Abstract

Toxic optic neuropathy (TON) refers to optic nerve involvement by toxins; however, retina and macula may also be involved. The toxins can be biological, chemical and iatrogenic agents. Toxic optic neuropathy can be aggravated by comorbidities especially nutritional and metabolic disorders. It manifests with vision loss, color vision defect and scotoma which may end up with optic atrophy. The retinal involvement may manifest with photopsia and metamorphopsia and may also result in optic nerve involvement. Iatrogenic etiology is the most common cause of TON and is mainly due to ethambutol, linezolid, amiodarone, etc. Chemotherapeutic agents such as methotrexate, cisplatin and vinca alkaloids are associated with TON. The diagnosis of TON is based on circumstantial evidence of exposure and known optic nerve toxicity and recovery on withdrawal. Monitoring of TON is done by serial evaluation of visual acuity, color vision and field charting. Majority of TON are associated with axonal changes which result in normal latency of P100 and small amplitude or non-recordable VEP. Retinal toxicity is dominated by chloroquine, topiramate, metronidazole, etc. It is important to have a high index of suspicion for the diagnosis of TON and withdraw the offending toxin as soon as possible.

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