Bezdicek O, Michalec J, Vaneckova M, Klempir J, Liskova I, Seidl Z, Janikova B, Miovsky M, Hubacek J, Diblik P, Kuthan P, Pilin A, Kurcova I, Fenclova Z, Petrik V, Navratil T, Pelclova D, Zakharov S, Ruzicka E
Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine and General University Hospital in Prague, Charles University in Prague, Czech Republic.
Department of Psychiatry, First Faculty of Medicine and General University Hospital, Charles University in Prague, Czech Republic.
Alcohol. 2017 Mar;59:27-35. doi: 10.1016/j.alcohol.2016.12.003. Epub 2016 Dec 10.
Methanol poisoning leads to lesions in the basal ganglia and subcortical white matter, as well as to demyelination and atrophy of the optic nerve. However, information regarding cognitive deficits in a large methanol sample is lacking. The principal aim of the present study was to identify the cognitive sequelae of methanol poisoning and their morphological correlates. A sample of 50 patients (METH; age 48 ± 13 years), 3-8 months after methanol poisoning, and 57 control subjects (CS; age 49 ± 13 years) were administered a neuropsychological battery. Forty-six patients were followed in 2 years' perspective. Patients additionally underwent 1.5T magnetic resonance imaging (MRI). Three biochemical and toxicological metabolic markers and a questionnaire regarding alcohol abuse facilitated the classification of 24 patients with methanol poisoning without alcohol abuse (METHna) and 22 patients with methanol poisoning and alcohol abuse (METHa). All groups were compared to a control group of similar size, and matched for age, education, premorbid intelligence level, global cognitive performance, and level of depressive symptoms. Using hierarchical multiple regression we found significant differences between METH and CS, especially in executive and memory domains. METHa showed a similar pattern of cognitive impairment with generally more severe executive dysfunction. Moreover, all METH patients with extensive involvement on brain MRI (lesions in ≥2 anatomical regions) had a more severe cognitive impairment. From a longitudinal perspective, we did not find any changes in their cognitive functioning after 2 years' follow-up. Our findings suggest that methanol poisoning is associated with executive dysfunction and explicit memory impairment, supposedly due to basal ganglia dysfunction and disruption of frontostriatal circuitry proportional to the number of brain lesions, and that these changes are persistent after 2 years' follow-up.
甲醇中毒会导致基底神经节和皮质下白质出现病变,以及视神经脱髓鞘和萎缩。然而,目前缺乏关于大量甲醇中毒患者认知缺陷的信息。本研究的主要目的是确定甲醇中毒的认知后遗症及其形态学关联。对50名甲醇中毒患者(METH组;年龄48±13岁,中毒后3 - 8个月)和57名对照者(CS组;年龄49±13岁)进行了一套神经心理学测试。对46名患者进行了为期2年的随访。患者还接受了1.5T磁共振成像(MRI)检查。通过三种生化和毒理学代谢标志物以及一份关于酒精滥用的问卷,将24名无酒精滥用的甲醇中毒患者(METHna)和22名有酒精滥用的甲醇中毒患者(METHa)进行了分类。将所有组与规模相似的对照组进行比较,并在年龄、教育程度、病前智力水平、整体认知表现和抑郁症状水平方面进行匹配。使用分层多元回归分析,我们发现METH组和CS组之间存在显著差异,尤其是在执行功能和记忆领域。METHa组表现出类似的认知障碍模式,总体上执行功能障碍更严重。此外,所有在脑MRI上有广泛病变(≥2个解剖区域有病变)的METH患者认知障碍更严重。从纵向角度来看,在2年的随访后,我们未发现他们的认知功能有任何变化。我们的研究结果表明,甲醇中毒与执行功能障碍和外显记忆损害有关,推测是由于基底神经节功能障碍以及额叶纹状体回路的破坏,且这种破坏与脑病变数量成正比,并且这些变化在2年的随访后仍然持续存在。