The consequences of traumatic brain injury on cerebral blood flow and autoregulation: A review

In this decade, the brain argueably stands as one of the most exciting and challenging organs to study. Exciting in as far as that it remains an area of research vastly unknown and challenging due to the very nature of its an atomical design: the skull provides a formidable barrier and direct observa tions of intraparenchymal function in vivo are impractical. Moreover, traum atic brain injury (TBI) brings with it added complexities and nuances. The development of irreversible damage following TBI involves a plethora of bio chemical events, including impairment of the cerebral vasculature, which re nder the brain at risk to secondary insults such as ischemia and intracrani al hypertension. The present review will focus on alterations in the cerebr ovasculature following TBI, and more specifically on changes in cerebral bl ood flow (CBF), mediators of CBF including local chemical mediators such as K+, pH and adenosine, endothelial mediators such as nitric oxide and neuro genic mediators such as catecholamines, as well as pressure autoregulation. It is emphasized that further research into these mechanisms may help atte nuate the prevalence of secondary insults and therefore improve outcome fol lowing TBI.