Department of Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Berlin Institute of Health (BIH), Berlin, Germany.
Nat Commun. 2024 Oct 1;15(1):8475. doi: 10.1038/s41467-024-52814-4.
Dystonia is a hyperkinetic movement disorder that has been associated with an imbalance towards the direct pathway between striatum and internal pallidum, but the neuronal underpinnings of this abnormal basal ganglia pathway activity remain unknown. Here, we report invasive recordings from ten dystonia patients via deep brain stimulation electrodes that allow for parallel recordings of several basal ganglia nuclei, namely the striatum, external and internal pallidum, that all displayed activity in the low frequency band (3-12 Hz). In addition to a correlation with low-frequency activity in the internal pallidum (R = 0.88, P = 0.001), we demonstrate that dystonic symptoms correlate specifically with low-frequency coupling between striatum and internal pallidum (R = 0.75, P = 0.009). This points towards a pathophysiological role of the direct striato-pallidal pathway in dystonia that is conveyed via coupling in the enhanced low-frequency band. Our study provides a mechanistic insight into the pathophysiology of dystonia by revealing a link between symptom severity and frequency-specific coupling of distinct basal ganglia pathways.
肌张力障碍是一种运动障碍，与纹状体和内苍白球之间的直接通路失衡有关，但这种异常基底节通路活动的神经元基础仍不清楚。在这里，我们报告了来自 10 名肌张力障碍患者的侵入性记录，这些记录通过深部脑刺激电极进行，允许对几个基底节核进行平行记录，即纹状体、外苍白球和内苍白球，所有这些核都显示出低频带（3-12 Hz）的活动。除了与内苍白球的低频活动相关（R=0.88，P=0.001）之外，我们还证明了肌张力障碍症状与纹状体和内苍白球之间的低频耦合特别相关（R=0.75，P=0.009）。这表明直接纹状体苍白球通路在肌张力障碍中具有病理生理学作用，这种作用是通过增强的低频带中的耦合来传递的。我们的研究通过揭示症状严重程度与不同基底节通路的特定频率耦合之间的联系，为肌张力障碍的病理生理学提供了一种机制上的见解。
