Can patients with Multiple Sclerosis (MS) experiencing an episode of optic neuritis develop peripheral vision loss?

Peripheral Vision Loss in MS-Associated Optic Neuritis

MS-associated optic neuritis characteristically causes central scotomas and central visual field defects, not peripheral vision loss—peripheral field defects should raise suspicion for atypical optic neuritis or alternative diagnoses.

Typical Visual Field Pattern in MS Optic Neuritis

Central scotomas are the hallmark visual field defect in MS-related optic neuritis, not peripheral field loss 1. The characteristic presentation includes:

• Central visual field defects with red-green color desaturation (dyschromatopsia) 1
• Central scotomas representing damage to the papillomacular bundle 1
• Retinal sensitivity depression that may extend beyond the central field, but primarily affects central vision 2

Red Flags: When Peripheral or Atypical Field Defects Suggest Alternative Diagnoses

Peripheral or altitudinal visual field defects are atypical for MS-related optic neuritis and mandate immediate investigation for other etiologies 3, 1. Specifically:

Neuromyelitis Optica Spectrum Disorder (NMOSD)

• Altitudinal field defects (superior or inferior half of visual field) strongly suggest NMOSD rather than MS 3, 4
• More severe vision loss with poorer recovery than MS 5
• Bilateral simultaneous involvement is common 1, 5
• Requires immediate AQP4-IgG testing 1, 6

Systemic Lupus Erythematosus (SLE)

• Can cause arcuate defects (nerve fiber bundle defects following the retinal nerve fiber layer pattern) 3
• Altitudinal field defects associated with antiphospholipid antibodies suggest ischemic/thrombotic mechanism 3
• Poor visual prognosis with only 30% maintaining acuity >20/25 3, 5, 6

MOG-Antibody Disease (MOGAD)

• Long optic nerve lesions on MRI 1, 5
• Bilateral involvement more common than MS 5
• Requires MOG-IgG testing 1, 6

Subclinical Visual Pathway Involvement in MS

While MS patients may have asymptomatic visual loss affecting the entire retino-cortical pathway 7, this represents:

• Approximately 20% loss of functional neural channels even without prior optic neuritis 7
• Peripheral zone retinal sensitivity depression detectable on automated perimetry 2
• This subclinical involvement is distinct from symptomatic peripheral field loss, which remains atypical for MS 2

Diagnostic Algorithm When Peripheral Field Defects Are Present

If a patient with suspected MS optic neuritis presents with peripheral or altitudinal visual field defects, immediately pursue:

1. Urgent serum antibody testing for AQP4-IgG and MOG-IgG 1, 6
2. MRI of orbits and brain with contrast looking for:
   • Posterior optic nerve/chiasmal involvement (suggests NMOSD) 1
   • Long optic nerve lesions (suggests NMOSD/MOGAD) 1, 5
   • Soft tissue enhancement extrinsic to nerve (suggests MOGAD or granulomatous disease) 5
3. Autoimmune workup including ANA, anti-dsDNA, antiphospholipid antibodies if SLE suspected 3, 6
4. Funduscopy to assess for optic disc edema (30-40% in SLE-related cases) 3

Critical Clinical Pitfall

Do not assume all optic neuritis in MS patients is MS-related—the presence of atypical features, particularly peripheral or altitudinal field defects, demands investigation for NMOSD, MOGAD, or SLE, as these conditions require fundamentally different treatment approaches than MS 1, 6. Treatment delay beyond 2 weeks worsens prognosis, particularly in SLE-related cases 3, 6.