Rare combination of bilateral putaminal necrosis, optic neuritis, and polyneuropathy in a case of acute methanol intoxication among patients met with hooch tragedy in Gujarat, India

Jarwani, Bhavesh; Motiani, Puja; Divetia, Ruchir; Thakkar, Gurudutta

doi:10.4103/0974-2700.102413

Cited by 10 publications

(10 citation statements)

References 6 publications

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“…Acidosis leads to tachypnoea or Kussmaul respiration as a compensator y mechanism. Acute methanol intoxication may progress to exitus due to nervous system depression (respiratory depression, cardiovascular collapse) [10,13].…”

Section: Results and Dscussionsmentioning

confidence: 99%

Study Regarding Correlation of the Methanol Intoxication and Tissues Necrosis

Knieling¹,

Matei²,

Iliescu³

et al. 2017

Rev. Chim.

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Methanol intoxication is a potentially fatal medical condition associated with basal ganglia and subcortical white matter necrosis. The authors present the case of a 34 years-old female with putaminal necrosis and haemorrhagic stroke secondary to methanol intoxication. The patient was hospitalized in the intensive care unit with severe metabolic acidosis and bilateral blindness after ingesting an unspecified amount of methanol. Computed tomography (CT) examination performed at hospital admission revealed a hypodense, inhomogeneous aspect of lenticular nuclei with ischemia in observation. In the 18th day post-ingestion the patient went into deep coma and a new CT examination was performed revealing an intracerebral hematoma involving the right lenticular nucleus, right external and extreme capsule, and right insula with uncal herniation. Neurosurgical decompression was attempted with unfavourable outcome and exitus. Necropsy examination revealed bilateral lenticular necrosis and a hematoma between the base of the right lenticular nucleus and insular cortex with destruction of the claustrum, external and extreme capsules. Methanol poisoning (mostly accidental) is not uncommon in our country and its metabolite, the formic acid, is a potent central nervous system toxin. Bilateral lenticular necrosis is a typical finding in methanol intoxication due to formic acid accumulation with decrease in mitochondrial adenosine triphosphate (ATP) synthesis responsible for cellular toxicity.

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Section: Results and Dscussionsmentioning

confidence: 99%

Study Regarding Correlation of the Methanol Intoxication and Tissues Necrosis

Knieling¹,

Matei²,

Iliescu³

et al. 2017

Rev. Chim.

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show abstract

“…Destek tedavi, kortikosteroid tedavi ve folik asid tedavisine rağmen duyu ve motor fonksiyonlarda düzelme görülmediği bildirilmiştir. Gelişen poliradikülopatinin patogenezinin tam olarak açıklanamayacağı bildirilmiştir (21). Santral ve periferik nörolojik sistemin tutulması nedeniyle literatüre dikkat çekici bir olgu olarak geçmiştir.…”

Section: Discussionunclassified

“…Santral ve periferik nörolojik sistemin tutulması nedeniyle literatüre dikkat çekici bir olgu olarak geçmiştir. Metanol intoksikasyonların-da bilateral putaminal nekroz ile birlikte polinöropatilerin de sekel olarak görülebileceği konusunda dikkatli olunması gerektiği ileri sürülmektedir (21). Bu çalışmada gelişen polinöropatinin etilen glikol intoksikasyonunda görülen polinö-ropati benzeri olduğu tartışılmış ancak öyküde etilen glikol alımı ile herhangi bir bilgi olmadığı görülmektedir.…”

Section: Discussionunclassified

Neuromuscular Functions on Experimental Acute Methanol Intoxication

Moral¹,

Çankayalı²,

Sergi̇n³

et al. 2015

Turk J Anaesth Reanim

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Objective: The incidence of accidental or suicidal ingestion of methyl alcohol is high and methyl alcohol intoxication has high mortality. Methyl alcohol intoxication causes severe neurological sequelae and appears to be a significant problem. Methyl alcohol causes acute metabolic acidosis, optic neuropathy leading to permanent blindness, respiratory failure, circulatory failure and death. It is metabolised in the liver, and its metabolite formic acid has direct toxic effects, causing oxidative stress, mitochondrial damage and increased lipid peroxidation associated with the mechanism of neurotoxicity. Methanol is known to cause acute toxicity of the central nervous system; however, the effects on peripheral neuromuscular transmission are unknown. In our study, we aimed to investigate the electrophysiological effects of experimentally induced acute methanol intoxication on neuromuscular transmission in the early period (first 24 h). Methods:After approval by the Animal Experiment Ethics Committee of Ege University, the study was carried out on 10 Wistar rats, each weighing about 200 g. During electrophysiological recordings and orogastric tube insertion, the rats were anaesthetised using intra-peritoneal (IP) injection of ketamine 100 mg kg −1 and IP injection of xylazine 10 mg kg −1 . The rats were given 3 g kg −1 methyl alcohol by the orogastric tube. Electrophysiological measurements from the gastrocnemius muscle were compared with baseline.Results: Latency measurements before and 24 h after methanol injection were 0.81±0.11 ms and 0.76±0.12 ms, respectively. CMAP amplitude measurements before and 24 h after methanol injection were 9.85±0.98 mV and 9.99±0.40 mV, respectively. CMAP duration measurements before and 24 h after methanol injection were 9.86±0.03 ms and 9.86±0.045 ms, respectively. Conclusion:It was concluded that experimental methanol intoxication in the acute phase (first 24 h) did not affect neuromuscular function.

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“…It is also used as a cheap adulterant of illicit liquors. The most severe consequences of methanol intoxication are blindness, a profound metabolic acidosis, and various forms of neurological impairment [63,64]. Its toxicity mainly stems from its toxic metabolites (formaldehyde and formic acid), which inhibit cytochrome oxidase in the retina and impair mitochondrial function [65,66].…”

Section: Methanolmentioning

confidence: 99%