In the skin surrounding a site of injury, hyperalgesia develops to mechanical stimuli. Two types of secondary hyperalgesia (to light touch and punctate stimuli) have recently been differentiated, based on different durations and sizes of the area involved. We studied secondary hyperalgesia in a subject who had a loss of myelinated afferent nerve fibres below the neck that spared the Aδ group. Stroking with a cotton swab was not perceived anywhere on affected skin either before or after injection of 60 μg of capsaicin. Thus, there was no hyperalgesia to light touch. Capsaicin injection into the volar forearm evoked normal pain and flare. A von Frey probe exerting a force of 40 mN was perceived as sharp. The sensation of sharpness was more pronounced up to 2 cm outside the flare zone for at least 16 min following the injection (tested with a 200 mN von Frey probe). Thus, hyperalgesia to punctate stimuli developed as in healthy subjects. These data support the model that hyperalgesia to light touch (allodynia) is due to sensitisation of central pain-signaling neurones to low-threshold mechanoreceptor input (Aβ fibres). In contrast, punctate hyperalgesia is likely to be due to sensitisation to nociceptor input (Aδ or C fibres).
∗Correspondence to: Dr. Rolf-Detlef Treede, Institute of Physiology and Pathophysiology, Johannes Gutenberg University Mainz, Duesbergweg 6, D-6500 Mainz, Germany. Tel.: (49-6131) 39-5715; FAX: (49-6131) 39-5774.
Submitted May 21, 1992; revised November 9, 1992; accepted November 24, 1992.
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