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Biomedical subjects

Rachel Yehuda

Publications and source records attributed to Rachel Yehuda.

86 records · Page 5Linked to original sources
PubMed2002

Biologic models of traumatic memories and post-traumatic stress disorder. The role of neural networks.

Neural networks and their behavior provide an information-processing model for initiation and maintenance of the biologic aspects of post-traumatic stress disorder (PTSD). The repeated replaying of the intrusive and distressing recollections that follow a trauma modifies the structure of the neural networks involved in the processing of traumatic memories. The hypothesis is proposed that this repetition instigates the mechanisms of iterative learning, top-down activation and pruning. The development of the symptoms of PTSD can be explained by current knowledge about modeling disturbances of parallel distributing processing. The noradrenergic neurons play a central role in coordinating the interaction of multiple cortical regions, which is an essential aspect of parallel distributed processing. Disturbances of this system in PTSD are likely to be manifest as a dysfunctional modulation of working memory and involuntary traumatic recollection. Modifications of neural networks have a secondary effect of kindling in the hippocampus that further moderates the individual's sensitivity to a range of stressors. Therefore, a neural network model of PTSD provides a method for conceptualizing the onset of PTSD symptoms and their subsequent modification with the passage of time.

Animals↗
PubMed2002

Neuroimaging studies in post-traumatic stress disorder.

The authors review some of the advances that have been made in understanding the structural, biochemical, and functional neuroanatomy of post-traumatic stress disorder (PTSD). First, the authors review the primary brain regions that had been hypothesized a priori, from the phenomenology and neurobiology of PTSD, to be implicated in the pathophysiology. Next, they review findings from neuroimaging studies of these brain regions in PTSD, and explain the various experimental methods and imaging technologies used in these studies. A broader perspective, including a discussion of additional brain areas that may be involved in PTSD, is synthesized. The authors conclude with a rationale and approach for studies testing sharply defined hypotheses and those using multidisciplinary strategies that integrate neuroimaging data with other cognitive, biologic, and genetic tools to study this complex disorder.

Amygdala↗
PubMed2002

Current status of cortisol findings in post-traumatic stress disorder.

This article summarizes findings of hypothalamic-pituitary-adrenal axis alterations in post-traumatic stress disorder (PTSD) and evaluates likely reasons for the lack of agreement among published studies. Sources of variance caused by methodologic and interpretative differences are highlighted, but the disparate findings are explained as illustrating a more complex neuroendocrinology of PTSD than has previously been described.

Arousal↗
PubMed2002

Treating survivors of the World Trade Center terrorist attacks of September 11, 2001.

As part of an established traumatic stress research and treatment program located in New York City, we experienced the September 11, 2001, terrorist attacks on the World Trade Center first as New Yorkers, but also as professionals with an interest in both treating the survivors and furthering scientific knowledge regarding the neurobiology and treatment of traumatic stress. This paper gives vignettes of calls to our program and the treatment of World Trade Center terrorist attack survivors.

Journal Article↗
PubMed2002

Clinical relevance of biologic findings in PTSD.

Posttraumatic stress disorder (PTSD) describes a syndrome in which a trauma survivor experiences an inability to get the event out of his/her mind. The symptoms of PTSD were initially conceptualized as resulting from the cascade of biological and psychological responses following the activation of fear and other brain systems. In the last decade, scientific developments have led to a better understanding of why only certain individuals develop this disorder. Furthermore, studies of the neurobiology of PTSD have delineated specific alterations that help shape our understanding of how biological and psychological responses at the time of traumatic events may have long-term consequences. This review will discuss these new findings and their treatment implications.

Arousal↗
PubMed2002

Longitudinal course of salivary cortisol in post-traumatic stress disorder.

OBJECTIVE: In chronic post-traumatic stress disorder (PTSD) lowered cortisol secretion and hypersuppression to dexamethasone has been described repeatedly. However, so far no longitudinal data on the natural course or on the effect of therapy are available. METHOD: We measured basal and post-dexamethasone morning salivary cortisol in a drug-free patient with chronic PTSD (DSM-IV) monthly for nearly 2 years and assessed PTSD and depressive symptoms. RESULTS: Salivary cortisol decreased dramatically 3 months after the traumatic event and in the further course showed an inverse relation to fluctuating but gradually improving PTSD symptoms. Post-dexa-methasone cortisol was suppressed below the detection limit early after trauma and rose again more than 1 year post-trauma. CONCLUSION: Both the potential renormalization of low cortisol levels in improving chronic PTSD and the putative vulnerability to develop PTSD in subjects with increased dexamethasone suppression need further research.

Adult↗
PubMed2002

Assessing dissociation as a risk factor for posttraumatic stress disorder: a study of adult offspring of holocaust survivors.

Dissociative symptoms are frequently present in trauma survivors with posttraumatic stress disorder (PTSD). However, the possibility that dissociative symptoms may comprise a risk factor for the development of PTSD has not been examined. The current research investigates this possibility by evaluating dissociative symptoms in a group of adult offspring of Holocaust survivors, whom we have previously shown to be at increased risk of PTSD. Eighty-seven Holocaust survivor offspring and 39 comparison participants completed the Dissociative Experiences Scale, and assessments of trauma exposure, psychopathology, and parental PTSD. Dissociative symptoms were elevated in individuals with current PTSD, but not in those with past PTSD or with the risk factor of parental PTSD. Dissociative symptoms were also associated with forms of psychopathology other than PTSD. The results suggest that dissociative symptoms are related to current psychiatric symptomatology, including PTSD, rather than representing an enduring trait or preexisting risk factor for the development of PTSD.

Adult↗
PubMed2002

Memory performance in Holocaust survivors with posttraumatic stress disorder.

OBJECTIVE: The authors evaluated memory performance in Holocaust survivors and its association with posttraumatic stress disorder (PTSD) and age. METHOD: Memory performance was measured in Holocaust survivors with PTSD (N=31) and without PTSD (N=16) and healthy Jewish adults not exposed to the Holocaust (N=35). Explicit and implicit memory were measured by paired-associate recall and word stem completion, respectively. RESULTS: The groups did not differ by age or gender, but the survivors with PTSD had significantly fewer years of education and had lower estimated IQs than the survivors without PTSD and the nonexposed group. There was a significant overall group effect for paired-associate recall but not word stem completion. The survivors with PTSD recalled fewer semantically unrelated words than did the survivors without PTSD and the nonexposed group and fewer semantically related words than the nonexposed group. Of the survivors with PTSD, 36% performed at a level indicative of frank cognitive impairment. Older age was significantly associated with poorer paired-associate recall in the survivors with PTSD but not in the other two groups. CONCLUSIONS: Markedly poorer explicit but not implicit memory was found in Holocaust survivors with PTSD, which may be a consequence of or a risk factor for chronic PTSD. Accelerated memory decline is one of several explanations for the significantly greater association of older age with poorer explicit memory in survivors with PTSD, which, if present, could increase the cognitive burden of this illness with aging.

Age Factors↗
PubMedDate not supplied

Relationship between dexamethasone-inhibited lysozyme activity in peripheral mononuclear leukocytes and the cortisol and glucocorticoid receptor response to dexamethasone.

The assessment of lysozyme activity in mononuclear leukocytes (MNLs) following the in vitro administration of dexamethasone (DEX) provides a measure of peripheral glucocorticoid sensitivity. The goal of the present study was to determine the relationship between the IC(50) of lysozyme activity following such challenge, and the cortisol response to oral administration of 0.50 mg DEX in 18 healthy subjects. The results demonstrated a robust association between the IC(50) and both cortisol decline and percent suppression of cortisol in response to low-dose DEX. However, this measure was uncorrelated with pre or post DEX cortisol levels or GR number. The high correlation between the inhibitory effect of DEX on lysozyme synthesis and two measures reflecting cortisol suppression in response to oral DEX reflects the similarities of GC responsiveness in both in vivo and in vitro models, and suggests that the in vitro assessment of lysozyme activity in MNLs may be useful in the study of neuropsychiatric or other clinical disorder.

Adult↗
PubMedDate not supplied

Cortisol levels in adult offspring of Holocaust survivors: relation to PTSD symptom severity in the parent and child.

We have previously demonstrated lower mean 24-h urinary cortisol excretion in adult offspring of Holocaust survivors with parental posttraumatic stress disorder (and lifetime PTSD), compared to offspring without parental PTSD, and to demographically similar comparison subjects. In the current study, we re-analyze data from our previously published report, plus four new subjects, to further examine the relationship between cortisol and severity of PTSD symptoms in offspring and their parents. We also examine the contribution of current depressive disorder to cortisol levels. Two-way analysis of variance revealed lifetime PTSD to be associated with significantly lower cortisol levels, while depressive disorder was associated with higher cortisol levels. The presence of parental PTSD was associated with lower cortisol excretion in the offspring only if both parents were affected. There were significant negative correlations between severity of parental PTSD and offspring urinary cortisol excretion, and between severity of offspring PTSD symptoms and urinary cortisol levels. The findings amplify our earlier descriptions of children of Holocaust survivors with PTSD as a sample 'at risk' for PTSD by demonstrating relationships between lowered cortisol excretion in these offspring and their experience of their parents' PTSD symptoms.

Adult↗
PubMedDate not supplied

Marked lability in urinary cortisol levels in subgroups of combat veterans with posttraumatic stress disorder during an intensive exposure treatment program.

OBJECTIVE: The objective of this study was to obtain longitudinal data on lability of cortisol levels in posttraumatic stress disorder (PTSD) because previous studies have largely been based on sampling at a single time point and have yielded varying results. METHODS: This study measured urinary cortisol levels at admission, midcourse, and discharge during a 90-day hospitalization period in male Vietnam combat veterans with PTSD (N = 51). RESULTS: Although there were no significant differences in the mean +/- SEM urinary cortisol levels between the admission (59.4 +/- 3.0 microg/d), midcourse (55.6 +/- 3.9 microg/d), and discharge (53.4 +/- 3.4 microg/d) values, marked lability of cortisol levels in individual patients was observed over time, with changes ranging from +93 to -58 microg/d from admission to midcourse. In addition, this hormonal lability defined discrete subgroups of patients on the basis of the longitudinal pattern of cortisol change during exposure treatment, and there were significant psychometric differences in the level of social functioning between these subgroups. CONCLUSIONS: The findings do not support the concept of either a static "hypocortisolism" or "hypercortisolism" in PTSD, but rather suggest a psychogenic basis for cortisol alterations in PTSD in relation to psychosocial stress and indicate a central regulatory dysfunction of the hypothalamic-pituitary-adrenal axis characterized by a dynamic tendency to overreact in both upward and downward directions. The longitudinal findings fit with recent observations that cortisol elevations occur when acutely superimposed stressful conditions emotionally engage patients and overwhelm the usually dominating disengaging coping mechanisms associated with suppression of cortisol levels in PTSD. The findings emphasize the importance of longitudinal data in studies of the hypothalamic-pituitary-adrenal axis in PTSD.

Adult↗
PubMedDate not supplied

Posttraumatic stress, nonadherence, and adverse outcome in survivors of a myocardial infarction.

OBJECTIVE: Posttraumatic stress disorder (PTSD) symptoms have been reported in patients with coronary vascular disease, after the trauma of a myocardial infarction (MI). The effect of these symptoms on post-MI disease control has not been elucidated. We conducted a study that sought to determine whether PTSD symptoms post-MI are associated with increased likelihood of cardiovascular readmission and with nonadherence to treatment recommendations. METHODS: Patients were recruited during a visit in a cardiology clinic 6 months post-MI and were followed for 1 year. Adherence to aspirin was measured by platelet thromboxane production (an indication of aspirin's effect). Medical outcome was measured as rate of admission due to cardiovascular causes during the follow-up period. Self-report measures of PTSD (Impact of Event Scale), Depression, and Global Distress (SCL-90-R) were administered at enrollment. RESULTS: Seventy-three patients were studied. Above-threshold PTSD symptom scores at enrollment, but not depression or global distress scores, were significant predictors of nonadherence to aspirin and of an increased likelihood of cardiovascular readmission over the course of the following year. CONCLUSIONS: PTSD symptoms predicted poor disease control in this cohort of MI survivors. The data suggest that screening MI survivors for symptoms of PTSD may be beneficial if this high-risk population is to be targeted for interventions.

Aspirin↗
PubMedDate not supplied

Symptoms of posttraumatic stress disorder in patients who have had a myocardial infarction.

Symptoms of posttraumatic stress disorder (PTSD) and risk factors for recurrent ischemia were evaluated in 65 survivors of a myocardial infarction (MI) at baseline and 6 months afterward. PTSD patients had more uncontrolled cardiovascular risk factors at baseline. Patients with PTSD (N=14) were offered trauma-focused cognitive-behavior treatment (CBT) plus a nonspecific intervention to improve adherence to medical recommendations. Adherence to aspirin improved in recipients of the nonspecific intervention (N=8); PTSD symptoms and cardiovascular risk improved in patients who received CBT (N=6). PTSD may be a treatable risk factor for poor post-MI outcome. Further research is needed to evaluate treatment options.

Aged↗