bluuebunny/crossref_metadata_2025 huggingface dataset:
The Relationship Between Cognitive and Brain Changes in Posttraumatic Stress Disorder
Authors: BREMNER J. DOUGLAS
Published: August 2006

Abstract: Preclinical studies show that stress is associated with changes in structure of the hippocampus, a brain area that plays a critical role in memory, inhibition of neurogenesis, and memory deficits. Studies in animals showed that both serotonin reuptake inhibitors (SSRIs) and the epilepsy medication phenytoin (dilantin) block the effects of stress on the hippocampus. Imaging studies in posttraumatic stress disorder (PTSD) have found smaller volume of the hippocampus as measured with magnetic resonance imaging (MRI) in patients with PTSD related to both combat and childhood abuse. These patients were also found to have deficits in memory on neuropsychological testing. Functional imaging studies using positron emission tomography (PET) found decreased hippocampal activation with memory tasks. In an initial study, we found that a year of treatment with paroxetine led to a 5% increase in hippocampal volume and a 35% increase in memory function. A second study showed that phenytoin was efficacious for symptoms of PTSD and led to a significant 6% increase in both right hippocampal and right whole brain volume, with no significant change in memory. These studies suggest that medications may counteract the effects of stress on the brain in patients with PTSD.
Neuroimaging Studies of Emotional Responses in PTSD
Authors: LIBERZON ISRAEL , MARTIS BRIAN
Published: August 2006

Abstract:  Neuroimaging research offers a powerful and noninvasive means to understand healthy as well as dysregulated emotional processing in healthy subjects and PTSD patients. Functional neuroimaging findings suggest specific roles for subregions of the medial prefrontal (mPFC), orbito frontal (OFC), anterior cingulate (ACC), and insular cortices as well as the sublenticular extended amygdala (SLEA) and hippocampus in various components of emotional processing. Some of the same regions appear to be associated with emotional response to trauma, and with symptom formation in PTSD. Neuroimaging findings of emotional processing in healthy subjects and PTSD patients are discussed, addressing the specific roles of cortical regions like mPFC, ACC, and insula, and their potential contribution to PTSD pathophysiology. Processes of cognitive–emotional interactions and social emotions are discussed in an attempt to synthesize the prefrontal findings in healthy subjects and PTSD patients. Further links between functional neuroanatomy of emotional responses and neuroendocrine stress regulation are proposed.
Toward a Psychobiology of Posttraumatic Self‐Dysregulation
Authors: FREWEN PAUL A. , LANIUS RUTH A.
Published: August 2006

Abstract:  In this article we propose a psychobiological model that construes PTSD fundamentally as a disorder of affect arousal regulation. Neuroimaging studies of emotion regulation in psychologically healthy populations are initially reviewed as a framework for interpreting the results of previously published investigations of the neural correlates of PTSD reexperiencing and dissociation. We then apply the emotion regulation framework toward understanding other perturbed affective states in PTSD. We conclude by discussing the clinical significance of this framework for psychological assessment and treatment of posttrauma psychopathology.
Advances in Understanding Neuroendocrine Alterations in PTSD and Their Therapeutic Implications
Authors: YEHUDA RACHEL
Published: August 2006

Abstract:  The findings from investigations of the neuroendocrinology of posttraumatic stress disorder (PTSD) have highlighted alterations that have not historically been associated with pathologic processes, and have, accordingly, raised several questions about the nature of the findings and their relationship to PTSD. The most infamous of these observations‐–low cortisol levels‐–has been the subject of much discussion and scrutiny because the finding has been both counterintuitive, and not uniformly reproducible. This fact notwithstanding, novel therapeutic approaches to the treatment of PTSD are in large part predicated on the assumption that glucocorticoid levels may be lower in PTSD. This article summarizes important neuroendocrine observations in cortisol and provides strategies for understanding what has emerged over the past two decades, to be a complex and sometimes contradictory literature.
Immune Function in PTSD
Authors: ALTEMUS MARGARET , DHABHAR FIRDAUS S. , YANG RUIRONG
Published: August 2006

Abstract:  Disturbed regulation of both the hypothalamic‐pituitary‐adrenal (HPA) axis and sympathoadrenomedullary system in posttraumatic stress disorder (PTSD) suggests that immune function, which is modulated by these systems, may also be dysregulated. Two dermatologic, in vivo measures of immune function, delayed‐type hypersensitivity (DTH) and skin barrier function recovery, were examined in female subjects with PTSD and compared to measures in healthy female comparison subjects. In addition, at the time of DTH test placement, circulating numbers of lymphocyte subtypes were assessed. In separate studies, the effects of acute psychological stress on DTH and skin barrier function recovery were examined in healthy volunteer subjects. Both DTH and barrier function recovery were enhanced in women with PTSD. These findings contrast with the effects of acute stress in healthy control subjects, which was associated with suppression of DTH responses and skin barrier function recovery. There was no difference between subjects with PTSD and healthy control subjects in proportions of circulating lymphocyte subsets or in expression of the lymphocyte markers CD62, CD25, and CD45RO/CD45RA. These results suggest that cell‐mediated immune function is enhanced in individuals with PTSD, a condition that imposes chronic physiologic and mental stress on sufferers. These findings contrast with suppression of DTH and skin barrier function recovery in healthy volunteers in response to acute psychological stress.
Alterations in Stress Reactivity After Long‐Term Treatment with Paroxetine in Women with Posttraumatic Stress Disorder
Authors: VERMETTEN ERIC , VYTHILINGAM MEENA , SCHMAHL CHRISTIAN , DE KLOET CARIEN , SOUTHWICK STEVEN M. , CHARNEY DENNIS S. , BREMNER J. DOUGLAS
Published: August 2006

Abstract:  Posttraumatic stress disorder (PTSD) is typically accompanied by both acute and chronic alterations in the stress response. These alterations have mostly been described in individuals under baseline conditions, but studies have also used a challenge model to assess the role of the hypothalamic‐pituitary‐adrenal (HPA) axis in the stress response. The purpose of this article was to assess the effect of long‐term treatment with the selective reuptake inhibitor (SSRI), paroxetine, on stress reactivity in patients with PTSD. We assessed diurnal salivary cortisol and urinary cortisol as well as cortisol, heart rate, and behavioral responses to a standardized cognitive stress challenge, in 13 female patients with chronic PTSD before and after 12 months of paroxetine treatment. Treatment resulted in a significant decrease in PTSD symptoms. Twenty‐four‐hour urinary cortisol was lower compared to base line after successful treatment. Treatment resulted in a decrease of salivary cortisol levels on all time points on a diurnal curve. Despite similar stress perception, cortisol response to the cognitive stress challenge resulted in a 26.5% relative decrease in stress‐induced salivary cortisol with treatment. These results suggest that successful treatment with SSRI in chronic PTSD is associated with a trend for a decrease in baseline diurnal cortisol and with reduced cortisol reactivity to stress.
Neuroendocrine Regulation of Sleep Disturbances in PTSD
Authors: NEYLAN THOMAS C. , OTTE CHRISTIAN , YEHUDA RACHEL , MARMAR CHARLES R.
Published: August 2006

Abstract:  Studies that have conducted quantitative analysis of the sleep electroencephalogram (EEG) have demonstrated decreased delta sleep in PTSD. Elevations in both hypothalamic (neurohormonal) and extrahypothalamic (neurotransmitter) corticotropin releasing factor (CRF) release is associated with decreased delta sleep activity. We present data from several studies examining the effect of metyrapone administration on the sleep EEG in PTSD and control subjects. Plasma ACTH, cortisol, and 11‐deoxycorticol were obtained the morning following polysomnographic sleep recordings before and after metyrapone administration. Delta sleep was measured by period amplitude analysis. The results demonstrate: a) decreased delta sleep in male subjects with PTSD; b) metyrapone administration resulted in an activation of the sleep EEG and a robust decrease in quantitative delta sleep; c) the sleep and endocrine (increase in ACTH) responses to metyrapone were significantly decreased in PTSD in two different study samples; and d) the metyrapone‐related disruption to sleep in both samples was predicted by the increase in ACTH measured the following morning. These findings strongly suggest that the delta sleep response to metyrapone is a measure of the brain response to a hypothalamic CRF challenge. The attenuated delta sleep and endocrine response to metyrapone challenge in PTSD is consistent with a model of enhanced negative feedback regulation or downregulation of CRF receptors in an environment of chronically increased CRF activity.
Glucocorticoid‐Induced Inhibition of Memory Retrieval
Authors: DE QUERVAIN DOMINIQUE J.‐F.
Published: August 2006

Abstract:  Posttraumatic stress disorder (PTSD) is characterized by traumatic memories that can manifest as daytime recollections, traumatic nightmares, or flashbacks in which components of the event are relived. These symptoms reflect excessive retrieval of traumatic memories that often retain their vividness and power to evoke distress for decades or even a lifetime. We have reported previously that elevated glucocorticoid levels inhibit memory retrieval in animals and healthy human subjects. We therefore hypothesized that the administration of cortisol might also inhibit the retrieval of traumatic memories in patients with PTSD. In a recent pilot study, we found the first evidence to support this hypothesis. During a 3‐month observation period, low‐dose cortisol (10 mg/day) was administered orally for 1 month to three patients with chronic PTSD using a double‐blind, placebo‐controlled, crossover design. In each patient investigated, there was a significant treatment effect with cortisol‐related reductions in one of the daily rated symptoms of traumatic memories without causing adverse side effects. Future studies with more patients and longer treatment periods are required to evaluate the efficacy of cortisol treatment for PTSD.
Neurobiological Research on Sleep and Stress Hormones in Epidemiological Samples
Authors: BRESLAU NAOMI
Published: August 2006

Abstract:  Information on stress hormones and sleep disturbance in posttraumatic stress disorder (PTSD) is on the basis of clinical samples and samples of other selective populations. Neurobiological studies nested in a large epidemiological community sample were recently reported. PTSD was compared with several control groups, defined by exposure and by diagnostic classification on the basis of comorbidity with Major Depression. Key findings were: (a) higher mean catecholamines in persons with PTSD versus controls; (b) no difference in mean cortisol between groups; (c) comorbid PTSD and depression was associated with higher cortisol in women; and (d) polysomnographic studies failed to detect clinically relevant sleep disturbance in PTSD, although an increase in brief arousal from REM was detected. Methodological questions raised by discrepancies between biological findings from epidemiologic versus clinical and other selective samples are discussed.
Social Context and the Psychobiology of Posttraumatic Stress
Authors: GALEA SANDRO , ACIERNO RON , RUGGIERO KENNETH , RESNICK HEIDI , TRACY MELISSA , KILPATRICK DEAN
Published: August 2006

Abstract:  A growing body of research is identifying the molecular and genetic correlates of psychopathology and holds tremendous promise in suggesting the biologic mechanisms that may explain emergent posttraumatic stress disorder (PTSD) phenotypes. Another body of research has begun to consider how elements of the social context may influence the risk of PTSD. It is likely that the social context and molecular/genetic factors jointly determine the risk of PTSD and as such scientific inquiry that considers the interrelationship of these factors stands to advance the field. However, there are particular conceptual and methodologic challenges to conducting and designing studies that adequately assess both the social context and the biologic determinants of PTSD. Much of the current research exploring the biology of PTSD is conducted with highly selective samples that were recruited on the basis of strict phenotypic or medical history criteria. In contrast, population‐based sampling represents an opportunity to obtain heterogenous samples that better represent the population distribution of relevant molecular, genotypic, and phenotypic parameters of interest. These sampling strategies also allow researchers to consider the role of the social context and in turn, how the social context influences the molecular determinants of PTSD. An example of our own work illustrates the feasibility of the population‐based sampling approach.
Developmental Epidemiology of PTSD
Authors: KOENEN KARESTAN C.
Published: August 2006

Abstract:  Epidemiologic and meta‐analytic studies point to consistent effects of pretrauma factors on risk for posttraumatic stress disorder (PTSD). However, our understanding of why only some individuals are vulnerable to the adverse effects of traumatic events remains limited. This article argues that a developmentally informed approach to the epidemiology of PTSD is needed to move this understanding forward. However, there are many challenges to such an approach including the historic conceptualization of PTSD as a normative response to traumatic events, the almost exclusive reliance on retrospective self‐report of PTSD risk factors, and the lack of attention to current knowledge of human development in selecting risk factors for epidemiologic studies. The developmental construct of self‐regulation may provide a key mechanism for understanding the effects of pretrauma factors on the vulnerability to PTSD. Pretrauma factors shown to have consistent effect on risk for PTSD in meta‐analytic studies include familial psychopathology, child abuse, and preexisting psychopathology. A preliminary framework integrating these pretrauma factors with self‐regulation as a central mechanism in the etiology of PTSD is presented. The implications of a developmentally informed epidemiologic approach to PTSD for theory, research, and practice are discussed.
Clinical Implications of Neuroscience Research in PTSD
Authors: VAN DER KOLK BESSEL A.
Published: August 2006

Abstract: The research showing how exposure to extreme stress affects brain function is making important contributions to understanding the nature of traumatic stress. This includes the notion that traumatized individuals are vulnerable to react to sensory information with subcortically initiated responses that are irrelevant, and often harmful, in the present. Reminders of traumatic experiences activate brain regions that support intense emotions, and decrease activation in the central nervous system (CNS) regions involved in (a) the integration of sensory input with motor output, (b) the modulation of physiological arousal, and (c) the capacity to communicate experience in words. Failures of attention and memory in posttraumatic stress disorder (PTSD) interfere with the capacity to engage in the present: traumatized individuals “lose their way in the world.” This article discusses the implications of this research by suggesting that effective treatment needs to involve (a) learning to tolerate feelings and sensations by increasing the capacity for interoception, (b) learning to modulate arousal, and (c) learning that after confrontation with physical helplessness it is essential to engage in taking effective action.
Establishing an Agenda for Translational Research on PTSD
Authors: MILLER MELINDA M. , McEWEN BRUCE S.
Published: August 2006

Abstract:  Animal research on brain mechanisms involved in psychiatric disorders presents an enormous challenge because it is impossible to precisely model symptoms of a human disorder in a rat or mouse. Nevertheless, there are uses for animal models as long as the limitations are recognized. Animal research related to posttraumatic stress disorder (PTSD) points to acute and chronic stressors, such as restraint or immobilization as being the most relevant stimuli to study how neural and endocrine systems are affected, both immediately and long term. Of particular relevance are the onset and duration of effects of stressors on brain areas subserving emotional memories, such as the amygdala, prefrontal cortex, and hippocampus. The hippocampus plays a role in memory and in vegetative functions of the body. The hippocampus receives input from the amygdala and its function in spatial memory is altered by amygdala activity. Repeated stress in the rat suppresses dentate gyrus neurogenesis and causes dendrites of hippocampal and medial prefrontal cortical neurons to shrink. Conversely, it causes basolateral amygdala neurons to increase in dendritic complexity and sprout new synapses. Repeated stress also increases fear and aggression, reduces spatial memory, and alters contextual fear conditioning. Antidepressants and mood stabilizers have diverse effects on these processes. New data indicate that a single stress episode can cause a delayed alteration in synapse formation in the basolateral amygdala without changing dendritic length and branching. Further studies are examining the structural changes in prefrontal cortex and hippocampus as a result of single traumatic stressors, which may reflect the functional interactions with the amygdala. Together with mechanistic studies of the role of adrenal glucocorticoids and catecholamines, these results may tell us how the brain is shaped by acute and repeated uncontrollable stress in ways that then can be investigated in human anxiety disorders.
Neurobiological Consequences of Early Stress and Childhood Maltreatment: Are Results from Human and Animal Studies Comparable?
Authors: TEICHER MARTIN H. , TOMODA AKEMI , ANDERSEN SUSAN L.
Published: August 2006

Abstract:  Recent studies have reported an association between exposure to childhood abuse or neglect and alterations in brain structure or function. One limitation of these studies is that they are correlational and do not provide evidence of a cause–effect relationship. Preclinical studies on the effects of exposure to early life stress can demonstrate causality, and can enrich our understanding of the clinical research if we hypothesize that the consequences of early abuse are predominantly mediated through the induction of stress responses. Exposure to early abuse and early stress has each been associated with the emergence of epileptiform electroencephalogram (EEG) abnormalities, alterations in corpous callosum area, and reduced volume or synaptic density of the hippocampus.
Further, there is evidence that different brain regions have unique periods when they are maximally sensitive to the effects of early stress. To date, preclinical studies have guided clinical investigations and will continue to provide important insight into studies on molecular mechanisms and gene–environment interactions.
Toward an Animal Model of Posttraumatic Stress Disorder
Authors: SIEGMUND ANJA , WOTJAK CARSTEN T.
Published: August 2006

Abstract:  Posttraumatic stress disorder (PTSD) belongs to the most frequent anxiety disorders. Despite a broad body of evidence concerning neurobiological correlates of this illness, the pathomechanisms of PTSD are still poorly understood. This illustrates the need to establish animal models of this disorder. Recently, PTSD model has become a somewhat fashionable term used in animal studies for almost every stress‐induced behavioral alteration. Only few cases, however, reflect the human disorder closely enough to deserve this term. Systematic research requires valid animal modeling with clearly defined criteria. This article outlines and discusses criteria for prospective PTSD models, based on a theoretical framework that emphasizes the involvement of both associative and nonassociative memory processes in the development and maintenance of PTSD.
The Contribution of an Animal Model Toward Uncovering Biological Risk Factors for PTSD
Authors: COHEN HAGIT , MATAR MICHAEL A. , RICHTER‐LEVIN GAL , ZOHAR JOSEPH
Published: August 2006

Abstract:  Clinical studies of posttraumatic stress disorder (PTSD) have elicited proposed risk factors for developing PTSD in the aftermath of stress exposure. Generally, these risk factors have arisen from retrospective analysis of premorbid characteristics of study populations. A valid animal model of PTSD can complement clinical studies and help to elucidate issues, such as the contribution of proposed risk factors, in ways which are not practicable in the clinical arena. Important qualities of animal models include the possibility to conduct controlled prospective studies, easy access to postmortem brains, and the availability of genetically manipulated subjects, which can be tailored to specific needs. When these qualities are further complemented by an approach which defines phenomenologic criteria to address the variance in individual response pattern and magnitude, enabling the animal subjects to be classified into definable groups for focused study, the model acquires added validity. This article presents an overview of a series of studies in such an animal model which examine the contribution of two proposed risk factors and the value of two early postexposure pharmacological manipulations on the prevalence rates of subjects displaying an extreme magnitude of behavioral response to a predator stress paradigm.
Glucocorticoid “Programming” and PTSD Risk
Authors: SECKL JONATHAN R. , MEANEY MICHAEL J.
Published: August 2006

Abstract:  Epidemiological data have linked an adverse fetal environment with increased risks of cardiovascular, metabolic, neuroendocrine, and psychiatric disorders in adulthood. Prenatal stress and/or glucocorticoid excess might underlie this link. In animal models, prenatal stress, glucocorticoid exposure or inhibition/knockout of 11ß‐hydroxysteroid dehydrogenase type 2 (11ß‐HSD‐2), the feto‐placental barrier to maternal glucocorticoids, reduces birth weight and causes permanent hypertension, hyperglycemia, increased hypothalamic‐pituitary‐adrenal (HPA) axis activity and behavior resembling of anxiety. In humans, 11ß‐HSD‐2 gene mutations cause low birth weight and placental 11ß‐HSD‐2 activity correlates directly with birth weight and inversely with infant blood pressure. Low birth weight babies have higher plasma cortisol levels throughout adult life, indicating HPA programming. In human pregnancy, severe maternal stress affects the offspring HPA axis and associates with neuropsychiatric disorders. Posttraumatic stress disorder (PTSD) appears to be a variable in the effects. Intriguingly, some of these effects appear to be ‘inherited’ into a further generation, itself unexposed to exogenous glucocorticoids at any point in the lifespan from fertilization, implying epigenetic marks persist into subsequent generation(s). Overall, the data suggest that prenatal exposure to excess glucocorticoids programs peripheral and CNS functions in adult life, predisposing to some pathologies, perhaps protecting from others, and these may be transmitted perhaps to one or two subsequent generations.
Developing an Agenda for Translational Studies of Resilience and Vulnerability Following Trauma Exposure
Authors: YEHUDA RACHEL , FLORY JANINE D. , SOUTHWICK STEVEN , CHARNEY DENNIS S.
Published: August 2006

Abstract:  Here we outline a translational research agenda for studies of resilience, defined as the process of adapting well in the face of adversity or trauma. We argue that an individual differences approach to the study of resilience, in which the full range of behavioral and biological responses to stress exposure is examined can be applied across human samples (e.g., people who have developed psychopathology versus those who have not; people who have been exposed to trauma versus those who have not) and even, in some cases, across species. We delineate important psychological resilience‐related factors including positive affectivity and optimism, cognitive flexibility, coping, social support, emotion regulation, and mastery. Key brain regions associated with stress‐related psychopathology have been identified with animal models of fear (e.g., extinction and fear conditioning; memory reconsolidation) and we describe how these regions can be studied in humans using neuroimaging technology. Finally, we cite recent research identifying neuroendocrine markers of resilience and recovery in humans (e.g., neuropeptide Y [NPY], dehydroepiandrosterone [DHEA]) that can also be measured, in some cases, in other species. That exposure to adversity or trauma does not necessarily lead to impairment and the development of psychopathology in all people is an important observation. Understanding why this is so will provide clues for the development of therapeutic interventions for those people who do develop stress‐related psychopathology, or even for the prevention of adverse outcomes.
Alexithymia in PTSD
Authors: FREWEN PAUL A. , PAIN CLAIRE , DOZOIS DAVID J. A. , LANIUS RUTH A.
Published: August 2006

Abstract:  Two studies examined correlates of alexithymia in posttraumatic stress disorder (PTSD). In study 1 (n= 77 individuals with PTSD and 45 controls) Toronto alexithymia scale (TAS‐20) scores were positively correlated with PTSD symptoms, dissociation, and childhood abuse and neglect. In study 2, TAS‐20 scores were examined as correlates of functional magnetic resonance imaging (fMRI) blood oxygen level dependent (BOLD) response to trauma script imagery. In 16 controls, TAS‐20 scores correlated positively with response in medial prefrontal cortex (mPFC), and negatively with response in anterior cingulate cortex (ACC) and thalamus. In 26 individuals with PTSD, TAS‐20 scores correlated positively with response in insula, posterior cingulate cortex (PCC), and thalamus, and negatively with response in ACC.
Neuroimaging of Pain Perception in Dutch Veterans With and Without Posttraumatic Stress Disorder: Preliminary Results
Authors: GEUZE ELBERT , VERMETTEN ERIC , JOCHIMS ANJA , BOHUS MARTIN , SCHMAHL CHRISTIAN , WESTENBERG HERMAN
Published: August 2006

Abstract:  This article presents initial data on the application of a pain protocol in posttraumatic stress disorder (PTSD) to assess the neural circuitry that is involved in the disorder, with a special interest in the role of the anterior cingulate cortex (ACC). Preliminary analysis demonstrated a specific and differentiated role for the ACC. Fixed affects analysis demonstrated that stimuli subjectively perceived as more painful resulted in increased activation of the caudal ACC, whereas less painful stimuli resulted in increased activation of the rostral ACC in both groups.
The Relationship Between Hippocampal Volume and Declarative Memory in a Population of Combat Veterans With and Without PTSD
Authors: TISCHLER LISA , BRAND SARAH R. , STAVITSKY KARINA , LABINSKY ELLEN , NEWMARK RANDALL , GROSSMAN ROBERT , BUCHSBAUM MONTE S. , YEHUDA RACHEL
Published: August 2006

Abstract:  Both reduced hippocampal volume and cognitive alterations have been found in posttraumatic stress disorder (PTSD). The purpose of this article was to examine the relationship between hippocampal volume, combat exposure, symptom severity, and memory performance in a sample of combat veterans with and without a history of PTSD. Subjects were 33 male veteran volunteers (16 PTSD+, 17 PTSD−) who underwent an MRI and neuropsychological testing with the California Verbal Learning Test (CVLT), a measure of declarative memory. Relationships between hippocampal volume (i.e., right + left hippocampal volume/whole brain volume) and performance on the CVLT were determined using partial correlational analysis controlled for age and Wechsler Adult Intelligence Scale, Third Edition (WAIS‐III) vocabulary scores. Percent hippocampal volume for the entire sample was positively associated with several aspects of memory performance as reflected by the CVLT. In the PTSD+ group, CVLT performance was negatively correlated with lifetime, but not current CAPS symptoms. CVLT performance appears to be strongly correlated with hippocampal volume in a group of trauma survivors with and without PTSD. Insofar as CVLT performance in the PTSD group was negatively associated with worst episode, but not to current PTSD symptoms, memory performance in combat veterans may reflect some aspect of risk related to the magnitude of the psychological response to trauma, rather than current symptoms that may be interfering with cognitive performance. It will be of interest to study cognitive abilities that may relate to the likelihood of specific PTSD symptoms and to track changes in CVLT performance and hippocampal volume over time in persons with and without a history of trauma exposure.
Moderators of PTSD‐Related Psychophysiological Effect Sizes
Authors: POLE NNAMDI
Published: August 2006

Abstract:  Though many studies have reported psychophysiological differences between individuals with and without posttraumatic stress disorder (PTSD), there have been inconsistencies in the magnitude of observed effect sizes across studies. Following a meta‐analysis of the effect of current PTSD on psychophysiology during resting baseline, startle, standard trauma cue, and idiographic trauma cue studies, the author examined moderators of the obtained effect sizes. Results revealed that, among several moderators examined, greater PTSD effects on psychophysiology were most consistently associated with trauma‐free control groups, greater PTSD symptom severity, and studies using earlier rather than more recent diagnostic criteria for PTSD (e.g., DSM‐III versus DSM‐IV).
Association Between Alexithymia and Neuroendocrine Response to Psychological Stress in Police Academy Recruits
Authors: McCASLIN SHANNON E. , INSLICHT SABRA S. , NEYLAN THOMAS C. , METZLER THOMAS J. , OTTE CHRISTIAN , LENOCI MARYANN , HENN‐HAASE CLARE , BEST SUZANNE , YEHUDA RACHEL , MARMAR CHARLES R.
Published: August 2006

Abstract:  Alexithymia has been associated with both posttraumatic stress disorder and neuroendocrine responses to stress. This study examined the relationship of alexithymia to salivary cortisol and 3‐methoxy‐4‐hydroxy‐phenylglycol (MHPG) in a sample of police academy recruits exposed to a video stress challenge. Alexithymia scores were negatively associated with catecholamine response to the video challenge but no association was found between alexithymia scores and cortisol reactivity.
Increased Cortisol in Women With Intimate Partner Violence‐Related Posttraumatic Stress Disorder
Authors: INSLICHT SABRA S. , MARMAR CHARLES R. , NEYLAN THOMAS C. , METZLER THOMAS J. , HART STACEY L. , OTTE CHRISTIAN , MCCASLIN SHANNON E. , LARKIN GREGORY LUKE , HYMAN KELLY B. , BAUM ANDREW
Published: August 2006

Abstract:  Intimate partner violence (IPV) is a chronic and recurrent traumatic stressor associated with PTSD; however, its biological correlates are not well understood. This study examined diurnal salivary cortisol and platelet catecholamines in women with lifetime IPV‐related PTSD and in women exposed to IPV who did not develop PTSD. Cortisol was elevated in women with lifetime PTSD compared to controls. No differences were found for platelet catecholamines.
Differential Effects of Subtypes of Trauma Symptoms on Couples' Hypothalamus‐Pituitary‐Adrenal (HPA) Axis Reactivity and Recovery in Response to Interpersonal Stress
Authors: POWERS SALLY I. , GUNLICKS MEREDITH , LAURENT HEIDEMARIE , BALABAN SUSAN , BENT EILEEN , SAYER ALINE
Published: August 2006

Abstract:  This article examined the relation of five subtypes of trauma symptoms to hypothalamus‐pituitary‐adrenal (HPA) functioning as assessed with salivary cortisol before, during, and after an experimentally induced interpersonal conflict task in 194 heterosexual young adult couples. Trauma history and symptoms were assessed through structured clinical interviews and standardized self‐report measures. Hierarchical linear modeling was used to analyze the effects of trauma symptoms on trajectories of cortisol reactivity to and recovery from the interpersonal stress. Trauma‐related anxiety, depression, sleep disturbances, and dissociation significantly predicted cortisol reactivity and recovery. Trauma‐related anxiety, sleep disturbances, and sexual problems significantly predicted partners' cortisol reactivity to interpersonal stress.
Effect of High‐Dose Cortisol on Memory Functions
Authors: BRUNNER ROMUALD , SCHAEFER DANIELE , HESS KLAUS , PARZER PETER , RESCH FRANZ , SCHWAB STEFAN
Published: August 2006

Abstract:  Although research indicates that hightened glucocorticoid levels impair long‐term memory functions and may inhibit traumatic memory retrieval in humans, the impact of acutely elevated glucocorticoid levels on learning and attentional functions is still unclear. Furthermore, the effect of glucocorticoids on executive functions as well as the recovery from long‐term memory deficits is insufficiently studied. The present study examined memory functions in patients with acute exacerbation of neurological diseases (multiple sclerosis, acute optic neuritis), who were treated with a high dose of glucocorticoids. All patients demonstrated a reversible impairment of long‐term memory functions, whereas measures of short‐term memory, attentional functions, and alertness remained unaffected. These findings indicate a selective cognitive disturbance, providing further evidence that the memory deficits reflect a receptor‐mediated effect of glucocorticoids on hippocampal function thereby supporting a potential association of stress‐induced elevated cortisol levels and memory disturbances in trauma‐related psychiatric disorders (psychogenic amnesia, PTSD).
Ecological Study of Sleep Disruption in PTSD
Authors: GERMAIN ANNE , HALL MARTICA , KATHERINE SHEAR M. , NOFZINGER ERIC A. , BUYSSE DANIEL J.
Published: August 2006

Abstract:  Laboratory‐based sleep studies have yielded inconsistent results regarding the presence and nature of objective sleep anomalies in posttraumatic stress disorder (PTSD). This pilot study aimed at assessing sleep in adult crime victims with PTSD by using in‐home polysomnography. Compared to healthy archival subjects, PTSD subjects showed longer sleep latency, reduced total sleep time, and increased duration of nocturnal awakening. Quantitative electroencephalography (EEG) measures of delta and beta activity also differed in PTSD and healthy subjects. These preliminary findings suggest that ambulatory methods can capture objective signs of sleep disruption, and corroborate subjective complaints of disrupted sleep in PTSD.
Allostatic Load in Women With and Without PTSD Symptoms
Authors: GLOVER DORIE A.
Published: August 2006

Abstract:  Allostatic load (AL) is the cumulative physiological “cost” of prolonged stress. An AL composite measure successfully predicts morbidity and mortality among the elderly but has not been reported in “high stress” samples with postraumatic stress disorder (PTSD). Accordingly, AL was measured in mothers (ages 29–55) of pediatric cancer survivors and control mothers of healthy children. A significant “dose‐response” pattern (high to low AL) emerged: cancer mothers meeting all PTSD criteria, cancer mothers with no/low symptoms, and controls, respectively. Results indicate elevated AL can be detected in relatively young women with high stress histories, and particularly those with PTSD.
The ACTH Response to Dexamethasone in Persian Gulf War Veterans
Authors: GOLIER JULIA A. , LEGGE JULIANA , YEHUDA RACHEL
Published: August 2006

Abstract:  The basis of postdeployment health symptoms in Gulf War veterans remains poorly understood. Alterations in the feedback regulation of the hypothalamic‐pituitary‐adrenal (HPA) axis have been demonstrated in posttraumatic stress disorder (PTSD) and other bodily disorders related to stress. The objective of this article was to examine whether similar HPA axis alterations are related to Gulf War deployment, postdeployment health symptoms, or PTSD. Plasma adrenocorticotropic hormone (ACTH) was measured on consecutive mornings at 08:00 h before and after a low dose of oral dexamethasone (DEX) at 23:00 h in Gulf War veterans with PTSD (n= 14), Gulf War veterans without PTSD (n= 11), and healthy veterans never deployed to a war zone (n= 12). Both Gulf War veterans with PTSD and Gulf War veterans without PTSD had significantly lower post‐DEX ACTH levels than the nonexposed veterans, in the absence of group differences in basal ACTH or DEX levels. Among Gulf War veterans, post‐DEX ACTH levels were significantly associated with musculoskeletal symptoms. Gulf War deployment and postdeployment health symptoms appear to be associated with alterations in feedback regulation of the pituitary gland that suggests a possible common link between postdeployment health symptoms and other chronic stress‐related conditions.
The Effect of Maternal PTSD Following in Utero Trauma Exposure on Behavior and Temperament in the 9‐Month‐Old Infant
Authors: BRAND SARAH R. , ENGEL STEPHANIE M. , CANFIELD RICHARD L. , YEHUDA RACHEL
Published: August 2006

Abstract:  In view of evidence of in utero glucocorticoid programming, and our prior observation of lower cortisol levels in 9‐month‐old infants of mothers with posttraumatic stress disorder (PTSD) compared to mothers without PTSD, we undertook an examination of the effect of in utero maternal stress, as determined by PTSD symptom severity, and maternal cortisol levels on behavioral outcomes in the infant. Methods: Ninety‐eight pregnant women directly exposed to the World Trade Center (WTC) collapse on 9/11 provided salivary cortisol samples and completed a PTSD symptom questionnaire and a behavior rating scale to measure infant temperament, including distress to limitations, and response to novelty. Results: Mothers who developed PTSD in response to 9/11 had lower morning and evening salivary cortisol levels, compared to mothers who did not develop PTSD. Maternal morning cortisol levels were inversely related to their rating of infant distress and response to novelty (i.e., loud noises, new foods, unfamiliar people). Also, mothers who had PTSD rated their infants as having greater distress to novelty than did mothers without PTSD (t= 2.77, df= 61, P= 0.007). Conclusion: Longitudinal studies are needed to determine how the association between maternal PTSD symptoms and cortisol levels and infant temperament reflect genetic and/or epigenetic mechanisms of intergenerational transmission.
Longitudinal Assessment of Dissociation in Holocaust Survivors With and Without PTSD and Nonexposed Aged Jewish Adults
Authors: LABINSKY ELLEN , BLAIR WILLIAM , YEHUDA RACHEL
Published: August 2006

Abstract:  The trajectory of posttraumatic stress disorder (PTSD) and PTSD‐related symptoms in relation to aging is not well understood. We previously observed higher levels of dissociation as measured by the Dissociative Experiences Scale (DES) among older Holocaust survivors with, compared to those without, PTSD, though scores on the DES in Holocaust survivors were markedly lower than those that had been reported for younger cohorts. We undertook a longitudinal evaluation of dissociation in Holocaust survivors.
Twenty‐six Holocaust survivors with current PTSD, 30 Holocaust survivors without current PTSD, and 19 nonexposed were evaluated at the initial evaluation and subsequently 8.11 years later. Repeated measures analysis of variance (ANOVA) on the DES scores from these times demonstrated a significant main effect for time and a significant group by time interaction, reflecting a marked decline in Holocaust survivors, particularly those with PTSD. Controlling for age obliterated the effect of time, but not the group by time interaction. A similar pattern was shown with The Clinician Administered PTSD Scale (CAPS) scores.
Different symptoms related to PTSD show different trajectories of change with age, with dissociation appearing to be less prominent with age.
World War II Never Ended in My House
Authors: CAVIN SUSAN
Published: August 2006

Abstract:  The author conducted sociological interviews of 12 OSS spies (7 male, 5 female) who were operatives in France during World War II (WW II). The Office of Strategic Services (OSS) existed from 1941 to 1945 and was later renamed the CIA in 1947. This paper includes family studies of six close relatives of OSS vets and observation of 400 OSS veterans at the 50th anniversary of WW II
. Three of the 12 OSS veterans who had been tortured by the Gestapo still suffered from PTSD‐startle symptoms after 50 years; those three also suffered massive strokes in later life. The majority of OSS vets, regardless of gender, exhibited “war excitement” when talking about the war 50 years later. Most saw the war as the highpoint of their lives. War excitement needs more careful study within PTSD circles.
Assessment of Posttraumatic Stress Symptoms in Children who are Medically Ill and Children Presenting to a Child Trauma Program
Authors: SHEMESH EYAL , ANNUNZIATO RACHEL A. , NEWCORN JEFFREY H. , ROCKMORE LORI , BIERER LINDA M. , COHEN JUDITH A. , SCHMEIDLER JAMES , YEHUDA RACHEL
Published: August 2006

Abstract:  To test the utility of the UCLA posttraumatic stress disorder (PTSD) Index for DSM‐IV (U‐PTSD‐I)© for predicting PTSD diagnosis in children with and without medical illnesses. The U‐PTSD‐I and a standard psychiatric interview were administered to medically ill children (n= 76) and children who experienced other traumatic events (n= 31). We found U‐PTSD‐I's sensitivity and specificity was better in the nonmedical illness cohort. Only intrusion symptoms were significantly associated with the diagnosis of PTSD in the medically ill. In conclusion, the U‐PTSD‐I performs better among general trauma versus medically ill patients. Intrusion symptoms should be focused on when assessing PTSD in medically ill children.
Medical Screenings as a Trigger for PTSD in Public Safety Workers
Authors: DEMARIA THOMAS , BARRETT MINNA , RYAN DIANE
Published: August 2006

Abstract:  Emotional distress appears to be a component of the medical screening process for 9/11 Public Safety Workers. A significant number of Public Safety Workers have found the anticipation of the medical examination process and actual examination to trigger reexperiencing and problems of emotional regulation. Selective Case examples are presented to illustrate how Public Safety Workers might be better prepared for this process.
Bio‐Psycho‐Social Assessment of 9/11‐Bereaved Children
Authors: DEMARIA THOMAS , BARRETT MINNA , KERASIOTIS BERNADINA , ROHLIH JEANNE , CHEMTOB CLAUDE
Published: August 2006

Abstract:  A comprehensive and integrated assessment bio‐psycho‐social model for the assessment of children who lost parents in the World Trade Center is necessary so that effective short‐term and long‐term care planning can be achieved. This model has been used to guide assessments of children in the Care Alliance project. Rationale for this model, as well as preliminary findings from the Care Alliance project are presented.
Are Adult Offspring Reliable Informants About Parental PTSD? A Validation Study
Authors: YEHUDA RACHEL , LABINSKY ELLEN , TISCHLER LISA , BRAND SARAH R. , LAVIN YONIT , BLAIR WILLIAM , BIERER LINDA M. , GOODMAN RACHEL Z. , GROSSMAN ROBERT A.
Published: August 2006

Abstract:  We developed a short questionnaire—Parental PTSD Questionnaire–(PPQ), designed to assess the presence of posttraumatic stress disorder (PTSD) symptoms in parents. Fifty‐eight adult offspring of Holocaust survivors (23 men and 35 women) completed the questionnaire about a parent who was independently evaluated by a trained clinician using the Clinician Administered PTSD Scale (CAPS). Only 5.2% of the offspring reported, “not knowing” if their parent had experienced 10 or fewer symptoms, while 56.9% provided estimates for all 17 items. There were no significant differences between lifetime frequencies of the individual symptoms as endorsed on the PPQ compared to the CAPS when subjects with completed PPQs were compared with CAPS. Interrater reliability between offspring and clinician was highly significant for each of the items when evaluated separately so as to include data for subjects who endorsed not knowing if a certain symptom had been present. Further studies are warranted to examine the psychometric properties of this measure.
Posttraumatic Stress Disorder With Amnesia Following Asphyxiation
Authors: LAYTON BARRY S. , KRIKORIAN ROBERT , DORI GALIT , MARTIN GREGG A. , WARDI KATHERINE
Published: August 2006

Abstract:  We describe five cases of traumatic asphyxiation injury, each meeting diagnostic criteria for posttraumatic stress disorder (PTSD) and characterized by a range of postinjury cognitive impairment. Four patients exhibited dense retrograde amnesia, including absence of conscious memory for the traumatic event. Appreciation of these asphyxiation cases, which involve temporally extended trauma exposure, may help resolve arguments regarding the possibility of co‐occurrence of PTSD and neurological amnesia based exclusively on observations of much briefer duration events (specifically, motor vehicle crashes). These five cases also provide evidence that cognitive symptoms of PTSD can develop in the absence of conscious memory for the event.
Women and Reproductive‐Related Trauma
Authors: BORN LESLIE , SOARES CLAUDIO N. , PHILLIPS SHAUNA‐DAE , JUNG MATT , STEINER MEIR
Published: August 2006

Abstract:  Women are at higher risk for developing posttraumatic stress disorder (PTSD) than men, leading to significant psychosocial burden and healthcare‐related costs. Research has shown an association between the negative impact of traumatic experiences and the reproductive life cycle in women. Pregnant women with a history of abuse/trauma frequently report intrusive reemergence of symptoms. Women who experience miscarriage may present with even higher prevalence rates of PTSD symptoms. Both psychologic and physiologic factors are believed to be relevant to the development of peripartum posttraumatic stress symptoms. Much less is known, however, about treatment. A case series of patients who presented with PTSD symptoms in the context of reproductive‐related traumatic events (e.g., miscarriage, stillbirth) or who experienced reemergence of symptoms during pregnancy is presented, including treatment strategies.
Posttraumatic Stress Disorder and Other Psychological Sequelae Among World Trade Center Clean Up and Recovery Workers
Authors: GROSS RAZ , NERIA YUVAL , TAO XUGUANG (GRANT) , MASSA JENNIFER , ASHWELL LESLIE , DAVIS KATHLEEN , GEYH ALISON
Published: August 2006

Abstract:  We assessed the health of workers exposed to the World Trade Center (WTC) site and of a comparison group of unexposed workers, by means of a mail survey. Exposed workers reported higher frequency of symptoms consistent with posttraumatic stress disorder (PTSD), depression, anxiety, and other psychological problems, approximately 20 months after the disaster. PTSD was positively associated with traumatic on‐site experiences and with respiratory problems. These findings may have important clinical and public health implications.