"MRI "
"haemolysis (e.g. glucose-6-phosphate dehydrogenase (G6PD) deficiency, ABO or Rh incompatibility)"
"MR spectroscopy has been infrequently reported in the literature on kernicterus; existing studies have reported increased levels of glutamine and glutamate, along with decreased levels of choline and N-acetylaspartate 9."
Expected headings
"MRI "
"Nearly all affected infants will have clinical features of acute bilirubin encephalopathy, such as jaundice, somnolence, hypertonia, opisthotonos, and retrocollis, before manifestation of these permanent neurological signs 1. These early signs are often unfortunately mistaken for mimics such as sepsis or hypoglycaemia 1."
"As a result, this unconjugated bilirubin deposits symmetrically in the brain, with a predilection for the globi pallidi, subthalamic nuclei, hippocampus (especially CA2-CA3), putamen, thalamus, and cranial nerve nuclei (especially of CN III, IV, and VI) 1,2,5-10. Macroscopically, these areas have a characteristic yellow appearance 1,2,5-10."
"There are numerous underlying causes for unconjugated hyperbilirubinaemia, and thus kernicterus, in infancy 1-3,5-10:"
"There is no disease-modifying treatment available, and the prognosis is poor 1,2,6. Early management of neonatal hyperbilirubinaemia, with therapies such as phototherapy and exchange transfusions, should be employed to prevent kernicterus 1,2,6."
"haemolysis (e.g. glucose-6-phosphate dehydrogenase (G6PD) deficiency, ABO or Rh incompatibility)"
"disorders of hepatic bilirubin metabolism (e.g. Crigler-Najjar syndrome)"
"acquired defects in bilirubin conjugation (e.g. Lucey-Driscoll syndrome)"
"MR spectroscopy has been infrequently reported in the literature on kernicterus; existing studies have reported increased levels of glutamine and glutamate, along with decreased levels of choline and N-acetylaspartate 9."