Abstract
Many causes of toxic optic neuropathy have been described to date and novel causes of toxicity are continuously being added to the current literature. The pathophysiological basis for the toxicity or a direct causal relationship is yet to be determined for many of these agents. This review highlights the reports made over the last year about the commonly reported agents, with emphasis on the mechanisms of toxicity. Mitochondria of retinal ganglion cells and papillomacular bundle in particular could be the common target of many causes of toxic optic neuropathy, if not all. Agents or their metabolites responsible for the toxicity seem to interfere with the oxidative phosphorylation in mitochondria, causing a buildup of reactive oxidation species, energy depletion, oxidative stress, and activation of apoptosis. Further data are still necessary to understand how some of the usual suspects cause damage to the optic nerve or whether they indeed cause damage or not. A basic algorithm, as proposed, could be a useful addition to discriminate the novel causes of toxic optic neuropathy. See the Supplemental Digital Content 1 (http://links.lww.com/COOP/A11).
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