Abstract
Botulinum neurotoxin (BoNT) is commonly used to manage focal spasticity in stroke survivors. This study aimed to a perform comprehensive assessment of the effects of BoNT injection. Twelve stroke subjects with spastic hemiplegia (age: 52.0 ± 10.1 year; 5 females) received 100 units of BoNT to the spastic biceps brachii muscles. Clinical, biomechanical, electrophysiological, and neuro-motor assessments were performed one week (wk) before (pre-injection), 3 weeks (wks) after, and 3 months (mons) after BoNT injection. BoNT injection significantly reduced spasticity, muscle strength, reflex torque, and compound muscle action potential (CMAP) amplitude of spastic elbow flexors (all p < 0.05) during the 3-wks visit, and these values return to the pre-injection level during the 3-mons visit. Furthermore, the degree of reflex torque change was negatively correlated to the amount of non-reflex component of elbow flexor resistance torque. However, voluntary force control and non-reflex resistance torque remained unchanged throughout. Our results revealed parallel changes in clinical, neurophysiological and biomechanical assessment after BoNT injection; BoNT injection would be more effective if hypertonia was mainly mediated by underlying neural mechanisms. BoNT did not affect voluntary force control of spastic muscles.
Highlights
Spasticity and weakness are disabling motor impairments after stroke
In contrast to weakness that occurs at the stroke onset, spasticity emerges in the subacute stage
In a recent study [17], we reported that force variability of voluntary elbow flexion remained unchanged 3 wks after botulinum toxin (BoNT) injections to the biceps muscles
Summary
Spasticity and weakness are disabling motor impairments after stroke. In contrast to weakness that occurs at the stroke onset, spasticity emerges in the subacute stage. During sustained voluntary elbow flexion on the spastic-paretic side of stroke survivors, Rymer and colleagues have reported that spinal motor neurons are hyperexcitable and even spontaneously firing. The spasticity-related spontaneous motor neuron firing is not under voluntary control, and could be viewed as “motor noise” during voluntary activation. As such, they may make it difficult for stroke survivors to perform voluntary actions with spastic muscles, such as to initiate or terminate a hand grip [13,14] or maintain a constant force output [12,15,16,17]. Spasticity interferes with motor performance of spastic muscles [9]
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