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Related Experiment Video

Updated: Apr 25, 2026

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
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Toxic optic neuropathies: an updated review.

Andrzej Grzybowski1,2, Magdalena Zülsdorff1, Helmut Wilhelm3

  • 1Department of Ophthalmology, Poznań City Hospital, Poznań, Poland.

Acta Ophthalmologica
|August 28, 2014
PubMed
Summary

Toxic optic neuropathy (TON) damages the optic nerve via toxins like drugs and solvents, or nutritional deficits. This review covers TON causes, symptoms, diagnosis, and treatments, focusing on drug-induced optic nerve damage.

Keywords:
Leber's hereditary optic neuropathyadalimumab optic neuropathyantitumor necrosis factor alpha optic neuropathycuban epidemic optic neuropathyethambutol optic neuropathyinfliximab optic neuropathynutritional optic neuropathytobacco-alcohol amblyopiatoxic optic neuropathy

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Area of Science:

  • Ophthalmology
  • Toxicology
  • Neurology

Background:

  • Toxic optic neuropathy (TON) results from optic nerve damage due to various exogenous and endogenous factors.
  • Common causes include exposure to drugs, metals, organic solvents, and nutritional deficiencies (e.g., B vitamins, folic acid).

Purpose of the Study:

  • To review and synthesize current knowledge on the etiology, clinical presentation, diagnostic approaches, and management of TON.
  • To specifically examine the association between various pharmaceutical agents and the development of optic neuropathy.

Main Methods:

  • Comprehensive literature review of studies investigating toxic optic neuropathy.
  • Analysis of reported cases and etiological factors, with a focus on drug-induced TON.
  • Synthesis of information on clinical manifestations, diagnostic criteria, and treatment strategies.

Main Results:

  • Identified a wide range of toxins implicated in TON, including industrial chemicals and medications.
  • Detailed the clinical spectrum of TON, emphasizing visual field defects and visual acuity reduction.
  • Highlighted the complex relationship between specific drug classes (e.g., tuberculostatic, antiepileptic, antiarrhythmic drugs) and optic nerve damage.

Conclusions:

  • TON is a significant cause of vision loss, often linked to specific toxic exposures, particularly medications.
  • Accurate diagnosis requires a thorough history of exposures and clinical evaluation.
  • Management strategies depend on the causative agent, with early identification and removal of the toxin being crucial.