Methanol poisoning is a cause of an acute toxic leukoencephalopathy that also has eventual chronic sequelae.


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 .

Clinical presentation

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

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


Methanol (CH3OH) is a clear and colourless simple liquid alkanol that can easily be mistaken for ethanol . Unlike ethanol, it is highly toxic (1 g/kg is considered a lethal dose of methanol) and not suitable for human consumption . It is instead used as a constituent of a large number of industrial and commercially available solvents, cleaning products and antifreeze liquids .

The increased toxicity compared to ethanol is due to its metabolism. Methanol is first metabolized into formaldehyde by alcohol dehydrogenase . Formaldehyde is then nearly completely metabolized into formate (formic acid) by aldehyde dehydrogenase . Formate is highly toxic respiratory chain metabolism toxin and inhibits cytochrome oxidase causing cell hypoxia (causing necrosis of tissue), metabolic acidosis, and optic nerve demyelination .

It is thought that the putamen is particularly affected by this process due to its high metabolic demands , but this remains a subject of ongoing research. As this metabolic process takes time, there is often a latency period of 12-24 hours before clinical features manifest .

Radiographic features

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 .


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


Regions of involvement are identical to those involved on CT. Signal characteristics of the characteristic putaminal necrosis in the acute setting include:

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

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

Treatment and prognosis

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

Differential diagnosis

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

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