Abstract
The objective of this study was to characterize the effects of intramuscular botulinum toxin (BT) injections on the electromechanical delay (EMD) in spastic human biceps muscles. The EMD is calculated as the time lag between the muscle activation onset, as recorded from the surface electromyogram (sEMG), and the onset of recorded force. In a cohort of chronic stroke survivors, we compared the computed EMD derived from the spastic (injected) biceps brachii with that from the contralateral muscle. Eight participants were tested before and up to 3 months after a BT injection. At each session, participants followed an isometric trapezoidal force trajectory at 50 and 30%, respectively, of the tested maximum voluntary contraction (MVC). Joint force and sEMG signals were recorded as well. The number of zero crossings (ZC) of the sEMG during the steady-state portion of the task was also computed. The EMD post-BT was found to increase by 64 ± 10% (at 50% MVC) and 93 ± 18% (at 30% MVC) when compared to pre-BT values, while the number of sEMG-ZC, the mean MVC values, and the force-EMD slope exhibited striking reductions. These parameters, calculated on the contralateral side, remained relatively constant across sessions, with the EMD significantly lower and the MVC values much higher. We discuss potential contributing factors to an increase in EMD values on the affected side, both pre- and post-BT. The observed co-variation across sessions of the increased EMD values with the decreased ZC estimates, a surrogate of motor outflow, and, potentially, more compliant muscle fascicles suggests that the altered motor unit (MU) behavior contributes, at least in part, to the delayed force production.
Highlights
The process of tension generation in the neurally activated muscle fiber begins at the neuromuscular junction, followed by a cascade of electromechanical events [1]
This study provides a quantitative characterization of changes in the electromechanical delay (EMD) and the number of zero-crossing in the surface electromyogram (sEMG) signal after the intramuscular botulinum toxin (BT) injections in stroke survivors, which allowed us to understand the effects of BT more clearly on voluntary contraction
The results suggest that the BT-induced reduction of spasticity results in a reduction in voluntary contraction capacity in association with the increased EMD value
Summary
The process of tension generation in the neurally activated muscle fiber begins at the neuromuscular junction, followed by a cascade of electromechanical events [1]. There is a finite lag after the neural activation of muscle fibers before there is detectable force generation by the muscle-tendon system [2, 3]. The electromechanical delay, which is partly a function of a muscle’s rate of force generation, depends on two major factors: (a) the number of recruited motor units, and (b) the electro-mechanical properties of the muscle-tendon unit (MTU). The latter is dominated by intrinsic stiffness of the muscle and tendon [2]. Intramuscular Botulinum toxin injections are increasingly used to treat focal spasticity, and are known to affect both neural and non-neural properties that are subsequent to injection in spastic muscles [11]
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