Effect of cerebral blood flow and cerebrovascular autoregulation on the distribution, type and extent of cerebral injury

Global cerebral blood flow (GCBF) is low in the human neonate compared to the adult. It is even lower in mechanically ventilated, preterm infants: 10-12 ml/100 g/minute, a level associated with brain infarction in adults. The reactivity, however, of global CBF to changes in cerebral metabolism, PaCO2, and arterial blood pressure is normal, except following severe birth asphyxia, or in mechanically ventilated preterm infants, who subsequently develop major germinal layer hemorrhage. The low level of cerebral blood flow (CBF) matches a low cerebral metabolism of glucose and a relatively small number of cortical synapses in the perinatal period. It has not been possible to define a threshold for GCBF below which electrical dysfunction or brain damage occurs (such as white matter and thalamic-basal ganglia necrosis). Three explanations for the lack of clear relation between GCBF and electrical brain activity of the preterm infant must be examined more closely: 1) low levels of CBF are adequate; 2) GCBF does not adequately reflect critically low perfusion of the white matter, and 3) acute white matter ischemia does not result in electrical silence. Two clinical patterns of brain damage following asphyxia may be explained by changes in the blood flow distribution induced by asphyxia: brainstem sparing and parasagittal cerebral injury. Hours to days after severe asphyxia, a state of marked global hyperperfusion may prevail. It is associated with poor neurological outcome and may be an entry point for trials of interventions aiming sat blocking the translation of asphyctic injury to cellular death and tissue damage.