848 resultados para Complex posttraumatic stress disorder


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Background: Impairments in explicit memory have been observed in Holocaust survivors with posttraumatic stress disorder. Methods: To evaluate which memory components are preferentially affected, the California Verbal Learning Test was administered to Holocaust survivors with (n = 36) and without (n = 26) posttraumatic stress disorder, and subjects not exposed to the Holocaust (n = 40). Results: Posttraumatic stress disorder subjects showed impairments in learning and short-term and delayed retention compared to nonexposed subjects; survivors without posttraumatic stress disorder did not. Impairments in learning, but not retention, were retained after controlling fir intelligence quotient. Older age was associated with poorer learning and memory performance in the posttraumatic stress disorder group only. Conclusions: The most robust impairment observed in posttraumatic stress disorder was in verbal learning, which may be a risk factor for or consequence of chronic posttraumatic stress disorder. The negative association between performance and age may reflect accelerated cognitive decline in posttraumatic stress disorder.

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Intrusive reexperiencing in posttraumatic stress disorder (PTSD) has been linked to perceptual priming for trauma-related material. A prospective longitudinal study (N = 69) investigated perceptual priming for trauma-related, general threat, and neutral words in assault survivors with and without PTSD, using a new version of the word-stem completion task. Survivors with PTSD showed enhanced priming for trauma-related words. Furthermore, priming for trauma-related words measured soon after the trauma was associated with subsequent PTSD severity at 3 6, and 9 months. The enhanced priming effect was specific to trauma-related words. Enhanced perceptual priming for traumatic material appears to be one of the cognitive processes operating in PTSD.

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Two studies of assault victims examined the roles of (a) disorganized trauma memories in the development of posttraumatic stress disorder (PTSD), (b) peritraumatic cognitive processing in the development of problematic memories and PTSD, and (c) ongoing dissociation and negative appraisals of memories in maintaining symptomatology. In the cross-sectional study (n = 81), comparisons of current, past, and no-PTSD groups suggested that peritraumatic cognitive processing is related to the development of disorganized memories and PTSD. Ongoing dissociation and negative appraisals served to maintain PTSD symptoms. The prospective study (n = 73) replicated these findings longitudinally. Cognitive and memory assessments completed within 12-weeks postassault predicted 6-month symptoms. Assault severity measures explained 22% of symptom variance; measures of cognitive processing, memory disorganization, and appraisals increased prediction accuracy to 71%.

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There is a high prevalence of traumatic events within individuals diagnosed with schizophrenia, and of auditory hallucinations within individuals diagnosed with posttraumatic stress disorder (PTSD). However, the relationship between the symptoms associated with these disorders remains poorly understood. We conducted a multidimensional assessment of auditory hallucinations within a sample diagnosed with schizophrenia and substance abuse, both with and without co-morbid PTSD. Results suggest a rate of co-morbid PTSD similar to those reported within other studies. Patients who suffered co-morbid PTSD reported more distressing auditory hallucinations. However, the hallucinations were not more frequent or of longer duration. The need for a multidimensional assessment is supported. Results are discussed within current theoretical accounts of traumatic psychosis.

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Contrary to expectations derived from preclinical studies of the effects of stress, and imaging studies of adults with posttraumatic stress disorder (PTSD), there is no evidence of hippocampus atrophy in children with PTSD. Multiple pediatric studies have reported reductions in the corpus callosum - the primary white matter tract in the brain. Consequently, in the present study, diffusion tensor imaging was used to assess white matter integrity in the corpus callosum in 17 maltreated children with PTSD and 15 demographically matched normal controls. Children with PTSD had reduced fractional anisotropy in the medial and posterior corpus, a region which contains interhemispheric projections from brain structures involved in circuits that mediate the processing of emotional stimuli and various memory functions - core disturbances associated with a history of trauma. Further exploration of the effects of stress on the corpus callosum and white matter development appears a promising strategy to better understand the pathophysiology of PTSD in children. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

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Research in rodents demonstrated that psychological stress increases circulating levels of alanine transaminase, aspartate transaminase, and alkaline phosphatase reflecting liver injury. Moreover, chronic posttraumatic stress disorder and transaminases predicted coronary heart disease.

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Inflammation might link posttraumatic stress disorder (PTSD) with an increased risk of cardiovascular events. We explored the association between PTSD and inflammatory biomarkers related to cardiovascular morbidity and the role of co-morbid depressive symptoms in this relationship.

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Chronic posttraumatic stress disorder (PTSD) has been associated with perturbed hypothalamic-pituitary-adrenal (HPA) axis function and a hyperadrenergic state. We hypothesized that patients with PTSD attributable to myocardial infarction (MI) would show peripheral hypocortisolemia and increased norepinephrine levels, whereby taking into account that depressive symptoms would affect this relationship.

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Posttraumatic stress disorder (PTSD) and circulating cellular adhesion molecules (CAMs) predict cardiovascular risk. We hypothesized a positive relationship between PTSD caused by myocardial infarction (MI) and soluble CAMs. We enrolled 22 post-MI patients with interviewer-rated PTSD and 22 post-MI patients with no PTSD. At 32±6months after index MI, all patients were re-scheduled to undergo the Clinician-Administered PTSD Scale (CAPS) interview and had blood collected to assess soluble CAMs at rest and after the CAPS interview. Relative to patients with no PTSD, those with PTSD had significantly higher levels of soluble vascular cellular adhesion molecule (sVCAM)-1 and intercellular adhesion molecule (sICAM)-1 at rest and, controlling for resting CAM levels, significantly higher sVCAM-1 and sICAM-1 after the interview. Greater severity of PTSD predicted significantly higher resting levels of sVCAM-1 and soluble P-selectin in patients with PTSD. At follow-up, patients with persistent PTSD (n=15) and those who had remitted (n=7) did not significantly differ in CAM levels at rest and after the interview; however, both these groups had significantly higher sVCAM-1 and sICAM-1 at rest and also after the interview compared to patients with no PTSD. Elevated levels of circulating CAMs might help explain the psychophysiologic link of PTSD with cardiovascular risk.

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Hypercoagulability of the blood might partially explain the increased cardiovascular disease risk in posttraumatic stress disorder (PTSD) and is also triggered by anticipatory stress. We hypothesized exaggerated procoagulant reactivity in patients with PTSD in response to a trauma-specific interview that would be moderated by momentary stress levels. We examined 23 patients with interviewer-diagnosed PTSD caused by myocardial infarction (MI) and 21 post-MI patients without PTSD. A second diagnostic (i.e., trauma-specific) interview to assess posttraumatic stress severity was performed after a median follow-up of 26 months (range 12-36). Before that interview patients rated levels of momentary stress (Likert scale 0-10) and had blood collected before and after the interview. The interaction between PTSD diagnostic status at study entry and level of momentary stress before the follow-up interview predicted reactivity of fibrinogen (P=0.036) and d-dimer (P=0.002) to the PTSD interview. Among patients with high momentary stress levels, PTSD patients had greater fibrinogen (P=0.023) and d-dimer (P=0.035) reactivity than non-PTSD patients. Among patients with low momentary stress levels, PTSD patients had less d-dimer reactivity than non-PTSD patients (P=0.024); fibrinogen reactivity did not significantly differ between groups. Momentary stress levels, but not severity of posttraumatic stress, correlated with d-dimer reactivity in PTSD patients (r=0.46, P=0.029). We conclude that momentary stress levels moderated the relationship between PTSD and procoagulant reactivity to a trauma-specific interview. Procoagulant reactivity in post-MI patients with PTSD confronted with their traumatically experienced MI was observed if patients perceived high levels of momentary stress before the interview.

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Based on a brief systematic review suggesting dyslipidemia in posttraumatic stress disorder (PTSD), we studied, for the first time, levels of blood lipids in patients with a DSM-IV diagnosis of PTSD caused by myocardial infarction (MI).

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In my thesis, I incorporate both psychological research and personal narratives in order to explain why, in the aftermath of the Vietnam War, the United States officially recognized Post-Traumatic Stress Disorder while the Vietnamese government did not. The absence of Vietnamese studies on the impact of PTSD on veterans, in comparison to the abundance of research collected on American soldiers, is reflective not of a disparity in the actual prevalence of the disorder, but of the influence of political policy on the scope of Vietnamese psychology. Personal narratives from Vietnamese civilians and soldiers thus reveal accounts of trauma otherwise hidden due to the absence of Vietnamese psychological research. Although these two nations conspicuously differed in their respective responses to the prevalence of psychological trauma in war veterans, these responses demonstrated that both the recognition and rejection of PTSD was a result of sociopolitical factors: political ideologies, rather than scientific reasons, dictated whether the postwar trajectory of psychological research focused on fully exploring the impact of PTSD on veteran populations. The association of military defeat with psychological trauma thus fixed attention on certain groups of veterans, including former American and South Vietnamese soldiers, while ignoring the impact of trauma on veterans of the Viet Cong and North Vietnamese Army. The correlation of a soldier¿s ideological background with psychological trauma, rather than exposure to actual traumatic experiences, demonstrates that cultural and sociopolitical factors are far more influential in the construction of PTSD than objective indicators of the disorder¿s prevalence. Culturally-constructed responses to disorders such as PTSD therefore account for the subjective treatment of mental illness. The American and Vietnamese responses to veterans suffering from PTSD both demonstrated that the evidence of mental health problems in an individual does not guarantee an immediate or appropriate diagnosis and treatment regimen. External authorities whose primary aims are not necessarily concerned with the objective treatment of all victims of mental illness subjectively dictate mental health care policy, and therefore risk ignoring or marginalizing the needs of individuals in need of proper treatment.