Nonalcoholic Wernicke Encephalopathy: An Entity Not to Be Missed

A high index of suspicion for WE is needed in the setting of poor nutrition (e.g. caused by gastrointestinal disturbances, bariatric surgery, hyperemesis gravidarum, or malignancy), regardless of whether there is a history of alcoholism.1-4 WE can also be triggered by administration of total parenteral nutrition.4 In this case, it is likely that both the gastrointestinal disturbances and total parenteral nutrition were culprits. Often, not all features of the classic triad of ataxia, nystagmus/ophthalmoplegia, and confusion are seen, especially in nonalcoholic cases (the full triad occurring in only 33.6% of such cases versus 53.9% in alcoholic patients).2 Therefore, WE is often clinically underdiagnosed.1-4 Reversible cytotoxic edema in WE causes distinctive lesions and brain MRI is very useful in aiding the clinical diagnosis.1 The typical and common MRI findings of WE are symmetrical lesions in the medial thalami/periventricular region of the third ventricle (seen in 85% of cases), periaqueductal region (65% of cases), and mamillary bodies (58% of cases). In cases of nonalcoholic WE, atypical MRI findings can be observed in the cerebellum, cranial nerve nuclei, red nuclei, dorsal medulla, caudate nuclei, splenium, and cerebral cortex.1,3 Measurements of blood thiamine concentration or red blood cell transketolase activity are limited by a lack of specificity and technical difficulty,4 and were not done in this case.