Botulinum toxin type A is an exotoxin produced by Clostridium botulinum. By permanently binding to the neuromuscular junction, the substance paralyses neuromuscular transmission through cleavage of the SNAP-25 protein (synaptosomal-associated protein). This protein is essential for the release of acetylcholine from presynaptic nerve terminals. Following intramuscular administration (by injection), the toxin rapidly binds to specific high-affinity cell surface receptors. The toxin is subsequently transported across the cell membrane via receptor-mediated endocytosis. In the final stage, the toxin is released into the intracellular fluid. This process is accompanied by inhibition of acetylcholine release from synaptic vesicles.
Following injection into muscles, maximal paralysis occurs after 2 weeks and persists for 2–4 months.
It is believed that at therapeutic doses of botulinum toxin type A, systemic distribution is minimal — standard pharmacokinetic studies have not been conducted.
Botulinum toxin type A is presumably metabolised by proteases, and its molecular components are incorporated into normal metabolic pathways.
⚠️ Warnings
Botulinum toxin type A should be used with caution in patients with subclinical or symptomatic neuromuscular transmission disorders, as there is a risk of excessive muscle weakness. Anaphylactic reactions may occur following the use of botulinum toxin type A. There have been rare reports of death due to aspiration pneumonia, dysphagia, and other complications following administration of botulinum toxin type A. Excessively frequent administration or use of excessive doses of botulinum toxin may lead to treatment resistance (due to the production of neutralising antibodies by the body). Patients should gradually increase their activity following treatment. Caution should be exercised in cases of significant weakness, muscle atrophy, or inflammation at the injection site. Botulinum toxin type A should be used with caution in patients with peripheral motor neuropathies. Application of the substance to the orbicularis oculi muscle may reduce the frequency of blinking. Caution is advised in patients at risk of angle-closure glaucoma, due to the anticholinergic effect of the substance. Investigation into the underlying cause of axillary hyperhidrosis is recommended in order to detect possible primary disease (hyperthyroidism, phaeochromocytoma).
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