Individuals with spinal cord injury (SCI) have a significantly increased risk for cognitive impairment that is associated with cerebrovascular remodeling and endothelial dysfunction. The sub-acute stage following high thoracic SCI is characterized by increased fibrosis and stiffness of cerebral arteries. However, a more prolonged duration after SCI exacerbates cerebrovascular injury by damaging endothelium. Endothelial dysfunction is associated with reduced expression of transient receptor potential cation channel 4 that mediates the production of nitric oxide and epoxyeicosatrienoic acids following shear stress and the response to carbachol and other endothelium-dependent vasodilators. Reduced expression of CD31 in cerebral arteries also suggests the loss of endothelial cell integrity following chronic SCI. Repetitively transient hypertension and intermittent hypotension contribute to cerebrovascular endothelial dysfunction in the animals with a sub-acute stage of high thoracic SCI. The increase in vascular remodeling and endothelial dysfunction ultimately reduce cerebral blood flow, which promotes cerebral hypoperfusion and cognitive dysfunction in the chronic phase of SCI. In conclusion, the duration and magnitude of fluctuations in blood pressure after SCI play a vital role in the onset and progress of cerebrovascular dysfunction, which promotes the development of cognitive impairment.
Keywords: Autoregulation; Blood pressure; Cerebral blood flow; Cerebrovasculature; Cognitive impairment; Endothelial dysfunction; Spinal cord injury; Vascular remodeling.