Keratitis associated with palsy of the ophthalmic division of the trigeminal nerve.
Palsy of the ophthalmic division of the trigeminal nerve is lessfrequent that facial nerve palsy.
The trigeminal nerve is responsible for the cornea’s sensitivity toexogenous influences. A conduction disturbance in the trigeminal nerve is usually a sequela of damage to the trigeminal ganglion from trauma, radiation therapy of an acoustic neurinoma, or surgery. It will lead to loss of corneal sen-sitivity. As a result of this loss of sensitivity, the patient will not feel any sensa-tion of drying in the eye, and the blinking frequency drops below the level required to ensure that the cornea remains moist. As in exposure keratitis, superficial punctate lesions will form initially, followed by larger epithelial defects that can progress to a corneal ulcer if bacterial superinfection occurs.
Because patients with loss of trigeminal function are free of pain,they will experience only slight symptoms such as a foreign body sensation or an eyelid swelling.
Corneal damage, usually central or slightlybelow the center of the cornea, may range from superficial punctate keratitis (visible after application of fluorescein dye) to a deep corneal ulcer with per-foration. The eye will be red and in extreme cases may be leaking aqueous humor.
Corneal ulcer due to herpes virus infection.
This is essentiallyidentical to treatment of exposure keratitis. Itincludes moistening the cornea, antibiotic protection as prophylaxis against infection, and, if conservative methods are unsuccessful, tarsorrhaphy.
These changes are generally the result of a corneal trauma.