Faculty Bibliography

BACKGROUND: Brain imaging research in posttraumatic stress disorder has been largely performed on patients with chronic disease, often heavily medicated, with current or past alcohol and substance abuse. Additionally, virtually only activation brain imaging paradigms have been done in posttraumatic stress disorder, whereas in other mental disorders both resting and activation studies have been performed. METHODS: Twenty-eight (11 posttraumatic stress disorder) trauma survivors underwent resting state hexamethylpropyleneamineoxime single photon emission computed tomography and magnetic resonance imaging 6 months after trauma. Eleven nontraumatized subjects served as healthy controls. RESULTS: Regional cerebral blood flow in the cerebellum was higher in posttraumatic stress disorder than in both control groups. Regional cerebral blood flow in right precentral, superior temporal, and fusiform gyri in posttraumatic stress disorder was higher than in healthy controls. Cerebellar and extrastriate regional cerebral blood flow were positively correlated with continuous measures of depression and posttraumatic stress disorder. Cortisol level in posttraumatic stress disorder was negatively correlated with medial temporal lobe perfusion. Anterior cingulate perfusion and cortisol level were positively correlated in posttraumatic stress disorder and negatively correlated in trauma survivors without posttraumatic stress disorder. CONCLUSIONS: Recent posttraumatic stress disorder is accompanied by elevated regional cerebral blood flow, particularly in the cerebellum. This warrants attention because the cerebellum is often used as a reference region in regional cerebral blood flow studies. The inverse correlation between plasma cortisol and medial temporal lobe perfusion may herald hippocampal damage

OBJECTIVE: Traumatic amnesia has been amply documented in the psychoanalytic literature but inconsistently in the research literature. METHOD: Six trauma were followed prospectively. Survivors were interviewed 7, 30, and 120 days following the traumatic event. Each interview documented in detail their recollections of the day of their trauma. RESULTS: In four subjects who did not develop posttraumatic stress disorder (PTSD), we found brief, stable, and persistent memory gaps, which coincided with the moment of greatest emotional intensity. In two subjects who developed PTSD, we found, in addition to the previous form of amnesia, longer, progressive, and unstable memory gaps. DISCUSSION: Neurobiological research offers two explanatory mechanisms for the observations: A failure of acquisition of episodic memories may account for the stable deficits seen in all subjects. This could coincide with stress-induced malfunction of the hippocampal declarative memory system. A failure of spontaneous recall may account for the more extended traumatic amnesia that was observed in PTSD patients. This resembles the psychoanalytic description of repression. CONCLUSION: These preliminary findings suggest that brief, irreversible memory gaps are common in trauma survivors, whereas longer, progressive, and potentially reversible amnesia occurs among survivors who develop PTSD

Traditional methods for analyzing trends in longitudinal data have typically emphasized average group change over time. In this article, we propose multilevel, regression-based methods for examining inter-individual differences in intra-individual change and apply these methods to research in trauma and posttraumatic stress disorder (PTSD). The outcome or dependent variable of interest is reconceptualized as an index of dynamic change reflecting the trend or trajectory of an individual's PTSD symptom severity scores across time. A basic statistical model is presented, and analyses and findings are demonstrated with an existing database used in previously published studies. The methods offer promise for future study of the natural course of PTSD chronicity or recovery, risk and resilience factors that influence individual growth or decline, and critical timepoints for intervention

Posttraumatic stress disorder (PTSD) is a prevalent anxiety disorder marked by behavioral, physiologic, and hormonal alterations. PTSD is disabling and commonly follows a chronic course. The etiology of PTSD is unknown, although exposure to a traumatic event constitutes a necessary, but not sufficient, factor. A twin study of Vietnam veterans has shown significant genetic contribution to PTSD. The fact that PTSD's underlying genotypic vulnerability is only expressed following trauma exposure limits the usefulness of family-based linkage approaches. In contrast to the other major psychiatric disorders, large studies for the search of underlying genes have not been described in PTSD to date. Complementary approaches for locating involved genes include association-based studies employing case-control or parental genotypes for transmission dysequilibrium analysis and quantitative trait loci studies in animal models. Identification of susceptibility genes will increase our understanding of traumatic stress disorders and help to elucidate their molecular basis. The current review provides an up-to-date outline of progress in the field of PTSD

Hypothalamic pituitary adrenal axis abnormalities have been described in posttraumatic stress disorder (PTSD), and among the recently traumatized. Plasma cortisol and continuous measures of PTSD symptoms were obtained from 21 survivors, at 1 week and 6 months after traumatic events. Eight survivors met Clinician Administered PTSD Scale criteria for PTSD at 6 months. Cortisol levels at 1 week did not predict subsequent PTSD. Survivors with and without PTSD had similar mean levels of cortisol at both time points. Cortisol levels at 6 months negatively correlated with self-reported PTSD symptoms within PTSD subjects

BACKGROUND: Larger heart rate responses to sudden, loud (startling) tones represent one of the best-replicated psychophysiologic markers for posttraumatic stress disorder (PTSD). This abnormality may be a pretrauma vulnerability factor, ie, it may have been present prior to the event's occurrence and increased the individual's likelihood of developing PTSD on traumatic exposure. Alternately, it may be an acquired PTSD sign, ie, it may have developed after the traumatic exposure, along with the PTSD. Studying identical twins discordant for traumatic exposure offers an opportunity to resolve these competing origins. METHODS: Subjects included pairs of Vietnam combat veterans and their non-combat-exposed, monozygotic twins. Combat veterans were diagnosed as having current PTSD (n = 50) or non-PTSD (ie, never had) (n = 53). All subjects listened to a series of 15 sudden, loud tone presentations while heart rate, skin conductance, and orbicularis oculi electromyogram responses were measured. RESULTS: Consistent with previous reports, averaged heart rate responses to the tones were larger in Vietnam combat veterans with PTSD. These larger responses were not shared by their non-combat-exposed co-twins, whose responses were similar to those of the non-PTSD combat veterans and their non-combat-exposed co-twins. This result remained significant after adjusting for a number of potentially confounding factors. CONCLUSIONS: The results suggest that larger heart rate responses to sudden, loud tones represent an acquired sign of PTSD rather than a familial vulnerability factor

BACKGROUND: Homeopathy is commonly used for the treatment of medical and psychological conditions. Such prevalent use, however, is not supported by robust, methodologically sound research. This study evaluates the effect of homeopathic treatment in generalized anxiety disorder, a prevalent mental disorder characterized by an enduring pattern of excessive apprehension and distress and by mental and bodily complaints. METHOD: Forty-four patients with DSM-IV generalized anxiety disorder participated in a randomized, double-blind, placebo-controlled 10-week trial of individually tailored homeopathic remedy. Homeopathic therapy was administered by an expert who followed the traditional routines of homeopathic diagnosis and prescription. Thirty-nine subjects completed the study (20 in the active treatment group and 19 in the placebo group). Subjects' symptoms were rated before treatment and after 5 and 10 weeks of treatment, with the Hamilton Rating Scale for Anxiety (HAM-A) as main outcome measure. Additional measures of outcome included the Brief Symptom Inventory, the Psychological General Well-Being Index, the Hamilton Rating Scale for Depression, the Beck Depression Inventory, Spielberger's State-Trait Anxiety Inventory, and a Visual Analogue Scale of subjective distress. RESULTS: Significant (p <.05) improvement in most measures, including the HAM-A, was observed in both the active treatment and placebo groups, yet no group effect was observed. CONCLUSION: The effect of homeopathic treatment on mental symptoms of patients with generalized anxiety disorder did not differ from that of placebo. The improvement in both conditions was substantial. Improvement of such magnitude may account for the current belief in the efficacy of homeopathy and the current increase in the use of this practice

Gender differences in psychological responses to motor vehicle accidents were examined as part of a large-scale prospective study of PTSD. Participants were recruited from an emergency room (n = 275) and interviewed 1 week, 1 month, and 4 months later. No gender differences were seen in the prevalence or recovery from PTSD, or in symptom levels at 1- and 4 months. Women had a higher prevalence of lifetime- and postaccident generalized anxiety disorder. Gender differences were found regarding the type, but not the total number, of potentially traumatic events previously experienced. These results suggest that gender differences in responses to traumatic events are not explained by exposure as such, but rather may result from gender-specific attributes of the event

Chronic post-traumatic stress disorder (PTSD) has been associated with cognitive impairments involving memory and attention. The association between cognitive impairment and early PTSD symptoms is unknown, yet such association may lead to poorer processing of traumatic memories and thereby contribute to subsequent PTSD. This study evaluated the relationship between PTSD symptoms and cognitive functioning within 10 days of traumatic events. Forty-eight survivors were assessed for symptoms of PTSD, anxiety, depression and dissociation and for immediate and delayed verbal and figural memory, attention, learning and IQ. Survivors with high levels of PTSD symptoms showed impaired attention and immediate recall for figural information and lower IQ. They did not show, however, an impairment of verbal recall and learning. The observed difference was not explained by anxiety or dissociation. It disappeared, however, when the effect of depressive symptoms was controlled for. Lower IQ and impaired attention are associated with early PTSD and depressive symptoms. Poorer attention may have a role in shaping traumatic memories