Perinatal cerebral ischaemia and developmental neurologic disorders.
In infants who die during the first months of life necrotic foci are almost invariably found. They are, as a rule, located in border zones between vascular territories, suggesting cerebral ischemia as a pathogenetic mechanism. Normally, the brain is protected against changes in perfusion pressure by autoregulation of cerebral perfusion. In utero, this mechanism is extremely fragile, and normal birth is a sufficient hypoxic insult to abolish autoregulation. Abolished autoregulation has been demonstrated in distressed newborns: Even mild hypotension, which is a common occurrence in these infants during the first few hours of life, is sufficient to induce ischemia. Follow-up studies at the ages of one and four years have shown neonatal ischemia to be the decisive factor in the development of atrophic encephalopathy and motor and cognitive dysfunction. This clarification of the pathogenetic process has important implications for prevention, which is briefly discussed.
D001794:Blood Pressure; D002545:Brain Ischemia / Q000150:complications* / Q000517:prevention & control; D002543:Cerebral Hemorrhage / Q000209:etiology; D002544:Cerebral Infarction / Q000473:pathology; D002552:Cerebral Ventricles / Q000473:pathology; D002560:Cerebrovascular Circulation; D002658:Developmental Disabilities / Q000503:physiopathology; D006706:Homeostasis; D006801:Humans; D007231:Infant, Newborn; D009422:Nervous System Diseases / Q000209:etiology; D010477:Perfusion