Biologic Differences

A component of the cerebral edema associated with an infarct is thought to be vasogenic, due to movement of water across the BBB into the interstitial space of the brain parenchyma. Although the BBB in neonates is generally considered "immature" and therefore "less effective," these concepts have been challenged by advances in developmental neuroanatomy, as well as by recent studies using MRI in rodent models (13). For example, the higher cerebral spinal fluid protein concentration found in neonates, as compared to adults, may not be due to an ineffective BBB, but rather a physiologic mechanism that promotes protein passage across the BBB, which becomes less effective as the brain matures (14). Endothelial tight junctions, which form the basis of the BBB, also undergo developmental changes that might contribute to a developmental decline in passive permeability (15,16).

Cerebrovascular autoregulation is important in the pathogenesis of a stroke, affecting cerebral blood flow during the acute thromboembolic event and playing a role in reperfusion injury. Although preterm infants have long been thought to have a "pressure-passive" cerebral circulation, term newborns also appear to have narrow autoregulatory windows, which might make them more susceptible to brain injury at extremes of blood pressure (17-19).

Glutamate receptors are developmentally regulated in both neurons and glia, and glu-tamatergic synaptic transmission is largely NMDA receptor mediated early in development (20). NMDA-receptor-subunit composition changes with development, with the NR2B subunit predominating early, followed by increasing expression of NR2A (21). This phenomenon is important for synaptogenesis because NMDA receptors in which NR2B is expressed have slower deactivation and higher conductance (21). Like the NMDA receptor, AMPA receptor subunit composition also changes during development, with decreased expression of the GluR2 subunit at early ages (22), leading to higher calcium permeability (23). The developing brain has high concentrations of unsaturated fatty acids, high rates of oxygen consumption, low concentrations of antioxidants, and increased availability of "free" redox-active iron (24). These and many other changes in neural cell phenotypes greatly influence the response of the neonatal brain to pathologic mechanisms, such as excitotoxicity, oxidative stress, and subsequent cell death.

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