Abstract
Botulinum Neurotoxin A (BoNT-A) injections have been used for the treatment of muscle contractures and spasticity. This study assessed the influence of (BoNT-A) injections on passive biomechanical properties of the muscle-tendon unit. Mousegastrocnemius muscle (GC) was injected with BoNT-A (n = 18) or normal saline (n = 18) and passive, non-destructive, in vivo load relaxation experimentation was performed to examine how the muscle-tendon unit behaves after chemical denervation with BoNT-A. Injection of BoNT-A impaired passive muscle recovery (15% vs. 35% recovery to pre-stretching baseline, p < 0.05) and decreased GC stiffness (0.531 ± 0.061 N/mm vs. 0.780 ± 0.037 N/mm, p < 0.05) compared to saline controls. The successful use of BoNT-A injections as an adjunct to physical therapy may be in part attributed to the disruption of the stretch reflex; thereby modulating in vivo passive muscle properties. However, it is also possible that BoNT-A injection may alter the structure of skeletal muscle; thus modulating the in vivo passive biomechanical properties of the muscle-tendon unit.
Highlights
Spasticity is a debilitating and complex hyperkinetic syndrome characterized by excessive excitability of the stretch reflex and loss of neuronal control leading to muscle overactivity with the inability of the muscle to rest [1,2,3]
The Botulinum Neurotoxin A (BoNT-A) injected group produced an average of 0.079 N ± 0.03 N for single twitch force and an average of 0.302 N ± 0.108 N for tetanic contraction force
Sample time histories for muscle-tendon unit displacements to 1 mm (Figure 2A), 2 mm (Figure 2B), and 4 mm (Figure 2C) during Protocol 1 showed that the BoNT-A injected muscle-tendon unit generated less passive tension throughout the displacement protocol
Summary
Spasticity is a debilitating and complex hyperkinetic syndrome characterized by excessive excitability of the stretch reflex (myotatic reflex) and loss of neuronal control leading to muscle overactivity with the inability of the muscle to rest [1,2,3]. Lesions to upper motor neurons, regardless of etiology or mechanism, affect the ability of the central nervous system to synchronize motor unit recruitment and to relax skeletal muscle [2]. Activation of the peripheral stretch reflex alters resting posture of the affected limb and impairs passive function [2], which leads to structural muscle changes over time that increase muscle stiffness and contribute to the clinical symptoms of spasticity [10]. Stretching has been shown to influence skeletal muscle by altering active contractility, passive biomechanical properties, and neural excitability [11]. Previous studies have documented decreased stiffness [12,13,14], improved movement control [15], and fewer contractures [16]
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