====== Periventricular-intraventricular hemorrhage etiology ======

[[Perinatal]] brain injury may lead to long-term morbidity and neurodevelopmental impairment. Improvements in perinatal care have resulted in the survival of more infants with perinatal brain injury. The effects of hypoxia-ischemia, inflammation, and infection during critical periods of development can lead to a common pathway of perinatal brain injury marked by neuronal excitotoxicity, cellular apoptosis, and microglial activation
((Novak CM, Ozen M, Burd I. Perinatal Brain Injury: Mechanisms, Prevention, and Outcomes. Clin Perinatol. 2018 Jun;45(2):357-375. doi: 10.1016/j.clp.2018.01.015. Epub 2018 Mar 21. PMID: 29747893.))

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Infants most at risk are those born before 33 weeks of gestational age, as after this time, the germinal matrix involutes.

The highly vascular [[germinal matrix]] is part of the primordial [[tissue]] of the developing [[brain]] and is the source of future [[neuron]]s and [[glial cell]]s. It is located just beneath the [[ependyma]]l lining of the [[lateral ventricle]]s, and undergoes progressive [[involution]] until 36 weeks gestational age (GA). Thus, the [[matrix]] may persist out of [[utero]] in [[premature]] infants. A disproportionate amount of the total [[CBF]] perfuses the [[periventricular]] circulation through these capillaries which are immature and fragile and have impaired [[autoregulation]]
((Lou HC, Lassen NA, Friis-Hansen B. Impaired [[Autoregulation]] of [[Cerebral Blood Flow]] in the Distressed [[Newborn]] Infant. J Pediatr. 1979; 94:118– 121))
((Milligan DWA. Failure of [[Autoregulation]] and [[Intraventricular Hemorrhage]] in [[Preterm]] Infants. Lancet. 1980; 1:896–898)).