Optic atrophy and cerebral infarcts caused by methanol intoxication: MRI

Hsu, Hui‐Chi; Chen, C. Y.; Chen, F. H.; Lee, C. C.; Chou, Ting-Ywan; Zimmerman, Robert A.

doi:10.1007/s002340050391

Cited by 43 publications

(38 citation statements)

References 7 publications

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“…1 CT and MR imaging demonstrate toxic effects of methanol in the central nervous system, and they have frequently been described in the literature. [1][2][3][4][5][6][7][8] The most well known CT and MRI finding of methanol intoxication is bilateral necrosis of the basal ganglia, primarily the putamen with or without haemorrhage. [1][2][3][4][5][6] Lesions can also extend into the corona radiata, centrum semiovale, hippocampus, optic nerve, tegmentum, cerebral grey matter and cerebellum, 1 optic nerves 4 and subcortical white matter, 1,5,6 produce diffuse cerebral oedema or separate necrotic lesions in the cerebral white matter.…”

Section: Discussionmentioning

confidence: 99%

Methanol Poisoning: An Unusual Case of White Matter Changes on MRI

Cader

Das

2015

J. Medicine

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A 47-year old Bangladeshi gentleman presented with the complaints of sudden onset bilateral blurring of visionfor 3 days with aggressive behaviour. The visual loss was acute, and the patient had become rather drowsy, with incoherent speech and tremors. There was no preceding history of trauma, fever, neck rigidity, limb weakness, seizures or other comorbidities requiring toxic drugs. On query, his relatives gave a history of chronic alcohol intake for over 10 years, possibly including methanol due to adulteration of ethyl alcohol. The patient had taken an alcoholic binge the night before to onset of symptoms. He was hypertensive, well controlled on amlodipine-atenolol combination.On examination, GCS was 15/15 (i.e. conscious) but he was delirious and extremely aggressive. Pulse was 96 beats/ min. Blood pressure was 95/60mmHg. Pupils were slightly dilated bilaterallywith sluggish reaction to light. Visual acuity was no perception of light (NPL). Ophthalmoscopy revealed bilateral optic atrophy (Figure 1). There was no nystagmus but extraocular muscles could not be tested owing to NPL. Other cranial nerves were intact and there was no focal neurological deficit, although higher psychic function was severely impaired. He also had retrograde amnesia. There were no abnormalities on other systemic examinations. Random blood sugar was 6.1mmol/L so hypoglycaemia as a cause for visual loss and delirium were effectively excluded. Serum electrolytes: Na + 141mmol/L. MRI of brain revealed lesions of subcortical white matter of both frontal lobes showing increased signal intensity signifying restricted diffusion on diffusion-weighted imaging (DWI), while on FSET2 and T2 FLAIR the same lesions showed hyperintensity.These findings were consistent with toxic myelinosis (Figure 2 a & b). Corpus callosum, optic chiasma, basal ganglia including the putamen, cerebellum, thalami, pituitary and para-sellar areas appeared normal in signal characteristics and morphology. J MEDICINE 2015; 16 : 64-66 . Fig. 2(a): MRI showing toxic myelinosis involving frontal lobe on DWI

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Section: Discussionmentioning

confidence: 99%

Methanol Poisoning: An Unusual Case of White Matter Changes on MRI

Cader

Das

2015

J. Medicine

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“…Its inhibition leads to anoxia and, furthermore, to cellular edema and cell death (histotoxic an-/hypoxia) [2,8,9,12].…”

Section: Discussionmentioning

confidence: 99%

“…The histotoxic an-/hypoxia causes a myelinoclastic effect. The loss of myelin leads to atrophy of the optic nerves and blindness [2,6,8,9,11].…”

Section: Discussionmentioning

confidence: 99%

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MRI of the Brain in Methanol Intoxication*

Albrecht

2008

Clin Neuroradiol

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“…Contrastenhanced MRI confirmed bilateral blood-brain barrier disruption on the putamina. We assumed that putaminal necrosis was associated with alcoholic intoxication such as methanol poisoning, but this finding is not specific and was also seen in a variety of conditions including Wilson and Leigh disease, Kearns-Sayre syndrome and various other neurodegenerative disorders [14][15][16][17][18] . The mechanism underlying selective putaminal necrosis is unknown.…”

Section: Discussionmentioning

confidence: 99%