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Myelinated afferents signal the hyperalgesia associated with nerve injury
James N Campbell1, Srinivasa N Raja, Richard A Meyer
1Department of Neurosurgery, Johns Hopkins University, Baltimore, MD 21205 U.S.A. Department of Anesthesiology and Critical Care Medicine,Johns Hopkins University, Baltimore, MD 21205 U.S.A. Applied Physics Laboratory, School of Medicine, Johns Hopkins University, Baltimore, MD 21205 U.S.A. Division of Plastic Surgery, University of Toronto, TorontoCanada.
Abstract:
Pain to light touching of the skin is a hallmark sign of causalgia. The purpose of this study was to determine whether myelinated or unmyelinated afferent fibers signal this hyperalgesia. Sensory testing was performed in 17 patients with long-standing hyperalgesia after nerve injury. The patients underwent a differential ischemic block of nerve function of the involved area. At a time when touch sensation in adjacent normal skin was eliminated, but when sensibility to warming and cooling stimuli was unaffected, the hyperalgesia to mechanical stimuli was abolished in 15 of the subjects. In 2 of these 15 patients, a differential local anesthetic block of the injured nerve was performed proximal to the site of injury. When temperature sensibility was absent, but when touch sensation was intact, hyperalgesia was present. In a third study, latency measurements in response to 400 micron stepped displacement stimuli were made in two patients who had hyperalgesia on the foot. The mean latency for detection of pain in the hyperalgesic region was 414 +/- 18 msec, compared to 458 +/- 16 msec for the detection of touch to the same stimuli applied to the opposite normal foot. These 3 lines of evidence indicate that myelinated primary afferents, perhaps A beta fibers, signal the hyperalgesic pain in causalgia. These fibers may be sensitized A beta nociceptors or low-threshold mechanoreceptors.