The toxicity of botulinum toxin has been known for centuries, and only in recent decades has it been known to be still beneficial. Records of botulism date back to medieval and Roman imperial manuscripts, but the first accurate and complete description of the clinical symptoms of foodborne botulism was published by the German physician Justinus Kerner in the early 1800s. The pathogenic bacterium, Clostridium botulinum, was first isolated in Belgium in 1895 by Emile Pierre van Ermengem from victims of food and food poisoning. This bacterium was responsible for the generalized muscle paralysis of the victims; these victims died of asphyxiation following chest muscle paralysis. In the United States, outbreaks of foodborne botulism were very rare in the early 1900s. The first attempt to purify botulinum toxin type A is generally believed to have been carried out in the 1920s by Herman Sommer at the Hooper Foundation of the University of California, San Francisco (DasGupta, 1994).Dr. Sommer precipitated botulinum toxin type A in a highly concentrated form from cultures of used neurotoxin microorganisms. This precipitate later provided the raw material for experiments on the toxin as a biological weapon, which were conducted under very strict security conditions at Fort Detrick near Frederick, Maryland, during World War II (Schantz, Johnson, 1994; Coffield et al, 1994). Edward J. Schantz, PhD conducted some of the early work with Clostridium botulinum at Fort Detrick. in 1946 the toxin was isolated as crystals of a high molecular weight protein of about 900 kilodaltons (KDa), which consisted of 150 KD toxin units bound to a nontoxic protein, and the nontoxic protein was considered important to stabilize the toxin units . Meanwhile, Schantz continued to focus on the production and purification of botulinum toxin type A (Schantz and Johnson, 1994; Coffield et al, 1994). In London in 1949, Burgen, Dichens and Zatman discovered that local injection of botulinum toxin type A blocked the release of acetylcholine at the neuromuscular junction (Naumann, 2003).Dr. Danniel Drachman later used botulinum toxin to study the neurotrophic effects of acetylcholine transmission on skeletal muscle, and he first found that local injections of botulinum toxin paralyzed the injected muscles (Naumann, 2003). Physiologist Dr. Vernon Brooks suggested to Dr. Schantz in the 1950s that the toxin might help reduce the activity level of overactive muscles. Inspired by this, when Alan Scott asked Dr. Schantz if he had a substance to correct strabismus, Dr. Schantz provided Scott with a sample of toxin type A. This collaboration continued until Dr. Schantz left Fort Detrick to transfer to the Department of Food Microbiology and Toxicology at the University of Wisconsin, where most of the early work in the preparation and characterization of botulinum toxin type A formulations for clinical use was done. After preclinical animal studies showed promise, Dr. Scott received FDA clearance to study botulinum toxin type A in humans for strabismus in the late 1970s. At that time, he started his own company, Oculinum, Inc. After more than 10 years of research, the FDA approved the product in 1989 for the treatment of strabismus and blepharospasm associated with myotonia in patients 12 years of age and older. One year prior to this (1988) Allergan acquired the rights to Oculinum and the product and initiated additional clinical studies for a large number of other indications. The product is currently sold under the trade name BOTOX? (botulinum toxin type A), and is approved for 25 different indications in 85 countries worldwide, with additional indications expected to be approved in the United States in the near future.