Optic neuropathy from amiodarone
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The antiarrhythmic agent, amiodarone (Cordone®, Pacerone®), has been reported to cause optic neuropathy. However, the clinical manifestations are similar to non-arteritic anterior ischemic optic neuropathy (AION), which makes diagnosing amiodarone optic neuropathy difficult. There is controversy whether or not amiodarone optic neuropathy actually exists as a distinct entity. The clinical manifestations and the proposed pathophysiology of amiodarone optic neuropathy are discussed.
Pathophysiology
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Teitelbaum, Bruce A. OD1; Castells, David D. OD1; Tresley, David J. MD2 Author Information
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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.
Discontinuation
Optic disc
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Abstract Toxic optic neuropathy ( TON ) is caused by the damage to the optic nerve through different toxins, including drugs, metals, organic solvents, methanol and carbon dioxide. A similar clinical picture may also be caused by nutritional deficits, including B vitamins, folic acid and proteins with sulphur‐containing amino acids. This review summarizes the present knowledge on disease‐causing factors, clinical presentation, diagnostics and treatment in TON . It discusses in detail known and hypothesized relations between drugs, including tuberculostatic drugs, antimicrobial agents, antiepileptic drugs, antiarrhythmic drugs, disulfiram, halogenated hydroquinolones, antimetabolites, tamoxifen and phosphodiesterase type 5 inhibitors and optic neuropathy.
Disulfiram
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