Beyond the Classic Triad: A Transdiagnostic Perspective on Wernicke's Encephalopathy Through Two Case Narratives

Background: Wernicke’s encephalopathy is a neuropsychiatric syndrome caused by thiamine deficiency, most often linked with chronic alco- hol use. Classically characterized by the triad of ophthalmoplegia, ataxia, and confusion, it frequently presents with incomplete or atypical features, making early diagnosis challenging. Post-surgical states, nutritional compromise, and alcohol withdrawal can further complicate its clinical presentation. A transdiagnostic clinical approach, integrating neurological, psychiatric, and neuroimaging perspectives, may enhance recognition and timely management. Method: We present a brief case series of two male patients with chronic alcohol dependence both of whom developed postoperative neuropsychiatric syndromes later confirmed as Wernicke’s encephalopathy. Both the cases were evaluated clinically and neuro- radiologically, with treatment initiated using parenteral thiamine supplementation alongside tailored psychiatric and neurologi- cal management. Results: The first case involved a 39-year-old male with 20 years of alcohol use, established dependence for 8–10 years, and comorbid generalized tonic-clonic epilepsy. Following an epididymal cystectomy, he developed withdrawal seizures, diplopia, ataxic gait, irrelevant speech, and bilateral papilledema. MRI revealed dorsomedial thalamic hyperintensities and a left frontal calcification. He responded promptly to intravenous thiamine (500 mg) and sodium valproate (1 g/day), achieving clinical stabilization. The second case was a 60-year-old male with 25 years of alcohol dependence, hypertension, antral gastritis, and hiatus hernia. After hernioplasty, he developed delirium tremens with marked fluctuations in consciousness, aggressive behavior, disorienta- tion, labile mood, insomnia, and significant memory deficits. MRI revealed periaqueductal hyperintensities, mammillary body degeneration, cerebellar involvement, and fronto-temporal cortical atrophy. Despite high-dose thiamine therapy (500 mg/day for 5 days, then 300 mg/day for 4 weeks), recovery was protracted, requiring adjunctive memantine (10 mg/day) and prolonged inpatient psychiatric care. Conclusion: This case series underscores the heterogeneity of WE presentations in alcohol-dependent individuals, particularly in postopera- tive contexts. The first case illustrates a rapid response to thiamine with near-complete recovery, while the second highlights chronic structural brain changes leading to persistent cognitive impairment despite aggressive supplementation. A transdiagnos- tic approach—recognizing overlapping neurological, psychiatric, and cognitive domains facilitates earlier diagnosis and im- proves prognosis. Clinicians should maintain high vigilance for WE in surgical and withdrawal states, as delayed recognition may result in irreversible deficits.