Background: Wernicke encephalopathy (WE) is an acute and potentially fatal neuropsychiatric disorder resulting from thiamine deficiency: its etiology and clinical presentation can be heterogeneous and arduously recognized, especially in children and adolescents.
Case Presentation: An 8-year-old girl arrived to the emergency room with ataxic gait, nystagmus, and mental confusion after a 10-day history of repeated severe vomiting; her recent clinical history was characterized by restricted nutrition due to a choking phobia, which caused substantial . Brain magnetic resonance imaging revealed a bilaterally increased T2 signal in the medial areas of the thalami and cerebral periaqueductal region. Diagnosis of WE based on clinical and neuroradiological findings was established and confirmed after labwork showing low serum thiamine. Following psychiatric evaluation, the patient was also diagnosed with avoidance-restrictive food intake disorder (ARFID), which required starting cognitive behavioral therapy and introducing aripiprazole. The patient displayed improvement of the radiological findings after one month and complete resolution of her neurological symptoms and signs.
Conclusions: Eating disorders like ARFID might forerun acute signs of WE; this possibility should be considered even in pediatric patients, especially when atypical neurological pictures or feeding issues come out.
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http://dx.doi.org/10.3390/diseases12060112 | DOI Listing |
BMJ Case Rep
January 2025
Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
We present a case of a male in his early 50s assessed in the emergency department with a seemingly clear alcohol history but with classic symptoms of Wernicke's encephalopathy (WE): disorientation, gait ataxia and vertical nystagmus. He also had significant bilateral hearing loss and profound anterograde amnesia. Neuroimaging revealed hallmark signs of WE, including symmetrical T2/fluid-attenuated inversion recovery hyperintensity in the medial thalami.
View Article and Find Full Text PDFPalliat Support Care
January 2025
Department of Psycho-Oncology, Saitama Medical University International Medical Center, Saitama, Japan.
Objectives: Wernicke encephalopathy (WE) is an acute neuropsychiatric disorder caused by thiamine deficiency. The classical triad of symptoms for WE include mental status changes, ataxia, and ophthalmoplegia. In contrast, more uncommon symptoms include hallucinations.
View Article and Find Full Text PDFJ Clin Med
January 2025
Department of Emergency Medicine, Henry Ford Health, Detroit, MI 48202, USA.
: Wernicke's encephalopathy can occur in oncology patients independent of alcohol use, likely resulting from poor dietary thiamine intake. High metabolic demands, such as those in acute illnesses seen in the emergency department (ED), can exacerbate thiamine deficiency. In this study, our objective was to assess the incidence of thiamine deficiency in ED oncology patients, which could lead to Wernicke's encephalopathy or other thiamine deficiency disorders if left untreated.
View Article and Find Full Text PDFPediatr Neurol
December 2024
University of Alabama, Birmingham, Children's of Alabama, Birmingham, Alabama.
Wernicke encephalopathy is a well-described neurological complication of thiamine deficiency that is classically characterized by a triad of mental confusion, ophthalmoplegia, and gait ataxia. Although most commonly linked to alcoholism and thiamine deficiency in adults, it can present in pediatric patients. Wernicke encephalopathy presenting as dysnatremias is not well described.
View Article and Find Full Text PDFCureus
December 2024
Critical Care Medicine, Springfield Clinic, Springfield, USA.
A 27-year-old male patient with chronic alcohol use disorder was diagnosed with Marchiafava-Bignami disease (MBD) after experiencing an episode of unconsciousness. MRI scans revealed lesions in the corpus callosum and adjacent white matter. Despite prompt initiation of intensive treatment with high-dose thiamine and corticosteroids, the patient only partially recovered, remaining disoriented and exhibiting persistent neurological deficits during follow-up.
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