Peripheral contributions to offset analgesia: effects of stimulus duration, intensity, and location.

Abstract

Offset analgesia (OA) is a substantial decrease in pain perception after a minor reduction in noxious stimulus intensity. The peripheral mechano- and heat-sensitive A-fibre nociceptors (AMH-I and AMH-II) and the C-fibre nociceptors (CMH) are hypothesised to contribute to OA. These nociceptors differ in initial response latency, peak response latency, and heat threshold, and the AMH-II fibres may be absent from the palm. Stimuli targeting those different nociceptive properties were used to decide which nociceptors critically contribute to OA. Healthy volunteers (N = 64) underwent 16 unique trials with continuous noxious heat (45-47°C). These trials included 3-second (short) or 12-second (long) periods of increased noxious heat (46-48°C), or an intense 0.2 seconds pulse of heat (51°C). Stimuli were delivered to the dorsum (back) and palm of the hands. Notable OA effects were observed for long-duration trials on both the dorsum and palm of the hand. Offset analgesia was inconsistently present and much smaller for the short-duration trials and for the pulse trials. Pain ratings generally increased more slowly during palm stimulation compared with dorsum stimulation. The demonstration of OA on the palm suggests that AMH-II nociceptors are either not critical for OA or that the AMH-II nociceptors are present in the palm. The small OA after the intense pulse and the substantial reduction in OA during the short trials suggests that AMH-I nociceptors are not necessary for OA and that the faster response of the AMH-II or CMH nociceptors is not sufficient to generate OA.