Alterations in autonomic cerebrovascular control after spinal cord injury.

Among chronic cardiovascular and metabolic sequelae of spinal cord injury (SCI) is an up-to four-fold increase in the risk of ischemic and hemorrhagic stroke, suggesting that individuals with SCI cannot maintain stable cerebral perfusion. In able-bodied individuals, the cerebral vasculature is able to regulate cerebral perfusion in response to swings in arterial pressure (cerebral autoregulation), blood gases (cerebral vasoreactivity), and neural metabolic demand (neurovascular coupling). This ability depends, at least partly, on intact autonomic function, but high thoracic and cervical spinal cord injuries result in disruption of sympathetic and parasympathetic cerebrovascular control. In addition, alterations in autonomic and/or vascular function secondary to paralysis and physical inactivity can impact cerebrovascular function independent of the disruption of autonomic control due to injury. Thus, it is conceivable that SCI results in cerebrovascular dysfunction that may underlie an elevated risk of stroke in this population, and that rehabilitation strategies targeting this dysfunction may alleviate the long-term risk of adverse cerebrovascular events. However, despite this potential direct link between SCI and the risk of stroke, studies exploring this relationship are surprisingly scarce, and the few available studies provide equivocal results. The focus of this review is to provide an integrated overview of the available data on alterations in cerebral vascular function after SCI in humans, and to provide suggestions for future research.