Offset analgesia is reduced on the palm and increases with stimulus duration

A noxious stimulus following a more intense stimulus often feels less painful than continuous noxious stimulation. This effect, known as offset analgesia (OA), may be due to descending inhibitory control, to changes in peripheral neural transmission or both. The timing and location of noxious thermal stimulation were manipulated to better understand the peripheral and central contributions to OA.

In a first experiment, participants (n = 29) provided continuous pain ratings as stimuli were delivered to the palm or dorsum of each hand. Offset trials included 44°C (T1), 45°C (T2) and 44°C (T3) stimulation periods. Baseline trials were identical except the T3 temperature fell to 35°C. Constant trials were 44°C throughout. The duration of T1 and T2 was either 1 s or 6 s, whereas T3 was always 12 s. In a second experiment, participants (n = 43) rated pain levels of noxious stimuli presented to the forearms with varying T1 and T2 durations (3, 6, 10 or 13 s) and a 20 s T3 period.

OA effects became stronger with increasing inducing durations. OA, however, was not found on the palm even at longer durations.

The increase in OA with duration suggests that accumulated nociceptive signalling is more important to triggering OA than is a decrease in nociceptors' instantaneous firing rates. The lack of OA on the palm, however, implies a key role for the rapidly adapting Type II AMH fibres that may be absent or not readily activated on the palm. Unravelling the relative central and peripheral contribution to OA requires further investigation.

Offset analgesia (OA) is a fundamentally temporal phenomenon dependent on dynamic changes in stimulus intensity. Here we demonstrate increased OA with increased stimulus duration. This finding implies the more slowly-responding AMH-I peripheral mechanoreceptors contribute to OA. The more rapidly responding AMH-II peripheral mechanoreceptors, however, may be absent or more difficult to activate in the palm where we did not observe OA. This finding implies that the AMH-II receptors are necessary for OA. Our studies suggest methods to unravel the different peripheral and central contributions to OA.