Wernicke's encephalopathy in mixed connective tissue disease triggered by persistent vomiting: a case report and literature review.

Wernicke's encephalopathy (WE) is an acute, reversible but potentially disabling neurological syndrome caused by thiamine deficiency. It is increasingly recognized in non-alcoholic settings, particularly when persistent vomiting, poor intake, malabsorption, or systemic illness rapidly depletes limited thiamine stores. Patients with mixed connective tissue disease (MCTD) may be vulnerable because esophageal/gastrointestinal dysmotility, gastroesophageal reflux, chronic inflammation, and reduced oral intake can overlap and obscure nutritional complications. A 38-year-old woman with a 4-year history of anti-U1 RNP-positive MCTD, interstitial lung disease, Raynaud's phenomenon, sclerodactyly, polyarthritis, GERD, and pre-existing sensory axonal neuropathy presented with two weeks of recurrent postprandial vomiting followed by excessive daytime somnolence, bilateral horizontal nystagmus, lower-limb weakness, and impaired vibration sense. Brain MRI showed symmetrical T2/FLAIR hyperintensities involving the bilateral dorsomedial thalami, mammillary bodies, and periaqueductal gray matter. CSF examination was non-inflammatory, CSF cytology was negative, anti-aquaporin-4 antibody was negative, spinal MRI was normal, and infectious, malignant, metabolic, and neuromyelitis optica spectrum disorder differentials were excluded. Empirical intravenous thiamine 500 mg three times daily was started on day 1; vomiting, alertness, and nystagmus improved within 72 h, and complete neurological recovery was documented at one month. This case highlights non-alcoholic WE as a treatable neurological mimic in autoimmune rheumatic disease. Persistent vomiting with new ocular, cognitive, gait, or motor findings in MCTD should prompt early empiric parenteral thiamine, even when the classical triad is incomplete and serum thiamine is unavailable.