Abstract

Spasticity is one component of the upper motor neuron (UMN) syndrome resulting from a multitude of neurologic conditions, such as stroke, brain injury, spinal cord injury, multiple sclerosis, and cerebral palsy. It is clinically recognized as a phenomenon of velocity-dependent increase in resistance, i.e., hypertonia. Recent advances in the pathophysiology of spasticity improve our understanding of mechanisms underlying this complex phenomenon and its relations to other components of UMN syndrome (weakness and disordered motor control), as well as the resultant clinical problems. This theoretical framework provides a foundation to set up treatment goals and to guide goal-oriented clinical assessment and treatment. Among a spectrum of treatment options, botulinum toxin (BoNT) therapy is the preferred treatment for focal spasticity. The evidence is very robust that BoNT therapy effectively reduces spasticity; however, it does not improve voluntary movement. In this chapter, we highlight a few issues on how to achieve the best clinical outcomes of BoNT therapy, such as dosing, dilution, guidance techniques, adjunctive therapies, early treatment, repeated injections, and central effects, as well as the ways to improve motor function in selected subgroups of patients with spasticity. We also discuss the reasons of poor responses to BoNT therapy and when not to use BoNT therapy.

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