Hypoxic-hemodynamic pathogenesis of brain lesions in the newborn.
For more than a century two opposing views on the pathogenetic mechanisms and the timing of the origin of cerebral palsy (CP) have prevailed: the idea first formulated by Little attributing CP to "difficult deliveries" has been opposed by the view by Freud recognizing fetal influences, and the issue seems to be unsettled. The present review seeks to bridge the gap by recognizing that late prenatal or perinatal hypoxic-hemodynamic insult is a dominating final common path in the pathogenesis of static encephalopathies during development, in particular in premature infants. In turn, however, such lesions are determined by early genetic and environmental influences. The pathogenesis of static encephalopathy should therefore be seen as a chain of events, with its origin before gestation.
Lou
H C
HC
Department of Pediatric Neurology, John F. Kennedy Institute, Glostrup, Denmark.
D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000196:embryology* / Q000254:growth & development; D001927:Brain Diseases / Q000196:embryology / Q000209:etiology*; D002545:Brain Ischemia / Q000150:complications*; D002543:Cerebral Hemorrhage / Q000150:complications; D002547:Cerebral Palsy / Q000196:embryology / Q000209:etiology; D005260:Female; D006801:Humans; D007022:Hypotension / Q000150:complications; D002534:Hypoxia, Brain / Q000150:complications*; D007223:Infant; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000209:etiology; D007969:Leukomalacia, Periventricular / Q000196:embryology / Q000209:etiology; D011247:Pregnancy; D011263:Pregnancy Trimester, Third