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Year : 2009  |  Volume : 57  |  Issue : 6  |  Page : 835--836

Methanol poisoning

Sameer Vyas1, Neeraj Kaur1, Navneet Sharma2, Paramjeet Singh1, Niranjan Khandelwal1,  
1 Department of Radiodiagnosis, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
Sameer Vyas
Department of Radiodiagnosis and Imaging, PGIMER, Chandigarh
India




How to cite this article:
Vyas S, Kaur N, Sharma N, Singh P, Khandelwal N. Methanol poisoning.Neurol India 2009;57:835-836


How to cite this URL:
Vyas S, Kaur N, Sharma N, Singh P, Khandelwal N. Methanol poisoning. Neurol India [serial online] 2009 [cited 2019 Jul 19 ];57:835-836
Available from: http://www.neurologyindia.com/text.asp?2009/57/6/835/59503


Full Text

A 22-year-old male presented with acute onset vomiting, diarrhea, abdominal pain and altered sensorium. He had a history of acute alcohol intake (locally made with solvent) a day prior to the presentation. Biochemical investigations revealed severe metabolic acidosis. Diagnosis of methanol poisoning was made on the basis of history and biochemical abnormality. Magnetic resonance imaging (MRI) done on fifth day revealed hemorrhagic putaminal necrosis, left occipital, corpus callosum and cerebellar cortical lesions [Figure 1],[Figure 2],[Figure 3],[Figure 4].

Acute methanol intoxication can occur as accidental or suicidal ingestion. Patients present acutely with acute neurological, visual and gastrointestinal symptoms. [1] Neuroimaging helps in establishing the clinical diagnosis of the methanol poisoning. MRI findings in methanol poisoning are characteristic and include hemorrhagic putaminal necrosis (most characteristic), subcortical and deep white matter lesions, cerebral and cerebellar cortical lesions, and midbrain lesions. [1],[2],[3],[4] Basal ganglia involvement is likely due to direct effect of metabolites of methanol as well as selective vulnerability of the basal ganglia to acidosis, as compared to rest of brain. Selective basal ganglia and white matter lesions are not specific to methanol intoxication and can be seen in hepatolenticular degeneration, carbon monoxide poisoning, hypoxic-ischemic insult and Leigh's disease. [4] Optic nerve lesions are considered to be due to myelinoclastic effect of formic acid and due to axonal loss. [3] Hemorrhage in methanol poisoning is seen in up to 14% of patients and diffusion restriction may be seen in the involved areas. [4] Index case showed almost entire spectrum of the MRI finding seen in the methanol poisoning.

References

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2Rubinstein D, Escott E, Kelly JP. Methanol intoxication with putaminal and white matter necrosis: MR and CT findings. AJNR Am J Neuroradiol 1995;16:1492-4.
3Hsu HH, Chen CY, Chen FH, Lee CC, Chou TY, Zimmerman RA. Optic atrophy and cerebral infarcts caused by methanol intoxication: MRI. Neuroradiology 1997;39:192-4.
4Sefidbakht S, Rasekhi AR, Kamali K, Borhani Haghighi A, Salooti A, Meshksar A, et al. Methanol poisoning: Acute MR and CT findings in nine patients. Neuroradiology 2007;49:427-35.