Objective:To present results of electrophysiologic investigations of the visual toxicity observed during the early stage of methanol poisoning.Design:Retrospective, clinical study.Setting:A 7-bed intensive care unit in a university hospital.Patients:Nineteen patients admitted with a diagnosis of acute methanol poisoning.Interventions:Visual evoked potentials were obtained within the first 48 hrs after admission; a clinical follow-up examination was performed in 11 patients, and 12 patients were followed up by visual evoked potentials beyond the same delay. Correlations between the occurrence of an optic neuropathy and clinical, biological, and electrophysiological data were studied.Measurements and Main Results:A significant correlation was found between arterial pH and blood formate concentration (r2= 0.58,p= .003), between blood formate and bicarbonate concentrations (r2= 0.36,p= .02), and between delay from ingestion and blood formate concentration (r2= 0.44,p= .017). Clinical outcome was correlated not only with the bicarbonate (p= .007), formate (p= .018), and methanol (p= .03) concentrations and arterial pH (p= .004) but also with a well-defined electrophysiologic pattern during the acute stage. An index of global cortical functioning ≥3 was associated with death, whereas a global cortical functioning index ≤2 was associated with survival (p= .0058). Moreover, a statistically significant difference in long-term visual impairment was found between the subgroup with abnormal wave III morphology or a global cortical functioning index of 1-2 and the subgroup with normal wave III morphology and a global cortical functioning index <1 (p= .015).Results of the electrophysiologic studies were expressed as retinal dysfunction and optic nerve injury. Five patients had normal findings on electrophysiologic examination. Ten patients had early signs of retinal dysfunction that were fully reversed in the eight patients who were followed. Ten patients had persistent electrophysiologic signs of optic neuropathy.Conclusions:Although reversible retinal dysfunction is evident in the early stage of human methanol poisoning, its absence does not preclude development of optic neuropathy. The occurrence of optic neuropathy and early electrophysiologic data are correlated.