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PTSD & Childhood Sexual Abuse: Psychobiology

PTSD & Childhood Sexual Abuse: Psychobiology
创伤后应激障碍
批准号:
6658007
负责人:
Michael Damingo De Bellis
金额:
$51.38万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2002
资助国家:
美国
项目状态:
已结题
起止时间:
2002-09-09 至 2007-08-31

项目摘要

项目成果

Michael Damingo De Bellis的其他基金

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中文摘要
翻译
描述(由申请人提供):本申请为5年期 一项横断面调查,前瞻性随访一年, 非侵入性地检查儿童创伤后压力的心理生物学 创伤后应激障碍(PTSD)继发于性虐待。在横向研究中,我们 报告说,临床上提到的虐待儿童与创伤后应激障碍, 24-小时尿儿茶酚胺和游离皮质醇水平和较小的颅内压 和大脑体积,胼胝体的更小的正中矢状区。和 与未滥用对照组相比,心室更大。创伤后应激障碍对大多数人来说 是性虐待开始受虐待的年龄较早, 滥用的持续时间和更大的PTSD症状与更多的 和正常人有很大的不同动物研究表明, 在发育过程中升高的儿茶酚胺和皮质醇水平可能导致 对大脑发育不利我们的试点研究并没有解决我们在多大程度上 结果是创伤后应激障碍或虐待的结果。我们会研究 创伤后应激障碍的诊断和严重程度对生物应激系统结果的影响 调节和大脑成熟。我们将研究3组70名儿童(35 男性/35名女性),6至12岁:继发于性行为的创伤后应激障碍儿童 虐待,性虐待儿童没有创伤后应激障碍,和非创伤的年龄, 社会人口统计学可比对照。生物胁迫系统调控 将通过24小时尿儿茶酚胺和游离皮质醇水平进行评估。 将通过以下方法评估脑成熟:基于磁共振波谱的 脑N-乙酰天冬氨酸浓度,反映神经元的完整性, 基于磁共振成像的脑形态测量(脑, 杏仁核/海马体积和胼胝体面积)和认知功能。 本研究包括入组时的横截面部分(时间-01)和 1年随访(Time-02)。滥用受试者的研究入组时间在3 几个月的滥用披露。时间-01和-02评估测量已知风险 PTSD的发展因素。具体目标是确定 有和没有PTSD的性虐待与这些结果之间的关系 在时间-01,并确定性虐待与创伤后应激障碍的一年影响, 没有创伤后应激障碍的性虐待对这些孩子的生物压力系统的影响 和神经心理功能。次要目标是:确定 PTSD持续性和对PTSD的恢复力的心理生物学预测因子 在滥用披露后的一年期间(时间-02)。我们假设 患有创伤后应激障碍的性虐待儿童将显示出改变的证据, 时间-01和02时的生物应激系统和脑成熟。我们 进一步假设时间-01时的某些风险因素(例如, 虐待、不良生活事件和生物学测量)将预测 时间02时PTSD的持续性。
英文摘要
DESCRIPTION (provided by applicant): This application is a 5-year cross-sectional investigation with a one-year prospective follow-up to non-invasively examine the psychobiology of childhood posttraumatic stress disorder (PTSD) secondary to sexual abuse. In cross-sectional studies, we reported that clinically referred maltreated children with PTSD had elevated 24-hour urinary catecholamine and free cortisol levels and smaller intracranial and cerebral volumes, smaller midsaggital areas of the corpus callosum. and larger ventricles compared to non-abused controls. PTSD trauma for the majority of these children was sexual abuse. Earlier age of onset of abuse, longer duration of abuse, and greater PTSD symptoms each were associated with more extreme difference from normals on these measures. Animal studies suggest that elevated levels of catecholamines and cortisol during development may lead to adverse brain development. Our pilot study did not address to what extent our results were PTSD specific or the result of abuse. We will examine the diagnosis and severity of PTSD on outcomes of biological stress system regulation and brain maturation. We will study 3 groups of 70 children (35 males/35 females), aged 6 to 12 years: children with PTSD secondary to sexual abuse, sexually abused children without PTSD, and non-traumatized age and sociodemographically comparable controls. Biological stress system regulation will be assessed by 24-hour urinary catecholamine and free cortisol levels. Brain maturation will be assessed by: magnetic resonance spectroscopy-based brain N-acetylaspartate concentrations, which reflect neuronal integrity, magnetic resonance imaging-based brain morphometry (cerebral, amygdala/hippocampal volumes and corpus callosum area), and cognitive function. This study includes a cross-sectional component at entry (Time-01) and a one-year follow-up (Time-02). Study entry for abused subjects is within 3 months of abuse disclosure. Time-01 and -02 assessments measure known risk factors for the development of PTSD. Specific aims are to determine the relationship between sexual abuse with PTSD and without PTSD and these outcomes at Time-01 and to determine the one-year effects of sexual abuse with PTSD and sexual abuse without PTSD on these same children's biological stress systems and neuropsychological function. Secondary aims are: to identify the psychobiological predictors of the persistence of PTSD and resiliency to PTSD at the one-year period after abuse disclosure (Time-02). We hypothesize that sexually abused children with PTSD will show evidence of alterations in biological stress systems and brain maturation at Time-01 and Time-02. We further hypothesize that certain risk factors at Time-01 (e.g. age of onset of abuse, adverse life events, and biological measures) will predict the persistence of PTSD at Time-02.
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会议论文
National Consortium on Alcohol and NeuroDevelopment in Adolescence: Duke
  • 批准号:
    8412987
  • 项目类别:
  • 资助金额:
    $73.36万
  • 财政年份:
    2012
  • 负责人:
    Michael Damingo De Bellis
  • 依托单位:
National Consortium on Alcohol and NeuroDevelopment in Adolescence: Duke
  • 批准号:
    8534003
  • 项目类别:
  • 资助金额:
    $68.74万
  • 财政年份:
    2012
  • 负责人:
    Michael Damingo De Bellis
  • 依托单位:
National Consortium on Alcohol and NeuroDevelopment in Adolescence: Duke
  • 批准号:
    8693886
  • 项目类别:
  • 资助金额:
    $71.63万
  • 财政年份:
    2012
  • 负责人:
    Michael Damingo De Bellis
  • 依托单位:
Prefrontal Function in Adolescent Limited vs Life Course Persistent SUD
  • 批准号:
    8069994
  • 项目类别:
  • 资助金额:
    $66.03万
  • 财政年份:
    2008
  • 负责人:
    Michael Damingo De Bellis
  • 依托单位: