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Individual differences in endogenous pain modulation as a risk factor for chronic pain

From the Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD.

Address correspondence and reprint requests to Dr Edwards, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 600 N. Wolfe St., Meyer 1-108, Baltimore, MD 21287; e-mail: redwar10{at}jhmi.edu

This review summarizes evidence, primarily from recent human studies, indirectly supporting a novel hypothesis: that the assessment of healthy individuals’ responses to standardized noxious stimuli in a controlled laboratory environment has important implications for the later risk of developing a broad spectrum of chronically painful conditions. Descriptions of many chronic pain syndromes note that the disorder (e.g., fibromyalgia, headache, complex regional pain syndrome) is associated with hypersensitivity to pain and with reduced endogenous inhibition of pain, implying that an individual’s processing of pain-related information changes with the onset of the syndrome. However, pain sensitivity and pain-inhibitory capacity are normally distributed along a wide continuum in the general population, and recent evidence suggests that heightened baseline pain sensitivity and reduced basal pain-inhibitory processing place individuals at greater risk for experiencing severe, acute, clinical pain (e.g., postoperative pain). More controversial is the hypothesis that such individual-difference characteristics confer risk for, or protection against, chronic pain; although only a single prospective study has been published, substantial indirect evidence supports the contention that greater basal pain sensitivity and reduced pain-inhibitory capacity may act as a diathesis for chronic pain. Long-term cohort studies are necessary to test this hypothesis; such research could yield insight into the nature of chronic pain and permit greater precision in selecting high-risk individuals for chronic pain prevention research.

Supported by a grant from the NIH (AR 051315), which provided salary support for the author.

Disclosure: The authors report no conflicts of interest.

Received November 11, 2004. Accepted in final form April 5, 2005.

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