CAS Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing, China.
Department of Psychology, University of Chinese Academy of Sciences, Beijing, China.
Ann N Y Acad Sci. 2021 Aug;1497(1):39-56. doi: 10.1111/nyas.14587. Epub 2021 Mar 10.
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.
疼痛对我们的生存至关重要，因为它有助于保护我们免受严重伤害。伤害性信号可能会因持续的身体活动而加剧，但也可以被身体运动打断或覆盖，这一过程称为运动诱发的镇痛。已经提出了几种神经机制来解释这种效应，包括重反射原理、非伤害性干扰和自上而下的下行调制。鉴于这些机制在运动执行过程中的镇痛效应在时间上重叠，目前尚不清楚运动诱发的镇痛是来自单一的神经机制，还是来自多个神经机制的共同作用。为了解决这个问题，我们通过评估运动执行后的镇痛效应，在 129 名健康人类中进行了五项实验。通过结合心理物理学和脑电图记录，我们量化了自愿运动强度与镇痛效应之间的关系，以及镇痛效应的时间和空间特征。我们的发现表明，运动诱发的镇痛是由多个神经机制的共同作用产生的。这项研究首次分离了不同神经机制对自愿运动镇痛效应的不同贡献，这扩展了我们对源于自愿运动的感觉衰减的理解，并可能有助于开发新的疼痛管理策略。
