Abstract
Botulinum neurotoxin is produced by the anaerobic bacterium Clostridium botulinum . It is the most poisonous biological substance known. Very small amounts of botulinum toxin can lead to botulism, a descending paralysis with prominent bulbar symptoms and often affecting the autonomic nervous system. Botulism can occur in two ways. It can result from infection with bacterial spores that produce and release the toxin in the body—as in enteric infectious botulism, when the bacteria grow in the intestine, and in wound botulism, when the wound becomes infected. Alternatively, botulism occurs after ingestion of the toxin (food borne botulism).1 Botulism has been recognised since the early 19th century, and there was speculation about what caused the condition. In 1822 it was suggested that a “fatty acid” in sausages was the culprit,2 and this led to the term botulism ( botulus being the Latin word for sausage). In 1897, Van Ermengen related botulism to a bacterial toxin.3 The discovery that botulinum toxin blocks neuromuscular transmission4 and thereby causes weakness laid the foundation for its development as a therapeutic tool. In 1981, the ophthalmologist Alan Scott pioneered treatment with botulinum toxin when he used it to treat strabismus.5 He paved the way for clinical research in many specialties. #### Summary points Botulinum toxin inhibits release of acetylcholine at the neuromuscular junction and in cholinergic sympathetic and parasympathetic neurones Local injections of toxin weaken overactive muscles and control hypersecretion of glands supplied by cholinergic neurones Botulinum toxin injections have an established role in some disorders of ocular motility Botulinum toxin is the treatment of choice for focal dystonias such as torticollis and writer's cramp and for hemifacial spasm and may complement the management of spasticity Local injections have also been shown to be beneficial in many other conditions including achalasia, chronic anal fissure, and …