A 60-YEAR-OLD MAN WAS ADMITTED TO THE INTENSIVE care unit (ICU) 18 hours after having ingested 100 ml of methanol. On arrival, he was conscious but complained of blurred vision and changes in color perception. His visual acuity was estimated 20/100 in both eyes. Pupils were 4 mm and reactive, and fundoscopy did not reveal any significant change. The blood methanol level was 28.7 mmol/l and the plasma formate concentration was 18.16 mmol/l, while blood pH was 7.14 and serum bicarbonate level was 7 mmol/l. The patient received 100 mEq NaHCO 3 and 50 mg folinic acid, and antidotal therapy with fomepizole was started immediately with an intrave- nous loading dose of 1,050 mg (15 mg/kg). Continuous infusion of fomepizole (1 mg/kg per hour) was maintained during hemodialysis, performed over 18 hours. An addi- tional dose of 700 mg fomepizole (10 mg/kg) was given 12 hours after the loading dose. Flash electroretinogram (fERG) and flash visual evoked potentials (fVEPs) were obtained at the bedside 2 hours after admission (day 0), on day 1, and on day 8 (Figure 1). Both were elicited by LED goggles (monocular stimulation, red light, flash duration 200 s; rate 0.9/s) and recorded from needle electrodes. Pattern-reversal visual evoked potentials (pVEPs) were obtained on day 1 and day 8 by reversal of a black-and-white checkerboard (monocular stimulation, 4 check sizes: 1 degree, 30', 15', 7'30, rate 1.7/s). The pVEPs were recorded at one occipital location (Oz) referred to Cz with the same parameters as those used for fVEPs, except for the analysis time (250 ms). The plasma formate concentration at the time of elec- trophysiological recordings on days 0, 1, and 8 were, respectively, 18.16, 0.08, and 0.08 mmol/l (Nl 0.11 mmol/l). On day 0, the VEP peak III was markedly delayed (134 ms, Nl 95 ms) and the b-wave of the fERG was present but of low amplitude (1.5 V). On days 1 and 8, the ERG amplitude normalized (10 V) and peak III latency returned to normal. The pVEPs were normal on days 1 and 8. Twenty hours after admission, the patient did not complain of any visual impairment. He had recovered color perception and was able to read a newspaper. He had an uneventful follow-up after several weeks. Our patient met three criteria of severity for poor visual prognosis: admission after 18 hours, blood bicarbonate 7 mmol/l, and plasma formate 18.16 mmol/l. 1 This observa- tion is in accordance with our previous report on 17 methanol-poisoned patients treated by ethanol as a first choice antidote: a reversible retinal dysfunction could be observed at the early stage of methanol poisoning inde- pendently of the development of optic neuropathy. 2 Fur- thermore, it shows that fomepizole, a potent and long- acting competitive inhibitor of alcohol dehydrogenase, is safe and effective for reversing methanol-induced visual toxicity in a patient who already exhibits signs of visual impairment. 3 There was some concern regarding the use of fomepizole for patients who might develop visual impair- ment. It seems that fomepizole has the potential to inhibit retinol dehydrogenase, an isoenzyme of alcohol dehydro- genase. 4 This potential interference with vitamin A me- tabolism never appeared clinically significant, either in animal studies or in humans. 5 REFERENCES 1. Mahieu P, Hassoun A, Lauwerys R. Predictors of methanol intoxication with unfavorable outcome. Hum Toxicol 1989; 8:135–137. 2. Hantson P, de Tourtchaninoff M, Simoe ¨ns G, et al. Evoked potentials investigation of visual dysfunction after methanol poisoning. Crit Care Med 1999;27:2707–2715. 3. Sivilotti MLA, Burns MJ, Aaron CK, McMartin KE, Brent J. Reversal of severe methanol-induced visual impairment: no evidence of retinal toxicity due to fomepizole. J Toxicol Clin Toxicol 2001;39:627–631. 4. Ingemansson SO. Studies on the effect of 4-methylpyrazole on retinal activity in the methanol poisoned monkey by record- ing the electroretinogram. Acta Ophtalmol 1983;158(Suppl): 3–24. 5. Brent J, McMartin K, Phillips S, Aaron C, Kulig K, for the Methylpyrazole for Toxic Alcohols Study Group. Fomepizole for the treatment of methanol poisoning. N Engl J Med 2001;344:424 – 429. Reversible Cortical Blindness in Preeclampsia Diana V. Do, MD, Vivian Rismondo, MD, and Quan Dong Nguyen, MD, MSc PURPOSE: To report the clinical course and magnetic resonance imaging (MRI) findings in a 28-year-old woman with preeclampsia and reversible cortical blind- ness. DESIGN: Interventional case report. METHODS: The patient presented at the 37th week of pregnancy with headache and hypertension. The next day, her visual acuity decreased to light perception in both eyes. After emergent cesarean section, examination revealed reactive pupils and normal fundi. RESULTS: Magnetic resonance imaging of the brain showed areas of increased signal in both occipital lobes. One month later, at which time the patient’s visual acuity had returned to 20/20, follow-up MRI showed complete resolution of radiologic abnormalities. CONCLUSIONS: Cortical blindness is a rare complication of preeclampsia. In this case, cortical blindness was revers- ible and most likely due to vasogenic edema rather than Accepted for publication July 22, 2002. From the Wilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, and the Department of Ophthalmol- ogy, Greater Baltimore Medical Center, Baltimore, Maryland. Inquiries to Diana V. Do, MD, The Wilmer Eye Institute, The Johns Hopkins Hospital, 600 North Wolfe St, Wilmer B-20, Baltimore, MD 21287; e-mail: dianavdo@yahoo.com AMERICAN JOURNAL OF OPHTHALMOLOGY 916 DECEMBER 2002