PURPOSE

To identify the specifics of structural and functional changes in patients with toxic optical neuropathy caused by acute methanol poisoning.

MATERIAL AND METHODS

One female patient with toxic optic neuropathy (TON), 2 male patients with partial optic atrophy caused by methanol poisoning, and 1 male patient with methanol intoxication after ethanol containing alcohol use were examined with kinetic perimetry and optical coherence tomography.

RESULTS

Patients with TON caused by acute methanol poisoning were observed to have decreasing visual acuity to the extent of complete blindness. OCT follow-up studies revealed thinning of the retinal nerve fiber layer (RNFL) as well as formation of microcysts in the inner retinal layers, destruction of ellipsoid zone and outer segments of photoreceptors. The patient with methanol intoxication after use of ethanol containing alcohol had retained his visual functions; he was found to have microcysts and RNFL thinning during the first few months after the intoxication, but they were within normal range of OCT parameters.

CONCLUSION

Patients with TON caused by acute methanol poisoning are common to have optic atrophy with either residual visual functions or complete blindness as well as microcysts formation, structural changes and destruction of the ellipsoid zone and outer segments of photoreceptors. In patient with methanol intoxication after use of ethanol, which is known to be an antidote, complete visual recovery was observed, although some microcystic changes and ganglion cells layer thinning were noted.