Dynamic progression of Wernicke encephalopathy in a gastric cancer patient: Multimodal MRI insights with arterial spin labeling perfusion imaging.

Wernicke encephalopathy (WE), a neurological emergency caused by thiamin deficiency, is traditionally diagnosed based on the triad of ophthalmoplegia, ataxia, and confusion. However, this classic presentation occurs in fewer than 10% of cases, complicating early recognition. Untreated cases risk irreversible brain damage or progression to Korsakoff syndrome. While magnetic resonance imaging (MRI) aids diagnosis, early-stage structural abnormalities may be subtle or absent. Arterial spin labeling (ASL), a noninvasive perfusion imaging technique, offers potential for detecting microcirculatory changes preceding cytotoxic edema. This case explores ASL's diagnostic utility in WE through a high-risk patient with atypical progression. A 50-year-old female with gastric adenocarcinoma developed persistent vomiting following chemotherapy. By hospital day 9, she rapidly deteriorated into a comatose state (Glasgow Coma Scale: E1V1M3), prompting neurological evaluation. No classic WE triad features were initially documented. Brain MRI revealed bilateral thalamic, periventricular, and periaqueductal gray matter hyperintensities on T2-FLAIR/DWI. ASL perfusion imaging demonstrated elevated cerebral blood flow (CBF) in these regions, extending to frontal and parietal lobes. Follow-up diffusion-weighted imaging (DWI) showed lesion progression involving cortical and medullary areas, with ASL hyperperfusion exceeding diffusion-restricted zones. Serum thiamin levels (<1 ng/mL) confirmed deficiency, establishing WE diagnosis. Initial supportive care: Vasopressors, fluid resuscitation, methylprednisolone (40 mg/day), granulocyte colony-stimulating factor critical intervention delay: Thiamine replacement deferred until day 11 due to pending laboratory confirmation family-directed care: Against medical advice, transferred to local hospital prior to initiating high-dose IV thiamin. Radiological progression: Lesion expansion from deep gray matter to cortical/medullary regions within 48 hours Therapeutic uncertainty: Final neurological recovery status unreported due to care discontinuity. ASL may identify perfusion alterations prior to DWI-detectable cytotoxic edema, suggesting a role in WE's early diagnostic algorithm. Rapid lesion progression in high-risk patients necessitates urgent thiamin repletion even without classic symptoms. Neuroimaging findings in WE may exhibit dynamic spatial-temporal evolution, requiring multimodal imaging interpretation. Serum thiamin levels remain critical for diagnostic confirmation in radiologically ambiguous cases.