Etiologic spectrum and predictors of visual acuity in non-glaucomatous optic atrophy

To determine the prevalence and underlying causes of nonglaucomatous optic atrophy (NGOA) in a tertiary referral center in southeastern Iran and to identify predictors of current visual acuity in this population.

In this descriptive cross-sectional study, patients with a confirmed diagnosis of NGOA were included. All cases had a definitive etiologic diagnosis based on clinical evaluation, paraclinical investigations, and thorough review of medical records. Patients were classified into etiologic categories including hereditary or developmental disorders; secondary or consecutive optic atrophy; traumatic optic neuropathy (TON); compressive lesions; raised intracranial pressure-related involvement; inflammatory or demyelinating disease; infiltrative processes; toxic exposure; and ischemic causes.

A total of 155 eyes from 155 patients with NGOA were analyzed, of whom 86 (55.5%) were male. Overall, 75 patients (48.4%) had a best-corrected visual acuity (BCVA) of ≥ 1.90 logMAR (logarithm of the minimum angle of resolution), corresponding to counting fingers vision or worse. Patients with toxic optic neuropathy demonstrated the poorest visual outcomes, with 5 of 6 cases (83.3%) having a BCVA of ≥ 1.90 logMAR. Ischemic causes were the most prevalent etiology, identified in 46 patients (29.7%), including 45 cases of non-arteritic anterior ischemic optic neuropathy (AION). TON was the second most common cause, observed in 37 patients (23.9%). In multivariate analysis, a longer duration from symptom onset was the sole independent predictor of poorer current visual acuity (β = 0.253, P = 0.010).

Previous non-arteritic AION was the most common cause of NGOA in this cohort, followed by TON. Toxic exposure was associated with the poorest visual acuities. Among all evaluated variables, the duration from symptom onset was the only independent predictor of current visual acuity.