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The aim of the study was to examine the presence of hyperalgesia to heat stimuli within the zone of secondary hyperalgesia to punctate mechanical stimuli. A burn was produced on the medial part of the non-dominant crus in 15 healthy volunteers with a 50×25 mm thermode (47°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 heat stimuli were examined by von Frey hairs and contact thermodes (3.75 and 12.5 cm2), and pain responses were rated with a visual analog scale (0–100). The area of secondary hyperalgesia to punctate stimuli was assessed with a rigid von Frey hair (462 mN). The heat pain responses to 45°C in 5 s (3.75 cm2) were tested in the area just outside the burn, where the subjects developed secondary hyperalgesia, and on the lateral crus where no subject developed secondary hyperalgesia (control area). The burns decreased pain thresholds and increased pain responses to both thermal and mechanical stimuli within the burn (P<10−5). Further, the burns induced secondary hyperalgesia (mean 89 cm2) to punctate mechanical stimuli (P<10−5), and increased the pain response to mechanical stimuli in the areas of secondary hyperalgesia (P<10−5). The pain response to heat stimuli increased over time 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). However, 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 more intense in the zone of primary hyperalgesia than in the zone of secondary hyperalgesia (P=0.004), in contrast to the mechanical pain response, which was not significantly different between the two zones of hyperalgesia. In conclusion, secondary hyperalgesia in man is not restricted to mechanical stimuli, as significant hyperalgesia to heat developed 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 mechanical stimuli, whereas secondary hyperalgesia to heat and mechanical stimuli may be explained by a common central mechanism.