Methanol poisoning

Methanol poisoning can cause an acute toxic leukoencephalopathy with eventual chronic sequelae. Methanol is a clear and colourless liquid that can easily be mistaken for ethanol 1. Unlike ethanol, it is highly toxic (1 g/kg is considered a lethal dose of methanol) and not suitable for human consumption 1,2. It is instead used as a constituent of a large number of industrial and commercially available solvents, cleaning products and antifreeze liquids 1.

Methanol poisoning or intoxication is rare, and often occurs after suicidal or accidental oral ingestion of methanol-containing agents, or after consumption of adulterated or "moonshine" alcoholic beverages 1,2.

Patients can present with a variety of devastatingly disabling clinical features, often after a 12-24 hour latency:

  • visual disturbances characterised by optic neuritis and eventual blindness 1,3 
  • CNS features such as headache, dizziness, fatigue, and eventual permanent neurological dysfunction 1-3
  • gastrointestinal symptoms such as nausea, vomiting, and abdominal pain 1,4
  • severe uncompensated metabolic acidosis with a high anion gap 1,2,4
  • eventual coma and death are common 1,2

Methanol (CH3OH) is a simple alkanol which is first metabolised into formaldehyde by alcohol dehydrogenase 4. Formaldehyde is then nearly completely metabolised into formate (formic acid) by aldehyde dehydrogenase 4. Formate is highly toxic and inhibits cytochrome oxidase causing cell hypoxia (causing necrosis of tissue), metabolic acidosis, and optic nerve demyelination 4. It is thought that the putamen is particularly affected by this process due to its high metabolic demands 1, but this remains a subject of ongoing research. As this metabolisation process takes time, there is often a latency period of 12-24 hours before clinical features manifest 1,4

Methanol poisoning characteristically tends to bilaterally affect the putamen, optic nerves, and retina, but can also affect other basal ganglia nuclei, subcortical white matter, and cerebellum 1-3

CT brain

Classically seen as hypo-attenuation bilaterally in the putamen, reflective of putaminal necrosis 1. Other features include diffuse hypo-attenuation in cerebral white matter and haemorrhages 1.

MRI brain

Regions of involvement are similar to CT. Signal characteristics of the characteristic putaminal necrosis in the acute setting include:

  • T1: variable signal depending on presence of haemorrhage (high signal if present, otherwise low signal) 1,2
  • T2/FLAIR: affected areas demonstrate high signal 1,2
  • T1 C+ (Gd): enhancement is variable 2
  • DWI: affected areas show restricted diffusion in the acute phase 3

Furthermore, similar acute signal changes secondary to tissue necrosis may be noted of the optic nerves (also due to demyelination), subcortical white matter, and cerebellum 1,2. In the chronic phase, cystic cavities may develop in the putamen 2.

Treatment classically involves administration of intravenous ethanol, which has a much higher affinity (10-20 times greater) for alcohol dehydrogenase compared to methanol 1,4, in an effort to reduce the production of formate. This can be enhanced by administration of fomepizole or folinic acid 4. Additional treatment options including correcting metabolic acidosis with intravenous sodium bicarbonate, gastric lavage, and haemodialysis 1,4

For involvement in and around the putamen or basal ganglia, consider:

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Article information

rID: 51680
Section: Pathology
Synonyms or Alternate Spellings:
  • Methanol intoxication

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