Direct Measurement of Motor Cortical Oscillations in Response to Transcranial Direct Current Stimulation

慢性脑卒中患者的神经调节方法是有限的。经颅直流电刺激 （tDCS）已显示出改善这一人群运动缺陷的潜力;然而，其效果尚未得到证实。 迄今为止，随机研究中的一致性，限制了广泛采用。我们知识中的一个关键差距是 详细了解tDCS如何影响运动皮层振荡，这在指导自愿 运动我们的长期目标是开发有效的基于神经调节的治疗系统， 基于对大脑皮层信号的神经调节如何改善恢复的更好理解， 的运动行为。在以前的研究中，我们记录了硬膜下皮层电图（sECoG）， 接受DBS手术的运动不能-僵硬型帕金森病（PD）患者，并观察到显著的调制 运动皮层的振荡与伸手任务的关系。因此，皮层振荡的变化支持了 改善该组的运动表现。基于这些结果，我们的中心假设是， 运动前和运动中的运动皮层振荡可能是tDCS促进运动的一种机制， 慢性运动性中风后的恢复。为了验证这一假设，在接受DBS手术的PD患者中，我们将 测量在暗示伸手过程中皮层β（13-30 Hz）和宽带γ（70-200 Hz）振荡 任务（目标1）和运动想象任务（目标2）之前和之后的初级运动皮层的阳极tDCS激活。 在这些患者中，将同时进行sECoG和EEG。为了确保我们在PD中的发现 将直接转化为中风模型，在目标3中，我们将使用组合tDCS和EEG收集试点数据 在目标1中执行与PD患者相同的手臂任务的慢性卒中患者队列中。目标1和2将 Aim 3将在NI Core EEG实验室进行。我们预计tDCS 将调节运动皮层振荡的方式，偏见的运动规划和启动在两个群体。 在神经外科手术中将联合收割机tDCS与sECoG和EEG相结合的建议是新颖的。如果我们的假设 经证实，这些发现可能有助于开发用于中风恢复的闭环形式的tDCS， 我们将有试点数据（来自目标3）来告知这种方法。此外，EEG的测量在两个 PD和慢性中风患者，使用相同的实验范式和记录方式，确保 结果将在两个模型之间直接解释。最后，我们的sECoG记录将提供详细的 EEG未捕获的空间和频域（70 Hz以上）信息。在未来，这些结果可能 潜在地为慢性中风患者的侵入性系统奠定基础， 病理性振荡，如已经在商业上可用于癫痫患者并且目前正在开发中的 对于PD。

Neuromodulatory approaches for chronic stroke patients are limited. Transcranial direct current stimulation (tDCS) has shown the potential to improve motor deficits in this population; however, its effects have not been consistent in randomized studies to date, limiting widespread adoption. A critical gap in our knowledge is a detailed understanding of how tDCS affects motor cortical oscillations, which are important in guiding voluntary movement. Our long-term goal is to develop effective neuromodulation-based therapeutic systems in chronic stroke patients based on a better understanding of how neuromodulation of cortical signals can improve recovery of motor behavior in this population. In a previous study, we recorded subdural electrocorticography (sECoG) in akinetic-rigid Parkinson’s disease (PD) patients undergoing DBS surgery, and observed significant modulation of motor cortical oscillations in relation to an arm-reaching task. Thus, changes in cortical oscillations supported improved motor performance in this group. Based on these results, our central hypothesis is that modulation of motor cortical oscillations both prior to and during movement may be one mechanism by which tDCS promotes recovery after chronic motor stroke. To test this hypothesis, in PD patients undergoing DBS surgery, we will measure cortical beta (13-30 Hz) and broadband gamma (70-200 Hz) oscillations during a cued arm-reaching task (Aim 1) and a motor imagery task (Aim 2) before and after anodal tDCS activation of primary motor cortex. In these patients, simultaneous sECoG and EEG will be performed. In order to ensure that our findings in PD will be directly translatable to a stroke model, in Aim 3 we will collect pilot data using combined tDCS and EEG in a cohort of chronic stroke patients performing the same arm task as PD patients in Aim 1. Aims 1 and 2 will be performed in the operating room, while Aim 3 will take place in the NI Core EEG lab. We anticipate that tDCS will modulate motor cortical oscillations in a way that biases movement planning and initiation in both populations. This proposal to combine tDCS with sECoG and EEG during neurosurgery is novel. If our hypotheses are confirmed, the findings may have use in developing a closed-loop form of tDCS for stroke recovery, for which we will have pilot data (from Aim 3) to inform such an approach. Furthermore, the measurement of EEG in both PD and chronic stroke patients, using an identical experimental paradigm and recording modality, ensures that the results will be directly interpretable between both models. Finally, our sECoG recordings will provide detailed spatial and frequency domain (above 70 Hz) information not captured by EEG. In the future, these results may potentially set the stage for an invasive system in chronic stroke patients based on sensing and responding to pathological oscillations, as is already commercially available for epilepsy patients and currently in development for PD.