Brain damage in the premature or full-term fetus or newborn infant encompasses multiple patterns of injury, many considered to be anomalous in origin. However, there is increasing evidence that such congenital lesions arise as a consequence of hypoxia or ischemia (reperfusion failure). Animal models have been helpful in elucidating the underlying cellular and molecular mechanisms responsible for perinatal brain damage. Ultimately, neuroprotective strategies will prevent or minimize the occurrence of these lesions and their consequent functional deficiencies.
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