Optic Neuritis
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Direct answer
Pain behind one eye that worsens on eye movement, with vision dropping over days in a young woman, is the textbook presentation of optic neuritis — demyelinating inflammation of the optic nerve. Examination shows a relative afferent pupillary defect, impaired colour vision with red desaturation, and a visual field defect (usually central scotoma); two-thirds have a normal disc (retrobulbar neuritis), giving the aphorism "the patient sees nothing and the doctor sees nothing". Magnetic resonance imaging of the brain is performed in every case, both to prognosticate the multiple sclerosis risk and to exclude compressive lesions. Per the Optic Neuritis Treatment Trial, intravenous methylprednisolone accelerates recovery but does not change final vision, while oral prednisolone alone is avoided; most patients recover well within weeks.
What you must remember
- Classic demographic: young adult, female preponderance, unilateral; children may have bilateral disease after viral infection, with better recovery. Pain on eye movements, present in the great majority, reflects inflammation of the nerve sheath within the orbit.
- Signs: relative afferent pupillary defect, red desaturation, central or centrocaecal scotoma on fields, and reduced contrast sensitivity.
- Disc appearance: papillitis (anterior neuritis) swells the disc; retrobulbar neuritis leaves a normal fundus — the majority in adults.
- ONTT protocol: intravenous methylprednisolone 1 g daily for three days followed by oral prednisone taper; oral prednisolone alone was associated with increased recurrence and is avoided.
- Recovery begins within weeks and final acuity is good in most patients despite residual colour and contrast deficits.
- MRI prognosticates: demyelinating white-matter lesions substantially raise the long-term risk of multiple sclerosis, converting the eye sign into a neurology referral and follow-up.
- Neuromyelitis optica spectrum disease (anti-aquaporin-4 antibody) presents with severe bilateral neuritis and longitudinally extensive myelitis, poor steroid response and plasma exchange need — check the antibody in atypical cases.
- Differentiate urgently from compressive lesions (progressive painless loss, proptosis, optic atrophy with pallor out of proportion) and from ischaemic optic neuropathy (sudden, painless, older patient, altitudinal defect).
A young woman with dim vision, worked through
A 28-year-old teacher reports three days of greying vision in the right eye with an ache behind the globe whenever she looks sideways. Acuity is 6/36; colour plates read incorrectly with a washed-out red target; the swinging torch test shows a right relative afferent pupillary defect; fields show a central scotoma; and the fundus is completely normal. Retrobulbar neuritis fits every finding, and the pain ties it to demyelination. Order the brain MRI with contrast: periventricular white-matter lesions would confirm a demyelinating tendency and stratify her multiple sclerosis risk, while a compressive mass at the orbital apex would redirect the case entirely. Treat with intravenous methylprednisolone 1 g daily for three days, then an oral taper — explaining honestly that the drip speeds recovery rather than improving the final outcome, which is usually 6/9 or better within weeks. Avoid plain oral prednisolone, the arm of the trial associated with more recurrences. Review at one and three months for acuity, colour and fields; a second event elsewhere — a spinal cord syndrome, new MRI lesions — moves her care into the multiple sclerosis pathway. Had this been a 62-year-old hypertensive with sudden painless superior field loss and a pale swollen disc, the diagnosis would be non-arteritic anterior ischaemic optic neuropathy, not neuritis, and the work-up would target giant cell arteritis instead. The pairing of pain with a normal fundus is what carries the mark.
Where candidates slip
Two answers cost marks repeatedly. The first is steroid route: "oral prednisolone" as sole therapy for optic neuritis is the historical arm that increased recurrence — the trial answer is intravenous methylprednisolone, then taper. The second is forgetting the MRI: it is not optional decoration but the prognostic and diagnostic core, quantifying multiple sclerosis risk and excluding compression. A third, subtler slip is missing atypical neuritis — severe, bilateral, or poorly recovering — where testing for neuromyelitis optica antibody changes both prognosis and treatment.
Frequently asked questions
What are the three cardinal signs of optic neuritis?
Reduced acuity with a relative afferent pupillary defect, red colour desaturation, and pain on eye movement — usually with a central scotoma on field testing.
What did the ONTT conclude about steroids?
Intravenous methylprednisolone 1 g daily for three days followed by oral taper accelerates visual recovery but does not improve final acuity; oral prednisolone alone increased recurrence risk.
Why is brain MRI performed in optic neuritis?
To quantify demyelinating lesions that predict conversion to multiple sclerosis and to exclude compressive or inflammatory alternatives that change management.
How does NMO optic neuritis differ from typical demyelinating neuritis?
It is often bilateral, severe and poorly responsive to steroids, associated with anti-aquaporin-4 antibodies and longitudinally extensive transverse myelitis, requiring plasma exchange and immunosuppression.
Which painless, sudden optic neuropathy occurs in the elderly?
Non-arteritic anterior ischaemic optic neuropathy — sudden altitudinal field loss with a pale swollen disc, in a hypertensive or diabetic patient.