AUAUpdateSeries. Lesson 19 Volume Treatment of Non-Neurogenic Overactive Bladder with Electrical Stimulation

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1 AUAUpdateSeries Lesson 19 Volume Treatment of Non-Neurogenic Overactive Bladder with Electrical Stimulation Learning Objective: At the conclusion of this continuing medical education activity, the participant will be able to describe the different types of electrical stimulation options used in the treatment of non-neurogenic overactive bladder, and understand the surgical technique and long-term outcomes of implantable sacral nerve stimulation for nonneurogenic bladder overactivity. TobyC.Chai,M.D. Disclosures: Nothing to disclose John D. Young Professor Division of Urology University of Maryland School of Medicine Baltimore, Maryland This self-study continuing medical education activity is Credit Designation Statement: The American Urological of the audience with information on which they can designed to provide urologists, Board candidates Association designates this educational activity for a make their own judgments. The program planners and/or residents affordable and convenient access to maximum of 1.0 AMA PRA Category 1 Credit. Each must resolve any conflicts of interest prior to the the most recent developments and techniques in physician should only claim credit commensurate with commencement of the educational activity. It remains urology. The American Urological Association (AUA) is the extent of their participation in the activity. for the audience to determine if the faculty s accredited by the Accreditation Council for Continuing AUA Disclosure Policy: As a provider accredited by the relationships may influence the educational content Medical Education (ACCME) to provide continuing ACCME, the AUA must insure balance, independence, with regard to exposition or conclusion. When medical education for physicians. The AUA takes objectivity and scientific rigor in all its activities. All unlabeled or unapproved uses of drugs or devices are responsibility for the content, quality and scientific faculty participating in an educational activity provided discussed, these are also indicated. integrity of this CME activity. by the AUA are required to disclose to the audience Unlabled/Unapproved Uses: It is the policy of the AUA any relevant financial relationships with any to require the disclosure of all references to commercial interest to the provider. The intent of this unlabeled or unapproved uses of drugs or devices disclosure is not to prevent faculty with relevant prior to the presentation of educational content. financial relationships from serving as faculty, but Please consult the prescribing information for full rather to provide members disclosure of approved uses. Publication date: June 2008 Expiration date: June American Urological Association, Education and Research Inc., Linthicum, MD

2 KEY WORDS: electric stimulation therapy; urinary bladder, overactive; urinary incontinence, urge INTRODUCTION Lower urinary tract symptoms include complaints by patients of urinary urgency, frequency and nocturia. Urge urinary incontinence is an involuntary loss of urine preceded by urgency. Urgency, as defined by the International Continence Society, is the complaint of a sudden compelling desire to pass urine which is difficult to defer. 1 According to this definition, urgency is a pathological sensation and not considered part of the normal sense of desire to urinate when the bladder is full. These symptoms (LUTS and/or UUI) together have been called overactive bladder, although some might insist that the ICS defined urgency must be present in all patients who are diagnosed with OAB. The debate over whether urgency as defined by the ICS should be the cornerstone of OAB was highlighted in a recent article. 2 All of these descriptive words are attempts to tersely summarize symptoms. For example, does a complaint of feeling like I have to urinate all the time mean frequency and/or urgency or neither? Can a patient have UUI without the precedent event of ICS defined urgency? Thus, while symptoms may be expressed by patients, these symptoms do not always necessarily rigidly fit within the definition of OAB. This review will focus on electrical stimulation, including intravaginal electrical stimulation, posterior tibial neurostimulation and sacral neuromodulation (InterStim, Medtronic, Inc., Minneapolis, Minnesota) for treating idiopathic or non-neurogenic OAB. The mechanisms of action of electrical stimulation are unknown. However, electrical stimulation by its nature must somehow modulate the neural reflexes (afferent and efferent pathways) of the lower urinary tract including the bladder, urethra and pelvic floor musculature. By modulating these lower urinary tract reflexes with electrical stimulation, bladder storage function can be augmented and thus alleviate LUTS and UUI. The use of IES and PTNS may be considered first line therapeutic options either alone or in conjunction with antimuscarinic therapy. InterStim, because of the invasive nature and the associated costs, is indicated in patients in whom conservative therapies, such as antimuscarinics, IES, PTNS and pelvic floor rehabilitation, have failed. Because antimuscarinics will fail in many patients, even when used with behaviorial modification, a comprehensive evaluation of the current literature on these therapies will help give the urologist a perspective of other options available. INTRAVAGINAL ELECTRICAL STIMULATION This technique involves the use of a probe within the vagina providing electrical stimulation, which patients are usually taught to self-administer at home. The electrical parameters used such as current, frequency and pulse-width may be adjusted, although the mechanisms of how these parameters may affect symptoms are unknown. Patients use the device every day or every other day for 10 to 30 minutes. Duration of use before effects were measured varied from 8 to 20 weeks. Data from a randomized placebo controlled trial 3 and non-randomized nonplacebo prospective trial, 4 in which large numbers of patients were studied, showed a benefit of IES for treating UUI. However, there was a major difference in the populations studied. In the study by Brubaker et al 50% of the cohort had pure stress urinary incontinence, 3 whereas none of the cohort had pure stress urinary incontinence (all had UUI or mixed urinary incontinence) in the study by Siegel et al. 4 In the latter study it is clear that 100% of the patients were treatment naïve because an exclusion criterion was current incontinence treatment. It is not clear in the study by Brubaker et al how many cases were treatment naïve or treatment failures (eg drugs or surgery). Smith reported that IES was no better than anticholinergic therapy, although the number of patients was small and the anticholinergic agent used was propantheline which is no longer widely used. 5 A more recent randomized, placebo controlled trial of IES revealed no benefit for mixed urinary incontinence (although most of these subjects had UUI). 6 This population was well defined as treatment naïve ( none of the patients had taken anticholinergics or tricyclic antidepressants, or had been treated using pelvic floor exercises or bladder training ). However, the fact that no statistical difference was found in outcome between sham stimulation and IES in this trial may be attributable to small sample size and thus insufficient power. Furthermore, the power analysis of this trial was not well stated. The use of IES can be contemplated in patients who present initially with LUTS and/or UUI and do not desire or cannot tolerate medical treatment. It is unknown whether IES would be effective for patients after multiple other treatments have failed. While this procedure is relatively non-invasive, the barriers to its use include patient compliance and inconsistent insurance coverage. However, IES should be considered a first line therapeutic option. POSTERIOR TIBIAL NERVE STIMULATION This technique involves placement of a 34 gauge needle over the posterior tibial nerve as it crosses the medial malleolus of the ankle. The needle is then attached to an electrical stimulator. A treatment of 30 minutes is given usually once a week for up to 12 weeks. The clinical use of this technique to treat LUTS/ UUI was first described by McGuire et al 7 and expanded to wider clinical use by Cooperberg and Stoller who have a US patent on the technique (U.S. Patent No. 6,493,588). 8 The results of several clinical trials on PTNS have been published. A prospective, non-placebo controlled trial showed that PTNS was effective in patients with refractory OAB defined as LUTS and UUI. 9 It is presumed that these subjects had nonneurogenic OAB but this was not explicitly stated in the article. Previous medical therapy, Kegel exercise, biofeedback and pelvic floor stimulators had failed in these 52 patients. The success rates were 25% reduction in day frequency, 21% reduc- ABBREVIATIONS: FDA (Food and Drug Administration), ICS (International Continence Society), IES (intravaginal electrical stimulation), IPG (implantable pulse generator), LUTS (lower urinary tract symptoms), OAB (overactive bladder), PNE (peripheral nerve evaluation), PTNS (posterior tibial neurostimulation), UUI (urge urinary incontinence) 170

3 tion in nocturia and 35% reduction of UUI after 12 weeks of PTNS. In a study from the Netherlands the outcomes of PTNS were examined in 37 patients with refractory non-neurogenic OAB (although there were more patients in this study who had other conditions including non-obstructive urinary retention). 10 Previous medical therapy including anticholinergics (mean 1.9 medications administered) failed in 91% of these 37 patients. Twelve weeks of PTNS therapy significantly improved subjective and objective OAB parameters. Neither of these studies was placebo controlled and so placebo effect, effect of behavioral modification from voiding diary, selection bias, etc were not controlled. A study on the changes in urodynamic parameters during PTNS (acute testing) revealed increased bladder capacity and increased bladder volume at which first detrusor overactivity was detected. 11 However this study involved 44 patients with the majority having neurogenic bladder and only 7 having non-neurogenic OAB. Similar results were reported in 90 consecutive patients with non-neurogenic OAB symptoms who underwent urodynamics after 12 PTNS sessions. 12 The authors found that PTNS cannot abolish urodynamic detrusor overactivity, although it can delay the volume of onset of the detrusor overactivity. Furthermore, the presence of urodynamic detrusor overactivity was associated with poorer outcomes with PTNS. Although there is no level 1 evidence (placebo controlled, randomized clinical trial) in the literature, the use of PTNS can be contemplated in patients with non-neurogenic OAB who are treatment naïve and in whom prior treatment has failed. Use of this therapy may be hindered by lack of familiarity by urologists. Another issue is the durability of benefits once PTNS treatment is completed. SACRAL NEUROMODULATION Historical review. The use of an implantable electrode in the S3 foramen to continuously electrically stimulate the S3 nerve root is called sacral neuromodulation. Sacral neuromodulation is marketed as InterStim by Medtronic, Inc. InterStim has been approved by the Food and Drug Administration for urinary urgency, frequency, urge incontinence and non-obstructive urinary retention in the United States since The company sponsored trials for OAB symptoms that resulted in FDA approval of InterStim have been published. These trials 13, 14 showed that InterStim was significantly effective in decreasing urinary frequency, urgency and episodes of urge incontinence. While these trials were not truly placebo controlled, there was a control group in which InterStim therapy was delayed (although no treatment was given, this was not a true placebo group since the subjects randomized to delayed treatment knew they were not getting treatment) and ultimately this delayed group crossed over to receive treatment. Prior multiple therapies for OAB symptoms had failed in these patients. From a historical perspective, InterStim evolved directly from the work of Schmidt and Tanagho in the late 1970s and early 1980s when they attempted to develop a bladder pacemaker in hopes of providing an on-demand stimulation of the sacral spinal nerves to induce voiding in patients with bladder areflexia secondary to spinal cord injury. 15, 16 From this early work, they provided convincing evidence of the important role of the pudendal nerve in modulating the micturition reflex, 17 which is important in understanding the theoretical mechanism of neuromodulation. The more widespread clinical application of S3 nerve root electrical stimulation/neuromodulation to treat urinary urge incontinence or the frequency urgency syndrome did not occur until the 1990s when Schmidt et al described a simple, percutaneous method to evaluate S3 nerve root integrity (peripheral nerve evaluation). 18 Schmidt et al were not intent on developing a sacral neuromodulation technique for therapeutic purposes, but rather as a diagnostic test to evaluate the sacral reflex arc. It was during this time that they realized the therapeutic potential of subchronic PNE of the S3 nerve root. Evolution of InterStim technique. PNE Followed by InterStim Implantable Pulse Generator Implantation: When InterStim was first approved by the FDA for OAB symptoms, the initial procedure was subchronic PNE of the S3 nerve root for 5 to 7 days. The procedure involved placing a floppy, temporary wire into 1 or both of the S3 foramen. The temporary wire(s) was taped to the patient s back and the patient recorded a voiding diary for 5 to 7 days to assess the effects of subchronic S3 nerve stimulation on voiding frequency, urgency and urge incontinent episodes. At the end of the 5 to 7 days the temporary wire(s) was removed. If the patient had >50% improvement in any of these parameters, he/she would receive a permanently implanted S3 lead (on the side with the best clinical response) and at the same time an IPG during 1 operative session. Problems with this approach included a high migration rate of the temporary leads during the 5 to 7 days of PNE testing leading to inability to assess whether S3 nerve neuromodulation would be effective. Often the PNE subchronic testing would have to be repeated. Another problem was matching the clinical response of the implanted permanent lead with the temporary lead since both leads are of different designs and placed at different times. Furthermore, the position of the permanent lead would not necessarily mirror that of the temporary lead as they are introduced through the S3 foramen in a different manner. Modifications With Fluoroscopy and Fascial Anchoring of Permanent Lead: An early modification of the subchronic S3 PNE with temporary wires was proposed in Instead of using the temporary wire electrode during the subchronic test phase, an implantable lead was used which could then be tested for 2 to 4 weeks. The lead was implanted using a minimally invasive technique, anchored to the lumbodorsal fascia and connected to an extension wire, which was tunneled subcutaneously and exited the skin at a distance from the implant site. The benefits of this modification included less chance of lead migration during the extended test phase period. Additionally, one could expect a completely identical clinical response rate between the sub-chronic phase and the chronic neuromodulation phase because the lead was the same for both phases. This modification was similar to that of staged implantation described by previous investigators. 20 Another modification was the development of fluoroscopy to help localize the S3 foramen. Current Technique of InterStim: The technique of InterStim therapy involves 2 stages. The first stage is percutaneous implan- 171

4 tation of a permanent tined lead which was first described in In the illustrations the patient is in a prone position with the head to the right and the feet to the left. The initial step is placement of the finder needle into the S3 foramen (fig. 1). The correct position is verified by stimulation of the finder needle and examining for a bellows response and/or toe flexion. Once the needle is confirmed to be in the S3 foramen, the tined lead is inserted using the Seldinger technique and cross-table lateral fluoroscopy. A wire is placed into the finder needle and the finder needle is removed (fig. 2, note wire is in left S3 foramen and a right tined lead has already been placed in the right S3 foramen). The introducer is then passed coaxially down the wire (fig. 3). Lateral fluoroscopy will help guide the depth of introducer passage. The wire and inner obturator from the introducer are then removed and the tined lead is placed down the introducer (fig. 4). Lateral fluoroscopy shows the position of both tined leads in good position with lead 1 (the longest lead in the quadripolar tined lead) straddling the anterior sacral cortex (fig. 5, note 2 leads in S3 on this lateral view). Both leads are tunneled out the right side (fig. 6). A pocket is made for the 2 external extension connectors and the extensions are brought out through a more superior position (fig. 7). Alternatively, the extension wires can be brought back across the midline to exit the left side to allow more distance between the extension wire exit site and the future IPG pocket (which will be where the pocket for FIG. 3 FIG. 4 FIG. 1 FIG. 5 FIG. 2 the connectors is made). This distance can help reduce IPG pocket infection risk. Figure 8 shows the conclusion of the case. Both leads will be tested in sequential fashion, with 1 week of stimulation for each S3 lead. The side that gives the best response will be the side that will be connected to the IPG during the second stage surgery. A unilateral tined lead can be placed instead of bilateral leads but bilateral testing can ensure a potentially better response. The IPG available in the United States is not a dual channel 172

5 FIG. 6 FIG. 9 FIG. 7 FIG. 8 stimulator and so only 1 lead can be stimulated but not both simultaneously. If the patient has >50% clinical response, stage 2 of the procedure is performed which is connection of a tined lead to the IPG and implantation of the IPG. The contralateral tined lead, if placed, is usually left indwelling as a spare and buried with the IPG. However, one can remove the non-stimulated tined lead if desired. A new IPG (IPG II) was recently made available which is smaller and thinner than the previous model (fig. 9). The subcutaneous pocket does not have to be made as large, which is tolerated better by the patients. Long-term results with InterStim. In a recent prospective study the 5-year post-implant data on InterStim were reviewed. 22 Of 163 patients enrolled in the study 5-year follow-up data were available for 105 (retention rate 64%). InterStim explantation was necessary in 16 patients due to lack of efficacy or complications (10%). For UUI pre-implant incontinence frequency was episodes a day, which decreased to at 1 year and was maintained at after 5 years. Pad use also was significantly decreased and maintained at 5 years. For urinary frequency and urgency symptoms the average number of voids a day decreased from before implant to a year after implant. Urinary frequency increased slightly to at 5 years after implantation. The volume per void increased significantly and was maintained at 5 years. Of the patients in this study 39.5% experienced an adverse event. The most common adverse events were device exchange (23.7%), reposition of IPG (7.9%), reposition of lead and IPG (6.6%), and reposition of lead only (6.6%). However, it should be noted that all of these patients received the earlier generation IPG and leads, and were not treated with the aforementioned current technique. Whether the percutaneously placed tined leads and IPG II will cause fewer adverse events remains to be reported. Based on empirical clinical experience, the tined leads rarely migrate and, therefore, complications related to lead revision with this newer lead will likely be minimal. Also, due to smaller size of the IPG II it is expected that the revision rate due to pain at the IPG site will decrease (most of the revision with the original IPG was related to pain at the implant site at least partly due to the larger size). However, in exchange for a smaller IPG is a shorter battery life and, therefore, earlier and more frequent battery replacement should be expected. Several other studies also support the long-term efficacy of InterStim. 23, 24 From these studies it appears that InterStim maintains its durability of beneficial effect for treating non-neurogenic OAB symptoms for up to 5 years. It should be noted that almost all studies on InterStim in the literature are from centers associated with Medtronic sponsored trials, although there are several independent studies reporting equivalent benefit of InterStim

6 InterStim future. The use of InterStim to treat non-neurogenic OAB by now is well established. However many questions remain, some of which have been addressed. Amundsen et al performed a retrospective review to determine prognostic factors related to predicting who may or may not benefit from InterStim. 28 They found that older age (>55 years), more than 3 chronic conditions and perhaps neurological disease were associated with poorer cure rates with InterStim. Cure was defined as no daily leakage episodes after permanent implantation. This was a small study population and a larger study is needed to confirm these findings. Recently, the return of PNE instead of staged implantation has become more popular, likely secondary to economic issues. However, a prospective randomized study between PNE and staged implantation revealed that the latter was significantly better at predicting progression of IPG implantation than PNE. 29 The subjects in the study were older (>55 years) and, therefore, cure was more difficult. PNE may be better than staged implantation for patients who prefer an office rather than a surgical procedure. South et al reported that urodynamic finding of detrusor overactivity has no prognostic significance on InterStim treatment. 30 Of their population with refractory UUI 64% responded with a >50% improvement in incontinence episodes to stage 1 stimulation and 36% did not. The responders were significantly younger than non-responders (age 59.7 versus 67.0 years). It does not appear that urodynamics add much to deciding who will benefit from InterStim therapy although a prospective, controlled randomized study would provide a higher evidence level than this report. 30 We do not yet know how IPG stimulation parameters of pulse width, frequency, amplitude (voltage), cycling and bipolar versus unipolar settings affect clinical responses. The use of bilateral S3 stimulation has not been explored fully because a dual channel IPG is only available in Europe. The longterm effects of stimulation on the S3 nerve root function are not known although long-term studies do not indicate any problems. 22 Other issues that remain unresolved include how to prevent electrical stimuli to other dermatomes. When this happens, patients often complain of dysesthesia or pain in the leg, ankle, foot or buttock. The best way to manage these minor complaints is not well established, and reprogramming the IPG becomes a trial and error process. Based on empirical experience, explantation of the InterStim is necessary in some cases due to intolerable dysesthesias. Long-term effects of sacral nerve stimulation on the pelvic floor are also unknown. Do the pelvic floor muscles hypertrophy? From the neural perspective, with long-term sacral nerve stimulation does the sacral reflex arc develop neuroplasticity? From an afferent perspective, it is also theorized that InterStim effects may be at the sensory cortex in the supraspinal central nervous system (cerebral cortex). The effects of long-term electrical stimulation on the brain are also unknown. CONCLUSIONS Electrical stimulation is a commonly used technique to treat bladder symptoms attributed to non-neurogenic OAB. The tech- niques for stimulation include intravaginal electrical stimulation, percutaneous posterior tibial nerve electrical stimulation and implantable S3 nerve root stimulation. There are data to support the efficacy of all 3 techniques. The pros and cons of these different techniques must be weighed against patient preferences, severity of symptoms and costs. REFERENCES 1. Abrams P, Cardozo L, Fall M et al: The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002; 21: Yamaguchi O, Honda K, Nomiya M et al: Defining overactive bladder as hypersensitivity. Neurourol Urodyn 2007; 26: Brubaker L, Benson JT, Bent A et al: Transvaginal electrical stimulation for female urinary incontinence. Am J Obstet Gynecol 1997; 177: Siegel SW, Richardson DA, Miller KL et al: Pelvic floor electrical stimulation for the treatment of urge and mixed urinary incontinence in women. Urology 1997; 50: Smith JJ 3rd: Intravaginal stimulation randomized trial. J Urol 1996; 155: Amaro JL, Gameiro MO, Kawano PR et al: Intravaginal electrical stimulation: a randomized, double-blind study on the treatment of mixed urinary incontinence. Acta Obstet Gynecol Scand 2006; 85: McGuire EJ, Shi-Chun Z, Horwinski ER et al: Treatment of motor and sensory detrusor instability by electrical stimulation. J Urol 1983; 129: Cooperberg MR and Stoller ML: Percutaneous neuromodulation. Urol Clin North Am 2005; 32: Govier FE, Litwiller S, Nitti V et al: Percutaneous afferent neuromodulation for the refractory overactive bladder: results of a multicenter study. J Urol 2001; 165: van Balken MR, Vandoninck V, Gisolf KW et al: Posterior tibial nerve stimulation as neuromodulative treatment of lower urinary tract dysfunction. J Urol 2001; 166: Amarenco G, Ismael SS, Even-Schneider A et al: Urodynamic effect of acute transcutaneous posterior tibial nerve stimulation in overactive bladder. J Urol 2003; 169: Vandoninck V, van Balken MR, Finazzi Agro E et al: Percutaneous tibial nerve stimulation in the treatment of overactive bladder: urodynamic data. Neurourol Urodyn 2003; 22: Hassouna MM, Siegel SW, Nyeholt AA et al: Sacral neuromodulation in the treatment of urgency-frequency symptoms: a multicenter study on efficacy and safety. J Urol 2000; 163: Schmidt RA, Jonas U, Oleson KA et al: Sacral nerve stimulation for treatment of refractory urinary urge incontinence. Sacral Nerve Stimulation Study Group. J Urol 1999; 162: Schmidt RA and Tanagho EA: Feasibility of controlled micturition through electric stimulation. Urol Int 1979; 34: Tanagho EA and Schmidt RA: Bladder pacemaker: scientific basis and clinical future. Urology 1982; 20: Tanagho EA and Schmidt RA: Electrical stimulation in the clinical management of the neurogenic bladder. J Urol 1988; 140: Schmidt RA, Senn E and Tanagho EA: Functional evaluation of sacral nerve root integrity. Report of a technique. Urology 1990; 35: Chai TC and Mamo GJ: Modified techniques of S3 foramen localization and lead implantation in S3 neuromodulation. Urology 2001; 58:

7 20. Janknegt RA, Weil EH and Eerdmans PH: Improving neuromodulation technique for refractory voiding dysfunctions: two-stage implant. Urology 1997; 49: Spinelli M, Giardiello G, Gerber M et al: New sacral neuromodulation lead for percutaneous implantation using local anesthesia: description and first experience. J Urol 2003; 170: van Kerrebroeck PE, van Voskuilen AC, Heesakkers JP et al: Results of sacral neuromodulation therapy for urinary voiding dysfunction: outcomes of a prospective, worldwide clinical study. J Urol 2007; 178: Janknegt RA, Hassouna MM, Siegel SW et al: Long-term effectiveness of sacral nerve stimulation for refractory urge incontinence. Eur Urol 2001; 39: Siegel SW, Catanzaro F, Dijkema HE et al: Long-term results of a multicenter study on sacral nerve stimulation for treatment of urinary urge incontinence, urgency-frequency, and retention. Urology, suppl., 2000; 56: Latini JM, Alipour M and Kreder KJ Jr: Efficacy of sacral neuromodulation for symptomatic treatment of refractory urinary urge incontinence. Urology 2006; 67: Starkman JS, Wolter CE, Scarpero HM et al: Management of refractory urinary urge incontinence following urogynecological surgery with sacral neuromodulation. Neurourol Urodyn 2007; 26: Sherman ND, Jamison MG, Webster GD et al: Sacral neuromodulation for the treatment of refractory urinary urge incontinence after stress incontinence surgery. Am J Obstet Gynecol 2005; 193: Amundsen CL, Romero AA, Jamison MG et al: Sacral neuromodulation for intractable urge incontinence: are there factors associated with cure? Urology 2005; 66: Borawski KM, Foster RT, Webster GD et al: Predicting implantation with a neuromodulator using two different test stimulation techniques: a prospective randomized study in urge incontinent women. Neurourol Urodyn 2007; 26: South MM, Romero AA, Jamison MG et al: Detrusor overactivity does not predict outcome of sacral neuromodulation test stimulation. Int Urogynecol J Pelvic Floor Dysfunct 2007; 18:

8 Study Questions Volume 27 Lesson The sacral peripheral nerve evaluation was developed to a. Treat urge incontinence b. Assess the sacral reflex arc c. Reduce bladder outlet obstruction d. Assess pelvic floor muscle spasms e. Stop detrusor overactivity 2. A motor response to S3 stimulation is a. Toe flexion b. Ankle rotation c. Gastrocnemius contraction d. Anal wink e. Knee flexion 3. The benefit of a staged implant using a tined lead compared to a temporary lead placement includes a. Easier placement b. Quicker recovery c. Lower costs d. Less migration e. No need for fluoroscopy 4. Which factor is associated with a better outcome with sacral neuromodulation? a. Age <55 years b. Detrusor overactivity on urodynamics c. Neurological disease d. More than 3 chronic problems e. Less pad weight 5. Parameters in the IPG of InterStim that can be adjusted include a. Amperes b. Voltage c. Impedance d. Capacitance e. Conductivity Take this test online at