Conte Antonella, Defazio Giovanni, Mascia Marcello, Belvisi Daniele, Pantano Patrizia, Berardelli Alfredo
Department of Human Neurosciences, Sapienza, University of Rome, Rome, Italy.
IRCCS Neuromed, Pozzilli (IS), Italy.
F1000Res. 2020 Jan 30;9. doi: 10.12688/f1000research.21029.2. eCollection 2020.
Focal dystonia is a movement disorder characterized by involuntary muscle contractions that determine abnormal postures. The traditional hypothesis that the pathophysiology of focal dystonia entails a single structural dysfunction (i.e. basal ganglia) has recently come under scrutiny. The proposed network disorder model implies that focal dystonias arise from aberrant communication between various brain areas. Based on findings from animal studies, the role of the cerebellum has attracted increased interest in the last few years. Moreover, it has been increasingly reported that focal dystonias also include nonmotor disturbances, including sensory processing abnormalities, which have begun to attract attention. Current evidence from neurophysiological and neuroimaging investigations suggests that cerebellar involvement in the network and mechanisms underlying sensory abnormalities may have a role in determining the clinical heterogeneity of focal dystonias.
局限性肌张力障碍是一种运动障碍,其特征为非自主性肌肉收缩,导致异常姿势。传统假说认为局限性肌张力障碍的病理生理学涉及单一结构功能障碍(即基底神经节),该假说最近受到了审视。提出的网络障碍模型表明,局限性肌张力障碍源于不同脑区之间的异常通信。基于动物研究的结果,小脑的作用在过去几年中引起了越来越多的关注。此外,越来越多的报道称,局限性肌张力障碍还包括非运动障碍,包括感觉处理异常,这已开始引起关注。神经生理学和神经影像学研究的当前证据表明,小脑参与感觉异常背后的网络和机制可能在决定局限性肌张力障碍的临床异质性方面发挥作用。