Mild symptomatic Wernicke’s Encephalopathy: a case report

Abstract

Wernicke’s encephalopathy (WE) is an acute, neuropsychiatric syndrome which results from a deficiency in vitamin B1 (thiamine), which in its biologically active form, thiamine pyrophosphate, is an essential coenzyme in several biochemical pathways in the brain, often due to alcohol abuse (alcoholic WE). Non-alcoholic WE variant manifests in many different clinical settings, such as gastrointestinal tumors, hyperemesis gravidarum, chemotherapy, acquired immunodeficiency syndrome, prolonged therapeutic fasting, protracted parenteral nutrition and bariatric surgery, anorexia nervosa and can even be secondary to socioeconomic factors. The classic triad of encephalopathy, oculomotor dysfunction, and gait ataxia is only seen in approximately one-third of patients and is more common in alcoholics; only some of these symptoms are usually present. Here we describe a case of an occasional neuroradiological finding of Wernicke Encephalopathy not related to symptoms or signs.

Wernicke's encephalopathy: A forgotten disease

“…The magnetic resonance imaging is the most important diagnostic tool for early diagnosis, prognostication, and identification of atypical cases and has a 53% sensitivity and 93% specificity (5). In our patient, there was a hyper-intensity surrounding the aqueduct detected on axial FLAIR sequences, while a bilateral, symmetrical hyper-intensity at dorsomedial of thalamus on DWI images was observed, but there was no increase in the signal intensity at the same localization on ADC images.…”