Methanol Induced Optic Neuropathy: Molecular Mysteries, Public Health Perspective, Clinical Insights and Treatment Strategies.

Abstract

Methanol-induced optic neuropathy (MION) represents a critical public health issue, particularly prevalent in lower socioeconomic populations and regions with restricted alcohol access. MION, characterized by irreversible visual impairment, arises from the toxic metabolization of methanol into formaldehyde and formic acid, leading to mitochondrial oxidative phosphorylation inhibition, oxidative stress, and subsequent neurotoxicity. The pathogenesis involves axonal and glial cell degeneration within the optic nerve and potential retinal damage. Despite advancements in therapeutic interventions, a significant proportion of affected individuals endure persistent visual sequelae. The study comprehensively investigates the pathophysiology of MION, encompassing the absorption and metabolism of methanol, subsequent systemic effects, and ocular impacts. Histopathological changes, including alterations in retinal layers and proteins, Müller cell dysfunction, and visual symptoms, are meticulously examined to provide insights into the disease mechanism. Furthermore, preventive measures and public health perspectives are discussed to highlight the importance of awareness and intervention strategies. Therapeutic approaches, such as decontamination procedures, ethanol and fomepizole administration, hemodialysis, intravenous fluids, electrolyte balance management, nutritional therapy, corticosteroid therapy, and erythropoietin (EPO) treatment, are evaluated for their efficacy in managing MION. This comprehensive review underscores the need for increased awareness, improved diagnostic strategies, and more effective treatments to mitigate the impact of MION on global health.