The potential contribution of stress systems to the transition to chronic whiplash-associated disorders.
METHODS
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.


BACKGROUND
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.


CONCLUSIONS
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.
Department of Anesthesiology, N2201 UNC Hospitals, Chapel Hill, NC 27599-7010, USA. smclean@aims.unc.edu
Samuel A
SA
McLean
D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D059350:Chronic Pain / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D018450:Disease Progression; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000502:physiology; D011941:Receptors, Adrenergic / Q000378:metabolism; D013312:Stress, Physiological / Q000502:physiology*; D014911:Whiplash Injuries / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*
D002395:Catecholamines; D011941:Receptors, Adrenergic