Wernicke’s encephalopathy (WE) is a neurological emergency related to a severe thiamine (vitamin B1) deficiency, an essential cofactor in cerebral energy metabolism. Although historically associated with chronic alcoholism, this condition can occur in any context of malnutrition, prolonged vomiting, or hypercatabolism. We conducted a retrospective descriptive study on seven patients admitted to our neurology department between 2015 and 2020, in order to de-scribe the clinical, radiological, and outcome characteristics of this pathology. The diagnosis was made in the presence of suggestive signs (at least two among confusion, ataxia, oculomotor disorders), a risk context of deficiency or malnutrition, typical MRI abnormalities and/or rapid improvement after thiamine ad-ministration. Our series included two male patients with chronic alcohol consumption, and five pregnant women with severe hyperemesis gravidarum, with an average age of 32.4 years. Mental confusion was the most frequent sign, followed by gait disturbances and oculomotor abnormalities. The most characteristic MRI lesions involved the thalamus, the periaqueductal region, and the mammillary bodies. All patients received high-dose intravenous thiamine supplementation (500 mg every eight hours for three days), followed by oral maintenance therapy. The outcome was favorable in five cases, while two patients had persistent memory disorders. These observations confirm that WE is not limited to alcoholic forms and must be considered in any situation with nutritional risk. Early diagnosis and rapid administration of intravenous thiamine remain essential to prevent irreversible neurological sequelae and improve functional prognosis.