Baroreflex Function after Spinal Cord Injury

1 Cardiovascular Physiology and Rehabilitation Laboratory, Physical Activity Promotion and Chronic Disease Prevention Unit, University of British Columbia , British Columbia, Canada .
Journal of neurotrauma (Impact Factor: 3.71). 08/2012; 29(15):2431-45. DOI: 10.1089/neu.2012.2507
Source: PubMed


Abstract Significant cardiovascular and autonomic dysfunction occurs after spinal cord injury (SCI). It is now recognized that cardiovascular disease is a leading cause of morbidity and mortality in SCI. Patients with SCI may also suffer severe orthostatic hypotension and autonomic dysreflexia. Baroreflex sensitivity (i.e., the capability of the autonomic nervous system to detect and respond effectively to acute changes in blood pressure) has been recognized as having predictive value for cardiovascular events, as well as playing a role in effective short-term regulation of blood pressure. The purpose of this article is to review the mechanisms underlying effective baroreflex function, describe the techniques available to measure baroreflex function, and summarize the literature examining baroreflex function after SCI. Finally, we describe the potential mechanisms responsible for baroreflex dysfunction after SCI and propose future avenues for research. Briefly, although cardiovagal baroreflex function is reduced markedly in those with high-level lesions (above the T6 level), the reduction appears to be partially mitigated in those with low-level lesions. Although no studies have examined the sympathetic arm of the baroreflex in those with SCI, despite this being arguably more important to blood pressure regulation than the cardiovagal baroreflex, nine articles have examined sympathetic responses to orthostatic challenges; these findings are reviewed. Future studies are needed to describe whether dysfunctional baroreflex sensitivity after SCI is due to arterial stiffening or a neural component. Further, measurement of forearm vascular conductance and/or muscle sympathetic nerve activity is required to directly evaluate the sensitivity of the sympathetic arm of the baroreflex in those with SCI.

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    • "The medullary region of the brainstem is the primary centre of autonomic control. Poor cerebrovascular regulation after SCI in the medullary region may exacerbate blood pressure and autonomic instability commonly found in this population [19,20]. Blood flow delivery to the medullary region of the brain is a combination of arterial branches (i.e., anterior spinal artery, posterior inferior cerebellar artery) deriving from the vertebral arteries. "
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    ABSTRACT: Purpose: To compare neurovascular coupling in the posterior cerebral artery (PCA) between those with spinal cord injury (SCI) and able bodied (AB) individuals. Methods: A total of seven SCI and seven AB were matched for age and sex. Measures included PCA velocity (PCAv), beat-by-beat blood pressure and end-tidal carbon dioxide. Posterior cerebral cortex activation was achieved by 10 cycles of (1) 30 s eyes closed (pre-stimulation), (2) 30 s reading (stimulation). Results: Blood pressure was significantly reduced in those with SCI (SBP: 100 ± 13 mmHg; DBP: 58 ± 13 mmHg) vs.
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    ABSTRACT: Disruption of autonomic control after spinal cord injury (SCI) results in life-threatening cardiovascular dysfunctions and impaired endurance performance; hence, an improved ability to recognize those at risk of autonomic disturbances is of critical clinical and sporting importance. PURPOSE: To assess the effect of neurological level, along with motor, sensory, and autonomic completeness of injury, on cardiovascular control in Paralympic athletes with SCI. METHODS: 52 highly-trained male Paralympic athletes (age 34.8 ± 7.1 y) from 14 countries with chronic SCI (C2-L2) completed 3 experimental trials. During trial 1, motor and sensory function was assessed according to the American Spinal Injury Association Impairment Scale (AIS). During trial 2, autonomic function was assessed via sympathetic skin responses (SSRs). During trial 3, cardiovascular control was assessed via the beat-by-beat blood pressure response to orthostatic challenge. RESULTS: Athletes with cervical SCI exhibited the lowest seated blood pressure and the most severe orthostatic hypotension (OH; p<0.025). There were no differences in cardiovascular function between athletes with different AIS grades (p>0.96). Conversely, those with the lowest SSR scores exhibited the lowest seated blood pressure and most severe OH (p<0.002). Linear regression demonstrated that the combined model of neurological level and autonomic completeness of SCI explained the most variance in all blood pressure indices. CONCLUSION: We demonstrate for the first time that neurological level and SSR score provides the optimal combination of assessments to identify those at risk of abnormal cardiovascular control. We advocate the use of autonomic testing in the clinical and sporting classification of SCI athletes.
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    ABSTRACT: Significant cardiovascular and autonomic dysfunction occurs following a 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 the potential drastic alterations in cerebral perfusion pressure. In the context of orthostatic hypotension and autonomic dysreflexia, the purpose of this review is to examine systematically the mechanisms underlying effective CBF following SCI and propose future avenues for research. Although only 15 studies have examined CBF control in those with high level SCI (above the 6th thoracic level), it appears that CBF regulation is markedly altered in this population. Cerebrovascular function is comprised of three major mechanisms: 1) cerebral autoregulation, which can be broken down into static cerebral autoregulation (i.e., the relative change in CBF responding to steady-state changes in blood pressure) and dynamic cerebral autoregulation (i.e., relative change in CBF responding to rapid changes in blood pressure); 2) cerebrovascular reactivity to changes in PaCO2 (i.e. relative change in CBF in response to altered blood gas concentration); and 3) neurovascular coupling (i.e., the relative change in CBF in response to altered metabolic demand). While static cerebral autoregulation is 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 increased parasympathetic activity. Future studies are needed to describe whether altered CBF responses after SCI aid or impede orthostatic tolerance. Further, simultaneous evaluation of extra- and intra cranial CBF, combined with modern structural and functional imaging, would allow for a more comprehensive evaluation of CBF regulatory processes.
    Full-text · Article · Jun 2013 · Journal of neurotrauma
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