Understanding motor impairment in the paretic lower limb after a stroke: a review of the literature

Abstract

In addition to muscle weakness caused by injury to supraspinal centers, several mechanisms may contribute to motor impairment in the paretic lower limb following a stroke. Physiological changes in the paretic muscles and their motor units, passive or active restraint of agonist activation, and abnormal muscle activation patterns have been shown to occur after a stroke and to reduce muscle force generation. Other factors such as increased passive tone may impede agonist and antagonist muscle torque generation, while abnormal motor activation and altered motor control of muscles can produce abnormal gait patterns. Co-activation of opposing lower limb muscles contributes to joint stiffness and postural stability; abnormal co-activation in paretic lower limbs can lead to deficits in postural stabilization. Abnormal timing of muscle activation can also yield reduced muscle work output and, in turn, reduced limb function. When sensory deficits accompany muscle weakness, impaired processing of afferent signals may contribute to abnormal muscle activation, abnormal gait patterns, and abnormal responses to perturbation during gait and stance. This article reviews the impact of these various factors, individually and in combination, on impaired motor function in the paretic lower limb after a stroke.