D. Garg, D. Vibha, Varun Reddy, Parthiban Balasundaram, Leve Joseph, A. Pandit, R. Rajan, A. Srivastava, G. Shukla, K. Prasad
{"title":"甲醇中毒的典型临床和神经影像学特征","authors":"D. Garg, D. Vibha, Varun Reddy, Parthiban Balasundaram, Leve Joseph, A. Pandit, R. Rajan, A. Srivastava, G. Shukla, K. Prasad","doi":"10.4172/2161-0495.1000i102","DOIUrl":null,"url":null,"abstract":"Figure 1: A 40-year-old male with chronic alcohol dependence presented to us with acute bilateral visual diminution, epigastric discomfort, and altered sensorium after a binge involving illicit liquor. Examination revealed a dehydrated male in encephalopathy without meningeal irritation, focal deficits or extrapyramidal involvement. Fundus showed bilateral papilledema. Non-contrast CT scan (Figure 1a) showed hypodensities involving putamen (black arrows) and subcortical white matter (red arrows), which were hypointense on T1-weighted (T1W) MRI (Figure 1b), hyperintense on T2 weighted image (Figure 1c) and FLAIR (Figure 1d). Diffusion restriction and microhemorrhages were seen on diffusion-weighted imaging (DWI) (Figures 1f, g) and susceptibility weighted imaging (SWI) (Figure 1g (yellow arrows)). T1W postgadolinium images showed peripheral putaminal enhancement (Figure 1h, (green arrows)). Ethanol supplementation led to gradual resolution of encephalopathy but not visual loss, over a period of two weeks. Accumulation of methanol metabolite formate leads to specific endorgan damage [1]. Fomepizole and ethanol are useful antidotes [2].","PeriodicalId":15433,"journal":{"name":"Journal of Clinical Toxicology","volume":"33 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Typical Clinical and Neuroimaging Features in Methanol Intoxication\",\"authors\":\"D. Garg, D. Vibha, Varun Reddy, Parthiban Balasundaram, Leve Joseph, A. Pandit, R. Rajan, A. Srivastava, G. Shukla, K. Prasad\",\"doi\":\"10.4172/2161-0495.1000i102\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Figure 1: A 40-year-old male with chronic alcohol dependence presented to us with acute bilateral visual diminution, epigastric discomfort, and altered sensorium after a binge involving illicit liquor. Examination revealed a dehydrated male in encephalopathy without meningeal irritation, focal deficits or extrapyramidal involvement. Fundus showed bilateral papilledema. Non-contrast CT scan (Figure 1a) showed hypodensities involving putamen (black arrows) and subcortical white matter (red arrows), which were hypointense on T1-weighted (T1W) MRI (Figure 1b), hyperintense on T2 weighted image (Figure 1c) and FLAIR (Figure 1d). Diffusion restriction and microhemorrhages were seen on diffusion-weighted imaging (DWI) (Figures 1f, g) and susceptibility weighted imaging (SWI) (Figure 1g (yellow arrows)). T1W postgadolinium images showed peripheral putaminal enhancement (Figure 1h, (green arrows)). Ethanol supplementation led to gradual resolution of encephalopathy but not visual loss, over a period of two weeks. Accumulation of methanol metabolite formate leads to specific endorgan damage [1]. Fomepizole and ethanol are useful antidotes [2].\",\"PeriodicalId\":15433,\"journal\":{\"name\":\"Journal of Clinical Toxicology\",\"volume\":\"33 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Clinical Toxicology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4172/2161-0495.1000i102\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Clinical Toxicology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4172/2161-0495.1000i102","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Typical Clinical and Neuroimaging Features in Methanol Intoxication
Figure 1: A 40-year-old male with chronic alcohol dependence presented to us with acute bilateral visual diminution, epigastric discomfort, and altered sensorium after a binge involving illicit liquor. Examination revealed a dehydrated male in encephalopathy without meningeal irritation, focal deficits or extrapyramidal involvement. Fundus showed bilateral papilledema. Non-contrast CT scan (Figure 1a) showed hypodensities involving putamen (black arrows) and subcortical white matter (red arrows), which were hypointense on T1-weighted (T1W) MRI (Figure 1b), hyperintense on T2 weighted image (Figure 1c) and FLAIR (Figure 1d). Diffusion restriction and microhemorrhages were seen on diffusion-weighted imaging (DWI) (Figures 1f, g) and susceptibility weighted imaging (SWI) (Figure 1g (yellow arrows)). T1W postgadolinium images showed peripheral putaminal enhancement (Figure 1h, (green arrows)). Ethanol supplementation led to gradual resolution of encephalopathy but not visual loss, over a period of two weeks. Accumulation of methanol metabolite formate leads to specific endorgan damage [1]. Fomepizole and ethanol are useful antidotes [2].