A PSYCHOPHYSICAL STUDY OF SECONDARY HYPERALGESIA - EVIDENCE FOR INCREASED PAIN TO INPUT FROM NOCICEPTORS

Substantial evidence suggests that the hyperalgesia to mechanical stim uli that occurs in an area of uninjured skin surrounding a site of inj ury (area of secondary hyperalgesia) arises from activity in low-thres hold mechanoreceptors (LTMs). In this study, we have investigated if a ctivity in mechanically sensitive nociceptors also contributes to this secondary hyperalgesia. It is known that all woollen fabrics excite L TMs, but that only the prickly ones activate mechanically sensitive no ciceptors. Therefore, we have conducted a psychophysical study using a range of prickly and non-prickly woollen fabrics applied to normal an d hyperalgesic skin to assess the roles of LTMs and nociceptors in sec ondary hyperalgesia. We have studied in 10 normal volunteers the sensa tions of fabric-evoked prickle and pain in normal and hyperalgesic ski n. Secondary hyperalgesia was produced by intradermal injection of cap saicin (25 mu g) into the volar skin of the forearm. Five woollen fabr ics (2 non-prickly, 2 prickly and 1 intermediate) were presented, in a blind manner, to the skin before and after the capsaicin injection. T he sensation of fabric-evoked prickle was not changed in hyperalgesic skin. On the other hand, little if any pain was evoked by the fabrics when applied to normal skin, but substantial pain was produced by all fabrics when applied to hyperalgesic skin. The pain ratings were grade d with the ratings of prickle so that fabrics that evoked the greatest prickle also evoked significantly more pain. The magnitude of pain in creased linearly with prickle sensation; the slope of this regression function increased substantially in hyperalgesic skin. The increased p ain produced by prickly fabrics in the hyperalgesic skin exceeded that which could be predicted by the acquired capacity of LTMs to evoke pa in plus the pain produced by the prickly fabrics in normal skin. We co nclude that the central alterations responsible for secondary hyperalg esia involve two components: an acquired capacity of LTMs to evoke pai n and an increased responsiveness of central neurones to input from me chanically sensitive nociceptors.