Neurotrophic keratitis is an inflammatory and dystrophic corneal changes that develop against the background of an infectious or traumatic lesion of the trigeminal nerve. Neurotrophic keratitis is manifested by a decrease or absence of corneal sensitivity, neuralgic pain, opacity and corneal ulcer. In the diagnosis of neurotrophic keratitis, biomicroscopy of the eye, a fluorescein test, determination of corneal sensitivity, examination of smears from the conjunctiva by culture and PCR method, ELISA are used. Treatment keratitis is mainly local; installations of antiviral drugs, the laying of antibacterial ointments, subconjunctival injections, novocaine blockades, vitamins; diathermy on the cervical sympathetic ganglia are prescribed.
The group of neurotrophic keratitis in ophthalmology includes neuroparalytic and neurotrophic keratitis. The pathogenesis is associated with damage to the trigeminal nerve, which leads to a sharp decrease or loss of corneal sensitivity, slowing of regenerative processes and recurrent inflammation of the cornea. In the outcome of neurotrophic keratitis, there is a decrease in the transparency of the cornea of varying degrees of severity and a decrease in its optical properties.
The pathogenesis of neurotrophic keratitis is based on the defeat of the first branch of the trigeminal nerve – the ocular nerve innervating the eyeball. The lesion occurs more often in the area of the Gasser node (ganglion of the trigeminal nerve), less often in the sensitive nuclei of the brain stem.
The immediate causes may be infectious or traumatic factors. In particular, blocking the conduction of the optic nerve is often caused by adenoviruses, herpesviruses (herpes simplex, herpes zoster), etc. Traumatic damage to the first branch of the trigeminal nerve may be caused by the intersection of the optic nerve during surgery, injection into the ganglion area, extirpation of the Gasser node, the presence of nerve-squeezing tumors and foreign bodies.
With such lesions of the first branch of the trigeminal nerve, there is a decrease in the protective movements of the eyelids (blinking), a decrease in sensitivity, a violation of trophic and corneal hydration. In the cornea that has lost sensitivity, dystrophic processes and sluggish inflammation develop over time – neurotrophic keratitis.
Unlike keratitis of other etiology, the clinic of neurotrophic keratitis has its own characteristic features. The course of neurotrophic keratitis may be asymptomatic for a long time. Due to a sharp decrease or absence of corneal sensitivity, pathognomonic corneal syndrome does not develop: there is no lacrimation, photophobia, blepharospasm, subjective sensations of a foreign body in the eye, pericorneal injection of blood vessels. Of the neurological symptoms in neurotrophic keratitis, a pain syndrome typical of trigeminal neuralgia may be noted. With herpesvirus etiology, lesions on the skin of the eyelid, forehead and nose and along the I branch of the trigeminal nerve, herpetic vesicles may appear.
With neurotrophic keratitis, over time, the surface of the cornea becomes rough and clouded. Neurotrophic changes initially develop in the central zone of the cornea: there is swelling and swelling of the surface epithelium, its peeling with the formation of erosions and an extensive drain defect of a saucer-shaped shape. The edges and bottom of the resulting ulcer can remain clean for a long time. With timely treatment of neurotrophic keratitis, the ulcer heals, leaving behind a slight local opacity of the cornea.
In the case of the addition of coccoid flora, a cloudy plaque of grayish-white or yellowish color appears, followed by the formation of a purulent corneal ulcer. With an unfavorable course of neurotrophic keratitis, ulceration of the cornea can lead to its perforation and complete destruction.
Neurotrophic changes in the cornea can develop at various times after the defeat of the first branch of the trigeminal nerve – from several days to many months. Usually, the course of neurotrophic keratitis is long and sluggish; the disease lasts for years: at the same time, the ulcer can then heal, then reappear.
When diagnosing neurotrophic keratitis, an ophthalmologist takes into account the connection of the disease with adenovirus or herpesvirus infections, mechanical damage to the eye and other possible factors. The patient’s examination plan includes ophthalmological examinations, laboratory tests, consultations with a neurologist and an otolaryngologist.
Morphological changes of the cornea in neurotrophic keratitis are evaluated using biomicroscopy of the eye, endothelial and confocal microscopy of the cornea. A fluorescein instillation test is performed to determine erosions and ulcers of the corneal surface. The corneal reflex in neurotrophic keratitis is evaluated by estesiometry or a corneal sensitivity test.
To identify infectious factors of neurotrophic keratitis, cytological and bacteriological examination of a smear from the conjunctiva, blood ELISA, PCR examination of the scraping epithelium are resorted to.
If necessary, to exclude tumor compression of the trigeminal nerve, radiography of the orbit, radiography of the skull, radiography of the paranasal sinuses can be prescribed.
When neurotrophic keratitis is detected, therapy is carried out aimed at improving the trophism of the cornea, stimulating metabolic processes and early epithelization of defects. For this purpose, instillation of eye drops (solutions of methylethylpyridinol, taurine, vitamin A), laying in the conjunctival cavity of eye ointments and gels based on hemodialysate of calves’ blood or dexpanthenol, subconjunctival injections of methylethylpyridinol or pentahydroxyethyl naphthoquinone are prescribed locally. Antiviral drugs (acyclovir, interferons, potassium polyriboadenylate) are additionally included in the therapy of neurotrophic keratitis of viral etiology. Laser stimulation and magnetotherapy with keratoplastic drugs, electrophoresis with potassium iodide are shown to stimulate reparative processes.
Systemic treatment is carried out by oral and intramuscular administration of NSAIDs (indomethacin, diclofenac, etc.), B vitamins, ascorbic acid. From physiotherapy procedures, diathermy is indicated for the area of the cervical sympathetic ganglia. To relieve neuralgic pain, novocaine blockades are carried out up to the course of the superficial temporal artery.
Prevention of secondary infection of the cornea requires the appointment of antibacterial drops, subconjunctival or parabulbar administration of antimicrobial solutions.
To protect the cornea from drying out and infection, it is recommended to wear semi-hermetic glasses or a protective bandage. With the threat of corneal perforation, blepharography (eyelid stitching) is resorted to, leaving a gap at the inner corner of the eye for instillation of medications.
Prognosis and prevention
The course of neurotrophic keratitis is more often chronic, recurrent. The outcome is a clouding of the cornea of various sizes and intensity (from a light cloud to an eyesore), which reduces visual acuity to one degree or another.
Prevention dictates the need to increase the overall reactivity of the body, prevent the development of infectious diseases, exclude eye injuries.