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Clostridium botulinum is a bacteria that causes botulism. It produces seven distinct neurotoxins that are neuromuscular paralyzing agents. The toxins are called botulinum toxin type A,B,C1,D,E,F, and G. Each neurotoxin consists of a 2 chain polypeptide linked by a disulfide bond as demonstrated in this picture. The larger polypeptide, called the heavy chain, is identical for all 7 toxin types. The smaller polypeptide, called the light chain, varies for each toxin subtype.

At the junction between the muscle and the nerve is an area called a neuromuscular junction. The impulses from the nervous system travel down the nerve and cause a chemical messenger, acetylcholine, to be released from synaptic vesicles stored with the nerve endings.

Within the nerve ending itself, seen in the picture on the right, are a series of proteins that are necessary to allow the synaptic vesicles to bind with the nerve endings to allow release of the acetylcholine. These proteins include SNAP-25, VAMP, and syntaxin. Botulinum toxin type A and E cut SNAP-25. Botulinum toxin B,D, F, and G cut VAMP. Botulinum toxin C1 cut syntaxin and SNAP-25.
Botulinum Toxin A, commonly referred to as Botox®, is an artificially produced neuromuscular paralyzing agent that is now licensed by the FDA for blepharospasm and wrinkles. Botulinum Toxin B, commonly referred to as Myobloc® or Neurobloc®, is an artificially produced neuromuscular paralyzing agent that was more recently licensed by the FDA for cervical dystonia. When either botulinum toxin is injected into muscle the heavy chain binds to the nerve ending.

It is then internalized into the nerve terminal. In the nerve terminal botulinum toxin type A cuts the protein SNAP-25 and botulinum toxin type B cuts VAMP. The nerve terminal is no longer able to release acetylcholine.

When acetylcholine is no longer able to be released, the nerve impulses no longer make the muscles contract. Over time, the nerve creates new endings in a process called sprouting.

These new nerve terminals establish contact with the muscle (or sweat gland) and the effect of botulinum toxin wears off.

In the doses we commonly use, it is rare to get any systemic side effects. If one overinjects a muscle, then that muscle can be weakened more than desired. Of course, this is not permanent as the nerve regenerates the damaged protein and the neuromuscular junction begins working again. Botulinum toxin type B commonly causes dry mouth.

In the case of hyperhidrosis, a condition where one produces excessive amount of sweat, the botulinum toxin is used to target the nerves that come into contact with the sweat gland. The process of sprouting occurs and the nerve-gland junction regenerates.

In the case of neuropathic pain, the presumed mechanism of botox is to block the sensory nerve release of Substance P and CGRP.

Botox is commonly used to treat cervical dystonia, hemifacial spasm, blepharospasm, hyperhidrosis, and migraine.