Secondary hyperalgesia is mediated by heat-insensitive A-fibre nociceptors

Abstract

Secondary hyperalgesia refers to the increase in sensitivity to mechanical nociceptive stimuli delivered outside the area of tissue injury. Previous studies suggested that secondary hyperalgesia is mediated by a specific class of myelinated nociceptors: slowly-adapting A-fibre mechano- and heat-sensitive (AMH) Type I nociceptors. Here, we tested this hypothesis by examining, whether long-lasting heat stimuli, which are known to activate AMH-type I nociceptors, elicit enhanced responses when delivered to the area of secondary hyperalgesia induced by high frequency electrical stimulation of the skin (HFS). Before and twenty minutes after HFS, sustained 30-s radiant heat stimuli were delivered to the area of increased mechanical pinprick sensitivity while participants continuously rated intensity of perception using an online visual-analogue scale (0-100 mm). After HFS, no significant enhancement of heat perception was observed in the area of increased pinprick sensitivity. To establish that myelinated nociceptors actually contribute to the perception of sustained heat, we conducted a second experiment in which sustained heat stimuli were presented before and during an A-fibre nerve conduction block, achieved by applying a rubber band with weights which compresses the superficial radial nerve against the radius. During the block, heat perception was significantly reduced 17–33 s after the onset of the heat stimulus (before: mean = 53 mm, during: mean = 31 mm; P = .03), matching the response profile of AMH-type I nociceptors. These results support the notion that AMH-type I nociceptors contribute to the perception of sustained heat, but also show that these afferents do not mediate secondary hyperalgesia.

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