The injury response in the term newborn brain: can we neuroprotect?

Curr Opin Neurol. 2003 Apr;16(2):147-54. doi: 10.1097/01.wco.0000063775.81810.79.

Abstract

Purpose of review: Perinatal hypoxia-ischemia is responsible for significant morbidity and mortality in term infants. The developing brain is uniquely vulnerable to hypoxic-ischemic injury, with a complex evolution of injury that affords opportunities for intervention, yet potentially jeopardizes normal maturational processes.

Recent findings: Data published over the past year have provided insights into the evolution of injury, and have suggested a greater role for oxidants and inflammatory mediators.

Summary: The search for ideal neuroprotective agents and techniques for timely injury detection is actively progressing and has led to advances in our understanding of pathogenesis.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Antioxidants / therapeutic use
  • Fetal Diseases / metabolism
  • Fetal Diseases / prevention & control
  • Glutamic Acid / metabolism
  • Humans
  • Hypothermia, Induced
  • Hypoxia-Ischemia, Brain / metabolism*
  • Hypoxia-Ischemia, Brain / prevention & control*
  • Infant, Newborn
  • Infant, Newborn, Diseases / metabolism
  • Infant, Newborn, Diseases / prevention & control
  • Inflammation / physiopathology
  • Neuroprotective Agents / therapeutic use
  • Oxidative Stress / drug effects
  • Receptors, N-Methyl-D-Aspartate / metabolism

Substances

  • Anti-Inflammatory Agents
  • Antioxidants
  • Neuroprotective Agents
  • Receptors, N-Methyl-D-Aspartate
  • Glutamic Acid