Botulinum toxin A, a neurotoxic protein produced by Clostridium botulinum, is being utilized by clinicians to decrease muscle hyperactivity for a multitude of therapeutic and cosmetic symptoms ranging from cervical dystonia to glabellar rhytids. Its use accounted for more than 25% of nonsurgical aesthetic procedures in the United States in 2008.1 There are eight serotypes of the toxin, synthesized as a single-chain polypeptide protoxin and “nicked” by proteases to activate binding at nerve terminal receptors. Once bound to synaptic receptor SNAP-25, the toxin inhibits release of acetylcholine, thus causing muscle paralysis.