[Mechanism of therapy effects by botulinum neurotoxin].
Botulinum neurotoxin (BoNT) is produced by Clostridium botulinum as a complex of proteins containing the neurotoxin itself and other nontoxic proteins. Activation of the neurotoxin occurs upon proteolytic cleavage into the heavy and light chains. This di-chain moiety is essential for neurotoxin and each chain is playing a unique role; the heavy chain mediates neurospecifics cell binding and entry, whereas the light chain, a protease, catalyzes the cleavage and inactivation of neuronal proteins that mediate neurotransmitter release. There are seven BoNT serotypes (A,B,CI,D,E,F, and G), all of which inhibit acetylcholine release, though their intracellular target proteins, the characteristics of their actions, and their potencies vary substantially. BoNT type A has been the most widely studied and applied serotype for therapeutic purposes. It has been a mainstay in the treatment of cervical dystonia, blepharospasm, and hemifacial spasm for years. BoNT has more recently emerged as an increasingly important therapeutic option in the clinical management of a broad array of conditions, including other focal dystonias, spasticity, cerebral palsy, equinovarus, gastrointestinal (GI) and urogenital disorders, hypersecretory disorders, facial lines due to hyperfunctional facial muscles and recently, musculoskeletal pain disorders and headache.