Martel Marylie, Harvey Marie-Philippe, Houde Francis, Balg Frédéric, Goffaux Philippe, Léonard Guillaume
Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, J1H 5N4, Canada.
Research Centre on Aging, CIUSSS de l'Estrie-CHUS, 1036, rue Belvédère Sud, Sherbrooke, QC, J1H 4C4, Canada.
Exp Brain Res. 2017 Apr;235(4):1223-1231. doi: 10.1007/s00221-017-4880-0. Epub 2017 Feb 10.
The interaction between pain and the motor system is well-known, with past studies showing that pain can alter corticomotor excitability and have deleterious effects on motor learning. The aim of this study was to better understand the cortical mechanisms underlying the interaction between pain and the motor system. Experimental pain was induced on 19 young and healthy participants using capsaicin cream, applied on the middle volar part of the left forearm. The effect of pain on brain activity and on the corticomotor system was assessed with electroencephalography (EEG) and transcranial magnetic stimulation (TMS), respectively. Compared to baseline, resting state brain activity significantly increased after capsaicin application in the central cuneus (theta frequency), left dorsolateral prefrontal cortex (alpha frequency), and left cuneus and right insula (beta frequency). A pain-evoked increase in the right primary motor cortex (M1) activity was also observed (beta frequency), but only among participants who showed a reduction in corticospinal output (as depicted by TMS recruitment curves). These participants further showed greater beta M1-cuneus connectivity than the other participants. These findings indicate that pain-evoked increases in M1 beta power are intimately tied to changes in the corticospinal system, and provide evidence that beta M1-cuneus connectivity is related to the corticomotor alterations induced by pain. The differential pattern of response observed in our participants suggest that the effect of pain on the motor system is variable from on individual to another; an observation that could have important clinical implications for rehabilitation professionals working with pain patients.
疼痛与运动系统之间的相互作用是众所周知的,过去的研究表明,疼痛会改变皮质运动兴奋性,并对运动学习产生有害影响。本研究的目的是更好地理解疼痛与运动系统相互作用背后的皮质机制。使用辣椒素乳膏对19名年轻健康的参与者进行实验性疼痛诱导,将其涂抹在左前臂掌侧中部。分别通过脑电图(EEG)和经颅磁刺激(TMS)评估疼痛对大脑活动和皮质运动系统的影响。与基线相比,在中央楔叶(θ频率)、左侧背外侧前额叶皮质(α频率)、左侧楔叶和右侧岛叶(β频率)涂抹辣椒素后,静息状态下的大脑活动显著增加。还观察到右侧初级运动皮层(M1)活动在疼痛诱发下增加(β频率),但仅在皮质脊髓输出减少的参与者中出现(如TMS募集曲线所示)。这些参与者进一步显示出比其他参与者更强的β频段M1 - 楔叶连接性。这些发现表明,疼痛诱发的M1区β功率增加与皮质脊髓系统的变化密切相关,并提供证据表明β频段M1 - 楔叶连接性与疼痛引起的皮质运动改变有关。我们参与者中观察到的不同反应模式表明,疼痛对运动系统的影响因人而异;这一观察结果可能对治疗疼痛患者的康复专业人员具有重要的临床意义。