Cerebral Oxidative Metabolism in Perinatal Post‐hemorrhagic Hydrocephalus

Publisher Website
Google Scholar
Abstract
Survivors of perinatal intraventricular hemorrhage often develop a distinct clinical syndrome chracterized by hydrocephalus and biochemical abnormalities in CSF. Human neonates (6) with post-hemorrhagic obstructive hydrocephalus were studied to identify cerebral metabolic disturbances responsible for the hypoglycorrhachia observed in this disorder. Lactic acid concentrations and lactate/pyruvate ratios in ventricular fluid were significantly elevated in infants with post-hemorrhagic hydrocephalus compared with the values in 5 with congenital (non-hemorrhagic) obstructive hydrocephalus. Comparable degrees of ventricular dilatation and intracranial hypertension were present in the 2 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. Apparently when periventricular hemorrhage occurs, the associated cerebral ischemia leads to focal anaerobic glycolysis and increased glucose requirement. With inadequate cerebral glucose delivery from the blood, glucose diffuses into the brain from the ventricular fluid, resulting hypoglycorrhachia. Cerebral lactic acid production is enhanced, which accumulates in ventricular fluid in the presence of ventricular obstruction.