Abstract
Clinical and experimental results are reviewed concerning muscle weakness in patients with hemiparesis after a stroke. The discussion includes the important role that alterations in the physiology of motor units, notably changes in firing rates and muscle fiber atrophy, play in the manifestation of muscle weakness. This role is compared with the lesser role that spasticity (defined as hyperactive stretch reflexes) of the antagonist muscle group appears to play in determining the weakness of agonist muscles. The contribution of other factors that result in mechanical restraint of the agonist by the antagonist (e.g., passive mechanical properties and inappropriate cocontraction) is discussed relative to muscle weakness in patients with hemiparesis.
