Neonatal brain hemorrhage (NBH) of prematurity is an unfortunate consequence of preterm
birth. Complications result in shunt dependence and long-term structural changes such as posthemorrhagic
hydrocephalus, periventricular leukomalacia, gliosis, and neurological dysfunction.
Several animal models are available to study this condition, and many basic mechanisms, etiological
factors, and outcome consequences, are becoming understood. NBH is an important clinical
condition, of which treatment may potentially circumvent shunt complication, and improve functional
recovery (cerebral palsy, and cognitive impairments). This review highlights key pathophysiological
findings of the neonatal vascular-neural network in the context of molecular mechanisms targeting the posthemorrhagic
hydrocephalus affecting this vulnerable infant population.
Keywords: Cerebral palsy, experimental, germinal matrix hemorrhage, hydrocephalus, mental retardation, neonatal rats, neurological
dysfunction, pathogenesis, stroke.
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