the impression that", "source": "dsm5.pdf"} {"id": "04255a3699f0-0", "page_content": "654 Personality Disorders\nthey lack emotion. Their lives sometimes se em directionless, an d they may appear to\n\u201cdrift\u201d in their goals. Such individuals ofte n react passively to adverse circumstances and\nhave difficulty responding appropriately to im portant life events. Because of their lack of\nsocial skills and lack of desire for sexual experiences, individuals with this disorder have\nfew friendships, date infreque ntly, and often do not marry. Occupational functioning may\nbe impaired, particularly if interpersonal involvement is required, but individuals with\nthis disorder may do well when they work un der conditions of soci al isolation. Particu-\nlarly in response to stress, individuals with this disorder may experience very brief psy-\nchotic episodes (lasting minutes to hours) . In some instances, schizoid personality\ndisorder may appear as the pr emorbid antecedent of delusional disorder or schizophre-\nnia. Individuals with this disorder may so metimes develop major depressive disorder.\nSchizoid personality disorder most often co-occurs with schi zotypal, paranoid, and avoid-\nant personality disorders.\nPrevalence\nSchizoid personality disorder is uncommon in clinical settings. A prevalence estimate for\nschizoid personality based on a probability su bsample from Part II of the National Co-\nmorbidity Survey Replication suggests a pr evalence of 4.9%. Data from the 2001\u20132002\nNational Epidemiologic Survey on Alcohol and Related Conditions suggest a prevalence of\n3.1%.\nDevelopment and Course\nSchizoid personality disorder may be first apparent in childhood and adolescence with\nsolitariness, poor peer relationships, and underachievement in school, which mark these\nchildren or adolescents as different and make them subject to teasing.\nRisk and Prognostic Factors\nGenetic and physiological. Schizoid personality disorder may have increased preva-", "source": "dsm5.pdf"} {"id": "04255a3699f0-1", "page_content": "Genetic and physiological. Schizoid personality disorder may have increased preva-\nlence in the relatives of individuals with schizophrenia or schizotypa l personality disorder.\nCulture-Related Diagnostic Issues\nIndividuals from a variety of cultural bac kgrounds sometimes exhibit defensive behaviors\nand interpersonal styles that may be erroneously labeled as \u201cschizoid.\u201d For example, those\nwho have moved from rural to metropolitan environments may react with \u201cemotional\nfreezing\u201d that may last for several months and manifest as solitary activities, constricted\naffect, and other deficits in communication. Immigrants from other countries are some-\ntimes mistakenly perceived as cold, hostile, or indifferent.\nGender-Related Diagnostic Issues\nSchizoid personality disorder is diagnosed slightly more often in males and may cause\nmore impairment in them.\nDifferential Diagnosis\nOther mental disorders with psychotic symptoms. Schizoid persona lity disorder can\nbe distinguished from delusional disorder, sc hizophrenia, and a bipolar or depressive dis-\norder with psychotic features because these d isorders are all characterized by a period of\npersistent psychotic symptoms (e .g., delusions and hallucinations). To give an additional\ndiagnosis of schizoid personality disorder, the personality disorder must have been present\nbefore the onset of psychotic symptoms an d must persist when the psychotic symptoms", "source": "dsm5.pdf"} {"id": "6615fe80001c-0", "page_content": "Schizotypal Personality Disorder 655\nare in remission. When an individual has a pe rsistent psychotic diso rder (e.g., schizophre-\nnia) that was preceded by schizoid person ality disorder, schizoid personality disorder\nshould also be recorded, followe d by \u201cpremorbid\u201d in parentheses.\nAutism spectrum disorder. There may be great difficulty di fferentiating individuals with\nschizoid personality disorder from those with milder forms of autism spectrum disorder,\nwhich may be differentiated by more severely impaired social inte raction and stereotyped\nbehaviors and interests.\nPersonality change due to another medical condition. Schizoid personality disorder\nmust be distinguished from personality ch ange due to another medical condition, in\nwhich the traits that emerge ar e attributable to the effects of another medical condition on\nthe central nervous system. \nSubstance use disorders. Schizoid personality disorder must also be distinguished\nfrom symptoms that may develop in a ssociation with persistent substance use.\nOther personality disorder s and personality traits. Other personality disorders may be\nconfused with schizoid personality disorder because they have certain features in com-\nmon. It is, therefore, import ant to distinguish among these disorders based on differences\nin their characteristic features. However, if an individual has personality features that\nmeet criteria for one or more personality disorders in addition to schizoid personality dis-\norder, all can be diagnosed. Although characteri stics of social isolation and restricted af-\nfectivity are common to schizoid, schizotypal, and paranoid personality disorders,\nschizoid personality disorder can be distin guished from schizotypa l personality disorder\nby the lack of cognitive and perceptual dist ortions and from paranoid personality disorder\nby the lack of suspiciousness and paranoid ideation. The social isolation of schizoid per-", "source": "dsm5.pdf"} {"id": "6615fe80001c-1", "page_content": "sonality disorder can be distinguished from th at of avoidant personality disorder, which is\nattributable to fear of being embarrassed or found inadequate and excessive anticipation\nof rejection. In contrast, people with schizoid personality disorder have a more pervasive\ndetachment and limited desire for social in timacy. Individuals with obsessive-compulsive\npersonality disorder may also show an apparent social detachment stemming from devo-\ntion to work and discomfort wi th emotions, but they do have an underlying capacity for\nintimacy.\nIndividuals who are \u201cloners\u201d may display pe rsonality traits that might be considered\nschizoid. Only when these trai ts are inflexible and maladaptive and cause significant func-\ntional impairment or subjective distress do they constitute schizoid personality disorder.\nSchizotypal Personality Disorder\nDiagnostic Criteria 301.22 (F21)\nA. A pervasive pattern of social and interpersonal deficits marked by acute discomfort\nwith, and reduced capacity for, close relationships as well as by cognitive or perceptual\ndistortions and eccentricities of behavior, beginning by early adulthood and present in\na variety of contexts, as indicated by five (or more) of the following:\n1. Ideas of reference (excluding delusions of reference).\n2. Odd beliefs or magical thinking that influences behavior and is inconsistent with\nsubcultural norms (e.g., superstitiousness, belief in clairvoyance, telepathy, or\n\u201csixth sense\u201d; in children and adolescents, bizarre fantasies or preoccupations).\n3. Unusual perceptual experiences, including bodily illusions.\n4. Odd thinking and speech (e.g., vague, circumstantial, metaphorical, overelaborate,\nor stereotyped).\n5. Suspiciousness or paranoid ideation.", "source": "dsm5.pdf"} {"id": "e10af770dd7e-0", "page_content": "656 Personality Disorders\n6. Inappropriate or constricted affect.\n7. Behavior or appearance that is odd, eccentric, or peculiar.\n8. Lack of close friends or confidants other than first-degree relatives.\n9. Excessive social anxiety that does not diminish with familiarity and tends to be as-\nsociated with paranoid fears rather than negative judgments about self.\nB. Does not occur exclusively during the course of schizophrenia, a bipolar disorder or\ndepressive disorder with psychotic features, another psychotic disorder, or autism\nspectrum disorder.\nNote: If criteria are met prior to the onset of schizophrenia, add \u201cpremorbid,\u201d e.g., \u201cschizo-\ntypal personality disorder (premorbid).\u201d\nDiagnostic Features\nThe essential feature of schizo typal personality disorder is a pervasive pattern of social\nand interpersonal deficits ma rked by acute discomfort with, and reduced capacity for,\nclose relationships as well as by cognitive or pe rceptual distortions and eccentricities of be-\nhavior. This pattern begins by early adulthoo d and is present in a variety of contexts.\nIndividuals with schizotypal personality disord er often have ideas of reference (i.e., in-\ncorrect interpretations of casual incidents and external events as having a particular and\nunusual meaning specifically for the person ) (Criterion A1). Th ese should be distin-\nguished from delusions of reference, in whic h the beliefs are held with delusional convic-\ntion. These individuals may be superstitiou s or preoccupied with paranormal phenomena\nthat are outside the norms of their subculture (Criterion A2). They may feel that they have\nspecial powers to sense events before they happen or to read others\u2019 thoughts. They may\nbelieve that they have magical control over others, which can be implemented directly", "source": "dsm5.pdf"} {"id": "e10af770dd7e-1", "page_content": "believe that they have magical control over others, which can be implemented directly\n(e.g., believing that their spouse\u2019s taking the do g out for a walk is the direct result of think-\ning an hour earlier it should be done) or in directly through compli ance with magical rit-\nuals (e.g., walking past a specific object three times to avoid a certain harmful outcome).\nPerceptual alterations may be present (e.g., se nsing that another person is present or hear-\ning a voice murmuring his or her name) (Criterion A3). Their speech may include unusual\nor idiosyncratic phrasing and construction. It is often loose, digressive, or vague, but with-\nout actual derailment or incoherence (Criteri on A4). Responses can be either overly con-\ncrete or overly abstract, and words or conc epts are sometimes applied in unusual ways\n(e.g., the individual may state that he or she was not \u201ctalkable\u201d at work).\nIndividuals with this disorder are often suspicious and may have paranoid ideation\n(e.g., believing their colleagues at work ar e intent on undermining their reputation with\nthe boss) (Criterion A5). They are usually not able to negotiate the fu ll range of affects and\ninterpersonal cuing required fo r successful relationships and thus often appear to interact\nwith others in an inappropriate, stiff, or constricted fashion (Criterion A6). These individ-\nuals are often considered to be odd or ecce ntric because of unusual mannerisms, an often\nunkempt manner of dress that does not quite \u201cfit together,\u201d and inattention to the usual\nsocial conventions (e.g., the in dividual may avoid eye contact, wear clothes that are ink\nstained and ill-fitting, and be unable to join in the give-and-take banter of co-workers)", "source": "dsm5.pdf"} {"id": "e10af770dd7e-2", "page_content": "(Criterion A7).\nIndividuals with schizotypal personality di sorder experience in terpersonal related-\nness as problematic and are uncomfortable relating to other people. Although they may\nexpress unhappiness about their lack of relationships, their behavior suggests a decreased\ndesire for intimate contacts. As a result, they usually have no or few close friends or con-\nfidants other than a first-degree relative (Cri terion A8). They are anxious in social situa-\ntions, particularly those invo lving unfamiliar people (Crite rion A9). They will interact", "source": "dsm5.pdf"} {"id": "7848217207d7-0", "page_content": "fidants other than a first-degree relative (Cri terion A8). They are anxious in social situa-\ntions, particularly those invo lving unfamiliar people (Crite rion A9). They will interact\nwith other individuals when they have to but prefer to keep to themselves because they\nfeel that they are different and just do not \u201cfit in.\u201d Their social anxiety does not easily abate,", "source": "dsm5.pdf"} {"id": "040c167c6714-0", "page_content": "Schizotypal Personality Disorder 657\neven when they spend more time in the setti ng or become more fa miliar with the other\npeople, because their anxiety tends to be assoc iated with suspiciousness regarding others\u2019\nmotivations. For example, when attending a dinner party, the individual with schizotypal\npersonality disorder will not become more rela xed as time goes on, but rather may become\nincreasingly tense and suspicious.\nSchizotypal personality disorder should not be diagnosed if the pattern of behavior oc-\ncurs exclusively during the course of schizo phrenia, a bipolar or de pressive disorder with\npsychotic features, another psychotic disorder, or autism spectrum disorder (Criterion B).\nAssociated Features Supporting Diagnosis\nIndividuals with schizotypal personality diso rder often seek treatment for the associated\nsymptoms of anxiety or depression rather than for the personality disorder features per se.\nParticularly in response to stress, individual s with this disorder may experience transient\npsychotic episodes (lasting minutes to hours), although they usually are insufficient in du-\nration to warrant an additional diagnosis such as brief psychotic disorder or schizophreni-\nform disorder. In some cases, clinically sig nificant psychotic symptoms may develop that\nmeet criteria for brief psychotic disorder, sc hizophreniform disorder, delusional disorder,\nor schizophrenia. Over half may have a hist ory of at least one ma jor depressive episode.\nFrom 30% to 50% of individuals diagnosed with this disorder have a concurrent diagnosis\nof major depressive disorder when admitted to a clinical setting. There is considerable co-\noccurrence with schizoid, paranoid, avoi dant, and borderline personality disorders.\nPrevalence\nIn community studies of schizotypal personality disorder, reported rates range from 0.6%", "source": "dsm5.pdf"} {"id": "040c167c6714-1", "page_content": "in Norwegian samples to 4.6% in a U.S. commu nity sample. The prevalence of schizotypal\npersonality disorder in clinical populations seems to be infrequent (0%\u20131.9%), with a\nhigher estimated prevalence in the general population (3.9%) found in the National Epi-\ndemiologic Survey on Alco hol and Related Conditions.\nDevelopment and Course\nSchizotypal personality disorder has a relative ly stable course, with only a small propor-\ntion of individuals going on to develop sc hizophrenia or another psychotic disorder.\nSchizotypal personality disorder may be firs t apparent in childhood and adolescence with\nsolitariness, poor peer relationships, social anxiety, underachievement in school, hyper-\nsensitivity, peculiar thoughts and language, an d bizarre fantasies. These children may ap-\npear \u201codd\u201d or \u201ceccentric\u201d and attract teasing. \nRisk and Prognostic Factors\nGenetic and physiological. Schizotypal personality disord er appears to aggregate fa-\nmilially and is more prevalent among the firs t-degree biological relatives of individuals\nwith schizophrenia than among the general po pulation. There may also be a modest in-\ncrease in schizophrenia and other psychotic disorders in the relatives of probands with\nschizotypal personality disorder.\nCultural-Related Diagnostic Issues\nCognitive and perceptual distortions must be evaluated in the context of the individual\u2019s\ncultural milieu. Pervasive cultur ally determined characteristic s, particularly those regard-\ning religious beliefs and rituals, can appear to be schizotypal to the uninformed outsider\n(e.g., voodoo, speaking in tongues, life beyo nd death, shamanism, mind reading, sixth\nsense, evil eye, magical beliefs related to health and illness).", "source": "dsm5.pdf"} {"id": "4e5e30675916-0", "page_content": "658 Personality Disorders\nGender-Related Diagnostic Issues\nSchizotypal personality disorder may be slightly more common in males.\nDifferential Diagnosis\nOther mental disorders with psychotic symptoms. Schizotypal personality disorder\ncan be distinguished from de lusional disorder, schizophrenia , and a bipolar or depressive\ndisorder with psychotic features because thes e disorders are all characterized by a period\nof persistent psychotic symptoms (e.g., delu sions and hallucinations). To give an addi-\ntional diagnosis of schizotypal personality disorder, the personality disorder must have\nbeen present before the onset of psychoti c symptoms and persis t when the psychotic\nsymptoms are in remission. Wh en an individual has a persist ent psychotic disorder (e.g.,\nschizophrenia) that was preceded by schizo typal personality disorder, schizotypal per-\nsonality disorder should also be recorded, followed by \u201cpremorbid\u201d in parentheses.\nNeurodevelopmental disorders. There may be great difficulty differentiating children\nwith schizotypal personality disorder from the heterogeneous group of solitary, odd chil-\ndren whose behavior is characterized by mark ed social isolation, eccentricity, or peculiar-\nities of language and whose diagnoses woul d probably include milder forms of autism\nspectrum disorder or language communicat ion disorders. Commun ication disorders may\nbe differentiated by the primacy and severity of the disorder in language and by the char-\nacteristic features of impaired language found in a specialized language assessment.\nMilder forms of autism spectrum disorder are differentiated by the even greater lack of so-\ncial awareness and emotional reciprocity and stereotyped behaviors and interests.\nPersonality change due to another medical condition. Schizotypal personality disor-\nder must be distinguished from personality change due to another medical condition, in", "source": "dsm5.pdf"} {"id": "4e5e30675916-1", "page_content": "der must be distinguished from personality change due to another medical condition, in\nwhich the traits that emerge ar e attributable to the effects of another medical condition on\nthe central nervous system. \nSubstance use disorders. Schizotypal personality disorder must also be distinguished\nfrom symptoms that may develop in a ssociation with persistent substance use.\nOther personality disorders and personality traits. Other personality disorders may\nbe confused with schizotypal personality diso rder because they have certain features in\ncommon. It is, therefore, important to distin guish among these disorders based on differ-\nences in their characteristic features. However, if an individual has personality features\nthat meet criteria for one or more personality disorders in addition to schizotypal person-\nality disorder, all can be diagnosed. Although paranoid and schizoid personality disor-\nders may also be characterized by social de tachment and restricted affect, schizotypal\npersonality disorder can be distinguished fr om these two diagnoses by the presence of\ncognitive or perceptual distortions and marked eccentricity or oddn ess. Close relation-\nships are limited in both schizotypal person ality disorder and avoidant personality dis-\norder; however, in avoidant personality disorder an active desire for relationships is\nconstrained by a fear of rejection, whereas in schizotypal personality disorder there is\na\u00a0lack of desire for relationships and persis tent detachment. Indivi duals with narcissistic\npersonality disorder may also display suspic iousness, social withdrawal, or alienation,\nbut in narcissistic personality disorder these qualities derive primarily from fears of hav-\ning imperfections or flaws revealed. Individu als with borderline personality disorder may\nalso have transient, psychotic-like symptoms, but these are usually more closely related to", "source": "dsm5.pdf"} {"id": "4e5e30675916-2", "page_content": "also have transient, psychotic-like symptoms, but these are usually more closely related to\naffective shifts in response to stress (e.g., intense anger, anxiety, disappointment) and are\nusually more dissociative (e.g., derealization, depersonalization). In contrast, individuals\nwith schizotypal personality disorder are more likely to have enduring psychotic-like symp-", "source": "dsm5.pdf"} {"id": "d33f346a9b4b-0", "page_content": "usually more dissociative (e.g., derealization, depersonalization). In contrast, individuals\nwith schizotypal personality disorder are more likely to have enduring psychotic-like symp-\ntoms that may worsen under stress but are less likely to be invariably associated with pro-\nnounced affective symptoms. Although social isolation may occur in borderline personality", "source": "dsm5.pdf"} {"id": "3c9ac610db0e-0", "page_content": "Antisocial Personality Disorder 659\ndisorder, it is usually secondary to repeated interpersonal failures due to angry outbursts\nand frequent mood shifts, rather than a result of a persistent lack of social contacts and de-\nsire for intimacy. Furt hermore, individuals with schizoty pal personality disorder do not\nusually demonstrate the impulsiv e or manipulative behaviors of the individual with bor-\nderline personality diso rder. However, there is a high ra te of co-occurren ce between the\ntwo disorders, so that making such distinctions is not always feasible. Schizotypal features\nduring adolescence may be reflective of transi ent emotional turmoil, rather than an endur-\ning personality disorder.\nCluster B Personality Disorders\nAntisocial Personality Disorder\nDiagnostic Criteria 301.7 (F60.2)\nA. A pervasive pattern of disregard for and violation of the rights of others, occurring since\nage 15 years, as indicated by three (or more) of the following:\n1. Failure to conform to social norms with respect to lawful behaviors, as indicated by\nrepeatedly performing acts that are grounds for arrest.\n2. Deceitfulness, as indicated by repeated lying, use of aliases, or conning others for\npersonal profit or pleasure.\n3. Impulsivity or failure to plan ahead.\n4. Irritability and aggressiveness, as indicated by repeated physical fights or assaults.\n5. Reckless disregard for safety of self or others.\n6. Consistent irresponsibility, as indicated by repeated failure to sustain consistent\nwork behavior or honor financial obligations.\n7. Lack of remorse, as indicated by being indifferent to or rationalizing having hurt,\nmistreated, or stolen from another.\nB. The individual is at least age 18 years.", "source": "dsm5.pdf"} {"id": "3c9ac610db0e-1", "page_content": "B. The individual is at least age 18 years.\nC. There is evidence of conduct disorder with onset before age 15 years.\nD. The occurrence of antisocial behavior is not exclusively during the course of schizo-\nphrenia or bipolar disorder.\nDiagnostic Features\nThe essential feature of antisocial personality disorder is a pervasive pattern of disregard\nfor, and violation of, the rights of others that begins in childhood or early adolescence and\ncontinues into adulthood. This pattern has also been referred to as psychopathy, sociopathy,\nor dyssocial personality disorder. Because deceit and manipulation are central features of an-\ntisocial personality disorder, it may be especially helpful to integrate information acquired\nfrom systematic clinical assessment with information collected from collateral sources.\nFor this diagnosis to be given, the individual must be at least age 18 years (Criterion B)\nand must have had a history of some symptoms of conduct disorder before age 15 years\n(Criterion C). Conduct disorder involves a repe titive and persistent pattern of behavior in\nwhich the basic rights of othe rs or major age-appropriate societal norms or rules are vio-\nlated. The specific behaviors characteristic of conduct disorder fall into one of four cate-\ngories: aggression to people and animals, destruction of proper ty, deceitfulness or theft, or\nserious violation of rules.", "source": "dsm5.pdf"} {"id": "e8e53618f3b6-0", "page_content": "660 Personality Disorders\nThe pattern of antisocial behavior continues into adulthood. Indi viduals with antiso-\ncial personality disorder fail to conform to social norms with respect to lawful behavior\n(Criterion A1). They may repeatedly perfor m acts that are grounds for arrest (whether\nthey are arrested or not), such as destroying property, harassing ot hers, stealing, or pur-\nsuing illegal occupations. Persons with this di sorder disregard the wishes, rights, or feel-\nings of others. They are freq uently deceitful and manipulative in order to gain personal\nprofit or pleasure (e.g., to obtain money, sex, or power) (Criterion A2). They may repeat-\nedly lie, use an alias, con others, or malinger. A pattern of impulsiv ity may be manifested\nby a failure to plan ahead (Criterion A3). Decisions are made on the spur of the moment,\nwithout forethought and without consideration fo r the consequences to self or others; this\nmay lead to sudden changes of jobs, residences , or relationships. Individuals with antiso-\ncial personality disorder tend to be irrita ble and aggressive and may repeatedly get into\nphysical fights or commit acts of physical assau lt (including spouse beating or child beat-\ning) (Criterion A4). (Aggressive acts that are required to defend oneself or someone else\nare not considered to be evidence for this it em.) These individuals also display a reckless\ndisregard for the safety of themselves or othe rs (Criterion A5). This may be evidenced in\ntheir driving behavior (i.e., recurrent speedi ng, driving while intoxicated, multiple acci-\ndents). They may engage in sexual behavior or substance use that has a high risk for harm-\nful consequences. They may neglec t or fail to care for a child in a way that puts the child in\ndanger.", "source": "dsm5.pdf"} {"id": "e8e53618f3b6-1", "page_content": "danger.\nIndividuals with antisocial personality disord er also tend to be consistently and ex-\ntremely irresponsible (Criterion A6). Irrespon sible work behavior may be indicated by sig-\nnificant periods of unemployme nt despite available job opportunities, or by abandonment\nof several jobs without a realistic plan for ge tting another job. There may also be a pattern\nof repeated absences fr om work that are not explained by illness either in themselves or in\ntheir family. Financial irresponsibility is indicated by acts such as defaulting on debts, fail-\ning to provide child support, or failing to support other dependents on a regular basis. In-\ndividuals with antisocial personality disorder show little remorse for the consequences of\ntheir acts (Criterion A7). They may be indifferent to, or provide a superficial rationaliza-\ntion for, having hurt, mistreated, or stolen from someone (e.g., \u201clife\u2019s unfair,\u201d \u201closers de-\nserve to lose\u201d). These individuals may blame the victims for being foolish, helpless, or\ndeserving their fate (e.g., \u201che had it coming anyway\u201d); they may minimize the harmful\nconsequences of their actions; or\u00a0they may simply indicate complete indifference. They\ngenerally fail to compensate or make amends for their behavior. They may believe that\neveryone is out to \u201chelp number one\u201d and that one should stop at nothing to avoid being\npushed around.\nThe antisocial behavior must not occur excl usively during the course of schizophrenia\nor bipolar disorder (Criterion D).\nAssociated Features Supporting Diagnosis\nIndividuals with antisocial personality disord er frequently lack empathy and tend to be\ncallous, cynical, and contempt uous of the feelings, rights, and sufferings of others. They", "source": "dsm5.pdf"} {"id": "e8e53618f3b6-2", "page_content": "may have an inflated and arrogant self-appraisa l (e.g., feel that ordinary work is beneath\nthem or lack a realistic concern about their current problems or th eir future) and may be\nexcessively opinionated, self-assured, or coc ky. They may display a glib, superficial charm\nand can be quite voluble and verbally facile (e.g., using technical terms or jargon that\nmight impress someone who is unfamiliar with th e topic). Lack of empathy, inflated self-", "source": "dsm5.pdf"} {"id": "629a240654ec-0", "page_content": "and can be quite voluble and verbally facile (e.g., using technical terms or jargon that\nmight impress someone who is unfamiliar with th e topic). Lack of empathy, inflated self-\nappraisal, and superficial charm are features that have been commonly included in tradi-\ntional conceptions of psychopathy that may be particularly distinguishing of the disorder\nand more predictive of recidivism in prison or forensic settings, where criminal, delin-\nquent, or aggressive acts are likely to be no nspecific. These individuals may also be irre-\nsponsible and exploitative in their sexual re lationships. They may have a history of many", "source": "dsm5.pdf"} {"id": "dd34679f3aa6-0", "page_content": "Antisocial Personality Disorder 661\nsexual partners and may never have sustained a monogamous relationship. They may be\nirresponsible as parents, as evidenced by maln utrition of a child, an illness in the child re-\nsulting from a lack of minimal hygiene, a ch ild\u2019s dependence on neighbors or nonresident\nrelatives for food or shelter, a failure to arrange for a caretaker for a young child when the\nindividual is away from home, or repeated squandering of money required for household\nnecessities. These individuals may receive di shonorable discharges from the armed ser-\nvices, may fail to be self-supporting, may be come impoverished or even homeless, or may\nspend many years in penal institutions. Indi viduals with antisocial personality disorder\nare more likely than people in the general po pulation to die prematurely by violent means\n(e.g., suicide, accidents, homicides).\nIndividuals with antisocial personality disorder may also experience dysphoria, in-\ncluding complaints of tension, inability to tolerate boredom, and depressed mood. They\nmay have associated anxiety disorders, depressive disorders, substa nce use disorders, so-\nmatic symptom disorder, gambli ng disorder, and other disord ers of impulse control. In-\ndividuals with antisocial personality disorder also often have personality features that\nmeet criteria for other personality disorders, particularly borderline, histrionic, and nar-\ncissistic personality disorders. The likelihood of developing antisocial personality disor-\nder in adult life is increased if the indivi dual experienced childhood onset of conduct\ndisorder (before age 10 years) and accompanyi ng attention-deficit/hyperactivity disorder.\nChild abuse or neglect, unstable or erratic parenting, or inconsistent parental discipline\nmay increase the likelihood that conduct disord er will evolve into antisocial personality\ndisorder.", "source": "dsm5.pdf"} {"id": "dd34679f3aa6-1", "page_content": "may increase the likelihood that conduct disord er will evolve into antisocial personality\ndisorder.\nPrevalence\nTwelve-month prevalence rates of antisocial personality diso rder, using criteria from pre-\nvious DSMs, are between 0.2% and 3.3%. The highest prevalence of antisocial personality\ndisorder (greater than 70%) is among most se vere samples of males with alcohol use dis-\norder and from substance abuse clinics, prison s, or other forensic settings. Prevalence is\nhigher in samples affected by adverse socioeconomic (i.e., poverty) or sociocultural (i.e.,\nmigration) factors.\nDevelopment and Course\nAntisocial personality disorder has a chronic course but may become less evident or remit\nas the individual grows older, particularly by the fourth deca de of life. Although this re-\nmission tends to be particularly evident with respect to engaging in criminal behavior,\nthere is likely to be a decrease in the full spectrum of antisocial behaviors and substance\nuse. By definition, antisocial personalit y cannot be diagnosed before age 18 years.\nRisk and Prognostic Factors\nGenetic and physiological. Antisocial personality disorder is more common among the\nfirst-degree biological relatives of those with the disorder than in the general population.\nThe risk to biological relatives of females with the disorder tends to be higher than the risk\nto biological relatives of males with the disorder. Biological relatives of individuals with\nthis disorder are also at in creased risk for somatic symptom disorder and substance use\ndisorders. Within a family that has a member with antisocial personality disorder, males\nmore often have antisocial personality disord er and substance use disorders, whereas fe-\nmales more often have somatic symptom disorder. However, in such families, there is an", "source": "dsm5.pdf"} {"id": "dd34679f3aa6-2", "page_content": "males more often have somatic symptom disorder. However, in such families, there is an\nincrease in prevalence of al l of these disorders in both males and females compared with\nthe general population. Adoption studies indi cate that both genetic and environmental\nfactors contribute to the risk of developing antisocial personality disorder. Both adopted\nand biological children of parents with antisocial personality disorder have an increased", "source": "dsm5.pdf"} {"id": "425086605bd6-0", "page_content": "662 Personality Disorders\nrisk of developing antisocial personality disorder, somatic symptom disorder, and sub-\nstance use disorders. Adopted-away children resemble their biological parents more than\ntheir adoptive parents, but the adoptive family environm ent influences the risk of devel-\noping a personality disorder and related psychopathology.\nCulture-Related Diagnostic Issues\nAntisocial personality disorder appears to be associated with low socioeconomic status\nand urban settings. Concerns have been raised that the diagnosis may at times be misap-\nplied to individuals in settings in which seemingly antisocial behavior may be part of a\nprotective survival stra tegy. In assessing antisocial traits, it is helpful for the clinician to\nconsider the social and economic co ntext in which the behaviors occur.\nGender-Related Diagnostic Issues\nAntisocial personality disorder is much more common in males than in females. There has\nbeen some concern that antisocial persona lity disorder may be underdiagnosed in fe-\nmales, particularly because of the emphasis on aggressive items in the definition of con-\nduct disorder.\nDifferential Diagnosis\nThe diagnosis of antisocial personality disorder is not given to individuals younger than\n18 years and is given only if there is a histor y of some symptoms of conduct disorder be-\nfore age 15 years. For individuals older than 18 years, a diagnosis of conduct disorder is\ngiven only if the criteria for antiso cial personality disorder are not met.\nSubstance use disorders. When antisocial behavior in an adult is associated with a\nsubstance use disorder, the diagnosis of antisoci al personality disorder is not made unless\nthe signs of antisocial personality disorder were also present in childhood and have con-\ntinued into adulthood. When substance use and antisocial behavior both began in childhood\nand continued into adulthood, both a substance use disorder and antisocial personality", "source": "dsm5.pdf"} {"id": "425086605bd6-1", "page_content": "and continued into adulthood, both a substance use disorder and antisocial personality\ndisorder should be diagnosed if the criteria fo r both are met, even though some antisocial\nacts may be a consequence of the substance us e disorder (e.g., illegal selling of drugs, thefts\nto obtain money for drugs).\nSchizophrenia and bipolar disorders. Antisocial behavior that occurs exclusively dur-\ning the course of schizophrenia or a bipolar disorder should not be diagnosed as antisocial\npersonality disorder. \nOther personality disorders. Other personality disorders may be confused with antiso-\ncial personality disorder because they have certain features in common. It is therefore im-\nportant to distinguish among these disorders based on differences in their characteristic\nfeatures. However, if an indivi dual has personality features that meet criteria for one or\nmore personality disorders in addition to antisocial personality disorder, all can be diag-\nnosed. Individuals with antisocial personalit y disorder and narcissistic personality disor-\nder share a tendency to be tough-minded, glib , superficial, exploitative, and lack empathy.\nHowever, narcissistic personality disorder does not include ch aracteristics of impulsivity,\naggression, and deceit. In addition, individuals with antisocial personality disorder may\nnot be as needy of the admiration and envy of others, and persons with narcissistic per-\nsonality disorder usually lack the history of conduct disorder in childhood or criminal\nbehavior in adulthood. Indivi duals with antisocial personality disorder and histrionic\npersonality disorder share a tendency to be impulsive, superficial, excitement seeking,\nreckless, seductive, and manipulative, but pe rsons with histrionic personality disorder\ntend to be more exaggerated in their emotions and do not characteristically engage in an-\ntisocial behaviors. Individuals with histrion ic and borderline pers onality disorders are", "source": "dsm5.pdf"} {"id": "c9054d3ba773-0", "page_content": "Borderline Personality Disorder 663\nmanipulative to gain nurturance, whereas thos e with antisocial personality disorder are\nmanipulative to gain profit, po wer, or some other material gratification. Individuals with\nantisocial personality disorder tend to be less emotionally unstable and more aggressive\nthan those with borderline personality disorder. Although antisocial behavior may be\npresent in some individuals with paranoid pe rsonality disorder, it is not usually moti-\nvated by a desire for personal gain or to exploit others as in antisocial personality disorder,\nbut rather is more often attributable to a desire for revenge.\nCriminal behavior not associated with a personality disorder. Antisocial personality\ndisorder must be distinguished from criminal behavior undertaken for gain that is not ac-\ncompanied by the personality features characteristic of this disorder. Only when antisocial\npersonality traits are inflexible, maladaptive, and persistent and cause significant func-\ntional impairment or subjective distress do th ey constitute antisocial personality disorder.\nBorderline Personality Disorder\nDiagnostic Criteria 301.83 (F60.3)\nA pervasive pattern of instability of interpersonal relationships, self-image, and affects,\nand marked impulsivity, beginning by early adulthood and present in a variety of contexts,\nas indicated by five (or more) of the following:\n1. Frantic efforts to avoid real or imagined abandonment. ( Note: Do not include suicidal\nor self-mutilating behavior covered in Criterion 5.)\n2. A pattern of unstable and intense interpersonal relationships characterized by alternat-\ning between extremes of idealization and devaluation.\n3. Identity disturbance: markedly and persistently unstable self-image or sense of self.\n4. Impulsivity in at least two areas that are potentially self-damaging (e.g., spending, sex,", "source": "dsm5.pdf"} {"id": "c9054d3ba773-1", "page_content": "substance abuse, reckless driving, binge eating). ( Note: Do not include suicidal or self-\nmutilating behavior covered in Criterion 5.)\n5. Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior.\n6. Affective instability due to a marked reactivity of mood (e.g., intense episodic dysphoria,\nirritability, or anxiety usually lasting a few hours and only rarely more than a few days).\n7. Chronic feelings of emptiness.\n8. Inappropriate, intense anger or difficulty controlling anger (e.g., frequent displays of\ntemper, constant anger, recurrent physical fights).\n9. Transient, stress-related paranoid ideation or severe dissociative symptoms.\nDiagnostic Features\nThe essential feature of borderline personality disorder is a pervasive pattern of instability\nof interpersonal relationships, self-image, an d affects, and marked impulsivity that begins\nby early adulthood and is present in a variety of contexts.\nIndividuals with borderline pe rsonality disorder make fran tic efforts to avoid real or\nimagined abandonment (Criterion 1). The perception of impending separation or rejection,\nor the loss of external structure, can lead to profound changes in sel f-image, affect, cognition,\nand behavior. These individuals are very sensitive to environmental circumstances. They ex-\nperience intense abandonment fears and inappropriate anger even when faced with a real-\nistic time-limited separation or when there are unavoidable changes in plans (e.g., sudden\ndespair in reaction to a clinician\u2019s announcing the end of the hour; panic or fury when some-\none important to them is just a few minutes la te or must cancel an appointment). They may\nbelieve that this \u201cabandonment\u201d implies they are \u201cbad.\u201d These abandonment fears are re-\nlated to an intolerance of being alone and a need to have other people with them. Their frantic", "source": "dsm5.pdf"} {"id": "400d0c4ecbb6-0", "page_content": "664 Personality Disorders\nefforts to avoid abandonment may include impulsive actions such as self-mutilating or sui-\ncidal behaviors, which are described separately in Criterion 5.\nIndividuals with borderline personality disord er have a pattern of unstable and intense\nrelationships (Criterion 2). They may idealize potential caregivers or lovers at the first or\nsecond meeting, demand to spend a lot of time together, and share the most intimate details\nearly in a relationship. Howeve r, they may switch quickly from idealizing other people to\ndevaluing them, feeling that the other person does not care enough, does not give enough,\nor is not \u201cthere\u201d enough. These individuals can empathize with and nurture other people,\nbut only with the expectation th at the other person will \u201cbe ther e\u201d in return to meet their\nown needs on demand. These indi viduals are prone to sudden and dramatic shifts in their\nview of others, who may alternatively be seen as beneficent supports or as cruelly punitive.\nSuch shifts often reflect disillusionment with a caregiver whose nurturing qualities had\nbeen idealized or whose rejectio n or abandonment is expected.\nThere may be an identity disturbance charac terized by markedly and persistently un-\nstable self-image or sense of self (Criterion 3). There are sudden and dramatic shifts in self-\nimage, characterized by shifting goals, values, and vocational aspirations. There may be\nsudden changes in opinions and plans about ca reer, sexual identity, values, and types of\nfriends. These individuals may suddenly chan ge from the role of a needy supplicant for\nhelp to that of a righteous av enger of past mistreat ment. Although they usually have a self-\nimage that is based on being bad or evil, individuals with this disorder may at times have", "source": "dsm5.pdf"} {"id": "400d0c4ecbb6-1", "page_content": "image that is based on being bad or evil, individuals with this disorder may at times have\nfeelings that they do not exist at all. Such experiences usually occur in situations in which\nthe individual feels a lack of a meaningful relationship, nurturing, and support. These in-\ndividuals may show worse performance in unstructured work or school situations.\nIndividuals with borderline pe rsonality disorder display impulsivity in at least two areas\nthat are potentially self-damaging (Criterion 4). They may gamble, spend money irrespon-\nsibly, binge eat, abuse substanc es, engage in unsafe sex, or drive recklessly. Individuals\nwith this disorder display recurrent suicidal behavior, gestures, or threats, or self-mutilat-\ning behavior (Criterion 5). Completed suicide occurs in 8%\u201310% of such individuals, and\nself-mutilative acts (e.g., cutting or burnin g) and suicide threats and attempts are very\ncommon. Recurrent suicidality is often the reason that these individuals present for help.\nThese self-destructive acts are usually precipit ated by threats of separation or rejection or\nby expectations that the individual assumes increased responsibility. Self-mutilation may\noccur during dissociative experiences and often brings relief by reaffirming the ability to\nfeel or by expiating the individual\u2019s sense of being evil.\nIndividuals with borderline personality disorder may display affective instability that\nis due to a marked reactivity of mood (e.g., intense episodic dysphoria, irritability, or anx-\niety usually lasting a few hours and only rarely more than a few days) (Criterion 6). The\nbasic dysphoric mood of those with borderline personality disorder is often disrupted by\nperiods of anger, panic, or de spair and is rarely relieved by periods of well-being or satis-", "source": "dsm5.pdf"} {"id": "400d0c4ecbb6-2", "page_content": "faction. These episodes may reflect the indivi dual\u2019s extreme reactivity to interpersonal\nstresses. Individuals with borderline personalit y disorder may be troubled by chronic feel-\nings of emptiness (Criterion 7). Easily bored, they may constantly seek something to do.\nIndividuals with this disorder frequently expr ess inappropriate, intense anger or have dif-\nficulty controlling their anger (Criterion 8) . They may display extreme sarcasm, enduring", "source": "dsm5.pdf"} {"id": "91e1e6e65657-0", "page_content": "Individuals with this disorder frequently expr ess inappropriate, intense anger or have dif-\nficulty controlling their anger (Criterion 8) . They may display extreme sarcasm, enduring\nbitterness, or verbal outbursts. The anger is often elicited when a caregiver or lover is seen\nas neglectful, withholding, uncaring, or abandoning. Such expressions of anger are often\nfollowed by shame and guilt and contribute to the feeling they have of being evil. During\nperiods of extreme stress , transient paranoid ideation or dissociative symptoms (e.g., de-\npersonalization) may occur (Criterion 9), but th ese are generally of insufficient severity or\nduration to warrant an addition al diagnosis. These episodes occur most frequently in re-\nsponse to a real or imagined abandonment. Symptoms tend to be transient, lasting min-\nutes or hours. The real or perceived return of the caregiver\u2019s nurturance may result in a\nremission of symptoms.", "source": "dsm5.pdf"} {"id": "9d3b98175d1e-0", "page_content": "Borderline Personality Disorder 665\nAssociated Features Supporting Diagnosis\nIndividuals with borderline personality disorder may have a pattern of undermining\nthemselves at the moment a goal is about to be realized (e.g., dropping out of school just\nbefore graduation; regressing se verely after a discussion of ho w well therapy is going; de-\nstroying a good relationship just when it is clear that the relationship could last). Some in-\ndividuals develop psychotic-like symptoms (e.g ., hallucinations, body-image distortions,\nideas of reference, hypnagogic phenomena) du ring times of stress. Individuals with this\ndisorder may feel more secure with transition al objects (i.e., a pet or inanimate possession)\nthan in interpersonal relationships. Prematur e death from suicide may occur in individu-\nals with this disorder, especially in those with co-occurring depressive disorders or sub-\nstance use disorders. Physical handicaps may result from self-inflicted abuse behaviors or\nfailed suicide attempts. Recurrent job losses, in terrupted education, and separation or di-\nvorce are common. Physical and sexual abuse, neglect, hostile conflict, and early parental\nloss are more common in the childhood histor ies of those with borderline personality dis-\norder. Common co-occurring disorders include depressive and bipolar disorders, sub-\nstance use disorders, eating disorders (not ably bulimia nervosa), posttraumatic stress\ndisorder, and attention-defici t/hyperactivity disorder. Bo rderline personality disorder\nalso frequently co-occurs with the other personality disorders.\nPrevalence\nThe median population prevalence of border line personality disorder is estimated to be\n1.6% but may be as high as 5.9%. The preval ence of borderline personality disorder is", "source": "dsm5.pdf"} {"id": "9d3b98175d1e-1", "page_content": "about 6% in primary care sett ings, about 10% among individual s seen in outpatient mental\nhealth clinics, and about 20% among psychiat ric inpatients. The prevalence of borderline\npersonality disorder may decrease in older age groups. \nDevelopment and Course\nThere is considerable variability in the course of borderline personality disorder. The most\ncommon pattern is one of chronic instability in early adulthoo d, with episodes of serious\naffective and impulsive dyscontrol and high levels of use of health and mental health re-\nsources. The impairment from the disorder and the risk of suicide are greatest in the\nyoung-adult years and gradually wane with advancing age. Although the tendency to-\nward intense emotions, impulsivity, and intens ity in relationships is often lifelong, indi-\nviduals who engage in therapeutic interv ention often show improvement beginning\nsometime during the first year. During their 30s and 40s, the majority of individuals with\nthis disorder attain greater stability in their relationships and vocational functioning. Fol-\nlow-up studies of individuals identified thr ough outpatient mental health clinics indicate\nthat after about 10 years, as many as half of the individuals no longer have a pattern of be-\nhavior that meets full criteria for borderline personality disorder.\nRisk and Prognostic Factors\nGenetic and physiological. Borderline personality disorder is about five times more\ncommon among first-degree biological relatives of those with the disorder than in the gen-\neral population. There is also an increased familial risk for substance use disorders, anti-\nsocial personality disorder, and depressive or bipolar disorders.\nCulture-Related Diagnostic Issues\nThe pattern of behavior seen in borderline personality disorder has been identified in many\nsettings around the world. Adolescents and youn g adults with identity problems (especially\nwhen accompanied by substance use) may transiently display behaviors that misleadingly", "source": "dsm5.pdf"} {"id": "c63ad0563e09-0", "page_content": "666 Personality Disorders\ngive the impression of borderline personality disorder. Such situations are characterized by\nemotional instability, \u201cexistential\u201d dilemmas, uncertainty, anxiety- provoking choices, con-\nflicts about sexual orientation, and competing social pressures to decide on careers. \nGender-Related Diagnostic Issues\nBorderline personality disord er is diagnosed predominantly (about 75%) in females.\nDifferential Diagnosis\nDepressive and bipolar disorders. Borderline personality disorder often co-occurs with\ndepressive or bipolar disorders, and when criteria for both are met, both may be diagnosed.\nBecause the cross-sectional presentation of bo rderline personality disorder can be mimicked\nby an episode of depressive or bipolar disord er, the clinician should avoid giving an addi-\ntional diagnosis of borderline personality diso rder based only on cr oss-sectional presenta-\ntion without having documented that the pattern of behavior had an early onset and a long-\nstanding course.\nOther personality disorders. Other personality disorders ma y be confused with border-\nline personality disorder because they have certain features in common. It is therefore im-\nportant to distinguish among these disorders based on differences in their characteristic\nfeatures. However, if an individual has person ality features that meet criteria for one or\nmore personality disorders in addition to bord erline personality disorder, all can be diag-\nnosed. Although histrionic personality disorder can also be characterized by attention seek-\ning, manipulative behavior, an d rapidly shifting emotions, borderline personality disorder\nis distinguished by self-destructiveness, an gry disruptions in close relationships, and\nchronic feelings of deep emptiness and loneline ss. Paranoid ideas or illusions may be pres-\nent in both borderline personality disorder an d schizotypal personality disorder, but these\nsymptoms are more transient, in terpersonally reactive, and responsive to external structur-", "source": "dsm5.pdf"} {"id": "c63ad0563e09-1", "page_content": "symptoms are more transient, in terpersonally reactive, and responsive to external structur-\ning in borderline personality disorder. Althou gh paranoid personalit y disorder and narcis-\nsistic personality disorder may also be charac terized by an angry reaction to minor stimuli,\nthe relative stability of self-ima ge, as well as the relative lack of self-destructiveness, impul-\nsivity, and abandonment concerns, distinguishe s these disorders from borderline person-\nality disorder. Although antisocial personality disorder and borderline personality disorder\nare both characterized by mani pulative behavior, in dividuals with antisocial personality\ndisorder are manipulative to gain profit, po wer, or some other material gratification,\nwhereas the goal in borderline personality disorder is directed more toward gaining the con-\ncern of caretakers. Both depe ndent personality disorder and borderline personality disorder\nare characterized by fear of abandonment; however, the individual with borderline person-\nality disorder reacts to abandonment with f eelings of emotional emptiness, rage, and de-\nmands, whereas the individual with dependent personality disorder re acts with increasing\nappeasement and submissiveness and urgently seeks a replacement relationship to provide\ncaregiving and support. Borderline personality disorder can further be distinguished from\ndependent personality disorder by the typical pattern of unstable and intense relationships.\nPersonality change due to another medical condition. Borderline personality disor-\nder must be distinguished from personality change due to another medical condition, in\nwhich the traits that emerge ar e attributable to the effects of another medical condition on\nthe central nervous system.\nSubstance use disorders. Borderline personality disorder must also be distinguished\nfrom symptoms that may develop in a ssociation with persistent substance use.\nIdentity problems. Borderline personality disorder sh ould be distinguished from an", "source": "dsm5.pdf"} {"id": "e38916bc2b28-0", "page_content": "from symptoms that may develop in a ssociation with persistent substance use.\nIdentity problems. Borderline personality disorder sh ould be distinguished from an\nidentity problem, which is re served for identity concerns related to a developmental phase\n(e.g., adolescence) and does no t qualify as a me ntal disorder.", "source": "dsm5.pdf"} {"id": "ca2769a5771b-0", "page_content": "Histrionic Personality Disorder 667\nHistrionic Personality Disorder\nDiagnostic Criteria 301.50 (F60.4)\nA pervasive pattern of excessive emotionality and attention seeking, beginning by early adult-\nhood and present in a variety of contexts, as indicated by five (or more) of the following:\n1. Is uncomfortable in situations in which he or she is not the center of attention.\n2. Interaction with others is often characterized by inappropriate sexually seductive or\nprovocative behavior.\n3. Displays rapidly shifting and shallow expression of emotions.\n4. Consistently uses physical appearance to draw attention to self.\n5. Has a style of speech that is excessively impressionistic and lacking in detail.\n6. Shows self-dramatization, theatricality, and exaggerated expression of emotion.\n7. Is suggestible (i.e., easily influenced by others or circumstances).\n8. Considers relationships to be more intimate than they actually are.\nDiagnostic Features\nThe essential feature of histrionic personalit y disorder is pervasiv e and excessive emotion-\nality and attention-seeking behavior. This pattern begins by early adulthood and is pres-\nent in a variety of contexts.\nIndividuals with histrionic personality diso rder are uncomfortabl e or feel unappreci-\nated when they are not the center of attentio n (Criterion 1). Often lively and dramatic, they\ntend to draw attention to themselves and ma y initially charm new acquaintances by their\nenthusiasm, apparent openness, or flirtatiousness. These qua lities wear thin, however, as\nthese individuals continually demand to be th e center of attention. They commandeer the\nrole of \u201cthe life of the party.\u201d If they are not the center of attention, they may do something", "source": "dsm5.pdf"} {"id": "ca2769a5771b-1", "page_content": "dramatic (e.g., make up stories, create a scene) to draw the fo cus of attention to themselves.\nThis need is often apparent in their behavior wi th a clinician (e.g., being flattering, bring-\ning gifts, providing dramatic descriptions of physical and psychological symptoms that\nare replaced by new symptoms each visit).\nThe appearance and behavior of individuals with this disorder are often inappropri-\nately sexually provocative or seductive (Criteri on 2). This behavior not only is directed to-\nward persons in whom the individual has a sexu al or romantic interest but also occurs in\na wide variety of social, occupational, and professional rela tionships beyond what is ap-\npropriate for the social context. Emotional ex pression may be shallow and rapidly shifting\n(Criterion 3). Individuals with this disorder consistently use physical appearance to draw\nattention to themselves (Criterion 4). They are overly concerned with impressing others by\ntheir appearance and expend an excessive am ount of time, energy, and money on clothes\nand grooming. They may \u201cfish for compliments\u201d regarding appearance and may be easily\nand excessively upset by a critical comment about how they look or by a photograph that\nthey regard as unflattering.\nThese individuals have a style of speech that is excessively impre ssionistic and lacking\nin detail (Criterion 5). Strong opinions are expressed with dramatic flair, but underlying\nreasons are usually vague and diffuse, with out supporting facts and details. For example,\nan individual with histrionic personality disorder may comment that a certain individual\nis a wonderful human being, yet be unable to provide any specific examples of good qual-\nities to support this opinion. Individuals with this disorder are characterized by self-\ndramatization, theatricality, and an exaggera ted expression of emotion (Criterion 6). They", "source": "dsm5.pdf"} {"id": "ca2769a5771b-2", "page_content": "may embarrass friends and acquaintances by an excessive public displa y of emotions (e.g.,\nembracing casual acquaintances with excessive ardor, sobbing uncontrollably on minor", "source": "dsm5.pdf"} {"id": "bf5859e7f3de-0", "page_content": "668 Personality Disorders\nsentimental occasions, having temper tantru ms). However, their emotions often seem to\nbe turned on and off too quickly to be deeply felt, which may lead others to accuse the in-\ndividual of faking these feelings.\nIndividuals with histrionic pers onality disorder have a high degree of suggestibility (Cri-\nterion 7). Their opinions and f eelings are easily influenced by others and by current fads.\nThey may be overly trusting, especially of st rong authority figures whom they see as mag-\nically solving their problems. They have a te ndency to play hunches and to adopt convic-\ntions quickly. Individuals with this disorder often consider relationships more intimate\nthan they actually are, describing almost every acquaintance as \u201cmy dear, dear friend\u201d or\nreferring to physicians met only once or twice under professional circumstances by their\nfirst names (Criterion 8). \nAssociated Features Supporting Diagnosis\nIndividuals with histrionic personality disord er may have difficulty achieving emotional in-\ntimacy in romantic or sexual relationships. Without being aware of it, they often act out a\nrole (e.g., \u201cvictim\u201d or \u201cprincess\u201d) in their rela tionships to others. They may seek to control\ntheir partner through emotional manipulation or seductiveness on one level, while display-\ning a marked dependency on them at another level. Individuals with this disorder often\nhave impaired relationships with same-sex friends because their sexually provocative inter-\npersonal style may seem a threat to their friends\u2019 relationsh ips. These individuals may also\nalienate friends with demands for constant a ttention. They often become depressed and up-\nset when they are not the center of attention. They may crave novelty, stimulation, and ex-", "source": "dsm5.pdf"} {"id": "bf5859e7f3de-1", "page_content": "citement and have a tendency to become bore d with their usual routine. These individuals\nare often intolerant of, or frustrated by, situ ations that involve delayed gratification, and\ntheir actions are often directed at obtaining immediate satisfac tion. Although they often ini-\ntiate a job or project with great enthusiasm, their interest may lag quickly. Longer-term re-\nlationships may be ne glected to make way for the ex citement of new relationships.\nThe actual risk of suicide is not known, bu t clinical experience suggests that individu-\nals with this disorder are at in creased risk for suicidal gestur es and threats to get attention\nand coerce better caregiving. Histrionic personality disorder has been associated with\nhigher rates of somatic symptom disorder, conversion disorder (functional neurological\nsymptom disorder), and major depressive disord er. Borderline, narcissistic, antisocial, and\ndependent personality disorders often co-occur.\nPrevalence\nData from the 2001\u20132002 National Epidemio logic Survey on Alcohol and Related Condi-\ntions suggest a prevalence of histrionic personality of 1.84%.\nCulture-Related Diagnostic Issues\nNorms for interpersonal behavior, personal appearance, and emotional expressiveness\nvary widely across cultures, genders, and age groups. Before considering the various traits\n(e.g., emotionality, seductiveness, dramatic interperso nal style, novelty seeking, sociabil-\nity, charm, impressionability, a tendency to somatization) to be evidence of histrionic per-\nsonality disorder, it is impo rtant to evaluate whether they cause clinically significant\nimpairment or distress. \nGender-Related Diagnostic Issues\nIn clinical settings, this disorder has been di agnosed more frequently in females; however,", "source": "dsm5.pdf"} {"id": "bf5859e7f3de-2", "page_content": "In clinical settings, this disorder has been di agnosed more frequently in females; however,\nthe sex ratio is not significantly different from the sex ratio of females within the respective\nclinical setting. In contrast, some studies using structured assessments report similar prev-\nalence rates among males and females.", "source": "dsm5.pdf"} {"id": "648fa46c4934-0", "page_content": "Narcissistic Personality Disorder 669\nDifferential Diagnosis\nOther personality disorder s and personality traits. Other personality disorders may\nbe confused with histrionic personality disorder because they have certain features in\ncommon. It is therefore important to distinguish among these disorders based on differ-\nences in their characteristic features. However, if an individual has personality features\nthat meet criteria for one or more personality disorders in addition to histrionic personal-\nity disorder, all can be diagnosed. Although borderline personality disorder can also be\ncharacterized by attention seeking, manipulati ve behavior, and rapidly shifting emotions,\nit is distinguished by self-destructiveness, angry disruptions in close relationships, and\nchronic feelings of deep emptiness and identi ty disturbance. Individuals with antisocial\npersonality disorder and histrionic personalit y disorder share a tend ency to be impulsive,\nsuperficial, excitement seeking, reckless, seductive, and manipulative, but persons with\nhistrionic personality disorder tend to be mo re exaggerated in their emotions and do not\ncharacteristically engage in antisocial behavi ors. Individuals with histrionic personality\ndisorder are manipulative to gain nurturance , whereas those with antisocial personality\ndisorder are manipulative to gain profit, powe r, or some other material gratification. Al-\nthough individuals with narcissistic personalit y disorder also crave attention from others,\nthey usually want praise for their \u201csuperiority,\u201d whereas individuals with histrionic per-\nsonality disorder are willing to be viewed as frag ile or dependent if this is instrumental in\ngetting attention. Individuals with narcissistic personality disorder may exaggerate the\nintimacy of their relationships with other pe ople, but they are more apt to emphasize the\n\u201cVIP\u201d status or wealth of th eir friends. In dependent personality disorder, the individual", "source": "dsm5.pdf"} {"id": "648fa46c4934-1", "page_content": "\u201cVIP\u201d status or wealth of th eir friends. In dependent personality disorder, the individual\nis excessively dependent on othe rs for praise and guidance, but is without the flamboyant,\nexaggerated, emotional features of individu als with histrionic personality disorder.\nMany individuals may display histrionic personality traits. Only when these traits are\ninflexible, maladaptive, and persisting and cause significant functional impairment or\nsubjective distress do they constitu te histrionic personality disorder.\nPersonality change due to another medical condition. Histrionic personality disorder\nmust be distinguished from personality ch ange due to another medical condition, in\nwhich the traits that emerge ar e attributable to the effects of another medical condition on\nthe central nervous system. \nSubstance use disorders. The disorder must also be distinguished from symptoms that\nmay develop in association with persistent substance use.\nNarcissistic Personality Disorder\nDiagnostic Criteria 301.81 (F60.81)\nA pervasive pattern of grandiosity (in fantasy or behavior), need for admiration, and lack\nof empathy, beginning by early adulthood and present in a variety of contexts, as indicated\nby five (or more) of the following:\n1. Has a grandiose sense of self-importance (e.g., exaggerates achievements and talents,\nexpects to be recognized as superior without commensurate achievements).\n2. Is preoccupied with fantasies of unlimited success, power, brilliance, beauty, or ideal\nlove.\n3. Believes that he or she is \u201cspecial\u201d and unique and can only be understood by, or\nshould associate with, other special or high-status people (or institutions).\n4. Requires excessive admiration.\n5. Has a sense of entitlement (i.e., unreasonable expectations of especially favorable\ntreatment or automatic compliance with his or her expectations).", "source": "dsm5.pdf"} {"id": "15c32779e4f0-0", "page_content": "670 Personality Disorders\n6. Is interpersonally exploitative (i.e., takes advantage of others to achieve his or her own\nends).\n7. Lacks empathy: is unwilling to recognize or identify with the feelings and needs of others.\n8. Is often envious of others or believes that others are envious of him or her.\n9. Shows arrogant, haughty behaviors or attitudes.\nDiagnostic Features\nThe essential feature of narcissistic personality disorder is a pervasive pattern of grandi-\nosity, need for admiration, and lack of empathy that begins by early adulthood and is pres-\nent in a variety of contexts.\nIndividuals with this disorder have a grandiose sense of self-impor tance (Criterion 1).\nThey routinely overestimate their abilities and in flate their accomplishme nts, often appearing\nboastful and pretentious. They may blithely assume that others attribute the same value to\ntheir efforts and may be surprised when the prai se they expect and feel they deserve is not\nforthcoming. Often implicit in the inflated ju dgments of their own accomplishments is an un-\nderestimation (devaluation) of the contributions of others. Individuals with narcissistic per-\nsonality disorder are often preo ccupied with fantasies of unlimit ed success, power, brilliance,\nbeauty, or ideal love (Criterion 2). They ma y ruminate about \u201clong overdue\u201d admiration and\nprivilege and compare themselves favora bly with famous or privileged people.\nIndividuals with narcissistic personality disorder believe that they are superior, spe-\ncial, or unique and expect others to recogniz e them as such (Criterion 3). They may feel\nthat they can only be understood by, and sh ould only associate with, other people who are\nspecial or of high status and may attribute \u201cunique,\u201d \u201cperfect,\u201d or \u201cgifted\u201d qualities to those", "source": "dsm5.pdf"} {"id": "15c32779e4f0-1", "page_content": "with whom they associate. Individuals with th is disorder believe that their needs are spe-\ncial and beyond the ken of ordinary people. Their own self-esteem is enhanced (i.e., \u201cmir-\nrored\u201d) by the idealized value that they assign to those with whom they associate. They are\nlikely to insist on having only the \u201ctop\u201d pers on (doctor, lawyer, hair dresser, instructor) or\nbeing affiliated with the \u201cbest\u201d institutions but may devalue the credentials of those who dis-\nappoint them.\nIndividuals with this disorder generally require excessiv e admiration (Criterion 4). Their\nself-esteem is almost invariably very fragile. They may be preoccupied with how well they\nare doing and how favorably they are regarded by others. This often takes the form of a need\nfor constant attention and admira tion. They may expect their arri val to be greeted with great\nfanfare and are astonished if others do not c ovet their possessions. Th ey may constantly fish\nfor compliments, often with great charm. A sens e of entitlement is ev ident in these individ-\nuals\u2019 unreasonable expectation of especially fa vorable treatment (Criterion 5). They expect\nto be catered to and are puzzled or furious when this does not happen. For example, they\nmay assume that they do not have to wait in line and that th eir priorities are so important\nthat others should defer to them, and then ge t irritated when others fail to assist \u201cin their\nvery important work.\u201d This sense of entitlement, combined with a lack of sensitivity to the\nwants and needs of others, may result in the conscious or unwitting exploitation of others\n(Criterion 6). They expect to be given whatever they want or feel they need, no matter what\nit might mean to others. For example, these individuals may expect great dedication from", "source": "dsm5.pdf"} {"id": "15c32779e4f0-2", "page_content": "it might mean to others. For example, these individuals may expect great dedication from\nothers and may overwork them wi thout regard for the impact on their lives. They tend to\nform friendships or romantic relationships only if the other person seems likely to advance\ntheir purposes or otherwise enhance their self -esteem. They often usurp special privileges\nand extra resources that they believe th ey deserve because they are so special.", "source": "dsm5.pdf"} {"id": "75be9ef228b0-0", "page_content": "their purposes or otherwise enhance their self -esteem. They often usurp special privileges\nand extra resources that they believe th ey deserve because they are so special.\nIndividuals with narcissistic personality disorder generally have a lack of empathy and\nhave difficulty recognizing the desires, subjective experiences, and feelings of others (Crite-\nrion 7). They may assume that others are tota lly concerned about their welfare. They tend to\ndiscuss their own concerns in inappropriate an d lengthy detail, while failing to recognize\nthat others also have feelings and needs. They are often contemptuous and impatient with", "source": "dsm5.pdf"} {"id": "3bb016315f66-0", "page_content": "Narcissistic Personality Disorder 671\nothers who talk about their ow n problems and concerns. These individuals may be oblivious\nto the hurt their remarks may in flict (e.g., exuberantly telling a former lover that \u201cI am now\nin the relationship of a lifetime !\u201d; boasting of health in front of someone who is sick). When\nrecognized, the needs, desires, or feelings of others are likely to be viewed disparagingly as\nsigns of weakness or vulnerability. Those who re late to individuals with narcissistic person-\nality disorder typically find an emotional coldness and lack of reciprocal interest.\nThese individuals are often envious of others or believe that others are envious of them\n(Criterion 8). They may begrudge others their su ccesses or possessions, fe eling that they better\ndeserve those achievements, admiration, or priv ileges. They may harshly devalue the contri-\nbutions of others, particularly when those individuals have received acknowledgment or\npraise for their accomplishments. Arrogant, haug hty behaviors characterize these individuals;\nthey often display snobbish, disdainful, or patr onizing attitudes (Criterion 9). For example, an\nindividual with this disorder may complain about a clumsy waiter\u2019s \u201crudeness\u201d or \u201cstupidity\u201d\nor conclude a medical evaluation with a condescending evaluation of the physician.\nAssociated Features Supporting Diagnosis\nVulnerability in self-esteem makes individuals with narcissistic personality disorder very\nsensitive to \u201cinjury\u201d from criticism or defe at. Although they may not show it outwardly,\ncriticism may haunt these individuals and ma y leave them feeling humiliated, degraded,\nhollow, and empty. They may react with disdain, rage, or defiant counterattack. Such ex-\nperiences often lead to social withdrawal or an appearance of humility that may mask and", "source": "dsm5.pdf"} {"id": "3bb016315f66-1", "page_content": "periences often lead to social withdrawal or an appearance of humility that may mask and\nprotect the grandiosity. Interpersonal relation s are typically impaired because of problems\nderived from entitlement, the need for admira tion, and the relative disregard for the sen-\nsitivities of others. Though overweening ambition and confidence may lead to high\nachievement, performance may be disrupted beca use of intolerance of criticism or defeat.\nSometimes vocational functioning can be very low, reflecting an unwillingness to take a\nrisk in competitive or other situations in wh ich defeat is possible. Sustained feelings of\nshame or humiliation and the attendant self-criticism may be associated with social with-\ndrawal, depressed mood, and persistent depr essive disorder (dysthymia) or major de-\npressive disorder. In contrast, sustained periods of grandiosity may be associated with a\nhypomanic mood. Narcissistic personality disorder is also associated with anorexia ner-\nvosa and substance use disorder s (especially related to cocaine). Histrionic, borderline,\nantisocial, and paranoid personality disorders may be associated with narcissistic person-\nality disorder.\nPrevalence\nPrevalence estimates for narcissistic person ality disorder, based on DSM-IV definitions,\nrange from 0% to 6.2% in community samples. \nDevelopment and Course\nNarcissistic traits may be particularly comm on in adolescents and do not necessarily in-\ndicate that the individual will go on to have narcissistic personality disorder. Individuals\nwith narcissistic personality disorder may have special difficulties adjusting to the onset of\nphysical and occupational limitations that are inherent in the aging process. \nGender-Related Diagnostic Issues\nOf those diagnosed with narcissistic personality disorder, 50%\u201375% are male.\nDifferential Diagnosis\nOther personality disorder s and personality traits. Other personality disorders may", "source": "dsm5.pdf"} {"id": "3bb016315f66-2", "page_content": "Differential Diagnosis\nOther personality disorder s and personality traits. Other personality disorders may\nbe confused with narcissistic personality disorder because they have certain features in", "source": "dsm5.pdf"} {"id": "d2e7729eae01-0", "page_content": "672 Personality Disorders\ncommon. It is, therefore, important to distin guish among these disorders based on differ-\nences in their characteristic features. However, if an individual has personality features\nthat meet criteria for one or more personalit y disorders in addition to narcissistic person-\nality disorder, all can be diagnosed. The most useful feature in discriminating narcissistic\npersonality disorder from histrionic, antisocial, and borderline personality disorders, in\nwhich the interactive styles are coquettish, callous, and needy, respectively, is the grandi-\nosity characteristic of narcissistic personalit y disorder. The relative stability of self-image\nas well as the relative lack of self-destruc tiveness, impulsivity, an d abandonment concerns\nalso help distinguish narcissistic personality disorder from borderline personality disor-\nder. Excessive pride in achievements, a relative lack of emotional display, and disdain for\nothers\u2019 sensitivities help distinguish narci ssistic personality disorder from histrionic\npersonality disorder. Although individuals wi th borderline, histrionic, and narcissistic\npersonality disorders may requir e much attention, those with narcissistic personality dis-\norder specifically need that attention to be admiring. Individuals with antisocial and nar-\ncissistic personality disorders share a tendency to be tough-minded, glib, superficial,\nexploitative, and unempathic. However, narciss istic personality disorder does not neces-\nsarily include characteristics of impulsivity, aggression, and deceit. In addition, individu-\nals with antisocial personality disorder may not be as needy of the admiration and envy of\nothers, and persons with narcissistic personal ity disorder usually lack the history of con-\nduct disorder in childhood or criminal behavior in adulthood. In both narcissistic person-\nality disorder and obsessive-compulsive personality disorder, the individual may profess", "source": "dsm5.pdf"} {"id": "d2e7729eae01-1", "page_content": "ality disorder and obsessive-compulsive personality disorder, the individual may profess\na commitment to perfectionism and believe that others cannot do things as well. In con-\ntrast to the accompanying self-criticism of those with obsessive-compulsive personality\ndisorder, individuals with narcissistic persona lity disorder are more likely to believe that\nthey have achieved perfection. Suspiciousness and social withdrawal usually distinguish\nthose with schizotypal or paranoid personalit y disorder from those with narcissistic per-\nsonality disorder. When these qualities are pres ent in individuals with narcissistic person-\nality disorder, they derive primarily from fear s of having imperfections or flaws revealed. \nMany highly successful individuals display pe rsonality traits that might be considered\nnarcissistic. Only when these traits are inflexible, maladaptive, and persisting and cause\nsignificant functional impairment or subjective distress do they constitute narcissistic per-\nsonality disorder.\nMania or hypomania. Grandiosity may emerge as part of manic or hypomanic episodes,\nbut the association with mood change or functional impairments helps distinguish these\nepisodes from narcissistic personality disorder. \nSubstance use disorders. Narcissistic personality disorder must also be distinguished\nfrom symptoms that may develop in a ssociation with persistent substance use.\nCluster C Personality Disorders\nAvoidant Personality Disorder\nDiagnostic Criteria 301.82 (F60.6)\nA pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to neg-\native evaluation, beginning by early adulthood and present in a variety of contexts, as in-\ndicated by four (or more) of the following:\n1. Avoids occupational activities that invo lve significant interpersonal contact because of\nfears of criticism, disapproval, or rejection.", "source": "dsm5.pdf"} {"id": "ac73b82717d9-0", "page_content": "Avoidant Personality Disorder 673\n2. Is unwilling to get involved with people unless certain of being liked.\n3. Shows restraint within intimate relationships because of the fear of being shamed or\nridiculed.\n4. Is preoccupied with being criticized or rejected in social situations.\n5. Is inhibited in new interpersonal situations because of feelings of inadequacy.\n6. Views self as socially inept, personally unappealing, or inferior to others.\n7. Is unusually reluctant to take personal risks or to engage in any new activities because\nthey may prove embarrassing.\nDiagnostic Features\nThe essential feature of avoidant personality disorder is a pervasive pa ttern of social inhi-\nbition, feelings of inadequacy, and hypersensitivity to negative evaluation that begins by\nearly adulthood and is present in a variety of contexts.\nIndividuals with avoidant personality disord er avoid work activities that involve sig-\nnificant interpersonal contact because of fears of criticism, disapprova l, or rejection (Cri-\nterion 1). Offers of job prom otions may be declined because the new responsibilities might\nresult in criticism from co-workers. These individuals avoid making new friends unless\nthey are certain they will be liked and accept ed without criticism (Criterion 2). Until they\npass stringent tests proving the contrary, other people are assumed to be critical and dis-\napproving. Individuals with this disorder will not join in group activities unless there are\nrepeated and generous offers of support and nurturance. Inte rpersonal intimacy is often\ndifficult for these individuals, although they are able to es tablish intimate relationships\nwhen there is assurance of uncritical acceptan ce. They may act with restraint, have diffi-\nculty talking about themselves, and withhold intimate feelings for fear of being exposed,\nridiculed, or shamed (Criterion 3).", "source": "dsm5.pdf"} {"id": "ac73b82717d9-1", "page_content": "ridiculed, or shamed (Criterion 3).\nBecause individuals with this disorder are preoccupied with being criticized or re-\njected in social situations, they may have a markedly low threshold for detecting such re-\nactions (Criterion 4). If someone is even s lightly disapproving or critical, they may feel\nextremely hurt. They tend to be shy, quiet, inhibited, and \u201cinvisible\u201d because of the fear\nthat any attention would be degrading or reject ing. They expect that no matter what they\nsay, others will see it as \u201cwrong,\u201d and so th ey may say nothing at all. They react strongly\nto subtle cues that are suggest ive of mockery or derision. Despite their longing to be active\nparticipants in social life, they fear placing their welfare in the hands of others. Individuals\nwith avoidant personality disorder are inhibi ted in new interpersonal situations because\nthey feel inadequate and have low self-esteem (Criterion 5). Doubts concerning social\ncompetence and personal appeal become especially manifest in settings involving inter-\nactions with strangers. These individuals believe themselves to be socially inept, person-\nally unappealing, or inferior to others (Cri terion 6). They are unusually reluctant to take\npersonal risks or to engage in any new activities because these may prove embarrassing\n(Criterion 7). They are prone to exaggerate the potential dangers of ordinary situations,\nand a restricted lifestyle may result from their need for certainty and security. Someone\nwith this disorder may cancel a job interview for fear of being embarrassed by not dressing\nappropriately. Marginal somatic symptoms or other problems may become the reason for\navoiding new activities.\nAssociated Features Supporting Diagnosis\nIndividuals with avoidant personality disorder often vigilantly appr aise the movements\nand expressions of those with whom they come into contact. Their fearful and tense de-", "source": "dsm5.pdf"} {"id": "ac73b82717d9-2", "page_content": "and expressions of those with whom they come into contact. Their fearful and tense de-\nmeanor may elicit ridicule an d derision from others, which in turn confirms their self-\ndoubts. These individuals are very anxious about the possibility that they will react to crit-", "source": "dsm5.pdf"} {"id": "3f8d9cbb6648-0", "page_content": "meanor may elicit ridicule an d derision from others, which in turn confirms their self-\ndoubts. These individuals are very anxious about the possibility that they will react to crit-\nicism with blushing or crying. They are described by others as being \u201cshy,\u201d \u201ctimid,\u201d", "source": "dsm5.pdf"} {"id": "b56240caaef8-0", "page_content": "674 Personality Disorders\n\u201clonely,\u201d and \u201cisolated.\u201d The major problems associated with this disorder occur in social\nand occupational functi oning. The low self-esteem and hy persensitivity to rejection are\nassociated with restricted in terpersonal contacts. These individuals may become relatively\nisolated and usually do not have a large social support ne twork that can help them weather\ncrises. They desire affection and acceptance and may fantasize about idealized relation-\nships with others. The avoidant behaviors can also adversely affect occupational function-\ning because these individuals try to avoid the types of social situations that may be\nimportant for meeting the basic dema nds of the job or for advancement.\nOther disorders that are commonly diagnosed with avoidant personality disorder in-\nclude depressive, bipolar, and anxiety disorders, especially social anxiety disorder (social\nphobia). Avoidant personality disorder is often diagnosed with dependent personality\ndisorder, because individuals with avoidant pe rsonality disorder become very attached to\nand dependent on those few other people wi th whom they are friends. Avoidant per-\nsonality disorder also tends to be diagnosed with borderline personality disorder and with\nthe Cluster A personality disorders (i.e., paranoid, schizoid, or schizotypal personality\ndisorders).\nPrevalence\nData from the 2001\u20132002 National Epidemio logic Survey on Alcohol and Related Condi-\ntions suggest a prevalence of about 2.4% for avoidant personality disorder.\nDevelopment and Course\nThe avoidant behavior often st arts in infancy or childhood with shyness, isolation, and\nfear of strangers and new situations. Although shyness in childhood is a common precur-\nsor of avoidant personality disorder, in most individuals it tends to gradually dissipate as\nthey get older. In contrast, individuals who go on to develop avoidant personality disor-", "source": "dsm5.pdf"} {"id": "b56240caaef8-1", "page_content": "der may become increasingly shy and avoidant during adolescence and early adulthood,\nwhen social relationships with new people become especially important. There is some\nevidence that in adults, avoi dant personality disorder tend s to become less evident or to\nremit with age. This diagnosi s should be used with great caution in children and adoles-\ncents, for whom shy and avoidant behavi or may be developmentally appropriate.\nCulture-Related Diagnostic Issues\nThere may be variation in the degree to whic h different cultural and ethnic groups regard\ndiffidence and avoidance as appropriate. Mo reover, avoidant behavior may be the result\nof problems in acculturat ion following immigration. \nGender-Related Diagnostic Issues\nAvoidant personality disorder appears to be equally frequent in males and females.\nDifferential Diagnosis\nAnxiety disorders. There appears to be a great deal of overlap between avoidant person-\nality disorder and social anxiety disorder (s ocial phobia), so much so that they may be\nalternative conceptualizations of the same or similar conditions. Avoidance also character-\nizes both avoidant personality disorder and agoraphobia, and they often co-occur. \nOther personality disorders and personality traits. Other personality disorders may\nbe confused with avoidant pers onality disorder because they have certain fe atures in com-\nmon. It is, therefore, important to distingu ish among these disorder s based on differences\nin their characteristic features. However, if an individual has personality features that\nmeet criteria for one or more personality diso rders in addition to avoidant personality dis-", "source": "dsm5.pdf"} {"id": "01e4faa09b32-0", "page_content": "Dependent Personality Disorder 675\norder, all can be diagnosed. Both avoidant personality disorder and dependent personal-\nity disorder are characterized by feelings of inadequacy, hypersensitivity to criticism, and\na need for reassurance. Although the primary focus of concern in avoidant personality\ndisorder is avoidance of humiliation and reject ion, in dependent pers onality disorder the\nfocus is on being taken care of. However, avoidant personality disorder and dependent\npersonality disorder are particularly likely to co-occur. Like avoidant personality disor-\nder, schizoid personality disorder and schizotypal personality disorder are characterized\nby social isolation. However, individuals with avoidant personality disorder want to have\nrelationships with others and feel their loneliness deeply, whereas those with schizoid or\nschizotypal personality disorder may be conten t with and even prefer their social isola-\ntion. Paranoid personality disorder and avoida nt personality disorder are both character-\nized by a reluctance to confide in others. Ho wever, in avoidant personality disorder, this\nreluctance is attributable more to a fear of being embarrassed or being found inadequate\nthan to a fear of others\u2019 malicious intent.\nMany individuals display avoidant personality traits. Only when these traits are in-\nflexible, maladaptive, and persisting and caus e significant functional impairment or sub-\njective distress do they constitu te avoidant personality disorder.\nPersonality change due to another medical condition. Avoidant personality disorder\nmust be distinguished from personality ch ange due to another medical condition, in\nwhich the traits that emerge ar e attributable to the effects of another medical condition on\nthe central nervous system. \nSubstance use disorders. Avoidant personality disorder must also be distinguished\nfrom symptoms that may develop in a ssociation with persistent substance use.\nDependent Personality Disorder", "source": "dsm5.pdf"} {"id": "01e4faa09b32-1", "page_content": "Dependent Personality Disorder\nDiagnostic Criteria 301.6 (F60.7)\nA pervasive and excessive need to be taken care of that leads to submissive and clinging\nbehavior and fears of separation, beginning by early adulthood and present in a variety of\ncontexts, as indicated by five (or more) of the following:\n1. Has difficulty making everyday decisions without an excessive amount of advice and\nreassurance from others.\n2. Needs others to assume responsibility for most major areas of his or her life.\n3. Has difficulty expressing disagreement with others because of fear of loss of support\nor approval. ( Note: Do not include realistic fears of retribution.)\n4. Has difficulty initiating projects or doing things on his or her own (because of a lack of\nself-confidence in judgment or abilities rather than a lack of motivation or energy).\n5. Goes to excessive lengths to obtain nurturance and support from others, to the point\nof volunteering to do things that are unpleasant.\n6. Feels uncomfortable or helpless when alone because of exaggerated fears of being\nunable to care for himself or herself.\n7. Urgently seeks another relationship as a source of care and support when a close re-\nlationship ends.\n8. Is unrealistically preoccupied with fears of being left to take care of himself or herself.\nDiagnostic Features\nThe essential feature of dependent personalit y disorder is a pervasive and excessive need\nto be taken care of that leads to submissive and clinging behavior and fears of separation.\nThis pattern begins by early ad ulthood and is present in a variety of contexts. The dependent", "source": "dsm5.pdf"} {"id": "4474d120399a-0", "page_content": "676 Personality Disorders\nand submissive behaviors are designed to elicit caregiving and arise from a self-perception\nof being unable to function adequately without the help of others.\nIndividuals with dependent personality disorder have grea t difficulty making every-\nday decisions (e.g., what color shirt to wear to work or whether to carry an umbrella) without\nan excessive amount of advice and reassurance from others (Criterion 1). These individu-\nals tend to be passive and to allow other people (often a single other person) to take the ini-\ntiative and assume responsibility for most majo r areas of their lives (Criterion 2). Adults\nwith this disorder typically depend on a pa rent or spouse to decide where they should\nlive, what kind of job they should have, and which neighbors to befriend. Adolescents\nwith this disorder may allow their parent(s) to decide what they should wear, with whom\nthey should associate, how they should spen d their free time, and what school or college\nthey should attend. This need for others to \u00a0assume responsibility goes beyond age-appro-\npriate and situation-appropriate requests fo r assistance from others (e.g., the specific\nneeds of children, elderly persons, and hand icapped persons). Dependent personality dis-\norder may occur in an individual who has a serious medical conditio n or disability, but in\nsuch cases the difficulty in taking responsib ility must go beyond what would normally be\nassociated with that condition or disability.\nBecause they fear losing support or approval, individuals with dependent personality\ndisorder often have difficulty expressing d isagreement with other individuals, especially\nthose on whom they are dependent (Criterion 3) . These individuals feel so unable to func-\ntion alone that they will agree with things that they feel are wrong rather than risk losing", "source": "dsm5.pdf"} {"id": "4474d120399a-1", "page_content": "tion alone that they will agree with things that they feel are wrong rather than risk losing\nthe help of those to whom they look for guidance. They do not get appropriately angry at\nothers whose support and nurturance they need for fear of alienating them. If the individ-\nual\u2019s concerns regarding the consequences of expressing disagreement are realistic (e.g.,\nrealistic fears of retribution from an abusiv e spouse), the behavior should not be consid-\nered to be evidence of dependent personality disorder.\nIndividuals with this disorder have difficulty initiating projects or doing things inde-\npendently (Criterion 4). They lack self-confidence and believe that they need help to begin\nand carry through tasks. They will wait for othe rs to start things because they believe that\nas a rule others can do them better. These in dividuals are convinced that they are incapable\nof functioning independently and present them selves as inept and requiring constant as-\nsistance. They are, however, lik ely to function adequately if given the assurance that some-\none else is supervising and approving. There ma y be a fear of becoming or appearing to be\nmore competent, because they may believe that this will lead to abandonment. Because\nthey rely on others to handle their problems, they often do not learn the skills of indepen-\ndent living, thus perpetuating dependency.\nIndividuals with dependent personality disord er may go to excessive lengths to obtain\nnurturance and support from others, even to the point of volunteering for unpleasant\ntasks if such behavior will bring the care they need (Criterion 5). They are willing to submit\nto what others want, even if the demands are unreasonable. Their need to maintain an im-\nportant bond will often re sult in imbalanced or distorted relationships. They may make ex-", "source": "dsm5.pdf"} {"id": "4474d120399a-2", "page_content": "traordinary self-sacrifices or tolerate verbal, physical, or sexual abuse. (It should be noted\nthat this behavior should be considered evid ence of dependent pers onality disorder only\nwhen it can clearly be established that other options are available to the individual.) Indi-\nviduals with this disorder feel uncomfortable or helpless when alone, because of their ex-", "source": "dsm5.pdf"} {"id": "5121c1ce709a-0", "page_content": "when it can clearly be established that other options are available to the individual.) Indi-\nviduals with this disorder feel uncomfortable or helpless when alone, because of their ex-\naggerated fears of being unable to care for th emselves (Criterion 6). They will \u201ctag along\u201d\nwith important others just to avoid being alone, even if they are not interested or involved\nin what is happening.\nWhen a close relationship ends (e.g., a breakup with a lover; the death of a caregiver), in-\ndividuals with dependent person ality disorder may urgently seek another relationship to\nprovide the care and support they need (Criterion 7). Their be lief that they are unable to\nfunction in the absence of a cl ose relationship motivates these individuals to become quickly\nand indiscriminately attached to another individual. Individuals with this disorder are often", "source": "dsm5.pdf"} {"id": "9fe0a99b8b6e-0", "page_content": "Dependent Personality Disorder 677\npreoccupied with fears of being left to care fo r themselves (Criterion 8). They see themselves\nas so totally dependent on the advice and help of an important other person that they worry\nabout being abandoned by that person when ther e are no grounds to justify such fears. To be\nconsidered as evidence of this criterion, the fears must be ex cessive and unrealistic. For ex-\nample, an elderly man with cancer who moves into his son\u2019s household for care is exhibiting\ndependent behavior that is appropriate given this person\u2019s life circumstances.\nAssociated Features Supporting Diagnosis\nIndividuals with dependent personality diso rder are often charac terized by pessimism\nand self-doubt, tend to belittl e their abilities and assets, and may constantly refer to them-\nselves as \u201cstupid.\u201d They take criticism and disapproval as proof of their worthlessness and\nlose faith in themselves. They may seek ov erprotection and dominance from others. Oc-\ncupational functioning may be impaired if in dependent initiative is required. They may\navoid positions of responsibility and become anxious when faced with decisions. Social re-\nlations tend to be limited to those few people on whom the individual is dependent. There\nmay be an increased risk of depressive disorders, anxiety disorders, and adjustment dis-\norders. Dependent personality disorder often co-occurs with other personality disorders,\nespecially borderline, avoidant, and histrion ic personality disorders. Chronic physical ill-\nness or separation anxiety disorder in childhood or adolescence may predispose the indi-\nvidual to the development of this disorder.\nPrevalence\nData from the 2001\u20132002 National Epidemio logic Survey on Alcohol and Related Condi-\ntions yielded an estimated prevalence of depe ndent personality disorder of 0.49%, and de-", "source": "dsm5.pdf"} {"id": "9fe0a99b8b6e-1", "page_content": "pendent personality was estimated, based on a probability subsample from Part II of the\nNational Comorbidit y Survey Replication, to be 0.6%.\nDevelopment and Course\nThis diagnosis should be used with great caution, if at all, in children and adolescents, for\nwhom dependent behavior may be developmentally appropriate.\nCulture-Related Diagnostic Issues\nThe degree to which dependen t behaviors are considered to be appropriate varies sub-\nstantially across different age and sociocultu ral groups. Age and cultural factors need to\nbe considered in evaluating the diagnostic threshold of each crit erion. Dependent behav-\nior should be considered characteristic of the disorder only when it is clearly in excess of\nthe individual\u2019s cultural norms or reflects unrealistic concerns. An emphasis on passivity,\npoliteness, and deferential treatment is characteristic of some societies and may be mis-\ninterpreted as traits of dependent personality disorder. Similarly, societies may differen-\ntially foster and discourage depend ent behavior in males and females. \nGender-Related Diagnostic Issues\nIn clinical settings, dependent personality d isorder has been diagnosed more frequently in\nfemales, although some studies report simila r prevalence rates among males and females. \nDifferential Diagnosis\nOther mental disorders and medical conditions. Dependent personality disorder must\nbe distinguished from dependen cy arising as a consequence of other mental disorders (e.g.,\ndepressive disorders, panic disorder, agoraphobia) and as a resu lt of other medical conditions.", "source": "dsm5.pdf"} {"id": "49c56438c354-0", "page_content": "678 Personality Disorders\nOther personality disorders and personality traits. Other personality disorders may be\nconfused with dependent personality disorder because they ha ve certain features in com-\nmon. It is therefore important to distinguis h among these disorders based on differences in\ntheir characteristic features. However, if an individual has personality features that meet cri-\nteria for one or more personality disorders in addition to dependent personality disorder, all\ncan be diagnosed. Although many personality disorders are characterized by dependent\nfeatures, dependent personality disorder can be distinguished by its predominantly submis-\nsive, reactive, and clinging be havior. Both dependent person ality disorder and borderline\npersonality disorder are characterized by fe ar of abandonment; however, the individual\nwith borderline personality disorder reacts to abandonment with feelings of emotional emp-\ntiness, rage, and demands, whereas the individual with dependent personality disorder re-\nacts with increasing appeasement and submissiveness and urgently seeks a replacement\nrelationship to provide caregiving and suppor t. Borderline personalit y disorder can further\nbe distinguished from dependen t personality disorder by a ty pical pattern of unstable and\nintense relationships. Individual s with histrionic personality disorder, like those with de-\npendent personality disorder, ha ve a strong need for reassu rance and approval and may ap-\npear childlike and clinging. However, unli ke dependent personality disorder, which is\ncharacterized by self-effacing and docile behavior, histrionic personality disorder is charac-\nterized by gregarious flamboyance with acti ve demands for attention. Both dependent\npersonality disorder and avoidant personality di sorder are characterized by feelings of in-\nadequacy, hypersensitivity to criticism, and a need for reassurance; however, individuals\nwith avoidant personality disorder have such a strong fear of humiliation and rejection that", "source": "dsm5.pdf"} {"id": "49c56438c354-1", "page_content": "with avoidant personality disorder have such a strong fear of humiliation and rejection that\nthey withdraw until they are certain they will be accepted. In contrast, individuals with de-\npendent personality disorder have a pattern of seeking and maintaining connections to im-\nportant others, rather than avoiding and withdrawing fr om relationships.\nMany individuals display dependent personalit y traits. Only when these traits are in-\nflexible, maladaptive, and persisting and caus e significant functional impairment or sub-\njective distress do they constitute dependent personality disorder. \nPersonality change due to another medical condition. Dependent personality disor-\nder must be distinguished from personality change due to another medical condition, in\nwhich the traits that emerge ar e attributable to the effects of another medical condition on\nthe central nervous system.\nSubstance use disorders. Dependent personality disorder must also be distinguished\nfrom symptoms that may develop in a ssociation with persistent substance use.\nObsessive-Compulsive Personality Disorder\nDiagnostic Criteria 301.4 (F60.5)\nA pervasive pattern of preoccupation with orderliness, perfectionism, and mental and in-\nterpersonal control, at the expense of flexibility, openness, and efficiency, beginning by\nearly adulthood and present in a variety of contexts, as indicated by four (or more) of the\nfollowing:\n1. Is preoccupied with details, rules, lists, order, organization, or schedules to the extent\nthat the major point of the activity is lost.\n2. Shows perfectionism that interferes with task completion (e.g., is unable to complete a\nproject because his or her own over ly strict standards are not met).\n3. Is excessively devoted to work and productivity to the exclusion of leisure activities and\nfriendships (not accounted for by obvious economic necessity).", "source": "dsm5.pdf"} {"id": "49c56438c354-2", "page_content": "friendships (not accounted for by obvious economic necessity).\n4. Is overconscientious, scrupulous, and inflexible about matters of morality, ethics, or\nvalues (not accounted for by cultural or religious identification).", "source": "dsm5.pdf"} {"id": "21207f0e70c3-0", "page_content": "Obsessive-Compulsive Personality Disorder 679\n5. Is unable to discard worn-out or worthless objects even when they have no sentimental\nvalue.\n6. Is reluctant to delegate tasks or to work with others unless they submit to exactly his\nor her way of doing things.\n7. Adopts a miserly spending style toward both self and others; money is viewed as\nsomething to be hoarded for future catastrophes.\n8. Shows rigidity and stubbornness.\nDiagnostic Features\nThe essential feature of obse ssive-compulsive personality disorder is a preoccupation\nwith orderliness, perfectionism, and mental and interpersonal control, at the expense of\nflexibility, openness, and efficiency. This patt ern begins by early adulthood and is present\nin a variety of contexts.\nIndividuals with obse ssive-compulsive personality disorder attempt to maintain a\nsense of control through painstaking attention to rules, trivial details, procedures, lists,\nschedules, or form to the extent that the major point of the activity is lost (Criterion 1). They\nare excessively careful and prone to repetiti on, paying extraordinary attention to detail\nand repeatedly checking for possible mistakes. They are oblivious to the fact that other\npeople tend to become very annoyed at the de lays and inconveniences that result from this\nbehavior. For example, when such individuals misplace a list of things to be done, they\nwill spend an inordinate amount of time looking for the list rather than spending a few\nmoments re-creating it from memory and proceeding to accomplish the tasks. Time is\npoorly allocated, and the most important tasks are left to the last moment. The perfection-\nism and self-imposed high standards of performance cause significant dysfunction and\ndistress in these individuals. They may beco me so involved in maki ng every detail of a", "source": "dsm5.pdf"} {"id": "21207f0e70c3-1", "page_content": "project absolutely perfect that the project is never finished (Criterion 2). For example, the\ncompletion of a written report is delayed by numerous time-consuming rewrites that all\ncome up short of \u201cperfection.\u201d Deadlines are missed, and aspects of the individual\u2019s life\nthat are not the current focus of activity may fall into disarray.\nIndividuals with obsessive-compulsive pers onality disorder display excessive devotion\nto work and productivity to th e exclusion of leisure activities and friendships (Criterion 3).\nThis behavior is not accounted for by economic necessity. They often f eel that they do not\nhave time to take an evening or a weekend day of f to go on an outing or to just relax. They\nmay keep postponing a pleasurable activity, such as a vacation, so that it may never occur.\nWhen they do take time for leisure activities or vacations, they are very uncomfortable un-\nless they have taken along some thing to work on so they do not \u201cwaste time.\u201d There may be\na great concentration on househ old chores (e.g., repeated excessive cleaning so that \u201cone\ncould eat off the floor\u201d). If they spend time with friends, it is likely to be in some kind of for-\nmally organized activity (e.g., sports). Hobbies or recreational activities are approached as\nserious tasks requiring careful organization and hard work to master. The emphasis is on\nperfect performance. These individuals turn play into a structured task (e.g., correcting an\ninfant for not putting ring s on the post in the right order; tell ing a toddler to ride his or her tri-\ncycle in a straight line; turning a baseball game into a harsh \u201clesson\u201d).\nIndividuals with obsessive-co mpulsive personality disord er may be excessively con-\nscientious, scrupulous, and infl exible about matters of moralit y, ethics, or values (Crite-", "source": "dsm5.pdf"} {"id": "21207f0e70c3-2", "page_content": "rion 4). They may force themselves and othe rs to follow rigid moral principles and very\nstrict standards of performance. They may al so be mercilessly self-c ritical about their own\nmistakes. Individuals with this disorder are rigidly deferential to authority and rules and\ninsist on quite literal compliance, with no ru le bending for extenuating circumstances. For", "source": "dsm5.pdf"} {"id": "9ff6454e36a6-0", "page_content": "mistakes. Individuals with this disorder are rigidly deferential to authority and rules and\ninsist on quite literal compliance, with no ru le bending for extenuating circumstances. For\nexample, the individual will not lend a quarte r to a friend who needs one to make a tele-\nphone call because \u201cneither a borrower nor a le nder be\u201d or because it would be \u201cbad\u201d for", "source": "dsm5.pdf"} {"id": "568c04f0fed7-0", "page_content": "680 Personality Disorders\nthe person\u2019s character. These qualities should not be accounted for by the individual\u2019s cul-\ntural or religious identification.\nIndividuals with this disorder may be unable to discard worn-out or worthless objects,\neven when they have no sentimental value (C riterion 5). Often these individuals will ad-\nmit to being \u201cpack rats.\u201d They regard discar ding objects as wastef ul because \u201cyou never\nknow when you might need something\u201d and will become upset if someone tries to get rid of\nthe things they have saved. Their spouses or roommates may complain about the amount of\nspace taken up by old parts, magazines, broken appliances, and so on. \nIndividuals with obsessive-compulsive pers onality disorder are reluctant to delegate\ntasks or to work with others (Criterion 6). They stubbornly and unreasonably insist that\neverything be done their way and that people conform to their way of doing things. They\noften give very detaile d instructions about how things should be done (e.g., there is one\nand only one way to mow the lawn, wash the dishes, build a doghouse) and are surprised\nand irritated if others suggest creative alternat ives. At other times they may reject offers of\nhelp even when behind schedule because th ey believe no one else can do it right.\nIndividuals with this disorder may be miserly and stingy and maintain a standard of\nliving far below what they can afford, believing that spending must be tightly controlled to\nprovide for future catastrophes (Criterion 7) . Obsessive-compulsive personality disorder\nis characterized by rigidity and stubbornness (Criterion 8). Individuals with this disorder\nare so concerned about having things done the one \u201ccorrect\u201d way that they have trouble\ngoing along with anyone else\u2019s ideas. These individuals plan ahead in meticulous detail", "source": "dsm5.pdf"} {"id": "568c04f0fed7-1", "page_content": "going along with anyone else\u2019s ideas. These individuals plan ahead in meticulous detail\nand are unwilling to consider changes. Totally wrapped up in their own perspective, they\nhave difficulty acknowledging the viewpoints of others. Friends and colleagues may be-\ncome frustrated by this constant rigidity. Even when individuals with obsessive-compul-\nsive personality disorder recognize that it may be in their interest to compromise, they\nmay stubbornly refuse to do so, arguing that it is \u201ct he principle of the thing.\u201d\nAssociated Features Supporting Diagnosis\nWhen rules and established procedures do not dictate the correct answer, decision making\nmay become a time-consuming, often painfu l process. Individuals with obsessive-\ncompulsive personality disorder may have such difficulty deciding which tasks take pri-\nority or what is the best way of doing some pa rticular task that they may never get started\non anything. They are prone to become upset or angry in situations in which they are not\nable to maintain control of their physical or interpersonal environment, although the an-\nger is typically not expressed di rectly. For example, an individual may be angry when ser-\nvice in a restaurant is poor, but instead of complaining to the management, the individual\nruminates about how much to leave as a tip. On other occasions, anger may be expressed\nwith righteous indignation over a seemingly minor matter. Individuals with this disorder\nmay be especially attentive to their relative status in dominance-submission relationships\nand may display excessive deference to an au thority they respect and excessive resistance\nto authority they do not respect.\nIndividuals with this disorder usually expres s affection in a highly controlled or stilted\nfashion and may be very uncomfortable in the presence of others who are emotionally ex-\npressive. Their everyday relationships have a formal and serious quality, and they may be", "source": "dsm5.pdf"} {"id": "568c04f0fed7-2", "page_content": "pressive. Their everyday relationships have a formal and serious quality, and they may be\nstiff in situations in which others would smile and be happy (e.g., greeting a lover at the\nairport). They carefully hold th emselves back until they are sure that whatever they say\nwill be perfect. They may be preoccupied with logic and intellect, and intolerant of affec-", "source": "dsm5.pdf"} {"id": "3e95fc110f4c-0", "page_content": "airport). They carefully hold th emselves back until they are sure that whatever they say\nwill be perfect. They may be preoccupied with logic and intellect, and intolerant of affec-\ntive behavior in others. They often have diffi culty expressing tender feelings, rarely pay-\ning compliments. Individuals with this disord er may experience occupational difficulties\nand distress, particularly when confronted with new situat ions that demand flexibility\nand compromise.\nIndividuals with anxiety disorders, including generalized anxiety disorder, social anx-\niety disorder (social phobia), and specific pho bias, and obsessive-compulsive disorder (OCD)", "source": "dsm5.pdf"} {"id": "660217b7611b-0", "page_content": "Obsessive-Compulsive Personality Disorder 681\nhave an increased likelihood of having a person ality disturbance that meets criteria for ob-\nsessive-compulsive personality disorder. Even so , it appears that the majority of individ-\nuals with OCD do not have a pattern of behavior that meets criteria for this personality\ndisorder. Many of the features of obsessive-compulsive pers onality disorder overlap with\n\u201ctype A\u201d personality characteristics (e.g., pr eoccupation with work, competitiveness, time\nurgency), and these features may be present in people at risk for myocardial infarction.\nThere may be an association between obsessiv e-compulsive personality disorder and de-\npressive and bipolar disorders and eating disorders.\nPrevalence\nObsessive-compulsive personalit y disorder is one of the mo st prevalent personality dis-\norders in the general population, with estimated prevalence ranging from 2.1% to 7.9%. \nCulture-Related Diagnostic Issues\nIn assessing an individual for obsessive-com pulsive personality disorder, the clinician\nshould not include those behaviors that reflect habits, customs, or interpersonal styles that\nare culturally sanctioned by the individual\u2019s reference group. Certain cultures place sub-\nstantial emphasis on work and productivity; the resulting behaviors in members of those\nsocieties need not be considered indications of obsessive-compulsive personality disorder.\nGender-Related Diagnostic Issues\nIn systematic studies, obsessiv e-compulsive personality disord er appears to be diagnosed\nabout twice as often among males.\nDifferential Diagnosis\nObsessive-compulsive disorder. Despite the similarity in names, OCD is usually easily\ndistinguished from obsessive-comp ulsive personality disorder by the presence of true ob-\nsessions and compulsions in OCD. When crit eria for both obsessive-compulsive person-\nality disorder and OCD are met, bo th diagnoses should be recorded.", "source": "dsm5.pdf"} {"id": "660217b7611b-1", "page_content": "ality disorder and OCD are met, bo th diagnoses should be recorded.\nHoarding disorder. A diagnosis of hoarding disorder should be considered especially\nwhen hoarding is extreme (e.g., accumulated st acks of worthless objects present a fire haz-\nard and make it difficult for others to walk through the house). When criteria for both ob-\nsessive-compulsive personality disorder and ho arding disorder are met, both diagnoses\nshould be recorded. \nOther personality disorder s and personality traits. Other personality disorders may\nbe confused with obsessive-compulsive person ality disorder because they have certain\nfeatures in common. It is, therefore, important to distingu ish among these disorders based\non differences in their characteristic features. However, if an individual has personality\nfeatures that meet criteria for one or more personality disorders in addition to obsessive-\ncompulsive personality disorder, all can be diagnosed. Individuals with narcissistic per-\nsonality disorder may also profess a commitmen t to perfectionism and believe that others\ncannot do things as well, but these individuals are more likely to believe that they have\nachieved perfection, whereas those with obse ssive-compulsive personality disorder are\nusually self-critical. Individuals with narcissi stic or antisocial personality disorder lack\ngenerosity but will indulge themselves, wher eas those with obsessive-compulsive person-\nality disorder adopt a miserly spending style toward both self and others. Both schizoid\npersonality disorder and obsessive-compulsive personality disorder may be characterized\nby an apparent formality and social detachme nt. In obsessive-compulsive personality dis-\norder, this stems from discomfort with emot ions and excessive devotion to work, whereas\nin schizoid personality disorder there is a fundamental lack of capacity for intimacy.", "source": "dsm5.pdf"} {"id": "fde9e2d13ad0-0", "page_content": "682 Personality Disorders\nObsessive-compulsive personality traits in moderation may be espe cially adaptive, par-\nticularly in situations that reward high perfor mance. Only when these traits are inflexible,\nmaladaptive, and persisting and cause significa nt functional impairment or subjective dis-\ntress do they constitute obsessive-compulsive personality disorder.\nPersonality change due to another medical condition. Obsessive-compulsive person-\nality disorder must be distin guished from personality change due to another medical con-\ndition, in which the traits emerge attributable to the effects of another medical condition\non the central nervous system.\nSubstance use disorders. Obsessive-compulsive personality disorder must also be dis-\ntinguished from symptoms that may develop in association with persistent substance use.\nOther Personality Disorders\nPersonality Change\n Due to Another Medical Condition\nDiagnostic Criteria 310.1 (F07.0)\nA. A persistent personality disturbance that represents a change from the individual\u2019s pre-\nvious characteristic personality pattern.\nNote: In children, the disturbance involves a marked deviation from normal devel-\nopment or a significant change in the child\u2019s usual behavior patterns, lasting at least\n1 year.\nB. There is evidence from the history, physical examination, or laboratory findings that the\ndisturbance is the direct pathophysiological consequence of another medical condition. \nC. The disturbance is not better explained by another mental disorder (including another\nmental disorder due to another medical condition).\nD. The disturbance does not occur exclusively during the course of a delirium.\nE. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nSpecify whether:\nLabile type: If the predominant feature is affective lability.\nDisinhibited type: If the predominant feature is poor impulse control as evidenced by", "source": "dsm5.pdf"} {"id": "fde9e2d13ad0-1", "page_content": "Disinhibited type: If the predominant feature is poor impulse control as evidenced by\nsexual indiscretions, etc.\nAggressive type: If the predominant feature is aggressive behavior.\nApathetic type: If the predominant feature is marked apathy and indifference.\nParanoid type: If the predominant feature is suspiciousness or paranoid ideation.\nOther type: If the presentation is not characterized by any of the above subtypes.\nCombined type: If more than one feature predominates in the clinical picture.\nUnspecified type\nCoding note: Include the name of the other medical condition (e.g., 310.1 [F07.0] person-\nality change due to temporal lobe epilepsy). The other medical condition should be coded\nand listed separately immediately before the personality disorder due to another medical\ncondition (e.g., 345.40 [G40.209] temporal lobe epilepsy; 310.1 [F07.0] personality\nchange due to temporal lobe epilepsy).", "source": "dsm5.pdf"} {"id": "82ef357811f4-0", "page_content": "Personality Change Due to Another Medical Condition 683\nSubtypes\nThe particular personality change can be sp ecified by indicating the symptom presenta-\ntion that predominates in the clinical presentation.\nDiagnostic Features\nThe essential feature of a personality change due to another medical condition is a persis-\ntent personality disturbance that is judged to be due to the direct pathophysiological ef-\nfects of a medical condition. The personality disturbance represents a change from the\nindividual\u2019s previous characteristic personalit y pattern. In children , this condition may be\nmanifested as a marked deviat ion from normal development rather than as a change in a\nstable personality pattern (Criterion A). There must be evidence from the history, physical\nexamination, or laboratory findings that the personality change is the direct physiological\nconsequence of another medical condition (Crite rion B). The diagnosis is not given if the\ndisturbance is better explained by another ment al disorder (Criterion C). The diagnosis is\nnot given if the disturbance occurs exclusively during the course of a delirium (Criterion\nD). The disturbance must also ca use clinically significant distress or impairment in social,\noccupational, or other important areas of functioning (Criterion E).\nCommon manifestations of the personality change include affective instability, poor\nimpulse control, ou tbursts of aggression or rage grossly out of proportion to any precipi-\ntating psychosocial stressor, marked apathy , suspiciousness, or paranoid ideation. The\nphenomenology of the change is indicated using the subtypes listed in the criteria set. An\nindividual with the disorder is often characte rized by others as \u201cnot himself [or herself].\u201d\nAlthough it shares the term \u201cpersonality\u201d with the other personality disorders, this diag-\nnosis is distinct by virtue of its specific et iology, different phenome nology, and more vari-", "source": "dsm5.pdf"} {"id": "82ef357811f4-1", "page_content": "able onset and course.\nThe clinical presentation in a given individual may depend on the nature and localiza-\ntion of the pathological process. For example, injury to the frontal lobes may yield symp-\ntoms such as lack of judgment or foresight, facetiousness, disinhibition, and euphoria.\nRight hemisphere strokes have often been shown to evoke personal ity changes in asso-\nciation with unilateral spatial neglect, anos ognosia (i.e., inability of the individual to\nrecognize a bodily or functional deficit, such as the existence of hemiparesis), motor im-\npersistence, and other ne urological deficits.\nAssociated Features Supporting Diagnosis\nA variety of neurological and other medica l conditions may cause personality changes,\nincluding central nervous system neoplasm s, head trauma, cerebrovascular disease,\nHuntington\u2019s disease, epilepsy, infectious conditions with central nervous system in-\nvolvement (e.g., HIV), endocrine conditions (e.g., hypothyroidism, hypo- and hyperadre-\nnocorticism), and autoimmune conditions with central nerv ous system involvement (e.g.,\nsystemic lupus erythematosus). The associat ed physical examination findings, laboratory\nfindings, and patterns of preval ence and onset reflec t those of the neurological or other\nmedical condition involved.\nDifferential Diagnosis\nChronic medical conditions associ ated with pain and disability. Chronic medical con-\nditions associated with pain and disability can also be associated with changes in person-\nality. The diagnosis of personality change du e to another medical condition is given only\nif a direct pathophysiological mechanism can be established. This diagnosis is not given if\nthe change is due to a behavioral or psycholo gical adjustment or response to another med-\nical condition (e.g., dependent behaviors that result from a need for the assistance of others", "source": "dsm5.pdf"} {"id": "82ef357811f4-2", "page_content": "ical condition (e.g., dependent behaviors that result from a need for the assistance of others\nfollowing a severe head trauma, card iovascular disease , or dementia).", "source": "dsm5.pdf"} {"id": "a2fd75c4a5ab-0", "page_content": "684 Personality Disorders\nDelirium or major neurocognitive disorder. Personality change is a frequently associated\nfeature of a delirium or major neurocognitive disorder. A separate diagnosis of personal-\nity change due to another medical condition is not given if the change occurs exclusively\nduring the course of a delirium. However, the diagnosis of personality change due to an-\nother medical condition may be given in additi on to the diagnosis of major neurocognitive\ndisorder if the personality change is a prom inent part of the clinical presentation.\nAnother mental disorder due to another medical condition. The diagnosis of person-\nality change due to another medical condition is not given if the disturbance is better ex-\nplained by another mental disorder due to another medical condition (e.g., depressive\ndisorder due to brain tumor).\nSubstance use disorders. Personality changes may also occur in the context of substance\nuse disorders, especially if the disorder is long -standing. The clinician should inquire carefully\nabout the nature and extent of substance use. If th e clinician wishes to indicate an etiological re-\nlationship between the personality change and su bstance use, the unspecified category for the\nspecific substance (e.g., unspecified st imulant-related disorder) can be used.\nOther mental disorders. Marked personality changes may also be an associated feature\nof other mental disorders (e.g., schizophrenia ; delusional disorder; depressive and bipolar\ndisorders; other specified and unspecified disruptive behavior, impulse-control, and con-\nduct disorders; panic disorder). However, in these disorders, no specific physiological fac-\ntor is judged to be et iologically related to the personality change.\nOther personality disorders. Personality change due to another medical condition can\nbe distinguished from a persona lity disorder by the requirement for a clinically significant\nchange from baseline personality functioning and the presence of a specific etiological\nmedical condition.", "source": "dsm5.pdf"} {"id": "a2fd75c4a5ab-1", "page_content": "change from baseline personality functioning and the presence of a specific etiological\nmedical condition.\nOther Specified Personality Disorder\n301.89 (F60.89)\nThis category applies to presentations in which symptoms characteristic of a personality\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the personality disorders diagno stic class. The other specified personality\ndisorder category is used in situations in which the clinician chooses to communicate the\nspecific reason that the presentation does not meet the criteria for any specific personality\ndisorder. This is done by recording \u201cother specified personality disorder\u201d followed by the\nspecific reason (e.g., \u201cmixed personality features\u201d).\nUnspecified Personality Disorder\n301.9 (F60.9)\nThis category applies to presentations in which symptoms characteristic of a personality\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the personality disorders diagnostic class. The unspecified personality\ndisorder category is used in situations in which the clinician chooses not to specify the rea-\nson that the criteria are not met for a specific personality disorder, and includes presenta-\ntions in which there is insufficient information to make a more specific diagnosis.", "source": "dsm5.pdf"} {"id": "68b44a7c3f28-0", "page_content": "685Paraphilic\n Disorders\nParaphilic disorders included in this manual are voyeuristic disorder (spying on\nothers in private activities), exhibitionisti c disorder (exposing th e genitals), frotteuristic\ndisorder (touching or rubbin g against a nonconsenting individual), sexual masochism\ndisorder (undergoing humiliation , bondage, or suffering), se xual sadism disorder (inflict-\ning humiliation, bondage, or suffering), pedophilic disorder (sexual focus on children), fe-\ntishistic disorder (using nonliv ing objects or having a highly specific focus on nongenital\nbody parts), and transvestic disorder (engaging in sexua lly arousing cross-dressing).\nThese disorders have tr aditionally been selected for specific listing and assignment of ex-\nplicit diagnostic criteria in DSM for two main reasons: they are relatively common, in re-\nlation to other paraphilic disorders, and some of them entail actions for their satisfaction\nthat, because of their noxiousness or potentia l harm to others, are classed as criminal of-\nfenses. The eight listed disorders do not exha ust the list of possible paraphilic disorders.\nMany dozens of distinct paraphilias have be en identified and named, and almost any of\nthem could, by virtue of its negative consequences for the individual or for others, rise to\nthe level of a paraphilic disorder. The diagno ses of the other specified and unspecified\nparaphilic disorders are therefore indispensable and will be required in many cases.\nIn this chapter, the order of presentation of the listed paraphilic disorders generally\ncorresponds to common classification scheme s for these conditions. The first group of\ndisorders is based on anomalous activi ty preferences. These disorders are subdivided into", "source": "dsm5.pdf"} {"id": "68b44a7c3f28-1", "page_content": "disorders is based on anomalous activi ty preferences. These disorders are subdivided into\ncourtship disorders, which resemble distorted components of human courtship behavior\n(voyeuristic disorder, exhibitionistic di sorder, and frotteuristic disorder), and algolagnic\ndisorders, which involve pain and suffering (sexual masochism disorder and sexual sadism\ndisorder). The second group of disorders is based on anomalous target preferences. These\ndisorders include one directed at other hu mans (pedophilic disorder) and two directed\nelsewhere (fetishistic disorder and tran svestic disorder).\nThe term paraphilia denotes any intense and persistent sexual interest other than sexual\ninterest in genital stimulation or preparator y fondling with phenotypically normal, phys-\nically mature, consenting human partners. In some circumstances, the criteria \u201cintense\nand persistent\u201d may be difficult to apply, su ch as in the assessment of persons who are\nvery old or medically ill and who may not have \u201cintense\u201d sexual interests of any kind. In\nsuch circumstances, the term paraphilia may be defined as any sexual interest greater than\nor equal to normophilic sexual interests. There are also spec ific paraphilias that are gen-\nerally better described as preferential sexual interests than as intense sexual interests.\nSome paraphilias primarily concern the indivi dual\u2019s erotic activities, and others pri-\nmarily concern the individual\u2019s erotic targets. Examples of the former would include in-\ntense and persistent interests in spanking, whipping, cutting, binding, or strangulating\nanother person, or an interest in these activiti es that equals or exceeds the individual\u2019s in-\nterest in copulation or equivalent interaction with another person. Examples of the latter", "source": "dsm5.pdf"} {"id": "68b44a7c3f28-2", "page_content": "terest in copulation or equivalent interaction with another person. Examples of the latter\nwould include intense or preferential sexual in terest in children, corp ses, or amputees (as\na class), as well as intense or preferential in terest in nonhuman animals, such as horses or\ndogs, or in inanimate obje cts, such as shoes or articles made of rubber.\nA paraphilic disorder is a paraphilia that is currently causing distress or impairment to the\nindividual or a paraphilia whose satisfaction has entailed personal harm, or risk of harm, to", "source": "dsm5.pdf"} {"id": "745744b42c05-0", "page_content": "686 Paraphilic Disorders\nothers. A paraphilia is a necessary but not a sufficient condition for having a paraphilic dis-\norder, and a paraphilia by itself does not nece ssarily justify or require clinical intervention.\nIn the diagnostic criteria set for each of the listed paraphilic disorder s, Criterion A specifies\nthe qualitative nature of the paraphilia (e.g., an erotic focus on children or on exposing the gen-\nitals to strangers), and Criterio n B specifies the negative conseq uences of the paraphilia (i.e.,\ndistress, impairment, or harm to others). In keeping with the distinction between paraphilias\nand paraphilic disorders, the term diagnosis should be reserved for individuals who meet both\nCriteria A and B (i.e., individuals who have a pa raphilic disorder). If an individual meets Cri-\nterion A but not Criterion B for a particular paraphilia\u2014a circumstance that might arise when\na benign paraphilia is discovered during the clinical investigation of some other condition\u2014\nthen the individual may be said to have that paraphilia but not a paraphilic disorder.\nIt is not rare for an individual to manifest tw o or more paraphilias. In some cases, the para-\nphilic foci are closely related and the connectio n between the paraphilias is intuitively com-\nprehensible (e.g., foot fetishism and shoe fetish ism). In other cases, th e connection between the\nparaphilias is not obvious, and the presence of mu ltiple paraphilias may be coincidental or else\nrelated to some generalized vulnerability to an omalies of psychosexual development. In any\nevent, comorbid diagnoses of separate paraphil ic disorders may be warranted if more than\none paraphilia is causing suffering to the individual or harm to others.", "source": "dsm5.pdf"} {"id": "745744b42c05-1", "page_content": "one paraphilia is causing suffering to the individual or harm to others.\nBecause of the two-pronged nature of diag nosing paraphilic disorders, clinician-rated\nor self-rated measures and se verity assessments could addre ss either the strength of the\nparaphilia itself or the seriousness of its co nsequences. Although the distress and impair-\nment stipulated in the Criterio n B are special in being the im mediate or ultimate result of\nthe paraphilia and not primarily the result of some other factor, the phenomena of reactive\ndepression, anxiety, guilt, poor work history, impaired social relations, and so on are not\nunique in themselves and may be quantified with multipurpose measures of psychosocial\nfunctioning or quality of life.\nThe most widely applicable framework for assessing the strength of a paraphilia itself\nis one in which examinees\u2019 paraphilic sexual fa ntasies, urges, or beha viors are evaluated in\nrelation to their normophilic sexual interests and behaviors. In a clinical interview or on\nself-administered questionnair es, examinees can be asked whether their paraphilic sexual\nfantasies, urges, or behaviors are weaker th an, approximately equal to, or stronger than\ntheir normophilic sexual intere sts and behaviors. This same type of comparison can be,\nand usually is, employed in psychophysiological measures of sexual interest, such as pe-\nnile plethysmography in males or viewing time in males and females.\nVoyeuristic Disorder\nDiagnostic Criteria 302.82 (F65.3)\nA. Over a period of at least 6 months, recurrent and intense sexual arousal from observ-\ning an unsuspecting person who is naked, in the process of disrobing, or engaging in\nsexual activity, as manifested by fantasies, urges, or behaviors.", "source": "dsm5.pdf"} {"id": "745744b42c05-2", "page_content": "sexual activity, as manifested by fantasies, urges, or behaviors. \nB. The individual has acted on these sexual urges with a nonconsenting person, or the\nsexual urges or fantasies cause clinically significant distress or impairment in social,\noccupational, or other important areas of functioning.\nC. The individual experiencing the arousal and/or acting on the urges is at least 18 years\nof age.\nSpecify if:\nIn a controlled environment: This specifier is primarily applicable to individuals living\nin institutional or other settings where opportunities to engage in voyeuristic behavior\nare restricted.", "source": "dsm5.pdf"} {"id": "81a3981a64ba-0", "page_content": "Voyeuristic Disorder 687\nIn full remission: The individual has not acted on the urges with a nonconsenting per-\nson, and there has been no distress or impairment in social, occupational, or other ar-\neas of functioning, for at least 5 years while in an uncontrolled environment.\nSpecifiers\nThe \u201cin full remission\u201d specifier does not address the continued presence or absence of\nvoyeurism per se, which may still be present af ter behaviors and dist ress have remitted. \nDiagnostic Features\nThe diagnostic criteria for voyeuristic disorder can apply both to individuals who more or less\nfreely disclose this paraphilic interest and to those who categorically deny any sexual arousal\nfrom observing an unsuspecting person who is na ked, disrobing, or engaged in sexual activity\ndespite substantial objective evidence to the cont rary. If disclosing individuals also report dis-\ntress or psychosocial problems because of thei r voyeuristic sexual pref erences, they could be\ndiagnosed with voyeuristic disorder. On the ot her hand, if they declare no distress, demon-\nstrated by lack of anxiety, obse ssions, guilt, or shame, about these paraphilic impulses and are\nnot impaired in other im portant areas of functioning because of this sexual interest, and their\npsychiatric or legal histories indicate that they do not act on it, they could be ascertained as\nhaving voyeuristic sexual interest but should not be diagnosed with voyeuristic disorder. \nNondisclosing individuals include, for example, individuals known to have been spy-\ning repeatedly on unsuspecting persons who ar e naked or engaging in sexual activity on\nseparate occasions but who deny any urges or fantasies concerning such sexual behavior,\nand who may report that known episodes of wa tching unsuspecting naked or sexually ac-", "source": "dsm5.pdf"} {"id": "81a3981a64ba-1", "page_content": "and who may report that known episodes of wa tching unsuspecting naked or sexually ac-\ntive persons were all accidental and nonsexual. Others may disclose past episodes of ob-\nserving unsuspecting naked or sexually ac tive persons but contest any significant or\nsustained sexual interest in this behavior. Since these individuals deny having fantasies or\nimpulses about watching others nude or involv ed in sexual activity, it follows that they\nwould also reject feeling subjectively distressed or socially impaired by such impulses. De-\nspite their nondisclosing stance, such individuals may be diagnosed with voyeuristic dis-\norder. Recurrent voyeuristic behavior cons titutes sufficient suppo rt for voyeurism (by\nfulfilling Criterion A) and simult aneously demonstrates that this paraphilically motivated\nbehavior is causing harm to ot hers (by fulfilling Criterion B).\n\u201cRecurrent\u201d spying on unsuspecting persons who are naked or engaging in sexual ac-\ntivity (i.e., multiple victims, each on a separate oc casion) may, as a general rule, be inter-\npreted as three or more victim s on separate occasions. Fewer victims can be interpreted as\nsatisfying this criterion if there were multiple occasions of watching the same victim or if\nthere is corroborating evidence of a distinct or preferential interest in secret watching of\nnaked or sexually acti ve unsuspecting persons. Note th at multiple victims, as suggested\nearlier, are a sufficient but not a necessary cond ition for diagnosis; the criteria may also be\nmet if the individual acknowledges intense voyeuristic sexual interest. \nThe Criterion A time frame, indicating that signs or symptoms of voyeurism must have\npersisted for at least 6 months , should also be understood as a general guideline, not a\nstrict threshold, to ensure that the sexual in terest in secretly watching unsuspecting naked", "source": "dsm5.pdf"} {"id": "81a3981a64ba-2", "page_content": "strict threshold, to ensure that the sexual in terest in secretly watching unsuspecting naked\nor sexually active others is not merely transient. \nAdolescence and puberty generally increase sexual curiosity and activity. To alleviate\nthe risk of pathologizing normative sexual in terest and behavior during pubertal adoles-\ncence, the minimum age for the diagnosis of voye uristic disorder is 18 years (Criterion C).\nPrevalence\nVoyeuristic acts are the most common of pote ntially law-breaking sexual behaviors. The", "source": "dsm5.pdf"} {"id": "c297cf07d384-0", "page_content": "cence, the minimum age for the diagnosis of voye uristic disorder is 18 years (Criterion C).\nPrevalence\nVoyeuristic acts are the most common of pote ntially law-breaking sexual behaviors. The\npopulation prevalence of voyeuristic disorder is unknown. However, based on voyeuris-", "source": "dsm5.pdf"} {"id": "021e622d6524-0", "page_content": "688 Paraphilic Disorders\ntic sexual acts in nonclinical samples, the highest possible lifetime prevalence for voyeuris-\ntic disorder is approximately 12% in males and 4% in females.\nDevelopment and Course\nAdult males with voyeuristic disorder often first become aware of their sexual interest in\nsecretly watching unsuspecti ng persons during adolescence. However, the minimum age\nfor a diagnosis of voyeuristic disorder is 18 years because there is substantial difficulty in\ndifferentiating it from age-appropriate pubert y-related sexual curiosity and activity. The\npersistence of voyeurism over time is unclear. Voyeuristic disorder, however, per defini-\ntion requires one or more contributing factors that may change over time with or without\ntreatment: subjective distress (e.g., guilt, sh ame, intense sexual fr ustration, loneliness),\npsychiatric morbidity, hypersex uality, and sexual impulsivit y; psychosocial impairment;\nand/or the propensity to act out sexually by spying on unsuspecting naked or sexually ac-\ntive persons. Therefore, the course of voyeuristic disorder is likely to vary with age.\nRisk and Prognostic Factors\nTemperamental. Voyeurism is a necessary precondition for voyeuristic disorder; hence,\nrisk factors for voyeurism sh ould also increase the rate of voyeuristic disorder.\nEnvironmental. Childhood sexual abuse, substance misuse, and sexual preoccupation/\nhypersexuality have been suggested as risk fa ctors, although the causal relationship to\nvoyeurism is uncertain and the specificity unclear. \nGender-Related Diagnostic Issues\nVoyeuristic disorder is very uncommon among females in clinical settings, while the male-\nto-female ratio for single sexually ar ousing voyeuristic acts might be 3:1.\nDifferential Diagnosis\nConduct disorder and antiso cial personality disorder. Conduct disorder in adolescents", "source": "dsm5.pdf"} {"id": "021e622d6524-1", "page_content": "Differential Diagnosis\nConduct disorder and antiso cial personality disorder. Conduct disorder in adolescents\nand antisocial personality disorder would be characterized by additional norm-breaking\nand antisocial behaviors, and the specific sexual interest in secretly watching unsuspect-\ning others who are naked or engaging in sexual activity should be lacking. \nSubstance use disorders. Substance use disorders might involve single voyeuristic ep-\nisodes by intoxicated individuals but should no t involve the typical sexual interest in se-\ncretly watching unsuspecting persons being na ked or engaging in sexual activity. Hence,\nrecurrent voyeuristic sexual fantasies, urges, or behaviors that occu r also when the indi-\nvidual is not intoxicated suggest that voyeuristic disorder might be present.\nComorbidity\nKnown comorbidities in voyeur istic disorder are largely b ased on research with males\nsuspected of or convicted for acts involving the secret watching of unsuspecting nude or\nsexually active persons. Hence, these comorb idities might not apply to all individuals with\nvoyeuristic disorder. Conditions that occur comorbidly with voyeuristic disorder include\nhypersexuality and other paraphilic disorders, particularly exhibitionistic disorder. De-\npressive, bipolar, anxiety, an d substance use disorders; a ttention-deficit/hyperactivity\ndisorder; and conduct disorder and antisocial personality disorder ar e also frequent co-\nmorbid conditions.", "source": "dsm5.pdf"} {"id": "8e1587d23c41-0", "page_content": "Exhibitionistic Disorder 689\nExhibitionistic Disorder\nDiagnostic Criteria 302.4 (F65.2)\nA. Over a period of at least 6 months, recurrent and intense sexual arousal from the ex-\nposure of one\u2019s genitals to an unsuspecting person, as manifested by fantasies, urges,\nor behaviors. \nB. The individual has acted on these sexual urges with a nonconsenting person, or the\nsexual urges or fantasies cause clinically significant distress or impairment in social,\noccupational, or other important areas of functioning.\nSpecify whether:\nSexually aroused by exposing ge nitals to prepubertal children\nSexually aroused by exposing genitals to physically mature individuals\nSexually aroused by exposing genitals to prepubertal children and to physically\nmature individuals\nSpecify if:\nIn a controlled environment: This specifier is primarily applicable to individuals living in\ninstitutional or other settings where opportunities to expose one\u2019s genitals are restricted.\nIn full remission: The individual has not acted on the urges with a nonconsenting per-\nson, and there has been no distress or impairment in social, occupational, or other ar-\neas of functioning, for at least 5 years while in an uncontrolled environment.\nSubtypes\nThe subtypes for exhibitionistic disorder are ba sed on the age or physical maturity of the non-\nconsenting individuals to whom the individual prefers to expose his or her genitals. The non-\nconsenting individuals could be prepubescent children, adults, or both. This specifier should\nhelp draw adequate attention to characteristics of victims of individuals with exhibitionistic\ndisorder to prevent co-occurring pedophilic di sorder from be ing overlooked. However, indi-\ncations that the individual with exhibitionistic disorder is\u00a0sexually attracted to exposing his or", "source": "dsm5.pdf"} {"id": "8e1587d23c41-1", "page_content": "cations that the individual with exhibitionistic disorder is\u00a0sexually attracted to exposing his or\nher genitals to children should not preclude a diagnosis of pedophilic disorder.\nSpecifiers\nThe \u201cin full remission\u201d specifier does not addr ess the continued presence or absence of ex-\nhibitionism per se, which may still be present after behaviors and distress have remitted. \nDiagnostic Features\nThe diagnostic criteria for exhibitionistic diso rder can apply both to individuals who more or\nless freely disclose this paraphilia and to those who categorically deny any sexual attraction to\nexposing their genitals to unsuspecting persons despite substantial objective evidence to the\ncontrary. If disclosing individuals also report ps ychosocial difficulties because of their sexual\nattractions or preferences for exposing, they ma y be diagnosed with exhibitionistic disorder. In\ncontrast, if they declare no distress (exemplified by absence of anxiety, obsessions, and guilt or\nshame about these paraphilic impulses) and are not impaired by this sexual interest in other\nimportant areas of functioning, and their self-rep orted, psychiatric, or legal histories indicate\nthat they do not act on them, they could be asce rtained as having exhibi tionistic sexual interest\nbut not be diagnosed with exhibitionistic disorder. \nExamples of nondisclosing individuals in clude those who have exposed themselves\nrepeatedly to unsuspecting persons on separa te occasions but who deny any urges or fan-", "source": "dsm5.pdf"} {"id": "464a9ef5dfac-0", "page_content": "690 Paraphilic Disorders\ntasies about such sexual behavior and who re port that known episodes of exposure were\nall accidental and nonsexual. Others may disclo se past episodes of sexual behavior involv-\ning genital exposure but refute any significant or sustained sexual interest in such behav-\nior. Since these individuals deny having urge s or fantasies involving genital exposure, it\nfollows that they would also deny feeling subjectively distressed or socially impaired by\nsuch impulses. Such individuals may be diagnosed with exhibitionistic disorder despite\ntheir negative self-report. Re current exhibitionistic behavior constitutes sufficient support\nfor exhibitionism (Criterion A) and simultaneously demonstrat es that this paraphilically\nmotivated behavior is causing harm to others (Criterion B).\n\u201cRecurrent\u201d genital exposure to unsuspecting others (i.e., multiple victims, each on a\nseparate occasion) may, as a ge neral rule, be interpreted as three or more victims on sep-\narate occasions. Fewer victims can be interpreted as satisfying this criterion if there were\nmultiple occasions of exposure to the same victim, or if th ere is corroborating evidence of\na strong or preferential interest in genital exposure to unsuspecting persons. Note that\nmultiple victims, as suggested earlier, are a sufficient but not a necessary condition for di-\nagnosis, as criteria may be met by an indi vidual\u2019s acknowledging intense exhibitionistic\nsexual interest with distress and/or impairment.\nThe Criterion A time frame, indicating that signs or sy mptoms of exhibitionism must\nhave persisted for at least 6 months, should also be understo od as a general guideline, not\na strict threshold, to ensure that the sexual interest in exposing one\u2019s genitals to unsuspect-\ning others is not merely transient. This migh t be expressed in clear evidence of repeated\nbehaviors or distress ov er a nontransient period shorter than 6 months.", "source": "dsm5.pdf"} {"id": "464a9ef5dfac-1", "page_content": "behaviors or distress ov er a nontransient period shorter than 6 months. \nPrevalence\nThe prevalence of exhibitionistic disorder is unknown. However, based on exhibitionistic\nsexual acts in nonclinical or general populati ons, the highest possible prevalence for exhi-\nbitionistic disorder in the male population is 2%\u20134%. The prevalence of exhibitionistic dis-\norder in females is even more uncertain but is generally believed to be much lower than in\nmales. \nDevelopment and Course\nAdult males with exhibitionistic disorder often report that they first became aware of sex-\nual interest in exposing their genitals to unsuspecting persons during adolescence, at a\nsomewhat later time than the typical development of normative sexual interest in women\nor men. Although there is no minimum age re quirement for the diagno sis of exhibitionis-\ntic disorder, it may be difficult to different iate exhibitionistic be haviors from age-appro-\npriate sexual curiosity in adolescents. Wher eas exhibitionistic impulses appear to emerge\nin adolescence or early adulthood, very little is known about persistence over time. By def-\ninition, exhibitionistic disord er requires one or more contributing factors, which may\nchange over time with or without treatment; subjective distress (e.g., guilt, shame, intense\nsexual frustration, lo neliness), mental disorder comorb idity, hypersexuality, and sexual\nimpulsivity; psychosocial impair ment; and/or the propensity to act out sexually by expos-\ning the genitals to unsuspecting persons. Ther efore, the course of exhibitionistic disorder\nis likely to vary with age. As with other sexual preferences, advancing age may be associ-\nated with decreasing exhibitionistic sexual preferences and behavior.\nRisk and Prognostic Factors\nTemperamental. Since exhibitionism is a necessary pr econdition for exhibitionistic dis-", "source": "dsm5.pdf"} {"id": "464a9ef5dfac-2", "page_content": "Temperamental. Since exhibitionism is a necessary pr econdition for exhibitionistic dis-\norder, risk factors for exhibiti onism should also increase the rate of exhibitionistic disor-\nder. Antisocial history, antisocial person ality disorder, alcohol misuse, and pedophilic\nsexual preference might increase risk of se xual recidivism in ex hibitionistic offenders.", "source": "dsm5.pdf"} {"id": "a824a02485f5-0", "page_content": "Frotteuristic Disorder 691\nHence, antisocial personality disorder, alco hol use disorder, and pedophilic interest may\nbe considered risk factors for exhibitionistic disorder in males with exhibitionistic sexual\npreferences.\nEnvironmental. Childhood sexual and emotional abus e and sexual preoccupation/hyper-\nsexuality have been suggested as risk factor s for exhibitionism, al though the causal rela-\ntionship to exhibitionism is unce rtain and the specificity unclear. \nGender-Related Diagnostic Issues\nExhibitionistic disorder is highly unusual in females, whereas single sexually arousing ex-\nhibitionistic acts might occur up to half as often among women compared with men.\nFunctional Consequences of Exhibitionistic Disorder\nThe functional consequences of exhibitionisti c disorder have not been addressed in re-\nsearch involving individuals who have not acte d out sexually by exposing their genitals to\nunsuspecting strangers but who fulfill Criterio n B by experiencing intense emotional dis-\ntress over these preferences.\nDifferential Diagnosis\nPotential differential diagnose s for exhibitionistic disorder sometimes occur also as co-\nmorbid disorders. Therefore, it is generally necessary to evaluate the evidence for exhibi-\ntionistic disorder and ot her possible conditions as separate questions. \nConduct disorder and antisocial personality disorder. Conduct disorder in adolescents\nand antisocial personality disorder would be characterized by additional norm-breaking and\nantisocial behaviors, and the specific sexual interest in exposing the genitals should be lacking. \nSubstance use disorders. Alcohol and substance use di sorders might involve single\nexhibitionistic episodes by intoxicated individuals but should not involve the typical sex-\nual interest in exposing the genitals to unsusp ecting persons. Hence, recurrent exhibition-\nistic sexual fantasies, urges, or behaviors that occur also when the individual is not\nintoxicated suggest that exhibitionistic disorder might be present.\nComorbidity", "source": "dsm5.pdf"} {"id": "a824a02485f5-1", "page_content": "intoxicated suggest that exhibitionistic disorder might be present.\nComorbidity\nKnown comorbidities in exhibitionistic disorder are largely based on research with indi-\nviduals (almost all males) convicted for criminal acts involving genital exposure to non-\nconsenting individuals. Hence, these comorbidities might not apply to all individuals who\nqualify for a diagnosis of exhibitionistic diso rder. Conditions that occur comorbidly with\nexhibitionistic disorder at high rates includ e depressive, bipolar, anxiety, and substance\nuse disorders; hypersexuality; attention-deficit/hyperactiv ity disorder; other paraphilic\ndisorders; and antisocial personality disorder. \nFrotteuristic Disorder\nDiagnostic Criteria 302.89 (F65.81)\nA. Over a period of at least 6 months, recurrent and intense sexual arousal from touching\nor rubbing against a nonconsenting person, as manifested by fantasies, urges, or be-\nhaviors.\nB. The individual has acted on these sexual urges with a nonconsenting person, or the\nsexual urges or fantasies cause clinically significant distress or impairment in social,\noccupational, or other important areas of functioning.", "source": "dsm5.pdf"} {"id": "ad37c0dddb4a-0", "page_content": "692 Paraphilic Disorders\nSpecify if:\nIn a controlled environment: This specifier is primarily applicable to individuals living\nin institutional or other settings where opportunities to touch or rub against a noncon-\nsenting person are restricted. \nIn full remission: The individual has not acted on the urges with a nonconsenting per-\nson, and there has been no distress or impairment in social, occupational, or other ar-\neas of functioning, for at least 5 years while in an uncontrolled environment.\nSpecifiers\nThe \u201cin remission\u201d specifier does not address the continued presence or absence of frot-\nteurism per se, which may still be present af ter behaviors and distress have remitted. \nDiagnostic Features\nThe diagnostic criteria for frotteuristic disord er can apply both to in dividuals who relatively\nfreely disclose this paraphilia and to those wh o firmly deny any sexual attraction from touch-\ning or rubbing against a nonconsenting individual regardless of considerable objective evi-\ndence to the contrary. If disclo sing individuals also report psychosocial impairment due to\ntheir sexual preferences for touching or ru bbing against a nonconsenting individual, they\ncould be diagnosed with frotteuristic disorder. In contrast, if they declare no distress (demon-\nstrated by lack of anxiety, ob sessions, guilt, or shame) about these paraphilic impulses and are\nnot impaired in other im portant areas of functioning because of this sexual interest, and their\npsychiatric or legal histories indicate that they do not act on it, they could be ascertained as\nhaving frotteuristic sexual interest but should not be diagnosed with frotteuristic disorder.\nNondisclosing individuals include, for in stance, individuals known to have been\ntouching or rubbing against nonconsenting individuals on separate occasions but who", "source": "dsm5.pdf"} {"id": "ad37c0dddb4a-1", "page_content": "touching or rubbing against nonconsenting individuals on separate occasions but who\ncontest any urges or fantasies concerning such sexual behavior. Such individuals may re-\nport that identified episodes of touching or rubbing against an unwilling individual were\nall unintentional and nonsexual. Others may disc lose past episodes of touching or rubbing\nagainst nonconsenting individuals but contest any major or persistent sexual interest in\nthis. Since these individuals deny having fant asies or impulses about touching or rubbing,\nthey would consequently reject feeling dist ressed or psychosocially impaired by such\nimpulses. Despite their nondisclosing position, such individuals may be diagnosed with\nfrotteuristic disorder. Recurrent frotteuristic behavior constitutes satisfactory support for\nfrotteurism (by fulfilling Criterion A) and co ncurrently demonstrates that this paraphili-\ncally motivated behavior is causing harm to others (by fulfilling Criterion B).\n\u201cRecurrent\u201d touching or rubbing against a no nconsenting individual (i.e., multiple vic-\ntims, each on a separate occasion) may, as a ge neral rule, be interpreted as three or more vic-\ntims on separate occasions. Fewer victims can be interpreted as satisfying this criterion if\nthere were multiple occasions of touching or rubbing agains t the same unwilling individ-\nual, or corroborating evidence of a strong or preferential interest in touching or rubbing\nagainst nonconsenting individuals. Note that mu ltiple victims are a sufficient but not a nec-\nessary condition for diagnosis; criteria may also be met if the individual acknowledges in-\ntense frotteuristic sexual inte rest with clinically significant distress and/or impairment. \nThe Criterion A time frame, indicating that si gns or symptoms of frotteurism must persist\nfor at least 6 months, should also be interpreted as a general guid eline, not a strict threshold, to", "source": "dsm5.pdf"} {"id": "ad37c0dddb4a-2", "page_content": "ensure that the sexual interest in touching or rubbing against a nonconsenting individual is not\ntransient. Hence, the duration part of Criterion A may also be met if there is clear evidence of\nrecurrent behaviors or distress over a shorter but nontrans ient time period. \nPrevalence", "source": "dsm5.pdf"} {"id": "97de5014054d-0", "page_content": "transient. Hence, the duration part of Criterion A may also be met if there is clear evidence of\nrecurrent behaviors or distress over a shorter but nontrans ient time period. \nPrevalence\nFrotteuristic acts, including the uninvited sexu al touching of or rubbing against another\nindividual, may occur in up to 30% of adult males in the general population. Approximately", "source": "dsm5.pdf"} {"id": "abb5a7940606-0", "page_content": "Frotteuristic Disorder 693\n10%\u201314% of adult males seen in outpatient se ttings for paraphilic disorders and hypersex-\nuality have a presentation that meets diagnost ic criteria for frotteuristic disorder. Hence,\nwhereas the population prev alence of frotteuristic disorder is unknown, it is not likely that\nit exceeds the rate found in selected clinical settings. \nDevelopment and Course\nAdult males with frotteuristic disorder often re port first becoming aware of their sexual in-\nterest in surreptitiously touching unsuspecting persons during late adolescence or emerging\nadulthood. However, children and adolescents may also touch or rub against unwilling oth-\ners in the absence of a diagnosis of frotteuris tic disorder. Although th ere is no minimum age\nfor the diagnosis, frotteuristic disorder can be difficult to di fferentiate from conduct-disor-\ndered behavior without sexual motivation in individuals at younger ages. The persistence of\nfrotteurism over time is unclear. Frotteuristic disorder, however, by de finition requires one\nor more contributing factors that may change over time with or without treatment: subjec-\ntive distress (e.g., guilt, shame, intense sexual frustration, loneliness); psychiatric morbidity;\nhypersexuality and sexual impulsivity; psycho social impairment; and/ or the propensity to\nact out sexually by touching or rubbing against unconsenting persons. Therefore, the course\nof frotteuristic disorder is like ly to vary with age. As with other sexual preferences, advanc-\ning age may be associated with decreasing fr otteuristic sexual preferences and behavior. \nRisk and Prognostic Factors\nTemperamental. Nonsexual antisocial behavior and sexual preoccupation/hypersexuality", "source": "dsm5.pdf"} {"id": "abb5a7940606-1", "page_content": "Temperamental. Nonsexual antisocial behavior and sexual preoccupation/hypersexuality\nmight be nonspecific risk factors, although the causal relationship to frotteurism is uncertain\nand the specificity unclear. However, frotteurism is a necessary precondition for frotteuristic\ndisorder, so risk factors for frot teurism should also increase the rate of frotteuristic disorder. \nGender-Related Diagnostic Issues\nThere appear to be substantially fewer female s with frotteuristic sexual preferences than\nmales. \nDifferential Diagnosis\nConduct disorder and antiso cial personality disorder. Conduct disorder in adolescents\nand antisocial personality disorder would be characterized by additional norm-breaking\nand antisocial behaviors, and the specific sexual interest in touching or rubbing against a\nnonconsenting individual should be lacking. \nSubstance use disorders. Substance use disorders, particularly those involving stimu-\nlants such as cocaine and amphetamines, might involve single frotteuristic episodes by in-\ntoxicated individuals but should not involve the typical sustained sexual interest in\ntouching or rubbing against unsuspecting persons. Hence, recurrent frotteuristic sexual\nfantasies, urges, or be haviors that occur also when the individual is not intoxicated sug-\ngest that frotteuristic d isorder might be present.\nComorbidity\nKnown comorbidities in frotteuristic disorder are largely based on research with males\nsuspected of or convicted for criminal acts involving sexually motivated touching of or\nrubbing against a nonconsentin g individual. Hence, these co morbidities might not apply\nto other individuals with a diagnosis of frotte uristic disorder based on subjective distress\nover their sexual interest. Conditions that o ccur comorbidly with frot teuristic disorder in-", "source": "dsm5.pdf"} {"id": "abb5a7940606-2", "page_content": "clude hypersexuality and other paraphilic disord ers, particularly exhibitionistic disorder\nand voyeuristic disorder. Conduct disorder, antisocial personality disorder, depressive", "source": "dsm5.pdf"} {"id": "7a15b3f0293d-0", "page_content": "694 Paraphilic Disorders\ndisorders, bipolar disorders, anxiety disorders, and substanc e use disorders also co-occur.\nPotential differential diagnoses for frotteuristic disorder so metimes occur also as comor-\nbid disorders. Therefore, it is generally necessary to evaluate the evidence for frotteuristic\ndisorder and possible comorbid co nditions as separate questions. \nSexual Masochism Disorder\nDiagnostic Criteria 302.83 (F65.51)\nA. Over a period of at least 6 months, recurrent and intense sexual arousal from the act\nof being humiliated, beaten, bound, or otherwise made to suffer, as manifested by fan-\ntasies, urges, or behaviors.\nB. The fantasies, sexual urges, or behaviors cause clinically significant distress or impair-\nment in social, occupational, or other important areas of functioning.\nSpecify if:\nWith asphyxiophilia: If the individual engages in the practice of achieving sexual\narousal related to restriction of breathing.\nSpecify if:\nIn a controlled environment: This specifier is primarily applicable to individuals living\nin institutional or other settings where opportunities to engage in masochistic sexual\nbehaviors are restricted.\nIn full remission: There has been no distress or impairment in social, occupational,\nor other areas of functioning for at last 5 years while in an uncontrolled environment.\nDiagnostic Features\nThe diagnostic criteria for sexual masochism disorder are intended to apply to individuals\nwho freely admit to having such paraphilic interests. Such individuals openly acknowl-\nedge intense sexual arousal from the act of being humiliated, beaten, bound, or otherwise\nmade to suffer, as manifested by fantasies, urges, or behaviors. If these individuals also re-\nport psychosocial difficulties because of thei r sexual attractions or preferences for being", "source": "dsm5.pdf"} {"id": "7a15b3f0293d-1", "page_content": "port psychosocial difficulties because of thei r sexual attractions or preferences for being\nhumiliated, beaten, bound, or otherwise made to suffer, they may be diagnosed with sex-\nual masochism disorder. In contrast, if they de clare no distress, exemplified by anxiety, ob-\nsessions, guilt, or shame, about these paraphi lic impulses, and are not hampered by them\nin pursuing other personal goals, they coul d be ascertained as having masochistic sexual\ninterest but should not be diagnosed with sexual masochism disorder.\nThe Criterion A time frame, indicating that the signs or symptoms of sexual masoch-\nism must have persisted for at least 6 months, should be understood as a general guideline,\nnot a strict threshold, to ensure that the sexual interest in being humiliated, beaten, bound,\nor otherwise made to suffer is not merely transient. However, the disorder can be diag-\nnosed in the context of a clearly sustained but shorter time period.\nAssociated Features Supporting Diagnosis\nThe extensive use of pornography involving the ac t of being humiliated, beaten, bound, or oth-\nerwise made to suffer is sometimes an asso ciated feature of sexual masochism disorder.\nPrevalence\nThe population prevalence of sexual masochis m disorder is unknown. In Australia, it has\nbeen estimated that 2.2% of males and 1.3% of females had been involved in bondage and\ndiscipline, sadomasochism, or dominance and submissio n in the past 12 months.", "source": "dsm5.pdf"} {"id": "fd43d4d30ee8-0", "page_content": "Sexual Sadism Disorder 695\nDevelopment and Course\nCommunity individuals with paraphilias have reported a mean age at onset for masoch-\nism of 19.3 years, although earlier ages, in cluding puberty and childhood, have also been\nreported for the onset of masochistic fantasi es. Very little is known about persistence over\ntime. Sexual masochism disorder per definition requires one or more contributing factors,\nwhich may change over time with or without treatment. These include subjective distress\n(e.g., guilt, shame, intense sexual frustration, loneliness), psychiatri c morbidity, hypersex-\nuality and sexual impulsivity, and psychosocial impairment. Therefore, the course of sex-\nual masochism disorder is likely to vary with age. Advancing age is likely to have the same\nreducing effect on sexual preference involvin g sexual masochism as it has on other para-\nphilic or normophilic sexual behavior. \nFunctional Consequences of Sexual Masochism Disorder\nThe functional consequences of sexual maso chism disorder are unknown. However, mas-\nochists are at risk of accidental death while practicing asphyxiophilia or other autoerotic\nprocedures. \nDifferential Diagnosis\nMany of the conditions that could be differ ential diagnoses for sexual masochism disorder\n(e.g., transvestic fetishism, sexual sadism di sorder, hypersexuality, alcohol and substance\nuse disorders) sometimes occur also as comorbid diagnoses. Therefore, it is necessary to\ncarefully evaluate the evidence for sexual masochism disorder, keep ing the possibility of\nother paraphilias or other mental disorders as part of the di fferential diagnosis. Sexual\nmasochism in the absence of distress (i.e., no disorder) is also includ ed in the differential,", "source": "dsm5.pdf"} {"id": "fd43d4d30ee8-1", "page_content": "as individuals who conduct the behaviors may be satisfied with thei r masochistic interest.\nComorbidity\nKnown comorbidities with sexu al masochism disorder are largely based on individuals in\ntreatment. Disorders that occur comorbidly wi th sexual masochism disorder typically in-\nclude other paraphilic disorders, such as transvestic fetishism.\nSexual Sadism Disorder\nDiagnostic Criteria 302.84 (F65.52)\nA. Over a period of at least 6 months, recurrent and intense sexual arousal from the phys-\nical or psychological suffering of another person, as manifested by fantasies, urges, or\nbehaviors.\nB. The individual has acted on these sexual urges with a nonconsenting person, or the\nsexual urges or fantasies cause clinically significant distress or impairment in social,\noccupational, or other important areas of functioning.\nSpecify if:\nIn a controlle d environment: This specifier is primarily applicable to individuals living\nin institutional or other settings where opportunities to engage in sadistic sexual behav-\niors are restricted.\nIn full remission: The individual has not acted on the urges with a nonconsenting per-\nson, and there has been no distress or impairment in social, occupational, or other ar-\neas of functioning, for at least 5 years while in an uncontrolled environment.", "source": "dsm5.pdf"} {"id": "66a6c678629f-0", "page_content": "696 Paraphilic Disorders\nDiagnostic Features\nThe diagnostic criteria for sexual sadism disord er are intended to apply both to individuals\nwho freely admit to having such paraphilic interests and to those who deny any sexual interest\nin the physical or psychological suffering of another individual despite substantial objective\nevidence to the contrary. Indivi duals who openly acknowledge in tense sexual interest in the\nphysical or psychological suffering of others are referred to as \u201cadmitting individuals.\u201d If these\nindividuals also report psychosocial difficulties because of their sexual attractions or prefer-\nences for the physical or psychological suffering of another individual, they may be diagnosed\nwith sexual sadism disorder. In contrast, if admitting individuals declare no distress, exempli-\nfied by anxiety, obsessions, gu ilt, or shame, about these para philic impulses, and are not ham-\npered by them in pursuing other goals, and thei r self-reported, psychiat ric, or legal histories\nindicate that they do not act on them, then they could be ascertained as having sadistic sexual\ninterest but they would not meet criteria for sexual sadism disorder.\nExamples of individuals who deny any interest in the physical or psychological suffering\nof another individual include in dividuals known to have inflicted pain or suffering on mul-\ntiple victims on separate occasions but who de ny any urges or fantasies about such sexual\nbehavior and who may further claim that known episodes of sexual assault were either un-\nintentional or nonsexual. Others may admit past episodes of sexual behavior involving the\ninfliction of pain or suffering on a nonconsenting individual but do not report any significant\nor sustained sexual interest in the physical or psychological suffering of another individual.\nSince these individuals deny having urges or fantasies involving sexual arousal to pain and\nsuffering, it follows that they would also deny feeling subjectively distressed or socially im-", "source": "dsm5.pdf"} {"id": "66a6c678629f-1", "page_content": "suffering, it follows that they would also deny feeling subjectively distressed or socially im-\npaired by such impulses. Such individuals may be diagnosed with sexual sadism disorder\ndespite their negative self-report. Their recurrent behavior constitutes clinical support for\nthe presence of the paraphilia of sexual sadi sm (by satisfying Criterion A) and simultane-\nously demonstrates that their paraphilically motivated behavior is causing clinically signif-\nicant distress, harm, or risk of harm to others (satisfying Criterion B).\n\u201cRecurrent\u201d sexual sadism invo lving nonconsenting others (i .e., multiple victims, each\non a separate occasion) may, as general rule , be interpreted as three or more victims on\nseparate occasions. Fewer victims can be interpre ted as satisfying this criterion, if there are\nmultiple instances of infliction of pain and su ffering to the same victim, or if there is cor-\nroborating evidence of a strong or preferential interest in pain and suffering involving\nmultiple victims. Note that multiple victims, as suggested earlier, are a sufficient but not\na necessary condition for diagnosis, as the crit eria may be met if the individual acknowl-\nedges intense sadistic sexual interest. \nThe Criterion A time frame, indicating that the signs or symptoms of sexual sadism\nmust have persisted for at least 6 months, should also be understood as a general guide-\nline, not a strict threshold, to ensure that the sexual interest in inflicting pain and suffering\non nonconsenting victims is not merely tran sient. However, the diagnosis may be met if\nthere is a clearly sustaine d but shorter period of sadistic behaviors. \nAssociated Features Supporting Diagnosis\nThe extensive use of pornography involving the inflic tion of pain and suffering is some-\ntimes an associated feature of sexual sadism disorder.", "source": "dsm5.pdf"} {"id": "66a6c678629f-2", "page_content": "times an associated feature of sexual sadism disorder.\nPrevalence\nThe population prevalence of sexual sadism disorder is unknown and is largely based on\nindividuals in forensic settings. Depending on the criteria for sexual sadism, prevalence", "source": "dsm5.pdf"} {"id": "414faa99d9a3-0", "page_content": "Prevalence\nThe population prevalence of sexual sadism disorder is unknown and is largely based on\nindividuals in forensic settings. Depending on the criteria for sexual sadism, prevalence\nvaries widely, from 2% to 30%. Among civi lly committed sexual offenders in the United\nStates, less than 10% have sexual sadism. Among individuals who have committed sexu-\nally motivated homicides, rates of sexual sadism disorder range from 37% to 75%.", "source": "dsm5.pdf"} {"id": "37e106bee657-0", "page_content": "Pedophilic Disorder 697\nDevelopment and Course\nIndividuals with sexual sadism in forensic samples are almost exclusively male, but a rep-\nresentative sample of the population in Aust ralia reported that 2.2% of men and 1.3% of\nwomen said they had been involved in bondage and discipline, \u201csadomasochism,\u201d or dom-\ninance and submission in the previous year . Information on the development and course\nof sexual sadism disorder is extremely lim ited. One study reported that females became\naware of their sadomasochistic interest as young adults, and another reported that the\nmean age at onset of sadism in a group of males was 19.4 years. Whereas sexual sadism per\nse is probably a lifelong characteristic, sexu al sadism disorder may fluctuate according to\nthe individual\u2019s subjective distress or his or her propensity to harm nonconsenting others.\nAdvancing age is likely to have the same reducing effect on this disorder as it has on other\nparaphilic or normophilic sexual behavior.\nDifferential Diagnosis\nMany of the conditions that could be diffe rential diagnoses for sexual sadism disorder\n(e.g., antisocial pers onality disorder, sexual masochism disorder, hypersexuality, sub-\nstance use disorders) sometime s occur also as comorb id diagnoses. Therefore, it is neces-\nsary to carefully evaluate the evidence for sexual sadism disorder, keeping the possibility\nof other paraphilias or mental disorders as pa rt of the differential diagnosis. The majority\nof individuals who are active in community networks that pr actice sadistic and masoch-\nistic behaviors do not express any dissatisfaction with their sexual interests, and their be-\nhavior would not meet DSM-5 criteria for sexual sadism disorder. Sadi stic interest, but not\nthe disorder, may be considered in the differential diagnosis.", "source": "dsm5.pdf"} {"id": "37e106bee657-1", "page_content": "the disorder, may be considered in the differential diagnosis.\nComorbidity\nKnown comorbidities with sexual sadism diso rder are largely based on individuals (al-\nmost all males) convicted for criminal acts involving sadistic acts against nonconsenting\nvictims. Hence, these comorbidities might not apply to all individuals who never engaged\nin sadistic activity with a nonconsenting vi ctim but who qualify for a diagnosis of sexual\nsadism disorder based on subjec tive distress over their sexual interest. Diso rders that are\ncommonly comorbid with sexual sadism diso rder include other paraphilic disorders.\nPedophilic Disorder\nDiagnostic Criteria 302.2 (F65.4)\nA. Over a period of at least 6 months, recurrent, intense sexually arousing fantasies, sex-\nual urges, or behaviors involving sexual activity with a prepubescent child or children\n(generally age 13 years or younger).\nB. The individual has acted on these sexual urges, or the sexual urges or fantasies cause\nmarked distress or interpersonal difficulty.\nC. The individual is at least age 16 years and at least 5 years older than the child or chil-\ndren in Criterion A.\nNote: Do not include an individual in late adolescence involved in an ongoing sexual\nrelationship with a 12- or 13-year-old.\nSpecify whether:\nExclusive type (attracted only to children)\nNonexclusive type", "source": "dsm5.pdf"} {"id": "0aefebff4384-0", "page_content": "698 Paraphilic Disorders\nSpecify if:\nSexually attracted to males\nSexually attracted to females\nSexually attracted to both\nSpecify if:\nLimited to incest\nDiagnostic Features\nThe diagnostic criteria for pedophilic disorder are intended to apply both to individuals who\nfreely disclose this paraphilia and to individuals who deny any sexual attraction to prepuber-\ntal children (generally age 13 years or younger) , despite substantial objective evidence to the\ncontrary. Examples of disclosing this paraphilia include candidly acknowledging an intense\nsexual interest in children and indicating that sexual interest in children is greater than or equal\nto sexual interest in physically mature individuals. If individuals also complain that their sex-\nual attractions or preferences for children are caus ing psychosocial difficulties, they may be di-\nagnosed with pedophilic disorder. However, if they report an absence of feelings of guilt,\nshame, or anxiety about these impulses and are not functionally limited by their paraphilic im-\npulses (according to self-repor t, objective assessment, or both), and their self-reported and le-\ngally recorded histories indicate that they ha ve never acted on their impulses, then these\nindividuals have a pedophilic sexual interest but not pedophilic disorder.\nExamples of individuals who deny attraction to children include individuals who are\nknown to have sexually approached multiple children on separate occasions but who deny\nany urges or fantasies about sexual behavior involving children, and who may further claim\nthat the known episodes of physical contact were all unintentional and nonsexual. Other indi-\nviduals may acknowledge past episodes of sexual behavior involving children but deny any\nsignificant or sustained sexual interest in children. Since these individuals may deny experi-\nences impulses or fantasies involving children, they may also deny feeling subjectively dis-\ntressed. Such individuals may still be diagnosed with pedophilic disorder despite the absence", "source": "dsm5.pdf"} {"id": "0aefebff4384-1", "page_content": "tressed. Such individuals may still be diagnosed with pedophilic disorder despite the absence\nof self-reported distress, provided that there is evidence of recurrent behaviors persisting for\n6 months (Criterion A) and evidence that the individual has acted on sexual urges or experi-\nenced interpersonal difficulties as a cons equence of the disorder (Criterion B).\nPresence of multiple victims, as discussed above, is su fficient but not necessary for di-\nagnosis; that is, the individual can still meet Criterion A by merely acknowledging intense\nor preferential sexual interest in children. \nThe Criterion A clause, indicating that the signs or symptoms of pedophilia have per-\nsisted for 6 months or longer, is intended to ensure that the sexual attraction to children is\nnot merely transient. However, the diagnosis ma y be made if there is clinical evidence of\nsustained persistence of the sexual attraction to children even if the 6-month duration can-\nnot be precisely determined.\nAssociated Features Supporting Diagnosis\nThe extensive use of pornography depicting prepubescent children is a useful diagnostic\nindicator of pedophilic disorder. This is a specific instance of the general case that individ-\nuals are likely to choose the kind of pornography that corresponds to their sexual interests.\nPrevalence\nThe population prevalence of pedophilic disorder is unknown. The highest possible prev-\nalence for pedophilic disorder in the male population is approximately 3%\u20135%. The pop-\nulation prevalence of pedophilic disorder in females is even more uncertain, but it is likely\na small fraction of the prevalence in males.", "source": "dsm5.pdf"} {"id": "f8e694c0b166-0", "page_content": "Pedophilic Disorder 699\nDevelopment and Course\nAdult males with pedophilic disorder may indi cate that they become aware of strong or\npreferential sexual interest in children arou nd the time of puberty\u2014the same time frame\nin which males who later prefer physically ma ture partners became aware of their sexual\ninterest in women or men. Attempting to diag nose pedophilic disorder at the age at which\nit first manifests is problematic because of th e difficulty during adolescent development in\ndifferentiating it from age-appropriate sexual interest in peers or from sexual curiosity.\nHence, Criterion C requires for diagnosis a minimum age of 16 years and at least 5 years\nolder than the child or children in Criterion A.\nPedophilia per se appears to be a lifelong condition. Pedophilic disorder, however,\nnecessarily includes other elements that may change over time with or without treatment:\nsubjective distress (e.g., guilt, shame, intense se xual frustration, or feelings of isolation) or\npsychosocial impairment, or the propensity to act out sexually with children, or both.\nTherefore, the course of pedophilic disorder may fluctuate, in crease, or decr ease with age.\nAdults with pedophilic disorder may report an awareness of sexual interest in children\nthat preceded engaging in sexual behavior invo lving children or self-identification as a pedo-\nphile. Advanced age is as likely to similarly di minish the frequency of sexual behavior involv-\ning children as it does other paraphilically motivated and normophilic sexual behavior.\nRisk and Prognostic Factors\nTemperamental. There appears to be an interaction between pedophilia and antisocial-\nity, such that males with both traits are more likely to act out sexually with children. Thus,\nantisocial personality disorder may be consid ered a risk factor for pedophilic disorder in", "source": "dsm5.pdf"} {"id": "f8e694c0b166-1", "page_content": "antisocial personality disorder may be consid ered a risk factor for pedophilic disorder in\nmales with pedophilia. \nEnvironmental. Adult males with pedophilia often repo rt that they were sexually abused\nas children. It is unclear, however, whether this correlation reflects a causal influence of\nchildhood sexual abuse on adult pedophilia.\nGenetic and physiological. Since pedophilia is a necessary condition for pedophilic dis-\norder, any factor that increase s the probability of pedophilia al so increases the risk of pe-\ndophilic disorder. There is some evidence that neurodevelopme ntal perturbation in utero\nincreases the probability of develo pment of a pedoph ilic interest.\nGender-Related Diagnostic Issues\nPsychophysiological laboratory measures of sexu al interest, which are sometimes useful in di-\nagnosing pedophilic disorder in males, are not necessarily useful in diagnosing this disorder in\nfemales, even when an identical procedure (e.g., viewing time) or anal ogous procedures (e.g.,\npenile plethysmography and vaginal photoplethysmography) are available.\nDiagnostic Markers\nPsychophysiological measures of sexual interest may sometimes be useful when an indi-\nvidual\u2019s history suggests the possible presence of pedophilic disorder but the individual\ndenies strong or preferential attraction to children. The most thoroughly researched and\nlongest used of such measures is penile plethysmography, although the sensitivity and spec-\nificity of diagnosis may vary from one site to another. Viewing time, using photographs of\nnude or minimally clothed person s as visual stimuli, is also used to diagnose pedophilic\ndisorder, especially in combination with self-report measures. Mental health professionals\nin the United States, however, should be aware that possession of such visual stimuli, even", "source": "dsm5.pdf"} {"id": "f8e694c0b166-2", "page_content": "in the United States, however, should be aware that possession of such visual stimuli, even\nfor diagnostic purposes, may violate American law regarding possession of child pornog-\nraphy and leave the mental health professio nal susceptible to criminal prosecution.", "source": "dsm5.pdf"} {"id": "a13a67dbdbfe-0", "page_content": "700 Paraphilic Disorders\nDifferential Diagnosis\nMany of the conditions that could be differ ential diagnoses for pedophilic disorder also\nsometimes occur as comorbid diagnoses. It is th erefore generally necessary to evaluate the\nevidence for pedophilic disord er and other possible condit ions as separate questions.\nAntisocial personality disorder. This disorder increases the li kelihood that a person who\nis primarily attracted to the mature physique will approach a child, on one or a few occa-\nsions, on the basis of relative availability. The individual often shows other signs of this\npersonality disorder, such as recurrent law-breaking.\nAlcohol and substance use disorders. The disinhibiting effects of intoxication may also\nincrease the likelihood that a person who is primarily attracted to th e mature physique will\nsexually approach a child.\nObsessive-compulsive disorder. There are occasional individuals who complain about\nego-dystonic thoughts and worries about possi ble attraction to children. Clinical inter-\nviewing usually reveals an absence of sexual thoughts about children during high states of\nsexual arousal (e.g., approaching orgasm during masturbation) and sometimes additional\nego-dystonic, intrusive se xual ideas (e.g., concerns about homosexuality).\nComorbidity\nPsychiatric comorbidity of pedophilic disorder includes substance use disorders; depres-\nsive, bipolar, and anxiety disorders; antisocial personality disorder; and other paraphilic\ndisorders. However, findings on comorbid disorders are largely among individuals con-\nvicted for sexual offenses involving childre n (almost all males) and may not be general-\nizable to other individuals wi th pedophilic disorder (e.g., individuals who have never\napproached a child sexually but who qualify for the diagnosis of pedophilic disorder on\nthe basis of subjective distress).\nFetishistic Disorder", "source": "dsm5.pdf"} {"id": "a13a67dbdbfe-1", "page_content": "the basis of subjective distress).\nFetishistic Disorder\nDiagnostic Criteria 302.81 (F65.0)\nA. Over a period of at least 6 months, recu rrent and intense sexual arousal from either\nthe use of nonliving objects or a highly specific focus on nongenital body part(s), as\nmanifested by fantasies, urges, or behaviors.\nB. The fantasies, sexual urges, or behaviors cause clinically significant distress or impair-\nment in social, occupational, or other important areas of functioning.\nC. The fetish objects are not limited to articles of clothing used in cross-dressing (as in\ntransvestic disorder) or devices specifical ly designed for the purpose of tactile genital\nstimulation (e.g., vibrator).\nSpecify:\nBody part(s)\nNonliving object(s)\nOther\nSpecify if:\nIn a controlled environment: This specifier is primarily applicable to individuals living\nin institutional or other settings where opportunities to engage in fetishistic behaviors\nare restricted.\nIn full remission: There has been no distress or impairment in social, occupational,\nor other areas of functioning for at least 5 years while in an uncontrolled environment.", "source": "dsm5.pdf"} {"id": "2c2ab539e3cd-0", "page_content": "Fetishistic Disorder 701\nSpecifiers\nAlthough individuals with fetishistic disord er may report intens e and recurrent sexual\narousal to inanimate objects or a specific body part, it is not unusual for non\u2013mutually ex-\nclusive combinations of fetishes to occur. Thus, an individual may have fetishistic disorder\nassociated with an inanimate object (e.g., fe male undergarments) or an exclusive focus on\nan intensely eroticized body part (e.g., feet, ha ir), or their fetishisti c interest may meet cri-\nteria for various combinations of these specifiers (e.g., socks, shoes and feet).\nDiagnostic Features\nThe paraphilic focus of fetishistic disorder involves the persistent and repetitive use of or de-\npendence on nonliving objects or a highly specif ic focus on a (typically nongenital) body part\nas primary elements associated with sexual arous al (Criterion A). A diagnosis of fetishistic dis-\norder must include clinically significant pers onal distress or psycho social role impairment\n(Criterion B). Common fetish objects include female undergarments, male or female footwear,\nrubber articles, leather cl othing, or other wearing apparel. Hi ghly eroticized body parts asso-\nciated with fetishistic disorder include feet, toes, and hair. It is not uncommon for sexualized\nfetishes to include both inanimate objects and bo dy parts (e.g., dirty socks and feet), and for\nthis reason the definition of feti shistic disorder now re-incorporates partialism (i.e., an exclusive\nfocus on a body part) into its boundaries. Part ialism, previously considered a paraphilia not\notherwise specified disorder, ha d historically been subsumed in fetishism prior to DSM-III.\nMany individuals who self-identify as fetish ist practitioners do not necessarily report", "source": "dsm5.pdf"} {"id": "2c2ab539e3cd-1", "page_content": "Many individuals who self-identify as fetish ist practitioners do not necessarily report\nclinical impairment in association with their fetish-associated behavi ors. Such individuals\ncould be considered as having a fetish but not fetishistic diso rder. A diagnosis of fetishistic\ndisorder requires concurrent fulfillment of both the behaviors in Criterion A and the clin-\nically significant distress or impairment in functioning noted in Criterion B.\nAssociated Features Supporting Diagnosis\nFetishistic disorder can be a multisensory ex perience, including holding, tasting, rubbing,\ninserting, or smelling the fetish object while ma sturbating, or preferring that a sexual part-\nner wear or utilize a fetish object during sexual encounters. Some individuals may acquire\nextensive collections of high ly desired fetish objects.\nDevelopment and Course \nUsually paraphilias have an onset during pube rty, but fetishes can develop prior to ado-\nlescence. Once established, fetish istic disorder tends to have a continuous course that fluc-\ntuates in intensity and freq uency of urges or behavior. \nCulture-Related Diagnostic Issues\nKnowledge of and appropriate consideration fo r normative aspects of sexual behavior are\nimportant factors to explore to establish a clinical diagnosis of fetishistic disorder and to\ndistinguish a clinical diagnosis from a socially acceptable sexual behavior.\nGender-Related Diagnostic Issues\nFetishistic disorder has not been systematically reported to occur in females. In clinical\nsamples, fetishistic disorder is ne arly exclusively re ported in males.\nFunctional Consequences of Fetishistic Disorder\nTypical impairments associated with fetishistic disorder include sexual dysfunction\nduring romantic reciprocal rela tionships when the preferred fe tish object or body part is", "source": "dsm5.pdf"} {"id": "25b74b136ce7-0", "page_content": "702 Paraphilic Disorders\nunavailable during foreplay or coitus. Some individuals with fetishistic disorder may pre-\nfer solitary sexual activity as sociated with their fetishistic preference (s) even while in-\nvolved in a meaningful reciprocal and affectionate relationship.\nAlthough fetishistic disorder is relatively uncommon among arrested sexual offenders\nwith paraphilias, males with fe tishistic disorder may steal an d collect their particular fe-\ntishistic objects of desire. Such individuals have been arrested and charged for nonsexual\nantisocial behaviors (e.g., breaking and enteri ng, theft, burglary) that are primarily moti-\nvated by the fetishistic disorder.\nDifferential Diagnosis\nTransvestic disorder. The nearest diagnostic neighbor of fetishistic diso rder is transves-\ntic disorder. As noted in the diagnostic criter ia, fetishistic disorder is not diagnosed when\nfetish objects are limited to ar ticles of clothing exclusively worn during cross-dressing (as\nin transvestic disorder), or when the object is genitally stimulating because it has been de-\nsigned for that purpose (e.g., a vibrator). \nSexual masochism disorder or other paraphilic disorders. Fetishes can co-occur with\nother paraphilic disorders, especially \u201csad omasochism\u201d and transvestic disorder. When\nan individual fantasizes about or engages in \u201cforced cross-dressing\u201d and is primarily sex-\nually aroused by the domination or humiliation associated with such fantasy or repetitive\nactivity, the diagnosis of sexual ma sochism disorder should be made.\nFetishistic behavior with out fetishistic disorder. Use of a fetish object for sexual arousal\nwithout any associated distress or psychosoci al role impairment or other adverse conse-\nquence would not meet criteria for fetishisti c disorder, as the threshold required by Crite-", "source": "dsm5.pdf"} {"id": "25b74b136ce7-1", "page_content": "quence would not meet criteria for fetishisti c disorder, as the threshold required by Crite-\nrion B would not be met. For example, an indi vidual whose sexual partner either shares or\ncan successfully incorporate his interest in caressing, smelling, or licking feet or toes as an\nimportant element of foreplay would not be diagnosed with fetishistic disorder; nor\nwould an individual who prefers, and is not di stressed or impaired by, solitary sexual be-\nhavior associated with wearing rubber garments or leather boots.\nComorbidity\nFetishistic disorder may co-occur with othe r paraphilic disorders as well as hypersexual-\nity. Rarely, fetishistic disorder may be associated with neurological conditions.\nTransvestic Disorder\nDiagnostic Criteria 302.3 (F65.1)\nA. Over a period of at least 6 months, recurrent and intense sexual arousal from cross-\ndressing, as manifested by fantasies, urges, or behaviors.\nB. The fantasies, sexual urges, or behaviors cause clinically significant distress or impair-\nment in social, occupational, or other important areas of functioning.\nSpecify if:\nWith fetishism: If sexually aroused by fabrics, materials, or garments.\nWith autogynephilia: If sexually aroused by thoughts or images of self as female.\nSpecify if:\nIn a controlled environment: This specifier is primarily applicable to individuals living\nin institutional or other settings where opportunities to cross-dress are restricted.\nIn full remission: There has been no distress or impairment in social, occupational,\nor other areas of functioning for at least 5 years while in an uncontrolled environment.", "source": "dsm5.pdf"} {"id": "e70ea08d26ac-0", "page_content": "Transvestic Disorder 703\nSpecifiers\nThe presence of fetishism decreases the likelih ood of gender dysphoria in men with trans-\nvestic disorder. The presence of autogynephilia increases the likelihood of gender dyspho-\nria in men with transvestic disorder. \nDiagnostic Features\nThe diagnosis of transvestic diso rder does not apply to all individuals who dress as the op-\nposite sex, even those who do so habitually. It applies to individuals whose cross-dressing\nor thoughts of cross-dressing are always or of ten accompanied by sexual excitement (Cri-\nterion A) and who are emotionally distressed by this pattern or feel it impairs social or in-\nterpersonal functioning (Crite rion B). The cross-dressing may involve only one or two\narticles of clothing (e.g., for men, it may pertain only to women\u2019s undergarments), or it\nmay involve dressing completely in the inner and outer garments of the other sex and (in\nmen) may include the use of women\u2019s wigs and make-up. Transvestic disorder is nearly\nexclusively reported in males. Sexual arousal, in its most obvious form of penile erection,\nmay co-occur with cross-dressing in various wa ys. In younger males, cross-dressing often\nleads to masturbation, following which any fe male clothing is removed. Older males often\nlearn to avoid masturbating or doing anything to stimulate the penis so that the avoidance\nof ejaculation allows them to prolong their cr oss-dressing session. Males with female part-\nners sometimes complete a cro ss-dressing session by having intercourse with their part-\nners, and some have difficult y maintaining a sufficient erec tion for intercourse without\ncross-dressing (or private fantasies of cross-dressing).\nClinical assessment of distress or impairme nt, like clinical assessment of transvestic", "source": "dsm5.pdf"} {"id": "e70ea08d26ac-1", "page_content": "Clinical assessment of distress or impairme nt, like clinical assessment of transvestic\nsexual arousal, is usually dependent on the in dividual\u2019s self-report. The pattern of behav-\nior \u201cpurging and acquisition\u201d often signifies the presence of distress in individuals with\ntransvestic disorder. During this behavioral pattern, an individual (usually a man) who\nhas spent a great deal of money on women\u2019s clothes and other apparel (e.g., shoes, wigs)\ndiscards the items (i.e., purges them) in an effort to overc ome urges to cross-dress, and\nthen begins acquiring a woman\u2019s wardrobe all over again.\nAssociated Features Supporting Diagnosis\nTransvestic disorder in men is often accompanied by autogynephilia (i.e., a male\u2019s para-\nphilic tendency to be sexually aroused by th e thought or image of himself as a woman).\nAutogynephilic fantasies and behaviors may focu s on the idea of exhibiting female phys-\niological functions (e.g., lactat ion, menstruation), engaging in stereotypically feminine be-\nhavior (e.g., knitting), or posses sing female anatomy (e.g., breasts).\nPrevalence\nThe prevalence of transvestic di sorder is unknown. Transvesti c disorder is rare in males\nand extremely rare in females. Fewer than 3% of males repo rt having ever been sexually\naroused by dressing in women\u2019s attire. The percentage of individuals who have cross-\ndressed with sexual arousal more than once or a few times in their lifetimes would be even\nlower. The majority of males with transvesti c disorder identify as heterosexual, although\nsome individuals have occasional sexual in teraction with other males, especially when\nthey are cross-dressed. \nDevelopment and Course", "source": "dsm5.pdf"} {"id": "e70ea08d26ac-2", "page_content": "they are cross-dressed. \nDevelopment and Course\nIn males, the first signs of transvestic disorder may begin in childhood, in the form of\nstrong fascination with a particular item of women\u2019s attire. Prior to puberty, cross-dress-\ning produces generalized feelings of pleasura ble excitement. With the arrival of puberty,\ndressing in women\u2019s clothes begins to elicit pe nile erection and, in some cases, leads di-", "source": "dsm5.pdf"} {"id": "e764a1c52501-0", "page_content": "704 Paraphilic Disorders\nrectly to first ejaculation. In many cases, cross-dressing elicits less and less sexual ex-\ncitement as the individual grows older; eventually it may produce no discernible penile\nresponse at all. The desire to cross-dress, at the same time, remains the same or grows even\nstronger. Individuals who report such a dimi nution of sexual response typically report\nthat the sexual excitement of cross-dressing has been replaced by feelings of comfort or\nwell-being.\nIn some cases, the course of transvestic disorder is contin uous, and in others it is epi-\nsodic. It is not rare for men with transvestic d isorder to lose interest in cross-dressing when\nthey first fall in love with a woman and be gin a relationship, but such abatement usually\nproves temporary. When the desire to cross-dr ess returns, so does the associated distress.\nSome cases of transvestic disorder progress to gender dysphoria. The males in these\ncases, who may be indistinguishable from othe rs with transvestic disorder in adolescence\nor early childhood, gradually develop desires to remain in the female role for longer pe-\nriods and to feminize their anatomy. The de velopment of gender dysphoria is usually ac-\ncompanied by a (self-reported) reduction or e limination of sexual arousal in association\nwith cross-dressing.\nThe manifestation of transvestism in penile erection and stimulation, like the manifesta-\ntion of other paraphilic as well as normophilic sexual interests, is most intense in adolescence\nand early adulthood. The severity of transvestic disorder is highest in adulthood, when the\ntransvestic drives are most likely to conflict with performance in he terosexual intercourse", "source": "dsm5.pdf"} {"id": "e764a1c52501-1", "page_content": "transvestic drives are most likely to conflict with performance in he terosexual intercourse\nand desires to marry and start a family. Middle -age and older men with a history of trans-\nvestism are less likely to present with transvestic disorder than with gender dysphoria.\nFunctional Consequences of Transvestic Disorder\nEngaging in transvestic behaviors can interfer e with, or detract from, heterosexual rela-\ntionships. This can be a source of distress to men who wish to maintain conventional mar-\nriages or romantic partnerships with women.\nDifferential Diagnosis\nFetishistic disorder. This disorder may resemble transv estic disorder, in particular, in\nmen with fetishism who put on women\u2019s unde rgarments while masturbating with them.\nDistinguishing transvestic disorder depends on the individual\u2019s specific thoughts during\nsuch activity (e.g., are there any ideas of be ing a woman, being like a woman, or being\ndressed as a woman?) and on the presence of othe r fetishes (e.g., soft, silky fabrics, whether\nthese are used for garments or for something else). \nGender dysphoria. Individuals with transvestic disorder do not report an incongruence be-\ntween their experienced gender and assigned gender nor a desire to be of the other gender; and\nthey typically do not have a history of chil dhood cross-gender behaviors, which would be\npresent in individuals with gender dysphoria. Individuals with a presentation that meets full\ncriteria for transvestic disorder as well as ge nder dysphoria should be given both diagnoses.\nComorbidity\nTransvestism (and thus transvestic disorder) is often found in associ ation with other para-\nphilias. The most frequently co-occurring paraphilias are fetishism and masochism. One", "source": "dsm5.pdf"} {"id": "e764a1c52501-2", "page_content": "particularly dangerous form of masochism, autoerotic asphyxia, is associated with transves-\ntism in a substantial proportion of fatal cases.", "source": "dsm5.pdf"} {"id": "bc1873f284aa-0", "page_content": "Other Specified Paraphilic Disorder 705\nOther Specified Paraphilic Disorder\n302.89 (F65.89)\nThis category applies to presentations in whic h symptoms characteristic of a paraphilic disor-\nder that cause clinically significant distress or impairment in social, occupational, or other im-\nportant areas of functioning predominate but do not meet the full criteria for any of the disorders\nin the paraphilic disorders diagnostic class. The other specified paraphilic disorder category is\nused in situations in which the clinician chooses to communicate the specific reason that the\npresentation does not meet the cr iteria for any specific paraphilic disorder. This is done by re-\ncording \u201cother specified paraphilic disorder\u201d followed by the spec ific reason (e.g., \u201czoophilia\u201d). \nExamples of presentations that can be specified using the \u201cother specified\u201d designation\ninclude, but are not limited to, recurrent and intense sexual arousal involving telephone\nscatologia (obscene phone calls), necrophilia (corpses), zoophilia (animals), coprophilia\n(feces), klismaphilia (enemas), or urophilia (urine) that has been present for at least 6 months\nand causes marked distress or impairment in social, occupational, or other important ar-\neas of functioning. Other specified paraphilic disorder can be specified as in remission\nand/or as occurring in a controlled environment.\nUnspecified Paraphilic Disorder\n302.9 (F65.9)\nThis category applies to presentations in which symptoms characteristic of a paraphilic\ndisorder that cause clinically significant distress or impairment in social, occupational, or\nother important areas of functioning predominate but do not meet the full criteria for any of", "source": "dsm5.pdf"} {"id": "bc1873f284aa-1", "page_content": "other important areas of functioning predominate but do not meet the full criteria for any of\nthe disorders in the paraphilic disorders diagnostic class. The unspecified paraphilic dis-\norder category is used in situations in which the clinician chooses not to specify the reason\nthat the criteria are not met for a specific paraphilic disorder, and includes presentations\nin which there is insufficient information to make a more specific diagnosis.", "source": "dsm5.pdf"} {"id": "d9802890f8a6-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "46f086507c3e-0", "page_content": "707Other Mental\nDisorders\nFour disorders are included in this chapter: ot her specified mental disorder due to\nanother medical condition; unsp ecified mental disorder due to another medical condition;\nother specified mental disorder; and unspecified mental disorder. This residual category\napplies to presentations in which symptoms char acteristic of a mental disorder that cause\nclinically significant distress or impairment in social, occupational, or other important ar-\neas of functioning predominate but do not meet the full criteria for any other mental dis-\norder in DSM-5. For other specified and un specified mental diso rders due to another\nmedical condition, it must be established that the disturbance is caused by the physiolog-\nical effects of another medica l condition. If other specified and unspecified mental disor-\nders are due to another medi cal condition, it is necessary to code and list the medical\ncondition first (e.g., 042 [B20] HIV disease), fo llowed by the other spec ified or unspecified\nmental disorder (use appropriate code).\nOther Specified Mental Disorder\nDue to Another Medical Condition\n294.8 (F06.8)\nThis category applies to presentations in whic h symptoms characteristic of a mental dis-\norder due to another medical condition that cause clinically significant distress or impair-\nment in social, occupational, or other impor tant areas of functioning predominate but do\nnot meet the full criteria for any specific mental disorder attributable to another medical\ncondition. The other specified mental disor der due to another medical condition category\nis used in situations in which the clinician chooses to communicate the specific reason that\nthe presentation does not meet the criteria for any specific mental disorder attributable to\nanother medical condition. This is done by recording the name of the disorder, with the\nspecific etiological medical condition inserted in place of \u201canother medical condition,\u201d fol-", "source": "dsm5.pdf"} {"id": "46f086507c3e-1", "page_content": "specific etiological medical condition inserted in place of \u201canother medical condition,\u201d fol-\nlowed by the specific symptomatic manifestation that does not meet the criteria for any\nspecific mental disorder due to another medical condition. Furthermore, the diagnostic\ncode for the specific medical condition must be listed immediately before the code for the\nother specified mental disorder due to anothe r medical condition. For example, dissocia-\ntive symptoms due to complex partial seizures would be coded and recorded as 345.40\n(G40.209), complex partial seizures 294.8 (F06. 8) other specified mental disorder due to\ncomplex partial seizures, dissociative symptoms.\nAn example of a presentation that can be specified using the \u201cother specified\u201d desig-\nnation is the following:\nDissociative symptoms: This includes symptoms occurring, for example, in the con-\ntext of complex partial seizures.", "source": "dsm5.pdf"} {"id": "6775b6f959e9-0", "page_content": "708 Other Mental Disorders\nUnspecified Mental Disorder\nDue to Another Medical Condition\n294.9 (F09)\nThis category applies to presentations in which symptoms characteristic of a mental dis-\norder due to another medical condition that cause clinically significant distress or impair-\nment in social, occupational, or other impor tant areas of functioning predominate but do\nnot meet the full criteria for any specific mental disorder due to another medical condition.\nThe unspecified mental disorder due to another medical condition category is used in sit-\nuations in which the clinician chooses not to specify the reason that the criteria are not met\nfor a specific mental disorder due to another medical condition, and includes presentations\nfor which there is insufficient information to make a more specific diagnosis (e.g., in emer-\ngency room settings). This is done by recording the name of the disorder, with the specific\netiological medical condition inserted in plac e of \u201canother medical condition.\u201d Furthermore,\nthe diagnostic code for the specific medical condition must be listed immediately before\nthe code for the unspecified mental disorder due to another medical condition. For exam-\nple, dissociative symptoms due to complex partial seizures would be coded and recorded\nas 345.40 (G40.209) complex partial seizures , 294.9 (F06.9) unspecified mental disorder\ndue to complex partial seizures. \nOther Specified Mental Disorder\n300.9 (F99)\nThis category applies to presentations in which symptoms characteristic of a mental dis-\norder that cause clinically significant distre ss or impairment in social, occupational, or oth-\ner important areas of functioning predominate but do not meet the full criteria for any\nspecific mental disorder. The other specified m ental disorder category is used in situations\nin which the clinician chooses to communicate the specific reason that the presentation\ndoes not meet the criteria for any specific mental disorder. This is done by recording \u201cother", "source": "dsm5.pdf"} {"id": "6775b6f959e9-1", "page_content": "does not meet the criteria for any specific mental disorder. This is done by recording \u201cother\nspecified mental disorder\u201d followed by the specific reason.\nUnspecified Mental Disorder\n300.9 (F99)\nThis category applies to presentations in which symptoms characteristic of a mental dis-\norder that cause clinically significant distre ss or impairment in social, occupational, or oth-\ner important areas of functioning predominate but do not meet the full criteria for any\nmental disorder. The unspecified mental disorder category is used in situations in which\nthe clinician chooses not to specify the reason that the criteria are not met for a specific\nmental disorder, and includes presentations for which there is insufficient information to\nmake a more specific diagnosis (e.g., in emergency room settings).", "source": "dsm5.pdf"} {"id": "aee65c948032-0", "page_content": "709Medication-Induced Movement\nDisorders and Other Adverse\nEffects of Medication\nMedication-induced movement disorders are included in Section II because of\ntheir frequent importance in 1) the management by medication of mental disorders or oth-\ner medical conditions and 2) the differential diagnosis of mental disorders (e.g., anxiety\ndisorder versus neuroleptic-induced akathisi a; malignant catatonia versus neuroleptic\nmalignant syndrome). Although these moveme nt disorders are labeled \u201cmedication in-\nduced,\u201d it is often difficult to establish the causal relationship between medication expo-\nsure and the development of the movement di sorder, especially because some of these\nmovement disorders also occu r in the absence of medicati on exposure. The conditions\nand problems listed in this ch apter are not mental disorders.\nThe term neuroleptic is becoming outdated because it highlights the propensity of an-\ntipsychotic medications to cause abnormal movements, and it is being replaced with the\nterm antipsychotic in many contexts. Nevertheless, the term neuroleptic remains appropri-\nate in this context. Although newer antipsychotic medications may be less likely to cause\nsome medication-induced move ment disorders, those disorders still occur. Neuroleptic\nmedications include so-called conventional, \u201ct ypical,\u201d or first-gene ration antipsychotic\nagents (e.g., chlorpromazine, haloperidol, fl uphenazine); \u201catypical\u201d or second-generation\nantipsychotic agents (e.g., clozapine, risperidone, olanzapine, quetiapine); certain dopa-\nmine receptor\u2013blocking drugs used in the tr eatment of symptoms such as nausea and gas-", "source": "dsm5.pdf"} {"id": "aee65c948032-1", "page_content": "mine receptor\u2013blocking drugs used in the tr eatment of symptoms such as nausea and gas-\ntroparesis (e.g., prochlorperazine, prometh azine, trimethobenzamide, thiethylperazine,\nmetoclopramide); and amoxapine, which is marketed as an antidepressant.\nNeuroleptic-Induced Parkinsonism\nOther Medication-Induced Parkinsonism\n332.1 (G21.11) Neuroleptic-Induced Parkinsonism\n332.1 (G21.19) Other Medication-Induced Parkinsonism\nParkinsonian tremor, muscular rigidity, akinesia (i.e., loss of movement or difficulty ini-\ntiating movement), or bradykinesia (i.e., slowing movement) developing within a few\nweeks of starting or raising the dosage of a me dication (e.g., a neuroleptic) or after reduc-\ning the dosage of a medication used to treat extrapyramidal symptoms.\nNeuroleptic Malignant Syndrome\n333.92 (G21.0) Neuroleptic Malignant Syndrome\nAlthough neuroleptic malignant syndrome is easily recognized in its classic full-blown\nform, it is often heterogeneous in onset, pres entation, progression, and outcome. The clin-\nical features described below are those consid ered most important in making the diagno-\nsis of neuroleptic malignant syndrome based on consensus recommendations.", "source": "dsm5.pdf"} {"id": "86b7b22ddf62-0", "page_content": "710 Medication-Induced Movement Disorders\nDiagnostic Features\nPatients have generally been exposed to a dopamine antagonist within 72 hours prior to\nsymptom development. Hyperthermia ( \uf03e100.4\uf0b0 F or \uf03e38.0\uf0b0C on at least two occasions,\nmeasured orally), associated with profuse dia phoresis, is a distinguishing feature of neu-\nroleptic malignant syndrome, sett ing it apart from other neurol ogical side effects of anti-\npsychotic medications. Extreme elevations in temperature, reflecting a breakdown in\ncentral thermoregulation, are more likely to support the diagnosis of neuroleptic malig-\nnant syndrome. Generalized rigidity, described as \u201clead pipe\u201d in its most severe form and\nusually unresponsive to antiparkinsonian agen ts, is a cardinal feature of the disorder and\nmay be associated with other neurological symptoms (e.g., tremor, sialorrhea, akinesia,\ndystonia, trismus, myoclonus, dysarthria, dysphagia, rhab domyolysis). Creatine kinase\nelevation of at least four times the upper limit of normal is commonly seen. Changes in\nmental status, characterized by delirium or altered consciousness ranging from stupor to\ncoma, are often an early sign. Affected indi viduals may appear alert but dazed and unre-\nsponsive, consistent with catatonic stupor. Autonomic activation and instability\u2014mani-\nfested by tachycardia (rate \uf03e25% above baseline), diaphoresis, blood pressure elevation\n(systolic or diastolic \uf0b325% above baseline) or fluctuation ( \uf0b320 mmHg diastolic change or", "source": "dsm5.pdf"} {"id": "86b7b22ddf62-1", "page_content": "\uf0b325 mmHg systolic change within 24 hours), urinary incontinence, and pallor\u2014may be\nseen at any time but provide an early clue to the diagnosis. Tachypnea (rate \uf03e50% above\nbaseline) is common, and respiratory distress \u2014resulting from metabolic acidosis, hyper-\nmetabolism, chest wall restriction, aspiration pneumonia, or pulmonary emboli\u2014can oc-\ncur and lead to sudden respiratory arrest.\nA workup, including laboratory investigation, to exclude other infectious, toxic, met-\nabolic, and neuropsychiatric et iologies or complications is essential (see the section \u201cDif-\nferential Diagnosis\u201d later in this discussion ). Although several laboratory abnormalities\nare associated with neuroleptic malignant synd rome, no single abnormality is specific to\nthe diagnosis. Individuals with neuroleptic malignant syndrome may have leukocytosis,\nmetabolic acidosis, hypoxia, decreased serum iron concentrations, and elevations in se-\nrum muscle enzymes and catecholamines. Findings from cerebrospinal fluid analysis and\nneuroimaging studies are generally normal, whereas electroencephalography shows gen-\neralized slowing. Autopsy findings in fatal ca ses have been nonspecific and variable, de-\npending on complications.\nDevelopment and Course\nEvidence from database studies suggests in cidence rates for neuroleptic malignant syn-\ndrome of 0.01%\u20130.02% among indi viduals treated with antips ychotics. The temporal pro-\ngression of signs and symptoms provides important clues to the diagnosis and prognosis\nof neuroleptic malignant syndrome. Alteration in mental status and other neurological\nsigns typically precede systemic signs. The on set of symptoms varies from hours to days\nafter drug initiation. Some cases develop with in 24 hours after drug initiation, most within", "source": "dsm5.pdf"} {"id": "86b7b22ddf62-2", "page_content": "after drug initiation. Some cases develop with in 24 hours after drug initiation, most within\nthe first week, and virtually all cases within 30 days. Once the syndrome is diagnosed and\noral antipsychotic drugs are d iscontinued, neuroleptic maligna nt syndrome is self-limited\nin most cases. The mean reco very time after drug discontinuation is 7\u201310 days, with most\nindividuals recovering within 1 week and nearly all within 30 days. The duration may be\nprolonged when long-acting antipsychotics are implicated. There have been reports of in-\ndividuals in whom residual neurological signs persisted for weeks after the acute hyper-\nmetabolic symptoms re solved. Total resolution of symp toms can be obtained in most\ncases of neuroleptic malignant syndrome; howe ver, fatality rates of 10%\u201320% have been", "source": "dsm5.pdf"} {"id": "72b863fdf50b-0", "page_content": "metabolic symptoms re solved. Total resolution of symp toms can be obtained in most\ncases of neuroleptic malignant syndrome; howe ver, fatality rates of 10%\u201320% have been\nreported when the disorder is not recogniz ed. Although many individuals do not experi-\nence a recurrence of neuroleptic malignant syndrome when rechallenged with antipsy-\nchotic medication, some do, especially when antipsychotics are reinstituted soon after an\nepisode.", "source": "dsm5.pdf"} {"id": "ec07b755c287-0", "page_content": "Medication-Induced Movement Disorders 711\nRisk and Prognostic Factors\nNeuroleptic malignant sy ndrome is a potential risk in an y individual after antipsychotic\ndrug administration. It is not specific to an y neuropsychiatric diagnosis and may occur in\nindividuals without a diagnosable mental disorder who receive dopamine antagonists.\nClinical, systemic, and metabolic factors associ ated with a heightened risk of neuroleptic\nmalignant syndrome include agitation, exhaus tion, dehydration, and iron deficiency. A\nprior episode associated with antipsychotics has been described in 15%\u201320% of index\ncases, suggesting underlying vulnerability in some patients; however, genetic findings\nbased on neurotransmitter receptor polymorphi sms have not been replicated consistently.\nNearly all dopamine antagonists have been associated with neuroleptic malignant\nsyndrome, although high-potency antipsychotics pose a greater risk compared with low-\npotency agents and newer atypical antipsychoti cs. Partial or milder forms may be associ-\nated with newer antipsychotics, but neurolep tic malignant syndrome varies in severity\neven with older drugs. Dopami ne antagonists used in medical settings (e.g., metoclopra-\nmide, prochlorperazine) have also been impl icated. Parenteral administration routes,\nrapid titration rates, and higher total drug dosages have been associated with increased\nrisk; however, neuroleptic malignant syndrome usually occurs within the therapeutic dos-\nage range of antipsychotics.\nDifferential Diagnosis\nNeuroleptic malignant syndrome must be di stinguished from other serious neurological\nor medical conditions, including central nerv ous system infections, inflammatory or au-\ntoimmune conditions, status ep ilepticus, subcortical structur al lesions, and systemic con-", "source": "dsm5.pdf"} {"id": "ec07b755c287-1", "page_content": "ditions (e.g., pheochromocytoma, thyrotoxicosis, tetanu s, heat stroke).\nNeuroleptic malignant syndrome also must be distinguished from similar syndromes\nresulting from the use of other substances or medications, such as serotonin syndrome;\nparkinsonian hyperthermia syndrome following abrupt discontinuation of dopamine ag-\nonists; alcohol or sedative withdrawal; malignant hyperthe rmia occurring during anes-\nthesia; hyperthermia associated with abuse of stimulants and hallucinogens; and atropine\npoisoning from anticholinergics.\nIn rare instances, individuals with schizophrenia or a mood diso rder may present with\nmalignant catatonia, which ma y be indistinguishable from neuroleptic malignant syn-\ndrome. Some investigators consider neurol eptic malignant syndrome to be a drug-\ninduced form of malignant catatonia.\nMedication-Induced Acute Dystonia\n333.72 (G24.02) Medication-Induced Acute Dystonia\nAbnormal and prolonged contract ion of the muscles of the ey es (oculogyric crisis), head,\nneck (torticollis or retrocollis), limbs, or trunk developing within a few days of starting or\nraising the dosage of a medication (such as a neuroleptic) or after reducing the dosage of a\nmedication used to treat extrapyramidal symptoms.\nMedication-Induced Acute Akathisia\n333.99 (G25.71) Medication-Induced Acute Akathisia\nSubjective complaints of restlessness, ofte n accompanied by observed excessive move-\nments (e.g., fidgety movements of the legs, rocking from foot to foot, pacing, inability to sit", "source": "dsm5.pdf"} {"id": "ec07b755c287-2", "page_content": "or stand still), developing within a few weeks of starting or raising the dosage of a medi-\ncation (such as a neuroleptic) or after reducing the dosage of a medication used to treat ex-\ntrapyramidal symptoms.", "source": "dsm5.pdf"} {"id": "19387b90f7cf-0", "page_content": "712 Medication-Induced Movement Disorders\nTardive Dyskinesia\n333.85 (G24.01) Tardive Dyskinesia\nInvoluntary athetoid or chorei form movements (lasting at le ast a few weeks) generally of\nthe tongue, lower face and jaw, and extremit ies (but sometimes involving the pharyngeal,\ndiaphragmatic, or trunk muscles) developing in association with the use of a neuroleptic\nmedication for at least a few months.\nSymptoms may develop after a shorter period of medication use in older persons. In\nsome patients, movements of this type may ap pear after discontinuation, or after change\nor reduction in dosage, of neuroleptic medica tions, in which case the condition is called\nneuroleptic withdrawal -emergent dyskinesia. Because withdrawal-emergent dyskinesia is\nusually time-limited, lasting less than 4\u20138 week s, dyskinesia that persists beyond this win-\ndow is considered to be tardive dyskinesia.\nTardive Dystonia\nTardive Akathisia\n333.72 (G24.09) Tardive Dystonia\n333.99 (G25.71) Tardive Akathisia\nTardive syndrome involving other types of movement problems, such as dystonia or\nakathisia, which are distinguished by their late emergence in the course of treatment and\ntheir potential persistence for months to years, even in the face of neuroleptic discontinu-\nation or dosage reduction.\nMedication-Induced Postural Tremor\n333.1 (G25.1) Medication-Induced Postural Tremor\nFine tremor (usually in the range of 8\u201312 Hz) occurring during attempts to maintain a pos-", "source": "dsm5.pdf"} {"id": "19387b90f7cf-1", "page_content": "ture and developing in associ ation with the use of medicati on (e.g., lithium, antidepres-\nsants, valproate). This tremor is very similar to the tremor seen with anxiety, caffeine, and\nother stimulants.\nOther Medication-Induced Movement Disorder\n333.99 (G25.79) Other Medication-Induced Movement Disorder\nThis category is for medication-induced movement disorders not captured by any of the\nspecific disorders listed above. Examples include 1) presentations resembling neuroleptic\nmalignant syndrome that are associated with medications other than neuroleptics and\n2) other medication-induc ed tardive conditions.\nAntidepressant Discontinuation Syndrome\n995.29 ( T43.205A )Initial encounter\n995.29 ( T43.205D )Subsequent encounter \n995.29 ( T43.205S )Sequelae\nAntidepressant discontinuation syndrome is a set of symptoms that can occur after an\nabrupt cessation (or marked re duction in dose) of an antide pressant medication that was\ntaken continuously for at least 1 month. Symp toms generally begin within 2\u20134 days and\ntypically include specific sensory, somatic, and cognitive-emotional manifestations. Fre-", "source": "dsm5.pdf"} {"id": "4bac07806f0f-0", "page_content": "Medication-Induced Movement Disorders 713\nquently reported sensory and somatic symptoms include flashes of lights, \u201celectric shock\u201d\nsensations, nausea, and hyperre sponsivity to nois es or lights. Nons pecific anxiety and\nfeelings of dread may also be reported. Symptoms are alleviated by restarting the same\nmedication or starting a different medication that has a similar mechanism of action\u2014\nfor example, discontinuation symptoms afte r withdrawal from a serotonin-norepineph-\nrine reuptake inhibitor may be alleviated by starting a tricyclic antidepressant. To qualify\nas antidepressant discontinuation syndrome, the symptoms should not have been present\nbefore the antidepressant dosa ge was reduced and are not be tter explained by another\nmental disorder (e.g., manic or hypomanic episode, substance intoxication, substance\nwithdrawal, somatic symptom disorder).\nDiagnostic Features\nDiscontinuation symptoms may occur following treatment with tricyclic antidepressants\n(e.g., imipramine, amitriptyline, desipramine) , serotonin reuptake in hibitors (e.g., fluox-\netine, paroxetine, sertraline), and monoamine oxidase inhibitors (e.g., phenelzine, selegi-\nline, pargyline). The incidence of this syndrome depends on the dosage and half-life of the\nmedication being taken, as well as the rate at which the medication is tapered. Short-acting\nmedications that are stopped ab ruptly rather than tapered gradually may pose the great-\nest risk. The short-acting selective serotonin reuptake inhibitor (SSRI) paroxetine is the\nagent most commonly associated with disconti nuation symptoms, but such symptoms oc-\ncur for all types of antidepressants.", "source": "dsm5.pdf"} {"id": "4bac07806f0f-1", "page_content": "cur for all types of antidepressants.\nUnlike withdrawal syndromes associated with opioids, alcohol, and other substances\nof abuse, antidepressant discontinuation sy ndrome has no pathognomonic symptoms. In-\nstead, the symptoms tend to be vague and variable and typically begin 2\u20134 days after the\nlast dose of the antidepressant. For SSRIs (e.g., paroxetine), symptoms such as dizziness,\nringing in the ears, \u201celectric shocks in the head ,\u201d an inability to sleep, and acute anxiety are\ndescribed. The antidepressant use prior to discontinuation must not have incurred hypo-\nmania or euphoria (i.e., there should be confidence that the discontinuation syndrome is\nnot the result of fluctuations in mood stabi lity associated with the previous treatment).\nThe antidepressant discontinuation syndrome is based solely on pharmacological factors\nand is not related to the reinforcing effects of an antidepressant. Also, in the case of stim-\nulant augmentation of an antidepressant, abru pt cessation may result in stimulant with-\ndrawal symptoms (see \u201cStimulant Withdraw al\u201d in the chapter \u201cSubstance-Related and\nAddictive Disorders\u201d) rather than the antide pressant discontinuation syndrome described\nhere.\nPrevalence\nThe prevalence of antidepressant discontinu ation syndrome is unknown but is thought to\nvary according to the dosage prior to discon tinuation, the half-life and receptor-binding\naffinity of the medication, and possibly the indi vidual\u2019s genetically influenced rate of me-\ntabolism for this medication.\nCourse and Development\nBecause longitudinal studies are lacking, little is known about the clinical course of anti-\ndepressant discontinuation syndrome. Sympto ms appear to abate over time with very\ngradual dosage reductions. After an episode, some individuals may pr efer to resume med-", "source": "dsm5.pdf"} {"id": "4bac07806f0f-2", "page_content": "gradual dosage reductions. After an episode, some individuals may pr efer to resume med-\nication indefinitely if tolerated.\nDifferential Diagnosis\nThe differential diagnosis of antidepressant discontinuation syndrome includes anxiety\nand depressive disorders, su bstance use disorders, and tolerance to medications.", "source": "dsm5.pdf"} {"id": "7a15019526a8-0", "page_content": "714 Medication-Induced Movement Disorders\nAnxiety and depressive disorders. Discontinuation symptoms often resemble symptoms\nof a persistent anxiety disorder or a return of somatic symptoms of depression for which\nthe medication was initially given.\nSubstance use disorders. Antidepressant discontinuatio n syndrome differs from sub-\nstance withdrawal in that antidepressants th emselves have no reinforcing or euphoric ef-\nfects. The medication dosage has usually not been increased without the clinician\u2019s\npermission, and the individual generally does no t engage in drug-seeking behavior to ob-\ntain additional medication. Criteria for a substance use disorder are not met.\nTolerance to medications. Tolerance and discontinuation symptoms can occur as a\nnormal physiological response to stopping medication after a substantial duration of\nexposure. Most cases of medication tolerance can be managed through carefully con-\ntrolled tapering.\nComorbidity\nTypically, the individual was initially started on the medication for a major depressive dis-\norder; the original symptoms may return during the discontinuation syndrome.\nOther Adverse Effect of Medication\n995.20 ( T50.905A )Initial encounter\n995.20 ( T50.905D )Subsequent encounter \n995.20 ( T50.905S )Sequelae\nThis category is available for optional use by clinicians to code side effects of medication\n(other than movement symptoms) when these ad verse effects become a main focus of clin-\nical attention. Examples include severe hypotension, cardia c arrhythmias, and priapism.", "source": "dsm5.pdf"} {"id": "775d491fdef6-0", "page_content": "715Other Conditions That May Be\na Focus of Clinical Attention\nThis discussion covers other conditions and proble ms that may be a focus of clini-\ncal attention or that may otherwise affect the diagnosis, course, prog nosis, or treatment of\na patient\u2019s mental disorder. These conditio ns are presented with their corresponding\ncodes from ICD-9-CM (usually V codes) and ICD-10-CM (usu ally Z codes). A condition\nor problem in this chapter may be coded if it is a reason for the current visit or helps to\nexplain the need for a test, procedure, or trea tment. Conditions and problems in this chap-\nter may also be included in the medical record as useful information on circumstances that\nmay affect the patient\u2019s care, regardless of their relevance to the current visit.\nThe conditions and problems listed in this chapter are not mental disorders. Their in-\nclusion in DSM-5 is meant to draw attention to the scope of additional issues that may be\nencountered in routine clinical practice and to provide a systematic listing that may be\nuseful to clinicians in documenting these issues.\nRelational Problems\nKey relationships, especially intimate adult partner relationships and parent/caregiver-\nchild relationships, have a significant impact on the health of the individuals in these re-\nlationships. These relationships can be health promoting and protective, neutral, or detri-\nmental to health outcomes. In the extreme, th ese close relationships can be associated with\nmaltreatment or neglect, which has signif icant medical and psyc hological consequences\nfor the affected individual. A relational problem may come to clinical attention either as\nthe reason that the individual seeks health care or as a pr oblem that affects the course,\nprognosis, or treatment of the individual\u2019s mental or other medical disorder.", "source": "dsm5.pdf"} {"id": "775d491fdef6-1", "page_content": "prognosis, or treatment of the individual\u2019s mental or other medical disorder.\nProblems Related to Family Upbringing\nV61.20 (Z62.820) Parent-Child Relational Problem\nFor this category, the term parent is used to refer to one of the child\u2019s primary caregivers,\nwho may be a biological, adoptive, or foster pa rent or may be another relative (such as a\ngrandparent) who fulfills a parent al role for the child. This ca tegory should be used when\nthe main focus of clinical atte ntion is to address the quality of the parent-child relationship\nor when the quality of the parent-child relati onship is affecting th e course, prognosis, or\ntreatment of a mental or other medical disorder. Typically, the parent-child relational\nproblem is associated with impaired functionin g in behavioral, cognitive, or affective do-\nmains. Examples of behavioral problems include inadequate parental control, supervision,\nand involvement with the child; parental over protection; excessive parental pressure; ar-\nguments that escalate to threats of physical violence; and avoidance without resolution of\nproblems. Cognitive problems may include negati ve attributions of th e other\u2019s intentions,\nhostility toward or scapegoating of the other, and unwarranted feelings of estrangement.\nAffective problems may include feelings of sadness, apathy, or anger about the other in-\ndividual in the relationship. Clinicians should take into account the developmental needs\nof the child and the cultural context.", "source": "dsm5.pdf"} {"id": "9b813454c31e-0", "page_content": "716 Other Conditions That May Be a Focus of Clinical Attention\nV61.8 (Z62.891) Sibling Relational Problem\nThis category should be used when the focus of clinical attention is a pattern of interaction\namong siblings that is associated with significan t impairment in individual or family function-\ning or with development of symptoms in one or more of the siblings, or when a sibling relational\nproblem is affecting the course, prognosis, or treatment of a sibling\u2019s mental or other medical\ndisorder. This category can be used for either children or adults if the focus is on the sibling re-\nlationship. Siblings in this context include fu ll, half-, step-, foster , and adopted siblings.\nV61.8 (Z62.29) Upbringing Away From Parents\nThis category should be used when the main focus of clinical attention pertains to issues\nregarding a child being raised away from the parents or when this separate upbringing af-\nfects the course, prognosis, or treatment of a mental or other medical disorder. The child\ncould be one who is under state custody and pl aced in kin care or foster care. The child\ncould also be one who is living in a nonparenta l relative\u2019s home, or with friends, but whose\nout-of-home placement is not mandated or sanctioned by the courts. Problems related to a\nchild living in a group home or orphanage are also included. This category excludes issues\nrelated to V60.6 (Z59.3) ch ildren in boarding schools.\nV61.29 (Z62.898) Child Affected by Parental Relationship Distress\nThis category should be used when the focus of clinical attention is the negative effects of\nparental relationship discord (e.g., high levels of conflict, distress, or disparagement) on a\nchild in the family, including effects on the child\u2019s mental or other medical disorders.", "source": "dsm5.pdf"} {"id": "9b813454c31e-1", "page_content": "child in the family, including effects on the child\u2019s mental or other medical disorders.\nOther Problems Related to Primary Support Group\nV61.10 (Z63.0) Relationship Distress With Spouse or Intimate Partner\nThis category should be used when the major fo cus of the clinical contact is to address the\nquality of the intimate (spouse or partner) relationship or when the quality of that rela-\ntionship is affecting the course, prognosis, or treatment of a mental or other medical dis-\norder. Partners can be of the same or differ ent genders. Typically, the relationship distress\nis associated with impaired functioning in beha vioral, cognitive, or affective domains. Ex-\namples of behavioral proble ms include conflict resolution difficulty, withdrawal, and\noverinvolvement. Cognit ive problems can manifest as chronic negative attributions of the\nother\u2019s intentions or dismissals of the part ner\u2019s positive behaviors. Affective problems\nwould include chronic sadness, apathy, and/or anger about the other partner.\nNote: This category excludes clinical encounte rs for V61.1x (Z69.1x) mental health ser-\nvices for spousal or partner abuse prob lems and V65.49 (Z70.9) sex counseling.\nV61.03 (Z63.5) Disruption of Family by Separation or Divorce\nThis category should be used when partners in an intimate adult couple are living apart\ndue to relationship problems or are in the process of divorce.\nV61.8 (Z63.8) High Expressed Emotion Level Within Family\nExpressed emotion is a construct used as a qualitat ive measure of the \u201camount\u201d of emo-\ntion\u2014in particular, hostility, emotional overin volvement, and criticism directed toward a", "source": "dsm5.pdf"} {"id": "9b813454c31e-2", "page_content": "tion\u2014in particular, hostility, emotional overin volvement, and criticism directed toward a\nfamily member who is an identified patient\u2014displayed in the family environment. This\ncategory should be used when a family\u2019s hi gh level of expressed emotion is the focus of\nclinical attention or is affecting the course, prognosis, or treatment of a family member\u2019s\nmental or other medical disorder.\nV62.82 (Z63.4) Uncomplicated Bereavement\nThis category can be used when the focus of cl inical attention is a normal reaction to the\ndeath of a loved one. As part of their reaction to such a loss, some grieving individuals\npresent with symptoms characteristic of a major depressive episode\u2014for example, feel-", "source": "dsm5.pdf"} {"id": "1f9cc6497a2a-0", "page_content": "Other Conditions That May Be a Focus of Clinical Attention 717\nings of sadness and associated symptoms su ch as insomnia, poor appetite, and weight\nloss. The bereaved individual typically re gards the depressed mood as \u201cnormal,\u201d al-\nthough the individual may seek professional help for relief of associated symptoms such\nas insomnia or anorexia. The duration and expression of \u201cnormal\u201d bereavement vary con-\nsiderably among different cultural groups. Fu rther guidance in distinguishing grief from\na major depressive episode is provided in the criteria for major depressive episode.\nAbuse and Neglect\nMaltreatment by a family member (e.g., caregiver, intimate adult partner) or by a nonrel-\native can be the area of current clinical focu s, or such maltreatment can be an important\nfactor in the assessment and treatment of pati ents with mental or other medical disorders.\nBecause of the legal implications of abuse and neglect, care should be used in assessing\nthese conditions and assigning these codes. Ha ving a past history of abuse or neglect can\ninfluence diagnosis and treatment response in a number of mental disorders, and may also\nbe noted along with the diagnosis.\nFor the following categories, in addition to listings of the confirmed or suspected event\nof abuse or neglect, other code s are provided for use if the cu rrent clinical encounter is to\nprovide mental health services to either the victim or the perpetrator of the abuse or ne-\nglect. A separate code is also provided for designating a past history of abuse or neglect.\nCoding Note for ICD-10-CM Abuse and Neglect Conditions\nFor T codes only, the 7th character should be coded as follows:\nA (initial encounter) \u2014Use while the patient is receiving active treatment for\nthe condition (e.g., surgical treatment, emergency department encounter, eval-", "source": "dsm5.pdf"} {"id": "1f9cc6497a2a-1", "page_content": "the condition (e.g., surgical treatment, emergency department encounter, eval-\nuation and treatment by a new clinician); or\nD (subsequent encounter) \u2014Use for encounters after the patient has received\nactive treatment for the condition and wh en he or she is receiving routine care\nfor the condition during the healing or re covery phase (e.g., cast change or re-\nmoval, removal of external or internal fixation device, medi cation adjustment,\nother aftercare and follow-up visits).\nChild Maltreatment and Neglect Problems\nChild Physical Abuse\nChild physical abuse is nonaccidental physical injury to a child\u2014ranging from minor bruises\nto severe fractures or death\u2014occurring as a re sult of punching, beating, kicking, biting,\nshaking, throwing, stabbing, choking, hitting (with a hand, stick, strap, or other object),\nburning, or any other method that is inflicted by a parent, caregiver, or other individual who\nhas responsibility for the child. Such injury is considered abuse regardless of whether the\ncaregiver intended to hurt the ch ild. Physical discipline, such as spanking or paddling, is not\nconsidered abuse as long as it is reasonable and causes no bodily injury to the child.\nChild Physical Abuse, Confirmed\n995.54 (T74.12XA) Initial encounter\n995.54 (T74.12XD) Subsequent encounter\nChild Physical Abuse, Suspected\n995.54 (T76.12XA) Initial encounter\n995.54 (T76.12XD) Subsequent encounter", "source": "dsm5.pdf"} {"id": "979832185969-0", "page_content": "718 Other Conditions That May Be a Focus of Clinical Attention\nOther Circumstances Related to Child Physical Abuse\nV61.21 (Z69.010) Encounter for mental health services for victim of child abuse by parent\nV61.21 (Z69.020) Encounter for mental health servic es for victim of nonparental child\nabuse\nV15.41 (Z62.810) Personal history (past history) of physical abuse in childhood\nV61.22 (Z69.011) Encounter for mental health services for perpetrator of parental child\nabuse\nV62.83 (Z69.021) Encounter for mental health servic es for perpetrator of nonparental\nchild abuse\nChild Sexual Abuse\nChild sexual abuse encompasses any sexual act involving a child that is intended to pro-\nvide sexual gratification to a parent, caregi ver, or other individual who has responsibility\nfor the child. Sexual abuse includes activities such as fondling a child\u2019s genitals, penetra-\ntion, incest, rape, sodomy, and indecent exposure. Sexual abuse also includes noncontact\nexploitation of a child by a parent or caregi ver\u2014for example, forcing, tricking, enticing,\nthreatening, or pressuring a child to participate in acts for the sexual gratification of others,\nwithout direct physical contact between child and abuser.\nChild Sexual Abuse, Confirmed\n995.53 (T74.22XA) Initial encounter\n995.53 (T74.22XD) Subsequent encounter\nChild Sexual Abuse, Suspected\n995.53 (T76.22XA) Initial encounter\n995.53 (T76.22XD) Subsequent encounter\nOther Circumstances Related to Child Sexual Abuse\nV61.21 (Z69.010) Encounter for mental health services for victim of child sexual abuse\nby parent", "source": "dsm5.pdf"} {"id": "979832185969-1", "page_content": "by parent\nV61.21 (Z69.020) Encounter for mental health servic es for victim of nonparental child\nsexual abuse\nV15.41 (Z62.810) Personal history (past history) of sexual abuse in childhood\nV61.22 (Z69.011) Encounter for mental health services for perpetrator of parental child\nsexual abuse\nV62.83 (Z69.021) Encounter for mental health servic es for perpetrator of nonparental\nchild sexual abuse\nChild Neglect\nChild neglect is defined as any confirmed or suspected egregious ac t or omission by a\nchild\u2019s parent or other caregiver that deprives the child of basic age-appropriate needs and\nthereby results, or has reasonab le potential to result, in physical or psychological harm to\nthe child. Child neglect encompasses abandonm ent; lack of appropriate supervision; fail-\nure to attend to necessary em otional or psychological needs; and failure to provide neces-\nsary education, medical care, nouris hment, shelter, and/or clothing.\nChild Neglect, Confirmed\n995.52 (T74.02XA) Initial encounter\n995.52 (T74.02XD) Subsequent encounter", "source": "dsm5.pdf"} {"id": "e1dedfff919f-0", "page_content": "Other Conditions That May Be a Focus of Clinical Attention 719\nChild Neglect, Suspected\n995.52 (T76.02XA) Initial encounter\n995.52 (T76.02XD) Subsequent encounter\nOther Circumstances Related to Child Neglect\nV61.21 (Z69.010) Encounter for mental health servic es for victim of child neglect by\nparent\nV61.21 (Z69.020) Encounter for mental health servic es for victim of nonparental child\nneglect\nV15.42 (Z62.812) Personal history (past history) of neglect in childhood\nV61.22 (Z69.011) Encounter for mental health services for perpetrator of parental child\nneglect\nV62.83 (Z69.021) Encounter for mental health servic es for perpetrator of nonparental\nchild neglect\nChild Psychological Abuse\nChild psychological abuse is nonaccidental verb al or symbolic acts by a child\u2019s parent or\ncaregiver that result, or have reasonable potential to result, in significant psychological\nharm to the child. (Physical and sexual abusive acts are not included in this category.) Ex-\namples of psychological abuse of a child include berating, disparaging, or humiliating\nthe child; threatening the child; harming/abandoning\u2014or indicating that the alleged\noffender will harm/abandon\u2014people or things that the child cares about; confining the\nchild (as by tying a child\u2019s arms or legs togeth er or binding a child to furniture or another\nobject, or confining a child to a small enclosed area [e.g., a closet]); egregious scapegoating\nof the child; coercing the child to inflict pain on himself or herself; and disciplining the\nchild excessively (i.e., at an extremely high fr equency or duration, even if not at a level of", "source": "dsm5.pdf"} {"id": "e1dedfff919f-1", "page_content": "physical abuse) through physical or nonphysical means.\nChild Psychological Abuse, Confirmed\n995.51 (T74.32XA) Initial encounter\n995.51 (T74.32XD) Subsequent encounter\nChild Psychological Abuse, Suspected\n995.51 (T76.32XA) Initial encounter\n995.51 (T76.32XD) Subsequent encounter\nOther Circumstances Related to Child Psychological Abuse\nV61.21 (Z69.010) Encounter for mental health services for victim of child psychological\nabuse by parent\nV61.21 (Z69.020) Encounter for mental health servic es for victim of nonparental child\npsychological abuse\nV15.42 (Z62.811) Personal history (past history) of psychological abuse in childhood\nV61.22 (Z69.011) Encounter for mental health services for perpetrator of parental child\npsychological abuse\nV62.83 (Z69.021) Encounter for mental health servic es for perpetrator of nonparental\nchild psychological abuse", "source": "dsm5.pdf"} {"id": "0d16aa6fc876-0", "page_content": "720 Other Conditions That May Be a Focus of Clinical Attention\nAdult Maltreatment and Neglect Problems\nSpouse or Partner Violence, Physical\nThis category should be used when nonaccidental acts of physical force that result, or have\nreasonable potential to result, in physical harm to an intimate partner or that evoke signif-\nicant fear in the partner have occurred during the past year. Nonaccidental acts of physical\nforce include shoving, slapping, hair pulling, pinching, restraining, shaking, throwing,\nbiting, kicking, hitting with the fist or an ob ject, burning, poisoning, applying force to the\nthroat, cutting off the air supply, holding th e head under water, and using a weapon. Acts\nfor the purpose of physically protecting oneself or one\u2019s partner are excluded.\nSpouse or Partner Violen ce, Physical, Confirmed\n995.81 (T74.11XA) Initial encounter\n995.81 (T74.11XD) Subsequent encounter\nSpouse or Partner Violence, Physical, Suspected\n995.81 (T76.11XA) Initial encounter\n995.81 (T76.11XD) Subsequent encounter\nOther Circumstances Related to Spou se or Partner Violence, Physical\nV61.11 (Z69.11) Encounter for mental health services for victim of spouse or partner\nviolence, physical\nV15.41 (Z91.410) Personal history (past history) of spouse or partner violence, physical\nV61.12 (Z69.12) Encounter for mental health services for perpetrator of spouse or\npartner violence, physical\nSpouse or Partner Violence, Sexual\nThis category should be used when forced or coerced sexual acts with an intimate partner\nhave occurred during the past year. Sexual violence may involve the use of physical force", "source": "dsm5.pdf"} {"id": "0d16aa6fc876-1", "page_content": "have occurred during the past year. Sexual violence may involve the use of physical force\nor psychological coercion to compel the partner to engage in a sexual act against his or her\nwill, whether or not the act is completed. Also included in this category are sexual acts\nwith an intimate partner who is unable to consent.\nSpouse or Partner Violence, Sexual, Confirmed\n995.83 (T74.21XA) Initial encounter\n995.83 (T74.21XD) Subsequent encounter\nSpouse or Partner Violence, Sexual, Suspected\n995.83 (T76.21XA) Initial encounter\n995.83 (T76.21XD) Subsequent encounter\nOther Circumstances Related to Sp ouse or Partner Violence, Sexual\nV61.11 (Z69.81) Encounter for mental health services for victim of spouse or partner\nviolence, sexual\nV15.41 (Z91.410) Personal history (past history) of spouse or partner violence, sexual\nV61.12 (Z69.12) Encounter for mental health services for perpetrator of spouse or\npartner violence, sexual", "source": "dsm5.pdf"} {"id": "3cd01544cb5a-0", "page_content": "Other Conditions That May Be a Focus of Clinical Attention 721\nSpouse or Partner Neglect\nPartner neglect is any egregious act or omission in the past year by one partner that de-\nprives a dependent partner of basic needs and thereby results, or has reasonable potential\nto result, in physical or psycho logical harm to the dependent pa rtner. This category is used\nin the context of relationships in which one partner is extremely dependent on the other\npartner for care or for assistance in navigating ordinary daily activities\u2014for example, a\npartner who is incapable of self-care owing to substantial physical, psychological/intel-\nlectual, or cultural limitations (e.g., inability to communicat e with others and manage ev-\neryday activities due to living in a foreign culture).\nSpouse or Partner Neglect, Confirmed\n995.85 (T74.01XA) Initial encounter\n995.85 (T74.01XD) Subsequent encounter\nSpouse or Partner Neglect, Suspected\n995.85 (T76.01XA) Initial encounter\n995.85 (T76.01XD) Subsequent encounter\nOther Circumstances Related to Spouse or Partner Neglect\nV61.11 (Z69.11) Encounter for mental health services for victim of spouse or partner\nneglect\nV15.42 (Z91.412) Personal history (past history) of spouse or partner neglect\nV61.12 (Z69.12) Encounter for mental health services for perpetrator of spouse or\npartner neglect\nSpouse or Partner Abuse, Psychological\nPartner psychological abuse encompasses nonaccidental verbal or symbolic acts by one\npartner that result, or have reasonable potentia l to result, in significant harm to the other\npartner. This category should be used when such psycholo gical abuse has occurred during", "source": "dsm5.pdf"} {"id": "3cd01544cb5a-1", "page_content": "partner. This category should be used when such psycholo gical abuse has occurred during\nthe past year. Acts of psycholo gical abuse include berating or humiliating the victim; inter-\nrogating the victim; restricting the victim\u2019s ability to come and go freely; obstructing the vic-\ntim\u2019s access to assistance (e.g., law enforcemen t; legal, protective, or medical resources);\nthreatening the victim with physical harm or sexual assault; harming, or threatening to\nharm, people or things that th e victim cares about; unwarranted restriction of the victim\u2019s ac-\ncess to or use of economic resources; isolating the victim from family, friends, or social sup-\nport resources; stalking the victim; and trying to make the victim think that he or she is crazy.\nSpouse or Partner Abuse, Psychological, Confirmed\n995.82 (T74.31XA) Initial encounter\n995.82 (T74.31XD) Subsequent encounter\nSpouse or Partner Abuse, Psychological, Suspected\n995.82 (T76.31XA) Initial encounter\n995.82 (T76.31XD) Subsequent encounter\nOther Circumstances Related to Spouse or Partner Abuse, Psychological\nV61.11 (Z69.11) Encounter for mental health services for victim of spouse or partner\npsychological abuse", "source": "dsm5.pdf"} {"id": "4dd0e2781dd6-0", "page_content": "722 Other Conditions That May Be a Focus of Clinical Attention\nV15.42 (Z91.411) Personal history (past history) of sp ouse or partner psychological abuse\nV61.12 (Z69.12) Encounter for mental health services for perpetrator of spouse or part-\nner psychological abuse\nAdult Abuse by Nons pouse or Nonpartner\nThese categories should be used when an ad ult has been abused by another adult who is\nnot an intimate partner. Such maltreatment may involve acts of physical, sexual, or emo-\ntional abuse. Examples of adult abuse include nonaccidental acts of physical force (e.g.,\npushing/shoving, scratching, slapping, thro wing something that could hurt, punching,\nbiting) that have resulted\u2014o r have reasonable potential to result\u2014in physical harm or\nhave caused significant fear; forced or coer ced sexual acts; and ve rbal or symbolic acts\nwith the potential to cause psychological harm (e.g., berating or humiliating the person;\ninterrogating the person; restricting the person \u2019s ability to come and go freely; obstructing\nthe person\u2019s access to assistance; threatening the person; harming or threatening to harm\npeople or things that the person cares about; restricting the person\u2019s access to or use of eco-\nnomic resources; isolating the person from fa mily, friends, or social support resources;\nstalking the person; trying to make the person think that he or she is crazy). Acts for the\npurpose of physically protecting oneself or the other person are excluded.\nAdult Physical Abuse by Nonspouse or Nonpartner, Confirmed\n995.81 (T74.11XA) Initial encounter\n995.81 (T74.11XD) Subsequent encounter\nAdult Physical Abuse by Nonspouse or Nonpartner, Suspected\n995.81 (T76.11XA) Initial encounter", "source": "dsm5.pdf"} {"id": "4dd0e2781dd6-1", "page_content": "995.81 (T76.11XA) Initial encounter\n995.81 (T76.11XD) Subsequent encounter\nAdult Sexual Abuse by Nonspo use or Nonpartner, Confirmed\n995.83 (T74.21XA) Initial encounter\n995.83 (T74.21XD) Subsequent encounter\nAdult Sexual Abuse by Nonspo use or Nonpartn er, Suspected\n995.83 (T76.21XA) Initial encounter\n995.83 (T76.21XD) Subsequent encounter\nAdult Psychological Abuse by Nonspouse or Nonpartner, Confirmed\n995.82 (T74.31XA) Initial encounter\n995.82 (T74.31XD) Subsequent encounter\nAdult Psychological Abuse by Nonspouse or Nonpartner, Suspected\n995.82 (T76.31XA) Initial encounter\n995.82 (T76.31XD) Subsequent encounter\nOther Circumstances Related to Adult Abuse by Nonspouse or Nonpartner\nV65.49 (Z69.81) Encounter for mental health services for victim of nonspousal or non-\npartner adult abuse\nV62.83 (Z69.82) Encounter for mental health services for perpetrator of nonspousal or\nnonpartner adult abuse", "source": "dsm5.pdf"} {"id": "8e3f1279a0b1-0", "page_content": "Other Conditions That May Be a Focus of Clinical Attention 723\nEducational and Occu pational Problems\nEducational Problems\nV62.3 (Z55.9) Academic or Educational Problem\nThis category should be used when an academic or educational problem is the focus of\nclinical attention or has an impact on the in dividual\u2019s diagnosis, tr eatment, or prognosis.\nProblems to be consider ed include illiteracy or low-level lit eracy; lack of access to school-\ning owing to unavailability or unattainability; problems with academ ic performance (e.g.,\nfailing school examinations, receiving failing marks or grades) or underachievement (be-\nlow what would be expected given the indivi dual\u2019s intellectual capacity); discord with\nteachers, school staff, or other students; an d any other problems related to education and/\nor literacy.\nOccupational Problems\nV62.21 (Z56.82) Problem Related to Current Military Deployment Status\nThis category should be used when an occupa tional problem directly related to an indi-\nvidual\u2019s military deployment status is the focus of clinical attention or has an impact on the\nindividual\u2019s diagnosis, treatment, or prognosi s. Psychological reactions to deployment are\nnot included in this category; such reactions would be better captured as an adjustment\ndisorder or another mental disorder.\nV62.29 (Z56.9) Other Problem Related to Employment\nThis category should be used when an occupational problem is the focus of clinical atten-\ntion or has an impact on the individual\u2019s treatment or prog nosis. Areas to be considered\ninclude problems with employment or in the work environment, including unemploy-\nment; recent change of job; threat of job loss; job dissatisfaction; stressful work schedule;\nuncertainty about career choices; sexual ha rassment on the job; other discord with boss,", "source": "dsm5.pdf"} {"id": "8e3f1279a0b1-1", "page_content": "supervisor, co-workers, or others in the wo rk environment; uncongenial or hostile work\nenvironments; other psychosocial stressors re lated to work; and any other problems re-\nlated to employment and/or occupation.\nHousing and Economic Problems\nHousing Problems\nV60.0 (Z59.0) Homelessness\nThis category should be used when lack of a regular dwelling or living quarters has an im-\npact on an individual\u2019s treatment or prognosi s. An individual is considered to be homeless\nif his or her primary nighttime residence is a homeless shelter, a warming shelter, a do-\nmestic violence shelter, a public space (e.g., tunnel, transportation st ation, mall), a build-\ning not intended for residential use (e.g., abandoned structure, unused factory), a\ncardboard box or cave, or some other ad hoc housing situation.\nV60.1 (Z59.1) Inadequate Housing\nThis category should be used when lack of adequate housing has an impact on an individ-\nual\u2019s treatment or prognosis. Examples of in adequate housing conditions include lack of\nheat (in cold temperatures) or electricity, infestation by insects or rodents, inadequate\nplumbing and toilet facilities , overcrowding, lack of adequa te sleeping space, and exces-\nsive noise. It is important to consider cultural norms before assigning this category.\nV60.89 (Z59.2) Discord With Neighbor, Lodger, or Landlord\nThis category should be used when discord with neighbors, lodgers, or a landlord is a fo-\ncus of clinical attention or has an impact on the individual\u2019s treatment or prognosis.", "source": "dsm5.pdf"} {"id": "58fa9316a8a2-0", "page_content": "724 Other Conditions That May Be a Focus of Clinical Attention\nV60.6 (Z59.3) Problem Related to Living in a Residential Institution\nThis category should be used when a problem (or problems) related to living in a residen-\ntial institution is a focus of clinical attention or has an impact on the individual\u2019s treatment\nor prognosis. Psychological reactions to a chan ge in living situation are not included in this\ncategory; such reactions would be better captured as an adjustment disorder.\nEconomic Problems\nV60.2 (Z59.4) Lack of Adequate Food or Safe Drinking Water\nV60.2 (Z59.5) Extreme Poverty\nV60.2 (Z59.6) Low Income\nV60.2 (Z59.7) Insufficient Social Insurance or Welfare Support\nThis category should be used for individuals wh o meet eligibility criter ia for social or wel-\nfare support but ar e not receiving such support, who rece ive support that is insufficient to\naddress their needs, or who otherwise lack access to needed insurance or support pro-\ngrams. Examples include inability to qualify for welfare support owing to lack of proper\ndocumentation or evidence of address, inability to obtain ad equate health insurance be-\ncause of age or a preexisting condition, and denial of support owing to excessively strin-\ngent income or other requirements.\nV60.9 (Z59.9) Unspecified Housing or Economic Problem\nThis category should be used when there is a problem related to hou sing or economic cir-\ncumstances other than as specified above.\nOther Problems Related to the Social Environment\nV62.89 (Z60.0) Phase of Life Problem\nThis category should be used when a problem adjusting to a life-cycle transition (a partic-\nular developmental phase) is the focus of clinic al attention or has an impact on the indi-", "source": "dsm5.pdf"} {"id": "58fa9316a8a2-1", "page_content": "vidual\u2019s treatment or prognosis. Examples of such transitions include entering or\ncompleting school, leaving parental control, getting married, starting a new career, be-\ncoming a parent, adjusting to an \u201cempty ne st\u201d after children leave home, and retiring.\nV60.3 (Z60.2) Problem Related to Living Alone\nThis category should be used when a problem associated with living alone is the focus of\nclinical attention or has an impact on the in dividual\u2019s treatment or prognosis. Examples of\nsuch problems include chronic feelings of lonelin ess, isolation, and lack of structure in car-\nrying out activities of daily living (e.g., i rregular meal and sleep schedules, inconsistent\nperformance of home maintenance chores).\nV62.4 (Z60.3) Acculturation Difficulty\nThis category should be used when difficulty in adjusting to a new culture (e.g., following\nmigration) is the focus of clinical attention or has an impact on the individual\u2019s treatment\nor prognosis.\nV62.4 (Z60.4) Social Exclusion or Rejection\nThis category should be used when there is an imbalance of social power such that there is\nrecurrent social exclusion or rejection by others. Examples of social rejection include bul-\nlying, teasing, and intimidation by others; be ing targeted by others for verbal abuse and\nhumiliation; and being purposefully excluded fr om the activities of peers, workmates, or\nothers in one\u2019s social environment.\nV62.4 (Z60.5) Target of (Perceived) Adverse Discrimination or Persecution\nThis category should be used when there is perceived or experienced discrimination\nagainst or persecution of the individual based on his or her membership (or perceived", "source": "dsm5.pdf"} {"id": "9d3154b63563-0", "page_content": "Other Conditions That May Be a Focus of Clinical Attention 725\nmembership) in a specific category. Typically , such categories include gender or gender\nidentity, race, ethnicity, religion, sexual orientation, country of origin, political beliefs, dis-\nability status, caste, social status , weight, and physical appearance.\nV62.9 (Z60.9) Unspecified Problem Related to Social Environment\nThis category should be used when there is a pr oblem related to the individual\u2019s social en-\nvironment other than as specified above.\nProblems Related to Crime or Interaction\n With the Legal System\nV62.89 (Z65.4) Victim of Crime\nV62.5 (Z65.0) Conviction in Civil or Criminal Proceedings Without Imprisonment\nV62.5 (Z65.1) Imprisonment or Other Incarceration\nV62.5 (Z65.2) Problems Related to Release From Prison\nV62.5 (Z65.3) Problems Related to Other Legal Circumstances\nOther Health Service Encounters for\nCounseling and Medical Advice\nV65.49 (Z70.9) Sex Counseling\nThis category should be used when the indi vidual seeks counseling related to sex educa-\ntion, sexual behavior, sexual orientation, sexual attitudes (embarrassment, timidity), oth-\ners\u2019 sexual behavior or orientation (e.g., spou se, partner, child), sexu al enjoyment, or any\nother sex-related issue.\nV65.40 (Z71.9) Other Counseling or Consultation\nThis category should be used when counseling is provided or advice/consultation is\nsought for a problem that is not specified above or elsewhere in this chapter. Examples in-\nclude spiritual or religious counseling, dietar y counseling, and counseling on nicotine use.", "source": "dsm5.pdf"} {"id": "9d3154b63563-1", "page_content": "clude spiritual or religious counseling, dietar y counseling, and counseling on nicotine use.\nProblems Related to Other Psychosocial, Personal,\nand Environmental Circumstances\nV62.89 (Z65.8) Religious or Spiritual Problem\nThis category can be used when the focus of clinical attention is a religious or spiritual\nproblem. Examples include distressing experi ences that involve lo ss or questioning of\nfaith, problems associated with conversion to a new faith, or questioning of spiritual val-\nues that may not necessarily be related to an organized church or religious institution.\nV61.7 (Z64.0) Problems Related to Unwanted Pregnancy\nV61.5 (Z64.1) Problems Related to Multiparity\nV62.89 (Z64.4) Discord With Social Service Provider, Including Probation Officer,\nCase Manager, or Social Services Worker\nV62.89 (Z65.4) Victim of Terrorism or Torture\nV62.22 (Z65.5) Exposure to Disaster, War, or Other Hostilities\nV62.89 (Z65.8) Other Problem Related to Psychosocial Circumstances\nV62.9 (Z65.9) Unspecified Problem Related to Un specified Psychosocial Circum-\nstances", "source": "dsm5.pdf"} {"id": "e9f555acab16-0", "page_content": "726 Other Conditions That May Be a Focus of Clinical Attention\nOther Circumstances of Personal History\nV15.49 (Z91.49) Other Personal History of Psychological Trauma\nV15.59 (Z91.5) Personal History of Self-Harm\nV62.22 (Z91.82) Personal History of Military Deployment\nV15.89 (Z91.89) Other Personal Risk Factors\nV69.9 (Z72.9) Problem Related to Lifestyle\nThis category should be used when a lifestyle pr oblem is a specific focus of treatment or di-\nrectly affects the course, prognosis, or treatmen t of a mental or other medical disorder. Ex-\namples of lifestyle problems include lack of physical exercise, inappropriate diet, high-risk\nsexual behavior, and poor sleep hygiene. A prob lem that is attributable to a symptom of a\nmental disorder should not be coded unless that problem is a specific focus of treatment or\ndirectly affects the course, prognosis, or treatmen t of the individual. In such cases, both the\nmental disorder and the lifesty le problem should be coded.\nV71.01 (Z72.811) Adult Antisocial Behavior\nThis category can be used when the focus of c linical attention is adult antisocial behavior\nthat is not due to a mental disorder (e.g., conduct disorder , antisocial personality disor-\nder). Examples include the behavior of some pr ofessional thieves, racketeers, or dealers in\nillegal substances.\nV71.02 (Z72.810) Child or Adolescent Antisocial Behavior\nThis category can be used when the focus of clinical attention is antisocial behavior in a\nchild or adolescent that is no t due to a mental disorder (e.g ., intermittent explosive disor-\nder, conduct disorder). Examples include isol ated antisocial acts by children or adoles-", "source": "dsm5.pdf"} {"id": "e9f555acab16-1", "page_content": "der, conduct disorder). Examples include isol ated antisocial acts by children or adoles-\ncents (not a pattern of antisocial behavior).\nProblems Related to Access to Medical \nand Other Health Care\nV63.9 (Z75.3) Unavailability or Inaccessibility of Health Care Facilities\nV63.8 (Z75.4) Unavailability or Inaccessibility of Other Helping Agencies\nNonadherence to Medical Treatment\nV15.81 (Z91.19) Nonadherence to Medical Treatment\nThis category can be used when the focus of clinical attention is nonadherence to an im-\nportant aspect of treatment for a mental diso rder or another medica l condition. Reasons\nfor such nonadherence may include discomfort resulting from treatment (e.g., medication\nside effects), expense of treatment, personal value judgments or religious or cultural be-\nliefs about the proposed treatment, age-related debility, and the presence of a mental dis-\norder (e.g., schizophrenia, personality disorder ). This category should be used only when\nthe problem is sufficiently severe to warrant independent clinical attention and does not\nmeet diagnostic criteria fo r psychological factors affect ing other medical conditions.\n278.00 (E66.9) Overweight or Obesity\nThis category may be used when overweight or obesity is a focus of clinical attention.\nV65.2 (Z76.5) Malingering\nThe essential feature of malingering is the inte ntional production of false or grossly exag-\ngerated physical or psychologi cal symptoms, motivated by external incentives such as\navoiding military duty, avoiding work, obta ining financial compensation, evading crimi-\nnal prosecution, or obtaining drugs. Under some circumstances, malingering may repre-", "source": "dsm5.pdf"} {"id": "322fea1998ba-0", "page_content": "Other Conditions That May Be a Focus of Clinical Attention 727\nsent adaptive behavior\u2014for example, feigni ng illness while a captive of the enemy during\nwartime. Malingering should be strongly suspected if any combination of the following is\nnoted:\n1. Medicolegal context of presentation (e.g., th e individual is referred by an attorney to\nthe clinician for examination, or the indivi dual self-refers while litigation or criminal\ncharges are pending).\n2. Marked discrepancy between the individual\u2019s claimed stress or disability and the ob-\njective findings and observations.\n3. Lack of cooperation during the diagnostic evaluation and in complying with the pre-\nscribed treatment regimen.\n4. The presence of antisocial personality disorder.\nMalingering differs from factitious disorder in that the motiva tion for the symptom\nproduction in malingering is an external ince ntive, whereas in factit ious disorder external\nincentives are absent. Malingering is differen tiated from conversion disorder and somatic\nsymptom\u2013related mental disorders by the inte ntional production of symptoms and by the\nobvious external incentives assoc iated with it. Definite evidence of feigning (such as clear\nevidence that loss of function is present du ring the examination but not at home) would\nsuggest a diagnosis of factitious disorder if the individual\u2019s apparent aim is to assume the\nsick role, or malingering if it is to obtain an incentive, such as money.\nV40.31 (Z91.83) Wandering Associated With a Mental Disorder\nThis category is used for individuals with a mental disorder whose desire to walk about\nleads to significant clinical management or safety concerns. For example, individuals with\nmajor neurocognitive or neurodevelopmental disorders may experience a restless urge to", "source": "dsm5.pdf"} {"id": "322fea1998ba-1", "page_content": "major neurocognitive or neurodevelopmental disorders may experience a restless urge to\nwander that places them at risk for falls and causes them to leave supervised settings with-\nout needed accompaniment. This category excl udes individuals whose intent is to escape\nan unwanted housing situation (e.g., childre n who are running away from home, patients\nwho no longer wish to remain in the hospital) or those who walk or pace as a result of med-\nication-induced akathisia.\nCoding note: First code associated mental disorder (e.g., major neurocognitive disor-\nder, autism spectrum disorder), then co de V40.31 (Z91.83) wandering associated with\n[specific mental disorder].\nV62.89 (R41.83) Borderline Intellectual Functioning\nThis category can be used when an individual\u2019s borderline intellectual functioning is the fo-\ncus of clinical attention or has an impact on the individual\u2019s treatmen t or prognosis. Differ-\nentiating borderline intellectual functioning and mild intellectual disability (intellectual\ndevelopmental disorder) requires careful asse ssment of intellectual and adaptive functions\nand their discrepanc ies, particularly in the presence of co-occurring mental disorders that\nmay affect patient compliance with standardized testing procedures (e.g., schizophrenia or\nattention-deficit/hyperactivity diso rder with severe impulsivity).", "source": "dsm5.pdf"} {"id": "ee4a08dc4a92-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "4e4e08541458-0", "page_content": "SECTION III\nEmerging Measures and Models\nAssessment Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .733\nCross-Cutting Symptom Measures . . . . . . . . . . . . . . . . . . . . . . . . . . .734\nDSM-5 Self-Rated Level 1 Cross-Cutting \nSymptom Measure\u2014Adult. . . . . . . . . . . . . . . . . . . . . . . . . . . . .738\nParent/Guardian-Rated DSM-5 Level 1 Cross-Cutting \nSymptom Measure\u2014Child Age 6\u201317 . . . . . . . . . . . . . . . . . . . .740\nClinician-Rated Dimensions of Psycho sis Symptom Severity . . . . . .742\nWorld Health Organization Disability Assessment Schedule 2.0 \n(WHODAS 2.0) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .745\nCultural Formulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .749\nCultural Formulation Interview (CFI). . . . . . . . . . . . . . . . . . . . . . . . . . .750\nCultural Formulation Interview (CFI)\u2014Informant Version . . . . . . . . . .755", "source": "dsm5.pdf"} {"id": "4e4e08541458-1", "page_content": "Alternative DSM-5 Model for Personality Disorders . . . . . . . . . . . . . . . .761\nConditions for Further Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .783\nAttenuated Psychosis Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . .783\nDepressive Episodes With Short-Duration Hypomania . . . . . . . . . . .786\nPersistent Complex Bereavement Disorder . . . . . . . . . . . . . . . . . . . .789\nCaffeine Use Disorder. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .792\nInternet Gaming Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .795\nNeurobehavioral Disorder Associated With \nPrenatal Alcohol Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .798\nSuicidal Behavior Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .801\nNonsuicidal Self-Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .803", "source": "dsm5.pdf"} {"id": "927e7dcc74de-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "29429cf3701f-0", "page_content": "This section contains tools and techniques to enhance the clinical deci-\nsion-making process, understand the cultural context of mental disorders, and\nrecognize emerging diagnoses for further study. It provides strategies to en-\nhance clinical practice and new criteria to stimulate future research, represent-\ning a dynamic DSM-5 that will evolve with advances in the field.\nAmong the tools in Section III is a Level 1 cross-cutting self/informant-rated\nmeasure that serves as a review of systems across mental disorders. A clini-\ncian-rated severity scale for schizophrenia and other psychotic disorders also\nis provided, as well as the World He alth Organization Disability Assessment\nSchedule, Version 2 (WHODAS 2.0). Level 2 severity measures are available\nonline (www.psychiatry.org/dsm5) and may be used to explore significant re-\nsponses to the Level 1 screen. A comprehensive review of the cultural context\nof mental disorders, and the Cultural Formulation Interview (CFI) for clinical use,\nare provided. \nProposed disorders for future study are provided, which include a new\nmodel for the diagnosis of personality disorders as an alternative to the estab-\nlished diagnostic criteria; the proposed m odel incorporates impairments in per-\nsonality functioning as well as pathological personality traits. Also included are\nnew conditions that are the focus of active research, such as attenuated psy-\nchosis syndrome and nonsuicidal self-injury.", "source": "dsm5.pdf"} {"id": "db831d07ca73-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "44b9b5fa9ce7-0", "page_content": "733 Assessment\n Measures\nA growing body of scientific evidence favors dimensional concepts in the diagnosis\nof mental disorders. The limitations of a cate gorical approach to diagnosis include the fail-\nure to find zones of rarity between diagnoses (i.e., delineation of mental disorders from one\nanother by natural boundaries), the need for in termediate categories like schizoaffective dis-\norder, high rates of comorbidity, frequent not-otherwise-specified (NOS) diagnoses, relative\nlack of utility in furthering the identification of unique antecedent validators for most men-\ntal disorders, and lack of treatment specif icity for the various di agnostic categories.\nFrom both clinical and research perspectiv es, there is a need for a more dimensional\napproach that can be combined with DSM\u2019s se t of categorical diagnoses. Such an approach\nincorporates variations of features within an in dividual (e.g., differential severity of indi-\nvidual symptoms both within and outside of a disorder\u2019s diagnostic criteria as measured\nby intensity, duration, or number of symptoms , along with other features such as type and\nseverity of disabilities) rather than relying on a simple yes-or-no approach. For diagnoses\nfor which all symptoms are needed for a diagnosis (a monothetic criteria set), different se-\nverity levels of the constituent symptoms may be noted. If a threshold endorsement of\nmultiple symptoms is needed, su ch as at least five of nine symptoms for major depressive\ndisorder (a polythetic criteria set), both severity levels and different combinations of the\ncriteria may identify more ho mogeneous diagnostic groups.\nA dimensional approach depending primarily on an individual\u2019s subjective reports of\nsymptom experiences along with the clinician\u2019s interpretation is consistent with current\ndiagnostic practice. It is expected that as our understanding of basic disease mechanisms", "source": "dsm5.pdf"} {"id": "44b9b5fa9ce7-1", "page_content": "diagnostic practice. It is expected that as our understanding of basic disease mechanisms\nbased on pathophysiology, neurocircuitry, ge ne-environment interactions, and laboratory\ntests increases, approaches that integrate both objective and subjective patient data will be\ndeveloped to supplement and enhance the accuracy of the diagnostic process.\nCross-cutting symptom measures modeled on general medicine\u2019s review of systems can\nserve as an approach for reviewing critical psychopathological domains. The general med-\nical review of systems is crucial to detecting subtle changes in different organ systems that\ncan facilitate diagnosis and treatment. A simi lar review of various mental functions can\naid in a more comprehensive mental status assessment by drawing attention to symptoms\nthat may not fit neatly into the diagnostic cr iteria suggested by the individual\u2019s presenting\nsymptoms, but may nonetheless be important to the individual\u2019s care. The cross-cutting\nmeasures have two levels: Level 1 questions ar e a brief survey of 13 symptom domains for\nadult patients and 12 domains for child and ad olescent patients. Level 2 questions provide\na more in-depth assessment of certain domains. These measures were developed to be\nadministered both at initial interview and ov er time to track the patient\u2019s symptom status\nand response to treatment.\nSeverity measures are disorder-specific, corresponding closely to the criteria that consti-\ntute the disorder definition. They may be ad ministered to individuals who have received\na diagnosis or who have a clinically signific ant syndrome that falls short of meeting full\ncriteria for a diagnosis. Some of the assess ments are self-completed by the individual,\nwhile others require a clinician to complete . As with the cross-cutting symptom measures,\nthese measures were developed to be administered both at initial interview and over time\nto track the severity of the individual\u2019s disorder and response to treatment.", "source": "dsm5.pdf"} {"id": "b3ae2d069704-0", "page_content": "734 Assessment Measures\nThe World Health Organization Disability Assessment Schedule , Version 2.0 (WHODAS 2.0)\nwas developed to assess a patient\u2019s ability to perform activities in six areas: understanding\nand communicating; getting around; self-care; getting along with people; life activities\n(e.g., household, work/school); and participat ion in society. The scale is self-administered\nand was developed to be used in patients with any medical disorder. It corresponds to\nconcepts contained in the WH O International Classification of Functioning, Disability\nand Health. This assessment can also be used over time to track changes in a patient\u2019s dis-\nabilities.\nThis chapter focuses on the DSM-5 Leve l 1 Cross-Cutting Symptom Measure (adult\nself-rated and parent/guardian versions); the Clinician-Rated Dimensions of Psychosis\nSymptom Severity; and the WHODAS 2.0. Cl inician instructions, scoring information,\nand interpretation guidelines are included for each. These measures and additional\ndimensional assessments, including those for diagnostic severity, can be found online at\nwww.psychiatry.org/dsm5.\nCross-Cutting Symptom Measures\nLevel 1 Cross-Cuttin g Symptom Measure\nThe DSM-5 Level 1 Cross-Cuttin g Symptom Measure is a patien t- or informant-rated mea-\nsure that assesses mental health domains th at are important across psychiatric diagnoses.\nIt is intended to help clinicians identify addi tional areas of inquiry that may have signifi-\ncant impact on the individual\u2019s treatment and prognosis. In addition, the measure may be\nused to track changes in the individu al\u2019s symptom presentation over time.\nThe adult version of the measure consists of 23 questions that assess 13 psychiatric do-", "source": "dsm5.pdf"} {"id": "b3ae2d069704-1", "page_content": "The adult version of the measure consists of 23 questions that assess 13 psychiatric do-\nmains, including depression, an ger, mania, anxiety, somatic symptoms, suicidal ideation,\npsychosis, sleep problems, memo ry, repetitive thoughts and behaviors, dissociation, per-\nsonality functioning, and substance use (Table 1). Each domain consists of one to three\nquestions. Each item inquires about how mu ch (or how often) the individual has been\nbothered by the specific symptom during the p ast 2 weeks. If the individual is of impaired\ncapacity and unable to complete the form (e .g., an individual with dementia), a knowl-\nedgeable adult informant may complete this measure. The measure was found to be clin-\nically useful and to have good reliability in the DSM-5 field trials that were conducted in\nadult clinical samples across the United States and in Canada.\nThe parent/guardian-rated ver sion of the measure (for childr en ages 6\u201317) consists of\n25 questions that assess 12 psychiatric domain s, including depression, anger, irritability,\nmania, anxiety, somatic symptoms, inattent ion, suicidal ideation/attempt, psychosis,\nsleep disturbance, repetitive thoughts and behaviors, an d substance use (Table 2). Each\nitem asks the parent or guardian to rate ho w much (or how often) his or her child has been\nbothered by the specific psychiatric symptom during the past 2 weeks. The measure was\nalso found to be clinically useful and to ha ve good reliability in the DSM-5 field trials that\nwere conducted in pediatric clinical samples across the United States. For children ages\n11\u201317, along with the parent/guardian rating of the child\u2019s sympto ms, the clinician may", "source": "dsm5.pdf"} {"id": "b3ae2d069704-2", "page_content": "consider having the child complete the child -rated version of the measure. The child-rated\nversion of the measure can be found online at www.psychiatry.org/dsm5.\nScoring and interpretation. On the adult self-rated version of the measure, each item is\nrated on a 5-point scale (0=none or not at all; 1=slight or rare, less than a day or two; 2=mild\nor several days; 3=moderate or more than half the days; and 4=severe or nearly every day).\nThe score on each item within a domain should be reviewed. However, a rating of mild (i.e.,\n2) or greater on any item within a domain, ex cept for substance use, suicidal ideation, and", "source": "dsm5.pdf"} {"id": "877033d68d74-0", "page_content": "The score on each item within a domain should be reviewed. However, a rating of mild (i.e.,\n2) or greater on any item within a domain, ex cept for substance use, suicidal ideation, and\npsychosis, may serve as a guide for additional inquiry and follow-up to determine if a more\ndetailed assessment is necessary, which may include the Level 2 cross-cutting symptom as-\nsessment for the domain (see Table 1). For substa nce use, suicidal idea tion, and psychosis, a", "source": "dsm5.pdf"} {"id": "271afa4d1be9-0", "page_content": "Assessment Measures 735\nrating of slight (i.e., 1) or greater on any item within the domain may serve as a guide for ad-\nditional inquiry and follow-up to determine if a more detailed a ssessment is needed. As\nsuch, indicate the highest score within a domain in the \u201cHighest domain score\u201d column.\nTable 1 outlines threshold scores that may guide further inquiry for the remaining domains.\nOn the parent/guardian-rated version of the measure (for children ages 6\u201317), 19 of the 25\nitems are each rated on a 5-point scale (0=none or not at all; 1=slight or rare, less than a day or\ntwo; 2=mild or several days; 3=moderate or mo re than half the days; and 4=severe or nearly\nevery day). The suicidal ideation, suicide atte mpt, and substance abuse items are each rated\non a \u201cYes, No, or Don\u2019t Know\u201d scale. The score on each item within a domain should be re-\nviewed. However, with the exception of inattentio n and psychosis, a rating of mild (i.e., 2) or\ngreater on any item within a domain that is scored on the 5-point scale may serve as a guide\nfor additional inquiry and follow-up to determin e if a more detailed assessment is necessary,\nwhich may include the Level 2 cross-cutting symptom assessment for the domain (see\nTable 2). For inattention or psychosis, a rating of slight or greater (i.e., 1 or greater) may beTABLE 1 Adult DSM-5 Self-Rated Level 1 Cross-Cutting Symptom Measure: \n13 domains, thresholds for further inquiry, and associated DSM-5 \nLevel 2 measures\nDomain Domain nameThreshold to guide", "source": "dsm5.pdf"} {"id": "271afa4d1be9-1", "page_content": "Level 2 measures\nDomain Domain nameThreshold to guide \nfurther inquiryDSM-5 Level 2 Cross-Cutting Symptom \nMeasurea\nI. Depression Mild or greater Lev el 2\u2014Depression\u2014Adult (PROMIS \nEmotional Distress\u2014Short Form)\nII. Anger Mild or greater Level 2\u2014Anger\u2014Adult (PROMIS Emo-\ntional Distress\u2014Anger\u2014Short Form)\nIII. Mania Mild or greater Level 2\u2014 Mania\u2014Adult (Altman Self-Rating \nMania Scale [ASRM])\nIV. Anxiety Mild or greater Level 2\u2014Anxiety\u2014Adult (PROMIS \nEmotional Distress\u2014Anxiety\u2014Short \nForm)\nV. Somatic symptoms Mild or greater Le vel 2\u2014Somatic Symptom\u2014Adult (Patient \nHealth Questionnaire\u201315 \n[PHQ-15] Somatic Symptom Severity \nScale)\nVI. Suicidal ideation Slight or greater None\nVII. Psychosis Slight or greater None\nVIII. Sleep problems Mild or greater Level 2\u2014Sleep Disturbance\u2014Adult \n(PROMIS Sleep Disturbance\u2014Short Form)\nIX. Memory Mild or greater None\nX. Repetitive thoughts \nand behaviorsMild or greater Level 2\u2014Repetitive Thoughts and \nBehaviors\u2014Adult (Florida Obsessive-\nCompulsive Inventory [FOCI] Severity \nScale)\nXI. Dissociation Mild or greater None\nXII. Personality \nfunctioningMild or greater None\nXIII. Substance use Slight or greater L evel 2\u2014Substance Us e\u2014Adult (adapted \nfrom the NIDA-Modified ASSIST)\nNote. NIDA=National Institute on Drug Abuse.", "source": "dsm5.pdf"} {"id": "271afa4d1be9-2", "page_content": "Note. NIDA=National Institute on Drug Abuse.\naAvailable at www.ps ychiatry.org/dsm5.", "source": "dsm5.pdf"} {"id": "01f44549660c-0", "page_content": "736 Assessment Measures\nused as an indicator for additional inquiry. A parent or guardian\u2019s ra ting of \u201cDon\u2019t Know\u201d on\nthe suicidal ideation, suicide a ttempt, and any of the substance use items, especially for chil-\ndren ages 11\u201317 years, may result in additional probing of the issues with the child, including\nusing the child-rated Level 2 Cross-Cutting Symptom Measure for the relevant domain. Be-\ncause additional inquiry is made on the basis of the highest score on any item within a do-\nmain, clinicians should indicate that score in the \u201cHighest Domain Score\u201d column. Table 2\noutlines threshold scores that may guide further inquiry for the remaining domains.TABLE 2 Parent/guardian-rated DSM-5 Level 1 Cross-Cutting Symptom Measure \nfor child age 6\u201317: 12 domains, thresholds for further inquiry, and \nassociated Level 2 measures\nDomain Domain nameThreshold to guide \nfurther inquiryDSM-5 Level 2 Cross-Cutting Symptom \nMeasurea\nI. Somatic symptoms Mild or greater Le vel 2\u2014Somatic Symptoms\u2014Parent/Guard-\nian of Child Age 6\u201317 (Patient Health \nQuestionnaire\u201315 Somatic Symptom Sever-\nity Scale [PHQ-15])\nII. Sleep problems Mild or greater Lev el 2\u2014Sleep Disturbance\u2014Parent/Guard-\nian of Child Age 6\u201317 (PROMIS Sleep \nDisturbance\u2014Short Form)\nIII. Inattention Slight or greater Level 2\u2014Inattention\u2014Parent/Guardian of \nChild Age 6\u201317 (Swanson , Nolan, and Pel-\nham, Version IV [SNAP-IV])\nIV. Depression Mild or greater Level 2\u2014Depression\u2014Parent/Guardian of", "source": "dsm5.pdf"} {"id": "01f44549660c-1", "page_content": "IV. Depression Mild or greater Level 2\u2014Depression\u2014Parent/Guardian of \nChild Age 6\u201317 (PROMIS Emotional Dis-\ntress\u2014Depression\u2014Parent Item Bank)\nV. Anger Mild or greater Level 2\u2014Anger\u2014Parent/Guardian of Child \n(PROMIS Calibrated Anger Measure\u2014Parent)\nVI. Irritability Mild or greater Level 2\u2014Irritability\u2014Parent/Guardian of \nChild (Affective Reactivity Index [ARI])\nVII. Mania Mild or greater Level 2\u2014 Mania\u2014Parent/Guardian of Child \nAge 6\u201317 (Altman Self-Rating Mania Scale \n[ASRM])\nVIII. Anxiety Mild or greater Level 2\u2014Anxiety\u2014Parent/Guardian of Child \nAge 6\u201317 (PROMIS Emotional Distress\u2014\nAnxiety\u2014Parent Item Bank)\nIX. Psychosis Slight or greater None\nX. Repetitive thoughts \nand behaviorsMild or greater None\nXI. Substance use Yes Level 2\u2014Substance Use\u2014Parent/Guardian of \nChild Age 6\u201317 (adapted from the NIDA-\nmodified ASSIST)\nDon\u2019t Know NIDA-modified ASSIST (adapted)\u2014\nChild-Rated (age 11\u201317 years)\nXII. Suicidal ideation/ \nsuicide attemptsYes None\nDon\u2019t Know None\nNote. NIDA=National Institute on Drug Abuse.\naAvailable at www.ps ychiatry.org/dsm5.", "source": "dsm5.pdf"} {"id": "e5260cbe10d1-0", "page_content": "Assessment Measures 737\nLevel 2 Cross-Cuttin g Symptom Measures\nAny threshold scores on the Level 1 Cross- Cutting Symptom Measure (as noted in Tables\n1 and 2 and described in \u201cScoring and Interpretation\u201d indicate a possible need for detailed\nclinical inquiry. Level 2 Cr oss-Cutting Symptom Measures provide one method of obtain-\ning more in-depth information on potentially significant symptoms to inform diagnosis,\ntreatment planning, and follow-up. They ar e available online at www.psychiatry.org/\ndsm5. Tables 1 and 2 outline each Level 1 domain and identify the domains for which\nDSM-5 Level 2 Cross-Cutting Symptom Measures are available for more detailed assess-\nments. Adult and pediatric (parent and child) versions are available online for most Level\n1 symptom domains at www.psychiatry.org/dsm5.\nFrequency of Use of the Cross-Cutting \nSymptom Measures\nTo track change in the individual\u2019s sympto m presentation over time , the Level 1 and rel-\nevant Level 2 cross-cutting symptom measures may be completed at regular intervals as\nclinically indicated, depending on the stab ility of the individual\u2019s symptoms and treat-\nment status. For individuals with impaired capacity and for children ages 6\u201317 years, it is\npreferable for the measures to be comple ted at follow-up appointments by the same\nknowledgeable informant and by the same parent or guardian. Consistently high scores\non a particular domain may indicate signif icant and problematic sy mptoms for the indi-\nvidual that might warrant further assessment, treatment, and follow-up. Clinical judg-\nment should guide decision making.", "source": "dsm5.pdf"} {"id": "cfdb665af90d-0", "page_content": "738 Assessment MeasuresDSM-5 Self-Rated Level 1 Cross-Cutting Symptom Measure\u2014Adult\nName:__________________________________________ ______________ Age: __________ Sex: [ ] Male [ ] Female Date:_____________\nIf the measure is being completed by an informant , what is your relationship with the individual?: __________________________ ____\nIn a typical week, approximately how much time do you spend with th e individual? _________________________ hours/week\nInstructions: The questions below ask about things that might have bothered you. For each question, circle the nu mber that best describes ho w much (or how \noften) you have been bothered by each problem during the past TWO (2) WEEKS.\nDuring the past TWO (2) WEEKS, how much (or how often) \nhave you been bothered by the following problems?None\nNot at \nallSlight\nRare, less than \na day or twoMild\nSeveral \ndaysModerate\nMore than\nhalf the daysSevere\nNearly \nevery dayHighest \nDomain Score\n(clinician)\nI. 1.Little interest or pleasure in doing things? 0 1 2 3 4\n2.Feeling down, depressed, or hopeless? 0 1 2 3 4\nII. 3. Feeling more irritated, gr ouchy, angry than usual? 0 1 2 3 4\nIII. 4.Sleeping less than usual, but still have a lot of energy? 0 1 2 3 4\n5.Starting lots more projects than usual or doing more risky things \nthan usual?0 1 2 3 4\nIV. 6.Feeling nervous, anxious, frig htened, worried, or on edge? 0 1 2 3 4", "source": "dsm5.pdf"} {"id": "cfdb665af90d-1", "page_content": "7.Feeling panic or being frightened? 0 1 2 3 4\n8.Avoiding situations that make you anxious? 0 1 2 3 4\nV. 9.Unexplained aches and pains (e.g., head, back, joints, abdomen, \nlegs)?0 1 2 3 4\n10. Feeling that your illnesses are not being taken seriously enough? 0 1 2 3 4\nVI. 11. Thoughts of actually hurting yourself? 0 1 2 3 4", "source": "dsm5.pdf"} {"id": "a8b0bad6dbaf-0", "page_content": "Assessment Measures 739VII. 12. Hearing things other people couldn\u2019t hear, such as voices even \nwhen no one was around?0 1 2 3 4\n13. Feeling that someone could hear your thoughts, or that you \ncould hear what another person was thinking?0 1 2 3 4\nVIII. 14. Problems with sleep that affect ed your sleep quality over all? 0 1 2 3 4\nIX. 15. Problems with memory (e.g., lear ning new information) or with \nlocation (e.g., finding your way home)?0 1 2 3 4\nX. 16. Unpleasant thoughts, urges, or images that repeatedly enter \nyour mind?0 1 2 3 4\n17. Feeling driven to perform certai n behaviors or mental acts over \nand over again?0 1 2 3 4\nXI. 18. Feeling detached or distant from yourself, your body, your phys-\nical surroundings, or your memories?0 1 2 3 4\nXII. 19. Not knowing who you really are or what you want out of life? 0 1 2 3 4\n20. Not feeling close to other people or enjoying your relationships \nwith them?01 23 4\nXIII. 21. Drink at least 4 drinks of any kind of alcohol in a single day? 0 1 2 3 4\n22. Smoke any cigarettes, a cigar, or pipe, or use snuff or chewing \ntobacco?0 1 2 3 4\n23. Use any of the following medicines ON YOUR OWN, that is, \nwithout a doctor\u2019s prescription, in greater amounts or longer", "source": "dsm5.pdf"} {"id": "a8b0bad6dbaf-1", "page_content": "without a doctor\u2019s prescription, in greater amounts or longer \nthan prescribed [e.g., painkillers (like Vicodin), stimulants (like \nRitalin or Adderall), sedatives or tranquilizers (like sleeping \npills or Valium), or drugs like marijuana, cocaine or crack, club \ndrugs (like ecstasy), hallucinogen s (like LSD), heroin, inhalants \nor solvents (like glue), or methamphetamine (like speed)]?0 1 2 3 4", "source": "dsm5.pdf"} {"id": "df530d728ceb-0", "page_content": "740 Assessment MeasuresParent/Guardian-Rated DSM-5 Level 1 Cros s-Cutting Symptom Measure\u2014Child Age 6\u201317\nChild\u2019s Name:__________________________________________ ___ Age: __________ Sex: [ ] Male [ ] Female Date:_____________\nRelationship to the child: ___________________________________\nInstructions (to parent or guardian of child): The questions below ask about things that might have bothered your child. For each question, circle the number that \nbest describes how much (or how often) your child has been bothered by each problem during t he past TWO (2) WEEKS.\nDuring the past TWO (2) WEEKS, how much (or how often) has your \nchild\u2026None\nNot at \nallSlight\nRare, less than \na day or twoMild\nSeveral \ndaysModerate\nMore than \nhalf the daysSevere\nNearly \nevery dayHighest \nDomain Score \n(clinician)\nI. 1.Complained of stomachaches, headaches, or other aches and \npains?0 1 2 3 4\n2.Said he/she was worried about hi s/her health or about getting \nsick?0 1 2 3 4\nII. 3. Had problems sleeping\u2014that is, trouble falling asleep, staying \nasleep, or waking up too early?01 23 4\nIII. 4.Had problems paying attention when he/she was in class or \ndoing his/her homework or read ing a book or playing a game?0 1 2 3 4\nIV. 5. Had less fun doing things than he/she used to? 0 1 2 3 4\n6. Seemed sad or depressed for several hours? 0 1 2 3 4\nV.\n and", "source": "dsm5.pdf"} {"id": "df530d728ceb-1", "page_content": "V.\n and\nVI.7.Seemed more irritated or easily annoyed than usual? 0 1 2 3 4\n8.Seemed angry or lost his/her temper? 0 1 2 3 4\nVII. 9. Starting lots more projects than usual or doing more risky things \nthan usual?01 23 4\n10. Sleeping less than usual for him/her but still has lots of energy? 0 1 2 3 4\nVIII. 11. Said he/she felt nervous, anxious, or scared? 0 1 2 3 4\n12. Not been able to stop worrying? 0 1 2 3 4\n13. Said he/she couldn\u2019t do things he/she wanted to or should have \ndone because they made him/her feel nervous? 0 1 2 3 4", "source": "dsm5.pdf"} {"id": "885e86617a12-0", "page_content": "Assessment Measures 741IX. 14. Said that he/she heard voices\u2014when there was no one there\u2014\nspeaking about him/her or tellin g him/her what to do or say-\ning bad things to him/her?01 23 4\n15. Said that he/she had a vision when he/she was completely awake\u2014\nthat is, saw something or someone that no one else could see?01 23 4\nX.16. Said that he/she had thoughts that kept coming into his/her \nmind that he/she would do so mething bad or that something \nbad would happen to him/her or to someone else?0 1 2 3 4\n17. Said he/she felt the need to chec k on certain things over and over \nagain, like whether a door was locked or whether the stove was \nturned off?0 1 2 3 4\n18. Seemed to worry a lot about things he/she touched being dirty or \nhaving germs or being poisoned?0 1 2 3 4\n19. Said that he/she had to do things in a certain way, like counting \nor saying special things out lo ud, in order to keep something \nbad from happening?0 1 2 3 4\nIn the past TWO (2) WEEKS, has your child\u2026\nXI. 20. Had an alcoholic beverage (beer, wine, liquor, etc.)? \u2751 Yes \u2751 No \u2751 Don\u2019t Know\n21. Smoked a cigarette, a cigar, or pipe, or used snuff or chewing \ntobacco?\u2751 Yes \u2751 No \u2751 Don\u2019t Know\n22. Used drugs like marijuana, cocaine or crack, club drugs (like \necstasy), hallucinogens (like LSD), heroin, inhalants or solvents", "source": "dsm5.pdf"} {"id": "885e86617a12-1", "page_content": "ecstasy), hallucinogens (like LSD), heroin, inhalants or solvents \n(like glue), or methamphetamine (like speed)?\u2751 Yes \u2751 No \u2751 Don\u2019t Know\n23. Used any medicine without a doctor \u2019s prescription (e.g., painkillers \n[like Vicodin], stimulants [like Ritalin or Adderall], sedatives or \ntranquilizers [like sleeping pills or Valium], or steroids)?\u2751 Yes \u2751 No \u2751 Don\u2019t Know\nXII. 24. In the past TWO (2) WEEKS, has he/she talked about wanting to \nkill himself/herself or about wanting to commit suicide?\u2751 Yes \u2751 No \u2751 Don\u2019t Know\n25. Has he/she EVER tried to kill himself/herself? \u2751 Yes \u2751 No \u2751 Don\u2019t Know", "source": "dsm5.pdf"} {"id": "34d83fe8abeb-0", "page_content": "742 Assessment Measures\nClinician-Rated Dimensions of\nPsychosis Symptom Severity\nAs described in the chapter \u201cSchizophrenia Spectrum and Other Psychotic Disorders,\u201d\npsychotic disorders are hetero geneous, and symptom severity can predict important as-\npects of the illness, such as the degree of cogn itive and/or neurobiological deficits. Dimen-\nsional assessments capture meaningful variation in the severity of symptoms, which may\nhelp with treatment planning, prognostic decision-making, and research on pathophysi-\nological mechanisms. The Clinician-Rated Dimensions of Psychosis Symptom Severity\nprovides scales for the dimensional assessment of the primary symptoms of psychosis, in-\ncluding hallucinations, delusions, disorganiz ed speech, abnormal psychomotor behavior,\nand negative symptoms. A scale for the dimensional assessment of cognitive impairment\nis also included. Many individuals with psyc hotic disorders have im pairments in a range\nof cognitive domains, which predict functional abilities. In addition, scales for dimensional\nassessment of depression and mania are provided , which may alert clinicians to mood pa-\nthology. The severity of mood symptoms in psychosis has prognostic value and guides\ntreatment. \nThe Clinician-Rated Dimensions of Psychosis Symptom Severity is an 8-item measure\nthat may be completed by the clinician at the time of the clinical assessment. Each item asks\nthe clinician to rate the severity of each sy mptom as experienced by the individual during\nthe past 7 days.\nScoring and Interpretation\nEach item on the measure is rated on a 5-poin t scale (0=none; 1=equivocal; 2=present, but\nmild; 3=present and moderate; and 4=present and severe) with a sy mptom-specific defi-", "source": "dsm5.pdf"} {"id": "34d83fe8abeb-1", "page_content": "nition of each rating level. The clinician may review all of the individual\u2019s available infor-\nmation and, based on clinical judgment, select (with checkmark) the level that most\naccurately describes the severity of the indivi dual\u2019s condition. The clinician then indicates\nthe score for each item in the \u201cScore\u201d column provided.\nFrequency of Use\nTo track changes in the indi vidual\u2019s symptom severity over time, the measure may be\ncompleted at regular intervals as clinically in dicated, depending on the stability of the in-\ndividual\u2019s symptoms an d treatment status. Consistently high scores on a particular do-\nmain may indicate significant and problematic areas for the individual that might warrant\nfurther assessment, treatment, and follow-up. Clinical judgment should guide decision\nmaking.", "source": "dsm5.pdf"} {"id": "da91e4712e4b-0", "page_content": "Assessment Measures 743Clinician-Rated Dimensions of Psychosis Symptom Severity \nName:______________________________________ ______ Age: __________ Sex: [ ] Male [ ] Female Date:________________\nInstructions: Based on all the information you have on the individual and usin g your clinical judgment, please rate (with checkmark) the pre sence and severity \nof the following symptoms as experienced by the in dividual in the past seven (7) days.\n\u00a0Domain 0 1 2 3 4 Score\nI. Hallucinations \u2751 Not present \u2751 Equivocal (severity or \nduration not sufficient \nto be considered psy-\nchosis)\u2751 Present, but mild (lit-\ntle pressure to act \nupon voices, not very \nbothered by voices)\u2751 Present and moderate \n(some pressure to \nrespond to voices, or \nis somewhat bothered \nby voices)\u2751 Present and severe \n(severe pressure to \nrespond to voices, or \nis very bothered by \nvoices)\nII. Delusions \u2751 Not present \u2751 Equivocal (severity or \nduration not sufficient \nto be considered psy-\nchosis)\u2751 Present, but mild (lit-\ntle pressure to act \nupon delusional \nbeliefs, not very both-\nered by beliefs)\u2751 Present and moderate \n(some pressure to act \nupon beliefs, or is \nsomewhat bothered \nby beliefs)\u2751 Present and severe \n(severe pressure to act \nupon beliefs, or is very \nbothered by beliefs)\nIII. Disorganized speech \u2751 Not present \u2751 Equivocal (severity or \nduration not sufficient \nto be considered dis-\norganization)\u2751 Present, but mild", "source": "dsm5.pdf"} {"id": "da91e4712e4b-1", "page_content": "to be considered dis-\norganization)\u2751 Present, but mild \n(some difficulty fol-\nlowing speech)\u2751 Present and moderate \n(speech often difficult \nto follow)\u2751 Present and severe \n(speech almost impos-\nsible to follow)\nIV. Abnormal psychomo-\ntor behavior\u2751 Not present \u2751 Equivocal (severity or \nduration not sufficient \nto be considered \nabnormal psychomo-\ntor behavior)\u2751 Present, but mild \n(occasional abnormal \nor bizarre motor \nbehavior or catatonia)\u2751 Present and moderate \n(frequent abnormal or \nbizarre motor behav-\nior or catatonia)\u2751 Present and severe \n(abnormal or bizarre \nmotor behavior or \ncatatonia almost con-\nstant)\nV. Negative symptoms \n(restricted emotional \nexpression or avolition)\u2751 Not present \u2751 Equivocal decrease in \nfacial expressivity, \nprosody, gestures, or \nself-initiated behavior\u2751 Present, but mild \ndecrease in facial \nexpressivity, pros-\nody, gestures, or self-\ninitiated behavior\u2751 Present and moderate \ndecrease in facial \nexpressivity, pros-\nody, gestures, or self-\ninitiated behavior\u2751 Present and severe \ndecrease in facial \nexpressivity, pros-\nody, gestures, or self-\ninitiated behavior", "source": "dsm5.pdf"} {"id": "9b9736ed12b6-0", "page_content": "744 Assessment Measures\u00a0Domain 0 1 2 3 4 Score\nVI. Impaired cognition \u2751 Not present \u2751 Equivocal (cognitive \nfunction not clearly \noutside the range \nexpected for age or \nSES; i.e., within 0.5 SD \nof mean)\u2751 Present, but mild \n(some reduction in \ncognitive function; \nbelow expected for \nage and SES, 0.5\u20131 SD \nfrom mean)\u2751 Present and moderate \n(clear reduction in \ncognitive function; \nbelow expected for \nage and SES, 1\u20132 SD \nfrom mean)\u2751 Present and severe \n(severe reduction in \ncognitive function; \nbelow expected for \nage and SES, >2 SD \nfrom mean)\nVII. Depression \u2751 Not present \u2751 Equivocal (occasion-\nally feels sad, down, \ndepressed, or hope-\nless; concerned about \nhaving failed some-\none or at something \nbut not preoccupied)\u2751 Present, but mild (fre-\nquent periods of feel-\ning very sad, down, \nmoderately \ndepressed, or hope-\nless; concerned about \nhaving failed some-\none or at something, \nwith some preoccupa-\ntion)\u2751 Present and moderate \n(frequent periods of \ndeep depression or \nhopelessness; preoc-\ncupation with guilt, \nhaving done wrong)\u2751 Present and severe \n(deeply depressed or \nhopeless daily; delu-\nsional guilt or unrea-\nsonable self-reproach \ngrossly out of propor-\ntion to circumstances)", "source": "dsm5.pdf"} {"id": "9b9736ed12b6-1", "page_content": "sonable self-reproach \ngrossly out of propor-\ntion to circumstances)\nVIII. Mania \u2751 Not present \u2751 Equivocal (occasional \nelevated, expansive, \nor irritable mood or \nsome restlessness)\u2751 Present, but mild (fre-\nquent periods of \nsomewhat elevated, \nexpansive, or irritable \nmood or restlessness)\u2751 Present and moderate \n(frequent periods of \nextensively elevated, \nexpansive, or irritable \nmood or restlessness)\u2751 Present and severe \n(daily and extensively \nelevated, expansive, \nor irritable mood or \nrestlessness)\nNote. SD=standard deviation; SES=socioeconomic status.", "source": "dsm5.pdf"} {"id": "c5013352fbcf-0", "page_content": "Assessment Measures 745\nWorld Health Organization\n Disability Assessment Schedule 2.0\nThe adult self-administered vers ion of the World Health Organization Disability Assessment\nSchedule 2.0 (WHODAS 2.0) is a 36-item measur e that assesses disability in adults age 18\nyears and older. It assesses disability across six domains, including understanding and\ncommunicating, getting around, self-care, gett ing along with people, life activities (i.e.,\nhousehold, work, and/or school activities), an d participation in society. If the adult indi-\nvidual is of impaired capacity and unable to complete the form (e.g., a patient with demen-\ntia), a knowledgeable informant may complete the proxy-administered version of the\nmeasure, which is available at www.psychiatry. org/dsm5. Each item on the self-administered\nversion of the WHODAS 2.0 asks the individual to rate how much difficulty he or she has\nhad in specific areas of functioning during the past 30 days.\nWHODAS 2.0 Scoring Instructions Provided by WHO\nWHODAS 2.0 summary scores. There are two basic options for computing the summary\nscores for the WHODAS 2.0 36-item full version.\nSimple: The scores assigned to each of the items\u2014\u201cnone\u201d (1), \u201cmild\u201d (2), \u201cmoderate\u201d (3),\n\u201csevere\u201d (4), and \u201cextreme\u201d (5 )\u2014are summed. This method is referred to as simple scoring\nbecause the scores from each of the items are simply added up withou t recoding or collaps-\ning of response categories; thus, there is no we ighting of individual items. This approach is", "source": "dsm5.pdf"} {"id": "c5013352fbcf-1", "page_content": "practical to use as a hand-scoring approach, and may be the method of choice in busy clin-\nical settings or in paper-and-pencil interview situations. As a result, the simple sum of the\nscores of the items across all domains constitutes a statistic that is suff icient to describe the\ndegree of functional limitations.\nComplex: The more complex method of scoring is called \u201citem-response-theory\u201d\n(IRT)\u2013based scoring. It takes into account mu ltiple levels of diffic ulty for each WHODAS\n2.0 item. It takes the coding for each item response as \u201cnone,\u201d \u201cmild,\u201d \u201cmoderate,\u201d \u201cse-\nvere,\u201d and \u201cextreme\u201d separately, and then uses a computer to determine the summary\nscore by differentially weighting the items and the levels of severity. The computer pro-\ngram is available from the WHO Web site. The scoring has three steps:\n\u2022 Step 1\u2014Summing of recoded item scores within each domain.\n\u2022 Step 2\u2014Summing of all six domain scores.\n\u2022 Step 3\u2014Converting the summary score in to a metric ranging from 0 to 100 \n(where 0=no disability; 100=full disability).\nWHODAS 2.0 domain scores. WHODAS 2.0 produces domain-specific scores for six\ndifferent functioning domains: cognition, mobilit y, self-care, getting along, life activities\n(household and work/school), and participation.\nWHODAS 2.0 population norms. For the population norms fo r IRT-based scoring of the\nWHODAS 2.0 and for the population distribution of IRT-based scores for WHODAS 2.0,\nplease see www.who.int/clas sifications/icf/Pop_norms_distrib_IRT_scores.pdf.", "source": "dsm5.pdf"} {"id": "c5013352fbcf-2", "page_content": "Additional Scoring and Inte rpretation Guidance for \nDSM-5 Users\nThe clinician is asked to review the individu al\u2019s response on each item on the measure\nduring the clinical interview and to indicate th e self-reported score for each item in the sec-\ntion provided for \u201cClinician Use Only.\u201d However, if the clinician determines that the score\non an item should be different based on the clinical interview and other information avail-", "source": "dsm5.pdf"} {"id": "2c58b025ce88-0", "page_content": "746 Assessment Measures\nable, he or she may indicate a corrected score in the raw item score box. Based on findings\nfrom the DSM-5 Field Trials in adult patient samples across si x sites in the United States\nand one in Canada, DSM-5 recommends calculation and use of average scores for each domain\nand for general disability. The average scores are comparab le to the WHODAS 5-point scale,\nwhich allows the clinician to think of the individual\u2019s disability in terms of none (1), mild\n(2), moderate (3), severe (4 ), or extreme (5). The averag e domain and general disability\nscores were found to be reliable, easy to use, and clinically useful to the clinicians in the\nDSM-5 Field Trials. The average domain score is calculated by dividing the raw domain score\nby the number of items in the domain (e.g., if all the items within the \u201cunderstanding and\ncommunicating\u201d domain are rated as being moderate then the average domain score\nwould be 18/6=3, indicating moderate disability). The average general disability score is cal-\nculated by dividing the raw overall score by nu mber of items in the measure (i.e., 36). The\nindividual should be encouraged to complete a ll of the items on the WHODAS 2.0. If no re-\nsponse is given on 10 or more items of the measure (i.e., more than 25% of the 36 total\nitems), calculation of the simple and average general disability scores may not be helpful.\nIf 10 or more of the total items on the measur e are missing but the items for some of the do-\nmains are 75%\u2013100% complete, the simple or aver age domain scores may be used for those\ndomains.", "source": "dsm5.pdf"} {"id": "2c58b025ce88-1", "page_content": "domains.\nFrequency of use. To track change in the individual\u2019s level of disability over time, the\nmeasure may be completed at regular intervals as clinically indicated, depending on the\nstability of the individual\u2019s symptoms and trea tment status. Consistently high scores on a\nparticular domain may indicate significant and problematic areas for the individual that\nmight warrant further assessment and intervention.", "source": "dsm5.pdf"} {"id": "35d3cd7355bb-0", "page_content": "Assessment Measures 747\nWHODAS 2.0 \nWorld Health Organization Disability Assessment Schedule 2.0 \n36-item version, self-administered \n3DWLHQW\u00031DPH\u001d\u0003 BBBBBBBBBBBBBBBBBBBBBBB$JH\u001d\u0003 BBBBBB\u0003 \u0003 6H[\u001d\u0003\u0089\u00030DOH\u0003\u0089\u0003)HPDOH\u0003\u0003 ' D W H \u001dBBBBBBBBBBBBB \u0003\nThis questionnaire asks about difficulties due to health /mental health conditions. Health conditions include diseases or \nillnesses, other health problems that may be short or long lasting, injuries, mental or emotional problems, and problems \nwith alcohol or drugs. Think back over the past 30 days and answer these questions thinking about how much difficulty you \nhad doing the following activities. For each question, please circle only one response. \n Clinician\u0003Use\u0003\nOnly\u0003\nNumeric scores assigned to each of the items: 1 2 3 4 5 \nRaw Item \nScore \nRaw \nDomain \nScore \nAverage \nDomain \nScore In the last 30 days, how much difficulty did you have in: \nUnderstanding and communicating \nD1.1 Concentrating on doing so mething for ten minutes? None Mild Moderate Severe Extreme or \ncannot do \n \n____ \n30 \n \n____ \n5 \n D1.2 Remembering to do important things? None Mild Moderate Severe Extreme or \ncannot do \nD1.3 Analyzing and finding solutions to problems in day-\nto-day life? None Mild Moderate Severe Extreme or \ncannot do \nD1.4 Learning a new task, for example, learning how to", "source": "dsm5.pdf"} {"id": "35d3cd7355bb-1", "page_content": "D1.4 Learning a new task, for example, learning how to \nget to a new place? None Mild Moderate Severe Extreme or \ncannot do \nD1.5 Generally understanding what people say? None Mild Moderate Severe Extreme or \ncannot do \nD1.6 Starting and maintaining a conversation? None Mild Moderate Severe Extreme or \ncannot do \nGetting around \nD2.1 Standing for long periods, such as 30 minutes? None Mild Moderate Severe Extreme or \ncannot do \n \n____ \n25 \n \n____ \n5 \n D2.2 Standing up from sitting down? None Mild Moderate Severe Extreme or \ncannot do \nD2.3 Moving around inside your home? None Mild Moderate Severe Extreme or \ncannot do \nD2.4 Getting out of your home? None Mild Moderate Severe Extreme or \ncannot do \nD2.5 Walking a long distance, such as a kilometer (or \nequivalent)? None Mild Moderate Severe Extreme or \ncannot do \nSelf-care \nD3.1 Washing your whole body? None Mild Moderate Severe Extreme or \ncannot do \n \n____ \n20 \n \n____ \n5 \n D3.2 Getting dressed? None Mild Moderate Severe Extreme or \ncannot do \nD3.3 Eating? None Mild Moderate Severe Extreme or \ncannot do \nD3.4 Staying by yourself for a few days? None Mild Moderate Severe Extreme or \ncannot do \nGetting along with people \nD4.1 Dealing with people you do not know? None Mild Moderate Severe Extreme or \ncannot do \n \n____ \n25 \n \n____", "source": "dsm5.pdf"} {"id": "35d3cd7355bb-2", "page_content": "cannot do \n \n____ \n25 \n \n____ \n5 \n D4.2 Maintaining a friendship? None Mild Moderate Severe Extreme or \ncannot do \nD4.3 Getting along with people who are close to you? None Mild Moderate Severe Extreme or \ncannot do \nD4.4 Making new friends? None Mild Moderate Severe Extreme or \ncannot do \nD4.5 Sexual activities? None Mild Moderate Severe Extreme or \ncannot do", "source": "dsm5.pdf"} {"id": "d2f2881a33f5-0", "page_content": "748 Assessment Measures\n Clinician\u0003Use\u0003\nOnly\u0003\nNumeric scores assigned to each of the items: 1 2 3 4 5 \nRaw Item \nScore \nRaw \nDomain \nScore \nAverage \nDomain \nScore In the last 30 days, how much difficulty did you have in: \nLife activities \u0376Household \nD5.1 Taking care of your household responsibilities? None Mild Moderate Severe Extreme or \ncannot do \n \n____ \n20 \n \n____ \n5 \n D5.2 Doing most important household tasks well? None Mild Moderate Severe Extreme or \ncannot do \nD5.3 Getting all of the household work done that you \nneeded to do? None Mild Moderate Severe Extreme or \ncannot do \nD5.4 Getting your household work done as quickly as \nneeded? None Mild Moderate Severe Extreme or \ncannot do \nLife activities \u0376School/Work \nIf you work (paid, non-paid, self-employed) or go to school, complete questions D5.5 \u0374D5.8, below. \nOtherwise, skip to D6.1. \nBecause of your health condition, in the past 30 days, how much difficulty did you have in: \nD5.5 Your day-to-day work/school? None Mild Moderate Severe Extreme or \ncannot do \n \n____ \n20 \n \n____ \n5 \n D5.6 Doing your most important work/school tasks well? None Mild Moderate Severe Extreme or \ncannot do \nD5.7 Getting all of the work done that you need to do? None Mild Moderate Severe Extreme or \ncannot do", "source": "dsm5.pdf"} {"id": "d2f2881a33f5-1", "page_content": "cannot do \nD5.8 Getting your work done as quickly as needed? None Mild Moderate Severe Extreme or \ncannot do \nParticipation in society \nIn the past 30 days: \nD6.1 How much of a problem did you have in joining in \ncommunity activities (for example, festivities, \nreligious, or other activities) in the same way as \nanyone else can? None Mild Moderate Severe Extreme or \ncannot do \n \n____ \n40 \n \n____ \n5 \n D6.2 How much of a problem did you have because of \nbarriers or hindrances around you? \nNone \nMild \nModerate \nSevere Extreme or \ncannot do \nD6.3 How much of a problem did you have living with \ndignity because of the attitudes and actions of \nothers? None Mild Moderate Severe Extreme or \ncannot do \nD6.4 How much time did you spend on your health \ncondition or its consequences? None Some Moderate A Lot Extreme or \ncannot do \nD6.5 How much have you been emotionally affected by \nyour health condition? None Mild Moderate Severe Extreme or \ncannot do \nD6.6 How much has your health been a drain on the \nfinancial resources of you or your family? None Mild Moderate Severe Extreme or \ncannot do \nD6.7 How much of a problem did your family have \nbecause of your health problems? None Mild Moderate Severe Extreme or \ncannot do \nD6.8 How much of a problem did you have in doing \nthings by yourself for relaxation or pleasure? None Mild Moderate Severe Extreme or \ncannot do \nGeneral Disability Score (Total): ____", "source": "dsm5.pdf"} {"id": "d2f2881a33f5-2", "page_content": "cannot do \nGeneral Disability Score (Total): ____ \n180 ____ \n5 \n\u008b\u0003:RUOG\u0003+HDOWK\u00032UJDQL]DWLRQ\u000f\u0003\u0015\u0013\u0014\u0015\u0011\u0003$OO\u0003ULJKWV\u0003UHVHUYHG\u0011\u00030HDVXUL QJ\u0003KHDOWK\u0003DQG\u0003GLVDELOLW\\\u001d\u0003PDQXDO\u0003IRU\u0003:+2\u0003'LVDELOLW\\\u0003\n$VVHVVPHQW\u00036FKHGXOH\u0003\u000b:+2'$6\u0003\u0015\u0011\u0013\f \u000f\u0003:RUOG\u0003+HDOWK\u00032UJDQL]DWLRQ\u000f\u0003\u0015\u0013 \u0014\u0013\u000f\u0003*HQHYD\u0011\u0003\n\u0003\n7KH\u0003:RUOG\u0003+HDOWK\u00032UJDQL]DWLRQ\u0003KD V\u0003JUDQWHG\u0003WKH\u00033XEOLVKHU\u0003SHUPLVV LRQ\u0003IRU\u0003WKH\u0003UHSURGXFWLRQ\u0003RI\u0003WKLV\u0003 LQVWUXPHQW\u0011\u00037KLV\u0003PDWHULDO\u0003FDQ\u0003\nEH\u0003UHSURGXFHG\u0003ZLWKRXW\u0003SHUPLVVLRQ\u0003E\\\u0003FOLQLFLDQV\u0003IRU\u0003XVH\u0003ZLWK\u0003WKH LU\u0003RZQ\u0003SDWLHQWV\u0011\u0003$Q\\\u0003RWKHU\u0003XVH\u000f\u0003LQFOXGLQJ\u0003HOHFWURQLF\u0003XVH\u000f\u0003", "source": "dsm5.pdf"} {"id": "d2f2881a33f5-3", "page_content": "UHTXLUHV\u0003ZULWWHQ\u0003SHUPLVVLRQ\u0003IURP\u0003:+2\u0011 \u0003\u00a9 World Health Organization, 2012. All rights reserved. Measuring health and disability: manual for WHO Disability\nAssessment Schedule (WHODAS 2.0), World Health Organization, 2010, Geneva.\nThe World Health Organization has granted the Publisher permission for the reproduction of this instrument. This material can\nbe reproduced without permission by clinicians for use with their own patients. Any other use, including electronic use,\nrequires written permission from WHO.", "source": "dsm5.pdf"} {"id": "679f1b2555ce-0", "page_content": "749Cultural\n Formulation\nUnderstanding the cultural context of illness experience is essential for effec-\ntive diagnostic assessment and clinical management. Culture refers to systems of knowl-\nedge, concepts, rules, and practices that ar e learned and transmitted across generations.\nCulture includes language, religion and spirit uality, family structur es, life-cycle stages,\nceremonial rituals, and customs, as well as moral and legal systems. Cultures are open,\ndynamic systems that undergo continuous ch ange over time; in the contemporary world,\nmost individuals and groups are exposed to mu ltiple cultures, which they use to fashion\ntheir own identities and make sense of experi ence. These features of culture make it cru-\ncial not to overgeneralize cultur al information or stereotype groups in terms of fixed cul-\ntural traits.\nRace is a culturally constructed category of identity that divides humanity into groups\nbased on a variety of superficia l physical traits attributed to some hypothetical intrinsic,\nbiological characteristics. Racial categories an d constructs have varied widely over history\nand across societies. The construct of race has no consistent biological definition, but it is\nsocially important because it supports racial ideologies, racism, discrimination, and social\nexclusion, which can have strong negative effe cts on mental health. There is evidence that\nracism can exacerbate many psychiatric disord ers, contributing to poor outcome, and that\nracial biases can affect diagnostic assessment.\nEthnicity is a culturally constructed group identity used to define peoples and communi-\nties. It may be rooted in a common history, geography, language, religion, or other shared\ncharacteristics of a group, which distinguish th at group from others. Ethnicity may be self-\nassigned or attributed by out siders. Increasing mobility, inte rmarriage, and intermixing of", "source": "dsm5.pdf"} {"id": "679f1b2555ce-1", "page_content": "cultures has defined new mixed, multiple, or hybrid ethnic identities.\nCulture, race, and ethnicity are related to economic inequities, racism, and discrimina-\ntion that result in health disparities. Cultural , ethnic, and racial identities can be sources of\nstrength and group support that enhance resilie nce, but they may also lead to psycholog-\nical, interpersonal, and intergen erational conflict or difficultie s in adaptation that require\ndiagnostic assessment.\nOutline for Cultural Formulation\nThe Outline for Cultural Formulation introduc ed in DSM-IV provided a framework for as-\nsessing information about cultural features of an individu al\u2019s mental health problem and\nhow it relates to a social and cultural context and history. DS M-5 not only includes an up-\ndated version of the Outline but also presents an approach to assessment, using the Cul-\ntural Formulation Interview (CFI), which has been field-tested for diagnostic usefulness\namong clinicians and for acceptability among patients.\nThe revised Outline for Cultur al Formulation calls for syst ematic assessment of the fol-\nlowing categories:\n\u2022Cultural identity of the individual: Describe the individual\u2019s racial, ethnic, or cultural\nreference groups that may influence his or he r relationships with others, access to re-", "source": "dsm5.pdf"} {"id": "fe6d24268681-0", "page_content": "750 Cultural Formulation\nsources, and developmental and current chal lenges, conflicts, or predicaments. For im-\nmigrants and racial or ethnic minorities, th e degree and kinds of involvement with both\nthe culture of origin and the ho st culture or majority cultur e should be noted separately.\nLanguage abilities, preferences, and patterns of use are relevant for identifying difficul-\nties with access to care, social integration, and the need fo r an interprete r. Other clini-\ncally relevant aspects of identity may in clude religious affiliation, socioeconomic\nbackground, personal and family places of birth and growing up, migrant status, and\nsexual orientation.\n\u2022Cultural conceptualizations of distress: Describe the cultural constructs that influence\nhow the individual experiences, understands, and communicates his or her symptoms\nor problems to others. These constructs may include cultural syndromes, idioms of dis-\ntress, and explanatory models or perceived causes. The level of severity and meaning of\nthe distressing experiences shou ld be assessed in relation to the norms of the individ-\nual\u2019s cultural reference groups. Assessment of coping and help-seeking patterns should\nconsider the use of profession al as well as traditional, alternative, or complementary\nsources of care.\n\u2022Psychosocial stressors and cultural feat ures of vulnerability and resilience: Identify\nkey stressors and supports in the individual \u2019s social environment (which may include\nboth local and distant events) and the role of religion, family, and other social networks\n(e.g., friends, neighb ors, coworkers) in providing emotional, instrumental, and infor-\nmational support. Social stressors and social supports vary with cultural interpreta-\ntions of events, family structure, developm ental tasks, and social context. Levels of", "source": "dsm5.pdf"} {"id": "fe6d24268681-1", "page_content": "functioning, disability, and resilience should be assessed in light of the individual\u2019s cul-\ntural reference groups.\n\u2022Cultural features of the relationship between the individual and the clinician: Iden-\ntify differences in culture, language, and social status between an individual and clini-\ncian that may cause difficulties in communication and may influence diagnosis and\ntreatment. Experiences of racism and discri mination in the larger society may impede\nestablishing trust and safety in the clinical diagnostic encounter. Effects may include\nproblems eliciting symptoms, misunderstanding of the cultural and clinical signifi-\ncance of symptoms and behaviors, and diffi culty establishing or maintaining the rap-\nport needed for an effe ctive clinical alliance.\n\u2022Overall cultural assessment: Summarize the implications of the components of the cul-\ntural formulation identified in earlier sections of the Ou tline for diagnosis and other\nclinically relevant issues or problems as well as appropriate management and treat-\nment intervention.\nCultural Formulation Interview (CFI)\nThe Cultural Formulation Interview (CFI) is a set of 16 questions that clinicians may use to\nobtain information during a me ntal health assessment about the impact of culture on key\naspects of an individual\u2019s clinical presentation and care. In the CFI, culture refers to\n\u2022 The values, orientations, kn owledge, and practices that individuals derive from mem-\nbership in diverse social groups (e.g., et hnic groups, faith communities, occupational\ngroups, veterans groups).\n\u2022 Aspects of an individual\u2019s background, de velopmental experiences, and current social\ncontexts that may affect his or her perspe ctive, such as geographical origin, migration,\nlanguage, religion, sexual orie ntation, or race/ethnicity.", "source": "dsm5.pdf"} {"id": "fe6d24268681-2", "page_content": "language, religion, sexual orie ntation, or race/ethnicity.\n\u2022 The influence of family, friends, and ot her community members (the individual\u2019s social\nnetwork ) on the individual\u2019s illness experience.", "source": "dsm5.pdf"} {"id": "a88293094aec-0", "page_content": "Cultural Formulation 751\nThe CFI is a brief semistructured interview for systematically assessing cultural factors\nin the clinical encounter that may be used with any individual. The CFI focuses on the in-\ndividual\u2019s experience and the so cial contexts of the clinical problem. The CFI follows a per-\nson-centered approach to cult ural assessment by eliciting information from the individual\nabout his or her own views and those of others in his or her social network. This approach\nis designed to avoid stereotyping, in that each individual\u2019s cultural knowledge affects how\nhe or she interprets illness experience and gu ides how he or she seeks help. Because the\nCFI concerns the individual\u2019s personal views, there are no right or wrong answers to these\nquestions. The interview follows and is available online at www.psychiatry.org/dsm5.\nThe CFI is formatted as two text columns. The left-hand column contains the instruc-\ntions for administering the CFI and describes the goals for each interview domain. The\nquestions in the right-hand column illustrate how to explore these domains, but they are\nnot meant to be exhaustive. Follow-up question s may be needed to clarify individuals\u2019 an-\nswers. Questions may be rephrased as needed. Th e CFI is intended as a guide to cultural as-\nsessment and should be used flexibly to maintain a natural flow of the interview and rapport\nwith the individual.\nThe CFI is best used in conjunction with demographic information obtained prior to\nthe interview in order to tailor the CFI ques tions to address the in dividual\u2019s background\nand current situation. Specific demographic do mains to be explored with the CFI will vary\nacross individuals and settings. A comprehens ive assessment may include place of birth,", "source": "dsm5.pdf"} {"id": "a88293094aec-1", "page_content": "across individuals and settings. A comprehens ive assessment may include place of birth,\nage, gender, racial/ethnic origin, marital stat us, family composition, education, language\nfluencies, sexual orientation, religious or sp iritual affiliation, occupation, employment, in-\ncome, and migration history.\nThe CFI can be used in the initial assessment of individuals in all clinical settings, regard-\nless of the cultural background of the individual or of the clinician. Individuals and clini-\ncians who appear to share the same cultural background may nevertheless differ in ways\nthat are relevant to care. The CFI may be used in its entirety, or components may be incor-\nporated into a clinical evaluation as needed. The CFI may be es pecially helpful when there is\n\u2022 Difficulty in diagnostic assessment owing to significant differences in the cultural, re-\nligious, or socioeconomi c backgrounds of clinician and the individual.\n\u2022 Uncertainty about the fit between culturally distinctive symptoms and diagnostic criteria.\n\u2022 Difficulty in judging illness severity or impairment.\n\u2022 Disagreement between the individual an d clinician on the course of care.\n\u2022 Limited engagement in and adherenc e to treatment by the individual.\nThe CFI emphasizes four domains of assessmen t: Cultural Definition of the Problem\n(questions 1\u20133); Cultural Perceptions of Caus e, Context, and Support (questions 4\u201310); Cul-\ntural Factors Affecting Self-Coping and Past Help Seeking (questions 11\u201313); and Cultural\nFactors Affecting Current Help Seeking (questions 14\u201316). Both the person-centered process\nof conducting the CFI and the information it el icits are intended to enhance the cultural va-\nlidity of diagnostic assessmen t, facilitate treatment planning , and promote the individual\u2019s", "source": "dsm5.pdf"} {"id": "a88293094aec-2", "page_content": "lidity of diagnostic assessmen t, facilitate treatment planning , and promote the individual\u2019s\nengagement and satisfaction. To achieve these goals, the info rmation obtained from the CFI\nshould be integrated with all other available clinical material into a comprehensive clinical\nand contextual evaluation. An In formant version of the CFI can be used to collect collateral\ninformation on the CFI domains from family members or caregivers.\nSupplementary modules have b een developed that expand on each domain of the CFI\nand guide clinicians who wish to explore th ese domains in greater depth. Supplementary", "source": "dsm5.pdf"} {"id": "ad63103ae703-0", "page_content": "Supplementary modules have b een developed that expand on each domain of the CFI\nand guide clinicians who wish to explore th ese domains in greater depth. Supplementary\nmodules have also been developed for specific populations, such as children and adoles-\ncents, elderly individuals, and immigrants and refugees. These supplementary modules\nare referenced in the CFI under the pertin ent subheadings and are available online at\nwww.psychiatry.org/dsm5.", "source": "dsm5.pdf"} {"id": "62b1e09c4392-0", "page_content": "752 Cultural Formulation\nCultural Formulation Interview (CFI)\nSupplementary modules used to expand each CFI subtopic are noted in parentheses.\nGUIDE TO INTERVIEWERINSTRUCTIONS TO THE INTERVIEWER ARE \nITALICIZED.\nThe following questions aim to clarify key aspects of \nthe presenting clinical pr oblem from the point of \nview of the individual and other members of the \nindividual\u2019s social network (i.e., family, friends, or \nothers involved in current problem). This includes \nthe problem\u2019s meaning, potential sources of help, \nand expectations for services.INTRODUCTION FOR THE INDIVIDUAL:\nI would like to understand the problems that \nbring you here so that I can help you more \neffectively. I want to know about your experi-\nence and ideas. I will ask some questions \nabout what is going on and how you are deal-\ning with it. Please remember there are no \nright or wrong answers.\nCULTURAL DEFINITION OF THE PROBLEM\nCULTURAL DEFINITION OF THE PROBLEM\n(Explanatory Model, Level of Functioning)\nElicit the individual\u2019s view of core problems and key \nconcerns.\nFocus on the individual\u2019s own way of understand-\ning the problem.\nUse the term, expression, or brief description elicited \nin question 1 to identify the problem in subsequent \nquestions (e.g., \u201cyour conflict with your son\u201d).1. What brings you here today?\nIF INDIVIDUAL GIVES FEW DETAILS OR \nONLY MENTIONS SYMPTOMS OR A \nMEDICAL DIAGNOSIS, PROBE:\nPeople often understand their problems in \ntheir own way, which may be similar to or \ndifferent from how doctors describe the", "source": "dsm5.pdf"} {"id": "62b1e09c4392-1", "page_content": "their own way, which may be similar to or \ndifferent from how doctors describe the \nproblem. How would you describe your \nproblem?\nAsk how individual frames the problem for members \nof the social network.2. Sometimes people have different ways of \ndescribing their problem to their family, \nfriends, or others in their community. How \nwould you describe your problem to them?\nFocus on the aspects of the problem that matter most \nto the individual.3. What troubles you mo st about your prob-\nlem?\nCULTURAL PERCEPTIONS OF CA USE, CONTEXT, AND SUPPORT\nCAUSES\n(Explanatory Model, Social Network, Older Adults)\nThis question indicates the meaning of the condition \nfor the individual, which may be relevant for clin-\nical care.4. Why do you think this is happening to \nyou? What do you think are the causes of \nyour [PROBLEM]?\nNote that individuals may identify multiple causes, \ndepending on the facet of the problem they are con-\nsidering.PROMPT FURTHER IF REQUIRED:\nSome people may explain their problem as \nthe result of bad things that happen in their \nlife, problems with others, a physical ill-\nness, a spiritual reason, or many other \ncauses.\nFocus on the views of memb ers of the in dividual\u2019s \nsocial network. These may be diverse and vary from \nthe individual\u2019s.5. What do others in your family, your \nfriends, or others in your community think \nis causing your [PROBLEM]?", "source": "dsm5.pdf"} {"id": "7ff32f19c4c3-0", "page_content": "Cultural Formulation 753\nSTRESSORS AND SUPPORTS\n(Social Network, Caregivers, Psychosocial Stre ssors, Religion and Spirituality, Immigrants and \nRefugees, Cultural Identity, Older Adults, Coping and Help Seeking)\nElicit information on the individual\u2019s life context, \nfocusing on resources, social supports, and resil-\nience. May also probe other supports (e.g., from co-\nworkers, from participation in religion or spiritu-\nality).6. Are there any kinds of support that make \nyour [PROBLEM] better, such as support \nfrom family, friends, or others?\nFocus on stressful aspects of the individual\u2019s envi-\nronment. Can also probe, e.g., relationship prob-\nlems, difficulties at work or school, or \ndiscrimination.7. Are there any kinds of stresses that make \nyour [PROBLEM] worse, such as difficul-\nties with money, or family problems?\nROLE OF CULTURAL IDENTITY\n(Cultural Identity, Psychosocial Stressors, Relig ion and Spirituality, Immigrants and Refugees, \nOlder Adults, Children and Adolescents)\nSometimes, aspects of people\u2019s back-\nground or identity can make their [PROB-\nLEM] better or worse. By background or \nidentity, I mean, for example, the commu-\nnities you belong to, the languages you \nspeak, where you or your family are from, \nyour race or ethnic background, your gen-\nder or sexual orientation, or your faith or \nreligion.\nAsk the individual to reflect on the most salient ele-\nments of his or her cult ural identity. Use this", "source": "dsm5.pdf"} {"id": "7ff32f19c4c3-1", "page_content": "ments of his or her cult ural identity. Use this \ninformation to tailor questions 9\u201310 as needed.8. For you, what are the most important \naspects of your back ground or identity?\nElicit aspects of identity that make the problem bet-\nter or worse.\nProbe as needed (e.g., cl inical worsening as a result \nof discrimination due to migration status, race/\nethnicity, or sexual orientation).9. Are there any aspects of your background \nor identity that make a difference to your \n[PROBLEM]?\nProbe as needed (e.g., migration-related problems; \nconflict across generations or due to gender roles).10. Are there any aspects of your background \nor identity that are causing other concerns \nor difficulties for you?\nCULTURAL FACTORS AFFECTING SELF- COPING AND PAST HELP SEEKING\nSELF-COPING\n(Coping and Help Seeking, Religion and Spirituality, Older Adults, Caregivers, \nPsychosocial Stressors)\nClarify self-coping for the problem. 11. Sometimes people have various ways of \ndealing with problems like [PROBLEM]. \nWhat have you done on your own to cope \nwith your [PROBLEM]?Cultural Formulation Interview (CFI) (continued)\nSupplementary modules used to expand each CFI subtopic are noted in parentheses.\nGUIDE TO INTERVIEWERINSTRUCTIONS TO THE INTERVIEWER ARE \nITALICIZED.", "source": "dsm5.pdf"} {"id": "d80052eda30a-0", "page_content": "754 Cultural Formulation\nPAST HELP SEEKING\n(Coping and Help Seeking, Religion and Spirituality, Older Adults, Care givers, Psychosocial \nStressors, Immigrants and Refu gees, Social Network, Clinician-Patient Relationship)\nElicit various sources of help (e.g., medical care, \nmental health treatment, support groups, work-\nbased counseling, folk healing, religious or spiri-\ntual counseling, other form s of traditional or alter-\nnative healing).\nProbe as needed (e.g., \u201cWhat other sources of help \nhave you used?\u201d).\nClarify the indivi dual\u2019s experience and regard for \nprevious help.12. Often, people look for help from many dif-\nferent sources, including different kinds of \ndoctors, helpers, or healers. In the past, \nwhat kinds of treatment, help, advice, or \nhealing have you sought for your [PROB-\nLEM]?\nPROBE IF DOES NOT DESCRIBE USE-\nFULNESS OF HELP RECEIVED:\nWhat types of help or treatment were most \nuseful? Not useful?\nBARRIERS\n(Coping and Help Seeking, Religion and Spirituality, Older Adults, Psychosocial Stressors, Immi-\ngrants and Refugees, Social Network, Clinician-Patient Relationship)\nClarify the role of social barriers to help seeking, \naccess to care, and problems engaging in previous \ntreatment.\nProbe details as needed (e.g., \u201cWhat got in the \nway?\u201d).13. Has anything prevented you from getting \nthe help you need?\nPROBE AS NEEDED:\nFor example, money, work or family com-\nmitments, stigma or discrimination, or lack \nof services that unde rstand your language \nor background?", "source": "dsm5.pdf"} {"id": "d80052eda30a-1", "page_content": "of services that unde rstand your language \nor background?\nCULTURAL FACTORS AFFECT ING CURRENT HELP SEEKING\nPREFERENCES\n(Social Network, Caregivers, Re ligion and Spirituality, Older Adults, Coping and Help Seeking)\nClarify individual\u2019s cu rrent perceived needs and \nexpectations of he lp, broadly defined.\nProbe if individual lists only one source of help (e.g., \n\u201cWhat other kinds of help would be useful to you \nat this time?\u201d).Now let\u2019s talk some more about the help \nyou need.\n14. What kinds of help do you think would be \nmost useful to you at this time for your \n[PROBLEM]?\nFocus on the views of the social network regarding \nhelp seeking.15. Are there other kinds of help that your fam-\nily, friends, or other people have suggested \nwould be helpful for you now?\nCLINICIAN -PATIENT RELATIONSHIP\n(Clinician-Patient Relationship, Older Adults)\nElicit possible concerns abou t the clinic or the clini-\ncian-patient relationship, including perceived rac-\nism, language barriers, or cultural differences that \nmay undermine goodwill, communication, or care \ndelivery.\nProbe details as needed (e.g., \u201cIn what way?\u201d).\nAddress possible barriers to care or concerns about \nthe clinic and the clinician-patient relationship \nraised previously.Sometimes doctors and patients misunder-\nstand each other because they come from \ndifferent backgrounds or have different \nexpectations.\n16. Have you been concerned about this and is \nthere anything that we can do to provide \nyou with the care you need?Cultural Formulation Interview (CFI) (continued)\nSupplementary modules used to expand each CFI subtopic are noted in parentheses.", "source": "dsm5.pdf"} {"id": "d80052eda30a-2", "page_content": "Supplementary modules used to expand each CFI subtopic are noted in parentheses.\nGUIDE TO INTERVIEWERINSTRUCTIONS TO THE INTERVIEWER ARE \nITALICIZED.", "source": "dsm5.pdf"} {"id": "7ec833c720c2-0", "page_content": "Cultural Formulation 755\nCultural Formulation Interview (CFI)\u2014Informant Version\nThe CFI\u2013Informant Version co llects collateral information from an informant who is\nknowledgeable about the clinical problems and life circumstances of the identified indi-\nvidual. This version can be used to suppleme nt information obtained from the core CFI or\ncan be used instead of the core CFI when the individual is unable to provide information\u2014\nas might occur, for example, with children or adolescents, floridly psychotic individuals,\nor persons with cognitive impairment.\nCultural Formulation Interv iew (CFI)\u2014Informant Version\nGUIDE TO INTERVIEWERINSTRUCTIONS TO THE INTERVIEWER ARE \nITALICIZED.\nThe following questions aim to clarify key aspects of \nthe presenting cl inical problem from the infor-\nmant\u2019s point of view. Th is includes the problem\u2019s \nmeaning, potential sources of help, and expecta-\ntions for services.INTRODUCTION FOR THE INFORMANT:\nI would like to understand the problems that \nbring your family me mber/friend here so \nthat I can help you and him/her more effec-\ntively. I want to know about your experience \nand ideas. I will ask some questions about \nwhat is going on and how you and your fam-\nily member/friend are dealing with it. There \nare no right or wrong answers.\nRELATIONSHIP WITH THE PATIENT\nClarify the informant\u2019s rela tionship with the indi-\nvidual and/or the individual\u2019s family.1. How would you describe your relationship \nto [INDIVIDUAL OR TO FAMILY]?\nPROBE IF NOT CLEAR:\nHow often do you see [INDIVIDUAL]?\nCULTURAL DEFINITION OF THE PROBLEM", "source": "dsm5.pdf"} {"id": "7ec833c720c2-1", "page_content": "CULTURAL DEFINITION OF THE PROBLEM\nElicit the informant\u2019s view of core problems and key \nconcerns.\nFocus on the informant\u2019s way of understanding the \nindividual\u2019s problem.\nUse the term, expression, or brief description elicited \nin question 1 to identify the problem in subsequent \nquestions (e.g., \u201cher conflict with her son\u201d).2. What brings your family member/friend \nhere today?\nIF INFORMANT GIVES FEW DETAILS OR \nONLY MENTIONS SYMPTOMS OR A \nMEDICAL DIAGNOSIS, PROBE:\nPeople often understand problems in their \nown way, which may be similar or differ-\nent from how doctors describe the prob-\nlem. How would you describe \n[INDIVIDUAL\u2019S] problem?\nAsk how informant frames the problem for members \nof the social network.3. Sometimes people have different ways of \ndescribing the problem to family, friends, \nor others in their community. How would \nyou describe [INDIVIDUAL\u2019S] problem to \nthem?\nFocus on the aspects of the problem that matter most \nto the informant.4. What troubles you most about [INDIVID-\nUAL\u2019S] problem?", "source": "dsm5.pdf"} {"id": "ee983968960a-0", "page_content": "756 Cultural Formulation\nCULTURAL PERCEPTIONS OF CA USE, CONTEXT, AND SUPPORT\nCAUSES\nThis question indicates the meaning of the condition \nfor the informant, which may be relevant for clini-\ncal care.\nNote that informants may identify multiple causes \ndepending on the facet of the problem they are con-\nsidering.5. Why do you think this is happening to \n[INDIVIDUAL]? What do you think are the \ncauses of his/her [PROBLEM]?\nPROMPT FURTHER IF REQUIRED:\nSome people may explain the problem as the \nresult of bad things that happen in their life, \nproblems with others, a physical illness, a \nspiritual reason, or many other causes.\nFocus on the views of me mbers of the in dividual\u2019s \nsocial network. These may be diverse and vary \nfrom the informant\u2019s.6. What do others in [INDIVIDUAL\u2019S] fam-\nily, his/her friends, or others in the com-\nmunity think is causing [INDIVIDUAL\u2019S] \n[PROBLEM]?\nSTRESSORS AND SUPPORTS\nElicit information on the individual\u2019s life context, \nfocusing on resources, so cial supports, and resil-\nience. May also probe oth er supports (e.g., from co-\nworkers, from participation in religion or spiritu-\nality).7. Are there any kinds of supports that make \nhis/her [PROBLEM] better, such as from \nfamily, friends, or others?\nFocus on stressful aspects of the individual\u2019s environ-\nment. Can also probe, e.g., relationship problems, dif-\nficulties at work or school, or discrimination.8. Are there any kinds of stresses that make", "source": "dsm5.pdf"} {"id": "ee983968960a-1", "page_content": "his/her [PROBLEM] worse, such as diffi-\nculties with money, or family problems?\nROLE OF CULTURAL IDENTITY\nSometimes, aspects of people\u2019s background \nor identity can make the [PROBLEM] better \nor worse. By background or identity, I mean, \nfor example, the commun ities you belong to, \nthe languages you speak, where you or your \nfamily are from, your race or ethnic back-\nground, your gender or sexual orientation, \nand your faith or religion.\nAsk the informant to reflect on the most salient ele-\nments of the individual\u2019s cu ltural identity. Use this \ninformation to tailor questions 10\u201311 as needed.9. For you, what are the most important \naspects of [INDIVIDUAL\u2019S] background or \nidentity?\nElicit aspects of identity that make the problem bet-\nter or worse.\nProbe as needed (e.g., cl inical worsening as a result \nof discrimination due to migration status, race/\nethnicity, or sexual orientation).10. Are there any aspects of [INDIVIDUAL\u2019S] \nbackground or identity that make a differ-\nence to his/her [PROBLEM]?\nProbe as needed (e.g., migration-related problems; \nconflict across generations or due to gender roles).11. Are there any aspects of [INDIVIDUAL\u2019S] \nbackground or identity that are causing \nother concerns or difficulties for him/her?Cultural Formulation Interv iew (CFI)\u2014Informant Version (continued)\nGUIDE TO INTERVIEWERINSTRUCTIONS TO THE INTERVIEWER ARE \nITALICIZED.", "source": "dsm5.pdf"} {"id": "3668495c6ff1-0", "page_content": "Cultural Formulation 757\nCULTURAL FACTORS AFFECTING SELF- COPING AND PAST HELP SEEKING\nSELF-COPING\nClarify individual\u2019s self-coping for the problem. 12. Sometimes people have various ways of \ndealing with problems like [PROBLEM]. \nWhat has [INDIVIDUAL] done on his/her \nown to cope with his/her [PROBLEM]?\nPAST HELP SEEKING\nElicit various sources of help (e.g., medical care, \nmental health treatment, support groups, work-\nbased counseling, folk healing, religious or spiri-\ntual counseling, other alternative healing).\nProbe as needed (e.g., \u201cWhat other sources of help \nhas he/she used?\u201d).\nClarify the indivi dual\u2019s experience and regard for \nprevious help.13. Often, people also look for help from many \ndifferent sources, including different kinds \nof doctors, helpers, or healers. In the past, \nwhat kinds of treatment, help, advice, or \nhealing has [INDIVIDUAL] sought for his/\nher [PROBLEM]?\nPROBE IF DOES NOT DESCRIBE USE-\nFULNESS OF HELP RECEIVED:\nWhat types of help or treatment were most \nuseful? Not useful?\nBARRIERS\nClarify the role of social barriers to help-seeking, \naccess to care, and problems engaging in previous \ntreatment.14. Has anything prevented [INDIVIDUAL] \nfrom getting the help he/she needs?\nProbe details as needed (e.g., \u201cWhat got in the \nway?\u201d).PROBE AS NEEDED:\nFor example, money, work or family com-\nmitments, stigma or discrimination, or lack \nof services that understand his/her lan-\nguage or background?", "source": "dsm5.pdf"} {"id": "3668495c6ff1-1", "page_content": "of services that understand his/her lan-\nguage or background?\nCULTURAL FACTORS AFFECT ING CURRENT HELP SEEKING\nPREFERENCES\nClarify individual\u2019s cu rrent perceived needs and \nexpectations of help, broadly defined, from the \npoint of view of the informant.\nProbe if informant lists only one source of help (e.g., \n\u201cWhat other kinds of help would be useful to \n[INDIVIDUAL] at this time?\u201d).Now let\u2019s talk about the help [INDIVID-\nUAL] needs.\n15. What kinds of help would be most useful to \nhim/her at this time for his/her [PROB-\nLEM]?\nFocus on the views of the social network regarding \nhelp seeking.16. Are there other kinds of help that [INDI-\nVIDUAL\u2019S] family, friends, or other people \nhave suggested would be helpful for him/\nher now?\nCLINICIAN -PATIENT RELATIONSHIP\nElicit possible concerns abou t the clinic or the clini-\ncian-patient relationship, including perceived rac-\nism, language barriers, or cultural differences that \nmay undermine goodwill, communication, or care \ndelivery.\nProbe details as needed (e.g., \u201cIn what way?\u201d).\nAddress possible barriers to care or concerns about \nthe clinic and the clinician-patient relationship \nraised previously.Sometimes doctors and patients misunder-\nstand each other because they come from \ndifferent backgrounds or have different \nexpectations.\n17. Have you been concerned about this, and is \nthere anything that we can do to provide \n[INDIVIDUAL] with the care he/she \nneeds?Cultural Formulation Interv iew (CFI)\u2014Informant Version (continued)", "source": "dsm5.pdf"} {"id": "3668495c6ff1-2", "page_content": "GUIDE TO INTERVIEWERINSTRUCTIONS TO THE INTERVIEWER ARE \nITALICIZED.", "source": "dsm5.pdf"} {"id": "1bce24b6e063-0", "page_content": "758 Cultural Formulation\nCultural Concepts of Distress\nCultural concepts of distress refers to ways that cultural groups experience, understand, and\ncommunicate suffering, behavioral problems, or troubling thoughts and emotions. Three\nmain types of cultural concepts may be distinguished. Cultural syndromes are clusters of\nsymptoms and attributions that tend to co -occur among individuals in specific cultural\ngroups, communities, or contexts and that ar e recognized locally as coherent patterns of\nexperience. Cultural idioms of distress are ways of expressing distress that may not involve\nspecific symptoms or syndromes, but that pr ovide collective, shared ways of experiencing\nand talking about personal or social concerns . For example, everyday talk about \u201cnerves\u201d\nor \u201cdepression\u201d may refer to widely varying forms of suffe ring without mapping onto a\ndiscrete set of symptoms, syndrome, or disorder. Cultural explanations or perceived causes\nare labels, attributions, or features of an ex planatory model that indicate culturally recog-\nnized meaning or etiology for symptoms, illness, or distress.\nThese three concepts\u2014syndromes, idioms, and explanations\u2014are more relevant to\nclinical practice than the older formulation culture-bound syndrome. Specifically, the term\nculture-bound syndrome ignores the fact that clinically important cultural differences often\ninvolve explanations or experience of distress rather than culturally distinctive configura-\ntions of symptoms. Furthermore, the term culture-bound overemphasizes the local partic-\nularity and limited distribution of cultural concepts of di stress. The current formulation\nacknowledges that all forms of distress are locally shaped, including the DSM disorders.\nFrom this perspective, many DSM diagnoses can be understood as operationalized proto-\ntypes that started out as cultural syndromes, and became widely accepted as a result of", "source": "dsm5.pdf"} {"id": "1bce24b6e063-1", "page_content": "types that started out as cultural syndromes, and became widely accepted as a result of\ntheir clinical and research utilit y. Across groups there remain culturally patterned differ-\nences in symptoms, ways of talking about dist ress, and locally perceived causes, which are\nin turn associated with coping strategies and patterns of help seeking.\nCultural concepts arise from local folk or professional diagnost ic systems for mental\nand emotional distress, and they may also re flect the influence of biomedical concepts.\nCultural concepts have four key featur es in relation to the DSM-5 nosology:\n\u2022 There is seldom a one-to-one correspondence of any cultural concept with a DSM diag-\nnostic entity; the correspondence is more lik ely to be one-to-many in either direction.\nSymptoms or behaviors that might be sort ed by DSM-5 into several disorders may be\nincluded in a single folk concept, and diverse presentations that might be classified by\nDSM-5 as variants of a single disorder may be sorted into several distinct concepts by an\nindigenous diagnostic system.\n\u2022 Cultural concepts may apply to a wide range of severity, including presentations that\ndo not meet DSM criteria for any mental disorder. For example, an individual with acute\ngrief or a social predicament may use the same idiom of distress or display the same\ncultural syndrome as another individual with more severe psychopathology.\n\u2022 In common usage, the same cultural term frequently denotes more than one type of\ncultural concept. A familiar example may be the concept of \u201cdepression,\u201d which may\nbe used to describe a syndrome (e.g., major depressive disorder), an idiom of distress\n(e.g., as in the common expression \u201cI feel depressed\u201d), or a perceived cause (similar to\n\u201cstress\u201d).\n\u2022 Like culture and DSM itself, cultural concepts may change over time in response to both", "source": "dsm5.pdf"} {"id": "1bce24b6e063-2", "page_content": "\u2022 Like culture and DSM itself, cultural concepts may change over time in response to both\nlocal and global influences.\nCultural concepts are important to ps ychiatric diagnosis for several reasons:\n\u2022To avoid misdiagnosis: Cultural variation in symptoms and in explanatory models as-\nsociated with these cultural co ncepts may lead clinicians to misjudge the severity of a", "source": "dsm5.pdf"} {"id": "e0841034f3ba-0", "page_content": "Cultural Formulation 759\nproblem or assign the wrong diagnosis (e.g., unfamiliar spiritual explanations may be\nmisunderstood as psychosis).\n\u2022To obtain useful clinical information: Cultural variations in symptoms and attribu-\ntions may be associated with particular fe atures of risk, res ilience, and outcome.\n\u2022To improve clinical rapport and engagement: \u201cSpeaking the language of the patient,\u201d\nboth linguistically and in terms of his or her dominant concepts and metaphors, can re-\nsult in greater communication and satisfac tion, facilitate treatment negotiation, and\nlead to higher rete ntion and adherence.\n\u2022To improve therapeutic efficacy: Culture influences the psychological mechanisms of\ndisorder, which need to be understood and addressed to improve clinical efficacy. For\nexample, culturally specific catastrophic co gnitions can contribute to symptom escala-\ntion into panic attacks.\n\u2022To guide clinical research: Locally perceived connections between cultural concepts\nmay help identify patterns of comorbidity and underlying biological substrates.\n\u2022To clarify the cu ltural epidemiology: Cultural concepts of distress are not endorsed\nuniformly by everyone in a given culture. Distinguishing syndromes, idioms, and ex-\nplanations provides an approach for studying the distribution of cultural features of ill-\nness across settings and regions, and over time. It also suggests qu estions about cultural\ndeterminants of risk, course, and outcome in clinical and community settings to en-\nhance the evidence base of cultural research.\nDSM-5 includes information on cultural conc epts in order to improve the accuracy of\ndiagnosis and the comprehensiveness of clinical assessment. Clinical assessment of indi-\nviduals presenting with thes e cultural concepts should determine whether they meet\nDSM-5 criteria for a spec ified disorder or an other specified or unspecified diagnosis. Once the", "source": "dsm5.pdf"} {"id": "e0841034f3ba-1", "page_content": "disorder is diagnosed, the cultural terms and explanations should be included in case for-\nmulations; they may help clarify symptoms and etiological a ttributions that could other-\nwise be confusing. Individuals whose sympto ms do not meet DSM criteria for a specific\nmental disorder may still expect and require treatment; this should be assessed on a case-\nby-case basis. In addition to the CFI and its supplementary modules, DSM-5 contains the\nfollowing information and tools that may be useful when integrating cultural information\nin clinical practice:\n\u2022Data in DSM-5 criteria and text for specific disorders: The text includes information\non cultural variations in prevalence, sy mptomatology, associate d cultural concepts,\nand other clinical aspects. It is important to emphasize that there is no one-to-one cor-\nrespondence at the categorical level between DSM disorders and cultural concepts. Dif-\nferential diagnosis for individuals must th erefore incorporate in formation on cultural\nvariation with information elicited by the CFI.\n\u2022Other Conditions That May Be a Focus of Clinical Attention: Some of the clinical con-\ncerns identified by the CFI may correspond to V codes or Z code s\u2014for example, accul-\nturation problems, parent-child relational pr oblems, or religious or spiritual problems.\n\u2022Glossary of Cultural Concepts of Distress: Located in the Appendix, this glossary pro-\nvides examples of well-studied cultural concepts of distress that illustrate the relevance\nof cultural information for c linical diagnosis and s ome of the interrelationships among\ncultural syndromes, idioms of di stress, and causal explanations.", "source": "dsm5.pdf"} {"id": "332991c95a1b-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "0e1dd5d449de-0", "page_content": "761Alternative DSM-5 Model for\nPersonality Disorders\nThe current approach to personality disorders appe ars in Section II of DSM-5,\nand an alternative model developed for DSM-5 is presented here in Section III. The inclu-\nsion of both models in DSM-5 reflects the de cision of the APA Board of Trustees to pre-\nserve continuity with current clinical practi ce, while also introducing a new approach that\naims to address numerous shor tcomings of the current approa ch to personality disorders.\nFor example, the typical patient meeting criter ia for a specific personality disorder fre-\nquently also meets criteria for other personalit y disorders. Similarly, other specified or un-\nspecified personality disorder is often the correct (but mostly uninformative) diagnosis, in\nthe sense that patients do not tend to present with patterns of symptoms that correspond\nwith one and only one personality disorder.\nIn the following alternative DSM-5 model, personality disorders are characterized by\nimpairments in personality functioning and pathological personality traits. The specific\npersonality disorder diagnoses that may be derived from this model include antisocial,\navoidant, borderline, narcissis tic, obsessive-compulsive, an d schizotypal personality dis-\norders. This approach also includes a diagno sis of personality disorder\u2014trait specified\n(PD-TS) that can be made when a personality disorder is considered present but the crite-\nria for a specific disorder are not met.\nGeneral Criteria for Personality Disorder\nGeneral Criteria for Personality Disorder\nThe essential features of a personality disorder are\nA. Moderate or greater impairment in personality (self/interpersonal) functioning.\nB. One or more pathological personality traits.\nC. The impairments in personality functioning and the individual\u2019s personality trait expres-\nsion are relatively inflexible and pervasive across a broad range of personal and social\nsituations.", "source": "dsm5.pdf"} {"id": "0e1dd5d449de-1", "page_content": "situations.\nD. The impairments in personality functioning and the individual\u2019s personality trait expres-\nsion are relatively stable across time, with onsets that can be traced back to at least\nadolescence or early adulthood.\nE. The impairments in personality functioning and the individual\u2019s personality trait expres-\nsion are not better explained by another mental disorder.\nF. The impairments in personality functioning and the individual\u2019s personality trait expres-\nsion are not solely attributable to the physiological effects of a substance or another\nmedical condition (e.g., severe head trauma).\nG. The impairments in personality functioning and the individual\u2019s personality trait expres-\nsion are not better understood as normal for an individual\u2019s developmental stage or so-\nciocultural environment.", "source": "dsm5.pdf"} {"id": "6913f78de7ae-0", "page_content": "762 Alternative DSM-5 Model for Personality Disorders\nA diagnosis of a personality disorder requires two determinations: 1) an assessment of\nthe level of impairment in personality functi oning, which is needed for Criterion A, and 2)\nan evaluation of pathological personality trai ts, which is required for Criterion B. The im-\npairments in personality functioning and person ality trait expression are relatively inflex-\nible and pervasive across a broad range of pers onal and social situations (Criterion C);\nrelatively stable across time, with onsets that can be traced back to at least adolescence or\nearly adulthood (Criterion D); not better explained by another mental disorder (Criterion\nE); not attributable to the effects of a substance or another medical condition (Criterion F);\nand not better understood as normal for an individual\u2019s developmental stage or sociocul-\ntural environment (Criterion G). All Section II I personality disorders described by criteria\nsets, as well as PD-TS, meet these general criteria, by definition.\nCriterion A: Level of Personality Functioning\nDisturbances in self and interpersonal functioning constitute the core of personality psy-\nchopathology and in this alternative diagnostic model they are evaluated on a continuum.\nSelf functioning involves identity and sel f-direction; interpersonal functioning involves\nempathy and intimacy (see Table 1). The Level of Personality Functioning Scale (LPFS; see\nTable 2, pp. 775\u2013778) uses each of these elements to differentiate five levels of impairment,\nranging from little or no impair ment (i.e., healthy, adaptive functioning; Level 0) to some\n(Level 1), moderate (Level 2), severe (Lev el 3), and extreme (Level 4) impairment.\nImpairment in personality functioning predicts the presence of a personality disorder,", "source": "dsm5.pdf"} {"id": "6913f78de7ae-1", "page_content": "Impairment in personality functioning predicts the presence of a personality disorder,\nand the severity of impairment predicts whet her an individual has more than one person-\nality disorder or one of the more typically se vere personality disorders. A moderate level\nof impairment in personality functioning is re quired for the diagnosis of a personality dis-\norder; this threshold is based on empirical ev idence that the moderate level of impairment\nmaximizes the ability of clinicians to accurate ly and efficiently identify personality disor-\nder pathology.\nCriterion B: Pathological Personality Traits\nPathological personality traits are organized into five broad domain s: Negative Affectiv-\nity, Detachment, Antagonism, Disinhibition, and Psychoticism. Within the five broad trait\ndomains are 25 specific trait facets that were developed initially from a review of existing\ntrait models and subsequently through iterat ive research with samples of persons who\nsought mental health services. The full trait taxonomy is presented in Table 3 (see pp. 779\u2013\n781). The B criteria for the spec ific personality disorders comp rise subsets of the 25 traitTABLE 1 Elements of personality functioning\nSelf:\n1. Identity: Experience of oneself as unique, with clear boundaries between self and others; sta-\nbility of self-esteem and accuracy of self-apprai sal; capacity for, and ability to regulate, a \nrange of emotional experience.\n2. Self-direction: Pursuit of coherent and meaningful short-term and life goals; utilization of \nconstructive and prosocial internal standards of behavior; ability to self-reflect productively.\nInterpersonal:\n1.Empathy: Comprehension and appreciation of others\u2019 experiences and motivations; tolerance \nof differing perspectives; understanding the effects of one\u2019s own behavior on others.", "source": "dsm5.pdf"} {"id": "6913f78de7ae-2", "page_content": "of differing perspectives; understanding the effects of one\u2019s own behavior on others.\n2. Intimacy: Depth and duration of connection with ot hers; desire and capa city for closeness; \nmutuality of regard reflected in interpersonal behavior.", "source": "dsm5.pdf"} {"id": "afd8536f8e98-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 763\nfacets, based on meta-analytic reviews and empi rical data on the relationships of the traits\nto DSM-IV personality disorder diagnoses.\nCriteria C and D: Perv asiveness and Stability\nImpairments in personality functioning an d pathological pers onality traits are relatively per-\nvasive across a range of personal and social contexts, as personality is defined as a pattern of\nperceiving, relating to, and thinking about the environm ent and oneself. The term relatively\nreflects the fact that all except the most extr emely pathological personalities show some de-\ngree of adaptability. The pattern in personality disorders is maladaptive and relatively inflex-\nible, which leads to disabilities in social, o ccupational, or other important pursuits, as\nindividuals are unable to modify their thinking or behavior, even in th e face of evidence that\ntheir approach is not working. The impairments in functioning and personality traits are also\nrelatively stable. Personality traits\u2014the dispositions to behave or feel in certain ways\u2014are\nmore stable than the symptomatic expressions of these dispositions, but personality traits can\nalso change. Impairments in personality fu nctioning are more stable than symptoms.\nCriteria E, F, and G: Al ternative Explanations for \nPersonality Pathology (D ifferential Diagnosis)\nOn some occasions, what appears to be a pe rsonality disorder may be better explained by\nanother mental disorder, the effects of a subs tance or another medica l condition, or a nor-\nmal developmental stage (e.g., adolescence, late life) or the individu al\u2019s sociocultural en-\nvironment. When another ment al disorder is present, the diagnosis of a personality\ndisorder is not made, if the manifestations of the personality disorder clearly are an ex-", "source": "dsm5.pdf"} {"id": "afd8536f8e98-1", "page_content": "disorder is not made, if the manifestations of the personality disorder clearly are an ex-\npression of the other mental disorder (e.g., if features of schizotypal personality disorder\nare present only in the context of schizophren ia). On the other hand, personality disorders\ncan be accurately diagnosed in the presence of another mental disord er, such as major de-\npressive disorder, and patients with other me ntal disorders should be assessed for comor-\nbid personality disorders because personality disorders often impact the course of other\nmental disorders. Therefore, it is always appropriate to assess personality functioning and\npathological personality traits to prov ide a context for other psychopathology.\nSpecific Personality Disorders\nSection III includes diagnostic criteria for antisocial, avoidant , borderline, narcissistic, ob-\nsessive-compulsive, and schizotypal personality disorders. Each pe rsonality disorder is\ndefined by typical impairments in personality functioning (Criterion A) and characteristic\npathological personality traits (Criterion B):\n\u2022 Typical features of antisocial personality disorder are a failure to conform to lawful\nand ethical behavior, and an egocentric, callous lack of concern for others, accompanied\nby deceitfulness, irresponsibility, manipulativeness, and/or risk taking.\n\u2022 Typical features of avoidant personality disorder are avoidance of social situations and\ninhibition in interpersonal relationships related to feelings of ineptitude and inade-\nquacy, anxious preoccupation with negative evaluation and rejection, and fears of rid-\nicule or embarrassment.\n\u2022 Typical features of borderline personality disorder are instability of self-image, per-\nsonal goals, interpersonal relationships, an d affects, accompanied by impulsivity, risk\ntaking, and/or hostility.\n\u2022 Typical features of narcissistic personality disorder are variable and vulnerable self-\nesteem, with attempts at regulation throug h attention and approval seeking, and either", "source": "dsm5.pdf"} {"id": "afd8536f8e98-2", "page_content": "esteem, with attempts at regulation throug h attention and approval seeking, and either\novert or covert grandiosity.", "source": "dsm5.pdf"} {"id": "26bc45432ab2-0", "page_content": "764 Alternative DSM-5 Model for Personality Disorders\n\u2022 Typical features of obsessive-compulsive personality disorder are difficulties in estab-\nlishing and sustaining close relationships, as sociated with rigid perfectionism, inflexi-\nbility, and restricted emotional expression.\n\u2022 Typical features of schizotypal personality disorder are impairments in the capacity\nfor social and close relationships, and eccent ricities in cognition, perception, and behav-\nior that are associated with distorted self-i mage and incoherent personal goals and ac-\ncompanied by suspiciousness and re stricted emotional expression.\nThe A and B criteria for the six specific pe rsonality disorders and for PD-TS follow. All\npersonality disorders also meet criteria C through G of the General Criteria for Personality\nDisorder.\nAntisocial Personality Disorder\nTypical features of antisocial personality diso rder are a failure to conform to lawful and\nethical behavior, and an egocentric, callous la ck of concern for others, accompanied by de-\nceitfulness, irresponsibility, manipulativeness, and/or risk taking. Characteristic difficul-\nties are apparent in identity, self-direction, empathy, and/or intimacy, as described below,\nalong with specific maladaptive traits in the domains of Antagonism and Disinhibition.\nProposed Diagnostic Criteria\nA. Moderate or greater impairment in personality functioning, manifested by characteristic\ndifficulties in two or more of the following four areas:\n1.Identity: Egocentrism; self-esteem derived from personal gain, power, or pleasure.\n2.Self-direction: Goal setting based on personal gratification; absence of prosocial\ninternal standards, associated with failure to conform to lawful or culturally norma-\ntive ethical behavior.\n3.Empathy: Lack of concern for feelings, needs, or suffering of others; lack of re-", "source": "dsm5.pdf"} {"id": "26bc45432ab2-1", "page_content": "morse after hurting or mistreating another.\n4.Intimacy: Incapacity for mutually intimate relationships, as exploitation is a primary\nmeans of relating to others, including by deceit and coercion; use of dominance or\nintimidation to control others.\nB. Six or more of the following seven pathological personality traits:\n1.Manipulativeness (an aspect of Antagonism): Frequent use of subterfuge to in-\nfluence or control others; use of seduction, charm, glibness, or ingratiation to\nachieve one\u2019s ends.\n2.Callousness (an aspect of Antagonism ): Lack of concern for feelings or problems\nof others; lack of guilt or remorse about the negative or harmful effects of one\u2019s ac-\ntions on others; aggression; sadism.\n3.Deceitfulness (an aspect of Antagonism): Dishonesty and fraudulence; misrepre-\nsentation of self; embellishment or fabrication when relating events.\n4.Hostility (an aspect of Antagonism): Persistent or frequent angry feelings; anger or\nirritability in response to minor slights and insults; mean, nasty, or vengeful behavior.\n5.Risk taking (an aspect of Disinhibition ): Engagement in dangerous, risky, and poten-\ntially self-damaging activities, unnecessarily and without regard for consequences;\nboredom proneness and thoughtless initiation of activities to counter boredom; lack of\nconcern for one\u2019s limitations and denial of the reality of personal danger.\n6.Impulsivity (an aspect of Disinhibition ): Acting on the spur of the moment in re-\nsponse to immediate stimuli; acting on a momentary basis without a plan or consid-\neration of outcomes; difficulty establishing and following plans.", "source": "dsm5.pdf"} {"id": "bd5d4acdbfee-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 765\n7.Irresponsibility (an aspect of Disinhibition ): Disregard for\u2014and failure to honor\u2014\nfinancial and other obligations or commitments; lack of respect for\u2014and lack of fol-\nlow-through on\u2014agreements and promises.\nNote. The individual is at least 18 years of age.\nSpecify if:\nWith psychopathic features.\nSpecifiers. A distinct variant often termed psychopathy (or \u201cprimary\u201d psychopathy) is\nmarked by a lack of anxiety or fear and by a bold interpersonal style that may mask mal-\nadaptive behaviors (e.g., fraudulence). This ps ychopathic variant is characterized by low\nlevels of anxiousness (Negative Affectivity domain) and withdrawal (Detachment do-\nmain) and high levels of attention seeking (Antagonism domain). High attention seeking\nand low withdrawal capture the social pote ncy (assertive/dominant) component of psy-\nchopathy, whereas low anxiousness captures the stress immunity (emotional stability/re-\nsilience) component.\nIn addition to psychopathic features, trait and personality functioning specifiers may be\nused to record other personality features that may be present in anti social personality dis-\norder but are not required for the diagnosis. For example, traits of Negative Affectivity (e.g.,\nanxiousness), are not diagnostic criteria for antisocial personality disorder (see Criterion B)\nbut can be specified when appropriate. Furthe rmore, although moderate or greater impair-\nment in personality functioning is required for the diagnosis of antisocial personality disor-\nder (Criterion A), the level of persona lity functioning can also be specified.\nAvoidant Person ality Disorder\nTypical features of avoidant personality disord er are avoidance of social situations and in-", "source": "dsm5.pdf"} {"id": "bd5d4acdbfee-1", "page_content": "Typical features of avoidant personality disord er are avoidance of social situations and in-\nhibition in interpersonal relationships related to feelings of inep titude and inadequacy,\nanxious preoccupation with negative evaluation and rejection, and fears of ridicule or em-\nbarrassment. Characteristic difficulties are apparent in identity, self-direction, empathy,\nand/or intimacy, as described below, along wi th specific maladaptiv e traits in the do-\nmains of Negative Affectivity and Detachment.\nProposed Diagnostic Criteria\nA. Moderate or greater impairment in personal ity functioning, manifest by characteristic\ndifficulties in two or more of the following four areas:\n1.Identity: Low self-esteem associated with self-appraisal as socially inept, person-\nally unappealing, or inferior; excessive feelings of shame.\n2.Self-direction: Unrealistic standards for behavior associated with reluctance to\npursue goals, take personal risks, or engage in new activities involving interper-\nsonal contact.\n3.Empathy: Preoccupation with, and sensitivity to, criticism or rejection, associated\nwith distorted inference of others\u2019 perspectives as negative.\n4.Intimacy: Reluctance to get involved with people unless being certain of being\nliked; diminished mutuality within intimate relationships because of fear of being\nshamed or ridiculed.\nB. Three or more of the following four pathological personality traits, one of which must\nbe (1) Anxiousness:\n1.Anxiousness (an aspect of Negative Affectivity): Intense feelings of nervous-\nness, tenseness, or panic, often in reaction to social situations; worry about the\nnegative effects of past unpleasant experiences and future negative possibilities;", "source": "dsm5.pdf"} {"id": "49e14d9a03e9-0", "page_content": "766 Alternative DSM-5 Model for Personality Disorders\nfeeling fearful, apprehensive, or threatened by uncertainty; fears of embarrass-\nment.\n2.Withdrawal (an aspect of Detachment ): Reticence in social situations; avoidance\nof social contacts and activity; lack of initiation of social contact.\n3.Anhedonia (an aspect of Detachment ): Lack of enjoyment from, engagement in,\nor energy for life\u2019s experiences; deficits in the capacity to feel pleasure or take in-\nterest in things.\n4.Intimacy avoidance (an aspect of Detachment ): Avoidance of close or romantic\nrelationships, interpersonal attachments, and intimate sexual relationships.\nSpecifiers. Considerable heterogeneity in the form of additional personality traits is\nfound among individuals diagnosed with avoida nt personality disorder. Trait and level of\npersonality functioning specifiers can be used to record additional personality features\nthat may be present in avoidant personality disorder. For example, other Negative Affec-\ntivity traits (e.g., depressivity, separation insecurity, submissiveness, suspiciousness, hos-\ntility) are not diagnostic criter ia for avoidant personality disorder (see Criterion B) but can\nbe specified when appropriate. Furthermore, although moderate or greater impairment in\npersonality functioning is required for the diag nosis of avoidant personality disorder (Cri-\nterion A), the level of personality functioning also can be specified.\nBorderline Personality Disorder\nTypical features of borderline personality disorder are instability of self-image, personal\ngoals, interpersonal relationships, and affect s, accompanied by impulsivity, risk taking,\nand/or hostility. Characteristic difficulties are apparent in identity, self-direction, empa-\nthy, and/or intimacy, as described below, along with specific maladaptive traits in the do-\nmain of Negative Affectivity, and also Antagonism and/or Disinhibition.\nProposed Diagnostic Criteria", "source": "dsm5.pdf"} {"id": "49e14d9a03e9-1", "page_content": "Proposed Diagnostic Criteria\nA. Moderate or greater impairment in personality functioning, manifested by characteristic\ndifficulties in two or more of the following four areas:\n1.Identity: Markedly impoverished, poorly developed, or unstable self-image, often\nassociated with excessive self-criticism; chronic feelings of emptiness; dissociative\nstates under stress.\n2.Self-direction: Instability in goals, aspirations, values, or career plans.\n3.Empathy: Compromised ability to recognize the feelings and needs of others asso-\nciated with interpersonal hypersensitivity (i.e., prone to feel slighted or insulted); per-\nceptions of others selectively biased toward negative attributes or vulnerabilities.\n4.Intimacy: Intense, unstable, and conflicted close relationships, marked by mistrust,\nneediness, and anxious preoccupation with real or imagined abandonment; close\nrelationships often viewed in extremes of idealization and devaluation and alternat-\ning between overinvolvement and withdrawal.\nB. Four or more of the following seven pathological personality traits, at least one of which\nmust be (5) Impulsivity, (6) Risk taking, or (7) Hostility:\n1.Emotional lability (an aspect of Negative Affectivity): Unstable emotional expe-\nriences and frequent mood changes; emotions that are easily aroused, intense,\nand/or out of proportion to events and circumstances.\n2.Anxiousness (an aspect of Negative Affectivity): Intense feelings of nervous-\nness, tenseness, or panic, often in reaction to interpersonal stresses; worry about\nthe negative effects of past unpleasant experiences and future negative possibili-", "source": "dsm5.pdf"} {"id": "45c86b4eee1c-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 767\nties; feeling fearful, apprehensive, or threatened by uncertainty; fears of falling\napart or losing control.\n3.Separation insecurity (an aspect of Negative Affectivity ): Fears of rejection by\u2014\nand/or separation from\u2014significant others, associated with fears of excessive de-\npendency and complete loss of autonomy.\n4.Depressivity (an aspect of Negative Affectivity): Frequent feelings of being down,\nmiserable, and/or hopeless; difficulty recovering from such moods; pessimism\nabout the future; pervasive shame; feelings of inferior self-worth; thoughts of sui-\ncide and suicidal behavior.\n5.Impulsivity (an aspect of Disinhibition ): Acting on the spur of the moment in re-\nsponse to immediate stimuli; acting on a momentary basis without a plan or consid-\neration of outcomes; difficulty establishing or following plans; a sense of urgency\nand self-harming behavior under emotional distress.\n6.Risk taking (an aspect of Disinhibition ): Engagement in dangerous, risky, and po-\ntentially self-damaging activities, unnecessarily and without regard to conse-\nquences; lack of concern for one\u2019s limitations and denial of the reality of personal\ndanger.\n7.Hostility (an aspect of Antagonism): Persistent or frequent angry feelings; anger\nor irritability in response to minor slights and insults.\nSpecifiers. Trait and level of personalit y functioning specifiers may be used to record ad-\nditional personality features that may be pres ent in borderline personality disorder but are\nnot required for the diagnosis. For example, traits of Psychoticism (e.g., cognitive and per-\nceptual dysregulation) are not diagnostic crit eria for borderline personality disorder (see", "source": "dsm5.pdf"} {"id": "45c86b4eee1c-1", "page_content": "ceptual dysregulation) are not diagnostic crit eria for borderline personality disorder (see\nCriterion B) but can be specif ied when appropriate. Furthermore, although moderate or\ngreater impairment in personality functioning is required for the di agnosis of borderline\npersonality disorder (Criterion A), the level of personality func tioning can also be specified.\nNarcissistic Personality Disorder\nTypical features of narcissistic personality disorder are variable and vulnerable self-esteem,\nwith attempts at regulation through attentio n and approval seeking, and either overt or\ncovert grandiosity. Characteristic difficulties are apparent in identity, self-direction, em-\npathy, and/or intimacy, as desc ribed below, along with specif ic maladaptive traits in the\ndomain of Antagonism.\nProposed Diagnostic Criteria\nA. Moderate or greater impairment in personality functioning, manifested by characteristic\ndifficulties in two or more of the following four areas:\n1.Identity: Excessive reference to others for self-definition and self-esteem regula-\ntion; exaggerated self-appraisal inflated or deflated, or vacillating between extremes;\nemotional regulation mirrors fl uctuations in self-esteem.\n2.Self-direction: Goal setting based on gaining approval from others; personal stan-\ndards unreasonably high in order to see oneself as exceptional, or too low based\non a sense of entitlement; often unaware of own motivations.\n3.Empathy: Impaired ability to recognize or identify with the feelings and needs of\nothers; excessively attuned to reactions of others, but only if perceived as relevant\nto self; over- or underestimate of own effect on others.\n4.Intimacy: Relationships largely superficial and exist to serve self-esteem regula-\ntion; mutuality constrained by little genuine interest in others\u2019 experiences and pre-\ndominance of a need for personal gain.", "source": "dsm5.pdf"} {"id": "83df1f1643bc-0", "page_content": "768 Alternative DSM-5 Model for Personality Disorders\nB. Both of the following pathological personality traits:\n1.Grandiosity (an aspect of Antagonism ): Feelings of entitlement, either overt or co-\nvert; self-centeredness; firmly holding to the belief that one is better than others;\ncondescension toward others.\n2.Attention seeking (an aspect of Antagonism ): Excessive attempts to attract and\nbe the focus of the attention of others; admiration seeking.\nSpecifiers. Trait and personality functioning specifie rs may be used to record additional\npersonality features that may be present in narcissistic person ality disorder but are not re-\nquired for the diagnosis. For example, other traits of Antagonism (e.g., manipulativeness, de-\nceitfulness, callousness) are not diagnostic criteria for narcissistic personality disorder (see\nCriterion B) but can be specified when more pervasive antagonistic features (e.g., \u201cmalignant\nnarcissism\u201d) are present. Other traits of Negative Affectivity (e.g., depressivity, anxiousness)\ncan be specified to record more \u201cvulnerable\u201d presentations. Furthermore, although moderate\nor greater impairment in person ality functioning is required for the diagnosis of narcissistic\npersonality disorder (Criterion A), the level of personality functioning can also be specified.\nObsessive-Compulsive Personality Disorder\nTypical features of obsessive-compulsive person ality disorder are difficulties in establish-\ning and sustaining close relationships, associated with rigid perfectionism, inflexibility,\nand restricted emotional expression. Characteristic difficulties are apparent in identity,\nself-direction, empathy, and/or intimacy, as described below, along with specific mal-\nadaptive traits in the domains of Ne gative Affectivity and/or Detachment.\nProposed Diagnostic Criteria", "source": "dsm5.pdf"} {"id": "83df1f1643bc-1", "page_content": "Proposed Diagnostic Criteria\nA. Moderate or greater impairment in personality functioning, manifested by characteristic\ndifficulties in two or more of the following four areas:\n1.Identity: Sense of self derived predominantly fr om work or productivity; constricted\nexperience and expression of strong emotions.\n2.Self-direction: Difficulty completing tasks and realizing goals, associated with rigid\nand unreasonably high and inflexible internal standards of behavior; overly consci-\nentious and moralistic attitudes.\n3.Empathy: Difficulty understanding and appreciating the ideas, feelings, or behav-\niors of others.\n4.Intimacy: Relationships seen as secondary to work and productivity; rigidity and\nstubbornness negatively affect relationships with others.\nB. Three or more of the following four pathological personality traits, one of which must\nbe (1) Rigid perfectionism:\n1.Rigid perfectionism (an aspect of extreme Conscientiousness [the opposite pole\nof Disinhibition]): Rigid insistence on everything being flawless, perfect, and without\nerrors or faults, including one\u2019s own and ot hers\u2019 performance; sacrificing of timeli-\nness to ensure correctness in every detail; believing that there is only one right way\nto do things; difficulty changing ideas and/or viewpoint; preoccupation with details,\norganization, and order.\n2.Perseveration (an aspect of Negative Affectivity ): Persistence at tasks long after\nthe behavior has ceased to be functional or effective; continuance of the same be-\nhavior despite repeated failures.\n3.Intimacy avoidance (an aspect of Detachment ): Avoidance of close or romantic\nrelationships, interpersonal attachments, and intimate sexual relationships.", "source": "dsm5.pdf"} {"id": "af360e7f1487-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 769\n4.Restricted affectivity (an aspect of Detachment ): Little reaction to emotionally\narousing situations; constricted emotional experience and expression; indifference\nor coldness.\nSpecifiers. Trait and personality functioning specifie rs may be used to record additional\npersonality features that may be present in obsessive-compulsive personality disorder but are\nnot required for the diagnosis. Fo r example, other traits of Negative Affectivity (e.g., anxious-\nness) are not diagnostic criteria for obsessive-compulsive personal ity disorder (see Criterion B)\nbut can be specified when appropriate. Furthe rmore, although moderate or greater impair-\nment in personality functioning is required for the diagnosis of obsessive-compulsive person-\nality disorder (Criterion A), the level of personality functioning can also be specified.\nSchizotypal Personality Disorder\nTypical features of schizotypal personality diso rder are impairments in the capacity for so-\ncial and close relationships and eccentricities in cognition, perception, and behavior that\nare associated with distorted self-image an d incoherent personal goals and accompanied\nby suspiciousness and restricted emotional ex pression. Characteristic difficulties are ap-\nparent in identity, self-direction, empathy, and/or intimacy, along with specific maladap-\ntive traits in the domains of Psychoticism and Detachment.\nProposed Diagnostic Criteria\nA. Moderate or greater impairment in personality functioning, manifested by characteristic\ndifficulties in two or more of the following four areas:\n1.Identity: Confused boundaries between self and others; distorted self-concept;\nemotional expression often not congruent with context or internal experience.\n2.Self-direction: Unrealistic or incoherent goals; no clear set of internal standards.\n3.Empathy: Pronounced difficulty understanding impact of own behaviors on others;", "source": "dsm5.pdf"} {"id": "af360e7f1487-1", "page_content": "3.Empathy: Pronounced difficulty understanding impact of own behaviors on others;\nfrequent misinterpretations of others\u2019 motivations and behaviors.\n4.Intimacy: Marked impairments in developing close relationships, associated with\nmistrust and anxiety.\nB. Four or more of the following six pathological personality traits:\n1.Cognitive and perceptual dysregulation (an aspect of Psychoticism ): Odd or\nunusual thought processes; vague, circumstantial, metaphorical, overelaborate, or\nstereotyped thought or speech; odd sensations in various sensory modalities.\n2.Unusual beliefs and experiences (an aspect of Psychoticism ): Thought content\nand views of reality that are viewed by others as bizarre or idiosyncratic; unusual\nexperiences of reality.\n3.Eccentricity (an aspect of Psychoticism ): Odd, unusual, or bizarre behavior or\nappearance; saying unusual or inappropriate things.\n4.Restricted affectivity (an aspect of Detachment ): Little reaction to emotionally\narousing situations; constricted emotional experience and expression; indifference\nor coldness.\n5.Withdrawal (an aspect of Detachment ): Preference for being alone to being with\nothers; reticence in social situations; avoidance of social contacts and activity; lack\nof initiation of social contact.\n6.Suspiciousness (an aspect of Detachment ): Expectations of\u2014and heightened\nsensitivity to\u2014signs of interpersonal ill-intent or harm; doubts about loyalty and fi-\ndelity of others; feelings of persecution.", "source": "dsm5.pdf"} {"id": "174827cc2d11-0", "page_content": "770 Alternative DSM-5 Model for Personality Disorders\nSpecifiers. Trait and personality functioning specifie rs may be used to record additional\npersonality features that may be present in sc hizotypal personality disorder but are not re-\nquired for the diagnosis. For ex ample, traits of Negative Affectivity (e.g., depressivity,\nanxiousness) are not diagnostic criteria for sc hizotypal personality disorder (see Criterion\nB) but can be specified when appropriate. Fu rthermore, although moderate or greater im-\npairment in personality functioning is required for the diagnosis of schizotypal personal-\nity disorder (Criterion A), the level of pe rsonality functioning can also be specified.\nPersonality Disorder \u2014Trait Specified\nProposed Diagnostic Criteria\nA. Moderate or greater impairment in personality functioning, manifested by difficulties in\ntwo or more of the following four areas:\n1.Identity\n2.Self-direction\n3.Empathy\n4.Intimacy\nB. One or more pathological personality trait domains OR specific trait facets within do-\nmains, considering ALL of the following domains:\n1.Negative Affectivity (vs. Emotional Stability): Frequent and intense experiences\nof high levels of a wide range of negative emotions (e.g., anxiety, depression, guilt/\nshame, worry, anger), and their behavioral (e.g., self-harm) and interpersonal (e.g.,\ndependency) manifestations.\n2.Detachment (vs. Extraversion): Avoidance of socioemotional experience, includ-\ning both withdrawal from interpersonal interactions, ranging from casual, daily in-\nteractions to friendships to intimate relationships, as well as restricted affective\nexperience and expression, particularly limited hedonic capacity.\n3.Antagonism (vs. Agreeableness): Behaviors that put the individual at odds with", "source": "dsm5.pdf"} {"id": "174827cc2d11-1", "page_content": "other people, including an exaggerated sense of self-importance and a concomi-\ntant expectation of special treatment, as well as a callous antipathy toward others,\nencompassing both unawareness of others\u2019 needs and feelings, and a readiness\nto use others in the service of self-enhancement.\n4.Disinhibition (vs. Conscientiousness): Orientation toward immediate gratification,\nleading to impulsive behavior driven by current thoughts, feelings, and external\nstimuli, without regard for past learning or consideration of future consequences.\n5.Psychoticism (vs. Lucidity): Exhibiting a wide range of culturally incongruent odd,\neccentric, or unusual behaviors and cognitions, including both process (e.g., per-\nception, dissociation) and content (e.g., beliefs).\nSubtypes. Because personality features vary continuously along multiple trait dimen-\nsions, a comprehensive set of potential expr essions of PD-TS can be represented by DSM-\n5\u2019s dimensional model of maladaptive personality trait variants (see Table 3, pp. 779\u2013781).\nThus, subtypes are unnecessary for PD-TS, and instead, the descriptiv e elements that con-\nstitute personality are provided, arranged in an empirically based model. This arrange-\nment allows clinicians to tailor the descript ion of each individual\u2019s personality disorder\nprofile, considering all five broad domains of personality trait variation and drawing on\nthe descriptive features of these domains as needed to characterize the individual.", "source": "dsm5.pdf"} {"id": "3cd7cede9156-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 771\nSpecifiers. The specific personality features of in dividuals are always recorded in eval-\nuating Criterion B, so the comb ination of personality features characterizing an individual\ndirectly constitutes the specifiers in each case. For example, two individuals who are both\ncharacterized by emotional lability, hostility, and depressivity may differ such that the\nfirst individual is characterized additionally by callousness, whereas the second is not.\nPersonality Disorder Scoring Algorithms\nThe requirement for any two of the four A criter ia for each of the six personality disorders\nwas based on maximizing the relationship of these criteria to their corresponding person-\nality disorder. Diagnostic thresholds for the B criteria were also set empirically to minimize\nchange in prevalence of the disorders from DSM-IV an d overlap with other personality\ndisorders, and to maximize relationships with functional impairment. The resulting diag-\nnostic criteria sets represent clinically usef ul personality disorders with high fidelity, in\nterms of core impairments in personality functioning of varying degr ees of severity and\nconstellations of pathological personality traits.\nPersonality Disorder Diagnosis\nIndividuals who have a pattern of impairment in personality functioning and maladaptive\ntraits that matches one of the six defined personality disorders should be diagnosed with\nthat personality disorder. If an individual also has one or even several prominent traits that\nmay have clinical relevance in addition to those requ ired for the diagnosis (e.g., see narcis-\nsistic personality disorder), the option exists for these to be noted as specifiers. Individuals\nwhose personality functioning or trait pattern is substantially different from that of any of\nthe six specific personality disorders should be diagnosed with PD-T S. The individual may\nnot meet the required number of A or B criter ia and, thus, have a su bthreshold presentation", "source": "dsm5.pdf"} {"id": "3cd7cede9156-1", "page_content": "of a personality disorder. The individual may have a mix of features of personality disorder\ntypes or some features that are less characteri stic of a type and more accurately considered\na mixed or atypical presentation. The specific level of impairment in personality function-\ning and the pathological personality traits that characterize the individual\u2019s personality can\nbe specified for PD-TS, using the Level of Personality Functioning Scale (Table 2) and the\npathological trait taxonomy (T able 3). The current diagnoses of paranoid, schizoid, histri-\nonic, and dependent personality disorders are represented also by the diagnosis of PD-TS;\nthese are defined by moderate or greater impairment in personality functioning and can be\nspecified by the relevant pathological personality trait combinations.\nLevel of Personality Functioning\nLike most human tendencies, personality func tioning is distributed on a continuum. Cen-\ntral to functioning and adaptation are indivi duals\u2019 characteristic ways of thinking about\nand understanding themselves and their intera ctions with others. An optimally function-\ning individual has a complex, fully elaborat ed, and well-integrated psychological world\nthat includes a mostly positive, volitional, and adaptive self-concept; a rich, broad, and ap-\npropriately regulated emotional life; and the ca pacity to behave as a productive member of\nsociety with reciprocal and fulfilling interper sonal relationships. At the opposite end of\nthe continuum, an individual with severe personality pathology has an impoverished, dis-\norganized, and/or conflicted psychological world that includes a weak, unclear, and mal-\nadaptive self-concept; a propensity to negative, dysregulated emotions; and a deficient\ncapacity for adaptive interpersona l functioning and social behavior.", "source": "dsm5.pdf"} {"id": "9c63d44be6f0-0", "page_content": "772 Alternative DSM-5 Model for Personality Disorders\nSelf- and Interpersonal Functioning \nDimensional Definition\nGeneralized severity may be the most import ant single predictor of concurrent and pro-\nspective dysfunction in assessing personalit y psychopathology. Pers onality disorders are\noptimally characterized by a generalized pers onality severity continuum with additional\nspecification of stylistic elem ents, derived from personalit y disorder symptom constella-\ntions and personality traits. At the same time , the core of personality psychopathology is\nimpairment in ideas and feelin gs regarding self and interper sonal relationships; this no-\ntion is consistent with multiple theories of personality disorder and their research bases. The\ncomponents of the Level of Personality Func tioning Scale\u2014identity, self-direction, empa-\nthy, and intimacy (see Table 1)\u2014are particularly central in describing a personality func-\ntioning continuum.\nMental representations of the self and interpersonal relationships are reciprocally in-\nfluential and inextricably tied , affect the nature of interaction with mental health pro-\nfessionals, and can have a significant impact on both treatment efficacy and outcome,\nunderscoring the importance of assessing an individual\u2019s characteristic self-concept as\nwell as views of other people and relationships. Although the degree of disturbance in the\nself and interpersonal functioning is continuous ly distributed, it is useful to consider the\nlevel of impairment in functioning for clinical characterization and for treatment planning\nand prognosis.\nRating Level of Pers onality Functioning\nTo use the Level of Personality Functioning Sc ale (LPFS), the clinician selects the level that\nmost closely captures the individual\u2019s current overall level of impairment in personality func-\ntioning. The rating is necessary for the diagnosi s of a personality disord er (moderate or greater", "source": "dsm5.pdf"} {"id": "9c63d44be6f0-1", "page_content": "impairment) and can be used to specify the seve rity of impairment pr esent for an individual\nwith any personality disorder at a given point in time. The LPFS may also be used as a global\nindicator of personality functi oning without specification of a personality disorder diagnosis,\nor in the event that personality impairment is subthreshold for a disorder diagnosis.\nPersonality Traits\nDefinition and Description\nCriterion B in the alternative model involves assessments of personality traits that are\ngrouped into five domains. A personality trait is a tendency to feel, perceive, behave, and\nthink in relatively consistent ways across time and across situations in which the trait may\nmanifest. For example, individuals with a high level of the personality trait of anxiousness\nwould tend to feel anxious readily, including in circumstances in which most people\nwould be calm and relaxed. Individuals high in trait anxiousness also would perceive sit-\nuations to be anxiety-provoking more freque ntly than would individuals with lower lev-\nels of this trait, and those high in the trait would tend to behave so as to avoid situations that\nthey think would make them anxious. They would thereby tend to think about the world as\nmore anxiety provoking than other people.\nImportantly, individuals high in trait anxiousness would not nece ssarily be anxious at\nall times and in all situations. Individuals\u2019 trait levels also can and do change throughout\nlife. Some changes are very general and reflect maturation (e.g., teenagers generally are\nhigher on trait impulsivity than are older ad ults), whereas other ch anges reflect individ-\nuals\u2019 life experiences.\nDimensionality of personality traits. All individuals can be located on the spectrum of\ntrait dimensions; that is, personality traits apply to everyone in different degrees rather", "source": "dsm5.pdf"} {"id": "e038f47d29f0-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 773\nthan being present versus absent. Moreover, personality traits, including those identified\nspecifically in the Section III model, exist on a spectrum with two opposing poles. For ex-\nample, the opposite of the trait of callousness is the tendency to be empathic and kind-\nhearted, even in circumstances in which most persons would not feel that way. Hence, al-\nthough in Section III th is trait is labeled callousness, because that pole of the dimension is\nthe primary focus, it coul d be described in full as callousness versus kind-heartedness. More-\nover, its opposite pole can be recognized and may not be adaptive in all circumstances\n(e.g., individuals who, due to extreme kind-heartedness, repeatedly allow themselves to\nbe taken advantage of by unscrupulous others).\nHierarchical structure of personality. Some trait terms are quite specific (e.g., \u201ctalkative\u201d)\nand describe a narrow range of behaviors, wh ereas others are quite broad (e.g., Detach-\nment) and characterize a wide range of beha vioral propensities. Broad trait dimensions\nare called domains, and specific trait dimensions are called facets. Personality trait domains\ncomprise a spectrum of more specific personality facets that tend to occur together. For ex-\nample, withdrawal and anhedonia are specific trait facets in the trait domain of Detachment.\nDespite some cross-cultural variation in pe rsonality trait facets, the broad domains they\ncollectively comprise are relati vely consistent across cultures.\nThe Personality Trait Model\nThe Section III personality trait system includ es five broad domains of personality trait\nvariation\u2014Negative Affectivity (vs. Emotiona l Stability), Detachment (vs. Extraversion),", "source": "dsm5.pdf"} {"id": "e038f47d29f0-1", "page_content": "Antagonism (vs. Agreeableness), Disinhibition (vs. Conscientiousness), and Psychoticism\n(vs. Lucidity)\u2014comprising 25 specific personalit y trait facets. Table 3 provides definitions\nof all personality domains and facets. These five broad domains are maladaptive variants\nof the five domains of the extensively valid ated and replicated personality model known\nas the \u201cBig Five\u201d, or Five Factor Model of pe rsonality (FFM), and are also similar to the do-\nmains of the Personality Psychopathology Five (PSY-5). The specific 25 facets represent a\nlist of personality facets chosen for their clinical relevance.\nAlthough the Trait Model focuses on persona lity traits associated with psychopathol-\nogy, there are healthy, adaptive, and resilien t personality traits identified as the polar\nopposites of these traits, as noted in the pa rentheses above (i.e., Em otional Stability, Ex-\ntraversion, Agreeableness, Conscientiousness, and Lucidity). Their presence can greatly\nmitigate the effects of mental disorders and facilitate coping and re covery from traumatic\ninjuries and other medical illness.\nDistinguishing Traits, Symptoms, and Specific Behaviors\nAlthough traits are by no means immutable and do change throughout the life span, they\nshow relative consistency compared with sy mptoms and specific behaviors. For example,\na person may behave impulsively at a specific ti me for a specific reason (e.g., a person who\nis rarely impulsive suddenly decides to spend a great deal of money on a particular item\nbecause of an unusual opportunity to purchase something of unique value), but it is only\nwhen behaviors aggregate across time and circumstance, such that a pattern of behavior\ndistinguishes between individuals, that they re flect traits. Nevertheless, it is important to", "source": "dsm5.pdf"} {"id": "e038f47d29f0-2", "page_content": "distinguishes between individuals, that they re flect traits. Nevertheless, it is important to\nrecognize, for example, that even people wh o are impulsive are not acting impulsively all\nof the time. A trait is a tendency or dispositio n toward specific behaviors; a specific behav-\nior is an instance or manifestation of a trait.\nSimilarly, traits are distin guished from most symptoms because symptoms tend to\nwax and wane, whereas traits are relatively more stable. For example, individuals with", "source": "dsm5.pdf"} {"id": "5684d1d4aa93-0", "page_content": "Similarly, traits are distin guished from most symptoms because symptoms tend to\nwax and wane, whereas traits are relatively more stable. For example, individuals with\nhigher levels of depressivity have a greater likelihood of experiencing discrete episodes of a\ndepressive disorder and of showing the sympto ms of these disorders, such difficulty con-\ncentrating. However, even patients who have a trait propensity to depressivity typically cy-\ncle through distinguishable episodes of mood disturbance, and specific symptoms such as", "source": "dsm5.pdf"} {"id": "43e2d6f93311-0", "page_content": "774 Alternative DSM-5 Model for Personality Disorders\ndifficulty concentrating tend to wax and wane in concert with specific episodes, so they do\nnot form part of the trait definition. Import antly, however, symptoms and traits are both\namenable to intervention, and many interven tions targeted at symptoms can affect the\nlonger term patterns of pers onality functioning that are ca ptured by personality traits.\nAssessment of the DSM-5 Section III \nPersonality Trait Model\nThe clinical utility of the Section III multidimensio nal personality trait model lies in its ability\nto focus attention on multiple relevant areas of personality variation in each individual patient.\nRather than focusing attention on the identification of one and only one optimal diagnostic\nlabel, clinical ap plication of the Section III personality trait model involves reviewing all five\nbroad personality domains portrayed in Table 3. The clinical approach to personality is similar\nto the well-known review of systems in clinical medicine. For example, an individual\u2019s pre-\nsenting complaint may focus on a specific ne urological symptom, yet during an initial\nevaluation clinicians still systematically review functioning in all relevant systems (e.g., car-\ndiovascular, respiratory, gastrointestinal), lest an important area of diminished functioning\nand corresponding opportunity for effective intervention be missed.\nClinical use of the Section III personality trait model proceeds similarly. An initial in-\nquiry reviews all five broad doma ins of personality. This systematic review is facilitated\nby the use of formal psychome tric instruments designed to me asure specific facets and do-\nmains of personality. For example, the person ality trait model is operationalized in the\nPersonality Inventory for DSM-5 (PID-5), which can be completed in its self-report form by\npatients and in its informant-report form by those who know the patient well (e.g., a", "source": "dsm5.pdf"} {"id": "43e2d6f93311-1", "page_content": "patients and in its informant-report form by those who know the patient well (e.g., a\nspouse). A detailed clinical assessment would involve collect ion of both patient- and in-\nformant-report data on all 25 facets of the pe rsonality trait model. However, if this is not\npossible, due to time or other co nstraints, assessment focused at the five-domain level is an\nacceptable clinical option when only a general (vs. detailed) portrait of a patient\u2019s person-\nality is needed (see Criterion B of PD-TS). Ho wever, if personality- based problems are the\nfocus of treatment, then it will be important to assess individual s\u2019 trait facets as well as do-\nmains.\nBecause personality traits are continuously distributed in the population, an approach\nto making the judgment that a specific trait is elevated (and therefor e is present for diag-\nnostic purposes) could involve comparing indi viduals\u2019 personality tr ait levels with pop-\nulation norms and/or clinical judgment. If a trait is elevated\u2014that is, formal psychometric\ntesting and/or interview data support the clinical judgment of elevation\u2014then it is con-\nsidered as contributing to meeting Criterion B of Section III personality disorders.\nClinical Utility of the Multidimensional Personality \nFunctioning a nd Trait Model\nDisorder and trait constructs each add value to the other in predicting important anteced-\nent (e.g., family history, hist ory of child abuse), concurrent (e.g., functional impairment,\nmedication use), and predictive (e.g., hospit alization, suicide attempts) variables. DSM-5\nimpairments in personality functioning and pa thological personality traits each contrib-\nute independently to clinical decisions about degree of disability; risks for self-harm, vio-", "source": "dsm5.pdf"} {"id": "43e2d6f93311-2", "page_content": "ute independently to clinical decisions about degree of disability; risks for self-harm, vio-\nlence, and criminality; reco mmended treatment type and intensity; and prognosis\u2014all\nimportant aspects of the utility of psychiatric diagnoses. Notably, knowing the level of an\nindividual\u2019s personality functioning and his or her pathological trait profile also provides\nthe clinician with a rich base of information and is valuable in treatment planning and in", "source": "dsm5.pdf"} {"id": "c271165b6d25-0", "page_content": "individual\u2019s personality functioning and his or her pathological trait profile also provides\nthe clinician with a rich base of information and is valuable in treatment planning and in\npredicting the course and outcome of many me ntal disorders in addition to personality\ndisorders. Therefore, assessment of persona lity functioning and pathological personality\ntraits may be relevant whether an indivi dual has a personality disorder or not.", "source": "dsm5.pdf"} {"id": "5494fabb05a4-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 775TABLE 2 Level of Personality Functioning Scale\nSELF INTERPERSONAL\nLevel of \nimpairment Identity Self-d irection Empathy Intimacy\n0\u2014Little or no \nimpairmentHas ongoing awareness of a \nunique self; maintains role-\nappropriate boundaries.\nHas consistent and self-regulated \npositive self-esteem, with accu-\nrate self-appraisal.\nIs capable of experiencing, toler-\nating, and regulating a full \nrange of emotions.Sets and aspires to reasonable \ngoals based on a realistic \nassessment of personal \ncapacities.\nUtilizes appropriate stan-\ndards of behavior, attaining \nfulfillment in multiple \nrealms.\nCan reflect on, and make con-\nstructive meaning of, inter-\nnal experience.Is capable of accurately under-\nstanding others\u2019 experiences \nand motivations in most situ-\nations.\nComprehends and appreciates \nothers\u2019 perspectives, even if \ndisagreeing.\nIs aware of the effect of own \nactions on others.Maintains multiple satisfying and \nenduring relationships in personal \nand community life.\nDesires and engages in a number of \ncaring, close, and reciprocal rela-\ntionships.\nStrives for cooperation and mutual \nbenefit and flexibly responds to a \nrange of others\u2019 ideas, emotions, \nand behaviors.\n1\u2014Some \nimpairmentHas relatively intact sense of self, \nwith some decrease in clarity of \nboundaries when strong emo-\ntions and mental distress are \nexperienced.\nSelf-esteem dimini shed at times, \nwith overly critical or some-\nwhat distorted self-appraisal.\nStrong emotions may be distress-", "source": "dsm5.pdf"} {"id": "5494fabb05a4-1", "page_content": "what distorted self-appraisal.\nStrong emotions may be distress-\ning, associated with a restric-\ntion in range of emotional \nexperience.Is excessively goal-directed, \nsomewhat goal-inhibited, or \nconflicted about goals.\nMay have an unrealistic or \nsocially inappropriate set of \npersonal standards, limiting \nsome aspects of fulfillment.\nIs able to reflect on internal \nexperiences, but may over-\nemphasize a single (e.g., \nintellectual, emotional) type \nof self-knowledge.Is somewhat compromised in \nability to appreciate and \nunderstand others\u2019 experi-\nences; may tend to see others \nas having unreasonable \nexpectations or a wish for \ncontrol.\nAlthough capable of consider-\ning and understanding dif-\nferent perspectives, resists \ndoing so.\nHas inconsistent awareness of \neffect of own behavior on \nothers.Is able to establish enduring rela-\ntionships in personal and commu-\nnity life, with some limitations on \ndegree of depth and satisfaction.\nIs capable of forming and desires to \nform intimate and reciprocal rela-\ntionships, but may be inhibited in \nmeaningful expression and some-\ntimes constrained if intense emo-\ntions or conflicts arise.\nCooperation may be inhibited by \nunrealistic standards; somewhat \nlimited in ability to respect or \nrespond to others\u2019 ideas, emo-\ntions, and behaviors.", "source": "dsm5.pdf"} {"id": "751ec0ea7c60-0", "page_content": "776 Alternative DSM-5 Model for Personality Disorders2\u2014Moderate \nimpairmentDepends excessively on others \nfor identity definition, with \ncompromised boundary delin-\neation.\nHas vulnerable self-esteem con-\ntrolled by exaggerated concern \nabout external evaluation, with \na wish for approval. Has sense \nof incompleteness or inferior-\nity, with compensatory \ninflated, or deflated, \nself-appraisal.\nEmotional regulation depends \non positive external appraisal. \nThreats to self-esteem may \nengender strong emotions such \nas rage or shame.Goals are more often a means \nof gaining external approval \nthan self-generated, and \nthus may lack coherence \nand/or stability.\nPersonal standards may be \nunreasonably high (e.g., a \nneed to be special or please \nothers) or low (e.g., not con-\nsonant with prevailing \nsocial values). Fulfillment is \ncompromised by a sense of \nlack of authenticity.\nHas impaired capacity to \nreflect on internal experi-\nence.Is hyperattuned to the experi-\nence of others, but only with \nrespect to perceived rele-\nvance to self.\nIs excessively self-referential; \nsignificantly compromised \nability to appreciate and \nunderstand others\u2019 experi-\nences and to co nsider alterna-\ntive perspectives.\nIs generally unaware of or \nunconcerned about effect of \nown behavior on others, or \nunrealistic appraisal of own \neffect.Is capable of forming and desires to \nform relationships in personal and \ncommunity life, but connections \nmay be largely superficial.\nIntimate relationships are predomi-", "source": "dsm5.pdf"} {"id": "751ec0ea7c60-1", "page_content": "may be largely superficial.\nIntimate relationships are predomi-\nnantly based on meeting self-regu-\nlatory and self-esteem needs, with \nan unrealistic expectation of being \nperfectly understood by others.\nTends not to view relationships in \nreciprocal terms, and cooperates \npredominantly for personal gain.TABLE 2 Level of Personality Functioning Scale (continued)\nSELF INTERPERSONAL\nLevel of \nimpairment Identity Self-d irection Empathy Intimacy", "source": "dsm5.pdf"} {"id": "6284d9d9aa06-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 7773\u2014Severe \nimpairmentHas a weak sense of autonomy/\nagency; experience of a lack of \nidentity, or emptiness. Bound-\nary definition is poor or rigid: \nmay show overidentification \nwith others, overemphasis on \nindependence from others, or \nvacillation between these.\nFragile self-esteem is easily influ-\nenced by events, and self-image \nlacks coherence. Self-appraisal \nis un-nuanced: self-loathing, \nself-aggrandizing, or an illogi-\ncal, unrealistic combination.\nEmotions may be rapidly shifting \nor a chronic, unwavering feel-\ning of despair.Has difficulty establishing \nand/or achieving personal \ngoals.\nInternal standards for behav-\nior are unclear or contradic-\ntory. Life is experienced as \nmeaningless or dangerous.\nHas significantly compro-\nmised ability to reflect on \nand understand own mental \nprocesses.Ability to consider and under-\nstand the thoughts, feelings, \nand behavior of other people \nis significantly limited; may \ndiscern very specific aspects \nof others\u2019 experience, particu-\nlarly vulnerabilities and suf-\nfering.\nIs generally unable to consider \nalternative perspectives; \nhighly threatened by differ-\nences of opinion or alterna-\ntive viewpoints.\nIs confused about or unaware \nof impact of own actions on \nothers; often bewildered \nabout peoples\u2019 thoughts and \nactions, with destructive \nmotivations frequently \nmisattributed to others.Has some desire to form relation-\nships in community and personal \nlife is present, but capacity for pos-\nitive and enduring connections is \nsignificantly impaired.", "source": "dsm5.pdf"} {"id": "6284d9d9aa06-1", "page_content": "itive and enduring connections is \nsignificantly impaired.\nRelationships are based on a strong \nbelief in the absolute need for the \nintimate other(s), and/or expecta-\ntions of abandonment or abuse. \nFeelings about intimate involve-\nment with others alternate \nbetween fear/rejection and des-\nperate desire for connection.\nLittle mutuality: others are concep-\ntualized primarily in terms of how \nthey affect the se lf (negatively or \npositively); cooperative efforts are \noften disrupted due to the percep-\ntion of slights from others.TABLE 2 Level of Personality Functioning Scale (continued)\nSELF INTERPERSONAL\nLevel of \nimpairment Identity Self-d irection Empathy Intimacy", "source": "dsm5.pdf"} {"id": "bafa2b223530-0", "page_content": "778 Alternative DSM-5 Model for Personality Disorders4\u2014Extreme \nimpairmentExperience of a unique self and \nsense of agency/autonomy are \nvirtually absent, or are orga-\nnized around perceived exter-\nnal persecution. Boundaries \nwith others are confused or \nlacking.\nHas weak or distorted self-image \neasily threatened by interac-\ntions with others; significant \ndistortions and confusion \naround self-appraisal.\nEmotions not congruent with \ncontext or internal experience. \nHatred and aggression may be \ndominant affects, although they \nmay be disavowed and attrib-\nuted to others.Has poor differentiation of \nthoughts from actions, so \ngoal-setting ability is \nseverely compromised, with \nunrealistic or incoherent \ngoals.\nInternal standards for behav-\nior are virtually lacking. \nGenuine fulfillment is virtu-\nally inconceivable.\nIs profoundly unable to con-\nstructively reflect on own \nexperience. Personal moti-\nvations may be unrecog-\nnized and/or experienced \nas external to self.Has pronounced inability to \nconsider and understand \nothers\u2019 experience and \nmotivation.\nAttention to others\u2019 perspec-\ntives is virtually absent \n(attention is hypervigilant, \nfocused on need fulfillment \nand harm avoidance).\nSocial interactions can be \nconfusing and disorienting.Desire for affiliation is limited \nbecause of profound disinterest or \nexpectation of harm. Engagement \nwith others is detached, disorga-\nnized, or consistently negative.\nRelationships are conceptualized \nalmost exclusively in terms of \ntheir ability to provide comfort or \ninflict pain and suffering.", "source": "dsm5.pdf"} {"id": "bafa2b223530-1", "page_content": "their ability to provide comfort or \ninflict pain and suffering.\nSocial/interpersonal behavior is not \nreciprocal; rather, it seeks fulfill-\nment of basic needs or escape from \npain.TABLE 2 Level of Personality Functioning Scale (continued)\nSELF INTERPERSONAL\nLevel of \nimpairment Identity Self-d irection Empathy Intimacy", "source": "dsm5.pdf"} {"id": "998d501529d1-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 779\nTABLE 3 Definitions of DSM-5 personality disorder trait domains \nand facets\nDOMAINS (Polar Opposites) \nand Facets Definitions\nNEGATIVE AFFECTIVITY \n(vs. Emotional Stability)Frequent and intense experiences of high levels of a wide range of \nnegative emotions (e.g., anxiet y, depression, guilt/ shame, worry, \nanger) and their behavioral (e.g., self-harm) and interpersonal (e.g., \ndependency) manifestations.\nEmotional lability Instability of emotional experiences and mood; emotions that are \neasily aroused, intense, and/or out of proportion to events and cir-\ncumstances.\nAnxiousness Feelings of nervousness, tensenes s, or panic in reaction to diverse situa-\ntions; frequent worry about the negative effects of past unpleasant \nexperiences and future negative possibilities; feeling fearful and \napprehensive about un certainty; expecting the worst to happen.\nSeparation insecurity Fears of being alone due to rejection by\u2014and /or separation from\u2014\nsignificant others, based in a lack of confidence in one\u2019s ability to \ncare for oneself, both ph ysically and emotionally.\nSubmissiveness Adaptation of one\u2019s behavior to the actual or perceived interests and \ndesires of others even when doing so is antithetical to one\u2019s own \ninterests, needs, or desires.\nHostility Persistent or frequent angry feelings; anger or irritability in response \nto minor slights and insults; mean, nasty, or vengeful behavior. See \nalso Antagonism.\nPerseveration Persistence at tasks or in a particular way of doing things long after the \nbehavior has ceased to be functional or effective; co ntinuance of the", "source": "dsm5.pdf"} {"id": "998d501529d1-1", "page_content": "behavior has ceased to be functional or effective; co ntinuance of the \nsame behavior despite repeated fail ures or clear reasons for stopping.\nDepressivity See Detachment.\nSuspiciousness See Detachment.\nRestricted affectivity \n(lack\u00a0of)The lack of this facet characterizes low levels of Negative Affectivity. \nSee Detachment for definition of this facet.\nDETACHMENT \n(vs. Extraversion)Avoidance of socioemotional experi ence, including both withdrawal \nfrom interpersonal interactions (ranging from casual, daily interac-\ntions to friendships to intimate relationships) and restricted affective \nexperience and expression, partic ularly limited hedonic capacity.\nWithdrawal Preference for bein g alone to being with others; reticence in social sit-\nuations; avoidance of social contacts and activity; lack of initiation \nof social contact.\nIntimacy avoidance Avoidance of close or ro mantic relationships, interpersonal attach-\nments, and intimate sexual relationships.\nAnhedonia Lack of enjoyment from, engagement in, or energy for life\u2019s experiences; \ndeficits in the capacity to feel pleasure and take interest in things.\nDepressivity Feelings of being down, mise rable, and/or hopeless; difficulty recov-\nering from such moods; pessimism about the future; pervasive \nshame and/or guilt; feelings of inferior self-worth; thoughts of sui-\ncide and suicidal behavior.\nRestricted affectivity Little reaction to emot ionally arousing situations; constricted emo-\ntional experience and expression; indifference and aloofness in nor-\nmatively engaging situations.\nSuspiciousness Expectations of\u2014and sensitivity to\u2014signs of interpersonal ill-\nintent or harm; doubts about loyalty and fidelity of others; feelings", "source": "dsm5.pdf"} {"id": "998d501529d1-2", "page_content": "intent or harm; doubts about loyalty and fidelity of others; feelings \nof being mistreated, used, and/or persecuted by others.", "source": "dsm5.pdf"} {"id": "7a51fd12eac6-0", "page_content": "780 Alternative DSM-5 Model for Personality Disorders\nANTAGONISM (vs. \nAgreeableness)Behaviors that put the individual at odds with other people, includ-\ning an exaggerated sense of self-importance and a concomitant \nexpectation of special treatment, as well as a callous antipathy \ntoward others, encompassing both an unawareness of others\u2019 \nneeds and feelings and a readiness to use others in the service of \nself-enhancement.\nManipulativeness Use of subterfuge to influence or control others; use of seduction, \ncharm, glibness, or ingratia tion to achieve one\u2019s ends.\nDeceitfulness Dishonesty and fraudulence; misrepresentation of self; embellish-\nment or fabrication when relating events.\nGrandiosity Believing that one is superior to others and deserves special treat-\nment; self-centeredness; feelings of entitlement; condescension \ntoward others.\nAttention seeking Engaging in behavior designed to attract notice and to make oneself \nthe focus of others\u2019 attention and admiration.\nCallousness Lack of concern for the feelings or problems of others; lack of guilt \nor remorse about the negative or harmful effects of one\u2019s actions \non others.\nHostility See Negative Affectivity.\nDISINHIBITION \n(vs. Conscientiousness)Orientation toward immediate gratification, leading to impulsive \nbehavior driven by current though ts, feelings, and external stim-\nuli, without regard fo r past learning or consideration of future \nconsequences.\nIrresponsibility Disregard for\u2014and failure to honor\u2014financial and other obliga-\ntions or commitments; lack of respect for\u2014and lack of follow-\nthrough on\u2014agreements and promises; carelessness with others\u2019 \nproperty.", "source": "dsm5.pdf"} {"id": "7a51fd12eac6-1", "page_content": "through on\u2014agreements and promises; carelessness with others\u2019 \nproperty.\nImpulsivity Acting on the spur of the moment in response to immediate stimuli; \nacting on a momentary basis with out a plan or consideration of \noutcomes; difficulty establishing and following plans; a sense of \nurgency and self-harming behavi or under emotional distress.\nDistractibility Difficulty concentrating and focusing on tasks; attention is easily \ndiverted by extraneous stimuli; difficulty maintaining goal-\nfocused behavior, including both planning and completing tasks.\nRisk taking Engagement in dangerous, risky, and potentially self-damaging \nactivities, unnecessarily and withou t regard to consequences; lack \nof concern for one\u2019s limitations and denial of the reality of per-\nsonal danger; reckless pursuit of goals regardless of the level of \nrisk involved.\nRigid perfectionism (lack of) Rigid insistence on everything being flawless, perfect, and without \nerrors or faults, including one\u2019s own and others\u2019 performance; sac-\nrificing of timeliness to ensure correctness in every detail; believ-\ning that there is only one right way to do things; difficulty \nchanging ideas and/or viewpoint; preoccupation with details, \norganization, and order. The lack of this facet characterizes low \nlevels of Disinhibition.TABLE 3 Definitions of DSM-5 personality disorder trait domains \nand facets (continued)\nDOMAINS (Polar Opposites) \nand Facets Definitions", "source": "dsm5.pdf"} {"id": "ad17133a99be-0", "page_content": "Alternative DSM-5 Model for Personality Disorders 781\nPSYCHOTICISM \n(vs. Lucidity)Exhibiting a wide range of cultura lly incongruent odd, eccentric, or \nunusual behaviors and cognitions, including both process (e.g., \nperception, dissociation) and content (e.g., beliefs).\nUnusual beliefs and \nexperiencesBelief that one has unusual abilities, such as mind reading, telekine-\nsis, thought-action fusion, unusual experiences of reality, includ-\ning hallucination-like experiences.\nEccentricity Odd, unusual, or bizarre behavior, appearance, and/or speech; \nhaving strange and unpredictable thoughts; saying unusual or \ninappropriate things.\nCognitive and perceptual \ndysregulationOdd or unusual thought processes and experiences, including \ndepersonalization, derealization, and dissociative experiences; \nmixed sleep-wake state experience s; thought-control experiences.TABLE 3 Definitions of DSM-5 personality disorder trait domains \nand facets (continued)\nDOMAINS (Polar Opposites) \nand Facets Definitions", "source": "dsm5.pdf"} {"id": "cc67c099d126-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "4e0663d0d8f9-0", "page_content": "783Conditions for\nFurther Study\nProposed criteria sets are presented fo r conditions on which future research is en-\ncouraged. The specific items, thresholds, and durations contained in these research crite-\nria sets were set by expert co nsensus\u2014informed by literature review, data reanalysis, and\nfield trial results, where available\u2014and are intended to provide a common language for\nresearchers and clinicians who are interested in studying these disord ers. It is hoped that\nsuch research will allow the field to better understand these conditions and will inform\ndecisions about possible placement in fort hcoming editions of DSM. The DSM-5 Task\nForce and Work Groups subjecte d each of these proposed crit eria sets to a careful empir-\nical review and invited wide commentary from the field as well as from the general public.\nThe Task Force determined that there was in sufficient evidence to warrant inclusion of\nthese proposals as official mental disorder diagnoses in Section II. These proposed criteria\nsets are not intended for clinical use; only th e criteria sets and disorders in Section II of\nDSM-5 are officially recognized and can be used for clinical purposes.\nAttenuated Psychosis Syndrome\nProposed Criteria \nA. At least one of the following symptoms is present in attenuated form, with relatively in-\ntact reality testing, and is of sufficient seve rity or frequency to warr ant clinical attention:\n1. Delusions.\n2. Hallucinations. \n3. Disorganized speech.\nB. Symptom(s) must have been present at least once per week for the past month.\nC. Symptom(s) must have begun or worsened in the past year.\nD. Symptom(s) is sufficiently distressing and disabling to\u00a0the individual to warrant clinical\nattention.\nE. Symptom(s) is not better explained by another mental disorder, including a depressive", "source": "dsm5.pdf"} {"id": "4e0663d0d8f9-1", "page_content": "E. Symptom(s) is not better explained by another mental disorder, including a depressive\nor bipolar disorder with psychotic features , and is not attributable to the physiological\neffects of a substance or another medical condition.\nF. Criteria for any psychotic disorder have never been met.\nDiagnostic Features\nAttenuated psychotic symptoms, as defined in Criterion A, are psychosis-like but below the\nthreshold for a full psychotic disorder. Comp ared with psychotic disorders, the symptoms\nare less severe and more transient, and insight is relatively maintained . A diagnosis of atten-\nuated psychosis syndrome requires state psychopathology associated with functional\nimpairment rather than long-standing trait pathology. The psychopathology has not pro-\ngressed to full psychotic severi ty. Attenuated psychosis syndrome is a disorder based on the\nmanifest pathology and impaired function and distress. Changes in experiences and behav-", "source": "dsm5.pdf"} {"id": "a4095b66e943-0", "page_content": "784 Conditions for Further Study\niors are noted by the individual and/or others, suggesting a change in mental state (i.e., the\nsymptoms are of sufficient severi ty or frequency to warrant clin ical attention) (Criterion A).\nAttenuated delusions (Criterion A1) may have suspiciousness /persecutory ideational con-\ntent, including persecutory ideas of reference. The individual may have a guarded, distrust-\nful attitude. When the delusions are moderate in severity, the individual views others as\nuntrustworthy and may be hyperv igilant or sense ill will in others. When the delusions are\nsevere but still within the attenuated range, the individual entertains loosely organized be-\nliefs about danger or hostile in tention, but the delusions do no t have the fixed nature that is\nnecessary for the diagnosis of a psychotic diso rder. Guarded behavior in the interview can\ninterfere with the ability to gath er information. Rea lity testing and perspective can be elic-\nited with nonconfirming evidence, but the prop ensity for viewing the world as hostile and\ndangerous remains strong. Attenuated delusions may have grandiose content presenting as\nan unrealistic sense of superior capacity. Wh en the delusions are moderate, the individual\nharbors notions of being gifted, influential, or special. When the delusions are severe, the in-\ndividual has beliefs of superiority that often alienate friends and worry relatives. Thoughts\nof being special may lead to unrealistic plans and investments, yet skepticism about these at-\ntitudes can be elicited with persis tent questioning and confrontation.\nAttenuated hallucinations (Criterion A2) include alterations in sensory perceptions,\nusually auditory and/or visual. When the hallucinations are moderate, the sounds and", "source": "dsm5.pdf"} {"id": "a4095b66e943-1", "page_content": "usually auditory and/or visual. When the hallucinations are moderate, the sounds and\nimages are often unformed (e.g ., shadows, trails, halos, mu rmurs, rumbling), and they are\nexperienced as unusual or puzzling. When the hallucinations are severe, these experiences\nbecome more vivid and frequent (i.e., recurring illusions or hallucinations that capture at-\ntention and affect thinking and concentratio n). These perceptual abnormalities may dis-\nrupt behavior, but skepticism about their reality can still be induced. \nDisorganized communica tion (Criterion A3) may manifest as odd speech (vague, meta-\nphorical, overelaborate, stereoty ped), unfocused speech (confuse d, muddled, too fast or too\nslow, wrong words, irrelevant context, off trac k), or meandering speech (circumstantial, tan-\ngential). When the disorganization is moderately severe, the individual frequently gets into\nirrelevant topics but re sponds easily to clarifying questi ons. Speech may be odd but under-\nstandable. At the moderately severe level, speech becomes meandering and circumstantial,\nand when the disorganization is severe, the in dividual fails to get to the point without\nexternal guidance (tangential). At the severe level, some thought blocking and/or loose as-\nsociations may occur infrequently, especially wh en the individual is under pressure, but re-\norienting questions quickly re turn structure and organiza tion to the conversation. \nThe individual realizes that changes in mental state and/or in relationships are taking\nplace. He or she maintains reasonable insigh t into the psychotic-like experiences and gen-\nerally appreciates that altered perceptions are not real and magical ideation is not compel-\nling. The individual must experience distress and/or impaired performance in social or role", "source": "dsm5.pdf"} {"id": "a4095b66e943-2", "page_content": "ling. The individual must experience distress and/or impaired performance in social or role\nfunctioning (Criterion D), and the individual or responsible others must note the changes\nand express concern, such that clinic al care is sought (Criterion A).\nAssociated Features Supporting Diagnosis\nThe individual may experience magical thinking, perceptual aberrations, difficulty in con-\ncentration, some disorganization in thought or behavior, excessive suspiciousness, anxi-\nety, social withdrawal, and disruption in sl eep-wake cycle. Impaired cognitive function", "source": "dsm5.pdf"} {"id": "685320d4fb81-0", "page_content": "centration, some disorganization in thought or behavior, excessive suspiciousness, anxi-\nety, social withdrawal, and disruption in sl eep-wake cycle. Impaired cognitive function\nand negative symptoms are often observed. Neuroimaging variables distinguish cohorts\nwith attenuated psychosis syndro me from normal control coho rts with patterns similar to,\nbut less severe than, that observed in schi zophrenia. However, neuroimaging data is not\ndiagnostic at the individual level.\nPrevalence\nThe prevalence of attenuated psychosis syndrome is unknown. Symptoms in Criterion A\nare not uncommon in the non-help-seeking population, ranging from 8%\u201313% for hallu-", "source": "dsm5.pdf"} {"id": "9ef416202c56-0", "page_content": "Conditions for Further Study 785\ncinatory experiences and delusional thinking. There appears to be a slight male prepon-\nderance for attenuated psychosis syndrome.\nDevelopment and Course\nOnset of attenuated psychosis syndrome is usually in mid-to-late adolescence or early\nadulthood. It may be preceded by normal development or evidence for impaired cogni-\ntion, negative symptoms, and/or impaired so cial development. In help-seeking cohorts,\napproximately 18% in 1 year and 32% in 3 years may progress symptomatically and met\ncriteria for a psychotic disorder . In some cases, the syndrome may transition to a depres-\nsive or bipolar disorder with psychotic featur es, but development to a schizophrenia spec-\ntrum disorder is more frequent. It appears that the diagnosis is best applied to individuals\nages 15\u201335 years. Long-term course is not yet describe d beyond 7\u201312 years.\nRisk and Prognostic Factors \nTemperamental. Factors predicting prognosis of attenuated psychosis syndrome have\nnot been definitively characterized, but the presence of negative symptoms, cognitive im-\npairment, and poor functionin g are associated with poor outcome and increase risk of\ntransition to psychosis.\nGenetic and physiological. A family history of psychosis places the individual with at-\ntenuated psychosis syndrome at increased risk for developing a full psychotic disorder.\nStructural, functional, and neurochemical im aging data are associated with increased risk\nof transition to psychosis.\nFunctional Consequences of \nAttenuated Psychosis Syndrome\nMany individuals may experience functional impairments. Modest-to-moderate impair-\nment in social and role functioning may pers ist even with abatement of symptoms. A sub-\nstantial portion of individuals with the diagnosis will improve over time; many continue", "source": "dsm5.pdf"} {"id": "9ef416202c56-1", "page_content": "stantial portion of individuals with the diagnosis will improve over time; many continue\nto have mild symptoms and impairment, and many others will have a full recovery.\nDifferential Diagnosis\nBrief psychotic disorder. When symptoms of attenuated psychosis syndrome initially\nmanifest, they may resemble sy mptoms of brief psychotic di sorder. However, in attenu-\nated psychosis syndrome, the symptoms do no t cross the psychosis threshold and reality\ntesting/insight remains intact. \nSchizotypal personality disorder. Schizotypal personality disorder, although having\nsymptomatic features that are similar to thos e of attenuated psychosis syndrome, is a rel-\natively stable trait disorder not meeting the st ate-dependent aspects (Criterion C) of atten-\nuated psychosis syndrome. In addition, a br oader array of symptoms is required for\nschizotypal personality disorder, although in the early stages of pr esentation it may re-\nsemble attenuated psychosis syndrome.\nDepressive or bipolar disorders. Reality distortions that are temporally limited to an\nepisode of a major depressive disorder or bipolar disorder and are descriptively more\ncharacteristic of those disorders do not me et Criterion E for attenuated psychosis syn-\ndrome. For example, feelings of low self-esteem or attributions of low regard from others\nin the context of major depressive disorder would not qualify fo r comorbid attenuated\npsychosis syndrome.\nAnxiety disorders. Reality distortions that are temporally limited to an episode of an\nanxiety disorder and are descriptively more ch aracteristic of an anxiety disorder do not", "source": "dsm5.pdf"} {"id": "08295bc77c5b-0", "page_content": "786 Conditions for Further Study\nmeet Criterion E for attenuated psychosis sy ndrome. For example, a feeling of being the\nfocus of undesired attention in the context of social anxiety disorder would not qualify for\ncomorbid attenuated psychosis syndrome.\nBipolar II disorder. Reality distortions that are temporal ly limited to an episode of ma-\nnia or hypomania and are descriptively more ch aracteristic of bipolar disorder do not meet\nCriterion E for attenuated psyc hosis syndrome. For example, inflated self-esteem in the\ncontext of pressured speech and reduced need for sleep would not qua lify for comorbid at-\ntenuated psychosis syndrome.\nBorderline personality disorder. Reality distortions that ar e concomitant with border-\nline personality disorder and are descriptively mo re characteristic of it do not meet Crite-\nrion E for attenuated psychosis syndrome. For example, a sense of being unable to\nexperience feelings in the context of an inte nse fear of real or im agined abandonment and\nrecurrent self-mutilation would not qualify fo r comorbid attenuated psychosis syndrome.\nAdjustment reaction of adolescence. Mild, transient symptoms typical of normal de-\nvelopment and consistent with the degree of stress experienced do not qualify for attenu-\nated psychosis syndrome.\nExtreme end of perceptual aberration and magical thinking in the non-ill population.\nThis diagnostic possibility should be strongly entertained when reality distortions are not\nassociated with distress and functional impairment and need for care.\nSubstance/medication-induced psychotic disorder. Substance use is common among\nindividuals whose symptoms meet attenuated psychosis syndrome criteria. When other-\nwise qualifying characteristic symptoms are strongly temporally related to substance use\nepisodes, Criterion E for attenuated psychosis syndrome may not be met, and a diagnosis", "source": "dsm5.pdf"} {"id": "08295bc77c5b-1", "page_content": "episodes, Criterion E for attenuated psychosis syndrome may not be met, and a diagnosis\nof substance/medication-induced ps ychotic disorder may be preferred.\nAttention-deficit/hyperactivity disorder. A history of attentional impairment does not\nexclude a current attenuated psychosis syndro me diagnosis. Earlier attentional impair-\nment may be a prodromal condit ion or comorbid at tention-deficit/hype ractivity disorder.\nComorbidity\nIndividuals with attenuated psychosis syndrome often experience anxiety and/or depres-\nsion. Some individuals with an attenuated psychosis syndrome diagnosis will progress to\nanother diagnosis, including anxi ety, depressive, bipolar, and personality disorders. In such\ncases, the psychopathology asso ciated with the attenuated psychosis syndrome diagnosis is\nreconceptualized as the prodromal phase of another disorder, not a comorbid condition.\nDepressive Episodes With Short-Duration Hypomania\nProposed Criteria \nLifetime experience of at least one majo r depressive episode meeting the following\ncriteria:\nA. Five (or more) of the following criteria have been present during the same 2-week pe-\nriod and represent a change from previous functioning; at least one of the symptoms\nis either (1) depressed mood or (2) loss of interest or pleasure. ( Note: Do not include\nsymptoms that are clearly attributable to a medical condition.)\n1. Depressed mood most of the day, nearly every day, as indicated by either subjec-\ntive report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g.,\nappears tearful). ( Note: In children and adolescents, can be irritable mood.)\n2. Markedly diminished interest or pleasure in al l, or almost all, activities most of the", "source": "dsm5.pdf"} {"id": "08295bc77c5b-2", "page_content": "day, nearly every day (as indicated by either subjective account or observation).", "source": "dsm5.pdf"} {"id": "18d764e62106-0", "page_content": "Conditions for Further Study 787\n3. Significant weight loss when not dieting or weight gain (e.g., a change of more than\n5% of body weight in a month), or dec rease or increase in appetite nearly every\nday. ( Note: In children, consider failure to make expected weight gain.)\n4. Insomnia or hypersomnia nearly every day.\n5. Psychomotor agitation or retardation nearly every day (observable by others, not\nmerely subjective feelings of restlessness or being slowed down).\n6. Fatigue or loss of energy nearly every day.\n7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delu-\nsional) nearly every day (not merely self-reproach or guilt about being sick).\n8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (ei-\nther by subjective account or as observed by others).\n9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation with-\nout a specific plan, or a suicide attempt or a specific plan for committing suicide.\nB. The symptoms cause clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nC. The disturbance is not attributable to the physiological effects of a substance or an-\nother medical condition.\nD. The disturbance is not better explained by schizoaffective disorder and is not superim-\nposed on schizophrenia, schizophreniform disorder , delusional disorder, or other spec-\nified or unspecified schizophrenia spectrum and other psychotic disorder.\nAt least two lifetime episodes of hypomanic periods that involve the required crite-\nrion symptoms below but are of insufficient duration (a t least 2 days but less than\n4 consecutive days) to meet criteria fo r a hypomanic episode. The criterion symp-", "source": "dsm5.pdf"} {"id": "18d764e62106-1", "page_content": "4 consecutive days) to meet criteria fo r a hypomanic episode. The criterion symp-\ntoms are as follows:\nA. A distinct period of abnormally and persistently elevated, expansive, or irritable mood\nand abnormally and persistently increased goal-directed activity or energy.\nB. During the period of mood disturbance and in creased energy and activity, three (or more)\nof the following symptoms have persisted (four if the mood is only irritable), represent a no-\nticeable change from usual behavior, and have been present to a significant degree:\n1. Inflated self-esteem or grandiosity.\n2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).\n3. More talkative than usual or pressured to keep talking.\n4. Flight of ideas or subjective experience that thoughts are racing.\n5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external\nstimuli), as reported or observed.\n6. Increase in goal-directed activity (either socially, at work or school, or sexually) or\npsychomotor agitation.\n7. Excessive involvement in activities that have a high potential for painful conse-\nquences (e.g., the individual engages in unrestrained buying sprees, sexual indis-\ncretions, or foolish business investments).\nC. The episode is associated with an unequivocal change in functioning that is uncharac-\nteristic of the individual when not symptomatic.\nD. The disturbance in mood and the change in functioning are observable by others.\nE. The episode is not severe enough to cause marked impairment in social or occupa-\ntional functioning or to necessitate hospitalization. If there are psychotic features, the\nepisode is, by definition, manic.", "source": "dsm5.pdf"} {"id": "18d764e62106-2", "page_content": "episode is, by definition, manic.\nF. The episode is not attributable to the physiological effects of a substance (e.g., a drug\nof abuse, a medication or other treatment).", "source": "dsm5.pdf"} {"id": "721538b8af02-0", "page_content": "788 Conditions for Further Study\nDiagnostic Features\nIndividuals with short-durati on hypomania have experienced at least one major depres-\nsive episode as well as at least two episodes of 2\u20133 days\u2019 duration in which criteria for a hy-\npomanic episode were met (except for symptom duration). These episodes are of sufficient\nintensity to be categorized as a hypomanic ep isode but do not meet the 4-day duration re-\nquirement. Symptoms are present to a signific ant degree, such that they represent a no-\nticeable change from the individual\u2019s normal behavior.\nAn individual with a history of a syndromal hypomanic episode and a major depres-\nsive episode by definition has bipolar II disord er, regardless of current duration of hypo-\nmanic symptoms.\nAssociated Features Supporting Diagnosis\nIndividuals who have experienced both shor t-duration hypomania and a major depres-\nsive episode, with their increased comorbidit y with substance use disorders and a greater\nfamily history of bipolar diso rder, more closely resemble in dividuals with bipolar disor-\nder than those with major depressive disorder. \nDifferences have also been found between individuals with short-duration hypomania\nand those with syndromal bipolar disorder. Work impairment was greater for individuals\nwith syndromal bipolar disorder, as was the es timated average number of episodes. Indi-\nviduals with short-duration hypomania may exhibit less se verity than individuals with\nsyndromal hypomanic episodes, including less mood lability.\nPrevalence\nThe prevalence of short-duration hypomania is un clear, since the criteria are new as of this\nedition of the manual. Using somewhat different criteria, however, it has been estimated", "source": "dsm5.pdf"} {"id": "721538b8af02-1", "page_content": "edition of the manual. Using somewhat different criteria, however, it has been estimated\nthat short-duration hypomania occurs in 2.8% of the population (compared with hypoma-\nnia or mania in 5.5% of the population). Short-duration hypomani a may be more common\nin females, who may present with more features of atypical depression. \nRisk and Prognostic Factors\nGenetic and physiological. A family history of mania is two to three times more common in\nindividuals with short-duration hypomania co mpared with the general population, but less\nthan half as common as in individuals with a history of syndromal mania or hypomania.\nSuicide Risk\nIndividuals with short-duration hypomania ha ve higher rates of suicide attempts than\nhealthy individuals, although not as high as the rates in individuals with syndromal bipo-\nlar disorder.\nFunctional Consequences of Short-Duration Hypomania\nFunctional impairments associated specifically with short-duration hypomania are as yet\nnot fully determined. However, research suggests that individuals with this disorder have\nless work impairment than individuals with syndromal bipolar disorder but more comor-\nbid substance use disorders, particularly alco hol use disorder, than individuals with major\ndepressive disorder. \nDifferential Diagnosis\nBipolar II disorder. Bipolar II disorder is characterized by a period of at least 4 days of\nhypomanic symptoms, whereas short-duration hypomania is characterized by periods of", "source": "dsm5.pdf"} {"id": "8c6f679b4d7c-0", "page_content": "Conditions for Further Study 789\n2\u20133 days of hypomanic symptoms. Once an individual has experienced a hypomanic ep-\nisode (4 days or more), the diagnosis beco mes and remains bipolar II disorder regardless\nof future duration of hy pomanic symptom periods. \nMajor depressive disorder. Major depressive disorder is al so characterized by at least\none lifetime major depressive ep isode. However, the additional presence of at least two life-\ntime periods of 2\u20133 days of hypomanic symptoms leads to a diagnosis of short-duration hy-\npomania rather than to major depressive disorder. \nMajor depressive disorder with mixed features. Both major depressive disorder with\nmixed features and short-duration hypomania are characterized by the presence of some\nhypomanic symptoms and a major depressive episode. However, major depressive disor-\nder with mixed features is characteri zed by hypomanic features present concurrently with\na major depressive episode, while individual s with short-duration hypomania experience\nsubsyndromal hypomania and fully syndroma l major depression at different times.\nBipolar I disorder. Bipolar I disorder is differentiat ed from short-duration hypomania\nby at least one lifetime manic episode, which is longer (at least 1 week) and more severe\n(causes more impaired social functioning) than a hypomanic episode. An episode (of any\nduration) that involves psychotic symptoms or necessitates hospitalization is by definition\na manic episode rather than a hypomanic one.\nCyclothymic disorder. While cyclothymic disorder is characterized by periods of de-\npressive symptoms and periods of hypomanic symptoms, the lifetime presence of a major\ndepressive episode precludes the di agnosis of cyclothymic disorder. \nComorbidity", "source": "dsm5.pdf"} {"id": "8c6f679b4d7c-1", "page_content": "Comorbidity\nShort-duration hypomania, similar to full hypomanic episodes, has been associated with\nhigher rates of comorbid anxi ety disorders and substance use disorders than are found in\nthe general population.\nPersistent Complex Bereavement Disorder\nProposed Criteria \nA. The individual experienced the death of someone with whom he or she had a close re-\nlationship.\nB. Since the death, at least one of the following symptoms is experienced on more days\nthan not and to a clinically significant degree and has persisted for at least 12 months\nafter the death in the case of bereaved adults and 6 months for bereaved children:\n1. Persistent yearning/longing for the deceased. In young children, yearning may be\nexpressed in play and behavior, including behaviors that reflect being separated\nfrom, and also reuniting with, a caregiver or other attachment figure.\n2. Intense sorrow and emotional pain in response to the death.\n3. Preoccupation with the deceased.\n4. Preoccupation with the circumstances of the death. In children, this preoccupation\nwith the deceased may be expressed through the themes of play and behavior and\nmay extend to preoccupation with possible death of others close to them.\nC. Since the death, at least six of the following symptoms are experienced on more days\nthan not and to a clinically significant degree, and have persisted for at least 12 months\nafter the death in the case of bereaved adults and 6 months for bereaved children:", "source": "dsm5.pdf"} {"id": "1b1b4fc52fde-0", "page_content": "790 Conditions for Further Study\nReactive distress to the death\n1. Marked difficulty accepting the death. In children, this is dependent on the child\u2019s\ncapacity to comprehend the meaning and permanence of death.\n2. Experiencing disbelief or emotional numbness over the loss.\n3. Difficulty with positive reminiscing about the deceased.\n4. Bitterness or anger related to the loss.\n5. Maladaptive appraisals about oneself in relation to the deceased or the death (e.g.,\nself-blame).\n6. Excessive avoidance of reminders of the loss (e.g., avoidance of individuals,\nplaces, or situations associated with the deceased; in children, this may include\navoidance of thoughts and feelings regarding the deceased).\nSocial/identity disruption\n7. A desire to die in order to be with the deceased.\n8. Difficulty trusting other individuals since the death.\n9. Feeling alone or detached from other individuals since the death.\n10. Feeling that life is meaningless or empty without the deceased, or the belief that\none cannot function without the deceased.\n11. Confusion about one\u2019s role in life, or a diminished sense of one\u2019s identity (e.g., feel-\ning that a part of oneself died with the deceased).\n12. Difficulty or reluctance to pursue interests since the loss or to plan for the future\n(e.g., friendships, activities).\nD. The disturbance causes clinically significant distress or impairment in social, occupa-\ntional, or other important areas of functioning.\nE. The bereavement reaction is out of proportion to or inconsistent with cultural, religious,\nor age-appropriate norms.\nSpecify if: \nWith traumatic bereavement: Bereavement due to homicide or suicide with persis-\ntent distressing preoccupations regarding the traumatic nature of the death (often in re-", "source": "dsm5.pdf"} {"id": "1b1b4fc52fde-1", "page_content": "tent distressing preoccupations regarding the traumatic nature of the death (often in re-\nsponse to loss reminders), including the deceased\u2019s last moments, degree of suffering\nand mutilating injury, or the malicious or intentional nature of the death.\nDiagnostic Features \nPersistent complex bereavement disorder is diagnosed only if at least 12 months (6 months\nin children) have elapsed since the death of someone with whom the bereaved had a close\nrelationship (Criterion A). This time fram e discriminates normal grief from persistent\ngrief. The condition typically involves a pe rsistent yearning/longing for the deceased\n(Criterion B1), which may be associated with intense sorrow and frequent crying (Crite-\nrion B2) or preoccupation with the deceased (Criterion B3). The individual may also be\npreoccupied with the manner in which the person died (Criterion B4). \nSix additional symptoms are required, includ ing marked difficulty accepting that the in-\ndividual has died (Criterion C1) (e.g. preparing meals for them), disbelief that the individual is\ndead (Criterion C2), distressing memories of the deceased (Criterion C3), anger over the loss\n(Criterion C4), maladaptive appraisals about oneself in relation to the deceased or the death\n(Criterion C5), and excessive avoidance of reminders of the loss (Criterion C6). Individuals\nmay also report a desire to die because they wish to be with the deceased (Criterion C7); be dis-\ntrustful of others (Criterion C8); feel isolated (Criterion C9); believe that life has no meaning or\npurpose without the deceased (C riterion C10); experience a di minished sense of identity in\nwhich they feel a part of themselves has died or been lost (Criterion C11); or have difficulty en-", "source": "dsm5.pdf"} {"id": "1b1b4fc52fde-2", "page_content": "gaging in activities, pursuing relationships, or planning for the future (Criterion C12).", "source": "dsm5.pdf"} {"id": "38031eef52c1-0", "page_content": "Conditions for Further Study 791\nPersistent complex bereavement disorder requires clinically significant distress or im-\npairment in psychosocial functioning (Criteri on D). The nature and severity of grief must\nbe beyond expected norms for the relevant cu ltural setting, religio us group, or develop-\nmental stage (Criterion E). Although there are variations in how grief can manifest, the\nsymptoms of persistent complex bereavement disorder occur in both genders and in di-\nverse social and cultural groups.\nAssociated Features Supporting Diagnosis \nSome individuals with persistent complex bereavement disorder experience hallucina-\ntions of the deceased (auditory or visual) in which they temporarily perceive the deceased\u2019s\npresence (e.g., seeing the deceased sitting in his or her favorite chai r). They may also ex-\nperience diverse somatic complaints (e.g., digestive complaints, pain, fatigue), including\nsymptoms experienced by the deceased. \nPrevalence\nThe prevalence of persistent complex bere avement disorder is approximately 2.4%\u20134.8%.\nThe disorder is more prevalent in females than in males.\nDevelopment and Course \nPersistent complex bereavement disorder can o ccur at any age, beginning after the age of\n1 year. Symptoms usually begin within the initial months af ter the death, although there\nmay be a delay of months, or even years, before the full syndrome a ppears. Although grief\nresponses commonly appear immediately following bereavemen t, these reactions are not\ndiagnosed as persistent comp lex bereavement disorder unless the symptoms persist be-\nyond 12 months (6 months for children). \nYoung children may experience the loss of a primary caregiver as traumatic, given the\ndisorganizing effects the caregiver\u2019s absence ca n have on a child\u2019s coping response. In chil-", "source": "dsm5.pdf"} {"id": "38031eef52c1-1", "page_content": "dren, the distress may be expressed in play and behavior, developmental regressions, and\nanxious or protest behavior at times of separation and reunion. Separation distress may be\npredominant in younger children, and social/i dentity distress and risk for comorbid de-\npression can increasingly manifest in older children and adolescents.\nRisk and Prognostic Factors \nEnvironmental. Risk for persistent complex bereavem ent disorder is heightened by in-\ncreased dependency on the deceased person pr ior to the death and by the death of a child.\nDisturbances in caregiver support increase the risk for bereaved children. \nGenetic and physiological. Risk for the disorder is height ened by the bereaved individ-\nual being female.\nCulture-Related Diagnostic Issues \nThe symptoms of persistent complex bereav ement disorder are observed across cultural\nsettings, but grief responses may manifest in cu lturally specific ways. Diagnosis of the dis-\norder requires that the persistent and severe responses go beyond cultural norms of grief\nresponses and not be better explained by culturally specific mourning rituals. \nSuicide Risk\nIndividuals with persistent complex bereavement disorder frequently report suicidal\nideation.", "source": "dsm5.pdf"} {"id": "93beca05d2ee-0", "page_content": "792 Conditions for Further Study\nFunctional Consequences of \nPersistent Complex Bereavement Disorder\nPersistent complex bereavement di sorder is associated with deficits in work and social func-\ntioning and with harmful health behaviors, such as increased tobacco and alcohol use. It is also\nassociated with marked increases in risks for serious medical conditions, including cardiac dis-\nease, hypertension, cancer, immunological deficiency, and reduced quality of life. \nDifferential Diagnosis\nNormal grief. Persistent complex bereavement diso rder is distinguished from normal\ngrief by the presence of severe grief reactions that persist at least 12 months (or 6 months in\nchildren) after the death of the bereaved. It is only when severe levels of grief response per-\nsist at least 12 months following the death an d interfere with the in dividual\u2019s capacity to\nfunction that persisten t complex bereavement disorder is diagnosed. \nDepressive disorders. Persistent complex bereavement disorder, major depressive dis-\norder, and persistent depressive disorder (dysthymia) share sadness, crying, and suicidal\nthinking. Whereas major depressi ve disorder and persistent de pressive disorder can share\ndepressed mood with persistent complex bereavement disorder, the latter is characterized\nby a focus on the loss. \nPosttraumatic stress disorder. Individuals who experience bereavement as a result of trau-\nmatic death may develop both posttraumatic stre ss disorder (PTSD) and persistent complex\nbereavement disorder. Both conditions ca n involve intrusive th oughts and avoidance.\nWhereas intrusions in PTSD revolve around the traumatic event, intrusive memories in per-\nsistent complex bereavement diso rder focus on thoughts about many aspects of the relation-\nship with the deceased, including positive asp ects of the relationship and distress over the", "source": "dsm5.pdf"} {"id": "93beca05d2ee-1", "page_content": "ship with the deceased, including positive asp ects of the relationship and distress over the\nseparation. In individuals with the traumatic be reavement specifier of persistent complex be-\nreavement disorder, the distressin g thoughts or feelings may be more overtly related to the\nmanner of death, with distressing fantasies of what happened. Both persistent complex be-\nreavement disorder and PTSD can involve avoi dance of reminders of distressing events.\nWhereas avoidance in PTSD is characterized by consistent avoidance of internal and external\nreminders of the traumatic experience, in persistent complex bereavement disorder, there is\nalso a preoccupation with the loss and yearning for the deceased, which is absent in PTSD. \nSeparation anxiety disorder. Separation anxiety disorder is characterized by anxiety\nabout separation from current attachment figures, whereas persistent complex bereavement\ndisorder involves distress about separation from a deceased individual. \nComorbidity \nThe most common comorbid disorders with pe rsistent complex bere avement disorder are\nmajor depressive disorder, PT SD, and substance use disorders. PTSD is more frequently\ncomorbid with persistent complex bereavement disorder when the deat h occurred in trau-\nmatic or violent circumstances.\nCaffeine Use Disorder\nProposed Criteria \nA problematic pattern of caffeine use leading to clinically significant impairment or distress, as\nmanifested by at least the first three of the following criteria occurring within a 12-month period: \n1. A persistent desire or unsuccessful efforts to cut down or control caffeine use.\n2. Continued caffeine use despite knowledge of having a persistent or recurrent physical\nor psychological problem that is likely to have been caused or exacerbated by caffeine.", "source": "dsm5.pdf"} {"id": "118993335c5b-0", "page_content": "Conditions for Further Study 793\n3. Withdrawal, as manifested by either of the following:\na. The characteristic withdrawal syndrome for caffeine. \nb. Caffeine (or a closely related) substance is taken to relieve or avoid withdrawal\nsymptoms.\n4. Caffeine is often taken in larger amounts or over a longer period than was intended.\n5. Recurrent caffeine use resulting in a failure to fulfill major role obligations at work,\nschool, or home (e.g., repeated tardiness or absences from work or school related to\ncaffeine use or withdrawal).\n6. Continued caffeine use despite having persist ent or recurrent social or interpersonal\nproblems caused or exacerbated by the effects of caffeine (e.g., arguments with\nspouse about consequences of use, medical problems, cost). \n7. Tolerance, as defined by either of the following: \na. A need for markedly increased amounts of caffeine to achieve desired effect.\nb. Markedly diminished effect with continued use of the same amount of caffeine. \n8. A great deal of time is spent in activities necessary to obtain caffeine, use caffeine, or\nrecover from its effects.\n9. Craving or a strong desire or urge to use caffeine.\nA diagnosis of substance dependence due to caffeine is recognized by the World Health\nOrganization in ICD-10. Since the publication of DSM-IV in 1994, considerable research on\ncaffeine dependence has been published, an d several recent reviews provide a current\nanalysis of this literature. There is now sufficie nt evidence to warran t inclusion of caffeine\nuse disorder as a research diagnosis in DSM-5 to encourage additional research. The work-\ning diagnostic algorithm propos ed for the study of caffeine use disorder differs from that\nof the other substance use disorders, reflecting the need to identify only cases that have", "source": "dsm5.pdf"} {"id": "118993335c5b-1", "page_content": "of the other substance use disorders, reflecting the need to identify only cases that have\nsufficient clinical importance to warrant the la beling of a mental disorder. A key goal of in-\ncluding caffeine use disorder in this section of DSM-5 is to stimulate research that will\ndetermine the reliability, validity, and preval ence of caffeine use disorder based on the\nproposed diagnostic schema, with particular attention to the association of the diagnosis\nwith functional impairments as part of validity testing. \nThe proposed criteria for caff eine use disorder reflect the need for a diagnostic thresh-\nold higher than that used for the other subs tance use disorders. Such a threshold is in-\ntended to prevent overdiagnosis of caffeine us e disorder due to the high rate of habitual\nnonproblematic daily caffeine use in the general population. \nDiagnostic Features\nCaffeine use disorder is characterized by the continued use of caffeine and failure to con-\ntrol use despite negative physical and/or psyc hological consequences. In a survey of the\ngeneral population, 14% of caffeine users met the criterion of use despite harm, with most\nreporting that a physician or counselor had advised them to stop or reduce caffeine use\nwithin the last year. Medical and psychological problems attributed to caffeine included\nheart, stomach, and urinary problems, and co mplaints of anxiety, depression, insomnia,\nirritability, and difficulty thinking. In the sam e survey, 45% of caffei ne users reported de-\nsire or unsuccessful efforts to control caffeine use, 18% repo rted withdrawal, 8% reported\ntolerance, 28% used more than intended, and 50% reported spending a great deal of time\nusing caffeine. In addition, 19% reported a strong desire for caffeine that they could not re-", "source": "dsm5.pdf"} {"id": "118993335c5b-2", "page_content": "sist, and less than 1% reported that caffein e had interfered with social activities. \nAmong those seeking treatment for quitting problematic caffeine use, 88% reported\nhaving made prior serious attempts to modify caffeine use, and 43% reported having been\nadvised by a medical professional to reduce or eliminate caffeine. Ninety-three percent\nendorsed signs and symptoms meeting DSM-IV criteria for caffeine dependence, with the", "source": "dsm5.pdf"} {"id": "94191dd9fc9c-0", "page_content": "794 Conditions for Further Study\nmost commonly endorsed criteria being withdr awal (96%), persistent desire or unsuccess-\nful efforts to control use (89%), and use de spite knowledge of physical or psychological\nproblems caused by caffeine (87%). The most common reasons for wanting to modify caf-\nfeine use were health-related (59%) and a desire to not be dependent on caffeine (35%).\nThe DSM-5 discussion of ca ffeine withdrawal in the Section II chapter \u201cSubstance-\nRelated and Addictive Disorders\u201d provides info rmation on the features of the withdrawal\ncriterion. It is well documented that habitual caffeine users can experience a well-defined\nwithdrawal syndrome upon ac ute abstinence from caffeine, and many caffeine-dependent\nindividuals report continued use of caffeine to avoid experiencing withdrawal symptoms. \nPrevalence\nThe prevalence of caffeine use di sorder in the general population is unclear. Based on all\nseven generic DSM-IV-TR criteria for dependence, 30% of current caffeine users may have\nmet DSM-IV criteria for a diagnosis of caffei ne dependence, with endorsement of three or\nmore dependence criteria, during the past year . When only four of the seven criteria (the\nthree primary criteria proposed above plus to lerance) are used, the prevalence appears to\ndrop to 9%. Thus, the expected prevalence of caffeine use disorder among regular caffeine\nusers is likely less than 9%. Given that approximately 75%\u201380% of the general population\nuses caffeine regularly, the estimated preval ence would be less than 7%. Among regular\ncaffeine drinkers at higher risk for caffeine use problems (e.g., high school and college stu-\ndents, individuals in drug treatment, and indi viduals at pain clinics who have recent his-\ntories of alcohol or illicit drug misuse), ap proximately 20% may have a pattern of use that", "source": "dsm5.pdf"} {"id": "94191dd9fc9c-1", "page_content": "meets all three of the proposed criteria in Criterion A.\nDevelopment and Course\nIndividuals whose patter n of use meets criteria for a ca ffeine use disorder have shown a\nwide range of daily caffeine intake and have been consumer s of various types of caffein-\nated products (e.g., coffee, soft drinks, tea) and medications. A diagnosis of caffeine use\ndisorder has been shown to prospectively pred ict a greater incidence of caffeine reinforce-\nment and more severe withdrawal.\nThere has been no longitudinal or cross-sect ional lifespan research on caffeine use dis-\norder. Caffeine use disorder has been identi fied in both adolescents and adults. Rates of\ncaffeine consumption and overa ll level of caffeine consumption tend to increase with age\nuntil the early to mid-30s and then level off. Age-related factors for caffeine use disorder\nare unknown, although concern is growing related to excessive caffeine consumption\namong adolescents and young adults through use of caffeinated energy drinks. \nRisk and Prognostic Factors \nGenetic and physiological. Heritabilities of heavy caffeine use, caffeine tolerance, and\ncaffeine withdrawal range from 35% to 77%. For caffeine use, alcohol use, and cigarette\nsmoking, a common genetic factor (polysubst ance use) underlies the use of these three\nsubstances, with 28%\u201341% of the heritable e ffects of caffeine use (or heavy use) shared\nwith alcohol and smoking. Caffeine and toba cco use disorders are associated and substan-\ntially influenced by genetic factors unique to these licit drugs. The magnitude of heritabil-\nity for caffeine use disorder ma rkers appears to be similar to that for alcohol and tobacco\nuse disorder markers.\nFunctional Consequences of Caffeine Use Disorder", "source": "dsm5.pdf"} {"id": "94191dd9fc9c-2", "page_content": "use disorder markers.\nFunctional Consequences of Caffeine Use Disorder\nCaffeine use disorder may predict greater use of caffeine during pregnancy. Caffeine with-\ndrawal, a key feature of caffeine use disorder, has been shown to produce functional im-", "source": "dsm5.pdf"} {"id": "d1949b79a911-0", "page_content": "Conditions for Further Study 795\npairment in normal daily activities. Caffeine intoxication may include symptoms of\nnausea and vomiting, as well as impairment of normal activities. Significant disruptions in\nnormal daily activities may occur during caffeine abstinence. \nDifferential Diagnosis\nNonproblematic use of caffeine. The distinction between nonproblematic use of caf-\nfeine and caffeine use disorder can be difficul t to make because social, behavioral, or psy-\nchological problems may be difficult to attribut e to the substance, espe cially in the context of\nuse of other substances. Regular, heavy caffeine use that can result in tolerance and with-\ndrawal is relatively common, which by itself sh ould not be sufficient for making a diagnosis. \nOther stimulant use disorder. Problems related to use of other stimulant medications\nor substances may approximate the fe atures of caffeine use disorder.\nAnxiety disorders. Chronic heavy caffeine use may mimi c generalized anxiety disorder,\nand acute caffeine cons umption may produce and mimic panic attacks. \nComorbidity\nThere may be comorbidity between caffeine use disorder and daily cigarette smoking, a\nfamily or personal history of alcohol use diso rder. Features of caffeine use disorder (e.g.,\ntolerance, caffeine withdrawal) may be positive ly associated with several diagnoses: ma-\njor depression, generali zed anxiety disorder, panic disorder, adult antisocial personality\ndisorder, and alcohol, cannab is, and cocaine use disorders.\nInternet Gaming Disorder\nProposed Criteria\nPersistent and recurrent\u00a0use of the Internet to engage in games, often with other players,\nleading to clinically significant impairment or distress as indicated by five (or more) of the\nfollowing in a 12-month period:\n1. Preoccupation with Internet games. (The individual thinks about previous gaming", "source": "dsm5.pdf"} {"id": "d1949b79a911-1", "page_content": "1. Preoccupation with Internet games. (The individual thinks about previous gaming\nactivity or anticipates playing the next game; Internet gaming becomes the dominant\nactivity in daily life).\nNote: This disorder is distinct from Internet gambling, which is included under gam-\nbling disorder. \n2. Withdrawal symptoms when Internet gami ng is taken away. (These symptoms are typ-\nically described as irritability, anxiety, or sadness, but there are no physical signs of\npharmacological withdrawal.)\n3. Tolerance\u2014the need to spend increasing amounts of time engaged in Internet games.\n4. Unsuccessful attempts to control the participation in Internet games.\n5. Loss of interests in previous hobbies and entertainment as a result of, and with the ex-\nception of, Internet games. \n6. Continued excessive use of Internet games despite knowledge of psychosocial problems.\n7. Has deceived family members, therapists, or others regarding the amount of Internet\ngaming.\n8. Use of Internet games to escape or relieve a negative mood (e.g., feelings of helpless-\nness, guilt, anxiety).\n9. Has jeopardized or lost a significant relationship, job, or educational or career oppor-\ntunity because of participation in Internet games.", "source": "dsm5.pdf"} {"id": "2dbbb1d7ce70-0", "page_content": "796 Conditions for Further Study\nNote: Only nongambling Internet games are included in this disorder. Use of the Internet\nfor required activities in a business or profe ssion is not included; nor is the disorder intend-\ned to include other recreational or social Internet use. Similarly, sexual Internet sites are\nexcluded.\nSpecify current severity:\nInternet gaming disorder can be mild, moderate, or severe depending on the degree\nof disruption of normal activities. Individuals with less severe Internet gaming disorder\nmay exhibit fewer symptoms and less disruption of their lives. Those with severe Inter-\nnet gaming disorder will have more hours spent on the computer and more severe loss\nof relationships or career or school opportunities. \nSubtypes \nThere are no well-researched subtypes for Inte rnet gaming disorder to date. Internet gam-\ning disorder most often involves specific Inte rnet games, but it co uld involve non-Internet\ncomputerized games as well, although these have been less researched. It is likely that pre-\nferred games will vary over time as new games are developed and popularized, and it is\nunclear if behaviors and consequence associat ed with Internet gaming disorder vary by\ngame type.\nDiagnostic Features\nGambling disorder is currently the only non-substance-related disorder proposed for in-\nclusion with DSM-5 substance-related and addi ctive disorders. However, there are other\nbehavioral disorders that show some similari ties to substance use disorders and gambling\ndisorder for which the word addiction is commonly used in nonmedical settings, and the\none condition with a considerab le literature is the compulsive playing of Internet games.\nInternet gaming has been reportedly define d as an \u201caddiction\u201d by the Chinese govern-\nment, and a treatment system has been set up. Reports of treatment of this condition have", "source": "dsm5.pdf"} {"id": "2dbbb1d7ce70-1", "page_content": "ment, and a treatment system has been set up. Reports of treatment of this condition have\nappeared in medical journals, mostly from A sian countries and some in the United States.\nThe DSM-5 work group reviewed more than 240 articles and found some behavioral\nsimilarities of Internet gaming to gambling disorder and to substance use disorders. The\nliterature suffers, howeve r, from lack of a standard defini tion from which to derive prev-\nalence data. An understanding of the natural histories of cases, with or without treatment,\nis also missing. The literature does describe many underlying similarities to substance ad-\ndictions, including aspects of tolerance, withdr awal, repeated unsuccessful attempts to cut\nback or quit, and impairment in normal func tioning. Further, the seemingly high preva-\nlence rates, both in Asian countries and, to a lesser extent, in the West, justified inclusion of\nthis disorder in Section III of DSM-5.\nInternet gaming disorder has significant public health importance, and additional re-\nsearch may eventually lead to evidence that Internet gaming disorder (also commonly re-\nferred to as Internet use disorder, Internet addiction, or gaming addiction ) has merit as an\nindependent disorder. As with gambling disord er, there should be epidemiological stud-\nies to determine prevalence, c linical course, possible geneti c influence, and potential bio-\nlogical factors based on, for example, brain imaging data. \nInternet gaming disorder is a pattern of exce ssive and prolonged Inte rnet gaming that re-\nsults in a cluster of cognitive and behavioral symptoms, including progressive loss of control\nover gaming, tolerance, and withdrawal sy mptoms, analogous to the symptoms of sub-\nstance use disorders. As with substance-related disorders, individuals with Internet gaming", "source": "dsm5.pdf"} {"id": "2dbbb1d7ce70-2", "page_content": "stance use disorders. As with substance-related disorders, individuals with Internet gaming\ndisorder continue to sit at a computer and en gage in gaming activi ties despite neglect of\nother activities. They typically de vote 8\u201310 hours or more per day to this activity and at least\n30 hours per week. If they are prevented from using a computer and returning to the game,\nthey become agitated and angry. They often go for long periods without food or sleep. Nor-", "source": "dsm5.pdf"} {"id": "b9765276ff71-0", "page_content": "Conditions for Further Study 797\nmal obligations, such as school or work, or family obligati ons are neglected. This condition is\nseparate from gambling disorder involving the Internet because mo ney is not at risk.\nThe essential feature of Internet gaming di sorder is persistent an d recurrent participa-\ntion in computer gaming, ty pically group games, for many hours. These games involve\ncompetition between groups of players (often in different global regions, so that duration\nof play is encouraged by the time-zone inde pendence) participating in complex structured\nactivities that include a significant aspect of social interactions during play. Team aspects\nappear to be a key motivation. Attempts to di rect the individual toward schoolwork or in-\nterpersonal activities are strongly resisted. Thus personal, family, or vocational pursuits\nare neglected. When individuals are asked, the major reasons given for using the com-\nputer are more likely to be \u201cavoiding boredo m\u201d rather than communicating or searching\nfor information.\nThe description of\u00a0criteria rela ted to this condition is\u00a0adapt ed from a study in China.\u00a0Un-\ntil the optimal criteria and threshold for di agnosis are determined empirically,\u00a0conserva-\ntive definitions ought to be used, such that diagnoses are considered for endorsement of\nfive or more of\u00a0nine criteria. \nAssociated Features Supporting Diagnosis \nNo consistent personality types associated with Internet gaming disorder have been iden-\ntified. Some authors describe associated diagnoses, such as depressive disorders, atten-\ntion-deficit/hyperactivity disorder (ADHD) , or obsessive-compulsive disorder (OCD).\nIndividuals with compulsive Internet gaming have demonstrated brain activation in spe-\ncific regions triggered by exposure to the Internet game but not limited to reward system\nstructures\nPrevalence\nThe prevalence of Internet gaming disorder is unclear because of the varying question-", "source": "dsm5.pdf"} {"id": "b9765276ff71-1", "page_content": "Prevalence\nThe prevalence of Internet gaming disorder is unclear because of the varying question-\nnaires, criteria and thresholds employed, but it seems to be highest in Asian countries and\nin male adolescents 12\u201320 years of age. There is an abundance of reports from Asian coun-\ntries, especially China and South Korea, bu t fewer from Europe and North America, from\nwhich prevalence estimates are highly variable . The point prevalence in adolescents (ages\n15\u201319 years) in one Asian study using a threshold of five criteria was 8.4% for males and\n4.5% for females.\nRisk and Prognostic Factors \nEnvironmental. Computer availability with Internet connection allows access to the\ntypes of games with which Internet gami ng disorder is most often associated.\nGenetic and physiological. Adolescent males seem to be at greatest risk of developing\nInternet gaming disorder, and it has been sp eculated that Asian environmental and/or ge-\nnetic background is another risk factor, but this remains unclear.\nFunctional Consequences of Internet Gaming Disorder\nInternet gaming disorder may lead to school failure, job loss, or marriage failure. The com-\npulsive gaming behavior tends to crowd out normal social, scholastic, and family activities.\nStudents may show declining grades and eventu ally failure in school. Family responsibil-\nities may be neglected. \nDifferential Diagnosis\nExcessive use of the Internet not involving playing of online games (e.g., excessive use of\nsocial media, such as Facebook; viewing porn ography online) is not considered analogous", "source": "dsm5.pdf"} {"id": "b31e57fd909b-0", "page_content": "798 Conditions for Further Study\nto Internet gaming disorder, and future rese arch on other excessive uses of the Internet\nwould need to follow similar guidelines as suggested herein. Excessive gambling online\nmay qualify for a separate diagnosis of gambling disorder.\nComorbidity\nHealth may be neglected due to compulsive ga ming. Other diagnoses that may be associ-\nated with Internet gaming disorder incl ude major depressive disorder, ADHD, and OCD.\nNeurobehavioral Disorder Associated\nWith Prenatal Alcohol Exposure\nProposed Criteria\nA. More than minimal exposure to alcohol during gestation, including prior to pregnancy\nrecognition. Confirmation of gestational exposure to alcohol may be obtained from ma-\nternal self-report of alcohol use in pregnancy, medical or other records, or clinical ob-\nservation. \nB. Impaired neurocognitive functioning as manifested by one or more of the following:\n1. Impairment in global intellectual performance (i.e., IQ of 70 or below, or a standard\nscore of 70 or below on a comprehensive developmental assessment).\n2. Impairment in executive functioning (e.g., poor planning and organization; inflexi-\nbility; difficulty with behavioral inhibition).\n3. Impairment in learning (e.g., lower academic achievement than expected for intel-\nlectual level; specific learning disability).\n4. Memory impairment (e.g., problems remembering information learned recently;\nrepeatedly making the same mistakes; difficulty remembering lengthy verbal in-\nstructions).\n5. Impairment in visual-spatial reasoning (e.g., disorganized or poorly planned draw-\nings or constructions; problems differentiating left from right).\nC. Impaired self-regulation as manifested by one or more of the following:\n1. Impairment in mood or behavioral regulation (e.g., mood lability; negative affect or\nirritability; frequent behavioral outbursts).", "source": "dsm5.pdf"} {"id": "b31e57fd909b-1", "page_content": "irritability; frequent behavioral outbursts).\n2. Attention deficit (e.g., difficulty shifting attention; difficulty sustaining mental effort).\n3. Impairment in impulse control (e.g., difficulty waiting turn; difficulty complying with\nrules).\nD. Impairment in adaptive functioning as manifested by two or more of the following, one\nof which must be (1) or (2):\n1. Communication deficit (e.g., delayed acquisition of language; difficulty understand-\ning spoken language).\n2. Impairment in social communication and interaction (e.g., overly friendly with strang-\ners; difficulty reading social cues; difficulty understanding social consequences).\n3. Impairment in daily living skills (e.g., delayed toileting, feeding, or bathing; difficulty\nmanaging daily schedule).\n4. Impairment in motor skills (e.g., poor fine motor development; delayed attainment\nof gross motor milestones or ongoing deficits in gross motor function; deficits in co-\nordination and balance).\nE. Onset of the disorder (symptoms in Criteria B, C, and D) occurs in childhood.", "source": "dsm5.pdf"} {"id": "629c087f2b46-0", "page_content": "Conditions for Further Study 799\nF. The disturbance causes clinically significant distress or impairment in social, aca-\ndemic, occupational, or other im portant areas of functioning.\nG. The disorder is not better explained by the direct physiological effects associated with\npostnatal use of a substance (e.g., a medication, alcohol or other drugs), a general\nmedical condition (e.g., traumatic brain injury, delirium, dementia), another known te-\nratogen (e.g., fetal hydantoin syndrome), a genetic condition (e.g., Williams syndrome,\nDown syndrome, Cornelia de Lange syndrome), or environmental neglect.\nAlcohol is a neurobehavioral te ratogen, and prenatal alcoho l exposure has teratogenic\neffects on central nervous system (CNS ) development and subsequent function. Neurobe-\nhavioral disorder associated with prenatal alcohol exposure (ND-PAE) is a new clarifying term,\nintended to encompass the full range of de velopmental disabilities associated with expo-\nsure to alcohol in utero. The current diagnost ic guidelines allow ND-PAE to be diagnosed\nboth in the absence and in the presence of th e physical effects of prenatal alcohol exposure\n(e.g., facial dysmorphology required for a diagnosis of fetal alcohol syndrome).\nDiagnostic Features\nThe essential features of ND-PAE are the mani festation of impairment in neurocognitive,\nbehavioral, and adaptive functioning associated with prenatal alcohol exposure. Impair-\nment can be documented based on past diagnostic evaluation s (e.g., psychological or ed-\nucational assessments) or medical records, reports by the in dividual or informants, and/\nor observation by a clinician.\nA clinical diagnosis of fetal alcohol synd rome, including specific prenatal alcohol-\nrelated facial dysmorphology and growth retardation, can be used as evidence of signifi-", "source": "dsm5.pdf"} {"id": "629c087f2b46-1", "page_content": "related facial dysmorphology and growth retardation, can be used as evidence of signifi-\ncant levels of prenatal alcohol exposure. Although both animal and human studies have\ndocumented adverse effects of lower levels of drinking, identifying how much prenatal\nexposure is needed to sign ificantly impact neurodevelop mental outcome remains chal-\nlenging. Data suggest that a history of more than minimal gestationa l exposure (e.g., more\nthan light drinking) prior to pregnancy reco gnition and/or following pregnancy recogni-\ntion may be required. Light drinking is defined as 1\u201313 drinks per month during preg-\nnancy with no more than 2 of these drinks co nsumed on any 1 drinking occasion. Identifying\na minimal threshold of drinking during preg nancy will require consideration of a variety\nof factors known to affect exposure and/or interact to influence developmental outcomes,\nincluding stage of prenatal development, gestational smoking, maternal and fetal genet-\nics, and maternal physical status (i.e., ag e, health, and certain obstetric problems). \nSymptoms of ND-PAE include marked impairment in global intellectual performance\n(IQ) or neurocognitive impair ments in any of the following areas: executive functioning,\nlearning, memory, and/or visual-spatial reasoning. Impairments in self-regulation are pres-\nent and may include impairment in mood or behavioral regulation, attention deficit, or\nimpairment in impulse control. Finally, impa irments in adaptive functioning include com-\nmunication deficits and impairment in soci al communication and interaction. Impairment\nin daily living (self-help) skills and impairment in motor skills may be present. As it may be\ndifficult to obtain an accurate assessment of the neurocogni tive abilities of very young chil-", "source": "dsm5.pdf"} {"id": "629c087f2b46-2", "page_content": "dren, it is appropriate to defer a diagnosi s for children 3 years of age and younger.\nAssociated Features Supporting Diagnosis\nAssociated features vary depending on age, degree of alcohol exposure, and the individ-\nual\u2019s environment. An individual can be diag nosed with this disorder regardless of socio-\neconomic or cultural background. However, ongoing parental alcohol/substance misuse,\nparental mental illness, exposure to domest ic or community violen ce, neglect or abuse,", "source": "dsm5.pdf"} {"id": "7ec756520a3e-0", "page_content": "economic or cultural background. However, ongoing parental alcohol/substance misuse,\nparental mental illness, exposure to domest ic or community violen ce, neglect or abuse,\ndisrupted caregiving relationships, multiple out-of-home placements, and lack of conti-\nnuity in medical or mental health care are often present.", "source": "dsm5.pdf"} {"id": "0c68bb35766d-0", "page_content": "800 Conditions for Further Study\nPrevalence\nThe prevalence rates of ND-PAE are unknown. However, estimated prevalence rates of clini-\ncal conditions associated with prenatal alco hol exposure are 2%\u20135% in the United States. \nDevelopment and Course\nAmong individuals with prenatal alcohol exposure, evidence of CNS dysfunction varies\naccording to developmental stage. Although about one-half of young children prenatally\nexposed to alcohol show marked developmental delay in the first 3 years of life, other chil-\ndren affected by prenatal alcohol exposure may not exhibit signs of CNS dysfunction until\nthey are preschool- or school-age. Additionally, impairments in higher order cognitive\nprocesses (i.e., executive functioning), which are often associated with prenatal alcohol ex-\nposure, may be more easily assessed in older children. When children reach school age,\nlearning difficulties, impairme nt in executive function, and problems with integrative lan-\nguage functions usually emerge more clearly, and both social skills deficits and challeng-\ning behavior may become more evident. In particular, as school and other requirements\nbecome more complex, greater deficits are no ted. Because of this, the school years repre-\nsent the ages at which a diagnosis of ND-PAE would be most likely. \nSuicide Risk\nSuicide is a high-risk outcome, with rates incr easing significantly in late adolescence and\nearly adulthood.\nFunctional Consequences of Neurobehavioral Disorder \nAssociated With Prenatal Alcohol Exposure\nThe CNS dysfunction seen in individuals with ND-PAE often leads to decrements in adap-\ntive behavior and to maladaptive behavior with lifelong consequences. Individuals\naffected by prenatal alcohol ex posure have a higher prevalence of disrupted school expe-\nriences, poor employme nt records, trouble with the law, confinement (legal or psychiat-", "source": "dsm5.pdf"} {"id": "0c68bb35766d-1", "page_content": "ric), and dependent living conditions. \nDifferential Diagnosis\nDisorders that are attributable to the physiolo gical effects associated with postnatal use\nof a substance, another medical condition, or environmental neglect. Other consid-\nerations include the physiological effects of po stnatal substance use, such as a medication,\nalcohol, or other substances; disorders due to another medical condition, such as traumatic\nbrain injury or other neurocognitive disorder s (e.g., delirium, majo r neurocognitive dis-\norder [dementia]); or environmental neglect.\nGenetic and teratogenic conditions. Genetic conditions such as Williams syndrome,\nDown syndrome, or Cornelia de Lange syndro me and other teratogeni c conditions such as\nfetal hydantoin syndrome and maternal phen ylketonuria may have similar physical and\nbehavioral characteristics. A careful review of prenatal exposure history is needed to clar-\nify the teratogenic agent, and an evaluation by a clinical geneticist may be needed to dis-\ntinguish physical characteristics associated with these and other genetic conditions. \nComorbidity\nMental health problems have been identified in more than 90% of individuals with histo-\nries of significant prenatal alcohol exposu re. The most common co-occurring diagnosis is\nattention-deficit/hyperactivity disorder, bu t research has shown that individuals with\nND-PAE differ in neuropsychological charac teristics and in their responsiveness to phar-", "source": "dsm5.pdf"} {"id": "f366de462031-0", "page_content": "Conditions for Further Study 801\nmacological interventions. Ot her high- probability co-occurring disorders include oppo-\nsitional defiant disorder and co nduct disorder, but the appropriateness of these diagnoses\nshould be weighed in the context of the sign ificant impairments in general intellectual and\nexecutive functioning that are often associa ted with prenatal al cohol exposure. Mood\nsymptoms, including symptoms of bipolar diso rder and depressive disorders, have been\ndescribed. History of prenatal alcohol exposure is associated with an increased risk for\nlater tobacco, alcohol, and other substance use disorders. \nSuicidal Behavior Disorder\nProposed Criteria \nA. Within the last 24 months, the individual has made a suicide attempt.\nNote: A suicide attempt is a self-initiated sequence of behaviors by an individual who,\nat the time of initiation, expected that the set of actions would lead to his or her own\ndeath. The \u201ctime of initiation\u201d is the time when a behavior took place that involved ap-\nplying the method.)\nB. The act does not meet criteria for nonsuicidal self-injury\u2014that is, it does not involve\nself-injury directed to the surface of the body undertaken to induce relief from a nega-\ntive feeling/cognitive state or to achieve a positive mood state.\nC. The diagnosis is not applied to suic idal ideation or to preparatory acts. \nD. The act was not initiated during a state of delirium or confusion. \nE. The act was not undertaken solely for a political or religious objective. \nSpecify if:\nCurrent: Not more than 12 months since the last attempt.\nIn early remission: 12\u201324 months since the last attempt.\nSpecifiers\nSuicidal behavior is often categorized in term s of violence of the method. Generally, over-", "source": "dsm5.pdf"} {"id": "f366de462031-1", "page_content": "doses with legal or illegal substances are cons idered nonviolent in method, whereas jump-\ning, gunshot wounds, and other methods are considered violent. Another dimension for\nclassification is medical consequences of the behavior, with high-lethality attempts being\ndefined as those requiring medical hospitalizat ion beyond a visit to an emergency depart-\nment. An additional dimension considered incl udes the degree of planning versus impul-\nsiveness of the attempt, a characteristic th at might have consequences for the medical\noutcome of a suicide attempt.\nIf the suicidal behavior occurred 12\u201324 mo nths prior to evaluation, the condition is\nconsidered to be in early remission. Individua ls remain at higher risk for further suicide at-\ntempts and death in the 24 months after a suicide attempt, and the period 12\u201324 months af-\nter the behavior took place is specified as \u201cearly remission.\u201d\nDiagnostic Features\nThe essential manifestation of suicidal be havior disorder is a suicide attempt. A suicide at-\ntempt is a behavior that the individual has undertak en with at least some intent to die. The\nbehavior might or might not le ad to injury or serious medi cal consequences. Several fac-\ntors can influence the medical consequences of the suicide a ttempt, including poor plan-\nning, lack of knowledge about the lethality of the method chosen, low intentionality or\nambivalence, or chance intervention by others after the behavior has been initiated. These\nshould not be considered in assigning the diagnosis.", "source": "dsm5.pdf"} {"id": "06fa565ecca5-0", "page_content": "802 Conditions for Further Study\nDetermining the degree of intent can be challenging. Individuals might not acknowl-\nedge intent, especially in situations where doin g so could result in hospitalization or cause\ndistress to loved ones. Markers of risk includ e degree of planning, including selection of a\ntime and place to minimize rescue or interrupt ion; the individual\u2019s mental state at the time\nof the behavior, with acute agitation being especially concerning; recent discharge from\ninpatient care; or recent discon tinuation of a mood stabilizer such as lithium or an anti-\npsychotic such as clozapine in the case of schizophrenia. Examples of environmental \u201ctrig-\ngers\u201d include recently learning of a potentia lly fatal medical diagnosis such as cancer,\nexperiencing the sudden and unexpected loss of a close relative or partner, loss of employ-\nment, or displacement from h ousing. Conversely, features su ch as talking to others about\nfuture events or preparedness to sign a contract for safety are less reliable indicators.\nIn order for the criteria to be met, the indivi dual must have made at least one suicide at-\ntempt. Suicide attempts can incl ude behaviors in which, after initiating the suicide attempt,\nthe individual changed his or her mind or so meone intervened. For example, an individual\nmight intend to ingest a given amount of medication or pois on, but either stop or be stopped\nby another before ingesting the full amount. If the individual is dissuaded by another or\nchanges his or her mind before initiating th e behavior, the diagnosis should not be made.\nThe act must not meet criteria for nonsuicidal self-i njury\u2014that is, it should not involve re-\npeated (at least five times within the past 12 months) self-injurious episodes undertaken to", "source": "dsm5.pdf"} {"id": "06fa565ecca5-1", "page_content": "induce relief from a negative feeling/cognitive state or to achieve a positive mood state. The\nact should not have been initiated during a st ate of delirium or confusion. If the individual\ndeliberately became intoxicated before initiating the behavior, to reduce anticipatory anxi-\nety and to minimize interference with the inte nded behavior, the diagnosis should be made.\nDevelopment and Course\nSuicidal behavior can occur at any time in the lifespan but is rarely seen in children under\nthe age of 5. In prepubertal children, the behavi or will often consist of a behavior (e.g., sit-\nting on a ledge) that a parent has forbidden because of the risk of accident. Approximately\n25%\u201330% of persons who attempt suicide will go on to make more attempts.There is sig-\nnificant variability in terms of frequency, me thod, and lethality of attempts. However, this\nis not different from what is observed in other illnesses, such as major depressive disorder,\nin which frequency of episode, subtype of episode, and impa irment for a given episode can\nvary significantly.\nCulture-Related Diagnostic Issues\nSuicidal behavior varies in frequency and form across cultures. Cultural differences might\nbe due to method availability (e.g., poisonin g with pesticides in developing countries;\ngunshot wounds in the southwestern United St ates) or the presence of culturally specific\nsyndromes (e.g., ataques de nervios, which in some Latino group s might lead to behaviors\nthat closely resemble suic ide attempts or might facilitate suicide attempts). \nDiagnostic Markers\nLaboratory abnormalities consequent to the suicidal attempt are of ten evident. Suicidal\nbehavior that leads to blood loss can be a ccompanied by anemia, hypotension, or shock.", "source": "dsm5.pdf"} {"id": "06fa565ecca5-2", "page_content": "Overdoses might lead to coma or obtundatio n and associated laboratory abnormalities\nsuch as electrolyte imbalances.\nFunctional Consequences of Suicidal Behavior Disorder\nMedical conditions (e.g., lacerations or skel etal trauma, cardiopulm onary instability, in-\nhalation of vomit and suffocation, hepatic fa ilure consequent to use of paracetamol) can\noccur as a consequence of suicidal behavior.", "source": "dsm5.pdf"} {"id": "23924defaef3-0", "page_content": "Conditions for Further Study 803\nComorbidity\nSuicidal behavior is seen in th e context of a variety of mental disorders, most commonly bipo-\nlar disorder, major depressive disorder, schizo phrenia, schizoaffective disorder, anxiety dis-\norders (in particular, panic disorders asso ciated with catastrophic content and PTSD\nflashbacks), substance use disorders (especially alcohol use disorders) , borderline personality\ndisorder, antisocial personality disorder, eating disorders, and adjustment disorders. It is\nrarely manifested by individual s with no discernible pathology, unless it is undertaken be-\ncause of a painful medical condition with the in tention of drawing attention to martyrdom for\npolitical or religious reasons, or in partners in a suicide pact, both of which are excluded from\nthis diagnosis, or when third-party informants wish to conceal the nature of the behavior. \nNonsuicidal Self-Injury\nProposed Criteria\nA. In the last year, the individual has, on 5 or more days, engaged in intentional self-inflicted\ndamage to the surface of his or her body of a sort likely to induce bleeding, bruising, or pain\n(e.g., cutting, burning, stabbing, hitting, excessive rubbing), with the expectation that the\ninjury will lead to only minor or moderate physi cal harm (i.e., there is no suicidal intent). \nNote: The absence of suicidal intent has either been stated by the individual or can be\ninferred by the individual\u2019s repeated engagement in a behavior that the individual\nknows, or has learned, is not likely to result in death.\nB. The individual engages in the self-injurious behavior with one or more of the following\nexpectations:\n1. To obtain relief from a negative feeling or cognitive state.\n2. To resolve an interpersonal difficulty.", "source": "dsm5.pdf"} {"id": "23924defaef3-1", "page_content": "2. To resolve an interpersonal difficulty.\n3. To induce a positive feeling state.\nNote: The desired relief or response is experienced during or shortly after the self-\ninjury, and the individual may display patterns of behavior suggesting a dependence\non repeatedly engaging in it.\nC. The intentional self-injury is associated with at least one of the following:\n1. Interpersonal difficulties or negative feelings or thoughts, such as depression, anx-\niety, tension, anger, generalized distress, or self-criticism, occurring in the period\nimmediately prior to the self-injurious act.\n2. Prior to engaging in the act, a period of preoccupation with the intended behavior\nthat is difficult to control.\n3. Thinking about self-injury that occurs frequently, even when it is not acted upon.\nD. The behavior is not socially sanctioned (e.g., body piercing, tattooing, part of a religious\nor cultural ritual) and is not restricted to picking a scab or nail biting.\nE. The behavior or its consequences cause clinically significant distress or interference in\ninterpersonal, academic, or other important areas of functioning.\nF. The behavior does not occur exclusively during psychotic episodes, delirium, sub-\nstance intoxication, or substance withdrawal. In individuals with a neurodevelopmental\ndisorder, the behavior is not part of a pattern of repetitive stereotypies. The behavior\nis not better explained by another mental disorder or medical condition (e.g., psychotic\ndisorder, autism spectrum disorder, intellectual disability, Lesch-Nyhan syndrome, ste-\nreotypic movement disorder with self-injur y, trichotillomania [hair-pulling disorder], ex-\ncoriation [skin-picking] disorder).", "source": "dsm5.pdf"} {"id": "870b78d07090-0", "page_content": "804 Conditions for Further Study\nDiagnostic Features\nThe essential feature of nonsuicidal self-injur y is that the individual repeatedly inflicts\nshallow, yet painful injuries to the surface of his or her body. Most commonly, the purpose\nis to reduce negative emotions, such as tensio n, anxiety, and self-reproach, and/or to re-\nsolve an interpersonal difficulty. In some cases, the injury is conceived of as a deserved\nself-punishment. The individual will often report an immediate sensation of relief that oc-\ncurs during the process. When the behavior o ccurs frequently, it mi ght be associated with\na sense of urgency and craving, the resultant behavioral pattern resembling an addiction.\nThe inflicted wounds can become deeper and more numerous. \nThe injury is most often inflicted with a knif e, needle, razor, or other sharp object. Com-\nmon areas for injury include the frontal area of the thighs and the dorsal side of the forearm.\nA single session of injury might involve a se ries of superficial, parallel cuts\u2014separated by\n1 or 2 centimeters\u2014on a visible or accessible location. The resulting cuts will often bleed and\nwill eventually leave a characteristic pattern of scars.\nOther methods used include stabbing an area , most often the upper arm, with a needle\nor sharp, pointed knife; inflicti ng a superficial burn with a lit cigarette end; or burning the\nskin by repeated rubbing with an eraser. En gagement in nonsuicidal self-injury with mul-\ntiple methods is associated with more severe psychopathology, including engagement in\nsuicide attempts. \nThe great majority of individuals who engage in nonsuicidal self-injury do not seek\nclinical attention. It is not known if this re flects frequency of engagement in the disorder,", "source": "dsm5.pdf"} {"id": "870b78d07090-1", "page_content": "because accurate reporting is seen as stigma tizing, or because the behaviors are experi-\nenced positively by the individual who engages in them, who is unmotivated to receive\ntreatment. Young children might experiment wi th these behaviors but not experience re-\nlief. In such cases, youths often report that the procedure is painful or distressing and\nmight then discontinue the practice.\nDevelopment and Course\nNonsuicidal self-injury most often starts in the early teen years and can continue for many\nyears. Admission to hospital for nonsuicida l self-injury reaches a peak at 20\u201329 years of\nage and then declines. However, research that has examined age at hospitalization did not\nprovide information on age at onset of the behavior, and prospective research is needed to\noutline the natural history of nonsuicidal self-injury and the factors that promote or in-\nhibit its course. Individuals often learn of th e behavior on the recommendation or observa-\ntion of another. Research has shown that wh en an individual who engages in nonsuicidal\nself-injury is admitted to an inpatient unit, other individuals may begin to engage in the\nbehavior.\nRisk and Prognostic Factors\nMale and female prevalence rates of nonsuicida l self-injury are closer to each other than in\nsuicidal behavior disorder, in which the female-to-male ratio is about 3:1 or 4:1.\nTwo theories of psychopathology\u2014based on functional behavioral analyses\u2014have been\nproposed: In the first, based on learning theo ry, either positive or negative reinforcement\nsustains the behavior. Positive reinforcement might result fr om punishing oneself in a way\nthat the individual feels is de served, with the behavior induci ng a pleasant and relaxed state", "source": "dsm5.pdf"} {"id": "870b78d07090-2", "page_content": "that the individual feels is de served, with the behavior induci ng a pleasant and relaxed state\nor generating attention and help from a signific ant other, or as an expression of anger. Neg-\native reinforcement results from affect regula tion and the reduction of unpleasant emotions\nor avoiding distressing thoughts, including th inking about suicide. In the second theory,\nnonsuicidal self-injury is thought to be a form of self-punishment, in which self-punitive ac-\ntions are engaged in to make up for acts that caused distress or harm to others.", "source": "dsm5.pdf"} {"id": "8ecda3cbacba-0", "page_content": "Conditions for Further Study 805\nFunctional Consequences of Nonsuicidal Self-Injury\nThe act of cutting might be performed with shared implements, raising the possibility of\nblood-borne disease transmission.\nDifferential Diagnosis\nBorderline personality disorder. As indicated, nonsuicidal se lf-injury has long been re-\ngarded as a \u201csymptom\u201d of borderline pers onality disorder, even though comprehensive\nclinical evaluations have found that most individuals with nonsuicidal self-injury have\nsymptoms that also meet criteria for other di agnoses, with eating disorders and substance\nuse disorders being especially common. Histor ically, nonsuicidal self-injury was regarded\nas pathognomonic of borderline personality d isorder. Both conditions are associated with\nseveral other diagnoses. Although frequently associated, borderline personality disorder\nis not invariably found in individuals with no nsuicidal self-injury. The two conditions dif-\nfer in several ways. Individuals with borderline personality disorder often manifest dis-\nturbed aggressive and hostile behaviors, whereas nonsuicidal self-injury is more often\nassociated with phases of closeness, collaborati ve behaviors, and positive relationships. At\na more fundamental level, there are difference s in the involvement of different neurotrans-\nmitter systems, but these will not be apparent on clinical examination. \nSuicidal behavior disorder. The differentiation between nonsuicidal self-injury and sui-\ncidal behavior disorder is base d either on the stated goal of the behavior being a wish to\ndie (suicidal behavior disorder) or, in nonsuicidal self-injury, to experience relief as de-\nscribed in the criteria. Depending on the ci rcumstances, individuals may provide reports\nof convenience, and several studies report high rates of false intent declaration. Individu-", "source": "dsm5.pdf"} {"id": "8ecda3cbacba-1", "page_content": "of convenience, and several studies report high rates of false intent declaration. Individu-\nals with a history of frequent nonsuicidal se lf-injury episodes have learned that a session\nof cutting, while painful, is, in the short-term, largely benign. Be cause individuals with\nnonsuicidal self-injury can and do attempt and commit suicide, it is important to check\npast history of suicidal behavior and to ob tain information from a third party concerning\nany recent change in stress exposure and mo od. Likelihood of suicide intent has been as-\nsociated with the use of multiple previous methods of self-harm. \nIn a follow-up study of cases of \u201cself-harm\u201d in males treated at one of several multiple\nemergency centers in the United Kingdom, in dividuals with nonsuicidal self-injury were\nsignificantly more likely to commit suicide th an other teenage individuals drawn from the\nsame cohort. Studies that have examined the relationship be tween nonsuicidal self-injury\nand suicidal behavior disorder are limited by being retrospe ctive and failing to obtain ver-\nified accounts of the method used during pr evious \u201cattempts.\u201d A significant proportion of\nthose who engage in nonsuicidal self-injury have responded positively when asked if they\nhave ever engaged in self-cutti ng (or their preferred means of self-injury) with an intention\nto die. It is reasonable to co nclude that nonsuicidal self-injury, while not presenting a high\nrisk for suicide when first manifested, is an especially dangerous form of self-injurious\nbehavior.\nThis conclusion is also supported by a mult isite study of depressed adolescents who had\npreviously failed to respond to antidepressant medi cation, which noted th at those with pre-", "source": "dsm5.pdf"} {"id": "8ecda3cbacba-2", "page_content": "vious nonsuicidal self-inj ury did not respond to cognitive-behavioral therapy, and by a study\nthat found that nonsuicida l self-injury is a predicto r of substance use/misuse. \nTrichotillomania (hair-pulling disorder). Trichotillomania is an injurious behavior con-\nfined to pulling out one\u2019s own hair, most commonly from the sc alp, eyebrows, or eyelashes.\nThe behavior occurs in \u201csessions\u201d that can last fo r hours. It is most likely to occur during a\nperiod of relaxation or distraction.", "source": "dsm5.pdf"} {"id": "585f8f51e3e2-0", "page_content": "806 Conditions for Further Study\nStereotypic self-injury. Stereotypic self-injury, which can include head banging, self-\nbiting, or self-hitting, is usually associated with intense concentration or under conditions\nof low external stimulation and might be associated with developmental delay.\nExcoriation (skin-picking) disorder. Excoriation disorder occurs mainly in females and\nis usually directed to picking at an area of th e skin that the individual feels is unsightly or\na blemish, usually on the face or the scalp. As in nonsuicidal self-injury, the picking is often\npreceded by an urge and is experienced as pleasurable, even thoug h the individual real-\nizes that he or she is harming himself or hersel f. It is not associated with the use of any im-\nplement.", "source": "dsm5.pdf"} {"id": "70a74dd69242-0", "page_content": "APPENDIX\nHighlights of Changes From DSM-IV to DSM-5 . . . . . . . . . . . . . . . . . . .809\nGlossary of Technical Terms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .817\nGlossary of Cultural Concepts of Distress . . . . . . . . . . . . . . . . . . . . . . .833\nAlphabetical Listing of DSM-5 Diagnoses and Codes \n(ICD-9-CM and ICD-10-CM) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .839\nNumerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM) . . . . . .863\nNumerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) . . . . .877\nDSM-5 Advisors and Other Contributors. . . . . . . . . . . . . . . . . . . . . . . . .897", "source": "dsm5.pdf"} {"id": "b9183b7a8a67-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "8d6c912c1cfc-0", "page_content": "809Highlights of Changes From\nDSM-IV to DSM-5\nChanges made to DSM-5 diagnostic criteria and text s are outlined in this chapter\nin the same order in which they appear in the DSM-5 classification. This abbreviated descrip-\ntion is intended to orient readers to only the most significant changes in each disorder cate-\ngory. An expanded description of nearly all changes (e.g., except minor text or wording\nchanges needed for clarity) is available online (www.psychiatry.org/ds m5). It should also be\nnoted that Section I contains a description of changes pertaining to the chapter organization\nin DSM-5, the multiaxial sy stem, and the introduction of dimensional assessments.\nNeurodevelopmental Disorders\nThe term mental retardation was used in DSM-IV. However, intellectual disability (intel-\nlectual developmental disorder) is the term that has come into common use over the past\ntwo decades among medical, ed ucational, and other professi onals, and by the lay public\nand advocacy groups. Diagnostic criteria em phasize the need for an assessment of both\ncognitive capacity (IQ) and adaptive functionin g. Severity is determined by adaptive func-\ntioning rather than IQ score.\nThe communication disorders, which are newly named from DSM-IV phonological dis-\norder and stuttering, respectively, include language disorder (which combines the previous\nexpressive and mixed receptive-ex pressive language disorders), speech sound disorder (pre-\nviously phonological disorder), and childhood-onset fluency disorder (previously stutter-\ning). Also included is social (pragmatic) communication disorder, a new condition involving\npersistent difficulties in the social us es of verbal and nonverbal communication.\nAutism spectrum disorder is a new DSM-5 disorder encompassing the previous DSM-", "source": "dsm5.pdf"} {"id": "8d6c912c1cfc-1", "page_content": "Autism spectrum disorder is a new DSM-5 disorder encompassing the previous DSM-\nIV autistic disorder (autism), Asperger\u2019s disorder, childhood disi ntegrative disorder,\nRett\u2019s disorder, and pervasive developmental di sorder not otherwise specified. It is char-\nacterized by deficits in two core domains: 1) deficits in social communication and social in-\nteraction and 2) restricted repetitive patterns of behavior, interests, and activities.\nSeveral changes have been made to the diagnostic criteria for attention-deficit/hyperactiv-\nity disorder (ADHD). Examples have been added to the criterion items to facilitate application\nacross the life span; the age at onset descri ption has been changed (from \u201csome hyperactive-\nimpulsive or inattentive symptoms that caused impairment were present before age 7 years\u201d\nto \u201cSeveral inattentive or hy peractive-impulsive symptoms we re present prior to age 12\u201d);\nsubtypes have been replaced with presentation specifiers that map directly to the prior sub-\ntypes; a comorbid diagnosis with autism spec trum disorder is now allowed; and a symptom\nthreshold change has been made for adults, to reflect the substantial evidence of clinically sig-\nnificant ADHD impairment, with the cutoff for ADHD of five symptoms, instead of six re-\nquired for younger persons, both for inatte ntion and for hyperactivity and impulsivity.\nSpecific learning disorder combines the DSM-IV diagnose s of reading disorder, math-\nematics disorder, disorder of written expression, and lear ning disorder not otherwise\nspecified. Learning deficits in the areas of reading, written expr ession, and mathematics\nare coded as separate specifiers. Acknowledgment is made in the text that specific types of\nreading deficits are described internationally in various ways as dyslexia and specific types", "source": "dsm5.pdf"} {"id": "8d6c912c1cfc-2", "page_content": "reading deficits are described internationally in various ways as dyslexia and specific types\nof mathematics deficits as dyscalculia.", "source": "dsm5.pdf"} {"id": "cd19f7537728-0", "page_content": "810 Highlights of Changes From DSM-IV to DSM-5\nThe following motor disorders are included in DSM-5: deve lopmental coordination disor-\nder, stereotypic movement disorder, Tourette\u2019s disorder, persistent (chronic) motor or vocal\ntic disorder, provisional tic disorder, other spec ified tic disorder, and un specified tic disorder.\nThe tic criteria have been standardized across all of these disorders in this chapter.\nSchizophrenia Spectrum and Other Psychotic Disorders\nTwo changes were made to Criterion A for schizophrenia: 1) the elimination of the special at-\ntribution of bizarre delusions and Schneiderian fi rst-rank auditory hallucinations (e.g., two or\nmore voices conversing), leadin g to the requirement of at least two Criterion A symptoms for\nany diagnosis of schizophrenia, and 2) the addition of the requirement that at least one of the\nCriterion A symptoms must be delusions, hallu cinations, or disorganized speech. The DSM-IV\nsubtypes of schizophrenia were eliminated due to their limited diagnostic stability, low reli-\nability, and poor validity. Instead, a dimensional approach to rating severity for the core symp-\ntoms of schizophrenia is includ ed in DSM-5 Section III to capt ure the important heterogeneity\nin symptom type and severity expressed across individual s with psychotic disorders.\nSchizoaffective disorder is reconceptualized as a longitudin al instead of a cross-sectional di-\nagnosis\u2014more comparable to schizophrenia, bipolar disorder, and majo r depressive disorder,\nwhich are bridged by this condition\u2014and requires that a major mood episode be present for a\nmajority of the total disorder \u2019s duration after Criterion A has been met. Criterion A for delu-\nsional disorder no longer has the requirement that th e delusions must be nonbizarre; a spec-", "source": "dsm5.pdf"} {"id": "cd19f7537728-1", "page_content": "ifier is now included for bizarre type delusions to provide continuity with DSM-IV. Criteria for\ncatatonia are described uniformly across DSM-5. Fu rthermore, catatonia may be diagnosed\nwith a specifier (for depressive, bipolar, and psychotic disorders, incl uding schizophrenia), in\nthe context of a known medical condition, or as an other specified diagnosis.\nBipolar and Related Disorders\nDiagnostic criteria for bipolar disorders now include both changes in mood and changes in\nactivity or energy. The DSM-IV diagnosis of bipolar I disorder, mixed episodes\u2014requiring\nthat the individual simultaneous ly meet full criteria for both mania and major depressive ep-\nisode\u2014is replaced with a new specifier \u201cwith mixed features.\u201d Particular conditions can\nnow be diagnosed under other specified bipolar and related disorder, including categori-\nzation for individuals with a past history of a major depressive di sorder whose symptoms\nmeet all criteria for hypomania except the duration criterion is not met (i.e., the episode lasts\nonly 2 or 3 days instead of the required 4 cons ecutive days or more). A second condition con-\nstituting an other specified bipolar and related disorder variant is that too few symptoms of\nhypomania are present to meet criteria for the full bipolar II syndrome, although the dura-\ntion, at least 4 consecutive days, is sufficient. Finally, in both this chapter and in the chapter\n\u201cDepressive Disorders,\u201d an anxious distress specifier is delineated.\nDepressive Disorders\nTo address concerns about potential overdiagno sis and overtreatment of bipolar disorder in\nchildren, a new diagnosis, disruptive mood dysregulation disorder, is included for children\nup to age 18 years who exhibit persistent irrita bility and frequent episodes of extreme behav-", "source": "dsm5.pdf"} {"id": "cd19f7537728-2", "page_content": "ioral dyscontrol. Premenstrual dysphoric disorder is now promoted from Appendix B, \u201cCri-\nteria Sets and Axes Provided for Further Study, \u201d in DSM-IV to the main body of DSM-5. What\nwas referred to as dysthymia in DSM-IV now falls under the category of persistent depressive\ndisorder, which includes both chronic major depre ssive disorder and the previous dysthymic", "source": "dsm5.pdf"} {"id": "2ba3c8cd0c16-0", "page_content": "was referred to as dysthymia in DSM-IV now falls under the category of persistent depressive\ndisorder, which includes both chronic major depre ssive disorder and the previous dysthymic\ndisorder. The coexistence within a major depressive episode of at least three manic symp-\ntoms (insufficient to satisfy cr iteria for a manic episode) is no w acknowledged by the specifier", "source": "dsm5.pdf"} {"id": "d71734b6821e-0", "page_content": "Highlights of Changes From DSM-IV to DSM-5 811\n\u201cwith mixed features.\u201d In DSM-IV, there was an exclusion criterion for a major depressive ep-\nisode that was applied to depressive symptoms lasting less than 2 months following the death\nof a loved one (i.e., the bereavement exclusion). This exclusion is omitted in DSM-5 for several\nreasons, including the recognitio n that bereavement is a severe psychosocial stressor that can\nprecipitate a major depressive episode in a vu lnerable individual, generally beginning soon\nafter the loss, and can add an additional risk for suffering, feelings of worthlessness, suicidal\nideation, poorer medical health, and worse interp ersonal and work functioning. It was critical\nto remove the implication that bereavement ty pically lasts only 2 months, when both physi-\ncians and grief counselors recognize that the duration is more commonly 1\u20132 years. A detailed\nfootnote has replaced the more simplistic DSM- IV exclusion to aid clinicians in making the\ncritical distinction between the symptoms characteristic of be reavement and those of a major\ndepressive disorder. Finally, a new specifier to indicate the presence of mixed symptoms has\nbeen added across both the bipo lar and the depressive disorders.\nAnxiety Disorders\nThe chapter on anxiety disorders no longer includes obsessive-compulsive disorder (which\nis in the new chapter \u201cObsessive-Compulsiv e and Related Disorders\u201d) or posttraumatic\nstress disorder (PTSD) and acut e stress disorder (which are in the new chapter \u201cTrauma-\nand Stressor-Related Disorders\u201d). Changes in criteria for specific phobia and social anxiety\ndisorder (social phobia) include deletion of the requirement that individuals over age 18\nyears recognize that their anxiet y is excessive or unreasonable . Instead, the anxiety must be", "source": "dsm5.pdf"} {"id": "d71734b6821e-1", "page_content": "years recognize that their anxiet y is excessive or unreasonable . Instead, the anxiety must be\nout of proportion to the actual danger or threat in the situation, after cultural contextual fac-\ntors are taken into account. In addition, the 6-month duration is now extended to all ages.\nPanic attacks can now be listed as a specifier that is applicable to all DSM-5 disorders. Panic\ndisorder and agoraphobia are unlinked in DSM-5. Thus, the former DSM-IV diagnoses of\npanic disorder with agoraphobia, panic disorder without agoraphobia, and agoraphobia\nwithout history of panic disorder are now replaced by two diagnoses, panic disorder and ag-\noraphobia, each with separate crit eria. The \u201cgeneralized\u201d specifier for social anxiety disor-\nder has been deleted and replaced with a \u201cperformance only\u201d specifier. Separation anxiety\ndisorder and selective mutism are now classified as anxiety di sorders. The wording of the\ncriteria is modified to more adequately repres ent the expression of se paration anxiety symp-\ntoms in adulthood. Also, in contrast to DSM-IV, the diagnostic criteria no longer specify that\nonset must be before age 18 years, and a duration statement\u2014\u201ctypically lasting for 6 months\nor more\u201d\u2014has been added for adults to minimize overdia gnosis of transient fears.\nObsessive-Compulsive and Related Disorders\nThe chapter \u201cObsessive-Compulsive and Related Disorders\u201d is new in DSM-5. New disor-\nders include hoarding disorder, excoriation (skin-pi cking) disorder, substance/medica-\ntion-induced obsessive-compulsive and related disorder, and obsessive-compulsive and\nrelated disorder due to another medical condition. The DSM-IV diagnosis of trichotillo-", "source": "dsm5.pdf"} {"id": "d71734b6821e-2", "page_content": "mania is now termed trichotillomania (hair-pulling disorder) and has been moved from a\nDSM-IV classification of impulse-control di sorders not elsewhere classified to obsessive-\ncompulsive and related disorders in DSM-5. The DSM-IV \u201cwith poor insight\u201d specifier for\nobsessive-compulsive disorder has been refined to allow a distinction between individuals\nwith good or fair insight, poor insight, and \u201cabsent insight/delusional\u201d obsessive-compul-\nsive disorder beliefs (i.e., comp lete conviction that obsessive-compulsive disorder beliefs", "source": "dsm5.pdf"} {"id": "5f78e1217629-0", "page_content": "with good or fair insight, poor insight, and \u201cabsent insight/delusional\u201d obsessive-compul-\nsive disorder beliefs (i.e., comp lete conviction that obsessive-compulsive disorder beliefs\nare true). Analogous \u201cinsight\u201d specifiers have been included for body dysmorphic disorder\nand hoarding disorder. A \u201ctic-related\u201d specifier for obsessive-compuls ive disorder has also\nbeen added, because presence of a comorbid tic disorder may have important clinical im-\nplications. A \u201cmuscle dy smorphia\u201d specifier for body dysmorphic disorder is added to re-\nflect a growing literature on the diagnostic validity and clinical utility of making this", "source": "dsm5.pdf"} {"id": "505b02a138f3-0", "page_content": "812 Highlights of Changes From DSM-IV to DSM-5\ndistinction in individuals with body dysmorphic disorder. The delusional variant of body\ndysmorphic disorder (which identifies individu als who are completely convinced that their\nperceived defects or flaws are truly abnormal ap pearing) is no longer coded as both delu-\nsional disorder, somatic type, and body dysmorph ic disorder; in DSM-5, this presentation is\ndesignated only as body dysmorphic disorder with the absent insight/delusional specifier.\nIndividuals can also be diagnosed with other specified obsessive-compulsive and related\ndisorder, which can include conditions such as body-focused repetitive behavior disorder\nand obsessional jealousy, or unspecified obsessive-compulsive and related disorder.\nTrauma- and Stressor-Related Disorders\nFor a diagnosis of acute stress disorder, qualifying traumatic events are now explicit as to\nwhether they were experienced directly, witnessed, or experienced indirectly. Also, the\nDSM-IV Criterion A2 regarding the subjective reaction to th e traumatic event (e.g., expe-\nriencing \u201cfear, helplessness, or horror\u201d) has been eliminated. Adjustment disorders are\nreconceptualized as a heterogeneous array of stress-response syndromes that occur after\nexposure to a distressing (traum atic or nontraumatic) event, rather than as a residual cat-\negory for individuals who exhibit clinically significant distress but whose symptoms do\nnot meet criteria for a more d iscrete disorder (as in DSM-IV).\nDSM-5 criteria for PTSD differ significantly from the DS M-IV criteria. The stressor cri-\nterion (Criterion A) is more ex plicit with regard to events that qualify as \u201ctraumatic\u201d ex-\nperiences. Also, DSM-IV Criterion A2 (subje ctive reaction) has been eliminated. Whereas", "source": "dsm5.pdf"} {"id": "505b02a138f3-1", "page_content": "there were three major symptom clusters in DSM-IV\u2014reexperiencing, avoidance/numb-\ning, and arousal\u2014there are no w four symptom clusters in DSM-5, because the avoidance/\nnumbing cluster is divided into two distinct clusters: avoidance and persistent negative al-\nterations in cognitions and mood. This latter category, which retains most of the DSM-IV\nnumbing symptoms, also includes new or re conceptualized symptoms, such as persistent\nnegative emotional states. The final cluster\u2014 alterations in arousal and reactivity\u2014retains\nmost of the DSM-IV arousal symptoms. It also includes irritable behavior or angry out-\nbursts and reckless or self-destructive beha vior. PTSD is now develo pmentally sensitive in\nthat diagnostic thresholds have been lowe red for children and adolescents. Furthermore,\nseparate criteria have been added for childre n age 6 years or younger with this disorder.\nThe DSM-IV childhood diagno sis reactive attachment di sorder had two subtypes:\nemotionally withdrawn/inhibited and indiscri minately social/disinhibited. In DSM-5,\nthese subtypes are defined as distinct disorders: reactive attachment disorder and disin-\nhibited social engagement disorder.\nDissociative Disorders\nMajor changes in dissociative disorders in DS M-5 include the following: 1) derealization is\nincluded in the name and symptom structure of what previously was called depersonali-\nzation disorder ( depersonalization/derealization disorder ); 2) dissociative fugue is now a\nspecifier of dissociative amnesia rather than a separate diagnosis, and 3) the criteria for\ndissociative identity disorder have been changed to indicate that symptoms of disruption\nof identity may be reported as well as observed, and that gaps in the recall of events may", "source": "dsm5.pdf"} {"id": "505b02a138f3-2", "page_content": "of identity may be reported as well as observed, and that gaps in the recall of events may\noccur for everyday and not just traumatic ev ents. Also, experiences of pathological pos-\nsession in some cultures are included in the description of identity disruption.\nSomatic Symptom and Related Disorders\nIn DSM-5, somatoform disorders are now referred to as somatic symptom and related dis-\norders. The DSM-5 classification reduces the number of these disorders and subcategories to\navoid problematic overlap. Diagnoses of somatization disorder, hypochondriasis, pain dis-", "source": "dsm5.pdf"} {"id": "6fe5171100cd-0", "page_content": "orders. The DSM-5 classification reduces the number of these disorders and subcategories to\navoid problematic overlap. Diagnoses of somatization disorder, hypochondriasis, pain dis-\norder, and undifferentiated somatoform diso rder have been removed. Individuals previ-", "source": "dsm5.pdf"} {"id": "4539faab96ac-0", "page_content": "Highlights of Changes From DSM-IV to DSM-5 813\nously diagnosed with somatization disorder wi ll usually have sympto ms that meet DSM-5\ncriteria for somatic symptom disorder, but only if they have th e maladaptive thoughts, feel-\nings, and behaviors that define the disorder, in addition to their somatic symptoms. Because\nthe distinction between somati zation disorder and undifferen tiated somatoform disorder\nwas arbitrary, they are merged in DSM-5 un der somatic symptom diso rder. Individuals pre-\nviously diagnosed with hypochondriasis who have high health anxiety but no somatic symp-\ntoms would receive a DSM-5 diagnosis of illness anxiety disorder (unless their health\nanxiety was better explained by a primary anxiety disorder, su ch as generalized anxiety dis-\norder). Some individuals with chronic pain w ould be appropriately di agnosed as having so-\nmatic symptom disorder, with predominant pain . For others, psychological factors affecting\nother medical conditions or an adjustment disorder would be more appropriate.\nPsychological factors affect ing other medical conditions is a new mental disorder in\nDSM-5, having formerly been listed in the DSM-IV chapter \u201cOther Conditions That May\nBe a Focus of Clinical At tention.\u201d This disorder and factitious disorder are placed among\nthe somatic symptom and related disorders because somatic symptoms are predominant\nin both disorders, and both are most often en countered in medical settings. The variants of\npsychological factors affecting other medical conditions are removed in favor of the stem\ndiagnosis. Criteria for conversion disorder (functional neurological symptom disorder)\nhave been modified to emphasize the essent ial importance of the neurological examina-\ntion, and in recognition that relevant psychological factors may not be demonstrable at the\ntime of diagnosis. Other spec ified somatic symptom disorder , other specified illness anx-", "source": "dsm5.pdf"} {"id": "4539faab96ac-1", "page_content": "time of diagnosis. Other spec ified somatic symptom disorder , other specified illness anx-\niety disorder, and pseudocyesis ar e now the only exemplars of the other specified somatic\nsymptom and related disorder classification.\nFeeding and Eating Disorders\nBecause of the elimination of the DSM-IV-TR chapter \u201cDisorders Us ually First Diagnosed\nDuring Infancy, Childhood, or Adolescence,\u201d th is chapter describes several disorders found in\nthe DSM-IV section \u201cFeeding and Eating Disord ers of Infancy or Early Childhood,\u201d such as\npica and rumination disorder. The DSM-IV category feeding disorder of infancy or early\nchildhood has been renamed avoidant/restrictive f ood intake disorder, and the criteria are\nsignificantly expanded. The core diagnostic criteria for anorexia nervosa are conceptually un-\nchanged from DSM-IV with one exception: the requirement for amenorrhea is eliminated. As\nin DSM-IV, individuals with this disorder are requ ired by Criterion A to be at a significantly\nlow body weight for their developmental stage. The wording of the criterion is changed for\nclarification, and guidan ce regarding how to judge whether an individual is at or below a sig-\nnificantly low weight is provided in the text. In DSM-5, Criterion B is expanded to include not\nonly overtly expressed fear of weight gain but also persistent behavior that interferes with\nweight gain. The only change in the DSM-IV criteria for bulimia nervosa is a reduction in the\nrequired minimum average frequency of binge eating and inappropri ate compensatory be-\nhavior frequency from twice to once weekly. The extensive research that followed the prom-\nulgation of preliminary criteria for binge-eating disorder in Appendix B of DSM-IV", "source": "dsm5.pdf"} {"id": "4539faab96ac-2", "page_content": "ulgation of preliminary criteria for binge-eating disorder in Appendix B of DSM-IV\ndocumented the clinical utility and validity of binge-eating disorder. The only significant dif-\nference from the prelimin ary criteria is that the minimum average frequency of binge eating re-\nquired for diagnosis is once weekly over the la st 3 months, identical to the frequency criterion\nfor bulimia nervosa (rather than at least 2 days a week for 6 months in DSM-IV).\nElimination Disorders", "source": "dsm5.pdf"} {"id": "011d7942f70b-0", "page_content": "for bulimia nervosa (rather than at least 2 days a week for 6 months in DSM-IV).\nElimination Disorders\nThere have been no significant changes in this diagnostic class from DSM-IV to DSM-5.\nThe disorders in this chapter were previously classified under disorders usually first di-\nagnosed in infancy, childhood, or adolescenc e in DSM-IV and exist now as an independent\nclassification in DSM-5.", "source": "dsm5.pdf"} {"id": "c23bd05e97cb-0", "page_content": "814 Highlights of Changes From DSM-IV to DSM-5\nSleep-Wake Disorders\nIn DSM-5, the DSM-IV diagnose s named sleep disorder related to another mental disorder\nand sleep disorder related to another medica l condition have been removed, and instead\ngreater specification of coexisting conditions is provided for each sleep-wake disorder. The\ndiagnosis of primary insomnia has been renamed insomnia disorder to avoid the differen-\ntiation between primary and secondary insomnia. DSM-5 also distinguishes narcolepsy \u2014\nnow known to be associated with hypocretin deficiency\u2014from other forms of hypersomno-\nlence (hypersomnolence disorder ). Finally, throughout the DSM-5 classification of sleep-\nwake disorders, pediatric and developmental cr iteria and text are integrated where existing\nscience and considerations of clinical utility support such integration. Breathing-related\nsleep disorders are divided into three relatively distinct disorders: obstructive sleep apnea\nhypopnea, central sleep apnea, and sleep-related hypoventilation. The subtypes of circadian\nrhythm sleep disorders are expanded to include advanced sleep phase type and irregular\nsleep-wake type, whereas the jet lag type has b een removed. The use of the former \u201cnot oth-\nerwise specified\u201d diagnoses in DSM- IV have been reduced by elevating rapid eye move-\nment sleep behavior disorder and restless legs syndrome to independent disorders.\nSexual Dysfunctions\nIn DSM-5, some gender-specifi c sexual dysfunctions have been added, and, for females,\nsexual desire and arousal disorders have been combined into one disorder: female sexual\ninterest/arousal disorder. All of the sexual dysfunctions (except substance/medication-in-\nduced sexual dysfunction ) now require a minimum duration of approximately 6 months and\nmore precise severity criteria. Genito-pelvic pain/p enetration disorder has been added to", "source": "dsm5.pdf"} {"id": "c23bd05e97cb-1", "page_content": "DSM-5 and represents a merging of vaginismus and dyspareunia, which were highly co-\nmorbid and difficult to distinguish. The diagno sis of sexual aversion disorder has been re-\nmoved due to rare use and la ck of supporting research.\nThere are now only two subtyp es for sexual dysfunctions: lifelong versus acquired\nand generalized versus situational. To indicate the presence and degree of medical and\nother nonmedical correlates, the following associated features have been added to the text:\npartner factors, relationship factors, individu al vulnerability factors, cultural or religious\nfactors, and medical factors.\nGender Dysphoria\nGender dysphoria is a new diagnostic class in DSM-5 and reflects a change in conceptual-\nization of the disorder\u2019s defining features by emphasizing the phenomenon of \u201cgender in-\ncongruence\u201d rather than cross-gender identification per se, as was the case in DSM-IV gender\nidentity disorder. Gender dyspho ria includes separate sets of criteria: for children and for\nadults and adolescents. For the adolescents an d adults criteria, the previous Criterion A\n(cross-gender identification) and Criterion B (aversion toward one\u2019s gender) are merged. In\nthe wording of the criteria, \u201cthe other sex\u201d is replaced by \u201cthe other gender\u201d (or \u201csome alter-\nnative gender\u201d).\u201d Gender instead of sex is used systematically because the concept \u201csex\u201d is in-\nadequate when referring to individuals with a disorder of sex development. In the child\ncriteria, \u201cstrong desire to be of the other gend er\u201d replaces the previous \u201crepeatedly stated de-\nsire to be...the other sex\u201d to capture the situat ion of some children who, in a coercive envi-", "source": "dsm5.pdf"} {"id": "c23bd05e97cb-2", "page_content": "ronment, may not verbalize the desire to be of another gender. For child ren, Criterion A1 (\u201ca\nstrong desire to be of the other gender or an in sistence that he or she is the other gender.. .)\u201d\nis now necessary (but not sufficient), which makes the diagnosi s more restrictive and conser-\nvative. The subtyping on the basis of sexual or ientation is removed because the distinction is", "source": "dsm5.pdf"} {"id": "8dbe481b8f3b-0", "page_content": "is now necessary (but not sufficient), which makes the diagnosi s more restrictive and conser-\nvative. The subtyping on the basis of sexual or ientation is removed because the distinction is\nno longer considered clinically useful. A posttransition specifier has been added to identify", "source": "dsm5.pdf"} {"id": "afedbdb377b1-0", "page_content": "Highlights of Changes From DSM-IV to DSM-5 815\nindividuals who have undergone at least one medical procedure or treatment to support the\nnew gender assignment (e.g., cross-sex hormon e treatment). Although the concept of post-\ntransition is modeled on the concept of full or partial remission, the term remission has impli-\ncations in terms of symptom reduction that do not apply directly to gender dysphoria.\nDisruptive, Impulse-Control, and Conduct Disorders\nThe chapter \u201cDisruptive, Impulse-Control, and Conduct Disorders\u201d is new to DSM-5 and\ncombines disorders that were pr eviously included in the chapte r \u201cDisorders Usually First Di-\nagnosed in Infancy, Childhood, or Adolescence\u201d (i.e., oppositional defiant disorder; conduct\ndisorder; and disruptive behavior disorder not otherwise specified, now categorized as other\nspecified and unspecified disrup tive, impulse-control, and cond uct disorders) and the chap-\nter \u201cImpulse-Control Disorders Not Elsewhere Cl assified\u201d (i.e., intermittent explosive disor-\nder, pyromania, and kleptomania). These diso rders are all characterized by problems in\nemotional and behavioral self-control. Notably, ADHD is frequently comorbid with the dis-\norders in this chapter but is listed with the neurodevelopmental disorders. Because of its\nclose association with co nduct disorder, antisocial personality disorder is listed both in this\nchapter and in the chapter \u201cPersonality Diso rders,\u201d where it is described in detail.\nThe criteria for oppositional defiant disorder are now grouped into three types: an-\ngry/irritable mood, argumentative/defiant be havior, and vindictiveness. Additionally,\nthe exclusionary criterion for conduct diso rder has been removed. The criteria for conduct", "source": "dsm5.pdf"} {"id": "afedbdb377b1-1", "page_content": "the exclusionary criterion for conduct diso rder has been removed. The criteria for conduct\ndisorder include a descriptive features specifier for individuals who meet full criteria for\nthe disorder but al so present with limited prosocial emotions. The primary change in in-\ntermittent explosive disorder is in the type of aggressive outbursts that should be consid-\nered: DSM-IV required physical aggression, whereas in DSM-5 verbal aggression and\nnondestructive/noninjurious physical aggression also meet criteria. DSM-5 also provides\nmore specific criteria defining frequency needed to meet the criteria and specifies that the\naggressive outbursts ar e impulsive and/or anger based in nature, and must cause marked\ndistress, cause impairment in occupational or interpersonal functioning, or be associated\nwith negative financial or legal consequences. Furthermore, a minimum age of 6 years (or\nequivalent developmental level) is now required.\nSubstance-Related and Addictive Disorders\nAn important departure from past diagnostic ma nuals is that the chapter on substance-related\ndisorders has been expanded to include gambling disorder. Another key change is that\nDSM-5 does not separate the diagnoses of substance abuse and dependence as in DSM-IV. Rather\ncriteria are provided for substance use disorder, accompanied by criteria for intoxication,\nwithdrawal, substance-induced disorders, and unspecified substance-related disorders,\nwhere relevant. Within substance use disorders, the DSM-IV recurrent substance-related legal\nproblems criterion has been dele ted from DSM-5, and a new criter ion\u2014craving, or a strong de-\nsire or urge to use a substance\u2014has been adde d. In addition, the thre shold for substance use\ndisorder diagnosis in DSM-5 is set at two or more criteria, in contrast to a threshold of one or", "source": "dsm5.pdf"} {"id": "afedbdb377b1-2", "page_content": "more criteria for a diagnosis of DSM-IV substance abuse and three or more for DSM-IV depen-\ndence. Cannabis withdrawal and caffeine withdrawal are new disorders (the latter was in\nDSM-IV Appendix B, \u201cCriteria Sets and Axes Provided for Further Study\u201d).\nSeverity of the DSM-5 substance use disorders is based on the number of criteria en-\ndorsed. The DSM-IV specifier fo r a physiological subtype is eliminated in DSM-5, as is the\nDSM-IV diagnosis of polysubstance dependence. Early remission from a DSM-5 substance", "source": "dsm5.pdf"} {"id": "9ffdab75c3de-0", "page_content": "dorsed. The DSM-IV specifier fo r a physiological subtype is eliminated in DSM-5, as is the\nDSM-IV diagnosis of polysubstance dependence. Early remission from a DSM-5 substance\nuse disorder is defined as at least 3 but less than 12 months without meeting substance use\ndisorder criteria (except crav ing), and sustained remission is defined as at least 12 months\nwithout meeting criteria (except craving). Additional new DSM-5 specifiers include \u201cin a\ncontrolled environment\u201d and \u201con maintenance therapy\u201d as the situation warrants.", "source": "dsm5.pdf"} {"id": "8316371fb6af-0", "page_content": "816 Highlights of Changes From DSM-IV to DSM-5\nNeurocognitive Disorders\nThe DSM-IV diagnoses of dementia and amnestic disorder are subsumed under the newly\nnamed entity major neurocognitive disorder (NCD). The term dementia is not precluded from\nuse in the etiological subtypes where that te rm is standard. Furthermore, DSM-5 now recog-\nnizes a less severe level of cognitive impairment, mild NCD, which is a new disorder that per-\nmits the diagnosis of less disabling syndromes that may nonetheless be the focus of concern\nand treatment. Diagnostic criteria are provided for both of these disorders, foll owed by diag-\nnostic criteria for different etiological subtypes. In DSM-IV, individual diagnoses were desig-\nnated for dementia of the Alzheimer\u2019s type , vascular dementia, and substance-induced\ndementia, whereas the other neurodegenerative disorders were classified as dementia due to\nanother medical condition, with HIV, head trauma, Parkinson\u2019s disease, Huntington\u2019s disease,\nPick\u2019s disease, Creutzfeldt-Jako b disease, and other medical co nditions specified. In DSM-5,\nmajor or mild NCD due to Alzheimer\u2019s disease and major or mild vascular NCD have been re-\ntained, while new separate criteria are now presented for major or mild frontotemporal NCD,\nNCD with Lewy bodies, and NCDs due to trau matic brain injury, a substance/medication,\nHIV infection, prion disease, Parkinson\u2019s diseas e, Huntington\u2019s disease, another medical con-\ndition, and multiple etiologies, respectively. Un specified NCD is also included as a diagnosis.\nPersonality Disorders\nThe criteria for personality disorders in Sectio n II of DSM-5 have not changed from those in", "source": "dsm5.pdf"} {"id": "8316371fb6af-1", "page_content": "DSM-IV. An alternative approach to the diag nosis of personality di sorders was developed\nfor DSM-5 for further study and can be found in Section III (see \u201cAlternative DSM-5 Model\nfor Personality Disorders\u201d). For the general criteria for personality disorder, presented in\nSection III, a revised personality functioning criterion (Criterion A) has been developed\nbased on a literature review of reliable clinical measures of core impa irments central to per-\nsonality pathology. A diagnosis of personality disorder\u2014trait specified, based on moderate\nor greater impairment in person ality functioning and the presence of pathological personal-\nity traits, replaces personality disorder not ot herwise specified and prov ides a much more in-\nformative diagnosis for individuals who are not optimally described as having a specific\npersonality disorder. A greater emphasis on pe rsonality functioning and trait-based criteria\nincreases the stability and empiri cal bases of the disorders. Personality functioning and per-\nsonality traits also can be assessed whether or not the individual has a personality disor-\nder\u2014a feature that provides clinically useful information about all individuals.\nParaphilic Disorders\nAn overarching change from DSM-IV is the addition of the course specifiers \u201cin a controlled\nenvironment\u201d and \u201cin remission\u201d to the diagnostic criteria se ts for all the paraphilic disor-\nders. These specifiers are added to indicate important changes in an individual\u2019s status. In\nDSM-5, paraphilias are not ipso facto mental disorders. There is a distinction between paraphil-\nias and paraphilic disorders. A paraphilic disorder is a paraphilia that is currently causing dis-\ntress or impairment to the individual or a pa raphilia whose satisfaction has entailed personal", "source": "dsm5.pdf"} {"id": "8316371fb6af-2", "page_content": "tress or impairment to the individual or a pa raphilia whose satisfaction has entailed personal\nharm, or risk of harm, to others. A paraphilia is a necessary but not a sufficient condition for\nhaving a paraphilic disorder, and a paraphilia by it self does not automatically justify or require\nclinical intervention. The distinction between paraphilias and paraphilic disorders was im-\nplemented without making any changes to the basi c structure of the diagnostic criteria as they\nhad existed since DSM-III-R. Th e change proposed for DSM-5 is that individuals who meet", "source": "dsm5.pdf"} {"id": "75773f079866-0", "page_content": "plemented without making any changes to the basi c structure of the diagnostic criteria as they\nhad existed since DSM-III-R. Th e change proposed for DSM-5 is that individuals who meet\nboth Criterion A and Criterion B would now be diagnosed as having a paraphilic disorder. A\ndiagnosis would not be given to individuals whose symptoms meet Criterion A but not Cri-\nterion B\u2014that is, to individuals who have a paraphilia but not a paraphilic disorder.", "source": "dsm5.pdf"} {"id": "7b09f2eb69db-0", "page_content": "817Glossary of\n Technical Terms\naffect A pattern of observable behaviors that is the expression of a subjectively experi-\nenced feeling state (emotion). Examples of af fect include sadness, elation, and anger. In\ncontrast to mood, which refers to a pervasive and sustained emotional \u201cclimate,\u201d affect\nrefers to more fluctuating changes in emot ional \u201cweather.\u201d What is considered the nor-\nmal range of the expression of affect varies considerably, both within and among dif-\nferent cultures. Disturba nces in affect include\nblunted Significant reduction in the inte nsity of emotional expression.\nflat Absence or near absence of an y sign of affective expression.\ninappropriate Discordance between affective expression and the content of speech\nor ideation.\nlabile Abnormal variability in affect with repeated, rapid, and abrupt shifts in af-\nfective expression.\nrestricted or constricted Mild reduction in the range and intensity of emotional ex-\npression.\naffective blunting See AFFECT .\nagitation (psychomotor) See PSYCHOMOTOR AGITATION .\nagnosia Loss of ability to recognize objects, persons, sounds, shapes, or smells that occurs\nin the absence of either impairment of the specific sense or significant memory loss.\nalogia An impoverishment in thinking that is inferred from observing speech and lan-\nguage behavior. There may be brief and concre te replies to questions and restriction in\nthe amount of spontaneous speech (termed poverty of speech ). Sometimes the speech is\nadequate in amount but conveys little inform ation because it is overconcrete, overab-\nstract, repetitive, or stereotyped (termed poverty of content ).\namnesia An inability to recall important autobiog raphical information that is inconsis-\ntent with ordinary forgetting.", "source": "dsm5.pdf"} {"id": "7b09f2eb69db-1", "page_content": "tent with ordinary forgetting.\nanhedonia Lack of enjoyment from, engagement in , or energy for life\u2019s experiences; def-\nicits in the capacity to feel pleasure and take interest in things. Anhedonia is a facet of\nthe broad personality trait domain D ETACHMENT .\nanosognosia A condition in which a person with an illness seems unaware of the exis-\ntence of his or her illness.\nantagonism Behaviors that put an individual at od ds with other people, such as an ex-\naggerated sense of self-importance with a concomitant expectation of special treat-\nment, as well as a callous antipathy toward others, encompassing both unawareness of\nothers\u2019 needs and feelings, and a readiness to use others in the service of self-enhance-\nment. Antagonism is one of the five broad PERSONALITY TRAIT DOMAINS defined in Sec-\ntion III \u201cAlternative DSM-5 Mo del for Personality Disorders.\u201d\nSMALL CAPS indicate term found elsewhere in this glossary. Glossary definitions were informed by\nDSM-5 Work Groups, publicly available Internet so urces, and previously published glossaries for\nmental disorders (World Heal th Organization and American Psychiatric Association).", "source": "dsm5.pdf"} {"id": "76478e3d13c1-0", "page_content": "818 Glossary of Technical Terms\nantidepressant discontinuation syndrome A set of symptoms that can occur after\nabrupt cessation, or marked reduction in dose, of an antidepressant medication that\nhad been taken continuously for at least 1 month.\nanxiety The apprehensive anticipation of future danger or misfortune accompanied by\na feeling of worry, distress, an d/or somatic symptoms of tension. The focus of antici-\npated danger may be internal or external.\nanxiousness Feelings of nervousness or tenseness in reaction to diverse situations; frequent\nworry about the negative effect s of past unpleasant experiences and future negative possi-\nbilities; feeling fearful and apprehensive about uncertainty; expecting the worst to happen.\nAnxiousness is a facet of the broad personality trait domain N EGATIVE AFFECTIVITY .\narousal The physiological and psychological state of being awake or reactive to stimuli.\nasociality A reduced initiative for interacting with other people.\nattention The ability to focus in a sustained manner on a particular stimulus or activity.\nA disturbance in attention ma y be manifested by easy DISTRACTIBILITY or difficulty in\nfinishing tasks or in concentrating on work.\nattention seeking Engaging in behavior designed to attract notice and to make oneself\nthe focus of others\u2019 attention and admiration . Attention seeking is a facet of the broad\npersonality trait domain ANTAGONISM .\nautogynephilia Sexual arousal of a natal male associated with the idea or image of being\na woman.\navoidance The act of keeping away from stress-rela ted circumstances; a tendency to cir-\ncumvent cues, activities, and situations that remind the individual of a stressful event\nexperienced.\navolition An inability to initiate and persist in go al-directed activities . When severe enough\nto be considered pathological, avolition is pervasive and prevents the person from com-", "source": "dsm5.pdf"} {"id": "76478e3d13c1-1", "page_content": "to be considered pathological, avolition is pervasive and prevents the person from com-\npleting many different types of activities (e.g., work, intellectual pursuits, self-care).\nbereavement The state of having lost through death someone with whom one has had\na close relationship. This state includes a range of grief and mourning responses.\nbiological rhythms See CIRCADIAN RHYTHMS .\ncallousness Lack of concern for the feelings or problems of others; lack of guilt or re-\nmorse about the negative or harmful effects of one\u2019s actions on others. Callousness is a\nfacet of the broad personality trait domain ANTAGONISM .\ncatalepsy Passive induction of a posture held against gravity. Compare with WAXY FLEX -\nIBILITY .\ncataplexy Episodes of sudden bilateral loss of mu scle tone resulting in the individual\ncollapsing, often occurring in association wi th intense emotions such as laughter, an-\nger, fear, or surprise.\ncircadian rhythms Cyclical variations in physiological and biochemical function, level\nof sleep-wake activity, and emotional state. Circadian rhythms have a cycle of about 24\nhours, ultradian rhythms have a cycle that is shorter than 1 day, and infradian rhythms\nhave a cycle that may last weeks or months.\ncognitive and perceptual dysregulation Odd or unusual thought processes and experi-\nences, including DEPERSONALIZATION , DEREALIZATION , and DISSOCIATION ; mixed sleep-\nwake state experiences; and thought-cont rol experiences. Cognitive and perceptual\ndysregulation is a facet of the broad personality trait domain P SYCHOTICISM .\ncoma State of complete loss of consciousness.", "source": "dsm5.pdf"} {"id": "01236d1cf0c4-0", "page_content": "Glossary of Technical Terms 819\ncompulsion Repetitive behaviors (e.g., hand wash ing, ordering, checking) or mental\nacts (e.g., praying, counting, repeating word s silently) that the individual feels driven\nto perform in response to an obsession, or according to rules that must be applied rig-\nidly. The behaviors or mental acts are aimed at preventing or redu cing anxiety or dis-\ntress, or preventing some dreaded event or situation; however, these behaviors or\nmental acts are not connected in a realistic way with what they are designed to neutral-\nize or prevent or are clearly excessive.\nconversion symptom A loss of, or alteration in, voluntary motor or sensory functioning,\nwith or without apparent impairment of consciousness. The symptom is not fully ex-\nplained by a neurological or another medical condition or the direct effects of a sub-\nstance and is not intentiona lly produced or feigned.\ndeceitfulness Dishonesty and fraudulence; misrep resentation of self; embellishment or\nfabrication when relating even ts. Deceitfulness is a facet of the broad personality trait\ndomain A NTAGONISM .\ndefense mechanism Mechanisms that mediate the indi vidual\u00b4s reaction to emotional\nconflicts and to external stressors. Some defense mechanisms (e.g., projection, splitting,\nacting out) are almost invariably maladapt ive. Others (e.g., suppression, denial) may\nbe either maladaptive or adaptive, dependin g on their severity, their inflexibility, and\nthe context in which they occur.\ndelusion A false belief based on incorrect inferenc e about external reality that is firmly\nheld despite what almost everyone else beli eves and despite what constitutes incontro-\nvertible and obvious proof or evidence to th e contrary. The belief is not ordinarily ac-", "source": "dsm5.pdf"} {"id": "01236d1cf0c4-1", "page_content": "vertible and obvious proof or evidence to th e contrary. The belief is not ordinarily ac-\ncepted by other members of the person\u2019s culture or subculture (i.e., it is not an article of\nreligious faith). When a false belief involves a value judgment, it is regarded as a delusion\nonly when the judgment is so extreme as to defy credibility. Delusional conviction can\nsometimes be inferred from an overvalued idea (in which case the individual has an un-\nreasonable belief or idea but does not hold it as firmly as is the case with a delusion). De-\nlusions are subdivided according to thei r content. Common types are listed below:\nbizarre A delusion that involves a phenomenon that the person\u2019s culture would re-\ngard as physically impossible.\ndelusional jealousy A delusion that one\u2019s sexual partner is unfaithful.\nerotomanic A delusion that another person, usually of higher status, is in love with\nthe individual.\ngrandiose A delusion of inflated worth, power, knowledge, identity, or special re-\nlationship to a deity or famous person.\nmixed type Delusions of more than one type (e.g., EROTOMANIC , GRANDIOSE , PERSE -\nCUTORY , SOMATIC ) in which no one theme predominates.\nmood-congruent See MOOD -CONGRUENT PSYCHOTIC FEATURES .\nmood-incongruent See MOOD -INCONGRUENT PSYCHOTIC FEATURES .\nof being controlled A delusion in which feelings, impulses, thoughts, or actions\nare experienced as being under the control of some external force rather than be-\ning under one\u2019s own control.\nof reference A delusion in which events, objects, or other persons in one\u2019s immedi-", "source": "dsm5.pdf"} {"id": "01236d1cf0c4-2", "page_content": "of reference A delusion in which events, objects, or other persons in one\u2019s immedi-\nate environment are seen as having a particular and unusual significance. These\ndelusions are usually of a negative or pejo rative nature but also may be grandiose\nin content. A delusion of reference differs from an idea of reference, in which the\nfalse belief is not as firmly held nor as fully organized into a true belief.\npersecutory A delusion in which the central theme is that one (or someone to whom\none is close) is being attacked, harassed, cheated, persecuted, or conspired against.", "source": "dsm5.pdf"} {"id": "08f51418bddd-0", "page_content": "820 Glossary of Technical Terms\nsomatic A delusion whose main content pertains to the appearance or functioning\nof one\u2019s body.\nthought broadcasting A delusion that one\u2019s thoughts are being broadcast out loud\nso that they can be perceived by others.\nthought insertion A delusion that certain of one\u2019s thoughts are not one\u00b4s own, but\nrather are inserted into one\u2019s mind.\ndepersonalization The experience of feeling detached from, and as if one is an outside\nobserver of, one\u2019s mental processes, body, or actions (e.g., feeling like one is in a dream;\na sense of unreality of self, perceptual al terations; emotional and/or physical numbing;\ntemporal distortions; sense of unreality).\ndepressivity Feelings of being intensely sad, mise rable, and/or hopeless. Some patients\ndescribe an absence of feelings and/or dy sphoria; difficulty recovering from such\nmoods; pessimism about the fu ture; pervasive shame and/or guilt; feelings of inferior\nself-worth; and thoughts of suicide and suicid al behavior. Depressivity is a facet of the\nbroad personality trait domain D ETACHMENT .\nderealization The experience of feeling detached from, and as if one is an outside ob-\nserver of, one\u2019s surroundings (e.g., individuals or obje cts are experienced as unreal,\ndreamlike, foggy, lifeless, or visually distorted).\ndetachment Avoidance of socioemotional experience, including both WITHDRAWAL from\ninterpersonal interactions (rangi ng from casual, daily interactions to friendships and inti-\nmate relationships [i.e., INTIMACY AVOIDANCE ]) and RESTRICTED AFFECTIVITY , particularly\nlimited hedonic capacity. Detachment is one of the five pathological PERSONALITY TRAIT", "source": "dsm5.pdf"} {"id": "08f51418bddd-1", "page_content": "limited hedonic capacity. Detachment is one of the five pathological PERSONALITY TRAIT\nDOMAINS defined in Section III \u201cAlternative DSM-5 Model for Personality Disorders.\u201d\ndisinhibition Orientation toward immediate gratification, leading to impulsive behav-\nior driven by current thoughts, feelings, an d external stimuli, without regard for past\nlearning or consideration of future consequences. R IGID PERFECTIONISM , the opposite\npole of this domain, reflects excessive constraint of impu lses, risk avoidance, hyper-\nresponsibility, hyperperfectio nism, and rigid, rule-govern ed behavior. Disinhibition\nis one of the five pathological PERSONALITY TRAIT DOMAINS defined in Section III \u201cAl-\nternative DSM-5 Model for Personality Disorders.\u201d\ndisorder of sex development Condition of significant inborn somatic deviations of the\nreproductive tract from the norm and/or of discrepancies among the biological indica-\ntors of male and female.\ndisorientation Confusion about the time of day, date, or season (time); where one is\n(place); or who one is (person).\ndissociation The splitting off of clusters of ment al contents from conscious awareness.\nDissociation is a mechanism central to dissocia tive disorders. The term is also used to\ndescribe the separation of an idea from its emotional significance and affect, as seen in\nthe inappropriate affect in schizophrenia. Of ten a result of psychic trauma, dissociation\nmay allow the individual to maintain allegiance to two contradictory truths while re-\nmaining unconscious of the contradiction. An extreme manifestatio n of dissociation is\ndissociative identity disorder, in which a person may exhibit several independent per-\nsonalities, each unaware of the others.\ndistractibility Difficulty concentrating and focusing on tasks; attention is easily divert-", "source": "dsm5.pdf"} {"id": "08f51418bddd-2", "page_content": "distractibility Difficulty concentrating and focusing on tasks; attention is easily divert-\ned by extraneous stimuli; difficulty main taining goal-focused behavior, including both\nplanning and completing tasks. Distractibilit y is a facet of the broad personality trait\ndomain D ISINHIBITION .\ndysarthria A disorder of speech sound production due to structural or motor impair-\nment affecting the articulatory apparatus. Such disorders include cleft palate, muscle", "source": "dsm5.pdf"} {"id": "92b020383421-0", "page_content": "Glossary of Technical Terms 821\ndisorders, cranial nerve disorders, and cerebr al palsy affecting bulbar structures (i.e.,\nlower and upper motor neuron disorders).\ndyskinesia Distortion of voluntary movements with involuntary muscle activity.\ndysphoria (dysphoric mood) A condition in which a person experiences intense feelings\nof depression, discontent, and in some case s indifference to th e world around them.\ndyssomnias Primary disorders of sleep or wakefulness characterized by INSOMNIA or\nHYPERSOMNIA as the major presenting symptom. Dyssomnias are disorders of the\namount, quality, or timing of sleep. Compare with PARASOMNIAS .\ndysthymia Presence, while depressed, of two or more of the following: 1) poor appetite\nor overeating, 2) insomnia or hypersomnia, 3) low energy or fatigue, 4) low self-esteem,\n5) poor concentration or difficulty making decisions, or 6) feelings of hopelessness.\ndystonia Disordered tonicity of muscles.\neccentricity Odd, unusual, or bizarre behavior , appearance, and/or speech having\nstrange and unpredictable thoughts; saying un usual or inappropriate things. Eccentric-\nity is a facet of the broad personality trait domain P SYCHOTICISM . \necholalia The pathological, parrotlike, and apparently senseless repetition (echoing) of\na word or phrase just spoken by another person.\nechopraxia Mimicking the movements of another.\nemotional lability Instability of emotional experience s and mood; emotions that are\neasily aroused, intense, and/or out of proportion to events and circumstances. Emo-\ntional lability is a facet of the broad personality trait domain NEGATIVE AFFECTIVITY .", "source": "dsm5.pdf"} {"id": "92b020383421-1", "page_content": "empathy Comprehension and appreciation of othe rs\u2019 experiences and motivations; tol-\nerance of differing perspectives; understand ing the effects of own behavior on others.\nepisode (episodic) A specified duration of time during which the patient has developed or\nexperienced symptoms that meet the diagnostic criteria for a given mental disorder. De-\npending on the type of mental disorder, episode may denote a certain number of symptoms\nor a specified severity or frequency of symptoms. Episodes may be further differentiated\nas a single (first) episode or a recurrence or relapse of mult iple episodes if appropriate.\neuphoria A mental and emotional condition in wh ich a person experiences intense feel-\nings of well-being, elation, happiness, excitement, and joy.\nfatigability Tendency to become easily fatigued. See also FATIGUE .\nfatigue A state (also called exhaustion, tiredness, lethargy, languidness, languor, lassi-\ntude, and listlessness) usually associated with a weakening or depletion of one\u2019s phys-\nical and/or mental resources, ranging from a general state of lethargy to a specific,\nwork-induced burning sensation within one\u2019s muscles. Physical fatigue leads to an in-\nability to continue functioning at one\u2019s norm al level of activity. Although widespread\nin everyday life, this state usually becomes particularly noticeable during heavy exer-\ncise. Mental fatigue, by contrast, most often manifests as SOMNOLENCE (sleepiness).\nfear An emotional response to perceived imminent threat or danger associated with\nurges to flee or fight.\nflashback A dissociative state during which aspe cts of a traumatic event are reexperi-\nenced as though they were occurring at that moment.\nflight of ideas A nearly continuous flow of accele rated speech with abrupt changes", "source": "dsm5.pdf"} {"id": "92b020383421-2", "page_content": "flight of ideas A nearly continuous flow of accele rated speech with abrupt changes\nfrom topic to topic that are usually based on understandable associations, distracting\nstimuli, or plays on words. When the cond ition is severe, speech may be disorganized\nand incoherent.", "source": "dsm5.pdf"} {"id": "12755d040623-0", "page_content": "822 Glossary of Technical Terms\ngender The public (and usually legally recogniz ed) lived role as boy or girl, man or\nwoman. Biological factors are seen as contri buting in interaction with social and psy-\nchological factors to gender development.\ngender assignment The initial assignment as male or female, which usually occurs at\nbirth and is subseque ntly referred to as the \u201cnatal gender.\u201d\ngender dysphoria Distress that accompanies the incongruence between one\u2019s experi-\nenced and expressed gender and one\u2019s assigned or natal gender.\ngender experience The unique and personal ways in which individuals experience their\ngender in the context of the gender roles provided by their societies.\ngender expression The specific ways in which indivi duals enact gender roles provided\nin their societies.\ngender identity A category of social identity that refers to an individual\u2019s identification\nas male, female or, occasionally, some category other than male or female.\ngender reassignment A change of gender that can be either medical (hormones, sur-\ngery) or legal (government reco gnition), or both. In case of medical interventions, often\nreferred to as sex reassignment.\ngeometric hallucination See HALLUCINATION .\ngrandiosity Believing that one is superi or to others and deserves special treatment; self-\ncenteredness; feelings of entitlement; co ndescension toward others. Grandiosity is a\nfacet of the broad personality trait domain ANTAGONISM .\ngrimace (grimacing) Odd and inappropriate facial expressions unrelated to situation\n(as seen in individuals with CATATONIA ).\nhallucination A perception-like experience with the clarity and impact of a true percep-\ntion but without the external stimulation of the relevant sensory organ. Hallucinations\nshould be distinguished from ILLUSIONS , in which an actual external stimulus is", "source": "dsm5.pdf"} {"id": "12755d040623-1", "page_content": "should be distinguished from ILLUSIONS , in which an actual external stimulus is\nmisperceived or misinterpreted. The person may or may not have insight into the non-\nveridical nature of the hallucination. One hallucinating person may recognize the false\nsensory experience, whereas another may be convinced that the ex perience is grounded\nin reality. The term hallucination is not ordinarily applied to the false perceptions that\noccur during dreaming, while falling asleep ( hypnagogic ), or upon awakening ( hypno-\npompic ). Transient hallucinatory experiences may occur without a mental disorder.\nauditory A hallucination involving the perception of sound, most commonly of\nvoice.\ngeometric Visual hallucinations involving geometric shapes such as tunnels and\nfunnels, spirals, la ttices, or cobwebs.\ngustatory A hallucination involving the percepti on of taste (usually unpleasant).\nmood-congruent See MOOD -CONGRUENT PSYCHOTIC FEATURES .\nmood-incongruent See MOOD -INCONGRUENT PSYCHOTIC FEATURES .\nolfactory A hallucination involving the perception of odor, such as of burning rub-\nber or decaying fish.\nsomatic A hallucination involving the perception of physical experience localized\nwithin the body (e.g., a feeling of electric ity). A somatic hallucination is to be dis-\ntinguished from physical sensations arisin g from an as-yet-u ndiagnosed general\nmedical condition, from hypochondriacal preoccupation with normal physical\nsensations, or from a tactile hallucination.\ntactile A hallucination involving the perception of being touched or of something\nbeing under one\u2019s skin. The most common tactile hallucinations are the sensation", "source": "dsm5.pdf"} {"id": "48263ef526e8-0", "page_content": "Glossary of Technical Terms 823\nof electric shocks and formication (the sensation of somethin g creeping or crawl-\ning on or under the skin).\nvisual A hallucination involving sight, which may consist of formed images, such as of\npeople, or of unformed images, such as fl ashes of light. Visual hallucinations should\nbe distinguished from ILLUSIONS , which are misperceptions of real external stimuli.\nhostility Persistent or frequent angry feelings; anger or irri tability in response to minor\nslights and insults; mean, nasty, or vengeful behavior. Hostility is a facet of the broad\npersonality trait domain ANTAGONISM .\nhyperacusis Increased auditory perception.\nhyperorality A condition in which inappropriate objects are placed in the mouth.\nhypersexuality A stronger than usual urge to have sexual activity.\nhypersomnia Excessive sleepiness, as evidenced by prolonged nocturnal sleep, difficul-\nty maintaining an alert awake state during the day, or undesired daytime sleep epi-\nsodes. See also SOMNOLENCE .\nhypervigilance An enhanced state of sensory sensit ivity accompanied by an exaggerated\nintensity of behaviors whose purpose is to dete ct threats. Hypervigilance is also accompa-\nnied by a state of increased anxiety which can cause exhaustion. Other symptoms include\nabnormally increased arousal, a high responsiveness to stimuli, and a continual scanning\nof the environment for threats. In hypervigilan ce, there is a perpetual scanning of the envi-\nronment to search for sights, sounds, people, beha viors, smells, or anything else that is rem-\niniscent of threat or trauma. The individual is placed on high alert in order to be certain", "source": "dsm5.pdf"} {"id": "48263ef526e8-1", "page_content": "iniscent of threat or trauma. The individual is placed on high alert in order to be certain\ndanger is not near. Hypervigil ance can lead to a variety of obsessive behavior patterns, as\nwell as producing difficulties with social interaction and relationships.\nhypomania An abnormality of mood resembling mania but of lesser intensity. See also\nMANIA .\nhypopnea Episodes of overly shallow breathing or an abnormally low respiratory rate.\nideas of reference The feeling that causal incidents and external events have a particu-\nlar and unusual meaning that is specific to th e person. An idea of reference is to be dis-\ntinguished from a DELUSION OF REFERENCE , in which there is a belief that is held with\ndelusional conviction.\nidentity Experience of oneself as unique, with cl ear boundaries betwee n self and others;\nstability of self-esteem and accu racy of self-appraisal; capaci ty for, and ability to regu-\nlate, a range of emotional experience.\nillusion A misperception or misinterpr etation of a real external stimulus, such as hear-\ning the rustling of leaves as the sound of voices. See also HALLUCINATION .\nimpulsivity Acting on the spur of the moment in response to immediate stimuli; acting\non a momentary basis without a plan or consid eration of outcomes; difficulty establish-\ning and following plans; a sense of urgenc y and self-harming behavior under emotion-\nal distress. Impulsivity is a facet of the broad personality trait domain D ISINHIBITION .\nincoherence Speech or thinking that is essentially incomprehensible to others because\nword or phrases are joined together without a logical or meaningful connection. This\ndisturbance occurs within clauses, in contrast to dera ilment, in which the disturbance", "source": "dsm5.pdf"} {"id": "48263ef526e8-2", "page_content": "disturbance occurs within clauses, in contrast to dera ilment, in which the disturbance\nis between clauses. This has sometimes been refe rred to a \u201cword salad\u201d to convey the\ndegree of linguistic disorgan ization. Mildly ungrammatica l constructions or idiomatic\nusages characteristic of a particular region al or cultural backgrounds, lack of educa-\ntion, or low intelligence should not be co nsidered incoherence. The term is generally\nnot applied when there is evidence that the disturbance in speech is due to an aphasia.\ninsomnia A subjective complaint of difficulty falling or staying asleep or poor sleep quality.", "source": "dsm5.pdf"} {"id": "7e02b178b8fc-0", "page_content": "824 Glossary of Technical Terms\nintersex condition A condition in which individuals have conflicting or ambiguous bi-\nological indicators of sex.\nintimacy Depth and duration of connection with others; desire and capacity for close-\nness; mutuality of regard reflected in interpersonal behavior.\nintimacy avoidance Avoidance of close or romantic relationships, interpersonal attach-\nments, and intimate sexual relationships. Intimacy avoidance is a facet of the broad\npersonality trait domain D ETACHMENT .\nirresponsibility Disregard for\u2014and failure to honor\u2014 financial and other obligations or\ncommitments; lack of respect for\u2014and lack of follow-through on\u2014agreements and\npromises; carelessness with others\u2019 property. Irresponsibility is a facet of the broad per-\nsonality trait domain D ISINHIBITION .\nlanguage pragmatics The understanding and use of language in a given context. For\nexample, the warning \u201cWatch your hands\u201d when issued to a child who is dirty is in-\ntended not only to prompt the child to look at his or her hands bu t also to communicate\nthe admonition \u201cDon\u2019t get anything dirty.\u201d\nlethargy A state of decreased mental activity, characterized by sluggishness, drowsi-\nness, inactivity, and reduced alertness.\nmacropsia The visual perception that objects are larger than they actually are. Compare\nwith MICROPSIA .\nmagical thinking The erroneous belief that one\u2019s thoug hts, words, or actions will cause\nor prevent a specific outcome in some way that defies commonly understood laws of\ncause and effect. Magical thinking may be a part of normal child development.\nmania A mental state of elevated, expansive, or irritable mood and persistently in-\ncreased level of activity or energy. See also HYPOMANIA .", "source": "dsm5.pdf"} {"id": "7e02b178b8fc-1", "page_content": "creased level of activity or energy. See also HYPOMANIA .\nmanipulativeness Use of subterfuge to influence or control others; use of seduction,\ncharm, glibness, or in gratiation to achieve one\u2019s ends. Manipulativeness is a facet of the\nbroad personality trait domain ANTAGONISM .\nmannerism A peculiar and characteristic individual style of movement, action, thought,\nor speech.\nmelancholia (melancholic) A mental state characterized by very severe depression.\nmicropsia The visual perception that objects are smaller than they actually are. Com-\npare with MACROPSIA .\nmixed symptoms The specifier \u201cwith mixed features\u201d is applied to mood episodes during\nwhich subthreshold symptoms from the oppo sing pole are present. Whereas these con-\ncurrent \u201cmixed\u201d symptoms are relatively simultaneous, they may also occur closely\njuxtaposed in time as a waxing and waning of individual symptoms of the opposite\npole (i.e., depressive symptoms during hypo manic or manic episodes, and vice versa).\nmood A pervasive and sustained em otion that colors the perception of the world. Com-\nmon examples of mood include depression, el ation, anger, and anxiety. In contrast to\naffect, which refers to more fluctuating change s in emotional \u201cweather,\u201d mood refers to\na pervasive and sustained emotional \u201cclimate.\u201d Types of mood include\ndysphoric An unpleasant mood, such as sad ness, anxiety, or irritability.\nelevated An exaggerated feeling of well-being, or euphoria or elation. A person\nwith elevated mood may desc ribe feeling \u201chigh,\u201d \u201cecstati c,\u201d \u201con top of the world,\u201d\nor \u201cup in the clouds.\u201d", "source": "dsm5.pdf"} {"id": "7e02b178b8fc-2", "page_content": "or \u201cup in the clouds.\u201d\neuthymic Mood in the \u201cnormal\u201d range, which implies the absence of depressed or\nelevated mood.", "source": "dsm5.pdf"} {"id": "17c862ccc430-0", "page_content": "Glossary of Technical Terms 825\nexpansive Lack of restraint in expressing one\u2019s feelings, frequently with an over-\nvaluation of one\u2019s significance or importance.\nirritable Easily annoyed and provoked to anger.\nmood-congruent psychotic features Delusions or hallucinations whose content is en-\ntirely consistent with the typi cal themes of a depressed or manic mood. If the mood is\ndepressed, the content of the delusions or hallucinations would involve themes of per-\nsonal inadequacy, guilt, disease, death, ni hilism, or deserved punishment. The content\nof the delusion may include themes of persec ution if these are based on self-derogatory\nconcepts such as deserved puni shment. If the mood is manic, the content of the delusions\nor hallucinations would involve themes of in flated worth, power, knowledge, or iden-\ntity, or a special relationship to a deity or a famous person. The content of the delusion\nmay include themes of persecution if thes e are based on concepts such as inflated\nworth or deserved punishment.\nmood-incongruent psychotic features Delusions or hallucinations whose content is not\nconsistent with the typical themes of a depr essed or manic mood. In the case of depres-\nsion, the delusions or hallucinations would not involve themes of personal inadequacy,\nguilt, disease, death, nihilism, or deserved punishment. In the case of mania, the delu-\nsions or hallucinations would not involve themes of inflated worth, power, knowledge,\nor identity, or a special relationsh ip to a deity or a famous person.\nmultiple sleep latency test Polysomnographic assessment of the sleep-onset period,\nwith several short sleep-wake cycles assessed during a single session. The test repeat-", "source": "dsm5.pdf"} {"id": "17c862ccc430-1", "page_content": "with several short sleep-wake cycles assessed during a single session. The test repeat-\nedly measures the time to daytime sleep on set (\u201csleep latency\u201d) and occurrence of and\ntime to onset of the rapid eye movement sleep phase.\nmutism No, or very little, verbal response (in the absence of known aphasia).\nnarcolepsy Sleep disorder characterized by period s of extreme drowsi ness and frequent\ndaytime lapses into sleep (sleep attacks). Th ese must have been occurring at least three\ntimes per week over the last 3 mont hs (in the absence of treatment).\nnegative affectivity Frequent and intense experiences of high levels of a wide range of\nnegative emotions (e.g., anxiety, depressio n, guilt/shame, worry, anger), and their be-\nhavioral (e.g., self-harm) and interpersonal (e.g., depe ndency) manifestations. Nega-\ntive Affectivity is one of the five pathological PERSONALITY TRAIT DOMAINS defined in\nSection III \u201cAlternative DSM-5 Mo del for Personality Disorders.\u201d\nnegativism Opposition to suggestion or advice; be havior opposite to that appropriate to\na specific situation or against the wishes of others, including direct resistance to efforts\nto be moved.\nnight eating syndrome Recurrent episodes of night eating, as manifested by eating after\nawakening from sleep or ex cessive food consumption afte r the evening meal. There is\nawareness and recall of the eating. The night eating is not better accounted for by ex-\nternal influences such as changes in the in dividual\u2019s sleep-wake cycle or by local social\nnorms.\nnightmare disorder Repeated occurrences of extended, extremely dysphoric, and well-\nremembered dreams that usually involve effo rts to avoid threats to survival, security", "source": "dsm5.pdf"} {"id": "17c862ccc430-2", "page_content": "remembered dreams that usually involve effo rts to avoid threats to survival, security\nor physical integrity and that generally occu r during the second half of the major sleep\nepisode. On awakening from the dysphoric dreams, the individual rapidly becomes\noriented and alert.\nnonsubstance addiction(s) Behavioral disorder (also called behavioral addiction) not re-\nlated to any substance of abuse that shar es some features with substance-induced\naddiction.", "source": "dsm5.pdf"} {"id": "7ecb06d12681-0", "page_content": "826 Glossary of Technical Terms\nobsession Recurrent and persistent thoughts, urges, or images that are experienced, at\nsome time during the disturbance, as intru sive and unwanted and that in most individ-\nuals cause marked anxiety or distress. The individual attempts to ignore or suppress\nsuch thoughts, urges, or images, or to neutralize them with some other thought or ac-\ntion (i.e., by performing a compulsion).\novereating Eating too much food too quickly.\novervalued idea An unreasonable and sustained belief that is maintained with less than\ndelusional intensity (i.e., the person is able to acknowledge the possibility that the be-\nlief may not be true). The belief is not one th at is ordinarily accept ed by other members\nof the person\u2019s culture or subculture.\npanic attacks Discrete periods of sudden onset of in tense fear or terror, often associated\nwith feelings of impending doom. During these attacks there are symptoms such as\nshortness of breath or smothering sensations; palpitations, pounding heart, or acceler-\nated heart rate; chest pain or discomfort; choking; and fear of going crazy or losing con-\ntrol. Panic attacks may be unexpected, in wh ich the onset of the attack is not associated\nwith an obvious trigger and instead occurs \u201c out of the blue,\u201d or expected, in which the\npanic attack is associated with an obvious trigger, either internal or external.\nparanoid ideation Ideation, of less than delusional proportions, involving suspicious-\nness or the belief that one is being hara ssed, persecuted, or unfairly treated.\nparasomnias Disorders of sleep involv ing abnormal behaviors or physiological events\noccurring during sleep or sleep-wake transitions. Compare with DYSSOMNIAS .", "source": "dsm5.pdf"} {"id": "7ecb06d12681-1", "page_content": "occurring during sleep or sleep-wake transitions. Compare with DYSSOMNIAS .\nperseveration Persistence at tasks or in particular way of doing things long after the be-\nhavior has ceased to be functional or effe ctive; continuance of the same behavior de-\nspite repeated failures or clear reasons fo r stopping. Perseveration is a facet of the\nbroad personality trait domain N EGATIVE AFFECTIVITY .\npersonality Enduring patterns of perceiving, relating to, and thinking about the envi-\nronment and oneself. P ERSONALITY TRAITS are prominent aspects of personality that are\nexhibited in relatively consist ent ways across time and across situations. Personality\ntraits influence self and interpersonal func tioning. Depending on their severity, im-\npairments in personality functioning and personality trait expression may reflect the\npresence of a personality disorder.\npersonality disord er\u2014trait specified In Section III \u201cAlternative DSM-5 Model for Per-\nsonality Disorders,\u201d a proposed diagnostic category for use when a personality disor-\nder is considered present but the criteria for a specific disorder ar e not met. Personality\ndisorder\u2014trait specified (PD-TS) is defined by significant impairment in personality\nfunctioning, as measured by the Level of Personality Functioning Scale and one or\nmore pathological PERSONALITY TRAIT DOMAINS or PERSONALITY TRAIT FACETS . PD-TS is\nproposed in DSM-5 Section III for further st udy as a possible future replacement for\nother specified personality disorder and unspecified personality disorder.\npersonality functioning Cognitive models of self and othe rs that shape patterns of emo-\ntional and affiliative engagement.\npersonality trait A tendency to behave, feel, perceive , and think in relatively consistent\nways across time and across situations in which the trait may be manifest.", "source": "dsm5.pdf"} {"id": "7ecb06d12681-2", "page_content": "ways across time and across situations in which the trait may be manifest.\npersonality trait facets Specific personality components that make up the five broad per-\nsonality trait domains in the dimensional ta xonomy of Section II I \u201cAlternative DSM-5\nModel for Personality Disorders.\u201d For exampl e, the broad domain antagonism has the\nfollowing component facets: MANIPULATIVENESS , DECEITFULNESS , GRANDIOSITY , ATTEN -\nTION SEEKING , CALLOUSNESS , and HOSTILITY .", "source": "dsm5.pdf"} {"id": "5ed78924e721-0", "page_content": "Glossary of Technical Terms 827\npersonality trait domains In the dimensional taxonomy of Section III \u201cAlternative DSM-\n5 Model for Personality Disorders,\u201d personalit y traits are organized into five broad do-\nmains: N EGATIVE AFFECTIVITY , DETACHMENT , ANTAGONISM , DISINHIBITION , and P SY-\nCHOTICISM . Within these five broad trait domains are 25 specific personality trait facets\n(e.g., IMPULSIVITY , RIGID PERFECTIONISM ).\nphobia A persistent fear of a specific object, ac tivity, or situation (i.e., the phobic stimu-\nlus) out of proportion to the actual danger posed by the specific object or situation that\nresults in a compelling desire to avoid it. If it cannot be avoided, the phobic stimulus is\nendured with marked distress.\npica Persistent eating of nonnutritive nonfood substances over a period of at least 1 month.\nThe eating of nonnutritive nonfood substances is inapprop riate to the developmental\nlevel of the individual (a minimum age of 2 years is suggested fo r diagnosis). The eat-\ning behavior is not part of a culturally supported or socially normative practice.\npolysomnography Polysomnography (PSG), also known as a sleep study, is a multipa-\nrametric test used in the study of sleep and as a diagnostic tool in sleep medicine. The\ntest result is called a polysomnogram, also abbreviated PSG. PSG monitors many body\nfunctions, including brain (electroencepha lography), eye movements (electro-oculog-\nraphy), muscle activity or skeletal muscle activation (electromyography), and heart\nrhythm (electrocardiography).", "source": "dsm5.pdf"} {"id": "5ed78924e721-1", "page_content": "rhythm (electrocardiography).\nposturing Spontaneous and active maintenance of a posture against gravity (as seen in\nCATATONIA ). Abnormal posturing may also be a si gn of certain injuries to the brain or\nspinal cord, including the following:\ndecerebrate posture The arms and legs are out straight and rigid, the toes point\ndownward, and the head is arched backward.\ndecorticate posture The body is rigid, the arms are stiff and bent, the fists are tight,\nand the legs are straight out.\nopisthotonus The back is rigid and arching, and the head is thrown backward.\nAn affected person may alternate between different postures as the condition changes.\npressured speech Speech that is increased in amount, a ccelerated, and difficult or impossi-\nble to interrupt. Usually it is also loud an d emphatic. Frequently th e person talks without\nany social stimulation and may continue to talk even though no one is listening.\nprodrome An early or premonitory sign or symptom of a disorder.\npseudocyesis A false belief of being pregnant that is associated with objective signs and\nreported symptoms of pregnancy.\npsychological distress A range of symptoms and experien ces of a person\u2019s internal life\nthat are commonly held to be troubling, confusing, or out of the ordinary.\npsychometric measures Standardized instruments such as scales, questionnaires, tests,\nand assessments that are designed to measu re human knowledge, abilities, attitudes,\nor personality traits.\npsychomotor agitation Excessive motor activity associated with a feeling of inner tension.\nThe activity is usually nonproductive and repetitious and consists of behaviors such as pac-\ning, fidgeting, wringing of the hands, pu lling of clothes, and inability to sit still.", "source": "dsm5.pdf"} {"id": "5ed78924e721-2", "page_content": "psychomotor retardation Visible generalized slowing of movements and speech.\npsychotic features Features characterized by delusions, hallucinations, and formal thought\ndisorder.\npsychoticism Exhibiting a wide range of culturally incongruent odd, eccentric, or un-\nusual behaviors and cognitions, including both process (e.g., perception, dissociation)", "source": "dsm5.pdf"} {"id": "d2397cef8140-0", "page_content": "828 Glossary of Technical Terms\nand content (e.g., beliefs). Psychoticism is one of the five broad PERSONALITY TRAIT DO-\nMAINS defined in Section III \u201cAlternative DSM-5 Model for Pers onality Disorders.\u201d\npurging disorder Eating disorder characterized by re current purging behavior to influ-\nence weight or shape, such as self-induced vomiting, misuse of laxatives, diuretics, or\nother medications, in the absence of binge eating.\nracing thoughts A state in which the mind uncontrollably brings up random thoughts\nand memories and switches between them ve ry quickly. Sometimes the thoughts are\nrelated, with one thought leading to anothe r; other times they are completely random.\nA person experiencing an episode of racing thoughts has no cont rol over them and is\nunable to focus on a single topic or to sleep.\nrapid cycling Term referring to bipolar disorder char acterized by the presence of at least\nfour mood episodes in the previous 12 months that meet the criteria for a manic, hypo-\nmanic, or major depressive episode. Episodes are demarcated either by partial or full\nremissions of at least 2 months or by a sw itch to an episode of the opposite polarity\n(e.g., major depressive episode to manic epis ode). The rapid cycling specifier can be ap-\nplied to bipolar I or bipolar II disorder.\nrapid eye movement (REM) A behavioral sign of the phase of sleep during which the\nsleeper is likely to be experiencing dreamlike mental activity.\nrepetitive speech Morphologically heterogeneous iterations of speech.\nresidual phase Period after an episode of schizophren ia that has partly or completed re-\nmitted but in which some symptoms may remain, and symptoms such as listlessness,\nproblems with concentrating, and withdrawal from social activities may predominate.", "source": "dsm5.pdf"} {"id": "d2397cef8140-1", "page_content": "problems with concentrating, and withdrawal from social activities may predominate.\nrestless legs syndrome An urge to move the legs, usually accompanied or caused by\nuncomfortable and unpleasant sensations in the legs (for pediatric restless legs syn-\ndrome, the description of these symptoms should be in the child\u2019s own words). The\nsymptoms begin or worsen during periods of rest or inactivity. Symptoms are partially\nor totally relieved by movement. Symptoms are worse in the evening or at night than\nduring the day or occur only in the night/evening.\nrestricted affectivity Little reaction to emotionally arousing situations; constricted\nemotional experience and expression; indiffer ence and aloofness in normatively engaging\nsituations. Restricted affectivity is a facet of the broad personality trait domain D ETACH -\nMENT .\nrigid perfectionism Rigid insistence on everything being flawless, perfect, and without\nerrors or faults, including one\u2019s own and ot hers\u2019 performance; sacrificing of timeliness\nto ensure correctness in every detail; believi ng that there is only one right way to do\nthings; difficulty changing ideas and/or viewpoint; preo ccupation with details, orga-\nnization, and order. Lack of rigid perfection ism is a facet of the broad personality trait\ndomain D ISINHIBITION .\nrisk taking Engagement in dangerous, risky, and po tentially self-damaging activities, un-\nnecessarily and without regard to consequences; lack of concern for one\u2019s limitations and\ndenial of the reality of personal danger; reck less pursuit of goals regardless of the level of\nrisk involved. Risk taking is a facet of the broad personality trait domain D ISINHIBITION .\nrumination (rumination disorders) Repeated regurgitation of food over a period of at", "source": "dsm5.pdf"} {"id": "d2397cef8140-2", "page_content": "rumination (rumination disorders) Repeated regurgitation of food over a period of at\nleast 1 month. Regurgitated food may be re-chewed, re-s wallowed, or spit out. In\nrumination disorders, there is no evidence that an associated gastrointestinal or an-\nother medical condition (e.g., gastroesophage al reflux) is sufficient to account for the\nrepeated regurgitation.", "source": "dsm5.pdf"} {"id": "db1c997ff1b3-0", "page_content": "Glossary of Technical Terms 829\nseasonal pattern A pattern of the occurrence of a sp ecific mental disorder in selected\nseasons of the year.\nself-directedness, self-direction Pursuit of coherent and meaningful short-term and life\ngoals; utilization of constructive and prosocial internal standards of behavior; ability to\nself-reflect productively.\nseparation insecurity Fears of being alone due to rejection by and/or separation from\nsignificant others, based in a lack of confidence in one\u2019s ability to care for oneself, both\nphysically and emotionally. Separation insecu rity is a facet of the broad personality\ntrait domain N EGATIVE AFFECTIVITY . \nsex Biological indication of male and female (understood in the context of reproductive\ncapacity), such as sex chromosomes, gona ds, sex hormones, and nonambiguous inter-\nnal and external genitalia.\nsign An objective manifestation of a pathological condition. Signs are observed by the\nexaminer rather than reported by th e affected individual. Compare with SYMPTOM .\nsleep-onset REM Occurrence of the rapid eye movement (REM) phase of sleep within\nminutes after falling asleep. Usually assessed by a polysomnographic MULTIPLE SLEEP\nLATENCY TEST .\nsleep terrors Recurrent episodes of abrupt terror ar ousals from sleep, usually occurring\nduring the first third of the major sleep episode and beginning with a panicky scream.\nThere is intense fear and signs of autonomi c arousal, such as mydriasis, tachycardia,\nrapid breathing, and sweating, during each episode.\nsleepwalking Repeated episodes of rising from bed during sleep and walking about,\nusually occurring during the first third of the major sleep episode. While sleepwalking,\nthe person has a blank, staring face, is relati vely unresponsive to the efforts of others to", "source": "dsm5.pdf"} {"id": "db1c997ff1b3-1", "page_content": "communicate with him or her, and can be awakened only with great difficulty.\nsomnolence (or \u201cdrowsiness\u201d) A state of near-sleep, a strong desire for sleep, or sleep-\ning for unusually long periods. It has two di stinct meanings, referring both to the usual\nstate preceding falling asleep and to the chro nic condition that involves being in that\nstate independent of a circadian rhythm. Compare with HYPERSOMNIA .\nspecific food cravings Irresistible desire for sp ecial types of food.\nstartle response (or \u201cstartle reaction\u201d) An involuntary (reflexive) reaction to a sudden\nunexpected stimulus, such as a loud noise or sharp movement.\nstereotypies, stereotyped behaviors/movements Repetitive, abnorma lly frequent, non-\ngoal-directed movements, seemingly driven , and nonfunctional motor behavior (e.g.,\nhand shaking or waving, body rock ing, head banging, self-biting).\nstress The pattern of specific and nonspecifi c responses a person makes to stimulus\nevents that disturb his or he r equilibrium and tax or exceed his or her ability to cope.\nstressor Any emotional, physical, social, economic, or other factor that disrupts the nor-\nmal physiological, cognitive, emotional, or behavioral balance of an individual.\nstressor, psychological Any life event or life change that may be associated temporally\n(and perhaps causally) with the onset, occurr ence, or exacerbation of a mental disorder.\nstupor Lack of psychomotor activity , which may range from not actively relating to the\nenvironment to complete immobility.\nsubmissiveness Adaptation of one\u2019s behavior to the actual or perceived interests and\ndesires of others even when doing so is antithetical to one\u2019s own interests, needs, or", "source": "dsm5.pdf"} {"id": "db1c997ff1b3-2", "page_content": "desires. Submissiveness is a facet of the broad personality trait domain N EGATIVE AF-\nFECTIVITY .", "source": "dsm5.pdf"} {"id": "9573097d7501-0", "page_content": "830 Glossary of Technical Terms\nsubsyndromal Below a specified level or threshold required to qualif y for a particular\ncondition. Subsyndromal conditions ( formes frustes) are medical condit ions that do not\nmeet full criteria for a diag nosis\u2014for example, because the symptoms are fewer or less\nsevere than a defined syndrome\u2014but that nevertheless can be identified and related to\nthe \u201cfull-blown\u201d syndrome.\nsuicidal ideas (suicidal ideation) Thoughts about self-harm, with deliberate consider-\nation or planning of possible techniques of causing one\u2019s own death.\nsuicide The act of intentionally causing one\u2019s own death.\nsuicide attempt An attempt to end one\u2019s own life, which may lead to one\u2019s death.\nsuspiciousness Expectations of\u2014and sensitivity to\u2014 signs of interpersonal ill intent or\nharm; doubts about loyalty and fidelity of ot hers; feelings of being mistreated, used,\nand/or persecuted by others. Suspiciousness is a facet of the broad personality trait do-\nmain D ETACHMENT .\nsymptom A subjective manifestation of a pathological condition. Symptoms are reported\nby the affected individual rather than observed by the examiner. Compare with SIGN .\nsyndrome A grouping of signs and symptoms, ba sed on their frequent co-occurrence\nthat may suggest a common underlying pathog enesis, course, familia l pattern, or treat-\nment selection.\nsynesthesias A condition in which stimulation of one sensory or cognitive pathway\nleads to automatic, involunt ary experiences in a second sensory or cognitive pathway.\ntemper outburst An emotional outburst (also calle d a \u201ctantrum\u201d), usually associated\nwith children or those in emotional distress, and typically characterized by stubborn-\nness, crying, screaming, defiance, angry rant ing, a resistance to attempts at pacifica-", "source": "dsm5.pdf"} {"id": "9573097d7501-1", "page_content": "tion, and in some cases hitting. Physical co ntrol may be lost, the person may be unable\nto remain still, and even if the \u201cgoal\u201d of th e person is met, he or she may not be calmed.\nthought-action fusion The tendency to treat thoughts and actions as equivalent.\ntic An involuntary, sudden, ra pid, recurrent, nonrhythmic motor movement or vocal-\nization.\ntolerance A situation that occurs with continued use of a drug in which an individual\nrequires greater dosages to achieve the same effect.\ntransgender The broad spectrum of individuals wh o transiently or permanently identify\nwith a gender different from their natal gender.\ntranssexual An individual who seeks, or has undergone, a social transition from male to\nfemale or female to male, which in many, but not all cases may also involve a somatic\ntransition by cross- sex hormone treatment and geni tal surgery (\u201csex reassignment\nsurgery\u201d).\ntraumatic stressor Any event (or events) that may cause or threaten death, serious injury,\nor sexual violence to an individual, a close family member, or a close friend.\nunusual beliefs and experiences Belief that one has unusual abilities, such as mind\nreading, telekinesis, or THOUGHT -ACTION FUSION ; unusual experiences of reality, in-\ncluding hallucinatory experiences. In genera l, the unusual beliefs are not held at the\nsame level of conviction as DELUSIONS . Unusual beliefs and experiences are a facet of\nthe personality trait domain P SYCHOTICISM .\nwaxy flexibility Slight, even resistance to positio ning by examiner. Compare with CAT-\nALEPSY .", "source": "dsm5.pdf"} {"id": "d715ede1404c-0", "page_content": "Glossary of Technical Terms 831\nwithdrawal, social Preference for being alone to being with others; reticence in social\nsituations; AVOIDANCE of social contacts and activity; lack of initiation of social contact.\nSocial withdrawal is a facet of th e broad personality trait domain D ETACHMENT .\nworry Unpleasant or uncomfortable thoughts th at cannot be consci ously controlled by\ntrying to turn the attention to other subjects. The worrying is often persistent, repeti-\ntive, and out of proportion to the topic worr ied about (it can even be about a triviality).", "source": "dsm5.pdf"} {"id": "12b55f78bb37-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "229023333520-0", "page_content": "833 Glossary of Cultural\nConcepts of Distress\nAtaque de nervios\nAtaque de nervios (\u201cattack of nerves\u201d) is a syndrome among individuals of Latino descent,\ncharacterized by symptoms of intense emotio nal upset, including acut e anxiety, anger, or\ngrief; screaming and shouting uncontrollably; a ttacks of crying; tremblin g; heat in the chest\nrising into the head; and becomi ng verbally and physically ag gressive. Dissociative experi-\nences (e.g., depersonalization, derealization, am nesia), seizure-like or fainting episodes, and\nsuicidal gestures are prominent in some ataques but absent in others. A general feature of an\nataque de nervios is a sense of being out of control. Attacks frequently occur as a direct result\nof a stressful event relating to the family, such as news of the death of a close relative, con-\nflicts with a spouse or childr en, or witnessing an accident involving a family member. For a\nminority of individuals, no partic ular social event triggers their ataques; instead, their vul-\nnerability to losing control comes from the accumulated experience of suffering.\nNo one-to-one relationship has been found between ataque and any specific psychiatric dis-\norder, although several disorders, including pani c disorder, other specif ied or unspecified dis-\nsociative disorder, and conversion diso rder, have symptomatic overlap with ataque .\nIn community samples, ataque is associated with suicidal ideation, disability, and out-\npatient psychiatric utilization, after adjustment for psychiatric diagnoses, traumatic expo-\nsure, and other covariates. However, some ataques represent normative expressions of", "source": "dsm5.pdf"} {"id": "229023333520-1", "page_content": "sure, and other covariates. However, some ataques represent normative expressions of\nacute distress (e.g., at a funeral) without clinical sequelae. The term ataque de nervios may\nalso refer to an idiom of distress that includ es any \u201cfit\u201d-like paroxysm of emotionality (e.g.,\nhysterical laughing) and may be used to indica te an episode of loss of control in response\nto an intense stressor.\nRelated conditions in other cultural contexts: Indisposition in Haiti, blacking out in\nthe Southern United States, and falling out in the West Indies.\nRelated conditions in DSM-5: Panic attack, panic disorder, other specified or unspec-\nified dissociative disorder, co nversion (functional neurologic symptom) disorder, inter-\nmittent explosive disorder, other specified or unspecified anxiety disorder, other specified\nor unspecified trauma and stressor-related disorder.\nDhat syndrome\nDhat syndrome is a term that was coined in South Asia little more than half a century ago to\naccount for common clinical presentations of young male patients who attributed their\nvarious symptoms to semen loss. Despite the name, it is not a discrete syndrome but rather\na cultural explanation of distress for patients who refer to diverse symptoms, such as anx-\niety, fatigue, weakness, weight loss, impotence, other multiple somatic complaints, and\ndepressive mood. The cardinal feature is an xiety and distress about the loss of dhat in the\nabsence of any identifiable physiological dysfunction. Dhat was identified by patients as\na white discharge that was noted on defecation or urination. Ideas about this substance\nare related to the concept of dhatu (semen) described in the Hindu system of medicine,\nAyurveda, as one of seven essential bodily fluids whose balance is necessary to maintain", "source": "dsm5.pdf"} {"id": "229023333520-2", "page_content": "Ayurveda, as one of seven essential bodily fluids whose balance is necessary to maintain\nhealth.", "source": "dsm5.pdf"} {"id": "1fc7a6e883fd-0", "page_content": "834 Glossary of Cultural Concepts of Distress\nAlthough dhat syndrome was formulated as a cultural guide to local clinical practice, related\nideas about the harmful effects of semen loss have been shown to be widespread in the general\npopulation, suggesting a cultural disposition for explaining health problems and symptoms\nwith reference to dhat syndrome. Research in health care settings has yielded diverse estimates\nof the syndrome\u2019s prevalence (e .g., 64% of men attending psychiatric clinics in India for sexual\ncomplaints; 30% of men attending general medical clinics in Pakistan). Although dhat syndrome\nis most commonly identified with young men from lower socioeconomic backgrounds, mid-\ndle-aged men may also be affe cted. Comparable concerns about white vaginal discharge (leu-\nkorrhea) have been associated with a variant of the concept for women.\nRelated conditions in other cultural contexts: koro in Southeast Asia, particularly Sin-\ngapore and shen-k\u2019uei (\u201ckidney deficiency\u201d) in China.\nRelated conditions in DSM-5: Major depressive disorder, persistent depressive disor-\nder (dysthymia), generalized anxiety disorder, somatic symptom disorder, illness anxiety\ndisorder, erectile disorder, early (premature) ejaculation, other specified or unspecified\nsexual dysfunction, academic problem.\nKhy\u00e2l cap\n\u201cKhy\u00e2l attacks\u201d ( khy\u00e2l cap ), or \u201cwind attacks,\u201d is a synd rome found among Cambodians in\nthe United States and Cambodia. Common symptoms include those of panic attacks, such\nas dizziness, palpitations, shortness of breath, and cold extremities, as well as other symp-\ntoms of anxiety and auto nomic arousal (e.g., tinnitus and neck soreness). Khy\u00e2l attacks in-", "source": "dsm5.pdf"} {"id": "1fc7a6e883fd-1", "page_content": "clude catastrophic cognitions centered on the concern that khy\u00e2l (a windlike substance)\nmay rise in the body\u2014along wi th blood\u2014and cause a range of serious effects (e.g., com-\npressing the lungs to cause shortness of breath and asphyxia; entering the cranium to\ncause tinnitus, dizziness, blurry vision, and a fatal syncope). Khy\u00e2l attacks may occur with-\nout warning, but are frequently brought abou t by triggers such as worrisome thoughts,\nstanding up (i.e., orthostasis), specific odor s with negative associations, and agoraphobic-\ntype cues like going to crowded spaces or riding in a car. Khy\u00e2l attacks usually meet panic\nattack criteria and may shape the experience of other anxiety and trauma- and stressor-\nrelated disorders. Khy\u00e2l attacks may be associated with considerable disability.\nRelated conditions in other cultural contexts: Laos ( pen lom), Tibet ( srog rlung gi nad ),\nSri Lanka ( vata), and Korea (hwa byung ).\nRelated conditions in DSM-5: Panic attack, panic disorder, generalized anxiety disor-\nder, agoraphobia, posttraumatic stre ss disorder, illness anxiety disorder.\nKufungisisa\nKufungisisa (\u201cthinking too much\u201d in Shona) is an id iom of distress and a cultural explana-\ntion among the Shona of Zimbabwe . As an explanation, it is considered to be causative of\nanxiety, depression, and somatic problems (e .g., \u201cmy heart is painful because I think too\nmuch\u201d). As an idiom of psychosocial distress, it is indicative of interpersonal and social\ndifficulties (e.g., marital problems, having no money to take care of children). Kufungisisa", "source": "dsm5.pdf"} {"id": "1fc7a6e883fd-2", "page_content": "involves ruminating on upsettin g thoughts, particularly worries.\nKufungisisa is associated with a range of psychopathology, including anxiety symp-\ntoms, excessive worry, panic atta cks, depressive symptoms, and ir ritability. In a study of a\nrandom community sample, two-thirds of the cases identified by a general psychopathol-\nogy measure were of this complaint.\nIn many cultures, \u201cthinking too much\u201d is considered to be damaging to the mind and\nbody and to cause specific symptoms like headache and dizziness. \u201cThinking too much\u201d\nmay also be a key component of cultural syndromes such as \u201cbrain fag\u201d in Nigeria. In the\ncase of brain fag, \u201cthinking too much\u201d is primarily attributed to excessive study, which is", "source": "dsm5.pdf"} {"id": "2ae6e6debabf-0", "page_content": "may also be a key component of cultural syndromes such as \u201cbrain fag\u201d in Nigeria. In the\ncase of brain fag, \u201cthinking too much\u201d is primarily attributed to excessive study, which is\nconsidered to damage the brain in particular, with symptoms including feelings of heat or\ncrawling sensations in the head.", "source": "dsm5.pdf"} {"id": "6ae14c6ac281-0", "page_content": "Glossary of Cultural Concepts of Distress 835\nRelated conditions in other cultural contexts: \u201cThinking too much \u201d is a common id-\niom of distress and cultural explanation acro ss many countries and ethnic groups. It has\nbeen described in Africa, th e Caribbean and Latin America, and among East Asian and\nNative American groups.\nRelated conditions in DSM-5: Major depressive disorder, pe rsistent depressive disorder\n(dysthymia), generalized anxiety disorder, pos ttraumatic stress disorder, obsessive-compul-\nsive disorder, persistent complex bereavement disorder (see \u201cConditions for Further Study\u201d).\nMaladi moun\nMaladi moun (literally \u201chumanly caused illness,\u201d also referred to as \u201csent sickness\u201d) is a\ncultural explanation in Haitian communitie s for diverse medical and psychiatric disor-\nders. In this explanatory mode l, interpersonal envy and malice cause people to harm their\nenemies by sending illnesses such as psychosis, depression, social or academic failure, and\ninability to perform activities of daily living. The etiological model assumes that illness\nmay be caused by others\u2019 envy and hatred, pr ovoked by the victim\u2019s economic success as\nevidenced by a new job or expensive purchase . One person\u2019s gain is assumed to produce\nanother person\u2019s loss, so visible success make s one vulnerable to attack. Assigning the la-\nbel of sent sickness depends on mode of on set and social status more than presenting\nsymptoms. The acute onset of new symptoms or an abrupt behavioral change raises sus-\npicions of a spiritual attack. Someone who is at tractive, intelligent, or wealthy is perceived\nas especially vulnerable, and even young healthy children are at risk.\nRelated conditions in other cultural contexts: Concerns about illness (typically, phys-", "source": "dsm5.pdf"} {"id": "6ae14c6ac281-1", "page_content": "Related conditions in other cultural contexts: Concerns about illness (typically, phys-\nical illness) caused by envy or social co nflict are common across cultures and often ex-\npressed in the form of \u201cevil eye\u201d (e.g. in Spanish, mal de ojo, in Italian, mal\u2019occhiu).\nRelated conditions in DSM-5: Delusional disorder, persecutory type; schizophrenia\nwith paranoid features.\nNervios\nNervios (\u201cnerves\u201d) is a common idiom of distress among Latinos in the United States and\nLatin America. Nervios refers to a general state of vulne rability to stressful life experiences\nand to difficult life circumstances. The term nervios includes a wide range of symptoms of\nemotional distress, somatic disturbance, an d inability to function. The most common\nsymptoms attributed to nervios include headaches and \u201cbrain aches\u201d (occipital neck ten-\nsion), irritability, stomach disturbances, slee p difficulties, nervousness, easy tearfulness,\ninability to concentrat e, trembling, tingling sensations, and mareos (dizziness with occa-\nsional vertigo-like exacerbations). Nervios is a broad idiom of distress that spans the range\nof severity from cases with no mental diso rder to presentations resembling adjustment,\nanxiety, depressive, dissociative, somatic symptom, or psychotic disorders. \u201cBeing ner-\nvous since childhood\u201d appears to be more of a trait and may precede social anxiety disor-\nder, while \u201cbeing ill with nerves\u201d is more related than other forms of nervios to psychiatric\nproblems, especially dissociation and depression.\nRelated conditions in other cultural contexts: Nevra among Greeks in North America,", "source": "dsm5.pdf"} {"id": "6ae14c6ac281-2", "page_content": "Related conditions in other cultural contexts: Nevra among Greeks in North America,\nnierbi among Sicilians in North America, and nerves among whites in Appalachia and\nNewfoundland.\nRelated conditions in DSM-5: Major depressive disorder, peristent depressive disor-\nder (dysthymia), generalized anxiety disorder, social anxiety disorder, other specified or\nunspecified dissociative disorder, soma tic symptom disorder, schizophrenia.\nShenjing shuairuo\nShenjing shuairuo (\u201cweakness of the nervous system\u201d in Mandarin Chines e) is a cultural\nsyndrome that integrates conceptual categori es of traditional Chinese medicine with the", "source": "dsm5.pdf"} {"id": "27d1f35400f9-0", "page_content": "836 Glossary of Cultural Concepts of Distress\nWestern diagnosis of neurasthenia. In the second, revised edition of the Chinese Classifica-\ntion of Mental Disorders (CCMD-2-R), shenjing shuairuo is defined as a syndrome composed\nof three out of five nonhierarchical symptom clusters: weak ness (e.g., mental fatigue),\nemotions (e.g., feeling vexed), excitement (e.g., increased recollections), nervous pain (e.g.,\nheadache), and sleep (e.g., insomnia). Fan nao (feeling vexed) is a form of irritability mixed\nwith worry and distress over conflicting thoug hts and unfulfilled desires. The third edi-\ntion of the CCMD retains shenjing shuairuo as a somatoform diagno sis of exclusion. Salient\nprecipitants of shenjing shuairuo include work- or family-rel ated stressors, loss of face\n(mianzi, lianzi ), and an acute sense of failure (e.g., in academic performance). Shenjing sh-\nuairuo is related to traditional concepts of weakness ( xu) and health imbalances related to\ndeficiencies of a vital essence (e.g., the depletion of qi [vital energy] following overstrain-\ning or stagnation of qi due to excessive worry). In the traditional interpretation, shenjing\nshuairuo results when bodily channels ( jing) conveying vital forces ( shen) become dysreg-\nulated as a result of various social and interpersonal stressors, such as the inability to\nchange a chronically frustrating and distressi ng situation. Various psychiatric disorders\nare associated with shenjing shuairuo, notably mood, anxiety, and somatic symptom disor-", "source": "dsm5.pdf"} {"id": "27d1f35400f9-1", "page_content": "ders. In medical clinics in China, however, up to 45% of patients with shenjing shuairuo do\nnot meet criteria for any DSM-IV disorder.\nRelated conditions in ot her cultural contexts: Neurasthenia-spectrum idioms and\nsyndromes are present in India ( ashaktapanna ) and Japan ( shinkei-suijaku ), among other set-\ntings. Other conditions, such as brain fag syndrome, burnout syndrome, and chronic fa-\ntigue syndrome, are also closely related.\nRelated conditions in DSM-5: Major depressive disorder, persistent depressive disor-\nder (dysthymia), generalized anxiety disorder, somatic symp tom disorder, social anxiety\ndisorder, specific phobia, po sttraumatic stress disorder.\nSusto\nSusto (\u201cfright\u201d) is a cultural explanation fo r distress and misfortune prevalent among\nsome Latinos in the United States and amon g people in Mexico, Central America, and\nSouth America. It is no t recognized as an illness catego ry among Latinos from the Carib-\nbean. Susto is an illness attributed to a frightenin g event that causes the soul to leave the\nbody and results in unhappiness and sickness, as well as difficulties functioning in key\nsocial roles. Symptoms may appear any time from days to years after the fright is experi-\nenced. In extreme cases, susto may result in death. There are no specific defining symp-\ntoms for susto; however, symptoms that are often reported by people with susto include\nappetite disturbances, inadequa te or excessive sleep, troubled sleep or dreams, feelings of\nsadness, low self-worth or dirtiness, interperso nal sensitivity, and lack of motivation to do", "source": "dsm5.pdf"} {"id": "27d1f35400f9-2", "page_content": "anything. Somatic symptoms accompanying susto may include muscle aches and pains,\ncold in the extremities, pallo r, headache, stomachache, and diarrhea. Precipitating events\nare diverse, and include natural phenomena, an imals, interpersonal situations, and super-\nnatural agents, among others.\nThree syndromic types of susto (referred to as cibih in the local Zapotec language) have\nbeen identified, each ha ving different relationships with psychiatric diagnoses. An interper-\nsonal susto characterized by feelings of loss, aban donment, and not being loved by family,\nwith accompanying symptoms of sadness, poor self-image, and suicidal ideation, seemed to\nbe closely related to major depressive disorder. When susto resulted from a traumatic event\nthat played a major role in shaping symptoms and in emotional processing of the experience,", "source": "dsm5.pdf"} {"id": "089cef73826b-0", "page_content": "be closely related to major depressive disorder. When susto resulted from a traumatic event\nthat played a major role in shaping symptoms and in emotional processing of the experience,\nthe diagnosis of posttrauma tic stress disorder appe ared more appropriate. Susto character-\nized by various recurrent somatic symptoms\u2014for which the person sought health care from\nseveral practitioners\u2014was thought to resemble a somatic symptom disorder.\nRelated conditions in other cultural contexts: Similar etiological concepts and symp-\ntom configurations are found globally. In the Andean region, susto is referred to as espanto .", "source": "dsm5.pdf"} {"id": "04aa3810a7d0-0", "page_content": "Glossary of Cultural Concepts of Distress 837\nRelated conditions in DSM-5: Major depressive disorder, posttraumatic stress disor-\nder, other specified or unspecified trauma and stressor-related di sorder, somatic symp-\ntom disorders.\nTaijin kyofusho\nTaijin kyofusho (\u201cinterpersonal fear disorder\u201d in Japa nese) is a cultural syndrome charac-\nterized by anxiety about and av oidance of interpersonal situations due to the thought, feel-\ning, or conviction that one\u2019s appearance and actions in social interactions are inadequate\nor offensive to others. In the United States, the variant involves having an offensive body\nodor and is termed olfactory reference syndrome. Individuals with taijin kyofusho tend to focus\non the impact of their symptoms and behavior s on others. Variants include major concerns\nabout facial blushing (erythrophobia), having an offensive body odor (olfactory reference\nsyndrome), inappropriate gaze (too much or too little eye co ntact), stiff or awkward facial\nexpression or bodily moveme nts (e.g., stiffening, trem bling), or body deformity.\nTaijin kyofusho is a broader construct than social an xiety disorder in DSM-5. In addition\nto performance anxiety, taijin kyofusho includes two culture-relate d forms: a \u201csensitive type,\u201d\nwith extreme social sensitivity and anxiety about interpersonal inte ractions, and an \u201cof-\nfensive type,\u201d in which the major concer n is offending others. As a category, taijin kyofusho\nthus includes syndromes with features of body dysmorphic disorder as well as delusional\ndisorder. Concerns may have a delusional qualit y, responding poorly to simple reassurance\nor counterexample.", "source": "dsm5.pdf"} {"id": "04aa3810a7d0-1", "page_content": "or counterexample.\nThe distinctive symptoms of taijin kyofusho occur in specific cultural contexts and, to\nsome extent, with more severe social anxiet y across cultures. Simila r syndromes are found\nin Korea and other societies that place a st rong emphasis on the self-conscious mainte-\nnance of appropriate social behavior in hierarchical interpersonal relationships. Taijin kyo-\nfusho \u2013like symptoms have also b een described in other cultural contexts, including the\nUnited States, Australia, and New Zealand.\nRelated conditions in other cultural contexts: Taein kong po in Korea.\nRelated conditions in DSM-5: Social anxiety disorder, bo dy dysmorphic disorder, de-\nlusional disorder, obsessive-co mpulsive disorder, olfactory re ference syndrome (a type of\nother specified obsessive-compulsive and related disorder ). Olfactory reference syndrome\nis related specifically to the jikoshu-kyofu variant of taijin kyofusho, whose core symptom is\nthe concern that the person emits an offensive body odor. This presentation is seen in var-\nious cultures outside Japan.", "source": "dsm5.pdf"} {"id": "45e67a95ef0e-0", "page_content": "This page intentionally left blank", "source": "dsm5.pdf"} {"id": "ddb56f72beb1-0", "page_content": "839Alphabetical Listing of\nDSM-5 Diagnoses and Codes\n(ICD-9-CM and ICD-10-CM)\nICD-9-CM codes are to be used for coding purposes in the United States through \nSeptember 30, 2014. ICD-10-CM codes are to be used starting October 1, 2014.\nICD-9-CM ICD-10-CM Disorder, condition, or problem\nV62.3 Z55.9 Academic or educational problem\nV62.4 Z60.3 Acculturation difficulty\n308.3 F43.0 Acute stress disorder \n\u00a0 \u00a0 Adjustment disorders\n309.24 F43.22 With anxiety\n309.0 F43.21 With depressed mood\n309.3 F43.24 With disturbance of conduct\n309.28 F43.23 With mixed anxiety and depressed mood\n309.4 F43.25 With mixed disturbanc e of emotions and conduct\n309.9 F43.20 Unspecified\nV71.01 Z72.811 Adult an tisocial behavior\n307.0 F98.5 Adult-onset fluency disorder\n\u00a0 \u00a0 Adult physical abuse by nonspouse or nonpartner, Confirmed\n995.81 T74.11XA Initial encounter\n995.81 T74.11XD Subsequent encounter\n\u00a0 \u00a0 Adult physical abuse by nonspouse or nonpartner, Suspected\n995.81 T76.11XA Initial encounter\n995.81 T76.11XD Subsequent encounter\n\u00a0 \u00a0 Adult psychological abuse by nonspouse or nonpartner, \nConfirmed\n995.82 T74.31XA Initial encounter\n995.82 T74.31XD Subsequent encounter\n\u00a0 \u00a0 Adult psychological abuse by nonspouse or nonpartner, Suspected\n995.82 T76.31XA Initial encounter", "source": "dsm5.pdf"} {"id": "ddb56f72beb1-1", "page_content": "995.82 T76.31XA Initial encounter\n995.82 T76.31XD Subsequent encounter\n\u00a0 \u00a0 Adult sexual abuse by nonspouse or nonpartner, Confirmed\n995.83 T74.21XA Initial encounter\n995.83 T74.21XD Subsequent encounter\n\u00a0 \u00a0 Adult sexual abuse by nonspo use or nonpartner, Suspected\n995.83 T76.21XA Initial encounter\n995.83 T76.21XD Subsequent encounter", "source": "dsm5.pdf"} {"id": "ba296aef4e47-0", "page_content": "840 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n300.22 F40.00 Agoraphobia\n291.89 \u00a0 Alcohol-induced anxiety disorder\n\u00a0 F10.180 With mild use disorder\n\u00a0 F10.280 With moderate or severe use disorder\n\u00a0 F10.980 Without use disorder\n291.89 \u00a0 Alcohol-induced bipo lar and related disorder\n\u00a0 F10.14 With mild use disorder\n\u00a0 F10.24 With moderate or severe use disorder\n\u00a0 F10.94 Without use disorder\n291.89 \u00a0 Alcohol-induced depressive disorder\n\u00a0 F10.14 With mild use disorder\n\u00a0 F10.24 With moderate or severe use disorder\n\u00a0 F10.94 Without use disorder\n291.1 \u00a0 Alcohol-induced major neuroc ognitive disorder, Amnestic \nconfabulatory type\n\u00a0 F10.26 With moderate or severe use disorder\n\u00a0 F10.96 Without use disorder\n291.2 \u00a0 Alcohol-induced major neuroc ognitive disorder, Nonamnestic \nconfabulatory type\n\u00a0 F10.27 With moderate or severe use disorder\n\u00a0 F10.97 Without use disorder\n291.89 \u00a0 Alcohol-induced mild neurocogniti ve disorder\n\u00a0 F10.288 With moderate or severe use disorder\n\u00a0 F10.988 Without use disorder\n291.9 \u00a0 Alcohol-induced psychotic disorder\n\u00a0 F10.159 With mild use disorder\n\u00a0 F10.259 With moderate or severe use disorder\n\u00a0 F10.959 Without use disorder\n291.89 \u00a0 Alcohol-induced sexual dysfunction\n\u00a0 F10.181 With mild use disorder\n\u00a0 F10.281 With moderate or severe use disorder\n\u00a0 F10.981 Without use disorder\n291.82 \u00a0 Alcohol-induc ed sleep disorder\n\u00a0 F10.182 With mild use disorder", "source": "dsm5.pdf"} {"id": "ba296aef4e47-1", "page_content": "F10.182 With mild use disorder\n\u00a0 F10.282 With moderate or severe use disorder\n\u00a0 F10.982 Without use disorder\n303.00 \u00a0 Alcohol intoxication\n\u00a0 F10.129 With mild use disorder\n\u00a0 F10.229 With moderate or severe use disorder\n\u00a0 F10.929 Without use disorder\n291.0 \u00a0 Alcohol intoxication delirium\n\u00a0 F10.121 With mild use disorder\n\u00a0 F10.221 With moderate or severe use disorder\n\u00a0 F10.921 Without use disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "b62f27d68b75-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 841\n\u00a0 \u00a0 Alcohol use disorder\n305.00 F10.10 Mild\n303.90 F10.20 Moderate\n303.90 F10.20 Severe\n291.81 \u00a0 Alcohol withdrawal\n\u00a0 F10.232 With perceptual disturbances\n\u00a0 F10.239 Without perceptual disturbances\n291.0 F10.231 Alcohol withdrawal delirium\n292.89 \u00a0 Amphetamine (or other stim ulant)\u2013induced anxiety disorder\n\u00a0 F15.180 With mild use disorder\n\u00a0 F15.280 With moderate or severe use disorder\n\u00a0 F15.980 Without use disorder\n292.84 \u00a0 Amphetamine (or other stimul ant)\u2013induced bipolar and related \ndisorder\n\u00a0 F15.14 With mild use disorder\n\u00a0 F15.24 With moderate or severe use disorder\n\u00a0 F15.94 Without use disorder\n\u00a0 F15.921 Amphetamine (or other stimulant)\u2013induced delirium\n292.84 \u00a0 Amphetamine (or other stimul ant)\u2013induced depressive disorder\n\u00a0 F15.14 With mild use disorder\n\u00a0 F15.24 With moderate or severe use disorder\n\u00a0 F15.94 Without use disorder\n292.89 \u00a0 Amphetamine (or other stimulan t)\u2013induced obsessive-compulsive \nand related disorder\n\u00a0 F15.188 With mild use disorder\n\u00a0 F15.288 With moderate or severe use disorder\n\u00a0 F15.988 Without use disorder\n292.9 \u00a0 Amphetamine (or other stimul ant)\u2013induced psychotic disorder\n\u00a0 F15.159 With mild use disorder\n\u00a0 F15.259 With moderate or severe use disorder\n\u00a0 F15.959 Without use disorder", "source": "dsm5.pdf"} {"id": "b62f27d68b75-1", "page_content": "F15.959 Without use disorder\n292.89 \u00a0 Amphetamine (or other stimul ant)\u2013induced sexual dysfunction\n\u00a0 F15.181 With mild use disorder\n\u00a0 F15.281 With moderate or severe use disorder\n\u00a0 F15.981 Without use disorder\n292.85 \u00a0 Amphetamine (or other stim ulant)\u2013induced sleep disorder\n\u00a0 F15.182 With mild use disorder\n\u00a0 F15.282 With moderate or severe use disorder\n\u00a0 F15.982 Without use disorder\n292.89 \u00a0 Amphetamine or other stimulant intoxication\n\u00a0 Amphetamine or other stimulant intoxication, With perceptual \ndisturbances\n\u00a0 F15.122 With mild use disorder\n\u00a0 F15.222 With moderate or severe use disorder\n\u00a0 F15.922 Without use disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "13f79b4dbb3a-0", "page_content": "842 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n\u00a0 Amphetamine or other stimulant intoxication, Without perceptual \ndisturbances\n\u00a0 F15.129 With mild use disorder\n\u00a0 F15.229 With moderate or severe use disorder\n\u00a0 F15.929 Without use disorder\n292.81 \u00a0 Amphetamine (or other stim ulant) intoxication delirium\n\u00a0 F15.121 With mild use disorder\n\u00a0 F15.221 With moderate or severe use disorder\n\u00a0 F15.921 Without use disorder\n292.0 F15.23 Amphetamine or other stimulant withdrawal\nAmphetamine-type substance use disorder\n305.70 F15.10 Mild\n304.40 F15.20 Moderate\n304.40 F15.20 Severe\n307.1 Anorexia nervosa\nF50.02 Binge-eating/purging type\nF50.01 Restricting type\n\u00a0 \u00a0 Antidepressant disc ontinuation syndrome\n995.29 T43.205A Initial encounter\n995.29 T43.205S Sequelae\n995.29 T43.205D Subsequent encounter\n301.7 F60.2 Antisocial personality disorder\n293.84 F06.4 Anxiety disorder due to another medical condition\n\u00a0 \u00a0 Attention-deficit/hy peractivity disorder\n314.01 F90.2 Combined presentation\n314.01 F90.1 Predominantly hyperactive/impulsive presentation\n314.00 F90.0 Predominantly inattentive presentation\n299.00 F84.0 Autism spectrum disorder\n301.82 F60.6 Avoidant personality disorder\n307.59 F50.8 Avoidant/restricti ve food intake disorder\n307.51 F50.8 Binge-eating disorder", "source": "dsm5.pdf"} {"id": "13f79b4dbb3a-1", "page_content": "307.51 F50.8 Binge-eating disorder\n\u00a0 \u00a0 Bipolar I disorder, Current or most recent episode depressed \n296.56 F31.76 In full remission\n296.55 F31.75 In partial remission\n296.51 F31.31 Mild\n296.52 F31.32 Moderate\n296.53 F31.4 Severe\n296.54 F31.5 With psychotic features\n296.50 F31.9 Unspecified\n296.40 F31.0 Bipolar I disorder, Current or most recent episode hypomanic\n296.46 F31.72 In full remission\n296.45 F31.71 In partial remission\n296.40 F31.9 UnspecifiedICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "fb46934e9950-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 843\n\u00a0 \u00a0 Bipolar I disorder, Current or most recent episode manic\n296.46 F31.74 In full remission\n296.45 F31.73 In partial remission\n296.41 F31.11 Mild\n296.42 F31.12 Moderate\n296.43 F31.13 Severe\n296.44 F31.2 With psychotic features\n296.40 F31.9 Unspecified\n296.7 F31.9 Bipolar I disorder, Current or most recent episode unspecified \n296.89 F31.81 Bipolar II disorder\n293.83 \u00a0 Bipolar and related disorder due to another medical condition\n\u00a0 F06.33 With manic features\n\u00a0 F06.33 With manic- or hypomanic-like episodes\n\u00a0 F06.34 With mixed features\n300.7 F45.22 Body dysmorphic disorder\nV62.89 R41.83 Borderline in tellectual functioning\n301.83 F60.3 Borderline personality disorder\n298.8 F23 Brief psyc hotic disorder\n307.51 F50.2 Bulimia nervosa\n292.89 \u00a0 Caffeine-induced anxiety disorder\n\u00a0 F15.180 With mild use disorder\n\u00a0 F15.280 With moderate or severe use disorder\n\u00a0 F15.980 Without use disorder\n292.85 \u00a0 Caffeine-indu ced sleep disorder\n\u00a0 F15.182 With mild use disorder\n\u00a0 F15.282 With moderate or severe use disorder\n\u00a0 F15.982 Without use disorder\n305.90 F15.929 Caffeine intoxication \n292.0 F15.93 Caffeine withdrawal \n292.89 \u00a0 Cannabis-induced anxiety disorder\n\u00a0 F12.180 With mild use disorder", "source": "dsm5.pdf"} {"id": "fb46934e9950-1", "page_content": "292.89 \u00a0 Cannabis-induced anxiety disorder\n\u00a0 F12.180 With mild use disorder\n\u00a0 F12.280 With moderate or severe use disorder\n\u00a0 F12.980 Without use disorder\n292.9 \u00a0 Cannabis-induced psychotic disorder\n\u00a0 F12.159 With mild use disorder\n\u00a0 F12.259 With moderate or severe use disorder\n\u00a0 F12.959 Without use disorder\n292.85 \u00a0 Cannabis-indu ced sleep disorder\n\u00a0 F12.188 With mild use disorder\n\u00a0 F12.288 With moderate or severe use disorder\n\u00a0 F12.988 Without use disorder\n292.89 \u00a0 Cannabis intoxicationICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "8dc69f6d6eaf-0", "page_content": "844 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n\u00a0 \u00a0 Cannabis intoxication, Wi th perceptual disturbances\n\u00a0 F12.122 With mild use disorder\n\u00a0 F12.222 With moderate or severe use disorder\n\u00a0 F12.922 Without use disorder\n\u00a0\u00a0 C annabis intoxication, Without percep tual disturbances\n\u00a0 F12.129 With mild use disorder\n\u00a0 F12.229 With moderate or severe use disorder\n\u00a0 F12.929 Without use disorder\n292.81 \u00a0 Cannabis intoxication delirium\n\u00a0 F12.121 With mild use disorder\n\u00a0 F12.221 With moderate or severe use disorder\n\u00a0 F12.921 Without use disorder\n\u00a0 \u00a0 Cannabis use disorder\n305.20 F12.10 Mild\n304.30 F12.20 Moderate\n304.30 F12.20 Severe\n292.0 F12.288 Cannabis withdrawal \n293.89 F06.1 Catatonia associated with another mental disorder (catatonia \nspecifier)\n293.89 F06.1 Catatonic disorder due to another medical condition\n\u00a0 \u00a0 Central sleep apnea\n780.57 G47.37 Central sleep apnea comorbid with opioid use\n786.04 R06.3 Cheyne-Stokes breathing\n327.21 G47.31 Idiopathic central sleep apnea\nV61.29 Z62.898 Child affected by parental relationship distress\n\u00a0 \u00a0 Child neglect, Confirmed\n995.52 T74.02XA Initial encounter\n995.52 T74.02XD Subsequent encounter\n\u00a0 \u00a0 Child neglect, Suspected\n995.52 T76.02XA Initial encounter\n995.52 T76.02XD Subsequent encounter\nV71.02 Z72.810 Child or adolescent antisocial behavior\n\u00a0 \u00a0 Child physical abuse, Confirmed", "source": "dsm5.pdf"} {"id": "8dc69f6d6eaf-1", "page_content": "Child physical abuse, Confirmed\n995.54 T74.12XA Initial encounter\n995.54 T74.12XD Subsequent encounter\n\u00a0 \u00a0 Child physical abuse, Suspected\n995.54 T76.12XA Initial encounter\n995.54 T76.12XD Subsequent encounter\n\u00a0 \u00a0 Child psychological abuse, Confirmed\n995.51 T74.32XA Initial encounter\n995.51 T74.32XD Subsequent encounter\n\u00a0 \u00a0 Child psychological abuse, Suspected\n995.51 T76.32XA Initial encounter\n995.51 T76.32XD Subsequent encounterICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "7e8b2958db4f-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 845\n\u00a0 \u00a0 Child sexual abuse, Confirmed\n995.53 T74.22XA Initial encounter\n995.53 T74.22XD Subsequent encounter\n\u00a0 \u00a0 Child sexual abuse, Suspected\n995.53 T76.22XA Initial encounter\n995.53 T76.22XD Subsequent encounter\n315.35 F80.81 Childhood-onset fluency disorder (stuttering)\n\u00a0 \u00a0 Circadian rhythm sl eep-wake disorders\n307.45 G47.22 Advanced sleep phase type\n307.45 G47.21 Delayed sleep phase type\n307.45 G47.23 Irregular sleep-wake type\n307.45 G47.24 Non-24-hour sleep-wake type\n307.45 G47.26 Shift work type\n307.45 G47.20 Unspecified type\n292.89 \u00a0 Cocaine-induced anxiety disorder\n\u00a0 F14.180 With mild use disorder\n\u00a0 F14.280 With moderate or severe use disorder\n\u00a0 F14.980 Without use disorder\n292.84 \u00a0 Cocaine-induced bipo lar and related disorder\n\u00a0 F14.14 With mild use disorder\n\u00a0 F14.24 With moderate or severe use disorder\n\u00a0 F14.94 Without use disorder\n292.84 \u00a0 Cocaine-induced depressive disorder\n\u00a0 F14.14 With mild use disorder\n\u00a0 F14.24 With moderate or severe use disorder\n\u00a0 F14.94 Without use disorder\n292.89 \u00a0 Cocaine-induced obsessive- compulsive and related disorder\n\u00a0 F14.188 With mild use disorder\n\u00a0 F14.288 With moderate or severe use disorder\n\u00a0 F14.988 Without use disorder\n292.9 \u00a0 Cocaine-induced psychotic disorder\n\u00a0 F14.159 With mild use disorder", "source": "dsm5.pdf"} {"id": "7e8b2958db4f-1", "page_content": "292.9 \u00a0 Cocaine-induced psychotic disorder\n\u00a0 F14.159 With mild use disorder\n\u00a0 F14.259 With moderate or severe use disorder\n\u00a0 F14.959 Without use disorder\n292.89 \u00a0 Cocaine-induced sexual dysfunction\n\u00a0 F14.181 With mild use disorder\n\u00a0 F14.281 With moderate or severe use disorder\n\u00a0 F14.981 Without use disorder\n292.85 \u00a0 Cocaine-induc ed sleep disorder\n\u00a0 F14.182 With mild use disorder\n\u00a0 F14.282 With moderate or severe use disorder\n\u00a0 F14.982 Without use disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "34bd1fa83b0f-0", "page_content": "846 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n292.89 \u00a0 Cocaine intoxication\n\u00a0 Cocaine intoxication, With perceptual disturbances\n\u00a0 F14.122 With mild use disorder\n\u00a0 F14.222 With moderate or severe use disorder\n\u00a0 F14.922 Without use disorder\n\u00a0 Cocaine intoxication, With out perceptual disturbances\n\u00a0 F14.129 With mild use disorder\n\u00a0 F14.229 With moderate or severe use disorder\n\u00a0 F14.929 Without use disorder\n292.81 \u00a0 Cocaine intoxication delirium\n\u00a0 F14.121 With mild use disorder\n\u00a0 F14.221 With moderate or severe use disorder\n\u00a0 F14.921 Without use disorder\nCocaine use disorder\n305.60 F14.10 Mild\n304.20 F14.20 Moderate\n304.20 F14.20 Severe\n292.0\u00a0 F14.23 Cocaine withdrawal\n\u00a0\u00a0 C onduct disorder\n312.82 F91.2 Adolescent-onset type\n312.81 F91.1 Childhood-onset type\n312.89 F91.9 Unspecified onset\n300.11 \u00a0 Conversion disorder (functional neurological symptom disorder)\nF44.4 With abnormal movement\nF44.6 With anesthesia or sensory loss\nF44.5 With attacks or seizures\nF44.7 With mixed symptoms\nF44.6 With special sensory symptoms \nF44.4 With speech symptoms \nF44.4 With swallowing symptoms\nF44.4 With weakness/paralysis\nV62.5 Z65.0 Conviction in civil or criminal proceedings without imprisonment\n301.13 F34.0 Cyclothymic disorder \n302.74 F52.32 Delayed ejaculation\n\u00a0\u00a0 D elirium", "source": "dsm5.pdf"} {"id": "34bd1fa83b0f-1", "page_content": "302.74 F52.32 Delayed ejaculation\n\u00a0\u00a0 D elirium\n293.0 F05 Delirium due to an other medical condition\n293.0 F05 Delirium due to multiple etiologies\n292.81 Medication-induced delirium (for ICD-10-CM codes, see specific \nsubstances )\nSubstance intoxication delirium (see specific substances for codes)\nSubstance withdrawal delirium (see specific subs tances for codes)\n297.1 F22 Delusional disorder\n301.6 F60.7 Dependent personality disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "3a22dd75298c-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 847\n300.6 F48.1 Depersonalization/derealization disorder\n293.83 \u00a0 Depressive disorder due to another medical condition\n\u00a0 F06.31 With depressive features\n\u00a0 F06.32 With major depr essive\u2013like episode\n\u00a0 F06.34 With mixed features\n315.4 F82 Developmental c oordination disorder \nV60.89 Z59.2 Discord with neighbor, lodger, or landlord\nV62.89 Z64.4 Discord with so cial service provider, including probation officer, \ncase manager, or social services worker\n313.89 F94.2 Disinhibited soci al engagement disorder\nV61.03 Z63.5 Disruption of family by separation or divorce\n296.99 F34.8 Disruptive mood dysregulation disorder \n300.12 F44.0 Dissociative amnesia\n300.13 F44.1 Dissociative amnesia, with dissoc iative fugue\n300.14 F44.81 Dissociative identity disorder\n307.7 F98.1 Encopresis\n307.6 F98.0 Enuresis\n302.72 F52.21 Erectile disorder\n698.4 L98.1\u00a0 Excoriation (s kin-picking) disorder\n302.4 F65.2 Exhibitionistic disorder\nV62.22 Z65.5 Exposure to disaster , war, or other hostilities\nV60.2 Z59.5 Extreme poverty\n300.19 F68.10 Factitious disorder\n302.73 F52.31 Female orgasmic disorder\n302.72 F52.22 Female sexual interest/arousal disorder\n302.81 F65.0 Fetishistic disorder", "source": "dsm5.pdf"} {"id": "3a22dd75298c-1", "page_content": "302.81 F65.0 Fetishistic disorder\n302.89 F65.81 Frotteuristic disorder\n312.31 F63.0 Gambling disorder\n302.85 F64.1 Gender dysphoria in adolescents and adults\n302.6 F64.2 Gender dysp horia in children\n300.02 F41.1 Generalized anxiety disorder \n302.76 F52.6 Genito-pelvic pain/penetration disorder\n315.8 F88 Global developmental delay\n292.89 F16.983 Hallucinog en persisting perception disorder \nV61.8 Z63.8 High expressed emotion level within family\n301.50 F60.4 Histrionic personality disorder\n300.3 F42 Hoarding disorder\nV60.0 Z59.0 Homelessness\n307.44 F51.11 Hypersomnolence disorder\n300.7 F45.21 Illness anxiety disorder\nV62.5 Z65.1 Imprisonment or other incarceration\nV60.1 Z59.1 Inadequate housingICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "0ee96eeffc71-0", "page_content": "848 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n292.89 \u00a0 Inhalant-induced anxiety disorder\n\u00a0 F18.180 With mild use disorder\n\u00a0 F18.280 With moderate or severe use disorder\n\u00a0 F18.980 Without use disorder\n292.84 \u00a0 Inhalant-induced depressive disorder\n\u00a0 F18.14 With mild use disorder\n\u00a0 F18.24 With moderate or severe use disorder\n\u00a0 F18.94 Without use disorder\n292.82 \u00a0 Inhalant-induced majo r neurocognitive disorder\n\u00a0 F18.17 With mild use disorder\n\u00a0 F18.27 With moderate or severe use disorder\n\u00a0 F18.97 Without use disorder\n292.89 \u00a0 Inhalant-induced mild neurocognitive disorder\n\u00a0 F18.188 With mild use disorder\n\u00a0 F18.288 With moderate or severe use disorder\n\u00a0 F18.988 Without use disorder\n292.9 \u00a0 Inhalant-induced psychotic disorder\n\u00a0 F18.159 With mild use disorder\n\u00a0 F18.259 With moderate or severe use disorder\n\u00a0 F18.959 Without use disorder\n292.89 \u00a0 Inhalant intoxication\n\u00a0 F18.129 With mild use disorder\n\u00a0 F18.229 With moderate or severe use disorder\n\u00a0 F18.929 Without use disorder\n292.81 \u00a0 Inhalant intoxication delirium\n\u00a0 F18.121 With mild use disorder\n\u00a0 F18.221 With moderate or severe use disorder\n\u00a0 F18.921 Without use disorder\n\u00a0 \u00a0 Inhalant use disorder\n305.90 F18.10 Mild\n304.60 F18.20 Moderate\n304.60 F18.20 Severe\n307.42 F51.01 Insomnia disorder\nV60.2 Z59.7 Insufficien t social insurance or welfare support", "source": "dsm5.pdf"} {"id": "0ee96eeffc71-1", "page_content": "V60.2 Z59.7 Insufficien t social insurance or welfare support\n\u00a0 Intellectual disability (intellectual developmental disorder)\n317\u00a0 F70 Mild\n318.0\u00a0 F71 Moderate\n318.1\u00a0 F72 Severe\n318.2\u00a0 F73 Profound\n312.34 F63.81 Intermittent explosive disorder \n312.32 F63.2 Kleptomania\nV60.2 Z59.4 Lack of adequate f ood or safe drinking water\n315.32 F80.2 Language disorder\nV60.2 Z59.6 Low incomeICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "dd89952964c0-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 849\n\u00a0 \u00a0 Major depressive disorder, Recurrent episode\n296.36 F33.42 In full remission\n296.35 F33.41 In partial remission\n296.31 F33.0 Mild\n296.32 F33.1 Moderate\n296.33 F33.2 Severe \n296.34 F33.3 With psychotic features\n296.30 F33.9 Unspecified\n\u00a0 \u00a0 Major depressive disorder, Single episode\n296.26 F32.5 In full remission\n296.25 F32.4 In partial remission\n296.21 F32.0 Mild\n296.22 F32.1 Moderate\n296.23 F32.2 Severe \n296.24 F32.3 With psychotic features\n296.20 F32.9 Unspecifed\n331.9 G31.9 Major frontotemporal neurocognitive disorder, Possible\nMajor frontotemporal neurocognitive disorder, Probable ( code first \n331.19 [G31.09] frontotemporal disease)\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without behavioral disturbance\n331.9 G31.9 Major neurocognitive disorder due to Alzheimer\u2019s disease, Possible\nMajor neurocognitive disorder due to Alzheimer\u2019s disease, \nProbable (code first 331.0 [G30.9] Alzheimer\u2019s disease)\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without behavioral disturbance\n\u00a0 \u00a0 Major neurocognitive disorder due to another medical condition\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without behavioral disturbance", "source": "dsm5.pdf"} {"id": "dd89952964c0-1", "page_content": "294.10 F02.80 Without behavioral disturbance\nMajor neurocognitive disorder due to HIV infection ( code first 042 \n[B20] HIV infection)\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without behavioral disturbance\nMajor neurocognitive disorder due to Huntington\u2019s disease ( code \nfirst 333.4 [G10] Huntington\u2019s disease)\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without behavioral disturbance\n331.9 G31.9 Major neurocogni tive disorder with Lewy bodies, Possible\nMajor neurocognitive disorder with Lewy bodies, Probable ( code \nfirst 331.82 [G31.83] Lewy body disease)\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without behavioral disturbance\n\u00a0 \u00a0 Major neurocognitive disord er due to multiple etiologies\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without behavioral disturbanceICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "03927ae52e78-0", "page_content": "850 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n331.9 G31.9 Major neurocognitive disorder due to Parkinson\u2019s disease, Possible\nMajor neurocognitive disorder due to Parkinson\u2019s disease, \nProbable (code first 332.0 [G20] Parkinson\u2019s disease)\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without beha vioral disturbance\nMajor neurocognitive disord er due to prion disease ( code first \n046.79 [A81.9] prion disease)\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without beha vioral disturbance\nMajor neurocognitive disorder due to trauma tic brain injury (code \nfirst 907.0 late effect of intracranial injury without skull fracture \n[S06.2X9S diffuse traumatic brain injury with loss of conscious-\nness of unspecified duration, sequela])\n294.11 F02.81 With behavioral disturbance\n294.10 F02.80 Without beha vioral disturbance\n331.9 G31.9 Major vascular neuroc ognitive diso rder, Possible\n\u00a0 \u00a0 Major vascular neurocog nitive disorder, Probable\n290.40 F01.51 With behavioral disturbance\n290.40 F01.50 Without beha vioral disturbance\n302.71 F52.0 Male hypoactive sexual desire disorder\nV65.2 Z76.5 Malingering\n333.99 G25.71 Medication-ind uced acute akathisia\n333.72 G24.02 Medication-induced acute dystonia\n292.81 \u00a0 Medication-induced delirium (for ICD-10-CM codes, see specific \nsubstances)", "source": "dsm5.pdf"} {"id": "03927ae52e78-1", "page_content": "substances)\n333.1 G25.1 Medication-indu ced postural tremor\n331.83 G31.84 Mild frontotemporal neurocognitive disorder\n331.83 G31.84 Mild neurocognitive diso rder due to Alzheimer\u2019s disease\n331.83 G31.84 Mild neurocognitive disord er due to another medical condition\n331.83 G31.84 Mild neurocognitive disorder due to HIV infection\n331.83 G31.84 Mild neurocognitive diso rder due to Huntington\u2019s disease\n331.83 G31.84 Mild neurocognitive disorder due to multiple etiologies\n331.83 G31.84 Mild neurocognitive diso rder due to Park inson\u2019s disease\n331.83 G31.84 Mild neurocognitive disorder due to prion disease\n331.83 G31.84 Mild neurocognitive diso rder due to traumatic brain injury\n331.83 G31.84 Mild neurocognitive disorder with Lewy bodies\n331.83 G31.84 Mild vascular neurocognitive disorder\n301.81 F60.81 Narcissistic personality disorder\n\u00a0\u00a0 N arcolepsy\n347.00 G47.419 Autosomal dominant ce rebellar ataxia, deafness, and \nnarcolepsy\n347.00 G47.419 Autosomal domi nant narcolepsy, obesity, and type 2 diabetes\n347.10 G47.429 Narcolepsy secondary to another medical condition\n347.01 G47.411 Narcolepsy wi th cataplexy but withou t hypocretin deficiency\n347.00 G47.419 Narcolepsy without catapl exy but with hypocretin deficiency\n332.1 G21.11 Neuroleptic-induced parkinsonismICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "0e098a70ec91-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 851\n333.92 G21.0 Neuroleptic malignant syndrome\n307.47 F51.5 Nightmare disorder\nV15.81 Z91.19 Nonadherence to medical treatment\n\u00a0 \u00a0 Non\u2013rapid eye movement sleep arousal disorders\n307.46 F51.4 Sleep terror type\n307.46 F51.3 Sleepwalking type\n300.3 F42 Obsessive-compulsive disorder\n301.4 F60.5 Obsessive-compuls ive personality disorder\n294.8 F06.8 Obsessive-compulsive and related disorder due to another \nmedical condition \n327.23 G47.33 Obstructive sleep apnea hypopnea\n292.89 \u00a0 Opioid-induced anxiety disorder\n\u00a0 F11.188 With mild use disorder\n\u00a0 F11.288 With moderate or severe use disorder\n\u00a0 F11.988 Without use disorder\n\u00a0 F11.921 Opioid-induced delirium\n292.84 \u00a0 Opioid-induced depressive disorder\n\u00a0 F11.14 With mild use disorder\n\u00a0 F11.24 With moderate or severe use disorder\n\u00a0 F11.94 Without use disorder\n292.89 \u00a0 Opioid-induced sexual dysfunction\n\u00a0 F11.181 With mild use disorder\n\u00a0 F11.281 With moderate or severe use disorder\n\u00a0 F11.981 Without use disorder\n292.85 \u00a0 Opioid-induce d sleep disorder\n\u00a0 F11.182 With mild use disorder\n\u00a0 F11.282 With moderate or severe use disorder\n\u00a0 F11.982 Without use disorder\n292.89 \u00a0 Opioid intoxication\n\u00a0 \u00a0 Opioid intoxicati on, With perceptual disturbances\n\u00a0 F11.122 With mild use disorder\n\u00a0 F11.222 With moderate or severe use disorder", "source": "dsm5.pdf"} {"id": "0e098a70ec91-1", "page_content": "F11.222 With moderate or severe use disorder\n\u00a0 F11.922 Without use disorder\n\u00a0 \u00a0 Opioid intoxicati on, Without percep tual disturbances\n\u00a0 F11.129 With mild use disorder\n\u00a0 F11.229 With moderate or severe use disorder\n\u00a0 F11.929 Without use disorder\n292.81 \u00a0 Opioid intoxication delirium\n\u00a0 F11.121 With mild use disorder\n\u00a0 F11.221 With moderate or severe use disorder\n\u00a0 F11.921 Without use disorder\n\u00a0 \u00a0 Opioid use disorder\n305.50 F11.10 Mild\n304.00 F11.20 Moderate\n304.00 F11.20 SevereICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "1d8bc3c620c0-0", "page_content": "852 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n292.0 F11.23 Opioid withdrawal \n292.0 F11.23 Opioid withdrawal delirium\n313.81 F91.3 Oppositional defiant disorder\n\u00a0 \u00a0 Other adverse effect of medication\n995.20 T50.905A Initial encounter\n995.20 T50.905S Sequelae\n995.20 T50.905D Subsequent encounter\n\u00a0\u00a0 Other circumstances related to adul t abuse by nonspouse or nonpartner\nV62.83 Z69.82 Encounter for mental health services for perpetrator of \nnonspousal adult abuse\nV65.49 Z69.81 Encounter for mental health services for victim of nonspousal \nadult abuse\n\u00a0\u00a0 Other circumstances related to child neglect\nV62.83 Z69.021 Encounter for mental health services for perpetrator of \nnonparental child neglect\nV61.22 Z69.011 Encounter for mental health services for perpetrator of parental \nchild neglect\nV61.21 Z69.010 Encounter for mental health se rvices for victim of child neglect by \nparent\nV61.21 Z69.020 Encounter for mental health services for victim of nonparental \nchild neglect\nV15.42 Z62.812 Personal history (past history) of neglect in childhood\n\u00a0\u00a0 Other circumstances related to child physical abuse\nV62.83 Z69.021 Encounter for mental health services for perpetrator of \nnonparental child abuse\nV61.22 Z69.011 Encounter for mental health services for perpetrator of parental \nchild abuse\nV61.21 Z69.010 Encounter for mental health services for victim of child abuse by \nparent", "source": "dsm5.pdf"} {"id": "1d8bc3c620c0-1", "page_content": "parent\nV61.21 Z69.020 Encounter for mental health services for victim of nonparental \nchild abuse\nV15.41 Z62.810 Personal histor y (past history) of phys ical abuse in childhood\n\u00a0\u00a0 Other circumstances related to child psychological abuse\nV62.83 Z69.021 Encounter for mental health services for perpetrator of \nnonparental child psychological abuse\nV61.22 Z69.011 Encounter for mental health services for perpetrator of parental \nchild psychological abuse\nV61.21 Z69.010 Encounter for mental health services for victim of child \npsychological abuse by parent\nV61.21 Z69.020 Encounter for mental health services for victim of nonparental \nchild psychological abuse\nV15.42 Z62.811 Personal histor y (past history) of psychological abuse in childhood\n\u00a0\u00a0 Other circumstances related to child sexual abuse\nV62.83 Z69.021 Encounter for mental health services for perpetrator of \nnonparental child sexual abuse\nV61.22 Z69.011 Encounter for mental health services for perpetrator of parental \nchild sexual abuseICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "5d3bf2722377-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 853\nV61.21 Z69.010 Encounter for mental health services for victim of child sexual \nabuse by parent\nV61.21 Z69.020 Encounter for mental health services for victim of nonparental \nchild sexual abuse\nV15.41 Z62.810 Personal his tory (past history) of se xual abuse in childhood\n\u00a0\u00a0 Other circumstances related to spou se or partner abuse, Psychological\nV61.12 Z69.12 Encounter for mental health services for perpetrator of spouse or \npartner psychological abuse\nV61.11 Z69.11 Encounter for mental health services for victim of spouse or \npartner psychological abuse\nV15.42 Z91.411 Personal hi story (past history) of spouse or partner \npsychological abuse\n\u00a0\u00a0 Other circumstances related to spouse or partner neglect\nV61.12 Z69.12 Encounter for mental health services for perpetrator of spouse or \npartner neglect\nV61.11 Z69.11 Encounter for mental health services for victim of spouse or \npartner neglect\nV15.42 Z91.412 Personal his tory (past history) of sp ouse or partner neglect\n\u00a0\u00a0 Other circumstances related to sp ouse or partner violence, Physical\nV61.12 Z69.12 Encounter for mental health services for perpetrator of spouse or \npartner violence, Physical\nV61.11 Z69.11 Encounter for mental health services for victim of spouse or \npartner violence, Physical\nV15.41 Z91.410 Personal histor y (past history) of spouse or partner violence, \nPhysical\n\u00a0\u00a0 Other circumstances related to sp ouse or partner violence, Sexual\nV61.12 Z69.12 Encounter for mental health services for perpetrator of spouse or", "source": "dsm5.pdf"} {"id": "5d3bf2722377-1", "page_content": "V61.12 Z69.12 Encounter for mental health services for perpetrator of spouse or \npartner violence, Sexual\nV61.11 Z69.81 Encounter for mental health services for victim of spouse or \npartner violence, Sexual\nV15.41 Z91.410 Personal histor y (past history) of spouse or partner violence, \nSexual\nV65.40 Z71.9 Other counseling or consultation\n292.89 \u00a0 Other hallucinogen\u2013i nduced anxiety disorder\n\u00a0 F16.180 With mild use disorder\n\u00a0 F16.280 With moderate or severe use disorder\n\u00a0 F16.980 Without use disorder\n292.84 \u00a0 Other hallucinogen\u2013induced bipolar and related disorder\n\u00a0 F16.14 With mild use disorder\n\u00a0 F16.24 With moderate or severe use disorder\n\u00a0 F16.94 Without use disorder\n292.84 \u00a0 Other hallucinogen\u2013ind uced depressive disorder\n\u00a0 F16.14 With mild use disorder\n\u00a0 F16.24 With moderate or severe use disorder\n\u00a0 F16.94 Without use disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "a0bcacd5b540-0", "page_content": "854 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n292.9 \u00a0 Other hallucinogen\u2013induced psychotic disorder\n\u00a0 F16.159 With mild use disorder\n\u00a0 F16.259 With moderate or severe use disorder\n\u00a0 F16.959 Without use disorder\n292.89 \u00a0 Other hallucinogen intoxication \n\u00a0 F16.129 With mild use disorder\n\u00a0 F16.229 With moderate or severe use disorder\n\u00a0 F16.929 Without use disorder\n292.81 \u00a0 Other hallucinogen intoxication delirium\n\u00a0 F16.121 With mild use disorder\n\u00a0 F16.221 With moderate or severe use disorder\n\u00a0 F16.921 Without use disorder\n\u00a0 \u00a0 Other hallucinogen use disorder\n305.30 F16.10 Mild\n304.50 F16.20 Moderate\n304.50 F16.20 Severe\n333.99 G25.79 Other medication-induced movement disorder\n332.1 G21.19 Other medicatio n-induced parkinsonism\nV15.49 Z91.49 Other personal hi story of psychological trauma\nV15.89 Z91.89 Other personal risk factors\nV62.29 Z56.9 Other problem related to employment\nV62.89 Z65.8 Other problem relate d to psychosocial circumstances\n300.09 F41.8 Other specif ied anxiety disorder\n314.01 F90.8 Other specified attentio n-deficit/hyperactivity disorder\n296.89 F31.89 Other specified bi polar and related disorder\n780.09 R41.0 Other sp ecified delirium\n311 F32.8 Other specified depressive disorder\n312.89 F91.8 Other specified disruptive, impulse-control, and conduct disorder\n300.15 F44.89 Other specifie d dissociati ve disorder", "source": "dsm5.pdf"} {"id": "a0bcacd5b540-1", "page_content": "300.15 F44.89 Other specifie d dissociati ve disorder\n\u00a0 \u00a0 Other specified elimination disorder\n787.60 R15.9 With fecal symptoms\n788.39 N39.498 With urinary symptoms\n307.59 F50.8 Other specified feeding or eating disorder\n302.6 F64.8 Other specifie d gender dysphoria\n780.54 G47.19 Other specified hypersomnolence disorder\n780.52 G47.09 Other specified insomnia disorder\n300.9 F99 Other specified mental disorder\n294.8 F06.8 Other specified mental disord er due to another medical condition\n315.8 F88 Other specified neur odevelopment al disorder\n300.3 F42 Other specified obsessive-compulsive and related disorder\n302.89 F65.89 Other specifie d paraphilic disorder\n301.89 F60.89 Other specifie d personality disorder\n298.8 F28 Other specified schizophrenia spectrum and other psychotic disorder\n302.79 F52.8 Other specifie d sexual dysfunctionICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "ef4b30ad0794-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 855\n780.59 G47.8 Other specified sleep-wake disorder\n300.89 F45.8 Other specified somati c symptom and related disorder\n307.20 F95.8 Other spec ified tic disorder\n309.89 F43.8 Other specified trauma - and stressor-related disorder\n292.89 \u00a0 Other (or unknown) subs tance\u2013induced anxiety disorder\n\u00a0 F19.180 With mild use disorder\n\u00a0 F19.280 With moderate or severe use disorder\n\u00a0 F19.980 Without use disorder\n292.84 \u00a0 Other (or unknown) substance\u2013induced bipolar and related disorder\n\u00a0 F19.14 With mild use disorder\n\u00a0 F19.24 With moderate or severe use disorder\n\u00a0 F19.94 Without use disorder\n\u00a0 F19.921 Other (or unknown) substance\u2013induced delirium\n292.84 \u00a0 Other (or unknown) substa nce\u2013induced depressive disorder\n\u00a0 F19.14 With mild use disorder\n\u00a0 F19.24 With moderate or severe use disorder\n\u00a0 F19.94 Without use disorder\n292.82 \u00a0 Other (or unknown) substance\u2013induced major neurocognitive \ndisorder\n\u00a0 F19.17 With mild use disorder\n\u00a0 F19.27 With moderate or severe use disorder\n\u00a0 F19.97 Without use disorder\n292.89 \u00a0 Other (or unknown) substance\u2013induced mild neurocognitive \ndisorder\n\u00a0 F19.188 With mild use disorder\n\u00a0 F19.288 With moderate or severe use disorder\n\u00a0 F19.988 Without use disorder\n292.89 \u00a0 Other (or unknown) substance\u2013induced obsessive-compulsive \nand related disorder\n\u00a0 F19.188 With mild use disorder", "source": "dsm5.pdf"} {"id": "ef4b30ad0794-1", "page_content": "and related disorder\n\u00a0 F19.188 With mild use disorder\n\u00a0 F19.288 With moderate or severe use disorder\n\u00a0 F19.988 Without use disorder\n292.9 \u00a0 Other (or unknown) substa nce\u2013induced psychotic disorder\n\u00a0 F19.159 With mild use disorder\n\u00a0 F19.259 With moderate or severe use disorder\n\u00a0 F19.959 Without use disorder\n292.89 \u00a0 Other (or unknown) substa nce\u2013induced sexual dysfunction\n\u00a0 F19.181 With mild use disorder\n\u00a0 F19.281 With moderate or severe use disorder\n\u00a0 F19.981 Without use disorder\n292.85 \u00a0 Other (or unknown) subs tance\u2013induced sleep disorder\n\u00a0 F19.182 With mild use disorder\n\u00a0 F19.282 With moderate or severe use disorder\n\u00a0 F19.982 Without use disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "735697569233-0", "page_content": "856 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n292.89 \u00a0 Other (or unknown) substance intoxication \n\u00a0 F19.129 With mild use disorder\n\u00a0 F19.229 With moderate or severe use disorder\n\u00a0 F19.929 Without use disorder\n292.81 \u00a0 Other (or unknown) subs tance intoxication delirium\n\u00a0 F19.121 With mild use disorder\n\u00a0 F19.221 With moderate or severe use disorder\n\u00a0 F19.921 Without use disorder\n\u00a0 \u00a0 Other (or unknown) substance use disorder\n305.90 F19.10 Mild\n304.90 F19.20 Moderate\n304.90 F19.20 Severe\n292.0 F19.239 Other (or unknown) substance withdrawal \n292.0 F19.231 Other (or unknown) su bstance withdrawal delirium\nOther or unspecified stimulant use disorder\n305.70 F15.10 Mild\n304.40 F15.20 Moderate\n304.40 F15.20 Severe\n278.00 E66.9 Overweight or obesity\nPanic attack specifier\n300.01 F41.0 Panic disorder \n301.0 F60.0 Paranoid pe rsonality disorder\nV61.20 Z62.820 Parent-child relational problem\n302.2 F65.4 Pedophilic disorder\n307.22 F95.1 Persistent (chronic) motor or vocal tic disorder\n300.4 F34.1 Persistent depressi ve disorder (dysthymia)\nV62.22 Z91.82 Personal history of military deployment\nV15.59 Z91.5 Personal history of self-harm\n310.1 F07.0 Personality change du e to another medical condition\nV62.89 Z60.0 Phase of life problem", "source": "dsm5.pdf"} {"id": "735697569233-1", "page_content": "V62.89 Z60.0 Phase of life problem\n292.89 \u00a0 Phencyclidine-induced anxiety disorder\n\u00a0 F16.180 With mild use disorder\n\u00a0 F16.280 With moderate or severe use disorder\n\u00a0 F16.980 Without use disorder\n292.84 \u00a0 Phencyclidine-i nduced bipolar an d related disorder\n\u00a0 F16.14 With mild use disorder\n\u00a0 F16.24 With moderate or severe use disorder\n\u00a0 F16.94 Without use disorder\n292.84 \u00a0 Phencyclidine-induc ed depressive disorder\n\u00a0 F16.14 With mild use disorder\n\u00a0 F16.24 With moderate or severe use disorder\n\u00a0 F16.94 Without use disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "fa5ebff99e99-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 857\n292.9 \u00a0 Phencyclidine-indu ced psychotic disorder\n\u00a0 F16.159 With mild use disorder\n\u00a0 F16.259 With moderate or severe use disorder\n\u00a0 F16.959 Without use disorder\n292.89 \u00a0 Phencyclidine intoxication\n\u00a0 F16.129 With mild use disorder\n\u00a0 F16.229 With moderate or severe use disorder\n\u00a0 F16.929 Without use disorder\n292.81 \u00a0 Phencyclidine intoxication delirium\n\u00a0 F16.121 With mild use disorder\n\u00a0 F16.221 With moderate or severe use disorder\n\u00a0 F16.921 Without use disorder\n\u00a0 \u00a0 Phencyclidine use disorder\n305.90 F16.10 Mild\n304.60 F16.20 Moderate\n304.60 F16.20 Severe\n307.52 \u00a0 Pica \n\u00a0 F50.8 In adults\n\u00a0 F98.3 In children\n309.81 F43.10 Posttraumatic stress disorder\n302.75 F52.4 Premature (early) ejaculation\n625.4 N94.3 Premenstrual dysphoric disorder \nV62.21 Z56.82 Problem related to cu rrent military deployment status\nV69.9 Z72.9 Problem related to lifestyle\nV60.3 Z60.2 Problem related to living alone\nV60.6 Z59.3 Problem related to living in a residential institution\nV61.5 Z64.1 Problems related to multiparity\nV62.5 Z65.3 Problems related to other legal circumstances\nV62.5 Z65.2 Problems related to release from prison\nV61.7 Z64.0 Problems related to unwanted pregnancy\n307.21 F95.0 Provisional tic disorder", "source": "dsm5.pdf"} {"id": "fa5ebff99e99-1", "page_content": "307.21 F95.0 Provisional tic disorder\n316 F54 Psychological factors affecting other medical conditions\n\u00a0 \u00a0 Psychotic dis order due to another medical condition\n293.81 F06.2 With delusions\n293.82 F06.0 With hallucinations\n312.33 F63.1 Pyromania\n327.42 G47.52 Rapid eye movement sleep behavior disorder\n313.89 F94.1 Reactive attachment disorder\nV61.10 Z63.0 Relationship distress wi th spouse or intimate partner\nV62.89 Z65.8 Religious or spiritual problem\n333.94 G25.81 Restless legs syndrome\n307.53 F98.21 Rumination disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "9356e8a99036-0", "page_content": "858 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n\u00a0 \u00a0 Schizoaffective disorder\n295.70 F25.0 Bipolar type\n295.70 F25.1 Depressive type\n301.20 F60.1 Schizoid pe rsonality disorder\n295.90 F20.9 Schizophrenia\n295.40 F20.81 Schizoph reniform disorder\n301.22 F21 Schizotypal personality disorder\n292.89 \u00a0 Sedative-, hypnotic-, or anxiolytic-induced anxiety disorder\n\u00a0 F13.180 With mild use disorder\n\u00a0 F13.280 With moderate or severe use disorder\n\u00a0 F13.980 Without use disorder\n292.84 \u00a0 Sedative-, hypnotic-, or anxiol ytic-induced bipolar and related \ndisorder\n\u00a0 F13.14 With mild use disorder\n\u00a0 F13.24 With moderate or severe use disorder\n\u00a0 F13.94 Without use disorder\n\u00a0 F13.921 Sedative-, hypnotic-, or anxiolytic-induced delirium\n292.84 \u00a0 Sedative-, hypnotic-, or anxiol ytic-induced depr essive disorder\n\u00a0 F13.14 With mild use disorder\n\u00a0 F13.24 With moderate or severe use disorder\n\u00a0 F13.94 Without use disorder\n292.82 \u00a0 Sedative-, hypnotic-, or anxiol ytic-induced major neurocognitive \ndisorder\n\u00a0 F13.27 With moderate or severe use disorder\n\u00a0 F13.97 Without use disorder\n292.89 \u00a0 Sedative-, hypnotic-, or anxiol ytic-induced mild neurocognitive \ndisorder\n\u00a0 F13.288 With moderate or severe use disorder\n\u00a0 F13.988 Without use disorder", "source": "dsm5.pdf"} {"id": "9356e8a99036-1", "page_content": "F13.988 Without use disorder\n292.9 \u00a0 Sedative-, hypnotic-, or anxiolytic-induced ps ychotic disorder\n\u00a0 F13.159 With mild use disorder\n\u00a0 F13.259 With moderate or severe use disorder\n\u00a0 F13.959 Without use disorder\n292.89 \u00a0 Sedative-, hypnotic-, or anxiol ytic-induced sexual dysfunction\n\u00a0 F13.181 With mild use disorder\n\u00a0 F13.281 With moderate or severe use disorder\n\u00a0 F13.981 Without use disorder\n292.85 \u00a0 Sedative-, hypnotic-, or an xiolytic-induced sleep disorder\n\u00a0 F13.182 With mild use disorder\n\u00a0 F13.282 With moderate or severe use disorder\n\u00a0 F13.982 Without use disorder\n292.89 \u00a0 Sedative, hy pnotic, or anxiolytic intoxication\n\u00a0 F13.129 With mild use disorder\n\u00a0 F13.229 With moderate or severe use disorder\n\u00a0 F13.929 Without use disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "090db13ebf7b-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 859\n292.81 \u00a0 Sedative, hypnot ic, or anxiolytic intoxication delirium\n\u00a0 F13.121 With mild use disorder\n\u00a0 F13.221 With moderate or severe use disorder\n\u00a0 F13.921 Without use disorder\n\u00a0 \u00a0 Sedative, hypnotic, or anxiolytic use disorder\n305.40 F13.10 Mild\n304.10 F13.20 Moderate\n304.10 F13.20 Severe\n292.0 \u00a0 Sedative, hypnotic, or anxiolytic withdrawal\n\u00a0 F13.232 With perceptual disturbances\n\u00a0 F13.239 Without perceptual disturbances\n292.0 F13.231 Sedative, hypnotic, or anxiolytic withdrawal delirium\n313.23 F94.0 Selective mutism \n309.21 F93.0 Separation anxiety disorder \nV65.49 Z70.9 Sex counseling\n302.83 F65.51 Sexual masochism disorder\n302.84 F65.52 Sexual sadism disorder\nV61.8 Z62.891 Sibling relational problem\n\u00a0 \u00a0 Sleep-related hypoventilation\n327.26 G47.36 Comorbid sleep-related hypoventilation\n327.25 G47.35 Congenital centra l alveolar hypoventilation\n327.24 G47.34 Idiopathic hypoventilation\n300.23 F40.10 Social anxiety disorder (social phobia)\nV62.4 Z60.4 Social exclusion or rejection\n315.39 F80.89 Social (pragmat ic) communication disorder\n300.82 F45.1 Somatic symptom disorder\n\u00a0 \u00a0 Specific learning disorder\n315.1 F81.2 With impairment in mathematics", "source": "dsm5.pdf"} {"id": "090db13ebf7b-1", "page_content": "Specific learning disorder\n315.1 F81.2 With impairment in mathematics\n315.00 F81.0 With impairment in reading\n315.2 F81.81 With impairment in written expression\n\u00a0 \u00a0 Specific phobia\n300.29 F40.218 Animal\n300.29 \u00a0 Blood-injection-injury\nF40.230 Fear of blood\nF40.231 Fear of injections and transfusions\nF40.233 Fear of injury\nF40.232 Fear of other medical care\n300.29 F40.228 Natural environment\n300.29 F40.298 Other\n300.29 F40.248 Situational \n315.39 F80.0 Speech sound disorder\n\u00a0 \u00a0 Spouse or partner abuse, Psychological, Confirmed\n995.82 T74.31XA Initial encounter\n995.82 T74.31XD Subsequent encounterICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "29ad84790755-0", "page_content": "860 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n\u00a0 \u00a0 Spouse or partner abuse, Psychological, Suspected\n995.82 T76.31XA Initial encounter\n995.82 T76.31XD Subsequent encounter\n\u00a0 \u00a0 Spouse or partner neglect, Confirmed\n995.85 T74.01XA Initial encounter\n995.85 T74.01XD Subsequent encounter\n\u00a0 \u00a0 Spouse or partner neglect, Suspected\n995.85 T76.01XA Initial encounter\n995.85 T76.01XD Subsequent encounter\n\u00a0 \u00a0 Spouse or partner viol ence, Physical, Confirmed\n995.81 T74.11XA Initial encounter\n995.81 T74.11XD Subsequent encounter\n\u00a0 \u00a0 Spouse or partner violence, Physical, Suspected\n995.81 T76.11XA Initial encounter\n995.81 T76.11XD Subsequent encounter\n\u00a0 \u00a0 Spouse or partner violence, Sexual, Confirmed\n995.83 T74.21XA Initial encounter\n995.83 T74.21XD Subsequent encounter\n\u00a0 \u00a0 Spouse or partner violence, Sexual, Suspected\n995.83 T76.21XA Initial encounter\n995.83 T76.21XD Subsequent encounter\n307.3 F98.4 Stereotypic movement disorder\n\u00a0 Stimulant in toxication (see amphetamine or cocaine intoxication for \nspecific codes)\n\u00a0 \u00a0 Stimulant use disorder (see amphetamine or cocaine use disorder for \nspecific codes)\n\u00a0S timulant withdrawal (see amphetamine or cocaine withdrawal for \nspecific codes)\n\u00a0 \u00a0 Substance intoxication delirium (see specific subs tances for codes)\n\u00a0 \u00a0 Substance withdrawal delirium (see specific subs tances for codes)", "source": "dsm5.pdf"} {"id": "29ad84790755-1", "page_content": "Substance withdrawal delirium (see specific subs tances for codes)\n\u00a0 \u00a0 Substance/medication-induced anxiety disorder (see specific \nsubstances for codes)\n\u00a0 \u00a0 Substance/medication-induced bipolar and related disorder (see \nspecific substa nces for codes)\n\u00a0 \u00a0 Substance/medication-induced depressive disorder (see specific \nsubstances for codes)\n\u00a0 \u00a0 Substance/medication-induced major or mild neurocognitive \ndisorder (see specific substances for codes)\n\u00a0 \u00a0 Substance/medication-induced ob sessive-compulsive and related \ndisorder (see specific substances for codes)\nSubstance/medication-induced psychotic disorder (see specific \nsubstances for codes)\nSubstance/medication-induced sexual dysfunction (see specific \nsubstances for codes)\nSubstance/medication-induced sleep disorder (see specific \nsubstances for codes)ICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "028b60709467-0", "page_content": "Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM) 861\n333.99 G25.71 Tardive akathisia\n333.85 G24.01 Tardive dyskinesia\n333.72 G24.09 Tardive dystonia\nV62.4 Z60.5 Target of (perceived) adve rse discrimination or persecution\n292.85 \u00a0 Tobacco-induc ed sleep disorder\n\u00a0 F17.208 With moderate or severe use disorder\n\u00a0 \u00a0 Tobacco use disorder\n305.1 Z72.0 Mild\n305.1 F17.200 Moderate\n305.1 F17.200 Severe\n292.0 F17.203 Tobacco withdrawal\n307.23 F95.2 Tourette\u2019s disorder \n302.3 F65.1 Transvestic disorder\n312.39 F63.3 Trichotillomania (hair-pulling disorder) \nV63.9 Z75.3 Unavailability or inaccessibility of health care facilities\nV63.8 Z75.4 Unavailability or inaccessibility of other helping agencies\nV62.82 Z63.4 Uncomplic ated bereavement\n291.9 F10.99 Unspecified alcohol-related disorder\n300.00 F41.9 Unspecified anxiety disorder\n314.01 F90.9 Unspecified attention- deficit/hyperacti vity disorder\n296.80 F31.9 Unspecified bipo lar and related disorder\n292.9 F15.99 Unspecified caffeine-related disorder\n292.9 F12.99 Unspecified cannabis-related disorder\n293.89 F06.1 Unspecified catatonia ( code first 781.99 [R29.818] other symptoms \ninvolving nervous and musculoskeletal systems)", "source": "dsm5.pdf"} {"id": "028b60709467-1", "page_content": "involving nervous and musculoskeletal systems)\n307.9 F80.9 Unspecified co mmunication disorder\n780.09 R41.0 Unspecified delirium\n311 F32.9 Unspecified depressive disorder\n312.9 F91.9 Unspecified disruptive, impu lse-control, and conduct disorder\n300.15 F44.9 Unspecified di ssociative disorder \n\u00a0 \u00a0 Unspecified elimination disorder \n787.60 R15.9 With fecal symptoms\n788.30 R32 With urinary symptoms\n307.50 F50.9 Unspecified feed ing or eating disorder\n302.6 F64.9 Unspecified gender dysphoria\n292.9 F16.99 Unspecified hallucinogen-related disorder\nV60.9 Z59.9 Unspecified hous ing or economic problem\n780.54 G47.10 Unspecified hy persomnolence disorder\n292.9 F18.99 Unspecified inhalant-related disorder\n780.52 G47.00 Unspecified insomnia disorder\n319 F79 Unspecified intellectual disability (intellectual developmental \ndisorder)\n300.9 F99 Unspecified mental disorder\n294.9 F09 Unspecified mental disorder due to another medical condition\n799.59 R41.9 Unspecified ne urocognitive disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "db847f1cebfd-0", "page_content": "862 Alphabetical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM and ICD-10-CM)\n315.9 F89 Unspecified neurodevelopmental disorder\n300.3 F42 Unspecified obsessive-co mpulsive and related disorder\n292.9 F11.99 Unspecified opioid-related disorder\n292.9 F19.99 Unspecified other (or unkn own) substance\u2013related disorder \n302.9 F65.9 Unspecified paraphilic disorder\n301.9 F60.9 Unspecified personality disorder\n292.9 F16.99 Unspecified phency clidine-related disorder\nV62.9 Z60.9 Unspecified problem related to social environment\nV62.9 Z65.9 Unspecified problem related to unspecified psychosocial \ncircumstances\n298.9 F29 Unspecified schizophrenia spec trum and other psychotic disorder\n292.9 F13.99 Unspecified sedative-, hypnot ic-, or anxiolytic-related disorder\n302.70 F52.9 Unspecified sexual dysfunction\n780.59 G47.9 Unspecified sleep-wake disorder\n300.82 F45.9 Unspecified somatic symptom and related disorder\n292.9 \u00a0 Unspecified stimul ant-related disorder\n\u00a0 F15.99 Unspecified amphetamine or other stimulant-related disorder\n\u00a0 F14.99 Unspecified cocaine-related disorder\n307.20 F95.9 Unspecifi ed tic disorder\n292.9 F17.209 Unspecified to bacco-related disorder\n309.9 F43.9 Unspecified trauma- an d stressor-related disorder\nV61.8 Z62.29 Upbringing away from parents\nV62.89 Z65.4 Victim of crime\nV62.89 Z65.4 Victim of terrorism or torture\n302.82 F65.3 Voyeuristic disorder", "source": "dsm5.pdf"} {"id": "db847f1cebfd-1", "page_content": "302.82 F65.3 Voyeuristic disorder\nV40.31 Z91.83 Wandering associat ed with a mental disorderICD-9-CM ICD-10-CM Disorder, condition, or problem", "source": "dsm5.pdf"} {"id": "9d691740e5d4-0", "page_content": "863Numerical Listing of\nDSM-5 Diagnoses and Codes\n(ICD-9-CM)\nICD-9-CM codes are to be used for coding purposes in the United States through \nSeptember 30, 2014. \nICD-9-CM Disorder, cond ition, or problem\n278.00 Overweight or obesity\n290.40 Probable major vascular neurocognitive disorder, With behavioral disturbance\n290.40 Probable major vascular neurocog nitive disorder, Without behavioral \ndisturbance\n291.0 Alcohol intoxication delirium\n291.0 Alcohol withdrawal delirium\n291.1 Alcohol-induced major ne urocognitive disorder, Amnestic confabulatory type\n291.2 Alcohol-induced major neurocognitive disorder, Nonamnestic confabulatory type\n291.81 Alcohol withdrawal\n291.82 Alcohol-induced sleep disorder\n291.89 Alcohol-induced anxiety disorder\n291.89 Alcohol-induced bipolar and related disorder\n291.89 Alcohol-induced depressive disorder\n291.89 Alcohol-induced mild neurocognitive disorder\n291.89 Alcohol-induced sexual dysfunction\n291.9 Alcohol-induced psychotic disorder\n291.9 Unspecified alco hol-related disorder\n292.0 Amphetamine or other stimulant withdrawal \n292.0 Caffeine withdrawal \n292.0 Cannabis withdrawal \n292.0 Cocaine withdrawal \n292.0 Opioid withdrawal \n292.0 Opioid withdrawal delirium\n292.0 Other (or unknown) substance withdrawal \n292.0 Other (or unknown) subs tance withdrawal delirium\n292.0 Sedative, hypnotic, or anxiolytic withdrawal\n292.0 Sedative, hypnotic, or anxiolytic withdr awal delirium\n292.0 Tobacco withdrawal", "source": "dsm5.pdf"} {"id": "9d691740e5d4-1", "page_content": "292.0 Tobacco withdrawal\n292.81 Amphetamine (or other stim ulant) intoxication delirium\n292.81 Cannabis intoxication delirium\n292.81 Cocaine intox ication delirium", "source": "dsm5.pdf"} {"id": "0593bf8b1f5c-0", "page_content": "864 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM)\n292.81 Inhalant intoxication delirium\n292.81 Medication-induced delirium\n292.81 Opioid intoxication delirium\n292.81 Other hallucinogen intoxication delirium\n292.81 Other (or unknown) subs tance intoxication delirium\n292.81 Phencyclidine intoxication delirium\n292.81 Sedative, hypnotic, or an xiolytic intoxication delirium\n292.82 Inhalant-induced majo r neurocognitive disorder\n292.82 Other (or unknown) substance\u2013in duced major neurocognitive disorder\n292.82 Sedative-, hypnotic-, or anxiolytic -induced major neurocognitive disorder\n292.84 Amphetamine (or other stimulant)\u2013i nduced bipolar an d related disorder\n292.84 Amphetamine (or other stimulan t)\u2013induced depressive disorder\n292.84 Cocaine-induced bipolar and related disorder\n292.84 Cocaine-induced depressive disorder\n292.84 Inhalant-induced depressive disorder\n292.84 Opioid-induced depressive disorder\n292.84 Other hallucinogen\u2013induced bipolar and related disorder\n292.84 Other hallucinogen\u2013indu ced depressi ve disorder\n292.84 Other (or unknown) substance\u2013in duced bipolar and related disorder\n292.84 Other (or unknown) substanc e\u2013induced depres sive disorder\n292.84 Phencyclidine-induced bi polar and related disorder\n292.84 Phencyclidine-induce d depressive disorder\n292.84 Sedative-, hypnotic-, or anxiolytic -induced bipolar and related disorder\n292.84 Sedative-, hypnotic-, or anxiol ytic-induced depr essive disorder", "source": "dsm5.pdf"} {"id": "0593bf8b1f5c-1", "page_content": "292.85 Amphetamine (or other stim ulant)\u2013induced sleep disorder\n292.85 Caffeine-induced sleep disorder\n292.85 Cannabis-induced sleep disorder\n292.85 Cocaine-induced sleep disorder\n292.85 Opioid-induced sleep disorder\n292.85 Other (or unknown) subs tance\u2013induced sleep disorder\n292.85 Sedative-, hypnotic-, or an xiolytic-induced sleep disorder\n292.85 Tobacco-induced sleep disorder\n292.89 Amphetamine (or other stimul ant)\u2013induced anxiety disorder\n292.89 Amphetamine (or other st imulant)\u2013induced obsessiv e-compulsive and related \ndisorder\n292.89 Amphetamine (or other stimulan t)\u2013induced sexual dysfunction\n292.89 Amphetamine or other stimulant intoxication\n292.89 Caffeine-induced anxiety disorder\n292.89 Cannabis-induced anxiety disorder\n292.89 Cannabis intoxication\n292.89 Cocaine-induced anxiety disorder\n292.89 Cocaine-induced obsessive-co mpulsive and related disorder\n292.89 Cocaine-induced sexual dysfunction\n292.89 Cocaine intoxication\n292.89 Hallucinogen persisti ng perception disorder ICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "89c7d79b1347-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM) 865\n292.89 Inhalant-induced anxiety disorder\n292.89 Inhalant-induced mild neurocognitive disorder\n292.89 Inhalant intoxication\n292.89 Opioid-induced anxiety disorder\n292.89 Opioid-induced sexual dysfunction\n292.89 Opioid intoxication\n292.89 Other hallucinogen\u2013induced anxiety disorder\n292.89 Other hallucinogen intoxication \n292.89 Other (or unknown) substance\u2013induced anxiety disorder\n292.89 Other (or unknown) substance\u2013in duced mild neurocognitive disorder\n292.89 Other (or unknown) substance\u2013induced obsessive-compulsive and related disorder\n292.89 Other (or unknown) substanc e\u2013induced sexual dysfunction\n292.89 Other (or unknown) substance intoxication \n292.89 Phencyclidine-indu ced anxiety disorder\n292.89 Phencyclidine intoxication\n292.89 Sedative-, hypnotic-, or anxi olytic-induced anxiety disorder\n292.89 Sedative-, hypnotic-, or anxiolytic-induced mild neurocognitive disorder\n292.89 Sedative-, hypnotic- , or anxiolytic-induced sexual dysfunction\n292.89 Sedative, hypnotic, or anxiolytic intoxication \n292.9 Amphetamine (or other stimul ant)\u2013induced ps ychotic disorder\n292.9 Cannabis-induced psychotic disorder\n292.9 Cocaine-induced psychotic disorder\n292.9 Inhalant-induced psychotic disorder\n292.9 Other hallucinogen\u2013induced psych otic disorder\n292.9 Other (or unknown) substa nce\u2013induced psychotic disorder\n292.9 Phencyclidine -induced psychotic disorder", "source": "dsm5.pdf"} {"id": "89c7d79b1347-1", "page_content": "292.9 Phencyclidine -induced psychotic disorder\n292.9 Sedative-, hypnotic-, or anxiol ytic-induced psychotic disorder\n292.9 Unspecified caffeine-related disorder\n292.9 Unspecified cannabis-related disorder\n292.9 Unspecified hallucin ogen-related disorder\n292.9 Unspecified inhalant-related disorder\n292.9 Unspecified opioid-related disorder\n292.9 Unspecified other (or unknown) substance\u2013related disorder \n292.9 Unspecified phencycl idine-related disorder\n292.9 Unspecified sedative-, hypnotic- , or anxiolytic-related disorder\n292.9 Unspecified stimulant-related disorder\n292.9 Unspecified tobacco-related disorder\n293.0 Delirium due to another medical condition\n293.0 Delirium due to multiple etiologies\n293.81 Psychotic disorder due to another medical condition, With delusions\n293.82 Psychotic disord er due to another medical condition, With hallucinations\n293.83 Bipolar and related disorder due to another medical condition\n293.83 Depressive disorder due to another medical condition\n293.84 Anxiety disorder due to another medical condition\n293.89 Catatonia associated with another mental disorder (catatonia specifier)ICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "12b8a8db3b1f-0", "page_content": "866 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM)\n293.89 Catatonic disorder due to another medical condition\n293.89 Unspecified catatonia ( code first 781.99 other symptoms involving nervous and \nmusculoskeletal systems)\n294.10 Major neurocognitive disorder due to another medical condition, Without \nbehavioral disturbance\n294.10 Major neurocognitive disorder due to HIV infection, Without behavioral \ndisturbance ( code first 042 HIV infection)\n294.10 Major neurocognitive disorder due to Huntington\u2019s disease, Without \nbehavioral disturbance ( code first 333.4 Huntington\u2019s disease)\n294.10 Major neurocognitive disorder due to multiple etiologies, Without behavioral \ndisturbance\n294.10 Major neurocognitive disorder probab ly due to Parkinson\u2019 s disease, Without \nbehavioral disturbance ( code first 332.0 Parkinson\u2019s disease)\n294.10 Major neurocognitive disorder due to prion disease, Without behavioral \ndisturbance ( code first 046.79 prion disease)\n294.10 Major neurocognitive disorder due to traumatic brain injury, Without \nbehavioral disturbance ( code first 907.0 late effect of intracranial injury without \nskull fracture)\n294.10 Probable major frontotemporal neurocognitive disorder, Without behavioral \ndisturbance ( code first 331.19 frontotemporal disease)\n294.10 Probable major neurocognitive disor der due to Alzheimer\u2019 s disease, Without \nbehavioral disturbance ( code first 331.0 Alzheimer\u2019s disease)\n294.10 Probable major neurocognitive disorder with Lewy bodies, Without behavioral \ndisturbance ( code first 331.82 Lewy body disease)", "source": "dsm5.pdf"} {"id": "12b8a8db3b1f-1", "page_content": "disturbance ( code first 331.82 Lewy body disease)\n294.11 Major neurocognitive disorder due to another medical condition, With \nbehavioral disturbance\n294.11 Major neurocognitive disorder due to HIV infection, With behavioral \ndisturbance ( code first 042 HIV infection)\n294.11 Major neurocognitive diso rder due to Huntington\u2019s disease, With behavioral \ndisturbance ( code first 333.4 Huntington\u2019s disease)\n294.11 Major neurocognitive disorder due to multiple etiologies, With behavioral \ndisturbance\n294.11 Major neurocognitive disorder prob ably due to Parkinso n\u2019s disease, With \nbehavioral disturbance ( code first 332.0 Parkinson\u2019s disease)\n294.11 Major neurocognitive disorder due to prion disease, With behavioral \ndisturbance ( code first 046.79 prion disease)\n294.11 Major neurocognitive diso rder due to traumatic brai n injury, With behavioral \ndisturbance ( code first 907.0 late effect of intracranial injury without skull \nfracture)\n294.11 Probable major frontotemporal neurocognitive disorder, With behavioral \ndisturbance ( code first 331.19 frontotemporal disease)\n294.11 Probable major neurocognitive disor der due to Alzheimer\u2019 s disease, With \nbehavioral disturbance ( code first 331.0 Alzheimer\u2019s disease)\n294.11 Probable major neurocog nitive disorder with Lewy bodies, With behavioral \ndisturbance ( code first 331.82 Lew y body disease)\n294.8 Obsessive-compulsive and related disorder due to another medical condition \n294.8 Other specified mental disorder due to another medical condition", "source": "dsm5.pdf"} {"id": "12b8a8db3b1f-2", "page_content": "294.8 Other specified mental disorder due to another medical condition\n294.9 Unspecified mental disorder due to another medical conditionICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "323b047f6be1-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM) 867\n295.40 Schizophreniform disorder\n295.70 Schizoaffective disorder, Bipolar type\n295.70 Schizoaffective diso rder, Depressive type\n295.90 Schizophrenia\n296.20 Major depressive disorder , Single episode, Unspecifed\n296.21 Major depressive disord er, Single episode, Mild\n296.22 Major depressive disorder , Single episode, Moderate\n296.23 Major depressive disorder , Single episode, Severe \n296.24 Major depressive disorder, Single episode, With psychotic features\n296.25 Major depressive disorder, Sing le episode, In partial remission\n296.26 Major depressive disorder, Si ngle episode, In full remission\n296.30 Major depressive disorder, Recurrent episode, Unspecified\n296.31 Major depressive disord er, Recurrent episode, Mild\n296.32 Major depressive disorder, Recurrent episode, Moderate\n296.33 Major depressive disorder, Recurrent episode, Severe \n296.34 Major depressive disorder, Recurr ent episode, With psychotic features\n296.35 Major depressive disorder, Recurr ent episode, In partial remission\n296.36 Major depressive disorder, Recu rrent episode, In full remission\n296.40 Bipolar I disorder, Current or most recent episode hypomanic\n296.40 Bipolar I disorder, Current or most recent episode hypomanic, Unspecified\n296.40 Bipolar I disorder, Current or most recent episode manic, Unspecified\n296.41 Bipolar I disorder, Current or most recent episode manic, Mild\n296.42 Bipolar I disorder, Current or most recent episode manic, Moderate\n296.43 Bipolar I disorder, Current or most recent episode manic, Severe", "source": "dsm5.pdf"} {"id": "323b047f6be1-1", "page_content": "296.43 Bipolar I disorder, Current or most recent episode manic, Severe\n296.44 Bipolar I disorder, Current or most recent episode manic, With psychotic features\n296.45 Bipolar I disorder, Current or most recent episode hypomanic, In partial remission\n296.45 Bipolar I disorder, Current or most re cent episode manic, In partial remission\n296.46 Bipolar I disorder, Current or most re cent episode hypomani c, In full remission\n296.46 Bipolar I disorder, Current or most re cent episode manic, In full remission\n296.50 Bipolar I disorder, Current or most recent episode depressed, Unspecified\n296.51 Bipolar I disorder, Current or most recent episode depressed, Mild\n296.52 Bipolar I disorder, Current or most recent episode depressed, Moderate\n296.53 Bipolar I disorder, Current or most recent episode depressed, Severe\n296.54 Bipolar I disorder, Current or most re cent episode depresse d, With psychotic \nfeatures\n296.55 Bipolar I disorder, Current or most recent episode depressed, In partial remission\n296.56 Bipolar I disorder, Current or most rece nt episode depressed, In full remission\n296.7 Bipolar I disorder, Current or most recent episode unspecified \n296.80 Unspecified bipolar and related disorder\n296.89 Bipolar II disorder\n296.89 Other specified bipo lar and related disorder\n296.99 Disruptive mood dy sregulation disorder \n297.1 Delusional disorder\n298.8 Brief psychotic disorder\n298.8 Other specified schizophrenia sp ectrum and other psychotic disorderICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "511cfee9071a-0", "page_content": "868 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM)\n298.9 Unspecified schizophrenia spectrum and other psychotic disorder\n299.00 Autism spectrum disorder\n300.00 Unspecified anxiety disorder\n300.01 Panic disorder \n300.02 Generalized anxiety disorder \n300.09 Other specified anxiety disorder\n300.11 Conversion disorder (functional neurological symptom disorder)\n300.12 Dissociative amnesia\n300.13 Dissociative amnesia, With dissociative fugue\n300.14 Dissociative identity disorder\n300.15 Other specified di ssociative disorder\n300.15 Unspecified dissociative disorder \n300.19 Factitious disorder\n300.22 Agoraphobia\n300.23 Social anxiety disorder (social phobia)\n300.29 Specific phobia, Animal\n300.29 Specific phobia, Blood-injection-injury\n300.29 Specific phobia, Natural environment\n300.29 Specific phobia, Other\n300.29 Specific phobia, Situational \n300.3 Hoarding disorder\n300.3 Obsessive-com pulsive disorder\n300.3 Other specified obsessive-compulsive and re lated disorder\n300.3 Unspecified obsessive-comp ulsive and re lated disorder\n300.4 Persistent depressive disorder (dysthymia)\n300.6 Depersonalization/derealization disorder\n300.7 Body dysmorphic disorder\n300.7 Illness anxiety disorder\n300.82 Somatic symptom disorder\n300.82 Unspecified somatic symptom and related disorder\n300.89 Other specified somatic symptom and related disorder\n300.9 Other specified mental disorder\n300.9 Unspecified mental disorder\n301.0 Paranoid personality disorder\n301.13 Cyclothymic disorder \n301.20 Schizoid personality disorder\n301.22 Schizotypal personality disorder", "source": "dsm5.pdf"} {"id": "511cfee9071a-1", "page_content": "301.20 Schizoid personality disorder\n301.22 Schizotypal personality disorder\n301.4 Obsessive-compulsiv e personality disorder\n301.50 Histrionic pe rsonality disorder\n301.6 Dependent personality disorder\n301.7 Antisocial pers onality disorder\n301.81 Narcissistic pe rsonality disorder\n301.82 Avoidant personality disorder\n301.83 Borderline personality disorder\n301.89 Other specified personality disorderICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "0ad41acaa373-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM) 869\n301.9 Unspecified pe rsonality disorder\n302.2 Pedophilic disorder\n302.3 Transvestic disorder\n302.4 Exhibitionistic disorder\n302.6 Gender dysphoria in children\n302.6 Other specified gender dysphoria\n302.6 Unspecified gender dysphoria\n302.70 Unspecified sexual dysfunction\n302.71 Male hypoactive sexual desire disorder\n302.72 Erectile disorder\n302.72 Female sexual interest/arousal disorder\n302.73 Female orgasmic disorder\n302.74 Delayed ejaculation\n302.75 Premature (early) ejaculation\n302.76 Genito-pelvic pain/penetration disorder\n302.79 Other specified sexual dysfunction\n302.81 Fetishistic disorder\n302.82 Voyeuristic disorder\n302.83 Sexual masochism disorder\n302.84 Sexual sadism disorder\n302.85 Gender dysphoria in adolescents and adults\n302.89 Frotteuristic disorder\n302.89 Other specified paraphilic disorder\n302.9 Unspecified paraphilic disorder\n303.00 Alcohol intoxication\n303.90 Alcohol use disorder, Moderate\n303.90 Alcohol use disorder, Severe\n304.00 Opioid use disorder, Moderate\n304.00 Opioid use disorder, Severe\n304.10 Sedative, hypnotic, or anxi olytic use disorder, Moderate\n304.10 Sedative, hypnotic, or an xiolytic use disorder, Severe\n304.20 Cocaine use disorder, Moderate\n304.20 Cocaine use disorder, Severe\n304.30 Cannabis use disorder, Moderate\n304.30 Cannabis use disorder, Severe\n304.40 Amphetamine-type substa nce use disorder, Moderate\n304.40 Amphetamine-type subs tance use disorder, Severe", "source": "dsm5.pdf"} {"id": "0ad41acaa373-1", "page_content": "304.40 Amphetamine-type subs tance use disorder, Severe\n304.40 Other or unspecified stimulant use diso rder, Moderate\n304.40 Other or unspecified st imulant use disorder, Severe\n304.50 Other hallucinogen use disorder, Moderate\n304.50 Other hallucinogen use disorder, Severe\n304.60 Inhalant use disorder, Moderate\n304.60 Inhalant use disorder, Severe\n304.60 Phencyclidine us e disorder, Moderate\n304.60 Phencyclidine us e disorder, SevereICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "26f0a076823d-0", "page_content": "870 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM)\n304.90 Other (or unknown) subs tance use disorder, Moderate\n304.90 Other (or unknown) subs tance use disorder, Severe\n305.00 Alcohol use disorder, Mild\n305.1 Tobacco use disorder, Mild\n305.1 Tobacco use disorder, Moderate\n305.1 Tobacco use disorder, Severe\n305.20 Cannabis use disorder, Mild\n305.30 Other hallucinogen use disorder, Mild\n305.40 Sedative, hypnotic, or an xiolytic use disorder, Mild\n305.50 Opioid use disorder, Mild\n305.60 Cocaine use disorder, Mild\n305.70 Amphetamine-type subs tance use disorder, Mild\n305.70 Other or unspecified st imulant use disorder, Mild\n305.90 Caffeine intoxication \n305.90 Inhalant use disorder, Mild\n305.90 Other (or unknown) su bstance use disorder, Mild\n305.90 Phencyclidine use disorder, Mild\n307.0 Adult-onset fluency disorder\n307.1 Anorexia nervosa\n307.20 Other specified tic disorder\n307.20 Unspecified tic disorder\n307.21 Provisional tic disorder \n307.22 Persistent (chronic) mo tor or vocal tic disorder\n307.23 Tourette\u2019s disorder \n307.3 Stereotypic movement disorder\n307.42 Insomnia disorder\n307.44 Hypersomnolence disorder\n307.45 Circadian rhythm sleep-wake di sorders, Advanced sleep phase type\n307.45 Circadian rhythm sleep-wake di sorders, Delayed sleep phase type\n307.45 Circadian rhythm sleep-wake di sorders, Irregula r sleep-wake type", "source": "dsm5.pdf"} {"id": "26f0a076823d-1", "page_content": "307.45 Circadian rhythm sleep-wake disorders, Non-24-hour sleep-wake type\n307.45 Circadian rhythm sleep-wake disorders, Shift work type\n307.45 Circadian rhythm sleep-wake disorders, Unspecified type\n307.46 Non\u2013rapid eye movement sleep ar ousal disorders, Sleep terror type\n307.46 Non\u2013rapid eye movement sleep ar ousal disorders, Sleepwalking type\n307.47 Nightmare disorder\n307.50 Unspecified feedin g or eating disorder\n307.51 Binge-eating disorder\n307.51 Bulimia nervosa\n307.52 Pica \n307.53 Rumination disorder\n307.59 Avoidant/restrictive food intake disorder\n307.59 Other specified feed ing or eating disorder\n307.6 Enuresis\n307.7 Encopresis\n307.9 Unspecified communication disorderICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "52d0606725fd-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM) 871\n308.3 Acute stress disorder \n309.0 Adjustment disorders , With depressed mood\n309.21 Separation anxiety disorder \n309.24 Adjustment disorders, With anxiety\n309.28 Adjustment disorders, With mixed anxiety and depressed mood\n309.3 Adjustment disorders, With disturbance of conduct\n309.4 Adjustment disorders, With mixed disturbance of em otions and conduct\n309.81 Posttraumatic stress disorder\n309.89 Other specified trauma- an d stressor-related disorder\n309.9 Adjustment disorders, Unspecified\n309.9 Unspecified trauma- and stressor-related disorder\n310.1 Personality change due to another medical condition\n311 Other specified depressive disorder\n311 Unspecified depressive disorder\n312.31 Gambling disorder\n312.32 Kleptomania\n312.33 Pyromania\n312.34 Intermittent ex plosive disorder \n312.39 Trichotillomania (h air-pulling disorder) \n312.81 Conduct disorder, Childhood-onset type\n312.82 Conduct disorder, Adolescent-onset type\n312.89 Conduct disorder, Unspecified onset\n312.89 Other specified disr uptive, impulse-control, and conduct disorder\n312.9 Unspecified disruptive, impuls e-control, and conduct disorder\n313.23 Selective mutism\n313.81 Oppositional defiant disorder\n313.89 Disinhibited social engagement disorder\n313.89 Reactive attachment disorder\n314.00 Attention-deficit/hyperactivity disorder, Predominantly inattentive presentation\n314.01 Attention-deficit/hyperactivity disorder, Combin ed presentation\n314.01 Attention-deficit/hyperactivity disorder, Predomin antly hyperactive/\nimpulsive presentation\n314.01 Other specified attention- deficit/hyperacti vity disorder", "source": "dsm5.pdf"} {"id": "52d0606725fd-1", "page_content": "impulsive presentation\n314.01 Other specified attention- deficit/hyperacti vity disorder\n314.01 Unspecified attention-de ficit/hyperactivity disorder\n315.00 Specific learning disorder , With impairment in reading\n315.1 Specific learning disorder, With impair ment in mathematics\n315.2 Specific learning di sorder, With impairment in written expression\n315.32 Language disorder\n315.35 Childhood-onset fluenc y disorder (stuttering)\n315.39 Social (pragmatic ) communication disorder\n315.39 Speech sound disorder\n315.4 Developmental coor dination disorder \n315.8 Global developmental delay\n315.8 Other specified neurodevelopmental disorder\n315.9 Unspecified neurodevelopmental disorder\n316 Psychological factors affecting other medical conditionsICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "6f023016b7e6-0", "page_content": "872 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM)\n317 Intellectual disability (intellectual developmental disorder), Mild\n318.0 Intellectual disability (intellectual developmental disorder), Moderate\n318.1 Intellectual disability (intelle ctual developmental disorder), Severe\n318.2 Intellectual disability (intellectual developmental disorder), Profound\n319 Unspecified intellectual disability (intellectual developmental disorder)\n327.21 Central sleep apnea, Idio pathic central sleep apnea\n327.23 Obstructive sleep apnea hypopnea\n327.24 Sleep-related hy poventilation, Idiopathic hypoventilation\n327.25 Sleep-related hypovent ilation, Congenital centra l alveolar hypoventilation\n327.26 Sleep-related hypoventilation, Como rbid sleep-relate d hypoventilation\n327.42 Rapid eye movement sleep behavior disorder\n331.83 Mild frontotemporal ne urocognitive disorder\n331.83 Mild neurocognitive disord er due to Alzheimer\u2019s disease\n331.83 Mild neurocognitive disorder due to another medical condition\n331.83 Mild neurocognitive disorder due to HIV infection\n331.83 Mild neurocognitive disorder due to Huntington\u2019s disease\n331.83 Mild neurocognitive disorder with Lewy bodies\n331.83 Mild neurocognitive disord er due to multiple etiologies\n331.83 Mild neurocognitive disord er due to Parkin son\u2019s disease\n331.83 Mild neurocognitive diso rder due to prion disease\n331.83 Mild neurocognitive disorder due to traumatic brain injury\n331.83 Mild vascular neur ocognitive disorder\n331.9 Major neurocognitive disorder possibly due to Parkinson\u2019s disease\n331.9 Possible major frontotempor al neurocognitive disorder\n331.9 Possible major neurocognitive di sorder due to Al zheimer\u2019s disease", "source": "dsm5.pdf"} {"id": "6f023016b7e6-1", "page_content": "331.9 Possible major neurocognitive di sorder due to Al zheimer\u2019s disease\n331.9 Possible major neurocognitive disorder with Lewy bodies\n331.9 Possible major vascular neurocognitive disorder\n333.1 Medication-induce d postural tremor\n332.1 Neuroleptic-ind uced parkinsonism\n332.1 Other medication-i nduced pa rkinsonism\n333.72 Medication-induced acute dystonia\n333.72 Tardive dystonia\n333.85 Tardive dyskinesia\n333.92 Neuroleptic ma lignant syndrome\n333.94 Restless legs syndrome\n333.99 Medication-induc ed acute akathisia\n333.99 Other medication-ind uced movement disorder\n333.99 Tardive akathisia\n347.00 Autosomal dominant cerebellar ataxia, deafness, and narcolepsy\n347.00 Autosomal dominant narcolepsy, obesity, and type 2 diabetes\n347.00 Narcolepsy withou t cataplexy but with hypocretin deficiency\n347.01 Narcolepsy with cataplexy but without hypocretin deficiency\n347.10 Narcolepsy secondary to another medical condition\n625.4 Premenstrual dysphoric disorder \n698.4 Excoriation (ski n-picking) disorderICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "8faec4a0a51e-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM) 873\n780.09 Other specified delirium\n780.09 Unspecified delirium\n780.52 Other specified insomnia disorder\n780.52 Unspecified insomnia disorder\n780.54 Other specified hy persomnolence disorder\n780.54 Unspecified hypersomnolence disorder\n780.57 Central sleep apnea, Central sl eep apnea comorbid with opioid use\n780.59 Other specified sleep-wake disorder\n780.59 Unspecified sleep-wake disorder\n786.04 Central sleep apnea, Cheyne-Stokes breathing\n787.60 Other specified elimination disorder, With fecal symptoms\n787.60 Unspecified elimination di sorder, With fecal symptoms\n788.30 Unspecified elimination di sorder, With urinary symptoms\n788.39 Other specified elimination disorder, With urinary symptoms\n799.59 Unspecified neur ocognitive disorder\n995.20 Other adverse effect of medication, Initial encounter\n995.20 Other adverse effect of medication, Sequelae\n995.20 Other adverse effect of me dication, Subsequent encounter\n995.29 Antidepressant di scontinuation syndrome, Initial encounter\n995.29 Antidepressant discontinuation syndrome, Sequelae\n995.29 Antidepressant disc ontinuation syndrome, Subsequent encounter\n995.51 Child psychological abuse, Confirmed, Initial encounter\n995.51 Child psychological abuse, Co nfirmed, Subsequent encounter\n995.51 Child psychological abuse, Suspected, Initial encounter\n995.51 Child psychological abuse, Su spected, Subsequent encounter\n995.52 Child neglect, Confirmed, Initial encounter\n995.52 Child neglect, Confirmed, Subsequent encounter\n995.52 Child neglect, Suspec ted, Initial encounter\n995.52 Child neglect, Suspecte d, Subsequent encounter", "source": "dsm5.pdf"} {"id": "8faec4a0a51e-1", "page_content": "995.52 Child neglect, Suspecte d, Subsequent encounter\n995.53 Child sexual abuse, Co nfirmed, Init ial encounter\n995.53 Child sexual abuse, Conf irmed, Subsequent encounter\n995.53 Child sexual abuse, Su spected, Initial encounter\n995.53 Child sexual ab use, Suspected, Subsequent encounter\n995.54 Child physical abuse, Co nfirmed, Initial encounter\n995.54 Child physical abuse, Conf irmed, Subsequent encounter\n995.54 Child physical abuse, Su spected, Initial encounter\n995.54 Child physical abuse, Susp ected, Subsequent encounter\n995.81 Adult physical abuse by nonspouse or nonpartner, Confirmed, Initial encounter\n995.81 Adult physical abuse by nonspouse or nonpartner , Confirmed, Subsequent \nencounter\n995.81 Adult physical abuse by nonspouse or nonpartner, Su spected, Initial encounter\n995.81 Adult physical abuse by nonspouse or nonpartner, Suspected, Subsequent \nencounterICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "e743961c18c6-0", "page_content": "874 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM)\n995.81 Spouse or partner violence, Phys ical, Confirmed, Initial encounter\n995.81 Spouse or partner violence, Physic al, Confirmed, Subsequent encounter\n995.81 Spouse or partner violence, Phys ical, Suspected, Initial encounter\n995.81 Spouse or partner violence, Physic al, Suspected, Subsequent encounter\n995.82 Adult psychological abuse by nonspo use or nonpartner, Confirmed, Initial \nencounter\n995.82 Adult psychological abuse by no nspouse or nonpartner, Confirmed, \nSubsequent encounter\n995.82 Adult psychological abuse by nonspo use or nonpartner, Suspected, Initial \nencounter\n995.82 Adult psychological abuse by no nspouse or nonpartner, Suspected, \nSubsequent encounter\n995.82 Spouse or partner abuse, Psycholo gical, Confirmed, Initial encounter\n995.82 Spouse or partner abuse, Psychological, Confirmed, Subsequent encounter\n995.82 Spouse or partner abuse, Psycholo gical, Suspected, Initial encounter\n995.82 Spouse or partner abuse, Psychologi cal, Suspected, Su bsequent encounter\n995.83 Adult sexual abuse by nonspouse or nonpartner, Confirmed, Initial encounter\n995.83 Adult sexual abuse by nonspouse or nonpartner, Confirmed, Subsequent \nencounter\n995.83 Adult sexual abuse by nonspouse or nonpartner, Suspected, Initial encounter\n995.83 Adult sexual abuse by nonspouse or nonpartner, Suspected, Subsequent \nencounter\n995.83 Spouse or partner violence, Se xual, Confirmed, Initial encounter", "source": "dsm5.pdf"} {"id": "e743961c18c6-1", "page_content": "995.83 Spouse or partner violence, Se xual, Confirmed, Initial encounter\n995.83 Spouse or partner violence, Sexu al, Confirmed, Subsequent encounter\n995.83 Spouse or partner violence, Se xual, Suspected, Initial encounter\n995.83 Spouse or partner violence, Sexu al, Suspected, Subsequent encounter\n995.85 Spouse or partner neglect, Confirmed, Initial encounter\n995.85 Spouse or partner neglect, Confirmed, Subsequent encounter\n995.85 Spouse or partner neglect, Suspected, Initial encounter\n995.85 Spouse or partner neglect, Suspected, Subsequent encounter\nV15.41 Personal history (p ast history) of physical abuse in childhood\nV15.41 Personal history (past history) of sexual abuse in childhood\nV15.41 Personal history (pas t history) of spouse or partner violence, Physical\nV15.41 Personal history (pas t history) of spouse or partner violence, Sexual\nV15.42 Personal histor y (past history) of neglect in childhood\nV15.42 Personal history (p ast history) of psychological abuse in childhood\nV15.42 Personal history (past history) of spou se or partner neglect\nV15.42 Personal history (pas t history) of spouse or partner psychological abuse\nV15.49 Other personal history of psychological trauma\nV15.59 Personal history of self-harm\nV15.81 Nonadherence to medical treatment\nV15.89 Other personal risk factors\nV40.31 Wandering associated with a mental disorder\nV60.0 Homelessness\nV60.1 Inadequate housing\nV60.2 Extreme povertyICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "643a8c94f60d-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM) 875\nV60.2 Insufficient social in surance or welfare support\nV60.2 Lack of adequate food or safe drinking water\nV60.2 Low income\nV60.3 Problem related to living alone\nV60.6 Problem related to living in a residential institution\nV60.89 Discord with neighbor, lodger, or landlord\nV60.9 Unspecified housin g or economic problem\nV61.03 Disruption of family by separation or divorce\nV61.10 Relationship distress with spouse or intimate partner\nV61.11 Encounter for mental health services for victim of spouse or partner neglect\nV61.11 Encounter for mental health servic es for victim of spouse or partner \npsychological abuse\nV61.11 Encounter for mental health services for victim of spouse or partner violence, \nPhysical\nV61.11 Encounter for mental health services for victim of spouse or partner violence, \nSexual\nV61.12 Encounter for mental health services for perpetrator of spouse or partner \nneglect\nV61.12 Encounter for mental health services for perpetrator of spouse or partner \npsychological abuse\nV61.12 Encounter for mental health services for perpetrator of spouse or partner \nviolence, Physical\nV61.12 Encounter for mental health services for perpetrator of spouse or partner \nviolence, Sexual\nV61.20 Parent-child relational problem\nV61.21 Encounter for mental health servic es for victim of child abuse by parent\nV61.21 Encounter for mental health services for victim of child neglect by parent\nV61.21 Encounter for mental health services for victim of child psychological abuse by \nparent\nV61.21 Encounter for mental health services for victim of child sexual abuse by parent", "source": "dsm5.pdf"} {"id": "643a8c94f60d-1", "page_content": "parent\nV61.21 Encounter for mental health services for victim of child sexual abuse by parent\nV61.21 Encounter for mental health services for victim of nonparental child abuse\nV61.21 Encounter for mental health services for victim of nonparental child neglect\nV61.21 Encounter for mental health services for victim of nonparental child \npsychological abuse\nV61.21 Encounter for mental health services for victim of nonparental child sexual \nabuse\nV61.22 Encounter for mental health services for perpetrator of parental child abuse\nV61.22 Encounter for mental health services for perpetrator of pa rental child neglect\nV61.22 Encounter for mental health servic es for perpetrator of parental child \npsychological abuse\nV61.22 Encounter for mental health services for perpetrator of pa rental chil d sexual \nabuse\nV61.29 Child affected by parental relationship distress\nV61.5 Problems related to multiparity\nV61.7 Problems related to unwanted pregnancy\nV61.8 High expressed emotion level within family\nV61.8 Sibling relational problemICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "01e00b417c9a-0", "page_content": "876 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-9-CM)\nV61.8 Upbringing away from parents\nV62.21 Problem related to current military deployment status\nV62.22 Exposure to disaster, war, or other hostilities\nV62.22 Personal history of military deployment\nV62.29 Other problem related to employment\nV62.3 Academic or educational problem\nV62.4 Acculturation difficulty\nV62.4 Social exclusion or rejection\nV62.4 Target of (perceived) advers e discrimination or persecution\nV62.5 Conviction in civil or crimin al proceedings wi thout imprisonment\nV62.5 Imprisonment or other incarceration\nV62.5 Problems related to other legal circumstances\nV62.5 Problems related to release from prison\nV62.82 Uncomplicated bereavement\nV62.83 Encounter for mental health services for perpetrator of nonparental child abuse\nV62.83 Encounter for mental health servic es for perpetrator of nonparental child \nneglect\nV62.83 Encounter for mental health servic es for perpetrator of nonparental child \npsychological abuse\nV62.83 Encounter for mental health servic es for perpetrator of nonparental child \nsexual abuse\nV62.83 Encounter for mental health services for perpetrator of nonspousal adult abuse\nV62.89 Borderline inte llectual functioning\nV62.89 Discord with social service provider, including probation officer, case manager, \nor social services worker\nV62.89 Other problem related to psychosocial circumstances\nV62.89 Phase of life problem\nV62.89 Religious or spiritual problem\nV62.89 Victim of crime\nV62.89 Victim of terrorism or torture\nV62.9 Unspecified problem related to social environment\nV62.9 Unspecified problem related to unspecified psychosocial circumstances", "source": "dsm5.pdf"} {"id": "01e00b417c9a-1", "page_content": "V62.9 Unspecified problem related to unspecified psychosocial circumstances\nV63.8 Unavailability or inaccessibility of other helping agencies\nV63.9 Unavailability or inaccessibility of health care facilities\nV65.2 Malingering\nV65.40 Other counseling or consultation\nV65.49 Encounter for mental health services for victim of nons pousal adult abuse\nV65.49 Sex counseling\nV69.9 Problem related to lifestyle\nV71.01 Adult antisocial behavior\nV71.02 Child or adolescent antisocial behaviorICD-9-CM Disorder, cond ition, or problem", "source": "dsm5.pdf"} {"id": "1f10cd8a1d71-0", "page_content": "877Numerical Listing of\n DSM-5 Diagnoses and Codes\n(ICD-10-CM)\nICD-10-CM codes are to be us ed for coding purposes in the United States starting \nOctober 1, 2014.\nICD-10-CM Disorder, co ndition, or problem\nE66.9 Overweight or obesity\nF01.50 Probable major vascular neurocognitive disorder, Without be havioral disturbance\nF01.51 Probable major vascular neurocognitive di sorder, With beha vioral disturbance\nF02.80 Major neurocognitive disorder du e to another medical condition, Without \nbehavioral disturbance\nF02.80 Major neurocognitive disorder du e to HIV infection, Without behavioral \ndisturbance ( code first B20 HIV infection)\nF02.80 Major neurocognitive disorder due to Hunting ton\u2019s disease, Without \nbehavioral disturbance ( code first G10 Huntington\u2019s disease)\nF02.80 Major neurocognitive disorder due to multiple etio logies, Without behavioral \ndisturbance\nF02.80 Major neurocognitive disorder probably due to Parkinson\u2019s disease, Without \nbehavioral disturbance ( code first G20 Parkinson\u2019s disease)\nF02.80 Major neurocognitive disorder du e to prion disease, Without behavioral \ndisturbance ( code first A81.9 prion disease)\nF02.80 Major neurocognitive disorder due to traumati c brain injury, Without \nbehavioral disturbance ( code first S06.2X9S diffuse traumatic brain injury \nwith loss of consciousness of unspecified duration, sequela)\nF02.80 Probable major frontotemporal neuroc ognitive disorder, Without behavioral \ndisturbance ( code first G31.09 frontotemporal disease)", "source": "dsm5.pdf"} {"id": "1f10cd8a1d71-1", "page_content": "disturbance ( code first G31.09 frontotemporal disease)\nF02.80 Probable major neurocognitive diso rder due to Alzheimer\u2019s disease, Without \nbehavioral disturbance ( code first G30.9 Alzheimer\u2019s disease)\nF02.80 Probable major neurocognitive disorder with Lewy bodies, Without \nbehavioral disturbance ( code first G31.83 Lewy body disease)\nF02.81 Major neurocognitive disorder du e to another medical condition, With \nbehavioral disturbance\nF02.81 Major neurocognitive disorder du e to HIV infection, With behavioral \ndisturbance ( code first B20 HIV infection)\nF02.81 Major neurocognitive disorder due to Huntington\u2019s disease, With behavioral \ndisturbance ( code first G10 Huntington\u2019s disease)\nF02.81 Major neurocognitive disorder due to multiple etiologies, With behavioral \ndisturbance", "source": "dsm5.pdf"} {"id": "6cd903b28c25-0", "page_content": "878 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nF02.81 Major neurocognitive disorder probably due to Parkinson\u2019s disease, With \nbehavioral disturbance ( code first G20 Parkinson\u2019s disease)\nF02.81 Major neurocognitive disorder du e to prion disease, With behavioral \ndisturbance ( code first A81.9 prion disease)\nF02.81 Major neurocognitive di sorder due to traumatic brain injury, With behavioral \ndisturbance ( code first S06.2X9S diffuse traumatic brain injury with loss of \nconsciousness of unspecified duration, sequela)\nF02.81 Probable major frontotemporal neur ocognitive disorder , With behavioral \ndisturbance ( code first G31.09 frontotemporal disease)\nF02.81 Probable major neurocognitive diso rder due to Alzheimer\u2019s disease, With \nbehavioral disturbance ( code first G30.9 Alzheimer\u2019s disease)\nF02.81 Probable major neurocognitive disord er with Lewy bodies, With behavioral \ndisturbance ( code first G31.83 Lewy body disease)\nF05 Delirium due to another medical condition\nF05 Delirium due to multiple etiologies\nF06.0 Psychotic disorder due to another medical condition, With hallucinations\nF06.1 Catatonia associated with another mental disord er (catatonia specifier)\nF06.1 Catatonic disorder due to another medical condition\nF06.1 Unspecified catatonia (code first R29.818 other symptoms involving nervous \nand musculoskeletal systems)\nF06.2 Psychotic disorder due to another medical condition, With delusions\nF06.31 Depressive disorder due to another medical condition, With depressive features", "source": "dsm5.pdf"} {"id": "6cd903b28c25-1", "page_content": "F06.31 Depressive disorder due to another medical condition, With depressive features\nF06.32 Depressive disorder due to anoth er medical condition, With major \ndepressive\u2013like episode\nF06.33 Bipolar and related disorder due to another medical condition, With manic features\nF06.33 Bipolar and related disorder due to another medical condition, With manic- or \nhypomanic-like episodes\nF06.34 Bipolar and related disorder due to another medical condition, With mixed \nfeatures\nF06.34 Depressive disorder due to another medical condition, With mixed features\nF06.4 Anxiety disorder due to another medical condition\nF06.8 Obsessive-compulsive and related disorder due to another medical condition \nF06.8 Other specified mental disorder due to another medical condition\nF07.0 Personality change due to another medical condition\nF09 Unspecified mental disorder due to another medical condition\nF10.10 Alcohol use disorder, Mild\nF10.121 Alcohol intoxication deli rium, With mild use disorder\nF10.129 Alcohol intoxication , With mild use disorder\nF10.14 Alcohol-induced bipolar and related disorder, With mild use disorder\nF10.14 Alcohol-induced depressive disorder, With mild use disorder\nF10.159 Alcohol-induced psychotic disorder, With mild use disorder\nF10.180 Alcohol-induced anxiety di sorder, With mild use disorder\nF10.181 Alcohol-induced sexual dysfunction, With mild use disorder\nF10.182 Alcohol-induced sleep disorder, With mild use disorder\nF10.20 Alcohol use disorder, Moderate\nF10.20 Alcohol use disorder, Severe\nF10.221 Alcohol intoxication delirium, Wi th moderate or severe use disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "b636bffe73c7-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 879\nF10.229 Alcohol intoxicati on, With moderate or severe use disorder\nF10.231 Alcohol withdrawal delirium\nF10.232 Alcohol withdrawal, Wi th perceptual disturbances\nF10.239 Alcohol withdrawal, With out perceptual disturbances\nF10.24 Alcohol-induced bipolar and related disorder, With moderate or severe use \ndisorder\nF10.24 Alcohol-induced depressive disorder, With moderate or severe use disorder\nF10.259 Alcohol-induced psychotic disorder, With moderate or severe use disorder\nF10.26 Alcohol-induced major neurocogniti ve disorder, Amnestic confabulatory \ntype, With moderate or severe use disorder\nF10.27 Alcohol-induced major neurocogniti ve disorder, Nonamnestic confabulatory \ntype, With moderate or severe use disorder\nF10.280 Alcohol-induced anxiety disorder, With moderate or severe use disorder\nF10.281 Alcohol-induced sexual dysfunction, With moderate or severe use disorder\nF10.282 Alcohol-induced sleep disorder, With moderate or severe use disorder\nF10.288 Alcohol-induced mild neurocognitive disorder, With moderate or severe use \ndisorder\nF10.921 Alcohol intoxication delirium, Without use disorder\nF10.929 Alcohol intoxicati on, Without use disorder\nF10.94 Alcohol-induced bipolar and related disorder, Without use disorder\nF10.94 Alcohol-induced depressive disorder, Without use disorder\nF10.959 Alcohol-induced psychotic disorder, Without use disorder\nF10.96 Alcohol-induced major neurocogniti ve disorder, Amnestic confabulatory \ntype, Without use disorder\nF10.97 Alcohol-induced major neurocogniti ve disorder, Nonamnestic confabulatory \ntype, Without use disorder\nF10.980 Alcohol-induced anxiety disorder, Without use disorder", "source": "dsm5.pdf"} {"id": "b636bffe73c7-1", "page_content": "type, Without use disorder\nF10.980 Alcohol-induced anxiety disorder, Without use disorder\nF10.981 Alcohol-induced sexual dysfunction, Without use disorder\nF10.982 Alcohol-induced sleep disorder, Without use disorder\nF10.988 Alcohol-induced mild neurocognitive disorder, Without use disorder\nF10.99 Unspecified alcohol-related disorder\nF11.10 Opioid use disorder, Mild\nF11.121 Opioid intoxication delirium, With mild use disorder\nF11.122 Opioid intoxication, With perceptu al disturbances, With mild use disorder\nF11.129 Opioid intoxication, Wi thout perceptual disturbanc es, With mild use disorder\nF11.14 Opioid-induced depressive disorder, With mild use disorder\nF11.181 Opioid-induced sexual dysfunction, With mild use disorder\nF11.182 Opioid-induced sleep disorder, With mild use disorder\nF11.188 Opioid-induced anxiety disorder, With mild use disorder\nF11.20 Opioid use disorder, Moderate\nF11.20 Opioid use disorder, Severe\nF11.221 Opioid intoxication delirium, With moderate or severe use disorder\nF11.222 Opioid intoxication, Wi th perceptual disturbances, With moderate or severe \nuse disorder\nF11.229 Opioid intoxication, Without percep tual disturbances, With moderate or \nsevere use disorder\nF11.23 Opioid withdrawal ICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "d60bbc55c1ef-0", "page_content": "880 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nF11.23 Opioid with drawal delirium\nF11.24 Opioid-induced depressive disorder, With moderate or severe use disorder\nF11.281 Opioid-induced sexual dysfunction, With moderate or severe use disorder\nF11.282 Opioid-induced sleep disorder, With moderate or severe use disorder\nF11.288 Opioid-induced anxiet y disorder, With moderate or severe use disorder\nF11.921 Opioid-induced delirium\nF11.921 Opioid intoxication delirium, Without use disorder\nF11.922 Opioid intoxication, With perceptual disturbances, Without use disorder\nF11.929 Opioid intoxication, Without percep tual disturbances, Without use disorder\nF11.94 Opioid-induced depressive disorder, Without use disorder\nF11.981 Opioid-induced sexual dy sfunction, Without use disorder\nF11.982 Opioid-induced sleep disorder, Without use disorder\nF11.988 Opioid-induced anxiety disorder, Without use disorder\nF11.99 Unspecified opioid-related disorder\nF12.10 Cannabis use disorder, Mild\nF12.121 Cannabis intoxication delirium, With mild use disorder\nF12.122 Cannabis intoxication, With perceptu al disturbances, With mild use disorder\nF12.129 Cannabis intoxication, Without percep tual disturbances, With mild use disorder\nF12.159 Cannabis-induced psychotic disorder, With mild use disorder\nF12.180 Cannabis-induced anxiety di sorder, With mild use disorder\nF12.188 Cannabis-induced sleep disorder, With mild use disorder\nF12.20 Cannabis use disorder, Moderate\nF12.20 Cannabis use disorder, Severe\nF12.221 Cannabis intoxication delirium, With moderate or severe use disorder", "source": "dsm5.pdf"} {"id": "d60bbc55c1ef-1", "page_content": "F12.221 Cannabis intoxication delirium, With moderate or severe use disorder\nF12.222 Cannabis intoxication, Wi th perceptual dist urbances, With moderate or severe \nuse disorder\nF12.229 Cannabis intoxication, Without perceptual disturbances, With moderate or \nsevere use disorder\nF12.259 Cannabis-induced psychotic disorder, With moderate or severe use disorder\nF12.280 Cannabis-induced anxiet y disorder, With moderate or severe use disorder\nF12.288 Cannabis-induced sleep disorder, With moderate or severe use disorder\nF12.288 Cannabis withdrawal \nF12.921 Cannabis intoxication delirium, Without use disorder\nF12.922 Cannabis intoxication, With perceptual disturbances, Without use disorder\nF12.929 Cannabis intoxica tion, Without percep tual disturbances, Without use disorder\nF12.959 Cannabis-induced psychotic disorder, Without use disorder\nF12.980 Cannabis-induced anxiety disorder, Without use disorder\nF12.988 Cannabis-induced sleep disorder, Without use disorder\nF12.99 Unspecified cannabis-related disorder\nF13.10 Sedative, hypnotic, or anxiolytic use disorder, Mild\nF13.121 Sedative, hypnotic, or anxiolytic intoxication deli rium, With mild use disorder\nF13.129 Sedative, hypnotic, or anxiolytic intoxication, With mild use disorder\nF13.14 Sedative-, hypnotic-, or anxiolytic-i nduced bipolar and related disorder, With \nmild use disorder\nF13.14 Sedative-, hypnotic-, or anxiolytic-induced depressive disorder, With mild use \ndisorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "3601037e9d75-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 881\nF13.159 Sedative-, hypnotic-, or anxiolytic-induced psych otic disorder, With mild use \ndisorder\nF13.180 Sedative-, hypnotic-, or anxiolytic -induced anxiety disorder, With mild use \ndisorder\nF13.181 Sedative-, hypnotic-, or anxiolytic-induced sexual dysfunction, With mild use \ndisorder\nF13.182 Sedative-, hypnotic-, or anxiolytic-ind uced sleep disorder, Wi th mild use disorder\nF13.20 Sedative, hypnotic, or an xiolytic use disorder, Moderate\nF13.20 Sedative, hypnotic, or an xiolytic use disorder, Severe\nF13.221 Sedative, hypnotic, or anxiolytic in toxication delirium, With moderate or \nsevere use disorder\nF13.229 Sedative, hypnotic, or anxiolytic intoxication, With mo derate or severe use disorder\nF13.231 Sedative, hypnotic, or an xiolytic withdrawal delirium\nF13.232 Sedative, hypnotic, or anxiolytic withdr awal, With perceptual disturbances\nF13.239 Sedative, hypnotic, or anxiolytic wi thdrawal, Without perceptual disturbances\nF13.24 Sedative-, hypnotic-, or anxiolytic-induced bipolar and related disorder, With \nmoderate or severe use disorder\nF13.24 Sedative-, hypnotic-, or anxiolytic-induced depressive disorder, With \nmoderate or severe use disorder\nF13.259 Sedative-, hypnotic-, or anxiolytic-induced psychotic disorder, With moderate \nor severe use disorder", "source": "dsm5.pdf"} {"id": "3601037e9d75-1", "page_content": "or severe use disorder\nF13.27 Sedative-, hypnotic-, or anxiolytic -induced major neurocognitive disorder, \nWith moderate or severe use disorder\nF13.280 Sedative-, hypnotic-, or anxiolytic-i nduced anxiety disorder, With moderate or \nsevere use disorder\nF13.281 Sedative-, hypnotic-, or anxiolytic-induced sexual dysfunction, With moderate \nor severe use disorder\nF13.282 Sedative-, hypnotic-, or anxiolytic-induced sleep disorder, With moderate or \nsevere use disorder\nF13.288 Sedative-, hypnotic-, or anxiolytic -induced mild neuroc ognitive disorder, \nWith moderate or severe use disorder\nF13.921 Sedative-, hypnotic-, or anxiolytic-induced delirium\nF13.921 Sedative, hypnotic, or anxiolytic in toxication delirium, Without use disorder\nF13.929 Sedative, hypnotic, or anxiolyt ic intoxication, Without use disorder\nF13.94 Sedative-, hypnotic-, or anxiolytic-induced bipolar and related disorder, \nWithout use disorder\nF13.94 Sedative-, hypnotic-, or anxiolytic -induced depressive disorder, Without use \ndisorder\nF13.959 Sedative-, hypnotic-, or anxiolytic -induced psychotic disorder, Without use \ndisorder\nF13.97 Sedative-, hypnotic-, or anxiolytic -induced major neurocognitive disorder, \nWithout use disorder\nF13.980 Sedative-, hypnotic-, or anxiolytic-i nduced anxiety disorder, Without use disorder\nF13.981 Sedative-, hypnotic-, or anxiolytic -induced sexual dysfunction, Without use \ndisorder", "source": "dsm5.pdf"} {"id": "3601037e9d75-2", "page_content": "disorder\nF13.982 Sedative-, hypnotic-, or anxiolytic-i nduced sleep disorder, Without use disorder\nF13.988 Sedative-, hypnotic-, or anxiolytic -induced mild neuroc ognitive disorder, \nWithout use disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "da701a1324ba-0", "page_content": "882 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nF13.99 Unspecified sedative-, hypnotic-, or anxiolytic-related disorder\nF14.10 Cocaine use disorder, Mild\nF14.121 Cocaine intoxication delirium, With mild use disorder\nF14.122 Cocaine intoxication, With perceptual disturbances, With mild use disorder\nF14.129 Cocaine intoxication, Wi thout perceptual disturbances, With mild use disorder\nF14.14 Cocaine-induced bipolar and related disorder, With mild use disorder\nF14.14 Cocaine-induced depressive disorder, With mild use disorder\nF14.159 Cocaine-induced psychotic disorder, With mild use disorder\nF14.180 Cocaine-induced anxiety disorder, With mild use disorder\nF14.181 Cocaine-induced sexual dysfunction, With mild use disorder\nF14.182 Cocaine-induced sleep disorder, With mild use disorder\nF14.188 Cocaine-induced obsessive-compulsive and related disorder, With mild use \ndisorder\nF14.20 Cocaine use disorder, Moderate\nF14.20 Cocaine use disorder, Severe\nF14.221 Cocaine intoxication delirium, With moderate or severe use disorder\nF14.222 Cocaine intoxication, Wi th perceptual disturbances, With moderate or severe \nuse disorder\nF14.229 Cocaine intoxication, Without perceptual disturbances, With moderate or \nsevere use disorder\nF14.23 Cocaine withdrawal\nF14.24 Cocaine-induced bipolar and related disorder, With moderate or severe use \ndisorder\nF14.24 Cocaine-induced depressive disorder, With moderate or severe use disorder\nF14.259 Cocaine-induced psychotic disorder, With moderate or severe use disorder\nF14.280 Cocaine-induced anxiety disorder, With moderate or severe use disorder", "source": "dsm5.pdf"} {"id": "da701a1324ba-1", "page_content": "F14.280 Cocaine-induced anxiety disorder, With moderate or severe use disorder\nF14.281 Cocaine-induced sexual dysfunction, With moderate or severe use disorder\nF14.282 Cocaine-induced sleep disorder, With moderate or severe use disorder\nF14.288 Cocaine-induced obsessive-compulsive and related disorder, With moderate \nor severe use disorder\nF14.921 Cocaine intoxication de lirium, Without use disorder\nF14.922 Cocaine intoxication, With perceptual disturba nces, Without use disorder\nF14.929 Cocaine intoxication, Without perceptual disturba nces, Without use disorder\nF14.94 Cocaine-induced bipolar and related disorder, Without use disorder\nF14.94 Cocaine-induced depressive disorder, Without use disorder\nF14.959 Cocaine-induced psychotic disorder, Without use disorder\nF14.980 Cocaine-induced anxiety disorder, Without use disorder\nF14.981 Cocaine-induced sexual dysfunction, Without use disorder\nF14.982 Cocaine-induced sleep disorder, Without use disorder\nF14.988 Cocaine-induced obsessive-compulsive and related disorder, Without use disorder\nF14.99 Unspecified stimulant-related disorder, Unspecified Cocaine-related disorder\nF15.10 Amphetamine-type su bstance use disorder, Mild\nF15.10 Other or unspecified stimulant use disorder, Mild\nF15.121 Amphetamine (or other stimulant) intoxication delirium, With mild use disorder\nF15.122 Amphetamine or other stimulant intoxication, With perceptual disturbances, \nWith mild use disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "1218c2ff7ddf-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 883\nF15.129 Amphetamine or ot her stimulant intoxicatio n, Without perceptual \ndisturbances, With mild use disorder\nF15.14 Amphetamine (or other stimulant)\u2013i nduced bipolar and related disorder, \nWith mild use disorder\nF15.14 Amphetamine (or other stimulant)\u2013induced depressive disorder, With mild \nuse disorder\nF15.159 Amphetamine (or other stimulant)\u2013ind uced psychotic disorder, With mild use \ndisorder\nF15.180 Amphetamine (or other stimulant)\u2013i nduced anxiety disorder, With mild use \ndisorder\nF15.180 Caffeine-induced anxiety disorder, With mild use disorder\nF15.181 Amphetamine (or other stimulant)\u2013induced sexual dysfunction, With mild \nuse disorder\nF15.182 Amphetamine (or other stimulant)\u2013induc ed sleep disorder, With mild use disorder\nF15.182 Caffeine-induced sleep disorder, With mild use disorder\nF15.188 Amphetamine (or other stimulant)\u2013induced obsessive-compulsive and related \ndisorder, With mild use disorder\nF15.20 Amphetamine-type subs tance use disorder, Moderate\nF15.20 Amphetamine-type subs tance use disorder, Severe\nF15.20 Other or unspecified st imulant use disorder, Moderate\nF15.20 Other or unspecified st imulant use disorder, Severe\nF15.221 Amphetamine (or other stimulant) intoxication delirium, With moderate or \nsevere use disorder\nF15.222 Amphetamine or other stimulant intoxication, With perceptual disturbances, \nWith moderate or severe use disorder", "source": "dsm5.pdf"} {"id": "1218c2ff7ddf-1", "page_content": "With moderate or severe use disorder\nF15.229 Amphetamine or ot her stimulant intoxicatio n, Without perceptual \ndisturbances, With moderate or severe use disorder\nF15.23 Amphetamine or ot her stimulan t withdrawal\nF15.24 Amphetamine (or other stimulant)\u2013i nduced bipolar and related disorder, \nWith moderate or severe use disorder\nF15.24 Amphetamine (or other stimulant) \u2013induced depressive disorder, With \nmoderate or severe use disorder\nF15.259 Amphetamine (or other stimulant) \u2013induced psychoti c disorder, With \nmoderate or severe use disorder\nF15.280 Amphetamine (or other stimulant)\u2013induced anxiety disorder, With moderate \nor severe use disorder\nF15.280 Caffeine-induced anxiety disorder, With moderate or severe use disorder\nF15.281 Amphetamine (or other stimulant)\u2013induced sexual dy sfunction, With \nmoderate or severe use disorder\nF15.282 Amphetamine (or other stimulant)\u2013induced sleep disorder, With moderate or \nsevere use disorder\nF15.282 Caffeine-induced sleep disorder, With moderate or severe use disorder\nF15.288 Amphetamine (or other stimulant)\u2013induced obsessive-compulsive and related \ndisorder, With moderate or severe use disorder\nF15.921 Amphetamine (or other stimulant)\u2013induced delirium\nF15.921 Amphetamine (or other stimulant) intoxication deli rium, Without use disorder\nF15.922 Amphetamine or other stimulant intoxication, With perceptual disturbances, \nWithout use disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "cdcf0f153ff3-0", "page_content": "884 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nF15.929 Amphetamine or ot her stimulant intoxicatio n, Without perceptual \ndisturbances, Without use disorder\nF15.929 Caffeine intoxication \nF15.93 Caffeine withdrawal \nF15.94 Amphetamine (or other stimulant)\u2013i nduced bipolar and related disorder, \nWithout use disorder\nF15.94 Amphetamine (or other stimulant)\u2013induced depressive disorder, Without use \ndisorder\nF15.959 Amphetamine (or other stimulant)\u2013i nduced psychotic disorder, Without use \ndisorder\nF15.980 Amphetamine (or other stimulant)\u2013i nduced anxiety disorder, Without use \ndisorder\nF15.980 Caffeine-induced anxiety disorder, Without use disorder\nF15.981 Amphetamine (or other stimulant)\u2013induced sexual dysfunction, Without use \ndisorder\nF15.982 Amphetamine (or other stimulant)\u2013ind uced sleep disorder, Without use disorder\nF15.982 Caffeine-induced sleep disorder, Without use disorder\nF15.988 Amphetamine (or other stimulant)\u2013induced obsessive-compulsive and related \ndisorder, Without use disorder\nF15.99 Unspecified amphetamine or other stimulant-related disorder\nF15.99 Unspecified caffeine-related disorder\nF16.10 Other hallucinogen use disorder, Mild\nF16.10 Phencyclidine use disorder, Mild\nF16.121 Other hallucinogen intoxication delirium, With mild use disorder\nF16.121 Phencyclidine intoxication delirium, With mild use disorder\nF16.129 Other hallucinogen intoxi cation, With mi ld use disorder", "source": "dsm5.pdf"} {"id": "cdcf0f153ff3-1", "page_content": "F16.129 Other hallucinogen intoxi cation, With mi ld use disorder\nF16.129 Phencyclidine intoxication, With mild use disorder\nF16.14 Other hallucinogen\u2013induced bipolar and related disorder, With mild use disorder\nF16.14 Other hallucinogen\u2013ind uced depressive disorder, With mild use disorder\nF16.14 Phencyclidine-induced bipolar and related disorder, With mild use disorder\nF16.14 Phencyclidine-induced depressive disorder, With mild use disorder\nF16.159 Other hallucinogen\u2013i nduced psychotic disorder, With mild use disorder\nF16.159 Phencyclidine-induced psychotic disorder, With mild use disorder\nF16.180 Other hallucinogen\u2013i nduced anxiety disorder, With mild use disorder\nF16.180 Phencyclidine-indu ced anxiety disorder, With mild use disorder\nF16.20 Other hallucinogen use disorder, Moderate\nF16.20 Other hallucinogen use disorder, Severe\nF16.20 Phencycl idine use disorder, Moderate\nF16.20 Phencyclidine use disorder, Severe\nF16.221 Other hallucinogen intoxication delirium, With moderate or severe use disorder\nF16.221 Phencyclidine intoxication delirium, With moderate or severe use disorder\nF16.229 Other hallucinogen intoxication, With moderate or severe use disorder\nF16.229 Phencyclidine intoxication, With moderate or severe use disorder\nF16.24 Other hallucinogen\u2013ind uced bipolar and related disorder, With moderate or \nsevere use disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "65be08cff400-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 885\nF16.24 Other hallucinogen\u2013ind uced depressive disorder, With moderate or severe \nuse disorder\nF16.24 Phencyclidine-induced bipolar and related disorder, With moderate or severe \nuse disorder\nF16.24 Phencyclidine-induced depressive disord er, With moderate or severe use disorder\nF16.259 Other hallucinog en\u2013induced psychotic disorder, With moderate or severe use \ndisorder\nF16.259 Phencyclidine-induced psychotic disord er, With moderate or severe use disorder\nF16.280 Other hallucinogen\u2013ind uced anxiety disorder, With moderate or severe use \ndisorder\nF16.280 Phencyclidine-induced anxiety disorder, With moderate or severe use disorder\nF16.921 Other hallucinogen intoxication delirium, Without use disorder\nF16.921 Phencyclidine intoxication delirium, Without use disorder\nF16.929 Other hallucinogen intoxication, Without use disorder\nF16.929 Phencyclidine intoxicat ion, Without use disorder\nF16.94 Other hallucinogen\u2013induced bipolar and related disorder, Without use disorder\nF16.94 Other hallucinogen\u2013i nduced depressive disorder, Without use disorder\nF16.94 Phencyclidine-induced bipolar and related disorder, Without use disorder\nF16.94 Phencyclidine-induced depressive disorder, Without use disorder\nF16.959 Other hallucinogen\u2013i nduced psychotic disord er, Without use disorder\nF16.959 Phencyclidine-induced psychotic disorder, Without use disorder\nF16.980 Other hallucinogen \u2013induced anxiety disord er, Without use disorder\nF16.980 Phencyclidine-in duced anxiety disorder , Without use disorder", "source": "dsm5.pdf"} {"id": "65be08cff400-1", "page_content": "F16.980 Phencyclidine-in duced anxiety disorder , Without use disorder\nF16.983 Hallucinogen persisting perception disorder \nF16.99 Unspecified halluc inogen-related disorder\nF16.99 Unspecified phencyclidine-related disorder\nF17.200 Tobacco use disorder, Moderate\nF17.200 Tobacco use disorder, Severe\nF17.203 Tobacco withdrawal\nF17.208 Tobacco-induced sleep disorder, Wi th moderate or severe use disorder\nF17.209 Unspecified tobac co-related disorder\nF18.10 Inhalant use disorder, Mild\nF18.121 Inhalant intoxication delirium, With mild use disorder\nF18.129 Inhalant intoxication, With mild use disorder\nF18.14 Inhalant-induced depressive disorder, With mild use disorder\nF18.159 Inhalant-induced psychotic disorder, With mild use disorder\nF18.17 Inhalant-induced major neurocogni tive disorder, With mild use disorder\nF18.180 Inhalant-induced anxiety di sorder, With mild use disorder\nF18.188 Inhalant-induced mild neurocognitive disorder, With mild use disorder\nF18.20 Inhalant use disorder, Moderate\nF18.20 Inhalant use disorder, Severe\nF18.221 Inhalant intoxication delirium, With moderate or severe use disorder\nF18.229 Inhalant intoxication, With moderate or severe use disorder\nF18.24 Inhalant-induced depressive disorder, With moderate or severe use disorder\nF18.259 Inhalant-induced psychotic disorder, With moderate or severe use disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "04001230c6c9-0", "page_content": "886 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nF18.27 Inhalant-induced major neurocognitive disorder, With moderate or severe use \ndisorder\nF18.280 Inhalant-induced anxiety disorder, With moderate or severe use disorder\nF18.288 Inhalant-induced mild neurocognitive disorder, With mode rate or severe use \ndisorder\nF18.921 Inhalant intoxication delirium, Without use disorder\nF18.929 Inhalant intoxicatio n, Without use disorder\nF18.94 Inhalant-induced depressive disorder, Without use disorder\nF18.959 Inhalant-induced psychotic disorder, Without use disorder\nF18.97 Inhalant-induced major neurocog nitive disorder, Wi thout use disorder\nF18.980 Inhalant-induced anxiety disorder, Without use disorder\nF18.988 Inhalant-induced mild neurocogni tive disorder, Without use disorder\nF18.99 Unspecified inhalant-related disorder\nF19.10 Other (or unknown) su bstance use disorder, Mild\nF19.121 Other (or unknown) substance intoxi cation delirium, With mild use disorder\nF19.129 Other (or unknown) substance in toxication, With mild use disorder\nF19.14 Other (or unknown) substance\u2013induced bipolar and related disorder, With \nmild use disorder\nF19.14 Other (or unknown) substance\u2013induced depressive disorder, With mild use \ndisorder\nF19.159 Other (or unknown) substance\u2013indu ced psychotic disorder, With mild use \ndisorder\nF19.17 Other (or unknown) substance\u2013induce d major neurocogniti ve disorder, With \nmild use disorder\nF19.180 Other (or unknown) substance\u2013induced anxiety disorder, With mild use disorder", "source": "dsm5.pdf"} {"id": "04001230c6c9-1", "page_content": "F19.181 Other (or unknown) substance\u2013induced sexual dysfunction, With mild use \ndisorder\nF19.182 Other (or unknown) substance\u2013induced sleep disorder, With mild use disorder\nF19.188 Other (or unknown) substance\u2013induce d mild neurocognitive disorder, With \nmild use disorder\nF19.188 Other (or unknown) substance\u2013induced obsessive-compulsive and related \ndisorder, With mild use disorder\nF19.20 Other (or unknown) substance use disorder, Moderate\nF19.20 Other (or unknown) su bstance use disorder, Severe\nF19.221 Other (or unknown) subs tance intoxication delirium, With moderate or severe \nuse disorder\nF19.229 Other (or unknown) substance intoxication, With moderate or severe use disorder\nF19.231 Other (or unknown) su bstance withdrawal delirium\nF19.239 Other (or unknown) substance withdrawal \nF19.24 Other (or unknown) substance\u2013induced bipolar and related disorder, With \nmoderate or seve re use disorder\nF19.24 Other (or unknown) substance\u2013induced depressive disorder, With moderate \nor severe use disorder\nF19.259 Other (or unknown) substance\u2013induce d psychotic disorder, With moderate or \nsevere use disorder\nF19.27 Other (or unknown) substance\u2013induce d major neurocogniti ve disorder, With \nmoderate or seve re use disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "419497a915bd-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 887\nF19.280 Other (or unknown) substance\u2013induce d anxiety disorder, With moderate or \nsevere use disorder\nF19.281 Other (or unknown) substance\u2013induced sexual dysfunction, With moderate or \nsevere use disorder\nF19.282 Other (or unknown) substance\u2013indu ced sleep disorder, With moderate or \nsevere use disorder\nF19.288 Other (or unknown) substance\u2013induce d mild neurocognitive disorder, With \nmoderate or severe use disorder\nF19.288 Other (or unknown) substance\u2013induced obsessive-compulsive and related \ndisorder, With moderate or severe use disorder\nF19.921 Other (or unknown) substance\u2013induced delirium\nF19.921 Other (or unknown) substance into xication delirium, Without use disorder\nF19.929 Other (or unknown) substance intoxication, With out use disorder\nF19.94 Other (or unknown) substance\u2013induced bipolar and related disorder, Without \nuse disorder\nF19.94 Other (or unknown) subs tance\u2013induced depressive disorder, Without use disorder\nF19.959 Other (or unknown) substance\u2013induced psychotic disorder, Without use disorder\nF19.97 Other (or unknown) substance\u2013in duced major neurocognitive disorder, \nWithout use disorder\nF19.980 Other (or unknown) substance\u2013induced anxiety disorder, Without use disorder\nF19.981 Other (or unknown) substance\u2013induced sexual dysfunction, Without use disorder\nF19.982 Other (or unknown) substance\u2013indu ced sleep disorder, Without use disorder\nF19.988 Other (or unknown) substance\u2013induced mild neurocognitive disorder, \nWithout use disorder", "source": "dsm5.pdf"} {"id": "419497a915bd-1", "page_content": "Without use disorder\nF19.988 Other (or unknown) substance\u2013induced obsessive-compulsive and related \ndisorder, Without use disorder\nF19.99 Unspecified other (or unknow n) substance\u2013related disorder \nF20.81 Schizophreniform disorder\nF20.9 Schizophrenia\nF21 Schizotypal personality disorder\nF22 Delusional disorder\nF23 Brief psychotic disorder\nF25.0 Schizoaffective disorder, Bipolar type\nF25.1 Schizoaffective disorder, Depressive type\nF28 Other specified schizophrenia sp ectrum and other psychotic disorder\nF29 Unspecified schizophrenia spec trum and other psychotic disorder\nF31.0 Bipolar I disorder, Current or most recent episode hypomanic\nF31.11 Bipolar I disorder , Current or most rece nt episode manic, Mild\nF31.12 Bipolar I disorder, Current or most recent episode manic, Moderate\nF31.13 Bipolar I disorder, Current or most recent episode manic, Severe\nF31.2 Bipolar I disorder, Current or most re cent episode manic, Wi th psychotic features\nF31.31 Bipolar I disorder, Current or most recent episode depressed, Mild\nF31.32 Bipolar I disorder, Cu rrent or most recent episode depressed, Moderate\nF31.4 Bipolar I disorder, Current or mo st recent episode depressed, Severe\nF31.5 Bipolar I disorder, Current or most recent episode depressed, With psychotic \nfeaturesICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "fae2a7e32c59-0", "page_content": "888 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nF31.71 Bipolar I disorder, Current or most rece nt episode hypomanic, In partial remission\nF31.72 Bipolar I disorder, Curr ent or most recent episode hypomanic, In full remission\nF31.73 Bipolar I disorder, Curre nt or most recent episode manic, In partial remission\nF31.74 Bipolar I disorder, Curre nt or most recent episode manic, In full remission\nF31.75 Bipolar I disorder, Current or most recent episode depressed, In partial remission\nF31.76 Bipolar I disorder, Current or most recent episode depressed, In full remission\nF31.81 Bipolar II disorder\nF31.89 Other specified bipolar and related disorder\nF31.9 Bipolar I disorder, Current or most recent episode depressed, Unspecified\nF31.9 Bipolar I disorder, Current or most recent episode hypomanic, Unspecified\nF31.9 Bipolar I disorder, Current or mo st recent episode manic, Unspecified\nF31.9 Bipolar I disorder, Current or most recent episode unspecified \nF31.9 Unspecified bipolar and related disorder\nF32.0 Major depressive disorder, Single episode, Mild\nF32.1 Major depressive disorder, Single episode, Moderate\nF32.2 Major depressive disorder, Single episode, Severe \nF32.3 Major depressive disorder, Single episode, With psychotic features\nF32.4 Major depressive disorder, Single episode, In partial remission\nF32.5 Major depressive disorder, Single episode, In full remission\nF32.8 Other specified depressive disorder\nF32.9 Major depressive disorder, Single episode, Unspecifed\nF32.9 Unspecified depressive disorder", "source": "dsm5.pdf"} {"id": "fae2a7e32c59-1", "page_content": "F32.9 Unspecified depressive disorder\nF33.0 Major depressive disorde r, Recurrent episode, Mild\nF33.1 Major depressive disorder, Recurrent episode, Moderate\nF33.2 Major depressive disorder, Recurrent episode, Severe \nF33.3 Major depressive disorder, Recurre nt episode, With psychotic features\nF33.41 Major depressive disorder, Recurrent episode, In partial remission\nF33.42 Major depressive disorder, Recurrent episode, In full remission\nF33.9 Major depressive disorder, Recurrent episode, Unspecified\nF34.0 Cyclothymic disorder \nF34.1 Persistent depressi ve disorder (dysthymia)\nF34.8 Disruptive mood dysregulation disorder \nF40.00 Agoraphobia\nF40.10 Social anxiety disorder (social phobia)\nF40.218 Specific phobia, Animal\nF40.228 Specific phobia, Natural environment\nF40.230 Specific phobia, Fear of blood\nF40.231 Specific phobia, Fear of injections and transfusions\nF40.232 Specific phobia, Fear of other medical care\nF40.233 Specific phobia, Fear of injury\nF40.248 Specific phobia, Situational \nF40.298 Specific phobia, Other\nF41.0 Panic disorder \nF41.1 Generalized anxiety disorder \nF41.8 Other specified anxiety disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "0a507111de98-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 889\nF41.9 Unspecified anxiety disorder\nF42 Hoarding disorder\nF42 Obsessive-compulsive disorder\nF42 Other specified obsessive-compulsive and related disorder\nF42 Unspecified obsessive-compulsive and related disorder\nF43.0 Acute stress disorder \nF43.10 Posttraumatic stress disorder\nF43.20 Adjustment disorders, Unspecified\nF43.21 Adjustment disorder s, With depressed mood\nF43.22 Adjustment diso rders, With anxiety\nF43.23 Adjustment disorders, With mixed anxiety and depressed mood\nF43.24 Adjustment disorders, With disturbance of conduct\nF43.25 Adjustment disorders, With mixed disturbance of emotions and conduct\nF43.8 Other specified trauma- and stressor-related disorder\nF43.9 Unspecified trauma- an d stressor-related disorder\nF44.0 Dissociative amnesia\nF44.1 Dissociative amnesia, With dissociative fugue\nF44.4 Conversion disorder (functional ne urological symptom disorder), With \nabnormal movement\nF44.4 Conversion disorder (functional ne urological symptom disorder), With \nspeech symptoms \nF44.4 Conversion disorder (functional ne urological symptom disorder), With \nswallowing symptoms\nF44.4 Conversion disorder (functional ne urological symptom disorder), With \nweakness/paralysis\nF44.5 Conversion disorder (functional ne urological symptom disorder), With \nattacks or seizures\nF44.6 Conversion disorder (functional ne urological symptom disorder), With \nanesthesia or sensory loss\nF44.6 Conversion disorder (functional ne urological symptom disorder), With \nspecial sensory symptoms \nF44.7 Conversion disorder (functional neurological symptom disorder), With mixed \nsymptoms", "source": "dsm5.pdf"} {"id": "0a507111de98-1", "page_content": "F44.7 Conversion disorder (functional neurological symptom disorder), With mixed \nsymptoms\nF44.81 Dissociative identity disorder\nF44.89 Other specified dissociative disorder\nF44.9 Unspecified diss ociative disorder \nF45.1 Somatic sy mptom disorder\nF45.21 Illness anxiety disorder\nF45.22 Body dysmorphic disorder\nF45.8 Other specified somatic symptom and related disorder\nF45.9 Unspecified somatic symptom and related disorder\nF48.1 Depersonalization/ derealization disorder\nF50.01 Anorexia nervosa, Restricting type\nF50.02 Anorexia nervosa, Binge-eating/purging type\nF50.2 Bulimia nervosa\nF50.8 Avoidant/restrictive food intake disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "bc12d37c8601-0", "page_content": "890 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nF50.8 Binge-eating disorder\nF50.8 Other specified feeding or eating disorder\nF50.8 Pica, in adults\nF50.9 Unspecified feeding or eating disorder\nF51.01 Insomnia disorder\nF51.11 Hypersomno lence disorder\nF51.3 Non\u2013rapid eye movement sleep arousal disorders, Sleepwalking type\nF51.4 Non\u2013rapid eye movement sleep arousal disorders, Sleep terror type\nF51.5 Nightmare disorder\nF52.0 Male hypoactive se xual desire disorder\nF52.21 Erectile disorder\nF52.22 Female sexual in terest/arous al disorder\nF52.31 Female orgasmic disorder\nF52.32 Delayed ejaculation\nF52.4 Premature (early) ejaculation\nF52.6 Genito-pelvic pain /penetration disorder\nF52.8 Other specified sexual dysfunction\nF52.9 Unspecified sexual dysfunction\nF54 Psychological factors affe cting other medical conditions\nF60.0 Paranoid personality disorder\nF60.1 Schizoid personality disorder\nF60.2 Antisocial personality disorder\nF60.3 Borderline personality disorder\nF60.4 Histrionic personality disorder\nF60.5 Obsessive-compulsiv e personality disorder\nF60.6 Avoidant personality disorder\nF60.7 Dependent personality disorder\nF60.81 Narcissistic personality disorder\nF60.89 Other specified personality disorder\nF60.9 Unspecified pe rsonality disorder\nF63.0 Gambling disorder\nF63.1 Pyromania\nF63.2 Kleptomania \nF63.3 Trichotillomania (hair-pulling disorder)\nF63.81 Intermittent explosive disorder", "source": "dsm5.pdf"} {"id": "bc12d37c8601-1", "page_content": "F63.81 Intermittent explosive disorder \nF64.1 Gender dysphoria in adolescents and adults\nF64.2 Gender dysphoria in children\nF64.8 Other specified gender dysphoria\nF64.9 Unspecified gender dysphoria\nF65.0 Fetishistic disorder\nF65.1 Transvestic disorder\nF65.2 Exhibitionistic disorder\nF65.3 Voyeuristic disorder\nF65.4 Pedophilic disorder\nF65.51 Sexual ma sochism disorder\nF65.52 Sexual sadism disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "0733103b9ce4-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 891\nF65.81 Frotteuristic disorder\nF65.89 Other specified paraphilic disorder\nF65.9 Unspecified pa raphilic disorder\nF68.10 Factitious disorder\nF70 Intellectual disability (intellectual developmental disorder), Mild\nF71 Intellectual disability (intellectual developmental disorder), Moderate\nF72 Intellectual disability (intellectual developmental disorder), Severe\nF73 Intellectual disability (intellectual developmental disorder), Profound\nF79 Unspecified intellectual disability (intellectual developmental disorder)\nF80.0 Speech sound disorder\nF80.2 Language disorder\nF80.81 Childhood-onset flue ncy disorder (stuttering)\nF80.89 Social (pragmatic ) communication disorder\nF80.9 Unspecified communication disorder\nF81.0 Specific learning disorder , With impairment in reading\nF81.2 Specific learning disorder, With impairment in mathematics\nF81.81 Specific learning disorder, With impairment in written expression\nF82 Developmental coordination disorder \nF84.0 Autism spectrum disorder\nF88 Global developmental delay\nF88 Other specified neurodevelopmental disorder\nF89 Unspecified neurod evelopmental disorder\nF90.0 Attention-deficit/hyperactivity disord er, Predominantly inattentive presentation\nF90.1 Attention-deficit/hyperactivity disorder, Predominantly hyperactive/\nimpulsive presentation\nF90.2 Attention-deficit/hyperactivity disorder, Combined presentation\nF90.8 Other specified attention- deficit/hyperactivity disorder\nF90.9 Unspecified attention-de ficit/hyperactivity disorder\nF91.1 Conduct disorder, Childhood-onset type\nF91.2 Conduct disorder, Adolescent-onset type\nF91.3 Oppositional defiant disorder", "source": "dsm5.pdf"} {"id": "0733103b9ce4-1", "page_content": "F91.3 Oppositional defiant disorder\nF91.8 Other specified disruptive, impulse-control, and conduct disorder\nF91.9 Conduct disorder, Unspecified onset\nF91.9 Unspecified disruptive, impulse-control, and conduct disorder\nF93.0 Separation anxiety disorder \nF94.0 Selective mutism\nF94.1 Reactive attachment disorder\nF94.2 Disinhibited social engagement disorder\nF95.0 Provisional tic disorder \nF95.1 Persistent (chronic) motor or vocal tic disorder\nF95.2 Tourette\u2019s disorder \nF95.8 Other specified tic disorder\nF95.9 Unspecified tic disorder\nF98.0 Enuresis\nF98.1 Encopresis\nF98.21 Rumination disorderICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "4a46e1901282-0", "page_content": "892 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nF98.3 Pica, in children\nF98.4 Stereotypic movement disorder\nF98.5 Adult-onset fluency disorder\nF99 Other specified mental disorder\nF99 Unspecified mental disorder\nG21.0 Neuroleptic malignant syndrome\nG21.11 Neuroleptic-induced parkinsonism\nG21.19 Other medication -induced parkinsonism\nG24.01 Tardive dyskinesia\nG24.02 Medication-ind uced acute dystonia\nG24.09 Tardive dystonia\nG25.1 Medication-induced postural tremor\nG25.71 Medication-induc ed acute akathisia\nG25.71 Tardiv e akathisia\nG25.79 Other medication-induced movement disorder\nG25.81 Restless legs syndrome\nG31.84 Mild frontotemporal neurocognitive disorder\nG31.84 Mild neurocogni tive disorder due to Alzheimer\u2019s disease\nG31.84 Mild neurocogniti ve disorder due to another medical condition\nG31.84 Mild neurocognitive di sorder due to HIV infection\nG31.84 Mild neurocogni tive disorder due to Huntington\u2019s disease\nG31.84 Mild neurocognitive disorder with Lewy bodies\nG31.84 Mild neurocognitive disorder due to multiple etiologies\nG31.84 Mild neurocogni tive disorder due to Parkinson\u2019s disease\nG31.84 Mild neurocognitive di sorder due to prion disease\nG31.84 Mild neurocognitive disord er due to traumatic brain injury\nG31.84 Mild vascular ne urocognitive disorder\nG31.9 Major neurocognitive disorder possibly due to Parkinson\u2019s disease", "source": "dsm5.pdf"} {"id": "4a46e1901282-1", "page_content": "G31.9 Major neurocognitive disorder possibly due to Parkinson\u2019s disease\nG31.9 Possible major frontotemp oral neurocognitive disorder\nG31.9 Possible major neurocognitive disorder due to Alzheimer\u2019s disease\nG31.9 Possible major neurocogniti ve disorder wi th Lewy bodies\nG31.9 Possible major vascular neurocogniti ve disorder\nG47.00 Unspecified insomnia disorder\nG47.09 Other specified insomnia disorder\nG47.10 Unspecified hypersomnolence disorder\nG47.19 Other specified hypersomnolence disorder\nG47.20 Circadian rhythm sleep-wak e disorders, Unspecified type\nG47.21 Circadian rhythm sleep-wake di sorders, Delayed sleep phase type\nG47.22 Circadian rhythm sleep-wake di sorders, Advanced sleep phase type\nG47.23 Circadian rhythm sleep-wake di sorders, Irregula r sleep-wake type\nG47.24 Circadian rhythm sleep-wake di sorders, Non-24-hour sleep-wake type\nG47.26 Circadian rhythm sleep-wak e disorders, Shift work type\nG47.31 Central sleep apnea, Id iopathic central sleep apneaICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "900fbdea249d-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 893\nG47.33 Obstructive sleep apnea hypopnea\nG47.34 Sleep-related hypoventilation, Idiopathic hypoventilation\nG47.35 Sleep-related hypoventilation, Cong enital central alveolar hypoventilation\nG47.36 Sleep-related hypoventilation, Comorbid sleep-related hypoventilation\nG47.37 Central sleep apnea comorbid with opioid use\nG47.411 Narcolepsy with cataplexy but without hypocretin deficiency\nG47.419 Autosomal dominant cerebellar ataxia, deafness, and narcolepsy\nG47.419 Autosomal dominant narcolep sy, obesity, and type 2 diabetes\nG47.419 Narcolepsy without cataple xy but with hypocretin deficiency\nG47.429 Narcolepsy secondary to another medical condition\nG47.52 Rapid eye movement sleep behavior disorder\nG47.8 Other specified sleep-wake disorder\nG47.9 Unspecified sleep-wake disorder\nL98.1\u00a0 Excoriation (skin-picking) disorder\nN39.498 Other specified elimination disorder, With urinary symptoms\nN94.3 Premenstrual dysphoric disorder \nR06.3 Central sleep apnea, Cheyne-Stokes breathing\nR15.9 Other specified elimination disorder, With fecal symptoms\nR15.9 Unspecified elimination disorder, With fecal symptoms\nR32 Unspecified elimination disorder, With urinary symptoms\nR41.0 Other specified delirium\nR41.0 Unspecified delirium\nR41.83 Borderline intellectual functioning\nR41.9 Unspecified neur ocognitive disorder\nT43.205A Antidepressant discontinuation syndrome, Initial encounter", "source": "dsm5.pdf"} {"id": "900fbdea249d-1", "page_content": "T43.205A Antidepressant discontinuation syndrome, Initial encounter\nT43.205D Antidepressant discontinuation syndrome, Subsequent encounter\nT43.205S Antidepressant discont inuation syndrome, Sequelae\nT50.905A Other adverse effect of medication, Initial encounter\nT50.905D Other adverse effect of medication, Subsequent encounter\nT50.905S Other adverse effect of medication, Sequelae\nT74.01XA Spouse or partner neglect, Confirmed, Initial encounter\nT74.01XD Spouse or partner neglect, Confirmed, Subsequent encounter\nT74.02XA Child neglect, Confirmed, Initial encounter\nT74.02XD Child neglect, Confirmed, Subsequent encounter\nT74.11XA Adult physical abuse by nonspouse or nonpartner, Confirme d, Initial encounter\nT74.11XA Spouse or partner violence, Physical, Confirmed, Initial encounter\nT74.11XD Adult physical abus e by nonspouse or nonpartn er, Confirmed, Subsequent \nencounter\nT74.11XD Spouse or partner violence, Phys ical, Confirmed, Subsequent encounter\nT74.12XA Child physical abuse, Confirmed, Initial encounter\nT74.12XD Child physical abuse, Confirmed, Subsequent encounter\nT74.21XA Adult sexual abuse by nonspouse or nonpartner, Confirmed, Initial encounter\nT74.21XA Spouse or partner violence, Sexual, Confirmed, Initial encounter\nT74.21XD Adult sexual abuse by nonspouse or nonpartner, Confirmed, Subsequent \nencounterICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "45e838104c6b-0", "page_content": "894 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nT74.21XD Spouse or partner violence, Se xual, Confirmed, Subsequent encounter\nT74.22XA Child sexual abuse, Confirmed, Initial encounter\nT74.22XD Child sexual abuse, Confirmed, Subsequent encounter\nT74.31XA Adult psychological abuse by nonspouse or nonpartner, Confirmed, Initial \nencounter\nT74.31XA Spouse or partner abuse, Psycho logical, Confirmed, Initial encounter\nT74.31XD Adult psychological abuse by nonspouse or nonpartner, Confirmed, \nSubsequent encounter\nT74.31XD Spouse or partner abuse, Psycholo gical, Confirmed, Subsequent encounter\nT74.32XA Child psychological abuse, Confirmed, Initial encounter\nT74.32XD Child psychological abuse, Confirmed, Subsequent encounter\nT76.01XA Spouse or partner neglec t, Suspected, Initial encounter\nT76.01XD Spouse or partner neglect, Suspected, Subsequent encounter\nT76.02XA Child neglect, Suspected, Initial encounter\nT76.02XD Child neglect, Suspected, Subsequent encounter\nT76.11XA Adult physical abuse by nonspouse or nonpartner, Suspected, Initial encounter\nT76.11XA Spouse or partner violence, Ph ysical, Suspected, Initial encounter\nT76.11XD Adult physical abus e by nonspouse or nonpartn er, Suspected, Subsequent \nencounter\nT76.11XD Spouse or partner violence, Phys ical, Suspected, Subsequent encounter\nT76.12XA Child physical abuse, Suspected, Initial encounter\nT76.12XD Child physical abuse, Suspected, Subsequent encounter", "source": "dsm5.pdf"} {"id": "45e838104c6b-1", "page_content": "T76.12XD Child physical abuse, Suspected, Subsequent encounter\nT76.21XA Adult sexual abuse by nonspouse or nonpartner, Suspected, Initial encounter\nT76.21XA Spouse or partner violence, Sexual, Suspected, Initial encounter\nT76.21XD Adult sexual abuse by nonspouse or nonpartner, Suspected, Subsequent \nencounter\nT76.21XD Spouse or partner violence, Se xual, Suspected, Subsequent encounter\nT76.22XA Child sexual abuse, Suspected, Initial encounter\nT76.22XD Child sexual abuse, Su spected, Subsequent encounter\nT76.31XA Adult psychological abuse by nonspouse or nonpartner, Suspected, Initial \nencounter\nT76.31XA Spouse or partner abuse, Psychological, Suspected, Initial encounter\nT76.31XD Adult psychological abuse by nonspouse or nonpartner, Suspected, \nSubsequent encounter\nT76.31XD Spouse or partner abuse, Psychological, Suspected, Subsequent encounter\nT76.32XA Child psychological abuse, Suspected, Initial encounter\nT76.32XD Child psychological abuse, Suspected, Subsequent encounter\nZ55.9 Academic or educational problem\nZ56.82 Problem related to current military deployment status\nZ56.9 Other problem related to employment\nZ59.0 Homelessness\nZ59.1 Inadequate housing\nZ59.2 Discord with neighbor, lodger, or landlord\nZ59.3 Problem related to living in a residential institution\nZ59.4 Lack of adequate food or safe drinking water\nZ59.5 Extreme povertyICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "62601fe857f9-0", "page_content": "Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM) 895\nZ59.6 Low income\nZ59.7 Insufficient social insurance or welfare support\nZ59.9 Unspecified housin g or economic problem\nZ60.0 Phase of life problem\nZ60.2 Problem related to living alone\nZ60.3 Acculturation difficulty\nZ60.4 Social exclusion or rejection\nZ60.5 Target of (perceived) advers e discrimination or persecution\nZ60.9 Unspecified problem related to social environment\nZ62.29 Upbringing away from parents\nZ62.810 Personal history (past histor y) of physical abuse in childhood\nZ62.810 Personal history (past history) of sexual abuse in childhood\nZ62.811 Personal history (past history) of psychological abuse in childhood\nZ62.812 Personal history (past history) of neglect in childhood\nZ62.820 Parent-child relational problem\nZ62.891 Sibling relational problem\nZ62.898 Child affected by pa rental relationship distress\nZ63.0 Relationship distress with spouse or intimate partner\nZ63.4 Uncomplicated bereavement\nZ63.5 Disruption of family by separation or divorce\nZ63.8 High expressed emotion level within family\nZ64.0 Problems related to unwanted pregnancy\nZ64.1 Problems related to multiparity\nZ64.4 Discord with social service provider, including probation officer, case \nmanager, or social services worker\nZ65.0 Conviction in civil or crimin al proceedings without imprisonment\nZ65.1 Imprisonment or other incarceration\nZ65.2 Problems related to release from prison\nZ65.3 Problems related to ot her legal circumstances\nZ65.4 Victim of crime\nZ65.4 Victim of terrorism or torture\nZ65.5 Exposure to disaster, war, or other hostilities", "source": "dsm5.pdf"} {"id": "62601fe857f9-1", "page_content": "Z65.5 Exposure to disaster, war, or other hostilities\nZ65.8 Other problem related to psychosocial circumstances\nZ65.8 Religious or spiritual problem\nZ65.9 Unspecified problem related to unspecified psychosocial circumstances\nZ69.010 Encounter for mental health services fo r victim of child abuse by parent\nZ69.010 Encounter for mental health services for victim of child neglect by parent\nZ69.010 Encounter for mental health services for victim of child psychological abuse by \nparent\nZ69.010 Encounter for mental he alth services for victim of child sexual abuse by parent\nZ69.011 Encounter for mental health services fo r perpetrator of parental child abuse\nZ69.011 Encounter for mental health services for perpetrator of parental child neglect\nZ69.011 Encounter for mental health serv ices for perpetrator of parental child \npsychological abuse\nZ69.011 Encounter for mental heal th services for perpetrator of parental child sexual abuse\nZ69.020 Encounter for mental health services fo r victim of nonparental child abuseICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "3b798e194b0b-0", "page_content": "896 Numerical Listing of DSM-5 Diagnoses and Codes (ICD-10-CM)\nZ69.020 Encounter for mental health services fo r victim of nonparental child neglect\nZ69.020 Encounter for mental health services fo r victim of nonparental child psycho-\nlogical abuse\nZ69.020 Encounter for mental he alth services for victim of nonparental child sexual abuse\nZ69.021 Encounter for mental he alth services for perpetrato r of nonparental child abuse\nZ69.021 Encounter for mental he alth services for perpetrator of nonparental child neglect\nZ69.021 Encounter for mental health services for perpetrator of nonparental child \npsychological abuse\nZ69.021 Encounter for mental health services for perpetrator of nonparental child \nsexual abuse\nZ69.11 Encounter for mental health services for victim of spouse or partner neglect\nZ69.11 Encounter for mental health servic es for victim of spouse or partner \npsychological abuse\nZ69.11 Encounter for mental health services for victim of spouse or partner violence, \nPhysical\nZ69.12 Encounter for mental heal th services for perpetrator of spouse or partner neglect\nZ69.12 Encounter for mental health services for perpetrator of spouse or partner \npsychological abuse\nZ69.12 Encounter for mental health services for perpetrator of spouse or partner \nviolence, Physical\nZ69.12 Encounter for mental health services for perpetrator of spouse or partner \nviolence, Sexual\nZ69.81 Encounter for mental health services for victim of nonspousal adult abuse\nZ69.81 Encounter for mental health services for victim of spouse or partner violence, \nSexual\nZ69.82 Encounter for mental he alth services for perpetrator of nonspousal adult abuse\nZ70.9 Sex counseling\nZ71.9 Other counseling or consultation", "source": "dsm5.pdf"} {"id": "3b798e194b0b-1", "page_content": "Z70.9 Sex counseling\nZ71.9 Other counseling or consultation\nZ72.0 Tobacco us e disorder, mild\nZ72.810 Child or adolesce nt antisocial behavior\nZ72.811 Adult antisocial behavior\nZ72.9 Problem related to lifestyle\nZ75.3 Unavailability or inaccessibility of health care facilities\nZ75.4 Unavailability or inaccessib ility of other helping agencies\nZ76.5 Malingering\nZ91.19 Nonadherence to medical treatment\nZ91.410 Personal history (past history) of spouse or partne r violence, Physical\nZ91.410 Personal history (past history) of spouse or partner violence, Sexual\nZ91.411 Personal history (past history) of spouse or partner psychological abuse\nZ91.412 Personal history (past histor y) of spouse or partner neglect\nZ91.49 Other personal history of psychological trauma\nZ91.5 Personal history of self-harm\nZ91.82 Personal history of military deployment\nZ91.83 Wandering associated with a mental disorder\nZ91.89 Other personal risk factorsICD-10-CM Disorder, co ndition, or problem", "source": "dsm5.pdf"} {"id": "89512ea02ed7-0", "page_content": "897DSM-5 Advisors and\n Other Contributors\nAPA Board of Trustees DSM-5 Review Committees\nScientific Review Committee (SRC)\nKenneth S. Kendler, M.D. (Chair)\nRobert Freedman, M.D. (Co-chair)\nDan G. Blazer, M.D., Ph.D., M.P.H. \nDavid Brent, M.D. (2011\u2013)\nEllen Leibenluft, M.D.\nSir Michael Rutter, M.D. (\u20132011)\nPaul S. Summergrad, M.D.\nRobert J. Ursano, M.D. (\u20132011)\nMyrna Weissman , Ph.D. (2011\u2013)\nJoel Yager, M.D.\nJill L. Opalesky M.S. (Administrative Support)\nClinical and Public Health Review \nCommittee (CPHC)\nJohn S. McIntyre, M.D. (Chair)\nJoel Yager, M.D. (Co-chair)\nAnita Everett M.D.\nCathryn A. Galanter, M.D.\nJeffrey M. Lyness, M.D.\nJames E. Nininger, M.D.\nVictor I. Reus, M.D.\nMichael J. Vergare, M.D.\nAnn Miller (Administrative Support)\nOversight Committee \nCarolyn Robinowitz, M.D. (Chair)\nMary Badaracco, M.D.\nRonald Burd, M.D.\nRobert Freedman, M.D.\nJeffrey A. Lieberman, M.D. \nKyla Pope, M.D.\nVictor I. Reus, M.D.\nDaniel K. Winstead, M.D.\nJoel Yager, M.D.\nAPA Assembly DSM-5 Review \nCommittee\nGlenn A. Martin, M.D. (Chair)", "source": "dsm5.pdf"} {"id": "89512ea02ed7-1", "page_content": "Committee\nGlenn A. Martin, M.D. (Chair)\nR. Scott Benson, M.D. (Speaker of the \nAssembly)\nWilliam Cardasis, M.D.\nJohn M. de Figueiredo, M.D.\nLawrence S. Gross, M.D.\nBrian S. Hart, M.D.Stephen A. McLeod Bryant, M.D.\nGregory A. Miller, M.D.\nRoger Peele, M.D.\nCharles S. Price, M.D.\nDeepika Sastry, M.D.\nJohn P.D. Shemo, M.D.\nEliot Sorel, M.D.\nDSM-5 Summit Group\nDilip V. Jeste, M.D. (Chair)\nR. Scott Benson, M.D.\nKenneth S. Kendler, M.D.\nHelena C. Kraemer, Ph.D.\nDavid J. Kupfer, M.D.\nJeffrey A. Lieberman, M.D.\nGlenn A. Martin, M.D.\nJohn S. McIntyre, M.D.\nJohn M. Oldham, M.D.\nRoger Peele, M.D.\nDarrel A. Regier, M.D., M.P.H.\nJames H. Scully Jr., M.D.\nJoel Yager, M.D. \nPaul S. Appelbaum, M.D. (Consultant)\nMichael B. First, M.D. (Consultant) \nDSM-5 Field Trials Review\nRobert D. Gibbons, Ph.D.\nCraig Nelson, M.D.\nDSM-5 Forensic Review\nPaul S. Appelbaum, M.D.\nLama Bazzi, M.D.\nAlec W. Buchanan, M.D., Ph.D.\nCarissa Cab\u00e1n Alem\u00e1n, M.D.", "source": "dsm5.pdf"} {"id": "89512ea02ed7-2", "page_content": "Carissa Cab\u00e1n Alem\u00e1n, M.D.\nMichael Champion, M.D.\nJeffrey C. Eisen, M.D.\nElizabeth Ford, M.D.\nDaniel T. Hackman, M.D.\nMark Hauser, M.D.\nSteven K. Hoge, M.D., M.B.A.\nDebra A. Pinals, M.D.\nGuillermo Portillo, M.D.\nPatricia Recupero, M.D., J.D.\nRobert Weinstock, M.D.\nCheryl Wills, M.D.\nHoward V. Zonana, M.D.", "source": "dsm5.pdf"} {"id": "21acfdac1bec-0", "page_content": "898 DSM-5 Advisors and Other Contributors\nPast DSM-5 APA Staff\nErin J. Dalder-Alpher\nKristin Edwards\nLeah I. EngelLenna Jawdat\nElizabeth C. Martin\nRocio J. Salvador\nWork Group Advisors\nADHD and Disruptive Behavior \nDisorders \nEmil F. Coccaro, M.D.\nDeborah Dabrick, Ph.D.\nPrudence W. Fisher, Ph.D.\nBenjamin B. Lahey, Ph.D.\nSalvatore Mannuzza, Ph.D.\nMary Solanto, Ph.D.\nJ. Blake Turner, Ph.D.\nEric Youngstrom, Ph.D.\nAnxiety, Obsessive-Compulsive \nSpectrum, Posttraumatic, and \nDissociative Disorders\nLynn E. Alden, Ph.D.\nDavid B. Arciniegas, M.D.\nDavid H. Barlow, Ph.D.\nKatja Beesdo-Baum, Ph.D.\nChris R. Brewin, Ph.D.\nRichard J. Brown, Ph.D.\nTimothy A. Brown, Ph.D.\nRichard A. Bryant, Ph.D.\nJoan M. Cook, Ph.D.\nJoop de Jong, M.D., Ph.D.\nPaul F. Dell, Ph.D.\nDamiaan Denys, M.D.\nBruce P. Dohrenwend, Ph.D.\nBrian A. Fallon, M.D., M.P.H. \nEdna B. Foa, Ph.D.\nMartin E. Franklin, Ph.D.\nWayne K. Goodman, M.D.\nJon E. Grant, J.D., M.D.\nBonnie L. Green, Ph.D.\nRichard G. Heimberg, Ph.D.\nJudith L. Herman, M.D.", "source": "dsm5.pdf"} {"id": "21acfdac1bec-1", "page_content": "Judith L. Herman, M.D.\nDevon E. Hinton, M.D., Ph.D.\nStefan G. Hofmann, Ph.D.\nCharles W. Hoge, M.D.\nTerence M. Keane, Ph.D.\nNancy J. Keuthen, Ph.D.\nDean G. Kilpatrick, Ph.D.\nKatharina Kircanski, Ph.D.\nLaurence J. Kirmayer, M.D.\nDonald F. Klein, M.D., D.Sc.\nAmaro J. Laria, Ph.D.\nRichard T. LeBeau, M.A.\nRichard J. Loewenstein, M.D.\nDavid Mataix-Cols, Ph.D.\nThomas W. McAllister, M.D.Harrison G. Pope, M.D., M.P.H.\nRonald M. Rapee, Ph.D. \nSteven A. Rasmussen, M.D. \nPatricia A. Resick, Ph.D.\nVedat Sar, M.D.\nSanjaya Saxena, M.D.\nPaula P. Schnurr, Ph.D.\nM. Katherine Shear, M.D.\nDaphne Simeon, M.D.\nHarvey S. Singer, M.D.\nMelinda A. Stanley, Ph.D.\nJames J. Strain, M.D.\nKate Wolitzky Taylor, Ph.D.\nOnno van der Hart, Ph.D.\nEric Vermetten, M.D., Ph.D.\nJohn T. Walkup, M.D.\nSabine Wilhelm, Ph.D.\nDouglas W. Woods, Ph.D.\nRichard E. Zinbarg, Ph.D.\nJoseph Zohar, M.D.\nChildhood and Adolescent \nDisorders\nAdrian Angold, Ph.D.", "source": "dsm5.pdf"} {"id": "21acfdac1bec-2", "page_content": "Childhood and Adolescent \nDisorders\nAdrian Angold, Ph.D.\nDeborah Beidel, Ph.D.\nDavid Brent, M.D.\nJohn Campo, M.D.\nGabrielle Carlson, M.D.\nPrudence W. Fisher, Ph.D.\nDavid Klonsky, Ph.D.\nMatthew Nock, Ph.D.\nJ. Blake Turner, Ph.D.\nEating Disorders\nMichael J. Devlin, M.D.\nDenise E. Wilfley, Ph.D.\nSusan Z. Yanovski, M.D.\nMood Disorders\nBoris Birmaher, M.D.\nYeates Conwell, M.D.\nEllen B. Dennehy, Ph.D.\nS. Ann Hartlage, Ph.D.\nJack M. Hettema, M.D., Ph.D.\nMichael C. Neale, Ph.D.\nGordon B. Parker, M.D., Ph.D., D.Sc.\nRoy H. Perlis, M.D. M.Sc.\nHolly G. Prigerson, Ph.D.\nNorman E. Rosenthal, M.D.\nPeter J. Schmidt, M.D.", "source": "dsm5.pdf"} {"id": "9c9f65d91410-0", "page_content": "DSM-5 Advisors and Other Contributors 899\nMort M. Silverman, M.D.\nMeir Steiner, M.D., Ph.D.\nMauricio Tohen, M.D., Dr.P.H., M.B.A.\nSidney Zisook, M.D.\nNeurocognitive Disorders\nJiska Cohen-Mansfield, Ph.D.\nVladimir Hachinski, M.D., C.M., D.Sc. \nSharon Inouye, M.D., M.P.H.\nGrant Iverson, Ph.D.\nLaura Marsh, M.D.\nBruce Miller, M.D.\nJacobo Mintzer, M.D., M.B.A.\nBruce Pollock, M.D., Ph.D.\nGeorge Prigatano, Ph.D.\nRon Ruff, Ph.D.\nIngmar Skoog, M.D., Ph.D.\nRobert Sweet, M.D.\nPaula Trzepacz, M.D.\nNeurodevelopmental Disorders\nAri Ne\u2019eman\nNickola Nelson, Ph.D.\nDiane Paul, Ph.D.\nEva Petrova, Ph.D.\nAndrew Pickles, Ph.D.\nJan Piek, Ph.D.\nHelene Polatajko, Ph.D.\nAlya Reeve, M.D.\nMabel Rice, Ph.D.\nJoseph Sergeant, Ph.D.\nBennett Shaywitz, M.D.\nSally Shaywitz, M.D.\nAudrey Thurm, Ph.D.\nKeith Widaman, Ph.D. \nWarren Zigman, Ph.D.\nPersonality and Personality \nDisorders\nEran Chemerinski, M.D.\nThomas N. Crawford, Ph.D.\nHarold W. Koenigsberg, M.D.\nKristian E. Markon, Ph.D.", "source": "dsm5.pdf"} {"id": "9c9f65d91410-1", "page_content": "Kristian E. Markon, Ph.D.\nRebecca L. Shiner, Ph.D.\nKenneth R. Silk, M.D.\nJennifer L. Tackett, Ph.D.\nDavid Watson, Ph.D.\nPsychotic Disorders\nKamaldeep Bhui, M.D.\nManuel J. Cuesta, M.D., Ph.D.\nRichard Douyon, M.D.\nPaolo Fusar-Poli, Ph.D.\nJohn H. Krystal, M.D.\nThomas H. McGlashan, M.D.\nVictor Peralta, M.D., Ph.D.\nAnita Riecher-R\u00f6ssler, M.D.\nMary V. Seeman, M.D.Sexual and Gender Identity \nDisorders\nStan E. Althof, Ph.D.\nRichard Balon, M.D.\nJohn H.J. Bancroft, M.D., M.A., D.P.M.\nHoward E. Barbaree, Ph.D., M.A.\nRosemary J. Basson, M.D.\nSophie Bergeron, Ph.D.\nAnita L. Clayton, M.D.\nDavid L. Delmonico, Ph.D.\nDomenico Di Ceglie, M.D.\nEsther Gomez-Gil, M.D.\nJamison Green, Ph.D.\nRichard Green, M.D, J.D.\nR. Karl Hanson, Ph.D.\nLawrence Hartmann, M.D.\nStephen J. Hucker, M.B.\nEric S. Janus, J.D.\nPatrick M. Jern, Ph.D.\nMegan S. Kaplan, Ph.D.\nRaymond A. Knight, Ph.D.\nEllen T.M. Laan, Ph.D.\nStephen B. Levine, M.D.\nChristopher G. McMahon, M.B.", "source": "dsm5.pdf"} {"id": "9c9f65d91410-2", "page_content": "Stephen B. Levine, M.D.\nChristopher G. McMahon, M.B.\nMarta Meana, Ph.D.\nMichael H. Miner, Ph.D., M.A.\nWilliam T. O\u2019Donohue, Ph.D.\nMichael A. Perelman, Ph.D.\nCaroline F. Pukall, Ph.D.\nRobert E. Pyke, M.D., Ph.D.\nVernon L. Quinsey, Ph.D. M.Sc.\nDavid L. Rowland, Ph.D., M.A.\nMichael Sand, Ph.D., M.P.H.\nLeslie R. Schover, Ph.D., M.A.\nPaul Stern, B.S, J.D.\nDavid Thornton, Ph.D.\nLeonore Tiefer, Ph.D.\nDouglas E. Tucker, M.D.\nJacques van Lankveld, Ph.D.\nMarcel D. Waldinger, M.D., Ph.D.\nSleep-Wake Disorders\nDonald L. Bliwise, Ph.D.\nDaniel J. Buysse, M.D.\nVishesh K. Kapur, M.D., M.P.H.\nSanjeeve V. Kothare, M.D.\nKenneth L. Lichstein, Ph.D.\nMark W. Mahowald, M.D.\nRachel Manber, Ph.D.\nEmmanuel Mignot , M.D., Ph.D.\nTimothy H. Monk, Ph.D., D.Sc.\nThomas C. Neylan, M.D.\nMaurice M. Ohayon, M.D., D.Sc., Ph.D.\nJudith Owens, M.D., M.P.H.\nDaniel L. Picchietti, M.D.\nStuart F. Quan, M.D.\nThomas Roth, Ph.D.\nDaniel Weintraub, M.D.", "source": "dsm5.pdf"} {"id": "325e8074e601-0", "page_content": "900 DSM-5 Advisors and Other Contributors\nTheresa B. Young, Ph.D.\nPhyllis C. Zee, M.D., Ph.D.\nSomatic Symptom Disorders\nBrenda Bursch, Ph.D.\nKurt Kroenke, M.D.\nW. Curt LaFrance, Jr., M.D., M.P.H.\nJon Stone, M.B., Ch.B., Ph.D.\nLynn M. Wegner, M.D.Substance-Related Disorders\nRaymond F. Anton, Jr., M.D.\nDeborah A. Dawson, Ph.D.\nRoland R. Griffiths, Ph.D.\nDorothy K. Hatsukami, Ph.D.\nJohn E. Helzer, M.D.\nMarilyn A. Huestis, Ph.D.\nJohn R. Hughes, M.D.\nLaura M. Juliano, Ph.D.\nThomas R. Kosten, M.D.\nNora D. Volkow, M.D.\nDSM-5 Study Group and Ot her DSM-5 Group Advisors\nLifespan Developmental \nApproaches\nChristina Bryant, Ph.D.\nAmber Gum, Ph.D.\nThomas Meeks, M.D.\nJan Mohlman, Ph.D.\nSteven Thorp, Ph.D.\nJulie Wetherell, Ph.D.\nGender and Cross-Cultural Issues\nNeil K. Aggarwal, M.D., M.B.A., M.A.\nSofie B\u00e4\u00e4rnhielm, M.D., Ph.D.\nJos\u00e9 J. Bauermeister, Ph.D.\nJames Boehnlein, M.D., M.Sc.\nJaswant Guzder, M.D.\nAlejandro Interian, Ph.D.\nSushrut S. Jadhav, M.B.B.S., M.D., Ph.D.", "source": "dsm5.pdf"} {"id": "325e8074e601-1", "page_content": "Laurence J. Kirmayer, M.D.\nAlex J. Kopelowicz, M.D.\nAmaro J. Laria, Ph.D.\nSteven R. Lopez, Ph.D.\nKwame J. McKenzie, M.D.\nJohn R. Peteet, M.D.Hans (J.G.B.M.) Rohlof, M.D.\nCecile Rousseau, M.D.\nMitchell G. Weiss, M.D., Ph.D.\nPsychiatric/General Medical \nInterface\nDaniel L. Coury, M.D.\nBernard P. Dreyer, M.D.\nDanielle Laraque, M.D.\nLynn M. Wegner, M.D.\nImpairment and Disability\nPrudence W. Fisher, Ph.D.\nMartin Prince, M.D., M.Sc.\nMichael R. Von Korff, Sc.D.\nDiagnostic Assessment \nInstruments\nPrudence W. Fisher, Ph.D.\nRobert D. Gibbons, Ph.D.\nRuben Gur, Ph.D.\nJohn E. Helzer, M.D.\nJohn Houston, M.D., Ph.D.\nKurt Kroenke, M.D.\nOther Contributo rs/Consultants\nADHD and Disruptive Behavior \nDisorders \nPatrick E. Shrout, Ph.D.\nErik Willcutt, Ph.D. \nAnxiety, Obsessive-Compulsive \nSpectrum, Posttraumatic, and \nDissociative Disorders \nEtzel Carde\u00f1a, Ph.D.\nRichard J. Castillo, Ph.D.\nEric Hollander, M.D. \nCharlie Marmar, M.D. \nAlfonso Mart\u00ednez-Taboas, Ph.D.\nMark W. Miller, Ph.D.\nMark H. Pollack, M.D.", "source": "dsm5.pdf"} {"id": "325e8074e601-2", "page_content": "Mark W. Miller, Ph.D.\nMark H. Pollack, M.D.\nHeidi S. Resnick, Ph.D.Childhood and Adolescent \nDisorders\nGrace T. Baranek, Ph.D.\nColleen Jacobson, Ph.D.\nMaria Oquendo, M.D.\nSir Michael Rutter, M.D.\nEating Disorders \nNancy L. Zucker, Ph.D.\nMood Disorders \nKeith Hawton, M.D., Ph.D.\nDavid A. Jobes, Ph.D.\nMaria A. Oquendo, M.D.\nAlan C. Swann, M.D.", "source": "dsm5.pdf"} {"id": "7d95399f4570-0", "page_content": "DSM-5 Advisors and Other Contributors 901\nNeurocognitive Disorders \nJ. Eric Ahlskog, M.D., Ph.D.\nAllen J. Aksamit, M.D.\nMarilyn Albert, Ph.D.\nGuy Mckhann, M.D.\nBradley Boeve, M.D. \nHelena Chui, M.D.\nSureyya Dikmen, Ph.D.\nDouglas Galasko, M.D.\nHarvey Levin, Ph.D. \nMark Lovell, Ph.D. \nJeffery Max, M.B.B.Ch. \nIan McKeith, M.D.\nCynthia Munro, Ph.D.\nMarlene Oscar-Berman, Ph.D. \nAlexander Troster, Ph.D.\nNeurodevelopmental Disorders \nAnna Barnett, Ph.D.\nMartha Denckla, M.D.\nJack M. Fletcher, Ph.D.\nDido Green, Ph.D.\nStephen Greenspan, Ph.D.\nBruce Pennington, Ph.D. \nRuth Shalev, M.D.\nLarry B. Silver, M.D.\nLauren Swineford, Ph.D.\nMichael Von Aster, M.D.\nPersonality and Personality \nDisorders \nPatricia R. Cohen, Ph.D. \nJaime L. Derringer, Ph.D. \nLauren Helm, M.D. \nChristopher J. Patrick, Ph.D. \nAnthony Pinto, Ph.D. \nPsychotic Disorders \nScott W. Woods, M.D.\nSexual and Gender Identity \nDisorders \nAlan J. Riley, M.Sc. \nRay C. Rosen, Ph.D.\nSleep-Wake Disorders \nJack D. Edinger, Ph.D. \nDavid Gozal, M.D.", "source": "dsm5.pdf"} {"id": "7d95399f4570-1", "page_content": "David Gozal, M.D. \nHochang B. Lee, M.D. \nTore A. Nielsen, Ph.D. \nMichael J. Sateia, M.D. \nJamie M. Zeitzer, Ph.D. \nSomatic Symptom Disorders \nChuck V. Ford, M.D. \nPatricia I. Rosebush, M.Sc.N., M.D. Substance-Related Disorders \nSally M. Anderson, Ph.D.\nJulie A. Kable, Ph.D.\nChristopher Martin, Ph.D.\nSarah N. Mattson, Ph.D.\nEdward V. Nunes, Jr., M.D. \nMary J. O\u2019Connor, Ph.D.\nHeather Carmichael Olson, Ph.D.\nBlair Paley, Ph.D.\nEdward P. Riley, Ph.D.\nTulshi D. Saha, Ph.D. \nWim van den Brink, M.D., Ph.D.\nGeorge E. Woody, M.D. \nDiagnostic Spectra and DSM/ICD \nHarmonization \nBruce Cuthbert, Ph.D. \nLifespan Developmental \nApproaches \nAartjan Beekman Ph.D.\nAlistair Flint, M.B.\nDavid Sultzer, M.D. \nEllen Whyte, M.D. \nGender and Cross-Cultural Issues \nSergio Aguilar-Gaxiola, M.D., Ph.D. \nKavoos G. Bassiri, M.S.\nVenkataramana Bhat, M.D.\nMarit Boiler, M.P.H. \nDenise Canso, M.Sc.\nSmita N. Deshpande, M.D., D.P.M. \nRavi DeSilva, M.D.", "source": "dsm5.pdf"} {"id": "7d95399f4570-2", "page_content": "Ravi DeSilva, M.D. \nEsperanza Diaz, M.D.\nByron J. Good, Ph.D. \nSimon Groen, M.A.\nLadson Hinton, M.D. \nLincoln I. Khasakhala, Ph.D.\nFrancis G. Lu, M.D. \nAthena Madan, M.A.\nAnne W. Mbwayo, Ph.D.\nOanh Meyer, Ph.D.\nVictoria N. Mutiso, Ph.D., D.Sc. \nDavid M. Ndetei, M.D.\nAndel V. Nicasio, M.S.Ed.\nVasudeo Paralikar, M.D., Ph.D.\nKanak Patil, M.A.\nFilipa I. Santos, H.B.Sc.\nSanjeev B. Sarmukaddam, Ph.D., M.Sc.\nMonica Z. Scal co, M.D., Ph.D.\nKatie Thompson, M.A. \nHendry Ton, M.D., M.Sc. \nRob C.J. van Dijk, M.Sc. \nWilliam A. Vega, Ph.D. \nJohann M. Vega-Dienstmaier, M.D.\nJoseph Westermeyer, M.D., Ph.D.", "source": "dsm5.pdf"} {"id": "b6e6978bd802-0", "page_content": "902 DSM-5 Advisors and Other Contributors\nPsychiatric/General Medical \nInterface\nDaniel J. Balog, M.D.\nCharles C. Engel, M.D., M.P.H.\nCharles D. Motsinger, M.D.\nImpairment and Disability \nCille Kennedy, Ph.D. \nDiagnostic Assessment \nInstruments\nPaul J. Pikonis, Ph.D. Other Conditions That May Be \na Focus of Clinical Attention\nWilliam E. Narrow, M.D., M.P.H., Chair\nRoger Peele, M.D.\nLawson R. Wulsin, M.D.\nCharles H. Zeanah, M.D.\nPrudence W. Fisher, Ph.D., Advisor\nStanley N. Caroff, M.D., Contributor/Consultant\nJames B. Lohr, M.D., Contributor/Consultant\nMarianne Wambolt, Ph.D., Contributor/Consultant\nDSM-5 Research Group\nAllan Donner, Ph.D.\nCPHC Peer Reviewers\nKenneth Altshuler, M.D.\nPedro G. Alvarenga, M.D.\nDiana J. Antonacci, M.D.\nRichard Balon, M.D.\nDavid H. Barlow, Ph.D.\nL. Jarrett Ba rnhill, M.D.\nKatja Beesdo-Baum, Ph.D.\nMarty Boman, Ed.D.\nJames Bourgeois, M.D.\nDavid Braff, M.D.\nHarry Brandt, M.D.\nKirk Brower, M.D.\nRachel Bryant-Waugh, Ph.D.\nJack D. Burke Jr., M.D., M.P.H.\nBrenda Bursch, Ph.D.\nJoseph Camilleri, M.D.\nPatricia Casey, M.D.", "source": "dsm5.pdf"} {"id": "b6e6978bd802-1", "page_content": "Joseph Camilleri, M.D.\nPatricia Casey, M.D.\nF. Xavier Castellanos, M.D.\nEran Chemerinski, M.D.\nWai Chen, M.D.\nElie Cheniaux, M.D., D.Sc.\nCheryl Chessick, M.D,\nJ. Richard Ciccone, M.D.\nAnita H. Clayton, M.D.\nTihalia J. Coleman, Ph.D.\nJohn Csernansky, M.D.\nManuel J. Cuesta M.D., Ph.D.\nJoanne L. Davis, M.D.\nDavid L. Delmonico, Ph.D.\nRay J. DePaulo, M.D.\nDimitris Dikeos, M.D.\nIna E. Djonlagic, M.D.\nC. Neill Epperson, M.D.\nJavier I. Escobar, M.D., M.Sc.\nSpencer Eth, M.D.\nDavid Fassler, M.D.\nGiovanni A. Fava, M.D.\nRobert Feinstein, M.D.\nMolly Finnerty, M.D.\nMark H. Fleisher, M.D.\nAlessio Florentini, M.D.Laura Fochtmann, M.D.\nMarshal Forstein, M.D.\nWilliam French, M.D.\nMaximillian Gahr, M.D.\nCynthia Geppert, M.D.\nAnn Germaine, Ph.D.\nMarcia Goin, M.D.\nDavid A. Gorelick, M.D., Ph.D.\nDavid Graeber, M.D.\nCynthia A. Graham, Ph.D.\nAndreas Hartmann, M.D.\nVictoria Hendrick, M.D.\nMerrill Herman, M.D.\nDavid Herzog, M.D.", "source": "dsm5.pdf"} {"id": "b6e6978bd802-2", "page_content": "Merrill Herman, M.D.\nDavid Herzog, M.D.\nMardi Horowitz, M.D.\nYa-fen Huang, M.D.\nAnthony Kales, M.D\nNiranjan S. Karnik, M.D., Ph.D.\nJeffrey Katzman, M.D.\nBryan King, M.D.\nCecilia Kjellgren, M.D.\nHarold W. Koenigsberg, M.D.\nRichard B. Krueger, M.D.\nSteven Lamberti, M.D.\nRuth A. Lanius, M.D.\nJohn Lauriello, M.D.\nAnthony Lehman, M.D.\nMichael Linden, M.D.\nMark W. Mahowald, M.D.\nMarsha D. Marcus, Ph.D.\nStephen Marder, M.D.\nWendy Marsh, M.D.\nMichael S. McCloskey, Ph.D.\nJeffrey Metzner, M.D.\nRobert Michels, M.D.\nLaura Miller, M.D.\nMichael C. Miller, M.D.\nFrederick Moeller, M.D.\nPeter T. Morgan, M.D., Ph.D.\nMadhav Muppa, M.D.\nPhilip Muskin, M.D.", "source": "dsm5.pdf"} {"id": "1721bdbb1057-0", "page_content": "DSM-5 Advisors and Other Contributors 903\nJoachim Nitschke, M.D.\nAbraham Nussbaum, M.D.\nAnn Olincy, M.D.\nMark Onslow, Ph.D.\nSally Ozonoff, Ph.D.\nJohn R. Peteet, M.D.\nIsmene L. Petrakis, M.D.\nChristophe M. Pfeiffer, M.D.\nKaren Pierce, M.D.\nBelinda Plattner, M.D.\nFranklin Putnam, M.D.\nStuart F. Quan, M.D.\nJohn Racy, M.D.\nPhillip Resnick, M.D.\nMichele Riba, M.D.\nJerold Rosenbaum, M.D.\nStephen Ross, M.D.\nLawrence Scahill, M.S.N., Ph.D. \nDaniel Schechter, M.D.\nMary V. Seeman, M.D.\nAlessandro Serretti, M.D.\nJianhua Shen, M.D.Ravi Kumar R. Singareddy, M.D.\nIngmar Skoog, M.D., Ph.D.\nGary Small, M.D.\nPaul Soloff, M.D.\nChristina Stadle r, M.D., Ph.D.\nNada Stotland, M.D.\nNeil Swerdlow, M.D.\nKim Tillery, Ph.D.\nDavid Tolin, Ph.D.\nJayne Trachman, M.D.\nLuke Tsai, M.D.\nMing T. Tsuang, M.D., Ph.D.\nRichard Tuch, M.D.\nJohan Verhulst, M.D.\nB. Timothy Walsh, M.D.\nMichael Weissberg, M.D.\nGodehard Weniger, M.D.\nKeith Widaman, Ph.D.", "source": "dsm5.pdf"} {"id": "1721bdbb1057-1", "page_content": "Godehard Weniger, M.D.\nKeith Widaman, Ph.D.\nThomas Wise, M.D.\nGeorge E. Woods, M.D.\nKimberly A. Yonkers, M.D.\nAlexander Young, M.D.\nDSM-5 Field Trials in Academic Clinical Centers\u2014\nAdult Samples\nDavid Geffen School of Medicine, Univ ersity of California, Los Angeles\nInvestigator\nHelen Lavretsky, M.D., Principal Investigator\nReferring and Interviewing \nClinicians\nJessica Brommelhoff, Ph.D.\nXavier Cagigas, Ph.D.\nPaul Cernin, Ph.D.\nLinda Ercoli, Ph.D.\nRandall Espinoza, M.D.Helen Lavretsky, M.D.\nJeanne Kim, Ph.D.\nDavid Merrill, M.D.\nKaren Miller, Ph.D.\nChristopher Nunez, Ph.D.\nResearch Coordinators\nNatalie St. Cyr, M.A., Lead Research \nCoordinator\nNora Nazarian, B.A.\nColin Shinn, M.A.\nCentre for Addiction and Mental Health, Toronto, Ontario, Canada\nInvestigators\nBruce G. Pollock, M.D., Ph.D., Lead Principal \nInvestigator\nR. Michael Bagby, Ph.D., Principal Investigator\nKwame J. McKenzie, M.D., Principal \nInvestigator\nTony P. George, M.D., Co-investigator\nLena C. Quilty, Ph.D., Co-investigator\nPeter Voore, M.D., Co-investigator\nReferring and Interviewing Clinicians\nDonna E. Akman, Ph.D.\nR. Michael Bagby, Ph.D.\nWayne C. V. Baici, M.D.", "source": "dsm5.pdf"} {"id": "1721bdbb1057-2", "page_content": "Wayne C. V. Baici, M.D.\nCrystal Baluyut, M.D.Eva W. C. Chow, M.D., J.D., M.P.H.\nZ. J. Daskalakis, M.D., Ph.D.\nPablo Diaz-Hermosillo, M.D.\nGeorge Foussias, M.Sc., M.D.\nPaul A. Frewen, Ph.D.\nAriel Graff-Guerrero, M.D., M.Sc., Ph.D.\nMargaret K. Hahn, M.D.\nLorena Hsu, Ph.D.\nJustine Joseph, Ph.D.\nSean Kidd, Ph.D.\nKwame J. McKenzie, M.D.\nMahesh Menon, Ph.D.\nRomina Mizrahi, M.D., Ph.D.\nDaniel J. Mueller, M.D., Ph.D.\nLena C. Quilty, Ph.D.\nAnthony C. Ruocco, Ph.D.", "source": "dsm5.pdf"} {"id": "8974fae8f0be-0", "page_content": "904 DSM-5 Advisors and Other Contributors\nJorge Soni, M.D.\nAristotle N. Voineskos, M.D., Ph.D.\nGeorge Voineskos, M.D.\nPeter Voore, Ph.D.\nChris Watson, Ph.D.\nReferring Clinicians \nOfer Agid, M.D.\nAsh Bender, M.D.\nPatricia Cavanagh, M.D.\nSarah Colman, M.D.\nVincenzo Deluca, M.D.\nJustin Geagea, M.D.\nDavid S. Goldbloom, M.D.\nDaniel Greben, M.D.\nMalati Gupta, M.D.\nKen Harrison, M.D.\nImraan Jeeva, M.D.\nJoel Jeffries, M.B. \nJudith Laposa, Ph.D.Jan Malat, M.D.\nShelley McMain, Ph.D.\nBruce Pollock, M.D., Ph.D.\nAndriy V. Samokhva lov, M.D., Ph.D.\nMartin Strassnig, M.D.\nAlbert H. C. Wong, M.D., Ph.D.\nResearch Coordinators\nGloria I. Leo, M.A., Lead Research Coordinator\nAnissa D. Bachan, B.A.\nBahar Haji-Khamneh, M.A.\nOlga Likhodi, M.Sc.\nEleanor J. Liu, Ph.D.\nSarah A. McGee Ng, B.B.A.\nOther Research Staff\nSusan E. Dickens, M.A., Clinical Research \nManager\nSandy Richards, B.Sc.N., Schizophrenia \nResearch Manager\nDallas VA Medical Center, Dallas, Texas\nInvestigators\nCarol S. North, M.D., M.P.E., Principal \nInvestigator", "source": "dsm5.pdf"} {"id": "8974fae8f0be-1", "page_content": "Investigators\nCarol S. North, M.D., M.P.E., Principal \nInvestigator\nAlina Suris, Ph.D., A.B.P.P., Principal \nInvestigator\nReferring and Interviewing Clinicians\nBarry Ardolf, Psy.D.\nAbila Awan, M.D.\nJoel Baskin, M.D.\nJohn Black, Ph.D.\nJeffrey Dodds, Ph.D.\nGloria Emmett, Ph.D.\nKarma Hudson, M.D.\nJamylah Jackson, Ph.D., A.B.P.P.\nLynda Kirkland-Culp, Ph.D., A.B.P.P.\nHeidi Koehler, Ph.D., A.B.P.P.\nElizabeth Lewis, Psy.D.\nAashish Parikh, M.D.\nReed Robinson, Ph.D.\nJheel Shah, M.D.\nGeetha Shivakumar, M.D.\nSarah Spain, Ph.D., A.B.P.P.Lisa Thoman, Ph.D.\nLia Thomas, M.D.\nJamie Zabukovec, Psy.D.\nMustafa Zaidi, M.D.\nAndrea Zartman, Ph.D.\nGeneral Referral Sources\nRobert Blake, L.M.S.W.\nEvelyn Gibbs, L.M.S.W.\nMichelle King-Thompson, L.M.S.W.\nResearch Coordinators\nJeannie B. Whitman, Ph.D., Lead Research \nCoordinator\nSunday Adewuyi, M.D.\nElizabeth Anderson, B.A.\nSolaleh Azimipour, B.S.\nCarissa Barney, B.S.\nKristie Cavazos, B.A.\nRobert Devereaux, B.S.\nDana Downs, M.S., M.S.W.\nSharjeel Farooqui, M.D.\nJulia Smith, Psy.D.", "source": "dsm5.pdf"} {"id": "8974fae8f0be-2", "page_content": "Sharjeel Farooqui, M.D.\nJulia Smith, Psy.D.\nKun-Ying H. Sung, B.S.\nSchool of Medicine, The University of Texas San Antonio, \nSan Antonio, Texas\nInvestigator\nMauricio Tohen, M.D., Dr.P.H., M.B.A., \nPrincipal Investigator \nReferring and Interviewing Clinicians\nSuman Baddam, Psy.D.\nCharles L. Bowden, M.D.Nancy Diazgranados, M.D., M.S.\nCraig A. Dike, Psy.D.\nDianne E. Dunn, Psy.D., M.P.H.\nElena Gherman, M.D.\nJodi M. Gonzalez, Ph.D.\nPablo Gonzalez, M.D.\nPhillip Lai, Psy.D.", "source": "dsm5.pdf"} {"id": "186d77032008-0", "page_content": "DSM-5 Advisors and Other Contributors 905\nNatalie Maples-Aguilar, M.A., L.P.A.\nMarlon P. Quinones, M.D.\nJeslina J. Raj, Psy.D.\nDavid L. Roberts, Ph.D.\nNancy Sandusky, R.N., F.P.M.H.N.P.-B.C., \nD.N.P.-C.\nDonna S. Stutes, M.S., L.P.C.\nMauricio Tohen, M.D., Dr.PH, M.B.A.\nDawn I. Velligan, Ph.D.\nWeiran Wu, M.D., Ph.D.\nReferring Clinicians\nAlbana Dassori, M.D.\nMegan Frederick, M.A.Robert Gonzalez, M.D.\nUma Kasinath, M.D.\nCamis Milam, M.D.\nVivek Singh, M.D.\nPeter Thompson, M.D.\nResearch Coordinators\nMelissa Hernandez, B.A., Lead Research \nCoordinator\nFermin Alejandro Carrizales, B.A.\nMartha Dahl, R.N., B.S.N.\nPatrick M. Smith, B.A. \nNicole B. Watson, M.A. \nMichael E. DeBakey VA Medical Center and the Menninger Clinic, \nHouston, Texas (Joint Study Site)\nMichael E. DeBakey VA Medical Center\nInvestigator\nLaura Marsh, M.D., Principal Investigator\nReferring and Interviewing Clinicians\nShalini Aggarwal, M.D.\nSu Bailey, Ph.D.\nMinnete (Helen) Beckner, Ph.D.\nCrystal Clark, M.D.\nCharles DeJohn, M.D.\nRobert Garza, M.D.\nAruna Gottumakkla, M.D.", "source": "dsm5.pdf"} {"id": "186d77032008-1", "page_content": "Robert Garza, M.D.\nAruna Gottumakkla, M.D.\nJanet Hickey, M.D.\nJames Ireland, M.D.\nMary Lois Lacey, A.P.R.N.\nWendy Leopoulos, M.D.\nLaura Marsh, M.D.\nDeleene Menefee, Ph.D.\nBrian I. Miller, Ph.D. \nCandy Smith, Ph.D.\nAvila Steele, Ph.D.\nJill Wanner, Ph.D.\nRachel Wells, Ph.D.\nKaki York-Ward, Ph.D.Referring Clinicians\nSara Allison, M.D.\nLeonard Denney, L.C.S.W.\nCatherine Flores, L.C.S.W.\nNathalie Marie, M.D.\nChristopher Martin, M.D.\nSanjay Mathew, M.D.\nErica Montgomery, M.D.\nGregory Scholl, P.A.\nJocelyn Ulanday, M.D., M.P.H. \nResearch Coordinators\nSarah Neely Torres, B.S., Lead Research \nCoordinator\nKathleen Grout, M.A.\nLea Kiefer, M.P.H.\nJana Tran, M.A.\nVolunteer Research Assistants\nCatherine Clark\nLinh Hoang\nMenninger Clinic \nInvestigator\nEfrain Bleiberg, M.D., Principal Investigator\nReferring and Interviewing Clinicians\nJennifer Baumgardner, Ph.D. \nElizabeth Dodd Conaway, L.C.S.W., B.C.D. \nWarren Christianson, D.O. \nWesley Clayton, L.M.S.W. \nJ. Christopher Fowler, Ph.D. \nMichael Groat, Ph.D. \nEdythe Harvey, M.D. \nDenise Kagan, Ph.D.", "source": "dsm5.pdf"} {"id": "186d77032008-2", "page_content": "Edythe Harvey, M.D. \nDenise Kagan, Ph.D. \nHans Meyer, L.C.S.W. Segundo Robert-Ibarra, M.D. \nSandhya Trivedi, M.D. \nRebecca Wagner, Ph.D. \nHarrell Woodson, Ph.D.\nAmanda Yoder, L.C.S.W. \nReferring Clinicians\nJames Flack, M.D.\nDavid Ness, M.D.\nResearch Coordinators\nSteve Herrera, B.S., M.T., Lead Research \nCoordinator\nAllison Kalpakci, B.A.", "source": "dsm5.pdf"} {"id": "6c80ab1389a6-0", "page_content": "906 DSM-5 Advisors and Other Contributors\nMayo Clinic, Rochester, Minnesota\nInvestigators\nMark A. Frye, M.D., Principal Investigator\nGlenn E. Smith, Ph.D.,\u00a0Principal Investigator\nJeffrey P. Staab M.D., M.S., Principal \nInvestigator\nReferring and Interviewing Clinicians\nOsama Abulseoud, M.D. \nJane Cerhan, Ph.D.\nJulie Fields, Ph.D. \nMark A. Frye, M.D.\nManuel Fuentes, M.D.\nYonas Geda, M.D. \nMaria Harmandayan, M.D.\nReba King, M.D. \nSimon Kung, M.D.\nMary Machuda, Ph.D. \nDonald McAlpine, M.D. \nAlastair McKean, M.D.\nJuliana Moraes, M.D.\nTeresa Rummans, M.D.James R. Rundell, M.D. \nRichard Seime, Ph.D. \nGlenn E. Smith, Ph.D.\u00a0\nChristopher Sola, D.O.\nJeffrey P. Staab M.D., M.S. \nMarin Veldic, M.D. \nMark D. Williams, M.D. \nMaya Yustis, Ph.D. \nResearch Coordinators\nLisa Seymour, B.S., Lead Research Coordinator\nScott Feeder, M.S.\nLee Gunderson, B.S.\nSherrie Hanna, M.A., L.P.\nKelly Harper, B.A.\nKatie Mingo, B.A.\nCynthia Stoppel, A.S.\nOther Study Staff\nAnna Frye\nAndrea Hogan\nPerelman School of Medicine, University of Pennsylvania, \nPhiladelphia, Pennsylvania\nInvestigators\nMahendra T. Bhati, M.D., Principal Investigator", "source": "dsm5.pdf"} {"id": "6c80ab1389a6-1", "page_content": "Investigators\nMahendra T. Bhati, M.D., Principal Investigator\nMarna S. Barrett, Ph.D., Co-investigator\nMichael E. Thase, M. D., Co-investigator\nReferring and Interviewing Clinicians\nPeter B. Bloom, M.D.\nNicole K Chalmers L.C.S.W.\nTorrey A. Creed, Ph.D.\nMario Cristancho, M.D.\nAmy Cunningham, Psy.D.\nJohn P. Dennis, Ph.D.\nJosephine Elia, M.D.\nPeter Gariti, Ph.D., L.C.S.W.\nPhilip Gehrman, Ph.D.\nLaurie Gray, M.D.\nEmily A.P. Haigh, Ph.D.\nNora J. Johnson, M.B.A., M.S., Psy.D.\nPaulo Knapp, M.D.\nYong-Tong Li, M.D.\nBill Mace, Ph.D.\nKevin S. McCarthy, Ph.D.\nDimitri Perivoliotis, Ph.D.\nLuke Schultz, Ph.D.\nTracy Steen, Ph.D.\nChris Tjoa, M.D.\nNancy A. Wintering, L.C.S.W.\nReferring Clinicians\nEleanor Ainslie, M.D.\nKelly C. Allison, Ph.D.Rebecca Aspden, M.D.\nClaudia F. Baldassano, M.D.\nVijayta Bansal, M.D.\nRachel A. Bennett, M.D.\nRichard Bollinger, Ph.D.\nAndrea Bowen, M.D.\nKarla Campanella, M.D.\nAnthony Carlino, M.D.\nNoah Carroll, M.S.S.\nAlysia Cirona, M.D.\nSamuel Collier, M.D.", "source": "dsm5.pdf"} {"id": "6c80ab1389a6-2", "page_content": "Alysia Cirona, M.D.\nSamuel Collier, M.D.\nAndreea Crauciuc, L.C.S.W.\nPilar Cristancho, M.D.\nTraci D'Almeida, M.D. \nKathleen Diller, M.D.\nBenoit Dub\u00e9, M.D.\nJon Dukes, M.S.W.\nLauren Elliott, M.D.\nMira Elwell, B.A.\nMia Everett, M.D.\nLucy F. Faulconbridge, Ph.D.\nPatricia Furlan, Ph.D.\nJoanna Goldstein, L.C.S.W.\nPaul Grant, Ph.D.\nJillian Graves, L.C.S.W.\nTamar Gur, M.D., Ph.D.\nAlisa Gutman, M.D., Ph.D.\nNora Hymowitz, M.D.\nSofia Jensen, M.D.\nTiffany King, M.S.W.\nKatherine Levine, M.D.", "source": "dsm5.pdf"} {"id": "bfae9e0e5f3f-0", "page_content": "DSM-5 Advisors and Other Contributors 907\nAlice Li, M.D.\nJanet Light, L.C.S.W.\nJohn Listerud, M.D., Ph.D.\nEmily Malcoun, Ph.D.\nDonovan Maust, M.D.\nAdam Meadows, M.D.\nMichelle Moyer, M.D.\nRebecca Naugle, L.C.S.W.\nCory Newman, Ph.D.\nJohn Northrop, M.D., Ph.D.\nElizabeth A. Ellis Ohr, Psy.D.\nJohn O'Reardon, M.D.\nAbraham Pachikara, M.D.\nAndrea Perelman, M.S.W.\nDiana Perez, M.S.W.\nBianca Previdi, M.D.\nJ. Russell Ramsay, Ph.D.\nJorge Rivera-Colon, M.D.\nJan Smedley, L.C.S.W.\nKatie Struble, M.S.W.\nAita Susi, M.D.\nYekaterina Tatarchuk, M.D.\nEllen Tarves, M.A.\nAllison Tweedie, M.D.\nHolly Valerio, M.D.Thomas A. Wadden, Ph.D.\nJoseph Wright, Ph.D.\nYan Xuan, M.D.\nDavid Yusko, Psy.D.\nResearch Coordinators\nJordan A. Coello, B.A., Lead Research \nCoordinator\nEric Wang, B.S.E.\nVolunteer Research Assistants/\nInterns\nJeannine Barker, M.A., A.T.R.\nJacqueline Baron\nKelsey Bogue \nAlexandra Ciomek\nMartekuor Dodoo, B.A.\nJulian Domanico\nLaura Heller, B.A.\nLeah Hull-Rawson, B.A.", "source": "dsm5.pdf"} {"id": "bfae9e0e5f3f-1", "page_content": "Laura Heller, B.A.\nLeah Hull-Rawson, B.A.\nJacquelyn Klehm, B.A.\nChristina Lam\nDante Proetto, B.S.\nMolly Roy\nCasey Shannon\nStanford University School of Medicine, Stanford, California\nInvestigators\nCarl Feinstein, M.D., Principal Investigator\nDebra Safer, M.D., Principal Investigator\nReferring and Interviewing Clinicians\nKari Berquist, Ph.D.\nEric Clausell, Ph.D.\nDanielle Colborn, Ph.D. \nWhitney Daniels, M.D.\nAlison Darcy, Ph.D.\nKrista Fielding, M.D.\nMina Fisher, M.D.\nKara Fitzpatrick, Ph.D.\nWendy Froehlich, M.D.\nGrace Gengoux, Ph.D.\nAnna Cassandra Golding, Ph.D.\nLisa Groesz, Ph.D. \nKyle Hinman, M.D.\nRob Holaway, Ph.D.\nMatthew Holve, M.D.\nRex Huang, M.D.\nNina Kirz, M.D.\nMegan Klabunde, Ph.D.\nJohn Leckie, Ph.D.\nNaomi Leslie, M.D.\nAdrianne Lona, M.D.\nRanvinder Rai, M.D.\nRebecca Rialon, Ph.D.\nBeverly Rodriguez, M.D., Ph.D.\nDebra Safer, M.D.\nMary Sanders, Ph.D.Jamie Scaletta, Ph.D.\nNorah Simpson, Ph.D.\nManpreet Singh, M.D.\nMaria-Christina Stewart, Ph.D.\nMelissa Vallas, M.D.\nPatrick Whalen, Ph.D.\nSanno Zack, Ph.D.\nReferring Clinicians", "source": "dsm5.pdf"} {"id": "bfae9e0e5f3f-2", "page_content": "Sanno Zack, Ph.D.\nReferring Clinicians\nRobin Apple, Ph.D.\nVictor Carrion, M.D.\nCarl Feinstein, M.D.\nChristine Gray, Ph.D. \nAntonio Hardan, M.D. \nMegan Jones, Psy.D. \nLinda Lotspeich, M.D.\nLauren Mikula, Psy.D. \nBrandyn Street, Ph.D. \nVioleta Tan, M.D.\nHeather Taylor, Ph.D. \nJacob Towery, M.D.\nSharon Williams, Ph.D. \nResearch Coordinators\nKate Arnow, B.A., Lead Research Coordinator\nNandini Datta, B.S.\nStephanie Manasse, B.A.\nVolunteer Research Assistants/\nInterns\nArianna Martin, M.S.\nAdriana Nevado, B.A.", "source": "dsm5.pdf"} {"id": "33b432e54e72-0", "page_content": "908 DSM-5 Advisors and Other Contributors\nChildren\u2019s Hospital Colorado, Aurora, Colorado\nInvestigator\nMarianne Wamboldt , M.D., Principal \nInvestigator\nReferring and Interviewing \nClinicians\nGalia Abadi, M.D.\nSteven Behling, Ph.D.\nJamie Blume, Ph.D.\nAdam Burstein, M.D.\nDebbie Carter, M.D.\nKelly Caywood, Ph.D.\nMeredith Chapman, M.D.\nPaulette Christian, A.P.P.M.H.N.\nMary Cook, M.D.\nAnthony Cordaro, M.D.\nAudrey Dumas, M.D.\nGuido Frank, M.D.\nKaren Frankel, Ph.D.\nDarryl Graham, Ph.D.\nYael Granader, Ph.D.\nIsabelle Guillemet, M.D.\nPatrece Hairston, Ph.D.\nCharles Harrison, Ph.D.\nTammy Herckner, L.C.S.W.\nCassie Karlsson, M.D.\nKimberly Kelsay, M.D.\nDavid Kieval, Ph.D.\nMegan Klabunde, Ph.D.\nJaimelyn Kost, L.C.S.W.\nHarrison Levine, M.D.\nRaven Lipmanson, M.D.\nSusan Lurie, M.D.\nAsa Marokus, M.D.\nIdalia Massa, Ph.D.\nChristine McDunn, Ph.D.\nScot McKay, M.D.\nMarissa Murgolo, L.C.S.W.\nAlyssa Oland, Ph.D.\nLina Patel, Ph.D.\nRheena Pineda, Ph.D.\nGautam Rajendran, M.D.\nDiane Reichmuth, Ph.D", "source": "dsm5.pdf"} {"id": "33b432e54e72-1", "page_content": "Gautam Rajendran, M.D.\nDiane Reichmuth, Ph.D\nMichael Rollin, M.D.Marlena Romero, L.C.S.W.\nMichelle Roy, Ph.D.\nCeleste St. John-Larkin, M.D.\nElise Sannar, Ph.D.\nDaniel Savin, M.D.\nClaire Dean Sinclair, Ph.D.\nAshley Smith, L.C.S.W.\nMindy Solomon, Ph.D.\nSally Tarbell, Ph.D.\nHelen Thilly, L.C.S.W.\nSara Tlustos-Carter, Ph.D.\nHolly Vause, A.P.P.M.H.N\nMarianne Wamboldt, M.D.\nAngela Ward, L.C.S.W.\nJason Williams, Ph.D.\nJason Willoughby, Ph.D.\nBrennan Young, Ph.D.\nReferring Clinicians\nKelly Bhatnagar, Ph.D.\nJeffery Dolgan, Ph.D.\nJennifer Eichberg, L.C.S.W.\nJennifer Hagman, M.D.\nJames Masterson, L.C.S.W.\nHy Gia Park, M.D.\nTami Roblek, Ph.D.\nWendy Smith, Ph.D.\nDavid Williams, M.D.\nResearch Coordinators\nLaurie Burnside, M.S.M., C.C.R.C., Lead \nResearch Coordinator\nDarci Anderson, B.A., C.C.R.C.\nHeather Kennedy, M.P.H.\nAmanda Millar, B.A.\nVanessa Waruinge, B.S.\nElizabeth Wallace, B.A.\nVolunteer Research Assistants/\nInterns\nWisdom Amouzou\nAshley Anderson\nMichael Richards\nMateya Whyte\nBaystate Medical Center, Springfield, Massachusetts\nInvestigators", "source": "dsm5.pdf"} {"id": "33b432e54e72-2", "page_content": "Michael Richards\nMateya Whyte\nBaystate Medical Center, Springfield, Massachusetts\nInvestigators\nBruce Waslick, M.D., Principal Investigator\nCheryl Bonica, Ph.D., Co-investigator \nJohn Fanton, M.D., Co-investigator \nBarry Sarvet, M.D. , Co-investigator Referring and Interviewing Clinicians\nJulie Bermant, R.N., M.S.N., N.P.\nCheryl Bonica, Ph.D.\nJodi Devine, L.I.C.S.W.\nWilliam Fahey, Ph.D.\nJohn Fanton, M.D.", "source": "dsm5.pdf"} {"id": "7d2f8f2a368f-0", "page_content": "DSM-5 Advisors and Other Contributors 909\nStephane Jacobus, Ph.D.\nBarry Sarvet, M.D.\nPeter Thunfors, Ph.D.\nBruce Waslick, M.D.\nVicki Weld, L.I.C.S.W.\nSara Wiener, L.I.C.S.W.\nShadi Zaghloul, M.D.\nReferring Clinicians\nSarah Detenber, L.I.C.S.W.\nGordon Garrison, L.I.C.S.W.\nJacqueline Humpreys, L.I.C.S.W.\nNoreen McGirr, L.I.C.S.W.Sarah Marcotte, L.C.S.W.\nPatricia Rogowski, R.N., C.N.S.\nResearch Coordinators\nJulie Kingsbury, C.C.R.P., Lead Research \nCoordinator\nBrenda Martin, B.A.\nVolunteer Research Assistant/\nIntern\nLiza Detenber\nNew York State Psychiatric Institute, New York, N.Y., Weill Cornell \nMedical College, Payne Whitney and Westchester Divisions, New York \nand White Plains, N.Y., and North Shore Child and Family Guidance \nCenter, Roslyn Heights, N.Y. (Joint Study Site)\nInvestigator\nPrudence W. Fisher, Ph.D., Principal \nInvestigator\nResearch Coordinators\nJulia K. Carmody, B.A., Lead Research \nCoordinator\nZvi R. Shapiro, B.A., Lead Research \nCoordinatorVolunteers\nPreeya Desai\nSamantha Keller\nJeremy Litfin, M.A.\nSarah L. Pearlstein, B.A.\nCedilla Sacher\nNew York State Psychiatric Institute\nReferring and Interviewing Clinicians\nMichele Cohen, L.C.S.W.\nEduvigis Cruz-Arrieta, Ph.D.", "source": "dsm5.pdf"} {"id": "7d2f8f2a368f-1", "page_content": "Eduvigis Cruz-Arrieta, Ph.D.\nMiriam Ehrensaft, Ph.D.\nLaurence Greenhill, M.D.\nSchuyler Henderson, M.D., M.P.H.\nSharlene Jackson, Ph.D.\nLindsay Moskowitz, M.D.\nSweene C. Oscar, Ph.D.\nXenia Protopopescu, M.D.\nJames Rodriguez, Ph.D.\nGregory Tau, M.D.\nMelissa Tebbs, L.C.S.W.\nCarolina Velez-Grau, L.C.S.W.\nKhadijah Booth Watkins, M.D.\nReferring Clinicians\nGeorge Alvarado, M.D.\nAlison Baker, M.D.\nElena Baron, Psy.D.\nLincoln Bickford, M.D., Ph.D.\nZachary Blumkin, Psy.D.\nColleen Cullen, L.C.S.W.\nChyristianne DeAlmeida, Ph.D.\nMatthew Ehrlich, M.D.Eve Friedl, M.D.\nClare Gaskins, Ph.D.\nAlice Greenfield, L.C.S.W.\nLiora Hoffman, M.D.\nKathleen Jung, M.D.\nKarimi Mailutha, M.D., M.P.H.\nValentina Nikulina, Ph.D.\nTal Reis, Ph.D. \nMoira Rynn, M.D.\nJasmine Sawhney, M.D.\nSarajbit Singh, M.D.\nKatherine Stratigos, M.D.\nOliver Stroeh, M.D.\nRussell Tobe, M.D.\nMeghan Tomb, Ph.D.\nMichelle Tricamo, M.D.\nResearch Coordinators\nAngel A. Caraballo, M.D.", "source": "dsm5.pdf"} {"id": "7d2f8f2a368f-2", "page_content": "Research Coordinators\nAngel A. Caraballo, M.D.\nErica M. Chin, Ph.D.\nDaniel T. Chrzanowski, M.D.\nTess Dougherty, B.A.\nStephanie Hundt, M.A.\nMoira A. Rynn, M.D.\nDeborah Stedge, R.N.", "source": "dsm5.pdf"} {"id": "4ad90be2bba4-0", "page_content": "910 DSM-5 Advisors and Other Contributors\nWeill Cornell Medical College, Payne Whitney and Westchester Divisions\nReferring and Interviewing Clinicians\nArchana Basu, Ph.D.\nShannon M. Bennett, M.D.\nMaria De Pena-Nowak, M.D.\nJill Feldman, L.M.S.W.\nDennis Gee, M.D.\nJo R. Hariton, Ph.D.\nLakshmi P. Reddy, M.D.\nMargaret Yoon, M.D.\nReferring Clinicians\nMargo Benjamin, M.D.\nVanessa Bobb, M.D.\nElizabeth Bochtler, M.D.\nKatie Cave, L.C.S.W.\nMaalobeeka Gangopadhyay, M.D.Jodi Gold, M.D.\nTejal Kaur, M.D.\nAaron Krasner, M.D.\nAmy Miranda, L.C.S.W.\nCynthia Pfeffer, M.D.\nJames Rebeta, Ph.D.\nSharon Skariah, M.D.\nJeremy Stone, Ph.D.\nDirk Winter, M.D.\nResearch Coordinators\nAlex Eve Keller, B.S., Lead Research Coordinator\nNomi Bodner (volunteer)\nBarbara L. Flye, Ph.D.\nJamie S. Neiman (volunteer)\nRebecca L. Rendleman, M.D.\nNorth Shore Child and Family Guidance Center\nReferring and Interviewing Clinicians\nCasye Brachfeld-Launer, L.C.S.W.\nSusan Klein Cohen, Ph.D.\nAmy Gelb, L.C.S.W.-R.\nJodi Glasser, L.C.S.W.\nElizabeth Goulding-Tag, L.C.S.W.\nDeborah B. Kassimir, L.C.S.W.", "source": "dsm5.pdf"} {"id": "4ad90be2bba4-1", "page_content": "Deborah B. Kassimir, L.C.S.W.\nMargo Posillico Messina, L.C.S.W.\nAndr\u00e9a Moullin-Heddle, L.M.S.W.\nLisa Pineda, L.C.S.W.\nElissa Smilowitz, L.C.S.W.\nReferring Clinicians\nRegina Barros-Rivera, L.C.S.W.-R. Assistant \nExecutive Director\nMaria Christiansen, B.S.\nAmy Davies-Hollander, L.M.S.W.\nEartha Hackett, M.S.Ed., M.Sc., B.Sc.Bruce Kaufstein, L.C.S.W.-R, Director of \nClinical Services\nKathy Knaust, L.C.S.W.\nJohn Levinson, L.C.S.W.-R, B.C.D.\nAndrew Maleckoff, L.C.S.W., Executive \nDirector/CEO\nSarah Rosen, L.C.S.W.-R, A.C.S.W.\nAbigail Rothenberg, L.M.S.W.\nChristine Scotten, A.C.S.W.\nMichelle Spatano, L.C.S.W.-R.\nDiane Straneri, M.S., R.N., C.S.\nRosara Torrisi, L.M.S.W.\nRob Vichnis, L.C.S.W.\nResearch Coordinators\nToni Kolb-Papetti, L.C.S.W.\nSheena M. Dauro (volunteer)\nDSM-5 Field Trials Pilot Study, \nJohns Hopkins Medical Institution, Baltimore, Maryland\nAdult Sample\nCommunity Psychiatry Outpatient Pr ogram, Department of Psychiatry \nand Behavioral Sciences Main Campus\nInvestigators\nBernadette Cullen, M.B., B.Ch., B.A.O., \nPrincipal Investigator\nHolly C. Wilcox, Ph.D., Principal Investigator", "source": "dsm5.pdf"} {"id": "4ad90be2bba4-2", "page_content": "Principal Investigator\nHolly C. Wilcox, Ph.D., Principal Investigator\nReferring and Interviewing \nClinicians\nBernadette Cullen, M.B., B.Ch., B.A.O. \nShane Grant, L.C.S.W.-C.\nCharee Green, L.C.P.C.Emily Lorensen, L.C.S.W.-C.\nKathleen Malloy, L.C.P.C.\nGary Pilarchik, L.C.S.W.-C\nHolly Slater, L.C.P.C.\nStanislav Spivak, M.D.\nTarcia Spencer Turner, L.C.P.C.\nNicholas Seldes Windt, L.C.S.W.-C.\nResearch Coordinators\nMellisha McKitty, B.A.\nAlison Newcomer, M.H.S.", "source": "dsm5.pdf"} {"id": "7cf0e7aa1d2b-0", "page_content": "DSM-5 Advisors and Other Contributors 911\nPediatric Sample\nChild and Adolescent Outpatient Progr am, Department of Psychiatry and \nBehavioral Sciences Bayview Medical Center\nInvestigators\nJoan P. Gerring, M.D., Principal Investigator\nLeslie Miller, M.D., Principal Investigator\nHolly C. Wilcox, Ph.D., Co-investigator\nReferring and Interviewing \nClinicians\nShannon Barnett, M.D.\nGwen Condon, L.C.P.C.\nBrijan Fellows, L.C.S.W.-C.\nHeather Garner, L.C.S.W.-C.\nJoan P. Gerring, M.D.Anna Gonzaga, M.D.\nDebra Jenkins, L.C.S.W.-C.\nPaige N. Johnston, L.C.P.C.\nBrenda Memel, D.N.P., R.N.\nLeslie Miller, M.D.\nRyan Moore, L.C.S.W.-C.\nShauna Reinblatt, M.D.\nMonique Vardi, L.C.P.C.\nResearch Coordinators\nMellisha McKitty, B.A.\nAlison Newcomer, M.H.S.\nDSM-5 Field Trials in Routin e Clinical Practice Settings: \nCollaborating Investigators\nArchil Abashidze, M.D.\nFrancis R. Abueg, Ph.D.\nJennifer Louise Accuardi, M.S.\nBalkozar S. Adam, M.D.\nMiriam E. Adams, Sc.D., M.S.W., L.I.C.S.W.\nSuzanna C. Adams, M.A.\nLawrence Adler, M.D.\nRownak Afroz, M.D.\nKhalid I. Afzal, M.D.\nJoseph Alimasuya, M.D.", "source": "dsm5.pdf"} {"id": "7cf0e7aa1d2b-1", "page_content": "Joseph Alimasuya, M.D.\nEmily\u00a0Allen, M.S.\nKatherine A. Alle n, L.M.F.T., M.A.\nWilliam D. Allen, M.S.\nJafar AlMashat, M.D.\nAnthony T. Al onzo, D.M.F.T.\nGuillermo\u00a0Alvarez, B.A., M.A.\nAngela\u00a0Amoia-Lutz, L.M.F.T.\nKrista A. Anderson, M.A., L.M.F.T.\nLisa R. Anderson, M.Ed., L.C.P.C.\nPamela M. Anderson, L.M.F.T.\nShannon N. Anderson, M.A., L.P.C., N.C.C.\nEric S. Andrews, M.A.\nVicki Arbuckle, M.S., Nursing(N.P.)\nNamita K. Arora, M.D.\nDarryl\u00a0Arrington, M.A.\nBearlyn Y. Ash, M.S.\nWylie J. Bagley, Ph.D.\nKumar D. Bahl, M.D.\nDeborah C. Bailey, M.A., M.S., Ph.D.\nCarolyn Baird, D.N.P., M.B.A., R.N.-B.C., \nC.A.R.N.-A.P., I.C.C.D.P.D.\nJoelle Bangsund M.S.W.\nMaria Baratta, M.S.W., Ph.D.\nStan Barnard, M.S.W.\nDeborah Barnes, M.S.Margaret L. Barnes, Ph.D.\nDavid Barnum, Ph.D.\nRaymond M. Baum, M.D.\nEdward Wescott Beal, M.D.\nMichelle Beaudoin, M.A.\nErnest E. Beckham, Ph.D.\nLori L. Beckwith, M.Ed", "source": "dsm5.pdf"} {"id": "7cf0e7aa1d2b-2", "page_content": "Ernest E. Beckham, Ph.D.\nLori L. Beckwith, M.Ed\nEmmet Bellville, M.A.\nRandall E. Bennett, M.A.\nLynn Benson, Ph.D.\nRobert Scott Benson, M.D.\nLinda Benton, M.S.W.\nDitza D. Berger, Ph.D.\nLouise I. Bertman, Ph.D.\nRobin Bieber, M.S., L.M.F.T.\nDiana M. Bigham, M.A.\nDavid R. Blackburn, Ph.D.\nKelley Blackwell, L.M.F.T.\nLancia Blatchley, B.A., L.M.F.T.\nStacey L. Block, L.M.S.W., A.C.S.W.\nKaren J. Bloodworth, M.S., N.C.C., L.P.C.\nLester Bloomenstiel, M.S.\nChristine M. Blue, D.O.\nMarina Bluvshtein, Ph.D.\nCallie Gray Bobbitt, M.S.W., L.C.S.W.\nMoses L. Boone, Jr., L.M.S.W., B.C.D.\nSteffanie Boudreau-T homas, M.A.-L.P.C.\nJay L. Boulter, M.A.\nAaron Daniel Bourne, M.A.\nHelen F. Bowden, Ph.D.\nAryn Bowley-Safranek, B.S., M.S.\nElizabeth Boyajian, Ph.D.\nBeth K. Boyarsky, M.D.\nGail M. Boyd, Ph.D.\nJeffrey M. Brandler, Ed.S., C.A.S., S.A.P.", "source": "dsm5.pdf"} {"id": "51e05e44f48b-0", "page_content": "912 DSM-5 Advisors and Other Contributors\nSandra L. Branton, Ed.D.\nKaren J. Brocco-Kish, M.D.\nKristin Brooks, P.M.H.N.P.\nAnn Marie Brown, M.S.W.\nPhilip Brown, M.S.W.\nKellie\u00a0Buckner, Ed.S.\nRichard\u00a0Bunt, M.D.\nNeil F. Buono, D.Min.\nJanice Bureau, M.S.W., L.C.S.W.\nKimlee Butterfield, M.S.W.\nClaudia Byrne, Ph.D.\nQuinn Callicott, M.S.W., L.C.S.W.\nAlvaro Camacho, M.D., M.P.H.\nSandra Cambra, Ph.D.\nHeather Campbell, M.A.\nNancy Campbell, Ph.D., M.S.W.\nKaren Ranee Canada, L.M.F.T.\nJoseph P. Cannavo, M.D.\nCatherine F. Caporale, Ph.D.\nFrederick Capps, Ph.D., M.S.\nRebecca J. Carney, M.B.A., M.A., L.M.H.C.\nKelly J. Carroll, M.S.W.\nRichard W. Carroll, Ph.D., L.P.C., A.C.S.\nSherry Casper, Ph.D.\nJoseph A. Catania, L.I.S.W.S., L.C.D.C. III\nManisha P. Cavendish, Ph.D.\nKenneth M. Certa, M.D.\nShambhavi Chandraiah, M.D.\nCalvin\u00a0Chatlos, M.D.\nDaniel C. Chen, M.D.\nDarlene Cheryl, M.S.W.\nMatthew R. Chirman, M.S.\nCarole A. Chisholm, M.S.W.", "source": "dsm5.pdf"} {"id": "51e05e44f48b-1", "page_content": "Carole A. Chisholm, M.S.W.\nShobha A. Chottera, M.D.\nJoseph Logue Christenson, M.D.\nPamela Christy, Psy.D.\nSharon M. Freeman Clevenger, Ph.D., \nP.M.H.C.N.S.-B.C.\nMary Ann Cohen, M.D.\nMitchell J. Cohen, M.D.\nDiego L. Coira, M.D.\nMelinda A. Lawless Coker, Psy.D.\nCarol Cole, M.S.W., L.C.S.W.\nCaron Collins, M.A., L.M.F.T.\nWanda Collins, M.S.N.\nLinda Cook Cason, M.A.\nAyanna Cooke-Chen, M.D., Ph.D.\nHeidi B. Cooperstein, D.O.\nIleana Corbelle, M.S.W.\nKimberly Corbett, Psy.D.\nAngelina Cordova, M.A.Ed.\nJennifer Carol Cox, L.P.C.\nSheree Cox, M.A., R.N., N.C.C., D.C.C., \nL.M.H.C.\nWilliam Frederick Cox, M.D.\nSally M. Cox, M.S.Ed.\nDebbie Herman Crane, M.S.W.\nArthur Ray Crawford, III, Ph.D.Roula Creighton, M.D.\nJohn R. Crossfield, L.M.H.C.\nSue Cutbirth, R.N., M.S.N, C.S., P.M.H.N.P.\nMarco Antonio Cuyar, M.S.\nRebecca Susan Daily, M.D.\nLori S. Danenberg, Ph.D.\nChan Dang-Vu, M.D.\nMary Hynes Danielak, Psy.D.\nCynthia A. Darby, M.Ed., Ed.S.", "source": "dsm5.pdf"} {"id": "51e05e44f48b-2", "page_content": "Cynthia A. Darby, M.Ed., Ed.S.\nDouglas Darnall, Ph.D.\nChristopher Davidson, M.D.\nDoreen Davis, Ph.D., L.C.S.W.\nSandra Davis, Ph.D., L.M.H.C., N.C.C.\nWalter Pitts Davis, M.Th.\nChristian J. Dean, Ph.D.\nKent Dean, Ph.D.\nElizabeth Dear, M.A.\nShelby DeBause, M.A.\nRebecca B. DeLaney, M.S.S.W., L.C.S.W., B.C.D.\nJohn R. Delatorre, M.A.\nFrank DeLaurentis, M.D.\nEric Denner, M.A., M.B.A.\nMary Dennihan, L.M.F.T.\nKenny Dennis, M.A.\nPamela L. Detrick, Ph.D., M.S., F.N.P.-B.C., \nP.M.H.N.P.-B.C., R.N.-B.C., C.A.P., \nG.C.A.C.\nRobert Detrinis, M.D.\nDaniel A. Deutschman, M.D.\nTania Diaz, Psy.D.\nSharon Dobbs, M.S.W., L.C.S.W.\nDavid Doreau, M.Ed.\nGayle L. Dosher, M.A.\nD'Ann Downey, Ph.D., M.S.W.\nBeth Doyle, M.A.\nAmy J. Driskill, M.S., L.C.M.F.T.\nJames Drury, M.D.\nBrenda-Lee Duarte, M.Ed.\nShane E. Dulemba, M.S.N.\nNancy R. G. Dunbar, M.D.\nCathy Duncan, M.A.", "source": "dsm5.pdf"} {"id": "51e05e44f48b-3", "page_content": "Cathy Duncan, M.A.\nRebecca S. Dunn, M.S.N., A.R.N.P.\nDebbie Earnshaw, M.A.\nShawna Eddy-Kissell, M.A.\nMomen El Nesr, M.D.\nJeffrey Bruce Elliott, Psy.D.\nLeslie Ellis, Ph.D.\nDonna M. Emfield, L.C.P.C.\nGretchen S. Enright, M.D.\nJohn C. Espy, Ph.D.\nRenuka\u00a0Evani, M.B.B.S., M.D.\nHeather Evans, M.S.Ed, L.P.C.N.C.C.\nCesar A. Fabiani, M.D.\nFahim Fahim, M.D.\nSamuel Fam, M.D.\nEdward H. Fankhanel, Ph.D., Ed.D.\nTamara Farmer, M.S.N, A.R.N.P.\nFarida Farzana, M.D.", "source": "dsm5.pdf"} {"id": "ce89a93a9253-0", "page_content": "DSM-5 Advisors and Other Contributors 913\nPhilip Fast, M.S.\nPatricia Feltrup-Exum, M.A.M.F.T.\nHector J. Fernandez-Barillas, Ph.D.\nJulie Ferry, M.S.W., L.I.C.S.W.\nJane Fink, Ph.D., M.S.S.A.\nKathy Finkle, L.P.C.M.H.\nSteven Finlay, Ph.D.\nRik\u00a0Fire, M.S.W., L.C.S.W.\nAnn Flood, Ph.D.\nJeanine Lee Foreman, M.S.\nThyra Fossum, Ph.D.\nKaren S. Franklin, L.I.C.S.W.\nSherre K. Franklin, M.A.\nHelen R. Frey, M.A., E.D.\nMichael L. Freytag, B.S., M.A.\nBeth Gagnon, M.S.W.\nPatrice L.R. Gallagher, Ph.D.\nAngela J. Gallien, M.A.\nRobert Gallo, M.S.W.\nMario Galvarino, M.D.\nVladimir I. Gasca, M.D.\nJoshua Gates, Ph.D.\nAnthony Gaudioso, Ph.D.\nMichelle S. Gauthier, A.P.R.N., M.S.N, \nP.M.H.N.P.-B.C.\nRachel E. Gearhart, L.C.S.W.\nStephen D. Gelfond, M.D.\nNancy S. Gerow, M.S.\nMichael J. Gerson, Ph.D.\nSusan M. A. Geyer, L.M.S.W.\nLorrie Gfeller-Strouts, Ph.D.\nShubu\u00a0Ghosh, M.D.\nRichard Dorsey Gillespie, M.Div.\nStuart A. Gitlin, M.S.S.A.", "source": "dsm5.pdf"} {"id": "ce89a93a9253-1", "page_content": "Stuart A. Gitlin, M.S.S.A.\nJeannette E. Given, Ph.D.\nFrances Gizzi, L.C.S.W.\nStephen I. Glicksman, Ph.D.\nMartha Glisky, Ph.D.\nSonia Godbole, M.D.\nHoward M. Gold fischer, Psy.D.\nMary Jane Gonzalez-Huss, Ph.D.\nMichael I. Good, M.D.\nDawn Goodman-Martin, M.A.-L.M.H.C.\nRobert Gorkin, Ph.D., M.D.\nJeff Gorski, M.S.W.\nLinda O. Graf, M.Ed., L.C.P.C.\nOna Graham, Psy.D.\nAubrie M. Graves, L.M.S.W., C.A.S.A.C.\nHoward S. Green, M.D.\nKaren Torry Green, M.S.W.\nGary Greenberg, Ph.D.\nMarjorie Greenhut, M.A. \nJames L. Greenstone, Ed.D., J.D.\nRaymond A. Griffin, Ph.D.\nJoseph Grillo, Ph.D.\nJaneane M. Grisez, A.A., B.A.\nLawrence S. Gross, M.D.\nRobert J. Gross, M.D.Sally J. Grosscup, Ph.D.\nPhilip A. Grossi, M.D.\nGabrielle Guedet, Ph.D.\nNicholas Guenzel, B.A., B.S., M.S.N.\nMary G. Hales, M.A.\nTara C. Haley, M.S., L.M.F.T.\nJohn D. Hall, M.D.\nAmy Hammer, M.S.W.\nMichael S. Hanau, M.D.\nLinda K.W. Hansen, M.A., L.P.", "source": "dsm5.pdf"} {"id": "ce89a93a9253-2", "page_content": "Linda K.W. Hansen, M.A., L.P.\nGenevieve R. Hansler, M.S.W.\nMary T. Harring ton, L.C.S.W.\nLois Hartman, Ph.D.\nSteven Lee Hartsock, Ph.D., M.S.W.\nVictoria Ann Harwood, M.S.W., L.C.S.W.\nRossi A. Hassad, Ph.D., M.P.H.\nErin V. Hatcher, M.S.N.\nRichard L. Hauger, M.D.\nKimberly M. Haverly, M.A. \nGale Eisner Heater, M.S., M.F.T.\nKatlin Hecox, M.A.\nBrenda Heideman, M.S.W.\nMelinda Heinen, M.Sc.\nMarie-Therese Heitkamp, M.S.\nMelissa B. Held, M.A.\nJessica Hellings, M.D.\nBonnie Helmick-O'Brien, M.A., L.M.F.T.\nMaLinda T. Henderson, M.S.N, F.P.M.H.N.P.\nGwenn Herman, M.S.W.\nMartha W. Hernandez, M.S.N, A.P.R.N., \nP.M.H.C.N.S.\nRobin L. Hewitt, M.S.\nKenneth Hoffman, Ph.D.\nPatricia E. Hogan, D.O.\nPeggy Holcomb, Ph.D.\nGarland H. Holloman, Jr., M.D.\nKimberly Huegel, M.S.W., L.C.S.W.\nJason Hughes, L.P.C.-S., N.C.C.\nJennifer C. Hughes, Ph.D., M.S.W., L.I.S.W.-S.\nMichelle K. Humke, M.A.\nJudith G. Hunt, L.M.F.T.", "source": "dsm5.pdf"} {"id": "ce89a93a9253-3", "page_content": "Judith G. Hunt, L.M.F.T.\nTasneem Hussainee, M.D.\nSharlene J. Hutchinson, M.S.N.\nMuhammad Ikram, M.D.\nSunday Ilechukwu, M.D., D.Psy. Cli.\nDouglas H. Ingram, M.D.\nMarilynn Irvine, Ph.D.\nMarjorie Isaacs, Psy.D.\nRaymond Isackila, Ed.S., P.C.C.-S., L.I.C.D.C.\nMohammed A. Issa, M.D.\nJohn L. Jankord, M.A.\nBarbara P. Jannah, L.C.S.W.\nC. Stuart\u00a0Johnson, M.S.\nDawn M. Johnson, M.A.\nDeanna V. Johnson, M.S., A.P.R.N., B.C.\nEric C. Johnson, M.F.T.\nJoy Johnson, Ph.D., L.C.S.W.\nWillard Johnson, Ph.D.", "source": "dsm5.pdf"} {"id": "0c456b87884d-0", "page_content": "914 DSM-5 Advisors and Other Contributors\nXenia Johnson-Bhembe, M.D.\nVann S. Joines, Ph.D.\nMargaret Jones, Psy.D.\nPatricia Jorgenson, M.S.W.\nSteven M. Joseph, M.D.\nTaylere Joseph, M.A.\nJeanette M. Joyner-Craddock, M.S.S.W.\nMelissa Kachapis, M.A.\nCharles T. Kaelber, M.D.\nAimee C. Kaempf, M.D.\nPeter Andrew Kahn, M.D.\nRobert P. Kahn-Rose, M.D.\nMaher Karam-Hage, M.D.\nTodd H. Kasdan, M .D.\nKaren Kaufman, M.S., L.M.F.T.\nRhesa Kaulia, M.A., M.F.T.\nDebbie Lynn Kelly, M.S.N, P.M.H.N.P.-B.C.\nW. Stephen Kelly, Ph.D.\nSelena Kennedy, M.A.\nJudith A. Kenney, M.S., L.P.C.\nMark Patrick Kerekes, M.D.\nAlyse Kerr, M.S., N.C.C., N.A.D.D.-C.C., L.P.C.\nKaren L. Kerschmann, L.C.S.W.\nMarcia Kesner, M.S.\nAshan Khan, Ph.D.\nShaukat Khan, M.D.\nAudrey Khatchikian, Ph.D.\nLaurie B. Kimmel, M.S.W.\nJason H. King, Ph.D.\nNancy Leigh King, M.S.W., L.C.S.W., L.C.A.S.\nKyle Kinne, M.S.C\nCassandra M. Klyman, M.D.\nDavid R. Knapp, L.C.S.W.", "source": "dsm5.pdf"} {"id": "0c456b87884d-1", "page_content": "David R. Knapp, L.C.S.W.\nMargaret Knerr, M.S.\nMichael R. Knox, Ph.D.\nCarolyn Koblin, M.S.\nValerie Kolbert, M.S., A.R.N.P.-B.C.\nHeather Koontz, M.S.W.\nFaye Koop, Ph.D., L.C.M.F.T.\nFern M. Kopakin, M.S.W., L.C.S.W.\nJoel Kotin, M.D.\nSharlene K. Kraemer, M.S.E.\nMarjorie Vego Krausz, M.A., Ed.D.\nNancy J. Krell, M.S.W.\nMindy E. Kronenberg, Ph.D.\nDwayne Kruse, M.S., M.F.T.\nAjay S. Kuchibhatla, M.D.\nShubha N. Kumar, M.D.\nHelen H. Kyomen, M.D., M.S.\nRebecca M. Lachut, M.Ed., Ed.S.\nAlexis Lake, M.S.S.\nRamaswamy Lakshmanan, M.D.\nBrigitta Lalone, L.C.S.W.-R\nJohn W. Lancaster, Ph.D.\nPatience R. Land, L.I.C.S.W., M.S.W., M.P.A.\nAmber Lange, M.A., Ph.D.\nJeff K. Larsen, M.A.\nNathan E. Lavid, M.D.Michelle Leader, Ph.D.\nStephen E. Lee, M.D.\nCathryn L. Leff, Ph.D., L.M.F.T.\nRachael Kollar Leombruno, L.M.F.T.\nArlene I. Lev, M.S.W., L.C.S.W.-R", "source": "dsm5.pdf"} {"id": "0c456b87884d-2", "page_content": "Arlene I. Lev, M.S.W., L.C.S.W.-R\nGregory K. Lewis, M.A.-L.M.F.T.\nJane Hart Lewis, M.S.\nMelissa S. Lewis, M.S.W., L.I.C.S.W.\nNorman Gerald Lewis, F.R.A.N.Z.C.P.\nRobin Joy Lewis, Ph.D.\nRyan Michael Ley, M.D.\nTammy R. Lias, M.A.\nRussell F. Lim, M.D.\nJana Lincoln, M.D.\nTed Lindberg, L.M.S.W., L.M.F.T., M.S.W.\nPeggy Solow Liss, M.S.W.\nAndrea Loeb, Psy.D.\nWilliam David Lohr, M.D.\nMary L. Ludy, M.A., L.M.H.C., L.M.F.T.\nNathan Lundin, M.A., L.P.C.\nVeena Luthra, M.D.\nPatti Lyerly, L.C.S.W.\nDenise E. Maas, M.A.\nSilvia MacAllister, L.M.F.T.\nNicola MacCallum, M.S., M.F.C. Therapy\nColin N. MacKenzie, M.D.\nCynthia Mack-Ernsdorff, Ph.D.\nJohn R. Madsen-Bibeau, M.S., M.Div\nChristopher J. Maglio, Ph.D.\nDeepak Mahajan, M.D.\nDebra Majewski, M.A.\nHarish Kumar Malhotra, M.D.\nPamela Marcus, R.N., M.S.\nMary P. Marshall, Ph.D.\nFlora Lynne Martin, M.A., L.P.C., A.D.C.\nRobert S. Martin, M.D.\nJennifer L. Martinez, M.S.", "source": "dsm5.pdf"} {"id": "0c456b87884d-3", "page_content": "Robert S. Martin, M.D.\nJennifer L. Martinez, M.S.\nNinfa Martinez-Aguilar, M.A., M.F.T.\nEmily Martinsen, M.S.W.\nFarhan A. Matin, M.D.\nJanus Maybee, P.M.H.N.P.\nKaren Mazarin-Stanek, M.A.\nEben L. McClenahan, M.D., M.S.\nJerlyn C. McCleod, M.D.\nSusan E. McCue, M.S.W., L.C.S.W.\nKent D. McDonald, M.S.\nDaniel McDonnell, M.S.N, P.M.H.-N.P.\nRobert McElhose, Ph.D.\nLisa D. McGrath, Ph.D.\nMark McGrosky, M.S.W.\nKatherine M. McKay, Ph.D.\nDarren D. McKinnis, M.S.W.\nMona McNelis-Broadley, M.S.W., L.C.S.W.\nRick McQuistion, Ph.D.\nSusan Joy Mendelsohn, Psy.D.\nBarbara S. Menninga, M.Ed.\nHindi Mermelstein, M.D., F.A.P.M.\nRachel B. Mich aelsen, M.S.W.", "source": "dsm5.pdf"} {"id": "547003e97325-0", "page_content": "DSM-5 Advisors and Other Contributors 915\nThomas F. Micka, M.D.\nTonya Miles, Psy.D.\nMatthew Miller, M.S.\nMichael E. Miller, M.D.\nNoel Miller, L.M.S.W., M.B.A., M.P.S.\nKalpana Miriyala, M.D.\nSandra Moenssens, M.S.\nErin Mokhtar, M.A.\nRobert E. Montgomery, M.Ed.\nSusan Moon, M.A.\nTheresa K. Moon, M.D.\nDavid B. Moore, B.A., M.Div., M.S.S.W., Ph.D.\nJoanne M. Moore, M.S.\nPeter I. M. Moran, M.B.B.Ch.\nAnna Moriarty, M.P.S., L.P.C., L.M.H.C.\nRichard Dean Morris, M.A.\nMichael M. Morrison, M.A.\nCarlton E. Munson, Ph.D.\nTimothy A. Murphy, M.D.\nBeth L. Murphy, Psy.D.\nMelissa A. Myers, M.D.\nStefan Nawab, M.D.\nAllyson Matney Neal, D.N.P.\nSteven Nicholas, M.A.\nAurelian N. Niculescu, M.D.\nEarl S. Nielsen, Ph.D.\nTerry Oleson, Ph.D.\nJulianne R. Oliver, B.S., M.S., Ph.D.\nRobert O. Olsen, M.D.\nAmy O'Neill, M.D.\nOscar H. Oo, Psy.D., A.B.P.P.\nLaurie Orlando, J.D., M.A.\nJill Osborne, M.S., Ed.S.\nKimberly Overlie, M.S.\nL. Kola Oyewumi, Ph.D.", "source": "dsm5.pdf"} {"id": "547003e97325-1", "page_content": "L. Kola Oyewumi, Ph.D.\nZachary J. Pa cha, M.S.W.\nSuzette R. Papadakis, M.S.\nAmanda C. Parsons, M.A., L.P.C.C.\nLee R. Pate, B.A., M.A.\nEric L. Patterson, L.P.C.\nSherri Paulson, M.Ed., L.S.C.W.\nPeter Dennis Pautz, B.A., M.S.W.\nMalinda J. Perkins, M.S.W., L.C.S.W.\nEleanor F. Perlman, M.S.W.\nDeborah K. Perry, M.S.W.\nAmanda Peterman, L.M.F.T.\nShawn Pflugardt, Psy.D.\nRobert J. Dean Phillips, M.S.\nLaura Pieper, M.S.W., L.C.S.W.\nLori D. Pink, M.S.W., B.C.D\nMichael G. Pipich, M.S., L.M.F.T.\nCynthia G. Pizzulli, M.S.W., Ph.D.\nKathy C. Points, M.A.\nMarya E. Pollack, M.D., M.P.H.\nSanford E. Pomerantz, M.D.\nEva Ponder, M.S.W., Psy.D.\nErnest Poortinga, M.D.\nDavid Post, M.D.Laura L. Post, M.D., Ph.D., J.D.\nPatrick W. Powell, Ed.D.\nBeth M. Prewett, Psy.D.\nRobert Price, D.C.C., M.Ed.\nJohn Pruett, M.D.\nAneita S. Radov, M.A.\nDawn M. Raffa, Ph.D.\nKavitha Raja, M.D.", "source": "dsm5.pdf"} {"id": "547003e97325-2", "page_content": "Kavitha Raja, M.D.\nRanjit Ram, M.D.\nMohamed Ibrahim Ramadan, M.D., M.S.\nChristopher S. Randolph, M.D.\nNancy Rappaport, M.Ed.\nJohn Moir Rauenhorst, M.D.\nLaurel Jean Rebenstock, L.M.S.W.\nEdwin Renaud, Ph.D.\nHeather J. Rhodes, M.A.\nJennifer S. Ritchie-Goodline, Psy.D.\nDaniel G. Roberts, M.A.\nBrenda Rohren, M.A., M.F.S., L.I.M.H.P., \nL.A.D.C., M.A.C.\nDonna G. Rolin-Kenny, Ph.D., A.P.R.N., \nP.M.H.C.N.S.-B.C.\nSylvia E. Rosario, M.Ed.\nMindy S. Rosenbloom, M.D.\nHarvey A. Rosenstock, M.D.\nThalia Ross, M.S.S.W.\nFernando Rosso, M.D.\nBarry H. Roth, M.D.\nThomas S. Rue, M.A., L.M.H.C.\nElizabeth Ruegg, L.C.S.W.\nDiane Rullo, Ph.D.\nAngie Rumaldo, Ph.D.\nEric Rutberg, M.A., D.H.Ed.\nJoseph A. Sabella, L.M.H.C.\nKemal Sagduyu, M.D.\nAdam H. Saltz, M.S.W.\nJennifer A. Samardak, L.I.S.W.-S.\nGeorge R. Samuels, M.A., M.S.W.\nCarmen Sanjurjo, M.A.\nJohn S. Saroyan, Ed.D.\nBrigid Kathleen Sboto, M.A., M.F.T.", "source": "dsm5.pdf"} {"id": "547003e97325-3", "page_content": "Brigid Kathleen Sboto, M.A., M.F.T.\nLori Cluff Schade, M.S.\nJoan E. Schaper, M.S.N.\nRae J. Schilling, Ph.D.\nLarry Schor, Ph.D.\nDonna J. Schwartz, M.S.W., L.I.C.S.W.\nAmy J. Schwarzenbart, P.M.H.-C.N.S., B.C., \nA.P.N.P.\nJohn V. Scialli, M.D.\nChad Scott, Ph.D., L.P.C.C.\nSabine Sell, M.F.T.\nMinal Shah, N.S., N.C.C., L.P.C.\nLynn Shell, M.S.N.\nDharmesh Navi n Sheth, M.D.\nS. Christopher Shim, M.D.\nMarta M. Shinn, Ph.D.\nAndreas Sidiropoulos, M.D., Ph.D.\nMichael Siegell, M.D.", "source": "dsm5.pdf"} {"id": "a06419415e85-0", "page_content": "916 DSM-5 Advisors and Other Contributors\nMichael G. Simonds, Psy.D.\nGagandeep Singh, M.D.\nMelissa Rae Skrzypchak, M.S.S.W., L.C.S.W.\nPaula Slater, M.D.\nWilliam Bill Slaughter, M.D., M.A.\nAki Smith, Ph.D.\nDeborah L. Smith, Ed.M.\nDiane E. Smith, M.A., L.M.F.T.\nJames S. Sommer, M.S. \nJ. Richard Spatafora, M.D.\nJudy Splittgerber, M.S.N., C.S., N.P.\nThiruneermalai T.G. Sriram, M.D.\nMartha W. St. John, M.D.\nSybil Stafford, Ph.D.\nTimothy Stambaugh, M.A.\nLaura A. Stamboni, M.S.W.\nCarol L. R. Stark, M.D.\nStephanie Steinman, M.S.\nClaudia M. Stevens, M.S.W.\nJennifer Boyer Stevens, Psy.D.\nDominique Stevens-Young, M.S.W., L.C.S.W.\nKenneth Stewart, Ph.D.\nDaniel Storch, M.D.\nSuzanne Straebler, A.P.R.N.\nDawn Stremel, M.A., L.M.F.T.\nEmel Stroup, Psy.D.\nJohn W. Stump, M.S., L.M.F.T.\nThomas G. Suk, M.A.\nElizabeth Sunzeri, M.S.\nLinnea Swanson, M.A., Psy.D.\nPatricia Swanson, M.A.\nFereidoon Taghizadeh, M.D.", "source": "dsm5.pdf"} {"id": "a06419415e85-1", "page_content": "Fereidoon Taghizadeh, M.D.\nBonnie L. Tardif, L.M.H.C., N.C.C., B.C.P.C.C.\nJoan Tavares, M.S.W.\nAnn Taylor, M.S.W.\nDawn O'Dwyer Taylor, Ph.D.\nChanel V. Tazza, L.M.H.C.\nMartha H. Teater, M.A.\nClark D. Terrell, M.D.\nMark R. Thelen, Psy.D.\nNorman E. Thibault, M.S., Ph.D.\nTojuana L. Thomason, Ph.D.\nPaula Thomson, Psy.D.\nD. Chadwick Thompson, M.A.\nSusan Thorne-Devin, A.M.\nJean Eva Thumm, M.A.P.C., M.A.T., L.M.F.T., \nB.C.C.\nJames E. Tille, Ph.D., D.Min.\nJacalyn G. Tippey, Ph.D.\nSaraswathi Tirumalasetty, M.D.\nJacqueline A. Torrance, M.S.\nTerrence Trobaugh, M.S.\nLouisa V. Troemel, Psy.D., L.M.F.T.Susan Ullman, M.S.W.\nJennifer M. Underwood, M.S.W., L.C.S.W.\nRodney Dale Veldhuizen, M.A.\nMichelle Voegels, B.S.N., M.S.N., B.C.\nWess Vogt, M.D.\nR. Christopher Votolato, Psy.D.\nJohn W. Waid, Ph.D.\nChrista A. Wallis, M.A.\nDominique Walmsley, M.A.\nBhupinder Singh Waraich, M.D.", "source": "dsm5.pdf"} {"id": "a06419415e85-2", "page_content": "Bhupinder Singh Waraich, M.D.\nJoseph Ward, N.C.C., L.P.C. M.Ed.\nRobert Ward, M.S.W.\nMarilee L. M. Wasell, Ph.D.\nGannon J. Watts, L.P.C.-S., L.A.C., N.C.C., \nN.C.S.C., A.A.D.C., I.C.A.A.D.C.\nSheila R. Webster, M.A., M.S.S.A.\nBurton Weiss, M.D.\nDennis V. Weiss, M.D.\nJonathan S. Weiss, M.D.\nRichard \u00a0Wendel, Ph.D.\nPaul L. West, Ed.D.\nKris Sandra Wheatley, M.A., L.P.C., N.C.C.\nLeneigh White, M.A.\nDanny R. Whitehead, L.I.C.S.W.\nJean Whitinger, M.A.\nPeter D. Wilk, M.D.\nVanessa Wilkinson, L.P.C.\nTim F. Willia, M.S., M.A.Ed., L.P.C.\nCathy E. Willis, M.A., L.M.F.T., C.A.D.C.\nJeffery John Wilson, M.D.\nJacquie Wilson, M.Ed.\nDavid D. Wines, M.S.W.\nBarbara A. Wirebaugh, M.S.W.\nDaniel L. Wise, Ph.D.\nChristina Wong, M.S.W., L.C.S.W.\nSusanna\u00a0Wood, M.S.W., L.C.S.W.\nLinda L. Woodall, M.D.\nLeoneen Woodard-Faust, M.D.\nSheryl E. Woodhouse, L.M.F.T.\nGregory J. Worthington, Psy.D.\nTanya Wozniak, M.D.", "source": "dsm5.pdf"} {"id": "a06419415e85-3", "page_content": "Tanya Wozniak, M.D.\nKimberly Isaac Wright, M.A.\nPeter Yamamoto, M.D.\nMaria Ruiza Ang Yee, M.D.\nMichael B. Zafrani, M.D.\nJafet E. Gonzalez Zakarchenco, M.D.\nJohn Zibert, Ph.D.\nKaren Zilberstein, M.S.W.\nCathi Zillmann, C.P.N.P., N.P.P.\nGerald A. Zimmerman, Ph.D.\nMichele Zimmerman, M.A., P.M.H.C.N.S.-B.C.\nJudith A. Zink, M.A.\nVanderbilt University REDCap Team\nPaul Harris, Ph.D.\nSudah Kashyap, B.E.\nBrenda MinorJon Scherdin, M.A.\nRob Taylor, M.A.\nJaney Wang, M.S.", "source": "dsm5.pdf"} {"id": "0e9f5f166e70-0", "page_content": "917Index \nPage numbers printed in boldface type refer to tables.\nAbuse and neglect, 22, 717\u2013722\nadult maltreatment and neglect problems, \n720\u2013722\nchild maltreatment and neglect problems, \n717\u2013719\nAccess to medica l and other health care, problems \nrelated to, 726\nAcute dissociative reacti ons to stressful events, \n306\u2013307\nAcute stress disorder, 265, 280\u2013286\nassociated features supporting diagnosis of, \n283\u2013284\nculture-related diagnostic issues in, 285\ndevelopment and course of, 284\ndiagnostic criteria for, 280\u2013281\ndiagnostic features of, 281\u2013283\ndifferential diagnosis of, 285\u2013286\nfunctional consequences of, 285\ngender-related diagnostic issues in, 285\nprevalence of, 284\nrisk and prognostic factors for, 284\u2013285\nAddiction. See Substance-related and addictive \ndisorders\nADHD. See Attention-deficit/hyperactivity \ndisorder\nAdjustment disorders, 265, 286\u2013289\ncomorbidity with, 289\nculture-related diagnostic issues in, 288\ndevelopment and course of, 287\ndiagnostic criteria for, 286\u2013287\ndiagnostic features of, 287\ndifferential diagnosis of, 288\u2013289\nfunctional consequences of, 288\nprevalence of, 287\nrisk and prognostic factors for, 288\nAdjustment-like disorders, 289\nAdult maltreatment and neglect problems, 720\u2013\n722\nadult abuse by nonspouse or nonpartner, 722\nspouse or partner abuse, psychological, 721\u2013\n722\nspouse or partner neglect, 721\nspouse or partner violence, physical, 720", "source": "dsm5.pdf"} {"id": "0e9f5f166e70-1", "page_content": "spouse or partner neglect, 721\nspouse or partner violence, physical, 720\nspouse or partner violence, sexual, 720Agoraphobia, 190, 217\u2013221\nassociated features supporting diagnosis of, \n219\ncomorbidity with, 221\ndevelopment and course of, 219\u2013220\ndiagnostic criteria for, 217\u2013218\ndiagnostic features of, 218\u2013219\ndifferential diagnosis of, 220\u2013221\nfunctional consequences of, 220\ngender-related diagnostic issues in, 220\nprevalence of, 219\nrisk and prognostic factors for, 220\nAkathisia, medication-induced, 22\nacute, 711\ntardive, 712\nAlcohol intoxication, 497\u2013499\nassociated features supporting diagnosis of, \n497\u2013498\ncomorbidity with, 499\nculture-related diagnostic issues in, 498\ndevelopment and course of, 498\ndiagnostic criteria for, 497\ndiagnostic features of, 497\ndiagnostic markers for, 499\ndifferential diagnosis of, 499\nfunctional consequences of, 499\ngender-related diagnostic issues in, 498\nprevalence of, 498\nrisk and prognostic factors for, 498\nAlcohol-related disorders, 481, 490\u2013503\nalcohol intoxication, 497\u2013499\nalcohol use disorder, 490\u2013497\nalcohol withdrawal, 484, 499\u2013501\ndiagnoses associated with, 482\nother alcohol-induced disorders, 502\u2013503\ndevelopment and course of, 502\u2013503\nfeatures of, 502\nunspecified alcohol-related disorder, 503\nAlcohol use disorder, 490\u2013497\nassociated features supporting diagnosis of, \n492\u2013493\ncomorbidity with, 496\u2013497", "source": "dsm5.pdf"} {"id": "0e9f5f166e70-2", "page_content": "492\u2013493\ncomorbidity with, 496\u2013497\nculture-related diagnostic issues in, 494\u2013495\ndevelopment and course of, 493\u2013494", "source": "dsm5.pdf"} {"id": "33599eeb10ab-0", "page_content": "918 Index\nAlcohol use disorder (continued)\ndiagnostic criteria for, 490\u2013491\ndiagnostic features of, 492\ndiagnostic markers for, 495\u2013496\ndifferential diagnosis of, 496\nfunctional consequences of, 496\nprevalence of, 493\nrisk and prognostic factors for, 494\nspecifiers for, 492\nAlcohol withdrawal, 499\u2013501\nassociated features supporting diagnosis of, 500\ncomorbidity with, 501\ndevelopment and course of, 501\ndiagnostic criteria for, 499\u2013500\ndiagnostic features of, 500\ndiagnostic markers for, 501\ndifferential diagnosis of, 501\nfunctional consequences of, 501\nprevalence of, 501\nrisk and prognostic factors for, 501\nspecifiers for, 500\nAlzheimer\u2019s disease, major or mild \nneurocognitive disorder due to, 591, 603, \n611\u2013614\nassociated features supporting diagnosis of, 612\ncomorbidity with, 614\nculture-related diagnostic issues in, 613\ndevelopment and course of, 612\u2013613\ndiagnostic criteria for, 611\u2013612\ndiagnostic features of, 612\ndiagnostic markers for, 613\ndifferential diagnosis of, 614\nfunctional consequences of, 614\nprevalence of, 612\nrisk and prognostic factors for, 613\nAmerican Psychiatric Association (APA), 5\u20137\nAnorexia nervosa, 329, 338\u2013345\nassociated features supporting diagnosis of, 341\natypical, 353\ncomorbidity with, 344\u2013345\nculture-related diagnostic issues in, 342\ndevelopment and course of, 341\u2013342\ndiagnostic criteria for, 338\u2013339\ndiagnostic features of, 339\u2013340", "source": "dsm5.pdf"} {"id": "33599eeb10ab-1", "page_content": "diagnostic criteria for, 338\u2013339\ndiagnostic features of, 339\u2013340\ndiagnostic markers for, 342\u2013343\ndifferential diagnosis of, 344\nfunctional consequences of, 343\nprevalence of, 341\nrisk and prognostic factors for, 342\nsubtypes of, 339\nsuicide risk in, 343\nAntidepressant discontinuation syndrome, 22, \n712\u2013714\ncomorbidity with, 714\ncourse and development of, 713diagnostic features of, 713\ndifferential diagnosis of, 713\u2013714\nprevalence of, 713\nAntisocial personality disorder, 461, 476, 645, 646, \n659\u2013663\nassociated features supporting diagnosis of, \n660\u2013661\nculture-related diagnostic issues in, 662\ndevelopment and course of, 661\ndiagnostic criteria for, 659\ndiagnostic features of, 659\u2013660\ndifferential diagnosis of, 662\u2013663\nfeatures and criteria in alternative DSM-5 \nmodel for personality disorders, 763, \n764\u2013765\ngender-related diagnostic issues in, 662\nprevalence of, 661\nrisk and prognostic factors for, 661\u2013662\nAnxiety disorder due to another medical \ncondition, 190, 230\u2013232\nassociated features supporting diagnosis of, \n231\ndevelopment and course of, 231\ndiagnostic criteria for, 230\ndiagnostic features of, 230\u2013231\ndiagnostic markers for, 231\ndifferential diagnosis of, 231\u2013232\nprevalence of, 231\nAnxiety disorders, 189\u2013264\nagoraphobia, 190, 217\u2013221\nanxiety disorder due to another medical \ncondition, 190, 230\u2013232", "source": "dsm5.pdf"} {"id": "33599eeb10ab-2", "page_content": "anxiety disorder due to another medical \ncondition, 190, 230\u2013232\ngeneralized anxiety disorder, 190, 222\u2013226\nhighlights of changes fr om DSM-IV to DSM-5, \n811\nother specified anxiety disorder, 233\npanic attack specifier, 214\u2013217\npanic disorder, 190, 208\u2013214\nselective mutism, 189, 195\u2013197\nseparation anxiety disorder, 189, 190\u2013195\nsocial anxiety disorder (social phobia), 190, \n202\u2013208\nspecific phobia, 189\u2013190, 197\u2013202\nsubstance/medication-induced anxiety \ndisorder, 190, 226\u2013230\nunspecified anxiety disorder, 233\nAPA (American Psychiatric Association), 5\u20137\nAssessment measures, 23\u201324, 733\u2013748\ncross-cutting symptom measures, 733\u2013741\nDSM-5 Level 1 Cross-Cutting Symptom \nMeasure, 734\u2013736, 738\u2013741\nDSM-5 Level 2 Cross-Cutting Symptom \nMeasures, 734, 735, 736, 737\nfrequency of use of, 737\nseverity measures, 733, 742", "source": "dsm5.pdf"} {"id": "6ac6fc95c202-0", "page_content": "Index 919\nClinician-Rated Dimensions of Psychosis \nSymptom Severity, 742\u2013744\nfrequency of use of, 742\nscoring and interpretation of, 742\nWHO Disability Assessment Schedule \n(WHODAS), 16, 21, 734, 745\u2013748\nAtaque de nervios, 14, 211\u2013212, 233, 833\nAttention-deficit/hyperactivity disorder \n(ADHD), 11, 32, 59\u201366\nassociated features supporting diagnosis of, 61\ncomorbidity with, 65\nculture-related diagnostic issues in, 62\ndevelopment and course of, 61\ndiagnostic criteria for, 59\u201361\ndiagnostic features of, 61\ndifferential diagnosis of, 63\u201365\nfunctional consequences of, 63\ngender-related diagnostic issues in, 63\nmedication-induced symptoms of, 65\nother specified attentio n-deficit/hyperactivity \ndisorder, 65\u201366\nprevalence of, 61\nrisk and prognostic factors for, 62\nunspecified attention- deficit/hyperactivity \ndisorder, 66\nAttenuated psychosis syndrome, 122, 783\u2013786\nassociated features supporting diagnosis of, 784\ncomorbidity with, 786\ndevelopment and course of, 785\ndiagnostic features of, 783\u2013784\ndifferential diagnosis of, 785\u2013786\nfunctional consequences of, 785\nprevalence of, 784\u2013785\nproposed criteria for, 783\nrisk and prognostic factors for, 785\nAutism spectrum disorder, 31\u201332, 50\u201359\nassociated features supporting diagnosis of, 55\ncomorbidity with, 58\u201359\nculture-related diagnostic issues in, 57\ndevelopment and course of, 55\u201356", "source": "dsm5.pdf"} {"id": "6ac6fc95c202-1", "page_content": "culture-related diagnostic issues in, 57\ndevelopment and course of, 55\u201356\ndiagnostic criteria for, 50\u201351\ndiagnostic features of, 53\u201355\ndifferential diagnosis of, 57\u201358\nfunctional consequences of, 57\ngender-related diagnostic issues in, 57\nprevalence of, 55\nrecording procedures for, 51\nrisk and prognostic factors for, 56\u201357\nspecifiers for, 51\u201353, 52\nAvoidant personality disorder, 645, 646, 672\u2013675\nassociated features supporting diagnosis of, \n673\u2013674\nculture-related diagnostic issues in, 674\ndevelopment and course of, 674\ndiagnostic criteria for, 672\u2013673diagnostic features of, 673\ndifferential diagnosis of, 674\u2013675\nfeatures and criteria in alternative DSM-5 \nmodel for personality disorders, 763, \n765\u2013766\ngender-related diagnostic issues in, 674\nprevalence of, 674\nAvoidant/restrictive food intake disorder, 329, \n334\u2013338\nassociated features supporting diagnosis of, 335\ncomorbidity with, 338\nculture-related diagnostic issues in, 336\ndevelopment and course of, 335\u2013336\ndiagnostic criteria for, 334\ndiagnostic features of, 334\u2013335\ndiagnostic markers for, 336\ndifferential diagnosis of, 336\u2013338\nfunctional consequences of, 336\ngender-related diagnostic issues in, 336\nrisk and prognostic factors for, 336\nBereavement, 125\u2013126, 134, 155, 161, 194\npersistent complex, 289, 789\u2013792\nBinge-eating disorder, 329, 350\u2013353\nassociated features supporting diagnosis of, 351", "source": "dsm5.pdf"} {"id": "6ac6fc95c202-2", "page_content": "associated features supporting diagnosis of, 351\ncomorbidity with, 353\nculture-related diagnostic issues in, 352\ndevelopment and course of, 352\ndiagnostic criteria for, 350\ndiagnostic features of, 350\u2013351\ndifferential diagnosis of, 352\u2013353\nfunctional consequences of, 352\nof low frequency and/or limited duration, 353\nprevalence of, 351\nrisk and prognostic factors for, 352\nBipolar I disorder, 123\u2013132\nassociated features supporting diagnosis of, 129\ncomorbidity with, 132\nculture-related diagnostic issues in, 130\ndevelopment and course of, 130\ndiagnostic criteria for, 123\u2013127\ndiagnostic features of, 127\u2013129\ndifferential diagnosis of, 131\u2013132\nfunctional consequences of, 131\ngender-related diagnostic issues in, 130\nprevalence of, 130\nrisk and prognostic factors for, 130\nsuicide risk and, 131\nBipolar II disorder, 123, 132\u2013139\nassociated features supporting diagnosis of, 136\ncomorbidity with, 139\ndevelopment and course of, 136\u2013137\ndiagnostic criteria for, 132\u2013135\ndiagnostic features of, 135\u2013136\ndifferential diagnosis of, 138\u2013139", "source": "dsm5.pdf"} {"id": "ed4791512826-0", "page_content": "920 Index\nBipolar II disorder (continued)\nfunctional consequences of, 138\ngender-related diagnostic issues in, 137\nprevalence of, 136\nrisk and prognostic factors for, 137\nsuicide risk in, 138\nBipolar and related disorder due to another \nmedical condition, 123, 145\u2013147\nassociated features supporting diagnosis of, 146\ncomorbidity with, 147\nculture-related diagnostic issues in, 147\ndevelopment and course of, 146\u2013147\ndiagnostic criteria for, 145\u2013146\ndiagnostic features of, 146\ndiagnostic markers for, 147\ndifferential diagnosis of, 147\nfunctional consequences of, 147\ngender-related diagnostic issues in, 147\nBipolar and related disorders, 123\u2013154\nbipolar I disorder, 123\u2013132\nbipolar II disorder, 123, 132\u2013139\nbipolar and related disorder due to another \nmedical condition, 123, 145\u2013147\ncyclothymic disorder, 123, 139\u2013141\nhighlights of changes fr om DSM-IV to DSM-5, \n810\nother specified bipolar and related disorder, \n123, 148\nspecifiers for, 149\u2013154\nsubstance/medication-induced bipolar and \nrelated disorder, 123, 142\u2013145\nunspecified bipolar and related disorder, 149\nBody dysmorphic disorder, 235, 236, 242\u2013247\nassociated features supporting diagnosis of, 244\ncomorbidity with, 247\nculture-related diagnostic issues in, 245\ndevelopment and course of, 244\ndiagnostic criteria for, 242\u2013243\ndiagnostic features of, 243\u2013244\ndifferential diagnosis of, 245\u2013247\nfunctional consequences of, 245", "source": "dsm5.pdf"} {"id": "ed4791512826-1", "page_content": "differential diagnosis of, 245\u2013247\nfunctional consequences of, 245\ngender-related diagnostic issues in, 245\nprevalence of, 244\nrisk and prognostic factors for, 245\nsuicide risk and, 245\nBody dysmorphic-like disorder with actual flaws, \n263\nBody dysmorphic-like disorder without repetitive \nbehaviors, 263\nBody-focused repetitive behavior disorder, 235, \n263\u2013264\nBorderline personality disorder, 645, 646, 663\u2013666\nassociated features supporting diagnosis of, 665\nculture-related diagnostic issues in, 665\u2013666\ndevelopment and course of, 665diagnostic criteria for, 663\ndiagnostic features of, 663\u2013664\ndifferential diagnosis of, 666\nfeatures and criteria in alternative DSM-5 \nmodel for personality disorders, 763, \n766\u2013767\ngender-related diagnostic issues in, 666\nprevalence of, 665\nrisk and prognostic factors for, 665\nBreathing-related sleep disorders, 361, 378\u2013390\ncentral sleep apnea, 383\u2013386\nobstructive sleep ap nea hypopnea, 378\u2013383\nsleep-related hypoventilation, 387\u2013390\nBrief illness anxiety disorder, 327\nBrief psychotic disorder, 94\u201396\nassociated features supporting diagnosis of, 95\nculture-related diagnostic issues in, 95\ndevelopment and course of, 95\ndiagnostic criteria for, 94\ndiagnostic features of, 94\u201395\ndifferential diagnosis of, 96\nduration of, 89, 94, 99\nfunctional consequences of, 95\nprevalence of, 95\nrisk and prognostic factors for, 95\nBrief somatic symptom disorder, 327", "source": "dsm5.pdf"} {"id": "ed4791512826-2", "page_content": "risk and prognostic factors for, 95\nBrief somatic symptom disorder, 327\nBulimia nervosa, 329, 345\u2013350\nassociated features supporting diagnosis of, 347\ncomorbidity with, 349\u2013350\nculture-related diagnostic issues in, 348\ndevelopment and course of, 347\u2013348\ndiagnostic criteria for, 345\ndiagnostic features of, 345\u2013347\ndiagnostic markers for, 348\ndifferential diagnosis of, 349\nfunctional consequences of, 349\ngender-related diagnostic issues in, 348\nof low frequency and/or limited duration, 353\nprevalence of, 347\nrisk and prognostic factors for, 348\nsuicide risk in, 349\nCaffeine intoxication, 503\u2013506\nassociated features supporting diagnosis of, 504\ncomorbidity with, 506\ndevelopment and course of, 505\ndiagnostic criteria for, 503\u2013504\ndiagnostic features of, 504\ndifferential diagnosis of, 505\nfunctional consequences of, 505\nprevalence of, 505\nrisk and prognostic factors for, 505\nCaffeine-related disorders, 481, 503\u2013509\ncaffeine intoxication, 503\u2013506\ncaffeine withdrawal, 506\u2013508", "source": "dsm5.pdf"} {"id": "12149abe69d2-0", "page_content": "Index 921\ndiagnoses associated with, 482\nother caffeine-indu ced disorders, 508\nunspecified caffeine- related disorder, 509\nCaffeine use disorder, 792\u2013795\ncomorbidity with, 795\ndevelopment and course of, 794\ndiagnostic features of, 793\u2013794\ndifferential diagnosis of, 795\nfunctional consequences of, 794\u2013795\nprevalence of, 794\nproposed criteria for, 792\u2013793\nrisk and prognostic factors for, 794\nCaffeine withdrawal, 506\u2013508\nassociated features supporting diagnosis of, 507\ncomorbidity with, 508\nculture-related diagnostic issues in, 508\ndevelopment and course of, 507\ndiagnostic criteria for, 506\ndiagnostic features of, 506\u2013507\ndifferential diagnosis of, 508\nfunctional consequences of, 508\nprevalence of, 507\nrisk and prognostic factors for, 507\u2013508\nCannabis intoxication, 516\u2013517\ndiagnostic criteria for, 516\ndiagnostic features of, 516\u2013517\ndifferential diagnosis of, 517\nfunctional consequences of, 517\nprevalence of, 517\nspecifiers for, 516\nCannabis-related disorders, 481, 509\u2013519\ncannabis intoxication, 516\u2013517\ncannabis use disorder, 509\u2013516\ncannabis withdrawal, 484, 517\u2013519\ndiagnoses associated with, 482\nother cannabis-induced disorders, 519\nunspecified cannabis-related disorder, 519\nCannabis use disorder, 509\u2013516\nassociated features supporting diagnosis of, 512\ncomorbidity with, 515\u2013516\nculture-related diagnostic issues in, 514\ndevelopment and course of, 513", "source": "dsm5.pdf"} {"id": "12149abe69d2-1", "page_content": "culture-related diagnostic issues in, 514\ndevelopment and course of, 513\ndiagnostic criteria for, 509\u2013510\ndiagnostic features of, 510\u2013512\ndiagnostic markers for, 514\nfunctional consequences of, 514\u2013515\nprevalence of, 512\nrisk and prognostic factors for, 513\u2013514\nspecifiers for, 510\nCannabis withdrawal, 517\u2013519\ndevelopment and course of, 518\ndiagnostic criteria for, 517\u2013518\ndiagnostic features of, 518\ndifferential diagnosis of, 519\nrisk and prognostic factors for, 519Case formulation, 19\u201320\ncultural, 749\u2013759 ( See also Cultural \nformulation)\nCatatonia, 89, 119\u2013121\nassociated with another mental disorder \n(catatonia specifier), 119\u2013120\ndiagnostic criteria for, 119\u2013120\ndiagnostic features of, 120\nunspecified, 89, 121\nCatatonic disorder due to another medical \ncondition, 120\u2013121\nassociated features supporting diagnosis of, 121\ndiagnostic criteria for, 120\u2013121\ndiagnostic features of, 121\ndifferential diagnosis of, 121\nCentral sleep apnea, 383\u2013386\nassociated features supporting diagnosis of, 385\ncomorbidity with, 386\ndevelopment and course of, 385\ndiagnostic criteria for, 383\u2013384\ndiagnostic features of, 384\u2013385\ndiagnostic markers for, 385\ndifferential diagnosis of, 386\nfunctional consequences of, 386\nprevalence of, 385\nrisk and prognostic factors for, 385\nspecifiers for, 384\nsubtypes of, 384\nCFI. See Cultural Formulation Interview", "source": "dsm5.pdf"} {"id": "12149abe69d2-2", "page_content": "subtypes of, 384\nCFI. See Cultural Formulation Interview\nCheyne-Stokes breathing, 383\u2013386. See also Central \nsleep apnea\nChildhood-onset fluency di sorder (stuttering), 31, \n45\u201347\nassociated features supporting diagnosis of, 46\ndevelopment and course of, 46\u201347\ndiagnostic criteria for, 45\u201346\ndiagnostic features of, 46\ndifferential diagnosis of, 47\nfunctional consequences of, 47\nrisk and prognostic factors for, 47\nChild maltreatment and neglect problems, 717\u2013719\nchild neglect, 718\u2013719\nchild physical abuse, 717\u2013718\nchild psychological abuse, 719\nchild sexual abuse, 718\nCircadian rhythm sleep-wake disorders, 361, \n390\u2013398\nadvanced sleep phase type, 393\u2013394\nassociated features supporting diagnosis \nof, 393\ncomorbidity with, 394\nculture-related diagnostic issues in, 394\ndevelopment and course of, 393\ndiagnostic features of, 393\ndiagnostic markers for, 394", "source": "dsm5.pdf"} {"id": "98ad50f7b918-0", "page_content": "922 Index\nCircadian rhythm sleep-wake disorders \n(continued)\nadvanced sleep phase type (continued)\ndifferential diagnosis of, 394\nfunctional consequences of, 394\nprevalence of, 393\nrisk and prognostic factors for, 394\nspecifiers for, 393\ndelayed sleep phase type, 391\u2013392\nassociated features supporting diagnosis \nof, 391\ncomorbidity with, 392\ndevelopment and course of, 391\ndiagnostic features of, 391\ndiagnostic markers for, 392\ndifferential diagnosis of, 392\nfunctional consequences of, 392\nprevalence of, 391\nrisk and prognostic factors for, 392\ndiagnostic criteria for, 390\u2013391\nirregular sleep-wake type, 394\u2013396\nassociated features supporting diagnosis \nof, 395\ncomorbidity with, 396\ndevelopment and course of, 395\ndiagnostic features of, 394\u2013395\ndiagnostic markers for, 395\ndifferential diagnosis of, 395\nfunctional consequences of, 395\nprevalence of, 395\nrisk and prognostic factors for, 395\nnon-24-hour sleep-wake type, 396\u2013397\nassociated features supporting diagnosis \nof, 396\ncomorbidity with, 397\ndevelopment and course of, 396\ndiagnostic features of, 396\ndiagnostic markers for, 397\ndifferential diagnosis of, 397\nfunctional consequences of, 397\nprevalence of, 396\nrisk and prognostic factors for, 396\u2013397\nrelationship to International Classification of \nSleep Disorders, 398\nshift work type, 397\u2013398\ncomorbidity with, 398\ndevelopment and course of, 398\ndiagnostic features of, 397", "source": "dsm5.pdf"} {"id": "98ad50f7b918-1", "page_content": "development and course of, 398\ndiagnostic features of, 397\ndiagnostic markers for, 398\ndifferential diagnosis of, 398\nfunctional consequences of, 398\nprevalence of, 397\nrisk and prognostic factors for, 398\nClinician-Rated Dimensions of Psychosis \nSymptom Severity, 742\u2013744Coding and reporting procedures, 12, 16, 22, 23, \n29\nCognitive disorders. See Neurocognitive disorders\nCommunication disorders, 31, 41\u201349\nchildhood-onset fluency disorder (stuttering), \n45\u201347\nlanguage disorder, 42\u201344\nsocial (pragmatic) communication disorder, \n47\u201349\nspeech sound disorder, 44\u201345\nunspecified communication disorder, 49\nComorbidity, 5\nCompulsions, 235\u2013236, 239. See also Obsessive-\ncompulsive and related disorders\nConditions for further study, 7, 11, 24, 783\u2013806\nattenuated psychosis syndrome, 783\u2013786\ncaffeine use disorder, 792\u2013795\ndepressive episodes with short-duration \nhypomania, 786\u2013789\nInternet gaming disorder, 795\u2013798\nneurobehavioral disorder associated with \nprenatal alcohol exposure, 798\u2013801\nnonsuicidal self-injury, 803\u2013805\npersistent complex bereavement disorder, \n789\u2013792\nsuicidal behavior disorder, 801\u2013803\nConduct disorder, 32, 461, 469\u2013475\nassociated features supporting diagnosis of, \n472\u2013473\ncomorbidity with, 475\nculture-related diagnostic issues in, 474\ndevelopment and course of, 473\ndiagnostic criteria for, 469\u2013471", "source": "dsm5.pdf"} {"id": "98ad50f7b918-2", "page_content": "development and course of, 473\ndiagnostic criteria for, 469\u2013471\ndiagnostic features of, 472\ndifferential diagnosis of, 474\u2013475\nfunctional consequences of, 474\ngender-related diagnostic issues in, 474\nprevalence of, 473\nrisk and prognostic factors for, 473\u2013474\nspecifiers for, 471\u2013472\nsubtypes of, 471\nConversion disorder (functional neurological \nsymptom disorder), 309, 310, 318\u2013321\nassociated features supporting diagnosis of, \n319\u2013320\ncomorbidity with, 321\nculture-related diagnostic issues in, 320\ndevelopment and course of, 320\ndiagnostic criteria for, 318\u2013319\ndiagnostic features of, 319\ndifferential diagnosis of, 321\nfunctional consequences of, 321\ngender-related diagnostic issues in, 320\nprevalence of, 320\nrisk and prognostic factors for, 320", "source": "dsm5.pdf"} {"id": "1013db57e035-0", "page_content": "Index 923\nCreutzfeldt-Jakob disease. See Prion disease, \nmajor or mild neurocognitive disorder due to\nCrime or interaction with the legal system, \nproblems related to, 725\nCriterion for clinical significance, 21\nCross-cutting symptom measures, 733\u2013741\nDSM-5 Level 1 Cross-Cutting Symptom \nMeasure, 734\u2013736, 738\u2013741\nDSM-5 Level 2 Cross-Cutting Symptom \nMeasures, 734, 735, 736, 737\nfrequency of use of, 737\nCultural concepts of distress, 750, 758, 759, 833\u2013837\nCultural explanations or perceived causes, 14, 758\nCultural formulation, 749\u2013759\ndefinitions related to, 749\ndiagnostic importance of, 758\u2013759\noutline for, 749\u2013750\nrelationship to DSM-5 nosology, 758\nCultural Formulation Interview (CFI), 17, 24, 749, \n750\u2013757\ndomains of assessment, 751\nindications for, 751\nInformant Version, 755\u2013757\nsupplementary modules of, 751\nCultural idioms of distress, 14, 758\nCultural issues, 14\u201315, 749\u2013759\nin anxiety disorders\ngeneralized anxiety disorder, 224\npanic attacks, 216\npanic disorder, 211\u2013212\nselective mutism, 196\nseparation anxiety disorder, 193\nsocial anxiety disorder (social phobia), \n205\u2013206\nspecific phobia, 201\nin bipolar and related disorders\nbipolar I disorder, 130\nbipolar and related disorder due to another \nmedical condition, 147\nin depressive disorders\nmajor depressive disorder, 166", "source": "dsm5.pdf"} {"id": "1013db57e035-1", "page_content": "medical condition, 147\nin depressive disorders\nmajor depressive disorder, 166\npremenstrual dysphoric disorder, 173\nin disruptive, impulse-control, and conduct \ndisorders\nconduct disorder, 474\nintermittent explosive disorder, 468\noppositional defiant disorder, 465\nin dissociative disorders\ndepersonalization/derealization disorder, \n304\ndissociative amnesia, 300\ndissociative identity disorder, 295\nin enuresis, 357\nin feeding and eating disorders\nanorexia nervosa, 342avoidant/restrictive f ood intake disorder, \n336\nbinge-eating disorder, 352\nbulimia nervosa, 348\npica, 331\nin fetishistic disorder, 701\nin gender dysphoria, 457\nin neurocognitive disorders, 609\ndue to Alzheimer\u2019s disease, 613\nin neurodevelopmental disorders\nattention-deficit/hyperactivity disorder, \n62\nautism spectrum disorder, 57\ndevelopmental coordination disorder, 76\nintellectual disabi lity (intellectual \ndevelopmental disorder), 39\nspecific learning disorder, 72\u201373\nstereotypic movement disorder, 79\ntic disorders, 83\nin obsessive-compulsive and related disorders\nbody dysmorphic disorder, 245\nhoarding disorder, 250\nobsessive-compulsive disorder, 240\ntrichotillomania (hair-pulling disorder), \n253\nin personality disorders, 648\nantisocial personality disorder, 662\navoidant personality disorder, 674\nborderline personality disorder, 665\u2013666\ndependent personality disorder, 677\nhistrionic personality disorder, 668\nobsessive-compulsive personality disorder, \n681\nparanoid personality disorder, 651", "source": "dsm5.pdf"} {"id": "1013db57e035-2", "page_content": "681\nparanoid personality disorder, 651\nschizoid personality disorder, 654\nschizotypal personality disorder, 657\nin schizophrenia spectrum and other psychotic \ndisorders\nbrief psychotic disorder, 95\ndelusional disorder, 93\nschizoaffective disorder, 108\u2013109\nschizophrenia, 103\nin sexual dysfunctions, 423\ndelayed ejaculation, 425\nerectile disorder, 428\nfemale orgasmic disorder, 432\nfemale sexual interest/arousal disorder, \n435\u2013436\ngenito-pelvic pain/penetration disorder, \n439\nmale hypoactive sexual desire disorder, \n442\npremature (early) ejaculation, 445\nsubstance/medication-induced sexual \ndysfunction, 449", "source": "dsm5.pdf"} {"id": "92b822a5e074-0", "page_content": "924 Index\nCultural issues (continued)\nin sleep-wake disorders\ncentral sleep apnea hypopnea, 381\ncircadian rhythm sleep-wake disorders, \nadvanced sleep phase type, 394\nnarcolepsy, 376\nnightmare disorder, 406\nsubstance/medication-induced sleep \ndisorder, 418\nin somatic symptoms and related disorders\nconversion disorder (functional \nneurological symptom disorder), 320\nillness anxiety disorder, 317\npsychological factors affecting other \nmedical conditions, 323\nsomatic symptom disorder, 313\nin substance-related and addictive disorders\nalcohol intoxi cation, 498\nalcohol use disorder, 495\ncaffeine withdrawal, 508\ncannabis use disorder, 514\ngambling disorder, 588\ninhalant use disorder, 536\nopioid use disorder, 544\nother hallucinogen use disorder, 526\nother (or unknown) substance use \ndisorder, 580\nother (or unknown) substance withdrawal, \n580\nphencyclidine use disorder, 522\nsedative, hypnotic, or anxiolytic use \ndisorder, 554\nstimulant use disorder, 565\ntobacco use disorder, 574\nin suicidal behavior disorder, 802\nin trauma- and stressor-related disorders\nacute stress disorder, 285\nadjustment disorders, 288\nposttraumatic stress disorder, 278\nreactive attachment disorder, 267\nCultural syndromes, 14, 758\nCulture-bound syndromes, 14, 758\nCyclothymic disorder, 123, 139\u2013141\ncomorbidity with, 141\ndevelopment and course of, 140\u2013141\ndiagnostic criteria for, 139\u2013140\ndiagnostic features of, 140", "source": "dsm5.pdf"} {"id": "92b822a5e074-1", "page_content": "diagnostic criteria for, 139\u2013140\ndiagnostic features of, 140\ndifferential diagnosis of, 141\nprevalence of, 140\nrisk and prognostic factors for, 141\nDefinition of a mental disorder, 20\nDelayed ejaculation, 423, 424\u2013426\nassociated features supporting diagnosis of, \n424\u2013425comorbidity with, 426\nculture-related diagnostic issues in, 425\ndevelopment and course of, 425\ndiagnostic criteria for, 424\ndiagnostic features of, 424\ndifferential diagnosis of, 425\u2013426\nfunctional consequences of, 425\nprevalence of, 425\nrisk and prognostic factors for, 425\nDelirium, 591, 596\u2013602\ndue to another medical condition, 597\nassociated features supporting diagnosis of, 600\ndevelopment and course of, 600\u2013601\ndiagnostic criteria for, 596\u2013598\ndiagnostic features of, 599\u2013600\ndiagnostic markers for, 601\ndifferential diagnosis of, 601\nfunctional consequences of, 601\nmedication-induced, 597, 599\ndue to multiple etiologies, 597\nother specified, 602\nprevalence of, 600\nrecording procedures for, 598\u2013599\nrisk and prognostic factors for, 601\nspecifiers for, 599\nsubstance intoxication, 596\u2013597, 598\nsubstance withdrawal, 597, 598\u2013599\nunspecified, 602\nDelusional disorder, 89, 90\u201393\nassociated features supporting diagnosis of, 92\nculture-related diagnostic issues in, 93\ndelusional symptoms in partner of individual \nwith, 122\ndevelopment and course of, 92\u201393\ndiagnostic criteria for, 90\u201391", "source": "dsm5.pdf"} {"id": "92b822a5e074-2", "page_content": "development and course of, 92\u201393\ndiagnostic criteria for, 90\u201391\ndiagnostic features of, 92\nfunctional consequences of, 93\nprevalence of, 92\nsubtypes of, 91\u201392\nDelusions, 87, 89, 90\u201393\nbizarre, 87, 91\nof control, 87\nerotomanic, 87, 90\ngrandiose, 87, 90\njealous, 90, 91\nmixed type, 91\nnihilistic, 87\nnonbizarre, 87\npersecutory, 87, 90\u201391\nreferential, 87\nwith significant overlapping mood episodes, \n122\nsomatic, 87, 90, 92\nunspecified type, 91\nDementia, 591. See also Neurocognitive disorders", "source": "dsm5.pdf"} {"id": "74bcd0b0cf90-0", "page_content": "Index 925\nDependent personality disorder, 645, 646, 675\u2013678\nassociated features supporting diagnosis of, 677\nculture-related diagnostic issues in, 677\ndevelopment and course of, 677\ndiagnostic criteria for, 675\ndiagnostic features of, 675\u2013677\ndifferential diagnosis of, 677\u2013678\ngender-related diagnostic issues in, 677\nprevalence of, 677\nDepersonalization/derealization disorder, 291, \n302\u2013306\nassociated features supporting diagnosis of, 303\ncomorbidity with, 306\nculture-related diagnostic issues in, 304\ndevelopment and course of, 303\u2013304\ndiagnostic criteria for, 302\ndiagnostic features of, 302\u2013303\ndifferential diagnosis of, 305\u2013306\nfunctional consequences of, 304\u2013305\nprevalence of, 303\nrisk and prognostic factors for, 304\nDepressive disorder du e to another medical \ncondition, 155, 180\u2013183\nassociated features supporting diagnosis of, 181\ncomorbidity with, 183\ndevelopment and course of, 181\u2013182\ndiagnostic criteria for, 180\u2013181\ndiagnostic features of, 181\ndiagnostic markers for, 182\ndifferential diagnosis of, 182\u2013183\nfunctional consequences of, 182\ngender-related diagnostic issues in, 182\nrisk and prognostic factors for, 182\nsuicide risk in, 182\nDepressive disorders, 155\u2013188\ndepressive disorder due to another medical \ncondition, 155, 180\u2013183\ndisruptive mood dysregulation disorder, 155, \n156\u2013160\nhighlights of changes fr om DSM-IV to DSM-5, \n810\u2013811\nmajor depressive disorder, 155, 160\u2013168", "source": "dsm5.pdf"} {"id": "74bcd0b0cf90-1", "page_content": "810\u2013811\nmajor depressive disorder, 155, 160\u2013168\nother specified depres sive disorder, 155, \n183\u2013184\npersistent depressive disorder (dysthymia), \n155, 168\u2013171\npremenstrual dysphoric disorder, 155, 171\u2013175\nspecifiers for, 184\u2013188\nsubstance/medication-induced depressive \ndisorder, 155, 175\u2013180\nunspecified depressive disorder, 155, 184\nDepressive episode or symptoms in bipolar and \nrelated disorders\nbipolar I disorder, 125\u2013126, 129\nbipolar II disorder, 133\u2013134, 135\u2013136cyclothymic disorder, 139, 140\nother specified bipolar and related disorder, \n148\nDepressive episodes with short-duration \nhypomania, 786\u2013789\nassociated features supporting diagnosis of, \n788\ncomorbidity with, 789\ndiagnostic features of, 788\ndifferential diagnosis of, 788\u2013789\nfunctional consequences of, 788\nprevalence of, 788\nproposed criteria for, 786\u2013787\nrisk and prognostic factors for, 788\nsuicide risk in, 788\nDevelopmental coordination disorder, 32, 74\u201377\nassociated features supporting diagnosis of, 75\ncomorbidity with, 76\nculture-related diagnostic issues in, 76\ndevelopment and course of, 75\u201376\ndiagnostic criteria for, 74\ndiagnostic features of, 74\u201375\ndifferential diagnosis of, 76\u201377\nfunctional consequences of, 76\nprevalence of, 75\nrisk and prognostic factors for, 76\nDhat syndrome, 833\u2013834\nDiagnosis, 5\u20136\nassessment and monitoring measures for,", "source": "dsm5.pdf"} {"id": "74bcd0b0cf90-2", "page_content": "Diagnosis, 5\u20136\nassessment and monitoring measures for, \n23\u201324, 733\u2013748\ncategorical, 5, 8, 12, 13, 19, 20\nclinical utility of, 20\ncoding and reporting procedures for, 12, 16, \n22, 23, 29\ncriterion for clinical significance, 21\nculture and, 14\u201315, 749\u2013759\ndefinition of a mental disorder, 20\ndiagnostic criteria and descriptors, 21\ndimensional approach to, 5, 8, 9, 12\u201313, 17\nelements of, 21\u201324\nin forensic settings, 25\nof medication-induced movement disorders, \n20, 22, 29, 709\u2013714\nof other conditions that may be a focus of \nclinical attention, 20, 22, 29, 715\u2013727\nprincipal, 22\u201323\nprovisional, 23\nDiagnostic criteria, 21, 29\ncase formulation and, 19\nproposed criteria for conditions for further \nstudy, 11, 783\nrevisions of, 6\u201310\nsubtypes and specifiers for, 21\u201322\nvalidators for, 5, 9, 11, 12, 20\nDiagnostic spectra, 6, 9, 12", "source": "dsm5.pdf"} {"id": "08b8c6b8b78e-0", "page_content": "926 Index\nDisinhibited social engagement disorder, 265, \n268\u2013270\nassociated features supporting diagnosis of, \n269\ndevelopment and course of, 269\u2013270\ndiagnostic criteria for, 268\u2013269\ndiagnostic features of, 269\ndifferential diagnosis of, 270\nfunctional consequences of, 270\nprevalence of, 269\nrisk and prognostic factors for, 270\nDisorganized thinking (speech), 88\nDisruptive, impulse-control, and conduct \ndisorders, 461\u2013480\nantisocial personality disorder, 461, 476, 645, \n646, 659\u2013663\nconduct disorder, 461, 469\u2013475\nhighlights of changes fr om DSM-IV to DSM-5, \n815\nintermittent explosive disorder, 461, 466\u2013469\nkleptomania, 461, 478\u2013479\noppositional defiant disorder, 461, 462\u2013466\nother specified disrupti ve, impulse-control, \nand conduct disorder, 461, 479\npyromania, 461, 476\u2013477\nunspecified disruptive, impulse-control, and \nconduct disorder, 480\nDisruptive mood dysregulation disorder, 155, \n156\u2013160\ncomorbidity with, 160\ndevelopment and course of, 157\ndiagnostic criteria for, 156\ndiagnostic features of, 156\u2013157\ndifferential diagnosis of, 158\u2013160\nfunctional consequences of, 158\ngender-related diagnostic issues in, 158\nprevalence of, 157\nrisk and prognostic factors for, 157\u2013158\nsuicide risk in, 158\nDissociative amnesia, 291, 298\u2013302\nassociated features supporting diagnosis of, 299\ncomorbidity with, 302", "source": "dsm5.pdf"} {"id": "08b8c6b8b78e-1", "page_content": "associated features supporting diagnosis of, 299\ncomorbidity with, 302\nculture-related diagnostic issues in, 300\ndevelopment and course of, 299\ndiagnostic criteria for, 298\ndiagnostic features of, 298\u2013299\ndifferential diagnosis of, 300\u2013302\nfunctional consequences of, 300\nprevalence of, 299\nrisk and prognostic factors for, 299\u2013300\nsuicide risk in, 300\nDissociative disorders, 291\u2013307\ndepersonalization/derealization disorder, 291, \n302\u2013306\ndissociative amnesia, 291, 298\u2013302dissociative identity disorder, 291\u2013298\nhighlights of changes fr om DSM-IV to DSM-5, \n812\nother specified dissoc iative disorder, 292, \n306\u2013307\nunspecified dissociative disorder, 307\nDissociative identity disorder, 291\u2013298\nassociated features supporting diagnosis of, \n294\ncomorbidity with, 297\u2013298\nculture-related diagnostic issues in, 295\ndevelopment and course of, 294\ndiagnostic criteria for, 292\ndiagnostic features of, 292\u2013294\ndifferential diagnosis of, 296\u2013297\nfunctional consequences of, 295\u2013296\ngender-related diagnostic issues in, 295\nprevalence of, 294\nrisk and prognostic factors for, 294\u2013295\nsuicide risk in, 295\nDissociative reactions to stressful events, acute, \n306\u2013307\nDissociative stupor or coma, 292\nDissociative trance, 292, 307\nDown syndrome, 38, 40, 44, 53\nDSM, history of, 5, 6\nDSM-5", "source": "dsm5.pdf"} {"id": "08b8c6b8b78e-2", "page_content": "DSM, history of, 5, 6\nDSM-5\ncultural issues in, 14\u201315, 749\u2013759\ndevelopmental and lifespan considerations in, \n13\nforensic use of, 25\ngender differences in, 15\nglossary of technical terms in, 817\u2013831\nharmonization with ICD-11, 11\u201312\nhighlights of changes from DSM-IV to, 809\u2013817\nanxiety disorders, 811\nbipolar and related disorders, 810\ndepressive disorders, 810\u2013811\ndisruptive, impulse-control, and conduct \ndisorders, 815\ndissociative disorders, 812\nelimination disorders, 813\nfeeding and eating disorders, 813\ngender dysphoria, 814\u2013815\nneurodevelopmental disorders, 809\u2013810\nobsessive-compulsive and related \ndisorders, 811\u2013812\nparaphilic disorders, 816\npersonality disorders, 816\nschizophrenia spectrum and other \npsychotic disorders, 810\nsexual dysfunctions, 814\nsleep-wake disorders, 814\nsomatic symptom and related disorders, \n812\u2013813", "source": "dsm5.pdf"} {"id": "e6a796502e70-0", "page_content": "Index 927\nsubstance-related and addictive disorders, \n815\u2013816\ntrauma- and stressor-related disorders, 812\nmultiaxial system and, 16\nonline enhancements of, 17\norganizational structure of, 10\u201311, 13\nother specified and unspecified mental \ndisorders in, 15\u201316, 19\u201320, 707\u2013708\nrevision process for, 5, 6\u201310\nexpert review, 8\u201310\nfield trials, 7\u20138\nproposals for revisions, 7\npublic and professional review, 8\nuse of, 19\u201324\nassessment and monitoring tools, 23\u201324, \n733\u2013748\ncase formulation, 19\u201320\ncoding and reporting procedures, 12, 16, \n22, 23, 29\ndefinition of a mental disorder, 20\u201321\nelements of a diagnosis, 21\u201324\nDSM-5 Level 1 Cross-Cutting Symptom Measure, \n734\u2013736\nadult self-rated version, 734, 735, 738\u2013739\nparent/guardian-rated version, 734, 736, \n740\u2013741\nscoring and interpretation of, 734\u2013736\nDSM-5 Level 2 Cross-Cutting Symptom \nMeasures, 734, 735, 736, 737\nDysthymia. See Persistent depressive disorder \n(dysthymia)\nDystonia, medication-induced, 22\nacute, 711\ntardive, 712\nEating disorders. See Feeding and eating disorders\nEconomic problems, 724\nEducational problems, 723\nEjaculation\ndelayed, 423, 424\u2013426\npremature (early), 423, 443\u2013446", "source": "dsm5.pdf"} {"id": "e6a796502e70-1", "page_content": "premature (early), 423, 443\u2013446\nElements of diagnosis, 21\u201324\nElimination disorders, 355\u2013360\nencopresis, 355, 357\u2013359\nenuresis, 355\u2013357\nhighlights of changes fr om DSM-IV to DSM-5, \n813\nother specified elimin ation disorder, 359\nunspecified elimination disorder, 360\nEncopresis, 355, 357\u2013359\nassociated features supporting diagnosis of, 358\ncomorbidity with, 359\ndevelopment and course of, 359\ndiagnostic criteria for, 357\u2013358\ndiagnostic features of, 358diagnostic markers for, 359\ndifferential diagnosis of, 359\nprevalence of, 359\nrisk and prognostic factors for, 359\nsubtypes of, 358\nEnuresis, 355\u2013357\nassociated features supporting diagnosis of, 356\ncomorbidity with, 356\nculture-related diagnostic issues in, 356\ndevelopment and course of, 356\ndiagnostic criteria for, 355\ndiagnostic features of, 355\u2013356\ndifferential diagnosis of, 356\nfunctional consequences of, 356\ngender-related diagnostic issues in, 356\nprevalence of, 356\nrisk and prognostic factors for, 356\nsubtypes of, 355\nErectile disorder, 423, 426\u2013429\nassociated features supporting diagnosis of, 427\ncomorbidity with, 429\nculture-related diagnostic issues in, 428\ndevelopment and course of, 427\u2013428\ndiagnostic criteria for, 426\u2013427\ndiagnostic features of, 427\ndiagnostic markers for, 428\ndifferential diagnosis of, 428\u2013429\nfunctional consequences of, 428\nprevalence of, 427", "source": "dsm5.pdf"} {"id": "e6a796502e70-2", "page_content": "functional consequences of, 428\nprevalence of, 427\nrisk and prognostic factors for, 428\nExcoriation (skin-picking) disorder, 235, 236, \n254\u2013257\nassociated features supporting diagnosis of, 255\ncomorbidity with, 257\ndevelopment and course of, 255\ndiagnostic criteria for, 254\ndiagnostic features of, 254\u2013255\ndiagnostic markers for, 255\ndifferential diagnosis of, 256\nfunctional consequences of, 256\nprevalence of, 255\nrisk and prognostic factors for, 255\nExhibitionistic disorder, 685, 689\u2013691\ncomorbidity with, 691\ndevelopment and course of, 690\ndiagnostic criteria for, 689\ndiagnostic features of, 689\u2013690\ndifferential diagnosis of, 691\nfunctional consequences of, 691\ngender-related diagnostic issues in, 691\nprevalence of, 690\nrisk and prognostic factors for, 690\u2013691\nspecifiers for, 689\nsubtypes of, 689\nExternalizing disorders, 13", "source": "dsm5.pdf"} {"id": "9ff3be3577f3-0", "page_content": "928 Index\nFactitious disorder, 309, 310, 324\u2013326\nassociated features supporting diagnosis of, \n325\u2013326\ndevelopment and course of, 326\ndiagnostic criteria for, 324\u2013325\ndiagnostic features of, 325\ndifferential diagnosis of, 326\nimposed on another, 310, 325\u2013325, 338\nprevalence of, 326\nrecording procedures for, 325\nFamily upbringing, problems related to, 715\u2013716\nFeeding and eating disorders, 329\u2013354\nanorexia nervosa, 329, 338\u2013345\navoidant/restrictive food intake disorder, 329, \n334\u2013338\nbinge-eating disorder, 329, 350\u2013353\nbulimia nervosa, 329, 345\u2013350\nhighlights of changes fr om DSM-IV to DSM-5, \n813\nother specified feeding or eating disorder, \n353\u2013354\npica, 329\u2013331\nrumination disorder, 329, 332\u2013333\nunspecified feeding or eating disorder, 354\nFemale orgasmic disorder, 423, 429\u2013432\nassociated features supporting diagnosis of, \n430\u2013431\ncomorbidity with, 432\nculture-related diagnostic issues in, 432\ndevelopment and course of, 431\ndiagnostic criteria for, 429\u2013430\ndiagnostic features of, 430\ndiagnostic markers for, 432\ndifferential diagnosis of, 432\nfunctional consequences of, 432\nprevalence of, 431\nrisk and prognostic factors for, 431\u2013432\nFemale sexual interest/arousal disorder, 423, \n433\u2013437\nassociated features supporting diagnosis of, \n434\u2013435\ncomorbidity with, 436\u2013437", "source": "dsm5.pdf"} {"id": "9ff3be3577f3-1", "page_content": "434\u2013435\ncomorbidity with, 436\u2013437\nculture-related diagnostic issues in, 435\u2013436\ndevelopment and course of, 435\ndiagnostic criteria for, 433\ndiagnostic features of, 433\u2013434\ndifferential diagnosis of, 436\nfunctional consequences of, 436\ngender-related diagnostic issues in, 436\nprevalence of, 435\nrisk and prognostic factors for, 435\nFetishistic disorder, 685, 700\u2013702\nassociated features supporting diagnosis of, 701\ncomorbidity with, 702\nculture-related diagnostic issues in, 701development and course of, 701\ndiagnostic criteria for, 700\ndiagnostic features of, 701\ndifferential diagnosis of, 702\nfunctional consequences of, 701\u2013702\ngender-related diagnostic issues in, 701\nspecifiers for, 701\nForensic settings, 25\nFormal thought disorder, 88\nFrontotemporal neurocognitive disorder, major or \nmild, 591, 603, 614\u2013618\nassociated features supporting diagnosis of, \n616\ndevelopment and course of, 616\ndiagnostic criteria for, 614\u2013615\ndiagnostic features of, 615\u2013616\ndiagnostic markers for, 616\u2013617\ndifferential diagnosis of, 617\u2013618\nfunctional consequences of, 617\nprevalence of, 616\nrisk and prognostic factors for, 616\nFrotteuristic disorder, 685, 691\u2013694\ncomorbidity with, 693\u2013694\ndevelopment and course of, 693\ndiagnostic criteria for, 691\u2013692\ndiagnostic features of, 692\ndifferential diagnosis of, 693\ngender-related diagnostic issues in, 693\nprevalence of, 692\u2013693", "source": "dsm5.pdf"} {"id": "9ff3be3577f3-2", "page_content": "gender-related diagnostic issues in, 693\nprevalence of, 692\u2013693\nrisk and prognostic factors for, 693\nspecifiers for, 692\nFunctional neurological symptom disorder. See \nConversion disorder\nGAF (Global Assessment of Functioning) scale, 16\nGambling disorder, 481, 585\u2013589\nassociated features supporting diagnosis of, \n587\ncomorbidity with, 589\nculture-related diagnostic issues in, 588\ndevelopment and course of, 587\u2013588\ndiagnostic criteria for, 585\u2013586\ndiagnostic features of, 586\u2013587\ndifferential diagnosis of, 589\nfunctional consequences of, 589\ngender-related diagnostic issues in, 588\nprevalence of, 587\nrisk and prognostic factors for, 588\nspecifiers for, 586\nGender differences, 15\nGender dysphoria, 451\u2013459\nassociated features supporting diagnosis of, \n454\ncomorbidity with, 458\u2013459\nculture-related diagnostic issues in, 457", "source": "dsm5.pdf"} {"id": "1829eef1b479-0", "page_content": "Index 929\ndevelopment and course of, 454\u2013456\nin association with a disorder of sex \ndevelopment, 456\nwithout a disorder of sex development, \n455\u2013456\ndiagnostic criteria for, 452\u2013453\ndiagnostic features of, 453\u2013454\ndiagnostic markers for, 457\ndifferential diagnosis of, 458\nfunctional consequences of, 457\u2013458\nhighlights of changes fr om DSM-IV to DSM-5, \n814\u2013815\nother specified, 459\nprevalence of, 454\nrisk and prognostic factors for, 456\u2013457\nspecifiers for, 453\nunspecified, 459\nGeneralized anxiety disorder, 190, 222\u2013226\nassociated features supporting diagnosis of, 223\ncomorbidity with, 226\nculture-related diagnostic issues in, 224\ndevelopment and course of, 223\u2013224\ndiagnostic criteria for, 222\ndiagnostic features of, 222\u2013223\ndifferential diagnosis of, 225\u2013226\nfunctional consequences of, 225\ngender-related diagnostic issues in, 224\u2013225\nprevalence of, 223\nrisk and prognostic factors for, 224\nGenito-pelvic pain/penetration disorder, 423, \n437\u2013440\nassociated features supporting diagnosis of, \n438\ncomorbidity with, 440\nculture-related diagnostic issues in, 439\ndevelopment and course of, 439\ndiagnostic criteria for, 437\ndiagnostic features of, 437\u2013438\ndifferential diagnosis of, 440\nfunctional consequences of, 439\ngender-related diagnostic issues in, 439\nprevalence of, 438\nrisk and prognostic factors for, 439\nGlobal Assessment of Functioning (GAF) scale, 16\nGlobal developmental delay, 31, 41", "source": "dsm5.pdf"} {"id": "1829eef1b479-1", "page_content": "Global developmental delay, 31, 41\nGlossary of technical terms, 817\u2013831\nHair pulling. See Trichotillomania (hair-pulling \ndisorder)\nHallucinations, 87\u201388\nauditory, 87, 103, 116, 122\ngustatory, 116\nhypnagogic, 87\nhypnopompic, 88\nolfactory, 116, 118tactile, 116\nvisual, 102, 103, 104, 116, 118\nHallucinogen persisting perception disorder, \n531\u2013532\nassociated features supporting diagnosis of, 531\ncomorbidity with, 532\ndevelopment and course of, 532\ndiagnostic criteria for, 531\ndiagnostic features of, 531\ndifferential diagnosis of, 532\nfunctional consequences of, 532\nprevalence of, 531\nrisk and prognostic factors for, 532\nHallucinogen-related disorders, 481, 520\u2013533\ndiagnoses associated with, 482\nhallucinogen persisting perception disorder, \n531\u2013532\nother hallucinogen-induced disorders, \n532\u2013533\nother hallucinogen intoxication, 529\u2013530\nother hallucinogen use disorder, 523\u2013527\nother phencyclidine-induced disorders, 532\nphencyclidine intoxication, 527\u2013529\nphencyclidine use disorder, 520\u2013523\nunspecified hallucinogen-related disorder, 533\nunspecified phencyclidine-related disorder, 533\nHistrionic personality disorder, 645, 646, 667\u2013669\nassociated features supporting diagnosis of, \n668\nculture-related diagnostic issues in, 668\ndiagnostic criteria for, 667\ndiagnostic features of, 667\u2013668", "source": "dsm5.pdf"} {"id": "1829eef1b479-2", "page_content": "diagnostic criteria for, 667\ndiagnostic features of, 667\u2013668\ndifferential diagnosis of, 669\ngender-related diagnostic issues in, 668\nprevalence of, 668\nHIV infection, major or mild neurocognitive \ndisorder due to, 591, 604, 632\u2013634\nassociated features supporting diagnosis of, 633\ncomorbidity with, 634\ndevelopment and course of, 633\ndiagnostic criteria for, 632\ndiagnostic features of, 632\ndiagnostic markers for, 634\ndifferential diagnosis of, 634\nfunctional consequences of, 634\nprevalence of, 633\nrisk and prognostic factors for, 633\nHoarding disorder, 235, 236, 247\u2013251\nassociated features supporting diagnosis of, 249\ncomorbidity with, 251\nculture-related diagnostic issues in, 250\ndevelopment and course of, 249\ndiagnostic criteria for, 247\ndiagnostic features of, 248\u2013249\ndifferential diagnosis of, 250\u2013251", "source": "dsm5.pdf"} {"id": "37cf93612bec-0", "page_content": "930 Index\nHoarding disorder (continued)\nfunctional consequences of, 250\ngender-related diagnostic issues in, 250\nprevalence of, 249\nrisk and prognostic factors for, 249\nspecifiers for, 248\nHousing problems, 723\u2013724\nHuntington\u2019s disease, 81, 117, 181, 182\nmajor or mild neurocognitive disorder due to, \n591, 604, 638\u2013641\nassociated features supporting diagnosis \nof, 639\ndevelopment and course of, 639\u2013640\ndiagnostic criteria for, 638\u2013639\ndiagnostic features of, 639\ndiagnostic markers for, 640\ndifferential diagnosis of, 640\u2013641\nfunctional consequences of, 640\nprevalence of, 639\nrisk and prognostic factors for, 640\nHypersomnolence disorder, 361, 368\u2013372\nassociated features supporting diagnosis of, \n370\ncomorbidity with, 372\ndevelopment and course of, 370\ndiagnostic criteria for, 368\u2013369\ndiagnostic features of, 369\u2013370\ndiagnostic markers for, 371\ndifferential diagnosis of, 371\u2013372\nfunctional consequences of, 371\nother specified, 421\nprevalence of, 370\nrelationship to International Classification of \nSleep Disorders, 372\nrisk and prognostic factors for, 370\u2013371\nunspecified, 421\nHypochondriasis, 310, 315\u2013316, 318. See also \nIllness anxiety disorder\nHypomanic episode or symptoms in bipolar and \nrelated disorders\nbipolar I disorder, 124\u2013125, 129\nbipolar II disorder, 132\u2013133, 135\u2013136\nbipolar and related disorder due to another", "source": "dsm5.pdf"} {"id": "37cf93612bec-1", "page_content": "bipolar and related disorder due to another \nmedical condition, 146\ncyclothymic disorder, 139, 140\ndepressive episodes with short-duration \nhypomania, 786\u2013789\nother specified bipolar and related disorder, \n148\nICD. See International Classification of Diseases\nICF (International Classification of Functioning, \nDisability and Health), 21, 734\nICSD-2. See International Classification of Sleep \nDisorders, 2nd EditionIdentity disturbance due to prolonged and intense \ncoercive persuasion, 306\nIllness anxiety disorder, 309, 310, 315\u2013318\nassociated features supporting diagnosis of, 316\nbrief, 327\ncomorbidity with, 318\nculture-related diagnostic issues in, 317\ndiagnostic criteria for, 315\ndiagnostic features of, 315\u2013316\ndifferential diagnosis of, 317\u2013318\nfunctional consequences of, 317\nprevalence of, 316\nrisk and prognostic factors for, 316\u2013317\nwithout excessive health-related behaviors, \n327\nInhalant intoxication, 538\u2013540\nassociated features supporting diagnosis of, \n539\ndiagnostic criteria for, 538\ndiagnostic features of, 538\ndifferential diagnosis of, 539\u2013540\nfunctional consequences of, 539\ngender-related diagnostic issues in, 539\nprevalence of, 539\nInhalant-related disorders, 481, 533\u2013540\ndiagnoses associated with, 482\ninhalant intoxication, 538\u2013540\ninhalant use disorder, 533\u2013538\nother inhalant-induced disorders, 540\nunspecified inhalant-related disorder, 540\nInhalant use disorder, 533\u2013538\nassociated features supporting diagnosis of, \n535", "source": "dsm5.pdf"} {"id": "37cf93612bec-2", "page_content": "associated features supporting diagnosis of, \n535\ncomorbidity with, 538\nculture-related diagnostic issues in, 536\ndevelopment and course of, 536\ndiagnostic criteria for, 533\u2013534\ndiagnostic features of, 535\ndiagnostic markers for, 536\u2013537\ndifferential diagnosis of, 537\nfunctional consequences of, 537\ngender-related diagnostic issues in, 536\nprevalence of, 535\u2013536\nrisk and prognostic factors for, 536\nspecifiers for, 535\nInsomnia disorder, 361, 362\u2013368\nassociated features supporting diagnosis of, \n364\nbrief, 420\ncomorbid ity w ith, 368\ndevelopment and course of, 365\ndiagnostic criteria for, 362\u2013363\ndiagnostic features of, 363\u2013364\ndiagnostic markers for, 366\u2013367\ndifferential diagnosis of, 367\u2013368", "source": "dsm5.pdf"} {"id": "f365361d917d-0", "page_content": "Index 931\nfunctional consequences of, 367\ngender-related diagnostic issues in, 366\nother specified, 420\nprevalence of, 364\u2013365\nrelationship to International Classification of \nSleep Disorders, 368\nrestricted to nonrestorative sleep, 420\nrisk and protective factors for, 366\nunspecified, 420\u2013421\nIntellectual disability (intellectual developmental \ndisorder), 31, 33\u201341\nassociated features supporting diagnosis of, 38\ncoding and reporting for, 33\ncomorbidity with, 40\nculture-related diagnostic issues in, 39\ndevelopment and course of, 38\u201339\ndiagnostic criteria for, 33\ndiagnostic features of, 37\u201338\ndiagnostic markers for, 39\ndifferential diagnosis of, 39\u201340\ngender-related diagnostic issues in, 39\nglobal developmental delay, 31, 41\nprevalence of, 38\nrelationship to other classifications, 40\u201341\nrisk and prognostic factors for, 39\nspecifiers for levels of severity of, 33, 34\u201336\nunspecified intellectual disability, 41\nIntermittent explosive disorder, 461, 466\u2013469\nassociated features supporting diagnosis of, \n467\ncomorbidity with, 469\nculture-related diagnostic issues in, 468\ndevelopment and course of, 467\ndiagnostic criteria for, 466\ndiagnostic features of, 466\u2013467\ndifferential diagnosis of, 468\u2013469\nfunctional consequences of, 468\ngender-related diagnostic issues in, 468\nprevalence of, 467\nrisk and prognostic factors for, 467\u2013468\nInternalizing disorders, 13\nInternational Classification of Diseases (ICD), 21\nrevision process for ICD-11, 6, 10, 11\u201312", "source": "dsm5.pdf"} {"id": "f365361d917d-1", "page_content": "revision process for ICD-11, 6, 10, 11\u201312\nuse of ICD-9-CM and ICD-10 codes, 12, 16, 22, \n23, 29\nInternational Classification of Functioning, \nDisability and Health (ICF), 21, 734\nInternational Classification of Sleep Disorders, 2nd \nEdition (ICSD-2), relationship of DSM-5 to, \n361\u2013362\ncircadian rhythm sleep-wake disorders, 398\nhypersomnolence disorder, 372\ninsomnia disorder, 368\nnarcolepsy, 378\nnightmare disorder, 407obstructive sleep ap nea hypopnea, 383\nrapid eye movement sleep behavior disorder, \n410\nrestless legs syndrome, 413\nsleep-related hypoventilation, 390\nsubstance/medication-induced sleep disorder, \n420\nInternet gaming disorder, 795\u2013798\nassociated features supporting diagnosis of, \n797\ncomorbidity with, 798\ndiagnostic features of, 796\u2013797\ndifferential diagnosis of, 797\u2013798\nfunctional consequences of, 797\nprevalence of, 797\nproposed criteria for, 795\u2013796\nrisk and prognostic factors for, 797\nsubtypes of, 796\nIntoxication, 481, 485\u2013487\nalcohol, 497\u2013499\nassociated with use of multiple substances, 486\ncaffeine, 503\u2013506\ncannabis, 516\u2013517\ndelirium due to, 598\ndevelopment and course of, 487\nduration of effects and, 486\ninhalant, 538\u2013540\nlaboratory findings associated with, 486\u2013487\nopioid, 546\u2013547", "source": "dsm5.pdf"} {"id": "f365361d917d-2", "page_content": "laboratory findings associated with, 486\u2013487\nopioid, 546\u2013547\nother hallucinogen, 529\u2013530\nother (or unknown) substance, 581\u2013582\nphencyclidine, 527\u2013529\nrecording procedures for, 487\nrelated to route of administration and speed of \nsubstance effects, 486\nsedative, hypnotic, or anxiolytic, 556\u2013557\nstimulant, 567\u2013569\nJealousy, obsessional, 264\nJikoshu-kyofu, 264\nKhy\u00e2l cap, 211, 212, 233, 834\nKleptomania, 461, 478\u2013479\nassociated features supporting diagnosis of, \n478\ncomorbidity with, 478\ndevelopment and course of, 478\ndiagnostic criteria for, 478\ndiagnostic features of, 478\ndifferential diagnosis of, 478\nfunctional consequences of, 478\nprevalence of, 478\nrisk and prognostic factors for, 478\nKoro, 264\nKufungisisa, 14, 834\u2013835", "source": "dsm5.pdf"} {"id": "4292add49d37-0", "page_content": "932 Index\nLanguage disorder, 31, 42\u201344\nassociated features supporting diagnosis of, 43\ncomorbidity with, 44\ndevelopment and course of, 43\ndiagnostic criteria for, 42\ndiagnostic features of, 42\ndifferential diagnosis of, 43\nrisk and prognostic factors for, 43\nLearning disorder. See Specific learning disorder\nLevel of Personality Fu nctioning Scale (LPFS), \n772, 775\u2013778\nLewy bodies, major or mild neurocognitive \ndisorder with, 591, 603, 618\u2013621\nassociated features supporting diagnosis of, 619\ncomorbidity with, 621\ndevelopment and course of, 619\u2013620\ndiagnostic criteria for, 618\u2013619\ndiagnostic features of, 619\ndiagnostic markers for, 620\ndifferential diagnosis of, 620\nfunctional consequences of, 620\nprevalence of, 619\nrisk and prognostic factors for, 620\nLPFS (Level of Personality Functioning Scale), \n772, 775\u2013778\nMajor depressive disorder, 155, 160\u2013168\nassociated features supporting diagnosis of, \n164\u2013165\ncomorbidity with, 168\nculture-related diagnostic issues in, 166\ndevelopment and course of, 165\u2013166\ndiagnostic criteria for, 160\u2013162\ndiagnostic features of, 162\u2013164\ndifferential diagnosis of, 167\u2013168\nfunctional consequences of, 167\ngender-related diagnostic issues in, 167\nprevalence of, 165\nrisk and prognostic factors for, 166\nsuicide risk in, 164, 167\nMajor depressive episode in bipolar and related \ndisorders\nbipolar I disorder, 125\u2013126, 129", "source": "dsm5.pdf"} {"id": "4292add49d37-1", "page_content": "disorders\nbipolar I disorder, 125\u2013126, 129\nbipolar II disorder, 133\u2013134, 135\u2013136\nother specified bipolar and related disorder, \n148\nMaladi moun, 14, 835\nMale hypoactive sexual desire disorder, 423, \n440\u2013443\nassociated features supporting diagnosis of, \n441\u2013442\ncomorbidity with, 443\nculture-related diagnostic issues in, 442\ndevelopment and course of, 442\ndiagnostic criteria for, 440\u2013441diagnostic features of, 441\ndifferential diagnosis of, 443\ngender-related diagnostic issues in, 442\u2013443\nprevalence of, 442\nrisk and prognostic factors for, 442\nManic episode\nin bipolar I disorder, 124, 127\u2013129\nin bipolar and related disorder due to another \nmedical cond ition, 146\nMedication-induced delirium, 597, 599\nMedication-induced movement disorders and \nother adverse effects of medication, 20, 22, \n29, 709\u2013714\nantidepressant discontinuation syndrome, 22, \n712\u2013714\nmedication-induced acute akathisia, 22, 711\nmedication-induced acute dystonia, 711\nmedication-induced postural tremor, 712\nneuroleptic-induced parkinsonism, 709\nneuroleptic malignant syndrome, 22, 709\u2013711\nother adverse effect of medication, 712\u2013714\nother medication-induced movement \ndisorder, 712\nother medication-induced parkinsonism, 709\ntardive akathisia, 712\ntardive dyskinesia, 22, 712\ntardive dystonia, 712\nMental disorder(s)", "source": "dsm5.pdf"} {"id": "4292add49d37-2", "page_content": "tardive dystonia, 712\nMental disorder(s)\nculture and, 14\u201315, 749\u2013759\ndefinition of, 20\ncriterion for clinical significance, 21\nin forensic settings, 25\ngender and, 15\nMotor disorders, neurodevelopmental, 32, 74\u201385\ndevelopmental coordination disorder, 74\u201377\nstereotypic movement disorder, 77\u201380\ntic disorders, 81\u201385\nMovement disorders, medication-induced. See \nMedication-induced movement disorders \nand other adverse effects of medication\nMuscle dysmorphia, 236, 243, 245\nNarcissistic personality disorder, 645, 646, \n669\u2013672\nassociated features supporting diagnosis of, \n671\ndevelopment and course of, 671\ndiagnostic criteria for, 669\u2013670\ndiagnostic features of, 670\u2013671\ndifferential diagnosis of, 671\u2013672\nfeatures and criteria in alternative DSM-5 \nmodel for personality disorders, 763, \n767\u2013768\ngender-related diagnostic issues in, 671\nprevalence of, 671", "source": "dsm5.pdf"} {"id": "077aa1dbf48f-0", "page_content": "Index 933\nNarcolepsy, 361, 372\u2013378\nassociated features supporting diagnosis of, \n374\u2013375\ncomorbidity with, 377\u2013378\nculture-related diagnostic issues in, 376\ndevelopment and course of, 375\ndiagnostic criteria for, 372\u2013373\ndiagnostic features of, 374\ndiagnostic markers for, 376\ndifferential diagnosis of, 376\u2013377\nfunctional consequences of, 376\nprevalence of, 375\nrelationship to International Classification of \nSleep Disorders, 378\nrisk and prognostic factors for, 375\u2013376\nsubtypes of, 373\u2013374\nNCDs. See Neurocognitive disorders\nNeglect\nchild, 718\u2013719\nspouse or partner, 721\nNervios, 835\nNeurobehavioral disorder associated with \nprenatal alcohol exposure, 798\u2013801\nassociated features supporting diagnosis of, 799\ncomorbidity with, 800\u2013801\ndevelopment and course of, 800\ndiagnostic features of, 799\ndifferential diagnosis of, 800\nfunctional consequences of, 800\nprevalence of, 800\nproposed criteria for, 798\u2013799\nsuicide risk in, 800\nNeurocognitive disorders (NCDs), 591\u2013643\ndelirium, 591, 596\u2013602\nother specified delirium, 602\nunspecified delirium, 602\nhighlights of changes fr om DSM-IV to DSM-5, \n816\nmajor and mild neurocognitive disorders, 591, \n602\u2013611, 611\u2013643\nassociated features supporting diagnosis \nof, 608\ncomorbidity with, 610\u2013611\nculture-related diagnostic issues in, 609\ndevelopment and course of, 608\u2013609", "source": "dsm5.pdf"} {"id": "077aa1dbf48f-1", "page_content": "culture-related diagnostic issues in, 609\ndevelopment and course of, 608\u2013609\ndiagnostic criteria for, 602\u2013606\ndiagnostic features of, 607\u2013608\ndiagnostic markers for, 609\u2013610\ndifferential diagnosis of, 610\nfunctional consequences of, 610\ngender-related diagnostic issues in, 609\nprevalence of, 608\nrisk and prognostic factors for, 609\nspecifiers for, 606\u2013607\nsubtypes of, 591, 603\u2013604, 606, 611\u2013643major or mild frontotemporal neuro-\ncognitive disorder, 591, 603, 614\u2013618\nmajor or mild neurocognitive disorder \ndue to Alzheimer\u2019s disease, 591, 603, \n611\u2013614\nmajor or mild neurocognitive disorder \ndue to another medical condition, \n591, 604, 641\u2013642\nmajor or mild neurocognitive disorder \ndue to HIV infection, 591, 604, 632\u2013\n634\nmajor or mild neurocognitive disorder \ndue to Huntington\u2019s disease, 591, \n604, 638\u2013641\nmajor or mild neurocognitive disorder \nwith Lewy bodies, 591, 603, 618\u2013621\nmajor or mild neurocognitive disorder \ndue to multiple etiologies, 591, 604, \n642\u2013643\nmajor or mild neurocognitive disorder \ndue to Parkinson\u2019s disease, 591, 604, \n636\u2013638\nmajor or mild neurocognitive disorder \ndue to prion disease, 591, 604, 634\u2013\n636\nmajor or mild neurocognitive disorder \ndue to traumatic brain injury, 591, \n603, 624\u2013627, 626\nmajor or mild substance/medication-", "source": "dsm5.pdf"} {"id": "077aa1dbf48f-2", "page_content": "603, 624\u2013627, 626\nmajor or mild substance/medication-\ninduced neurocognitive disorder, \n591, 603, 627\u2013632\nunspecified neurocognitive disorder, \n591, 604, 643\nvascular neurocogniti ve disorder, 591, \n603, 621\u2013624\nneurocognitive domains, 592, 593\u2013595\nNeurodevelopmental disorders, 11, 13, 31\u201386\nattention-deficit/hyperactivity disorder, 11, \n32, 59\u201366\nautism spectrum disorders, 31\u201332, 50\u201359\ncommunication disorders, 31, 41\u201349\nhighlights of changes fr om DSM-IV to DSM-5, \n809\u2013810\nintellectual disabilities, 31, 33\u201341\nmotor disorders, 32, 74\u201385\nother specified neurodevelopmental disorder, \n86\nspecific learning disorder, 32, 66\u201374\nspecifiers for, 32\u201333\ntic disorders, 32, 81\u201385\nunspecified neurodevelopmental disorder, 86\nNeurodevelopmental motor disorders, 32, 74\u201385\ndevelopmental coordination disorder, 74\u201377\nstereotypic movement disorder, 77\u201380\ntic disorders, 81\u201385", "source": "dsm5.pdf"} {"id": "5ece3f32df98-0", "page_content": "934 Index\nNeuroleptic-induced parkinsonism, 709\nNeuroleptic malignant syndrome, 22, 709\u2013711\ndevelopment and course of, 710\ndiagnostic features of, 710\ndifferential diagnosis of, 711\nrisk and prognostic factors for, 711\nNight eating syndrome, 354\nNightmare disorder, 361, 404\u2013407\nassociated features supporting diagnosis of, 405\ncomorbidity with, 407\nculture-related diagnostic issues in, 406\ndevelopment and course of, 405\ndiagnostic criteria for, 404\ndiagnostic features of, 404\u2013405\ndiagnostic markers for, 406\ndifferential diagnosis of, 406\u2013407\nfunctional consequences of, 406\ngender-related diagnostic issues in, 406\nprevalence of, 405\nrelationship to International Classification of \nSleep Disorders, 407\nrisk and prognostic factors for, 405\nNonadherence to medical treatment, 22, 726\u2013727\nNon\u2013rapid eye movement sleep arousal \ndisorders, 361, 399\u2013404\nassociated features supporting diagnosis of, \n400\u2013401\ncomorbidity with, 403\ndevelopment and course of, 401\ndiagnostic criteria for, 399\ndiagnostic features of, 400\ndiagnostic markers for, 402\ndifferential diagnosis of, 402\u2013403\nfunctional consequences of, 402\ngender-related diagnostic issues in, 401\nprevalence of, 401\nrelationship to International Classification of \nSleep Disorders, 404\nrisk and prognostic factors for, 401\nNonsuicidal self-injury, 803\u2013805\ndevelopment and course of, 804\ndiagnostic features of, 804\ndifferential diagnosis of, 805\u2013806\nfunctional consequences of, 805", "source": "dsm5.pdf"} {"id": "5ece3f32df98-1", "page_content": "differential diagnosis of, 805\u2013806\nfunctional consequences of, 805\nproposed criteria for, 803\nrisk and prognostic factors for, 804\nObesity, 22\nfeeding and eating disorders and, 329, 344, \n348, 351\u2013353\nsleep-wake disorders and, 413\nhypersomnia, 372, 373, 375, 376, 377\nobstructive sleep apnea hypopnea, \n379\u2013380, 382\nsleep-related hypoventilation, 387\u2013388, 389Obsessional jealousy, 264\nObsessive-compulsive disorder (OCD), 235\u2013236, \n237\u2013242\nassociated features supporting diagnosis of, \n238\u2013239\ncomorbidity with, 243\nculture-related diagnostic issues in, 240\ndevelopment and course of, 239\ndiagnostic criteria for, 237\ndiagnostic features of, 238\ndifferential diagnosis of, 242\u2013243\nfunctional consequences of, 241\u2013242\ngender-related diagnostic issues in, 239, 240\nprevalence of, 239\nrisk and prognostic factors for, 239\u2013240\nspecifiers for, 236, 238\nsuicide risk in, 240\nObsessive-compulsive personality disorder, 645, \n646, 678\u2013682\nassociated features supporting diagnosis of, \n680\u2013681\nculture-related diagnostic issues in, 681\ndiagnostic criteria for, 678\u2013679\ndiagnostic features of, 679\u2013680\ndifferential diagnosis of, 681\u2013682\nfeatures and criteria in alternative DSM-5 \nmodel for personality disorders, 764, \n768\u2013769\ngender-related diagnostic issues in, 681\nprevalence of, 681\nObsessive-compulsive and related disorder due to", "source": "dsm5.pdf"} {"id": "5ece3f32df98-2", "page_content": "prevalence of, 681\nObsessive-compulsive and related disorder due to \nanother medical condition, 235, 236, 260\u2013263\nassociated features supporting diagnosis of, \n262\ndevelopment and course of, 262\ndiagnostic criteria for, 260\u2013261\ndiagnostic features of, 261\u2013262\ndiagnostic markers for, 262\ndifferential diagnosis of, 262\u2013263\nObsessive-compulsive and related disorders, \n235\u2013264\nbody dysmorphic disorder, 235, 236, 242\u2013247\nexcoriation (skin-picking) disorder, 235, 236, \n254\u2013257\nhighlights of changes fr om DSM-IV to DSM-5, \n811\u2013812\nhoarding disorder, 235, 236, 247\u2013251\nobsessions and compulsions in, 235\u2013236, 239\nobsessive-compulsive disorder, 235\u2013236, \n237\u2013242\nobsessive-compulsive and related disorder \ndue to another medical condition, \n235.236, 260\u2013263\nother specified obsess ive-compulsive and \nrelated disorder, 235, 236, 263\u2013264", "source": "dsm5.pdf"} {"id": "7dae11871449-0", "page_content": "Index 935\nsubstance/medication-induced obsessive-\ncompulsive and related disorder, 235, \n236, 257\u2013260\ntrichotillomania (hair-pulling disorder), 235, \n236, 251\u2013254\nunspecified obsessive-compulsive and related \ndisorder, 235, 236\nObstructive sleep apnea hypopnea, 378\u2013383\nassociated features supporting diagnosis of, \n379\ncomorbidity with, 383\nculture-related diagnostic issues in, 381\ndevelopment and course of, 379\u2013380\ndiagnostic criteria for, 378\ndiagnostic features of, 379\ndiagnostic markers for, 381\ndifferential diagnosis of, 381\u2013383\nfunctional consequences of, 381\ngender-related diagnostic issues in, 381\nprevalence of, 379\nrelationship to International Classification of \nSleep Disorders, 383\nrisk and prognostic factors for, 380\u2013381\nspecifiers for, 378\u2013379\nOccupational problems, 723\nOCD. See Obsessive-compulsive disorder\nOlfactory reference syndrome, 246, 264, 837\nOnline enhancements, 17\nOpioid intoxication, 546\u2013547\ndiagnostic criteria for, 546\u2013547\ndiagnostic features of, 547\ndifferential diagnosis of, 547\nspecifiers for, 547\nOpioid-related disorders, 481, 540\u2013550\ndiagnoses associated with, 482\nopioid intoxication, 546\u2013547\nopioid use disorder, 541\u2013546\nopioid withdrawal, 484, 547\u2013549\nother opioid-induced disorders, 549\nunspecified opioid-related disorder, 550\nOpioid use disorder, 541\u2013546\nassociated features supporting diagnosis of, 543\ncomorbidity with, 546", "source": "dsm5.pdf"} {"id": "7dae11871449-1", "page_content": "associated features supporting diagnosis of, 543\ncomorbidity with, 546\nculture-related diagnostic issues in, 544\ndevelopment and course of, 543\ndiagnostic criteria for, 541\u2013542\ndiagnostic features of, 542\ndiagnostic markers for, 544\ndifferential diagnosis of, 545\u2013546\nfunctional consequences of, 544\u2013545\ngender-related diagnostic issues in, 544\nprevalence of, 543\nrisk and prognostic factors for, 543\u2013544\nspecifiers for, 542\nsuicide risk in, 544Opioid withdrawal, 484, 547\u2013549\nassociated features supporting diagnosis of, 549\ndevelopment and course of, 549\ndiagnostic criteria for, 547\u2013548\ndiagnostic features of, 548\ndifferential diagnosis of, 549\nprevalence of, 549\nOppositional defiant disorder, 32, 461, 462\u2013466\nassociated features supporting diagnosis of, \n464\ncomorbidity with, 466\nculture-related diagnostic issues in, 465\ndevelopment and course of, 464\ndiagnostic criteria for, 462\u2013463\ndiagnostic features of, 463\ndifferential diagnosis of, 465\nfunctional consequences of, 465\nprevalence of, 464\nrisk and prognostic factors for, 464\nspecifiers for, 463\nOther circumstances of personal history, 726\nOther conditions that may be a focus of clinical \nattention, 20, 22, 29, 715\u2013727\nabuse and neglect, 717\u2013722\nadult maltreatment and neglect problems, \n720\u2013722\nchild maltreatment and neglect problems, \n717\u2013719\neducational and occupational problems, 723\nhousing and economic problems, 723\u2013724", "source": "dsm5.pdf"} {"id": "7dae11871449-2", "page_content": "educational and occupational problems, 723\nhousing and economic problems, 723\u2013724\nnonadherence to medical treatment, 726\u2013727\nother circumstances of personal history, 726\nother health service encounters for counseling \nand medical advice, 725\nother problems related to the social \nenvironment, 724\u2013725\nproblems related to access to medical and \nother health care, 726\nproblems related to crime or interaction with \nthe legal system, 725\nproblems related to other psychosocial, \npersonal, and environmental \ncircumstances, 725\nrelational problems, 715\u2013717\nother problems relate d to primary support \ngroup, 716\u2013717\nproblems related to family upbringing, \n715\u2013716\nOther hallucinogen intoxication, 529\u2013530\ndiagnostic criteria for, 529\ndiagnostic features of, 529\ndifferential diagnosis of, 530\nfunctional consequences of, 530\nprevalence of, 530\nsuicide risk in, 530", "source": "dsm5.pdf"} {"id": "133f79e33be3-0", "page_content": "936 Index\nOther hallucinogen use disorder, 523\u2013527\nassociated features supporting diagnosis of, \n525\ncomorbidity with, 527\nculture-related diagnostic issues in, 526\ndevelopment and course of, 525\u2013526\ndiagnostic criteria for, 523\u2013524\ndiagnostic features of, 524\u2013525\ndiagnostic markers for, 526\ndifferential diagnosis of, 527\nfunctional consequences of, 527\ngender-related diagnostic issues in, 526\nprevalence of, 525\nrisk and prognostic factors for, 526\nspecifiers for, 524\nOther health service encounters for counseling \nand medical advice, 725\nOther mental disorders, 707\u2013708\nother specified mental disorder, 15\u201316, 19, \n708\nother specified mental di sorder due to another \nmedical condition, 707\nunspecified mental disorder, 15\u201316, 19\u201320, 708\nunspecified mental disorder due to another \nmedical condition, 708\nOther problems related to primary support group, \n716\u2013717\nOther problems related to social environment, \n724\u2013725\nOther psychosocial, personal, and environmental \ncircumstances, problems related to, 725\nOther specified mental disorder, 15\u201316, 19, 708\ndue to another medical condition, 707\nOther (or unknown) substance intoxication, \n581\u2013582\ncomorbidity with, 582\ndevelopment and course of, 581\u2013582\ndiagnostic criteria for, 581\ndiagnostic features of, 581\ndifferential diagnosis of, 582\nfunctional consequences of, 582\nprevalence of, 581\nOther (or unknown) substance\u2013related disorders, \n577\u2013585\ndiagnoses associated with, 482", "source": "dsm5.pdf"} {"id": "133f79e33be3-1", "page_content": "577\u2013585\ndiagnoses associated with, 482\nother (or unknown) substance\u2013induced \ndisorders, 584\u2013585\nother (or unknown) substance intoxication, \n581\u2013582\nother (or unknown) substance use disorder, \n577\u2013580\nother (or unknown) substance withdrawal, \n583\u2013584\nunspecified other (or unknown) substance\u2013\nrelated disorder, 585Other (or unknown) substance use disorder, \n577\u2013580\nassociated features supporting diagnosis of, 579\ncomorbidity with, 580\nculture-related diagnostic issues in, 580\ndevelopment and course of, 580\ndiagnostic criteria for, 577\u2013578\ndiagnostic features of, 579\ndiagnostic markers for, 580\ndifferential diagnosis of, 580\nprevalence of, 579\nrisk and prognostic factors for, 580\nspecifiers for, 578\nOther (or unknown) substance withdrawal, \n583\u2013584\ncomorbidity with, 584\nculture-related diagnostic issues in, 583\ndevelopment and course of, 583\ndiagnostic criteria for, 583\ndiagnostic features of, 583\ndifferential diagnosis of, 584\nfunctional consequences of, 584\nprevalence of, 583\nPanic attacks, 189, 190, 208\u2013209, 214\u2013217\nassociated features with, 215\ncomorbidity with, 217\nculture-related diagnostic issues in, 216\ndevelopment and course of, 215\u2013216\ndiagnostic markers for, 216\ndifferential diagnosis of, 217\nexpected vs. unexpected, 215\nfeatures of, 214\u2013215\nfunctional consequences of, 217\ngender-related diagnostic issues in, 216\nnocturnal, 209, 215", "source": "dsm5.pdf"} {"id": "133f79e33be3-2", "page_content": "gender-related diagnostic issues in, 216\nnocturnal, 209, 215\nin older adults, 210\u2013211, 215\u2013216\nprevalence of, 215\nrisk and prognostic factors for, 216\nspecifier for, 214\u2013217\nsuicide risk and, 215\nsymptoms of, 214\nPanic disorder, 190, 208\u2013214\nassociated features supporting diagnosis of, 210\nculture-related diagnostic issues in, 211\u2013212\ndevelopment and course of, 210\u2013211\ndiagnostic criteria for, 208\u2013209\ndiagnostic features of, 209\ndiagnostic markers for, 212\ndifferential diagnosis of, 212\u2013213\nfunctional consequences of, 212\ngender-related diagnostic issues in, 210.212\nprevalence of, 210\nrisk and prognostic factors for, 211\nsuicide risk in, 212", "source": "dsm5.pdf"} {"id": "8c139841c06c-0", "page_content": "Index 937\nParanoid personality disorder, 645, 646, 649\u2013652\nassociated features supporting diagnosis of, \n650\u2013651\nculture-related diagnostic issues in, 651\ndevelopment and course of, 651\ndiagnostic criteria for, 649\ndiagnostic features of, 649\u2013650\ndifferential diagnosis of, 652\nprevalence of, 651\nrisk and prognostic factors for, 651\nParaphilic disorders, 685\u2013705\nexhibitionistic disorder, 685, 689\u2013691\nfetishistic disorder, 685, 700\u2013702\nfrotteuristic disorder, 685, 691\u2013694\nhighlights of changes fr om DSM-IV to DSM-5, \n816\nother specified para philic disorder, 705\npedophilic disorder, 685, 697\u2013700\nsexual masochism disorder, 685, 694\u2013695\nsexual sadism disorder, 685, 695\u2013697\ntransvestic disorder, 685, 702\u2013704\nunspecified paraphilic disorder, 705\nvoyeuristic disorder, 685, 686\u2013688\nParasomnias, 361, 399\u2013410\nnightmare disorder, 361, 404\u2013407\nnon\u2013rapid eye movement sleep arousal \ndisorders, 361, 399\u2013404\nrapid eye movement sleep behavior disorder, \n361, 407\u2013410\nParkinsonism\nneuroleptic-induced, 709\nother medication-induced, 709\nParkinson\u2019s disease\nanxiety disorders and, 203, 205, 207, 218, 221\ndepressive disorders and, 181, 182\nmajor or mild neurocognitive disorder due to, \n591, 604, 636\u2013638\nassociated features supporting diagnosis", "source": "dsm5.pdf"} {"id": "8c139841c06c-1", "page_content": "591, 604, 636\u2013638\nassociated features supporting diagnosis \nof, 637\ncomorbidity with, 638\ndevelopment and course of, 637\ndiagnostic criteria for, 636\u2013637\ndiagnostic features of, 637\ndiagnostic markers for, 637\u2013638\ndifferential diagnosis of, 638\nprevalence of, 637\nrisk and prognostic factors for, 637\nsleep-wake disorders and, 372, 383, 395, 413, \n421\nREM sleep behavior disorder, 361, 408, 410\nPedophilic disorder, 685, 697\u2013700\nassociated features supporting diagnosis of, 698\ncomorbidity with, 700\ndevelopment and course of, 699\ndiagnostic criteria for, 697\u2013698diagnostic features of, 698\ndiagnostic markers for, 699\ndifferential diagnosis of, 700\ngender-related diagnostic issues in, 699\nprevalence of, 698\nrisk and prognostic factors for, 699\nPersistent complex bereavement disorder, 289, \n789\u2013792\nassociated features supporting diagnosis of, \n791\ncomorbidity with, 792\nculture-related diagnostic issues in, 791\ndevelopment and course of, 791\ndiagnostic features of, 790\u2013791\ndifferential diagnosis of, 792\nfunctional consequences of, 792\nprevalence of, 791\nproposed criteria for, 789\u2013790\nrisk and prognostic factors for, 791\nsuicide risk in, 791\nPersistent depressive disorder (dysthymia), 155, \n168\u2013171\ncomorbidity with, 171\ndevelopment and course of, 170\ndiagnostic criteria for, 168\u2013169\ndiagnostic features of, 169\u2013170", "source": "dsm5.pdf"} {"id": "8c139841c06c-2", "page_content": "diagnostic criteria for, 168\u2013169\ndiagnostic features of, 169\u2013170\ndifferential diagnosis of, 170\u2013171\nfunctional consequences of, 170\nprevalence of, 170\nrisk and prognostic factors for, 170\nPersonality change due to another medical \ncondition, 645, 682\u2013684\nassociated features supporting diagnosis of, \n683\ndiagnostic criteria for, 682\ndiagnostic features of, 683\ndifferential diagnosis of, 683\u2013684\nsubtypes of, 683\nPersonality disorders, 645\u2013684\nCluster A, 646, 649\u2013659\nparanoid personality disorder, 645, 646, \n649\u2013652\nschizoid personality disorder, 645, 646, \n652\u2013655\nschizotypal personality disorder, 87, 89, 90, \n645, 646, 655\u2013659\nCluster B, 646, 659\u2013672\nantisocial personality disorder, 461, 476, \n645, 646, 659\u2013663\nborderline personality disorder, 645, 646, \n663\u2013666\nhistrionic personality disorder, 645, 646, \n667\u2013669\nnarcissistic personality disorder, 645, 646, \n669\u2013672", "source": "dsm5.pdf"} {"id": "39ab86ff24a2-0", "page_content": "938 Index\nPersonality disorders (continued)\nCluster C, 646, 672\u2013682\navoidant personality disorder, 645, 646, \n672\u2013675\ndependent personality disorder, 645, 646, \n675\u2013678\nobsessive-compulsive personality disorder, \n645, 646, 678\u2013682\ngeneral personality disorder, 646\u2013649\ncriteria for, 646\u2013647\nculture-related diagnostic issues in, 648\ndevelopment and course of, 647\u2013648\ndiagnostic features of, 647\ndifferential diagnosis of, 648\u2013649\ngender-related diagnostic issues in, 648\nhighlights of changes fr om DSM-IV to DSM-5, \n816\nother specified personality disorder, 645\u2013646, \n684\npersonality change due to another medical \ncondition, 645, 682\u2013684\nunspecified personality disorder, 645\u2013646, 684\nPersonality disorders: alternative DSM-5 model, \n761\u2013781\ndiagnosis of, 771\ngeneral criteria for personality disorder, \n761\u2013763\nCriterion A: level of personality \nfunctioning, 762, 762\nCriterion B: pathological personality traits, \n762\u2013763\nCriteria C and D: pervasiveness and \nstability, 763\nCriteria E, F, and G: alternative \nexplanations for personality \npathology, 763\nlevel of personality functioning, 762, 762, \n771\u2013772\nLevel of Personality Functioning Scale for \nrating of, 772, 775\u2013778\nself- and interpersonal functioning \ndimensional definition, 772\npersonality traits, 772\u2013774\nassessment of Personality Trait Model, 774\nclinical utility of multidimensional \npersonality functioning and trait \nmodel, 774", "source": "dsm5.pdf"} {"id": "39ab86ff24a2-1", "page_content": "clinical utility of multidimensional \npersonality functioning and trait \nmodel, 774\ndefinition and description of, 772\u2013773\ndefinitions of personality disorder trait \ndomains and facets, 779\u2013781\ndimensionality of, 772\u2013773\ndistinguishing traits, symptoms, and \nspecific behaviors, 773\u2013774\nhierarchical structure of personality, 773\nPersonality Trait Model, 773scoring algorithms for, 771\nspecific personality disorders, 763\u2013771\nantisocial personality disorder, 763, 764\u2013765\navoidant personality disorder, 763, 765\u2013766\nborderline personality disorder, 763, 766\u2013\n767\nnarcissistic personality disorder, 763, \n767\u2013768\nobsessive-compulsive personality disorder, \n764, 768\u2013769\npersonality disorder\u2014trait specified, 761, \n770\u2013771\nschizotypal personality disorder, 764, \n769\u2013770\nPhencyclidine intoxication, 527\u2013529\ndiagnostic criteria for, 527\u2013528\ndiagnostic features of, 528\ndiagnostic markers for, 528\ndifferential diagnosis of, 528\u2013529\nfunctional consequences of, 528\nprevalence of, 528\nPhencyclidine-related disorders, 481\ndiagnoses associated with, 482\nother phencyclidine-induced disorders, 532\nphencyclidine intoxication, 527\u2013529\nphencyclidine use disorder, 520\u2013523\nunspecified phencyclidine-related disorder, 533\nPhencyclidine use disorder, 520\u2013523\nassociated features supporting diagnosis of, 522\nculture-related diagnostic issues in, 522\ndiagnostic criteria for, 520\u2013521\ndiagnostic features of, 521\u2013522\ndiagnostic markers for, 522", "source": "dsm5.pdf"} {"id": "39ab86ff24a2-2", "page_content": "diagnostic features of, 521\u2013522\ndiagnostic markers for, 522\ndifferential diagnosis of, 523\nfunctional consequences of, 522\ngender-related diagnostic issues in, 522\nprevalence of, 522\nrisk and prognostic factors for, 522\nspecifiers for, 521\nPhobic disorders\nagoraphobia, 190, 217\u2013221\nsocial anxiety disorder (social phobia), 190, \n202\u2013208\nspecific phobia, 189\u2013190, 197\u2013202\nPhysical abuse\nchild, 717\u2013718\nnonspouse or nonpartner, 722\nspouse or partner, 720\nPica, 329\u2013331\nassociated features supporting diagnosis of, \n330\ncomorbidity with, 331\nculture-related diagnostic issues in, 331\ndevelopment and course of, 330\ndiagnostic criteria for, 329\u2013330", "source": "dsm5.pdf"} {"id": "b2eff1a92825-0", "page_content": "Index 939\ndiagnostic features of, 330\ndiagnostic markers for, 331\ndifferential diagnosis of, 331\nfunctional consequences of, 331\ngender-related diagnostic issues in, 331\nprevalence of, 330\nrisk and prognostic factors for, 330\nPosttraumatic stress disorder (PTSD), 265, 271\u2013280\nassociated features supporting diagnosis of, \n276\ncomorbidity with, 280\nculture-related diagnostic issues in, 278\ndevelopment and course of, 276\u2013277\ndiagnostic criteria for, 271\u2013274\ndiagnostic features of, 274\u2013276\ndifferential diagnosis of, 279\u2013280\nfunctional consequences of, 278\u2013279\ngender-related diagnostic issues in, 278\nprevalence of, 276\nrisk and prognostic factors for, 277\u2013278\nsuicide risk in, 278\nPostural tremor, medication-induced, 712\nPremature (early) ejaculation, 423, 443\u2013446\nassociated features supporting diagnosis of, \n444\ncomorbidity with, 446\nculture-related diagnostic issues in, 445\ndevelopment and course of, 444\u2013445\ndiagnostic criteria for, 443\u2013444\ndiagnostic features of, 444\ndiagnostic markers for, 445\ndifferential diagnosis of, 445\u2013446\nfunctional consequences of, 445\ngender-related diagnostic issues in, 445\nprevalence of, 444\nrisk and prognostic factors for, 445\nPremenstrual dysphoric disorder, 155, 171\u2013175\nassociated features supporting diagnosis of, 173\ncomorbidity with, 175\nculture-related diagnostic issues in, 173\ndevelopment and course of, 173\ndiagnostic criteria for, 171\u2013172\ndiagnostic features of, 172\u2013173", "source": "dsm5.pdf"} {"id": "b2eff1a92825-1", "page_content": "diagnostic criteria for, 171\u2013172\ndiagnostic features of, 172\u2013173\ndiagnostic markers for, 173\u2013174\ndifferential diagnosis of, 174\u2013175\nfunctional consequences of, 174\nprevalence of, 173\nrecording procedures for, 172\nrisk and prognostic factors for, 173\nPrincipal diagnosis, 22\u201323\nPrion disease, major or mild neurocognitive \ndisorder due to, 591, 604, 634\u2013636\ndevelopment and course of, 635\ndiagnostic criteria for, 634\u2013635\ndiagnostic features of, 635diagnostic markers for, 636\ndifferential diagnosis of, 636\nprevalence of, 635\nrisk and prognostic factors for, 636\nProblems related to access to medical and other \nhealth care, 726\nProblems related to crime or interaction with the \nlegal system, 725\nProblems related to family upbringing, 715\u2013716\nProblems related to other psychosocial, personal, \nand environmental circumstances, 725\nProvisional diagnosis, 23\nPseudocyesis, 310, 327\nPsychological abuse\nchild, 719\nnonspouse or nonpartner, 722\nspouse or partner abuse, 721\u2013722\nPsychological factors af fecting other medical \nconditions, 309, 310, 322\u2013324\ncomorbidity with, 324\nculture-related diagnostic issues in, 323\ndevelopment and course of, 323\ndiagnostic criteria for, 322\ndiagnostic features of, 322\u2013323\ndifferential diagnosis of, 323\u2013324\nfunctional consequences of, 323\nprevalence of, 323\nPsychotic disorder due to another medical \ncondition, 89, 115\u2013118", "source": "dsm5.pdf"} {"id": "b2eff1a92825-2", "page_content": "Psychotic disorder due to another medical \ncondition, 89, 115\u2013118\nassociated features supporting diagnosis of, 116\ncomorbidity with, 118\ndevelopment and course of, 117\ndiagnostic criteria for, 115\u2013116\ndiagnostic features of, 116\ndiagnostic markers for, 117\ndifferential diagnosis of, 118\nfunctional consequences of, 118\nprevalence of, 116\u2013117\nrisk and prognostic factors for, 117\nspecifiers for, 116\nsuicide risk in, 118\nPsychotic disorders. See Schizophrenia spectrum \nand other psychotic disorders\nPTSD. See Posttraumatic stress disorder\nPurging disorder, 353\nPyromania, 461, 476\u2013477\nassociated features supporting diagnosis of, \n476\u2013477\ncomorbidity with, 477\ndevelopment and course of, 477\ndiagnostic criteria for, 476\ndiagnostic features of, 476\ndifferential diagnosis of, 477\ngender-related diagnostic issues in, 477\nprevalence of, 477", "source": "dsm5.pdf"} {"id": "9c7aee51ad74-0", "page_content": "940 Index\nRapid eye movement (REM) sleep behavior \ndisorder, 361, 407\u2013410\nassociated features supporting diagnosis of, 408\ncomorbidity with, 410\ndevelopment and course of, 408\u2013409\ndiagnostic criteria for, 407\u2013408\ndiagnostic features of, 408\ndiagnostic markers for, 409\ndifferential diagnosis of, 409\u2013410\nfunctional consequences of, 409\nprevalence of, 408\nrelationship to International Classification of \nSleep Disorders, 410\nrisk and prognostic factors for, 409\nReactive attachment disorder, 265\u2013268\nassociated features supporting diagnosis of, 266\ncomorbidity with, 268\nculture-related diagnostic issues in, 267\ndevelopment and course of, 266\ndiagnostic criteria for, 265\u2013266\ndiagnostic features of, 266\ndifferential diagnosis of, 267\u2013268\nfunctional consequences of, 267\nprevalence of, 266\nrisk and prognostic factors for, 267\nRecurrent brief depression, 183\nRelational problems, 22, 715\u2013717\nother problems relate d to primary support \ngroup, 716\u2013717\nproblems related to family upbringing, 715\u2013716\nREM sleep behavior disorder. See Rapid eye \nmovement sleep behavior disorder\nRestless legs syndrome (RLS), 361, 410\u2013413\nassociated features supporting diagnosis of, \n411\ncomorbidity with, 413\ndevelopment and course of, 411\u2013412\ndiagnostic criteria for, 410\ndiagnostic features of, 411\ndiagnostic markers for, 412\ndifferential diagnosis of, 413\nfunctional consequences of, 412\u2013413\ngender-related diagnostic issues in, 412\nprevalence of, 411\nrelationship to International Classification of", "source": "dsm5.pdf"} {"id": "9c7aee51ad74-1", "page_content": "prevalence of, 411\nrelationship to International Classification of \nSleep Disorders, 413\nrisk and prognostic factors for, 412\nRett syndrome, 33, 38, 51, 53, 56, 57, 79, 80\nRLS. See Restless legs syndrome\nRumination disorder, 329, 332\u2013333\nassociated features supporting diagnosis of, \n332\u2013333\ncomorbidity with, 333\ndevelopment and course of, 333\ndiagnostic criteria for, 332diagnostic features of, 332\ndifferential diagnosis of, 333\nfunctional consequences of, 333\nprevalence of, 333\nrisk and prognostic factors for, 333\nSchizoaffective disorder, 89\u201390, 105\u2013110\nassociated features supporting diagnosis of, 107\ncomorbidity with, 110\nculture-related diagnostic issues in, 108\u2013109\ndevelopment and course of, 108\ndiagnostic criteria for, 105\u2013106\ndiagnostic features of, 106\u2013107\ndifferential diagnosis of, 109\u2013110\nfunctional consequences of, 109\nprevalence of, 107\u2013108\nrisk and prognostic factors for, 108\nsuicide risk in, 109\nSchizoid personality disorder, 645, 646, 652\u2013655\nassociated features supporting diagnosis of, \n653\u2013654\nculture-related diagnostic issues in, 654\ndevelopment and course of, 654\ndiagnostic criteria for, 652\u2013653\ndiagnostic features of, 653\ndifferential diagnosis of, 654\u2013655\ngender-related diagnostic issues in, 654\nprevalence of, 654\nrisk and prognostic factors for, 654\nSchizophrenia, 87, 99\u2013105\nassociated features supporting diagnosis of,", "source": "dsm5.pdf"} {"id": "9c7aee51ad74-2", "page_content": "Schizophrenia, 87, 99\u2013105\nassociated features supporting diagnosis of, \n101\u2013102\nwith catatonia, 88, 100\ncomorbidity with, 105\nculture-related diagnostic issues in, 103\ndevelopment and course of, 102\u2013103\ndiagnostic features of, 87\u201388, 100\u2013101\ndifferential diagnosis of, 104\u2013105\nfunctional consequences of, 104\ngender-related diagnostic issues in, 103\u2013104\nprevalence of, 102\nrisk and prognostic factors for, 103\nsuicide risk in, 104\nSchizophrenia spectrum and other psychotic \ndisorders, 87\u2013122\nbrief psychotic disorder, 89, 94\u201396\ncatatonia, 88, 89, 119\u2013121\nclinician-rated assessment of symptoms and \nrelated clinical phenomena in, 89\u201390\ndelusional disorder, 89, 90\u201393\nhighlights of changes fr om DSM-IV to DSM-5, \n810\nkey features of, 87\u201388\ndelusions, 87\ndisorganized thinking (speech), 88", "source": "dsm5.pdf"} {"id": "c4fd8a35eeb5-0", "page_content": "Index 941\ngrossly disorganized or abnormal motor \nbehavior (including catatonia), 88\nhallucinations, 87\u201388\nnegative symptoms, 88\nother specified schizo phrenia spectrum and \nother psychotic disorder, 122\npsychotic disorder due to another medical \ncondition, 89, 115\u2013118\nschizoaffective disorder, 89\u201390, 105\u2013110\nschizophrenia, 87, 99\u2013105\nschizophreniform disorder, 89, 96\u201399\nschizotypal (personality) disorder, 87, 89, 90\nsubstance/medication-induced psychotic \ndisorder, 89, 110\u2013115\nunspecified schizophrenia spectrum and other \npsychotic disorder, 122\nSchizophreniform disorder, 89, 96\u201399\nassociated features supporting diagnosis of, 98\ndevelopment and course of, 98\ndiagnostic criteria for, 96\u201397\ndiagnostic features of, 97\u201398\ndifferential diagnosis of, 98\u201399\nfunctional consequences of, 98\nprevalence of, 98\nprovisional diagnosis of, 97\nrisk and prognostic factors for, 98\nSchizotypal personality disorder, 87, 89, 90, 645, \n646, 655\u2013659\nassociated features supporting diagnosis of, \n657\nculture-related diagnostic issues in, 657\ndevelopment and course of, 657\ndiagnostic criteria for, 655\u2013656\ndiagnostic features of, 656\u2013657\ndifferential diagnosis of, 658\u2013659\nfeatures and criteria in alternative DSM-5 \nmodel for personality disorders, 764, \n769\u2013770\ngender-related diagnostic issues in, 658\nprevalence of, 657", "source": "dsm5.pdf"} {"id": "c4fd8a35eeb5-1", "page_content": "gender-related diagnostic issues in, 658\nprevalence of, 657\nrisk and prognostic factors for, 657\nSedative, hypnotic, or an xiolytic intoxication, \n556\u2013557\nassociated features supporting diagnosis of, 557\ndiagnostic criteria for, 556\ndiagnostic features of, 556\u2013557\ndifferential diagnosis of, 557\nprevalence of, 557\nSedative-, hypnotic-, or anxiolytic-related \ndisorders, 481, 550\u2013560\ndiagnoses associated with, 482\nother sedative-, hypnotic-, or anxiolytic-\ninduced disorders, 560\nsedative, hypnotic, or anxiolytic intoxication, \n556\u2013557sedative, hypnotic, or anxiolytic use disorder, \n550\u2013556\nsedative, hypnotic, or anxiolytic withdrawal, \n484, 557\u2013560\nunspecified sedative-, hy pnotic-, or anxiolytic-\nrelated disorder, 560\nSedative, hypnotic, or anxiolytic use disorder, \n550\u2013556\nassociated features supporting diagnosis of, \n553\ncomorbidity with, 555\u2013556\nculture-related diagnostic issues in, 554\ndevelopment and course of, 553\u2013554\ndiagnostic criteria for, 550\u2013552\ndiagnostic features of, 552\u2013553\ndiagnostic markers for, 554\u2013555\ndifferential diagnosis of, 555\nfunctional consequences of, 555\ngender-related diagnostic issues in, 554\nprevalence of, 553\nrisk and prognostic factors for, 554\nspecifiers for, 552\nSedative, hypnotic, or anxiolytic withdrawal, 484, \n557\u2013560", "source": "dsm5.pdf"} {"id": "c4fd8a35eeb5-2", "page_content": "557\u2013560\nassociated features supporting diagnosis of, 559\ndiagnostic criteria for, 557\u2013558\ndiagnostic features of, 558\ndiagnostic markers for, 559\ndifferential diagnosis of, 559\u2013560\nprevalence of, 559\nSelective mutism, 189, 195\u2013197\nassociated features supporting diagnosis of, \n195\u2013196\ncomorbidity with, 197\nculture-related diagnostic issues in, 196\ndevelopment and course of, 196\ndiagnostic criteria for, 195\ndiagnostic features of, 195\ndifferential diagnosis of, 197\nfunctional consequences of, 196\u2013197\nprevalence of, 196\nrisk and prognostic factors for, 196\nSeparation anxiety disorder, 189, 190\u2013195\nassociated features supporting diagnosis of, 192\ncomorbidity with, 195\nculture-related diagnostic issues in, 193\ndevelopment and course of, 192\u2013193\ndiagnostic criteria for, 190\u2013191\ndiagnostic features of, 191\u2013192\ndifferential diagnosis of, 194\u2013195\nfunctional consequences of, 193\u2013194\ngender-related diagnostic issues in, 193\nprevalence of, 192\nrisk and prognostic factors for, 193\nsuicide risk in, 193", "source": "dsm5.pdf"} {"id": "2d3097fdbf72-0", "page_content": "942 Index\nSeverity measures, 733, 742\nClinician-Rated Dimensions of Psychosis \nSymptom Severity, 742\u2013744\nfrequency of use of, 742\nscoring and interpretation of, 742\nSexual abuse\nchild, 718\nnonspouse or nonpartner, 722\nspouse or partner, 720\nSexual dysfunctions, 423\u2013450\ndelayed ejaculation, 423, 424\u2013426\nerectile disorder, 423, 426\u2013429\nfemale orgasmic disorder, 423, 429\u2013432\nfemale sexual interest/arousal disorder, 423, \n433\u2013437\ngenito-pelvic pain/penetration disorder, 423, \n437\u2013440\nhighlights of changes fr om DSM-IV to DSM-5, \n814\nmale hypoactive sexual desire disorder, 423, \n440\u2013443\nother specified sexual dysfunction, 423, 450\npremature (early) ejaculation, 423, 443\u2013446\nsubstance/medication-induced sexual \ndysfunction, 423, 446\u2013450\nsubtypes of, 423\nunspecified sexual dysfunction, 423, 450\nSexual masochism disorder, 685, 694\u2013695\nassociated features supporting diagnosis of, 694\ncomorbidity with, 695\ndevelopment and course of, 695\ndiagnostic criteria for, 694\ndiagnostic features of, 694\ndifferential diagnosis of, 695\nfunctional consequences of, 695\nprevalence of, 694\nSexual sadism disorder, 685, 695\u2013697\nassociated features supporting diagnosis of, 696\ncomorbidity with, 697\ndevelopment and course of, 697\ndiagnostic criteria for, 695\ndiagnostic features of, 696", "source": "dsm5.pdf"} {"id": "2d3097fdbf72-1", "page_content": "diagnostic criteria for, 695\ndiagnostic features of, 696\ndifferential diagnosis of, 697\nprevalence of, 696\nShenjing shuairuo, 835\u2013836\nShubo-kyofu, 264\nSkin picking. See Excoriation (skin-picking) \ndisorder\nSleep-related hypoventilation, 387\u2013390\nassociated features supporting diagnosis of, \n387\u2013388\ncomorbidity with, 389\u2013390\ndevelopment and course of, 388\ndiagnostic criteria for, 387\ndiagnostic features, 387diagnostic markers for, 389\ndifferential diagnosis of, 389\nfunctional consequences of, 389\ngender-related diagnostic issues in, 389\nprevalence of, 388\nrelationship to International Classification of \nSleep Disorders, 390\nrisk and prognostic factors for, 388\nsubtypes of, 387\nSleep terrors, 399\u2013403. See also Non\u2013rapid eye \nmovement sleep arousal disorders\nSleep-wake disorders, 361\u2013422\nbreathing-related sleep disorders, 361, 378\u2013390\ncentral sleep apnea, 383\u2013386\nobstructive sleep ap nea hypopnea, 378\u2013383\nsleep-related hypoventilation, 387\u2013390\ncircadian rhythm sleep-wake disorders, 361, \n390\u2013398\nadvanced sleep phase type, 393\u2013394\ndelayed sleep phase type, 391\u2013392\nirregular sleep-wake type, 394\u2013396\nnon-24-hour sleep-wake type, 396\u2013397\nshift work type, 397\u2013398\nhighlights of changes fr om DSM-IV to DSM-5, \n814\nhypersomnolence disorder, 361, 368\u2013372\nother specified, 421", "source": "dsm5.pdf"} {"id": "2d3097fdbf72-2", "page_content": "other specified, 421\nunspecified, 421\ninsomnia disorder, 361, 362\u2013368\nother specified, 420\nunspecified, 420\u2013421\nnarcolepsy, 361, 372\u2013378\nother specified sleep-wake disorder, 421\nparasomnias, 399\u2013410\nnightmare disorder, 361, 404\u2013407\nnon\u2013rapid eye movement sleep arousal \ndisorders, 361, 399\u2013404\nrapid eye movement sleep behavior \ndisorder, 361, 407\u2013410\nrelationship to International Classification of \nSleep Disorders, 361\u2013362 ( See also specific \nsleep-wake disorders )\nrestless legs syndrome, 361, 410\u2013413\nsubstance/medication-induced sleep disorder, \n413\u2013420\nunspecified sleep-wake disorder, 422\nSleepwalking, 399\u2013403. See also Non\u2013rapid eye \nmovement sleep arousal disorders\nSmoking. See Tobacco-related disorders\nSocial anxiety disorder (social phobia), 190, \n202\u2013208\nassociated features supporting diagnosis of, \n204\ncomorbidity with, 208\nculture-related diagnostic issues in, 205\u2013206", "source": "dsm5.pdf"} {"id": "eef782649831-0", "page_content": "Index 943\ndevelopment and course of, 205\ndiagnostic criteria for, 202\u2013203\ndiagnostic features of, 203\u2013204\ndifferential diagnosis of, 206\u2013207\nfunctional consequences of, 206\ngender-related diagnostic issues in, 204, 206\nprevalence of, 204\nrisk and prognostic factors for, 205\nspecifiers for, 203\nSocial (pragmatic) communication disorder, 31, \n47\u201349\nassociated features supporting diagnosis of, 48\ndevelopment and course of, 48\ndiagnostic criteria for, 47\u201348\ndiagnostic features of, 48\ndifferential diagnosis of, 49\nrisk and prognostic factors for, 48\nSomatic symptom disorder, 309, 310, 311\u2013315\nassociated features supporting diagnosis of, \n312\ncomorbidity with, 314\u2013315\nculture-related diagnostic issues in, 313\ndevelopment and course of, 312\u2013313\ndiagnostic criteria for, 311\ndiagnostic features of, 311\u2013312\ndifferential diagnosis of, 314\nprevalence of, 312\nrisk and prognostic factors for, 313\nSomatic symptoms and related disorders, 309\u2013327\nconversion disorder (functional neurological \nsymptom disorder), 309, 310, 318\u2013321\nfactitious disorder, 309, 310, 324\u2013326\nhighlights of changes fr om DSM-IV to DSM-5, \n812\u2013813\nillness anxiety disorder, 309, 310, 315\u2013318\nother specified somatic symptom and related \ndisorder, 309, 310, 327\npsychological factors affecting other medical \nconditions, 309, 310, 322\u2013324", "source": "dsm5.pdf"} {"id": "eef782649831-1", "page_content": "conditions, 309, 310, 322\u2013324\nsomatic symptom disorder, 309, 310, 311\u2013315\nunspecified somatic symptom and related \ndisorder, 309, 310, 327\nSpecific learning disorder, 32, 66\u201374\nassociated features supporting diagnosis of, 70\ncomorbidity with, 72, 74\nculture-related diagnostic issues in, 72\u201373\ndevelopment and course of, 70\u201372\ndiagnostic criteria for, 66\u201368\ndiagnostic features of, 68\u201370\ndifferential diagnosis of, 73\u201374\nfunctional consequences of, 73\ngender-related diagnostic issues in, 73\nprevalence of, 70\nrecording procedures for, 68\nrisk and prognostic factors for, 72Specific phobia, 189\u2013190, 197\u2013202\nassociated features supporting diagnosis of, 199\ncomorbidity with, 202\nculture-related diagnostic issues in, 201\ndevelopment and course of, 199\u2013200\ndiagnostic criteria for, 197\u2013198\ndiagnostic features of, 198\u2013199\ndifferential diagnosis of, 201\u2013202\nfunctional consequences of, 201\nprevalence of, 199\nrisk and prognostic factors for, 200\nspecifiers for, 198\nsuicide risk in, 201\nSpecifiers, 21\u201322\nSpecifiers for bipolar and related disorders, \n149\u2013154\nSpecifiers for depressive disorders, 184\u2013188\nSpeech sound disorder, 31, 44\u201345\nassociated features supporting diagnosis of, 44\ndevelopment and course of, 44\u201345\ndiagnostic criteria for, 44\ndiagnostic features of, 44\ndifferential diagnosis of, 45\nSpouse or partner abuse, psychological, 721\u2013722", "source": "dsm5.pdf"} {"id": "eef782649831-2", "page_content": "Spouse or partner abuse, psychological, 721\u2013722\nSpouse or partner neglect, 721\nSpouse or partner violence\nphysical, 720\nsexual, 720\nStereotypic movement disorder, 32, 77\u201380\ncomorbidity with, 80\nculture-related diagnostic issues in, 79\ndevelopment and course of, 79\ndiagnostic criteria for, 77\u201378\ndiagnostic features of, 78\u201379\ndifferential diagnosis of, 79\u201380\nprevalence of, 79\nrecording procedures for, 78\nrisk and prognostic factors for, 79\nspecifiers for, 78\nStimulant intoxication, 567\u2013569\nassociated features supporting diagnosis of, 568\ndiagnostic criteria for, 567\u2013568\ndiagnostic features of, 568\ndifferential diagnosis of, 568\u2013569\nStimulant-related disorders, 481, 561\u2013570\ndiagnoses associated with, 482\nother stimulant-indu ced disorders, 570\nstimulant intoxication, 567\u2013569\nstimulant use disorder, 561\u2013567\nstimulant withdrawal, 484, 569\u2013570\nunspecified stimulant-related disorder, 570\nStimulant use disorder, 561\u2013567\nassociated features supporting diagnosis of, \n563\u2013564\ncomorbidity with, 566\u2013567", "source": "dsm5.pdf"} {"id": "162bdb5e8349-0", "page_content": "944 Index\nStimulant use disorder (continued)\nculture-related diagnostic issues in, 565\ndevelopment and course of, 564\u2013565\ndiagnostic criteria for, 561\u2013562\ndiagnostic features of, 563\ndiagnostic markers for, 565\u2013566\ndifferential diagnosis of, 566\nfunctional consequences of, 566\nprevalence of, 564\nrisk and prognostic factors for, 565\nspecifiers for, 563\nStimulant withdrawal, 484, 569\u2013570\nassociated features supporting diagnosis of, 570\ndiagnostic criteria for, 569\ndifferential diagnosis of, 570\nStroke, 46, 73, 117\nbipolar disorder and, 146, 147\ndepressive disorders and, 164, 167, 181\u2013182\nStuttering. See Childhood-onset fluency disorder \n(stuttering)\nSubstance-induced disorders, 481, 485\u2013490. See \nalso specific substances of abuse\nalcohol-related, 497\u2013503\ncaffeine-related, 503\u2013508\ncannabis-related, 516\u2013519\nhallucinogen-related, 527\u2013533\ninhalant-related, 538\u2013540\nopioid-related, 546\u2013549\nother (or unknown) substance\u2013related, 581\u2013585\nsedative-, hypnotic-, or anxiolytic-related, \n556\u2013560\nsubstance intoxication and withdrawal, 481, \n485\u2013487 ( See also Intoxication; \nWithdrawal from substance)\nassociated with use of multiple substances, \n486\ndevelopment and course of, 487\nduration of effects and, 486\nlaboratory findings associated with, \n486\u2013487\nrecording procedures for, 487\nrelated to route of administration and", "source": "dsm5.pdf"} {"id": "162bdb5e8349-1", "page_content": "486\u2013487\nrecording procedures for, 487\nrelated to route of administration and \nspeed of substance effects, 486\nsubstance/medication-induced mental \ndisorders, 481, 487\u2013490\ndevelopment and course of, 489\nfeatures of, 488\u2013489\nfunctional consequences of, 490\nrecording procedures for, 490\ntobacco-related, 575\u2013576\nSubstance intoxication delirium, 596\u2013597, 598\nSubstance/medication-ind uced anxiety disorder, \n190, 226\u2013230\nassociated features supporting diagnosis of, \n228\u2013229diagnostic criteria for, 226\u2013227\ndiagnostic features of, 228\ndiagnostic markers for, 229\ndifferential diagnosis of, 229\u2013230\nprevalence of, 229\nrecording procedures for, 227\u2013228\nSubstance/medication-induced bipolar and \nrelated disorder, 123, 142\u2013145\nassociated features supporting diagnosis of, 144\ncomorbidity with, 146\ndevelopment and course of, 144\u2013145\ndiagnostic criteria for, 142\u2013143\ndiagnostic features of, 144\ndiagnostic markers for, 145\ndifferential diagnosis of, 145\nprevalence of, 144\nrecording procedures for, 143\u2013144\nSubstance/medication-induced depressive \ndisorder, 155, 175\u2013180\ncomorbidity with, 180\ndevelopment and course of, 178\ndiagnostic criteria for, 175\u2013176\ndiagnostic features of, 177\u2013178\ndiagnostic markers for, 179\ndifferential diagnosis of, 179\u2013180\nprevalence of, 178\nrecording procedures for, 176\u2013177\nrisk and prognostic factors for, 178\u2013179", "source": "dsm5.pdf"} {"id": "162bdb5e8349-2", "page_content": "risk and prognostic factors for, 178\u2013179\nsuicide risk in, 179\nSubstance/medication-induced neurocognitive \ndisorder, 591, 603, 627\u2013632\nassociated features supporting diagnosis of, 630\ncomorbidity with, 632\ndevelopment and course of, 631\ndiagnostic criteria for, 627\u2013629\ndiagnostic features of, 629\u2013630\ndiagnostic markers for, 631\ndifferential diagnosis of, 631\nfunctional consequences of, 631\nprevalence of, 630\nrecording procedures for, 629\nrisk and prognostic factors for, 631\nSubstance/medication-induced obsessive-\ncompulsive and related disorder, 235, 236, \n257\u2013260\nassociated features supporting diagnosis of, 259\ndiagnostic criteria for, 257\u2013258\ndiagnostic features of, 259\ndifferential diagnosis of, 259\u2013260\nprevalence of, 259\nrecording procedures for, 258\u2013259\nSubstance/medication-induced psychotic \ndisorder, 89, 110\u2013115\nassociated features supporting diagnosis of, 113\ndevelopment and course of, 114", "source": "dsm5.pdf"} {"id": "699a2340ba99-0", "page_content": "Index 945\ndiagnostic criteria for, 110\u2013111\ndiagnostic features of, 112\u2013113\ndiagnostic markers for, 114\ndifferential diagnosis of, 114\u2013115\nfunctional consequences of, 114\nprevalence of, 113\nrecording procedures for, 112\nSubstance/medication-induced sexual \ndysfunction, 423, 446\u2013450\nassociated features supporting diagnosis of, \n448\u2013449\nculture-related diagnostic issues in, 449\ndevelopment and course of, 449\ndiagnostic criteria for, 446\u2013447\ndiagnostic features of, 448\ndifferential diagnosis of, 450\nfunctional consequences of, 450\ngender-related diagnostic issues in, 449\nprevalence of, 449\nrecording procedures for, 447\u2013448\nSubstance/medication-ind uced sleep disorder, \n413\u2013420\nassociated features supporting diagnosis of, \n416\u2013418\ncomorbidity with, 420\nculture-related diagnostic issues in, 418\ndevelopment and course of, 418\ndiagnostic criteria for, 413\u2013415\ndiagnostic features of, 416\ndiagnostic markers for, 419\ndifferential diagnosis of, 419\u2013420\nfunctional consequences of, 419\ngender-related diagnostic issues in, 418\nrecording procedures for, 415\u2013416\nrelationship to International Classification of \nSleep Disorders, 420\nrisk and prognostic factors for, 418\nSubstance-related and addictive disorders, \n481\u2013589\ngambling disorder, 481, 585\u2013589\nhighlights of changes fr om DSM-IV to DSM-5, \n815\nsubstance-related disorders, 481\u2013585 ( See also \nspecific substances of abuse )\nalcohol-related disorders, 490\u2013503\ncaffeine-related disorders, 503\u2013509", "source": "dsm5.pdf"} {"id": "699a2340ba99-1", "page_content": "alcohol-related disorders, 490\u2013503\ncaffeine-related disorders, 503\u2013509\ncannabis-related disorders, 509\u2013519\ndiagnoses associated with substance class, \n482\ndrug classes in, 481\nhallucinogen-related disorders, 520\u2013533\ninhalant-related disorders, 533\u2013540\nopioid-related disorders, 540\u2013550\nother (or unknown) substance\u2013related \ndisorders, 577\u2013585sedative-, hypnotic- or anxiolytic-related \ndisorders, 550\u2013560\nstimulant-related disorders, 561\u2013570\nsubstance-induced disorders, 481, 485\u2013490\nsubstance use disorders, 481, 483\u2013485, \n490\u2013585\ntobacco-related disorders, 571\u2013577\nSubstance use disorders, 481, 483\u2013485\nalcohol use disorder, 490\u2013497\ncaffeine use disorder, 792\u2013795\ncannabis use disorder, 509\u2013516\nfeatures of, 483\u2013484\ninhalant use disorder, 533\u2013538\nopioid use disorder, 541\u2013546\nother hallucinogen use disorder, 523\u2013527\nother (or unknown) substance use disorder, \n577\u2013580\nphencyclidine use disorder, 520\u2013523\nrecording procedures for, 485\nsedative, hypnotic, or anxiolytic use disorder, \n550\u2013556\nseverity and specifiers for, 484\nstimulant use disorder, 561\u2013567\ntobacco use disorder, 571\u2013574\ntolerance and withdrawal in, 484\nSubstance withdrawal delirium, 597, 598\u2013599\nSuicidal behavior disorder, 801\u2013803\ncomorbidity with, 803\nculture-related diagnostic issues in, 802", "source": "dsm5.pdf"} {"id": "699a2340ba99-2", "page_content": "comorbidity with, 803\nculture-related diagnostic issues in, 802\ndevelopment and course of, 802\ndiagnostic features of, 801\u2013802\ndiagnostic markers for, 802\nfunctional consequences of, 802\nproposed criteria for, 801\nspecifiers for, 801\nSuicide risk\nanorexia nervosa and, 343\nbipolar I disorder and, 131\nbipolar II disorder and, 138\nbody dysmorphic disorder and, 245\nbulimia nervosa and, 349\ndepressive disorder due to another medical \ncondition and, 182\ndepressive episodes with short-duration \nhypomania and, 788\ndisruptive mood dysregulation disorder and, \n158\ndissociative amnesia and, 300\ndissociative identity disorder and, 295\nmajor depressive disorder and, 164, 167\nneurobehavioral disorder associated with \nprenatal alcohol exposure and, 800\nobsessive-compulsive disorder and, 240\nopioid use disorder and, 544\nother hallucinogen intoxication and, 530", "source": "dsm5.pdf"} {"id": "de293eff5eda-0", "page_content": "946 Index\nSuicide risk (continued)\npanic attacks and, 215\npanic disorder and, 212\npersistent complex bereavement disorder and, \n791\nposttraumatic stress disorder and, 278\npsychotic disorder due to another medical \ncondition and, 118\nschizoaffective disorder and, 109\nschizophrenia and, 104\nseparation anxiety disorder and, 193\nspecific phobia and, 201\nsubstance/medication-induced depressive \ndisorder and, 180\nSusto, 836\u2013837\nTaijin kyofusho, 205, 837\nTardive akathisia, 712\nTardive dyskinesia, 22, 712\nTardive dystonia, 712\nTechnical terms, glossary of, 817\u2013831\nTic disorders, 32, 81\u201385\ncomorbidity with, 83, 85\nculture-related diagnostic issues in, 83\ndevelopment and course of, 83\ndiagnostic criteria for, 81\ndiagnostic features of, 81\u201382\ndifferential diagnosis of, 84\nfunctional consequences of, 84\ngender-related diagnostic issues in, 83, 84\nother specified tic disorder, 85\nprevalence of, 83\nrisk and prognostic factors for, 83\nspecifiers for, 81\nunspecified tic disorder, 85\nTobacco-related disorders, 481, 571\u2013577\ndiagnoses associated with, 482\nother tobacco-induced disorders, 576\ntobacco use disorder, 571\u2013574\ntobacco withdrawal, 484, 575\u2013576\nunspecified tobacco-related disorder, 577\nTobacco use disorder, 571\u2013574\nassociated features supporting diagnosis of, 573\ncomorbidity with, 574", "source": "dsm5.pdf"} {"id": "de293eff5eda-1", "page_content": "associated features supporting diagnosis of, 573\ncomorbidity with, 574\nculture-related diagnostic issues in, 574\ndevelopment and course of, 573\ndiagnostic criteria for, 571\u2013572\ndiagnostic features of, 572\u2013573\ndiagnostic markers for, 574\nfunctional consequences of, 574\nprevalence of, 573\nrisk and prognostic factors for, 573\u2013574\nspecifiers for, 572\nTobacco withdrawal, 484, 575\u2013576\nassociated features supporting diagnosis of, 575development and course of, 576\ndiagnostic criteria for, 575\ndiagnostic features of, 575\ndiagnostic markers for, 576\ndifferential diagnosis of, 576\nfunctional consequences of, 576\nprevalence of, 576\nrisk and prognostic factors for, 576\nTolerance to substance effects, 484\nTourette\u2019s disorder, 32. See also Tic disorders\ndiagnostic criteria for, 81\ndiagnostic features of, 81\u201382\nfunctional consequences of, 84\nprevalence of, 83\nrisk and prognostic factors for, 83\nTransvestic disorder, 685, 702\u2013704\nassociated features supporting diagnosis of, \n703\ncomorbidity with, 704\ndevelopment and course of, 703\u2013704\ndiagnostic criteria for, 702\ndiagnostic features of, 703\ndifferential diagnosis of, 704\nfunctional consequences of, 704\nprevalence of, 703\nspecifiers for, 703\nTrauma- and stressor-related disorders, 265\u2013290\nacute stress disorder, 265, 280\u2013286\nadjustment disorders, 265, 286\u2013289\ndisinhibited social engagement disorder, 265, \n268\u2013270", "source": "dsm5.pdf"} {"id": "de293eff5eda-2", "page_content": "disinhibited social engagement disorder, 265, \n268\u2013270\nhighlights of changes fr om DSM-IV to DSM-5, \n812\nother specified trauma- and stressor-related \ndisorder, 289\nposttraumatic stress disorder, 265, 271\u2013280\nreactive attachment disorder, 265\u2013268\nunspecified trauma- and stressor-related \ndisorder, 290\nTraumatic brain injury\nbipolar disorder and, 146\ndepressive disorders and, 181\ndissociative amnesia and, 298, 299, 301\nhoarding disorder and, 247, 250\nmajor or mild neurocognitive disorder due to, \n591, 603, 624\u2013627, 626\nassociated features supporting diagnosis \nof, 625\ncomorbidity with, 627\ndevelopment and course of, 625\u2013626\ndiagnostic criteria for, 624\ndiagnostic features of, 625\ndiagnostic markers for, 627\ndifferential diagnosis of, 627\nfunctional consequences of, 627", "source": "dsm5.pdf"} {"id": "c1049761fc1c-0", "page_content": "Index 947\nprevalence of, 625\nrisk and prognostic factors for, 626\u2013627\nspecifiers for, 625\nneurodevelopmental disorders and, 38, 39, 44, \n73\npsychotic disorders and, 99, 117\nseverity ratings for, 625, 626\ntrauma- and stressor-related disorders and, \n280, 281, 284, 286\nTremor, medication-induced, 712\nTrichotillomania (hair-pulling disorder), 235, 236, \n251\u2013254\nassociated features supporting diagnosis of, \n252\ncomorbidity with, 254\nculture-related diagnostic issues in, 253\ndevelopment and course of, 253\ndiagnostic criteria for, 251\ndiagnostic features of, 251\u2013252\ndiagnostic markers for, 253\ndifferential diagnosis of, 253\u2013254\nfunctional consequences of, 253\nprevalence of, 252\nrisk and prognostic factors for, 253\nTr\u00fang gi\u00f3, 211, 212\nUnspecified mental disorder, 15\u201316, 19\u201320, 708\ndue to another medical condition, 708\nVascular neurocognitive disorder, major or mild, \n591, 603, 621\u2013624\nassociated features supporting diagnosis of, \n622\ncomorbidity with, 624\ndevelopment and course of, 623\ndiagnostic criteria for, 621\ndiagnostic features of, 621\u2013622\ndiagnostic markers for, 623\ndifferential diagnosis of, 623\u2013624\nfunctional consequences of, 623\nprevalence of, 622\u2013623\nrisk and prognostic factors for, 623Voyeuristic disorder, 685, 686\u2013688\ncomorbidity with, 688", "source": "dsm5.pdf"} {"id": "c1049761fc1c-1", "page_content": "comorbidity with, 688\ndevelopment and course of, 688\ndiagnostic criteria for, 686\u2013687\ndiagnostic features of, 687\ndifferential diagnosis of, 688\ngender-related diagnostic issues in, 688\nprevalence of, 687\u2013688\nrisk and prognostic factors for, 688\nspecifiers for, 687\nWithdrawal from substance, 481, 485\u2013487\nalcohol, 499\u2013501\ncaffeine, 506\u2013508\ncannabis, 517\u2013519\ndelirium due to, 598\ndevelopment and course of, 487\nduration of effects and, 486\nlaboratory findings associated with, 486\u2013487\nmultiple substances, 486\nopioids, 484, 547\u2013549\nother (or unknown) substance, 583\u2013584\nrecording procedures for, 487\nrelated to route of administration and speed of \nsubstance effects, 486\nsedative, hypnotic, or anxiolytic, 484, 557\u2013560\nstimulant, 484, 569\u2013570\ntobacco, 484, 575\u2013576\nWorld Health Organization (WHO), 6, 23\nInternational Classification of Diseases (ICD), 21\nrevision process for ICD-11, 6, 10, 11\u201312\nuse of ICD-9-CM and ICD-10 codes, 12, 16, \n22, 23, 29\nInternational Classification of Functioning, \nDisability and Health (ICF), 21, 734\nWorld Health Organization Disability Assessment \nSchedule 2.0 (WHODAS), 16, 21, 734, \n745\u2013748\nadditional scoring and interpretation guidance \nfor DSM-5 users, 745\u2013746", "source": "dsm5.pdf"} {"id": "c1049761fc1c-2", "page_content": "additional scoring and interpretation guidance \nfor DSM-5 users, 745\u2013746\nfrequency of use of, 746\nscoring instructions provided by WHO for, 745", "source": "dsm5.pdf"}