What are the typical symptoms, signs, and first‑line treatment of optic neuritis in a young adult (20‑40 years, slight female predominance)?

Symptoms of Optic Neuritis

Core Clinical Presentation

Optic neuritis in young adults (20-40 years, female predominance) classically presents with the triad of subacute visual loss developing over hours to days, periocular pain that worsens with eye movement, and red-green color desaturation (dyschromatopsia). 1, 2, 3

Visual Symptoms

• Subacute visual impairment progressing over hours to days (not instantaneous) is the hallmark feature, distinguishing it from vascular causes like retinal artery occlusion 1, 3
• Central scotomas (central visual field defects) are the most characteristic pattern in MS-related optic neuritis, representing papillomacular bundle damage 4
• Red-green color desaturation (dyschromatopsia) is a defining feature that often persists even after visual acuity recovers 1, 2, 5
• Blurred vision and distortion are common presenting complaints 6
• Visual symptoms typically stabilize after the initial worsening phase, then may resolve spontaneously even without treatment in 95% of typical cases 1, 3

Pain Characteristics

• Periocular pain worsening with eye movement is present in the majority of cases and is a key diagnostic feature 1, 2, 3
• Pain typically precedes or accompanies visual loss 3, 5
• The pain originates from inflammation along the optic nerve itself, not from ocular surface pathology 1

Additional Symptoms

• Photophobia is a commonly associated symptom 1
• Scotomas (blind spots) may be reported 6
• Visual field changes beyond central scotomas can occur 6

Objective Clinical Findings

Pupillary Abnormalities

• Relative afferent pupillary defect (RAPD) is present in unilateral cases, with weaker direct pupillary light reflex in the affected eye 3

Optic Disc Appearance

• One-third of patients present with mild optic disc edema (papillitis) on funduscopy 3
• Two-thirds have a normal-appearing disc initially (retrobulbar optic neuritis) 3
• Prominent optic disc edema or papilledema is a red flag for atypical optic neuritis (NMOSD or MOGAD) rather than typical MS-related disease 1, 2
• Optic nerve atrophy or pallor develops in chronic cases 1

Red Flag Symptoms Suggesting Atypical Optic Neuritis

The presence of any of these features mandates immediate investigation for NMOSD, MOGAD, or systemic lupus erythematosus, as these conditions require fundamentally different treatment approaches than MS. 4, 1, 2

High-Risk Clinical Features

• Bilateral simultaneous involvement strongly suggests NMOSD or MOGAD rather than MS 4, 1, 7, 2
• Severe vision loss with poor recovery after steroids or steroid dependence indicates atypical disease 1, 2
• Peripheral or altitudinal visual field defects (rather than central scotomas) are atypical for MS and suggest NMOSD or SLE 4
• Prominent optic disc edema/papilledema is more characteristic of NMOSD or MOGAD 1, 2
• Painless presentation with bilateral involvement suggests rare autoimmune causes like GFAP or CRMP5 autoimmunity 2

First-Line Treatment

Acute Management

High-dose intravenous methylprednisolone is the first-line treatment, which speeds visual recovery but does not improve the final visual outcome. 3, 5

• IV methylprednisolone accelerates recovery and reduces the short-term risk of MS conversion 3, 5
• Oral prednisone alone is contraindicated as it increases the risk of recurrent episodes 3, 5
• Typical MS-related optic neuritis recovers well even without treatment in 95% of cases, though steroids expedite recovery 1, 3

Atypical Optic Neuritis Treatment

• NMOSD and severe atypical cases require IV steroids and often plasma exchange for acute attacks, plus long-term immunosuppression (commonly rituximab) to prevent devastating relapses 1, 7, 2
• MOGAD has a 50-60% relapse rate during corticosteroid taper, necessitating maintenance immunosuppressive therapy 1, 7
• Treatment delay beyond 2 weeks is an unfavorable prognostic factor, particularly in SLE-related cases 4, 1

Essential Diagnostic Workup

Immediate Testing Required

• MRI of orbits and brain with contrast is the primary diagnostic study, showing T2 hyperintensity, optic nerve swelling, and gadolinium enhancement in 95% of cases 1, 7
• Serum AQP4-IgG and MOG-IgG antibody testing must be obtained at initial presentation when atypical features are present, as these have significant therapeutic consequences 1, 7, 2
• Cell-based assays using full-length human MOG are the gold standard for antibody testing 1, 7

Prognostic Assessment

• Brain MRI is critical for MS risk stratification even in isolated optic neuritis; even one clinically silent T2 hyperintense brain lesion dramatically increases MS conversion risk (hazard ratio 5.1 for 1-3 lesions, 11.3 for ≥10 lesions) 1
• Visual evoked potentials (VEPs) confirm optic nerve dysfunction with delayed conduction and provide objective evidence even when imaging is equivocal 1
• Optical coherence tomography (OCT) documents retinal nerve fiber layer thinning as evidence of optic nerve damage 1

Selective Use of Lumbar Puncture

• Routine lumbar puncture is not required for first-episode optic neuritis; reserve it for atypical presentations where CSF findings would directly alter management 1
• CSF oligoclonal bands combined with brain MRI lesions dramatically reduce the likelihood of monophasic illness 1

Critical Clinical Pitfalls

• Do not confuse the subacute evolution (hours to days) with truly sudden vision loss, which suggests vascular causes requiring different urgent management 1
• Do not dismiss peripheral or altitudinal field defects as typical MS-related optic neuritis; these patterns demand urgent antibody testing for NMOSD and SLE workup 4
• Do not use oral prednisone alone, as this increases recurrence risk compared to IV methylprednisolone or no treatment 3, 5
• Do not delay antibody testing in bilateral cases, as NMOSD requires aggressive immunosuppression to prevent devastating relapses, while MS-directed therapies (interferon-β) can worsen NMOSD and MOGAD 1, 7, 2