Pudendal Nerve Stimulation Research Articles

Real-Time Bladder Pressure Estimation for Closed-Loop Control in a Detrusor Overactivity Model.

Overactive bladder (OAB) patients suffer from a frequent urge to urinate, which can lead to a poor quality of life. Current neurostimulation therapy uses open-loop electrical stimulation to alleviate symptoms. Continuous stimulation facilitates habituation of neural pathways and consumes battery power. Sensory feedback-based closed-loop stimulation may offer greater clinical benefit by driving bladder relaxation only when bladder contractions are detected, leading to increased bladder capacity. Effective delivery of such sensory feedback, particularly in real-time, is necessary to accomplish this goal. We implemented a Kalman filter-based model to estimate bladder pressure in real-time using unsorted neural recordings from sacral-level dorsal root ganglia, achieving a 0.88 ± 0.16 correlation coefficient fit across 35 normal and simulated OAB bladder fills in five experiments. We also demonstrated closed-loop neuromodulation using the estimated pressure to trigger pudendal nerve stimulation, which increased bladder capacity by 40% in two trials. An offline analysis indicated that unsorted neural signals had a similar stability over time as compared to sorted single units, which would require a higher computational load. We believe this paper demonstrates the utility of decoding bladder pressure from neural activity for closed-loop control; however, real-time validation during behavioral studies is necessary prior to clinical translation.

Low pressure voiding induced by a novel implantable pudendal nerve stimulator.

To validate the functionality of an implantable pudendal nerve stimulator under development for Food and Drug Administration approval to restore bladder function after spinal cord injury. In nine cats under anesthesia, two tripolar cuff electrodes were implanted bilaterally on the pudendal nerves and one bipolar cuff electrode was implanted on the right pudendal nerve central to the tripolar cuff electrode. The pudendal nerve stimulator was implanted subcutaneously on the left lower back along the lumbosacral spine and connected to the cuff electrodes. In five cats, a double lumen catheter was inserted into the bladder through the urethra to infuse saline and measure bladder pressure and another catheter was inserted into the distal urethra to perfuse and measure the back pressure caused by urethral contraction. In four cats, a bladder catheter was inserted into the bladder dome and the urethra was left open so that voiding could occur without urethral outlet obstruction. The implantable pudendal nerve stimulator was controlled wirelessly and successfully provided the required stimulation waveforms to different cuff electrodes. Pudendal nerve stimulation (PNS) at 5 Hz increased bladder capacity to about 200% of control capacity. PNS at 20 to 30 Hz induced large (80-100 cmH2 O) bladder contractions under isovolumetric conditions. When combined with ipsilateral or bilateral pudendal nerve block induced by 6 to 10 kHz stimulation, PNS at 20 to 30 Hz elicited low pressure (<40 cmH 2 O) efficient (70%) voiding. The implantable stimulator generated the required stimulation waveforms and successfully induced low pressure efficient voiding in anesthetized cats.

Comparison of efficacy and safety between electroacupuncture at ‘four sacral points’ and conventional electroacupuncture for the treatment of urinary incontinence after stroke: study protocol for a randomised controlled trial

IntroductionElectroacupuncture at ‘four sacral points’, also known as electrical pudendal nerve stimulation therapy, combines the advantages of pudendal nerve neuromodulation and the technique of deep insertion of long acupuncture needles....

Sensory pudendal nerve stimulation increases bladder capacity through sympathetic mechanisms in cyclophosphamide-induced cystitis rats.

Interstitial cystitis and bladder pain syndrome is a prevalent health concern with inadequate treatments. Neuromodulation has emerged as a therapeutic option to treat patients refractory to standard care. The objective of this study was to determine the efficacy and mechanism(s) of sensory pudendal nerve stimulation on bladder function in cystitis rats. Female rats were administered saline (n = 8) or cyclophosphamide (CYP, 150 mg/kg IP, n = 16) and single-trial cystometry experiments were conducted under urethane anesthesia 48 h after injection. Electrical stimulation (0.02-0.22 mA, 10-20 Hz) was delivered to the sensory branch of the pudendal nerve and its effect on the bladder and external urethral sphincter were measured. Stimulation trials were also conducted following bilateral hypogastric nerve transection (HGNT) or pharmacological inhibition of beta-adrenergic receptors (propranolol, 1 mg/kg IV) to determine the mechanisms of bladder inhibition. CYP-induced cystitis decreased bladder capacity (P = 0.0352) and bladder compliance (P = 0.024) by up to 38% of control. Electrical stimulation of the sensory pudendal nerve increased bladder capacity (P < 0.0001) in control and CYP rats by up to 51-52% of their respective baselines. HGNT did not influence bladder inhibition generated by sensory pudendal nerve stimulation in control rats, whereas HGNT and propranolol decreased the efficacy of electrical stimulation in CYP rats. Sympathetic reflex activity mediates sensory pudendal nerve stimulation in CYP treated but not control rats. These studies demonstrate an alternative approach to neuromodulation in cystitis and establish mechanistic changes during stimulation that may enable the development of novel therapeutics.

Spinal mechanisms of pudendal nerve stimulation-induced inhibition of bladder hypersensitivity in rats

Bilateral electrical pudendal nerve stimulation (bPNS) reduces bladder hypersensitivity in rat models of bladder pain and anecdotally reduces pain in humans with pelvic pain of urologic origin. The spinal neurochemical mechanisms of this antinociception are unknown. In the present study, bladder hypersensitivity was produced by neonatal bladder inflammation in rat pups coupled with a second inflammatory insult as an adult. Visceromotor responses (VMRs; abdominal muscle contractions) to urinary bladder distension (UBD) were used as a nociceptive endpoint under urethane-isoflurane anesthesia. bPNS consisted of bilateral biphasic electrical stimulation of the mixed motor/sensory component of the pudendal nerves. Following determination of the inhibitory effect of bPNS on VMRs, pharmacological antagonists were administered via an intrathecal catheter onto the lumbosacral spinal cord and bPNS effects on VMRs redetermined. bPNS resulted in statistically significant inhibition of VMRs to UBD in hypersensitive rats that was statistically reduced by the intrathecal administration of methysergide, WAY100636, CGP35348 and strychnine but was unaffected by naloxone, bicuculline, phentolamine, ondansetron and normal saline. This study suggests that inhibitory effects of bPNS may include serotonergic, GABA-B-ergic and glycinergic mechanisms suggesting the potential for interaction of the neuromodulatory effect with concommitant drug therapies.

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 βII-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 βII-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.

Spinal interneuronal mechanisms underlying pudendal and tibial neuromodulation of bladder function in cats

This study examined the mechanisms underlying pudendal and tibial neuromodulation of bladder function at the single neuron level in the spinal cord. A microelectrode was inserted into the S2 spinal cord of anesthetized cats to record single neuron activity induced by bladder distention over a range of constant intravesical pressures (10–40 cmH2O). Pudendal nerve stimulation (PNS) or tibial nerve stimulation (TNS) was applied at 5 Hz frequency and 0.2 ms pulse width and at multiples of the threshold (T) intensities for inducing anal or toe twitches. A total of 14 spinal neurons from 11 cats were investigated. Both PNS and TNS at 2 T intensity significantly (p < .05) reduced by 40–50% the frequency of firing induced by bladder distention at 20–40 cmH2O in the same spinal neurons. This reduction was not changed by blocking opioid receptors with naloxone (1 mg/kg, i.v.). Activation of pudendal afferents by repeatedly stroking (3–5 times per second) the genital skin using a cotton swab also inhibited the neuron activity induced by bladder distention. Prolonged (30 min) TNS at 4 T intensity produced a short lasting (10–18 min) post-stimulation inhibition that reduced by 40–50% bladder-related neuron activity at different bladder pressures. These results indicate that PNS and TNS inhibition of reflex bladder activity may be mediated in part by convergence of inhibitory inputs onto the same population of bladder-related interneurons in laminae V-VII of the S2 spinal cord and that an opioid receptor mechanism is not involved in the inhibition.

PD55-04 TIBIAL AND PUDENDAL NEUROMODULATION OF SPINAL NEURON ACTIVITY INDUCED BY BLADDER DISTENTION

You have accessJournal of UrologyBladder & Urethra: Anatomy, Physiology & Pharmacology II1 Apr 2018PD55-04 TIBIAL AND PUDENDAL NEUROMODULATION OF SPINAL NEURON ACTIVITY INDUCED BY BLADDER DISTENTION Todd Yecies, Shun Li, Yan Zhang, Daniel Cai, Bing Shen, Jicheng Wang, James Roppolo, William De Groat, and Changfeng Tai Todd YeciesTodd Yecies More articles by this author , Shun LiShun Li More articles by this author , Yan ZhangYan Zhang More articles by this author , Daniel CaiDaniel Cai More articles by this author , Bing ShenBing Shen More articles by this author , Jicheng WangJicheng Wang More articles by this author , James RoppoloJames Roppolo More articles by this author , William De GroatWilliam De Groat More articles by this author , and Changfeng TaiChangfeng Tai More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2018.02.2624AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Neuromodulation is an FDA-approved treatment for overactive bladder (OAB), however the mechanisms underlying neuromodulation are not completely understood. Prior studies have suggested that perigenital stimulation (PGS), pudendal nerve stimulation (PNS) and tibial nerve stimulation (TNS) can alter afferent sensory signaling from the bladder, however the sites of action (spinal or supraspinal) for bladder neuromodulation are not clear. We present a novel approach to identify individual bladder related neurons (BRNs) and assess the effect of PGS, PNS, and TNS on BRN activity. METHODS The S2 level of the spinal cord was exposed in α-chloralose anesthetized cats. Bladder pressure was modulated using a urethral catheter attached to an adjustable height reservoir. Using a tungsten micro-electrode lowered into the S2 spinal cord, individual neurons with firing patterns that changed with bladder pressure were identified. The effect of PGS, PNS (5Hz, 0.2 ms) at 2 times the threshold to induce anal twitch (2T), and TNS (5Hz, 0.2 ms) at 2 and 4 times the threshold to induce toe movement (2 and 4T) on BRN activity were studied. Naloxone, an opioid receptor antagonist, was administered intravenously (1.0mg/kg) to a subset of cats to determine the role of opiate signaling in PNS and TNS inhibition of BRN signaling. RESULTS A total of 19 BRNs were identified in 12 cats. Of these, 18 were positively stimulated by increased bladder pressure, while 1 was inhibited by rises in bladder pressure. BRNs demonstrated increased activity with increased bladder pressure (p<0.01). Both PNS and TNS at 2T significantly inhibited BRN activity at bladder pressures of 10, 20, 30, and 40 cm H2O (p<0.05). Perigenital stimulation inhibited BRN activity at all tested bladder pressures (p=0.037). TNS at 4T for a 30 minute period provided a brief post-stimulation inhibitory effect at 20-40cm H2O (p<0.01) which dissipated within a 5 minute recovery window. Administration of IV naloxone increased background neuron activity (p=0.04) but had no effect on PNS and TNS-mediated inhibition of BRN activity. CONCLUSIONS Individual BRNs could be reliably identified within the feline S2 spinal cord. Perigenital stimulation, TNS and PNS significantly inhibited BRN activity at different bladder pressures. TNS and PNS inhibition was not effected by naloxone, suggesting non-opiate mediated inhibition. Through this novel technique of measuring BRN activity, the effect of pharmacologic or neuromodulatory interventions to manage OAB can be more precisely delineated to reveal the potential sites of action. © 2018FiguresReferencesRelatedDetails Volume 199Issue 4SApril 2018Page: e1057 Advertisement Copyright & Permissions© 2018MetricsAuthor Information Todd Yecies More articles by this author Shun Li More articles by this author Yan Zhang More articles by this author Daniel Cai More articles by this author Bing Shen More articles by this author Jicheng Wang More articles by this author James Roppolo More articles by this author William De Groat More articles by this author Changfeng Tai More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

(142) - Effect of spinal neurotransmitter antagonists on inhibition due to pudendal nerve stimulation in rats

(142) - Effect of spinal neurotransmitter antagonists on inhibition due to pudendal nerve stimulation in rats

The value of synchro-cystourethrometry for evaluating the relationship between urethral instability and overactive bladder.

To investigate the correlation between urethral instability (URI) and overactive bladder (OAB) in children. We retrospectively investigated 126 children with OAB and 36 children without OAB using synchro-cystourethrometry. The prevalence of detrusor overactivity (DO) and URI, and the diagnostic sensitivity of DO alone and DO combined with URI, was compared. The OAB children with URI voluntarily received transcutaneous electrical pudendal nerve stimulation with anisodamine (stimulation group, SG) or anisodamine alone (non-stimulation group, NSG). The effectiveness of treatment was evaluated. Average voided volume (AVV), maximum voided volume (MVV), and number of voids per day (NV) were collected and analyzed. In OAB children, the prevalence of DO and URI was 51.6 and 32.5%, respectively. The prevalence of URI was 5.6% in controls. The prevalence of URI was significantly higher in OAB children. The diagnostic sensitivity and Youden index of DO combined with URI were higher than DO alone. In SG, 45.7% of children were cured, with a ≥50% improvement rate of 82.9%, while no child was cured, with a ≥50% improvement rate of 36.8% in NSG. A significant increase in AVV and MVV together, with a decrease in NV, was seen in SG. There was a significant difference in visual analogue scale values between SG and NSG (P<0.01). Urethral instability plays an essential role in the pathogenesis and progression of OAB in children. Synchro-cystourethrometry is a useful urodynamic technology to precisely diagnose OAB, and transcutaneous electrical pudendal nerve stimulation may be an effective treatment for OAB children induced by URI.

Urethral function and histopathology in aged female rats as a stress urinary incontinence model.

Stress urinary incontinence (SUI) is a common disease condition in elderly women, suggesting that its etiology may be linked to aging. To investigate the hypothesis that urethral dysfunction and histopathological changes are possible contributors to SUI in elderly women, several parameters of urethral function, as well as histological parameters, were compared between young and aged rats. Virgin female rats were examined at 3 different ages, namely 3, 12, and 24 months, corresponding to young, middle-aged, and aged rats, respectively. Urethral function was assessed by measuring the leak point pressure (LPP), pudendal nerve stimulation (PNS)-induced elevation in urethral pressure, and phenylephrine-induced increase in urethral perfusion pressure (UPP). Histopathological assessments were performed following hematoxylin and eosin (HE), Masson's trichrome, and immunofluorescence staining of urethral tissue. LPP of aged rats was significantly reduced compared to that of both young and middle-aged rats. PNS-induced elevation in urethral pressure in aged rats was also significantly lower than that in young rats. In contrast, there were no significant differences in the phenylephrine-induced increase in UPP between young and aged rats. Connective tissue area in the external urethral sphincter (EUS) layer was increased in aged rats, whereas the smooth muscle layer was histologically similar to that in young rats. The number of EUS fibers was significantly reduced in aged rats, whereas the cross-sectional area of EUS fibers increased from differed compared with young rats. We have demonstrated age-related changes in EUS function and morphology in the rat urethra, which are considered to be etiological risk factors for SUI in humans.

Time-Frequency Analysis of Increases in Vaginal Blood Perfusion Elicited by Long-Duration Pudendal Neuromodulation in Anesthetized Rats

Female sexual dysfunction (FSD) affects a significant portion of the population. Although treatment options for FSD are limited, neuromodulation for bladder dysfunction has improved sexual function in some women. A few studies have investigated peripheral neuromodulation for eliciting changes in vaginal blood flow, as a proxy for modulating genital sexual arousal, however results are generally transient. Our central hypothesis is that repeated or extended-duration pudendal nerve stimulation can elicit maintained vaginal blood flow increases. Under ketamine anesthesia, the pudendal nerve of 14 female rats was stimulated at varying frequencies (1-100 Hz) and durations (0.15-60 min). Vaginal blood perfusion was measured with a laser Doppler flowmetry probe. Changes in blood perfusion were determined through raw signal analysis and increases in the energy of neurogenic (0.076-0.200 Hz) and myogenic (0.200-0.740 Hz) frequency bands through wavelet analysis. Additionally, a convolution model was developed for a carry-over stimulation effect. Each experiment had significant increases in vaginal blood perfusion due to pudendal nerve stimulation. In addition, there were large concurrent increases in neurogenic and myogenic frequency-band energy in 11/14 experiments, with an average maximal response at 31.3 min after stimulation initiation. An effective stimulation model with a 30-min carry-over effect had a stronger correlation to blood perfusion than the stimulation period itself. Repeated or extended-duration pudendal nerve stimulation can elicit maintained increases in vaginal blood perfusion. This work indicates the potential for pudendal neuromodulation as a method for increasing genital arousal as a potential treatment for FSD.

Short-term Clinical Efficacy of Electric Pudendal Nerve Stimulation on Neurogenic Lower Urinary Tract Disease: A Pilot Research

To compare the short-term efficacy of electrical pudendal nerve stimulation (EPNS) vs anogenital electrical stimulation (AES) for neurogenic lower urinary tract disease. Sixty eligible participants were randomized at a ratio of 2:1 to the test group of 40 patients and the control group of 20. The test group was treated with EPNS and the control group was treated with AES. After 12 sessions of treatment, therapeutic effects were evaluated based on self-assessed questionnaire scores. All patients with a residual urine volume >50 mL were also assessed by the post-treatment residual urine volume. At the end of treatment, the median symptom score and the quality of life score were 11 (range 3-23) and 4.26 (range 1.00-5.81) in the test group, and the median post-treatment residual urine volume was 46 (range 0-223) mL. By contrast, the median severity of symptoms and quality of life scores were 15 (range 8-33) and 3.84 (range 0.89-5.84) in the control group, and the median post-treatment residual urine volume was 105 (range 28-340) mL. Significant differences between the test group and the control group could be observed in the post-treatment symptom score, the quality of life score, and the residual urine volume (with P = .005, P <.001, P = .02, respectively). Compared with AES, EPNS is more effective in treating neurogenic lower urinary tract disease in the short term.

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.

Laparoscopic implantation of electrodes for bilateral neuromodulation of the pudendal nerves and S3 nerve roots for treating pelvic pain and voiding dysfunction.

The objective of this video is to describe the technique for laparoscopic implantation of electrodes for bilateral neuromodulation of S3 and pudendal nerves. We report a successful case of a 48-year-old woman with spina bifida occulta referred with a 14-year history of intense acyclic pelvic pain, urinary hesitancy, and intermittent flow refractory to various conservative measures. The procedure began with the removal of two previously placed InterStims. A quadripolar electrode was then laparoscopically inserted into Alcock's canal and attached to the pelvic pectineal line. Another lead was placed juxtaneurally to S3. Lead contacts were then exteriorized, and the peritoneum closed. The same procedure was then performed on the contralateral side. The leads were connected to a 16-pole rechargeable pulse generator. Postoperatively, the patient developed an acute dissection and partial thrombosis of the external iliac artery, which was treated endovascularly. Complete pain resolution was observed with simultaneous S3 and pudendal stimulation, with pudendal stimulation turned off for voiding. We conclude that laparoscopic implantation of neuromodulation electrodes allows simultaneous stimulation of S3 and pudendal nerves, providing more programming options and possibly increasing success rates in complex pelvic floor dysfunction cases.

Clinical utility of neurostimulation devices in the treatment of overactive bladder: current perspectives.

ObjectivesThis review describes the evidence from established and experimental therapies that use electrical nerve stimulation to treat lower urinary tract dysfunction.MethodsClinical studies on established treatments such as percutaneous posterior tibial nerve stimulation (P-PTNS), transcutaneous electrical nerve stimulation (TENS), sacral nerve stimulation (SNS) and sacral anterior root stimulation (SARS) are evaluated. In addition, clinical evidence from experimental therapies such as dorsal genital nerve (DGN) stimulation, pudendal nerve stimulation, magnetic nerve stimulation and ankle implants for tibial nerve stimulation are evaluated.ResultsSNS and P-PTNS have been investigated with high-quality studies that have shown proven efficacy for the treatment for overactive bladder (OAB). SARS has proven evidence-based efficacy in spinal cord patients and increases the quality of life. TENS seems inferior to other OAB treatments such as SNS and P-PTNS but is noninvasive and applicable for ambulant therapy. Results from studies on experimental therapies such as pudendal nerve stimulation seem promising but need larger study cohorts to prove efficacy.ConclusionNeurostimulation therapies have proven efficacy for bladder dysfunction in patients who are refractory to other therapies.SignificanceRefinement of neurostimulation therapies is possible. The aim should be to make the treatments less invasive, more durable and more effective for the treatment of lower urinary tract dysfunction.

Glutamatergic Mechanisms Involved in Bladder Overactivity and Pudendal Neuromodulation in Cats.

The involvement of ionotropic glutamate receptors in bladder overactivity and pudendal neuromodulation was determined in α-chloralose anesthetized cats by intravenously administering MK801 (a NMDA receptor antagonist) or CP465022 (an AMPA receptor antagonist). Infusion of 0.5% acetic acid (AA) into the bladder produced bladder overactivity. In the first group of 5 cats, bladder capacity was significantly (P < 0.05) reduced to 55.3±10.0% of saline control by AA irritation. Pudendal nerve stimulation (PNS) significantly (P < 0.05) increased bladder capacity to 106.8 ± 15.0% and 106.7 ± 13.3% of saline control at 2T and 4T intensity, respectively. T is threshold intensity for inducing anal twitching. MK801 at 0.3 mg/kg prevented the increase in capacity by 2T or 4T PNS. In the second group of 5 cats, bladder capacity was significantly (P < 0.05) reduced to 49.0 ± 7.5% of saline control by AA irritation. It was then significantly (P < 0.05) increased to 80.8±13.5% and 79.0±14.0% of saline control by 2T and 4T PNS, respectively. CP465022 at 0.03-1 mg/kg prevented the increase in capacity by 2T PNS and at 0.3-1 mg/kg prevented the increase in capacity by 4T PNS. In both groups, MK801 at 0.3 mg/kg and CP465022 at 1 mg/kg significantly (P < 0.05) increased the prestimulation bladder capacity (about 80% and 20%, respectively) and reduced the amplitude of bladder contractions (about 30 and 20 cmH2O, respectively). These results indicate that NMDA and AMPA glutamate receptors are important for PNS to inhibit bladder overactivity and that tonic activation of these receptors also contributes to the bladder overactivity induced by AA irritation.

MP26-12 MOTOR UNIT NUMBER ESTIMATION OF THE PUBORECTALIS MUSCLE

You have accessJournal of UrologyUrodynamics/Lower Urinary Tract Dysfunction/Female Pelvic Medicine: Basic Research & Pathophysiology I1 Apr 2017MP26-12 MOTOR UNIT NUMBER ESTIMATION OF THE PUBORECTALIS MUSCLE Nicholas Dias, Yun Peng, Jinbao He, Charles Popeney, and Yingchun Zhang Nicholas DiasNicholas Dias More articles by this author , Yun PengYun Peng More articles by this author , Jinbao HeJinbao He More articles by this author , Charles PopeneyCharles Popeney More articles by this author , and Yingchun ZhangYingchun Zhang More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2017.02.783AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Motor unit number estimation (MUNE) techniques estimate the number of functioning motor units (MUs) in a muscle, and serve as a biomarker for neuromuscular and muscular atrophy. Application of current MUNE techniques to the pelvic floor is impractical because of the need for either multiple stimulations or invasive needle electrodes. The objective is to propose a novel MUNE technique applicable to pelvic floor muscles, by combining a high-density surface EMG (HD-sEMG) decomposition approach with pudendal nerve stimulation, negating the need for invasive needles or multiple stimulations. METHODS All procedures were approved by UH IRB. The pudendal nerve was stimulated transrectally with a St. Mark′s electrode mounted on the operator′s glove. HD-sEMG recordings were acquired from the puborectalis muscle with a vaginal EMG probe (Figure 1b) during supramaximal stimulation and three maximal voluntary contractions of pelvic floor muscles. Firstly, single motor unit action potentials (SMUPs) were decomposed from EMG recordings during muscle contraction using our recently developed K-Means Clustering Convolution Kernel Compensation (KmCKC) Algorithm. All SMUPs were grouped into left or right side by visually checking their innervation zone locations following an established procedure. Next, mean SMUPs were derived for both sides by averaging all HD-sEMG profiles of grouped SMUPs. Last, MUNE was calculated as the weighted average of compound muscle action potential (CMAP) size to mean SMUP size ratios for both sides. RESULTS Left and right branches of the pudendal nerve were simulated. Four SMUPs were decomposed from HD-sEMG signals (left: 3 and right: 1). MUNE for the left and right sides were 22.8 and 27.0, respectively. CONCLUSIONS This pilot study proves the feasibility of a novel MUNE technique for muscles in the pelvic floor region. The KmCKC algorithm enables a non-invasive collection of SMUPs, negating the need for repeated electrical stimulation or invasive needle electrodes. Results from more subjects will be available from our ongoing subject recruitment. © 2017FiguresReferencesRelatedDetails Volume 197Issue 4SApril 2017Page: e324 Advertisement Copyright & Permissions© 2017MetricsAuthor Information Nicholas Dias More articles by this author Yun Peng More articles by this author Jinbao He More articles by this author Charles Popeney More articles by this author Yingchun Zhang More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Efficacy of Electrical Pudendal Nerve Stimulation versus Transvaginal Electrical Stimulation in Treating Female Idiopathic Urgency Urinary Incontinence

We compared the efficacy of electrical pudendal nerve stimulation vs transvaginal electrical stimulation to treat female idiopathic urgency urinary incontinence. A total of 120 female patients with idiopathic urgency urinary incontinence refractory to medication were randomized at a ratio of 2:1 to group 1 of 80 patients and group 2 of 40. Groups 1 and 2 were treated with electrical pudendal nerve stimulation and transvaginal electrical stimulation, respectively. To perform electrical pudendal nerve stimulation long acupuncture needles were deeply inserted into 4 sacrococcygeal points and electrified to stimulate pudendal nerves. Outcome measures were the 24-hour pad test and a questionnaire to measure the severity of symptoms and quality of life in women with urgency urinary incontinence. The median severity of symptoms and quality of life score on the urgency urinary incontinence questionnaire (urgency urinary incontinence total score) was 13 (range 7 to 18.75) in group 1 and 11 (range 8 to 16) in group 2 before treatment, which decreased to 2 (range 0 to 6.75) in group 1 and 6.5 (range 3.25 to 10.75) in group 2 (both p <0.01) after the completion of treatment. At the end of treatment in group 1 complete symptom resolution was noted in 34 patients (42.5%), with a 50% or greater symptom improvement rate in 70.1%. In group 2 complete symptom resolution was noted in 1 patient (2.5%) with a 50% or greater symptom improvement rate in 45.0%. The posttreatment urgency urinary incontinence total score was lower and the therapeutic effect was better in group 1 than in group 2 (both p <0.01). Electrical pudendal nerve stimulation is more effective than transvaginal electrical stimulation in treating drug refractory, female idiopathic urgency urinary incontinence.