Program of Neural Computation, Carnegie Mellon University, Pittsburgh, PA 15213, USA.
Medical Scientist Training Program, University of Pittsburgh and Carnegie Mellon University, Pittsburgh, PA 15213, USA.
Cereb Cortex. 2022 Oct 8;32(20):4480-4491. doi: 10.1093/cercor/bhab496.
The mechanism of action of deep brain stimulation (DBS) to the basal ganglia for Parkinson's disease remains unclear. Studies have shown that DBS decreases pathological beta hypersynchrony between the basal ganglia and motor cortex. However, little is known about DBS's effects on long range corticocortical synchronization. Here, we use machine learning combined with graph theory to compare resting-state cortical connectivity between the off and on-stimulation states and to healthy controls. We found that turning DBS on increased high beta and gamma band synchrony (26 to 50 Hz) in a cortical circuit spanning the motor, occipitoparietal, middle temporal, and prefrontal cortices. The synchrony in this network was greater in DBS on relative to both DBS off and controls, with no significant difference between DBS off and controls. Turning DBS on also increased network efficiency and strength and subnetwork modularity relative to both DBS off and controls in the beta and gamma band. Thus, unlike DBS's subcortical normalization of pathological basal ganglia activity, it introduces greater synchrony relative to healthy controls in cortical circuitry that includes both motor and non-motor systems. This increased high beta/gamma synchronization may reflect compensatory mechanisms related to DBS's clinical benefits, as well as undesirable non-motor side effects.
深部脑刺激(DBS)对基底神经节治疗帕金森病的作用机制尚不清楚。研究表明,DBS 可降低基底神经节与运动皮层之间病理性β超同步性。然而,对于 DBS 对远距离皮质同步性的影响知之甚少。在这里,我们使用机器学习结合图论来比较关闭和开启刺激状态下的静息状态皮质连接,并与健康对照组进行比较。我们发现,开启 DBS 可增加跨越运动、顶枕颞和前额皮质的皮质回路中的高β和γ频带同步性(26 至 50 Hz)。与 DBS 关闭和对照组相比,该网络中的同步性在 DBS 开启时更高,而 DBS 关闭和对照组之间没有显著差异。与 DBS 关闭和对照组相比,开启 DBS 还可增加β和γ频带中的网络效率、强度和子网络模块性。因此,与 DBS 对病理性基底神经节活动的亚皮质正常化不同,它在包括运动和非运动系统在内的皮质回路中引入了与健康对照组相比更高的同步性。这种增加的高β/γ同步性可能反映了与 DBS 的临床益处相关的补偿机制,以及不希望出现的非运动副作用。