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可塑性与肌张力障碍:一个充满变异性的假说。

Plasticity and dystonia: a hypothesis shrouded in variability.

机构信息

Motor Control and Movement Disorders Group, St George's University of London, London, UK.

Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, UK.

出版信息

Exp Brain Res. 2020 Aug;238(7-8):1611-1617. doi: 10.1007/s00221-020-05773-3. Epub 2020 Mar 23.

Abstract

Studying plasticity mechanisms with Professor John Rothwell was a shared highlight of our careers. In this article, we discuss non-invasive brain stimulation techniques which aim to induce and quantify plasticity, the mechanisms and nature of their inherent variability and use such observations to review the idea that excessive and abnormal plasticity is a pathophysiological substrate of dystonia. We have tried to define the tone of our review by a couple of Professor John Rothwell's many inspiring characteristics; his endless curiosity to refine knowledge and disease models by scientific exploration and his wise yet humble readiness to revise scientific doctrines when the evidence is supportive. We conclude that high variability of response to non-invasive brain stimulation plasticity protocols significantly clouds the interpretation of historical findings in dystonia research. There is an opportunity to wipe the slate clean of assumptions and armed with an informative literature in health, re-evaluate whether excessive plasticity has a causal role in the pathophysiology of dystonia.

摘要

与约翰·罗思韦尔教授一起研究可塑性机制是我们职业生涯的共同亮点。在本文中,我们讨论了旨在诱导和量化可塑性的非侵入性脑刺激技术,以及它们内在变异性的机制和性质,并利用这些观察结果来回顾过度和异常可塑性是肌张力障碍病理生理学基础的观点。我们试图通过约翰·罗思韦尔教授的几个令人鼓舞的特点来定义我们的评论基调;他通过科学探索不断完善知识和疾病模型的无尽好奇心,以及当证据支持时,他明智而谦逊地准备修改科学教义的意愿。我们的结论是,非侵入性脑刺激可塑性方案的反应高度可变,极大地模糊了肌张力障碍研究中历史发现的解释。现在有机会清除假设,并且在健康方面拥有丰富的信息文献,可以重新评估过度的可塑性是否在肌张力障碍的病理生理学中起因果作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df68/7413892/2fbcd41b0178/221_2020_5773_Fig1_HTML.jpg

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