Abstract
The incidence of facial nerve paralysis is approximately 30 per 100,000 persons annually. Although it is often idiopathic, as in Bell's palsy, it can also result from infections, trauma, or neoplasms. Facial nerve paralysis may present with partial or total facial paresis, lagophthalmos, denervation of the lacrimal gland, and other ocular abnormalities. While dry eye is a commonly expected outcome of facial nerve injury, some patients may paradoxically experience epiphora and hyperlacrimation. In this review, we examine this phenomenon and its mechanisms in facial nerve injury. Several mechanisms have been proposed for epiphora and hyperlacrimation, including aberrant axonal regeneration, which is known to cause crocodile tears syndrome; ocular irritation due to dry eye, resulting in increased reflex lacrimation due to disruption of the tear film; and impaired drainage of tears caused by paralysis of the orbicularis oculi muscle and malposition of the eyelids. Understanding the pathophysiology of these symptoms is crucial in guiding the management of patients with facial nerve injury. Further experimental and clinical studies focusing on the quantification of tear production and localization of nerve damage will help improve our understanding of the neuroanatomical correlates of this paradoxical manifestation.