Reflexes That Promote Bladder Storage

Two important reflexes may play an important role in modulation of bladder function: the guarding reflex and the bladder afferent loop reflex. Both reflexes promote urine storage (guarding reflex under somatic influence and bladder loop reflex under sympathetic tone). The guarding reflex guards or prevents urine loss from times of cough or other physical stress that would normally trigger a micturition episode. Suprapontine input from the brain turns off the guarding reflex during micturition to allow efficient and complete emptying. The bladder afferent reflex works through sacral interneurons that then activate storage through pudendal nerve efferent pathways directed toward the urethral sphincter. As such, the activity has truly been realized only in cats but has been postulated to exist in humans and to function the same. Similar to the guarding reflex, the bladder afferent reflex promotes continence during periods of bladder filling and is quiet during micturition (Fig. 70–1).

Figure 70–1 The guarding reflex promotes continence and allows the outlet to contract the urinary sphincter during periods of stress (e.g., cough). The brain can turn this reflex off during voiding.

(Modified from Leng WW, Chancellor MB. How sacral nerve stimulation neuromodulation works. Urol Clin North Am 2005;32:11–8.)

Reflexes That Promote Bladder Emptying

Signals from the bladder that may modulate the need to void with fullness, pain, pressure, or stretch may elicit bladder afferent activity through the Aδ or even C fibers. These bladder afferent nerve fibers then synapse with both parasympathetic efferents (bladder-bladder reflex) and parasympathetic urethral efferents (bladder-urethral) reflex. The urge to void may then be translated as an initial activity (inhibitory) of the bladder-urethral reflex to allow the pressure in the urethral outlet to drop immediately before a bladder contraction ensues and simultaneously permit the bladder-bladder reflex to allow a smooth bladder contraction to occur as the reflex is maintained throughout the entire void (de Groat, 1978; de Groat et al, 1981, 1996).

Putative Mechanism of Action of Sacral Neuromodulation

Although our knowledge of how neuromodulation works is evolving, two main theories exist: (1) direct activation of efferent fibers to the striated urethral sphincter reflexively causes detrusor relaxation and (2) selective activation of afferent fibers causes inhibition at spinal and supraspinal levels. Accumulating evidence suggests that activation of somatic sacral afferent inflow at the sacral root level that in turn affects the storage and emptying reflexes in the bladder and central nervous system accounts for the positive effects of neuromodulation on both storage and emptying functions of the bladder (Yoshimura and de Groat, 1992, 1997; Leng and Chancellor, 2005). Malaguti and coworkers (2003), using detection of somatosensory evoked potentials during sacral neuromodulation, concluded that sacral neuromodulation therapy works by sacral afferent activity and concomitant activation of the somatosensory cortex. Because sacral neuromodulation has been clinically proven for both storage (urgency/frequency and urgency urinary incontinence) and emptying (nonobstructive urinary retention) dysfunctions of the bladder, isolating the mechanism of action to the micturition reflex pathway of sacral afferent and efferent pathways alone is challenging. However, by understanding the reflexes that influence the promotion of urine storage or emptying of the sacral micturition reflex pathway one begins to realize how neuromodulation may affect these reflexes and elicit symptomatic and functional improvement of voiding function (Fowler et al, 2000). Animal models of sacral neuromodulation for detrusor overactivity are now being developed and may shed more light on how this technology achieves its benefits (Riazimand and Mense, 2004; Vignes et al, 2009)

Putative Mechanism of Action of Sacral Neuromodulation in Overactive Bladder

The bladder storage and emptying reflexes are modulated by several centers in the brain and may be altered by neurologic injury that effectively unmasks involuntary bladder contractions. Thus, sacral neuromodulation of these primitive reflexes may restore normal micturition (de Groat, 1976). Animal data exist to support the fact that somatic afferent input to the spinal cord can affect the guarding and bladder-bladder reflexes (de Groat, 1978; Chen et al, 1993). It is believed that suppression of interneuronal transmission in the bladder reflex pathway may be how sacral neuromodulation affects detrusor overactivity (de Groat, 1976; Kruse and de Groat, 1993; Leng and Chancellor, 2005). The inhibition by electrical neuromodulation may, in part, modulate the sensory outflow from the bladder through the ascending pathways to the pontine micturition center, thereby preventing involuntary contractions by modulating the micturition reflex circuit but allowing voluntary voiding to occur (Fig. 70–2). The preservation of voluntary voiding may be due to selective avoidance of normal sensory ascending outflow pathways of the bladder from Aδ fibers to the pontine micturition center as well as initiation of the descending pathways from the pontine micturition center to sacral efferent outflow pathways. Therefore, as is seen in clinical practice, sacral neuromodulation may affect and improve the abnormal bladder sensations, involuntary voids, and detrusor contractions but still maintain normal bladder sensations and voluntary voiding patterns.

Figure 70–2 Pudendal nerve afferent firing can modulate and accordingly inhibit the bladder micturition reflex. SNS, sacral nerve stimulation.

(Modified from Leng WW, Chancellor MB. How sacral nerve stimulation neuromodulation works. Urol Clin North Am 2005;32:11–8.)

Putative Mechanism of Action of Sacral Neuromodulation in Urinary Retention

Sphincteric activity can be turned off by brain pathways to allow efficient and complete bladder emptying. If the suprasacral pathways are altered, the guarding and urethral reflexes still exist and cannot be turned off. This may cause retention, as in the spinal cord–injured patient who in turn has detrusor-sphincter dyssynergia resulting in urinary retention. Thus, inhibition of the guarding reflexes may allow urinary retention states to be improved (Fig. 70–3). Originally for urinary retention due to functional outlet obstruction, sacral neuromodulation was thought to directly turn off excitatory flow to the urethral outlet and facilitate bladder emptying. This may be an efferent effect of the primary afferent mechanism of sacral neuromodulation as reported by Dasgupta and colleagues (2005), who described novel neuroimaging evidence for the existence of abnormal interaction between the brainstem and cortical centers in women with urinary retention due to Fowler syndrome or overactive sphincteric activity. The direct therapeutic effect of sacral neuromodulation in patients with sphincter overactivity or functional outlet obstruction appears to be in the afferent restoration of a normal pattern of midbrain activity and decreased cortical activity leading to inhibition of the guarding reflexes.

Figure 70–3 In neurologic disease the supraspinal circuitry is “disconnected” and therefore cannot turn off the spinal guarding reflex, and thus retention occurs. Sacral neuromodulation (SNS) can restore the normal voluntary pattern of micturition by inhibition of the spinal guarding reflex.

(Modified from Leng WW, Chancellor MB. How sacral nerve stimulation neuromodulation works. Urol Clin North Am 2005;32:11–8.)

Criteria for Selection of Patients

Because many lower urinary tract symptoms and dysfunctions are secondary to a neuromuscular etiology, a thorough history and physical examination will often reveal the nature (acute vs. chronic) and help classify the cause (neurogenic, anatomic, postsurgical, functional, inflammatory, or idiopathic). In addition to the unique evaluation of pelvic floor muscle dysfunction (Siegel, 2005), a urinalysis is routinely performed; urine cytology should be considered in patients who present with refractory symptoms of dysuria, urgency, or frequency of urination, because carcinoma in situ and bladder tumors may present as irritative bladder symptoms without hematuria. Further assessment of the bladder function, urodynamic studies including cystometrography, pressure-flow studies, and electromyography of sphincters and pelvic floor muscles are performed on a selected basis, because most non-neurogenic assessments are completed routinely with the use of a voiding diary and a focused physical examination of the pelvis. Electromyography is recommended in suspected cases of neurogenic bladder dysfunction, detrusor-sphincter dyssynergia, or Fowler syndrome and may be considered for evaluation of inappropriate pelvic floor muscle behavior (Dasgupta and Fowler, 2003). As of now, urodynamics have not yielded adequate predictive factors that allow enhanced selection for patients undergoing sacral neuromodulation (Groenendijk et al, 2007). The characteristics of neurogenic bladders, as seen in patients with multiple sclerosis and spinal cord injury, can change with time and disease progression. Therefore, reevaluation with urodynamics and assessment of the upper urinary tracts may be needed when symptoms change despite active medical intervention.

Cystourethroscopy may yield information helpful in making a diagnosis. Anatomic lesions such as urethral stricture, bladder neck fibrosis, trabeculation, and bladder lesions have been found even in women with bladder outlet obstruction. Baseline upper tract imaging is performed in patients with neurologic disease or, if indicated, by physical or baseline studies or a patient’s history.

Sacral neuromodulation is frequently attempted in patients in whom traditional conservative measures (e.g., bladder retraining, pelvic floor biofeedback, and medications) have failed and before more invasive surgical procedures (e.g., enterocystoplasty and urinary diversion). Despite all the studies done to date there are no defined preclinical factors, such as urodynamic findings, that can predict which patients will or will not respond to sacral neuromodulation.

Although most patients are considered candidates for neurostimulation and neuromodulation therapies when more conservative treatment has failed there are some clinical considerations for excluding patients from this therapy. These include significant anatomic abnormalities in the spine or sacrum that may present challenges to gaining access; mental incapacitation of patients who cannot manage their device or judge the clinical outcome; physical limitations that prevent the patient from achieving normal pelvic organ function, such as functional urinary incontinence; and noncompliance of the patient.

Relative contraindications for patients who may be considering or who have an implantable electrical stimulation device are magnetic resonance imaging (MRI) and pregnancy. Magnetic fields produce currents in neuroelectrodes, and there is some concern that the magnetic field from MRI may damage the pulse generator, as discussed later. Many radiologists are reluctant to provide MRI services for patients with implantable electrical stimulation devices despite the anecdotal evidence that no adverse event has occurred when MRI has inadvertently or purposefully been done for emergent reasons or in small trials (Hassouna and Elkelini, 2005). For patients who have InterStim devices in place (see later), the authors advocate removal of the device in preparation for elective MRI based on current manufacturer recommendations. After the MRI procedure, a new neuroelectrode and generator may be placed. Anecdotal reports of patients safely undergoing the study (MRI) with the InterStim implant in place have occurred, but patients should have the devices turned off in anticipation. Because of the potential for teratogenicity or abortion from the effect of electrical stimulation, electrical stimulation has been considered contraindicated in pregnant women with various voiding dysfunctions. However, whether electrical stimulation can cause abortion or malformation is not known. Wang and Hassouna (1999) reported no adverse effects of electrical stimulation on pregnant rats and that termination of pregnancy is not advised for prospective mothers when electrical stimulation has been performed unknowingly in early pregnancy. Women with electrical stimulation devices for pelvic health conditions who become pregnant may simply turn off their devices during pregnancy.

Electrical Stimulation of the Bladder

Transurethral electrical bladder stimulation (TEBS) has been pursued not only for initiating sensory awareness of bladder filling and stimulating detrusor contractility (see later section) but also for increasing bladder capacity at low pressure in pediatric patients with myelomeningocele (Kaplan et al, 1989; Decter et al, 1994). The authors in these two cited references carried on an interesting point-counterpoint discussion in publications regarding the practical benefit of TEBS (Kaplan, 2000; Decter, 2000), which remains controversial.

Both authors seem to be saying the same thing with respect to results but attach a totally different significance to the practical implications of the results. Kaplan (2000) points out that when the procedure was initiated the goal was to provide children with neurogenic bladder dysfunction, mostly secondary to spina bifida, enough sensation to detect a filling or full bladder and to have them synergistically void or catheterize in a timely manner. As the results of treatment have been evaluated over the years, the real benefit of this program, to Kaplan at least, was the potential to increase bladder capacity while maintaining or decreasing end-filling bladder pressure (in essence, improving compliance). Decter (2000) gives what seems to be a reasonable summation of the largest multi-institutional report of this therapy involving 568 patients who underwent TEBS at 11 institutions, only 335 of whom had adequate pretreatment and post-treatment urodynamics for evaluation. Bladder capacity increased by 20% or more in 56% of the 335 patients, whereas pressure at bladder capacity decreased by 25% or more in 16% of those in whom the bladder capacity increased. Decter (2000) calculated that only 30 of 335 patients had both a 20% or more increase in bladder capacity and a 25% decrease in compliance. He reports his experience with 25 patients during a 4-year period as showing that bladder capacity increased more than 20% (values referred to a comparison to age-adjusted bladder capacity) and end-filling bladder pressures showed clinically significant decreases in 29% of patients. Putting this in perspective, he believes “the practical benefits our patients derive seem limited…the urodynamic improvements we achieved after stimulation did not materially alter daily voiding routine (i.e., clean intermittent catheterization) of these children.” Pugach and associates (2000) also reported the results of TEBS in a group of pediatric patients; only 7 of 44 (16%) had safe storage pressures with continence after treatment. There exist limited new data since 2000 on this treatment modality probably owing to other better potential nerve targets.

Sacral Rhizotomy

In most cases, bilateral anterior and posterior sacral rhizotomy or conusectomy converts a overactive detrusor to an areflexic one. This alone may be inappropriate therapy because it also adversely affects the rectum, anal and urethral sphincters, sexual function, and the lower extremities. In an attempt to leave sphincter and sexual function intact, selective motor nerve section was originally introduced as a treatment to increase bladder capacity by abolishing only the motor supply responsible for involuntary contractions. The initial use of this procedure followed the observation that the third anterior (ventral) sacral root provided the dominant motor innervation of the human bladder. To enhance the clinical response and to minimize side effects, differential sacral rhizotomy should always be preceded by stimulation and blockade of the individual sacral roots with cystometric and sphincterometric control.

Although technique refinements, such as percutaneous radiofrequency selective sacral rhizotomy and cryoneurolysis, have occurred, there is still controversy about the role of anterior rhizotomy procedures within a treatment plan for detrusor overactivity. Torrens (1985) summarized successful results in collected groups of patients that ranged from 48% for idiopathic overactivity to 81% for patients classified as having a “paraplegic bladder.” However, as he astutely pointed out, the definition of success varies from one series and from one patient to another. When these procedures are used, they should certainly be preceded by urodynamics and urologic evaluation of the effects of selective nerve blocks before performance, especially in patients without fixed neurologic disease or injury. Even then, unintended effects on pelvic and lower extremity sensory or motor functions may occur with disastrous medical and legal sequelae.

Both Tanagho and Schmidt (Tanagho and Schmidt, 1988; Tanagho et al, 1989) and Brindley (Brindley and Rushton, 1990) have popularized the concept of sensory deafferentation by dorsal or posterior rhizotomy to increase bladder capacity as part of their overall plan to simultaneously rehabilitate storage and emptying problems in patients with significant spinal cord injury or disease. These are patients in whom electrical stimulation also was used to alleviate emptying deficits (see section on emptying disorders). McGuire and Savastano (1984) also mentioned dorsal root ganglionectomy alone in such patients to increase bladder capacity.

Gasparini and colleagues (1992) reported durability of the deafferentation response to selective dorsal sacral rhizotomy up to 64 months after section. The technique involves selecting nerve roots whose intraoperative stimulation provokes an adequate detrusor response. The dorsal and ventral components of these roots are then separated and the dorsal root or roots severed. An increase in bladder capacity of 259 to 377 mL was noted in 16 of 17 patients studied (24 in the original series), with an increase in the volume to the first contraction of 99 to 270 mL. Fourteen patients were cured of incontinence, and 2 improved; the technique failed in 1 patient. Of seven potent men, two experienced a decrease in erectile frequency but were still able to achieve penetration. Bowel and sphincter function were unaffected. Koldewijn and associates (1994) reported on the effects of intradural bilateral posterior root rhizotomies from S2 to S5 with implantation of an anterior root stimulator in a group of patients with suprasacral spinal cord injury. All showed persistent detrusor areflexia afterward, although 2 required subsequent secondary rhizotomy at the level of the conus. A majority showed decreased bladder compliance up to 5 days postoperatively, followed by a rapid increase thereafter.

Brindley (1994) summarized the advantages of bilateral posterior sacral rhizotomy in treatment of voiding dysfunction after spinal cord injury as abolishing reflex incontinence, improving compliance, and abolishing striated sphincter dyssynergia without altering resting tone. Partial or selective procedures are considered only in such patients who retain some sensation or have excellent reflex erections. Madersbacher (2000) comments that posterior sacral rhizotomy for sacral deafferentation of the bladder is best achieved by the intradural approach, which has the advantage that, in this location, motor and sensory fibers can easily be separated, whereas distal to the spinal ganglion, motor and sensory fibers are intermingled and a clear separation is no longer possible. If an intradural procedure is not possible, he believes that a deafferentation at the level of the conus medullaris is preferable to an extradural sacral approach. He mentions that he has treated 65 tetraplegic or paraplegic patients with post–spinal cord injury reflex urinary incontinence who were resistant to all other means of conservative treatment. Incontinence was abolished in 90% of these patients.

Sacral Neuromodulation

Neuromodulation is an innovative treatment of lower urinary tract symptoms and dysfunctions of bladder storage secondary to neuromuscular causes. In addition to the application of evolving technologies for sacral neuromodulation therapy, expanding clinical indications such as neurogenic detrusor overactivity, post–sling-related voiding dysfunction, interstitial cystitis, pelvic pain, pediatric voiding dysfunction, and bowel disorders as well as novel forms of transcutaneous and implantable neuromodulation devices for different nerve roots are under investigation.

Technique

Sacral nerve stimulation (SNS) by the InterStim (Medtronic, Minneapolis, MN) procedure is performed in two stages: stage I, a clinical trial of a temporary or permanent lead for external stimulation; and stage II, implantation of a subcutaneous implantable pulse generator (IPG). Each stage can be performed with monitored anesthesia care supplemented by local anesthesia. During the initial introduction of sacral neuromodulation therapy, patients underwent a percutaneous nerve evaluation by the placement of a unilateral percutaneous lead in the S3 foramen with use of local injectable anesthesia. The lead was connected to an external pulse generator and worn by the patient for several days. A large number of false-negative results with therapy are attributed to improper lead placement and migration. Whereas some physicians still prefer to perform the first stage by a percutaneous nerve evaluation approach, most have adopted a permanent tined lead placement for the first stage in an attempt to avoid the issues related to high false-negative results with the first stage and high false-positive results with the second stage. Changes in lower urinary tract symptoms and postvoid residuals are recorded in a detailed bladder diary. If improvement is minimal or absent, revision or bilateral percutaneous lead placement may be attempted. If more than 50% improvement in symptoms of urgency/frequency or urgency urinary incontinence is attained, a permanent IPG is implanted. The length of the trial with the external pulse generator may vary slightly from patient to patient, by the indication, and by the surgeon’s practice preference. In patients with urgency/frequency and urgency urinary incontinence, a 1- to 2-week trial is generally adequate. For retention, a longer trial of 3 to 4 weeks or more may be necessary before a desired clinical response is obtained.

Previous lead placement required a more time-consuming surgical dissection of the layers above the sacral foramen and unreliable lead fixation with anchors. Recent technical advances have made implantation of the percutaneous lead easier and less prone to migration. Spinelli and colleagues (2003) were the first to present the advantages of the tined lead that used a percutaneous approach for placement and fixation (Fig. 70–4). Subsequent large-scale clinical experience worldwide confirms that the tined lead is less prone to migration and has decreased false-negative results with the screening trial. Furthermore, the false-positive rate of the screening trial is reduced when placement of a permanent lead with reliable fixation during the screening trial ensures that the same location of stimulation is achieved when the IPG is implanted. With a percutaneous nerve evaluation or similar temporary lead electrode during the screening trial, a different clinical outcome may occur when the permanent lead is placed at the time of the IPG implantation.

Figure 70–4 The tined lead is introduced typically into the S3 nerve foramen. The “tines” allow the lead to be fixed into the fascial layers above the sacrum. This lead has a quadripolar configuration (four contact points).

(Courtesy of Medtronic, Minneapolis, MN.)

For the first stage of the procedure, preoperative intravenous antibiotics are given before the procedure and aseptic techniques of foreign body implants are implemented. The patient is placed in the prone position, and the buttocks are held apart by wide tape retraction so that the anus is visible during test stimulation. The anus and tape are prepared in a sterile fashion and then covered with a separate plastic drape until visualization is needed during the procedure. The sterile drape covering the feet must be folded back such that the feet can be visualized during the procedure as well.

The location of the S3 foramen is approximated by measuring 9 cm cephalad to the dropoff of the sacrum and 1 to 2 cm lateral to the midline on either side. Alternatively, the site may also be localized by palpating the cephalad portions of the sciatic notches bilaterally and drawing a connecting line that intersects the midline of the sacrum; one fingerbreadth on either side of the midline of the sacrum at this intersection will define the location of the S3 foramen (Fig. 70–5). The foramen needle is then inserted into the S3 foramen. The pelvic plexus and pudendal nerve run alongside the pelvis, and therefore the needle should be placed just inside the ventral foramen. The position of the needle is confirmed by fluoroscopy. The nerve is tested for the appropriate motor response, which is dorsiflexion of the great toe and bellows contraction of the perineal area, which represents contraction of the levator muscles (bellows reflex). Simultaneous sensory responses determined at the time of lead placement help optimize positioning. Although this is controversial, if one can localize the stimulation at the time of lead positioning to the vagina-rectum juncture in females and perineoscrotal area in males this is proper localization of the device. The foramen needle stylet is then removed and replaced with the introducer sheath. The distal aspect of the lead consists of four electrodes numbered 0 through 3. The lead is placed into the introducer sheath as directed to expose the electrodes. Typically, electrodes are positioned such that electrodes 2 and 3 straddle the ventral surface of the sacrum (Fig. 70–6). Test stimulation is repeated on each electrode, and the responses are observed. An S3 response should be noted on at least two of the electrodes (see Table 70–2). Once the surgeon is satisfied with the position, the sheath is removed, releasing the tines that anchor the lead. A sensory response, sensation of stimulation in the perineum, is not needed to confirm proper placement if the correct S3 motor response is observed. However, when a motor response is absent, raising the conscious level of the patient during the procedure and detecting the correct sensory response will confirm proper localization, and a clinical response may still be obtained during the screening trial period despite the absence of the motor response.

Figure 70–5 A, The percutaneous test stimulation is performed in an outpatient setting. A small lead wire is placed into S3 and connected to an external stimulator for 1 week to administer stimulation to the nerve roots. B, Measurement of the S3 nerve foramen is typically 9 cm to the coccyx and 11 cm to the anal verge. One measures 1 to 2 cm lateral to this mark to find the rough site of the S3 nerve foramen. The “cross hair” technique can be used to find the midline fluoroscopically and the lower aspect of the sacroiliac joints laterally to find the S3 nerve foramen as well.

(Courtesy of Medtronic, Minneapolis, MN.)

Figure 70–6 Fluoroscopy is used to confirm lead placement, typically with the lead configurations to obtain optimal muscle (bellows response and ipsilateral toe contractions) and sensory (vaginal, penile, or scrotal “pulsating” feeling) responses. The lead may then be deployed.

A 3- to 4-cm incision into the subcutaneous tissues in the upper lateral buttock is made below the beltline or below the level of the ischial wings for connecting the permanent lead to the percutaneous extension lead wire. If the screening trial is successful, this connection site will be the site of implantation for the IPG. With use of the tunneling device provided in the commercial kit, the permanent lead is transferred to the medial aspect of the lateral buttock incision. The lead is then connected to the extension wire, and the tunneling device is used again to transpose the extension wire from the medial aspect of the incision to an exit point on the contralateral side of the back. This transfer and long tunnel reduce the occurrence of infection from the percutaneous exit site of the wire. The extension wire is connected to the external pulse generator. Patients are able to resume their normal activities immediately but are advised to limit excessive movement-related activities, such as high-impact exercises, for the duration of the trial period.

The external generator can be flexibly programmed for the duration of the intended trial while the patient records symptoms and bladder function in a voiding diary. If there is more than 50% improvement in the symptoms or voiding function, a stage II procedure is performed.

A stage II procedure entails placement of the IPG. No fluoroscopy is required during stage II when a permanent neuroelectrode has been placed for the stage I procedure; however, if a percutaneous nerve evaluation was performed for stage I, fluoroscopic confirmation of the neuroelectrode placement is advised. The patient may be placed in the prone position or a lateral position with the site of the previous lateral incision for the lead connections placed upward (Fig. 70–7). The lateral position may improve ventilation during sedation. The previous buttock incision overlying the lead connections is opened, the percutaneous extension wire is removed, and the extension lead is secured to the permanent lead and subsequently to the IPG. A pocket is made in the subcutaneous tissue that is large enough to avoid tension on closure and at a depth to provide a covering layer of subcutaneous tissue anterior to the pulse generator to prevent erosion.

Figure 70–7 A 3- to 4-cm counterincision in the upper gluteal crease is made for a deep subcutaneous pocket to allow implantation of the implantable pulse generator.

Special Populations

With the success of neuromodulatory therapies for refractory detrusor overactivity and urinary retention it should be no surprise that indications are expanding. Despite the fact that there is no true FDA-approved indication for neuromodulation in select populations, these groups all have some component of the indicated symptom-complex that includes urgency, frequency, urgency urinary incontinence, or urinary retention. The current expansion of indications for neuromodulation has developed into areas of neurogenic bladder (Parkinson disease, multiple sclerosis, spinal cord injury), interstitial cystitis (painful bladder syndrome), pelvic pain, fecal incontinence and bowel disorders, and pediatric voiding dysfunction.

Neurogenic Bladder

Patients with neurogenic bladder may have several urodynamic events that lead to their symptomatic voiding dysfunction. This may include neurogenic detrusor overactivity, detrusor-sphincter dyssynergia, and flaccid areflexia. Whereas neuromodulation has not been well examined in cases of obvious areflexia (possibly because of the need for some end-organ response for neuromodulation to have any benefit), it has been studied in small subgroups of patients with detrusor overactivity and possibly detrusor–external sphincter dyssynergia, although few published reports exist.

Because the spectrum of neurologic diseases with potential bladder manifestations is wide, one must be cognizant of a few important relative contraindications before contemplating current neuromodulatory therapies, as follows: significant bone abnormalities in the spine or sacrum that may present challenges to gaining access; mental incapacity of patients, who cannot manage the device; physical limitations that prevent voiding (functional incontinence); future need of MRI; and noncompliance.

Multiple Sclerosis

Multiple sclerosis (MS) is a chronic demyelinating disease of the central and peripheral nervous system that can cause a variety of voiding dysfunction scenarios including neurogenic detrusor overactivity, detrusor-sphincter dyssynergy, areflexia, and combinations of these. Because many patients have been refractory to standard therapies, neuromodulation or neurostimulation (to be addressed later in the section on neurostimulation for retention) may be considered a part of their treatment options. In an appropriately selected patient with MS, neuromodulation truly has some promise because it may balance the function of the bladder itself as well as that of the outlet (two of the main components of MS-related voiding dysfunction). This may be considered off-label use of neuromodulation because it is not approved specifically for MS-related voiding dysfunction, but approval may be based on symptoms such as urgency, frequency, or often urgency urinary incontinence and even nonobstructive urinary retention.

No prospective randomized trials exist on the use of neuromodulation in management of MS-related bladder dysfunction. Small series with encouraging results in patients with MS demonstrate that neuromodulation may have a role in treatment of MS-related voiding dysfunction (Bosch and Groen, 1996; Wallace et al, 2007). It appears that the best candidates are ones with mild, nonprogressive MS, with few functional issues, who also have detrusor overactivity or even retention but not areflexia. One of the major issues that arises in the patient with MS in particular is the potential change in the disease state that may be potentiated by neuromodulation. Although this may be theoretical, it was one of the factors cited by the FDA in the original sacral neuromodulation trials and precluded MS patients from being enrolled (Hassouna et al, 2000).

A secondary issue that may arise if a patient with MS is implanted with the lead and IPG system is the potential need for MRI in the future. One should maintain close contact with the patient’s neurologist as to the decision to place a neuromodulatory device to prevent any future need for MRI or selection of a patient in an active phase of disease who requires routine MRI. The main concern with MRI and implantable stimulator or pacemaker-type devices is that heating of the leads has been demonstrated in vivo and in vitro (Roguin et al, 2004; Martin, 2005). Whereas some question the clinical significance of the small temperature changes with the leads, the potential exists to elicit nerve damage with heating of the lead, and the magnetic field may change the generator itself (Gimbel and Kanal, 2004). At present, it is contraindicated to perform MRI of a patient with an implantable neurostimulator system.

Spinal Cord Injury

Many specialists who treat neurogenic disorders due to spinal cord injury realize that a patient may present with a variety of clinical and urodynamic findings. Many patients have neurogenic detrusor areflexic situations, but perhaps more often and sometimes more challenging is the subset who may be incontinent from neurogenic detrusor overactivity with or without concomitant sphincteric dyssynergy. Furthermore, the adverse sequelae of treated or untreated spinal cord injury may include infections, urolithiasis, reflux, or obstruction. The goal, then, is not only to prevent these adverse events but also to ensure a bladder that functions well, empties at a low pressure to protect the upper tracts, and maintains a good capacity and continence. Whereas it is implied that an intact reflex arc should be in place for neuromodulation to work, this has not been proved in clinical studies. Basic science data suggest that at least some communication should exist between sacral outflow and the pontine micturition center to allow processing for the reflexes that may be inhibited by the brain

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