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帕金森病和肌张力障碍中的运动皮质回路。

Motor cortical circuits in Parkinson disease and dystonia.

作者信息

Udupa Kaviraja, Chen Robert

机构信息

Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences, Bangalore, India.

Division of Neurology, Department of Medicine, University of Toronto, Toronto, ON, Canada.

出版信息

Handb Clin Neurol. 2019;161:167-186. doi: 10.1016/B978-0-444-64142-7.00047-3.

Abstract

We review the motor cortical and basal ganglia involvement in two important movement disorders: Parkinson's disease (PD) and dystonia. Single and paired pulse transcranial magnetic stimulation studies showed altered excitability and cortical circuits in PD with decreased silent period, short interval intracortical inhibition, intracortical facilitation, long afferent inhibition, interhemispheric inhibition, and cerebellar inhibition, and increased long interval intracortical inhibition and short interval intracortical facilitation. In dystonia, there is decreased silent period, short interval intracortical inhibition, long afferent inhibition, interhemispheric inhibition, and increased intracortical facilitation. Plasticity induction protocols revealed deficient plasticity in PD and normal and exaggerated plasticity in dystonia. In the basal ganglia, there is increased β (14-30Hz) rhythm in PD and characteristic 5-18Hz band synchronization in dystonia. These motor cortical circuits, cortical plasticity, and oscillation profiles of the basal ganglia are altered with medications and deep brain stimulation treatment. There is considerable variability in these measures related to interindividual variations, different disease characteristics, and methodological considerations. Nevertheless, these pathophysiologic studies have expanded our knowledge of cortical excitability, plasticity, and oscillations in PD and dystonia, improved our understanding of disease pathophysiology, and helped to develop new treatments for these conditions.

摘要

我们回顾了运动皮层和基底神经节在两种重要运动障碍中的表现

帕金森病(PD)和肌张力障碍。单脉冲和双脉冲经颅磁刺激研究表明,PD患者的兴奋性和皮层回路发生改变,静息期缩短、短间隔皮层内抑制、皮层内易化、长传入抑制、半球间抑制和小脑抑制减弱,长间隔皮层内抑制和短间隔皮层内易化增强。在肌张力障碍中,静息期缩短、短间隔皮层内抑制、长传入抑制、半球间抑制减弱,皮层内易化增强。可塑性诱导方案显示,PD患者的可塑性不足,而肌张力障碍患者的可塑性正常且增强。在基底神经节,PD患者的β(14 - 30Hz)节律增强,肌张力障碍患者则有特征性的5 - 18Hz频段同步化。这些运动皮层回路、皮层可塑性和基底神经节的振荡模式会因药物治疗和深部脑刺激治疗而改变。这些测量结果存在相当大的变异性,这与个体差异、不同的疾病特征以及方法学考虑因素有关。尽管如此,这些病理生理学研究扩展了我们对PD和肌张力障碍中皮层兴奋性、可塑性和振荡的认识,增进了我们对疾病病理生理学的理解,并有助于开发针对这些疾病的新治疗方法。

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