The findings described in the present study are summarized in Table 1. It may be noted that anoxia or total asphyxia, whether in the newborn animal or in the (see article) adult, leads to patterns of injury in the brainstem. Hemispheral structures outside the thalamus seem to be entirely spared in those animals which survive. In contrast to this, situations leading to hypoxia associated with severe acidosis, usually of a mixed respiratory and metabolic type, cause brain edema; and when the edema is limited in its distribution, the damage is restricted to specific cortical loci. When the cerebral edema becomes more generalized owing to spread of the process, more and more extensive regions of the hemispheres are damaged until the entire cerebrum may become necrotic. On the other hand, clinical circumstances which lead to hypoxia but without acidosis of any great magnitude--usually due to the indolence of the process or to an associated hyperventilation of the mother--produce lesions which may be restricted to the white matter. These processes may be characterized by perivenular white matter hemorrhage and/or focal areas of periventricular leucomalacia. Finally, those clinical circumstances which lead to combined episodes of hypoxia plus anoxia with acidosis favor a predominance of lesions that affect the basal ganglia.