Viscerosympathetic reflexes in human spinal cord injury: relationships between detrusor pressure, blood pressure and skin blood flow during bladder distension
Authors: Wallin B. Gunnar , Burton Alexander R. , Elam Mikael , Tamaddon Kadi , Millard Richard , Macefield Vaughan G. 
Published: February 2013

New Findings

What is the central question of this study?

Dangerous increases in blood pressure (autonomic dysreflexia) can be caused by visceral stimuli in spinal cord injury, but it is not known how cutaneous vasoconstriction is related to increases in bladder and blood pressures during bladder distension.

What is the main finding and its importance?

We show that an increase in bladder pressure causes cutaneous vasoconstriction in the fingers that is inversely related to the bladder pressure. Skin blood flow was inversely related to the increase in blood pressure in nine of 15 patients. Monitoring finger blood flow therefore provides a useful, supplementary, non‐invasive means of assessing sympathetic outflow below the lesion in high thoracic or cervical spinal cord injury.

Autonomic dysreflexia, a dangerous and sustained increase in blood pressure brought about by widespread, reflexly generated vasoconstriction, can be induced by visceral or somatic sensory inputs originating below the lesion following spinal cord injury (SCI). We assessed whether cutaneous vasoconstriction below the lesion could serve as a proxy marker of incipient autonomic dysreflexia during bladder distension. Skin blood flow (pulse plethysmography), sweat release, blood pressure, heart rate, bladder and rectal pressures were recorded during routine cystometry (urodynamics) in 16 patients with SCI. Eight urological patients without SCI served as control subjects. In all SCI patients, who had sustained injuries 2 months to 44 years previously at levels C3–T3, bladder filling (mean ± SD, 339 ± 132 ml) induced increases in detrusor (bladder–rectal) pressure (52 ± 25 cmH2O) and cutaneous vasoconstriction in the fingers, but no consistent increases in sweat release. This occurred irrespective of whether the spinal lesions were complete [American Spinal Injury Association (ASIA) grade A, n = 6] or incomplete (ASIA B–D; n = 10). Group mean blood pressure for the SCI patients increased by 17 ± 15 mmHg, but in four patients the pressure decreased or did not change. Despite similar bladder volumes (423 ± 126 ml) in the control patients, the increases in detrusor pressure (14 ± 8 cmH2O) and blood pressure (9 ± 12 mmHg) were significantly smaller than in the SCI patients; moreover, there were no consistent changes in skin blood flow in the control subjects. In all SCI patients, changes in finger pulse amplitudes were inversely correlated to changes in detrusor pressure (mean r = −0.62 ± 0.17). Changes in finger pulse amplitudes correlated inversely to changes in blood pressure in nine of 15 patients. It is concluded that cystometry in SCI patients is associated with detrusor and cardiovascular reflex effects that are exaggerated compared with those in intact subjects and that measurement of skin blood flow from the fingers in patients with a high spinal lesion provides a supplementary, clinically useful, non‐invasive and continuous marker of spinally mediated viscerosympathetic reflex activity below the lesion in such patients.