In 1820, Justinus Kerner, a small-town German medical officer and romantic poet, gave the first complete description of clinical botulism based on extensive clinical observations of so-called “sausage poisoning”. Following experiments on animals and on himself, he concluded that the toxin acts by interrupting signal transmission in the somatic and autonomic motor systems, without affecting sensory signals or mental functions. He observed that the toxin develops under anaerobic conditions, and can be lethal in minute doses.His prescience in suggesting that the toxin might be used therapeutically to block both abnormal movements and hypersecretions earned him recognition as the intellectual founder of modern botulinum toxin therapy.
Seventy-five years later, Émile van Ermengem, professor of bacteriology and a student of Robert Koch, correctly described Clostridium botulinum as the bacterial source of the toxin. Thirty-four attendees at a funeral were poisoned by eating partially salted ham, an extract of which was found to cause botulism-like paralysis in laboratory animals. Van Ermengem isolated and grew the bacterium, and described its toxin,which was later purified by P Tessmer Snipe and Hermann Sommer.
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Ophthalmologists specializing in eye muscle disorders (strabismus) had developed the method of EMG-guided injection (using the electromyogram, the electrical signal from an activated muscle, to guide injection) of local anesthetics as a diagnostic technique for evaluating an individual muscle’s contribution to an eye movement.Because strabismus surgery frequently needed repeating, a search was undertaken for non-surgical, injection treatments using various anesthetics, alcohols, enzymes, enzyme blockers, and snake neurotoxins. Finally, inspired by Daniel Drachman’s work with chicks at Johns Hopkins,Alan B Scott and colleagues injected botulinum toxin into monkey extraocular muscles. The result was remarkable: a few picograms induced paralysis that was confined to the target muscle, long in duration, and without side-effects.
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In 1987, Alastair divided his Vancouver dermatology practice between surgery for skin cancer and cosmetic procedures. He shared his office with Jean, an eye doctor who treated pediatric disorders as well as adult conditions such as blepharospasm. An uncontrollable blinking and spasming of the eye and surrounding area, blepharospasm was treated with a dilute solution of botulinum toxin, which, injected into the skin, temporarily paralyzes the spasming muscles. One day, by Jean’s account, one of her blepharospasm patients became irate that her forehead was not being injected. “But your forehead isn’t spasming,” Jean responded, and asked why she cared. “Because when you inject my forehead,” the patient said, “my wrinkles go away.”
At dinner that night, Jean mentioned to Alastair the woman’s reaction. He and his dermatology patients had been frustrated in their attempts to erase vertical frown lines between the eyebrows, known to doctors as “glabellar lines.” The fillers available at the time didn’t last long and could be painful. The next day, Jean talked their receptionist, Cathy Bickerton, into being the first guinea pig for the cosmetic use of botulinum toxin. Once Alastair saw the results, he needed no persuasion. “I had the patients,” he says, summing up what would become one of the most successful symbioses in late-20th-century cosmetic medicine, “and Jean had the toxin.”