![]() These manifestations include resting hypotension, a drop in BP in response to an orthostatic challenge (orthostatic hypotension, OH) and episodes of transient hypertension (autonomic dysreflexia, AD), which is a reflex response to noxious or non-noxious afferent stimuli from below the level of injury, such as a full bladder, constipation, or sexual stimulation. Consequently, debilitating cardiovascular impairments commonly manifest in these individuals ( Phillips and Krassioukov, 2015). Indeed, an SCI at or above the sixth thoracic level (≥ T6) can disrupt supraspinal sympathetic control to the heart (preganglionic neurons exiting between T1 - T5 spinal segments) and vascular tone of blood vessels in the trunk and lower extremities (preganglionic neurons exiting between T1 - L2 spinal segments). The cerebrovascular health consequences (i.e., elevated risk-of-stroke and cognitive dysfunction) associated with chronic SCI are likely a result of altered autonomic cardiovascular control ( Kim and Tan, 2018 Sachdeva et al., 2019). A recent systematic review also indicated that up to 60% of individuals with SCI suffer from global cognitive deficits ( Sachdeva et al., 2018). Large population studies have indicated an increased incidence of cerebrovascular disease, such as stroke, in individuals with spinal cord injury. Collectively, these results may partially explain the increased cerebrovascular health burden in individuals with SCI. Our preliminary findings reveal an important difference between the cohorts in the dynamic CVR component, tau. Thus, living with a SCI for a longer period of time, having a higher NLI and lower blood pressure are linked with poorer CVR outcomes. Lower CVR whole and ssCVR in the SCI-cohort was significantly (P<0.05) correlated with lower daytime blood pressure (R S≥ 0.81) and a higher frequency of hypotensive episodes (R S≥ -0.83). Neurological level of injury (NLI), modified into an ascending, continuous numeric variable, was positively correlated with GM CVR whole (R S=0.85, p=0.016), GM ssCVR (R S=0.95, p=0.001) and brainstem ssCVR (R S=0.90, p=0.006). Time since injury (TSI) displayed negative correlations with ssCVR in the GM and brainstem of SCI participants: R S=-0.77, p=0.041 and R S=-0.76, p=0.049, respectively, where R S is the Spearman’s rank Correlation Coefficient. Our results showed a longer tau in the GM of SCI participants compared to controls (median of the difference = 3.0 seconds p<0.05). A 24-hour ambulatory blood pressure monitor was worn to capture free-living blood pressure outcomes. In addition, CVR was further decomposed into its dynamic (tau) and static components (steady state CVR ssCVR). Initially, CVR was calculated as is standard, via the linear, least-squares fit across the whole gas challenge protocol (CVR whole). The CVR outcome measure was assessed in three ways. CVR was measured by assessing the MRI-blood oxygen level–dependent signal with hypercapnic challenge (controlled CO 2 inhalation). Thirteen participants (7 chronic SCI (all male, median age of 42 years), 6 controls (all male, median age of 33 years) were studied cross-sectionally. carbon dioxide, CO 2) or altered metabolic demand. CVR represents the capacity of brain parenchyma to change cerebral blood flow in response to a vasoactive stimulus (e.g. The aim of this study was to assess cerebrovascular reactivity (CVR) in both the grey matter (GM) and brainstem using functional magnetic resonance imaging (fMRI) in participants with SCI compared to non-injured controls. These impairments can lead to alterations in blood flow, cerebral perfusion pressure and ultimately tissue perfusion, which can lead to an elevated risk of stroke and global cognitive deficits. Cervical and upper-thoracic spinal cord injury (SCI) commonly results in autonomic cardiovascular impairments.
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