The Neural and Biomechanical Changes Underlying Weakness in the Paretic Upper Limb in Individuals with Chronic Hemiparetic Stroke

Garmirian, Lindsay

doi:https://doi.org/10.21985/n2-2k3s-br87

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The Neural and Biomechanical Changes Underlying Weakness in the Paretic Upper Limb in Individuals with Chronic Hemiparetic Stroke

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A stroke occurs when blood flow in the brain is impaired and often causes damage to corticospinal tract projections that control the muscles of the upper-extremity. Due to this damage, 50-70% of stroke survivors experience long-term upper-extremity functional deficits(Faria-Fortini, Michaelsen, Cassiano, & Teixeira-Salmela, 2011). These deficits result from motor impairments such as paresis (weakness), loss of independent joint control and muscle hypertonicity. For decades, we have known that the paretic upper extremity is weak post stroke, however, quantitative data is lacking to explain the underlying causes of this weakness. To address the current gap in knowledge, we quantified strength of the paretic and non-paretic upper-extremity, as well as differences in the ability to voluntarily activate muscle, muscle volume and antagonist co-activation of the wrist and elbow flexors and extensors. Voluntary activation was assessed using twitch interpolation, a measure that employs electrical stimulation to quantify the ability to fully activate a muscle. Muscle volume was quantified using magnetic resonance imaging, including the Dixon method to account for intramuscular fat. Antagonist co-activation was quantified using surface EMG. Strength, voluntary activation and muscle volume were all significantly reduced in the paretic upper extremity, while antagonist co-activation was increased. Deficits in strength were explained more by deficits in voluntary activation than muscle volume or antagonist co-contraction. Deficits in voluntary activation and hence strength, were greater distally compared to proximally but deficits in muscle volume and antagonist co-activation did not differ significantly across joints. We postulate that deficits in voluntary activation were greater distally compared to proximally because of losses in corticospinal projections which is the main system that controls the more distal muscles (Lawrence & Kuypers, 1968; Lemon, 2008) of the upper limb. The disparity between voluntary activation and muscle volume deficits distally (compared to proximally, larger deficits in voluntary activation but not volume), may be explained by involuntary activation (muscle hypertonicity) throughout the day and due to mass activation, especially of the flexors, during shoulder abduction due to a loss of independent joint control.

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