Among 592 infants examined at autopsy during a four-year period, 32 (5.4%) had cerebral infarcts. Excluded were cases of traumatic hemorrhages and softening, periventricular leukomalacia, venous lesions, and any mass, including encephaloceles, with arterial distortion and infarction. Histological abnormalities were similar to those of infarcts in adults. Relatively advanced histopathological changes in some infants living only a few hours indicated that some infactions may have occurred in utero. The most common cause of arterial occlusion was embolization, with sepsis and disseminated intravascular coagulation playing a major role. The brains of term neonates were more frequently involved than those of premature infants. Multiple small infarcts occurred more often in premature infants. In most cases autonomic dysfunction with prolonged apnea, episodic seizures, and metabolic acidosis were the major associated clinical features, rather than focal neurological deficits. Similar cerebral infarcts in infants who survive with less severe systemic complications may lead to porecephaly, hemiplegia, mental and motor retardation, and recurrent seizures.