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慢性深部脑刺激可使孤立性肌张力障碍患者的头皮脑电图活动正常化。

Chronic deep brain stimulation normalizes scalp EEG activity in isolated dystonia.

机构信息

Department of Neurology, Emory University, Atlanta, GA, United States.

Department of Neurological Surgery, University of California San Francisco, San Francisco, CA, United States.

出版信息

Clin Neurophysiol. 2018 Feb;129(2):368-376. doi: 10.1016/j.clinph.2017.11.011. Epub 2017 Nov 26.

DOI:10.1016/j.clinph.2017.11.011
PMID:29288993
Abstract

OBJECTIVE

To investigate cortical activity using scalp EEG in patients with isolated dystonia treated with chronic deep brain stimulation (DBS), on and off stimulation.

METHODS

We analyzed 64-channel scalp EEG in 12 isolated dystonia patients treated with chronic DBS (7 generalized, 5 cervical/segmental; 7 globus pallidus (GP), 5 subthalamic nucleus (STN)), and 20 healthy age-matched controls. Recordings during rest and movement task, and clinical motor scores, were collected with DBS-on and during a 90-min DBS washout.

RESULTS

Resting state alpha power in the dominant (or contralateral to more dystonic side) motor cortex channel during DBS was comparable to healthy controls, but it increased when DBS was stopped. Resting state and movement-related alpha coherence between bilateral motor cortex channels was increased off DBS.

CONCLUSIONS

Chronic DBS reduces exaggerated alpha oscillations and interhemispheric alpha coherence in the motor cortex of patients with isolated dystonia.

SIGNIFICANCE

These findings complement related studies in Parkinson's disease and support the view that network desynchronization is a prominent mechanism of DBS in movement disorders.

摘要

目的

通过头皮 EEG 研究接受慢性深部脑刺激 (DBS) 治疗的孤立性肌张力障碍患者的皮质活动,刺激开启和关闭时的情况。

方法

我们分析了 12 例接受慢性 DBS 治疗的孤立性肌张力障碍患者(7 例全身性,5 例颈部/节段性;7 例苍白球,5 例丘脑底核)和 20 例年龄匹配的健康对照者的 64 通道头皮 EEG。在 DBS 开启和 90 分钟 DBS 冲洗期间,收集休息和运动任务期间的记录以及临床运动评分。

结果

DBS 时优势(或对侧更为痉挛侧)运动皮质通道的静息状态α功率与健康对照组相当,但 DBS 停止时会增加。双侧运动皮质通道的静息状态和运动相关的α相干性在 DBS 关闭时增加。

结论

慢性 DBS 可降低孤立性肌张力障碍患者运动皮质中过度的α振荡和半球间α相干性。

意义

这些发现补充了帕金森病相关研究,支持了网络去同步化是 DBS 治疗运动障碍的主要机制的观点。

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