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Intraventricular hemorrhage in premature infants: mechanism of disease

Praveen Ballabh1

  • 1Department of Pediatrics, Anatomy and Cell Biology, New York Medical College-Westchester Medical Center, Valhalla, New York 10595, USA. Pballabh@msn.com

Pediatric Research
|October 10, 2009
PubMed

Insights

Intraventricular hemorrhage (IVH) in premature infants stems from fragile germinal matrix vessels. Stabilizing these vessels and restoring cerebral blood flow (CBF) may prevent IVH.

Area of Science:

  • Neonatal neuroscience
  • Vascular biology
  • Developmental neurobiology

Background:

  • Intraventricular hemorrhage (IVH) is a significant complication in premature infants.
  • IVH originates in the germinal matrix, a highly vascularized area of precursor cells in the developing brain.
  • The causes of IVH are complex, involving fragile germinal matrix vasculature and altered cerebral blood flow (CBF).

Purpose of the Study:

  • To review the pathogenesis of IVH.
  • To focus on recent molecular mechanisms underlying germinal matrix vascular fragility.
  • To identify potential strategies for IVH prevention.

Main Methods:

  • Review of existing literature on IVH pathogenesis.
  • Analysis of molecular mechanisms contributing to germinal matrix vascular fragility.
  • Examination of the roles of angiogenic factors and hypoxia.

Main Results:

  • Germinal matrix microvasculature is fragile due to abundant immature angiogenic vessels lacking pericytes.
  • Deficiencies in basal lamina and glial fibrillary acidic protein (GFAP) in astrocyte endfeet contribute to fragility.
  • Elevated VEGF and angiopoietin-2 levels promote rapid angiogenesis, potentially due to germinal matrix hypoxia.

Conclusions:

  • The fragility of germinal matrix vasculature is a key factor in IVH development.
  • High levels of angiogenic factors, possibly driven by hypoxia, exacerbate vascular immaturity.
  • Stabilizing angiogenic vessels and normalizing CBF early in life are promising strategies for IVH prevention.

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