PTSD & Childhood Sexual Abuse: Psychobiology

描述(申请人提供)：本申请为期5年 横断面调查，为期一年的前瞻性随访 非侵入性检查儿童创伤后应激的心理生物学 性虐待引起的精神障碍(PTSD)。在横断面研究中，我们 报告称，经临床转介的患有创伤后应激障碍的虐待儿童的比例上升 24小时尿儿茶酚胺和游离皮质醇水平与较小的颅内 和大脑体积，较小的胼胝体中部矢状区。和 与未滥用的对照组相比，脑室更大。大多数人的创伤后应激障碍 其中一名儿童是性虐待。开始虐待的年龄越早，时间越长 虐待的持续时间和更严重的创伤后应激障碍症状都与更多的 在这些衡量标准上与正常标准有极大的差异。动物研究表明 发育过程中儿茶酚胺和皮质醇水平升高可能会导致 大脑发育不良。我们的初步研究没有解决我们的 结果是创伤后应激障碍特有的或滥用的结果。我们将研究 创伤后应激障碍的诊断和严重程度对生物应激系统结局的影响 调节和大脑成熟。我们将研究3组70名儿童(35名 男/35女)，6至12岁：继发性创伤后应激障碍儿童 虐待，没有创伤后应激障碍的性虐待儿童，以及未受创伤的年龄和 社会人口学上具有可比性的对照。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。 大脑成熟度将通过以下方式进行评估：基于磁共振波谱 大脑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(大脑， 杏仁核/海马体体积和穹隆体区)，以及认知功能。 这项研究包括进入时的横截面成分(时间-01)和 一年随访(TIME-02)。被虐待对象的研究条目在3个以内 几个月来的虐待行为曝光。TIME-01和-02评估衡量已知风险 影响创伤后应激障碍发生的因素。具体目标是确定 伴发与不伴发创伤后应激障碍的性虐待与预后的关系 在TIME-01，并确定患有创伤后应激障碍的性虐待和 没有创伤后应激障碍的性虐待对这些儿童的生物压力系统 和神经心理功能。次要目标是：确定 创伤后应激障碍持久性和抗创伤后应激障碍的心理生物学预测因子 在披露滥用后的一年期间(Time-02)。我们假设 患有创伤后应激障碍的性虐待儿童将显示出 时间-01和时间-02的生物应激系统和大脑成熟。我们 进一步假设时间-01的某些危险因素(如发病年龄 虐待、不良生活事件和生物测量)将预测 持续时间为-02的创伤后应激障碍。

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.