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小脑刺激无法调节书写性肌张力障碍中运动皮层的可塑性。

Cerebellar stimulation fails to modulate motor cortex plasticity in writing dystonia.

作者信息

Sadnicka Anna, Hamada Masashi, Bhatia Kailash P, Rothwell John C, Edwards Mark J

机构信息

Shared first authorship, London, United Kingdom; Sobell Department of Motor Neuroscience and Movement Disorders, University College London, London, United Kingdom.

出版信息

Mov Disord. 2014 Sep;29(10):1304-7. doi: 10.1002/mds.25881. Epub 2014 May 5.

Abstract

BACKGROUND

Primary dystonia is characterized neurophysiologically by reduced inhibitory mechanisms and abnormal regulation of plasticity responses. The potential of anodal cerebellar transcranial direct current stimulation as a therapeutic tool in writing dystonia was examined, after the observation that cerebellar stimulation reduces responses to an associative plasticity protocol in healthy subjects.

METHODS

Ten patients with writing dystonia completed a two-part study (sham and anodal) in which cerebellar stimulation was given simultaneously with paired associative stimulation. Electrophysiological and clinical parameters were measured before and after stimulation.

RESULTS

Clinical symptoms were unchanged by cerebellar stimulation. Patients exhibited much variability in the size and direction of their plasticity responses. Excessive or topographically abnormal plasticity responses were not observed. In the subgroup of patients with facilitatory responses to paired associative stimulation in the sham condition, anodal cerebellar stimulation retained its ability to reduce the magnitude of plasticity response.

CONCLUSIONS

Our limited understanding of intersubject variability of plasticity responses in writing dystonia currently undermines cerebellar stimulation as a novel treatment in this subset of dystonia. Cerebellar stimulation may be beneficial in other neurological disorders with consistently exaggerated plasticity.

摘要

背景

原发性肌张力障碍在神经生理学上的特征是抑制机制减弱和可塑性反应调节异常。在观察到小脑刺激可降低健康受试者对联合可塑性方案的反应后,研究了阳极小脑经颅直流电刺激作为书写性肌张力障碍治疗工具的潜力。

方法

10名书写性肌张力障碍患者完成了一项分为两部分的研究(假刺激和阳极刺激),其中在给予配对联合刺激的同时进行小脑刺激。在刺激前后测量电生理和临床参数。

结果

小脑刺激并未改变临床症状。患者在可塑性反应的大小和方向上表现出很大的变异性。未观察到过度或地形异常的可塑性反应。在假刺激条件下对配对联合刺激有促进反应的患者亚组中,阳极小脑刺激仍能降低可塑性反应的幅度。

结论

目前我们对书写性肌张力障碍中可塑性反应个体间变异性的了解有限,这削弱了小脑刺激作为该类型肌张力障碍新治疗方法的作用。小脑刺激可能对其他可塑性持续过度增强的神经系统疾病有益。

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