Case of the Week
Section Editors: Matylda Machnowska1 and Anvita Pauranik2
1University of Toronto, Toronto, Ontario, Canada
2BC Children's Hospital, University of British Columbia, Vancouver, British Columbia, Canada
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December 26, 2019
Wernicke Encephalopathy after Bariatric Surgery
- Background:
- Wernicke encephalopathy (WE) is caused by thiamine (vitamin B1) deficiency.
- Although it is usually encountered in malnourished patients or those with alcoholism, WE may occur in patients who undergo bariatric surgery secondary to intestinal malabsorption.
- Clinical Presentation:
- WE is characterized by a clinical triad: confusion, ataxia, and ophthalmoplegia.
- Our patient also presented with bilateral hearing loss and sixth cranial nerve palsy, presumably from more extensive brain stem involvement.
- Key Diagnostic Features:
- On MR images, symmetric T2-FLAIR hyperintensities are seen in medial thalamic regions, periaqueductal gray, colliculi, the floor of the fourth ventricle, and mammillary bodies, with or without restriction of diffusion.
- After gadolinium administration, the lesions can show mild enhancement on T1-weighted images.
- Posttherapeutic images usually demonstrate resolution of the abnormalities.
- Differential Diagnoses:
- Stroke (artery of Percheron) and other causes of encephalopathy (infectious, inflammatory, metabolic) are the main differential diagnoses.
- The clinical context and the typical anatomic distribution of the lesions on the MR images are key clues to the diagnosis of WE.
- Treatment:
- Thiamine administration is the only required treatment.
- Recognition of this diagnosis is important because treatment delays can lead to irreversible neurologic deficits.
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