Du poison au remède

La toxine botulique est le plus puissant poison naturel connu. Il suffirait d'un gramme d'aérosol pour tuer au moins 1,5 million de personnes. Cette substance est fabriquée par une bactérie, le Clostridium botulinum, lorsqu'elle est infectée par un virus. En thérapie, la toxine botulique, utilisée bien évidemment à des doses infimes (de l'ordre de quelques nanogrammes), supprime pour plusieurs semaines la transmission de l'influx nerveux et produit un affaiblissement musculaire au lieu de l'injection.

Ce traitement s'est imposé ces dernières années pour traiter les dystonies focales. Répété en moyenne tous les trois mois, il améliore considérablement 90% environ des blépharo-spasmes, 70% des dystonies oro-mandibulaires, des spasmes hémifaciaux et des torticolis spasmodiques, et 50% des dystonies des extrémités. Les résultats sont moins bons dans la crampe des écrivains.

L' historique du BOTOX

From Toxin to Therapeutic Agent

Clostridium botulinum produces 7 distinct toxins, types A through G. Botulinum toxin type A is the most potent of the 7 serotypes produced by the anaerobic bacterium Clostridium botulinum. Minute quantities of botulinum toxin type A offer significant potential in treating a wide variety of disorders associated with muscle overactivity.

History of Botulinum Toxin Type A

Work with botulinum toxin type A as a therapeutic agent to treat human disease began in the late 1960s through the collaboration of Alan B. Scott, MD, of the Smith-Kettlewell Eye Research Foundation and Edward J. Schantz, PhD, director of food microbiology and toxicology at the University of Wisconsin. This is when botulinum toxin type A was first considered not as an agent of human sickness and disease but as a powerful therapeutic agent to treat symptoms of neurological disorders.

In 1989, the rights to a form of botulinum toxin type A, currently commercialized under the trade name BOTOX®, were acquired by Allergan, Inc. In December of that same year, BOTOX® was approved for use in strabismus and blepharospasm associated with dystonia in patients 12 years of age and above. Through the collaboration of Drs. Scott and Schantz, and the pioneering efforts of Allergan, BOTOX® was added to the armamentarium of drugs used to treat these conditions.

Mechanism of Action–Blockade of Neuromuscular Transmission in the Treatment of Blepharospasm and Strabismus

At a normal neuromuscular junction, a nerve impulse triggers the release of acetylcholine, which causes the muscle to contract. Hyperactive muscle contraction is characterized by excessive release of acetylcholine at the neuromuscular junction. The use of BOTOX® (Botulinum Toxin Type A) Purified Neruotoxin Complex can be effective in reducing the excessive activity by blocking the release of acetylcholine at the neuromuscular junction.

BOTOX® is injected directly into the muscles surrounding the eye. It exerts its effect on the peripheral nerve terminal at the neuromuscular junction by blocking the release of acetylcholine. Affected terminals are inhibited from stimulating muscle contraction, resulting in a reduction in muscle tone.

Clinical effects of BOTOX® are usually seen within 1 week of injection. The typical duration of symptomatic relief averages 12.5 weeks. Repeat injections of BOTOX® may be required to maintain the desired clinical effect.

Muscles treated with BOTOX® eventually recover as new nerve sprouts develop. A nerve sprout establishes a new neuromuscular junction, and neuromuscular transmission gradually returns over a period of several months.

The most frequently reported side effects with BOTOX® include drooping of the eyelids, superficial punctate keratitis, and eye dryness. Reduced blinking can lead to corneal exposure. Sedentary patients should be cautioned to resume activity slowly following BOTOX® injections.


The clinical use of BOTOX® represents one of the most dramatic role reversals in modern medicine: a potent biologic toxin transformed into a therapeutic agent.

BOTOX® offers potential as a powerful and versatile tool in the treatment of a wide variety of disorders characterized by muscle hyperactivity