Abstract
In presenting the neuropathology of asphyxia neonatorum and some related conditions, as illustrated in experiments with monkeys (12), I have tried to make six principal points. (i) Newborn monkeys need not be asphyxiated to the point of terminal apnea to suffer structural brain damage. Mental retardation has not been proved, but neither has it been excluded, in these monkeys. (ii) Asphyxia neonatorum requiring resuscitation of the offspring, which otherwise would die, is associated with a remarkably constant syndrome of bilaterally symmetrical, nonhemorrhagic lesions in thalamic and brain-stem nuclei, mainly those of afferent systems. The individuals in this category clearly are retarded. (iii) Asphyxia neonatorum of this second degree may be associated with postpartum complications leading to neocortical atrophy, often of considerable magnitude. The individuals are markedly retarded, often palsied, epileptic, and in a few instances even comatose. (iv) Increased intrauterine pressure in the monkey during prolonged labor leads to fetal and postpartum depression, in connection with which cerebral cortical injury occurs in the absence of typical asphyxial lesions. (v) The relationship of cerebral hemorrhages to mental retardation is not clear, but their presence at autopsy probably signifies trauma during birth, or is an agonal artifact associated with death after postpartum depression. (vi) Finally, kernicterus, a condition in which bile pigment escapes into the brain tissues from the blood when the bilirubin level is high and when there is, in combination with it, some depressing factor such as asphyxia, has been produced in the newborn monkey. It, too, is associated with mental retardation.