DISSOCIATED SECONDARY HYPERALGESIA IN A SUBJECT WITH A LARGE-FIBER SENSORY NEUROPATHY

In the skin surrounding a site of injury, hyperalgesia develops to mec hanical stimuli. Two types of secondary hyperalgesia (to light touch a nd punctate stimuli) have recently been differentiated, based on diffe rent durations and sizes of the area involved. We studied secondary hy peralgesia in a subject who had a loss of myelinated afferent nerve fi bres below the neck that spared the Adelta group. Stroking with a cott on swab was not perceived anywhere on affected skin either before or a fter injection of 60 mug of capsaicin. Thus, there was no hyperalgesia to light touch. Capsaicin injection into the volar forearm evoked nor mal pain and flare. A von Frey probe exerting a force of 40 mN was per ceived as sharp. The sensation of sharpness was more pronounced up to 2 cm outside the flare zone for at least 16 min following the injectio n (tested with a 200 mN von Frey probe). Thus, hyperalgesia to punctat e stimuli developed as in healthy subjects. These data support the mod el that hyperalgesia to light touch (allodynia) is due to sensitisatio n of central pain-signaling neurones to low-threshold mechanoreceptor input (Abeta fibres). In contrast, punctate hyperalgesia is likely to be due to sensitisation to nociceptor input (Adelta or C fibres).