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韦尼克脑病中的胼胝体萎缩

Corpus callosum atrophy in Wernicke's encephalopathy.

作者信息

Lee Soon-Tae, Jung Young-Min, Na Duk L, Park Seong Ho, Kim Manho

机构信息

Department of Neurology, Seoul National University Hospital, 28 Youngon-Dong, Chongno-gu, Seoul 110-744, South Korea.

出版信息

J Neuroimaging. 2005 Oct;15(4):367-72. doi: 10.1177/1051228405278352.

DOI:10.1177/1051228405278352
PMID:16254403
Abstract

BACKGROUND AND PURPOSE

Neuropathologic changes in Wernicke's encephalopathy (WE) involve variable brain structures. Corpus callosum involvement in WE, however, is largely unknown. The authors investigated the degree and the pattern of corpus callosum changes in WE according to the etiologies.

METHODS

Nineteen patients with WE (between 34 and 81 years) and 19 age- and sex-matched control participants were included. The total cross-sectional callosal area and 5 callosal subregions (C1-C5) were measured by tracing outer margins in the midsagittal sections. Subregions were determined by placing radial dividers with 10 rays. The pixel numbers for corpus callosums were calculated, and the values obtained were adjusted for head size variations.

RESULTS

The causes of WE were alcoholism (10), intestinal surgery (5), anorexia (3), and hyperemesis gravidarum (1). The mean size of the total corpus callosum was significantly reduced in alcoholic WE (P< .001; 527.8 +/- 70.8 mm2 for alcoholic WE; 664.6 +/- 58.1 mm2 for the corresponding controls), but not in nonalcoholic WE. In subregion analysis, prefrontal callosum (C2) atrophy was the most prominent in alcoholic WE. In contrast, only splenium (C5) was atrophied in nonalcoholic WE. The degree of atrophy did not change throughout the follow-up period (mean 5.3 weeks).

CONCLUSION

This study suggests that the extent and location of corpus callosum atrophy differs between alcoholic WE and nonalcoholic WE, implying separate contribution of alcohol neurotoxicity and nutritional deficiency.

摘要

背景与目的

韦尼克脑病(WE)的神经病理变化涉及多种脑结构。然而,胼胝体在WE中的受累情况在很大程度上尚不清楚。作者根据病因研究了WE中胼胝体变化的程度和模式。

方法

纳入19例WE患者(年龄在34至81岁之间)和19名年龄及性别匹配的对照参与者。通过在正中矢状面追踪外缘来测量胼胝体的总横截面积和5个胼胝体亚区域(C1 - C5)。亚区域通过放置有10条射线的径向分隔器来确定。计算胼胝体的像素数,并对获得的值进行头部大小变化的校正。

结果

WE的病因包括酒精中毒(10例)、肠道手术(5例)、厌食症(3例)和妊娠剧吐(1例)。酒精性WE患者胼胝体的平均大小显著减小(P <.001;酒精性WE为527.8±70.8mm²;相应对照组为664.6±58.1mm²),而非酒精性WE患者则不然。在亚区域分析中,前额叶胼胝体(C2)萎缩在酒精性WE中最为明显。相比之下,非酒精性WE中仅压部(C5)萎缩。在整个随访期(平均5.3周)内,萎缩程度没有变化。

结论

本研究表明,酒精性WE和非酒精性WE中胼胝体萎缩的程度和位置不同,这意味着酒精神经毒性和营养缺乏有不同的作用。

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