Abstract
Background
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.
Methods
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 1s or 6s, whereas T3 was always 12s. 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 13s) and a 20s T3 period.
Results
OA effects became stronger with increasing inducing durations. OA, however, was not found on the palm even at longer durations.
Conclusions
The increase of 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.
from Wiley: European Journal of Pain: Table of Contents https://ift.tt/3gC6tOM
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