Müller Eli J, Robinson Peter A
School of Physics, The University of Sydney, Sydney, NSW, Australia.
Center for Integrative Brain Function, The University of Sydney, Sydney, NSW, Australia.
Front Comput Neurosci. 2018 Dec 11;12:98. doi: 10.3389/fncom.2018.00098. eCollection 2018.
A neural field model of the corticothalamic-basal ganglia system is developed that describes enhanced beta activity within subthalamic and pallidal circuits in Parkinson's disease (PD) via system resonances. A model of deep brain stimulation (DBS) of typical clinical targets, the subthalamic nucleus (STN) and globus pallidus internus (GPi), is added and studied for several distinct stimulation protocols that are used for treatment of the motor symptoms of PD and that reduce pathological beta band activity (13-30 Hz) in the corticothalamic-basal ganglia network. The resulting impact of DBS on enhanced beta activity in the STN and GPi, as well as cortico-subthalamic and cortico-pallidal coherence, are studied. Both STN-DBS and GPi-DBS are found to be effective for suppressing peak STN and GPi power in the beta band, with GPi-DBS being slightly more effective in both the STN and the GPi for all stimulus protocols tested. The largest decrease in cortico-STN coherence is observed during STN-DBS, whereas GPi-DBS is most effective for reducing cortico-GPi coherence. A reduction of the pathologically large STN connection strengths that define the parkinsonian state results in enhanced 6 Hz activity and could thus represent a compensatory mechanism that has the side effect of driving parkinsonian tremor-like oscillations. This model provides a method for systematically testing effective DBS protocols that agrees with experimental and clinical findings. Furthermore, the model suggests GPi-DBS and STN-DBS have distinct impacts on elevated synchronization between the basal ganglia and motor cortex in PD.
构建了一个皮质丘脑 - 基底神经节系统的神经场模型，该模型通过系统共振描述了帕金森病（PD）中丘脑底核和苍白球回路内增强的β活动。添加了针对典型临床靶点丘脑底核（STN）和内侧苍白球（GPi）的深部脑刺激（DBS）模型，并针对几种不同的刺激方案进行了研究，这些方案用于治疗PD的运动症状并降低皮质丘脑 - 基底神经节网络中病理性β频段活动（13 - 30 Hz）。研究了DBS对STN和GPi中增强的β活动以及皮质 - 丘脑底核和皮质 - 苍白球相干性的影响。发现STN - DBS和GPi - DBS在抑制β频段中STN和GPi的峰值功率方面均有效，对于所有测试的刺激方案，GPi - DBS在STN和GPi中均略为有效。在STN - DBS期间观察到皮质 - STN相干性的最大降低，而GPi - DBS在降低皮质 - GPi相干性方面最有效。定义帕金森状态的病理性大的STN连接强度的降低导致6 Hz活动增强，因此可能代表一种具有引发帕金森样震颤振荡副作用的补偿机制。该模型提供了一种系统测试有效DBS方案的方法，与实验和临床发现一致。此外，该模型表明GPi - DBS和STN - DBS对PD中基底神经节和运动皮层之间增强的同步有不同影响。
