To report a case of non-alcoholic Wernicke’s encephalopathy presenting with psychosis.

Wernicke’s encephalopathy is a neurological syndrome secondary to thiamine deficiency. Although most commonly associated with chronic alcoholism, it is also seen with nutritional deficiencies. It is characterized by a classic triad of encephalopathy, ophthalmoplegia, and ataxia. Although confusion is common, psychosis as a presenting sign hasn’t been reported. Typical MRI findings include symmetric changes in the thalami, mammillary bodies, and periaqueductal region, but atypical areas can be involved including rare cortical involvement.

A 39-year-old male with a 6-month history of vomiting was admitted for acute-onset psychosis one week following a cholecystectomy. On presentation, the patient was paranoid of family members’ motives, having delusions of infidelity, and had vertical nystagmus. His initial vital signs, CSF studies, EEG, and MRI Brain were normal. He was incidentally found to have lung nodules on CT Chest, which were biopsied, revealing pulmonary sarcoidosis. He became progressively apathetic, encephalopathic, ultimately becoming nonverbal, developed profound neuropathy, and hypophonia. A course of Methylprednisolone was tried due to concern for neurosarcoidosis with no improvement.

A third MRI Brain, three weeks after presentation revealed cortical ribboning in bilateral frontal lobes and FLAIR hyperintensity along thalami, mammillary bodies, and periaqueductal region. It took three weeks from symptom onset to recognition of Wernicke’s encephalopathy and thiamine repletion. On discharge, the patient had slight improvement in his mentation, had vertical nystagmus, was hypophonic, and apathetic. Fifteen months following discharge, the patient is residing in a skilled nursing facility with severe memory deficits.

It is important to recognize psychosis as a potential predominant presenting feature of Wernicke's encephalopathy since symptoms could be reversible with early recognition and treatment. Cortical ribboning, while typically seen in prion disease, can be seen in severe cases of Wernicke’s encephalopathy.