Secondary hyperalgesia to punctate mechanical stimuli

E. A. Ziegler, W. Magerl, R. A. Meyer, R.-D. Treede
1999 Brain  
Tissue injury induces enhanced pain sensation to light completely but C-fibre conduction was fully intact, pricking pain to punctate stimuli was reduced by 75%, touch and punctate stimuli in adjacent, uninjured skin but burning pain to capsaicin injection remained (secondary hyperalgesia). Whereas hyperalgesia to light unchanged. In normal skin without A-fibre blockade, touch (allodynia) is mediated by A-fibre low-threshold pain ratings to the punctate probes increased significantly
more » ... icantly mechanoreceptors, hyperalgesia to punctate stimuli may by a factor of two after adjacent capsaicin injection. In be mediated by A-or C-fibre nociceptors. To disclose contrast, pain ratings to the punctate probes were not the relative contributions of A-and C-fibres to the increased after capsaicin injection when A-fibre conduchyperalgesia to punctate stimuli, the superficial radial tion was selectively blocked. However, hyperalgesia to nerve was blocked by pressure at the wrist in nine punctate stimuli was detectable immediately after block healthy subjects. Secondary hyperalgesia was induced release, when A-fibre conduction returned to normal. by intradermal injection of 40 µg capsaicin, and pain In conclusion, the pricking pain to punctate stimuli sensitivity in adjacent skin was tested with 200 µm is predominantly mediated by A-fibre nociceptors. In diameter probes (35-407 mN) . The progress of conduction secondary hyperalgesia, this pathway is heterosynaptically blockade was monitored by touch, cold, warm and first facilitated by conditioning C-fibre input. Thus, secondary pain detection and by compound sensory nerve action hyperalgesia to punctate stimuli is induced by nociceptive C-fibre discharge but mediated by nociceptive A-fibres. potential. When A-fibre conduction was blocked
doi:10.1093/brain/122.12.2245 pmid:10581220 fatcat:44r32iw4djg2zpu3p4wnjvaqge