Abstract

The aim of this study was to investigate changes in the tear film lipid layer thickness (LLT) and aqueous tear production after botulinum neurotoxin A (BoNT) injection in patients with benign essential blepharospasm (BEB) and hemifacial spasm (HFS). Eleven and six patients with BEB and HFS, respectively, who received BoNT injection were consecutively enrolled in this prospective study. The blepharospasm disability index (BSDI), blink pattern, dry eye symptoms, Schirmer test 1 findings, LLT, eyelid performance, and corneal integrity were evaluated before and after treatment. Both BEB and HSF patients experienced remarkable relief from spasms and ocular discomfort after BoNT injection. LLT, the partial blink rate, the snap-back time, the lid distraction distance, and lateral canthal laxity were significantly increased at 1 month after treatment. There were no significant changes in Schirmer test 1 findings and meibomian gland dropout. Our findings suggest that LLT, a decisive factor for tear film stability, significantly increases at 1 month after BoNT injection for BEB and HFS. A decrease in BSDI and an increase in the snap-back time may contribute to the increase in LLT; this mechanism is probably responsible for the relief from dryness after BoNT injection in patients with facial movement disorders.

Highlights

  • Benign essential blepharospasm (BEB) and hemifacial spasm (HFS) are associated with overactivity of the facial nerve and are the two most common facial movement disorders[1]

  • There were no significant differences in most parameters associated with meibomian gland function and eyelid functional performance between the BEB and HFS groups

  • We found that aqueous tear deficiency was common, both before and after botulinum neurotoxin A (BoNT) injection, in patients with facial movement disorders

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Summary

Introduction

Benign essential blepharospasm (BEB) and hemifacial spasm (HFS) are associated with overactivity of the facial nerve and are the two most common facial movement disorders[1]. BoNT is an exotoxin produced by the bacterium Clostridium botulinum (an anaerobic, gram-positive bacillus)[9] It blocks the release of acetylcholine at the neuromuscular junction of cholinergic nerves, causing temporary paralysis of the target muscles. Dry eye disease is the most common complication of BoNT injection for BEB and HFS, but the reported incidence greatly varies from 7.5% to 70%19–22,24. Functional changes in the meibomian glands and alterations in the tear film lipid layer thickness (LLT) after BoNT injection for BEB and HFS remain unclear.

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