Abstract

BackgroundSpasticity is a key motor impairment that affects many hemispheric stroke survivors. Intramuscular botulinum toxin (BT) injections are used widely to clinically manage spasticity-related symptoms in stroke survivors by chemically denervating muscle fibers from their associated motor neurons. In this study, we sought to understand how BT affects muscle activation, motor unit composition and voluntary force generating capacity over a time period of 3 months. Our purpose was to characterize the time course of functional changes in voluntary muscle activity in stroke survivors who are undergoing BT therapy as part of their physician-prescribed clinical plan.MethodOur assessment of the effects of BT was based on the quantification of surface electromyogram (sEMG) recordings in the biceps brachii (BB), an upper arm muscle and of voluntary contraction force. We report here on voluntary force and sEMG responses during isometric elbow contractions across consecutive recording sessions, spread over 12 weeks in three segments, starting with a preliminary session performed just prior to the BT injection. At predetermined time points, we conducted additional clinical assessments and we also recorded from the contralateral limbs of our stroke cohort. Eight subjects were studied for approximately 86 experimental recording sessions on both stroke-affected and contralateral sides.ResultsWe recorded an initial reduction in force and sEMG in all subjects, followed by a trajectory with a progressive return to baseline over a maximum of 12 weeks, although the minimum sEMG and minimum force were not always recorded at the same time point. Three participants were able to complete only one to two segments. Slope values of the sEMG-force relations were also found to vary across the different time segments. While sEMG-force slopes provide assessments of force generation capacity of the BT injected muscle, amplitude histograms from novel sEMG recordings during the voluntary tasks provide additional insights about differential actions of BT on the overall motor unit (MU) population over time.ConclusionsThe results of our study indicate that there are potential short term as well as long term decrements in muscle control and activation properties after BT administration on the affected side of chronic stroke survivors. Muscle activation levels as recorded using sEMG, did not routinely return to baseline even at three months’ post injection. The concurrent clinical measures also did not follow the same time course, nor did they provide the same resolution as our experimental measures. It follows that even 12 weeks after intramuscular BT injections muscle recovery may not be complete, and may thereby contribute to pre-existing paresis.

Highlights

  • Spasticity is a key motor impairment that affects many hemispheric stroke survivors

  • We recorded an initial reduction in force and surface electromyogram (sEMG) in all subjects, followed by a trajectory with a progressive return to baseline over a maximum of 12 weeks, the minimum sEMG and minimum force were not always recorded at the same time point

  • It follows that even 12 weeks after intramuscular botulinum toxin (BT) injections muscle recovery may not be complete, and may thereby contribute to pre-existing paresis

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Summary

Introduction

Spasticity is a key motor impairment that affects many hemispheric stroke survivors. Intramuscular botulinum toxin (BT) injections are used widely to clinically manage spasticity-related symptoms in stroke survivors by chemically denervating muscle fibers from their associated motor neurons. Botulinum toxin is a metalloproteinase that induces cholinergic blockade at the presynaptic level of the neuromuscular junction This chemo-denervation reduces hypertonia as well as hyper-reflexia by reducing global motor outflow [5]. An initial reduction of voluntary muscle capacity is to be expected, quantification of the initial reduction, as well as quantification of the subsequent return to baseline values could provide insight regarding neuromuscular recovery (the time course, voluntary capacity level and neural control of muscle) subsequent to chemical denervation. This information could be used to assist in driving decisions about timing and dosage of repeated doses of BT as well as the need for other rehabilitative therapies due to the potential of further weakening paretic muscle. While BT is used to reduce spasticity, BT broadly targets motor outflow so more extensive impairment of motor function is possible

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