Authors: G Abbruzzese A Berardelli
Publish Date: 2009/03/07
Volume: 9, Issue: 2-3, Pages: 109-114
Abstract
Botulinum toxin type A BoNTA acts peripherally by inhibiting acetylcholine release from the presynaptic neuromuscular terminals thus weakening muscle contraction and its clinical benefit depends primarily on the toxin’ peripheral action In addition to acting directly at the neuromuscular junction the toxin alters sensory inputs to the central nervous system thus indirectly inducing secondary central changes Some of the longterm clinical benefits of BoNTA treatment may also reflect plastic changes in motor output after the reorganization of synaptic density
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