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Neuromodulation with Botulinum Toxin in Eyelid-Associated Ocular Surface Disease
Kaleb S Abbott1, Roshni J Echharam2, Laura M Periman3
1Department of Ophthalmology, University of Colorado School of Medicine; Kaleb.abbott@cuanschutz.edu.
None:
Ocular surface disease (OSD) encompasses a range of conditions that not only include the well-described dry eye disease (DED) components - such as hyperosmolarity, inflammation, ocular surface damage, and neurosensory compromise - but also eyelid-related disorders. These can stem from anatomical abnormalities or as consequences of DED, leading to various mechanical and inflammatory issues. These may include friction between the eyelids and the globe; irregular blink mechanics; and incomplete protection or even frank exposure of the ocular surface. Eyelid-associated ocular surface disease (EAOSD) includes conditions such as superior limbic keratoconjunctivitis, orbicularis oculi spasm (Jumping Orbicularis Sign), lid wiper epitheliopathy, and tight eyelid syndrome. Botulinum toxin, produced by the bacterium Clostridium botulinum, works by blocking the release of acetylcholine at the neuromuscular junction, leading to temporary muscle weakening. When mindfully injected into the orbicularis oculi, frontalis, or tarsal plate, botulinum toxin may reduce muscle tension around the eyelids, which improves eyelid tone and anatomic apposition between the eyelid and ocular surface tissues. Botulinum toxin can also be used to address abnormal blink patterns, incomplete blinking, nocturnal lid seal insufficiency, and lagophthalmos. Such interventions may alleviate symptoms associated with EAOSD. This paper examines the applications of botulinum toxin in the treatment of EAOSD. Other applications of botulinum toxin for addressing photophobia and excess trigeminal nerve tone are separately addressable topics.
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