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Impact of Botulinum Toxin on Ocular Surface Parameters in Patients with Orbicularis Spasm: A Systematic Review and
Davi Marçola Veiga1, Alexandre Yamada Fujimura Júnior1, Laura Goldfarb Cyrino2
1University of Marília Faculty of Medicine and Nursing, Marília, SP, Brazil.
Topic:
While botulinum toxin (BTX) is the primary treatment for facial dystonias and spasms, its effects on the ocular surface and corneal metrics are poorly defined and contradictory in current literature.
Clinical Significance:
This systematic review and meta-analysis provides standardized evidence to support interpretation of BTX-related ocular surface outcomes in patients with blepharospasm and hemifacial spasm.
Methods:
We searched PubMed, Embase, and Cochrane up to June 2025 using terms related to orbicularis spasm and ocular surface parameters. Eligible articles enrolled ≥7 patients with orbicularis spasm and reported pre and post-treatment outcomes. Primary endpoints included Schirmer I (ST1), tear break-up time (TBUT), ocular surface disease index (OSDI), Fluorescein Staining, and Astigmatism. A single-arm random-effects model in R was used to estimate mean differences.
Results:
Twenty-six studies (820 patients, 1,147 eyes) were included. OSDI scores significantly improved at 1-4 weeks (MD -11.77; 95% CI [-19.93, -0.28]; p < 0.001) and 3 months (MD -7.43; p < 0.0001). TBUT showed a significant increase at 3 months (MD 0.81; 95% CI [0.20, 1.43]; p < 0.01). ST1 and fluorescein staining remained stable across all intervals (p > 0.05), though meta-regression revealed that more injection sites correlated with higher ST1 at 1 month (R² = 80.3%; p < 0.001). Additionally, BTX was associated with a small but significant reduction in astigmatism (MD -0.14; p < 0.01).
Conclusion:
BTX improves ocular surface symptoms and tear film stability in orbicularis oculi spasm, with neutral effects on Schirmer tests and reduced astigmatism. However, since these effects are likely influenced by the the reduction of involuntary eyelid contractions, these findings should not be interpreted as evidence of a direct biological effect of BTX on ocular surface physiology. Future studies incorporating objective ocular surface and spasm assessments are needed to clarify the underlying mechanisms.
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