OBJECTIVE Spastic co-contraction is a motor-disabling form of muscle overactivity occurring after a stroke, contributing to a limitation in active movement and a certain level of motor impairment. The cortical mechanisms underlying spastic co-contraction remain to be more fully elucidated, the present study aimed to investigate the role of the cortical beta oscillations in spastic co-contraction after a stroke. METHOD We recruited fifteen post-stroke participants and nine healthy controls. The participants were asked to perform active elbow extensions. In the study, multimodal analysis was performed to combine the evaluation of three-dimensional elbow kinematics, the elbow muscles electromyographic activations, and the cortical oscillatory activity. RESULTS The movement-related beta desynchronization was significantly decreased in post-stroke participants compared to healthy participants. We found a significant correlation between the movement-related beta desynchronization and the elbow flexors activation during the active elbow extension in post-stroke participants. When compared to healthy participants, post-stroke participants exhibited significant alterations in the elbow kinematics and greater muscle activation levels. CONCLUSIONS Cortical beta oscillation alterations may reflect an important neural mechanism underlying spastic co-contraction after a stroke. SIGNIFICANCE Measuring the cortical oscillatory activity could be useful to further characterize neuromuscular plasticity induced by recovery or therapeutic interventions.

中文翻译：

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痉挛性联合收缩与中风后皮质β振荡的改变直接相关

目的 痉挛性共同收缩是中风后肌肉过度活动的一种运动功能障碍形式，导致主动运动受限和一定程度的运动障碍。痉挛性共收缩的皮层机制仍有待更充分地阐明，本研究旨在调查皮质β振荡在中风后痉挛性共收缩中的作用。方法 我们招募了 15 名中风后参与者和 9 名健康对照者。参与者被要求进行主动肘部伸展。在这项研究中，进行了多模态分析，以结合对三维肘关节运动学、肘部肌肉肌电图激活和皮质振荡活动的评估。结果 与健康参与者相比，中风后参与者的运动相关β去同步显着降低。我们发现中风后参与者在活动肘部伸展过程中，运动相关的 β 不同步与肘部屈肌激活之间存在显着相关性。与健康参与者相比，中风后参与者在肘部运动学和肌肉激活水平方面表现出显着改变。结论皮质β振荡改变可能反映了中风后痉挛性共同收缩的重要神经机制。意义 测量皮质振荡活动可能有助于进一步表征由恢复或治疗干预引起的神经肌肉可塑性。我们发现中风后参与者在活动肘部伸展过程中，运动相关的 β 不同步与肘部屈肌激活之间存在显着相关性。与健康参与者相比，中风后参与者在肘部运动学方面表现出显着改变，肌肉激活水平更高。结论皮质β振荡改变可能反映了中风后痉挛性共同收缩的重要神经机制。意义 测量皮质振荡活动可能有助于进一步表征由恢复或治疗干预引起的神经肌肉可塑性。我们发现中风后参与者在活动肘部伸展过程中，运动相关的 β 不同步与肘部屈肌激活之间存在显着相关性。与健康参与者相比，中风后参与者在肘部运动学和肌肉激活水平方面表现出显着改变。结论皮质β振荡改变可能反映了中风后痉挛性共同收缩的重要神经机制。意义 测量皮质振荡活动可能有助于进一步表征由恢复或治疗干预引起的神经肌肉可塑性。中风后参与者表现出肘部运动学的显着改变和更大的肌肉激活水平。结论皮质β振荡改变可能反映了中风后痉挛性共同收缩的重要神经机制。意义 测量皮质振荡活动可能有助于进一步表征由恢复或治疗干预引起的神经肌肉可塑性。中风后参与者表现出肘部运动学的显着改变和更大的肌肉激活水平。结论皮质β振荡改变可能反映了中风后痉挛性共同收缩的重要神经机制。意义 测量皮质振荡活动可能有助于进一步表征由恢复或治疗干预引起的神经肌肉可塑性。