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In order to function effectively, the brain requires a constant supply of oxygen at a finely balanced concentration and tension. A reduction of oxygen supply (hypoxia) can occur acutely, chronically and/or intermittently during childhood, and may range in severity from a mild decline from the normal percentage of oxyhaemoglobin saturation (95–100%) to severe hypoxia coupled with ischaemia and leading to infarction. Importantly, there is increasing recognition (e.g. Bass, Corwin, Gozal, Moore, Nishida, Parker, Schonwald, Wilker, Stehle & Kinane, 2004 ) that even mild desaturation, if present persistently and/or intermittently, is sufficient to alter the otherwise expected course of cognitive and behavioural development. In this Special Issue we build upon earlier reviews of neurological and cognitive outcome in humans following experimental and clinical hypoxia ( Tune, 1964 ; Nyakas, Buwalda & Luiten, 1996 ; Wilson, 1996 ; Caine & Watson, 2000 ) to specifically consider the detrimental effects of altered oxygen delivery to the brain on neurocognitive development in childhood. Each paper focuses on a different condition, ranging in severity of hypoxia. Despite the disparate aetiology on which this Special Issue is based, evidence is marshalled to suggest that hypoxia is the common pathophysiological pathway across the conditions leading
Developmental Science – Wiley
Published: Jul 1, 2006
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