Division of Physical Therapy, Department of Rehabilitation Medicine, 12239Emory University, Atlanta, GA, USA.
Atlanta VA Visual and Neurocognitive Center of Excellence, Decatur, GA, USA.
Neurorehabil Neural Repair. 2021 Dec;35(12):1065-1075. doi: 10.1177/15459683211046272. Epub 2021 Sep 27.
The inability to flexibly modulate motor behavior with changes in task demand or environmental context is a pervasive feature of motor impairment and dysfunctional mobility after stroke. The purpose of this study was to test the reactive and modulatory capacity of lower-limb primary motor cortical (M1) networks using electroencephalography (EEG) measures of cortical activity evoked by transcranial magnetic stimulation (TMS) and to evaluate their associations with clinical and biomechanical measures of walking function in chronic stroke. TMS assessments of motor cortex excitability were performed during rest and active ipsilateral plantarflexion in chronic stroke and age-matched controls. TMS-evoked motor cortical network interactions were quantified with simultaneous EEG as the post-TMS (0-300 ms) beta (15-30 Hz) coherence between electrodes overlying M1 bilaterally. We compared TMS-evoked coherence between groups during rest and active conditions and tested associations with poststroke motor impairment, paretic propulsive gait deficits, and the presence of paretic leg motor evoked potentials (MEPs). Stroke ( = 14, 66 ± 9 years, = 4) showed lower TMS-evoked cortical coherence and activity-dependent modulation compared to controls ( = 9, 68 ± 6 years, = 3). Blunted reactivity and atypical modulation of TMS-evoked coherence were associated with lower paretic ankle moments for propulsive force generation during walking and absent paretic MEPs. Impaired flexibility of motor cortical networks to react to TMS and modulate during motor activity is distinctly associated with paretic limb biomechanical walking impairment, and may provide useful insight into the neuromechanistic underpinnings of chronic post-stroke mobility deficits.
无法根据任务需求或环境变化灵活调节运动行为是运动障碍和卒中后运动功能障碍的普遍特征。本研究旨在使用经颅磁刺激（TMS）诱发的皮质活动的脑电图（EEG）测量来测试下肢初级运动皮质（M1）网络的反应性和调节能力，并评估其与慢性卒中行走功能的临床和生物力学测量的相关性。在慢性卒中患者和年龄匹配的对照组中，在休息和主动同侧跖屈期间进行 TMS 评估运动皮质兴奋性。使用同时的 EEG 量化 TMS 诱发的运动皮质网络相互作用，将电极置于双侧 M1 上，以记录 TMS 后（0-300ms）的β（15-30Hz）相干性。我们比较了两组在休息和主动状态下的 TMS 诱发相干性，并测试了其与卒中后运动障碍、瘫痪推进步态缺陷以及瘫痪肢体运动诱发电位（MEPs）的相关性。与对照组（n=9，68±6 岁，n=3）相比，卒中患者（n=14，66±9 岁，n=4）的 TMS 诱发皮质相干性和与运动相关的调制均较低。TMS 诱发相干性的反应性和调制减弱与步行时瘫痪踝关节力矩生成的推进力降低以及瘫痪 MEPs 缺失有关。运动皮质网络对 TMS 的反应性和运动过程中的调制灵活性受损与瘫痪肢体的生物力学步行障碍明显相关，可能为慢性卒中后运动功能障碍的神经机制提供有用的见解。
