Abstract
The phenomenon of exaggerated motor overflow is well documented in stroke survivors with spasticity. However, the mechanism underlying the abnormal motor overflow remains unclear. In this study, we aimed to investigate the possible mechanisms behind abnormal motor overflow and its possible relations with post-stroke spasticity. 11 stroke patients (63.6 ± 6.4 yrs; 4 women) and 11 healthy subjects (31.18 ± 6.18 yrs; 2 women) were recruited. All of them were asked to perform unilateral isometric elbow flexion at submaximal levels (10, 30, and 60% of maximum voluntary contraction). Electromyogram (EMG) was measured from the contracting biceps (iBiceps) muscle and resting contralateral biceps (cBiceps), ipsilateral flexor digitorum superficialis (iFDS), and contralateral FDS (cFDS) muscles. Motor overflow was quantified as the normalized EMG of the resting muscles. The severity of motor impairment was quantified through reflex torque (spasticity) and weakness. EMG-EMG coherence was calculated between the contracting muscle and each of the resting muscles. During elbow flexion on the impaired side, stroke subjects exhibited significant higher motor overflow to the iFDS muscle compared with healthy subjects (ipsilateral or intralimb motor overflow). Stroke subjects exhibited significantly higher motor overflow to the contralateral spastic muscles (cBiceps and cFDS) during elbow flexion on the non-impaired side (contralateral or interlimb motor overflow), compared with healthy subjects. Moreover, there was significantly high EMG-EMG coherence in the alpha band (6–12 Hz) between the contracting muscle and all other resting muscles during elbow flexion on the non-impaired side. Our results of diffuse ipsilateral and contralateral motor overflow with EMG-EMG coherence in the alpha band suggest subcortical origins of motor overflow. Furthermore, correlation between contralateral motor overflow to contralateral spastic elbow and finger flexors and their spasticity was consistently at moderate to high levels. A high correlation suggests that diffuse motor overflow to the impaired side and spasticity likely share a common pathophysiological process. Possible mechanisms are discussed.
Highlights
When a stroke survivor with spastic hemiplegia is asked to squeeze the hand or flex the elbow joint on the non-impaired side as shown in Figure 1, there is involuntary activation of spastic finger and elbow flexors on the impaired side (Figures 1A, B)
There was no significant difference in maximum voluntary contraction (MVC) values between the dominant and non-dominant sides of the healthy subjects for elbow flexion tasks (42.1 ± 10.7 N-m vs. 37.9 ± 6.9 N-m; p = 0.14)
We found that stroke subjects exhibited greater motor overflow to the impaired side in general, either from the proximal to distal muscle during elbow flexion on the impaired side or from the nonimpaired to impaired side during elbow flexion on the nonimpaired side
Summary
When a stroke survivor with spastic hemiplegia is asked to squeeze the hand or flex the elbow joint on the non-impaired side as shown in Figure 1, there is involuntary activation of spastic finger and elbow flexors on the impaired side (Figures 1A, B). When a stroke survivor with spastic hemiplegia is asked to squeeze the hand or flex the elbow joint on the non-impaired side as shown, there is involuntary activation of spastic finger and elbow flexors on the impaired side (Figures 1A, B). This phenomenon of involuntary activation of spastic muscles can occur in about 30% of hemiplegic stroke [1]. It is often referred as motor overflow or associated reaction [1,2,3,4,5,6,7,8]. Other types of muscle overactivity are seen clinically, such as spastic dystonia, co-contraction [9, 10]
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