Study Design: A narrative description highlighting preclinical and clinical evidence that physiologic stress systems contribute to whiplash-associated disorders (WAD) pathogenesis.
Objective: To present several lines of evidence supporting the hypothesis that physiologic stress systems contribute to WAD pathogenesis.
Summary Of Background Data: In addition to subjecting soft tissue to biomechanical strain, a motor vehicle collision (MVC) event is also an acute stressor which activates physiologic stress systems. Increasing data from animal and human studies suggest that the activation of these stress systems may contribute to long-lasting changes in pain sensitivity after tissue injury.
Methods: Nonsystematic review of several lines of evidence that together suggest that physiologic systems involved in the stress response may contribute to the development of WAD.
Results: Stress systems which appear capable of producing hyperalgesia and allodynia include catecholaminergic systems, serotonin systems, and the hypothalamic-pituitary-adrenocortical system. Evidence for the role of these systems comes, in part, from studies examining the association between genetic variants and chronic pain outcomes. For example, in a recent study of acute neck pain after MVC, patients with certain genotypes of an enzyme involved in catecholamine metabolism were more than twice as likely to report moderate or severe neck pain in the emergency department. Such pain vulnerability because of stress system function may interact with the effects of biomechanical injury and psychobehavioral responses to influence the development of WAD.
Conclusion: More research examining the influence of stress systems on WAD are needed. If these systems do influence WAD outcomes, then treatments which diminish the adverse effects of stress systems may be a useful component of multimodal therapeutic interventions for individuals at risk of chronic pain development after MVC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232298 | PMC |
| http://dx.doi.org/10.1097/BRS.0b013e3182387fb4 | DOI Listing |
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