Passive Properties of the Wrist and Fingers Following Chronic Hemiparetic Stroke: Interlimb Comparisons in Persons With and Without a Clinical Treatment History That Includes Botulinum Neurotoxin.

Benjamin I Binder-Markey,Wendy M Murray,Julius P A Dewald

doi:10.3389/fneur.2021.687624

Abstract

Background: Neural impairments that follow hemiparetic stroke may negatively affect passive muscle properties, further limiting recovery. However, factors such as hypertonia, spasticity, and botulinum neurotoxin (BoNT), a common clinical intervention, confound our understanding of muscle properties in chronic stroke.Objective: To determine if muscle passive biomechanical properties are different following prolonged, stroke-induced, altered muscle activation and disuse.Methods: Torques about the metacarpophalangeal and wrist joints were measured in different joint postures in both limbs of participants with hemiparetic stroke. First, we evaluated 27 participants with no history of BoNT; hand impairments ranged from mild to severe. Subsequently, seven participants with a history of BoNT injections were evaluated. To mitigate muscle hypertonia, torques were quantified after an extensive stretching protocol and under conditions that encouraged participants to sleep. EMGs were monitored throughout data collection.Results: Among participants who never received BoNT, no significant differences in passive torques between limbs were observed. Among participants who previously received BoNT injections, passive flexion torques about their paretic wrist and finger joints were larger than their non-paretic limb (average interlimb differences = +42.0 ± 7.6SEM Ncm, +26.9 ± 3.9SEM Ncm, respectively), and the range of motion for passive finger extension was significantly smaller (average interlimb difference = −36.3° ± 4.5°SEM; degrees).Conclusion: Our results suggest that neural impairments that follow chronic, hemiparetic stroke do not lead to passive mechanical changes within the wrist and finger muscles. Rather, consistent with animal studies, the data points to potential adverse effects of BoNT on passive muscle properties post-stroke, which warrant further consideration.

Highlights

Following a hemiparetic stroke, induced damage to corticofugal motor pathways result in an increased reliance on indirect contralesional corticoreticulospinal (CRS) pathways [1,2,3,4,5]
After stroke, prolonged altered use and neural inputs to muscle do not substantially increase or negatively impact the passive torques about either the wrist or fingers, nor significantly limit passive extension at the fingers, unless an individual has received Botulinum neurotoxin (BoNT)
This suggests that clinically observed stiffness and loss of range of motion (ROM) is likely due to either neurally driven muscle hypertonia or long-lasting detrimental increases in muscle stiffness following BoNT injections

Summary

Introduction

Following a hemiparetic stroke, induced damage to corticofugal motor (i.e., corticospinal and corticobulbar) pathways result in an increased reliance on indirect contralesional corticoreticulospinal (CRS) pathways [1,2,3,4,5] This loss of corticofugal input have been shown to be linked to muscle weakness [6,7,8], whereas the increase reliance on CRS pathways is postulated to result in a loss of independent joint control, or abnormal limb synergies [9,10,11,12,13], and motor neuron hyperactivity [14] manifesting as hypertonia (increased muscle tone due to constant neural drive) and spasticity (hyperactive muscle stretch reflexes) [15,16,17,18,19]. Factors such as hypertonia, spasticity, and botulinum neurotoxin (BoNT), a common clinical intervention, confound our understanding of muscle properties in chronic stroke

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Results

Discussion

Conclusion