Introduction

Wernicke's encephalopathy is an acute neuropsychiatric syndrome caused by thiamine (vitamin B1) deficiency. It is classically characterized by a triad of altered mental status, ataxia, and ophthalmoplegia. This article presents the second case in a series, highlighting the clinical presentation, diagnostic challenges, and management strategies.

Case Presentation

A 52-year-old male with a history of chronic alcohol use disorder presented to the emergency department with confusion, gait instability, and double vision. His family reported a two-week history of progressive lethargy, poor oral intake, and repeated vomiting.

On examination, the patient was disoriented to time and place, with horizontal nystagmus and bilateral abducens nerve palsy. He was unable to stand without support due to severe ataxia. Vital signs were stable except for mild tachycardia and hypotension. Laboratory investigations revealed low serum thiamine levels, elevated liver enzymes, and a blood alcohol level of 0.08%.

Diagnostic Workup

Magnetic resonance imaging of the brain showed symmetric hyperintensities in the medial thalami, mammillary bodies, and periaqueductal gray matter on T2-weighted and FLAIR sequences, a finding highly specific for Wernicke's encephalopathy. No evidence of stroke or other focal lesions was observed. Cerebrospinal fluid analysis was unremarkable.

The clinical diagnosis was confirmed as Wernicke's encephalopathy, classified as Case 2 in our series due to the presence of the full triad with characteristic MRI changes.

Treatment and Outcome

Intravenous thiamine at a dose of 500 mg three times daily for two days was initiated immediately, followed by 250 mg daily thereafter. Magnesium and other electrolytes were supplemented as needed. The patient showed rapid improvement in ophthalmoplegia within 24 hours and gradual resolution of ataxia over the following week. His cognitive status improved more slowly, requiring supportive care and nutritional rehabilitation.

At two-week follow-up, residual gait difficulty and mild short-term memory impairment persisted, underscoring the importance of early recognition and aggressive thiamine replacement.

Discussion

This case emphasizes that Wernicke's encephalopathy is a medical emergency with significant morbidity if untreated. The classic triad is present in only about one-third of cases, and atypical presentations are common. In this Case 2, the presence of bilateral abducens nerve palsy served as a prominent ocular manifestation, which is a key component of the ophthalmoplegia often seen in this condition.

Risk factors include chronic alcoholism, malnutrition, hyperemesis gravidarum, prolonged fasting, and bariatric surgery. Thiamine is a cofactor for several enzymes involved in glucose metabolism, and its deficiency leads to focal brain damage in areas with high metabolic demand.

Clinicians should maintain a low threshold for empirical thiamine administration in any patient with unexplained encephalopathy, especially when risk factors are present. Unfortunately, delayed treatment can result in permanent neurological deficits such as Korsakoff syndrome, a chronic amnesic state.

Keywords

The following keywords are relevant to this case: thiamine deficiency, Wernicke-Korsakoff syndrome, ophthalmoplegia, nystagmus, ataxia, confusion, abducens nerve palsy, mammillary bodies, periaqueductal gray matter, alcohol use disorder, intravenous thiamine, and neuroimaging.

Conclusion

Case 2 of Wernicke's encephalopathy demonstrates a classic presentation with full clinical triad and characteristic imaging findings. Prompt recognition and high-dose thiamine therapy are crucial to prevent irreversible neurological damage. This case serves as a reminder for healthcare professionals to consider Wernicke's encephalopathy in all patients with acute neurological symptoms and nutritional risk factors.