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Short-latency afferent inhibition is reduced in people with multiple sclerosis during fatiguing muscle contractions
European Journal of Neroscience ( IF 3.4 ) Pub Date : 2024-01-17 , DOI: 10.1111/ejn.16253
Emily J. Brotherton 1 , Surendran Sabapathy 2 , Lisa M. Dempsey 1 , Justin J. Kavanagh 1
Affiliation  

Understanding how inhibitory pathways influence motor cortical activity during fatiguing contractions may provide valuable insight into mechanisms associated with multiple sclerosis (MS) muscle activation. Short-latency afferent inhibition (SAI) reflects inhibitory interactions between the somatosensory cortex and the motor cortex, and although SAI is typically reduced with MS, it is unknown how SAI is regulated during exercise-induced fatigue. The current study examined how SAI modulates motor evoked potentials (MEPs) during fatiguing contractions. Fourteen people with relapsing–remitting MS (39 ± 6 years, nine female) and 10 healthy individuals (36 ± 6 years, six female) participated. SAI was induced by stimulation of the median nerve that was paired with TMS over the motor representation of the abductor pollicis brevis. A contraction protocol was employed that depressed force generating capacity using a sustained 3-min 15% MVC, immediately followed by a low-intensity (15% MVC) intermittent contraction protocol so that MEP and SAI could be measured during the rest phases of each duty cycle. Similar force, electromyography and MEP responses were observed between groups. However, the MS group had significantly reduced SAI during the contraction protocol compared to the healthy control group (p < .001). Despite the MS group reporting greater scores on the Fatigue Severity Scale and Modified Fatigue Impact Scale, these scales did not correlate with inhibitory measures. As there were no between-group differences in SSEPs, MS-related SAI differences during the fatiguing contractions were most likely associated with disease-related changes in central integration.

中文翻译:

多发性硬化症患者在肌肉收缩疲劳期间,短潜伏期传入抑制减少

了解抑制通路如何影响疲劳收缩期间的运动皮层活动可能为了解与多发性硬化症 (MS) 肌肉激活相关的机制提供有价值的见解。短潜伏期传入抑制 (SAI) 反映了体感皮层和运动皮层之间的抑制性相互作用,尽管 SAI 通常会因 MS 而降低,但尚不清楚在运动引起的疲劳期间 SAI 是如何调节的。当前的研究探讨了 SAI 如何在疲劳收缩期间调节运动诱发电位 (MEP)。 14 名复发缓解型 MS 患者(39 ± 6 岁,9 名女性)和 10 名健康个体(36 ± 6 岁,6 名女性)参与了研究。 SAI 是通过刺激正中神经而诱发的,正中神经与拇短展肌的运动表现上的 TMS 配对。采用收缩方案,使用持续 3 分钟 15% MVC 抑制力产生能力,然后立即进行低强度 (15% MVC) 间歇性收缩方案,以便可以在每次任务的其余阶段测量 MEP 和 SAI循环。各组之间观察到相似的力、肌电图和 MEP 反应。然而,与健康对照组相比,MS 组在收缩方案期间的 SAI 显着降低 ( p  < .001)。尽管 MS 组报告的疲劳严重程度量表和改良疲劳影响量表得分更高,但这些量表与抑制措施并不相关。由于 SSEP 没有组间差异,因此疲劳收缩期间与 MS 相关的 SAI 差异很可能与疾病相关的中枢整合变化有关。
更新日期:2024-01-17
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