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Optic Neuritis

URGENT — Neuro

Symptoms

  • typical age 18–45 years; usually unilateral
  • vision loss progressing over hours to days (nadir at ~1 week)
  • retro-orbital pain, especially with eye movement (>90% of cases)
  • acquired loss of color vision (red desaturation)
  • uhthoff sign: worsening of symptoms with exercise or increased body temperature
  • pulfrich phenomenon: altered perception of moving objects
  • atypical: advanced age, bilateral onset, or severe loss without recovery (suspect nmosd/mogad)

Clinical Findings

Clinical examination

  • relative afferent pupillary defect (rapd) in unilateral cases
  • decreased color vision on ishihara plates
  • central, cecocentral, or arcuate visual field defects

Nerve appearance

  • retrobulbar (2/3): normal optic disc appearance (adults)
  • papillitis (1/3): swollen optic disc (children/young adults)
  • absence of peripapillary hemorrhages is typical for demyelinating on

Etiology

Demyelinating disease

  • multiple sclerosis (ms): frequently the initial manifestation
  • nmosd (anti-aqp4) and mogad (anti-mog): critical atypical causes

Other causes

  • viral: measles, mumps, varicella, mononucleosis
  • granulomatous: sarcoidosis, syphilis, tb, lyme
  • contiguous inflammation: meninges, orbit, or sinuses

Red Flags

  • lack of pain: present in >90% of typical on; absence suggests ischemia or sarcoid
  • vision loss progressing >2 weeks: rule out compressive or infiltrative etiology
  • poor recovery at 4–6 weeks: consider nmosd or mogad
  • systemic features (rash, arthritis): evaluate for lupus or sarcoidosis

Investigations

Imaging

  • mri brain + orbits with gadolinium and fat suppression (essential to see enhancement)

Laboratory workup

  • anti-aqp4 and anti-mog antibodies: draw on all first-presentation cases
  • targeted: ace (sarcoid), rpr/fta-abs (syphilis), lyme titer, esr/cbc

Functional testing

  • automated visual field (hvf 24-2 or 30-2)
  • oct rnfl: baseline and monitoring for axonal loss
  • csf oligoclonal bands: predictive of ms if mri is inconclusive

Treatment

Acute phase

  • iv methylprednisolone 1 g/day × 3 days, followed by oral prednisone taper
  • gastric prophylaxis: omeprazole 20 mg po daily
  • plasmapheresis: if poor steroid response in suspected nmosd

Long-term management

  • ms disease-modifying therapy (dmt): interferons, glatiramer acetate, ocrelizumab, etc.
  • nmosd/mogad: chronic immunosuppression (e.g., rituximab, azathioprine)

Clinical Pearl

ontt (optic neuritis treatment trial): iv steroids speed recovery but don't improve 1-year vision. 15-year data: 50% develop ms if mri abnormal; 25% if normal mri. mri at presentation is most important prognostic test. vep latency remains prolonged even after clinical recovery — useful for diagnosing subclinical or previous optic neuritis.

Differential Diagnosis

  • • ischemic optic neuropathy (naion/aaion)
  • • acute papilledema
  • • leber hereditary optic neuropathy (lhon)
  • • toxic or metabolic optic neuropathy

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