Bore Joyce Chelangat, Toth Carmen, Campbell Brett A, Cho Hanbin, Pucci Francesco, Hogue Olivia, Machado Andre G, Baker Kenneth B
Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United States.
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH, United States.
Front Neurosci. 2022 Mar 4;16:831055. doi: 10.3389/fnins.2022.831055. eCollection 2022.
Parkinson's disease is a neurological disease with cardinal motor signs including bradykinesia and tremor. Although beta-band hypersynchrony in the cortico-basal ganglia network is thought to contribute to disease manifestation, the resulting effects on network connectivity are unclear. We examined local field potentials from a non-human primate across the naïve, mild, and moderate disease states (model was asymmetric, left-hemispheric dominant) and probed power spectral density as well as cortico-cortical and cortico-subthalamic connectivity using both coherence and Granger causality, which measure undirected and directed effective connectivity, respectively. Our network included the left subthalamic nucleus (L-STN), bilateral primary motor cortices (L-M1, R-M1), and bilateral premotor cortices (L-PMC, R-PMC). Results showed two distinct peaks (Peak A at 5-20 Hz, Peak B at 25-45 Hz) across all analyses. Power and coherence analyses showed widespread increases in power and connectivity in both the Peak A and Peak B bands with disease progression. For Granger causality, increases in Peak B connectivity and decreases in Peak A connectivity were associated with the disease. Induction of mild disease was associated with several changes in connectivity: (1) the cortico-subthalamic connectivity in the descending direction (L-PMC to L-STN) decreased in the Peak A range while the reciprocal, ascending connectivity (L-STN to L-PMC) increased in the Peak B range; this may play a role in generating beta-band hypersynchrony in the cortex, (2) both L-M1 to L-PMC and R-M1 to R-PMC causalities increased, which may either be compensatory or a pathologic effect of disease, and (3) a decrease in connectivity occurred from the R-PMC to R-M1. The only significant change seen between mild and moderate disease was increased right cortical connectivity, which may reflect compensation for the left-hemispheric dominant moderate disease state.
帕金森病是一种具有运动迟缓、震颤等主要运动症状的神经疾病。尽管皮质 - 基底神经节网络中的β波段超同步化被认为与疾病表现有关，但其对网络连接性的影响尚不清楚。我们研究了一只非人类灵长类动物在未患病、轻度和中度疾病状态下（模型不对称，左半球占主导）的局部场电位，并使用相干性和格兰杰因果关系分别探测功率谱密度以及皮质 - 皮质和皮质 - 丘脑底核的连接性，这两种方法分别测量无向和有向有效连接性。我们的网络包括左侧丘脑底核（L - STN）、双侧初级运动皮层（L - M1、R - M1）和双侧运动前区皮层（L - PMC、R - PMC）。结果显示在所有分析中出现两个不同的峰值（峰值A在5 - 20赫兹，峰值B在25 - 45赫兹）。功率和相干性分析表明，随着疾病进展，峰值A和峰值B频段的功率和连接性普遍增加。对于格兰杰因果关系，峰值B连接性增加而峰值A连接性降低与疾病相关。轻度疾病的诱发与连接性的若干变化有关：（1）在峰值A范围内，下行方向（L - PMC至L - STN）的皮质 - 丘脑底核连接性降低，而反向的上行连接性（L - STN至L - PMC）在峰值B范围内增加；这可能在皮层中产生β波段超同步化中起作用，（2）L - M1至L - PMC和R - M1至R - PMC的因果关系均增加，这可能是一种补偿或疾病的病理效应，并且（3）从R - PMC到R - M1的连接性降低。在轻度和中度疾病之间观察到的唯一显著变化是右侧皮质连接性增加，这可能反映了对左半球占主导的中度疾病状态的补偿。
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