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Effect of Disrupted Autonomic Control on the Cardiovascular System

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An intact spinal cord is required for optimal autonomic function and cardiovascular stability (Furlan & Fehlings, 2008). Changes in cardiovascular function are lesion-dependent and unique to each SCI patient. Generally, higher-level spinal cord injuries result in the greatest degree of cardiovascular impairment and as such, cardiovascular complications subsequent to SCI are directly related to the neurological level of injury. After SCI, autonomic control of regions below the level of the lesion can be severely disrupted. Higher-level SCIs, particularly cervical or high-thoracic (T6 or above) injuries, are associated with significant SNS dysfunction as a consequence of the loss of supraspinal control of the SNS; this is considered the major cause of post-SCI hemodynamic imbalance and regulatory changes. Parasympathetic control of cardiac function is preserved following SCI as innervation to the heart is carried out via the vagal nerve and does not transmit through the spinal cord. Disruption of autonomic function caused by SCI results in disproportionate involvement of the SNS in comparison to the PNS in terms of hemodynamic regulation. Hypoactive sympathetic outflow together with unopposed parasympathetic activity through the intact vagal nerve leads to imbalanced autonomic control and disordered cardiac function, including clinical manifestations such as bradycardia, low resting blood pressure, and even cardiac arrest , which is particularly prominent in the acute phase post-SCI (Furlan & Fehlings, 2008; Phillips et al., 2012; Teasell et al., 2000; West et al., 2012). Regardless of the level of spinal cord injury, all blood vessels are still innervated. The SCI does not result in denervation, simply the central control is lost.

The relationship between injury severity (complete versus incomplete) and resulting cardiovascular dysregulation is less well understood and no clear association has yet been established (West et al., 2013). One of the consistent trends which has been observed is that baroreflex function and sensitivity is disrupted after SCI, although this is a more regular finding in high-level injuries (Phillips et al., 2012). Baroreflex dysfunction in SCI is thought to be influenced by increased stiffening of arteries, where stretch-receptors are located that transmit information on systemic BP (Phillips et al., 2014). Other observed alterations in cardiac function include electrocardiographic abnormalities, mean arterial blood pressure, increased BP during the night, and white matter loss (Furlan et al., 2016; Furlan, Fehlings et al., 2003; Summers et al., 2013; Goh et al., 2015).

The association between physiological dysfunction and cardiovascular complications occurring during acute SCI has been evaluated by five studies.

An observational study by Krstačić et al. (2013) assessed autonomic dysfuntion after SCI and the effect of the resulting altered sympathetic activity on the cardiovascular system. Acute cervical SCI patients were monitored beginning on their first day of hospital admission. The patients were evaluated for cardiac autonomic balance using an electrocardiogram to analyze heart rate variability (HRV) in time and frequnecy domains. As a parameter of HRV, the ratio of low to high freqencies represents sympathovagal balance, and was significantly reduced in the SCI patient group compared to the control group (0.41 versus 1.71, p<0.001); this indicates the presence of altered sympathetic activity in acute cervical SCI patients. Goh et al. (2017) observed that tetraplegics consistently had reduced blood pressure compared to paraplegics, and mobilizing controls in the acute phase. This difference, however, was no longer observable one year post admission.

Furlan et al. (2003) demonstrated an association between the location and severity of pathology in the spinal cord and cardiovascular dysfunction following SCI. This observational study retrospectively compared cervical SCI patients who developed severe cardiovascular dysfunction (Group 1) to those with no or minor cardiovascular dysfunction (Group 2). A control group of patients (Group 3) who had intact central nervous systems was also included for comparison purposes, and all patient information was collected during a 5-week post-injury period. Axonal preservation in the dorsal aspects of the lateral funiculus (Area I) and in the white matter adjacent to the dorsolateral aspects of the intermediolateral cell column (Area II) was significantly lower in Group 1 than in Group 2 participants (p<0.034 and p=0.013, respectively). There was an observed axonal loss of ~70% in Area I in Group 1 compared to 20% in Group 2 patients, and a 20% loss in Area II in Group 1 compared to 15% in Group 2 patients, suggesting the dorsal aspects of the lateral funiculus were the more likely site of descending vasomotor pathways contributing to cardiovascular dysfunction after SCI. Furlan et al. (2016) later found that there was no association between severity of SCI and cardiovascular dysfunction detectible by electrocardiograms. This suggests cardiovascular complications as a result of SCI may not be related to the severity of SCI but that the majority of those with an SCI are vulnerable to cardiac complications.

Finally, in an observational study by Summers et al. (2013), SCI patients were studied within the early stages of their emergency department resuscitation to determine the pathophysiology underlying neurogenic shock. Hemodynamic variables were collected from patients who were diagnosed with neurogenic shock using impedance cardiography. Etiology was variable; it was observed as a decrease in peripheral vascular resistance in 33% of patients, a loss of vascular capacitance in 22% of patients, or a combination of both, as seen in 33% of patients. Etiology was solely cardiac in the remaining 11% of patients.