Stroke is a leading cause of long-term disability. Approximately 610,000 people suffer a new stroke each year in the US,¹ often resulting in disability due to motor impairment and consequences of the upper motor neuron (UMN) syndrome. UMN syndrome results in both positive and negative motor effects. The positive features include muscle overactivity including spasticity, clonus, flexor/extensor spasm, and hyper-reflexia. Negative features consist of weakness, loss of dexterity, and decreased co-ordination.² The combination of these effects often leads to complications of contractures at the involved joints.

Spasticity is characterized by a velocity-dependent increase in resistance to muscle stretch associated with attempts to flex or extend a limb.³ It is a leading cause of morbidity and long-term post-stroke disability. Observational cohort studies have estimated that post-stroke spasticity (PSS) may affect 17–43% of the 6.5 million American stroke survivors.^4,5–9 These patients often present with characteristic antigravity postural patterns with shoulder adduction, elbow and wrist flexion, hip adduction, knee extension, ankle plantar flexion, and foot inversion. Symptoms vary in localization and severity and may include hypertonicity (increased muscle tone), clonus (a series of rapid muscle contractions), exaggerated deep tendon reflexes, muscle spasms, scissoring (involuntary crossing of the legs), and fixed joints. The degree of spasticity may vary from mild muscle stiffness to severe, painful, and uncontrollable muscle spasms.¹⁰ Spasticity may be associated with disabling pain, and over time may lead to permanent contractures that may eventually result in posture and joint deformities. Therefore, early intervention for spasticity may be critical for the preservation of muscle reactivity.¹¹

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