Levinson Lila H, Caldwell David J, Cronin Jeneva A, Houston Brady, Perlmutter Steve I, Weaver Kurt E, Herron Jeffrey A, Ojemann Jeffrey G, Ko Andrew L
Graduate Program in Neuroscience, University of Washington, Seattle, WA, United States.
Center for Neurotechnology, University of Washington, Seattle, WA, United States.
Front Hum Neurosci. 2021 Mar 11;15:590251. doi: 10.3389/fnhum.2021.590251. eCollection 2021.
Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a clinically effective tool for treating medically refractory Parkinson's disease (PD), but its neural mechanisms remain debated. Previous work has demonstrated that STN DBS results in evoked potentials (EPs) in the primary motor cortex (M1), suggesting that modulation of cortical physiology may be involved in its therapeutic effects. Due to technical challenges presented by high-amplitude DBS artifacts, these EPs are often measured in response to low-frequency stimulation, which is generally ineffective at PD symptom management. This study aims to characterize STN-to-cortex EPs seen during clinically relevant high-frequency STN DBS for PD. Intraoperatively, we applied STN DBS to 6 PD patients while recording electrocorticography (ECoG) from an electrode strip over the ipsilateral central sulcus. Using recently published techniques, we removed large stimulation artifacts to enable quantification of STN-to-cortex EPs. Two cortical EPs were observed - one synchronized with DBS onset and persisting during ongoing stimulation, and one immediately following DBS offset, here termed the "start" and the "end" EPs respectively. The start EP is, to our knowledge, the first long-latency cortical EP reported during ongoing high-frequency DBS. The start and end EPs differ in magnitude ( < 0.05) and latency ( < 0.001), and the end, but not the start, EP magnitude has a significant relationship ( < 0.001, adjusted for random effects of subject) to ongoing high gamma (80-150 Hz) power during the EP. These contrasts may suggest mechanistic or circuit differences in EP production during the two time periods. This represents a potential framework for relating DBS clinical efficacy to the effects of a variety of stimulation parameters on EPs.
丘脑底核(STN)的深部脑刺激(DBS)是治疗药物难治性帕金森病(PD)的一种临床有效工具,但其神经机制仍存在争议。先前的研究表明,STN DBS可在初级运动皮层(M1)诱发诱发电位(EP),提示皮层生理调节可能参与其治疗效果。由于高振幅DBS伪迹带来的技术挑战,这些EP通常是在低频刺激时测量的,而低频刺激对PD症状管理通常无效。本研究旨在描述在临床上相关的高频STN DBS治疗PD期间观察到的STN到皮层的EP。术中,我们对6例PD患者进行STN DBS,同时从同侧中央沟上方的电极条记录皮层脑电图(ECoG)。使用最近发表的技术,我们去除了大的刺激伪迹,以能够对STN到皮层的EP进行量化。观察到两种皮层EP——一种与DBS开始同步并在持续刺激期间持续存在,另一种紧跟在DBS结束后,这里分别称为“起始”和“结束”EP。据我们所知,起始EP是在持续高频DBS期间首次报道的长潜伏期皮层EP。起始和结束EP在幅度(<0.05)和潜伏期(<0.001)上存在差异,并且结束EP的幅度(而非起始EP)与EP期间持续的高伽马(80 - 150 Hz)功率有显著关系(<0.001,根据受试者的随机效应进行调整)。这些差异可能表明两个时间段内EP产生的机制或回路存在差异。这代表了一个将DBS临床疗效与各种刺激参数对EP的影响相关联的潜在框架。