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关于书写痉挛中可塑性研究的思考。

A reflection on plasticity research in writing dystonia.

作者信息

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

机构信息

Sobell Department of Motor Neuroscience and Movement Disorders, University College London, London, UK.

出版信息

Mov Disord. 2014 Jul;29(8):980-7. doi: 10.1002/mds.25908. Epub 2014 May 13.

Abstract

Much attention has focused on the hypothesis that there is enhanced plasticity of sensorimotor circuits in patients with dystonia. A common experimental method to assess plasticity in dystonia research is paired associative stimulation (PAS). Excessive, nonfocal effects of PAS were observed in early studies of dystonia; however, these large effects have not been uniformly replicated. In this viewpoint, data from 15 patients with writing dystonia are presented. We suggest that, as in healthy individuals, the effects of PAS are highly variable. A review of previous studies examining PAS in writing dystonia highlights the range of results that have been observed. We conclude that current experimental evidence cannot be fully explained by the notion that PAS responses in writing dystonia are consistently excessive or nonspecific. The variability of PAS responses is such that enhanced plasticity should not be considered a dystonic fingerprint, because the direction of response can vary, and there is overlap between patient and healthy data. We also discuss evidence questioning the assumption that PAS responses are a clear correlate to levels of synaptic plasticity; we need to define more specifically what PAS responses signify in the dystonic brain. Our conclusions are limited to PAS in writing dystonia; however, much variation exists with other plasticity protocols. Large multicenter studies of both focal and generalized forms of dystonia, probing variability of individual neurophysiological profiles, are encouraged. This will reveal the true role of plasticity in the pathophysiology of dystonia and may expose subject-specific therapeutic interventions that are currently concealed.

摘要

许多注意力都集中在这样一种假说上,即肌张力障碍患者的感觉运动回路具有增强的可塑性。在肌张力障碍研究中评估可塑性的一种常见实验方法是配对联想刺激(PAS)。在肌张力障碍的早期研究中观察到了PAS的过度、非局灶性效应;然而,这些显著效应并未得到一致的重复验证。在本文中,我们展示了15例书写痉挛患者的数据。我们认为,与健康个体一样,PAS的效应具有高度变异性。对先前研究书写痉挛中PAS的回顾突出了所观察到的结果范围。我们得出结论,目前的实验证据不能完全用书写痉挛中PAS反应始终过度或非特异性这一观点来解释。PAS反应的变异性使得增强的可塑性不应被视为肌张力障碍的特征,因为反应方向可能不同,且患者与健康个体的数据存在重叠。我们还讨论了质疑PAS反应与突触可塑性水平明显相关这一假设的证据;我们需要更具体地定义PAS反应在肌张力障碍大脑中的意义。我们的结论仅限于书写痉挛中的PAS;然而,其他可塑性方案也存在很大差异。鼓励对局限性和全身性肌张力障碍进行大型多中心研究,探究个体神经生理特征的变异性。这将揭示可塑性在肌张力障碍病理生理学中的真正作用,并可能揭示目前隐藏的针对个体的治疗干预措施。

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