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Drug-induced optical neuropathies
Last reviewed: 07.07.2025
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Ethambutol-induced drug-induced optic neuropathy
Ethambutol in combination with isoniazid and rifampicin is used to treat tuberculosis. Toxicity depends on the dose and duration of treatment and is 6% at a daily dose of 25 mg/kg (a dose of 15 mg/kg is rarely toxic). Toxicity may occur after 2 months of treatment (average 7 months).
Isoniazid may also cause toxic optic neuropathy, especially in combination with ethambutol.
It manifests itself as a symmetrical gradual deterioration of vision and dyschromatopsia,
Symptoms: normal or slightly edematous disc with streaky hemorrhages.
Visual field defects: central or centrocecal scotomas, may also have bitemporal or peripheral narrowing.
The prognosis after treatment is good, but recovery may take up to 12 months. In a small number of patients, persistent vision loss is associated with the development of optic nerve atrophy.
Screening should be performed at 3-month intervals if the daily dose exceeds 15 mg/kg. If symptoms of optic neuropathy occur, the drug should be stopped immediately.
Amiodarone-induced drug-induced optic neuropathy
Amiodarone is used to treat cardiac arrhythmias. Vortex keratopathy, which is harmless, occurs in almost everyone. Optic neuropathy develops in only 1-2% of patients, regardless of the dose.
It manifests itself as a gradual unilateral or bilateral deterioration of vision.
Symptoms: Bilateral papilledema persisting for several months after drug discontinuation.
Visual field defects may be small and reversible or large and permanent.
The prognosis is difficult, since discontinuing the drug may not result in improvement.
Screening is not performed because it does not help identify risk. However, patients should be warned of the possible risk of drug toxicity and should report any changes in vision,
Drug-induced optic neuropathy due to vigabatrin
Vigabatrin is an antiepileptic drug used as a second-line drug, except in cases of infantile spasm (Wesl syndrome). Many patients develop dyschromatopsia and visual field defects at a total dose of 1500 g or more. Defects develop within 1 month to several years after the start of treatment and often persist despite discontinuation of the drug. Visual field examinations are recommended at 6-month intervals.
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