The Effects of Botulinum Toxin Injections on Spasticity and Motor Performance in Chronic Stroke with Spastic Hemiplegia

Chuan Zhang,Gerard E Francisco,Elaine Magat,Sheng Li,Yang Liu,Yen-Ting Chen,Ping Zhou,Monica Verduzco-Gutierrez,Yingchun Zhang

doi:10.3390/toxins12080492

Abstract

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.

Highlights

Spasticity and weakness are primary motor impairments and impose significant challenges for patient care
Spasticity is estimated to be present in about 20–40% of all stroke survivors [3], but in up to 97% of those with moderate to severe motor impairment [4]
Post-stroke spasticity is recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes

Summary

Introduction

Spasticity and weakness (i.e., spastic hemiparesis) are primary motor impairments and impose significant challenges for patient care. Toxins 2020, 12, 492 pathways and lack of central activation [1], weakness is the primary contributor of motor impairments and disabilities [2]. Post-stroke spasticity is recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (‘muscle tone’) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex [5]. Such phenomenon of increased resistance is commonly assessed by passive stretch in clinical practice using clinical scales, such as Modified Ashworth Scale (MAS) and Tardieu scale [6]. Quantification of resistance torques in response to motorized stretch in laboratory settings is often able to differentiate neural (i.e., stretch reflex) and non-neural components of hypertonia [8,9,10,11]

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