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Toxic optic neuropathies

Ugur E Altiparmak

    Current Opinion in Ophthalmology
    |October 9, 2013
    PubMed
    Abstract

    Insights

    Toxic optic neuropathy can stem from various agents, often targeting retinal mitochondria. Recent findings suggest these agents disrupt cellular energy production, leading to oxidative stress and cell death, though mechanisms require further study.

    Area of Science:

    • Ophthalmology
    • Neuroscience
    • Toxicology

    Background:

    • Toxic optic neuropathy encompasses a range of conditions with diverse etiologies.
    • The precise mechanisms underlying optic nerve damage by many causative agents remain incompletely understood.

    Purpose of the Study:

    • To review recent literature on toxic optic neuropathy, focusing on commonly reported agents.
    • To elucidate the mechanisms of toxicity for various agents implicated in optic nerve damage.

    Main Methods:

    • Literature review of reports from the past year concerning toxic optic neuropathy.
    • Analysis of proposed pathophysiological mechanisms, with an emphasis on mitochondrial dysfunction.

    Main Results:

    • Mitochondria, particularly in retinal ganglion cells and the papillomacular bundle, are identified as a potential common target.
    • Agents or their metabolites appear to inhibit mitochondrial oxidative phosphorylation, leading to reactive oxygen species accumulation, energy depletion, oxidative stress, and apoptosis.

    Conclusions:

    • Further research is needed to confirm the causative role and specific mechanisms of common agents in optic nerve damage.
    • A proposed diagnostic algorithm may aid in identifying novel cases of toxic optic neuropathy.

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