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左旋多巴诱导的帕金森病运动障碍:当前和不断发展的概念。

Levodopa-induced dyskinesia in Parkinson disease: Current and evolving concepts.

机构信息

UC Gardner Neuroscience Institute and Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, OH.

Institute of Molecular and Clinical Sciences, St George's University of London, London, United Kingdom.

出版信息

Ann Neurol. 2018 Dec;84(6):797-811. doi: 10.1002/ana.25364. Epub 2018 Nov 30.

Abstract

Levodopa-induced dyskinesia is a common complication in Parkinson disease. Pathogenic mechanisms include phasic stimulation of dopamine receptors, nonphysiological levodopa-to-dopamine conversion in serotonergic neurons, hyperactivity of corticostriatal glutamatergic transmission, and overstimulation of nicotinic acetylcholine receptors on dopamine-releasing axons. Delay in initiating levodopa is no longer recommended, as dyskinesia development is a function of disease duration rather than cumulative levodopa exposure. We review current and in-development treatments for peak-dose dyskinesia but suggest that improvements in levodopa delivery alone may reduce its future prevalence. Ann Neurol 2018;84:797-811.

摘要

左旋多巴诱导的运动障碍是帕金森病的常见并发症。致病机制包括多巴胺受体的阶段性刺激、血清素能神经元中不生理的左旋多巴向多巴胺的转化、皮质纹状体谷氨酸能传递的过度活跃以及多巴胺释放轴上烟碱乙酰胆碱受体的过度刺激。不再推荐延迟开始使用左旋多巴,因为运动障碍的发展是疾病持续时间的函数,而不是累积左旋多巴暴露的函数。我们回顾了目前和正在开发的治疗峰值剂量运动障碍的方法,但建议单独改善左旋多巴的输送可能会降低其未来的患病率。《神经病学年鉴》2018 年;84:797-811。

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