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.

Spastic muscles are weak muscles. It is known that muscle weakness is linked to poor motor performance. Botulinum neurotoxin (BoNT) injections are considered as the first-line treatment for focal spasticity. The purpose of this study was to quantitatively investigate the effects of BoNT injections on force control of spastic biceps brachii muscles in stroke survivors. Ten stroke survivors with spastic hemiplegia (51.7 ± 11.5 yrs; 5 men) who received 100 units of incobotulinumtoxinA or onabotulinumtoxinA to the biceps brachii muscles participated in this study. Spasticity assessment (Modified Ashworth Scale (MAS) and reflex torque) and muscle strength of elbow flexors, as well as motor performance assessment (force variability of submaximal elbow flexion) were performed within one week before (pre-injection) and 3~4 weeks (3-wk) after BoNT injections. As expected, BoNT injections reduced the MAS score and reflex torque, and elbow flexor strength on the spastic paretic side. However, motor performance remained within similar level before and after injections. There was no change in muscle strength or motor performance on the contralateral arm after BoNT injections. The results of this study provide evidence that BoNT injections can reduce spasticity and muscle strength, while motor performance of the weakened spastic muscle remains unchanged.

Spasticity is a common post-stroke syndrome that imposes significant adverse impacts on patients and caregivers. This study aims to improve the efficiency of botulinum toxin (BoNT) in managing spasticity, by utilizing a three-dimensional innervation zone imaging (3DIZI) technique based on high-density surface electromyography (HD-sEMG) recordings. Stroke subjects were randomly assigned to two groups: the control group ([Formula: see text]) which received standard ultrasound-guided injections, and the experimental group ([Formula: see text]) which received 3DIZI-guided injections. The amount of BoNT given was consistent for all subjects. The Modified Ashworth Scale (MAS), compound muscle action potential (CMAP) and muscle activation volume (MAV) from bilateral biceps brachii muscles were obtained at the baseline, 3 weeks, and 3 months after injection. Intra-group and inter-group comparisons of MAS, CMAP amplitude and MAV were performed. An overall improvement in MAS of spastic elbow flexors was observed during the 3-week visit ([Formula: see text]), yet no statistically significant difference found with intra-group or inter-group analysis. Compared to the baseline, a significant reduction of CMAP amplitude and MAV were observed in the spastic biceps muscles of both groups at 3-week post-injection, and returned to approximate baseline value at 12-week post injection. A significantly higher reduction was found in CMAP amplitude ([Formula: see text]% versus [Formula: see text]%, [Formula: see text]) and MAV ([Formula: see text]% versus [Formula: see text]%, [Formula: see text]) in the experimental group compared to the control group. The study has demonstrated preliminary evidence that precisely directing BoNT to the innervation zones (IZs) localized by 3DIZI leads to a significantly higher treatment efficiency improvement in spasticity management. Results have also shown the feasibility of developing a personalized BoNT injection technique for the optimization of clinical treatment for post-stroke spasticity using proposed 3DIZI technique.