Objective:

To present an atypical case of Wernicke encephalopathy manifesting with acute ascending flaccid paralysis, emphasizing the diagnostic challenges and importance of early recognition.

Background:

Wernicke encephalopathy is an acute syndrome requiring emergent treatment resulting from thiamine deficiency, classically characterized by the triad of confusion, oculomotor dysfunction, and gait ataxia. However, atypical presentations can obscure timely diagnosis and delay treatment, leading to irreversible neurological deficits.

Design/Methods:

Case report

Results:

A 34-year-old male presented with a 3–4 day history of progressive muscle weakness, advancing to bilateral lower extremity flaccid paralysis, loss of gross sensation, and nystagmus. He reported a similar prior episode that improved after hydration and electrolytes replacement. Also reported a history of heavy alcohol use, with cessation three months earlier, accompanied by poor nutrition and weight loss. Lumbar puncture results were unremarkable. MRI brain (T2/FLAIR) revealed subtle hyperintense signal changes in the bilateral medial thalami and periventricular regions surrounding the third ventricle that was noticed later in the admission, consistent with Wernicke encephalopathy. High-dose thiamine therapy (500 mg IV TID for 3 days, followed by 100 mg daily with multivitamins) was initiated on hospital day 3. Within 24 hours, the patient demonstrated cognitive clarity, allowing a more accurate history—revealing ongoing alcohol use and one month of the onset of symptoms. Gradual motor recovery ensued, though areflexia persisted. The patient was subsequently discharged to an inpatient rehabilitation facility for continued recovery.

Conclusions:

This case underscores the need to maintain a high index of suspicion for Wernicke encephalopathy even in the absence of its classic triad. Thiamine deficiency can present with atypical neurological findings, including flaccid paralysis, mimicking other neuromuscular disorders. Prompt recognition and early thiamine replacement remain essential to optimize neurological recovery and prevent permanent sequelae.