Wernicke encephalopathy presenting with rare clinical findings: bilateral VI cranial nerve palsy and pontine lesion

Wernicke encephalopathy (WE) is a serious acute neurological condition that is commonly associated with vitamin B1 (thiamine) deficiency due to alcohol abuse, albeit it can also occur in non-alcoholic settings. In cases of thiamine deficiency, a clinical diagnosis of WE is considered when two or more of the classic features—such as ophthalmoplegia, gait ataxia, and confusion—are present. A rare clinical manifestation of WE, including bilateral sixth cranial nerve palsy, ataxia, and pontine involvement on MRI, is described in this report. A 36-year-old male was admitted with complaints of diplopia for five days, along with a one-month history of hallucinations and insomnia. His medical history revealed chronic alcohol dependence, including recent consumption of homemade alcohol shortly before his complaints began. On neurological examination, bilateral restricted lateral gaze was observed. Axial T2-weighted MRI images of the brain showed a hyperintense lesion at the pontine midline. The patient was admitted with a preliminary diagnosis of WE and started on thiamine therapy at 500 mg/day for five days, followed by 200 mg/day and then 100 mg/day, each administered for an additional five days. During the early stages of WE, patients typically exhibit characteristic symptoms such as alterations in mental status, ophthalmoplegia, and ataxia. On T2-weighted MRI, Wernicke encephalopathy is indicated by hyperintense lesions in brain regions with high carbohydrate metabolism, particularly involving the ventral thalamus, hypothalamus, mammillary bodies, periaqueductal gray matter, and the floor of the fourth ventricle. This case has been presented to highlight a rare clinical presentation of Wernicke encephalopathy.