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Author | Affiliation | Title | Comment | Disclosure | commentStatusID | datePublished | publishingUserID | volume | issue | page | dateSubmitted | siteID | userID | creationDate | updateDate
[NAME],  Masters student  National University |  |  | Hello, I am a student in a masters program and I am researching Bipolar assessment ools for a assessment class. I am hoping to obtain a copy of your tool SADS.   thank you   [NAME] [EMAIL] 4711 elkridge road weed, ca 96094    Conflict of Interest: None declared |  | NR |  |  | 35 | 7 | 837
IMTIAZ S. BASRAI,  MD  COUNTY OF LOS ANGELES,  [NAME], [NAME], |  |  | To the Editor:   In the March 2011 issue [NAME] et al1 present a strong case for the cost effectiveness of combined CBT + a different SSRI for depressed adolescents who did not respond to a first line SSRI in the TORDIA study.2 The authors noted that the most favorable outcomes were evident in non-abused, non-co morbid and "low levels of hopelessness" groups of youths.   The increased risk of depression in abused youths is well known.3 The authors of this important study do not do so, but others may conclude from this study that CBT and/or combined treatment is not cost-effective for depressed abused youth. It is relevant to consider the defining elements of the CBT in TORDIA vs. those used in effective CBT for abused youth such as [NAME] (TF-CBT). The major components of TORDIA CBT4 were cognitive restructuring, behavioral activation, emotional regulation, psychoeducation and mood monitoring. In contrast TF-CBT incorporates a trauma focus into all components, e.g., gradual exposure in skill-based components; development of a trauma narrative; cognitive processing of the abuse experience(s); joint child-parent sessions and parent management skills of abuse-related problems.4 These elements are essential components in the recovery process of an abused youth and may be a highly cost effective approach in ameliorating the underlying cause of depression.   One explanation for the modest outcomes in the abused subset of youths is that the TORDIA CBT was not designed to address abuse-related issues. While not assessing diagnostic depression, both TF-CBT and a related trauma-focused group CBT model significantly improved youth depressive symptoms.5-6 In light of concerns about the overuse of medications in maltreated youth7 more research is needed to determine the most effective and cost-effective treatments for these youth.   References   1. [NAME], [NAME], [NAME], [NAME], [NAME], Wagner KD, [NAME], MD; Asarnow JR, [NAME], Birmaher B, [NAME], [NAME], Mayes T, DeBar L, McCracken JT, [NAME], [NAME], [NAME], Onorato M, Zelazny J, Iyengar S, Brent D. Incremental Cost-effectiveness of Combined Therapy vs Medication Only for Youth With Selective Serotonin Reuptake Inhibitor-Resistant Depression, Treatment of SSRI-Resistant Depression in Adolescents Trial Finding. Arch. Gen. [NAME]. 2011;68:253-262.   2. Brent D, [NAME], [NAME], Wagner KD, Asarnow JR, [NAME], Vitiello B, [NAME], Iyengar S, [NAME], Birmaher B, Ryan N, [NAME], Hughes C, DeBar L, McCracken J, Strober M, [NAME] R, [NAME], [NAME], Melhem N, Porta G, Onorato M, [NAME] to Another SSRI or to Venlafaxine With or Without Cognitive Behavioral Therapy for Adolescents With SSRI-Resistant Depression- The TORDIA Randomized Controlled Trial. [NAME]. 2008;299(8):901-913.   3. [NAME], Shugart M, Craighead WE, Nemeroff CB. Neurobiological and Psychiatric Consequences of Child Abuse and Neglect. Developmental Psychobiology. 52(7), 2010.   4. [NAME], [NAME], Weersing VR, Asarnow JA, Shamseddeen W, [NAME], Berk M, Hughes JL, [NAME], Emslie GJ, [NAME], Wagner KD, Brent DA. Journal of Consulting and Clinical Psychology. 2009;Vol.77,No.6:1033-1041.   5. [NAME], Deblinger E, [NAME], [NAME]. A Multisite, Randomized Controlled Trial for Children With Sexual Abuse-Related PTSD Symptoms. J. Am Acad. Child Adolesc. Psychiatry. 2004;43:4,393-402.   6. [NAME], BD, Jaycox, LH, Kataoka, SH, [NAME], M, Tu, W, Elliott, MN, Fink, A. A mental health intervention for school children exposed to violence: A randomized controlled trial. [NAME]. 2003;290:603-611.   7. [NAME], Safer DJ, [NAME], [NAME], [NAME], Coombes P, Dubowski M, Mendez-Lewis, M. Psychotropic medication patterns among youth in foster care. Pediatrics. 2008; 121(1):e157-63.    Conflict of Interest: [NAME] and [NAME] have no potential conflicts or relevant financial interests. [NAME] has received grant support from NIMH, SAMHSA, and the Annie E Casey Foundation for research related to TF-CBTand book royalties from Guilford Press for the TF-CBT treatment book. |  | NR |  |  | 68 | 2 | 253
[NAME],  MA PhD  University College London |  |  | Gold et al1 report that schizophrenic patients store fewer items in working memory (~2.4 versus 2.75 for controls), but have no impairment of memory precision. It’s pleasing to see current cognitive neuroscience methods2-4 being applied directly to psychiatry, but for correct interpretation it’s crucial to be aware of all experimental details.  In this study, participants viewed a briefly-presented array of colored squares. After a delay, the location of one square was cued and participants clicked on a color wheel to indicate the color they recalled at that location. Responses were assumed to fall into two categories: (a) trials where the cued color was stored, so responses were distributed (with some variability) around the correct color, and (b) those where the cued color was not stored, so responses were scattered randomly around the color wheel3.  However, to respond correctly on this task, one must remember not only the colors presented, but also which color was where. This introduces a third category of ‘misreporting’ responses: (c) where the cued color is stored but, because of errors in remembering its location, participants respond with one of the other (uncued) colors presented. We have shown that these errors make up the majority of supposedly ‘random’ responses4, implying that the recall task probes limits on precision of [NAME] (for both color and location) rather than how many items are stored.  In our study, misreporting errors were evident as a peak in response frequency centered on each uncued color4. In contrast, Gold et al report this distribution was “essentially flat” in their data, leading them to discount misreporting as a significant source of error. However, this ignores a critical difference from some previous versions of the task2,4. In Gold et al, all colors to-be-remembered were separated by a minimum angle (24°) rather than selected randomly from the color wheel. As a consequence, if subjects really were responding to only the cued item – uninfluenced by uncued items – their responses would rarely fall close to an uncued color. Therefore, the predicted frequency of responses centered on each uncued color should actually show a sharp decrease.  Indeed for this distribution to be uniform, as [NAME], for four-item arrays we calculate >25% responses would need to have been misreporting errors, i.e. responding to uncued colors. Taking into account this additional source of error might result in radically different conclusions regarding working memory in schizophrenia, as for normal performance4.  Paul M Bays & Masud Husain UCL Institute of Cognitive Neuroscience & Institute of Neurology, [NAME], London, WC1N 3AR, UK  References  1. Gold JM et al. Reduced capacity but spared precision and maintenance of working memory representations in schizophrenia. [NAME]. 2010; 67, 570-577.  2. Wilken P, Ma WJ. A detection theory account of change detection. J Vis. 2004; 4, 1120-1135.  3. [NAME], Luck SJ. Discrete fixed-resolution representations in visual working memory. Nature. 2008; 453, 233-235.  4. Bays PM, Catalao RFG, [NAME] The precision of visual working memory is set by allocation of a shared resource. J Vis. 2009; 9, 7.  5. Bays, PM, [NAME] shifts of limited working memory resources in human vision. Science. 2008; 321, 851-854.  (No relevant conflicts of interest) |  | P |  |  | 67 | 5 | 570
[NAME],  MD, PhD  Cologne Center for Genomics, University of Cologne, Cologne, Germany.,  Edmund T Rolls; [NAME] |  |  | A computational neuroscience approach to schizophrenia: working memory and attentional deficits   ET Rolls, Ph.D., D.Sc.,1 [NAME], Ph.D.,2,3 and [NAME], MD, Ph.D4,5   1. Oxford Centre for Computational Neuroscience, Oxford, UK. [EMAIL]. URL: http://www.oxcns.org   2. [NAME], Universitat Pompeu Fabra, Barcelona, Spain   3. Institució [NAME] i Estudis Avançats, Barcelona, Spain   4. Cologne Center for Genomics, University of Cologne, Cologne, Germany. [EMAIL]   5. Institute of Neurosciences and Medicine, Juelich Research Centre, Juelich, Germany   Correspondence to: [NAME], Cologne Center for Genomics, University of Cologne, Cologne, Germany. [EMAIL]   We have recently described a computational neuroscience approach to understanding the symptoms and neural bases of schizophrenia.1-4 In the stochastic neurodynamical approach, we consider the stability of neural systems in different cortical areas, and how different factors affect the stability in the face of the noise or randomness introduced into the system by the almost random spiking times of neurons for a given mean firing rate. We postulate that the cognitive symptoms, including impaired short-term memory especially in the presence of distracting events, which in turn impairs attention due to instability of the short-term memory systems that provide the source of the bias for top-down attentional control,5-8 are related to instability in attractor networks in the prefrontal cortex that implement short-term memory and control attention. The stability of the attractors is reduced by factors that reduce the firing rates of the neurons when they are in the high firing rate state that normally maintains the attractor-based short-term memory. The factors in schizophrenia that may produce these effects include reductions in the efficacy of cortical glutamate systems,9 of dopamine systems acting through the D1 receptors3,10 and a reduced synaptic spine density.4 (The loss of excitatory synapses in the prefrontal cortex at adolescence is especially great in those diagnosed with schizophrenia, amounting to 60%11-13). We postulate that the negative symptoms including the reduced affect are produced by decreased firing rates (produced by similar mechanisms) in the orbitofrontal and anterior cingulate cortex,14 which are involved in emotion and motivation.14-16 We postulate that the positive symptoms are related not only to instability of the high firing rate attractor states, but also to instability of the low firing rate spontaneous states, which even in the absence of input may jump into a high firing rate state which might represent a hallucination or intrusive thought when occurring in semantic and long-term memory systems in for example the temporal lobes.1, 3, 7, 17 This instability of the low firing rate states we ascribe for example to the reduced inhibitory GABAergic functionality, especially of the cortical parvalbumin-containing neurons, in schizophrenia.9, 18, 19   It is important that computational theories, and their predictions, should be tested. We therefore welcome a recent investigation of working memory representations in chronic patients with schizophrenia who were mostly treated with clozapine.20 In line with what might be predicted from our computational approach, a reduced capacity (in terms of the number of items that could be correctly remembered) was found in a working memory task. We interpret this as less stable and more noisy attractors of the recurrent networks that implement short-term memory, making different attractors susceptible to interference, and thereby reducing the working memory capacity.7 Although these investigators did not find a greater difference between performance at a 1 s and 4 s short-term memory interval for patients, we note that at both delays the schizophrenic patients were impaired relative to controls, and that the controls themselves did not show an effect of this change in the delay. Whether one obtains an effect of different delays does of course depend on a number of factors, such as the design of the task, the task difficulty, the duration of the delay, and, importantly, whether distracting stimuli are present, for attractor neural networks with reduced firing rates become more susceptible to distracting stimuli,1 and under these conditions especially short-term memory may be impaired. We therefore believe that future studies with distracting stimuli present would be of interest, and indeed note that the same research group have reported that, as predicted, schizophrenia patients fail to overcome distractors during a working memory task, showing a deficit of top-down attentional control.21 In future studies we believe that it would also be useful to combine behavioral studies of this kind with signal to noise measures of brain function, 22-25 and to select clinically homogenous patient groups or subjects who are unmedicated or subjects at risk for schizophrenia.   References   1. [NAME], Rolls ET, [NAME] A dynamical systems hypothesis of schizophrenia. [NAME]. 2007;3(11):e228. doi:210.1371/[NAME].   2. [NAME], Rolls ET, [NAME] fluctuations in attractor networks related to schizophrenia. Pharmacopsychiatry. 2007;40:S78-S84.   3. Rolls ET, [NAME], [NAME], [NAME] models of schizophrenia and dopamine modulation in the prefrontal cortex. [NAME]. 2008;9:696-709.   4. Rolls ET, [NAME] A computational neuroscience approach to schizophrenia and its onset. [NAME] Rev. Sep 17 2010.   5. [NAME], Rolls ET, [NAME] dynamics as a principle of brain function. Progress in Neurobiology. 2009;88:1-16.   6. Rolls ET, [NAME] of Vision. Oxford: Oxford University Press; 2002.   7. Rolls ET. Memory, Attention, and Decision-Making: A Unifying Computational Neuroscience Approach. Oxford: Oxford University Press; 2008.   8. Grabenhorst F, Rolls ET. Attentional modulation of affective vs sensory processing: functional connectivity and a top-down biased activation theory of selective attention. Journal of Neurophysiology. 2010;104:1649- 1660.   9. Coyle JT, [NAME], Benneyworth M, Basu A, [NAME] the dopamine receptor: novel therapeutic targets for treating schizophrenia. [NAME]. 2010;12(3):359-382.   10. [NAME], Seamans JK. The dual-state theory of prefrontal cortex dopamine function with relevance to COMT genotypes and schizophrenia. Biological Psychiatry. Jul 10 2008;64:739-749.   11. [NAME], [NAME]. Decreased dendritic spine density on prefrontal cortical pyramidal neurons in schizophrenia. [NAME]. Jan 2000;57(1):65-73.   12. [NAME], Gilmore JH, Hamer RM, [NAME], [NAME]. [NAME] and postsynaptic density protein 95 in the human prefrontal cortex from mid-gestation into early adulthood. Neuroscience. Nov 9 2007;149(3):582-591.   13. [NAME] MR. Synapse formation and regression in the cortex during adolescence and in schizophrenia. [NAME]. Feb 16 2009;190(4 Suppl):S14-16.   14. Rolls ET. Emotion Explained. Oxford: Oxford University Press; 2005.   15. Grabenhorst F, Rolls ET. Value, pleasure, and choice systems in the prefrontal cortex. Trends in Cognitive Sciences. 2011.   16. Rolls ET, [NAME] The orbitofrontal cortex and beyond: from affect to decision-making. Progress in Neurobiology. 2008;86:216-244.   17. Rolls ET, [NAME] The Noisy Brain: Stochastic Dynamics as a Principle of Brain Function. Oxford: Oxford University Press; 2010.   18. [NAME], Hashimoto T, [NAME]. Cortical inhibitory neurons and schizophrenia. Nat Rev Neurosci. Apr 2005;6(4):312-324.   19. Benes FM. Amygdalocortical circuitry in schizophrenia: from circuits to molecules. Neuropsychopharmacology. Jan 2010;35(1):239-257.   20. Gold JM, Hahn B, [NAME], et al. Reduced capacity but spared precision and maintenance of working memory representations in schizophrenia. [NAME]. [NAME].   21. Hahn B, Robinson BM, Kaiser ST, et al. Failure of schizophrenia patients to overcome salient distractors during working memory encoding. Biol Psychiatry. Oct 1 2010;68(7):603-609.   22. [NAME], Coppola R, Goldberg TE, et al. Prefrontal broadband noise, working memory, and genetic risk for schizophrenia. Am J Psychiatry. Mar 2004;161(3):490-500.   23. [NAME], [NAME], Beckmann C, et al. Instability of prefrontal signal processing in schizophrenia: an event-related fMRI study. Am J Psychiatry. Nov 2006;163(11):1960-1968.   24. [NAME], [NAME]. Genes, dopamine and cortical signal-to-noise ratio in schizophrenia. [NAME]. Nov 2004;27(11):683-690.   25. [NAME], [NAME], Dorn H, et [NAME]. [NAME]: reduced signal-to- noise ratio and impaired phase-locking during information processing. [NAME]. May 2000;111(5):837-849.    Conflict of Interest: None declared |  | P |  |  | 67 | 5 | 570