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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 ...