Superficial peroneal neuromodulation of nonobstructive urinary retention induced by prolonged pudendal afferent activity in cats.

The purpose of this study is to determine whether superficial peroneal nerve stimulation (SPNS) can improve nonobstructive urinary retention (NOUR) induced by prolonged pudendal nerve stimulation (PNS). In this exploratory acute study using eight cats under anesthesia, PNS and SPNS were applied by nerve cuff electrodes. Skin surface electrodes were also used for SPNS. A double lumen catheter was inserted via the bladder dome for bladder infusion and pressure measurement and to allow voiding without a physical urethral outlet obstruction. The voided and postvoid residual (PVR) volumes were also recorded. NOUR induced by repetitive (4-13 times) application of 30-min PNS significantly (P < 0.05) reduced voiding efficiency by 49.5 ± 16.8% of control (78.3 ± 7.9%), with a large PVR volume at 208.2 ± 82.6% of control bladder capacity. SPNS (1 Hz, 0.2 ms) at 1.5-2 times threshold intensity (T) for inducing posterior thigh muscle contractions was applied either continuously (SPNSc) or intermittently (SPNSi) during cystometrograms to improve the PNS-induced NOUR. SPNSc and SPNSi applied by nerve cuff electrodes significantly (P < 0.05) increased voiding efficiency to 74.5 ± 18.9% and 67.0 ± 15.3%, respectively, and reduced PVR volume to 54.5 ± 39.0% and 88.3 ± 56.0%, respectively. SPNSc and SPNSi applied noninvasively by skin surface electrodes also improved NOUR similar to the stimulation applied by a cuff electrode. This study indicates that abnormal pudendal afferent activity could be a pathophysiological cause for the NOUR occurring in Fowler's syndrome and a noninvasive superficial peroneal neuromodulation therapy might be developed to treat NOUR in patients with Fowler's syndrome.

Superficial peroneal neuromodulation of persistent bladder underactivity induced by prolonged pudendal afferent nerve stimulation in cats.

The purpose of this study is to determine whether superficial peroneal nerve stimulation (SPNS) can reverse persistent bladder underactivity induced by prolonged pudendal nerve stimulation (PNS). In 16 α-chloralose-anesthetized cats, PNS and SPNS were applied by nerve cuff electrodes. Skin surface electrodes were also used for SPNS. Bladder underactivity consisting of a significant increase in bladder capacity to 157.8 ± 10.9% of control and a significant reduction in bladder contraction amplitude to 56.0 ± 5.0% of control was induced by repetitive (4-16 times) application of 30-min PNS. SPNS (1 Hz, 0.2 ms) at 1.5-2 times threshold intensity (T) for inducing posterior thigh muscle contractions was applied either continuously (SPNSc) or intermittently (SPNSi) during a cystometrogram (CMG) to determine whether the stimulation can reverse the PNS-induced bladder underactivity. SPNSc or SPNSi applied by nerve cuff electrodes during the prolonged PNS inhibition significantly reduced bladder capacity to 124.4 ± 10.7% and 132.4 ± 14.2% of control, respectively, and increased contraction amplitude to 85.3 ± 6.2% and 75.8 ± 4.7%, respectively. Transcutaneous SPNSc and SPNSi also significantly reduced bladder capacity and increased contraction amplitude. Additional PNS applied during the bladder underactivity further increased bladder capacity, whereas SPNSc applied simultaneously with the PNS reversed the increase in bladder capacity. This study indicates that a noninvasive superficial peroneal neuromodulation therapy might be developed to treat bladder underactivity caused by abnormal pudendal nerve somatic afferent activation that is hypothesized to occur in patients with Fowler's syndrome.

Ambulatory urodynamic monitoring assessment of dorsal genital nerve stimulation for suppression of involuntary detrusor contractions following spinal cord injury: a pilot study.

STUDY DESIGN: A prospective interventional pilot study using within-individual comparisons. OBJECTIVES: To assess the effect of dorsal genital nerve stimulation (DGNS) on urine-storage parameters in participants with spinal cord injury (SCI) and neurogenic detrusor overactivity (NDO) during natural bladder filling. SETTING: The London Spinal Cord Injuries Centre at the Royal National Orthopaedic Hospital, Stanmore, UK. METHODS: Ambulatory urodynamic monitoring (AUM) was carried out with and without DGNS, before and after a week of using DGNS at home. DGNS was applied on-demand by four participants with bladder sensation, and both continuously and intermittently by one participant with absent sensation. A Wilcoxon sign-rank test was used to test paired results of changes within an AUM session. RESULTS: Urodynamic outcomes were improved using DGNS. Bladder capacity was increased from 244 ± 59 to 346 ± 61 ml (p = 0.0078), a mean change of 46 ± 25%. Maximum detrusor pressure was decreased from 58 ± 18 to 47 ± 18 cmH2O (p = 0.0156), a change of 17 ± 13%, and average peak detrusor pressure was decreased from 56 ± 16 to 31 ± 128 cmH2O (p = 0.0156), a mean reduction of 50 ± 19%. There was an increase in the number of detrusor contractions from the first involuntary detrusor contraction to a strong desire, urgency or incontinence, from 1.5 ± 1.4 to 4.3 ± 1.7, and an increase in time of 23 ± 22 min. There were no changes in baseline outcomes following home use of DGNS. CONCLUSIONS: DGNS may be applied on-demand, intermittently or continuously, to increase bladder capacity, decrease storage pressures and provide extra time. Improvements were made in addition to existing antimuscarinic medication regimes.

A novel, nonopiod-based treatment approach to men with urologic chronic pelvic pain syndrome using ultrasound-guided nerve hydrodissection and pelvic floor musculature trigger point injections.

INTRODUCTION: Urological chronic pelvic pain syndrome (UCPPS) represents a group of pain symptoms relating to patients with pelvic pain for which treatment is largely unsatisfactory. The objective of this study is to analyze the effects of a novel treatment strategy in males suffering from UCPPS. METHODS: This retrospective, institutional review board-approved study analyzed eight male patients aged 24 to 61 with UCPPS. All the patients had a trial of antibiotic therapy, NSAIDs, and pelvic floor physical therapy before the study. The Visual Analog scale (VAS) and Functional Pelvic Pain scale (FPPS) were collected pretreatment. While continuing physical therapy, patients underwent weekly ultrasound-guided pelvic floor trigger point injections to the iliococcygeus, pubococcygeus, and puborectalis with lidocaine 1%. Concomitantly, patients received peripheral nerve hydrodissection performed on the pudendal nerve and the posterior femoral cutaneous nerve. The first two injections combined 1% lidocaine with dexamethasone, while the next four injections consisted of 1% lidocaine with traumeel (a homeopathic, plant-derived anti-inflammatory medication). At the 6-week follow-up, each patient retook the VAS and FPPS. RESULTS: The mean age of our patients was 31.8 years and the average duration of symptoms of the UCPPS was 21 months. Pretreatment, the mean VAS was 3.3 (STD 1.7) and the mean VAS posttreatment was 1.8 (STD 1.4); P < .05; 95% CI, 0.73 to 2.27. The mean FPPS pretreatment was 11.0 (STD 8.0) and the mean FPPS posttreatment was 6.3 (STD 5.3); P < .05; 95% CI, 0.03 to 9.22. CONCLUSION: Our results show promise for a novel, nonopioid-based treatment for UCPPS.

A Novel Approach to Managing Post Retropubic Vaginal Sling Pain.

OBJECTIVE: To describe a novel technique of using peripheral nerve neuromodulation (PNNM) for the treatment of refractory, mesh-induced chronic pelvic pain. Chronic pelvic pain associated with mesh can be a debilitating complication and there is currently no consensus on treatment. PNNM has been shown to be successful in the treatment of post-traumatic neuralgias but has yet to be studied in mesh complications. MATERIALS AND METHODS: We present a case of a 50-year-old woman who had unrelenting pelvic pain after retropubic sling placement. She failed multiple therapies including medications, mesh removal, pelvic floor physical therapy, pudendal neuromodulation, and pelvic floor onabotulinumtoxinA trigger point injections. RESULTS: The only treatment that provided temporary relief of this patient's pain was transvaginal trigger point injections along with a right pudendal nerve block using 40 mg triamcinolone and 0.5% ropivacaine. To help define if treatment at the site of her pain would provide relief, a series of blocks were done by advancing a needle retropubically to her area of pain and injecting triamcinolone and 0.5% ropivacaine. This injection, which corresponded to the previous tract of her retropubic sling, provided temporary, but profound, relief. PNNM was then done with placement of the electrode in the retropubic space at the site of her pain. This provided instantaneous relief of almost all of her pain symptoms. Twelve months postoperatively, the patient continued to have >90% improvement in her pain. CONCLUSION: Focused PNNM is a simple procedure and can provide symptomatic relief for refractory postvaginal mesh pain.

Electrical stimulation of the pudendal nerve promotes neuroregeneration and functional recovery from stress urinary incontinence in a rat model.

The pudendal nerve can be injured during vaginal delivery of children, and slowed pudendal nerve regeneration has been correlated with development of stress urinary incontinence (SUI). Simultaneous injury to the pudendal nerve and its target muscle, the external urethral sphincter (EUS), during delivery likely leads to slowed neuroregeneration. The goal of this study was to determine if repeat electrical stimulation of the pudendal nerve improves SUI recovery and promotes neuroregeneration in a dual muscle and nerve injury rat model of SUI. Rats received electrical stimulation or sham stimulation of the pudendal nerve twice weekly for up to 2 wk after injury. A separate cohort of rats received sham injury and sham stimulation. Expression of brain-derived neurotrophic factor (BDNF) and ßII-tubulin expression in Onuf's nucleus were measured 2, 7, and 14 days after injury. Urodynamics, leak point pressure (LPP), and EUS electromyography (EMG) were recorded 14 days after injury. Electrical stimulation significantly increased expression of BDNF at all time points and ßII-tubulin 1 and 2 wk after injury. Two weeks after injury, LPP and EUS EMG during voiding and LPP testing were significantly decreased compared with sham-injured animals. Electrical stimulation significantly increased EUS activity during voiding, although LPP did not fully recover. Repeat pudendal nerve stimulation promotes neuromuscular continence mechanism recovery possibly via a neuroregenerative response through BDNF upregulation in the pudendal motoneurons in this model of SUI. Electrical stimulation of the pudendal nerve may therefore improve recovery after childbirth and ameliorate symptoms of SUI by promoting neuroregeneration after injury.

ICS Educational Module: Electromyography in the assessment and therapy of lower urinary tract dysfunction in adults.

AIM: To present the teaching module "Electromyography in the assessment and therapy of lower urinary tract dysfunction in adults." This teaching module embodies a presentation, in combination with this manuscript. This manuscript serves as a scientific background review; the evidence base made available on ICS website to summarize current knowledge and recommendations. METHODS: This review has been prepared by a Working Group of The ICS Urodynamics Committee. The methodology used included comprehensive literature review, consensus formation by the members of the Working Group, and review by members of the ICS Urodynamics Committee core panel. RESULTS: Electromyography (EMG) is a method to record spontaneous or artificially induced electrical activity of the nerve-muscle unit or to test nerve conductivity. EMG of the anal sphincter using surface electrode is most widely used screening technique to detect detrusor-sphincter dyssynergia in urology. It is non-invasive and easy to perform. EMG methods using needle electrodes are reserved for diagnostics in well selected group of mainly neurogenic patients. These methods require expertise in the field of general EMG and are usually performed by neurologist and neuro-physiologist. The evidence in many aspects of use of EMG in urology remains sparse. CONCLUSIONS: Currently EMG methods rarely play a decision making role in selecting proper treatment of lower urinary tract dysfunction. With the current efforts to improve phenotyping of these patients in order to provide individualized treatment, the role of EMG could increase.

Stimulation of the sensory pudendal nerve increases bladder capacity in the rat.

Pudendal nerve stimulation is a promising treatment approach for lower urinary tract dysfunction, including symptoms of overactive bladder. Despite some promising clinical studies, there remain many unknowns as to how best to stimulate the pudendal nerve to maximize therapeutic efficacy. We quantified changes in bladder capacity and voiding efficiency during single-fill cystometry in response to electrical stimulation of the sensory branch of the pudendal nerve in urethane-anesthetized female Wistar rats. Increases in bladder capacity were dependent on both stimulation amplitude and rate. Stimulation that produced increases in bladder capacity also led to reductions in voiding efficiency. Also, there was a stimulation carryover effect, and increases in bladder capacity persisted during several nonstimulated trials following stimulated trials. Intravesically administered PGE2 reduced bladder capacity, producing a model of overactive bladder (OAB), and sensory pudendal nerve stimulation again increased bladder capacity but also reduced voiding efficiency. This study serves as a basis for future studies that seek to maximize the therapeutic efficacy of sensory pudendal nerve stimulation for the symptoms of OAB.

Sacral neuromodulation blocks pudendal inhibition of reflex bladder activity in cats: insight into the efficacy of sacral neuromodulation in Fowler's syndrome.

This study tested the hypothesis that sacral neuromodulation, i.e., electrical stimulation of afferent axons in sacral spinal root, can block pudendal afferent inhibition of the micturition reflex. In α-chloralose-anesthetized cats, pudendal nerve stimulation (PNS) at 3-5 Hz was used to inhibit bladder reflex activity while the sacral S1 or S2 dorsal root was stimulated at 15-30 Hz to mimic sacral neuromodulation and to block the bladder inhibition induced by PNS. The intensity threshold (T) for PNS or S1/S2 dorsal root stimulation (DRS) to induce muscle twitch of anal sphincter or toe was determined. PNS at 1.5-2T intensity inhibited the micturition reflex by significantly ( P < 0.01) increasing bladder capacity to 150-170% of control capacity. S1 DRS alone at 1-1.5T intensity did not inhibit bladder activity but completely blocked PNS inhibition and restored bladder capacity to control level. At higher intensity (1.5-2T), S1 DRS alone inhibited the micturition reflex and significantly increased bladder capacity to 135.8 ± 6.6% of control capacity. However, the same higher intensity S1 DRS applied simultaneously with PNS, suppressed PNS inhibition and significantly ( P < 0.01) reduced bladder capacity to 126.8 ± 9.7% of control capacity. S2 DRS at both low (1T) and high (1.5-2T) intensity failed to significantly reduce PNS inhibition. PNS and S1 DRS did not change the amplitude and duration of micturition reflex contractions, but S2 DRS at 1.5-2T intensity doubled the duration of the contractions and increased bladder capacity. These results are important for understanding the mechanisms underlying sacral neuromodulation of nonobstructive urinary retention in Fowler's syndrome.

The effects of neuromodulation in a novel obese-prone rat model of detrusor underactivity.

Obesity is a global epidemic associated with an increased risk for lower urinary tract dysfunction. Inefficient voiding and urinary retention may arise in late-stage obesity when the expulsive force of the detrusor smooth muscle cannot overcome outlet resistance. Detrusor underactivity (DUA) and impaired contractility may contribute to the pathogenesis of nonobstructive urinary retention. We used cystometry and electrical stimulation of peripheral nerves (pudendal and pelvic nerves) to characterize and improve bladder function in urethane-anesthetized obese-prone (OP) and obese-resistant (OR) rats following diet-induced obesity (DIO). OP rats exhibited urinary retention and impaired detrusor contractility following DIO, reflected as increased volume threshold, decreased peak micturition pressure, and decreased voiding efficiency (VE) compared with OR rats. Electrical stimulation of the sensory branch of the pudendal nerve did not increase VE, whereas patterned bursting stimulation of the motor branch of the pudendal nerve increased VE twofold in OP rats. OP rats required increased amplitude of electrical stimulation of the pelvic nerve to elicit bladder contractions, and maximum evoked bladder contraction amplitudes were decreased relative to OR rats. Collectively, these studies characterize a novel animal model of DUA that can be used to determine pathophysiology and suggest that neuromodulation is a potential management option for DUA.

Can intraurethral stimulation inhibit micturition reflex in normal female rats?

OBJECTIVE: The study was designed to determine the effect of low frequency (2.5Hz) intraurethral electrical stimulation on bladder capacity and maximum voiding pressures. MATERIALS AND METHODS: The experiments were conducted in 15 virgin female Sprague-Dawley rats (220-250g). The animals were anesthetized by intraperitoneal injection of urethane (1.5g/kg). Animal care and experimental procedures were reviewed and approved by the Institutional Animal Care and Use Committee of Antwerp University (code: 2013-50). Unipolar square pulses of 0.06mA were used to stimulate urethra at frequency of 2.5Hz (0.2ms pulse width) in order to evaluate the ability of intraurethral stimulation to inhibit bladder contractions. Continuous stimulation and intermitente stimulation with 5sec ''on'' and 5sec ''off'' duty cycle were applied during repeated saline cystometrograms (CMGs). Maximum voiding pressures (MVP) and bladder capacity were investigated to determine the inhibitory effect on bladder contraction induced by intraurethral stimulation. RESULTS: The continuous stimulation and intermittent stimulation significantly (p<0.05) decreased MVP and increased bladder capacity. There was no significant difference in MVP and bladder capacity between continuous and intermittent stimulation group. CONCLUSIONS: The present results suggest that 2.5Hz continuous and intermittent intraurethral stimulation can inhibit micturition reflex, decrease MVP and increase bladder capacity. There was no significant difference in MVP and bladder capacity between continuous and intermittent stimulation group.

Can intraurethral stimulation inhibit micturition reflex in normal female rats?

ABSTRACT Objective The study was designed to determine the effect of low frequency (2.5Hz) intraurethral electrical stimulation on bladder capacity and maximum voiding pressures. Materials and Methods The experiments were conducted in 15 virgin female Sprague-Dawley rats (220–250g). The animals were anesthetized by intraperitoneal injection of urethane (1.5g/kg). Animal care and experimental procedures were reviewed and approved by the Institutional Animal Care and Use Committee of Antwerp University (code: 2013-50). Unipolar square pulses of 0.06mA were used to stimulate urethra at frequency of 2.5Hz (0.2ms pulse width) in order to evaluate the ability of intraurethral stimulation to inhibit bladder contractions. Continuous stimulation and intermittent stimulation with 5sec ‘‘on’’ and 5sec ‘‘off’’ duty cycle were applied during repeated saline cystometrograms (CMGs). Maximum voiding pressures (MVP) and bladder capacity were investigated to determine the inhibitory effect on bladder contraction induced by intraurethral stimulation. Results The continuous stimulation and intermittent stimulation significantly (p<0.05) decreased MVP and increased bladder capacity. There was no significant difference in MVP and bladder capacity between continuous and intermittent stimulation group. Conclusions The present results suggest that 2.5Hz continuous and intermittent intraurethral stimulation can inhibit micturition reflex, decrease MVP and increase bladder capacity. There was no significant difference in MVP and bladder capacity between continuous and intermittent stimulation group.

Minimizing Stimulus Current in a Wearable Pudendal Nerve Stimulator Using Computational Models.

After spinal cord injury, functions of the lower urinary tract may be disrupted. A wearable device with surface electrodes which can effectively control the bladder functions would be highly beneficial to the patients. A trans-rectal pudendal nerve stimulator may provide such a solution. However, the major limiting factor in such a stimulator is the high level of current it requires to recruit the nerve fibers. Also, the variability of the trajectory of the nerve in different individuals should be considered. Using computational models and an approximate trajectory of the nerve derived from an MRI study, it is demonstrated in this paper that it may be possible to considerably reduce the required current levels for trans-rectal stimulation of the pudendal nerve compared to the values previously reported in the literature. This was corroborated by considering an ensemble of possible and probable variations of the trajectory. The outcome of this study suggests that trans-rectal stimulation of the pudendal nerve is a plausible long term solution for treating lower urinary tract dysfunctions after spinal cord injury.

Neural network based forward prediction of bladder pressure using pudendal nerve electrical activity.

Individuals with spinal cord injury or neurological disorders have problems in urinary bladder storage and in voiding function. In these people, the detrusor of bladder contracts at low volume and this causes incontinence. The goal of bladder control is to increase the bladder capacity by electrical stimulation of relative nerves such as pelvic nerves, sacral nerve roots or pudendal nerves. For this purpose, the bladder pressure has to be monitored continuously. In this paper, we propose a method for real-time estimating the bladder pressure using artificial neural network. The method is based upon measurements of electroneurogram (ENG) signal of pudendal nerve. This approach yields synthetic bladder pressure estimates during bladder contraction. The experiments were conducted on three rats. The results show that neural predictor can provide accurate estimation and prediction of bladder pressure with good generalization ability. The average error of 1-second and 5-second ahead prediction of bladder pressure are 9.62% and 10.54%, respectively.

The effect of sacral neuromodulation on pudendal nerve function and female sexual function.

AIMS: To quantify changes in pudendal nerve function with sacral neuromodulation (SNM). To understand the relationship of pudendal nerve function to SNM treatment response for overactive bladder. To assess the relationship between female sexual function and pudendal nerve function after SNM. METHODS: Women undergoing SNM between January 2010 and May 2011 were enrolled. Baseline pudendal nerve terminal motor latencies (PNTML) were measured bilaterally. Subjects underwent peripheral nerve evaluation (PNE) prior to SNM therapy. PNTML was measured at 1 and 6 weeks after sacral neuromodulator implant. Women who did not undergo permanent implantation were reassessed at the end of the 1-week PNE testing phase. Pelvic floor and sexual function questionnaires were administered at baseline and follow-up to assess pelvic floor and sexual function. RESULTS: Of 34 women enrolled, 31 were evaluated. Mean age was 67.4 ± 14.2 years with 29/34 (85.3%) treated for refractory overactive bladder. Thirty of 31 (96.7%) went on to a permanent implant. PNE success rate was 73.5% (25/33). Mean PNTML changed from 2.74 ± 0.52 msec at baseline to 2.57 ± 0.50 msec at 6 weeks postop (P = 0.198). Baseline amplitude remained stable at 1 and 6 weeks. At 6 weeks PISQ-12 scores showed improved sexual function (P = 0.034) and PFDI-20 and PFIQ-7 scores showed improved pelvic floor, colorectal and urinary symptoms (P < 0.05). CONCLUSIONS: Women with refractory overactive bladder and non-obstructive urinary retention have abnormal pudendal nerve function, which showed a non-significant trend toward improvement after SNM. Sexually active women undergoing sacral neuromodulation experienced improvement in sexual function. Quality of life improved due to improvement in urinary and colorectal function.

Sacral neuromodulation as a treatment for pudendal neuralgia.

Pudendal neuralgia is a debilitating pain syndrome, and finding long-lasting treatment modalities has been challenging in pain management. The pudendal nerve has sensory and motor functions, and influences autonomic functions. Thus, entrapment or damage of this nerve can have multiple serious implications. The constellation of symptoms which result from injury to this nerve is commonly referred to as pudendal neuralgia. When conservative therapy does not provide adequate pain relief and surgical procedures fail or are not viable options, central and peripheral nerve stimulation can be effective treatment modalities. More recent approaches to treatment include the use of peripheral nerve stimulation through the use of an electrical lead placed next to the pudendal nerve in the ischioanal fossa. Also, epidural stimulation of the conus medullaris and pulsed radiofrequency ablation of the pudendal nerve have been shown to be effective in small patient populations. We present the case of a 36-year-old woman who sustained pudendal nerve injury during a hysterectomy and subsequently developed intractable pelvic pain and pudendal neuralgia. Conservative treatment measures failed, but she obtained excellent results from peripheral nerve stimulator therapy. Permanent implantation consisted of 4 tined Interstim leads, individually placed into the bilateral S3 and S4 foramina. The patient has been followed for approximately 4 years since her procedure, demonstrating increased function as she is able to stand and sit for prolonged periods of time. She has returned to her usual daily activities, including horseback riding. This is the first reported case of transforminal sacral neurostimulation providing excellent relief of pudendal neuralgia related symptoms.

Pudendal neuralgia.

Pudendal neuralgia is a painful condition affecting the nerve distribution of the pudendal nerve. The Nantes criteria give some structure for making this diagnosis. A step-ladder approach to therapy, as described, is suggested when treating these patients.

Baseline factors predictive of patient satisfaction with sacral neuromodulation for idiopathic fecal incontinence.

PURPOSE: Sacral neuromodulation (SNM) is an established treatment for fecal incontinence (FI). A recent study from our group found that the relationship between patient satisfaction and clinical outcome is complex and does not match the traditional used success criteria. Therefore, the ability to predict patient satisfaction must be given priority. The aim of the present study is to identify baseline factors predictive of patient satisfaction, with SNM, for idiopathic FI. METHODS: We analyzed data from patients treated with SNM for idiopathic FI in Aarhus, Denmark, and Maastricht, The Netherlands. A questionnaire considering self-reported satisfaction was mailed to these patients and compared to baseline characteristics. Logistic regression was used to determine the predictive value of baseline demographic and diagnostic variables. RESULTS: In total, 131 patients were included in the analysis. Patient satisfaction with the current treatment result was reported in 75 patients. Fifty-six patients were dissatisfied with SNM treatment, after median 46 months (range 11-122) with permanent implantation. Pudendal nerve terminal motor latency (PNTML) was the solely identified predictor for long-term patient satisfaction. A subgroup univariate-logistic regression analysis showed that PNTML ≤ 2.3 ms at the side of lead implantation was a statistically significant predictor for patient satisfaction (odds ratio (OR) 2.3, 95% confidence interval (CI) 1.01-5.24, p = 0.048). CONCLUSION: Baseline PNTML measurement may be predictive of long-term satisfaction with SNM therapy for idiopathic FI. Further studies are needed to confirm this result.

A novel implantation technique for pudendal nerve stimulation for treatment of overactive bladder and urgency incontinence.

Herein is described laparoscopic implantation of a neuroprosthesis to the pudendal nerve for treatment of non-neurogenic bladder overactivity. This case series study was performed at a tertiary referral unit that specializes in advanced gynecologic surgery and neuropelveology. Fourteen consecutive male and female patients underwent laparoscopic implantation of an electrode to the endopelvic portion of the pudendal nerve for pudendal neuromodulation. All procedures were performed successfully via laparoscopy, without any complications. The mean operative time for the entire procedure was 18 minutes. After a successful test phase of external stimulation, 11 patients (78.57%) underwent implantation of a permanent generator. These patients demonstrated a mean (SD) decreased micturition frequency, from 25 (11.7; range, 13-50) per day on average to 10.18 (2.7; range, 7-15) at final evaluation (mean follow-up, 18 months; range 9-49 months). Nocturia decreased from 5.82 (4.2; range, 3-18) to 2.18 (1.08; range, 1-5) micturitions per night. Cystometric bladder capacities increased from 159 mL (53; range, 80-230 mL) to 312 mL (104.9;160-500 mL). Mean incontinence episodes at the initial evaluation, based on a 3-day voiding diary, were 8.1. At final evaluation, 6 patients were completely dry. Number of pads used per day decreased from 7.3 (4.2) to 1.6 (2.3). No lead dislocation or migration occurred. It was concluded that laparoscopic implantation of a neuroprosthesis to the pudendal nerve is an effective, safe, and reproducible day procedure for treatment of intractable non-neurogenic overactive bladder with urinary urgency incontinence.