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Results for “PUDENDAL NERVE”

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PubMed2000

New, simple approach for maximal pudendal nerve exposure: anomalies and prospects for functional reconstruction.

PURPOSE: Functional neosphincters after pudendal nerve anastomosis proved possible in animal models and may be applicable in humans, but access is a recognized problem. We report the occurrence of pudendal nerve anomalies, its implications for reconstruction, and describe a new approach for maximal exposure. METHODS: Adult human cadavers were positioned prone and dissected via a gluteal approach. Pudendal nerve variations and physical measurements were analyzed statistically. RESULTS: A new, simple, four-step approach (surface landmarks and exposure of gluteus maximus muscle, sacrotuberous ligament, and pudendal neurovascular bundle) permitted optimal pudendal nerve exposure in all 14 human cadavers (28 limbs). Six were males and had a mean age of 82 (range, 58-102) years. Two anomalies, Type 1 (2-trunked) and Type 2 (3-trunked), of the pudendal nerve were recognized in 30 percent of cadavers, with a left-to-right ratio of 2.5:1. Mean pudendal nerve length over the ischial spine was 23.9 (range, 19-28) mm right, 24.2 (range, 19-28) mm left (P = 0.54), but its diameter measured 5.2 mm (right) and 4.9 mm (left; P = 0.04). Mean length of pudendal nerve trunk exposed after reflection of the sacrotuberous ligament was 55 (range, 44-75) mm on either side before division into terminal branches. The number and percent frequency of inferior rectal nerve on both sides were 1 (13 percent), 2 (76 percent), and 3 (11 percent), respectively, with a mean length of 27.1 (range, 21-34) mm right and 27.9 (range, 20-33) mm left (P = 0.31). CONCLUSION: A simple four-step approach to the pudendal nerve contributes to improved access in all cases. It facilitates reconstruction because it allows accurate nerve selection and recognition of potential anomalies that might influence functional outcome.

Aged↗

PubMed2002

Pudendal nerve terminal motor latency testing: assessing the educational learning curve: can we teach our own?

PURPOSE: Pudendal nerve terminal motor latency testing is useful as a diagnostic tool in fecal incontinence. It has also been used as a predictive factor in sphincteroplasty repairs. The technique is seldom taught and mastered in colorectal training programs. The purpose of this study was to assess a learning curve for teaching this procedure. METHODS: The student was a formally trained colorectal surgeon with no pudendal nerve terminal motor latency experience; the instructor has performed more than 3,000 pudendal nerve terminal motor latency studies. Fifty consecutive patients had manometry and pudendal nerve terminal motor latency testing. Both the student and instructor performed pudendal nerve terminal motor latency in a sequential fashion. Variables collected included pudendal nerve terminal motor latency, completion of test, time to complete test, and accuracy of the test. Variables were analyzed with paired t-test and chi-squared analysis. RESULTS: The study group included 41 female and 9 male patients. The average age of the patients was 53 years. Bowel complaints included constipation in 16 and incontinence in 34 patients. Data were analyzed in their entirety and at ten-patient intervals. The student tended to record longer latencies (P < 0.001). This led to false-positive rates of 23 and 21 percent, respectively, for left and right pudendal nerve terminal motor latency. On average, the time to complete the procedure was three times longer for the student than for the instructor (P < 0.001). At ten-patient intervals, the pudendal nerve terminal motor latency difference between the two groups disappeared at the 41-to-50-patient mark. CONCLUSION: Given the proper learning environment, pudendal nerve terminal motor latency testing can be mastered in a relatively short period. On the basis of this study, our estimation is 40 patients are required for a student to master this technique. The novice examiner can expect false-positive results early in the learning curve, and these should be validated accordingly.

Constipation↗

PubMed2005

Anal sphincter reconstruction using a transposed gracilis muscle with a pudendal nerve anastomosis: a preliminary anatomic study.

PURPOSE: Few studies have demonstrated the feasibility of cross innervating a skeletal muscle neosphincter with the pudendal nerve in an animal model. This study was designed to evaluate in humans the technical feasibility of anastomosing the nerve of the gracilis muscle and the pudendal nerve when the gracilis muscle is transposed around the anus. METHODS: Anatomic assessment was made in 30 cases. The gracilis muscle and its principal neurovascular pedicle were dissected and the nerve to the gracilis divided at its origin. The gracilis muscle, accompanied by its nerve, was then transposed around the anus. The pudendal nerve was dissected in its extrapelvic portion and divided at its termination. Gracilis reinnervation was considered feasible when the proximal end of the nerve to the gracilis muscle and the distal end of the pudendal nerve were able to be placed into tension-free contact. RESULTS: The mean lengths of the nerve to the gracilis and the pudendal nerve were 126.5 +/- 20.6 mm and 57.5 +/- 16.3 mm. Anastomosing the nerve of the gracilis muscle and the pudendal nerve was possible in 28 cases. There was a total mean surplus nerve length of 25.1 +/- 20.9 mm. In 26 cases, the distal end of the pudendal nerve (mean, 3.3 +/- 1.1 mm) was similar or larger than the end of the nerve to the gracilis (mean, 3 +/- 0.8 mm). CONCLUSIONS: Anal sphincter reconstruction using transposed gracilis muscle with pudendal nerve anastomosis is anatomically achievable in cadavers, and supports the potential applications of this technique for perineal reconstruction in clinical practice.

Aged↗

PubMed2005

Contribution of the pudendal nerve to sensation of the distal rectum.

BACKGROUND: Anal and rectal sensory mechanisms and pudendal nerve function are important in the control of faecal continence. The contribution of the pudendal nerve to sensation of the distal rectum was investigated. METHODS: Heat thresholds in the anal canal, distal and mid rectum were measured using a specially designed thermoprobe. Rectal sensory threshold volumes were measured using the balloon distension method. Needle electrodes were inserted into the external anal sphincter. Pudendal nerve block was performed through a perineal approach, and completeness assessed by loss of electromyographic activity. Heat and rectal volume thresholds were measured again following unilateral and bilateral pudendal nerve block. RESULTS: The technique was successful in four of six volunteers. Bilateral pudendal nerve block produced complete anaesthesia to heat in the anal canal (P = 0.029), but had no effect on heat thresholds in the distal or mid rectum. Rectal sensory threshold volumes were also unaffected by pudendal nerve anaesthesia. CONCLUSION: Anal canal sensation is subserved by the pudendal nerve, but this nerve is not essential to nociceptive sensory mechanisms in the distal or mid rectum. The transition between visceral control mechanisms in the lower rectum and somatic mechanisms in the anal canal may have functional importance in the initiation of defaecation and the maintenance of continence.

Adult↗

PubMed1993

The effect of vaginal dissection on the pudendal nerve.

OBJECTIVE: To determine the effect of vaginal dissection on the pudendal nerve. METHODS: Pudendal and perineal nerve terminal motor latencies were measured before and at least 6 weeks after either abdominal or vaginal surgery for genital tract prolapse with or without urinary and fecal incontinence. Forty-eight women were studied prospectively in a randomized, blinded fashion. RESULTS: All women in this study had pelvic floor prolapse, and their mean preoperative pudendal and perineal nerve terminal motor latencies were prolonged compared to previously established normal values. The 27 women undergoing vaginal dissection demonstrated significant mean increases in pudendal nerve terminal motor latency (0.63 milliseconds, 95% confidence interval [CI] 0.33-0.93; P = .001) and perineal nerve terminal motor latency (1.33 milliseconds, 95% CI 0.80-1.86; P = .0001). In the 21 who had abdominal operations without vaginal dissection, essentially no mean change was noted. Clinically significant increases (more than 2 standard deviations) in pudendal or perineal nerve terminal motor latency occurred in 20 women (74%) in the vaginal dissection group and in seven women (33%) in the abdominally operated group. The odds ratio of producing such neuropathy by vaginal dissection compared to operating abdominally without vaginal dissection was 5.78 (95% CI 1.6-20). CONCLUSIONS: All women had abnormal preoperative pudendal nerve function, supporting previous reports linking pudendal neuropathy with pelvic floor prolapse. Pelvic floor surgery involving vaginal dissection produces neuropathy of the pudendal nerve as measured by terminal motor latency.

Abdomen↗

PubMed1996

Prospective comparative study of abnormal distal rectoanal excitatory reflex, pudendal nerve terminal motor latency, and single fiber density as markers of pudendal neuropathy.

PURPOSE: This study was undertaken to determine the role of abnormal distal rectoanal excitatory reflex (RAER) as a marker of pudendal neuropathy and to compare results with pudendal nerve terminal motor latency (PNTML) and single fiber density (SFD) estimation. METHODS: Fifteen female patients (mean age, 47.1 (range, 20-70) years) referred to the pelvic floor laboratory with pelvic floor disorders (fecal incontinence, 13 patients; constipation, 2 patients) were evaluated prospectively with neurophysiologic tests and balloon reflex manometry for evidence of pudendal neuropathy. RESULTS: Pudendal nerve terminal motor latency provided evidence of pudendal neuropathy in ten patients (67 percent) and was normal in five patients (33 percent). Increased SFD confirmed denervation of the external anal sphincter in 12 patients (80 percent), being normal in 3 patients (20 percent). Distal RAER was abnormal in 13 patients (87 percent) and was normal in 2 patients (13 percent). In ten patients (67 percent), the three diagnostic modalities were in complete agreement, correctly identifying neuropathy in nine patients (60 percent) and excluding nerve damage in one patient (7 percent). Distal RAER was normal despite prolonged PNTML and increased SFD in one patient (7 percent). In two patients (13 percent), distal RAER was abnormal or absent despite normal PNTML and SFD. Pudendal nerve terminal motor latency was normal in the presence of abnormal distal RAER and increased SFD on electromyography in two patients (13 percent). CONCLUSIONS: Abnormal distal RAER compares favorably with current neurophysiologic tests used to diagnose pudendal neuropathy.

Adult↗

PubMed2003

Afferent fibers of the pudendal nerve modulate sympathetic neurons controlling the bladder neck.

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.

Adrenergic Fibers↗

PubMed2000

Delayed pudendal nerve conduction and endosonographic appearance of the anal sphincter complex.

PURPOSE: The aim of this study was to test the hypothesis that a delay in pudendal nerve conduction as measured by pudendal nerve terminal motor latency should be associated with atrophy of the external anal sphincter as measured using endoanal ultrasound. METHODS: Sixty-two adult females (median age, 58.9 (range, 22-88) years) presenting for evaluation of fecal incontinence with no evidence of an external anal sphincter tear on ultrasound were recruited. Ultrasound was performed with a 7.5-MHz radial rotating axial endoprobe in the left lateral position. Four measurements were made in the transverse plane--the external anal sphincter thickness in the midanal canal at the 6 o'clock and 9 o'clock positions, the internal sphincter at the 9 o'clock position, and the external anal sphincter in the low canal at the 9 o'clock position. Pudendal nerve terminal motor latency was measured using a transrectal nerve stimulation technique with measurement of the evoked muscle response. RESULTS: Although there was a trend toward thinner external sphincter muscles in those with bilateral prolonged pudendal nerve terminal motor latency, independent sample t-tests and Pearson correlation coefficients showed no statistically significant relationship (right pudendal nerve terminal motor latency: P = 0.083, 0.184, 0.128, 0.910; r = 0.228, 0.175, -0.201, -0.015; left pudendal nerve terminal motor latency: P = 0.946, 0.276, 0.510, 0.123; r = -0.009, -0.143, -0.087, -0.201). CONCLUSIONS: No statistically significant relationship between ultrasound-measured anal sphincter muscle thickness and pudendal nerve terminal motor latency was identified. Although a trend was suggested that could be further evaluated by a study with a larger sample size and a control group with asymptomatic patients, the small differences in muscle thickness involved and the difficulties in measurement suggest that the establishment of clinically useful ultrasound criteria for the detection of the neuropathic anal sphincter complex is unlikely.

Adult↗

PubMed2000

End-to-side pudendal nerve anastomosis for the creation of a new reinforcing anal sphincter in dogs.

BACKGROUND: An ideal reinforcing neo-sphincter should be innervated by the pudendal nerve to work in coordination with the external anal sphincter. The aim of this study was to create a skeletal muscle innervated by the pudendal nerve without inducing external anal sphincter morbidity. METHODS: Seven dogs were used. On the right side of each dog, the distal end of the transected nerve innervating the biceps femoris muscle was anastomosed to the perineural window of the pudendal nerve, where the epineurium was excised over a small area without injuring the funiculus. Reinnervation was studied 5 months after the operations. The left side of the dogs was used as a control. RESULTS: For all 7 dogs, there was no macroscopic difference detected in the external anal sphincter. For 6 dogs, the biceps femoris muscle was preserved after end-to-side pudendal nerve anastomosis. After the pudendal nerve central to the anastomosis site was electrically stimulated, the external anal sphincter contracted in all dogs. After end-to-side pudendal nerve anastomosis, the biceps femoris muscle contracted with the evoked potential in 5 dogs (71%) and demonstrated electric activity at rest in 3 dogs (43%), but there was no reflex activity after anal stimulation. The ratio of type 1 to type 2 muscle fiber in the biceps femoris muscle after end-to-side pudendal nerve anastomosis significantly changed and became the same as that in the external anal sphincter. The diameter of type 2 muscle fibers in the biceps femoris muscle significantly decreased after surgery. In addition, regenerated myelinated axons were observed in a cross section of the anastomosed nerve in 6 dogs. CONCLUSIONS: End-to-side pudendal nerve anastomosis is a promising technique for the creation of an anal sphincter in patients who have fecal incontinence. The technique preserved the original external anal sphincter and created a skeletal muscle that was innervated by the pudendal nerve in 71% of the dogs studied. This newly innervated skeletal muscle was capable of contracting in coordination with the original external anal sphincter on electric stimulation and also demonstrated characteristics closely similar to those of the external anal sphincter.

Anal Canal↗

PubMed2003

Pudendal nerve entrapment as source of intractable perineal pain.

Perineal pain caused by pudendal nerve entrapment is a rarely reported entity, with only a handful of cases in the modern literature. A 25-yr-old male medical student had refractory unilateral orchialgia for 32 mo and concomitant proctalgia for 14 mo. Pain was positional in nature, exacerbated by sitting and partially relieved when standing or recumbent. Pudendal nerve entrapment was diagnosed clinically, with computed tomography-guided nerve blocks providing temporary relief. A prolonged left pudendal nerve distal motor latency on electrodiagnostic testing later confirmed the diagnosis. At surgery, the left pudendal nerve was found flattened in the pudendal canal of Alcock and in contact with the sharp inferior border of the sacrospinous ligament. After surgical decompression and rehabilitation, the patient experienced significant relief of pain and returned to medical school. This case suggests pudendal nerve entrapment should be considered in the differential diagnosis of chronic urogenital or anorectal pain, particularly if the pain is aggravated by sitting or if there is a history of bicycle riding.

Adult↗

PubMed1998

No correlation between perineal position and pudendal nerve terminal motor latency in healthy perimenopausal women.

BACKGROUND: Significant associations between perineal descent and pudendal nerve latency have previously been described in fecally incontinent patients. This has led to the hypothesis that pelvic floor muscle and nerve injury initiated by childbirth might progress and cause fecal incontinence. PURPOSE: The study contained herein was undertaken to test whether changes in perineal position and pudendal nerve latency were associated in a population of healthy middle-aged women. METHODS: A cross-sectional study of 144 women were selected randomly from the Danish National Register; they had a mean age of 50 (range, 45-57) years and a mean parity of 2 (range, 0-6). Perineal position at rest and during simulated defecation and pudendal nerve terminal motor latency were measured. All examinations were performed by one of the authors (AMR) and without the knowledge of parity. RESULTS: The perineal position both at rest and during straining was significantly lowered, and the pudendal nerve terminal motor latency was significantly prolonged with increasing numbers of vaginal deliveries (data not shown). There was, however, no association between pudendal nerve terminal motor latency and perineal position at rest (correlation coefficient, r = -0.15, P = 0.1) or during simulated defecation (r = -0.08, P = 0.4). CONCLUSION: Small but significant effects of vaginal deliveries were detected in a random population of healthy perimenopausal women. However, because perineal descent and pudendal nerve latency were not associated, our findings do not support the hypothesis that damage induced by vaginal delivery to the pudendal nerves and pelvic floor will progress.

Anal Canal↗

PubMed2001

Monitoring pudendal nerve function during labor.

BACKGROUND: To determine methodology and feasibility of pudendal nerve monitoring during labor and delivery. METHODS: With Institutional Review Board approval, 13 low-risk, singleton pregnant women were recruited. The latency and amplitude of the perineal branch of the pudendal nerve compound muscle action potential were recorded during the second stage of labor and after delivery. With the first two patients, a wire electrode was used to stimulate the pudendal nerve continuously at the ischial spine. For the remaining 11 patients, a St. Mark's electrode was used to stimulate transvaginally. Aurethral ring electrode on a 14 French foley catheter monitored the response from the urethral sphincter. All patients received prophylactic antibiotics. EXPERIENCE: Twelve patients delivered vaginally, and one by cesarean. In two patients, continuous wire stimulation showed a gradual decrease in amplitude. Changes were minimal over 15-minute intervals. Wire electrode placement was technically difficult and dislodged easily. With the remaining 11 patients, all had data available for interpretation, and of the 85 potential perineal branch of the pudendal nerve compound muscle action potentials, 53 were obtained. No patients developed cystitis. CONCLUSION: Intrapartum assessment of pudendal nerve function is feasible. Continuous wire stimulation is technically more difficult and does not provide additional information beyond that available from intermittent stimulation.

Action Potentials↗

PubMed1998

[Traction on the orthopedic table and pudendal nerve injury. Importance of electrophysiologic examination].

PURPOSE OF THE STUDY: We performed a retrospective study about perioperative pudendal nerve palsy following fracture table tractions. MATERIAL: Six palsies were investigated. Mean age was 26 years. All of them presented sensitive and motor dysfunctions secondary to nerve compression following tractions on the fracture table. METHODS: All of them had complete electrophysiological recordings including perineal electromyogram, measurement of sacral roots latencies, sensory velocity of the dorsal nerve of the penis, somatosensory evoked potentials of the pudendal nerve and measurement of its terminal branches. RESULTS: Neurological symptoms were stereotyped associating sensory signs and sexual disorders, must of them being transient. Perineal electrophysiological examination always confirmed reality of pudendal nerve palsy. DISCUSSION: We discuss incidence, mechanism, etiology and prevention of this pudendal nerve palsy. CONCLUSION: Emergence of stereotyped perineal symptoms following orthopaedic surgery, especially after tractions on fracture table, must prevail on physicians to search for pudendal nerve palsy. Usual outcome is good in the six months following surgery, but definitive aftermath does occur. Perineal electrophysiological examination can confirm pudendal nerve palsy and give prognosis elements.

Adolescent↗

PubMed2006

Unusual origin of dorsal nerve of penis and abnormal formation of pudendal nerve--clinical significance.

The nerve roots of the sacral plexus are fascinating and critical in the functions of defecation, micturition, parturition, and even participate in the mechanism of male sexual functions of erection and ejaculation. During our routine cadaveric dissection of the right gluteal region of a 45-year-old male cadaver, we came across an unusual origin of the dorsal nerve of the penis (DNP) and abnormal formation of the pudendal nerve. The clinical aspects of the particular variations are discussed.

Cadaver↗

PubMed1998

Spinal and pudendal nerve modulation of human corticoanal motor pathways.

We investigated the effects of lumbosacral and pudendal nerve stimulation on the corticofugal pathways to the human external anal sphincter. In 11 healthy subjects, anal sphincter electromyographic responses, evoked to transcranial magnetic stimulation of the motor cortex, were recorded 5-500 ms after lumbosacral root or pudendal nerve stimulation. Lumbosacral and pudendal nerve stimulation alone evoked responses with amplitudes of 293 +/- 73 and 401 +/- 153 microV and latencies of 3.2 +/- 0.2 and 2.2 +/- 0.2 ms, respectively. Cortical stimulation also evoked responses with amplitudes of 351 +/- 104 microV and latencies of 20.9 +/- 1.1 ms. When lumbosacral or pudendal nerve stimulation preceded cortical stimulation, the cortically evoked responses were facilitated (P < 0.01), with the effect appearing greatest at 5-20 ms after both lumbosacral and pudendal excitation and at 50-100 ms after lumbosacral excitation alone. Our results demonstrate that cortical pathways to the external anal sphincter are facilitated by prior lumbosacral and pudendal nerve stimulation, indicating that sensorimotor interactions are important in the central neural control of sphincter function.

Adult↗

PubMed1991

Pudendal nerve evoked potential monitoring in procedures involving low sacral fixation.

Pudendal nerve evoked potentials were used in orthopaedic surgical procedures involving fixation below the S1 level. Pudendal nerve stimulation was used to monitor 154 patients. Eleven patients (7.14%) had responses that were either difficult or impossible to interpret in that they were not consistently replicable. In one case (0.65%), responses were lost during surgery, and there were no subsequent neurologic sequelae (false-positive response). No patients had postoperative deficit to the sacral roots or to the global cord. Although it is possible to obtain definitive dermatomal responses down to S1, the use of pudendal nerve stimulation was found to provide additional means of monitoring lower sacral roots. Since the pudendal nerve is intimately associated with bowel, bladder, and sexual dysfunction, easily obtainable routine monitoring of this nerve can provide significant safety that the conventional somatosensory and dermatomal responses give to higher spinal levels.

Adolescent↗

PubMed2001

The relationship of pudendal nerve terminal motor latency to squeeze pressure in patients with idiopathic fecal incontinence.

PURPOSE: With the advent of transanal ultrasonography it has been possible to identify those incontinent patients without sphincter defects. The majority of these patients are now thought to have neurogenic fecal incontinence secondary to pudendal neuropathy. They have been found to have reduced anal sphincter pressures and increased pudendal nerve terminal motor latencies. The aim of this study was to determine whether in those incontinent patients who do not have a sphincter defect, prolonged pudendal nerve terminal motor latency correlates with anal manometry, in particular maximum squeeze pressure. METHODS: Sixty-six incontinent patients were studied with transanal ultrasonography, anorectal manometry, and pudendal nerve terminal motor latency. Twenty-seven continent controls had anorectal manometry and pudendal nerve terminal motor latency measured. RESULTS: Maximum resting pressure and maximum squeeze pressure were significantly lower in the group of incontinent patients with bilateral prolonged pudendal nerve terminal motor latency (median maximum resting pressure = 26.5 mmHg; median maximum squeeze pressure = 60 mmHg) when compared with incontinent patients with normal bilateral pudendal nerve terminal motor latencies (median maximum resting pressure = 46 mmHg; median maximum squeeze pressure = 79 mmHg; maximum resting pressure P = 0.004; and maximum squeeze pressure P = 0.04). In incontinent patients with no sphincter defects no correlation between pudendal nerve terminal motor latency and maximum squeeze pressure was found (r = -0.109, P = 0.48) and maximum squeeze pressure did not correlate with bilateral or unilateral prolonged pudendal nerve terminal motor latency (r = -0.148, P = 0.56 and r = 0.355, P = 0.19 respectively). CONCLUSIONS: In patients with idiopathic fecal incontinence damage to the pelvic floor is more complex than damage to the pudendal nerve alone. Although increased pudendal nerve terminal motor latency may indicate that neuropathy is present, in patients with neuropathic fecal incontinence, pudendal nerve terminal motor latency does not correlate with maximum squeeze pressure. Normal pudendal nerve terminal motor latency does not exclude weakness of the pelvic floor.

Adult↗

PubMed2005

Sacral versus pudendal nerve stimulation for voiding dysfunction: a prospective, single-blinded, randomized, crossover trial.

AIMS: The objective of the study was to compare sacral nerve stimulation (SNS) to pudendal nerve stimulation (PNS) for voiding dysfunction. METHODS: Thirty subjects with voiding dysfunction had a tined lead placed at S3 and a second electrode implanted at the pudendal nerve via a posterior approach. In a blinded, randomized fashion, each lead was tested for 7 days. Voiding diaries and questionnaires were completed and outcomes monitored. RESULTS: The time to place a sacral lead was 25.85 min, pudendal lead 23.71 min (P = 0.57). Twenty-four of 30 (80%) subjects responded and had a permanent implant placed. PNS was chosen as a superior lead in 79.2%, SNS was superior in 20.8%. The order in which the lead was simulated had no impact on the final lead implanted and no carry over effect was seen. Overall reduction in symptoms was 63% for PNS and 46% for SNS (P = 0.02). On a 7-point scale from markedly worse to markedly better, the pudendal lead was superior to sacral for pelvic pain (P = 0.024), urgency (P = 0.005), frequency (P = 0.007), and bowel function (P = 0.049). Complications were minimal. CONCLUSIONS: This is the first blinded study of sacral versus pudendal stimulation for voiding dysfunction. Successful implantation of a pudendal lead was achieved in all subjects. The majority of subjects chose PNS to be superior to SNS. More patients and longer term data is needed to confirm these promising results.

Adult↗