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Increasing data suggest that these <jats:italic>chronic<\/jats:italic> deficits primarily reflect <jats:italic>acute<\/jats:italic> neuronal and glial injury sustained during adverse in utero events, such as exposure to severe hypoxia\u2013ischemia and inflammation. In the present review we examine recent evidence that this chronic impairment is partly due to upregulation of physiological apoptosis, related to input deprivation, and output isolation secondary to acute white and gray matter damage and axonal injury. However, progenitor cells in the subventricular zone (SVZ) are also vulnerable to injury, and loss of part of this critical population likely further compromises brain development. Based on these concepts the impact of proposed interventions such as induced hypothermia and endogenous growth factors are likely to be complex, but potentially offer focused ways of improving the outcomes of premature birth. 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