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NEURORADIOLOGY Table of Contents   
Year : 2005  |  Volume : 15  |  Issue : 3  |  Page : 341-342
Bilateral putaminal necrosis caused by methanol intoxication- A case report

From the Nijjar Scan & Diagnostic Centre, Amritsar, India

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Keywords: Putaminal necrosis; Methanol intoxication

How to cite this article:
Arora V, Nijjar I S, Thukral H, Roopa. Bilateral putaminal necrosis caused by methanol intoxication- A case report. Indian J Radiol Imaging 2005;15:341-2

How to cite this URL:
Arora V, Nijjar I S, Thukral H, Roopa. Bilateral putaminal necrosis caused by methanol intoxication- A case report. Indian J Radiol Imaging [serial online] 2005 [cited 2021 Mar 2];15:341-2. Available from:
Methanol, a highly toxic substance, is readily available as a component of many household products like antifreeze, paint removers, various solvents, cleaners and cologne. Its similarity to ethanol in appearance and odour leads to accidental use. Acute methanol poisoning produces severe metabolic acidosis and serious neurologic symptoms including severe visual impairment, extrapyramidal signs and coma. We describe a twenty eight year old man with methanol intoxication whose MRI showed bilateral necrosis of the putamen.

   Case report Top

A twenty eight year old man accidentally ingested spirit mistaking it for alcohol.

Twelve hours after ingestion he had nausea with vomiting and extreme drowsiness. He was referred for an MRI twenty four hours after ingestion.

MRI demonstrated bilateral Putaminal lesions, appearing hypointense on T1 W images [Figure - 1] and hyperintense on T2 W images [Figure - 2] suggestive of non haemorrhagic necrosis. No abnormal signal was identified in the optic nerves.

About ten hours after MRI examination, the patient developed blurred vision and motor dysfunction including rigidity and hypokinesis.

Now, five months later, the patient is well oriented but has persisting visual and extrapyramidal symptoms.

   Discussion Top

For more than 80 yrs, methanol has been known to produce several types of toxicity in the human nervous system [1]. Major methanol poisoning is one that affects the optic nerve and the CNS with a predilection for basal ganglia, showing symptoms of visual disturbance, blindness, drowsiness, seizure and coma [2],[3]. When a large amount of methanol is ingested, death usually occurs within 3 days [4]. Rarely complete recovery can follow after even a severe intoxication if prompt treatment is instituted early [5].

The mechanism of methanol toxicity has closely been linked to the effect of formic acid generated from methanol by alcohol dehydrogenase [4].

Characteristic clinical- pathological findings of methanol intoxication are optic neuropathy and bilateral Putaminal haemorrhagic and non haemorrhagic necrosis [6].

However, bilateral putaminal necrosis is by no means specific to methanol toxicity and can also be seen in Wilson's disease, Leigh Disease, Kearns-Sayre Syndrome and strial degeneration associated with Leber's optic atrophy [7]. In addition to these pathologies, carbon monoxide inhalation and hypoxic/anoxic injuries such as near-drowning should be considered as differential diagnosis. Moreover in carbon monoxide poisoning specific focus of toxicity is the globus pallidus and hypoxic/anoxic injuries additionally involve the caudate nucleus and other central grey nuclei [6].

In methanol intoxication putaminal necrosis is usually permanent, however in some series significant regression of neurologic findings and disappearance of extrapyramidal symptoms are reported [6].

Treatment is by drug elimination (for example, haemodialysis) and inhibition of metabolism of methanol to toxic formic acid by competitive inhibition of the enzyme alcohol dehydrogenase (ethyl alcohol or fomepizole) [8].

Our report illustrates the usual consequences of methanol intoxication on the nervous system. The lesion site is restricted to the bilateral putamen, as in most similar reports in the literature. In conclusion, when symmetrical lesions are detected in the basal ganglia along with visual disturbance, methanol intoxication should be considered in the differential diagnosis. Early diagnosis may improve the prognosis in the acute phase.

   References Top

1.Roe O. Methanol Poisoning. Acta med Scand. 1946 Supl. 182: 1-253.  Back to cited text no. 1    
2.Koopmans RA, Li DKB, Paty DW. Basal ganglia lesion in methanol poisoning: MR appearance. J ComputTomogr 1988; 12:168-9.  Back to cited text no. 2    
3.Pelletier J, Habib MH, Khalil R, Salamon G, Bartoli D, Jean P. Putaminal necrosis after methanol intoxication. J Neurol Neurosurg Psychiatry 1992 55(3):234-5.  Back to cited text no. 3    
4.David S Younger. Pollutants and industrial hazards. In: Merritt's Textbook of Neurology. Ed, Lewis P. Rowland. Ninth edition. Baltimore: Williams and Wilkins, 1995; pp 992-993.  Back to cited text no. 4    
5.Aquilonius SM, Askmark H, Enoksson P, Lundberg PO, Mostrom U. Computerised tomography in severe methanol intoxication. Br Med J 1978; Sep 30;2(6142):929-30.  Back to cited text no. 5    
6.Hantson P, Duprez T, Mahieu P. Neurotoxicity to the basal ganglia shown by magnetic resonance imaging (MRI) following poisoning by methanol and other substances. J Toxicol Clin Toxicol. 1997;35(2):151-61.  Back to cited text no. 6    
7.Koopmans RA, Li DK, Paty DW. Basal ganglia lesions in methanol poisoning: MR appearance. J Comput Assist Tomogr. 1988 Jan-Feb;12(1):168-9.  Back to cited text no. 7    
8.Cursiefen C, Bergua A. Acute bilateral blindness caused by accidental methanol intoxication during fire "eating". British Journal of Ophthalmology. 2002;86:1064-1065.  Back to cited text no. 8    

Correspondence Address:
V Arora
Nijjar Scan & Diagnostic Centre, Amritsar 143001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-3026.29149

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[Figure - 1], [Figure - 2]

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