Candidate neuroinflammatory markers of cerebral autoregulation dysfunction in human acute brain injury

Abstract

The loss of cerebral autoregulation (CA) is a common and detrimental secondary injury mechanism following acute brain injury and has been associated with worse morbidity and mortality. However patient outcomes have not as yet been conclusively proven to have improved as a result of CA-directed therapy. While CA monitoring has been used to modify CPP targets, this approach cannot work if the impairment of CA is not simply related to CPP but involves other underlying mechanisms and triggers, which at present are largely unknown. Neuroinflammation, particularly inflammation affecting the cerebral vasculature, is an important cascade that occurs following acute injury. We hypothesise that disturbances to the cerebral vasculature can affect the regulation of CBF, and hence the vascular inflammatory pathways could be a putative mechanism that causes CA dysfunction. This review provides a brief overview of CA, and its impairment following brain injury. We discuss candidate vascular and endothelial markers and what is known about their link to disturbance of the CBF and autoregulation. We focus on human traumatic brain injury (TBI) and subarachnoid haemorrhage (SAH), with supporting evidence from animal work and applicability to wider neurologic diseases.