While Wernicke encephalopathy (WE) is well-recognized as a condition most frequently associated with chronic excessive alcohol consumption, non-alcoholic WE (NAWE) remain underrecognized despite their clinical importance. An 85-year-old nursing home resident was brought to the Emergency Department (ED) with impaired consciousness. She had been taking furosemide 40 mg and spironolactone 25 mg daily for chronic heart failure for five months prior to presentation. One month before admission, she began receiving parenteral nutrition without thiamine due to poor oral intake accompanied by vomiting. On arrival, her Glasgow Coma Scale score was 3, exhibiting flaccid quadriplegia and absent deep tendon and oculocephalic reflexes. Brain MRI demonstrated hyperintensities in the peri-central sulcus cortex as well as typical WE-related regions, including the periaqueductal gray and bilateral medial thalami, on diffusion-weighted imaging (DWI) and T2-weighted imaging. Intravenous high-dose thiamine therapy was initiated based on a clinical diagnosis of WE, subsequently confirmed by a thiamine level below the detection limit (/mL). Although follow-up MRI showed radiological improvement after seven days, neurological recovery remained minimal despite 35 days of treatment. Nonspecific clinical manifestation of NAWE makes early diagnosis difficult, often resulting in progression to more advanced stages with cortical lesions. To prevent irreversible and potentially fatal neurological sequelae, it is crucial to be aware of NAWE in its early stages, particularly in patients with known risk factors, such as malnutrition (poor nutritional intake), parenteral nutrition without thiamine, gastric bypass surgery, malabsorption, dialysis, diuretic use, infections/sepsis, and hyperthyroidism.
Hongo et al. (Mon,) studied this question.
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