Corpus Callosum Atrophy in Wernicke's Encephalopathy

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 mm 2for alcoholic WE; 664.6 ± 58.1 mm 2for 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.