Wernicke’s Encephalopathy with Normal Neuroimaging - Suspect and Treat - A Case Report

Abstract

Wernicke’s encephalopathy (WE) is an unrecognized nutritional deficiency which often goes unnoticed. WE is clinically often composed of a triad including nystagmus, ophthalmoplegia and altered mental status. Although this triad practically is present only in a handful of cases1 it is also described as an acute neuropsychiatric presentation of thiamine deficiency. Early diagnosis and prompt treatment are of utmost importance here as it can prevent chronic brain damage which is often the end effect of thiamine deficiency. Wernicke’s encephalopathy is most commonly found in patients with chronic alcoholism, less frequent in non-alcoholic patients. In non-alcoholic patients, Wernicke’s encephalopathy might develop due to erosion of upper portion of gastrointestinal tract or secondary to intractable vomiting, inadequate dietary intake or malabsorption. Other causes include malignancies (gastric cancer, leukaemia, lymphoma), hyperemesis, anorexia, thyroid conditions.1,2 Wernicke’s encephalopathy is caused due to thiamine (B1) deficiency. B1 is a water-soluble vitamin which acts as a co-factor for carbohydrate metabolism. It is also important for neuronal cell function.2 This vitamin can’t be synthesised in the human body and thus dietary intake play a very important role. Symptoms of thiamine deficiency Include - Nystagmus, ataxia, encephalopathy, mental confusion. Early onset includes symptoms like: - headache, irritability, fatigue and abdominal discomfort. Prophylactic thiamine supplementation forms a major treatment for patients at risk for developing refeeding syndrome (RFS). RFS is an underdiagnosed condition which is characterised by potential shift in the fluid and electrolytes.

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