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.