Optic neuritis: urgent referral, GCA exclusion, and the IV steroid decision

Optic neuritis is the most common cause of subacute vision loss in adults under 50. It arises from inflammation of the optic nerve — most often the retrobulbar segment, which means the disc looks normal on fundoscopy while the patient loses vision. The hallmark features are monocular, subacute-onset vision loss over hours to days, pain behind or around the eye that is worse on eye movement, and a disproportionate loss of colour saturation: red in particular looks washed out or brown, even when white-light acuity is only mildly reduced.

The Royal Australian and New Zealand College of Ophthalmologists (RANZCO) and Therapeutic Guidelines (eTG) both emphasise that optic neuritis is a same-day referral — to ophthalmology, neurology, or the ED depending on local access — and that the most dangerous task in general practice is not missing giant cell arteritis (GCA) as an alternative diagnosis in any patient aged 50 or over.

A. Core clinical — the AU general-practice framework

History

Take a focused optic neuritis history covering:

• Onset and tempo — subacute (hours to 1–2 days) favours inflammatory; sudden onset favours vascular (CRAO, NAION, GCA); gradual and progressive over weeks to months favours compressive or toxic.
• Pain — retro-orbital aching, worse with eye movement, present in ~92% of MS-related optic neuritis; GCA may cause orbital pain too but also jaw claudication and scalp tenderness.
• Colour desaturation — ask whether red objects look faded or brown compared to the other eye.
• Visual field defect — a curtain, shadow, or blurring in the central or pericentral field.
• Bilateral simultaneous involvement — strongly suggests NMOSD or MOGAD rather than typical MS-related disease.
• Past history — known MS, NMOSD, MOGAD; prior episode of optic neuritis; autoimmune disease; cancer; recent immunotherapy (immune checkpoint inhibitors cause optic neuritis as an immune-related adverse event).
• Drug history — ethambutol (toxic optic neuropathy), sildenafil, methanol exposure, prior radiation to the orbit.
• Family history — MS, autoimmune disease, hereditary optic neuropathy (Leber hereditary optic neuropathy, or LHON, is maternally inherited and affects young males).
• GCA red flags (age ≥50) — jaw claudication, scalp tenderness, temporal artery pulsation or tenderness, shoulder/hip girdle ache (PMR), weight loss, night sweats.

Examination

Even without specialist equipment, a GP can perform a meaningful bedside assessment:

• Visual acuity each eye separately with a Snellen chart or near-vision card.
• Colour vision — Ishihara plates one eye at a time; a reduced score in the affected eye relative to the other eye is a sensitive early sign of optic neuropathy.
• Relative afferent pupillary defect (RAPD) via the swinging-flashlight test in a dim room: alternate two seconds of illumination on each eye; if the affected eye dilates rather than constricts when light moves to it, the test is positive — this is the most reliable bedside sign of unilateral optic neuropathy.
• Visual fields by confrontation — central or centrocaecal scotoma typical for optic neuritis; altitudinal defect suggests NAION; bitemporal hemianopia suggests chiasmal compression.
• Fundoscopy — the disc is normal in ~67% of optic neuritis (retrobulbar ON); disc swelling (papillitis) in ~33% is more typical of MOGAD and paediatric cases. Cherry-red spot suggests CRAO. Flame haemorrhages plus disc swelling suggest arteritic anterior ischaemic optic neuropathy (GCA).
• Neurological screen — brisk reflexes, upgoing plantar, sensory level, cerebellar signs, gait, bladder symptoms — features of MS or NMOSD.
• GCA screen — temporal artery thickening, tenderness, or absent pulsation; scalp tenderness; jaw claudication; shoulder girdle tenderness.

Initial management in general practice

If optic neuritis is suspected: arrange same-day ophthalmology or neurology referral. Before the referral letter leaves the practice, send bloods for AQP4-IgG (cell-based assay) and MOG-IgG (cell-based assay) — these results guide long-term treatment and must be sent before steroids wherever possible, as steroids transiently suppress antibody titres. Also send ESR and CRP in any patient aged 50 or over.

If GCA is suspected in a patient aged 50 or over: start prednisolone 60 mg orally immediately — do not wait for ESR/CRP, do not wait for the temporal artery biopsy, do not wait for the ophthalmology appointment. The fellow eye can be permanently blinded within days. Arrange same-day rheumatology or ophthalmology review and organise temporal artery biopsy within 5–7 days (steroid treatment does not invalidate biopsy for the first week).

B. Evidence appraisal — the ONTT and beyond

IV methylprednisolone

The Optic Neuritis Treatment Trial (ONTT; Beck, NEJM 1992) remains the cornerstone evidence base. This randomised trial of 457 patients found that IV methylprednisolone 1 g/day for 3 days accelerated visual recovery by approximately 1–2 Snellen lines at 2 weeks compared to oral prednisone and placebo. Crucially, the trial found no difference in long-term visual outcome at 6 or 12 months — all three groups ended up with similar final acuity. IV methylprednisolone is therefore standard first-line in acute MS-related optic neuritis because it shortens the acute episode, not because it changes the final result.

The critical finding from ONTT was that the oral prednisolone alone arm had a significantly increased rate of recurrent optic neuritis compared with both the IV and placebo arms. Oral prednisolone monotherapy is consequently contraindicated for acute optic neuritis — never prescribe oral steroids without IV methylprednisolone induction.

Time-critical treatment for NMOSD and MOGAD

For NMOSD-related optic neuritis, the situation is fundamentally different. Stiebel-Kalish et al. (Neurology NI 2019) demonstrated that delays of 7 or more days from onset to IV methylprednisolone are associated with markedly worse visual recovery — the window for preserving function is narrow. NMOSD-ON frequently fails to respond to IV methylprednisolone alone and requires plasma exchange (PLEX) within 5–7 days of steroid failure. NEMOS NMOSD recommendations 2023 (Trebst et al.) recommend maintenance immunosuppression after the first NMOSD attack — rituximab, eculizumab, satralizumab, or inebilizumab — to prevent further attacks.

For MOGAD-related optic neuritis, the MOGAD International Consensus (Banwell et al., Lancet Neurology 2023) recommends IV methylprednisolone acutely and selective maintenance treatment after a second episode or in patients with severe first-attack visual loss or persistently positive MOG-IgG.

C. Distinguishing causes — practical differential

The differential diagnosis of acute vision loss includes several conditions that mimic optic neuritis but require entirely different management:

Condition	Discriminating features
GCA / arteritic AION	Age ≥50; jaw claudication; scalp tenderness; markedly elevated ESR + CRP; disc swelling; arteritic history — prednisolone immediately
NAION (non-arteritic)	Sudden painless altitudinal vision loss; older + vasculopathy; no inflammation
CRAO	Sudden painless profound vision loss; cherry-red spot; retinal whitening; minutes-to-hours surgical window
NMOSD-ON	Severe pain; sequential or bilateral; AQP4-IgG positive; poor natural recovery
MOGAD-ON	Often bilateral; papillitis on fundoscopy; MOG-IgG positive
Toxic optic neuropathy	Gradual bilateral; ethambutol, methanol, B12 deficiency
Leber hereditary optic neuropathy (LHON)	Young male; painless; sequential bilateral; maternal family history
Compressive optic neuropathy	Gradually progressive; pituitary or meningioma; bitemporal field defect
Migraine aura	Bilateral, scintillating zigzag, self-limiting 15–30 min, headache follows

The most dangerous missed diagnosis is GCA in a patient over 50 — treat first, confirm second.

D. Australian operations

MBS items: standard consultations 23, 36, 44; GPCCMP 965/967 for established MS/NMOSD; MHCP 2715/2717 for vision-loss adjustment; ATSI 715; telehealth 91890/91891 for stable follow-up coordination.

PBS: IV methylprednisolone is hospital-only; oral prednisolone is PBS General Schedule; disease-modifying therapies for MS and NMOSD are PBS Authority-listed (see MS Australia for the current PBS tier list). Rituximab for NMOSD is PBS-listed under Section 100 for eligible patients.

Driving: Austroads Assessing Fitness to Drive requires visual acuity ≥6/12 in the better eye and binocular visual fields for an unconditional licence. Document driving cessation advice and refer the patient back to their licencing authority. Conditional driving licences are possible during recovery — neurology to advise on timeline.

NDIS / Vision Australia: patients with permanent vision impairment under 65 may qualify for NDIS support. Vision Australia provides low-vision rehabilitation, orientation and mobility training, assistive technology, and employment support.

E. Special populations

Older adults. GCA must be in the differential for every patient aged 50 or over presenting with new visual symptoms. NAION (non-arteritic) is more common than optic neuritis in this age group; it presents with painless, sudden, altitudinal vision loss and a small crowded optic disc. NAION is not treated with steroids and has no proven acute intervention.

Children and adolescents. Paediatric optic neuritis has a higher rate of disc swelling (papillitis) and bilateral involvement, and a higher probability of MOGAD rather than MS. Visual outcomes are generally favourable but require specialist paediatric ophthalmology or neuro-ophthalmology assessment.

ATSI communities. Coordinate with the Aboriginal Community Controlled Health Organisation (ACCHO) for specialist referral and cultural safety in the context of acute vision loss, which may have significant functional and social impact. Closing the Gap PBS Co-payment applies.

Pregnancy. MS relapse (including optic neuritis) can occur post-partum. IV methylprednisolone is used with specialist guidance — brief-duration administration is generally considered lower risk than untreated relapse. Specialist obstetric and neurology co-management required.

When to escalate

Refer same-day to ophthalmology/ED for: any new subacute monocular vision loss + pain on eye movement + colour desaturation; RAPD present; bilateral simultaneous vision loss.

In patients aged 50 or over with any features of GCA: start prednisolone 60 mg orally NOW and arrange same-day rheumatology or ophthalmology.

Refer urgently to neurology within 24–48 h for: confirmed or highly suspected optic neuritis with brain MRI lesions (CIS conversion decision); known NMOSD or MOGAD with new attack; incomplete recovery at 4–6 weeks.

What this article is and is not

This is general health information drawn from current Australian general practice guidelines — eTG, RANZCO, and major optic neuritis trial evidence including ONTT (Beck, NEJM 1992), NEMOS NMOSD 2023, and MOGAD Consensus 2023. It is not personal medical advice and does not create a doctor–patient relationship.

For Australian consumer information: MS Australia, Vision Australia, HealthDirect, Better Health Channel.

For acute crisis: Lifeline 13 11 14.

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Sources cited

1. RANZCO
2. Therapeutic Guidelines (eTG)
3. Beck RW et al. — ONTT (NEJM 1992)
4. Trebst C et al. — NEMOS NMOSD recommendations 2023
5. Banwell B et al. — MOGAD International Consensus (Lancet Neurology 2023)
6. Stiebel-Kalish H et al. — Time to treatment in AQP4/MOG ON (Neurology 2019)
7. Frontiers in Neurology — Comprehensive optic neuritis review 2025
8. MS Australia
9. Vision Australia
10. Austroads — Assessing Fitness to Drive
11. HealthDirect
12. Better Health Channel