Neural and muscular determinants of dorsiflexor weakness in chronic stroke survivors

Few examined the contribution of neural and muscular deficits to weakness in the same stroke subject. We determined maximal voluntary contraction (MVC) and 50 Hz torques, activation (twitch interpolation), electromyographic (EMG) amplitude and antagonist coactivation, and muscle volume using magneti...

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Bibliographic Details
Published in:Motor control 2013-07, Vol.17 (3), p.283-297
Main Authors: Klein, Cliff S, Power, Geoffrey A, Brooks, Dina, Rice, Charles L
Format: Article
Language:English
Subjects:
Adult
Aged
Case-Control Studies
Chronic Disease
Electric Stimulation - methods
Electromyography - methods
Evoked Potentials, Motor - physiology
Female
Gait - physiology
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Muscle Contraction - physiology
Muscle Weakness - etiology
Muscle Weakness - physiopathology
Muscle, Skeletal - pathology
Muscle, Skeletal - physiopathology
Muscular Atrophy - physiopathology
NMR
Nuclear magnetic resonance
Stroke - complications
Stroke - physiopathology
Survivors
Torque
Walking - physiology
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Summary:Few examined the contribution of neural and muscular deficits to weakness in the same stroke subject. We determined maximal voluntary contraction (MVC) and 50 Hz torques, activation (twitch interpolation), electromyographic (EMG) amplitude and antagonist coactivation, and muscle volume using magnetic resonance imaging (MRI) of the dorsiflexors bilaterally in 7 chronic stroke subjects (40-67 y). Recordings of MVC and 50 Hz torque were also done in 7 control subjects (24-69 y) without stroke. The MVC torque was smaller in the contralesional than ipsilesilesional limb (29.8 ± 21.3 Nm vs. 42.5 ± 12.0 Nm, p = .04), and was associated with deficits in activation (r2 = .77) and EMG amplitude (r2 = .71). Antagonist coactivation percentage was not significantly different between limbs. Muscle volume, 50 Hz torque, and specific torque (50Hz torque/muscle volume) were also not different between sides. The concept that atrophy is commonplace after stroke is not supported by the results. Our findings indicate that dorsiflexor weakness in mobile stroke survivors is not explained by atrophy or reduced torque generating capacity suggesting an important role for central factors.
ISSN:1087-1640
1543-2696
DOI:10.1123/mcj.17.3.283