neurogenic keratitis
Introduction
Introduction to neurogenic keratitis Neurotrophic keratitis is a degenerative disease of corneal epithelial healing disorder characterized by loss of corneal sensation leading to dissolution and perforation of the corneal stroma. There are many reasons for the loss of corneal sensation, which may be affected from the trigeminal nucleus to the corneal nerve endings. Among them, herpes virus infection and damage to the trigeminal ocular branch are the most common causes. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: keratitis
Cause
Cause of neurogenic keratitis
(1) Causes of the disease
Normal corneal innervation is essential for maintaining the integrity of the corneal epithelial layer. The metabolism and mitotic rate of corneal epithelial cells depend to some extent on the normal dominance of the trigeminal nerve. The sensory innervation of the cornea, conjunctiva and ocular appendages comes from In the Vth pair of cranial nerves - trigeminal nerve, trigeminal nerve from the half-moon ganglion, trigeminal nerve is divided into ocular branch, maxillary branch and mandibular branch, the trigeminal nerve branch is subdivided into three branches, namely lacrimal gland nerve, frontal nerve And nasal ciliary nerve, through the supraorbital fissure into the orbit, the lacrimal gland innervates the lacrimal gland, the frontal nerve dominates the upper conjunctiva through the supraorbital nerve and the upper trunk of the trochlear, the upper eyelid and forehead, the nasal ciliary nerve enters the total ankle ring, its 1 Branches - the ciliary long nerves are distributed as sensory nerves in the ciliary body, the iris and the cornea. This sensory nerve distribution acts as the afferent branch of the two reflex arcs, respectively, to manipulate the reflex secretion of tears (via the VII pair of brains) The parasympathetic branch of the nerve) and the blinking and closure of the eyelid (after the movement of the VII pair of cranial nerves), this coordinated reflex arc constitutes the entire ocular surface defense Neuroanatomical basis of integrity.
Lesions of the trigeminal ocular branch can cause abnormal or disruption of afferent nerves in the corneal sensation, which is characterized by loss of corneal sensation or disappearance, obstruction of corneal epithelial remodeling, and a series of corneal lesions, collectively referred to as neurogenic keratitis.
Neurogenic keratitis can be caused by a variety of reasons. Common causes are:
Local lesions of the cornea (45%):
Such as herpes zoster infection, herpes simplex virus infection, chemical burn of the cornea, etc., the herpes infection of herpes zoster virus is most likely to cause corneal sensation loss or loss, at least 25% of patients have a permanent corneal sensation Lost.
Trigeminal nerve palsy (25%):
Trigeminal nerve palsy, such as tumors (acoustic neuroma, aneurysm, meningeal disease, neurofibromatosis), intracranial surgery, head trauma, congenital diseases (such as familial autonomic dysfunction, family) Sexual corneal sensation, etc.).
Iatrogenic factors, systemic diseases (25%):
Such as long-term local application of anti-glaucoma (timolol, betaxolol), sulfa drugs, sodium diclofenac, etc., long-term wear contact lenses. Systemic diseases such as diabetes, vitamin A deficiency, leprosy, carbon disulfide poisoning, hydrogen sulfide poisoning, etc.
The above-mentioned various causes can cause neurogenic keratitis. The exact pathophysiological mechanism is still unclear, but the results are no more than two aspects. One is to cause dryness of the ocular surface, and the other is neurotrophic loss.
(two) pathogenesis
Studies have shown that the amount of tear secretion in patients with neurogenic keratitis is significantly reduced. When the topical anesthetic is used to make the ocular surface anesthesia, the amount of tear secretion can be reduced by 60% to 75%. After corneal denervation, accompanied by tear secretion. Decreased, the osmotic pressure of tears increased significantly, the goblet cell density of the conjunctiva decreased, the length of microvilli increased, the glycogen of corneal epithelial cells decreased, the permeability of corneal epithelial cells increased, and the content of mucin in tears changed. The morphological changes of corneal epithelial cells are similar to keratoconjunctivitis, the microvilli of epithelial cells in the epithelial cells, and the chemical changes of the mucus in the tears, which impair the adhesion of the tear film and the residual epithelial cells in the epithelial cells. When bilateral corneal sensation is absent, the blink frequency is significantly reduced, and the corneal surface is keratinized. The pathological changes of the cornea and conjunctival epithelium are not proportional to the extent of the lesion.
Normal innervation is very important for the metabolism of the corneal epithelium. Wright's experiments show that after corneal denervation, the mitosis of corneal epithelial cells is reduced by 20%, the mechanism is due to the regulation of epithelial cell proliferation, acetylcholine The level of intracellular cells is decreased, and at the same time, due to sensory denervation, the neuropeptide substance P in the cornea which stimulates the growth of corneal epithelial cells is also reduced.
The function of the trigeminal nerve plays an important role in maintaining the attachment of the corneal epithelial basement membrane to the anterior elastic layer. Experiments have shown that the trigeminal nerve can affect the synthesis of type VII gelatin of the corneal epithelial cells, and the adhesion of the epithelial basement membrane to the anterior elastic layer depends on Anchor-like fibrous structure, which is composed of type VII gel.
Herpes zoster eye infections often have scars on the eyelids, which can cause eyelash loss, trichiasis, varus or valgus valgus, eye contracture, loss of limbal tissue or destruction of the meibomian glands. These complications can cause Abnormal tear film and lesions of the corneal epithelium.
It can be considered that corneal lesions caused by loss of corneal sensation are caused by various mechanisms.
Prevention
Neurogenic keratitis prevention
Should pay attention to the history of topical medication, history of corneal surgery, history of head trauma and head and face surgery, history of diabetes, herpes virus infection, etc., should be used with caution when using the eye, corneal surgery should have strict surgical procedures, postoperative care should pay special attention In the life to avoid head trauma, diabetes, herpes should seek medical advice in time to prevent further deterioration of the condition.
Complication
Neurogenic keratitis complications Complications keratitis
Corneal perforation, aseptic anterior chamber empyema, atrophy of the eyeball, etc.
Corneal perforation is more common in corneal trauma. Perforation of sharp instruments, foreign objects in the ball, etc. can cause corneal perforation injuries. The postoperative effect depends on the cause and degree of injury. If it is caused by foreign matter in the ball, the corneal perforation injury will cause traumatic cataract after healing.
Anterior chamber empyema is characterized by acute onset of acute eye irritation, grayish yellow or yellowish infiltration of the cornea or ulceration. Early anterior chamber, iritis reaction develops in severe stage, yellowish white suppurative ulcer is often one Lateral expansion of the anterior chamber of the anterior chamber may have abscess formation in the base of the empyema. The main symptoms may be foreign body tingling or even burning. The conjunctiva is mixed with severe congestion. The edema ulcer first appears in the damaged cornea after trauma. The initial gray-white or yellow-white dense infiltration point is usually around the gray-colored edema area around the size of the rice or mung bean.
Symptom
Neurogenic keratitis symptoms Common symptoms Conjunctival hyperemia Corneal ulcer Herpes keratitis Uveitis
Corneal sensation diminished or disappeared is a necessary condition for the diagnosis of neurogenic keratitis. In the inquiry of medical history, it should be carefully and comprehensively, in order to find the cause of the disease, attention should be paid to the history of local medication, history of corneal surgery, history of head trauma and head and face surgery. , history of diabetes, herpes virus infection, etc., should pay attention to eyelid conditions, blink frequency, pupil and cranial nerves, tear secretion, etc. The earliest manifestation of neurogenic keratitis is congestion and edema of the limbus, followed by immediate appearance Ocular edema of the corneal epithelium, due to epithelial cell shedding, punctate epithelial defects, the most common site of cleft palate, punctate epithelial defects gradually merge, forming a large area of corneal epithelial loss and ulcer, the epithelium of the edge of the ulcer is slightly swelled, no ulcer around Significant matrix infiltration, its ulcer has a relatively characteristic, different from infectious ulcers, known as "nutritive ulcers", also known as "inert ulcers", when secondary infection or topical use of corticosteroids and other inappropriate treatment At the time, matrix melting, ulcer progression, severe corneal perforation may occur, and epithelial defects persist When, hypopyon sterility can occur, it can be associated with the Descemet folds.
Examine
Examination of neurogenic keratitis
Conduct laboratory tests for systemic diseases such as diabetes, cancer and congenital diseases.
Imaging studies can rule out trigeminal nerve palsy caused by many tumors, etc. The Cochet-Bonnet tactile tester can measure the sensitivity of the cornea by extracting blink reflex. The degree of corneal sensory loss is very important for the diagnosis of the disease. of.
Diagnosis
Diagnosis and differentiation of neurogenic keratitis
According to the clinical signs of the cornea, it is particularly proven that the original disease can be clearly diagnosed.
Other findings from eye examinations are also helpful in finding potential causes of corneal sensation. Iris atrophy is common in corneal uveitis caused by herpes zoster and herpes simplex virus. It can also be seen in leprosy, when neurogenic corneal sensation is absent. The anterior chamber can have a small amount of cells and mild aqueous humor. When the herpes zoster virus causes corneal sensation loss, it can also have a decrease in regulation, because the virus can infect the ciliary motor fibers of the ciliary ganglia.
