This survey of a group of individual cerebral lesions originating in early life and which are the evident cause of crippling clinical states (cerebral palsy, mental deficiency and epilepsy) was made with the primary objective of determining their etiology and pathogenesis. Selection of the lesion to be evaluated was based upon the opinions of previous investigators and the present writer's own experience in the realm of anoxic and ischemic lesions of the brain. After what seems to be a fairly comprehensive effort to elicit evidence from various source, certain of these lesions (uniform and widespread cerebral atrophies, cortical, cortical-subcortical, subtotal and total cerebral softenings, nodular cortical atrophy, porencephaly, chronic cystic degeneration of the cerebral white matter, diffuse myelinating disorders of early life, and certain striatal disorders), were believed to have their origin in generalized or localized disturbances in the circulation. The nature, value and completeness of the evidence pointing to this conclusion vary in the individual groups of lesions. For example, the anoxic origin of the widespread and uniform cerebral atrophies rests chiefly on the demonstration of similar changes in experimental animals after simulated natal anoxemia. The generalized softenings on the other hand appear to be due either to an impairment of the carotid circulation (as incident to absent or small carotid arteries) or to severe anoxemia (as demonstrated in the counterparts of these lesions of anoxic etiology in later life). This conclusion seems to be further supported by similar lesions produced by experimental carotid occlusion in young animals. Nodular cortical atrophy and porencephalic defects, quite commonly associated in a single specimen, are almost certainly the result of arterial occlusion as indicated both by the disclosure of similar lesions in later life and by their experimental production. The circulatory (anoxic) genesis of chronic cystic degeneration of the white matter is still somewhat in question as is widespread myelinopathy of early life. Comparative studies on similar lesions of postnatal life as residuals of severe anoxemin brings out comparisons which should not be lightly ignored. Similar lesions have also been produced by cerebral anoxia in experimental animals. The anoxic etiology of structural changes in the corpus striatum and thalamus, producing somewhat less common but typical clinical syndromes of early life, is suggested by the well known vulnerability of these structures to oxygen want. The nature of the resultant lesions (with the exception of status marmoratus) in both early and late cases are quite similar which strongly implies a common pathogenetic mechanism. In the isolated case of status marmoratus, there are no comparable lesions in adult life to guide one in evaluating either its etiology or pathogenesis. In this instance, the unusually high incidence of a history of dystocia with “brain injury” suggests either a traumatic or anoxemic origin. Experimental findings suggest that the aberrant location and the hypertrophy of the myelin sheaths as well as an increase in their number in the basal ganglia may be the result of a parenchymatous deficit in the regional cortex. This lesion may therefore be an indirect or secondary one resulting from a primary anoxic or ischemic disorder. Its genesis in a venous thrombosis with resultant hemorrhages in the affected structures seems most unlikely. The writer knows of no possible biological alchemy by which focal hemorrhages can be tansformed into bundles of myelinated nerve fibers.