PURPOSE: The present report describes previously undocumented changes in the electroretinogram (ERG) and visual-evoked response (VER) following acute methanol ingestion and highlights the ocular effects of methanol poisoning. METHODS: Two cases of acute ocular damage following methanol ingestion are presented. One patient underwent extensive electrophysiological and psychophysical testing. RESULTS: Both patients reported transient visual disturbances. In each patient vision was 6/6 in both eyes at presentation but subsequently improved to 6/4. Colour vision (Ishihara plates) and pupillary reactions were normal. The optic discs were hyperaemic and swollen and retinal oedema extended along the major vascular arcades. There was cystoid macular oedema and 'pseudo cherry red spots' were observed. Automated field analysis revealed a generalized depression of retinal sensitivity, an enlargement of one blind spot and paracentral scotomas. The scotopic ERG was subnormal with diminished a- and b-waveforms and the cone response to flicker was reduced. The pattern VER P2 waveform was normal in latency but decreased in amplitude. CONCLUSIONS: Acute methanol ingestion can cause characteristic ocular damage, together with widespread electrophysiological dysfunction. The data presented suggest that methanol affects the photoreceptors, Muller cells and the retrolaminar portion of the optic nerve.
PURPOSE: The present report describes previously undocumented changes in the electroretinogram (ERG) and visual-evoked response (VER) following acute methanol ingestion and highlights the ocular effects of methanolpoisoning. METHODS: Two cases of acute ocular damage following methanol ingestion are presented. One patient underwent extensive electrophysiological and psychophysical testing. RESULTS: Both patients reported transient visual disturbances. In each patient vision was 6/6 in both eyes at presentation but subsequently improved to 6/4. Colour vision (Ishihara plates) and pupillary reactions were normal. The optic discs were hyperaemic and swollen and retinal oedema extended along the major vascular arcades. There was cystoid macular oedema and 'pseudo cherry red spots' were observed. Automated field analysis revealed a generalized depression of retinal sensitivity, an enlargement of one blind spot and paracentral scotomas. The scotopic ERG was subnormal with diminished a- and b-waveforms and the cone response to flicker was reduced. The pattern VER P2 waveform was normal in latency but decreased in amplitude. CONCLUSIONS: Acute methanol ingestion can cause characteristic ocular damage, together with widespread electrophysiological dysfunction. The data presented suggest that methanol affects the photoreceptors, Muller cells and the retrolaminar portion of the optic nerve.