Pharmacology and Mechanism of Action
Botulinum toxin type A paralyzes muscles by blocking the release of acetylcholine at the neuromuscular junction. This agent has a number of uses, but it was originally developed for the treatment of strabismus. Within 24–48 hours of injection, botulinum toxin is bound and internalized within local motor nerve terminals, where it remains active for many weeks. Paralysis of the injected EOM begins within 2–4 days of injection and lasts clinically for at least 5–8 weeks. This produces, in effect, a pharmacologic recession: the EOM lengthens while it is paralyzed by botulinum toxin, and its antagonist contracts. These changes may produce long-term improvement in the alignment of the eyes. The recent introduction of bupivacaine injection into the antagonist muscle to provide a chemical resection effect may extend the durability of the correction and expand the range of deviations in which chemodenervation can be successfully used.
Debert I, Miller JM, Danh KK, Scott AB. Pharmacologic injection treatment of comitant strabismus. J AAPOS. 2016;20(2):106–111.
Scott AB. Botulinum toxin injection of eye muscles to correct strabismus. Trans Am Ophthalmol Soc. 1981;79:734–770.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.