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JAMA. 1965;194(8):905. doi:10.1001/jama.1965.03090210069020.
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Subependymal cerebral hemorrhage with intraventricular inundation, a condition peculiar to premature infants who die in the perinatal period, has been recognized for many years as a result of anoxia. The frequent occurrence of subependymal bleeding in premature infants suggests that a predisposing developmental factor exists in the subependymal matrix which results in bleeding into the primitive undifferentiated tissue. Possible predisposing factors previously considered include large thin-walled veins that lack adequate supporting fibers, congenital vascular defects, and terminal veins that are unusually susceptible to venous congestion and damage secondary to anoxia.

In the November issue of the American Journal of the Diseases of Children1 a reassessment of the natural history and pathology of subependymal bleeding suggests that the bleeding is a pathological response in premature infants to a combination of complications during pregnancy, at delivery, and after birth which cause trauma and anoxia, of which anoxia appears to be most


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