Typical Clinical and Neuroimaging Features in Methanol Intoxication

D. Garg, D. Vibha, Varun Reddy, Parthiban Balasundaram, Leve Joseph, A. Pandit, R. Rajan, A. Srivastava, G. Shukla, K. Prasad
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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].
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甲醇中毒的典型临床和神经影像学特征
图1:一名慢性酒精依赖的40岁男性在非法饮酒后出现急性双侧视力下降、上腹不适和感觉改变。检查发现一个脱水的男性脑病没有脑膜刺激,局灶性缺陷或锥体外受累。眼底显示双侧乳头水肿。非对比CT扫描(图1a)显示低密度涉及壳核(黑色箭头)和皮层下白质(红色箭头),其在t1加权(T1W) MRI上呈低密度(图1b),在T2加权(图1c)和FLAIR(图1d)上呈高密度(图1d)。扩散加权成像(DWI)(图1f、g)和敏感性加权成像(SWI)(图1g(黄色箭头))可见扩散受限和微出血。T1W增强后图像显示外周壳层增强(图1h,(绿色箭头))。在两周的时间内,乙醇补充导致脑病逐渐消退,但没有导致视力丧失。甲醇代谢物甲酸酯的积累导致特异性内器官损伤[1]。福美唑和乙醇是有用的解毒剂。
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