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Match and Mismatch: Identifying the Neuronal Determinants of Pain

Kenneth L. Casey, MD
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From Veterans Affairs Medical Center, Ann Arbor, Michigan. For the current author address, see end of text. Grant Support: By Merit Review grants from the Department of Veterans Affairs. Requests for Reprints: Kenneth L. Casey, MD, Neurology Service, Veterans Affairs Medical Center, 2215 Fuller Road, Ann Arbor, MI 48105.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1996;124(11):995-998. doi:10.7326/0003-4819-124-11-199606010-00007
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Despite the increased intensity and sophistication of research on pain mechanisms in the past three decades, serious uncertainties remain about the neuronal origin of pain, especially in painful clinical conditions. Although a positive correlation between nociceptive afferent activity and the subjective perception of pain has been seen under controlled experimental conditions, important mismatches point to the critical importance of central nervous system processes as determinants of pain. Multiple peripheral, segmental, and supraspinal neuronal activities control nociceptive processing at all levels of the neuraxis. Three studies in this issue highlight the problem of identifying the neuronal determinants of pain by addressing contrasting mismatches: angina-like chest pain without an obvious cause and a potential source of angina (myocardial ischemia) without pain. The results of these studies suggest that selective visceral hyperalgesia and hypoalgesia of peripheral or central origin may be present without other clinical evidence for neurologic abnormality. Complex mechanisms interacting at several levels of the nervous system appear to be involved.







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