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RELATIONSHIP BETWEEN BIO. AND PSYCH. CORRELATES OF PTSD

RELATIONSHIP BETWEEN BIO. AND PSYCH. CORRELATES OF PTSD
生物之间的关系。
批准号:
6528640
负责人:
EDNA B FOA
金额:
$37.79万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-09-01 至 2006-07-31

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中文摘要
翻译
描述(申请人提供):拨款建议采用纵向设计 检查创伤后应激障碍的生物学变化,其症状为 预计在长期暴露治疗(PE)后会有所改善。因为一个伟大的 大多数接受PE的创伤受害者在 临床症状,检查治疗前、治疗中和治疗后的生物学指标 这种操作提供了一个机会来探索 生物学改变、创伤后应激障碍症状严重程度和认知的变化 与这种疾病有关。因此,本研究对这一关系感兴趣 生物变化和心理因素(包括 对世界的危险和自我无能的功能障碍的认知) 与慢性创伤后应激障碍有牵连,特别是当它们可能随着 创伤后应激障碍症状的减少。此外,该研究将评估是否 与慢性创伤后应激障碍相关的生物学改变预测,或在 与治疗结果的关系。多重纵向设计 测量将使我们能够获得解决时间问题的数据 症状严重程度的变化与生物学和认知的关系 变量。如果生物变化主要与症状有关 严重程度和/或认知因素,维持创伤后应激障碍,然后成功 治疗这些症状应该改变生物学发现的方向 正常。但是,可能会发生症状严重性的变化 在神经内分泌特征没有显著变化的情况下,表明 与潜在风险相关的模式,而不是与症状表现相关的模式 这种紊乱。这些问题的解决对以下方面具有重要影响 了解创伤后应激障碍的病理生理学,有助于深入了解创伤后应激障碍 与成功的心理治疗相关的机制 无序。
英文摘要
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.
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