Optic neuropathy: amiodarone-induced or anterior ischemic optic neuropathy?

Optic neuropathy in patients taking amiodarone presents a diagnostic challenge. The changes at the optic discs and the optic nerve dysfunction could be induced directly by amiodarone, could be the result of a nonarteritic anterior ischemic optic neuropathy or could be a combination of these two factors. Various clinical criteria for the diagnosis of amiodarone-induced optic neuropathy have been described during the past 5 years. These include bilateral, usually insidious, visual loss and protracted optic disc edema over several months. Ophthalmological examinations should be carried out within the first 12 months (and particularly within 4 months) of initiating amiodarone and subsequently. Discontinuation of amiodarone should be considered in patients presenting with clinical features of amiodarone-induced optic neuropathy. However, in those patients in whom the mechanism of optic neuropathy is indeterminate or likely to be due to anterior ischemia, continuation with amiodarone therapy would be appropriate. Future studies aimed at understanding the effect of amiodarone on optic nerve axon biochemistry, physiology and structure leading to optic neuropathy, as well as identifying the influence of amiodarone in the perfusion of the anterior optic nerve by altering the blood flow in the short posterior ciliary arteries, will improve our understanding of the association between amiodarone intake and optic neuropathy.