Preliminary Observations on the Diffusion of Botulinum Toxin from the Site of Injection in Laryngeal Muscles
Botulinum neurotoxin A is a very potent neurotoxin which causes a flaccid paralysis upon ingestion or injection. Although it has been a feared food poisoning for years, clinical uses in medicine have been developed and refined so that localized injection is now an accepted form of treatment of various neuromuscular disorders. The clinical use of botulinum toxin was pioneered by Scott1, who developed it as a treatment modality for strabismus and blepharospasm. It has been used in ophthalmology since about 1980. The implications for otolaryngology and neurology have also been noted and it has since been used for such disorders as hemifacial spasm, torticollis, and spasmodic dysphonia2,3,4,5,6,7. Despite the known systemic effects from ingestion of the toxin, very few systemic effects from local injection have been reported. Ingestion is known to cause symptoms which suggest CNS involvement (e.g. dizziness, lethargy, general locomotor dysfunction), however the toxin has not been shown unequivocally to cross the blood brain barrier8. Antibody production has been noted in patients who received the larger doses (200–300 Units) used in the treatment of torticollis3. In addition, a patient with parkinsonism was noted in one study3 to develop fatigue after two series of injections (81.7 total units). Those studies that have explored the systemic effects physiologically have involved single fiber EMG studies at sites distant from the injection9,10. These studies have shown increased “jitter” in distant muscles, but no clinically apparent effects. A recent study looking at spread of the toxin after intramuscular injection looked at whether or not the toxin crossed fascial planes11. The results showed that botulinum toxin passed through muscle fascia even at subclinical doses, with fascia reducing the spread of toxin by only 23%.
KeywordsPermeability Fatigue Iodine Electrophoresis Syringe
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