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Therapeutic Approaches for Toxic Optic Neuropathies: Insights from Methanol-Induced Optic Neuropathy and NAION Treatments
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Therapeutic Approaches for Toxic Optic Neuropathies: Insights from Methanol-Induced Optic Neuropathy and NAION Treatments
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Journal Article
Therapeutic Approaches for Toxic Optic Neuropathies: Insights from Methanol-Induced Optic Neuropathy and NAION Treatments
2025
Overview
Background/Objectives: Toxic optic neuropathy (TON) represents a spectrum of optic nerve damage caused by exposure to toxins, including drugs, alcohol, and industrial chemicals. It is characterized by progressive vision loss, dyschromatopsia, and optic nerve pallor and poses a clinical challenge in diagnosis and management due to overlapping features with other optic neuropathies. Non-arteritic anterior ischemic optic neuropathy (NAION), although distinct, shares common pathophysiological mechanisms such as oxidative stress and mitochondrial dysfunction. This review aims to evaluate therapeutic strategies applied in TON and discuss the potential role of NAION-targeted treatments in TON management. Methods: We reviewed medical therapies previously used in NAION patients, including corticosteroids and neuroprotective substances, and analyzed their relevance in the context of TON. Particular focus was given to emerging interventions targeting oxidative stress and mitochondrial health, including experimental drugs. Results: Evidence indicates that early diagnosis and toxin removal are essential in preventing irreversible vision impairment in TON. Therapies for methanol-induced and drug-related ocular neuropathies have demonstrated inconsistent efficacy, especially when integrated with antioxidant and neuroprotective approaches. However, the search for potential synergy between detoxification protocols and NAION-targeted treatments offers a promising direction for comprehensive management strategies. Conclusions: While current therapeutic options remain controversial and often unsatisfactory, integrating detoxification with interventions aimed at oxidative stress and mitochondrial function may improve outcomes. Further research is needed to develop targeted therapies for TON and bridge gaps in clinical decision-making.
