Altered Mayer wave and baroreflex profiles in high spinal cord injury

Abstract

Spinal sympathetic neurons are distributed in cord segments from Th1 to L3. High spinal cord injury demonstrates severe orthostatic hypotension, but not lower cord injury. It remains to be clarified as to where is the critical spinal level disturbing neural cardiovascular regulations in response to orthostatic stress. To address this issue, beat-to-beat blood pressure (BP) (measured using a Finapres device) and RR interval (measured electrocardiographically) were recorded at rest and in a 60 degree head-up position in 26 patients with varying levels of spinal cord injury (C4 to Th12) and in 15 healthy (control) subjects. Sympathetic vascular tone was examined by the Mayer wave power spectrum of systolic blood pressure (SBP) variability. Baroreflex sensitivity was examined by transfer function analysis of SBP and RR interval variabilities. The Mayer wave power spectrum increased in response to postural shift in most patients injured at Th4 or below, whereas this parameter either remained unchanged or decreased in patients with higher-level injury. Baroreflex sensitivity tended to decrease with postural shift in patients injured at Th3 or below, whereas this parameter increased in all patients with higher-level injury. We divided spinal patients into high-level injury (Th3 or above, n = 14) and low-level injury (Th4 or below, n = 12) groups. Systolic blood pressure significantly fell (-10 +/- 4 mm Hg, P < .05) with postural shift in high-level injury group but did not change in low-level injury group or in control subjects. The low-level injury group and the control group demonstrated essentially similar autonomic nervous responses to postural shift, ie, a significant increase in Mayer wave power and an insignificant decrease in baroreflex sensitivity. On the contrary, the high-level injury group showed opposite responses, ie, an insignificant decrease in Mayer wave power and a significant increase in baroreflex sensitivity in response to postural shift. We conclude that spinal cord injury at Th3 or above eliminates normal neural cardiovascular responses to mild orthostatic stress in humans.

Orthostatic hypotension in the first month following acute spinal cord injury

“…21,22 Supraspinal control of at least one-quarter of spinal sympathetic neurons can preserve blood pressure regulation and prevent development of OH in patients with cervical SCI. 23 Our present findings show that in contrast to patients with cervical complete SCI, patients with cervical incomplete SCI had a significantly lower prevalence of OH, which resolved by the end of the acute rehabilitation period (1 month after injury). Similar results were reported by Frisbie 24 where patients with complete cervical injuries showed greater instability of cutaneous microcirculation than patients with incomplete cervical injuries.…”

Peripheral vascular function in spinal cord injury: a systematic review

“…27,28 It is, therefore, likely that both sympathetic hypoactivity and altered baroreceptor sensitivity are the primary causes of orthostatic hypotension following cervical SCI. 29,30 However, a lack of skeletal muscle pump, 31 cardiovascular deconditioning 32 and/or altered salt and water balance 33 have also been hypothesized to contribute to hypotension.…”

Orthostatic hypotension following spinal cord injury: understanding clinical pathophysiology

“…Sympathetic nervous system dysfunction 6,28 Altered baroreceptor sensitivity 62,64 Lack of skeletal muscle pumps [49][50][51] Cardiovascular deconditioning 69 Altered salt and water balance 74 The level and severity of spinal cord injury, and the extent to which other systems are affected will play a significant role in the development of orthostatic hypotension of cervical SCI individuals in whom catecholamine levels failed to increase following head-upright tilting. 53,54 These data suggest that there is severe impairment of descending tonic cardiovascular control to the spinal autonomic circuits in individuals with cervical SCI, such that there is insufficient sympathetic outflow to release noradrenaline, and consequently impaired vascoconstriction.…”

“…[59][60][61] In support of this notion, baroreflex function (assessed using spectral analysis of oscillations in heart period and blood pressure) during orthostatic stress was found to be abnormal in SCI patients with lesions at T3 or above. 62 Furthermore, individuals with tetraplegia are also reported to have impaired baroreceptor responses to discrete stimulation of the carotid sinus using neck suction or neck pressure, whereby both the baroreceptor sensitivity and range of operation were reduced. 63 However, the impairment in baroreceptor control may not be restricted to those individuals with high-level lesions.…”