Case Report: Wernicke’s encephalopathy induced by prolonged fasting due to apparent psychogenic dysphagia

TL;DR

A 26-year-old woman developed Wernicke’s encephalopathy from prolonged fasting due to psychogenic dysphagia, highlighting the need for early thiamine treatment even with atypical symptoms.

Contribution

This case report highlights WE caused by psychogenic dysphagia, emphasizing the importance of early thiamine treatment despite atypical presentations.

Findings

WE can occur from functional or psychogenic dysphagia leading to malnutrition.

Early thiamine repletion improved the patient’s neurological symptoms despite initial inconclusive imaging.

Psychiatric evaluation is important in cases of unexplained dysphagia and neurological symptoms.

Abstract

Wernicke’s encephalopathy (WE) is an acute neurologic emergency resulting from thiamine deficiency that can cause irreversible injury if treatment is delayed. Although often associated with alcohol use, WE also occurs in the setting of malnutrition, dysphagia, chronic illness, and malignancy. Dysphagia-related WE is rare and typically linked to impaired oral intake. We report a case of a 26-year-old woman with 3 months of dysphagia and subsequent poor oral intake who developed WE.

A 26-year-old woman with type 2 diabetes and hypothyroidism presented for confusion, speech incoherence, and gait instability following 3 months of dysphagia. She was hemodynamically stable, and her thyroid, autoimmune, toxic, and infectious workups were negative. Although repeated computed tomography was negative, magnetic resonance imaging showed signal changes in the mammillary bodies, posterior midbrain, and medial thalami, indicating Wernicke’s encephalopathy. Her thiamine, folate, and B12 levels were replaced, and her mentation and coordination improved. A swallow study showed no physiologic dysphagia. She was discharged on oral thiamine supplementation and referred to psychiatry for the presumed psychogenic etiology of her dysphagia, given the distressing life events prior to hospitalization.

The classic WE triad of confusion, oculomotor abnormalities, and ataxia presents in a minority of patients; hence, atypical presentations may be overlooked. Our patient demonstrated how WE can be induced by nutritional deficiencies secondary to functional or psychogenic dysphagia. Furthermore, this case highlights the importance of prompt clinical intervention via thiamine repletion despite inconclusive initial imaging, as delayed treatment can result in permanent complications.

Figures