Autonomic dysreflexia in response to pudendal nerve stimulation

Abstract

Study design: Pudendal nerve stimulation in complete spinal cord injury (SCI). Objective: To evaluate the influence of pudendal nerve stimulation on the cardiovascular system in SCI patients in order to assess the underlying neuronal mechanism and the potential risk during stimulation. Setting: Swiss Paraplegic Center, and University Hospital, Zurich. Methods: A total of 22 male patients with a complete SCI were divided into two groups according to the level of lesion: group A (C6-T6, n ¼ 15) and group B (T7-L2, n ¼ 7). A total of 66 stimulations using biphasic rectangular impulses (0.2 ms, 10 Hz) with intensities up to 100 mA were applied to the dorsal penile nerve. Of these, 15 stimulations in five patients were repeated after intravenous application of 7 mg of phentolamine. Heart rate (HR) and blood pressure (BP) were recorded by a Finapres s cuff applied to the right index finger. Results: Significant increased diastolic and systolic BP accompanied by significant decreased HR suggested the occurrence of autonomic dysreflexia (AD) during pudendal nerve stimulation. These cardiovascular changes corresponded with the subjective sensation of AD symptoms in patients of group A. Intravenous phentolamine lowered the resting BP and prevented severe hypertension during stimulation. Patients in group B presented with mild HR and BP changes in response to pudendal nerve stimulation and reported no AD symptoms. Conclusion: Our results show a considerable effect of electrical pudendal nerve stimulation on HR and BP in patients with high SCI. This may indicate that sacral somatic afferent fibers of the pudendal nerve are involved in the neuronal mechanism of AD in SCI patients with high neurological level. Intravenous phentolamine enables pudendal nerve stimulation without the risk of severe hypertension.

The effect of semiconditional dorsal penile nerve electrical stimulation on capacity and compliance of the bladder with deformity in spinal cord injury patients: a pilot study

“…These pain sensations induced by electrical stimulation increased the sympathetic outflow. 20 In this study, AD during semiconditional stimulation on the DPN was not observed in the six subjects.…”

Input–output relationships of a somatosympathetic reflex in human spinal injury

“…Values are presented as the mean of the peak response ±SE n the number of subjects who responded to a given stimulus Clin Auton Res (2009) 19:213-220 217 [3,5,9,20,21]. An increase in blood pressure can infer an increase in muscle and/or splanchnic vasoconstrictor drive, while cutaneous vasoconstriction and sweat release can infer an increase in cutaneous sympathetic nerve activity.…”

Somatosympathetic Vasoconstrictor Reflexes in Human Spinal Cord Injury: Responses to Innocuous and Noxious Sensory Stimulation below Lesion

“…Nevertheless, recording the effector-organ responses does provide a means of assessing sympathetic function indirectly: an increase in muscle and/or splanchnic vasoconstrictor drive can be inferred from an increase in blood pressure (assuming heart rate does not increase in parallel), while an increase in cutaneous vasoconstrictor or sudomotor drive can be inferred by a decrease in skin blood flow (measured by laser Doppler or photoelectric plethysmography) or by an increase in sweat release (measured indirectly from changes in electrical resistance, conductance, or potential of the skin – termed the galvanic skin response or the skin sympathetic response ). Indeed, there have been several attempts to assess the autonomic completeness of a spinal lesion by recording the electrodermal responses to electrical stimulation below and above lesion (Fuhrer, 1975; Cariga et al, 2002; Reitz et al, 2003; Ogura et al, 2004). While each of these studies found that a complete spinal lesion abolishes sudomotor responses in the lower limbs to electrical stimulation above lesion, Cariga et al (2002) concluded that the isolated spinal cord cannot generate cutaneous sympathetic responses, as demonstrated by the absence of electrodermal responses in the lower limbs to stimuli delivered below lesion.…”