Pain is essential for our survival because it helps to protect us from severe injuries. Nociceptive signals may be exacerbated by continued physical activities but can also be interrupted or overridden by physical movements, a process called movement-induced hypoalgesia. Several neural mechanisms have been proposed to account for this effect, including the reafference principle, non-nociceptive interference, and top-down descending modulation. Given that the hypoalgesic effects of these mechanisms temporally overlap during movement execution, it is unclear whether movement-induced hypoalgesia results from a single neural mechanism or from the joint action of multiple neural mechanisms. To address this question, we conducted five experiments on 129 healthy humans by assessing the hypoalgesic effect after movement execution. Combining psychophysics and electroencephalographic recordings, we quantified the relationship between the strength of voluntary movement and the hypoalgesic effect, as well as the temporal and spatial characteristics of the hypoalgesic effect. Our findings demonstrated that movement-induced hypoalgesia results from the joint action of multiple neural mechanisms. This investigation is the first to disentangle the distinct contributions of different neural mechanisms to the hypoalgesic effect of voluntary movement, which extends our understanding of sensory attenuation arising from voluntary movement and may prove instrumental in developing new strategies for pain management.
Keywords: electroencephalography; hypoalgesia; pain; sensory attenuation; voluntary movement.
© 2021 New York Academy of Sciences.