Objectives: Persistent pain and psychological sequelae are common after motor vehicle collision (MVC), but their etiology remains poorly understood. Such common sequelae include whiplash-associated disorders (WAD), fibromyalgia, and posttraumatic stress disorder (PTSD). Increasing evidence suggests that these disorders share overlapping epidemiologic and clinical features. A model is proposed in which central neurobiological systems, including physiologic systems and neuroanatomical structures involved in the stress response, are an important substrate for the development of all 3 disorders and interact with psychosocial and other factors to influence chronic symptom development.
Methods: Epidemiologic and clinical characteristics regarding the development of these disorders after MVC are reviewed. Evidence suggesting a role for stress response systems in the development of these disorders is presented.
Results: Contemporary evidence supports a model of chronic symptom development that incorporates the potential for interactions between past experience, acute stress responses to trauma, post-MVC behavior, and cognitive/psychosocial consequences to alter activity within brain regions which process pain and to result in persistent pain, as well as psychological sequelae, after MVC. Such a model incorporates factors identified in prior biopsychosocial theories and places them in the landscape of our rapidly developing understanding of stress systems and CNS pain-modulating pathways.
Conclusion: New models are needed to stimulate deeper examination of the interacting influences of initial tissue damage, acute pain, psychosocial contingencies, and central stress pathways during chronic symptom development after MVC. Deeper understanding could contribute to improved treatment approaches to reduce the immense personal and societal burdens of common trauma-related disorders.
CRH = corticotrophin-releasing hormone; MVC = motor vehicle collision; WAD = whiplash-associated disorders; PTSD = posttraumatic stress disorder; HPA = hypothalamic-pituitary-adrenal; LC/NE=locus ceruleus/norepinephrine-sympathetic.
From the Departments of Emergency Medicine (S.A.M.), Medicine (Rheumatology) (D.J.C.), and Psychiatry (I.L., J.L.A.) and the Chronic Pain and Fatigue Research Center (S.A.M., D.J.C.), University of Michigan Medical Center, Ann Arbor, Michigan.
Address correspondence and reprint requests to Samuel A. McLean, MD, University of Michigan Chronic Pain and Fatigue Research Center, 24 Frank Lloyd Wright Drive, PO Box 385, Ann Arbor, MI 48106. E-mail: email@example.com
Received for publication August 11, 2004; revision received April 15, 2005.
Funding for this study was provided by the National Institutes of Health Grant K12 RR017607-01 (to S.A.M.), Department of Army Grant DAMD-17002-0018 (to D.J.C.), National Institutes of Health Grant R01 MH52724-06 (to J.L.A.), and National Institutes of Health Grant R01 MH63092 (I.L.).