ACUTE OCULAR METHANOL TOXICITY - CLINICAL AND ELECTROPHYSIOLOGICAL FEATURES

Citation
Mj. Mckellar et al., ACUTE OCULAR METHANOL TOXICITY - CLINICAL AND ELECTROPHYSIOLOGICAL FEATURES, Australian and New Zealand journal of ophthalmology, 25(3), 1997, pp. 225-230
Citations number
22
Categorie Soggetti
Ophthalmology
ISSN journal
08149763
Volume
25
Issue
3
Year of publication
1997
Pages
225 - 230
Database
ISI
SICI code
0814-9763(1997)25:3<225:AOMT-C>2.0.ZU;2-W
Abstract
Purpose: The present report describes previously undocumented changes in the electroretinogram (ERG) and visual-evoked response (VER) follow ing acute methanol ingestion and highlights the ocular effects of meth anol poisoning. Methods: Two cases oi acute ocular damage following me thanol ingestion are presented. One patient underwent extensive electr ophysiological and psychophysical testing. Results: Both patients repo rted transient visual disturbances. In each patient vision was 6/6 in both eyes at presentation but subsequently improved to 6/4. Colour vis ion (Ishihara plates) and pupillary reactions were normal. The optic d iscs 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 g eneralized depression of retinal sensitivity, an enlargement of one bl ind spot and paracentral scotomas. The scotopic ERG was subnormal with diminished a-and b-waveforms and the cone response to flicker was red uced. The pattern VER P2 waveform was normal in latency but decreased in amplitude. Conclusions: Acute methanol ingestion can cause characte ristic ocular damage, together with widespread electrophysiological dy sfunction. The data presented suggest that methanol affects the photor eceptors, Muller cells and the retrolaminar portion of the optic nerve .