**Background:** Wernicke encephalopathy (WE) is an acute neurological emergency caused by thiamine (vitamin B1) deficiency, leading to biochemical injury of the central nervous system. The classic triad of ophthalmoplegia, ataxia, and confusion is present in only a minority of cases. In hyperemesis gravidarum, increased thiamine demand coupled with persistent vomiting rapidly depletes reserves, typically between the 14th and 20th weeks of gestation. This case report describes an atypical presentation of WE in pregnancy revealed by areflexic flaccid tetraparesis.
**Methods:** This is a single case report following SCARE (Surgical CAse REport) guidelines. The patient was a 25-year-old primigravid woman (G1P0) with no significant medical history, no alcohol use, but an unbalanced diet since pregnancy. She began vomiting at 8 weeks gestation and was treated with antiemetics without resolution. At 17 weeks, she developed tetraparesis and was initially treated with intravenous fluids including dextrose and metoclopramide before referral to the intensive care unit. On admission, neurological examination revealed ataxia, loss of equilibrium, areflexia, and motor deficits including thumb-index clamp weakness, wrist dorsiflexion deficit, and lower limb dorsiflexion at 3/5 and extension at 4/5. Cranial nerves, sensory exam, and Babinski reflex were normal. Laboratory findings showed serum potassium 2.8 mEq/L and a markedly low thiamine level of 10 nmol/L (normal range 74–222 nmol/L). Cranial MRI, spinal MRI, and electroneuromyography (ENMG) were all normal. Hypokalemia was corrected without clinical improvement. Once WE was diagnosed, the patient received intravenous thiamine 500 mg three times daily for 3 days, followed by 100 mg daily for 14 days.
**Key Results:** By the 19th day of hospitalization, the patient showed significant neurological improvement and was able to walk. She was discharged home on the 37th day with only mild residual ataxia. The authors note that MRI is abnormal in only 60% of WE cases, and that normal imaging does not exclude the diagnosis. Typical MRI findings, when present, include symmetrical T2, FLAIR, and diffusion hypersignals around the aqueduct of Sylvius, the third ventricle, the medial thalami, and the mammillary bodies. Diffusion-weighted imaging abnormalities predict long-term neurological sequelae.
**Clinical Implications:** WE is a medical emergency with 10–20% mortality and high morbidity, yet it is often missed due to atypical presentations. In pregnancy, delayed diagnosis can lead to miscarriage, preterm birth, and intrauterine growth retardation. This case demonstrates that WE can present with areflexic flaccid tetraparesis as the dominant feature, without the classic triad. Clinicians should maintain a high index of suspicion in pregnant women with hyperemesis and neurological symptoms, even when MRI is normal. Early parenteral thiamine administration can reverse symptoms and prevent permanent neurological damage. The authors emphasize that treatment should not be delayed while awaiting diagnostic confirmation.