A Review of the Paradoxical Manifestations from Facial Nerve Injury: Epiphora and Hyperlacrimation
Shreya Bhatt is currently a second year medical student at Nova Southeastern University (NSU) Dr. Kiran C. Patel College of Osteopathic Medicine. She graduated with a Bachelor of Science degree in Neurobiology from Penn State University and received her Masters in Biomedical Sciences from NSU in 2021. She is very interested in pursuing ophthalmology after medical school and thoroughly enjoys conducting research in this field as well as Neurobiology and research related to the head and neck. Outside of her courses and research, Shreya is the president of her medical school’s Ophthalmology Club, Random Acts of Kindness organization, and the Medical Students for Individuals with Possibilities organization. She also serves as a peer mentor for the underclassmen, served as a Teaching Assistant in Public Health for the undergraduate students, and enjoys volunteering at various service events, baking, cooking, and spending time with friends and family in her spare time.
Abstract
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Summary
The incidence of facial nerve paralysis is roughly 30 per 100,000 persons annually. Despite being frequently idiopathic in nature, as is commonly seen with Bell’s palsy, it may also be caused by infection, trauma, or neoplasm. It manifests with lagophthalmos, partial or total facial paresis, and dry eye due to denervation of the lacrimal gland alongside other ocular abnormalities. In this study, we examine the incidence and mechanisms of epiphora and hyperlacrimation in facial nerve injury by reviewing historical publications dating back to the 19th century as well as recent literature. Several mechanisms have been proposed, including aberrant axonal regeneration known to cause the syndrome of “crocodile tears”, ocular irritation due to dry eye with disruption of the tear film resulting in increased reflex lacrimation, and reduced drainage of tears as a result of paralysis of the orbicularis oculi muscle and malpositioning of the eyelids. The mechanisms of excess tearing in some types of facial nerve lesions, for example in patients with certain brainstem tumors, remain unknown. Understanding the pathophysiology of epiphora and hyperlacrimation is crucial in guiding management of patients presenting with these aforementioned signs of facial nerve injury. Further experimental and clinical studies focusing on the quantification of tear production and precise localization of facial nerve damage via modalities such as the Schirmer test and electromyography will help improve our understanding of these paradoxical manifestations from facial nerve dysfunction.