Previous neuroimaging studies on motor restoration after stroke using positron emission tomography (PET), functional magnetic resonance (fMRI) imaging, and transcranial magnetic stimulation (TMS) have identified that post-stroke patients exhibit a reduction in brain activities at the lesioned side and a propensity to recruit the contralesional motor cortex when conducting tasks involving the arms ( 9– 11). Although such post-stroke behavioral deviation can further exacerbate motor impairments, the interaction between the cortical plasticity in chronic stroke and the dynamic muscular coordination in the upper limb has not yet been well-investigated. However, Jones concluded that proximal compensations can be mistaken for recovery and constrain the potential motor restoration at the distal segments, leading to “learned non-use” or “learned dis-use” ( 8). In our previous study ( 6, 7), we found that the dyscoordination observed following chronic stroke was particularly evident during distal UE joint motion tasks, and that stroke patients frequently relied on compensatory contractions from proximal UE muscles to substitute for a loss or reduction in hand function. Specifically, patients' distal UE segments, e.g., fingers and wrist, usually exhibit poorer functional recovery than the proximal elbow and shoulder parts ( 5). Patients with chronic stroke (first onset over 6 months) regain the independence of the activities of daily living but always sustain upper extremity (UE) motor dysfunctions, e.g., muscle weakness, spasticity, and discoordination ( 4). Existing studies have found that the majority of motor recovery observed via cerebral plasticity reaches a plateau within the first 6 months after the onset ( 2, 3). Cerebral plasticity is the process by which the human body reorganizes neural networks and pathways after a stroke. Post-stroke motor recovery is usually associated with the cortical reorganization and adaptive learning experiences ( 1). EMG parameters showed higher EMG activation levels in TRI and BIC muscles ( P < 0.05), and higher CI values in the muscle pairs involving TRI and BIC during all the extension and flexion tasks in the stroke group than those in the control group ( P < 0.05).Ĭonclusion: The post-stroke proximal muscular compensations from the elbow to the finger movements were cortically originated, with the center mainly located in the contralesional hemisphere. No significant inter- or intra-group difference was observed in peak CMCoh during finger flexions. The stroke subjects showed significant differences in peak TRI and BIC CMCohs ( P < 0.01). The unimpaired controls exhibited significant intragroup differences between 20 and 40% levels in extensions for peak ED and FD CMCohs ( P < 0.05). Significant differences ( P < 0.05) were observed in both peak ED and FD CMCohs during finger extensions between the two groups. Result: The peak CMCoh with statistical significance ( P < 0.05) was found shifted from the ipsilesional side to the contralesional side in the proximal UE muscles, while to the central regions in the distal UE muscle in chronic strokes. EMG parameters, i.e., the EMG activation level and co-contraction index (CI), were analyzed to evaluate the compensatory muscular patterns in the upper limb. Electroencephalogram (EEG) data were recorded from the sensorimotor area and EMG signals were captured from extensor digitorum (ED), flexor digitorum (FD), triceps brachii (TRI), and biceps brachii (BIC) to investigate the CMCoh peak values in the Beta band. Method: Fourteen chronic stroke subjects and 10 age-matched unimpaired controls conducted isometric finger extensions and flexions at 20 and 40% of maximal voluntary contractions. In this study, corticomuscular coherence (CMCoh) and electromyography (EMG) analysis were adopted to investigate the corticomuscular coordinating pattern of proximal UE compensatory activities when conducting distal UE movements in chronic stroke. However, the cortical origin of this compensation has not been well-understood.
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