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Published on: August 5, 2017
Hyperbilirubinemia: subcortical mechanisms of cognitive and behavioral dysfunction
Leonard F Koziol1, Deborah Ely Budding, Dana Chidekel
1lfkoziol@aol.com
Insights
Neonatal jaundice, even without kernicterus, may pose risks for later neurodevelopmental disorders. This study predicts cognitive features linked to bilirubin neurotoxicity in infant brain regions.
Area of Science:
- Neonatal neurology
- Neuroscience
- Developmental pediatrics
Background:
- Neonatal jaundice is common, but kernicterus is rare.
- Debate exists on neurodevelopmental risks from moderate neonatal hyperbilirubinemia.
- Established brain pathology sites link bilirubin neurotoxicity to specific regions.
Purpose of the Study:
- To predict cognitive deficits in infants with hyperbilirubinemia based on brain-behavior relationships.
- To explore neurodevelopmental abnormalities beyond full kernicterus.
- To elucidate neuropathologic mechanisms driving these abnormalities.
Main Methods:
- Applying neuroscientific principles to known bilirubin neurotoxicity brain regions.
- Correlating affected brain areas with potential cognitive and behavioral outcomes.
- Reviewing neuropathologic mechanisms of hyperbilirubinemia-induced brain injury.
Main Results:
- Identified specific brain regions vulnerable to bilirubin.
- Predicted cognitive features associated with damage in these regions.
- Established a framework for understanding neurodevelopmental risks in hyperbilirubinemia.
Conclusions:
- Elevated neonatal bilirubin, even below kernicterus levels, may cause subtle neurodevelopmental issues.
- Understanding brain-behavior links is crucial for predicting outcomes.
- This research provides a blueprint for future studies to improve infant neurodevelopmental outcomes.
Abstract:
Although development of the full syndrome of kernicterus is relatively rare, neonatal jaundice continues to occur frequently. Controversy remains concerning whether or not infants with moderate elevations in bilirubin are at risk for neurodevelopmental disorders in later childhood. Sites of brain pathology associated with bilirubin neurotoxicity are identified and well established. Based on these regions of brain involvement, we apply neuroscientific principles of brain-behavior relationships to predict types of cognitive features that may accompany hyperbilirubinemia. We address a range of neurodevelopmental abnormalities that can arise as a function of elevated neonatal bilirubin levels affecting these brain regions, even in the absence of full kernicterus syndrome. Moreover, we explain the neuropathologic mechanisms that would drive these abnormalities. We thus attempt to establish a blueprint for future investigations of these conditions, to improve neurodevelopmental outcomes.
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