A 24-year-old man presented with acute encephalopathy, hematemesis, and rigidity of
the extremities. He had anion gap metabolic acidosis. Osmolar gap was normal. Plasma
methanol level was 40 mg/dL. The [Figure] shows his neuroimaging findings.
Figure Hemorrhagic necrosis of bilateral lentiform nuclei (arrows) was present on head CT
(Panel A) and on non-contrast brain MRI (Panel B, T1-weighted; Panel C, T2/FLAIR-weighted;
Panel D, susceptibility-weighted imaging). Subcortical white matter hyperintensities
were also noted (Panel C, asterisks).
Treatment with fomepizole and hemodialysis improved his encephalopathy. No obvious
visual deficits were noted. There was generalized hypertonia and hyperreflexia, and
dystonia of the right arm.
Formic acid, an end product of methanol metabolism, contributes to metabolic acidosis
following methanol poisoning. Formate inhibits mitochondrial cytochrome oxidase, causing
histotoxic hypoxia that preferentially affects the retina, optic nerve, subcortical
white matter, and lentiform nucleus. Survivors may develop ophthalmologic abnormalities,
dystonia or parkinsonism[1],[2],[3].
