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Hypoxic-Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy is a special form of fetal injury whose prevalence is only now being fully appreciated because neuroimaging enables examination of the fetal brain during pregnancy. Injury is attributable to hemodynamic mechanisms in up to 25% of preterm newborns (<1,500 g) at birth and in a much smaller but still meaningful proportion of more mature infants (Del Toro et al. 1991). Injury is caused by a wide spectrum of prenatal pathologic conditions, maternal, fetal, and placental, including ischemia (Callahan et al. 1990), hypertension (leading to peri- and intra-ventricular hemorrhages), and reperfusion after ischemia (leading to peri- and in-tra-ventricular hemorrhage and hemorrhagic peri-ventricular leukomalacia). Hemorrhagic periven-tricular leukomalacia can also occur secondary to venous infarction if massive peri- and intra-ven-tricular hemorrhage has obstructed draining veins (Volpe 2001). The hemorrhaging can also be delayed (cf. Darrow et al. 1988). The factors associated with neuropathological findings in immature newborns are summarized in Table 21.1.

The basic principles of ischemic brain injury may be explained at the molecular level. Oxidative stress is suggested to be involved in normal aging, especially also in the human fetal brain (Yamamoto et

Fig. 21.3a, b. Malformation due to abnormal neuronal migration. a Polymicrogyria; b glial nodules within the enlarged ventricular system by the vascular anatomy: the periventricular white matter (germinal matrix) is a vascular end zone supplied by long penetrating arteries arising from pial arteries on the brain surface. The oligodendrocytes in particular are injured (Liu et al. 2002). Moreover, the subependymal veins appear vulnerable to rupture. The structural immaturity of the veins in premature neonates is causally related to the high incidence of germinal matrix hemorrhage (Figs. 21.4c, d, 21.5a, b) (Anstrom et al. 2004). An additional increase in excitatory amino acids plus additional biochemical alterations are thought to mediate the pathogenesis of this type of encephalopathy.

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