SECONDARY HYPERALGESIA TO HEAT STIMULI AFTER BURN INJURY IN MAN

The aim of the study was to examine the presence of hyperalgesia to he at stimuli within the zone of secondary hyperalgesia to punctate mecha nical stimuli. A burn was produced on the medial part of the non-domin ant crus in 15 healthy volunteers with a 50 x 25 mm thermode (47 degre es C, 7 min), and assessments were made 70 min and 40 min before, and 0, 1, and 2 h after the burn injury. Hyperalgesia to mechanical and he at stimuli were examined by von Frey hairs and contact thermodes (3.75 and 12.5 cm(2)), and pain responses were rated with a visual analog s cale (0-100). The area of secondary hyperalgesia to punctate stimuli w as assessed with a rigid von Prey hair (462 mN). The heat pain respons es to 45 degrees C in 5 s (3.75 cm(2)) were tested in the area just ou tside the burn, where the subjects developed secondary hyperalgesia, a nd on the lateral crus where no subject developed secondary hyperalges ia (control area). The burns decreased pain thresholds and increased p ain responses to both thermal and mechanical stimuli within the burn ( P < 10(-5)). Further, the bums induced secondary hyperalgesia (mean 89 cm(2)) to punctate mechanical stimuli (P < 10(-5)), and increased the pain response to mechanical stimuli in the areas of secondary hyperal gesia (P < 10(-5)). The pain response to heat stimuli increased over t ime in the area of secondary hyperalgesia (P < 10(-5)), and so did the pain response to heat on the lateral part of the crus (P < 10(-3)). H owever, the heat pain response increased more (P = 0.006) and was more intense (P = 0.001) within the zone of secondary hyperalgesia than on the lateral part of the crus. Further, the heat pain response was mor e intense in the zone of primary hyperalgesia than in the zone of seco ndary hyperalgesia (P = 0.004), in contrast to the mechanical pain res ponse, which was not significantly different between the two zones of hyperalgesia. In conclusion, secondary hyperalgesia in man is not rest ricted to mechanical stimuli, as significant hyperalgesia to heat deve loped within the zone of secondary hyperalgesia to punctate mechanical stimuli. The data, combined with other evidence, suggest differences in the mechanisms accounting for primary hyperalgesia to heat and mech anical stimuli, whereas secondary hyperalgesia to heat and mechanical stimuli may be explained by a common central mechanism. (C) 1998 Inter national Association for the Study of Pain. Published by Elsevier Scie nce B.V.