Atypical Wernicke's encephalopathy with remarkable cerebellar lesions on diffusion-weighted MRI.

sphere and posterior vermis, simulating acute bilateral cerebellar infarctions ( fig. 1 A). An initial diagnosis was made based on a history of chronic alcohol abuse, with typical symptoms that included altered mental state and ophthalmoplegia, and combined lesions on bilateral thalamus and periaqueductal gray matter on DWI ( fig. 1 B). Immediate administration of 300 mg thiamine commenced. On the second hospital day, he became drowsy and did respond to simple commands. Mild horizontal gaze palsy, gaze-evoked nystagmus, and limb dysmetria were evident. A follow-up DWI performed 8 days after onset showed that the previously high signal intensities in the cerebellum ( fig. 1 A), medial thalamus, and periaqueductal gray matter ( fig. 1 B) had mostly resolved. Follow-up T 2 -weighted images showed no high signal intensity, but severe atrophy of the cerebellar vermis and anterior hemisphere were evident ( fig. 1 A). MR angiography showed no definite stenosis or occlusion in the vertebrobasilar circulation. Over several days of hospitalization, he regained alertness, but showed considerable memory impairment and gait ataxia.