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Botulinum toxins are potent neurotoxins produced by the bacteria Clostridium botulinum. The most widely studied effect of botulinum toxins is at the neuromuscular junction where they block the release of acetylcholine preventing muscle contraction and causing local flaccid paralysis (rather than rigid, or tetanic, paralysis caused by a related clostridial protein, tetanus toxin). This results in a temporary (months) chemodenervation and the loss or reduction in activity in the target organ (muscle, sweat gland, or sphincter) with minimal risk of systemic adverse effects. However, botulinum toxins work not only at the neuromuscular junction but also alter the sensory input, producing secondary changes at the central level. The broadening clinical role of botulinum toxins depends on the multiple direct and indirect effects that the toxin exerts in both the peripheral nervous system and in the central nervous system (CNS).

In 1989, the FDA approved botulinum toxin type A (BTX-A) for use in treating strabismus, blepharospasm and hemifacial spasm. In 2000–2001, both BTX-A (Allergan, Inc.) and botulinum toxin type B (BTX-B; Elan Pharmaceuticals) were FDA-approved for use in treating cervical dystonia, and in 2002, BTX-A was approved by the FDA for treatment of glabellar frown lines. Besides the FDA-approved indications, botulinum toxins have been used in a vast array of clinical problems, including achalasia; anismus; benign prostatic hypertrophy; dysphonia; dystonias; essential tremor; hyperhidrosis; kyphoscoliosis; low back pain; migraine and tension-type headache; myofascial pain; pancreatitis; pelvic floor disorders; rectal fissures; sialorrhea; spasticity; temporomandibular joint syndrome; urinary sphincter dysfunction; wrinkles; and various other movement disorders.

Clostridium botulinum was first identified as a causative agent in food poisoning by Van Ermengem following a fatal outbreak in 1895.1 In the 1920s, additional outbreaks lead to the isolation of a relatively crude form of botulinum toxin (BTX),2 the neurotoxin responsible for food-borne botulism.

Early development of BTX began during WW II in the course of studying the nature of certain toxins, including BTX, and the means for protecting against them.3 Although much of this initial work was carried out on BTX-A, other types of botulinum toxin were also studied, including types B, C, D, and E. The purpose was to develop a polyvalent toxoid for immunization purposes. After the war, a crystallized form of BTX-A became available and stimulated considerable scientific interest. Dr. Alan B. Scott, of the Smith-Kettlewell Eye Research Foundation, initiated efforts to study BTX in a monkey model of strabismus in the late 1960s.4 Sufficient data was collected by 1978 to file an investigational new drug (IND) application for human clinical studies.5 The passage of the Orphan Drug Act of 1983 and FDA approval aided clinical development of BTX-A as an orphan drug in December 1989.

There are two types of commercial botulinum toxins presently available in the United States: Botox (Botulinum toxin type A Purified Neurotoxin Complex, Allergan, Inc., 2525 Dupont Drive, Irvine, CA) and BTX-B (Myobloc, Elan Pharmaceuticals, ...

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