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图雷特综合征中苍白球内侧前区活动的紧张性和相位性变化。

Tonic and phasic changes in anteromedial globus pallidus activity in Tourette syndrome.

作者信息

Israelashvili Michal, Smeets Anouk Y J M, Bronfeld Maya, Zeef Dagmar H, Leentjens Albert F G, van Kranen-Mastenbroek Vivianne, Janssen Marcus L F, Temel Yasin, Ackermans Linda, Bar-Gad Izhar

机构信息

The Leslie & Susan Goldschmied (Gonda) Multidisciplinary Brain Research Center, Bar-Ilan University, Ramat-Gan, Israel.

Department of Neurosurgery, Maastricht University Medical Center, Maastricht, The Netherlands.

出版信息

Mov Disord. 2017 Jul;32(7):1091-1096. doi: 10.1002/mds.27043. Epub 2017 May 29.

Abstract

BACKGROUND

Tourette syndrome is a hyperkinetic neurodevelopmental disorder characterized by tics.

OBJECTIVE

Assess the neuronal changes in the associative/limbic GP associated with Tourette syndrome.

METHODS

Neurophysiological recordings were performed from the anterior (associative/limbic) GPe and GPi of 8 awake patients during DBS electrode implantation surgeries.

RESULTS

The baseline firing rate of the neurons was low in a state-dependent manner in both segments of the GP. Tic-dependent transient rate changes were found in the activity of individual neurons of both segments around the time of the tic. Neither oscillatory activity of individual neurons nor correlations in their interactions were observed.

CONCLUSIONS

The results demonstrate the involvement of the associative/limbic pathway in the underlying pathophysiology of Tourette syndrome and point to tonic and phasic modulations of basal ganglia output as a key mechanisms underlying the abnormal state of the disorder and the expression of individual tics, respectively. © 2017 International Parkinson and Movement Disorder Society.

摘要

背景

抽动秽语综合征是一种以抽动为特征的多动性神经发育障碍。

目的

评估与抽动秽语综合征相关的联合/边缘苍白球内侧部的神经元变化。

方法

在8例清醒患者进行脑深部电刺激(DBS)电极植入手术期间,从前部(联合/边缘)苍白球外侧部(GPe)和苍白球内侧部(GPi)进行神经生理学记录。

结果

在GP的两个节段中,神经元的基线放电率呈状态依赖性降低。在抽动发生时,两个节段的单个神经元活动中均发现了与抽动相关的瞬时速率变化。未观察到单个神经元的振荡活动及其相互作用的相关性。

结论

结果表明联合/边缘通路参与了抽动秽语综合征的潜在病理生理学过程,并分别指出基底神经节输出的紧张性和相位性调制是该疾病异常状态和个体抽动表达的关键机制。©2017国际帕金森病和运动障碍协会。

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