Cortical and basal ganglia local field potentials in human movement disorders

人类运动障碍中的皮质和基底神经节局部场电位

• 批准号: 8259791
• 负责人: PHILIP Andrew STARR
• 金额: $ 33.12万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8259791
• 关键词: Abbreviations; Address; Affect; Analysis of Variance; Area; Basal Ganglia; Basal Ganglia Diseases; Behavioral; Bradykinesia; Brain; Cues; Deep Brain Stimulation; Disease; Dystonia; Effectiveness; Elbow; Electrocorticogram; Electrodes; Electromyography; Epilepsy; Essential Tremor; Frequencies; Functional disorder; Globus Pallidus; Goals; Hand; Human; Implant; Inpatients; Jaw; Joints; Knowledge; Lead; Location; Monitor; Motor; Motor Cortex; Movement; Movement Disorders; Neurologist; Neurons; Operative Surgical Procedures; Parkinson Disease; Parkinsonian Disorders; Pathology; Patients; Pattern; Persons; Presynaptic Terminals; Primary Dystonias; Property; Resolution; Rest; Scalp structure; Sensory; Shoulder; Somatosensory Evoked Potentials; Structure of subthalamic nucleus; Surface; Techniques; Thinking; Work; Wrist; abstracting; arm; awake; base; brain electrical activity; comparison group; cranium; deep brain stimulator; density; foot; implantation; improved; novel; postsynaptic; programs; sensory cortex; sensory feedback; sensory system; theories; vibration

Abstract The goal of this project is to advance the understanding of movement disorders pathophysiology through studies of basal ganglia and cortical local field potentials (LFPs) in humans. The LFP represents synchronized sub- and supra-threshold activity in presynaptic terminals and postsynaptic neurons. Recent studies of subthalamic nucleus (STN) LFPs in Parkinson's disease (PD) produced a novel hypothesis: that parkinsonian bradykinesia is due to excessive basal ganglia synchronized oscillatory activity in the beta frequency range (13-30 Hz), and that suppression of beta oscillations is the mechanism for the effectiveness of STN deep brain stimulation (DBS). However, this framework leaves unanswered questions. Can the beta oscillation hypothesis be confirmed by comparison to subjects without movement disorders? Are excessive beta oscillations unique to PD, or are they associated with other movement disorders of basal ganglia origin? Are abnormal beta oscillations present in motor cortex as well, reflecting a network property of the basal ganglia-thalamocortical (BGTC) circuit? Here, we address these questions by comparing primary motor (M1) and primary sensory (S1) cortex LFPs in patients with a basal ganglia disorder (PD and primary dystonia), with two comparison groups without basal ganglia pathology (essential tremor (ET) and epilepsy). Movement disorders patients are studied while undergoing awake placement of DBS electrodes. Epilepsy patients are studied while undergoing inpatient video monitoring. We hypothesize that PD and dystonia both are characterized by broad beta band cortical activity which distinguishes these disorders from ET and from subjects without movement disorders. Our second major goal is to understand BGTC oscillations in primary dystonia, which has been less studied than PD. Our approach is simultaneous recording of STN and cortical LFPs in M1 and S1. We hypothesize: (1) Dystonic patients have an excess of high beta (21-30) and low gamma (30-55 Hz) oscillations in the STN during voluntary movement, while PD patients have predominant low beta (13- 20 Hz) activity, particularly at rest. 2.) Similar patterns are seen in M1 and S1, and in STN-cortical coherence. 3.) Movement related abnormalities in dystonia will be reproduced under conditions in which sensory feedback is activated. The novel features of this proposal are the use of electrocorticography in movement disorders, the introduction of a new target, STN, into the study of dystonia, and the analysis of cortex-basal ganglia interactions through simultaneous LFP recording in both areas. The proposed work should expand the framework for the "oscillation hypothesis" of PD to include the other major movement disorders, improve the rationale for choice of stimulation frequencies in DBS and could provide a basis for cortically based therapies for PD and dystonia.

抽象的 该项目的目的是提高对运动障碍病理生理学的理解 通过研究人类的基底神经节和皮质局部田间电位（LFP）。 LFP 代表突触前终端和突触后的同步子和上阈值活动 神经元。帕金森氏病（PD）中丘脑核（STN）LFP的最新研究产生了 新颖的假设：帕金森氏菌头肌障碍是由于基底神经节的过度同步 Beta频率范围（13-30 Hz）中的振荡活性，抑制β振荡的抑制作用是 STN深脑刺激（DBS）有效性的机制。 但是，该框架留下了未解决的问题。 β振荡假设可以 通过与没有运动障碍的受试者进行比较确认？过度β振荡 PD独有，还是与基底神经节的其他运动障碍有关？是 运动皮层中也存在异常的β振荡，反映了基础的网络特性 神经节 - 丘脑皮质（BGTC）电路？在这里，我们通过比较主电机来解决这些问题 基底神经节障碍患者（PD和原发性的患者）（M1）和原发性感觉（S1）皮质LFP 肌张力障碍），有两个没有基础神经节病理学的比较组（Essential Tremor（ET）和 癫痫）。运动障碍患者在醒着的DBS时进行了研究 电极。在进行住院视频监测时，研究了癫痫患者。我们假设 PD和Dystonia均以广泛的Beta带皮质活性为特征 这些疾病来自ET和没有运动障碍的受试者。 我们的第二个主要目标是了解原发性肌张力障碍的BGTC振荡 比PD少。我们的方法是在M1和S1中同时记录STN和皮质LFP。 我们假设：（1）障碍患者的高β（21-30）和低γ（30-55 Hz）过量过量 自愿运动期间STN的振荡，而PD患者主要具有低β（13-- 20 Hz）活动，尤其是在休息时。 2.）在M1和S1中也可以看到类似的模式 连贯性。 3.）在条件下，肌张力障碍的运动异常将在 激活哪种感觉反馈。该提案的新颖特征是使用 运动障碍中的皮质学，将新目标stn引入到研究中 肌张力障碍，以及通过同时在 这两个领域。拟议的工作应扩大PD的“振荡假设”的框架 包括其他主要运动障碍，提高选择刺激频率的理由 在DBS中，可以为PD和肌张力障碍基于皮质的疗法提供基础。

项目成果

Patterns of Cortical Synchronization in Isolated Dystonia Compared With Parkinson Disease.

• DOI: 10.1001/jamaneurol.2015.2561
• 发表时间: 2015-11
• 期刊: JAMA neurology
• 影响因子: 29
• 作者: Miocinovic S;de Hemptinne C;Qasim S;Ostrem JL;Starr PA
• 通讯作者: Starr PA

Acute effects of thalamic deep brain stimulation and thalamotomy on sensorimotor cortex local field potentials in essential tremor.

• DOI: 10.1016/j.clinph.2012.04.020
• 发表时间: 2012-11
• 期刊: Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
• 作者: Air EL;Ryapolova-Webb E;de Hemptinne C;Ostrem JL;Galifianakis NB;Larson PS;Chang EF;Starr PA
• 通讯作者: Starr PA

Intraoperative electrocorticography for physiological research in movement disorders: principles and experience in 200 cases.

• DOI: 10.3171/2015.11.jns151341
• 发表时间: 2017-01
• 期刊: Journal of neurosurgery
• 影响因子: 4.1
• 作者: Panov F;Levin E;de Hemptinne C;Swann NC;Qasim S;Miocinovic S;Ostrem JL;Starr PA
• 通讯作者: Starr PA

Subthalamic nucleus neurons are synchronized to primary motor cortex local field potentials in Parkinson's disease.

• DOI: 10.1523/jneurosci.4676-12.2013
• 发表时间: 2013-04-24
• 期刊: The Journal of neuroscience : the official journal of the Society for Neuroscience
• 作者: Shimamoto SA;Ryapolova-Webb ES;Ostrem JL;Galifianakis NB;Miller KJ;Starr PA
• 通讯作者: Starr PA

Therapeutic deep brain stimulation reduces cortical phase-amplitude coupling in Parkinson's disease.

治疗性深部脑刺激可减少帕金森病的皮层相位-幅度耦合。

• DOI: 10.1038/nn.3997
• 发表时间: 2015-05
• 期刊: NATURE NEUROSCIENCE
• 影响因子: 25
• 作者: de Hemptinne, Coralie;Swann, Nicole C.;Ostrem, Jill L.;Ryapolova-Webb, Elena S.;San Luciano, Marta;Galifianakis, Nicholas B.;Starr, Philip A.
• 通讯作者: Starr, Philip A.