Werner Lucy M, Schnitzler Alfons, Hirschmann Jan
Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf 40225, Germany.
Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf 40225, Germany
J Neurosci. 2025 Feb 26;45(9):e1366242024. doi: 10.1523/JNEUROSCI.1366-24.2024.
Recordings from Parkinson's disease (PD) patients show strong beta-band oscillations (13-35 Hz), which can be modulated by deep brain stimulation (DBS). While high-frequency DBS (>100 Hz) ameliorates motor symptoms and reduces beta activity in the basal ganglia and motor cortex, the effects of low-frequency DBS (<30 Hz) are less clear. Clarifying these effects is relevant for the debate about the role of beta oscillations in motor slowing, which might be causal or epiphenomenal. Here, we investigated how subthalamic nucleus (STN) beta-band DBS affects cortical beta oscillations and motor performance. We recorded the magnetoencephalogram of 14 PD patients (nine males) with DBS implants while on their usual medication. Following a baseline recording (DBS OFF), we applied bipolar DBS at beta frequencies (10, 16, 20, 26, and 30 Hz) via the left electrode in a cyclic fashion, turning stimulation on (5 s) and off (3 s) repeatedly. Cyclic stimulation was applied at rest and during right-hand finger tapping. In the baseline recording, we observed a negative correlation between the strength of hemispheric beta power lateralization and the tap rate. Importantly, beta-band DBS accentuated the lateralization and reduced the tap rate proportionally. The change in lateralization was specific to the alpha/beta range (8-26 Hz), outlasted stimulation, and did not depend on the stimulation frequency, suggesting a remote-induced response rather than entrainment. Our study demonstrates that cortical beta oscillations can be manipulated by STN beta-band DBS. This manipulation has consequences for motor performance, supporting a causal role of beta oscillations.
帕金森病（PD）患者的记录显示出强烈的β波段振荡（13 - 35赫兹），这种振荡可通过深部脑刺激（DBS）进行调节。虽然高频DBS（>100赫兹）可改善运动症状并降低基底神经节和运动皮层中的β活动，但低频DBS（<30赫兹）的效果尚不清楚。阐明这些效果对于关于β振荡在运动迟缓中作用的争论具有重要意义，β振荡在运动迟缓中可能是因果性的或附带现象的。在此，我们研究了丘脑底核（STN）β波段DBS如何影响皮层β振荡和运动表现。我们记录了14名植入DBS的PD患者（9名男性）在服用常规药物时的脑磁图。在基线记录（DBS关闭）后，我们通过左侧电极以循环方式在β频率（10、16、20、26和30赫兹）施加双极DBS，反复开启刺激（5秒）和关闭刺激（3秒）。在休息和右手手指敲击期间施加循环刺激。在基线记录中，我们观察到半球β功率侧化强度与敲击速率之间呈负相关。重要的是，β波段DBS加剧了侧化并按比例降低了敲击速率。侧化的变化特定于α/β范围（8 - 26赫兹），在刺激结束后仍持续存在，并且不依赖于刺激频率，这表明是一种远程诱导反应而非夹带作用。我们的研究表明，皮层β振荡可通过STNβ波段DBS进行操纵。这种操纵对运动表现有影响，支持了β振荡的因果作用。
