Objective: To analyze the clinical characteristics, dynamic imaging changes, and treatment responses of methanol-induced toxic neuropathy. Additionally, it sought to explore the correlation between poisoning severity, intervention timing, and visual functional outcomes, so as to evidence-based insights for optimizing clinical diagnosis and treatment strategies. Methods: A case-series study combined with a literature review was conducted. Nine patients (18 eyes) diagnosed with methanol-induced toxic neuropathy at Zhongshan Ophthalmic Center, Sun Yat-sen University from 2017 to 2024, were retrospectively included. Clinical data, including pupillary changes, fundus photography, optical coherence tomography (OCT), visual field tests, and visual evoked potentials (VEP), were collected and integrated with findings from the literature. The inclusion criteria were a confirmed history of methanol exposure, acute vision loss accompanied by optic disc edema or retinal nerve fiber layer (RNFL) thickening, and elevated blood/urine methanol or formic acid levels. Patients with pre-existing poor vision or retinal diseases were excluded. Multimodal imaging was employed to evaluate the characteristics of optic nerve injury, and treatment responses and prognostic factors were analyzed. Results: The nine patients (18 eyes) ranged in age from 23–51 years (7 males, 2 females), with the time from poisoning to consultation spanning from 3 days to 3 months. The best-corrected visual acuity (BCVA) ranged from no light perception (NLP, 11 eyes) to 1.0. Pupillary abnormalities were observed in 66.7% (12/18 eyes) of the cases. Fundus examination showed optic disc edema, while VEP revealed reduced amplitude and visual field defects. OCT demonstrated RNFL thickening in the acute phase and progressive atrophy with an increased cup-to-disc ratio (C/D) in the chronic phase. After treatment, 12 eyes showed visual improvement (followed at 2 months; 4 eyes with post-poisoning BCVA of 1.0 were excluded from this analysis). Among patients with extended follow-up (4 months to 3 years), most reached a visual acuity plateau after acute-phase intervention, although a minority remained at risk of delayed neurodegenerative decline. Early intervention with systemic high-dose steroid therapy, hemodialysis, and neuroprotective treatment might improve visual function in some patients, whereas delayed treatment often led to irreversible vision loss. Patients with preserved pupillary light reflexes had more favorable prognoses. Conclusions: The prognosis of methanol-induced optic neuropathy is closely related to poisoning severity, intervention timing, and pupillary reflex status. Early high-dose steroid therapy combined with neuroprotective treatment may enhance outcomes in some patients; however, prolonged poisoning typically results in irreversible neurovisual damage. Personalized staged treatment and long-term visual function monitoring are essential for preserving residual vision.
