One of the most lethal biological chemicals known as botulinum toxin is a neurotoxin created by the bacterium Clostridium botulinum. Eight exotoxins with distinct antigens are produced by C. botulinum (A, B, C1, C2, D, E, F and G). The main neurotransmitter at the neuromuscular junction, acetylcholine, is blocked by all serotypes, interfering with neuronal transmission and paralysing muscles. Botulinum toxin A injection-induced weakness often lasts for three months. Strabismus, focal dystonias, hemifacial spasm, various spastic movement disorders, headaches, hypersalivation, hyperhidrosis, and some chronic conditions that only partially respond to medical treatment are just a few of the many medical conditions that can now be managed with the help of Botulinum Toxin. The number of potential new symptoms is growing quickly. Cosmetological applications range from dermatological ones like hyperhidrosis to correcting lines, creases, and wrinkles all over the face, chin, neck, and chest. Botulinum toxin injections are often well tolerated and have few adverse effects. One of the most toxic biological molecules known as "wonder poison" is botulinum toxin. It is a neurotoxin created by the anaerobic, gram-positive rod-shaped bacterium Clostridium botulinum, which is typically found on plants, in soil, water, and animal intestinal tracts. Botulinum Toxin type A's efficiency in treating human strabismus was first demonstrated by Scott First. Botulinum toxin was subsequently authorised for the treatment of several spasticity problems as well as a variety of other ailments. It is currently utilised in practically all medical subspecialties. In order to temporarily reduce glabellar forehead frown lines for cosmetic reasons, the FDA approved the use of Botox® (Botulinum toxin-A) in 2002. Eight exotoxins with distinct antigens are produced by C. botulinum (A, B, C1, C2, D, E, F and G). The most powerful toxin is type A, followed by kinds B and F toxin. Botulism of types A, B, and E is frequently linked to systemic botulism in people. With a high degree of amino acid sequence homology amongst the toxin types, all botulinum neurotoxins are generated as relatively inactive, single polypeptide chains with a molecular mass of roughly 150 kDa. A disulfide bond connects the polypeptide chain's heavy (H) and light (L) chains, which are respectively 100 and 50 kDa in weight. Other benign proteins that may also have hemagglutinating activities are connected to the botulinum toxin neurotoxic complex. Botulinum toxin weakens striated muscles by preventing alpha motor neuron transmission at the neuromuscular junction. This has led to its use in diseases like dystonia that have overactive muscles. Additionally, muscle spindles' gamma neurones are hindered in transmission, which could change reflex overactivity. Additionally, the toxin prevents all parasympathetic and cholinergic postganglionic sympathetic neurons from releasing acetylcholine. This has sparked interest in using it to treat aberrant gland activity or overactive smooth muscles, such as in achalasia. The toxin takes between 24 to 72 hours to start working, which corresponds to how long it takes to stop the synaptosomal process. In extremely uncommon situations, some people could need up to five days to notice the full effect. The effects of botulinum toxin peak at about 10 days and extend for almost 8–12 weeks.
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