Risk and Resilience in Urban Black American Acute Trauma Survivors

美国城市黑人急性创伤幸存者的风险和复原力

• 批准号: 10379585
• 负责人: Christine L Larson
• 金额: $ 79.2万
• 依托单位: UNIVERSITY OF WISCONSIN MILWAUKEE
• 依托单位国家: 美国
• 财政年份: 2021
• 资助国家: 美国
• 起止时间: 2021-09-16 至 2026-07-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10379585
• 关键词: Accident and Emergency department; Acute; Adult; Affect; African American; Amines; Amygdaloid structure; Anxiety; Arousal; Behavioral; Biological; Brain; Child Abuse and Neglect; Chronic; Chronic Post Traumatic Stress Disorder; Communities; Complement; Data; Disadvantaged; Discrimination; Distress; Early Intervention; Early identification; Endocannabinoids; Environmental Risk Factor; Exposure to; Goals; Health; Hospitals; Image; Individual; Inflammatory; Intervention; Knowledge; Lead; Light; Link; Machine Learning; Measures; Mental Depression; Mental Health; Mental disorders; Minority; Minority Groups; Nature; Neighborhoods; Neurobiology; Outcome; Partner in relationship; Pathology; Patient Self-Report; Play; Population; Post-Traumatic Stress Disorders; Predictive Factor; Process; Prognosis; Public Health; Quality of life; Race; Recording of previous events; Recovery; Regulation; Research; Resources; Risk; Risk Factors; Role; Sampling; Sensitivity and Specificity; Social Environment; Specific qualifier value; Stress; Suicide; Survivors; Symptoms; System; Trauma; United States; Violence; Visit; Wisconsin; Work; adverse outcome; allostatic load; base; biological adaptation to stress; brain health; cytokine; deprivation; emotion regulation; ethnic minority population; experience; high risk; improved; indexing; innovation; intersectionality; medical schools; neural circuit; neurobehavioral; neurobiological mechanism; neuroimaging marker; neuromechanism; pediatric trauma; physical conditioning; post-trauma; predictive marker; preventive intervention; protective factors; racial and ethnic; racial minority; recruit; relating to nervous system; resilience; risk prediction; socioenvironmental factor; stress management; stressor; trauma exposure; trauma symptom; violence exposure

PROJECT ABSTRACT Trauma is common and increases risk for a host of negative health outcomes, most notably posttraumatic stress disorder (PTSD). Given the potential harmful sequelae of trauma exposure, it is crucial to identify acute post-trauma risk factors that predict chronic PTSD. Moreover, urban racial/ethnic minorities can experience significant environmental stress that puts them at particularly high risk for PTSD. At this juncture relatively little data exists to aid in prediction of risk specific to urban racial minorities, or that takes into account how disadvantage and minority stress may impact neurobiological stress systems in the months following trauma, and how that affects risk for long-term distress. Thus, under the guidance of a community advisory board our team will 1) identify acute post-trauma neurobehavioral predictors of risk for chronic PTSD among urban Black Americans, with a focus on prefrontal-subcortical function during processing of threat, 2) characterize how the longitudinal interaction of socioenvironmental risk and resilience factors and biological stress markers following trauma impacts risk, and 3) use machine learning to identify the most robust set of predictors of chronic PTSD drawn from a comprehensive assessment of neuroimaging, biomarkers, self-report and geocoded risk and resilience variables. We will recruit 190 adults who identify as Black or African American from the Emergency Department at Froedtert Hospital/Medical College of Wisconsin in Milwaukee, and conduct comprehensive assessments at 2 weeks, and 3, 6, and 12 months following trauma exposure. The two-week and 12-month assessments will include measures of neural systems for threat processing, including both anticipation of and reactivity to threat. All visits will include measures of PTSD and other symptoms, neurobiological stress markers, particularly endocannabinoids, and socioenvironmental risk and resilience factors, especially those relevant for urban Black Americans. We will examine how acute post-trauma neurocircuitry variables (2 week) predict PTSD and other outcomes twelve months later, and how pre-trauma environmental variables (resource deprivation, child maltreatment, violence exposure) moderate this relationship (Aim 1). We will also assess how, in the months following trauma, socio-environmental risk and resilience factors influence neurobiological stress systems, and how this interaction impacts risk for PTSD, poor physical health, and emotion regulation neurocircuitry at twelve months (Aim 2). We will use both hypothesis-driven analyses focusing on a priori specified predictors (Aims 1 and 2), as well as comprehensive data-driven machine learning analyses (Aim 3). This approach will allow for determination of the additional utility of neurobiological markers for predicting risk beyond previously identified self-report indicators. We expect this project to lead to identification of predictors of PTSD following trauma for urban Black Americans at high risk that are linked to underlying processes (hyper-responsivity to threat, aberrant neurobiological stress response) that can inform preventive interventions, ultimately improving the quality of life for urban Black American trauma survivors.

项目摘要 创伤很常见，增加了许多负面健康结果的风险，最著名的是创伤后 应激障碍（PTSD）。鉴于创伤暴露的潜在有害后遗症，至关重要的是识别急性 可预测慢性PTSD的创伤后风险因素。此外，城市种族/族裔少数民族可以体验 巨大的环境压力使他们对PTSD的风险特别高。在这个关头相对较少 存在数据是为了帮助预测城市种族少数群体的风险，或者考虑到如何 在创伤后的几个月中，劣势和少数压力可能会影响神经生物学压力系统， 以及这如何影响长期困扰的风险。因此，在社区顾问委员会的指导下 团队将1）确定城市黑色慢性PTSD风险的急性创伤后神经行为预测指标 美国人，重点是在威胁处理期间的前额叶和皮质功能，2）表征如何 社会环境风险和弹性因素和生物压力标志物的纵向相互作用 创伤会影响风险，3）使用机器学习来识别慢性PTSD的最强大预测因子 从对神经影像，生物标志物，自我报告和地理编码风险的全面评估中得出 弹性变量。我们将在紧急情况下招募190名成年人 密尔沃基威斯康星州Froedtert医院/医学院的系，并进行全面 创伤暴露后2周，3、6和12个月的评估。为期两个星期和12个月 评估将包括对威胁处理的神经系统的衡量标准，包括预期和 对威胁的反应性。所有访问都将包括PTSD和其他症状的措施，神经生物学压力 标记物，特别是内源性大麻素以及社会环境风险和韧性因素，尤其是那些 与城市黑人美国人有关。我们将研究急性急性创伤后神经通路变量（2周） 预测PTSD和其他成果十二个月后，以及创伤前的环境变量（资源） 剥夺，儿童虐待，暴力暴露）适应这种关系（目标1）。我们还将评估 在创伤后的几个月中，社会环境风险和弹性因素影响神经生物学 压力系统，以及这种相互作用如何影响PTSD的风险，身体健康状况不佳和情绪调节 十二个月时的神经通路（AIM 2）。我们将使用针对先验的假设驱动的分析 指定的预测因子（目标1和2）以及全面的数据驱动机器学习分析（AIM 3）。 这种方法将允许确定神经生物学标记的额外效用以预测风险 超越先前确定的自我报告指标。我们希望该项目能够识别预测因子 PTSD的创伤后针对城市黑人美国人高风险的创伤，与基础过程有关 （对威胁的高反应性，异常神经生物学压力反应），可以告知预防性 干预措施，最终改善了城市黑人美国创伤幸存者的生活质量。