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ing in an increased rate at which an individual performs tasks under stress. This, in turn, could result in more rapid and forceful responses during work tasks, thereby potentially increasing exposure to biomechanical risks.

Release of neurotransmitters may also play a role in the exacerbation of muscle pain. It has been observed that serotonin, which is released in response to stress (Stratakis, Gold, and Chrousos, 1995), potentiates the effects of endogenous pain mediators, such as bradykinin (Babenko et al., 1999). The infusion of both serotonin and bradykinin into the tibialis anterior muscle in humans has been associated with elevated pain intensity and prolonged pain in response to mechanical stimulation. This preliminary evidence suggests that exposure to stress could exert a nociceptor sensitization effect on muscle. In addition to the peripheral effect of stress on pain, data exist to support a direct role of the central nervous system (Fields and Basbaum, 1994). This may help explain how psychological processes, such as attention and emotion, influence pain and pain tolerance. In addition, the peripheral vasoconstriction induced by circulating catecholamines could further inhibit blood flow to a potentially compromised nerve in the case of carpal tunnel syndrome.

It has also been shown that exposure to stress exerts an inhibitory effect on inflammatory or immune responses (Chrousos and Gold, 1992). Glucocorticoids (cortisol) decrease the production of cytokines and other mediators of inflammation and inhibit the effects of these agents on target tissues. It is possible that the repeated elicitation of the stress response does not allow for the pain-sensitive tissues to recover following mechanical insult. Although the exact mechanism of injury differs from most work-related upper extremity disorders, it has recently been demonstrated that recovery from an oral puncture wound is significantly delayed following exposure to stress (Marucha, Kiecolt-Glaser, and Favagehi, 1998). Production of interleukin-1ρ, a proinflammatory cytokine important in cell recruitment and activation of fibroblasts, was noted to decrease by 68 percent following exposure to a stressor.

As indicated earlier, the potential pathways described above are speculative and represent a series of hypotheses that require rigorous scientific scrutiny. A critical element in validating these models is the determination of the time course between job stressor exposure, physiological changes, and symptom expression. Given the role that job stress plays in work-related symptoms in both the back and upper extremities, it is critical to identify the biobehavioral pathways underlying this effect, in order to understand how job stress can result in the symptom expressions characteristic of these disorders and in order to develop effective prevention and management strategies. The models reviewed need to be carefully tested using both laboratory and workplace studies.

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