Botox

Botulinum toxin is a neurotoxin protein produced by the bacterium Clostridium botulinum. It is one of the most poisonous naturally occurring substances in the world, and it is the most toxic protein.^[1] Though it is highly toxic, it is used in minute doses both to treat painful muscle spasms, and as a cosmetic treatment in some parts of the world. It is sold commercially under the brand names Botox and Dysport for this purpose. The terms Botox and Dysport are trade names and are not used generically to describe the neurotoxins produced by the clostridia species.

Medical uses

Cosmetically desirable effects of Botox were quickly discovered thereafter when the frown lines between the eyebrows were observed to soften following treatment for eye muscle disorders, leading to clinical trials and subsequent FDA approval for cosmetic use in April 2002. As of 2006, Botox injection is the most common cosmetic operation in the United States.

Besides its cosmetic application, Botox is used in the treatment of

• migraine headaches

• cervical dystonia (a neuromuscular disorder involving the head and neck)^[2]

• blepharospasm (involuntary contraction of the eye muscles)^[3]

• severe primary axillary hyperhidrosis (excessive sweating)^[4]

• achalasia (failure of the lower esophageal sphincter to relax)

Other uses of botulinum toxin type A that are widely known but not specifically approved by FDA include treatment of:

• involuntary microexpression facial triggers (concealing a lie)^{[citation needed]}

• pediatric incontinence^[5], incontinence due to overactive bladder,^[6] and incontinence due to neurogenic bladder.^[7]

• anal fissure^[8]

• spastic disorders associated with injury or disease of the central nervous system including trauma, stroke, multiple sclerosis, Parkinson's disease, or cerebral palsy

• focal dystonias affecting the limbs, face, jaw, or vocal cords

• TMJ pain disorders

• diabetic neuropathy

• wound healing

• excessive salivation

In the Journal of Dermatologic Surgery, Eric Finzi claims to have treated clinically depressed patients with botox. On Good Morning America, he claimed that by taking away the ability to frown, he was somehow taking away the ability to feel depressed.^[9]

Treatment and prevention of chronic headache^[10] and chronic musculoskeletal pain^[11] are emerging uses for botulinum toxin type A. In addition, there is evidence that Botox may aid in weight loss by increasing the gastric emptying time.^[12]

Biochemical mechanism of toxicity

Target molecules of botulinum (BoNT) and tetanus (TeNT) toxins inside the axon terminal.[1]

The heavy chain of the toxin is particularly important for targeting the toxin to specific types of axon terminals. The toxin must get inside the axon terminals in order to cause paralysis. Following the attachment of the toxin heavy chain to proteins on the surface of axon terminals, the toxin can be taken into neurons by endocytosis. The light chain is able to leave endocytotic vesicles and reach the cytoplasm. The light chain of the toxin has protease activity. The type A toxin proteolytically degrades the SNAP-25 protein, a type of SNARE protein. The SNAP-25 protein is required for the release of neurotransmitters from the axon endings.^[18] Botulinum toxin specifically cleaves these SNAREs, and so prevents neuro-secretory vesicles from docking/fusing with the nerve synapse plasma membrane and releasing their neurotransmitters.

Though it affects the nervous system, common nerve agent treatments (namely the injection of atropine and 2-pam-chloride) will increase mortality by enhancing botulin toxin's mechanism of toxicity. Attacks involving botulinum toxin are distinguishable from those involving nerve agent in that NBC detection equipment (such as M-8 paper or the ICAM) will not indicate a "positive" when a sample of the agent is tested. Furthermore, botulism symptoms develop relatively slowly, over several days compared to nerve agent effects, which can be instantaneous.

Source :
en.wikipedia.org
www.botox.co.in/myths.htm