RELATIONSHIP BETWEEN BIO. AND PSYCH. CORRELATES OF PTSD

描述（由申请人提供）：赠款建议采用纵向设计 研究PTSD的生物学改变， 预期在延长暴露治疗（PE）后改善。因为一个伟大的 大多数接受PE的创伤受害者在以下方面表现出显着改善： 临床症状，检查生物学参数之前，期间和之后 这种操作提供了一个机会，探索之间的关系， 生物学改变，PTSD症状严重程度和认知的变化 与疾病有关。因此，本研究关注 生理变化和心理因素（包括 对世界的危险和自我无能的功能失调的认知） 与慢性创伤后应激障碍有关，特别是因为它们可能会随着 减少PTSD症状。此外，研究将评估是否 与慢性创伤后应激障碍相关的生物学改变预测，或改变 与治疗结果的关系。纵向设计， 测量将使我们能够获得解决时间问题的数据， 症状严重程度变化与生物和认知的关系 变量如果生物学改变主要与症状有关， 严重程度和/或认知因素，维持创伤后应激障碍，然后成功地 治疗症状应该改变生物学发现的方向， 常态然而，有可能发生症状严重程度的变化 在神经内分泌特征没有显著变化的情况下， 与潜在风险相关的模式，而不是与 这种混乱。这些问题的解决对以下方面具有重要意义： 了解PTSD的病理生理学，并可能提供深入了解 与成功的心理治疗相关的机制 disorder.

DESCRIPTION (provided by applicant): The grant proposes to employ a longitudinal design to examine alterations in the biology of PTSD in individuals whose symptoms are expected to improve following prolonged exposure therapy (PE). Because a great majority of trauma victims who receive PE show significant improvement in clinical symptoms, examining biological parameters before, during, and after this manipulation provides an opportunity to explore the relationships among biological alterations, changes in PTSD symptom severity, and cognitions related to the disorder. Thus, this study is interested in the relationship between biological alterations and psychological factors (including dysfunctional cognitions about the danger of the world and self- incompetence) that have been implicated in chronic PTSD, particularly as they may change with reduction in PTSD symptoms. Furthermore, the study will assess whether biological alterations associated with chronic PTSD predict, or are altered in relation to, therapeutic outcome. The longitudinal design with multiple measurements will allow us to obtain data that address the temporal relationship between changes in symptom severity with biological and cognitive variables. If biological alterations are principally related to symptom severity and/or cognitive factors that maintain PTSD, then successfully treating the symptoms should alter biological findings in the direction of normality. However, it is possible that changes in symptom severity may occur in the absence of significant shifts in neuroendocrine profile, suggesting a pattern related to underlying risk rather than to symptomatic expression in this disorder. The resolution of these questions has important implications for understanding the pathophysiology of PTSD, and may provide insight into the mechanisms associated with successful psychological treatment for this disorder.