CNS changes in hyperbilirubinemia. Functional implications
J. Y. Jew and D. Sandquist
Hyperbilirubinemia is a recognized etiologic factor in motor and hearing
disorders associated with cerebral palsy. Its role in more subtle forms of
neurological impairment is more controversial. Using a mutant animal model,
which develops symptoms and signs closely resembling the human kernicterus
syndrome, neurons of hippocampus, cerebral cortex, cochlear nuclei, losuc
ceruleus, and olfactory bulb were examined by electron microscopy.
Pathological changes, observed in all areas studied, consisted of
mitochondrial and endoplasmic enlargement and vacuolation, with glycogen
deposition; increased extracellular space; myelin figures; and degenerating
changes in nerve terminals. If we make the assumption that pathologic
changes in the human infant with neonatal jaundice are similar to changes
in the animal model, then the widespread involvement of CNS neurons in all
cortical areas examined may well help to explain the syndromes of minimal
cerebral dysfunction reported in clinical studies.
