Botulinum neurotoxins are produced by the gram-positive anaerobic bacteria Clostridium botulinum, of which several different serotypes have been identified 1,2 . Botulinum neurotoxin type A (BTA) is clinically used the most due to the longer duration of its effect 3,4 and is the focus of this article. One of the first to investigate BTA was Brooks, as he in 1953, showed that when injecting BTA in muscle tissue it inhibited the release of Acetylcholine (ACh) at the neuromuscular junction and rendered motor nerve filaments unexcitable 3 . It has since been shown that BTA inhibits synaptosomal nerve-associated protein 25 (SNAP-25), a protein involved in the release of ACh filled vesicles into the synaptic cleft through the assembly of the soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptors (SNARE) complex, which is necessary for docking and fusing neurotransmitter vesicles with neuronal membranes.