Acute Wernicke's encephalopathy (WE) is caused by profound vitamin B1 (thiamine) 
deficiency and commonly presents with the classic clinical triad of mental 
confusion, ataxia, and ophthalmoplegia. This characteristic presentation results 
from the propensity of acute thiamine deficiency to preferentially injure 
specific brain regions: the dorsomedial thalamus, periaqueductal gray, and 
mamillary bodies. In these regions, abnormal magnetic resonance signaling on 
conventional sequences has been well described; however, diffusion restriction 
has only recently been reported. The authors demonstrate diffusion-weighted 
imaging (DWI) abnormalities of the splenium of the corpus callosum in a patient 
with acute WE, which has not been reported previously, and suggest a potential 
pathological mechanism. With the recent addition of DWI, MRI is becoming more 
sensitive to the changes in acute WE. Furthermore, the use of apparent diffusion 
coefficient mapping to evaluate the extent of likely underlying cytotoxic injury 
may help determine long-term response to vitamin therapy and, thus, disability.