Methanol Damages the Optic Nerve
Methanol (wood alcohol), not ethanol (drinking alcohol), is the type of alcohol that causes toxic optic neuropathy and can result in permanent, severe vision loss or blindness. 1, 2, 3
Mechanism of Optic Nerve Damage
Methanol itself is not directly toxic—the damage occurs through its metabolic byproduct:
- Formic acid (formaldehyde metabolite) causes histotoxic anoxia in watershed areas of the optic nerve circulation, leading to selective demyelination of the retrobulbar optic nerve segment just behind the lamina cribrosa 4
- The papillomacular bundle is preferentially affected because these small-caliber axons are rich in mitochondria and particularly vulnerable to metabolic toxicity 1
- Demyelination disrupts saltatory conduction, causing rapid vision loss, while axons may initially be preserved 4
Clinical Presentation
Vision loss from methanol is rapid, typically bilateral and symmetric, affecting central or centrocecal visual fields most severely: 3
- Fixed, dilated pupils are the most ominous prognostic sign and predict severe permanent vision loss even with treatment 3
- Initial fundus examination shows optic disc swelling in the acute phase 2
- Late-stage findings include optic atrophy with severe disc cupping (cup-to-disc ratios >0.9), mimicking glaucomatous damage due to ganglion cell loss 2
Diagnostic Findings
OCT demonstrates highly selective involvement of the papillomacular bundle: 1
- Ganglion cell layer (GCL) shows selective loss of nasal fibers corresponding to the papillomacular bundle 1
- Inner nuclear layer (INL) microcysts may appear in areas of GCL loss, representing non-specific damage 1
- RNFL may be initially preserved in milder cases, with selective GCL involvement 1
MRI findings include: 5
- Bilateral contrast enhancement in the retrobulbar segments of optic nerves 5
- Restricted diffusion on diffusion-weighted imaging in the retrobulbar optic nerves 5
Critical Distinction from Ethanol
The provided evidence regarding ethanol (drinking alcohol) and glaucoma is not relevant to toxic optic neuropathy. While chronic ethanol consumption shows weak associations with open-angle glaucoma through elevated intraocular pressure mechanisms 6, this represents a completely different pathophysiologic process than methanol's direct toxic demyelination of the optic nerve.
Prognosis
Even with prompt treatment (IV ethanol, hemodialysis, sodium bicarbonate), permanent severe vision loss frequently occurs if pupils are fixed and dilated at presentation 3. The pupillary status provides the best prognostic information for both visual morbidity and mortality 3.