权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

A critical test of neural models of risk among adolescent assault victims

对青少年袭击受害者风险神经模型的关键测试

基本信息

批准号：
8868347
负责人：
Joshua M Cisler
金额：
$ 23.16万
依托单位：
UNIV OF ARKANSAS FOR MED SCIS
依托单位国家：
美国
项目类别：
财政年份：
2015
资助国家：
美国
起止时间：
2015-04-15 至 2017-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8868347
关键词：
Adolescence Adolescent Adult Anterior Behavioral Bilateral Brain Clinical Data Decision Making Detection Development Dorsal Early-life trauma Emotions Employee Strikes Exploratory/Developmental Grant Exploratory/Developmental Grant for Diagnostic Cancer Imaging Female Adolescents Fright Functional Magnetic Resonance Imaging Future Goals Individual Intervention Lead Life Light Measures Mediating Mental Depression Mental Health Mental disorders Modeling National Institute of Mental Health Outcome Participant Perception Performance Pilot Projects Population Populations at Risk Post-Traumatic Stress Disorders Prevention program Process Psychopathology Recruitment Activity Research Risk Risk Factors Role Social Behavior Social Functioning Substance Use Disorder Symptoms Testing Theoretical model Toxic effect Trauma Trust Variant Violence Writing assault base behavior measurement cingulate cortex cognitive development functional disability high risk sexual behavior improved learning extinction longitudinal course neural correlate neural model neuromechanism novel peer physical assault programs public health relevance relating to nervous system response revictimization risk perception sexual assault social social learning social situation social skills treatment program

项目摘要

DESCRIPTION (provided by applicant): This proposal for a NIMH Exploratory/Developmental Grant Award (R21) seeks to critically evaluate and expand upon leading neurocircuitry models of trauma and PTSD among assaulted adolescent girls. Existing neurocircuitry models of trauma and PTSD focus almost exclusively on identifying the neural mechanisms that explain observed hypervigilance for threat and deficits in fear extinction learning. While these models have ample empirical support, they do not explain known deficits in risk perceptions of social situations and increased rates of revictimization among assault-exposed and PTSD populations. By contrast, our pilot study demonstrated that assaulted adolescent girls display both worse behavioral performance and decreased activation of anterior cingulate cortex and bilateral anterior insular cortex during a social learning task, which suggests a novel mechanism to explain known social functioning deficits in these populations. Based on these pilot data, we hypothesize that expanding existing neurorcircuitry models to include weakened brain and behavioral correlates of social prediction error encoding increases explanatory power for PTSD symptoms and functional deficits among assaulted adolescent girls. We propose to recruit control, assaulted without PTSD, and assaulted with PTSD adolescent girls and administer both a threat processing task and our previously used social learning task during fMRI. Participants would also complete a standardized risk perception task, in which they are presented with written vignettes depicting increasingly dangerous social situations. Aim 1 seeks to demonstrate that weakened encoding of social prediction errors among assaulted adolescent girls mediates decreased risk perceptions to the standardized risk social situation vignettes when controlling for variance explained by neural mechanisms on the threat processing task. Aim 2 seeks to demonstrate that weakened encoding of social prediction errors among assaulted adolescent girls predicts 3-month trajectories of PTSD symptoms when controlling for variance explained by neural mechanisms on the threat detection task. The overarching purpose of the proposed project is to demonstrate increased explanatory power of a neurocircuitry model that includes social processing deficits. Successful completion of the proposed project would stimulate new conceptualizations of the toxic effects of early life trauma and PTSD, and hopefully lead to improved prevention and treatment programs.

描述（由申请人提供）：NIMH探索/发展补助金（R21）的提案旨在批判性地评估和扩展受攻击少女中创伤和创伤后应激障碍的主要神经回路模型。现有的创伤和创伤后应激障碍的神经回路模型几乎完全集中在确定神经机制，解释观察到的过度警觉的威胁和恐惧消退学习的缺陷。虽然这些模型有充分的实证支持，他们不解释已知的赤字在社会情况下的风险认知和攻击暴露和创伤后应激障碍人群之间的再受害率增加。相比之下，我们的初步研究表明，被攻击的青春期女孩在社会学习任务中表现出更差的行为表现和前扣带皮层和双侧前岛叶皮层的激活减少，这表明了一种新的机制来解释这些人群中已知的社会功能缺陷。基于这些试点数据，我们假设，扩大现有的神经回路模型，包括削弱的大脑和行为相关的社会预测错误编码增加的解释力创伤后应激障碍的症状和功能缺陷的攻击青春期女孩。我们建议招募控制，袭击没有创伤后应激障碍，并与创伤后应激障碍的青春期女孩和管理的威胁处理任务和我们以前使用的社会学习任务在功能磁共振成像。参与者还将完成一项标准化的风险认知任务，在这项任务中，他们将看到描述日益危险的社会情况的书面小插曲。目的1旨在证明，弱化编码的社会预测错误之间的攻击青春期少女介导降低风险的看法，标准化的风险社会情况的小插曲时，控制方差解释的神经机制的威胁处理任务。目的2旨在证明，弱化的编码的社会预测错误的攻击青春期女孩预测3个月的轨迹PTSD症状时，控制方差解释的神经机制的威胁检测任务。所提出的项目的首要目的是证明增加的解释能力的神经回路模型，包括社会处理缺陷。成功完成拟议的项目将激发对早期生活创伤和创伤后应激障碍的毒性影响的新概念，并有望改善预防和治疗方案。