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Botox Injections and Spasmodic Dysphonia Botox is a commercial preparation of a toxin from the bacterium Clostridium botulinum. Although this toxin can be responsible for severe cases of food poisoning, in the clinical setting botulism toxin (Botox) can bring great relief to patients suffering from the vocal disorder spasmodic dysphonia or SD.
SD is a vocal disorder that results from improper communication between nerve cells and muscle cells. There are two types of SD, named for the laryngeal (voice box) muscles that are affected: adductor SD and abductor SD. In adductor SD, the muscles of the larynx that are responsible for closing the vocal folds during speaking receive too much signal to contract and cause excessive closure of the folds. Patients with adductor SD have great difficulty speaking, and their speech patterns are characterized by uncontrolled voice and pitch breaks. Abductor SD is due to intermittent opening of the vocal folds because of over contraction of the abductor muscles that open the vocal folds resulting in a decrease in volume and a hoarse, breathy voice. Botox works by eliminating the signal from the nerve cells that tells the muscle to contract. Nerve cells communicate with skeletal muscle cells through chemical signals. The nerve cell releases a chemical called acetylcholine that diffuses across a narrow space between the nerve cell and the muscle cell . When the acetylcholine binds to the membrane of the muscle cell it signals the muscle cell fibers to contract. Botox is composed of two small protein molecules. One recognizes the nerve cell membrane helps the second enter the nerve cell. Once inside the cell, the toxin prevents membrane vesicles from releasing the chemical signal acetylcholine. Since no acetylcholine is released, there is no signal telling the muscle cell to contract. Eliminating the over contraction of the laryngeal muscles allows the vocal folds to relax in SD patients. A small quantity of Botox is injected directly into the affected muscle where it can diffuse to the nerve cell endings and stop the signals coming from the nerve. The effect of the toxin lasts from 3-4 months with varying results in each individual patient. The most effective treatments for SD involve both the Botox injections and behavior/speech therapy to maximize the action of the toxin. Botox
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