Applying Biopsychosocial Model to Post-MVC Pain Development in African Americans

描述（由申请人提供）：每年大约有600万美国人在机动车碰撞（MVC）后到美国急诊科（ED）接受治疗。超过90%的人没有严重的身体伤害，在ED评估后出院回家。10-20%的欧洲裔美国人（EA）患有持续性肌肉骨骼疼痛，仅在美国每年就造成290亿美元的经济影响。经历MVC的非裔美国人（AA）慢性疼痛发展的发生率从未报道过。然而，大量证据（以及研究者的试验数据）表明，嗜酒者的慢性疼痛负担增加。人们对这种负担增加的原因知之甚少。MVC后慢性肌肉骨骼疼痛的发病机制被描述为生物心理社会模型，其中最著名的是Vlaeyen的恐惧-回避模型（FAM），该模型得到了大量研究的支持。歧视经历可能会影响FAM过程，并通过多种机制导致AA经历MVC的慢性疼痛发生率增加。例如，歧视经历可能：(1)导致应激诱导的生理变化，增加MVC反应的初始疼痛，(2)增加随后的抑郁和残疾，(3)增加残疾和抑郁反应的慢性疼痛易感性。此外，过去与歧视相关的不良结果可能会增加MVC后的负面预期，这反过来可能会恶化疼痛相关的结果。现有数据表明，个人种族认同的强度可能会缓和这些歧视的影响。迄今为止，FAM从未在AA过渡到恢复与持续疼痛的队列中进行过评估，歧视和种族认同对FAM机制的影响也从未被评估过。此外，遗传易感性因素对FAM概念和过程的影响很少被评估，在AA中也从未被评估过。评估影响影响FAM过程的生理系统功能的遗传因素可以促进我们对体质因素如何与认知、心理和经验因素相互作用以形成疼痛结果的理解。肾上腺素能神经系统是一个很好的生理系统，因为它在疼痛感知中的重要性，在应激反应中的关键作用，以及在慢性疼痛发展过程中与FAM过程的相互作用。拟议的研究将招募1000名AA，在小型MVC之后向ED站点的研究网络展示。参与者将在第6周、第6个月和第12个月接受初始ED评估和随访访谈。结构方程模型将用于检验FAM中描述的多变量预测关系。还将评估歧视经历和种族认同对特定FAM概念和过程的影响，以及影响肾上腺素能系统功能的遗传因素的影响。总之，这些分析结果将大大提高我们对AA慢性疼痛发病机制的认识。

DESCRIPTION (provided by applicant): Approximately 6 million Americans present to US Emergency Departments (ED) each year for care after motor vehicle collision (MVC). More than 90% of these individuals do not have serious physical injury and are discharged to home after ED evaluation. Persistent musculoskeletal pain develops in 10-20% of European Americans (EA) who experience such MVCs, with an economic impact of $29 billion per year in the US alone. The incidence of chronic pain development in African Americans (AA) experiencing MVC has never been reported. However, substantial evidence (and the investigator's pilot data) indicate that AA experience an increased burden of chronic pain. Reasons for this increased burden are poorly understood. Mechanisms of chronic musculoskeletal pain pathogenesis after MVC are described in biopsychosocial models, most notably Vlaeyen's fear-avoidance model (FAM), which is supported by substantial research. Experiences of discrimination may influence FAM processes and contribute to an increased incidence of chronic pain in AA experiencing MVC via a number of mechanisms. For example, discrimination experiences may: (1) cause stress-induced physiologic changes which increase initial pain in response to MVC, (2) increase subsequent depression and disability, and (3) increase chronic pain vulnerability in response to disability and depression. In addition, past adverse outcomes related to discrimination may increase negative expectations after MVC, which in turn may worsen pain-related outcomes. Available data suggest that the strength of an individual's ethnic identification may moderate these discrimination influences. To date, the FAM has never been evaluated in a cohort of AA transitioning to recovery vs. persistent pain, and the influence of discrimination and ethnic identity on FAM mechanisms has never been assessed. In addition, the influence of genetic vulnerability factors on FAM concepts and processes has rarely been evaluated, and never in AA. Evaluating genetic factors which influence the function of a physiologic system affecting FAM processes can advance our understanding of how constitutional factors interact with cognitive, psychological, and experiential factors to shape pain outcomes. The adrenergic nervous system is an excellent physiologic system to assess in this regard, because of its importance in pain perception, its critical role in the stress response, and its demonstrated interaction with FAM processes during chronic pain development. The proposed study will recruit one thousand AA presenting to a research network of ED sites after minor MVC. Participants will receive initial ED evaluation and follow-up interviews at 6 weeks and 6 and 12 months. Structural equation modeling will be used to test the multivariate predictive relationships described in the FAM. The influence of experiences of discrimination and ethnic identity on specific FAM concepts and processes will also be assessed, as will the influence of genetic factors affecting adrenergic system function. Together, the results of these analyses will substantially advance our knowledge of chronic pain pathogenesis in AA.