Optic neuritis denotes inflammation of the optic nerve, most commonly demyelinating in nature. The classic presentation includes acute or subacute monocular vision loss developing over hours to days (typically reaching nadir within 1-2 weeks), pain on eye movement (90% of cases), dyschromatopsia (impaired color vision, particularly red desaturation), and a relative afferent pupillary defect (RAPD) on the affected side. Visual field defects vary widely, with central scotoma being most common but altitudinal, arcuate, or hemianopic patterns possible. Funduscopy may show a swollen optic disc (papillitis) in approximately one-third of cases, while two-thirds have a normal-appearing disc (retrobulbar neuritis).
The differential diagnosis is broad, with idiopathic demyelinating optic neuritis being most common in young adults. Multiple sclerosis (MS) is the most important association: optic neuritis is the presenting feature in 20-25% of MS patients, and 50-75% of patients with isolated optic neuritis develop MS within 15 years (with brain MRI lesions being the strongest predictor). Neuromyelitis optica spectrum disorders (NMOSD), associated with aquaporin-4 IgG antibodies, cause more severe and bilateral optic neuritis with poor recovery. Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease represents a distinct entity with often bilateral optic neuritis, prominent disc swelling, and good steroid responsiveness. Other etiologies include infections (syphilis, Lyme, viral), autoimmune diseases (lupus, sarcoidosis), and toxic/nutritional causes.
Modern diagnostic evaluation includes comprehensive ophthalmic examination with visual acuity, color vision testing, automated perimetry, optical coherence tomography (showing acute peripapillary edema then chronic retinal nerve fiber layer thinning), and visual evoked potentials demonstrating prolonged latency. Brain and orbital MRI with gadolinium identifies optic nerve enhancement and is essential for MS risk stratification through detection of demyelinating lesions. Serum autoantibody testing for AQP4-IgG and MOG-IgG should be performed in atypical cases (bilateral, severe, poor recovery, recurrent). Treatment with high-dose intravenous methylprednisolone (1 g/day for 3-5 days) accelerates visual recovery without affecting final outcome in idiopathic disease, while NMOSD and MOG-AD often require additional therapies (plasma exchange, immunosuppression). Long-term disease-modifying therapy is initiated for high MS risk patients.