Cerebral oxidative metabolism in perinatal post-hemorrhagic hydrocephalus / Robert C. VANNUCCI in Developmental Medicine & Child Neurology, 22-3 (June 1980)

Public ISBD [article]  inDevelopmental Medicine & Child Neurology > 22-3 (June 1980) . - p.308-316 Titre : Cerebral oxidative metabolism in perinatal post-hemorrhagic hydrocephalus Type de document : Texte imprimé et/ou numérique Auteurs : Robert C. VANNUCCI, Auteur ; Jonathan HELLMAN, Auteur ; Orest DUBYNSKY, Auteur Année de publication : 1980 Article en page(s) : p.308-316 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Survivors of perinatal intraventricular hemorrhage often develop a distinct clinical syndrome characterized by hydrocephalus and biochemical abnormalities in cerebrospinal fluid. The authors investigated six neonates with post-hemorrhagic obstructive hydrocephalus in order to identify cerebral metabolic disturbances responsible for the hypoglycorrhachia observed in this disorder. Lactic acid concentraions and lactate/pyruvate ratios in ventricular fluid were significantly elevated in infants with post-hemorrhagic hydrocephalus compared with the values in five with congenital (non-hemorrhagic) obstructive hydrocephalus. Comparable degrees of ventricular dilatation and intracranial hypertension were present in the two groups. There is evidence that neither residual cellular elements in ventricular fluid nor a disrupted blood-CSF barrier can fully explain the observed alterations in ventricular-fluid glucose, lactate or lactate/pyruvate ratios. It is suggested that when periventricular hemorrhage occurs, the associated cerebral ischemia leads to focal anaerobic glycolysis and increased glucose requirement. With inadequate cerebral glucose glycolysis and increased glucose requirement. With inadequate cerebral glucose delivery from the blood, glucose diffuses into the brain from the ventricular fluid, resulting in hypoglycorrhachia. Cerebral lactic acid production is enhanced, which accumulates in ventricular fluid in the presence of ventricular obstruction. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=509 [article] Cerebral oxidative metabolism in perinatal post-hemorrhagic hydrocephalus [Texte imprimé et/ou numérique] / Robert C. VANNUCCI, Auteur ; Jonathan HELLMAN, Auteur ; Orest DUBYNSKY, Auteur . - 1980 . - p.308-316. Langues : Anglais (eng) in Developmental Medicine & Child Neurology > 22-3 (June 1980) . - p.308-316 Index. décimale : PER Périodiques Résumé : Survivors of perinatal intraventricular hemorrhage often develop a distinct clinical syndrome characterized by hydrocephalus and biochemical abnormalities in cerebrospinal fluid. The authors investigated six neonates with post-hemorrhagic obstructive hydrocephalus in order to identify cerebral metabolic disturbances responsible for the hypoglycorrhachia observed in this disorder. Lactic acid concentraions and lactate/pyruvate ratios in ventricular fluid were significantly elevated in infants with post-hemorrhagic hydrocephalus compared with the values in five with congenital (non-hemorrhagic) obstructive hydrocephalus. Comparable degrees of ventricular dilatation and intracranial hypertension were present in the two groups. There is evidence that neither residual cellular elements in ventricular fluid nor a disrupted blood-CSF barrier can fully explain the observed alterations in ventricular-fluid glucose, lactate or lactate/pyruvate ratios. It is suggested that when periventricular hemorrhage occurs, the associated cerebral ischemia leads to focal anaerobic glycolysis and increased glucose requirement. With inadequate cerebral glucose glycolysis and increased glucose requirement. With inadequate cerebral glucose delivery from the blood, glucose diffuses into the brain from the ventricular fluid, resulting in hypoglycorrhachia. Cerebral lactic acid production is enhanced, which accumulates in ventricular fluid in the presence of ventricular obstruction. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=509

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