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CNS changes in hyperbilirubinemia. Functional implications.

J Y Jew, D Sandquist

    Archives of Neurology
    |March 1, 1979
    PubMed
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    Neonatal jaundice (hyperbilirubinemia) can cause subtle neurological impairments. This study in a kernicterus animal model revealed widespread neuronal damage, suggesting a link to minimal cerebral dysfunction in infants.

    Area of Science:

    • Neuroscience
    • Toxicology
    • Developmental Biology

    Background:

    • Neonatal jaundice (hyperbilirubinemia) is a known cause of motor and hearing deficits in cerebral palsy.
    • The role of hyperbilirubinemia in subtler neurological impairments remains debated.

    Purpose of the Study:

    • To investigate the neuropathological effects of hyperbilirubinemia in a rodent model of kernicterus.
    • To explore the potential link between neonatal jaundice and minimal cerebral dysfunction.

    Main Methods:

    • Utilized a mutant animal model exhibiting kernicterus-like symptoms.
    • Examined neurons in the hippocampus, cerebral cortex, cochlear nuclei, locus ceruleus, and olfactory bulb via electron microscopy.

    Main Results:

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  • Observed pathological changes in all examined CNS areas.
  • These changes included mitochondrial and endoplasmic reticulum enlargement, vacuolation, glycogen deposition, increased extracellular space, myelin figures, and degenerating nerve terminals.

    • Conclusions:

    • The widespread neuronal pathology in the animal model suggests a potential explanation for minimal cerebral dysfunction observed in jaundiced infants.
    • Findings support the hypothesis that hyperbilirubinemia can induce subtle, widespread central nervous system (CNS) neuronal damage.