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Neonatal germinal matrix hemorrhage/intraventricular hemorrhage (GMH/IVH) remains a common form of intracranial hemorrhage in preterm infants. It is an important cause of long-term morbidities among survivors of neonatal intensive care. The hemorrhage is typically located in the cerebral ventricles. However, hemorrhage in its least severe form may be restricted to the germinal matrix area or subependyma without blood in the ventricles. Germinal matrix hemorrhage may evolve to rupture into the ventricular space.

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GMH/IVH is a neurological disorder unique to preterm infants.1 Its incidence decreases as gestational age birth weight increase.2 Because of improvement in perinatal and neonatal care, the incidence of GMH/IVH has decreased over the past several years but to a lesser extent than the decline in neonatal mortality.3,4 About 3 decades ago, GMH/IVH was noted in 45% of those with birth weight of 1500 grams or less and in greater than 60% of those with birth weight of 750 grams or less.5 In the 1990s, the incidence of GMH/IVH remained around 40% among the extremely low-birth-weight survivors,6 decreasing to 22% between 2000 and 2002.7 The more severe hemorrhages, grades III and IV, were reported to occur in 12% to 17% of the extremely low-birth-weight infants3 and in as high as 24% of those with birth weight of 750 grams or less.2 These severe hemorrhages occur in 17% to 28% of those with gestational age 22 to 26 weeks and in 9% to 14% of those 27 to 32 weeks’ gestation.8 Also, as to gender predisposition, boys are reported more likely to sustain GMH/IVH and are at higher risk for neurological sequelae.9

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The pathogenesis of GMH/IVH is complex1 and involves multiple risk factors and disorders that may cause biochemical, inflammatory, and hemodynamic alterations, predisposing to the development of hemorrhage. Further, the mechanisms for predisposition to hemorrhage, and the relationship among GMH/IVH and white matter and neuronal injury have recently been linked to generation of free radicals, reactive oxygen and nitrogen species, and genes-environment interactions.10,11 The origin of hemorrhage is the germinal matrix, a prominent structure in the preterm brain in the second and early third trimesters, which undergoes involution as gestation reaches term. The germinal matrix structure contains neuronal precursor cells prior to 20 weeks of gestation. As development progresses, the differentiating glioblasts give rise to oligodendroglial cells, which are important to myelination. The germinal matrix is supplied by a complex capillary network but is a low blood flow structure.12,13 The susceptibility of the thin-walled germinal matrix capillaries to rupture may be due to their large diameter, which offers lesser resistance to changes in intravascular pressure,14 and to endothelial cell tight junctions, which are still undergoing maturation of their specialized function through the third trimester.15 Rupture of the capillaries results when the endothelial wall loses integrity and or when there is imbalance of pressure between the intravascular lumen and ...

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