Secondary hyperalgesia to punctate mechanical stimuli - Central sensitization to A-fibre nociceptor input

Tissue injury induces enhanced pain sensation to light touch and punctate s timuli in adjacent, uninjured skin (secondary hyperalgesia). Whereas hypera lgesia to light touch (allodynia) is mediated by A-fibre low-threshold mech anoreceptors, hyperalgesia to punctate stimuli may be mediated by A- or C-f ibre nociceptors. To disclose the relative contributions of A- and C-fibres to the hyperalgesia to punctate stimuli, the superficial radial nerve was blocked by pressure at the wrist in nine healthy subjects. Secondary hypera lgesia was induced by intradermal injection of 40 mu g capsaicin, and pain sensitivity in adjacent skin was tested with 200 mu m diameter probes (35-4 07 mN). The progress of conduction blockade was monitored by touch, cold, w arm and first pain detection and by compound sensory nerve action potential . When A-fibre conduction was blocked completely but C-fibre conduction was fully intact, pricking pain to punctate stimuli was reduced by 75%, but bu rning pain to capsaicin injection remained unchanged. In normal skin withou t A-fibre blockade, pain ratings to the punctate probes increased significa ntly by a factor of two after adjacent capsaicin injection. In contrast, pa in ratings to the punctate probes were not increased after capsaicin inject ion when A-fibre conduction was selectively blocked. However, hyperalgesia to punctate stimuli was detectable immediately after block release, when A- fibre conduction returned to normal. In conclusion, the pricking pain to pu nctate stimuli is predominantly mediated by A-fibre nociceptors. In seconda ry hyperalgesia, this pathway is heterosynaptically facilitated by conditio ning C-fibre input. Thus, secondary hyperalgesia to punctate stimuli is ind uced by nociceptive C-fibre discharge but mediated by nociceptive A-fibres.