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

慢性中风患者的神经调节方法有限。经颅直流电刺激 (Tdcs)已经显示出改善这一人群运动缺陷的潜力；然而，它的效果并没有 到目前为止，在随机研究中保持一致，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如何影响运动皮质振荡，这对引导自愿行为很重要。 有动静。我们的长期目标是开发有效的以神经调节为基础的治疗系统 基于对皮质信号的神经调节如何促进康复的更好理解的中风患者 在这群人中的运动行为。在先前的一项研究中，我们记录了 接受DBS手术的僵硬性帕金森病(PD)患者，并观察到显著的调制 与伸臂任务有关的运动皮质振荡。因此，支持大脑皮层振荡的变化 改善了这一组的运动能力。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质振荡可能是tdcs促进运动的一种机制。 慢性运动中风后的康复。为了验证这一假设，在接受DBS手术的PD患者中，我们将 在提示性伸臂过程中测量皮质β(13-30赫兹)和宽带伽马(70-200赫兹)振荡 任务(目标1)和运动表象任务(目标2)在初级运动皮质阳极tdcs激活前后。 在这些患者中，将同时进行sCoG和EEG。为了确保我们在帕金森州的调查结果 将可直接转换为中风模型，在目标3中，我们将使用组合的tDCS和EEG收集飞行员数据 在一组慢性中风患者中，执行与目标1中的帕金森病患者相同的手臂任务。目标1和2将 手术将在手术室进行，而AIM 3将在NI Core EEG实验室进行。我们预计tdcs 将以一种偏向于两个种群的运动计划和启动的方式来调节运动皮质振荡。 这项在神经外科手术中将tDCs与sECoG和EEG相结合的建议是新颖的。如果我们的假设是 经证实，这些发现可能有助于开发用于中风恢复的闭环式tdcs，为此 我们将拥有试点数据(来自AIM 3)来为这种方法提供信息。此外，两组患者的脑电测量 帕金森病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录音将提供详细的 脑电没有捕捉到的空间和频域信息(高于70赫兹)。在未来，这些结果可能 潜在地为慢性中风患者建立基于感知和响应的侵入性系统奠定了基础 病理振荡，已可用于癫痫患者，目前正在开发中 对警局来说。

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.