Nonarteritic Anterior Ischaemic Optic Neuropathy – A Practical Overview for Junior Doctors

Zain Girach

Introduction

Non-arteritic anterior ischaemic optic neuropathy (NAION) is an important cause of sudden, usually painless monocular visual loss in adults over 50. It results from ischaemic injury to the optic nerve head and may leave a lasting visual field defect even when central acuity is relatively preserved. For the junior doctor, the immediate task is to recognise an acute optic neuropathy and arrange urgent ophthalmic assessment, with particular attention to excluding giant cell arteritis (GCA). This overview outlines the clinical features, investigation and management of NAION, including the recent safety advice concerning semaglutide (1,2).

Pathophysiology and risk factors

The precise initiating mechanism remains uncertain. Reduced perfusion of the optic nerve head, supplied largely by the short posterior ciliary circulation, is thought to trigger axonal swelling. In a structurally crowded optic disc, swelling may further compromise local perfusion and amplify injury. A small or absent physiological cup in the unaffected eye, often termed a “disc at risk”, supports this anatomical predisposition. NAION is not usually explained by an embolus in a large artery (1).

Associated conditions include hypertension, diabetes mellitus, dyslipidaemia and obstructive sleep apnoea. The history should therefore extend beyond the presenting eye complaint to vascular health, sleep symptoms and medication use. A patient may first notice the deficit on waking, but this is not a diagnostic requirement. The contribution of nocturnal hypotension remains debated; its proposed role should not prompt an automatic change to antihypertensive treatment (1–3).

Clinical presentation and examination

Patients commonly describe a fixed shadow, dimness or blurring in one eye. Loss of the upper or lower visual field can be more conspicuous than difficulty reading letters. Examination usually shows a relative afferent pupillary defect in unilateral disease, impaired visual function and sectoral or diffuse optic disc swelling, sometimes with peripapillary splinter haemorrhages. Automated perimetry frequently demonstrates an altitudinal or arcuate defect. An altitudinal defect is suggestive, but not specific to NAION (2,3).

Record visual acuity in each eye, colour vision, pupillary responses and visual fields, and examine both optic discs. Pain on eye movement, simultaneous bilateral involvement, an unusual age at presentation or a prolonged progressive course should prompt reconsideration of the diagnosis. Optic neuritis, compressive disease and other causes of disc swelling must remain in the differential (2,4).

Excluding arteritic disease

GCA is the most consequential alternative diagnosis in an older patient with acute optic neuropathy. Ask specifically about a new headache, scalp tenderness, jaw or tongue claudication, constitutional symptoms and symptoms of polymyalgia rheumatica. Severe visual loss with a pale swollen disc should increase concern. The absence of headache or other systemic symptoms does not reliably exclude GCA (5,6).

When GCA is suspected, obtain an urgent full blood count with platelet count, erythrocyte sedimentation rate and C-reactive protein. Normal inflammatory markers reduce the likelihood but do not eliminate it. Strong clinical suspicion, particularly with visual symptoms, requires immediate senior assessment and high-dose systemic glucocorticoids through the local GCA pathway. Treatment must not wait for temporal artery ultrasound or biopsy. This urgency differs fundamentally from the management of established NAION (5,6).

Table 1. Features that help distinguish acute optic neuropathies (2,4–7).

FeatureNAIONArteritic AION due to GCATypical demyelinating optic neuritis
Usual contextOlder adult with vascular risk factorsAdult over 50; systemic symptoms may be absentOften a younger adult
PainUsually absentHeadache or scalp tenderness may occurPain on eye movement is common
Optic discSwollen; haemorrhages may occurOften pale and swollenMay appear normal or swollen
Visual patternAltitudinal or arcuate loss is commonOften profound visual lossColour and central vision commonly affected
Immediate priorityUrgent assessment and exclusion of mimicsImmediate GCA assessment and treatmentSpecialist assessment; MRI and further tests as indicated

These are typical patterns rather than exclusion criteria. AION, anterior ischaemic optic neuropathy; MRI, magnetic resonance imaging.

Investigations

NAION is a clinical diagnosis; no single scan or blood test confirms it. Optical coherence tomography documents acute retinal nerve fibre layer swelling and subsequent thinning, while visual field testing provides a functional baseline. Neither should replace clinical assessment. MRI of the brain and orbits is useful when pain, persistent swelling or other atypical features raise concern for inflammation, compression or infiltration. Routine neuroimaging is not necessary in every typical presentation (2–4).

Systemic assessment should include blood pressure, glycaemic status and lipid profile. Ask about loud snoring, witnessed apnoeas and daytime sleepiness, and arrange assessment for suspected sleep apnoea. Observational studies have linked poor adherence to continuous positive airway pressure (CPAP) with fellow-eye involvement. This supports identifying and treating sleep apnoea, although it does not establish that CPAP reliably prevents a second NAION event (3,8).

Management and the limits of treatment

No treatment has been convincingly shown to restore vision reliably after NAION. This should be explained clearly, alongside the reasons for continued assessment and follow-up. The absence of a proven restorative treatment does not remove the need to exclude treatable alternative diagnoses or address systemic disease (3,4).

Optic nerve decompression surgery should not be offered for NAION. In the Ischemic Optic Neuropathy Decompression Trial, surgery failed to improve outcomes and was associated with more patients losing three or more lines of vision than careful follow-up alone. The trial also demonstrated why uncontrolled treatment reports are difficult to interpret: some patients improve spontaneously (9).

Corticosteroids remain controversial, but they are not an established routine treatment for NAION. A double-blind randomised trial involving 38 patients without diabetes found no significant difference in final visual acuity at six months between oral steroid and placebo groups. Faster resolution of disc swelling did not translate into a convincing clinical benefit. These findings should not be confused with the clear indication for urgent glucocorticoids in suspected GCA (5,10).

Longer-term care includes management of vascular risk factors, smoking cessation and treatment of sleep apnoea. These measures have wider health benefits, but should not be presented as proven protection against fellow-eye NAION. Review possible hypotension and relevant medicines with the prescribing clinician rather than stopping cardiovascular treatment indiscriminately. Aspirin has no established role in restoring sight or reliably preventing fellow-eye disease; any prescription should be justified by the individual’s cardiovascular indication and bleeding risk (3,4,11).

Semaglutide and NAION

Semaglutide has brought renewed attention to NAION. In February 2026, the Medicines and Healthcare products Regulatory Agency (MHRA) advised that semaglutide may very rarely be associated with the condition. Its review describes an approximately two-fold relative risk in adults with type 2 diabetes, corresponding to around one additional case per 10,000 treated people per year. The MHRA also notes conflicting evidence. Relative risk should therefore be discussed alongside the small absolute excess, rather than in isolation (12).

Medication history should include privately prescribed weight-loss treatments, which may be absent from the usual record. The MHRA advises urgent ophthalmic examination for sudden visual loss during semaglutide treatment and discontinuation if NAION is confirmed. Suspected adverse reactions should be reported through the Yellow Card scheme. These recommendations concern semaglutide specifically; the cited review did not establish an equivalent risk for every GLP-1 receptor agonist (12).

Prognosis and follow up

Recovery varies, and improvement in central acuity does not necessarily mean restoration of the visual field. Follow-up should assess function as well as the appearance of the optic disc. Persistent or renewed deterioration warrants reassessment rather than an assumption that it represents the expected course (3,4).

The possibility of involvement of the other eye is often a patient’s main concern. In the IONDT follow-up cohort, 48 of 326 patients at risk developed fellow-eye NAION over a median of 5.1 years, a cumulative proportion of 14.7%. Diabetes was associated with increased risk. This estimate provides a useful basis for counselling, but is not an individual prediction (11).

For junior doctors, the most useful approach is to recognise acute optic nerve dysfunction, actively consider GCA and ensure timely specialist assessment. Once NAION is established, honest discussion of treatment limitations, attention to systemic health and support for the functional effects of visual loss remain central to care.

References

1. Miller NR, Arnold AC. Current concepts in the diagnosis, pathogenesis and management of nonarteritic anterior ischaemic optic neuropathy. Eye (Lond). 2015;29(1):65–79. doi:10.1038/eye.2014.144.

2. Berry S, Lin WV, Sadaka A, Lee AG. Nonarteritic anterior ischemic optic neuropathy: cause, effect, and management. Eye Brain. 2017;9:23–28. doi:10.2147/EB.S125311.

3. North American Neuro-Ophthalmology Society. Non-Arteritic Anterior Ischemic Optic Neuropathy [Internet). (cited 2026 Oct 11). Available from: https://www.nanosweb.org/NAION/

4. American Academy of Ophthalmology. Non-Arteritic Anterior Ischemic Optic Neuropathy (NAION). EyeWiki [Internet). (cited 2026 Oct 11). Available from: https://eyewiki.aao.org/Non-Arteritic_Anterior_Ischemic_Optic_Neuropathy_(NAION)

5. Mackie SL, Dejaco C, Appenzeller S, et al. British Society for Rheumatology guideline on diagnosis and treatment of giant cell arteritis. Rheumatology (Oxford). 2020;59(3): e1–e23. doi:10.1093/rheumatology/kez672.

6. North American Neuro-Ophthalmology Society. Giant Cell Arteritis [Internet). (cited 2026 Oct 11). Available from: https://www.nanosweb.org/i4a/pages/index.cfm?pageid=4161

7. North American Neuro-Ophthalmology Society. Optic Neuritis [Internet). (cited 2026 Oct 11). Available from: https://www.nanosweb.org/i4a/pages/index.cfm?pageid=4191

8. Chang MY, Keltner JL. Risk factors for fellow eye involvement in nonarteritic anterior ischemic optic neuropathy. J Neuroophthalmol. 2019;39(2):147–152. doi:10.1097/WNO.0000000000000715.

9. The Ischemic Optic Neuropathy Decompression Trial Research Group. Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful. JAMA. 1995;273(8):625–632. doi:10.1001/jama.1995.03520320035038.

10. Saxena R, Singh D, Sharma M, James M, Sharma P, Menon V. Steroids versus no steroids in nonarteritic anterior ischemic optic neuropathy: a randomized controlled trial. Ophthalmology. 2018;125(10):1623–1627. doi:10.1016/j.ophtha.2018.03.032.

11. Newman NJ, Scherer R, Langenberg P, et al. The fellow eye in NAION: report from the ischemic optic neuropathy decompression trial follow-up study. Am J Ophthalmol. 2002;134(3):317–328. doi:10.1016/S0002-9394(02)01639-2.

12. Medicines and Healthcare products Regulatory Agency. Semaglutide (Wegovy, Ozempic and Rybelsus): risk of Non-arteritic Anterior Ischemic Optic Neuropathy (NAION). Drug Safety Update [Internet). 2026 Feb 5 [cited 2026 Oct 11). Available from: https://www.gov.uk/drug-safety-update/semaglutide-wegovy-ozempic-and-rybelsus-risk-of-non-arteritic-anterior-ischemic-optic-neuropathy-naion

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