Altered Mayer wave and baroreflex profiles in high spinal cord injury.

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.