Regulation of Cerebral Blood Flow after Spinal Cord Injury

Abstract

Significant cardiovascular and autonomic dysfunction occurs after era spinal cord injury (SCI). Two major conditions arising from autonomic dysfunction are orthostatic hypotension and autonomic dysreflexia (i.e., severe acute hypertension). Effective regulation of cerebral blood flow (CBF) is essential to offset these drastic changes in cerebral perfusion pressure. In the context of orthostatic hypotension and autonomic dysreflexia, the purpose of this review is to critically examine the mechanisms underlying effective CBF after an SCI and propose future avenues for research. Although only 16 studies have examined CBF control in those with high-level SCI (above the sixth thoracic spinal segment), it appears that CBF regulation is markedly altered in this population. Cerebrovascular function comprises three major mechanisms: (1) cerebral autoregulation, (i.e., ΔCBF/Δ blood pressure); (2) cerebrovascular reactivity to changes in PaCO2 (i.e. ΔCBF/arterial gas concentration); and (3) neurovascular coupling (i.e., ΔCBF/Δ metabolic demand). While static cerebral autoregulation appears to be well maintained in high-level SCI, dynamic cerebral autoregulation, cerebrovascular reactivity, and neurovascular coupling appear to be markedly altered. Several adverse complications after high-level SCI may mediate the changes in CBF regulation including: systemic endothelial dysfunction, sleep apnea, dyslipidemia, decentralization of sympathetic control, and dominant parasympathetic activity. Future studies are needed to describe whether altered CBF responses after SCI aid or impede orthostatic tolerance. Further, simultaneous evaluation of extracranial and intracranial CBF, combined with modern structural and functional imaging, would allow for a more comprehensive evaluation of CBF regulatory processes. We are only beginning to understand the functional effects of dysfunctional CBF regulation on brain function on persons with SCI, which are likely to include increased risk of transient ischemic attacks, stroke, and cognitive dysfunction.