Botulinum Toxin Treatment for Filamentary Keratitis Associated with Corneal Occlusion by Lids

Abstract

Botulinum toxin injections were performed to evaluate its effectiveness in treating filamentary keratitis caused by corneal occlusion by lids in 15 consecutive patients including 13 with essential blepharospasm, one with Meige syndrome and one with paralytic esotropia. After 5.7 ± 1.6 days following the injection, all patients showed subjective improvements with total resolution of corneal occlusion and filaments. Before injections, TBUT was 4.8 ± 3.2 sec and Schirmer I test without anesthetics was 3.9 ± 2.9 mm, both of which were significantly increased to 8.6 ± 3.1 sec and 7.7 ± 3.8 mm, respectively, after injections. A fluorescein clearance test was performed to prove that the increase of tear secretion after injections was caused by further slowing of the preexistent delayed tear clearance after injections. Impression cytology revealed that filaments were composed of a central core surrounded by PAS-positive amorphous materials and small epithelial cells, and the base of the filament was attached to metaplastic superficial epithelial cells. Therefore, it was speculated that excessive lid blinking might have aggravated aqueous tear deficiency, a condition frequently associated with essential blepharospasm, by facilitating tear clearance. Furthermore, filamentary keratitis, a condition associated with diverse diseases, might result from a common vicious cycle established by mechanical trauma from uncontrolled or excessive blinking and corneal occlusion by lids onto the surface epithelial cells with squamous metaplasia. The arrest and breakdown of such a cycle by the botulinum toxin might explain its efficacy in treating filamentary keratitis.