• J H Huang, Z Ali, T G Travison, J N Campbell, and R A Meyer.
• Department of Neurosurgery, Johns Hopkins University, Baltimore, MD 21287, USA.
• Pain. 2000 May 1;86(1-2):33-42.

AbstractThe purpose of this study was to examine how pain to punctate mechanical stimuli varies with position within the zone of secondary hyperalgesia. Secondary hyperalgesia was produced by an intradermal injection of capsaicin (50 microg) into the volar forearm of human volunteers (n=9). Before and at 20, 60 and 100 min after the capsaicin injection, a computer-controlled electromechanical stimulator was used to deliver controlled-force stimuli to the skin via a 12-mm wide, 100-microm thick blade probe. Three forces (16, 32 and 64 g; 1 s) were each applied in a random order to 10 sites spaced in 1-cm increments along a line starting 1 cm from the injection site and ending near the wrist. At 40 and 80 min after capsaicin injection the 'zone of hyperalgesia' was determined with use of a hand-held 20-g von Frey probe. Whereas, before capsaicin, the blade probe produced little or no pain, after capsaicin the 32-g and 64-g stimuli evoked pain consistently within but not outside the border of secondary hyperalgesia determined with the von Frey probe. Within the zone of hyperalgesia the average pain ratings to the 64-g stimulus decreased exponentially with distance from the injection site. Surprisingly, the space constant for this exponential decay was large (about 18 cm), and thus the decrease in pain ratings from the center to the edge of the secondary zone was small (37%). However, pain ratings dropped precipitously just outside the zone of secondary hyperalgesia. This finding unlikely reflects a ceiling effect because pain ratings within the zone of secondary hyperalgesia increased linearly with force. The relatively uniform pain ratings to the blade stimuli within the zone of secondary hyperalgesia and the sharp border that delimits the zone of hyperalgesia indicate that this sensory disturbance approaches being an 'all-or-nothing' phenomenon. Thus, a two-state model for central plasticity is needed to explain secondary hyperalgesia.

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