Neurobiology of Hypoxic-Ischemic Injury in the Developing Brain

Pediatr Res. 2001 Jun;49(6):735-41. doi: 10.1203/00006450-200106000-00003.

Abstract

Hypoxic ischemia is a common cause of damage to the fetal and neonatal brain. Although systemic and cerebrovascular physiologic factors play an important role in the initial phases of hypoxic-ischemic injuries, the intrinsic vulnerability of specific cell types and systems in the developing brain may be more important in determining the final pattern of damage and functional disability. Excitotoxicity, a term applied to the death of neurons and certain other cells caused by overstimulation of excitatory, mainly glutamate, neurotransmitter receptors, plays a critical role in these processes. Selected neuronal circuits as well as certain populations of glia such as immature periventricular oligodendroglia may die from excitotoxicity triggered by hypoxic ischemia. These patterns of neuropathologic vulnerability are associated with clinical syndromes of neurologic disability such as the extrapyramidal and spastic diplegia forms of cerebral palsy. The cascade of biochemical and histopathologic events triggered by hypoxic ischemia can extend for days to weeks after the insult is triggered, creating the potential for therapeutic interventions.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Brain / embryology
  • Brain / growth & development*
  • Brain Injuries / etiology*
  • Brain Injuries / pathology
  • Brain Injuries / physiopathology
  • Brain Ischemia / pathology
  • Brain Ischemia / physiopathology
  • Cerebral Palsy / etiology
  • Cerebral Palsy / pathology
  • Cerebral Palsy / physiopathology
  • Fetal Hypoxia / pathology
  • Fetal Hypoxia / physiopathology
  • Glucose / metabolism
  • Glutamic Acid / metabolism
  • Humans
  • Hypoxia, Brain / pathology
  • Hypoxia, Brain / physiopathology
  • Mitochondria / metabolism
  • Nerve Degeneration

Substances

  • Glutamic Acid
  • Glucose