WE is an acute neurological syndrome caused by thiamine deficiency. The classic triad of symptoms includes altered consciousness, oculomotor dysfunction, and gait ataxia; all are present in only 16% of cases. WE is seen in both alcoholic and non-alcoholic patients, with differing radiographic findings. Typical MRI findings include T2/FLAIR hyperintensities and diffusion weighted restriction (DWI) changes of symmetrical dorsomedial thalami, mammillary bodies, tectal plate, and periaqueductal area. Atypical locations include the cerebellar hemispheres, vermis, cranial nuclei, and cerebral cortex.  Atypical locations are rare in alcoholics, and when present are reported to be invariably associated with involvement of typical regions.

Case Report. WE diagnosed using CAINE criteria.

A 63 year old male with a history of alcohol abuse and six months of cognitive decline presented with two months of wide-based gait followed by marked disorientation, visual and auditory hallucinations, appetite loss, and severe hearing loss. Neurological exam showed poor attention, horizontal direction-changing nystagmus, lower extremity weakness, and gait ataxia. MRI Brain showed symmetric DWI signal in bilateral cerebellar hemispheres and vermis, along with mammillary bodies and fornix atrophy. TSH, B12, HIV, RPR, ANA, lumbar puncture (autoimmune panel, tau/amyloid, neuron specific enolase), and EEG were all unremarkable. RBC thiamin was decreased. High-dose thiamine was initiated, and his nystagmus improved within 24 hours. His presentation was consistent with WE. He was followed in neurocognitive clinic and demonstrated gradual cognitive improvement.