Abstract
The utility of botulinum neurotoxins as therapeutic and esthetic agents depends on their ability to inhibit neurotransmitter release from selected neurons, remain localized at the site of injection, and evade the body's immunologic defenses. The clinical correlates of these actions, respectively, are efficacy, safety, and a low rate of antibody formation. These properties have long formed the basis for the use of botulinum toxin type A (BTX-A) in the treatment of movement disorders such as focal dystonias, spasticity, and cerebral palsy 1 and, more recently, in the treatment of glabellar lines 2—all of which are characterized by excessive muscle activity.
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