Matt Lallas1, Jay Desai. 1. Division of Neurology, Children's Hospital Los Angeles, Los Angeles, California, USA.
Abstract
BACKGROUND: Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency. It is generally considered to be a disease of adult alcoholics. However, it is known to occur in the pediatric population and in non-alcoholic conditions. DATA SOURCES: We searched PubMed with the key words Wernicke, thiamine, pediatric, children and adolescents and selected publications that were deemed appropriate. RESULTS: The global prevalence rates of hunger, poverty and resultant nutrient deprivation have decreased in the 21st century. However, several scenarios which may predispose to Wernicke encephalopathy may be increasingly prevalent in children and adolescents such as malignancies, intensive care unit stays and surgical procedures for the treatment of obesity. Other predisposing conditions include magnesium deficiency and defects in the SLC19A3 gene causing thiamine transporter-2 deficiency. The classic triad consists of encephalopathy, oculomotor dysfunction and gait ataxia but is not seen in a majority of patients. Treatment should be instituted immediately when the diagnosis is suspected clinically without waiting for laboratory confirmation. Common magnetic resonance findings include symmetric T2 hyperintensities in dorsal medial thalamus, mammillary bodies, periaqueductal gray matter, and tectal plate. CONCLUSIONS: Wernicke encephalopathy is a medical emergency. Delay in its recognition and treatment may lead to significant morbidity, irreversible neurological damage or even death. This article aims to raise the awareness of this condition among pediatricians.
BACKGROUND:Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency. It is generally considered to be a disease of adult alcoholics. However, it is known to occur in the pediatric population and in non-alcoholic conditions. DATA SOURCES: We searched PubMed with the key words Wernicke, thiamine, pediatric, children and adolescents and selected publications that were deemed appropriate. RESULTS: The global prevalence rates of hunger, poverty and resultant nutrient deprivation have decreased in the 21st century. However, several scenarios which may predispose to Wernicke encephalopathy may be increasingly prevalent in children and adolescents such as malignancies, intensive care unit stays and surgical procedures for the treatment of obesity. Other predisposing conditions include magnesiumdeficiency and defects in the SLC19A3 gene causing thiamine transporter-2 deficiency. The classic triad consists of encephalopathy, oculomotor dysfunction and gait ataxia but is not seen in a majority of patients. Treatment should be instituted immediately when the diagnosis is suspected clinically without waiting for laboratory confirmation. Common magnetic resonance findings include symmetric T2 hyperintensities in dorsal medial thalamus, mammillary bodies, periaqueductal gray matter, and tectal plate. CONCLUSIONS:Wernicke encephalopathy is a medical emergency. Delay in its recognition and treatment may lead to significant morbidity, irreversible neurological damage or even death. This article aims to raise the awareness of this condition among pediatricians.
Authors: A B Mukherjee; S Svoronos; A Ghazanfari; P R Martin; A Fisher; B Roecklein; D Rodbard; R Staton; D Behar; C J Berg Journal: J Clin Invest Date: 1987-04 Impact factor: 14.808
Authors: Luísa Camacho; Sherry M Lewis; Michelle M Vanlandingham; Beth E Juliar; Greg R Olson; Ralph E Patton; Gonçalo Gamboa da Costa; Kellie Woodling; Estatira Sepehr; Matthew S Bryant; Daniel R Doerge; Mallikarjuna S Basavarajappa; Robert P Felton; K Barry Delclos Journal: Food Chem Toxicol Date: 2016-05-24 Impact factor: 6.023
Authors: Taryn J Smith; Casey R Johnson; Roshine Koshy; Sonja Y Hess; Umar A Qureshi; Mimi Lhamu Mynak; Philip R Fischer Journal: Ann N Y Acad Sci Date: 2020-12-10 Impact factor: 5.691