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帕利达和运动皮质相互作用决定了帕金森病中的步态启动动态

Jessica E Bath, Kenneth H Louie, Hamid Fekri Azgomi

medRxiv : the preprint server for health sciences

|December 23, 2024

概括

帕金森病通过改变基底和运动皮层活动来破坏步行启动,影响姿势调整. 这些神经变化,特别是皮皮质电路,是步行功能障碍和跌倒风险的关键.

科学领域:

神经科学是一个神经科学.
发动机控制器的控制器
帕金森病研究帕金森病研究

背景情况:

步行启动依赖于预期性姿势调整 (APA),这些在帕金森病 (PD) 中受到损害,增加了跌倒风险.
运动皮质和基底质在步行启动期间调节APAs中的作用以及它们对药物的反应仍然不清楚.

研究的目的:

在患有PD的个体中,在步行启动过程中调查基底 - 运动皮质电路的神经动力学.
为了确定神经活动,APA指标 (振幅和时间) 和莱沃多巴药物的作用之间的关系.

主要方法:

电皮质图 (ECoG) 和局部场势 (LFPs) 分别从运动皮质和球记录在五名PD患者中,在指导步行启动任务中.
强力板测量了APA,与神经数据同步,在ON和LOW莱沃多巴条件下.
线性混合模型分析了神经振荡,连贯性和APA特征之间的关联.

主要成果:

帕利达尔β功率下降,马功率增加,而皮质低频功率 (theta,alpha,β) 在步行启动过程中下降,不论是乐伏多巴.
在APA发作之前观察到增加的皮皮层连贯性.
帕利达尔马功率预测了APA振幅,而帕利达尔-皮层和皮层内连贯性预测了APA时间.

结论:

基本节 - 皮质电路动力学,包括功率和连贯性变化,在PD的步态开始期间发生了根本性的变化.
这些神经变化是功能失调的APA幅度和时间的基础,这表明了PD相关的行走障碍的潜在病理生理机制.
确定的神经机制似乎独立于levodopa对运动症状的急性影响.

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