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Methyl alcohol poisoning III. Ocular toxicity
Archives of Ophthalmology (Chicago, Ill. : 1960)
|October 1, 1977
Summary
Methyl alcohol (methanol) causes optic disc edema in rhesus monkeys, mimicking increased intracranial pressure. This ocular toxicity is linked to axoplasmic flow stasis, impacting vision.
Area of Science:
- Ophthalmology
- Toxicology
- Neuroscience
Background:
- Methyl alcohol (methanol) is a known toxic substance with severe systemic effects.
- Ocular toxicity, particularly optic nerve damage, is a critical concern in methanol poisoning.
- Understanding the mechanism of methanol-induced optic neuropathy is essential for effective treatment.
Purpose of the Study:
- To investigate the ocular toxicity of methyl alcohol in a non-human primate model.
- To characterize the fundus changes associated with methyl alcohol ingestion.
- To elucidate the potential mechanism behind methyl alcohol-induced optic disc edema.
Main Methods:
- Six rhesus monkeys ingested methyl alcohol.
- Ophthalmoscopy and fundus photography were used to monitor ocular changes.
- Fluorescein fundus angiography was performed to assess retinal and choroidal circulation.
Main Results:
- All monkeys developed optic disc edema and associated fundus changes within 43-171 hours.
- Fluorescein angiography confirmed optic disc edema but showed normal retinal and choroidal circulation.
- The observed optic disc edema was clinically indistinguishable from that caused by increased intracranial pressure, though no such increase was detected.
Conclusions:
- Methyl alcohol ingestion causes significant optic disc edema in rhesus monkeys.
- The ocular findings in methanol poisoning resemble those of raised intracranial pressure but are not caused by it.
- Axoplasmic flow stasis is postulated as the underlying mechanism for optic disc edema in methyl alcohol poisoning.