Secondary Logo

Share this article on:

Sacral Nerve Stimulation as a Therapy for Patients With Refractory Voiding and Bowel Dysfunction

Noblett, Karen L., MD; Buono, Kristen, MD

doi: 10.1097/AOG.0000000000002968
Contents: Urogynecology: Clinical Expert Series
Editors' Pick Podcast
Take CME Test

Sacral nerve stimulation delivers nonpainful electrical pulses to the sacral nerves that modulate the reflexes that control the bladder, bowels, and pelvic floor musculature. This relatively simple procedure was generated to improve and restore function in patients with a variety of pelvic floor disorders. Currently this therapy is approved for use in patients with urgency urinary incontinence, urinary urgency–frequency, nonobstructive urinary retention, and fecal incontinence. This review includes the history of this treatment modality, explains the mechanism of action, and describes the procedure for implantation of this device. Additionally, advancements in this treatment over the past two decades and landmark literature to date regarding sacral nerve stimulation are reviewed. Current literature regarding off-label uses of this treatment modality for a variety of pelvic floor disorders is also discussed.

Sacral nerve stimulation for refractory voiding and bowel dysfunction has provided an effective minimally invasive therapy for patients for whom more conservative treatments have failed.

Division of Female Pelvic Medicine and Reconstructive Surgery, Department of Obstetrics and Gynecology, University of California Irvine, Orange, California.

Corresponding author: Karen L. Noblett, MD, 333 City Boulevard West, Suite 1400, Orange, CA 92868; email: knoblett@uci.edu.

Financial Disclosure Dr. Noblett is the Chief Medical Officer for Axonics Modulation Technologies, Inc. The other author did not report any potential conflicts of interest.

Continuing medical education for this article is available at http://links.lww.com/AOG/B186.

Each author has indicated that she has met the journal's requirements for authorship.

Received December 13, 2017

Received in revised form February 11, 2018

Accepted April 26, 2018

Sacral nerve stimulation delivers nonpainful, electrical pulses to the sacral nerves to modulate the reflexes that influence the bladder, bowels, sphincters, and pelvic floor musculature to improve or restore function. Sacral nerve stimulation has been an available treatment for refractory urgency urinary incontinence (UUI) and nonobstructive urinary retention in the United States since 1997 and 1999, respectively. In 2011, it gained approval from the U.S. Food and Drug Administration (FDA) for the treatment of fecal incontinence. More than 225,000 patients worldwide have received sacral nerve stimulation,1 and currently the American Urological Association lists sacral nerve stimulation as a tier-three treatment option for UUI. Since its inception, the therapy has evolved to a minimally invasive procedure that can be performed under local anesthesia in an outpatient setting. Currently, InterStim is the only implantable device approved for sacral nerve stimulation in the United States. Because this therapy is becoming increasingly used for patients with pelvic floor disorders, there is a growing body of literature studying the long-term outcomes, side effects, comparison with other treatment modalities, and cost-effectiveness analyses. This article reviews the history of sacral nerve stimulation as well as the recent updates to the literature regarding this treatment modality.

Back to Top | Article Outline

HISTORY OF SACRAL NERVE STIMULATION

Mathias Saxtorph,2 a Danish general surgeon, introduced the idea of electrical stimulation for the treatment of bladder dysfunction in 1878; since then, multiple variations of pelvic floor electrical stimulation techniques have been introduced. Nashold demonstrated that direct spinal cord stimulation facilitated micturition.3,4 Their work was met with suboptimal clinical outcomes as a result of concomitant contraction of the external urethral sphincter resulting in high outlet resistance. To overcome the problem of simultaneous stimulation of the detrusor muscle and striated urethral sphincter, investigators sought more peripheral targets. In 1979 Tanagho5 demonstrated that stimulation of the ventral portion of the sacral nerve root was most effective in achieving micturition. The finding that a detrusor contraction could be achieved separately from activation of the urethral sphincter allowed the possibility of a therapeutic application.6 This landmark research ultimately led to the technique for sacral nerve stimulation and initiation of clinical trials.7,8

Back to Top | Article Outline

MECHANISM OF ACTION

Although the exact mechanism of action of sacral nerve stimulation is not completely understood, more insights have been gained over time. A frequently encountered question is how does a single intervention resolve both storage and emptying disorders? Addressing this question requires an understanding of normal voiding patterns. For infants who have not yet achieved voluntary control over bladder function, a specific level of bladder distention is required to stimulate the voiding reflex. Within the pontine micturition center, this sensory input simultaneously allows for a coordinated detrusor contraction and urethral sphincter relaxation, which results in micturition. In addition to voluntary control, continence is also maintained through an intact guarding reflex, which is an involuntary increase in the activity of the external urethral sphincter during bladder filling. Voluntary micturition is facilitated through stimulation of the excitatory efferent pathway, resulting in inhibition of the sympathetic system and activation of the sacral parasympathetics.9

Urinary urgency–frequency and UUI are included within the umbrella term of overactive bladder (OAB). A recent study estimated that one third of American adults experience bothersome symptoms of OAB, and the prevalence increases with age.10 Although the etiology of OAB is considered to be idiopathic, animal studies suggest there may be improper signaling from the bladder urothelium leading to subsequent voiding dysfunction.11 deGroat demonstrated that sacral preganglionic outflow to the bladder receives inhibitory input from both somatic and visceral afferents12–16 and that stimulation of the somatic afferents in the pudendal nerve induces inhibitory mechanisms.17 As a result of the low level of stimulation associated with sacral nerve stimulation, it likely functions through the somatic afferents because these nerves are depolarized at lower levels than autonomic nerves.

For patients with nonobstructive urinary retention, sacral nerve stimulation is believed to activate the pudendal nerve afferents originating from the pelvic organs. At the level of the spinal cord, pudendal afferents turn on voiding reflexes by suppressing exaggerated guarding reflexes, thus relieving urinary retention. In patients with OAB, it is thought that pudendal afferents can activate the inhibitory reflexes that promote bladder storage by inhibiting the afferent limb of an abnormal voiding reflex.

In patients with fecal incontinence, the mechanism of action is still not completely understood. A small study demonstrating the use of sacral nerve stimulation was associated with higher tolerance of rectal distention, but the neurologic mechanism behind this is unclear.18 Pudendal afferent somatic fibers are believed to inhibit colonic motility and activate the internal anal sphincter.19 A mechanism related to colonic motility explains why patients with significant anal sphincter defects may still demonstrate benefit from sacral nerve stimulation. Notably, chronic constipation is also an approved indication for sacral nerve stimulation in Europe. Dinning demonstrated increased colonic peristalsis and frequency of bowel movements in patients with slow-transit constipation after undergoing sacral nerve stimulation.20,21 As with the bladder, sacral nerve stimulation may be effective in treating both storage and emptying disorders of the bowels, but the exact mechanism is unknown.

Back to Top | Article Outline

PROCEDURE

Sacral nerve stimulation involves a two-stage procedure. The initial phase, the test stimulation period, is where the patient is allowed to evaluate whether or not the therapy is effective. The test stimulation can be performed by one of two techniques. The first option is percutaneous nerve evaluation, which is an office-based procedure in which a temporary electrode wire is passed through the S3 foramen under local anesthesia, with or without fluoroscopic guidance. The wire is connected to an external pulse generator and is worn for a trial period of 3–7 days (Fig. 1). Those with at least 50% improvement in their symptoms during the test phase are candidates for implant of the permanent lead wire and implantable pulse generator.22 The advantage is that this is an incision-free procedure performed in the office using local anesthesia, but because the wire is not securely anchored in place, the risk of migration of the wire away from the S3 nerve is increased.

Fig. 1

Fig. 1

The second option is a staged implant introduced by Spinelli in 2003,23,24 which is typically performed as an outpatient procedure using local anesthesia, intravenous sedation, and intraoperative fluoroscopy (Figs. 2 and 3). This procedure involves placement of the permanent, self-anchoring, quadripolar lead wire adjacent to a sacral nerve root (typically S3). The lead wire is connected to an external pulse generator and is worn for a trial period of 7–14 days. The advantage of this technique is that it allows for a longer trial period with minimal risk of lead migration. The permanent wire also has four electrodes, each of which can be trialed to achieve an optimal clinical outcome. During the second stage, the previously placed lead wire remains in place and is simply connected to the implantable pulse generator. This eliminates the chance of variable lead placement between the test and implantation phases. The disadvantage of the staged implant is that it requires two operations and may lead to more expense if the trial is ultimately unsuccessful because the lead wire requires surgical removal. However, in a prospective study comparing the percutaneous nerve evaluation with the staged implant, there was a significantly higher rate of conversion to an implant with the staged procedure compared with percutaneous nerve evaluation (88% vs 46%).25

Fig. 2

Fig. 2

Fig. 3

Fig. 3

The most common nerve targeted for stimulation is the S3 nerve root. Benson (Benson JT. Human sacral neuroanatomy: electrophysiologic determination. Presented as a poster at the 21st annual AUGS meeting, October 6–10, 2000, Vancouver, British Columbia, Canada) demonstrated that the third sacral nerve root provided the majority of innervation to the pelvic organs of interest. However, the sacral anatomy is extremely variable and thus occasionally the S4 or S2 nerve roots are stimulated. To determine optimal lead placement, both motor and sensory responses are desired. The typical sensory response is a tapping or vibratory sensation in the vagina, rectum, or perineum. The motor response includes a pulling in of the pelvic floor muscles known as a bellows response or flexion of the great toe. The ideal goal with placement is to obtain motor responses at all four electrodes at thresholds under 2–3 volts. There has been no definitive study to determine whether sensory or motor responses are more predictive of success. Recent investigation comparing patients evaluated with both sensory and motor response with those evaluated with motor response alone demonstrated similar rates of successful trial stimulation and device explant between groups with 4-year follow-up.26 Pizarro-Berdichevsky27 demonstrated a reduced risk of lead wire revision in patients with higher total motor response scores and great toe scores, but not bellows scores, in a recent retrospective review. The authors suggest that a great toe response reflects stimulation of a more therapeutically relevant target nerve, whereas a pelvic bellows response reflects stimulation of any portion of a broader target, which could include multiple nerves.

Back to Top | Article Outline

THERAPY ADVANCEMENTS

Since its introduction, sacral nerve stimulation has undergone significant improvements in design and application. The initial implantation technique required general anesthesia, a larger incision over the sacrum (often 5–7 cm), and dissection to the periosteum. With the introduction of the tined lead wire in 2003, currently the procedure requires only a 2-mm incision and can be performed under local anesthesia.24 In 2006, a smaller, second-generation implantable pulse generator was introduced. Additionally, it was postulated that a curved stylet would mimic the natural path of the sacral nerve root (Fig. 3) and was added to the tined lead kit after a randomized crossover trial demonstrated superiority of the curved over the straight stylet in achieving motor response at lower amplitudes.28

Another important component of sacral nerve stimulation device implantation is infection prevention. The American Urological Association recommends perioperative antibiotic prophylaxis with a first-generation cephalosporin before placement of the lead wire to cover for skin flora; however, data supporting this recommendation are lacking.29 A large retrospective cohort analysis of sacral nerve stimulation procedures noted a significant reduction in surgical site infections after the implementation of a chlorhexidine scrub the night before and the morning of the procedure. The infection rate decreased from 7.4% to 1.7% after institution of the chlorhexidine scrub.30 Additionally, 82% of devices that were explanted as a result of an infection were noted to be colonized with methicillin-resistant Staphylococcus aureus, which may influence the selection of prophylactic postoperative antibiotics.

Back to Top | Article Outline

CLINICAL TREATMENT OF OVERACTIVE BLADDER AND URINARY RETENTION

Before gaining approval from the FDA, Medtronic conducted a prospective, multicenter, randomized study evaluating the efficacy and safety of sacral nerve stimulation between 1993 and 1997 (MDT-103). This study included 23 centers worldwide and recruited 76 patients with urge incontinent, 50 with urgency–frequency, and 51 with urinary retention. All patients were required to have had a successful percutaneous nerve evaluation trial, defined as 50% or greater improvement from their baseline symptoms. They were randomized to implantation either immediately or 6 months after the percutaneous nerve evaluation trial.22

Regardless of the indication for sacral nerve stimulation, findings in the implant groups were encouraging. For the 38 participants with urge incontinence randomized to immediate implantation, the mean number of leakage episodes decreased from 10.8 to 2.9 per day. Overall, 45% of the patients remained completely dry and 34% achieved a 50% or greater reduction in leaking episodes. When the stimulation was turned off at 6 months, the mean number of baseline incontinent episodes went back up to 10.2. For those with urinary urgency–frequency, the mean number of daily voids decreased from 16.9 to 8.8 and 33% experienced a 50% or greater reduction in voids. At 6 months with the stimulation turned off, the number of voids increased to 13.5 voids per day. In patients with urinary retention, 61% were able to eliminate catheter use.

In 2007, van Kerrebroeck31 reported the results of a 5-year prospective, multicenter trial that evaluated the long-term efficacy and safety of sacral nerve stimulation. Seventeen centers of the original 23 from the MDT-103 study participated. A total of 163 patients were enrolled and 152 went on to implantation (129 were from the original trial). Overall the authors reported success rates at 5 years in 86% of patients with urge incontinence, 71% with urge–frequency, and 78% with urinary retention. Reported adverse events included a 7.9% rate of infection, 5.3% rate of lead migration, a 7.9% rate of pain at the lead wire site, and a 19.1% rate of pain at the implantable pulse generator site. Of note, this cohort included patients with an abdominal implantable pulse generator. At the time of data collection, 96% of all adverse events were resolved and no life-threatening or irreversible complications occurred. Bosch32 also published long-term results of sacral nerve stimulation therapy for urge incontinence in 45 patients who were followed by a mean duration of 47.8 months. Overall 40% of patients were cured, 30% were more than 50% improved, and in 30% treatment had failed. Of note, the study population included patients with underlying neurologic disease.

In a systematic literature review of sacral nerve stimulation therapy for the treatment of UUI, Brazelli33 found that, in the four controlled trials in the literature, there was an 80% success rate, whereas, in the 37 case series, there was an overall success of 67%. Amundsen34 conducted a prospective study to determine whether there were factors predictive of complete cure and found that age older than 55 years and the presence of more than three chronic conditions were independently associated with lower cure rates for patients with intractable UUI.

The InSite Trial was a randomized multicenter study evaluating the success rate of sacral nerve stimulation compared with standard medical therapy in patients with OAB. Standard medical therapy was defined as antimuscarinic therapy, and inclusion criteria included failure of at least one medication without having tried every available antimuscarinic medication. The InSite Trial, which was implemented in two phases, reflects current standard practices including minimally invasive technique, routine fluoroscopy use, and exclusive use of a staged implantation of the tined lead.

Phase 1 was a prospective, multicenter, randomized trial comparing sacral nerve stimulation with standard medical therapy and the primary objective was to compare the therapeutic success rate at 6 months, which was defined as 50% or greater improvement from baseline symptoms.35 In contrast to the MDT-103 trial in which all available therapies had failed and patients had more severe baseline symptoms, the patient population in the InSite trial had milder symptoms. Overall, 147 patients were randomized. For patients who were incontinent at baseline, 71% of those treated with sacral nerve stimulation responded compared with 47% of patients treated with standard medical therapy. Rates of complete continence were higher in those treated with sacral nerve stimulation (39% vs 21%) and this group showed statistically significant improvement over the standard medical therapy group in all measures of quality of life. The patient population was a less refractory group than previously studied, suggesting that sacral nerve stimulation is a successful option for patients throughout the OAB spectrum. The implication of the study is that after unsuccessful treatment with anticholinergic medication, patients with OAB may be more likely to benefit from sacral nerve stimulation than an additional anticholinergic medication.

Phase 2 of the InSite trial was a prospective evaluation of safety and efficacy of sacral neuromodulation over 5 years.36 During the study period, 340 patients received test stimulation and of those, 272 (80%) had the sacral nerve stimulation system implanted. The overall therapeutic success rate at 5 years was 82%. Given that the therapeutic success rate was 85% at 1 year,37 this demonstrates the long-term durability of sacral nerve stimulation for patients with OAB. Complete continence at 5 years was achieved in 45% of patients. Sustained improvements in quality-of-life measurements were reported from baseline to 5 years in all domains. The 5-year cumulative rate of adverse events that required surgical intervention after the full sacral nerve stimulation system was implanted was 22% with the most common adverse event being an undesirable change in stimulation. This study, which is one of the first to evaluate outcome data and continuation rates of sacral nerve stimulation beyond 36 months, demonstrates that this therapy provides a durable treatment effect 60 months after implantation of the system.

The Relax OAB trial is the first study describing outcomes of a rechargeable sacral nerve stimulation device. This was a prospective, single-stage implant of the lead wire and implantable pulse generator in patients with refractory OAB.38 The results reported at 3 months are comparable with results in the literature and an infection rate of less than 2% (Fig. 4). Ninety-eight percent of patients were able to recharge the device within the first month.

Fig. 4

Fig. 4

In 2013, the FDA approved intradetrusor onabotulinum toxin A (Botox) injections for the treatment of UUI. The Rosetta Trial, a randomized multicenter trial comparing intradetrusor Botox injections with sacral nerve stimulation in patients with refractory UUI, demonstrated that intradetrusor Botox injections resulted in a greater daily reduction of urgency incontinence episodes (−3.9 vs −3.3)39 (Fig. 5). Although this finding was noted to be statistically significant, the authors of the trial comment that this finding is of uncertain clinical importance. Additionally, urinary tract infections and the need for self-catheterization postoperatively were higher among the patients who underwent intradetrusor Botox injections. A secondary analysis of the Rosetta Trial revealed that older women with multiple comorbidities and decreased functional and health-related quality of life had decreased treatment response and satisfaction with intradetrusor Botox injections compared with sacral nerve stimulation.40 Recently the American Urological Association updated its guidelines in 2015 to include intradetrusor Botox injections as a standard third-line therapy for patients with refractory OAB.41

Fig. 5

Fig. 5

Back to Top | Article Outline

CLINICAL TREATMENT OF FECAL INCONTINENCE

In 2011, the FDA approved sacral nerve stimulation for the indication of fecal incontinence. In the multicenter, nonrandomized trial precipitating its approval, 133 participants underwent a 2-week trial of sacral nerve stimulation with 120 (90%) progressing to full device implantation.42 That group experienced a drop in weekly symptoms from 9.4 at baseline to 1.9 at 1 year. Forty-one percent were completely continent and 83% were at least 50% improved, which was sustained over 5 years after implantation.43 Surgical device revision, replacement, or explant, however, occurred in 35.5% of patients. Given the high recurrence and morbidity of other surgical options for the treatment of fecal incontinence, sacral nerve stimulation may be an appealing alternative for patients.44

Another study supporting the use of sacral nerve stimulation for fecal incontinence is a randomized prospective trial of this therapy compared with optimal medical management (dietary therapy and pelvic floor strengthening).45 Ninety percent of those randomized to sacral nerve stimulation had a successful trial and went on to full implantation. Patients were monitored for 12 months; the sacral nerve stimulation group demonstrated a reduction in weekly fecal incontinence episodes from 9.5 to 3.1, whereas the medical therapy group demonstrated no change from baseline, having more than nine incontinent episodes per week at the end of the trial. Interestingly, patients with sphincter defects up to 120° were included, and two thirds of those with sphincter defects demonstrated at least a 75% response rate. This supports a central mechanism rather than direct stimulation of the anal sphincter.

Back to Top | Article Outline

SACRAL NERVE STIMULATION DURING PREGNANCY

A recent systematic review of sacral nerve stimulation during pregnancy evaluated eight studies of 22 patients who underwent one or more pregnancies after implantation.46 Sacral nerve stimulation was continued during eight of the pregnancies and in the remaining 18 pregnancies in which the device was deactivated, seven patients experienced recurrent urinary tract infections and two patients requested reactivation during the second trimester. Sixteen patients were delivered by cesarean and nine were delivered vaginally. Sacral nerve stimulation functioned appropriately after 15 of the 25 pregnancies. Four patients required reprogramming, three required replacement, and three decided to remove the device after delivery as a result of lack of symptoms after deactivation. Based on this limited evidence, the use of sacral nerve stimulation during pregnancy appears to be safe and did not result in significant maternal or fetal morbidity.

Back to Top | Article Outline

FUTURE DIRECTIONS

A review article from 2011 demonstrated a 40–72% reduction in pelvic pain after implantation of a sacral nerve stimulation device.47 Martellucci48 published a cohort study of 16 patients with chronic pelvic pain who underwent sacral nerve stimulation implantation. The mean preoperative visual analog scale was 8.1, which decreased to 2.1 after 6 months. This improvement persisted for up to 24 months for 13 patients and up to 60 months for 3 patients. A recent case report of patients with a history of surgically treated deep infiltrating endometriosis who underwent staged sacral nerve stimulation testing49 demonstrated that three of the four patients went on to permanent implantation and all three patients continued to report improved quality of life 30 months after the implantation.

Although not currently approved for patients with interstitial cystitis, sacral nerve stimulation may provide an alternative therapy. In a prospective study of 37 patients with interstitial cystitis, 70% had a successful trial and went on to have the permanent lead wire implanted. Overall 24-hour voids decreased from 24.7 to 12.2 and 96% of the participants said they would undergo the procedure again.50 In a subsequent study of patients with interstitial cystitis, Peters51 demonstrated a 36% reduction in narcotic use with 22% stopping altogether. Zabihi52 prospectively evaluated 30 patients with interstitial cystitis and chronic pelvic pain and found a 41% improvement in symptoms 6 months after sacral nerve stimulation implantation.

The original trials with sacral nerve stimulation excluded patients with underlying neurologic disease. However, patients with neurologic conditions included in Bosch’s study had equivalent success during the trial as neurologically intact patients.32 A report of 33 patients with various neurologic conditions (primarily multiple sclerosis) demonstrated a similar implant rate as neurologically intact patients.53 More recently, a study of 62 patients with neurogenic bladder dysfunction demonstrated that two thirds had a positive response to the trial.54 Among the 37 participants implanted for a mean of 4.3 years, investigators found the effect of sacral nerve stimulation to be sustained in 75.7%, partially altered in 8.1%, and lost in 16.2%.

More peripheral sites of stimulation are currently being evaluated. In a randomized crossover trial of sacral compared with pudendal stimulation, the pudendal implant was found to be superior to a sacral implant in 79% of the cohort.55 All patients had successful placement of the pudendal lead through a posterior approach and there was no difference in time to implantation when compared with the sacral lead.

Some members of the health care community have expressed concern regarding the cost of sacral nerve stimulation. In a retrospective review of patients receiving sacral nerve stimulation, health care utilization was determined for the year before and after implantation.56 The investigators found that sacral nerve stimulation was associated with a 92% reduction in outpatient physician visits, diagnostic and procedure costs along with a 30% reduction in drug expenditures. Dutch investigators modeled the cost of adding sacral nerve stimulation to the treatment algorithm for fecal incontinence and found that adding this therapy decreased cost and improved treatment success, resulting in higher quality-adjusted life-years.57 A recently published cost–consequence model predicted that, over a 15-year period, the per-patient cost of treatment with a rechargeable, as compared with a nonrechargeable, sacral nerve stimulation device would result in an estimated payer cost savings of $27,121.58 Adoption of a rechargeable sacral nerve stimulation device was projected to result in health care expenditure savings up to $12 billion.

Back to Top | Article Outline

DISCUSSION

The advent of sacral nerve stimulation for the treatment of refractory voiding and bowel dysfunction has provided an effective and safe alternative therapy for patients for whom more conservative treatments have failed. Emerging research indicates that sacral nerve stimulation may be a future therapeutic option for patients with chronic pelvic pain and interstitial cystitis. As sacral nerve stimulation therapy continues to advance with the possible expansion to more direct sites of stimulation and widening therapeutic indications, more women with pelvic floor disorders may benefit from this effective, minimally invasive treatment option.

Back to Top | Article Outline

REFERENCES

2. Saxtorph MH. Strictura urethrae-fistula perinei-retentio urinae. Clinisk Chirurgi. Gyldendalske Forlag 1878:265–80.
3. Nashold BS Jr, Friedman H, Boyarsky S. Electrical activation of micturition by spinal cord stimulation. J Surg Res 1971;11:144–7.
4. Jonas U, Heine JP, Tanagho EA. Studies on the feasibility of urinary bladder evacuation by direct spinal cord stimulation. I. Parameters of most effective stimulation. Invest Urol 1975;13:142–50.
5. Schmidt RA, Bruschini H, Tanagho EA. Sacral root stimulation in controlled micturition. Peripheral somatic neurotomy and stimulated voiding. Invest Urol 1979;17:130–4.
6. Tanagho EA, Schmidt RA. Bladder pacemaker: scientific basis and clinical future. Urology 1982;20:614–9.
7. Schmidt RA, Senn E, Tanagho EA. Functional evaluation of sacral nerve root integrity. Report of a technique. Urology 1990;35:388–92.
8. Tanagho EA, Schmidt RA. Electrical stimulation in the clinical management of the neurogenic bladder. J Urol 1988;140:1331–9.
9. Chancellor MB, Chartier-Kastler EJ. Principles of sacral nerve stimulation (SNS) for the treatment of bladder and urethral sphincter dysfunctions. Neuromodulation 2000;3:16–26.
10. Coyne KS, Sexton CC, Vats V, Thompson C, Kopp ZS, Milsom I. National community prevalence of overactive bladder in the United States stratified by sex and age. Urology 2011;77:1081–7.
11. Birder L, Wyndaele JJ. From urothelial signalling to experiencing a sensation related to the urinary bladder. Acta Physiol (Oxf) 2013;207:34–9.
12. De Groat WC. Nervous control of the urinary bladder of the cat. Brain Res 1975;87:201–11.
13. de Groat WC. Mechanisms underlying recurrent inhibition in the sacral parasympathetic outflow to the urinary bladder. J Physiol 1976;257:503–13.
14. De Groat WC, Ryall RW. The identification and characteristics of sacral parasympathetic preganglionic neurones. J Physiol 1968;196:563–77.
15. De Groat WC, Ryall RW. Recurrent inhibition in sacral parasympathetic pathways to the bladder. J Physiol 1968;196:579–91.
16. DeGroat WC. Inhibition and excitation of sacral parasympathetic neurons by visceral and cutaneous stimuli in the cat. Brain Res 1971;33:499–503.
17. deGroat WC. Changes in the organization of the micturition reflex pathway of the cat after transection of the spinal cord. Exp Neurol 1981;71:22.
18. Abdel-Halim MR, Crosbie J, Engledow A, Windsor A, Cohen CR, Emmanuel AV. Temporary sacral nerve stimulation alters rectal sensory function: a physiological study. Dis Colon Rectum 2011;54:1134–40.
19. Gourcerol G, Vitton V, Leroi AM, Michot F, Abysique A, Bouvier M. How sacral nerve stimulation works in patients with faecal incontinence. Colorectal Dis 2011;13:e203–11.
20. Dinning PG, Fuentealba SE, Kennedy ML, Lubowski DZ, Cook IJ. Sacral nerve stimulation induces pan-colonic propagating pressure waves and increases defecation frequency in patients with slow-transit constipation. Colorectal Dis 2007;9:123–32.
21. Dinning PG, Hunt LM, Arkwright JW, Patton V, Szczesniak MM, Wiklendt L, et al. Pancolonic motor response to subsensory and suprasensory sacral nerve stimulation in patients with slow-transit constipation. Br J Surg 2012;99:1002–10.
22. Hassouna MM, Siegel SW, Anyehoult AA, Elhilali MM, van Kerrebrodeck PE, Das AK, et al. Sacral neuromodulation in the treatment of urgency-frequency symptoms: a multicenter study on efficacy and safety. J Urol 2000;163:1849–54.
23. Spinelli M, Giardiello G, Arduini A, van den Hombergh U. New percutaneous technique of sacral nerve stimulation has high initial success rate: preliminary results. Eur Urol 2003;43:70–4.
24. Spinelli M, Giardiello G, Gerber M, Arduini A, van den Hombergh U, Malaguti S. New sacral neuromodulation lead for percutaneous implantation using local anesthesia: description and first experience. J Urol 2003;170:1905–7.
25. Borawski KM, Foster RT, Webster GD, Amundsen CL. Predicting implantation with a neuromodulator using two different test stimulation techniques: a prospective randomized study in urge incontinent women. Neurourol Urodyn 2007;26:14–8.
26. Peters KM, Killinger KA, Boura JA. Is sensory testing during lead placement crucial for achieving positive outcomes after sacral neuromodulation? Neurourol Urodyn 2011;30:1489–92.
27. Pizarro-Berdichevsky J, Gill B, Clifton M, Okafor HT, Faris AE, Vasavada SP, et al. Motor response matters: optimizing lead placement improves sacral neuromodulation outcomes. J Urol 2018;199:1032–6.
28. Jacobs SA, Lane FL, Osann KE, Noblett KL. Randomized prospective cross-over study of Interstim lead wire placement with curved versus straight stylet. Neurourol Urodyn 2014;33:488–92.
29. Wolf JS Jr, Bennett CJ, Dmochowski RR, Hollenbeck BK, Pearle MS, Schaeffer AJ, et al. Best practice policy statement on urologic surgery antimicrobial prophylaxis. J Urol 2008;179:1379–90.
30. Brueseke T, Livingston B, Warda H, Osann K, Noblett K. Risk factors for surgical site infection in patients undergoing sacral nerve modulation therapy. Female Pelvic Med Reconstr Surg 2015;21:198–204.
31. van Kerrebroeck PE, van Voskuilen AC, Heesakkers JP, Lycklama á Nijholt AA, Siegel S, Jonas U, et al. Results of sacral neuromodulation therapy for urinary voiding dysfunction: outcomes of a prospective, worldwide clinical study. J Urol 2007;178:2029–34.
32. Bosch JL, Groen J. Sacral nerve neuromodulation in the treatment of patients with refractory motor urge incontinence: long-term results of a prospective longitudinal study. J Urol 2000;163:1219–22.
33. Brazzelli M, Murray A, Fraser C. Efficacy and safety of sacral nerve stimulation for urinary urge incontinence: a systematic review. J Urol 2006;175:835–41.
34. Amundsen CL, Romero AA, Jamison MG, Webster GD. Sacral neuromodulation for intractable urge incontinence: are there factors associated with cure? Urology 2005;66:746–50.
35. Siegel S, Noblett K, Mangel J, Griebling TL, Sutherland SE, Bird ET, et al. Results of a prospective, randomized, multicenter study evaluating sacral neuromodulation with InterStim therapy compared to standard medical therapy at 6-months in subjects with mild symptoms of overactive bladder. Neurourol Urodyn 2015;34:224–30.
36. Siegel S, Noblett K, Mangel J, Bennett J, Griebling TL, Sutherland SE, et al. Five year follow-up results of a prospective, multicenter study of patients with overactive bladder subjects treated with sacral neuromodulation. J Urol 2018;199:229–36.
37. Noblett K, Siegel S, Mangel J, Griebling TL, Sutherland SE, Bird ET, et al. Results of a prospective, multicenter study evaluating the quality of life, safety, and efficacy of sacral neuromodulation at twelve months in subjects with symptoms of overactive bladder. Neurourol Urodyn 2016;35:246–51.
38. Blok B, Van Kerrebroeck P, de Wachter S, Ruffion A, Van der Aa F, Jairam R, et al. Three month clinical results with a rechargeable sacral neuromodulation system for the treatment of overactive bladder. Neurourol Urodyn 2018;37(S2):S9–S16.
39. Amundsen CL, Richter HE, Menefee SA, Komesu YM, Arya LA, Gregory WT, et al. OnabotulinumtoxinA vs sacral neuromodulation on refractory urgency urinary incontinence in women: a randomized clinical trial. JAMA 2016;316:1366–74.
40. Richter HE, Amundsen CL, Erickson SW, Jelovsek JE, Komesu Y, Chermansky C, et al. Characteristics associated with treatment response and satisfaction in women undergoing onabotulinumtoxinA and sacral neuromodulation for refractory urgency urinary incontinence. J Urol 2017;198:890–6.
41. Gormley EA, Lightner DJ, Faraday M, Vasavada SP; American Urological Association; Society of Urodynamics, Female Pelvic Medicine. Diagnosis and treatment of overactive bladder (non-neurogenic) in adults: AUA/SUFU guideline amendment. J Urol 2015;193:1572–80.
42. Wexner SD, Coller JA, Devroede G, Hull T, McCallum R, Chan M, et al. Sacral nerve stimulation for fecal incontinence: results of a 120-patient prospective multicenter study. Ann Surg 2010;251:441–9.
43. Mellgren A, Wexner SD, Coller JA, Devroede G, Lerew DR, Madoff RD, et al. Long-term efficacy and safety of sacral nerve stimulation for fecal incontinence. Dis Colon Rectum 2011;54:1065–75.
44. Madoff RD, Parker SC, Varma MG, Lowry AC. Faecal incontinence in adults. Lancet 2004;364:621–32.
45. Tjandra JJ, Chan MK, Yeh CH, Murray-Green C. Sacral nerve stimulation is more effective than optimal medical therapy for severe fecal incontinence: a randomized, controlled study. Dis Colon Rectum 2008;51:494–502.
46. Mahran A, Soriano A, Safwat AS, Hijaz A, Mahajan ST, Trabuco EC, et al. The effect of sacral neuromodulation on pregnancy: a systematic review. Int Urogynecol J 2017;28:1357–65.
47. Marcelissen T, Jacobs R, van Kerrebroeck P, de Wachter S. Sacral neuromodulation as a treatment for chronic pelvic pain. J Urol 2011;186:387–93.
48. Martellucci J, Naldini G, Carriero A. Sacral nerve modulation in the treatment of chronic pelvic pain. Int J Colorectal Dis 2012;27:921–6.
49. Lavonius M, Suvitie P, Varpe P, Huhtinen H. Sacral neuromodulation: foray into chronic pelvic pain in end stage endometriosis. Case Rep Neurol Med 2017;2017:2197831.
50. Peters KM, Carey JM, Konstandt DB. Sacral neuromodulation for the treatment of refractory interstitial cystitis: outcomes based on technique. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:223–8.
51. Peters KM, Konstandt D. Sacral neuromodulation decreases narcotic requirements in refractory interstitial cystitis. BJU Int 2004;93:777–9.
52. Zabihi N, Mourtzinos A, Maher MG, Raz S, Rodriguez LV. Short-term results of bilateral S2-S4 sacral neuromodulation for the treatment of refractory interstitial cystitis, painful bladder syndrome, and chronic pelvic pain. Int Urogynecol J Pelvic Floor Dysfunct 2008;19:553–7.
53. Wallace PA, Lane FL, Noblett KL. Sacral nerve neuromodulation in patients with underlying neurologic disease. Am J Obstet Gynecol 2007;197:96.e1–5.
54. Chaabane W, Guillotreau J, Castel-Lacanal E, Abu-Anz S, De Boissezon X, Malavaud B, et al. Sacral neuromodulation for treating neurogenic bladder dysfunction: clinical and urodynamic study. Neurourol Urodyn 2011;30:547–50.
55. Peters KM, Feber KM, Bennett RC. Sacral versus pudendal nerve stimulation for voiding dysfunction: a prospective, single-blinded, randomized, crossover trial. Neurourol Urodyn 2005;24:643–7.
56. Aboseif SR, Kim DH, Rieder JM, Rhee EY, Menefee SA, Kaswick JR, et al. Sacral neuromodulation: cost considerations and clinical benefits. Urology 2007;70:1069–73.
57. van Wunnik BP, Visschers RG, van Asselt AD, Baeten CG. Cost-effectiveness analysis of sacral neuromodulation for faecal incontinence in The Netherlands. Colorectal Dis 2012;14:e807–14.
58. Noblett KL, Dmochowski RR, Vasavada SP, Garner AM, Liu S, Pietzsch JB. Cost profiles and budget impact of rechargeable versus non-rechargeable sacral neuromodulation devices in the treatment of overactive bladder syndrome. Neurourol Urodyn 2017;36:727–33.

Supplemental Digital Content

Back to Top | Article Outline
© 2018 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.