Many stroke survivors have residual sensorimotor deficits that impact negatively on balance and quality of life. The purpose of this review is to provide an overview of the impairments in motor control following stroke and the impact of those impairments on muscle activation patterns during postural control in stroke. Motor control impairments following stroke result in force production that is slow, weak and lacking in precision making it difficult to produce a fast rate of force development with sufficient magnitude to be effective for postural responses. Whether postural perturbations require feedback or feedforward responses, there is impairment to the timing, magnitude and sequencing of muscle activation following stroke. The impairment in muscle activation is dependent on the extent of the motor control impairments and strategies used by the individuals following stroke to compensate for the impairments. The central nervous system uses a variety of mechanisms to improve the muscle activation patterns needed for the recovery of postural responses following stroke.

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Purpose : To provide a comprehensive review of changes that occur in the muscle after stroke and how these changes influence the force-generating capacity of the muscle. Methods: A literature search of PubMed, CINAHL, MEDLINE, and Embase was conducted using the search terms stroke, hemiparesis, muscle structure, cross sectional area, atrophy, force, velocity, and torque. There were 27 articles included in this review. Results: Three changes occur in the muscle after stroke: a decrease in muscle mass, a decrease in fibre length, and a smaller pennation angle. In addition, the tendon is stretched and becomes more compliant. All of these factors reduce the affected muscle's ability to generate forces similar to controls or to non-paretic muscles. The result is a leftward shift in the length-tension curve, a downward shift in the torque-angle curve, and a downward shift in the force-velocity curve. Conclusion: Changes in muscle architecture contributing to weakness, such as muscle-fibre length, pennation angle, muscle atrophy, and tendon compliance, should be prevented or reversed by means of an appropriate rehabilitation programme.

The results of this efficacy study demonstrated that fast movement exercises improved postural responses to perturbations that were not practiced.

A single session of exercises emphasizing speed of movement can be used to improve muscle activation in persons with mild to moderately severe strokes.

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Background: Atherosclerosis of the carotid bifurcation with plaque formation causes asymptomatic carotid artery stenosis (ACAS), which may also be associated with cerebral hypoperfusion. Cerebral hypoperfusion adversely affects multiple aspects of mobility and