Graduate Program in Health and Rehabilitation Sciences, University of Western Ontario, London, ON N6G 1H1, Canada.
Exp Brain Res. 2011 Oct;214(2):303-15. doi: 10.1007/s00221-011-2826-5. Epub 2011 Aug 17.
Fatigue post-stroke is a disabling and persistent symptom affecting many stroke survivors. Despite its high prevalence, the pathophysiology underlying this phenomenon remains obscure. The aim of the present study was to investigate the origins of neuromuscular fatigue post-stroke. Ten chronic stroke survivors and 10 controls sustained an isometric contraction at 30% of maximal voluntary contraction (MVC) with the ankle dorsiflexors. Motor evoked potential (MEP), cortical silent period (SP), voluntary activation, M wave and contractile properties were evaluated before, during and after fatigue among the paretic, non-paretic and control limbs. The pattern of response to fatigue in the non-paretic and control limbs was comparable; therefore, results are presented between the paretic and non-paretic limbs. Before fatigue, reduced MVC peak torque and MEP amplitude were observed on the paretic side in comparison with the non-paretic side. During fatigue, the cortical SP duration increased significantly in both limbs, whereas the MEP amplitude significantly increased only in the non-paretic limb. After fatigue, MVC peak torque decreased significantly in both limbs. Significant reductions in M wave and twitch peak torque were observed in both limbs, pointing to the development of peripheral fatigue. However, central fatigue, evident by a significant reduction in voluntary activation, was greater in the paretic than in the non-paretic limb. After stroke, an inability to increase central excitability in response to an increased cortical inhibition associated with the fatiguing contraction may contribute to central fatigue observed in the paretic limb, which may also be linked to increased self-reported fatigue during activities of daily living. These findings advance our understanding of the neuromuscular basis of fatigue post-stroke.
脑卒中后疲劳是一种致残性且持续存在的症状，影响许多脑卒中幸存者。尽管其发病率很高，但这一现象的病理生理学基础仍不清楚。本研究旨在探讨脑卒中后神经肌肉疲劳的起源。10 名慢性脑卒中幸存者和 10 名对照者以 30%最大随意收缩（MVC）的踝关节背屈肌进行等长收缩。在疲劳前、疲劳期间和疲劳后评估运动诱发电位（MEP）、皮质静息期（SP）、自愿激活、M 波和收缩特性。非瘫痪侧和对照组的反应模式相似；因此，结果在瘫痪侧和非瘫痪侧之间呈现。在疲劳之前，与非瘫痪侧相比，瘫痪侧的 MVC 峰值扭矩和 MEP 幅度降低。在疲劳期间，双侧皮质 SP 持续时间显著增加，而 MEP 幅度仅在非瘫痪侧显著增加。疲劳后，双侧 MVC 峰值扭矩均显著降低。双侧 M 波和抽搐峰值扭矩均显著降低，表明出现了外周疲劳。然而，在瘫痪侧，由于与疲劳收缩相关的皮质抑制增加而导致的自愿激活显著降低，表明存在中枢疲劳，这也可能与日常生活活动中自我报告的疲劳增加有关。这些发现加深了我们对脑卒中后疲劳的神经肌肉基础的理解。
