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人类局灶性肌张力障碍的神经生理异常十年反思。

Ten-Year Reflections on the Neurophysiological Abnormalities of Focal Dystonias in Humans.

机构信息

Department of Human Neurosciences, Sapienza, University of Rome, Rome, Italy.

IRCCS Neuromed, Pozzilli (IS), Italy.

出版信息

Mov Disord. 2019 Nov;34(11):1616-1628. doi: 10.1002/mds.27859. Epub 2019 Oct 8.

Abstract

The physiological landscape of dystonia has changed considerably over the past 10 years. Initial ideas that dystonic motor symptoms could be explained by a combination of loss of inhibition and increased plasticity, together with subtle deficits in sensory processing, have been questioned, whereas the possible role of the cerebellum has risen in importance. In addition, it has been recognized that symptoms affect more than just the motor and sensory systems and encompass independent cognitive and psychological changes. Finally, it has become clear that, despite similarities in symptoms, there may be pathophysiological differences between idiopathic, inherited, and acquired forms of dystonia. In other words, progress in the pathophysiology of dystonia has followed the usual pattern from an initial phase in which core deficits are readily explained by highly simplified models to a realization that within a highly interconnected network, effects are more nuanced with widespread changes that might either compensate or contribute to the clinical symptoms to different degrees in different individuals. © 2019 International Parkinson and Movement Disorder Society.

摘要

过去 10 年来,肌张力障碍的生理学景观发生了重大变化。最初的观点认为,由抑制丧失和可塑性增加以及感觉处理的细微缺陷共同引起的肌张力障碍运动症状可以得到解释,而小脑的可能作用则变得更加重要。此外,人们已经认识到,症状不仅影响运动和感觉系统,还包括独立的认知和心理变化。最后,很明显,尽管症状相似,但特发性、遗传性和获得性肌张力障碍之间可能存在病理生理学差异。换句话说,肌张力障碍的病理生理学进展遵循了一个常见的模式,从最初的核心缺陷很容易用高度简化的模型来解释的阶段,到认识到在高度互联的网络中,影响更加微妙,广泛的变化可能在不同程度上补偿或导致不同个体的临床症状。 © 2019 国际帕金森病和运动障碍协会。

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