What Is Optic Neuritis?

Optic neuritis is a general term for inflammation of any part of the optic nerve. It refers to diseases such as inflammatory demyelinating, infection and non-specific inflammation of the optic nerve. Optic neuritis can be divided into intra-global and posterior-global according to the location of the lesions. The former refers to discitis and the latter is posterior optic neuritis. Optic neuritis is mostly unilateral. Optic papillitis is more common in children. Posterior optic neuritis is more common in young adults.

Basic Information

English name: Optic Neuritis
Visiting department: Ophthalmology
Multiple groups: Optic papillitis is more common in children, and posterior optic neuritis is more common in young adults.

Common locations: Optic nerve
Common causes: Inflammatory demyelinating, infection, autoimmune diseases, etc. can cause
Common symptoms: Decreased vision, eye pain, changes in light reflection, changes in fundus, etc.

Causes of Optic Neuritis

Inflammatory demyelinating

Is the more common cause. The exact etiology of inflammatory demyelinating neuritis is unknown. It is likely that some precursor factors such as upper respiratory tract or digestive tract virus infection, mental shock, and vaccination caused the body's autoimmune response, producing autoantibodies that attack the myelin sheath of the optic nerve. Lost and getting sick.

2. infection

Both local and systemic infections can affect the optic nerve and cause infectious optic neuritis.

(1) Local infections Intraocular, intraorbital inflammation, oral inflammation, middle ear and mastoiditis, and intracranial infections can be directly caused by local spread of optic neuritis.

(2) Systemic infection of certain infectious diseases can cause optic neuritis, such as: diphtheria (diphtheria), scarlet fever (streptococcus), pneumonia (pneumococcus, staphylococcus), dysentery (dysentery), typhoid (typhoid), Tuberculosis (tuberculosis), pyogenic meningitis, sepsis and other systemic bacterial infectious diseases, their pathogens can enter the bloodstream, grow and reproduce in the blood, release toxins, and cause optic nerve inflammation. Viral diseases such as influenza, measles, mumps, shingles, chicken pox, etc., as well as parasitic infections such as Lyme Treponema, Leptospira, Treponema pallidum, Toxoplasmosis, Toxoplasmosis, and Coccidiosis, all cause optic neuritis. Report.

3. Autoimmune diseases

Such as systemic lupus erythematosus, Wegener's granulomatosis, Behcet's disease, Sjogren's syndrome, and sarcoidosis can all cause non-specific inflammation of the optic nerve. In addition to the above reasons, the cause is not found in some cases in clinical practice; some of them may be Leber's hereditary optic nerve.

Clinical manifestations of optic neuritis

Optic neuritis is a common ophthalmic disease. In an age when everyone is advocating health, optic neuritis has brought serious threats to everyone's eye health, making patients live in pain and inconvenience.

(I) Classification

Understanding the clinical classification of optic neuritis can provide a clearer understanding of optic neuritis. According to clinical manifestations, it is divided into two types: simple optic atrophy and non-simple optic atrophy.

1. Non-simple optic nerve atrophy

The main manifestation is that the optic nerve papilla boundary is blurred, and it is grayish white or waxy yellow. Due to the proliferation of glial tissue, the physiological depression disappears, and the scleral sieve hole cannot be seen. White sheaths of retinal blood vessels can be seen around the nipples or the entire fundus, and the filling can be tortuous or thin. In some cases, there are choroidal atrophy spots and pigmentation, including: optic neuritis secondary to optic atrophy. Optic nerve papillary edema secondary to optic nerve atrophy. Retinitis pigmentosa is secondary to atrophy of the optic nerve.

2. Simple optic nerve atrophy

Mainly manifested by the optic nerve papilla boundary is clear, all or part of pale, scleral sieve apical membrane is clearly visible. Except for the optic nerve papilla, there were no other changes in the fundus, including: secondary optic nerve atrophy secondary to retrobulbar optic neuritis. Demyelination disease and white matter malnutrition cause optic nerve atrophy. Traumatic optic nerve bone canal fracture, severed or contused optic nerve. Compressive optic nerve atrophy caused by intracranial inflammation, which is common in those with tuberculous meningitis, recessive bacterial meningitis, or optic cross arachnoid inflammation limited to the intracranial segment of the optic nerve.

(B) the main clinical manifestations

Vision loss

Most of the eyesight suddenly drops, even a few days after the onset can be reduced to light or no light.

2. Eye pain

Traction-like pain in the back of the eyeball and deep orbital tenderness during eyeball rotation.

3. Change in light reflection

Pupils are slow or absent from light reflections, or do not respond long to light.

4. Fundus changes

In the case of papillitis, the papillary hyperemia, slight bulge (below 3D), unclear edges, disappearance of physiological depression, tortuous retinal vein filling, turbid retinal edema around the papillary, flame-like bleeding, and yellowish white exudation may sometimes affect the macular Causes radial macular edema and wrinkles. In retrobulbar optic neuritis, the fundus is basically normal in the early stage, the optic nipples become lighter in the later stage, and the optic nerve atrophies.

Optic Neuritis Examination

Eye examination

The pupil of the affected eye is often dilated, the direct photoreaction is dull or disappears, and the indirect photoreaction exists. Patients with monocular involvement usually have relative afferent pupillary disorder, which is a sign that the affected eye responds slowly to light relative to healthy eyes, especially when the examiner irradiates light alternately between the two eyes. Good eyes. Fundus examination showed that the optic disc was congested and slightly edema in patients with papillitis. There were small bleeding spots on or around the optic disc, but there was little exudate. The retinal veins are thickened and the arteries are generally unchanged. There were no abnormal changes in the fundus of posterior optic neuritis.

Visual field inspection

Various types of visual field damage can occur, but the more typical is the dark spot in the center of the visual field or the centripetal reduction of the visual field.

3. Visual evoked potential

It can be shown that P100 wave (P1 wave) has an increased incubation period and a reduced amplitude. In the case of retrobulbar optic neuritis, there is no change in the fundus. In order to identify whether it is pseudo-blind, objective VEP can be used to assist diagnosis. According to research, when optic neuritis develops, VEP changes in 90% of patients, and only 10% of VEP returns to normal after vision recovery.

4. Magnetic resonance imaging

Orbital fat suppression sequence MRI can show thickened and enhanced signals of the affected optic nerve; head MRI can help to identify the oppressive optic neuropathy caused by intracranial diseases such as tumors in the saddle area, as well as understand the conditions of the sphenoid sinus and ethmoid sinus, and help Differential diagnosis of the etiology; more importantly, understanding the presence or absence of demyelinating plaques in the white matter of the brain through MRI is of reference significance in the selection of treatment options and the prognosis of patients. For typical inflammatory demyelinating optic neuritis, systemic examination is not required for clinical diagnosis, but other causes of disease should be looked for, such as local or systemic infections and autoimmune diseases; the following guidelines require systemic examination and other vision Identification of neuropathy: the age of onset is outside the range of 20 to 50 years old; both eyes are onset simultaneously; vision persists after 14 days of onset.

5. Electrophysiological examination

The visual evoked potential showed that the P wave latency was prolonged and the wave amplitude decreased.

6. Fundus fluorescein angiography

In the early stage of optic papillitis, the papillary surface of the venous phase leaks fluorescence and the edges are blurred. The vein phase showed strong fluorescence.

Optic neuritis diagnosis

The diagnosis can be made based on the etiology, clinical manifestations, and fundus examination.

Optic Neuritis Treatment

Cause treatment

2. Corticosteroid treatment

In acute cases, due to inflammation and swelling of the optic nerve fibers, if the time is too long or the inflammatory response is too severe, the optic nerve fibers can be degenerated and necrotic. Therefore, it is extremely important to control the inflammatory response early and avoid the involvement of optic nerve fibers.

Some patients with inflammatory demyelinating optic neuritis can recover without treatment. The purpose of using glucocorticoids is to reduce relapse and shorten the course of disease. According to research, the recurrence rate of prednisone alone is twice that of the combined intravenous group. The principle of use is as follows:

(1) The patient is the first onset and has no previous history of multiple sclerosis or optic neuritis. If MRI finds demyelinating at least one place, glucocorticoid shock therapy can be used to accelerate vision recovery and reduce the chance of recurrence; normal MRI The possibility of multiple sclerosis (MS) is very low, but intravenous glucocorticoid shock treatment can still be used to accelerate vision recovery.

(2) For patients with previous diagnosis of multiple sclerosis or optic neuritis, glucocorticoid shock therapy can be applied during the relapse period, or immunosuppressive agents, gamma globulins, etc. can be selected as appropriate, and vitamin B group drugs and vasodilators can be used during the recovery period .

For infectious optic neuritis, cooperation with relevant departments should be given to treat the cause and protect the optic nerve; autoimmune optic neuropathy should also be regular and full-course glucocorticoid therapy for systemic autoimmune diseases.

3. Vasodilator

After the ball injection, tolasurin or oral tolasurin, niacin and so on.

4. Supportive Therapy

Vitamin B ₁ and Vitamin B _{12 are} injected intramuscularly once a day, and adenosine triphosphate can be injected intramuscularly once a day.

5. Anti-infective treatment

Antibiotics (penicillin, vanguardin) can be used if infected.