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Botulinum toxins (BTX) are potent neurotoxins produced by the bacterial spores of Clostridium botulinum. The major effect of BTX is at the neuromuscular junction, where they block the release of acetylcholine, preventing muscle contraction and causing dose-dependent weakness (rather than titanic weakness caused by tetanus toxin, a related clostridial protein). This blockade results in a temporary loss or reduction in activity in the target organ (muscle, sweat gland, and sphincter) with minimal risk of systemic adverse effects. However, BTX work not only work at the neuromuscular junction but also alter the sensory input, producing secondary changes at the central level. Clinical use of BTX depends on the multiple direct and indirect effects that the toxin exerts in the peripheral nervous system and the central nervous system (CNS).


C. botulinum was identified as a causative agent in food poisoning by Van Ermengem after a fatal outbreak in 1895.1 In the 1920s, additional outbreaks led to the isolation of a relatively crude form of BTX,2 the neurotoxin responsible for botulism.

Development of BTX began during World War II in the study of the nature of certain toxins, including BTX, and ways of protecting against them.3 Although much of the early work focused on BTX-A, also studied were BTX 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. 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 were 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.

In 1989, the U.S. Food and Drug Administration (FDA) approved BTX-A (Botox) for the treatment of strabismus, blepharospasm, and hemifacial spasm. In 2000-2001, both BTX-A and BTX-B (Myobloc) were FDA-approved for treatment of cervical dystonia, and in 2002, Botox was approved by the FDA for treatment of glabellar frown lines. In addition to the FDA-approved indications in the United States, BTX-A has been used for treatment of a number of painful conditions, including achalasia, anismus, benign prostatic hypertrophy, dysphonia, other dystonias, tremor, hyperhidrosis, kyphoscoliosis, low back pain, migraine and tension-type headache, myofascial pain syndrome (MPS), pancreatitis, pelvic floor pain, anal fissures, sialorrhea, spasticity, temporomandibular joint disorder, sphincter dysfunction, wrinkles, and other movement disorders.


There are several BTX preparations available in the US: Botox (BTX-A, Allergan, Inc.) and Myobloc. Botox is currently FDA-approved for the treatment of overactive bladder, detrusor overactivity associated with a neurologic condition (e.g., spinal cord injury [SCI], multiple ...

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