Neuroparalytic keratitis refers to a condition where the trigeminal nerve is damaged due to trauma, surgery, inflammation, or tumors, resulting in the loss of sensory innervation and reflex blinking of the cornea. This leads to sensory impairment and nutritional deficiency in the cornea, reducing its defense mechanisms against external harmful factors. As a result, the corneal epithelium becomes dry and prone to mechanical damage. Hereditary factors, such as congenital sensory nerve deficiencies and familial autonomic neuropathies, are also associated with this condition.
Clinical Manifestations
Despite severe inflammation of the cornea, patients may exhibit minimal or no subjective symptoms due to the loss of corneal sensation. In the early stages, the corneal epithelium in the exposed area within the palpebral fissure develops punctate epithelial erosions, which progressively enlarge into patchy epithelial defects. In severe cases, large epithelial-free areas may emerge, leading to ulcer formation. Secondary infections can result in the development of suppurative corneal ulcers, which are highly prone to perforation. Affected eyes may demonstrate reduced reflexive blinking, accompanied by hyperemia, vision loss, and increased ocular discharge.
Treatment
Treatment strategies include the use of preservative-free artificial tears to maintain ocular surface hydration. Antibiotic eye drops and ointments are used to prevent infection. Interventions such as amniotic membrane transplantation, application of soft contact lenses, or eye patching may facilitate the healing of epithelial defects. However, medical management often shows limited effectiveness. In such cases, tarsorrhaphy may be performed to protect the cornea. If suppurative corneal ulcers have developed, treatment follows the guidelines for corneal ulcer management. Additionally, the underlying primary condition responsible for trigeminal nerve damage should be actively addressed.