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 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.

Neural and Muscular Determinants of Dorsiflexor Weakness in Chronic Stroke Survivors Journal Articles