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Sacral Neuromodulation

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Last Update: April 18, 2024.

Continuing Education Activity

Sacral neuromodulation is a well-established, safe, effective, and minimally invasive advanced therapy for managing various lower urinary tract and bowel dysfunctions, including urinary and fecal incontinence, urgency, frequency, and retention. Sacral neuromodulation is especially advantageous for patients who have not seen improvement with conservative treatments. The procedure involves implanting a neurostimulator that delivers electrical impulses to the sacral nerves, thereby effectively modulating neural pathways and restoring bladder and bowel function. 

Sacral neuromodulation demonstrates notable effectiveness in addressing refractory urinary tract dysfunction and has proven efficacy in patients experiencing neurogenic bladder symptoms, including those associated with Parkinson disease. Furthermore, sacral neuromodulation is recommended for chronic fecal incontinence, providing patients with a minimally invasive option that holds significant promise for symptom improvement and an enhanced quality of life. This activity offers clinicians a comprehensive understanding of sacral neuromodulation, encompassing patient selection, pre- and postoperative management, surgical techniques, and programming optimization, while also mastering evidence-based strategies for conducting lead placement procedures, addressing complications, and coordinating multidisciplinary care. This activity enables clinicians to offer more effective and personalized treatment options for patients with complex lower urinary tract and bowel dysfunction by enhancing their competence in sacral neuromodulation, ultimately leading to improved patient outcomes and satisfaction.


  • Identify suitable candidates for sacral neuromodulation therapy based on clinical presentations, history, symptoms, and responsiveness to conservative treatments.
  • Implement lead placement procedures for sacral neuromodulation with precision and adherence to best practices.
  • Select appropriate programming parameters for sacral neuromodulation devices based on individual patient needs and responses.
  • Collaborate with other healthcare professionals to coordinate comprehensive care plans and devise postoperative management strategies for patients undergoing sacral neuromodulation.
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Sacral neuromodulation is a well-established, safe, effective, and minimally invasive advanced therapy used to treat various lower urinary tract and bowel dysfunctions, including urinary and fecal incontinence and urinary urgency, frequency, and retention in the United States. Sacral neuromodulation is especially advantageous for patients who have not seen improvement with conservative treatments and have not responded to behavioral and pharmacological treatments. In addition, sacral neuromodulation is indicated for chronic constipation in Canada and Europe.[1]

Sacral neuromodulation therapy, developed in 1982 by Tanagho and Schmidt, gained approval from the United States Food and Drug Administration (FDA) in 1997.[2][3] More than 300,000 patients have been treated with sacral neuromodulation implants worldwide.[4] Reviews suggest that between 16% and 29% of the population (with some estimates as high as 75%) experience some level of overactive bladder, including symptoms of urinary incontinence, urgency, or frequency.[5][6] Moreover, an estimated 25% to 40% of patients experiencing overactive bladder do not achieve satisfactory results after first- and second-line therapies (behavioral modifications and pharmacotherapy, respectively).[7] These patients have a refractory overactive bladder and may be eligible for sacral neuromodulation therapy.

Sacral neuromodulation has demonstrated significant clinical efficacy, particularly in otherwise intractable cases. In a study by Siegel et al, which evaluated 340 patients using sacral neuromodulation for 36 months, the success rate for overactive bladder was 83% among those who underwent sacral neuromodulation implantation (95% CI). Furthermore, 80% of patients reported improvement in all urinary symptoms.[8][9]

Although the mechanism of action of sacral neuromodulation remains not fully understood, the therapy appears to modulate spinal cord reflexes and brain involvement via afferent signaling rather than direct motor stimulation of the detrusor or urethral sphincter muscles.[10] The prevailing theory suggests that sacral neuromodulation blocks or otherwise interferes with the afferent input to the sacral spinal cord, thereby inhibiting detrusor overactivity and resulting in clinical relief of urinary frequency and urgency.[11]

Anatomy and Physiology

Lower Urinary Tract

The lower urinary tract performs 2 primary functions—storing and voiding urine, both regulated by a complex neuronal control system. Disruptions to this system can result in neurogenic bladder, characterized by voiding dysfunction. Notably, significant voiding dysfunction can manifest even without identifiable neurological lesions.[11] Symptoms may include difficult voiding, postvoid complications, and bladder storage issues such as frequency, urgency, urge incontinence, difficult urination, and incomplete emptying.[12]

Efferent Pathways of Lower Urinary Tract

Parasympathetic preganglionic fibers, originating from the sacral spinal cord (S2-S4), are pivotal in initiating micturition. They stimulate contraction of the bladder detrusor muscle while inhibiting the urethral sphincter. Postganglionic fibers release acetylcholine and synapse with M2 and M3 receptors in the bladder. M2 receptors, prevalent in the detrusor, primarily mediate bladder smooth muscle contraction. In contrast, parasympathetic innervation to the urethral smooth muscle, controlling the internal urinary sphincter, is inhibitory and mediated by nitric oxide.[11] Thus, anticholinergics such as oxybutynin and tolterodine, which inhibit M2 and M3 receptors, can serve as pharmacotherapy for overactive bladder, urgency, frequency, and urge incontinence.[5] Conversely, cholinergic agonists such as bethanechol can be utilized for nonobstructive urinary retention caused by detrusor hypoactivity.[13] 

Sympathetic preganglionic fibers originate from the intermediolateral nuclei in the thoracolumbar region of the spinal cord. These fibers traverse the hypogastric nerve and either synapse in the inferior mesenteric ganglion or join the pelvic nerves via the paravertebral chain. The activation of sympathetic pathways inhibits micturition, resulting in detrusor relaxation and constriction of the urethral sphincter.[11] Postganglionic sympathetic axons synapse with β2 and β3 receptors in the detrusor wall and α1 receptors of the urethral sphincter.[14] Medical treatments utilizing β3 sympathetic agonists, such as mirabegron and vibegron, effectively address symptoms of urinary urgency, frequency, overactivity, and urge incontinence without inducing anticholinergic adverse effects.[5][15][16]

Somatic efferent fibers originate from the Onuf nucleus at S2-S4 and travel as the pudendal nerve to the external urinary sphincter, releasing acetylcholine upon activation. The sphincter is composed of skeletal muscle and contains cholinergic receptors. Acetylcholine stimulation induces sphincter contraction, mechanically and reflexively inhibiting micturition. Moreover, the pudendal and hypogastric nerves transmit sensory input from the bladder neck, urethra, and perineum to the brain and spinal cord.[11]

The guarding reflex prevents accidental leakage caused by sudden or involuntary increases in bladder pressure, commonly known as stress incontinence. When bladder pressure abruptly rises, such as during coughing, sneezing, standing, or laughing, excitatory afferent fibers stimulate the Onuf nucleus to activate somatic efferent fibers, leading to contraction of the external urinary sphincter.[11]

Afferent Pathways of Lower Urinary Tract

Sensory signals from the bladder travel to the dorsal horn of the spinal cord via the pelvic and hypogastric nerves. Afferent fibers transmit electrical impulses from tension receptors and nociceptors in the bladder wall. Typically, myelinated Aδ fibers facilitate bladder distension. However, unmyelinated C fibers may become hyperactive during inflammation and neurogenic conditions.[11]

Sensory signals from the urethra travel to the spinal cord via the pelvic and pudendal nerves. Urethral afferent nerves are activated by the passage of urine through the urethra, enhancing the parasympathetic input to the bladder. This causes a positive feedback mechanism to ensure complete bladder emptying.[11]

Sensory input from the lower urinary tract reaches the pontine micturition center in the brainstem, where it interacts with the frontal micturition inhibiting center in the cerebrum. This process suppresses micturition until voluntary voiding is initiated in the cerebrum, which inhibits the micturition center.[17]

Rectum and Anal Sphincters

The rectum serves as the connection between the gastrointestinal tract and the anus, facilitating both stool storage and passage. Defecation involves a combination of voluntary and involuntary muscle actions, with sensory input mediated by pelvic nerves.[18] Neurogenic disruptions in the lower gastrointestinal tract can lead to symptoms such as diarrhea, constipation, and fecal incontinence, with obstetric anal trauma being 1 of the most prevalent and well-recognized contributing factors for fecal incontinence.[19] A recent study involving 221 patients with fecal incontinence revealed that 80% of those who underwent implantation experienced a lasting improvement of at least 50% in their leakage issues.[20]

Defecation Reflexes

Rectoanal sampling, also known as the rectoanal inhibitory reflex, is a cyclic process that recurs approximately every 8 to 10 minutes when rectal contents stimulate the anal sensory mucosa.[21] The relaxation of the internal anal sphincter during this reflex varies depending on the degree of rectal distension.[22] As rectal contents move into the upper anal canal, sensory discrimination between solid, liquid, or gaseous materials occurs.[23]

Defecation initiates upon reaching a critical threshold of rectal distension, signaling the cerebral cortex.[24] Sensory stimulation and distension within the rectum trigger a parasympathetic-mediated reflex, resulting in relaxation of the anal sphincters and pelvic floor, thereby facilitating stool passage into the lower rectum and anal canal.[25] As the final stool bolus traverses the anal canal, the external sphincter reflexively initiates closure in response to the relief of rectal distension.[26]

The somatic nervous system controls the external anal sphincter via the pudendal nerve.[27] Deferment of defecation occurs through contraction of the external anal sphincter, resisting the increase in rectal pressure sufficiently to enable muscle adaptation, leading to a reduction in rectal pressure and the feeling of urgency.[28]

Mechanism of Sacral Neuromodulation

Although a complete understanding of the mechanisms of sacral neuromodulation remains elusive due to its likely multifaceted nature, several theories have been proposed, including:

  • In neurogenic bladder conditions such as multiple sclerosis, meningomyelocele, and spinal cord injury, afferent C fibers can become more active due to neurologic and inflammatory disorders. C fibers can respond to bladder distension and activate voiding reflexes.[29] Sacral neuromodulation is thought to block C fiber activity, inhibiting irregular voiding responses.[30] 
  • As previously described, the urethral guarding reflex serves as a protective mechanism against stress urinary incontinence. Sacral neuromodulation is believed to inhibit the guarding reflex and induce voiding in patients with urinary retention.[31]
  • Sacral neuromodulation appears to stimulate the relaxation of pelvic floor muscles and the urethra, which helps initiate micturition in patients with impaired bladder pressure, retention, and incomplete emptying.[11][32]
  • A possible central mechanism has also been suggested. Patients with refractory overactive bladder who have been successfully treated with sacral neuromodulation have exhibited significant activation of Brodmann area 9 (specifically the left dorsolateral prefrontal cortex) following sacral neuromodulation treatment.[33]
  • Additional mechanisms are proposed for urinary urgency and frequency. When stimulated, the afferent portion of the pudendal nerve may inhibit bladder afferent pathways. Similarly, inhibiting preganglionic neurons in efferent bladder pathways may also decrease incontinence. The sustained ability to voluntarily void throughout therapy indicates that inhibition of the micturition reflex is a component of the sacral neuromodulation mechanism.[11]
  • The precise mechanisms underlying how sacral neuromodulation aids in controlling fecal incontinence remain poorly understood. Most research suggests that placing the sacral neuromodulation lead in the S3 region stimulates afferent fibers from the anal sphincter, rectum, and pelvic floor. This stimulation of afferents decreases the activation of C fibers during rectal filling, thus blocking inputs from the rectum to the pontine center.[34] Additionally, sacral neuromodulation may activate somatic afferent fibers, leading to the inhibition of colonic activity and the enhancement of internal anal sphincter tone through a somatovisceral reflex mechanism.[35][36]


Sacral neuromodulation is indicated for refractory urinary tract dysfunction, including symptoms of nonobstructive urinary retention, urgency, frequency, and urge incontinence. Sacral neuromodulation has shown efficacy in Parkinson patients with neurogenic bladder symptoms, who are often refractory to treatment. In a recent study, 82% of Parkinson's patients with neurogenic bladders responded positively to sacral neuromodulation therapy, with many discontinuing their oral medications for overactive bladder.[37] Additionally, sacral neuromodulation is indicated for chronic fecal incontinence.[38][39][40][41]

Patient Selection

Patients eligible for sacral neuromodulation therapy for urinary incontinence must have refractory nonobstructive urinary retention, urgency, urge incontinence, or severe frequency that have failed to respond to behavioral modifications and pharmacotherapy despite undergoing more than one medical therapy for a duration of 8 to 12 weeks.[42] Individuals undergoing sacral neuromodulation therapy are encouraged to maintain a voiding diary to track urinary and fecal symptoms and establish a baseline. This diary should be consistently updated throughout the clinical trial period to evaluate any improvement, with a reduction in symptoms of 50% or more considered successful.[43]

Sacral neuromodulation is not recommended by the American Urological Association Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction (2021) for patients with spina bifida or spinal cord injuries due to the significant variability in bladder function and progression.[44] However, sacral neuromodulation may be considered for patients with other types of neurogenic bladder. This includes cases causing urgency, frequency, or urge incontinence that are not effectively managed with more conservative measures.[44]


Sacral neuromodulation is contraindicated in patients with urinary obstruction or current pelvic infection. Additionally, patients with severe or rapidly progressive neurologic disease are relatively contraindicated from undergoing sacral neuromodulation therapy.[45]

Additional contraindications for sacral neuromodulation therapy include shortwave diathermy, microwave diathermy, therapeutic ultrasound, mechanical obstruction, and the patient's inability to operate the programmer.[46] In earlier iterations of sacral neuromodulation systems, not all devices were fully compatible with magnetic resonance imaging (MRI). As of 2020, all new implants are compatible with full-body MRIs. However, some implants manufactured before the fall of 2019 lack full MRI compatibility, necessitating limitations on MRI evaluations and imaging to just the head and neck for these patients. A comprehensive listing of MRI-compatible sacral neuromodulation devices has recently been published.[4][47]

Although age and comorbidities are not considered contraindications, there is evidence suggesting that patients aged 55 or older with 3 or more chronic comorbid conditions may experience reduced success rates in improving their voiding symptoms with sacral neuromodulation.[48]


Essential equipment for sacral neuromodulation procedures includes a sacral neuromodulation kit containing the tined lead, foramen needle, and internal pulse generator (IPG). Surgical supplies such as sterile surgical drapes and a basic surgical instrument tray are necessary. Furthermore, a C-arm fluoroscopic unit is essential for precise lead placement during the procedure.


During the peripheral nerve evaluation stage (step 1), the procedure requires the presence of a surgeon, a nurse, and an x-ray technician. Subsequently, during the implant stage (step 2), the procedure necessitates the participation of a surgeon, nurse, scrub technician, and either an anesthesiologist or a nurse anesthetist. Optionally, a representative from the sacral neuromodulation manufacturer may be present during the procedure to prepare and test the product for implantation, interrogate the IPG, and verify the leads for a motor response.

Technique or Treatment


The evaluation stage allows for a trial of therapy before opting for the complete implant. This procedure is conducted under local anesthesia to ensure sensory innervation is an important indicator of lead placement. The patient is positioned prone, and a C-arm fluoroscopy is positioned accordingly. General landmarks of the sacrum are then identified, including:

  • The base of the sacrum, which is located by following the iliac crest medially.
  • The apex of the sacrum, which is located at the sacrococcygeal articulation.
  • The median sacral crest, which is located along the sacrum midline between the sacral foramina[46]

During sacral neuromodulation lead placement, a foramen needle is angled at 60° and inserted into the S3 foramen. The desired motor response includes dorsiflexion of the great toe and contraction in the perineum and anus, known as the bellows reflex. Sensory responses may include fluttering or vibration sensations or pulling sensations in the scrotum, vagina, perineum, or inner gluteal fold. In addition, the clinician must be familiar with S2 and S4 nerve root responses, as they may not result in optimal therapy outcomes. Stimulation of the S2 root typically induces pinching of the anal sphincter, plantar flexion, and lateral foot rotation, accompanied by sensations in the leg and buttock area. In contrast, stimulation of the S4 root triggers the bellows reflex without lower extremity movement and elicits a pulling sensation around the perineum.[49]

After removing the stylet from the foramen needle, it is substituted with a directional guide. While maintaining the guide in position, the foramen needle is withdrawn. A small transverse incision is made at the skin entry point to facilitate the introducer's passage into the S3 foramen. Once advanced, the directional guide is removed, leaving the introducer sheath in place. Subsequently, the tined lead is inserted so that electrodes 2 and 3 straddle the sacral foramen, with electrode 3 positioned as the most proximal. Electrodes 0 and 1 are situated anterior to the bony sacrum, with electrode 0 being the most distal.[50] Recent studies recommend inserting the tined lead to occupy the most superior and medial space in the foramen, resulting in electrode 3 being positioned just beyond the foramen rather than straddling it.[51] Finally, the lead stylet and introducer sheath are withdrawn to allow the tines to deploy and secure the lead in place.

After testing all electrodes, motor and sensory responses are ideally observed at 2 mA or less. Subsequently, the lead is tunneled through a small gluteal incision over the iliac crest and connected to a percutaneous extension cable passed subcutaneously to the contralateral side below the hip. The percutaneous extension is then plugged into the external neurostimulator for the trial period.[46] The trial for evaluating the tined lead lasts for 7 to 14 days. Stage 2, which involves either complete implantation or removal of the leads, must be scheduled separately and will depend on the trial results.[46]

The precise placement of the tined lead during the procedure is crucial to ensure it follows the S3 root for optimal outcomes. Accurate identification of sacral landmarks is essential for success. Video guides can assist in learning and troubleshooting the lead placement process, thereby enhancing procedural precision and efficacy.[52]

In select cases, computed tomography (CT) guidance is an alternative to C-arm fluoroscopy for electrode placement.[53] Recent advancements include computer-assisted lead placement, which utilizes surgical navigation systems with electromagnetic tracking to precisely guide leads to the S3 nerve roots. These innovations facilitate optimal lead positioning, especially in challenging clinical scenarios, thereby enhancing procedural accuracy and efficacy.[54]

Good prognostic indicators that suggest maximal success with sacral neuromodulation include optimal lead placement, ideal motor threshold levels, and the utilization of curved stylets.[55] Monopolar configurations are generally more effective and stimulate more motor nerve fibers at lower sensory thresholds, leading to greater therapeutic efficacy. Moreover, in addition to reprogramming, changing the polarity or the position of the cathode lead can significantly alter sensory and motor responses.[56]


Following a successful trial period demonstrating at least a 50% improvement in symptoms, the IPG is implanted. The previous gluteal incision site is enlarged to accommodate the insertion of the IPG. The lead is then connected directly to the IPG at the neurostimulator head. Typically, the IPG is not sutured into the pocket to prevent the sensation of pulling or tugging, as dislocation of the IPG is rare.[46] Optionally, an antimicrobial mesh pouch can be sutured into the pocket to stabilize the device and prevent infection.

Commonly reported adverse events associated with sacral neuromodulation that necessitate revision include pain at the neurostimulator site (11.8% of patients with implants) and lead migration (7.9% of patients with implants).[57]

Neurostimulators are equipped with preprogrammed factory settings for lower urinary tract disorders and fecal incontinence. These programs include specific parameters such as pulse width, frequency, active electrodes, and cycling pattern. Patients have the flexibility to switch between preset programs and adjust the device's amplitude settings. Various variables can be used to program the patient's IPG, necessitating collaboration between the patient and the medical team to fine-tune program parameters for optimal therapy.[58] During office visits, providers can customize all settings using a physician programmer to meet each patient's unique requirements. Regular yearly follow-up appointments post-implantation are recommended to ensure ongoing symptom management.

The duration of treatment is directly related to the longevity of the implantable battery. Nonrechargeable implants typically last around 5 years on average.[59] By utilizing lower settings, the battery's lifespan can be extended. Recent technological advancements have introduced higher-capacity batteries in newer devices, allowing for wireless recharging and a lifespan of up to 15 years.[60] Additionally, there have been advancements in neuromodulation technology, including enhanced programming capabilities, single-stage outpatient implantation to reduce invasiveness, and the development of lower-cost implantable devices.[39]


The most severe complications of sacral neuromodulation are typically associated with lead migration, implant site pain, or infection.[61] These issues can significantly impact the effectiveness of treatment and may require further intervention or device removal.

The most common concern is that the patient no longer benefits from the therapy. Initially, the neurostimulator should be interrogated to confirm it is turned on. Subsequently, the resistances of the electrodes should be checked to rule out an open or short circuit. Assuming the device is activated, and there is no short circuit, adjustments to the programs should be made. The program encodes the active electrodes, including stimulation frequency, amplitude, and pulse width.[61] Additionally, adjusting the pulse width, alongside standard programming changes, can assist in pain relief and addressing efficacy issues.[62]

Lead migration or improper placement is possible and can be identified with an x-ray. However, lead revision surgery should be considered only as a last resort.[52] Before proceeding with surgery, it is crucial to review the issue with the manufacturing representative of the device and troubleshoot the flow process to explore alternative solutions.

Bilateral sacral electrical pudendal nerve stimulation has been successfully used in patients who, despite initial success, eventually fail standard sacral neuromodulation.[63][64][65]

Clinical Significance

Combination Therapy

Tang et al conducted a study on women with overactive bladders treated with a combination of sacral neuromodulation and tolterodine—an M2 and M3 antimuscarinic agent. After 3 months, the combination therapy demonstrated significant superiority over tolterodine alone, showing key improvements in various bladder parameters such as daily average single voided volume, daily maximum single volume of urination, first desire to void, and maximum cystometric capacity, indicating the bladder's tolerance volume before experiencing a strong, uncontrollable urge to urinate.[66]

Alternate Treatments

Percutaneous tibial nerve stimulation: Percutaneous tibial nerve stimulation (PTNS) is an alternative neuromodulation therapy for intractable overactive bladder. This procedure targets the tibial nerve by gently stimulating it with a needle connected to a low-voltage stimulator near the medial malleolus in the foot. This stimulation indirectly influences the sacral nerves responsible for bladder function. Patients typically experience sensations such as "tingling" or "pulsing" in the foot or ankle during treatment, which is generally painless.

Treatment sessions last for 30 minutes and are conducted weekly. Although some patients may notice symptomatic improvement as early as the second session, many require multiple treatments before experiencing significant benefits. Patients are advised to complete the full 12-week regimen initially, followed by clinical evaluation. Intermittent additional treatments may be needed for long-term symptomatic relief.

PTNS can significantly improve urinary frequency, urgency, urge incontinence, and nocturia, benefiting 60% to 80% of patients, according to research.[67] Unlike anticholinergics or sacral neuromodulation, PTNS provides a carryover effect of continued symptom improvement even when the nerve is not actively stimulated.[68] However, its limitations include the necessity for patients to be present in a clinical office for therapy sessions and commit to a full 12-week therapeutic trial.

Although PTNS and sacral neuromodulation are generally well-tolerated, PTNS may entail fewer adverse effects and is notably less invasive than sacral neuromodulation. However, PTNS lacks the long-term testing that sacral neuromodulation has undergone.[69] Therefore, the choice between the 2 is primarily based on equipment availability and patient preference regarding clinic proximity and surgical tolerance.[70] Despite its effectiveness in addressing fecal incontinence in other countries, PTNS lacks FDA approval for this indication in the United States.[20][41]

A wearable closed-loop transcutaneous tibial neuromodulation system has demonstrated efficacy, significantly reducing urinary frequency, urgency, and incontinence episodes over 12 weeks.[71] The response of this system remains durable up to 1 year of follow-up, and the device has received FDA approval.[71] Patients demonstrate increased compliance and satisfaction compared to alternative therapy delivery methods. Another wearable tibial nerve neuromodulation device utilizing an ankle strap and an implantable electrode has shown similar efficacy.

Chemical denervation of the detrusor using the onabotulinum A toxin: The FDA has approved botulinum toxin for therapeutic use.[72] Botulinum toxin injections can effectively manage overactive bladder and urinary urge incontinence, with results typically lasting 6 to 12 months, after which further injections can be administered.[73] Disadvantages of this treatment modality include possible urinary tract infections and urinary retention, affecting 5% to 15% of patients.[74] 

A recent cost-effectiveness comparison between sacral neuromodulation and onabotulinum A toxin was published for managing refractory overactive bladder issues.[75] The study examined various healthcare systems across 5 countries over 5- and 10-year periods. However, industry-sponsored studies, prevalent in the available literature, may influence outcomes. Although overall costs are similar, botulinum toxin seemed more cost-effective in the short term, while longer-term studies favor sacral neuromodulation.[75] 

Pelvic Pain

Several studies suggest sacral neuromodulation's efficacy in improving pelvic pain, including interstitial cystitis. In a study by Siegel et al, 9 out of 10 patients with interstitial cystitis experienced reduced pain after sacral neuromodulation at 19 months of follow-up.[76] T Pain levels decreased from an average of 9.7 to 4.4 on a scale of 0 to 10, with a decreasing trend in hours of pain.[76] However, sacral neuromodulation for interstitial cystitis lacks FDA approval, supported only by grade C evidence.[77]

While the precise mechanisms of action of sacral neuromodulation for pelvic pain still need to be elucidated, most research supports the theory of afferent signaling modulation to achieve symptomatic improvement. Several distinct mechanisms for symptom relief seem to exist, and therapy likely functions differently for each clinical indication.

Future Use

Some patients with spinal cord injuries appear to have benefitted from the early use of sacral neuromodulation in preventing functional deterioration of the bladder. Detrusor overactivity and incontinence were prevented while bowel function, erectile activity, and a normal bladder capacity were maintained.[78][79][80] However, despite these promising outcomes, the early use of sacral neuromodulation to alter the course of spinal cord injury and preserve bladder function is still considered investigational.[81] 


Sacral neuromodulation offers a reasonable, safe, effective, and reversible alternative for refractory overactive bladder, nonobstructive urinary retention, and fecal incontinence.[55]

Enhancing Healthcare Team Outcomes

Effective care in sacral neuromodulation requires a collaborative effort among healthcare professionals to optimize patient-centered outcomes, safety, and team performance. Physicians, advanced practitioners, nurses, pharmacists, and other healthcare team members contribute distinct skills and strategies to enhance patient care. Physicians and advanced practitioners utilize their expertise in patient assessment, diagnosis, and treatment planning to ensure sacral neuromodulation is appropriately indicated and executed. Nurses play a vital role in patient education, pre- and postoperative care, and ongoing support, fostering patient engagement and adherence.

Pharmacists contribute by ensuring appropriate medication management, addressing drug interactions, and providing patient counseling. Effective interprofessional communication among healthcare team members ensures seamless care coordination, facilitates shared decision-making, and mitigates errors. By fostering a patient-centered approach and promoting collaboration among team members, healthcare professionals can optimize sacral neuromodulation outcomes, improve patient satisfaction, and elevate overall team performance in delivering high-quality care.

Review Questions


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Disclosure: Michael Feloney declares no relevant financial relationships with ineligible companies.

Disclosure: Kari Stauss declares no relevant financial relationships with ineligible companies.

Disclosure: Stephen Leslie declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

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Bookshelf ID: NBK567751PMID: 33620828


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