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


RESULTS
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.


CONCLUSIONS
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.
Hamrick
Shannon E G
SE
Department of Pediatrics, Division of Child Neurology, University of California-San Francisco, 521 Parnassus Avenue, C215 San Francisco, CA 94143-0663, USA.
Ferriero
Donna M
DM
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D005315:Fetal Diseases / Q000378:metabolism / Q000517:prevention & control; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007036:Hypothermia, Induced; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism* / Q000517:prevention & control*; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000378:metabolism / Q000517:prevention & control; D007249:Inflammation / Q000503:physiopathology; D018696:Neuroprotective Agents / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D018696:Neuroprotective Agents; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid