Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, UK.
State Key Laboratory of Reliability and Intelligence of Electrical Equipment, School of Electrical Engineering, Hebei University of Technology, Tianjin, China.
J Physiol. 2021 May;599(9):2471-2482. doi: 10.1113/JP278536. Epub 2019 Nov 2.
We compare the effects on corticospinal excitability of repeatedly delivering peripheral nerve stimulation at three time points (-30 ms, 0 ms, +50 ms) relative to muscle onset in a cue-guided task. Plastic changes in excitability are only observed when stimuli are delivered immediately before the time when muscles activate, while stimuli delivered at muscle onset or shortly later (0, +50 ms) have no effect. Plastic effects are abolished if there is ongoing volitional electromyogram activity in the muscles prior to the onset of the phasic contraction. The plastic effects induced by timing peripheral stimulation relative to electromyographic markers of muscle activation are as effective as those that occur if stimulation is timed relative to electroencephalographic markers of motor cortical activation. We provide a simple alternative protocol to induce plasticity in people in whom electroencephalogram recording is difficult.
Plastic changes in corticospinal excitability (CSE) and motor function can be induced in a targeted and long-term manner if afferent volleys evoked by peripheral nerve stimulation are repeatedly associated with the peak of premovement brain activity assessed with an electroencephalogram (EEG). The present study investigated whether other factors might also characterize this optimal brain state for plasticity induction. In healthy human volunteers (n = 24), we found that the same reliable changes in CSE can be induced by timing peripheral afferent stimulation relative to the onset of electromyogram (EMG) activity rather than using the EEG peak. Specifically, we observed an increase in CSE when peripheral stimulation activated the cortex just before movement initiation. By contrast, there was no effect on CSE if the afferent input reached the cortex at the same time or after EMG onset, consistent with the idea that the temporal order of synaptic activation from afferent input and voluntary movement is important for production of plasticity. Finally, in 14 volunteers, we found that background voluntary muscle activity prior to movement also abolished the effect on CSE. One possible explanation is that the intervention strengthens synapses that are inactive at rest but change their activity in anticipation of movement, and that the intervention fails when the synapses are tonically active during background EMG activity. Overall, we demonstrate that, in individuals with voluntary control of muscles targeted by our intervention, EMG signals are a suitable alternative to an EEG for inducing plasticity by coupling movement-related brain states with peripheral afferent input.
我们比较了在 cue-guided 任务中，三次时间点（-30ms、0ms 和+50ms）相对于肌肉起始点重复施加外周神经刺激对皮质脊髓兴奋性的影响。只有当刺激在肌肉激活之前立即施加时，才能观察到兴奋性的可塑性变化，而在肌肉起始时或稍后施加刺激（0ms 和+50ms）则没有效果。如果在相位收缩开始之前肌肉中存在持续的自愿肌电图活动，则会消除塑性效应。相对于肌肉激活的肌电图标记来定时外周刺激引起的塑性效应与如果刺激相对于运动皮质激活的脑电图标记来定时是一样有效的。我们提供了一种简单的替代方案，可在脑电图记录困难的人群中诱导可塑性。
如果外周神经刺激引起的传入冲动反复与使用脑电图（EEG）评估的运动前脑活动的峰值相关联，则可以以靶向和长期的方式诱导皮质脊髓兴奋性（CSE）和运动功能的可塑性变化。本研究调查了其他因素是否也可以表征这种诱导可塑性的最佳大脑状态。在健康的人类志愿者（n=24）中，我们发现，通过定时外周传入刺激相对于肌电图（EMG）活动的起始来诱导 CSE 的相同可靠变化，而不是使用 EEG 峰值。具体而言，当外周刺激在运动起始前激活皮层时，我们观察到 CSE 增加。相比之下，如果传入输入在同一时间或在 EMG 起始后到达皮层，则对 CSE 没有影响，这与突触从传入输入和自愿运动的激活的时间顺序对于产生可塑性很重要的观点一致。最后，在 14 名志愿者中，我们发现运动前肌肉的背景自愿活动也消除了对 CSE 的影响。一种可能的解释是，该干预措施增强了在休息时处于非活动状态但在预期运动时改变其活动的突触，并且当突触在背景 EMG 活动期间持续活跃时，该干预措施会失败。总的来说，我们证明了在我们干预的目标肌肉具有自愿控制能力的个体中，肌电图信号是一种合适的替代方案，可通过将与运动相关的大脑状态与外周传入输入耦合来诱导可塑性。
