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Toxic optic neuropathy
Neuro-Ophthalmology
Key Points
- •Toxic optic neuropathy presents as bilateral, symmetric, painless, progressive visual loss with cecocentral scotomas and dyschromatopsia - the papillomacular bundle is selectively vulnerable due to high metabolic demand and thin myelination
- •Ethambutol is the most important drug cause - baseline screening (VA, color vision, visual fields) BEFORE starting treatment and monthly monitoring during use; stop immediately at first sign of toxicity
- •Methanol poisoning is a medical emergency - metabolized to formic acid which inhibits cytochrome c oxidase; treat with fomepizole (alcohol dehydrogenase inhibitor), hemodialysis, and folate
- •Color vision loss (Ishihara plates) is often the earliest detectable sign of toxic optic neuropathy - it may precede visual acuity drop and is the key screening tool for ethambutol monitoring
- •All toxic/nutritional optic neuropathies share a common final pathway of mitochondrial dysfunction - this explains the clinical overlap with LHON (primary mitochondrial DNA defect)
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17 more sections are included with the Clinical plan.
- Definition
- Epidemiology
- Aetiology and causes
- Pathogenesis
- Classification
- Risk factors and associations