Secondary hyperalgesia persists in capsaicin desensitized skin

Several lines of evidence suggest that secondary hyperalgesia to punctate m echanical stimuli arises from central sensitization to the input from prima ry afferent nociceptors. Conventional C-fiber nociceptors respond to heat s timuli and yet heat hyperalgesia is absent in the region of secondary hyper algesia. This evidence suggests that the central sensitization to nocicepto r input does not involve heat sensitive nociceptors, To test this hypothesi s, we investigated whether desensitization of heat sensitive nociceptors by topical application of capsaicin led to an alteration in the secondary hyp eralgesia. Two 2 x 2 cm areas on the volar forearm, separated by 1 cm, were treated in 10 healthy volunteers. One of the areas was desensitized by tre atment with 10% topical capsaicin (6 h/day for 2 days). The other site serv ed as vehicle control, Hyperalgesia was produced 2 days later by an intrade rmal injection of capsaicin (50 mu g, 10 mu l) at a point midway between th e two treatment areas. Secondary hyperalgesia to noxious mechanical stimuli was investigated by using a blade probe (32 and 64 g) attached to a comput er-controlled mechanical stimulator. In the area of topical capsaicin treat ment, there was a marked increase in heat pain threshold and decrease:in he at pain ratings indicating a pronounced desensitization of heat sensitive n ociceptors. However, touch threshold and pain to pinching stimuli were not significantly altered. The intradermal capsaicin injection led to the devel opment of a similar degree of secondary hyperalgesia at both the vehicle an d capsaicin treatment areas, These results:indicate that capsaicin insensit ive nociceptive afferents play a dominant role not only in normal mechanica l pain but also in secondary hyperalgesia to noxious mechanical stimuli. (C ) 2000 International Association for the Study of Pain. Published by Elsevi er Science B.V.