In the article referenced above, you opine that efficacy was due only to medication spreading close to region of the pundendal nerves?
The pudendal nerve modulates sympathetic neurons as well as contain sympathetic fibers (see articles below). Are we seeing over stimulation of sympathetic pathways secondary to pudendal neuropathy? Then it would seem that blocking components of the sympathetic neurons in the pelvic cavity may be of benefit in some.
Additionally, it has been shown that trauma to the vasa nervorum can lead to micro-infliammation promoting nerve sprouting. Don't forget that the nervous system is plexus.
As far as blocking the pudendal nerve....fairly straight forward with fluoroscopy.
Colorectal Dis. 2013 Nov;15(11):1410-5. doi: 10.1111/codi.12368.
Prolonged pudendal nerve terminal motor latency is associated with decreased resting and squeeze pressures in the intact anal sphincter.
Loganathan A1,
Schloithe AC,
Hakendorf P,
Liyanage CM,
Costa M,
Wattchow D.
Author information
Abstract
AIM:
To determine the contribution of the pudendal nerve to the anal continence mechanism by determining the correlation between pudendal nerve terminal motor latency (PNTML) and resting and squeeze anal canal pressures.
METHOD:
In all, 1051 patients were investigated with anorectal physiology studies between January 1998 and July 2010. Of these, 213 patients had intact anal sphincters on endoanal ultrasound and had undergone PNTML testing and anal manometry with measurement of resting and squeeze pressures. The relationship between PNTML and mean resting and squeeze pressures was compared in these patients with an intact anal sphincter. Values were compared using a two-sample t test with equal variances. A P value of < 0.05 was considered significant.
RESULTS:
Of these patients 40.8% had normal PNTML bilaterally, 9.9% had slow PNTML bilaterally and 21.6% had a unilateral slow PNTML. Mean resting pressure was significantly reduced in patients with unilateral slow and bilateral slow PNTML compared with normal. The magnitude of the reduction was 28% and 19% respectively. Mean squeeze pressure was significantly reduced in patients with unilateral slow and bilateral slow PNTML compared with normal. The magnitude of the reduction was 18% and 23% respectively.
CONCLUSION:
In patients with an intact anal sphincter, either unilaterally or bilaterally prolonged PNTMLs are associated with significantly decreased resting and squeeze pressures. Our results suggest that both internal and external sphincter function is impaired with pudendal nerve injury. The inhibition of internal sphincter function may be due to damage of autonomic,
principally sympathetic fibres carried in the pudendal nerve.
Neurourol Urodyn. 2003;22(6):597-601.
Afferent fibers of the pudendal nerve modulate sympathetic neurons controlling the bladder neck.
Reitz A1,
Schmid DM,
Curt A,
Knapp PA,
Schurch B.
Author information
Abstract
AIMS:
Pudendal nerve stimulation is known to have a potential modulative effect on bladder function. However, even if its efficiency has been established for various neurogenic and non-neurogenic bladder dysfunctions, the underlying neuronal mechanism, and the involved pathways in humans remain unknown. In this prospective study we focused on the effects of pudendal nerve stimulation in complete spinal cord injured patients to identify neuromodulative processes that occur on spinal level.
METHODS:
Twenty complete spinal male presenting with upper motor neuron lesion and neurogenic incontinence underwent pudendal nerve stimulation. Bladder, bladder neck (BN), and external urethral sphincter (EUS) pressures were continuously recorded with a three channel microtip pressure transducer catheter. Fifty six pudendal stimulations using biphasic rectangular impulses (0.2 ms, 10 Hz) with intensities up to 100 mA were applied to the dorsal penile nerve. In six patients, 18 stimulations were repeated after intravenous (i.v.) administration of 7 mg phentolamine.
RESULTS:
Mean BN and EUS pressure increased during stimulation significantly (P < 0.001). The latencies to the EUS responses range between 27 and 41 ms and those to the BN responses between 188 and 412 ms. Phentolamine decreased initial BN pressure and reduced the pressure rise during stimulation significantly (P < 0.05).
CONCLUSIONS:
Pudendal nerve stimulation evoked somatic responses in the EUS and autonomic responses in the smooth muscle sphincter controlling the BN. Longer latencies of the BN responses and the sensitivity to the alpha-blocking agent phentolamine suggest that sympathetic alpha-adrenergic fibers are involved. Somatic afferent fibers of the pudendal nerve are supposed to project on sympathetic thoracolumbar neurons to the BN and modulate their function. This neuromodulative effect works exclusively at the spinal level and appears to be at least partly responsible for BN competence and at least continence.
