晚期帕金森病的生理变化:运动皮质可塑性的改变及其在病理生理和临床症状中的意义

IF 0.4 Q4 CLINICAL NEUROLOGY
Takahiro Shimizu, R. Hanajima
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引用次数: 0

摘要

帕金森病(PD)是一种以黑质多巴胺能神经变性为特征的进行性神经退行性疾病。多巴胺在突触可塑性的诱导中起着重要作用,PD中大脑的可塑性变化已被广泛研究。在人类中,非侵入性经颅磁刺激(TMS)已被广泛用于运动皮层的可塑性诱导。在这篇综述中,我们将讨论多巴胺受体如何参与神经可塑性的诱导,PD模型动物皮质纹状体可塑性的变化,多巴胺对健康人运动皮质可塑性的影响,PD患者运动皮质可塑性的变化及其与运动症状的关系,最后,左旋多巴诱导的运动障碍的可塑性改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Physiological changes in advanced Parkinson's disease: Altered motor cortical plasticity and its significance in pathophysiology and clinical symptoms
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neurodegeneration in the substantia nigra. Dopamine plays an important role in the induction of synaptic plasticity, and plastic changes in the brain have been broadly investigated in PD. In humans, non‐invasive transcranial magnetic stimulation (TMS) has been widely used for plasticity induction in the motor cortex. In this review, we will discuss how dopamine receptors are involved in the induction of neuroplasticity, changes in corticostriatal plasticity in PD model animals, effects of dopamine on motor cortical plasticity in healthy humans, changes in motor cortical plasticity in PD patients including its relationship to motor symptoms, and, finally, altered plasticity in levodopa‐induced dyskinesia.
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来源期刊
CiteScore
0.80
自引率
0.00%
发文量
76
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