基底神经节
帕金森病
快速眼动睡眠行为障碍
神经科学
睡眠(系统调用)
医学
疾病
心理学
内科学
中枢神经系统
计算机科学
操作系统
作者
Zixiao Yin,Tianshuo Yuan,Anchao Yang,Yichen Xu,Guanyu Zhu,Q. An,Ruoyu Ma,Yifei Gan,Lin Shi,Yutong Bai,Ning Zhang,Chunxue Wang,Yin Jiang,Fangang Meng,Wolf‐Julian Neumann,Huiling Tan,Jianguo Zhang
标识
DOI:10.1136/jnnp-2023-332014
摘要
Rapid eye movement (REM) sleep behaviour disorder (RBD) is one of the most common sleep problems and represents a key prodromal marker in Parkinson's disease (PD). It remains unclear whether and how basal ganglia nuclei, structures that are directly involved in the pathology of PD, are implicated in the occurrence of RBD.Here, in parallel with whole-night video polysomnography, we recorded local field potentials from two major basal ganglia structures, the globus pallidus internus and subthalamic nucleus, in two cohorts of patients with PD who had varied severity of RBD. Basal ganglia oscillatory patterns during RBD and REM sleep without atonia were analysed and compared with another age-matched cohort of patients with dystonia that served as controls.We found that beta power in both basal ganglia nuclei was specifically elevated during REM sleep without atonia in patients with PD, but not in dystonia. Basal ganglia beta power during REM sleep positively correlated with the extent of atonia loss, with beta elevation preceding the activation of chin electromyogram activities by ~200 ms. The connectivity between basal ganglia beta power and chin muscular activities during REM sleep was significantly correlated with the clinical severity of RBD in PD.These findings support that basal ganglia activities are associated with if not directly contribute to the occurrence of RBD in PD. Our study expands the understanding of the role basal ganglia played in RBD and may foster improved therapies for RBD by interrupting the basal ganglia-muscular communication during REM sleep in PD.
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