Background: Facial nerve palsy is a common cause of acute unilateral facial paralysis that impairs eyelid closure (lagophthalmos), placing the ocular surface at risk for exposure-related injury and vision loss. This review aims to summarize the mechanisms underlying ocular surface disease in facial nerve palsy and to evaluate current management strategies.
Methods: A structured literature search of PubMed and Google Scholar was conducted (February–April 2026) using keywords including facial nerve palsy, lagophthalmos, exposure keratopathy, and ocular surface disease. Studies were included if they described pathophysiologic mechanisms or clinical management of ocular surface complications. Articles lacking mechanistic or clinical relevance were excluded. Evidence was synthesized narratively.
Results: Facial nerve palsy contributes to ocular surface injury through lagophthalmos, reduced blink reflex, and tear film instability. Orbicularis oculi dysfunction impairs eyelid closure, while reduced corneal sensation diminishes reflexive blinking, increasing exposure. These changes promote epithelial breakdown, inflammation, and infection risk, potentially progressing to corneal ulceration and vision loss. Evidence, largely from observational studies, supports stepwise management with lubrication, eyelid taping, and surgical interventions in refractory cases.
Conclusions: Early recognition and intervention are critical to preventing ocular surface complications. This review integrates pathophysiology with management and highlights the need for higher-quality evidence to guide treatment selection.
Methods: A structured literature search of PubMed and Google Scholar was conducted (February–April 2026) using keywords including facial nerve palsy, lagophthalmos, exposure keratopathy, and ocular surface disease. Studies were included if they described pathophysiologic mechanisms or clinical management of ocular surface complications. Articles lacking mechanistic or clinical relevance were excluded. Evidence was synthesized narratively.
Results: Facial nerve palsy contributes to ocular surface injury through lagophthalmos, reduced blink reflex, and tear film instability. Orbicularis oculi dysfunction impairs eyelid closure, while reduced corneal sensation diminishes reflexive blinking, increasing exposure. These changes promote epithelial breakdown, inflammation, and infection risk, potentially progressing to corneal ulceration and vision loss. Evidence, largely from observational studies, supports stepwise management with lubrication, eyelid taping, and surgical interventions in refractory cases.
Conclusions: Early recognition and intervention are critical to preventing ocular surface complications. This review integrates pathophysiology with management and highlights the need for higher-quality evidence to guide treatment selection.