Thiamine Deficiency and Brain Injury: Neuroanatomical Changes in the Wernicke-Korsakoff Syndrome

Thiamine deficiency triggers an acute neurological emergency, Wernicke's encephalopathy, which, if left untreated, can progress to the chronic amnestic Korsakoff syndrome. While chronic alcohol misuse remains the classic risk factor, thiamine deficiency is increasingly documented in malnutrition, hyperemesis gravidarum, post-bariatric surgery, chronic gastrointestinal disease, and malignancy. This expanded etiological spectrum underscores the need for a broader clinical perspective. This review included studies indexed in EMBASE, PubMed, Scopus, Web of Science, and Google Scholar databases. Whether the tools were magnetic resonance imaging, diffusion tensor imaging, positron emission tomography, autopsy, or memory testing, the narrative stayed consistent: the mammillary bodies, thalamus, hippocampus, and cerebellum take the greatest hit. Imaging reveals symmetrical atrophy, micro-hemorrhages, and fraying white-matter tracts deeper in alcohol-related Wernicke-Korsakoff syndrome, while non-alcoholic cases show extracortical or cerebellar lesions. Clinically, presentations range from acute confusion and gait instability to subtle executive lapses, with severe anterograde amnesia marking the chronic stage. The best scanner cannot outmatch a timely intravenous dose of thiamine. Hours separate reversible Wernicke's encephalopathy from lifelong Korsakoff syndrome. Building automatic thiamine checks into nutritional, surgical, oncological, and obstetric pathways and giving supplementation the moment deficiency is suspected can keep memories, independence, and quality of life intact.