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骑自行车抑制帕金森氏基底神经节中的异常β同步。

Bicycling suppresses abnormal beta synchrony in the Parkinsonian basal ganglia.

机构信息

Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.

Donders Institute for Brain, Cognition, and Behavior, Radboud University, Nijmegen, the Netherlands.

出版信息

Ann Neurol. 2017 Oct;82(4):592-601. doi: 10.1002/ana.25047. Epub 2017 Oct 10.

Abstract

OBJECTIVE

Freezing of gait is a poorly understood symptom of Parkinson disease, and can severely disrupt the locomotion of affected patients. However, bicycling ability remains surprisingly unaffected in most patients suffering from freezing, suggesting functional differences in the motor network. The purpose of this study was to characterize and contrast the oscillatory dynamics underlying bicycling and walking in the basal ganglia.

METHODS

We present the first local field potential recordings directly comparing bicycling and walking in Parkinson disease patients with electrodes implanted in the subthalamic nuclei for deep brain stimulation. Low (13-22Hz) and high (23-35Hz) beta power changes were analyzed in 22 subthalamic nuclei from 13 Parkinson disease patients (57.5 ± 5.9 years old, 4 female). The study group consisted of 5 patients with and 8 patients without freezing of gait.

RESULTS

In patients without freezing of gait, both bicycling and walking led to a suppression of subthalamic beta power (13-35Hz), and this suppression was stronger for bicycling. Freezers showed a similar pattern in general. Superimposed on this pattern, however, we observed a movement-induced, narrowband power increase around 18Hz, which was evident even in the absence of freezing.

INTERPRETATION

These results indicate that bicycling facilitates overall suppression of beta power. Furthermore, movement leads to exaggerated synchronization in the low beta band specifically within the basal ganglia of patients susceptible to freezing. Abnormal ∼18Hz oscillations are implicated in the pathophysiology of freezing of gait, and suppressing them may form a key strategy in developing potential therapies. Ann Neurol 2017;82:592-601.

摘要

目的

冻结步态是一种尚未被充分理解的帕金森病症状,会严重扰乱受影响患者的运动。然而,在大多数受冻结步态影响的患者中,骑自行车的能力仍然出人意料地未受影响,这表明运动网络存在功能差异。本研究的目的是描述和对比基底神经节中骑自行车和步行的振荡动力学。

方法

我们首次展示了在接受深部脑刺激的电极植入丘脑底核的帕金森病患者中,直接比较骑自行车和步行的局部场电位记录。在 13 名帕金森病患者(57.5±5.9 岁,4 名女性)的 22 个丘脑底核中分析了低(13-22Hz)和高(23-35Hz)β 频段的功率变化。研究组包括 5 名有冻结步态的患者和 8 名无冻结步态的患者。

结果

在无冻结步态的患者中,骑自行车和步行均导致丘脑底核β频段功率降低(13-35Hz),而骑自行车时抑制作用更强。冻结者通常也表现出类似的模式。然而,叠加在这种模式上,我们观察到一个运动诱导的、约 18Hz 的窄带功率增加,即使在没有冻结的情况下也很明显。

解释

这些结果表明,骑自行车可以促进β频段功率的整体抑制。此外,运动导致基底神经节中低β频段的同步明显增强,特别是在易冻结的患者中。异常的 18Hz 振荡与冻结步态的病理生理学有关,抑制它们可能是开发潜在治疗方法的关键策略。

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