TWO BASIC forms of hypoxic brain damage make their appearance in the fetus and newborn. The lesions, located in the cerebrum, distributed through the cortical and deep structures, are not of random occurrence. The cerebral damage evolves in precise patterns; the location of lesions is governed by the gestational age of the fetus or neonate at the time of the hypoxic event. This temporal factor is of significance not only in determining the anatomic pattern of the cerebral damage, but correspondingly, has a direct bearing on the ultimate form of the neurologic defect in infants who survive. Accordingly, the findings here offer an organic basis for correlating the occurrence of gestational complications, particularly prematurity, with the presence clinically of cerebral palsy, mental retardation, and other nervous system defects in infants who survive. Traditionally the occurrence of hypoxic damage in the neonatal brain has been minimized.