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Wernicke’s encephalopathy (WE) is an acute neuropsychiatric syndrome caused by thiamine (vitamin B1) deficiency, classically presenting with a triad of:

1. Encephalopathy
2. Oculomotor dysfunction
3. Gait ataxia </aside>

It is a medical emergency and potentially reversible, but may progress to Korsakoff syndrome if left untreated.

Wernicke Korsakoff Syndrome (Year of the Zebra)

https://youtu.be/ZxI-ieuJCGM

https://www.youtube.com/watch?v=yQnxREpGILk

Biochemistry

Metabolic pathway of thiamine:

![Metabolic pathway related to thiamine

Ota, Y., Capizzano, A.A., Moritani, T. et al. Comprehensive review of Wernicke encephalopathy: pathophysiology, clinical symptoms and imaging findings. Jpn J Radiol 38, 809–820 (2020). https://doi.org/10.1007/s11604-020-00989-3](attachment:ab34cc07-7b5a-44ee-b686-93d918574a5c:11604_2020_989_Fig1_HTML.webp)

Metabolic pathway related to thiamine

Ota, Y., Capizzano, A.A., Moritani, T. et al. Comprehensive review of Wernicke encephalopathy: pathophysiology, clinical symptoms and imaging findings. Jpn J Radiol 38, 809–820 (2020). https://doi.org/10.1007/s11604-020-00989-3

Interactions between alcohol consumption and thiamine deficiency:

Zahr, N., Kaufman, K. & Harper, C. Clinical and pathological features of alcohol-related brain damage. Nat Rev Neurol 7, 284–294 (2011). https://doi.org/10.1038/nrneurol.2011.42

Etiology

Pathophysiology

• Thiamine is a coenzyme for carbohydrate metabolism (e.g., pyruvate dehydrogenase)
• Deficiency → neuronal energy failure, oxidative stress, lactic acidosis
• Selective vulnerability of regions with high thiamine turnover and metabolic demand
• Vasogenic and cytotoxic edema, demyelination, and gliosis