Anoxic-ischemic encephalopathy in the human neonatal period. The significance of brain stem involvement.
Although the human brain stem is considered relatively invulnerable to ischemic anoxia, evaluation of 16 cases of a single acute asphyxial episode either at or following birth indicates that such involvement is a frequent and characteristic aspect of anoxic encephalopathy in the infant. Ischemic cell change, neuronal loss, and nuclear or reticular formation gliosis were present in the brain stem of all but one infant. At least two topographic patterns of anoxic encephalopathy exist: (1) a rostrocaudal pattern of decreasing vulnerability, with the cerebral cortex being most sensitive and the brain stem least sensitive, and (2) a pattern of brain stem and thalamic damage. Of the two, the latter pattern appears to follow most acute asphyxial episodes in the human neonate and infant.
D000293:Adolescent; D001921:Brain / Q000098:blood supply*; D001933:Brain Stem / Q000473:pathology*; D002540:Cerebral Cortex / Q000473:pathology; D002675:Child, Preschool; D003342:Corpus Striatum / Q000473:pathology; D005829:Geniculate Bodies / Q000473:pathology; D005917:Globus Pallidus / Q000473:pathology; D006801:Humans; D002534:Hypoxia, Brain / Q000473:pathology*; D007223:Infant; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000473:pathology*; D007245:Inferior Colliculi / Q000473:pathology; D007511:Ischemia / Q000473:pathology*; D013787:Thalamic Nuclei / Q000473:pathology