在患有多发性硬化症的人群中,在疲劳的肌肉收缩期间,短延迟的 afferent 抑制减少
Emily J Brotherton1, Surendran Sabapathy2, Lisa M Dempsey1
1Neural Control of Movement Laboratory, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
The European journal of neuroscience
|January 18, 2024
概括
患有多发性硬化症 (MS) 的人在疲劳性收缩期间表现出短延迟关节抑制 (SAI) 的降低,这表明运动皮层调节受损. 这表明与疾病相关的中央整合变化,而不是疲劳本身,是MS中这些抑制途径差异的基础.
科学领域:
- 神经科学是一个神经科学.
- 发动机控制器的控制器
- 临床神经学 临床神经学
背景情况:
- 短延迟附带抑制 (SAI) 测量了体感皮层和运动皮层之间的抑制相互作用.
- 在多发性硬化症 (MS) 中,SAI通常会降低,但在运动引起的疲劳期间,SAI的调节情况尚不清楚.
- 了解这些机制对于了解MS肌肉激活至关重要.
研究的目的:
- 研究SAI如何调节MS患者和健康对照者疲劳收缩期间的运动唤起潜力 (MEP).
- 为了确定运动引起的疲劳是否对MS的SAI有不同的影响.
- 探索MS中疲劳度表和抑制措施之间的关系.
主要方法:
- 参与者包括14名复发性复发性多发性硬化症患者和10名健康对照.
- 通过将中枢神经刺激与跨磁性刺激 (TMS) 配对在吸收器pollicis brevis运动皮层上进行SAI评估.
- 在休息阶段使用疲劳收缩方案 (持续和间歇性低强度收缩) 来测量MEP和SAI.
主要成果:
- 实力,肌电图或MEP的响应之间没有发现显著差异.
- 与健康对照组相比,MS组在疲劳收缩方案期间显著减少了SAI (p < .001).
- 疲劳严重程度量表和修改疲劳影响量表的得分与MS组的抑制措施没有相关性.
结论:
- 患有多发性硬化症的人在疲劳性收缩期间表现出受损的SAI,这表明与疾病相关的中心整合发生了变化.
- 这些发现突出了运动期间运动皮质抑制的疾病特异性缺陷,独立于感知疲劳水平.
- 结果强调了考虑中枢神经系统变化的重要性,以了解MS中运动控制挑战.
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