glycogen and Attention-Deficit-Disorder-with-Hyperactivity

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.

Topics: Age Factors; Animals; Attention Deficit Disorder with Hyperactivity; Brain; Cerebral Cortex; Cochlear Nerve; Extracellular Space; Glycogen; Hippocampus; Humans; Hyperbilirubinemia; Locus Coeruleus; Mitochondria; Nerve Degeneration; Nerve Endings; Neurons; Olfactory Bulb; Rats