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AJNR Awards, New Junior Editors, and more. Read the latest AJNR updates

Case of the Week

Section Editors: Matylda Machnowska1 and Anvita Pauranik2
1University of Toronto, Toronto, Ontario, Canada
2BC Children's Hospital, University of British Columbia, Vancouver, British Columbia, Canada

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March 10, 2022
  • Description
  • Legends
  • Diagnosis
  • Brain Teaser
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Methanol Toxicity

  • Background:
    • Methanol is oxidized into toxic formaldehyde and formic acid by alcohol dehydrogenase and formaldehyde dehydrogenase, respectively.
    • The toxic metabolites are neurotoxic, particularly to the optic nerves and putamina.
    • Note: After the neuroradiologist suggested methanol toxicity, the family confirmed methanol ingestion on the day the patient presented with myocardial infarction.
  • Clinical Presentation:
    • Dose-dependent and nonspecific manifestations range from blurry vision, nausea, vomiting, abdominal pain, drowsiness, confusion, seizures, coma, and even death if not treated.
  • Key Diagnostic Features:
    • Bilateral putaminal T2 prolongation and diffusion restriction, which can evolve to hemorrhagic necrosis
    • Similar changes are seen in the optic nerves, subcortical white matter, and caudate nuclei.
    • Uncommon areas of involvement are the corpus callosum, brainstem, and cerebellum.
  • Differential Diagnoses:
    • Carbon monoxide poisoning: Likely to involve the globus pallidus more than the putamen; injury of the cerebral cortex and subcortical white matter can also occur.
    • Anoxic brain injury: Variable pattern of involvement depending on brain maturity and severity of the ischemic insult; it can involve the basal ganglia, thalami, hippocampi, and cerebellum, or it can present as watershed infarcts; mostly nonhemorrhagic
    • Uremic encephalopathy: Symmetric swelling and edema of the lentiform nuclei with characteristic T2-hyperintense signal of the internal capsule, external capsule, and lamina terminalis (lentiform fork sign)
    • Osmotic demyelination syndrome: T2 prolongation of the central pons and/or extrapontine sites
    • Hypertensive hemorrhage: Basal ganglia hemorrhage is typically unilateral.
  • Treatment:
    • Antidote: Fomepizole or ethanol, which inhibit alcohol dehydrogenase, preventing the buildup of toxic metabolites
    • Supportive: Intravenous fluids and correction of electrolyte disturbances and acidemia

Suggested Reading

  1. Blanco M, Casado R, Vázquez F, et al. CT and MR imaging findings in methanol intoxication. AJNR Am J Neuroradiol 2006;27:452–54
  2. Halavaara J, Valanne L, Setälä K. Neuroimaging supports the clinical diagnosis of methanol poisoning. Neuroradiology 2002;44:924–28
  3. Rubinstein D, Escott E, Kelly JP. Methanol intoxication with putaminal and white matter necrosis: MR and CT findings. AJNR Am J Neuroradiol 1995;16:1492–94

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American Journal of Neuroradiology: 46 (6)
American Journal of Neuroradiology
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