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对侧初级运动皮层在中风后上肢恢复中的作用:一项遵循PRISMA-ScR指南的范围综述

The role of the contralesional primary motor cortex in upper limb recovery after stroke: a scoping review following PRISMA-ScR guidelines.

作者信息

Suputtitada Peerapat, Costa Valton, Fregni Felipe

机构信息

School of Biomedical Sciences, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.

Laboratory of Neurosciences and Neurological Rehabilitation, Physical Therapy Department, Federal University of Sao Carlos, Sao Carlos, SP, Brazil.

出版信息

BMC Neurosci. 2025 May 25;26(1):31. doi: 10.1186/s12868-025-00950-y.

DOI:10.1186/s12868-025-00950-y
PMID:40414854
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12105408/
Abstract

BACKGROUND

Stroke often results in motor impairments, with recovery involving complex interactions between the lesioned (ipsilesional) and non-lesioned (contralesional) hemispheres. This scoping review investigates the role of the contralesional primary motor cortex (M1) in motor recovery of the paretic upper limb following stroke, examining its structural and functional changes and compensatory roles.

METHODS

A systematic search for scoping review was conducted in PubMed, Embase, Web of Science, and Google Scholar following PRISMA-ScR guidelines. Studies examining contralesional M1 contributions to upper limb recovery in humans and animal models were included. Data were extracted, synthesized qualitatively, and assessed for risk of bias using SYRCLE and Cochrane tools.

RESULTS

A total of 38 studies were included in the analysis, consisting of 34 focused on stroke patients and 4 utilizing animal models. The findings revealed the dual and task-specific role of the contralesional primary motor cortex (M1) in upper limb recovery after stroke. In patients with severe motor impairments, contralesional M1 supported recovery through compensatory mechanisms, such as increased neuronal recruitment and functional reorganization. However, in cases with mild impairments, its activation was associated with inhibitory effects on ipsilesional reorganization, potentially delaying optimal recovery. Animal studies provided evidence of structural and functional plasticity, including dendritic remodeling and enhanced neuronal connectivity, which paralleled improvements in motor function. In human studies, contralesional M1 activation was task-dependent, with pronounced engagement during demanding tasks and unimanual movements. Ipsilateral motor deficits, including reduced dexterity, strength, and coordination, were commonly reported and underscored the disrupted interhemispheric dynamics influencing recovery. Neuromodulation techniques showed promise in modulating interhemispheric interactions and enhancing motor outcomes. These results emphasize the complex interplay between compensatory and inhibitory processes mediated by contralesional M1 in stroke recovery.

CONCLUSION

The contralesional M1 plays a complex, task-specific role in upper limb recovery after stroke, acting as both a compensatory resource and a potential inhibitory factor. Future research should stratify patients by impairment severity to refine therapeutic approaches.

CLINICAL TRIAL NUMBER

Not applicable.

摘要

背景

中风常导致运动功能障碍,恢复过程涉及受损(患侧)半球和未受损(健侧)半球之间的复杂相互作用。本综述探讨健侧初级运动皮层(M1)在中风后上肢运动恢复中的作用,研究其结构和功能变化以及代偿作用。

方法

按照PRISMA-ScR指南,在PubMed、Embase、Web of Science和谷歌学术上进行系统检索以进行综述。纳入研究健侧M1对人类和动物模型上肢恢复作用的研究。提取数据,进行定性综合,并使用SYRCLE和Cochrane工具评估偏倚风险。

结果

分析共纳入38项研究,其中34项聚焦于中风患者,4项使用动物模型。研究结果揭示了健侧初级运动皮层(M1)在中风后上肢恢复中的双重且特定任务的作用。在严重运动功能障碍患者中,健侧M1通过代偿机制支持恢复,如增加神经元募集和功能重组。然而,在轻度功能障碍的情况下,其激活与对患侧重组的抑制作用相关,可能会延迟最佳恢复。动物研究提供了结构和功能可塑性的证据,包括树突重塑和增强的神经元连接,这与运动功能的改善平行。在人体研究中,健侧M1的激活取决于任务,在要求较高的任务和单手运动中表现出明显的参与。常见的同侧运动缺陷包括灵活性、力量和协调性下降,这突出了影响恢复的半球间动力学紊乱。神经调节技术在调节半球间相互作用和改善运动结果方面显示出前景。这些结果强调了健侧M1介导的中风恢复中代偿和抑制过程之间的复杂相互作用。

结论

健侧M1在中风后上肢恢复中发挥复杂的、特定任务的作用,既是一种代偿资源,也是一个潜在的抑制因素。未来的研究应根据损伤严重程度对患者进行分层,以完善治疗方法。

临床试验编号

不适用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af20/12105408/b39048e88a02/12868_2025_950_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af20/12105408/b39048e88a02/12868_2025_950_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af20/12105408/b39048e88a02/12868_2025_950_Fig1_HTML.jpg

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