卒中相关性肌萎缩发生机制与研究进展

王丽晶; 詹青

doi:10.12022/jnnr.2016-0045

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神经病学与神经康复学杂志 ›› 2016, Vol. 12 ›› Issue (2) : 102-105. DOI: 10.12022/jnnr.2016-0045

综述

卒中相关性肌萎缩发生机制与研究进展

王丽晶^{1, 2}, 詹青^{1, 2}

作者信息 +

Research progress in pathogenesis of stroke-related sarcopenia

WANG Lijing^{1, 2}, ZHAN Qing^{1, 2}

Author information +

文章历史 +

摘要

脑卒中后残障发生率较高。卒中后出现的肌萎缩严重影响着康复治疗方法的选择与疗效,一定程度上制约了患者的有效康复。目前有关卒中后肌萎缩的发生机制尚无统一结论。有学者提出卒中相关性肌萎缩的概念,但对于其发生机制尚不完全明确。目前认为,卒中相关性肌萎缩可能与发病后活动减少、摄入不足以及泛素蛋白酶体通路激活有关。本文通过结合近年来肌萎缩的相关研究,对卒中相关性肌萎缩发生机制进行综述,同时与其他疾病所致的肌萎缩进行鉴别,以期为卒中后肌萎缩的预防和治疗提供参考依据。

Abstract

Physical disability is common in stroke survivors. Sarcopenia after stroke has a strong impact on the decision and efficiency of rehabilitation and it may lead to the delayed recovery of patients. The pathogenesis of sarcopenia has not been investigated in details. “Stroke-related sarcopenia” was proposed in 2013 and several factors have been well known to contribute to sarcopenia, such as immobilization, impaired feeding and the activation of ubiquitin proteasome pathway. This paper reviews the recent studies on pathogenesis of stroke-related sarcopenia and distinguishes it from sarcopenia induced by other diseases, providing a basis for the prevention and therapy of sarcopenia after stroke.

导出引用

王丽晶, 詹青. 卒中相关性肌萎缩发生机制与研究进展[J]. 神经病学与神经康复学杂志. 2016, 12(2): 102-105 https://doi.org/10.12022/jnnr.2016-0045

WANG Lijing, ZHAN Qing. Research progress in pathogenesis of stroke-related sarcopenia[J]. Journal of Neurology and Neurorehabilitation. 2016, 12(2): 102-105 https://doi.org/10.12022/jnnr.2016-0045

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