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Optic neuritis is most common among adults 20 to 40 years. Most cases result from demyelinating disease, particularly multiple sclerosis, in which case there may be recurrences. Optic neuritis is often the presenting manifestation of multiple sclerosis. Other causes include:

• Neuromyelitis optica (NMO) (1)

• Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) (2)

• Infectious diseases (eg, viral encephalitis [particularly in children], sinusitis, meningitis, tuberculosis [TB], syphilis, human immunodeficiency virus [HIV])

• Tumor metastasis to the optic nerve

• Systemic lupus erythematosus

Chemicals and drugs such as lead. methanol, quinine, arsenic, ethambutol, and antibiotics cause optic neuropathies rather than true optic neuritis. TNF-alpha inhibitors and immune checkpoint inhibitors can cause optic neuritis.

Rare causes include pernicious anemia and systemic autoimmune diseases. Often, the cause remains idiopathic despite thorough evaluation.

The main symptom of optic neuritis is vision loss, frequently maximal within several days and varying from a small central or paracentral scotoma to complete blindness. Most patients have mild eye pain, which often feels worse with eye movement.

The most characteristic findings include reduced visual acuity, a visual field deficit, and disturbed color vision (often out of proportion to loss of visual acuity). An afferent pupillary defect is usually detectable if the contralateral eye is unaffected or involved to a lesser degree. Testing of color vision is a useful adjunct, although 10% of males have congenital color blindness, producing false-positive results. In about two thirds of patients, inflammation is entirely retrobulbar, causing no visible changes to the optic nerve head. In the rest, disk hyperemia, edema in or around the disk, vessel engorgement, or a combination is present. A few exudates and hemorrhages may be present near or on the optic disk, but this is rare for most cases of optic neuritis.

• Clinical evaluation

• Magnetic resonance imaging (MRI)

Optic neuritis is suspected in patients with characteristic pain and vision loss, particularly if they are young. Neuroimaging, preferably with gadolinium-enhanced MRI of the brain and orbits, is usually done and may show an enlarged, enhancing optic nerve. MRI may also help diagnose multiple sclerosis, myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and neuromyelitis optica (NMO). There is usually more extensive enhancement of the optic nerve(s) in NMO and MOGAD. Fluid attenuating inversion recovery (FLAIR) MRI sequences may show typical demyelinating lesions in a periventricular location if optic neuritis is related to multiple sclerosis. Spinal cord involvement can be seen in any of the demyelinating diseases but is usually more extensive in NMO and MOGAD. NMO and MOG antibodies in the serum should be checked for any atypical or severe optic neuritis.

Prognosis depends on the underlying condition. Most episodes of typical optic neuritis improve spontaneously with significant recovery of vision in 2 to 3 months. The recurrence rate among patients with optic neuritis is variable and depends on the etiology. Patients with an underlying disease, such as NMO or MOGAD, have higher rates of recurrence in the same eye or in the other eye, and recovery of vision can be worse, especially for NMO (1). MRI is used to determine future risk of demyelinating disease, especially multiple sclerosis.

• Corticosteroids

Corticosteroids are an option, especially if multiple sclerosis or neuromyelitis optica are suspected. Treatment with methylprednisolone (1000 mg intravenously once a day) or the bioequivalent dose of oral prednisone (1250 mg once a day; [1]) for 3 days followed by prednisone (1 mg/kg orally once a day) for 11 days may speed recovery, but ultimate vision results are no different from those with observation alone for multiple sclerosis or idiopathic optic neuritis. Early high-dose corticosteroids may improve outcomes in atypical causes of optic neuritis, such as neuromyelitis optica (NMO) or myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD; [2]). Plasma exchange is often used for NMO attacks and is sometimes used for severe optic neuritis from other causes if the optic neuritis does not recover after high-dose corticosteroids. Treatment with low-dose oral prednisone alone does not improve vision outcome and may increase the rate of recurrent episodes. Low-vision aids (eg, magnifiers, large-print devices, talking watches) may be helpful. Multiple sclerosis disease-modifying treatments should be given to patients with multiple sclerosis, and NMO-specific treatments should be used in patients with NMO. MOGAD patients with relapsing disease may need chronic immunotherapy. It is important to note that patients with NMO and MOGAD should not be given certain multiple sclerosis disease-modifying agents, which may be ineffective or even worsen the outcome.