Amongst stroke patients, more than a third will develop spasticity, especially those that involve the paretic upper limbs. Despite establish intensive rehabilitaion programs in place, spasticity still affect a post-stroke patient's quality of life and create significant economic and caregiver burdens. The rationale for botulinum toxin type A (BoNT-A) use in spasticity is hinged on the toxin's ability to reduce muscle overactivity via a dual cholinergic blockede of extrafusal and intrafusal muscle. Efficacy and safety of BoNT-A in established post-stroke spasticity have been widely published, effectively establishing robustness of data and first line recommendation. Consensus guidelines and algorithms on the clinical use of BoNT-A for symptomatic upper limb spasticity are now also available. While BoNT-A has been universally shown to reduce muscle tone in spasticity, optimizing therapy requires judicious use of the toxin, while raising one's consciousness of adverse event, including muscle weakness, unwanted or desired in therapy. BoNT-A should not be administered alone in post-stroke spasticity, and its effects are best optimized in concert with a comprehensive neurorehabilitation program.

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