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|Year : 2013 | Volume
| Issue : 3 | Page : 243-244
Bilateral putaminal hemorrhagic necrosis with rapid recovery of sensorium in a patient with methanol intoxication
T Srivastava, N Kadam
Department of Neurology, SMS Medical College and Hospitals, Jaipur, Rajasthan, India
|Date of Web Publication||12-Sep-2013|
Department of Neurology, SMS Medical College and Hospitals, Jaipur, Rajasthan
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Srivastava T, Kadam N. Bilateral putaminal hemorrhagic necrosis with rapid recovery of sensorium in a patient with methanol intoxication. J Postgrad Med 2013;59:243-4
|How to cite this URL:|
Srivastava T, Kadam N. Bilateral putaminal hemorrhagic necrosis with rapid recovery of sensorium in a patient with methanol intoxication. J Postgrad Med [serial online] 2013 [cited 2019 Oct 21];59:243-4. Available from: http://www.jpgmonline.com/text.asp?2013/59/3/243/118058
We present a case of acute methanol intoxication who presented with acute onset blindness after consumption of country liquor followed by encephalopathy. Magnetic resonance imaging (MRI) showed bilateral putaminal hemorrhagic necrosis. There was complete improvement in sensorium with residual visual deficit in the form of complete blindness initially at the time of presentation with absent perception of light (PL) and projection of light (PR) to finger counting at 1 feet on day 30 of presentation.
A 35-year-old man developed acute onset blindness 6 h after a binge of country liquor followed by encephalopathy. There were no focal deficits or meningeal signs. Electrocardiogram, hemogram, electrolytes, liver, and renal function tests and arterial blood gas analysis were normal. He was treated with intravenous fluids and supportive treatment in the form of thiamine and multivitamin oral preparations. The sensorium improved within 5 days. Visual acuity after 1 month was finger counting at one feet. Fundus examination showed bilateral optic atrophy. There was mild cogwheel rigidity in upper limbs. Brain computed tomography on day 30 showed hypodensity in both putamen [Figure 1]a. Brain MRI on day 30 revealed hyperintensity in both putamen on T1W image consistent with hemorrhagic necrosis [Figure 1]b, MRI T2W image showed hypointensity at putamen with surrounding mild edema [Figure 1]c. The differential diagnoses of putaminal necrosis with optic neuropathy are methanol intoxication, hydrogen sulfide toxicity, and Leigh's disease and other mitochondrial diseases. In this patient, diagnosis of methanol intoxication was considered in view of the temporal history of intake of binge of alcohol and encephalopathy with evidence of optic atrophy, Parkinsonism More Details, and bilateral putamen hemorrhage. Bilateral putaminal hemorrhagic necrosis is characteristic of methanol intoxication although not frequently encountered. Methanol is used as a solvent and antifreeze. Poisoning occurs due to accidental or suicidal ingestion and it is a common adulterant in country liquor. It is oxidized in the liver to formaldehyde, then to formic acid, which contributes to the profound metabolic acidosis, obtundation, visual disturbance, and sometime death. The imaging findings of bilateral hemorrhagic necrosis, cerebral and intra-ventricular hemorrhage, cerebellar necrosis, and diffuse cerebral edema have been described as sequelae to severe methanol intoxication.
|Figure 1: (a) Brain computed tomography on day 3 showed hypodensity in both putamen; (b) Brain magnetic resonance imaging (MRI) T1WI on day 30 revealed hyperintensity in both putamen consistent with hemorrhagic necrosis; (c) Brain MRI T2WI showed hypointensity at putamen with surrounding hyperintensity consistent with edema|
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Putaminal hemorrhagic necrosis results from direct toxic effect of methanol metabolites and metabolic acidosis. It has a poor prognosis, i.e., either death or vegetative state. ,,,, Most patients have white matter necrosis and diffuse cerebral edema along with putaminal hemorrhagic necrosis documented on MRI or at autopsy. ,,,, This is a case report of methanol intoxication with putaminal hemorrhagic necrosis, where the patient became conscious and alert. This could be attributed to the absence of diffuse cerebral edema.
| :: References|| |
|1.||Sefidbakht 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. |
|2.||Blanco M, Casado R, Vázquez F, Pumar JM. CT and MR imaging findings in methanol intoxication. AJNR Am J Neuroradiol 2006;27:452-4. |
|3.||Kuteifan K, Oesterlé H, Tajahmady T, Gutbub AM, Laplatte G. Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI. Neuroradiology 1998;40:158-60. |
|4.||Gaul HP, Wallace CJ, Auer RN, Fong TC. MR findings in methanol intoxication. AJNR Am J Neuroradiol 1995;16:1783-6. |
|5.||Feany MB, Anthony DC, Frosch MP, Zane W, De Girolami U. August 2000: Two cases with necrosis and hemorrhage in the putamen and white matter. Brain Pathol 2001;11:121-2, 125. |
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