Methanol poisoning is a rare but extremely hazardous form of intoxication, generally occurring after suicidal or accidental events. Acute methanol poisoning produces severe metabolic acidosis and serious neurological symptoms including severe visual impairment, extrapyramidal signs, coma and death. The extent of permanent damage to CNS, retina and optic nerve depend on the amount of methanol ingested. Long term sequelae include optic neuropathy, blindness, Parkinsonism, dystonia, toxic encephalopathy, dementia and axonal polyneuropathy. We report a case of 40-year-old Indian man with methanol intoxication whose CT and MR imaging findings are described.

Introduction

Acute methanol poisoning produces severe metabolic acidosis and serious neurological symptoms including severe visual impairment, extrapyramidal signs, coma and death. The extent of permanent damage to CNS, retina and optic nerve depend on the amount of methanol ingested.1 Blindness is the most common symptom and persists after recovery from the intoxication. The occurrence of visual loss is probably related to individual idiosyncrasy to the drug because it does not occur in all cases of intoxication.2 Recently all of us have come across a number of newspaper reports of mortality and morbidity due to consumption of illicit liquor. But the history of alcohol intake may not always be forthcoming. We report a case of 40-year-old man with methanol intoxication whose CT and MR imaging finding provided a clue to the correct diagnosis. The toxicologic mechanisms of methanol poisoning are reviewed, the clinical findings and brain imaging studies with regard to diagnosis and prognosis has been discussed.

Case Report
A 40 yr old, non-diabetic, non-hypertensive chronic alcoholic Indian male, was referred for MR of brain and orbit to our hospital. Patient had a history of sudden onset of diminution of vision in both the eyes seven days ago associated with headache and episodes of vomiting. There was gradual loss of vision over a period of 7 days with almost complete blindness on admission. On examination, pupils were constricted with poor reaction to light. Fundoscopy revealed blurring of the optic disc. The blood pressure was 120/80 mmHg, pulse rate 90/min, respiration rate 30/min and temperature 37oC. The general and systemic examination otherwise did not reveal any abnormality. A chest radiograph, electrocardiograph, urinalysis, complete blood count, electrolytes, and blood glucose concentration were normal. CT scan of brain done on the previous day, revealed hypodense areas in the posteromedial aspect of the putamina bilaterally (Fig. 1A). MRI done in our hospital on a 1.5 Tesla scanner (GE Signa, Echospeed, Milwaukee, Wisc, USA) revealed, well-defined hypointense signal in the postero-medial aspect of the putamina bilateraly on T1 weighted images (Fig. 1B). These were hyperintense on T2 weighted images (Fig. 1C) and Flair images (Fig. 1D) and revealed subtle hyperintensity on the diffusion weighted images (Fig. 1E). Both the optic nerves appeared symmetrical and revealed normal signal on coronal STIR images (Fig. 1F). Taking CT and MR findings in consideration, possibility of substance abuse/toxicity was suspected. On enquiring in detail, history of drinking country liquor on the day prior to onset of symptoms was elicited. Taking the clnical and radiological findings in consideration, methanol intoxication was diagnosed which had occurred as a result of ingestion of illicit liquor. Arterial blood pH analysis done later, revealed severe metabolic acidosis with pH of 7.22 with increased anion gap. The blood methanol level was 120 mg/ml. The patient was put on haemodialysis. Marked visual deficit persisted with mere perception of light and hand movement.

Fig. 1 : A) Axial CT image through the basal ganglia reveals hypodense areas in the posteromedial aspect of the putamina bilaterally (marked by small white arrows) (B) Axial T1 W MR image reveals hypointense on axial T2 W image (C) (marked by small white arrows) and coronal flair image (D) (marked by small white arrows) (E) subtle hyperintensity on diffusion W images. (F) Both the optic nerves reveal normal signal intensity on coronal STIR image (marked by small white arrows).

Discussion

Methanol poisoning is a rare but extremely hazardous form of intoxication, generally occurring after suicidal or accidental events due to similarity of methanol to ethanol in appearance and odour.3 Methanol (wood spirit or methyl alcohol), a highly toxic substance, is used as industrial solvent in automobiles, in windshield wiper fluid, gasoline antifreeze, paint remover, de-icing solutions, varnish, photocopying fluid and in some eau de cologne.3 Besides being found in many household products and readily available at low cost, it has the general characteristics of being colourless, sweet smell and pleasant taste. This in a way attracts young children, and chronic alcoholic drinkers.4 Poisoning most commonly occurs via oral ingestion (accidental or deliberate), but may also occur by transdermal absorption or by inhalation. Methyl alcohol is also used as an inexpensive substitute during manufacture of illicit alcohol or in adulterated beverages which can result in poisoning.

Symptoms of methanol intoxication include nausea, vomiting, abdominal pain, dyspnoea, headache, dizziness, visual symptoms including blurring, dimming or blindness, flashes of light, “snowfield”, unsteadiness, confusion, coma, seizures and death. The lethal dose is 30-50 ml (0.5 ml/kg). Blindness can occur with as less as 10 ml.4 Signs of methanol intoxication include depressed level of consciousness, altered mental status, decreased visual acuity, visual field defects/scotomata, mydriasis, decreased pupillary response, hyperaemia of optic discs, peripapillary and retinal oedema (early) or glaucoma-like cupped/atrophic discs (late). Long term sequelae include optic neuropathy/blindness, Parkinsonism, dystonia, toxic encephalopathy, dementia and axonal polyneuropathy.3

Methanol itself is not toxic and depresses the brain to a lesser degree compared to ethanol. The mechanism of methanol toxicity is due to direct toxic effect of formic acid which is generated from methanol as well as injury secondary to anoxia and acidosis. Methanol is metabolized to formaldehyde by hepatic alcohol dehydrogenase and formaldehyde is converted to formic acid by aldehyde dehydrogenase, which in turn inhibits cytocrome oxidase, resulting in blockage of mitochondrial electron transport and ATP formation. High levels of formaldehyde do not appear in the blood, and toxic effects appear to be related to high levels of formic acid.5 The latent period (12 to 36 hrs) for the onset of symptoms corresponds to the time period in which the methanol is converted to formic acid.6 The clinical presentation of methanol intoxication can vary from patient to patient.7 Optic neuropathy and putaminal necrosis (haemorrhagic or nonhaemorrhagic) are two main complications of methanol poisoning.8 Putaminal necrosis is usually permanent, however in some series significant regression of neurologic findings and disappearance of extrapyramidal symptoms are reported. In addition to the optic nerve and putaminal lesions, brain oedema, brain necrosis, brain atrophy, caudate nucleus necrosis, and cerebral and cerebellar white matter signal changes can be seen in methanol intoxication. These changes are due to metabolites of methanol, hypoxaemia, severe acidosis and coexistent circulatory depression. Putaminal haemorrhagic necrosis, subcortical white matter changes, tegmental changes and optic nerve findings may indicate a poor prognosis. The defined changes in methanol intoxication can be seen with CT and MR. Ischaemic necrotic changes in the putamen are well seen on T2-weighted and IR (inversion recovery) sequences on MR1 as hyperintensities. Rarely complete recovery can occur even after severe intoxication if prompt early treatment is instituted.9

One hypothesis attributes the predilection for putaminal damage to the pattern of poor venous drainage.10 A recent hypothesis suggests that the greater susceptibility of optic nerve, macular area of retina and basal ganglia to anoxia and ischaemia following methanol intoxication is possibly due to their high metabolic rate. The pathogenesis of the white matter haemorrhagic necrosis remains unexplained.10

Bilateral putaminal lesions are found on MR in a variety of conditions including Wilson’s disease, hypoxic-ischaemic insults, encephalitis, Leigh’s syndrome, Kearns-Sayre syndrome, striatal degeneration associated with Leber’s optic atrophy and certain types of metabolic disorders. In addition, carbon monoxide inhalation and hypoxic - anoxic injuries such as near-drowning should be considered in the differential diagnosis. However in carbon monoxide poisoning specific focus of toxicity is the globus pallidus while hypoxic - anoxic injuries additionally involve the caudate nucleus and other central gray nuclei.1 The combination of optic atrophy and bilateral putaminal haemorrhagic infarctions is unique to methanol intoxication.

In conclusion, when symmetrical lesions are detected in the basal ganglia in cases of sudden blindness, methanol intoxication should be considered in the differential diagnosis. Early diagnosis may improve the prognosis in the acute phase.

References

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