Biomedical subjects

J D Bremner

Publications and source records attributed to J D Bremner.

At least 55 records · Page 3Linked to original sources

PubMed1997

Scholastic impairments among traumatized adolescents.

This investigation sought to determine if exposure to exceptional stress is associated with academic deficits or whether academic deficits are specifically associated with post-traumatic stress disorder (PTSD). In order to address these questions, the Metropolitan Achievement Test (MAT) as well as a measure of intelligence were administered to three groups of Lebanese adolescents. The first group met diagnostic criteria for PTSD. The second group had been exposed to qualitatively and quantitatively similar stressors but did not meet diagnostic criteria for PTSD. The third group consisted of nontraumatized controls. Data analysis using IQ as a covariate determined that the MAT scores of the PTSD subjects were significantly lower than the scores of the stress exposed PTSD negatives and controls. No significant differences were observed when the MAT scores of the stress exposed PTSD negatives and controls were compared.

Achievement↗

PubMed1997

Trauma-related dissociative states and long-term psychopathology in posttraumatic stress disorder.

Dissociative responses to trauma have been hypothesized to be associated with long-term increases in psychopathology. The purpose of this study was to examine dissociative responses to premilitary, combat-related and postmilitary traumatic events and long-term psychopathology in Vietnam combat veterans with (n = 34) and without (n = 28) posttraumatic stress disorder (PTSD). PTSD patients reported higher levels of dissociative states at the time of combat-related traumatic events than non-PTSD patients. Higher levels of dissociative states persisted in PTSD patients in the form of higher levels of dissociative states in-response to postmilitary traumatic events. In addition, dissociative responses to combat trauma were associated with higher long-term general dissociative symptomatology as measured by scores on the Dissociative Experience Scale, as well as increases in the number of flashbacks since the time of the war. These findings are consistent with previous formulations that dissociation in the face of trauma is a marker of long-term psychopathology.

Adult↗

PubMed1997

Elevated CSF corticotropin-releasing factor concentrations in posttraumatic stress disorder.

OBJECTIVE: Corticotropin-releasing factor (CRF) and somatostatin both play important roles in mediating responses to acute and chronic stress. The purpose of this study was to measure CSF concentrations of CRF and somatostatin in patients with chronic combat-related post-traumatic stress disorder (PTSD) and comparison subjects. METHOD: Lumbar punctures for collection of CSF were performed in Vietnam combat veterans with PTSD (N = 11) and comparison subjects (N = 17). CSF concentrations of CRF and somatostatin were compared between the two groups. RESULTS: CSF concentrations of CRF were higher in the PTSD patients than in the comparison subjects (mean = 29.0 pg/ml, SD = 7.8, versus mean = 21.9 pg/ml, SD = 6.0). This group difference remained significant after covariance for age. CSF somatostatin concentrations in PTSD patients were higher than those of the comparison subjects (mean = 19.9 pg/ml, SD = 5.4, versus mean = 13.7 pg/ml, SD = 8.0). However, covarying for age reduced the level of significance. CONCLUSIONS: Higher CSF CRF concentrations in patients with PTSD may reflect alterations in stress-related neurotransmitter systems. The higher CSF CRF concentrations may play a role in disturbances of arousal in patients with PTSD.

Adult↗

PubMed1996

Noradrenergic mechanisms in stress and anxiety: I. Preclinical studies.

There is considerable preclinical evidence for a relationship between noradrenergic brain systems and behaviors associated with stress and anxiety. The majority of noradrenergic neurons are located in the locus coeruleus (pons), with projections throughout the cerebral cortex and multiple subcortical areas, including hippocampus, amygdala, thalamus, and hypothalamus. This neuroanatomical formation of the noradrenergic system makes it well suited to rapidly and globally modulate brain function in response to changes in the environment, as occurs during the presentation of stressors. Stress exposure is associated with an increase in firing of the locus coeruleus and with associated increased release and turnover of norepinephrine in brain regions which receive noradrenergic innervation. Increased firing of the locus coeruleus is also associated with behavioral manifestations of fear, such as arched back and piloerection in the cat. Exposure to chronic stress results in long-term alterations in locus coeruleus firing and norepinephrine release in target brain regions of the locus coeruleus. Norepinephrine is also involved in neural mechanisms such as sensitization and fear conditioning, which are associated with stress. These findings are relevant to an understanding of psychiatric disorders, such as panic disorder and post-traumatic stress disorder (PTSD), the symptoms of which have been hypothesized to be related to alterations in noradrenergic function.

Adrenergic Fibers↗

PubMed1996

Noradrenergic mechanisms in stress and anxiety: II. Clinical studies.

Studies in animals have shown a relationship between alterations in noradrenergic brain system function and behaviors of anxiety and fear. These findings have generated the hypothesis that the symptoms seen in patients with anxiety disorders may be related to alterations in noradrenergic function. A number of clinical studies have tested this hypothesis, utilizing measures of catecholaminergic function such as heart rate and blood pressure, measurement of norepinephrine and its metabolites in urine and plasma and adrenergic receptor binding in platelets, as well as pharmacological challenge to the noradrenergic system. Acute stressors, such as public speaking, have been associated with an increase in heart rate, blood pressure, and norepinephrine and its metabolites in urine and plasma. Findings in patients with panic disorder at baseline related to heart rate, blood pressure, baseline norepinephrine and its metabolites, and platelet adrenergic receptors have been mixed, while the most consistent findings have been blunted growth hormone response to clonidine and increased 3-methoxy-4-hydroxy-phenylethylene-glucol (MHPG) and anxiety following stimulation of the noradrenergic system with yohimbine. Baseline measures of noradrenergic function in patients with posttraumatic stress disorder (PTSD) have also been mixed, while an increased heart, blood pressure and norepinephrine response to traumatic reminders, as well as increased behavioral (as well as different brain metabolic) response to yohimbine, have been found in PTSD. There are fewer studies of noradrenergic function in the other anxiety disorders, and the findings there have not been consistent. These studies provide evidence for increased noradrenergic responsiveness in panic disorder and PTSD, although there does not appear to be an alteration in baseline noradrenergic function in these patients.

Adrenergic Fibers↗

PubMed1996

Chronic PTSD in Vietnam combat veterans: course of illness and substance abuse.

OBJECTIVE: The purpose of this study was to measure the longitudinal course of specific symptoms of posttraumatic stress disorder (PTSD) and related symptoms of alcohol and substance abuse and the effects of alcohol and substances on the symptoms of PTSD. METHOD: A structured interview for the assessment of PTSD and alcohol and substance abuse, as well as other factors such as life stressors and treatment, was administered to 61 Vietnam combat veterans with PTSD. RESULTS: Onset of symptoms typically occurred at the time of exposure to combat trauma in Vietnam and increased rapidly during the first few years after the war. Symptoms plateaued within a few years after the war, following which the disorder became chronic and unremitting. Hyperarousal symptoms such as feeling on guard and feeling easily startled developed first, followed by avoidant symptoms and finally by symptoms from the intrusive cluster. The onset of alcohol and substance abuse typically was associated with the onset of symptoms of PTSD, and the increase in use paralleled the increase of symptoms. Patients reported a tendency for alcohol, marijuana, heroin, and benzodiazepines to make PTSD symptoms better, while cocaine made symptoms in the hyperarousal category worse. There was no relationship between treatment interventions and the natural course of PTSD. CONCLUSIONS: These findings suggest that symptoms of PTSD begin soon after exposure to trauma, that hyperarousal symptoms are the first symptoms to occur, that the natural course of alcohol and substance abuse parallels that of PTSD, and that specific substances have specific effects on PTSD symptoms.

Alcoholism↗

PubMed1996

Neural mechanisms in dissociative amnesia for childhood abuse: relevance to the current controversy surrounding the "false memory syndrome".

OBJECTIVE: There is considerable controversy about delayed recall of childhood abuse. Some authors have claimed that there is a "false memory syndrome," in which therapists suggest to patients events that never actually occurred. These authors point to findings that suggest that memory traces are susceptible to modification. The purpose of this paper is to review the literature on the potential vulnerability of memory traces to modification and on the effects of stress on the neurobiology of memory. METHOD: The authors review findings on mechanisms involved in normal memory function, effects of stress on memory in normal persons, children's memory of stressful events, and alterations of memory function in psychiatric disorders. The effects of stress on specific brain regions and brain chemistry are also examined. RESULTS: Neuropeptides and neurotransmitters released during stress can modulate memory function, acting at the level of the hippocampus, amygdala, and other brain regions involved in memory. Such release may interfere with the laying down of memory traces for incidents of childhood abuse. Also, childhood abuse may result in long-term alterations in the function of these neuromodulators. CONCLUSIONS: John Nemiah pointed out several years ago that alterations in memory in the form of dissociative amnesia are an important part of exposure to traumatic stressors, such as childhood abuse. The studies reviewed here show that extreme stress has long-term effects on memory. These findings may provide a model for understanding the mechanisms involved in dissociative amnesia, as well as a rationale for phenomena such as delayed recall of childhood abuse.

Amnesia↗

PubMed1995

Deficits in short-term memory in adult survivors of childhood abuse.

Exposure to stress has been associated with alterations in memory function, and we have previously shown deficits in short-term verbal memory in patients with a history of exposure to the stress of combat and the diagnosis of posttraumatic stress disorder (PTSD). Few studies of any kind have focused on adult survivors of childhood physical and sexual abuse. The purpose of this study was to investigate short-term memory function in adult survivors of childhood abuse. Adult survivors of severe childhood physical and sexual abuse (n = 21), as defined by specific criteria derived from the Early Trauma Inventory (ETI), who were presenting for psychiatric treatment were compared with healthy subjects (n = 20) matched for several variables including age, alcohol abuse, and years of education. All subjects were assessed with the Wechsler Memory Scale (WMS) Logical (verbal memory) and Figural (visual memory) components, the Verbal and Visual Selective Reminding Tests (SRT), and the Wechsler Adult Intelligence Scale-Revised (WAIS-R). Adult survivors of childhood abuse had significantly lower scores on the WMS Logical component for immediate and delayed recall in comparison to normal subjects, with no difference in visual memory, as measured by the WMS or the SRT, or IQ, as measured by the WAIS-R. Deficits in verbal memory, as measured by the WMS, were associated with the severity of abuse, as measured by a composite score on the ETI. Our findings suggest that childhood physical and sexual abuse is associated with long-term deficits in verbal short-term memory. These findings of specific deficits in verbal (and not visual) memory, with no change in IQ, are similar to the pattern of deficits that we have previously found in patients with combat-related PTSD.

Adult↗

PubMed1995

Effects of the benzodiazepine antagonist flumazenil in PTSD.

OBJECTIVE: Evidence from preclinical and clinical studies suggests a role for alterations in the benzodiazepine/GABAA receptor complex in stress and anxiety. Flumazenil is a relatively pure benzodiazepine/GABAA antagonist with limited intrinsic activity. In panic disorder patients, but not healthy controls, flumazenil has been demonstrated to provoke panic attacks. METHOD: Vietnam combat veterans with PTSD (n = 14) received 90-second intravenous infusions of flumazenil 2 mg or placebo in a double-blind, crossover study design. PTSD symptomology was assessed using the PTSD Symptom Scale, and anxiety symptoms were measured with visual analogue rating scales. RESULTS: There was no significant difference in PTSD and anxiety symptoms between administration of flumazenil and placebo. CONCLUSION: Flumazenil administration does not produce an increase in anxiety and PTSD symptoms in patients with PTSD. This suggests that PTSD and panic disorder are dissimilar in terms of benzodiazepine/GABAA system function.

Anxiety Disorders↗

PubMed1995

Functional neuroanatomical correlates of the effects of stress on memory.

Recently there has been an increase in interest in the relationship between stress and memory. Brain regions which are involved in memory function also effect the stress response. Traumatic stress results in changes in these brain regions; alterations in these brain regions in turn may mediate symptoms of posttraumatic stress disorder (PTSD). Neural mechanisms which are relevant to the effects of stress on memory, such as fear conditioning, stress sensitization, and extinction, are reviewed in relation to their implications for PTSD. Special topics including neural mechanisms in dissociation, neurobiological approaches to the validity of childhood memories as they apply to controversies over the "False Memory Syndrome," and implications of the effects of stress on memory for psychotherapy, are also reviewed. The findings discussed in this paper are consistent with the formulation that stress-induced alterations in brain regions and systems involved in memory may underlie many of the symptoms of PTSD, as well as dissociative amnesia, seen in survivors of traumatic stress.

Adult↗

PubMed1995

Synthesis and PET imaging of the benzodiazepine receptor tracer [N-methyl-11C]iomazenil.

The central benzodiazepine receptor tracer [N-methyl-11C]iomazenil (Ro 16-0154) was synthesized by alkylation of the desmethyl precursor noriomazenil with [11C]methyl iodide. The [11C]CH3I (prepared by reduction of [11C]CO2 with LiA1H4 followed by reaction with HI) was reacted with noriomazenil in N,N-dimethylformamide and Bu4N+OH- for 1 min at 80 degrees C and purified by HPLC (C18, 34% CH3CN/H2O 7 mL/min). The product was obtained with synthesis time 35 +/- 5 min (mean +/- SD, n = 7), radiochemical yield (EOB) 36 +/- 16%, radiochemical purity 99 +/- 1%, and specific activity 5100 +/- 2800 mCi/mumol. Absorbed radiation doses were calculated from previously acquired human biodistribution data. The urinary bladder wall received the highest dose (0.099 mGy/MBq) for 4.8 h voiding interval and the effective dose equivalent was 0.015 mSv/MBq. After i.v. injection of [11C]iomazenil in an adult baboon or healthy human volunteer, radioactivity accumulated in the cortex with time-activity curves in agreement with results obtained with [11C]flumazenil PET and [123I]iomazenil SPECT studies. The count rate was sufficient to obtain quantitative images up to 2 h post-injection with a 14 mCi injection. These results suggest that [11C]iomazenil will be a useful agent for measuring benzodiazepine receptors in vivo by positron emission tomography.

Adult↗

PubMed1995

MRI-based measurement of hippocampal volume in patients with combat-related posttraumatic stress disorder.

OBJECTIVE: Studies in nonhuman primates suggest that high levels of cortisol associated with stress have neurotoxic effects on the hippocampus, a brain structure involved in memory. The authors previously showed that patients with combat-related posttraumatic stress disorder (PTSD) had deficits in short-term memory. The purpose of this study was to compare the hippocampal volume of patients with PTSD to that of subjects without psychiatric disorder. METHOD: Magnetic resonance imaging was used to measure the volume of the hippocampus in 26 Vietnam combat veterans with PTSD and 22 comparison subjects selected to be similar to the patients in age, sex, race, years of education, socioeconomic status, body size, and years of alcohol abuse. RESULTS: The PTSD patients had a statistically significant 8% smaller right hippocampal volume relative to that of the comparison subjects, but there was no difference in the volume of other brain regions (caudate and temporal lobe). Deficits in short-term verbal memory as measured with the Wechsler Memory Scale were associated with smaller right hippocampal volume in the PTSD patients only. CONCLUSIONS: These findings are consistent with a smaller right hippocampal volume in PTSD that is associated with functional deficits in verbal memory.

Adult↗

PubMed1995

A double-blind comparison of Org 3770, amitriptyline, and placebo in major depression.

BACKGROUND: A 6-week, double-blind, dose titration study was performed to evaluate efficacy and safety of the new antidepressant Org 3770 in comparison with amitriptyline and placebo. METHOD: One hundred fifty outpatients of both sexes, 18 years and older, with a DSM-III diagnosis of major depressive episode, were randomly assigned to 6 weeks of treatment with Org 3770, amitriptyline, or placebo. RESULTS: At baseline, mean 17-item Hamilton Rating Scale for Depression (HAM-D) scores of all treatment groups were higher than 25, thus indicating that a large proportion of severely depressed patients entered the study. The overall mean daily doses were 22 mg/day for Org 3770, 133 mg/day for amitriptyline, and 4.9 capsules/day for placebo. The majority of times assessments were made, both active drugs produced significantly greater improvements than placebo on all efficacy variables (17-item HAM-D, Montgomery-Asberg Depression Rating Scale, Clinical Global Impressions, and Zung Self-Rating Depression Scale). After 6 weeks of treatment, significantly greater (p < or = .05) proportions of patients in both active treatment groups (70% in the Org 3770- and 58% in the amitriptyline-treatment groups) than in the placebo-treatment group (33%) were HAM-D responders. Org 3770 was well tolerated in this study; dry mouth and somnolence were the only adverse experiences that occurred significantly more frequently with Org 3770- than with placebo-treated patients. By contrast, treatment with amitriptyline was related to significantly higher rates of dry mouth, constipation, and dyspepsia as compared with both Org 3770 and placebo, and significantly higher rates of somnolence as compared with placebo. CONCLUSION: In this study, Org 3770 was as effective as amitriptyline in the treatment of major depression, with advantages regarding improvements of depressed mood (HAM-D Item 1), responder rates, and safety.

Amitriptyline↗

PubMed1994

Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses.

BACKGROUND: To characterize further behavioral, cognitive, neuroendocrine, and physiological effects of subanesthetic doses of ketamine hydrochloride in healthy human subjects. Ketamine, a phencyclidine hydrochloride derivative, is a dissociative anesthetic and a noncompetitive antagonist of the N-methyl-D-aspartate subtype of excitatory amino acid receptor. METHODS: Nineteen healthy subjects recruited by advertisements from the community participated in this randomized, double-blind, placebo-controlled study. Subjects completed three test days involving the 40-minute intravenous administration of placebo, ketamine hydrochloride (0.1 mg/kg), or ketamine hydrochloride (0.5 mg/kg). Behaviors associated with the positive and negative symptoms of schizophrenia were assessed by using the Brief Psychiatric Rating Scale. Changes in perception and behaviors associated with dissociative states were assessed by the Perceptual Aberration Subscale of the Wisconsin Psychosis Proneness Scale and the Clinician-Administered Dissociative States Scale. Cognitive function was assessed by using the (1) Mini-Mental State Examination; (2) tests sensitive to frontal cortical dysfunction, including a continuous performance vigilance task, a verbal fluency task, and the Wisconsin Card Sorting Test; and (3) tests of immediate and delayed recall. Plasma levels of cortisol, prolactin, homovanillic acid, and 3-methoxy-4-hydroxyphenethyleneglycol were measured. RESULTS: Ketamine (1) produced behaviors similar to the positive and negative symptoms of schizophrenia; (2) elicited alterations in perception; (3) impaired performance on tests of vigilance, verbal fluency, and the Wisconsin Card Sorting Test; (4) evoked symptoms similar to dissociative states; and (5) preferentially disrupted delayed word recall, sparing immediate recall and postdistraction recall. Ketamine had no significant effect on the Mini-Mental State Examination at the doses studied. Ketamine also had no effect on plasma 3-methoxy-4-hydroxyphenethyleneglycol levels, although it blunted a test day decline in plasma homovanillic acid levels at the higher dose. It also dose dependently increased plasma cortisol and prolactin levels. Ketamine produced small dose-dependent increases in blood pressure. CONCLUSIONS: These data indicate that N-methyl-D-aspartate antagonists produce a broad range of symptoms, behaviors, and cognitive deficits that resemble aspects of endogenous psychoses, particularly schizophrenia and dissociative states.

Adult↗

PubMed1994

SPECT measurement of benzodiazepine receptors in human brain with iodine-123-iomazenil: kinetic and equilibrium paradigms.

UNLABELLED: Iodine-123-iomazenil binding to benzodiazepine receptors in human brain was measured with SPECT using kinetic and equilibrium methods. METHODS: In the kinetic experiments (n = 6), regional time-activity curves after a single bolus injection of the tracer were fit to a three-compartment model to provide estimates of the rate constants K1 to k4. The binding potential (equal to the product of the receptor density and affinity) was derived from the rate constants. In the equilibrium method (n = 8), the tracer bolus injection was followed by a constant tracer infusion to induce a sustained equilibrium state. The regional equilibrium volume of distribution was calculated as the ratio of the regional brain concentration-to-the free parent tracer steady-state plasma concentration. In three experiments, a receptor-saturating dose of flumazenil was injected for direct measurement of the nondisplaceable compartment distribution volume. RESULTS: The kinetic and equilibrium method results were in good agreement in all regions investigated. Iodine-125-iomazenil binding potential measured in vitro in 12 postmortem samples was found to be consistent with SPECT in vivo measurements. CONCLUSION: These studies demonstrated the feasibility of quantification of receptor binding with SPECT.

Adult↗

PubMed1993

[123I]iomazenil SPECT imaging demonstrates significant benzodiazepine receptor reserve in human and nonhuman primate brain.

SPECT imaging with [123I]iomazenil was used to measure benzodiazepine (BZ) neuroreceptor occupancy of the agonist lorazepam administered at therapeutically relevant doses in humans and supratherapeutic doses in monkeys. Lorazepam at therapeutic doses (0.03 mg/kg, i.v.) administered 90 min after the bolus injection of [123I]iomazenil had no statistically significant effect (P > 0.12) on the washout rates of regional brain activities compared to that in control subjects, although human subjects demonstrated marked sedation from the lorazepam. In baboons, the effects of higher doses of lorazepam (cumulative 0.5 mg/kg) were examined in a stepwise displacement paradigm. The in vivo potency was expressed as the ED50 (or dose required to displace 50% of receptor bound activity) and was equal to 0.34 +/- 0.01 mg/kg (mean +/- SD, n = 12). Log-logit analyses of displacement data corrected for endogenous washout showed that therapeutic doses of lorazepam were associated with < 3% BZ receptor occupancy. To examine if endogenous GABA modulates potency of the BZ agonist, the ED50 of lorazepam was compared with and without concurrent administration of tiagabine, a GABA reuptake inhibitor. These experiments were designed to measure an in vivo GABA shift of agonist potency. In vivo microdialysis demonstrated that tiagabine (up to 1 mg/kg, i.v.) increased extracellular GABA levels up to 200% of baseline, but these doses had only a minimal enhancement of lorazepam's potency to displace [123I]iomazenil. This study strongly suggests that single therapeutically relevant doses of lorazepam occupy a relatively small percentage (i.e. < 3%) of BZ receptors and that BZ binding sites have a significant (i.e. > 97%) receptor reserve.

Adult↗

PubMed1993

Childhood physical abuse and combat-related posttraumatic stress disorder in Vietnam veterans.

OBJECTIVE: Early trauma in the form of childhood physical or sexual abuse has been associated with adult psychopathology. The purpose of this study was to compare rates of childhood abuse in Vietnam veterans with and without combat-related posttraumatic stress disorder (PTSD). METHOD: Premilitary stressful and traumatic events including childhood abuse and other potential predisposing factors were assessed in Vietnam combat veterans who sought treatment for PTSD (N = 38) and Vietnam combat veterans without PTSD who sought treatment for medical disorders (N = 28). Stressful and traumatic events including childhood physical abuse were assessed with the Checklist of Stressful and Traumatic Events and a clinician-administered interview for the assessment of childhood abuse. Level of combat exposure was measured with the Combat Exposure Scale. RESULTS: Vietnam veterans with PTSD had higher rates of childhood physical abuse than Vietnam veterans without PTSD (26% versus 7%). The association between childhood abuse and PTSD persisted after controlling for the difference in level of combat exposure between the two groups. Patients with PTSD also had a significantly higher rate of total traumatic events before joining the military than patients without PTSD (mean = 4.6, SD = 4.5, versus mean = 2.8, SD = 2.9). CONCLUSIONS: These findings suggest that patients seeking treatment for combat-related PTSD have higher rates of childhood physical abuse than combat veterans without PTSD. Childhood physical abuse may be an antecedent to the development of combat-related PTSD in Vietnam combat veterans.

Causality↗

PubMed1993

Use of the Structured Clinical Interview for DSM-IV Dissociative Disorders for systematic assessment of dissociative symptoms in posttraumatic stress disorder.

OBJECTIVE: This study compared dissociative symptom areas in Vietnam combat veterans with posttraumatic stress disorder (PTSD) and in Vietnam combat veterans without PTSD. METHOD: The Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D) was used to compare dissociative symptoms in 40 Vietnam combat veterans with PTSD and 15 Vietnam combat veterans without PTSD. The SCID-D yields a total score and scores in five symptom areas: amnesia, depersonalization, derealization, identity confusion, and identity alteration. RESULTS: The PTSD patients had more severe dissociative symptoms in each of the five symptom areas of the SCID-D and higher total symptom scores. Amnesia was the symptom area with the greatest difference in scores between the PTSD patients (mean = 3.68, SD = 0.73) and the non-PTSD veterans (mean = 1.06, SD = 0.26). CONCLUSIONS: The finding of higher levels of dissociative symptoms in Vietnam combat veterans with PTSD than in Vietnam veterans without PTSD is consistent with a level of dissociative symptoms in PTSD similar to that in dissociative disorders.

Adult↗