Synopsis
Recognise an acute optic neuropathy, distinguish typical demyelinating optic neuritis from ischaemic, compressive, infectious and antibody-associated disease and coordinate urgent eye and neurological investigation.
- Typical demyelinating optic neuritis usually causes subacute monocular visual loss over hours to days, pain worsened by eye movement, reduced colour saturation, a central or caecocentral field defect and a relative afferent pupillary defect.
- The optic disc is often normal because inflammation is retrobulbar. A normal-looking disc does not exclude substantial optic-nerve dysfunction; marked swelling, haemorrhage or exudate is atypical and broadens the differential.
- Measure corrected acuity in each eye, red or colour perception, pupils, confrontation fields and fundi. A binocular acuity result or vague statement that vision is blurred cannot localise the lesion.
- Pain with eye movement supports optic neuritis but is not specific; sinus, orbital and ocular inflammatory disease can cause pain, while some demyelinating and antibody-associated neuritis is painless.
- A relative afferent pupillary defect is expected in unilateral or asymmetric optic neuropathy. It may be absent when disease is bilaterally symmetric and does not arise from refractive error alone.
- Typical recovery begins within weeks. Progressive loss beyond roughly two weeks, absence of early recovery, recurrence in the same nerve, severe bilateral disease or steroid-dependent relapse is atypical.
- Younger age and painful central visual loss favour demyelinating neuritis; sudden painless altitudinal loss with a swollen disc in an older vascular-risk patient favours anterior ischaemic optic neuropathy.
- Ask about previous neurological episodes, myelitis, persistent vomiting or hiccups, autoimmune disease, infection, medicines, nutritional and toxic exposure, cancer, headache, jaw claudication and polymyalgic symptoms.
- MRI of brain and orbits with dedicated fat-suppressed post-contrast optic-nerve sequences supports the diagnosis, identifies lesions suggesting multiple sclerosis and helps characterise long or chiasmal inflammation.
- Aquaporin-4 and MOG antibody testing is reserved for phenotypes such as bilateral, severe, recurrent, longitudinally extensive, chiasmal or markedly swollen neuritis and is interpreted by neuroimmunology specialists.
- High-dose corticosteroid can hasten recovery in selected demyelinating attacks but does not justify low-dose oral steroid treatment, which is not a substitute for correct diagnosis and may be inappropriate in infection.
- Provide driving, work and safety advice based on current acuity and fields, and ensure both final visual outcome and the risk of future demyelinating events are reviewed.
Key red flags
Subacute unilateral central visual loss, dyschromatopsia, eye-movement pain and a relative afferent pupil defect with a normal or mildly swollen disc in a younger adult supports typical optic neuritis.
Severe optic-disc swelling, bilateral or recurrent attacks, long anterior optic-nerve enhancement and good steroid responsiveness with relapse on withdrawal can suggest MOG-antibody-associated disease.
Profound visual loss, posterior or chiasmal involvement, poor spontaneous recovery and associated longitudinally extensive myelitis or area-postrema symptoms raises neuromyelitis optica spectrum disorder.
Sudden painless monocular loss, often altitudinal, with a swollen disc in an older adult suggests ischaemic rather than inflammatory optic neuropathy; giant-cell-arteritis symptoms make treatment an immediate emergency.
Progressive painless loss, optic pallor, proptosis, dysmotility, asymmetrical disc change or a junctional field pattern suggests orbital, canalicular or chiasmal compression and needs targeted imaging.
Photopsia, metamorphopsia, retinal whitening, haemorrhage, vascular occlusion or detachment signs point to retina rather than optic nerve. A relative afferent defect can occur in severe asymmetric retinal disease.
Investigation priorities
Confirm objective afferent dysfunction, quantify severity and provide a baseline for recovery.
Management branches
Vision declines over minutes to days with pain, colour change, field loss or an afferent pupil defect.
- Obtain exact onset and systemic symptoms and perform corrected monocular acuity, colour, fields, pupils, fundi and a complete neurological and ocular-motor examination.
- Arrange same-day ophthalmic or neuro-ophthalmic assessment to exclude retinal vascular, giant-cell-arteritis, pressure and structural emergencies, sending ESR, CRP and platelets immediately when arteritis is possible.
- Use dedicated MRI brain and orbits and specialist-selected serology or CSF to phenotype inflammation, then agree whether observation, high-dose steroid or another urgent treatment is appropriate.