S4129 Exploring the Link Between Functional Dysphagia and Wernicke's Encephalopathy

Introduction: Functional dysphagia is characterized by the sensation of food sticking or delay in food passage through the esophagus, as defined by the Rome criteria. Wernicke's encephalopathy is a degenerative brain disorder caused by thiamine (vitamin B1) deficiency, presenting acutely with the classic triad of ophthalmoplegia, ataxia, and confusion. We report a case of Wernicke's encephalopathy in a nonalcoholic patient with functional dysphagia. Case Description: A 34-year-old woman presented to the emergency department with altered mental status, which began 2 days prior. Her family reported that she had not been acting like herself and had experienced significant weight loss of over 25 lbs in the past 3 months due to poor oral intake secondary to dysphagia. Ten days prior, she was evaluated in the hospital for dysphagia and odynophagia, at which time she underwent an esophagogastroduodenoscopy (EGD) with empiric 51 Fr dilation. Biopsies taken during the procedure were negative for eosinophilic esophagitis or Helicobacter pylori infection. A modified barium swallow study revealed no evidence of oral or pharyngeal dysphagia. Additionally, a repeat EGD and a computed tomography scan of the neck showed no obstructive pathology. Magnetic resonance imaging of the brain with intravenous (IV) contrast revealed abnormal fluid-attenuated inversion recovery signal in the medial thalami, periaqueductal region, and tectal plate in a symmetric pattern, suggestive of metabolic or toxic abnormalities, most notably thiamine deficiency, Wernicke’s encephalopathy, or West Nile virus infection. However, cerebrospinal fluid analysis was negative for bacterial, viral, or autoimmune etiologies. Laboratory workup revealed low plasma thiamine levels. Given her vision changes, confusion, ataxia, and prolonged history of dysphagia leading to poor dietary intake and weight loss, Wernicke’s encephalopathy was diagnosed. She was started on IV thiamine for 3 days, followed by oral thiamine supplementation. Her ocular abnormalities and gait ataxia improved; however, dysphagia persisted despite treatment. Discussion: Our case is unique, as functional dysphagia leading to vitamin B1 deficiency is rare. To our knowledge, only a few case reports have described Wernicke's encephalopathy presenting with dysphagia. However, in our patient, all evidence suggests that dysphagia was the primary cause of thiamine deficiency. This case also underscores the importance of further investigating and advancing our understanding of functional dysphagia and other functional esophageal disorders.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001143976.35774.c3
Primary Topic
Alcoholism and Thiamine Deficiency
Type
article
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article

S4129 Exploring the Link Between Functional Dysphagia and Wernicke's Encephalopathy

Haniya Waseem, Sagar Patil, Fnu Naina
The American Journal of Gastroenterology
Alcoholism and Thiamine Deficiency
article

S4129 Exploring the Link Between Functional Dysphagia and Wernicke's Encephalopathy

Haniya Waseem, Sagar Patil, Fnu Naina
article en

Abstract

Introduction: Functional dysphagia is characterized by the sensation of food sticking or delay in food passage through the esophagus, as defined by the Rome criteria. Wernicke's encephalopathy is a degenerative brain disorder caused by thiamine (vitamin B1) deficiency, presenting acutely with the classic triad of ophthalmoplegia, ataxia, and confusion. We report a case of Wernicke's encephalopathy in a nonalcoholic patient with functional dysphagia. Case Description: A 34-year-old woman presented to the emergency department with altered mental status, which began 2 days prior. Her family reported that she had not been acting like herself and had experienced significant weight loss of over 25 lbs in the past 3 months due to poor oral intake secondary to dysphagia. Ten days prior, she was evaluated in the hospital for dysphagia and odynophagia, at which time she underwent an esophagogastroduodenoscopy (EGD) with empiric 51 Fr dilation. Biopsies taken during the procedure were negative for eosinophilic esophagitis or Helicobacter pylori infection. A modified barium swallow study revealed no evidence of oral or pharyngeal dysphagia. Additionally, a repeat EGD and a computed tomography scan of the neck showed no obstructive pathology. Magnetic resonance imaging of the brain with intravenous (IV) contrast revealed abnormal fluid-attenuated inversion recovery signal in the medial thalami, periaqueductal region, and tectal plate in a symmetric pattern, suggestive of metabolic or toxic abnormalities, most notably thiamine deficiency, Wernicke’s encephalopathy, or West Nile virus infection. However, cerebrospinal fluid analysis was negative for bacterial, viral, or autoimmune etiologies. Laboratory workup revealed low plasma thiamine levels. Given her vision changes, confusion, ataxia, and prolonged history of dysphagia leading to poor dietary intake and weight loss, Wernicke’s encephalopathy was diagnosed. She was started on IV thiamine for 3 days, followed by oral thiamine supplementation. Her ocular abnormalities and gait ataxia improved; however, dysphagia persisted despite treatment. Discussion: Our case is unique, as functional dysphagia leading to vitamin B1 deficiency is rare. To our knowledge, only a few case reports have described Wernicke's encephalopathy presenting with dysphagia. However, in our patient, all evidence suggests that dysphagia was the primary cause of thiamine deficiency. This case also underscores the importance of further investigating and advancing our understanding of functional dysphagia and other functional esophageal disorders.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 54%
Alcoholism and Thiamine Deficiency
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