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Context Data from animal models demonstrate a link between stress exposure and hypertrophic changes in the amygdala; however, studies of adults with posttraumatic stress disorder (PTSD) have failed to find analogous structural alterations. Objectives To compare amygdala volumes between a sample of combat veterans with and without PTSD (analysis 1) and examine whether our observation of larger amygdala volume in individuals with PTSD could be accounted for by the presence of trauma exposure in childhood and the severity of combat exposure in adulthood (analysis 2). Design Cross-sectional magnetic resonance imaging. Setting Veterans Affairs Palo Alto Health Care System Inpatient Trauma Recovery Program and Veterans Affairs New England Health Care System Outpatient PTSD program. Participants Ninety-nine combat-exposed veterans from the Vietnam Conflict or the Persian Gulf War who had been exposed to substantial military operational stress. Main Outcome Measures Amygdala volume adjusted for total cerebral volume, Life Events Checklist, and the Combat Exposure Scale. Results Analysis 1 indicated that combat-exposed individuals with PTSD exhibited larger total amygdala volume compared with their non-PTSD counterparts (99 individuals, P = .047). Analysis 2 indicated that greater severity of combat exposure (87 individuals, P = .02), as well as the interaction between the presence of early life trauma and the severity of combat exposure (87 individuals, P = .008), were significantly associated with smaller total amygdala volume. The PTSD diagnosis continued to explain larger amygdala volume (87 individuals, P = .006). Conclusions Posttraumatic stress disorder is associated with enlarged amygdala volume, above the variance accounted for by a history of early life trauma and severity of adult trauma exposure. The discrepancy between our and prior findings may be explained by variability in these trauma indices in previous investigations. These findings support additional study of amygdala structure in human stress disorders and further delineation of the role of early and adult trauma on associated neurologic changes.

Event-related potentials (ERPs) to spoken sentences were recorded from young and elderly subjects. Sentences ended in semantically typical or atypical words. Subjects listened to the sentences during two attention conditions. In a semantic attention task, subjects listened to the meanings of the sentences for a subsequent memory test. In a phonemic attention task, subjects counted words beginning with the letter "p". Following these tasks, the sentence-final words were presented in isolation. A conventional auditory oddball paradigm was also presented. The N4 components elicited by semantically atypical sentence-final words were slightly attenuated and delayed in the older group. N4 was not influenced by the attention manipulation. Young but not older subjects' N4s were attenuated by repetition. When the sentence-final words were presented a third time in isolation, the N4s elicited were similar in amplitude and latency to those elicited in sentence context, but were not attenuated by repetition. In young and older subjects, the peak amplitude of the sentence-elicited N4 difference wave form was highly correlated with the number of correct recognitions of typical words, but not atypical sentence-final words. In young but not older subjects, sentence-elicited N4 amplitude was correlated with the amplitude of the P3 elicited in the auditory oddball paradigm.

Background Posttraumatic stress disorder (PTSD) is associated with structural and functional compromise of the anterior cingulate cortex (ACC), which may in turn be associated with impairment of its ability to regulate the amygdala. The Val158Met polymorphism in the catechol- O -methyltransferase gene, which substantially influences dopamine inactivation in the frontal lobe in general and in ACC in particular, may moderate ACC integrity in PTSD. Methods We tested this hypothesis in a sample of Vietnam and Persian Gulf War veterans who experienced substantial military operational stress, including 51 who met criteria for PTSD and 48 matched controls who did not. Results Participants with PTSD were previously reported to have smaller ACC volumes than controls in this sample. A novel repeated-measures analysis of variance was conducted with PTSD diagnosis, Val158Met genotype, and their interaction predicting left and right ACC volume. Genotype was not directly related to ACC volume, but it did significantly interact with the PTSD diagnosis. The difference in ACC volume between the participants without PTSD and participants with PTSD was greater among individuals homozygous for the Val allele than among carriers of the Met allele. This finding was driven largely by the right ACC. Analyses of Caucasian-only, non–Caucasian-only, and male-only subsamples indicated similar patterns. Conclusions Our findings suggest Val158Met genotype moderates the effect of PTSD-related processes on right ACC volume.

Data were collected shedding light on the brain electrical activity underlying word recognition. Subjects listened to a list of 48 spoken words in six random orders under two instructional sets: first to “think about the meanings of the words,” and second, to learn the list. The scalp EEG associated with hearing and identifying the words was recorded at F3, F4, Cz, P3, P4, Pz, and Oz. Standard within-subjects time-locked averaging across words showed a late negative-positive complex with N2-P3 topography, the negative component peaking around 480 msec, the positive component peaking around 830 msec. Averaging within words across subjects uncovered considerable latency variability in both components. Within-word N2 and P3 component latencies covaried with word durations and with the “recognition points” predicted for the words by the “cohort theory” of word recognition. N2 latencies corresponded closely to the “N400” effect elicited with semantically incongruous sentence-final spoken words. Implications for ERP investigations of language processing are discussed.

Psychobiological studies of posttraumatic stress disorder (PTSD) often challenge participants to assess the dynamics of systems evolved to organize responses to extreme events. Informed consent insures that volunteers have every opportunity to preevaluate the conditions of the research experience and decline if made uncomfortable by them. Notwithstanding their necessity, these protections set the stage for self-selection phenomena that may bias study outcomes. This study compared prospectively obtained psychometric data from 196 participants and 1229 nonparticipants in sleep and psychophysiological studies of PTSD. Lower subjective nightmare severity was endorsed by persons who later agreed to participate in a study of baseline sleep, an observation consistent with the low nightmare frequencies observed in most laboratories studies of sleep in PTSD.

This article describes a method for extracting heart rate (HR) and respiratory sinus arrhythmia (RSA) from the kinetocardiogram (KCG) recorded from accelerometers embedded in a mattress topper. Validation has been performed via comparison with simultaneously recorded ECG. All-night estimates of HR and RSA magnitude derived from both methods were highly correlated. KCG-derived estimates of HR were slightly lower, and those of RSA magnitude higher, than those derived from ECG. These biases are consistent with the need to constrain KCG estimation to periods free of body movement. Mattress actigraphy represents a zero-burden method of obtaining intensive longitudinal indices of cardiac status.

Studies imposing rigorous control over lifetime alcohol intake have usually not found smaller hippocampal volumes in persons with posttraumatic stress disorder. Because the majority of negative studies have used adolescent samples, it has been suggested that chronicity is a necessary condition for such findings. To test the hypothesis that a smaller hippocampus in PTSD is unrelated to comorbid alcoholism or to chronicity, this study estimated hippocampal volume in a relatively large group (N=99) of combat veterans in which PTSD, lifetime alcohol abuse/dependence, and Vietnam versus Gulf War service were crossed. In subjects with histories of alcoholism, unadjusted hippocampal volume was 9% smaller in persons with PTSD than in those without PTSD. In nonalcoholic subjects, the PTSD-related difference in hippocampal volume was 3%. The failure to observe a strong association between PTSD and hippocampal volume in nonalcoholic subjects was not ascribable to younger age, reduced PTSD chronicity, or lower PTSD symptom severity. The possibility that smaller hippocampal volume is limited to groups in which PTSD is compounded by comorbid alcoholism is not necessarily incompatible with results suggesting a smaller hippocampus is predispositional to PTSD. Further examination of the role of alcoholism and other comorbid conditions in studies of brain structure and function in PTSD appears warranted.

Background Neuroanatomical data point to functional relationships between the anterior cingulate cortex (ACC) and subcortical centers regulating fear, in particular, the amygdala. Functional brain imaging has disclosed divergent patterns of ACC activation in persons with posttraumatic stress disorder (PTSD). In addition, two preliminary structural imaging studies have found evidence of smaller ACC volume in PTSD. We explored associations between PTSD and ACC volume in a relatively large sample of adult combat veterans in which PTSD, lifetime alcohol abuse/dependence, and Vietnam versus Gulf War service were crossed. Methods Subjects were US military combat veterans of the Vietnam and Gulf Wars recruited from two metropolitan areas served by allied Department of Veterans Affairs PTSD treatment/research centers. Anterior cingulate cortex volume was analyzed as a function of grouping factors with and without adjustment for body size. Results Posttraumatic stress disorder was associated with smaller anterior cingulate cortex volume. This effect persisted in subjects without histories of alcoholism, did not interact with cohort effects, and was not modified by adjustment for body size. Conclusions Anterior cingulate cortex volume is substantially smaller in association with combat-related PTSD, a finding broadly consistent with cingulate hypofunctionality in that disorder.

Disturbed sleep is a common clinical problem in anxiety disorders, particularly in patients with post-traumatic stress disorder (PTSD) and panic disorder (PD). Several studies have attempted to validate the subjective sleep complaints of these disorders using laboratory polysomnography. These attempts, typically focusing on PTSD or PD independently, have demonstrated inconsistent results. To our knowledge, no such studies have attempted to directly compare and contrast sleep disturbances in PTSD and PD together. Our review of the studies of subjective sleep disturbances, sleep architecture, and sleep-related biologic phenomena suggests that a comparative characterization of sleep disturbances in these two disorders is timely. Such an inference is based on our identification of several areas of convergence and divergence between PTSD and PD found in the published literature, as well as our own preliminary investigations. Specifically, PTSD and PD seem to converge on several sleep-related parameters, namely, sleep quality, presence of episodic parasomnias, and movement time. They also appear to diverge in other important sleep-related areas such as respiratory disturbances and the particular phenomenological nature of episodic parasomnias, namely nightmares or nocturnal panic attacks. Investigations focusing on such overlapping phenomena may provide groundwork for further elucidation of central fear systems underlying these two disorders. Additionally, such sleep studies have the potential to provide important insights into ongoing efforts to develop a cohesive conceptual framework into the pathophysiologies of these disorders. Depression and Anxiety 18:187–197, 2003. © 2003 Wiley-Liss, Inc.

Objective: Patients with post-traumatic stress disorder (PTSD) are frequently diagnosed with other psychiatric comorbid conditions. This study tested the hypothesis that PTSD patients suffer a greater proportion of sleep problems according to comorbid diagnoses. Method: National Comorbidity Survey (NCS) data from 591 individuals diagnosed with PTSD were analyzed. Revised versions of the Diagnostic Interview Schedule and Composite International Diagnostic Interview were administered to a representative sample of males and females. Groups consisted of patients diagnosed with lifetime PTSD and with current comorbid panic disorder, major depressive disorder, generalized anxiety disorder, and alcohol dependence. Results: Patients diagnosed with PTSD/panic disorder reported a significantly greater proportion of nightmare complaints (96%) and insomnia (100%) compared with the other comorbid groups. Conclusions: A greater proportion of PTSD patients with comorbid panic disorder complain of sleep-related problems than other comorbid groups. This effect appears unique to panic, rather than other general anxiety disorder or depression. Prospective sleep studies are needed to differentiate the role of sleep in PTSD and PD, as well as to examine the role of psychiatric comorbidity in worsening sleep in PTSD patients.

The objective of this study was to assess, via heart rate, the arousal levels of participants in group trauma reexposure therapy for posttraumatic stress disorder, and so to better understand this common mode of treatment, particularly in regards to its presumed curative factor, extinction. Six Vietnam combat-related PTSD inpatients participated twice weekly in group trauma reexposure therapy during which their electrocardiograms were recorded. Heart rate was quantified continuously off-line. Heart rates of participants not directly engaged in imaginal reexposure to their personal combat traumas consistently exhibited mild linear declines from the beginnings to the ends of the approximately 2.5 hour sessions. Participants actively engaged in personal combat trauma reexposure exhibited higher whole-session heart rates. Most also exhibited more specific elevation extending over the later portions of therapy sessions during which intensive reexposure usually occurred. Surprisingly, no patients exhibited focal increases in heart rate concurrent with periods of most intensive traumatic incident review as judged from videotape. Administering imaginal reexposure in a group context does not preclude substantial physiological (sympathetic) arousal, as is preconditional for extinction. Under conditions in which the actively engaged reexposure patient is reliably identified, group trauma reexposure therapy may not provide an opportunity for "vicarious" flooding in nonengaged participants.

The status of semantic priming in Alzheimer's disease (AD) was examined using the speech elicited N400 component of the event-related brain potential (ERP). Speech was naturally paced, with 1 s of silence before the final word. In the semantic task, subjects attended to the meaning of the sentences for a subsequent memory test. In the phonemic monitoring task, they counted the words beginning with the letter 'p'. The effects of age were assessed by comparing young and elderly, and the effects of disease by comparing elderly and AD subjects. In healthy young and elderly subjects, N400s were large to semantically unprimed words and small to semantically primed words. In AD subjects, N400s were large to primed words, reflecting a failure of the sentence stem to prime the final word, and probably an impairment in semantic knowledge. The N400 priming effect was not smaller during the phonemic than semantic task in any group, suggesting that the semantic qualities of speech are processed even when subjects are attending to phonemic qualities. N400 latency was delayed with age and further delayed with dementia.

Life, some contend, is punctuated by accidental as well as developmental crises (Caplan, 1964). Developmental crises are disruptive but reasonably predictable life changes experienced as milestones in growth and cognitive development. Accidental crises, by contrast, almost always occur at unpredictable times, are disruptive, and involve some primary loss, such as the death of loved ones, loss of job, or debilitating illness. With both types of crises, however, how well an individual manages the crisis influences future functioning. If a crisis is resolved successfully, the individual may become more confident, more skilled, and better able to handle future crises. If not, an individual may become less confident and able in managing future crises (Caplan, 1964).

CONTEXT: Two sets of findings predict smaller cerebral cortical gray matter volume in adult posttraumatic stress disorder (PTSD). Measures of intracranial tissue volume and cerebral tissue volume have been observed to be smaller in adolescents with maltreatment-related PTSD. Second, lower intelligence, a risk factor for PTSD, is associated with smaller cerebral tissue volumes. Nevertheless, to our knowledge, only 1 study has observed globally smaller cerebral tissue volume in adults with PTSD. OBJECTIVES: To apply a recently developed method providing improved estimates of cortical volume and to estimate associations between adult PTSD and selected regional cortical volumes not yet investigated. DESIGN: Between-group comparison of global and regional cerebral cortical volumes in adult patients with combat-related PTSD and controls. SETTING: Two Department of Veterans Affairs medical centers with large inpatient and outpatient PTSD catchments. PARTICIPANTS: Ninety-seven combat-exposed veterans of the Vietnam and Persian Gulf wars. MAIN OUTCOME MEASURE: Global and regional cortical volumes determined using the FreeSurfer software program and the Desikan et al parcellation (modified). RESULTS: Cerebral cortical volume, thickness, and area were observed to be smaller in association with adult combat-related PTSD. Robust associations were observed between PTSD and smaller cortical volumes in the parahippocampal gyrus, superior temporal cortex, lateral orbital frontal cortex, and pars orbitalis of the inferior frontal gyrus. CONCLUSIONS: Cerebral cortical volume, thickness, and area may be smaller in adult chronic severe PTSD; however, the extracted structural variables did not mediate relations between intelligence and PTSD. The 4 regions exhibiting especially smaller cortical volumes in this sample share involvement in mechanisms subserving "top-down" facilitation of the identification of objects and words. Compromise of these regions may result in difficulty in relearning pretrauma schemata for interpreting the civilian physical and social environments. Language: en