Neurotoxicity to the Basal Ganglia Shown by Magnetic Resonance Imaging (MRI)

Hantson, Philippe; Duprez, T.; Mahieu, Paul

doi:10.3109/15563659709001186

Cited by 43 publications

(19 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[9][10][11][12][13][14] The earlier appropriate therapy is initiated for methanol or ethylene glycol ingestions, the better the outcome in preventing the serious consequences of blindness, renal dysfunction, neurotoxicity, acidemia, metabolic acidosis, pancreatitis, and death. [15][16][17] Therapies include altering the toxic alcohol's metabolism with antidotal treatment using ethanol, 8,15,18 fomepizole, 19,20 removal of the alcohols by hemodialysis, 13,18,21,22 supportive care with sodium bicarbonate, 13 and fluid resuscitation, 13 and the administration of adjuvant therapies (thiamine, pyridoxine, and leucovorin 2 ) appropriate to the toxin ingested.…”

mentioning

confidence: 99%

The Utility of an Alcohol Oxidase Reaction Test to Expedite the Detection of Toxic Alcohol Exposures

Hack

Chiang

Howland

et al. 2000

Academic Emergency Medicine

View full text Add to dashboard Cite

mentioning

confidence: 99%

The Utility of an Alcohol Oxidase Reaction Test to Expedite the Detection of Toxic Alcohol Exposures

Hack

Chiang

Howland

et al. 2000

Academic Emergency Medicine

View full text Add to dashboard Cite

“…[18] The characteristic clinicopathological fi ndings of methanol intoxication are optic neuropathy, bilateral putaminal hemorrhagic and non-hemorrhagic necrosis. [4] In two other reported cases, CT scans on the 1 st day appeared normal, but latter showed putaminal necrosis. [19] Bilateral putaminal necrosis is by no means specifi c to methanol toxicity and can also be seen in Wilson's disease, Leigh disease, Kearns-Sayre syndrome, striatal degeneration associated with Leber's optic atrophy, hypoxic-anoxic injuries and carbon monoxide poisoning.…”

Section: Discussionmentioning

confidence: 94%

“…[3] Putaminal necrosis is a characteristic fi nding in cases of methanol intoxication. [4] Clustering of all above defi cits in a sole patient has very rarely been described.…”

Section: Introductionmentioning

confidence: 97%

Methanol poisoning induced acute onset Parkinsonism, optic neuritis and peripheral neuropathy in a patient

Mangaraj¹,

Sethy²,

Sen³

et al. 2014

Int J Med Public Health

View full text Add to dashboard Cite

Methanol poisoning is a rare, but potentially life-threatening condition. It can result in signifi cant neurological toxicities such as optic neuritis, encephalopathy, ataxia, polyneuropathy and parkinsonism. Concomitant presence of optic neuritis, parkinsonism and peripheral neuropathy in a patient of methanol intoxication has been very rarely reported in the literature. We report a case of a young male who developed acute onset parkinsonism, optic neuritis and peripheral neuropathy with evidence of putaminal necrosis following methanol poisoning. Early therapy can salvage a patient as well as minimize potentially catastrophic complications. Despite adequate management, a signifi cant proportion of patients do develop devastating neurological defi cits, which plague them for the rest of their lives. Abstract Access this article onlineWebsite: www.ijmedph.org

show abstract

“…[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. 1,2,5 The basis for the selective vulnerability of these regions remains unknown.…”

Section: Discussionmentioning

confidence: 99%

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

Cader

Das

2015

J. Medicine

View full text Add to dashboard Cite

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

show abstract

Neurotoxicity to the Basal Ganglia Shown by Magnetic Resonance Imaging (MRI)

Abstract: Magnetic resonance imaging appeared as a well suited neuroimaging modality in methanol intoxicated patients both in revealing a specific pattern of brain lesions and in demonstrating valuable correlation between evolution of brain changes on magnetic resonance images and clinical outcome.

Cited by 43 publications

References 23 publications

The Utility of an Alcohol Oxidase Reaction Test to Expedite the Detection of Toxic Alcohol Exposures

The Utility of an Alcohol Oxidase Reaction Test to Expedite the Detection of Toxic Alcohol Exposures

Methanol poisoning induced acute onset Parkinsonism, optic neuritis and peripheral neuropathy in a patient

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

Contact Info

Product

Resources

About