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Suppression of Parkinsonian Beta Oscillations by Deep Brain Stimulation: Determination of Effective Protocols

机译:通过深部脑刺激抑制帕金森氏β振荡:有效协议的确定。

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摘要

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.
机译:建立了皮质丘脑-基底神经节系统的神经场模型,该模型描述了通过系统共振在帕金森病(PD)的丘脑下和苍白环内增强的β活性。添加了典型临床目标的深脑刺激(DBS)模型,丘脑下丘脑核(STN)和苍白球内侧(GPi),并研究了几种不同的刺激方案,这些方案可用于治疗PD的运动症状,以及减少皮质丘脑-基底神经节网络中的病理性β谱带活动(13–30 Hz)。研究了DBS对STN和GPi中增强的β活性以及皮质-丘脑下和皮质-苍白细胞相干性的影响。发现STN-DBS和GPi-DBS均可有效抑制β波段的峰值STN和GPi功率,而GPi-DBS在STN和GPi中对于所有测试的刺激方案均稍有效。在STN-DBS期间观察到最大的皮质STN相干性降低,而GPi-DBS对于降低皮质GPN相干性最有效。限定帕金森状态的病理性大STN连接强度的降低导致增强的6 Hz活性,因此可能代表一种补偿机制,其具有驱动帕金森震颤状振荡的副作用。该模型提供了一种系统地测试有效DBS方案的方法,该方案与实验和临床发现相符。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的高度同步具有明显的影响。

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