Plastic Changes in Human Motor Cortical Output Induced by Random but not Closed-Loop Peripheral Stimulation: the Curse of Causality.

Plastic Changes in Human Motor Cortical Output Induced by Random but not Closed-Loop Peripheral Stimulation: the Curse of Causality.
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人类运动皮质输出的塑性变化是由随机但不是闭环外围刺激引起的:因果关系的诅咒。

DOI:
10.3389/fnhum.2016.00590
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发表时间:
2016
影响因子:
2.9
通讯作者:
Baker SN
Baker SN
中科院分区:
医学3区
文献类型:
--
作者:
Brown KI;Williams ER;de Carvalho F;Baker SN

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以前的工作表明,重复的周围神经刺激可以诱导运动皮质输出的可塑性变化。从自然活动中触发对中央结构的电刺激也可以产生可塑性。在这项研究中,我们测试了肌肉活动触发周围神经刺激是否同样会导致运动输出的变化。我们开发了一种能够记录肌电(EMG)并在闭环控制下提供电刺激的可穿戴电子设备。这使得成对的刺激可以在比标准的基于实验室的方案更长的时间内传递。我们在健康的人类志愿者身上测试了这个设备。放松的大鱼际肌的运动皮质输出首先通过对侧经颅磁刺激反应的招募曲线进行评估。然后将可穿戴设备配置为记录大鱼际肌电信号并刺激腕部的正中神经(运动阈值附近的强度,频率~0.66 Hz)。受试者进行4~7h的日常活动,然后返回实验室进行重复招募曲线评估。测试了四种刺激方案(每组9-14名受试者):无STIM,不传递刺激;活动,由高于阈值的肌电活动触发的刺激;保存,根据同一受试者之前的活动时段计时的刺激;休息,当EMG静默时给予刺激。正如预期的那样,No Stim没有修改征聘曲线。活动和休息条件对不同受试者没有显著影响,尽管一些个体发生了变化。SAVE产生了显著和显著的增加,当刺激器强度超过阈值30%时,平均反应增加2.14倍。我们认为,闭环反馈中不可避免的延迟,主要是由于中枢和外周传导时间,意味着活动范式中的刺激在皮质激活后到达太晚,无法产生一致的可塑性变化。相比之下,在保存的范例中,基本上随机提供的刺激可能导致皮质兴奋性的普遍增加,类似于随机共振,导致皮质脊髓输出的可塑性变化。我们的研究表明,非侵入性的闭环刺激可能受到传导延迟和不可避免的因果关系约束的严重限制。
Previous work showed that repetitive peripheral nerve stimulation can induce plastic changes in motor cortical output. Triggering electrical stimulation of central structures from natural activity can also generate plasticity. In this study, we tested whether triggering peripheral nerve stimulation from muscle activity would likewise induce changes in motor output. We developed a wearable electronic device capable of recording electromyogram (EMG) and delivering electrical stimulation under closed-loop control. This allowed paired stimuli to be delivered over longer periods than standard laboratory-based protocols. We tested this device in healthy human volunteers. Motor cortical output in relaxed thenar muscles was first assessed via the recruitment curve of responses to contralateral transcranial magnetic stimulation. The wearable device was then configured to record thenar EMG and stimulate the median nerve at the wrist (intensity around motor threshold, rate ~0.66 Hz). Subjects carried out normal daily activities for 4–7 h, before returning to the laboratory for repeated recruitment curve assessment. Four stimulation protocols were tested (9–14 subjects each): No Stim, no stimuli delivered; Activity, stimuli triggered by EMG activity above threshold; Saved, stimuli timed according to a previous Activity session in the same subject; Rest, stimuli given when EMG was silent. As expected, No Stim did not modify the recruitment curve. Activity and Rest conditions produced no significant effects across subjects, although there were changes in some individuals. Saved produced a significant and substantial increase, with average responses 2.14 times larger at 30% stimulator intensity above threshold. We argue that unavoidable delays in the closed loop feedback, due mainly to central and peripheral conduction times, mean that stimuli in the Activity paradigm arrived too late after cortical activation to generate consistent plastic changes. By contrast, stimuli delivered essentially at random during the Saved paradigm may have caused a generalized increase in cortical excitability akin to stochastic resonance, leading to plastic changes in corticospinal output. Our study demonstrates that non-invasive closed loop stimulation may be critically limited by conduction delays and the unavoidable constraint of causality.
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