Mirpour Koorosh, Pouratian Nader
Department of Neurological Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Brain. 2025 Mar 6;148(3):886-895. doi: 10.1093/brain/awae300.
Recent progress in the study of Parkinson's disease has highlighted the pivotal role of beta oscillations within the basal ganglia-thalamo-cortical network in modulating motor symptoms. Predominantly manifesting as transient bursts, these beta oscillations are central to the pathophysiology of Parkinson's disease motor symptoms, especially bradykinesia. Our central hypothesis is that increased bursting duration in cortex, coupled with kinematics of movement, disrupts the typical flow of neural information, leading to observable changes in motor behaviour in Parkinson's disease. To explore this hypothesis, we employed an integrative approach, analysing the interplay between moment-to-moment brain dynamics and movement kinematics and the modulation of these relationships by therapeutic deep brain stimulation (DBS). Local field potentials were recorded from the hand motor (M1) and premotor cortical (PM) areas and internal globus pallidus (GPi) in 26 patients with Parkinson's disease undergoing DBS implantation surgery. Participants executed rapid alternating hand movements in 30-s blocks, both with and without therapeutic pallidal stimulation. Behaviourally, the analysis revealed bradykinesia, with hand movement cycle width increasing linearly over time during DBS-OFF blocks. Crucially, there was a moment-to-moment correlation between M1 low beta burst duration and movement cycle width, a relationship that dissipated with therapeutic DBS. Further analyses suggested that high gamma activity correlates with enhanced motor performance with DBS-ON. Regardless of the nature of coupling, DBS's modulation of cortical bursting activity appeared to amplify the brain signals' informational content regarding instantaneous movement changes. Our findings underscore that DBS significantly reshapes the interaction between motor behaviour and neural signals in Parkinson's disease, not only modulating specific bands but also expanding the system's capability to process and relay information for motor control. These insights shed light on the possible network mechanisms underlying DBS therapeutic effects, suggesting a profound impact on both neural and motor domains.
帕金森病研究的最新进展凸显了基底神经节 - 丘脑 - 皮质网络中的β振荡在调节运动症状方面的关键作用。这些β振荡主要表现为短暂爆发，是帕金森病运动症状病理生理学的核心，尤其是运动迟缓。我们的核心假设是，皮质中爆发持续时间的增加，再加上运动学因素，会扰乱神经信息的典型流动，导致帕金森病患者运动行为出现可观察到的变化。为了探究这一假设，我们采用了一种综合方法，分析瞬间脑动力学与运动学之间的相互作用，以及治疗性脑深部电刺激（DBS）对这些关系的调节作用。在26名接受DBS植入手术的帕金森病患者中，记录了手部运动（M1）和运动前皮质（PM）区域以及内侧苍白球（GPi）的局部场电位。参与者在30秒的时间段内执行快速交替手部运动，分别在有和没有苍白球治疗性刺激的情况下进行。行为学分析显示存在运动迟缓，在DBS关闭阶段，手部运动周期宽度随时间呈线性增加。至关重要的是，M1低β爆发持续时间与运动周期宽度之间存在瞬间相关性，这种关系在治疗性DBS时消失。进一步分析表明，高伽马活动与DBS开启时运动表现的增强相关。无论耦合的性质如何，DBS对皮质爆发活动的调节似乎放大了关于即时运动变化的脑信号信息内容。我们的研究结果强调，DBS显著重塑了帕金森病中运动行为与神经信号之间的相互作用，不仅调节特定频段，还扩展了系统处理和传递运动控制信息的能力。这些见解揭示了DBS治疗效果背后可能的网络机制，表明对神经和运动领域都有深远影响。
