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Botulinum neurotoxins (BTXs) inhibit the presynaptic release of acetylcoline causing a chemical denervation that results in sustained muscle weakness and have been used in the past 20 years to induce selective blocking of hyperactive striatal (and smooth) muscles.1 All the different seven serotypes of BTXs have in common the mechanism of action (block of the neuroexocytosis machinery inside the end plate, responsible for the release of acetylcholine into the neuromuscular junction), acting on different targets. The two commercially available serotypes, botulinum toxin type A and botulinum toxin type B (abbreviated BTX-A and BTX-B, respectively) are reported to act as zinc dependent endopeptidases on different intraneuronal target proteins.
The clinical value of BTX-A has been recognised for a long time and is widely demonstrated by hundreds of clinical reports. More recently a clinical usefulness of BTX-B has been investigated. Two controlled clinical trials have demonstrated that local intramuscular injections of BTX-B are effective in the treatment of cervical dystonia in patients with BTX-A responsive disease,2 as well as in patients with BTX-A resistant disease (secondary non-responders).3 BTX-B was found to be effective in both studies, with a significant improvement observed in all the parameters investigated (severity, disability, and pain); action was found to last as long as 16 weeks.2,3
Based on these favourable results, we investigated BTX-B treatment …