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Hypoxic-ischemic brain injury: addressing the disconnect between pathophysiology and public policy.

Hypoxic-ischemic brain injury (HI-BI) denotes a physiologically significant disruption of brain function due to a deficient supply of oxygen to the brain resulting from a reduced level of circulating arterial oxygen or diminished blood-oxygen saturation or insufficiency of hemoglobin (i.e., hypoxia), failure of cerebral perfusion (i.e., ischemia), or a combination of these factors (i.e., hypoxia-ischemia) [9]. The causes and the neurological consequences of hypoxia and hypoxia-ischemia are complex, and they vary with the relative contributions of these pathophysiologic processes and their durations in a given individual [4]. The pathophysiologic, etiologic, and demographic heterogeneity of HI-BI is reflected in the wide variety of neurological, neurobehavioral, and functional outcomes associated with this category of brain injuries [2,8,10,12–14]. Although this general definition and understanding of HI-BI is used commonly by neurologists and neurorehabilitation specialists, it is important that we acknowledge at the outset of this issue of NeuroRehabil-