SCOPE OF THE PROBLEM

Pelvic floor dysfunction (PFD) is a highly prevalent functional disorder, affecting both women and men, which may manifest in diverse clinical symptoms including urinary frequency, urgency with or without incontinence, and/or retention, as well as rectal incontinence and pelvic pain. Overactive bladder (OAB), a constellation of symptoms defined by “urgency, with or without urge incontinence, usually with frequency and nocturia,”¹ is one of the most common manifestations of PFD, and it the best-studied epidemiologically. OAB affects approximately 16.5% of adult men and women in population-based studies conducted in both the United States² and Europe.³ Some 9.3% of women and 2.6% of men, respectively, suffer from OAB associated with urge incontinence.² These figures translate to an estimated 33 million affected adults in the United States alone, a prevalence similar to that of other major chronic conditions such as hypertension and heart disease.⁴ The global costs of treating OAB are estimated at $12 to $17 billion per year, comparable to those attributed to pneumonia, osteoporosis, or arthritis.^2,⁵

Pharmaceutical remedies for urinary complaints referable to PFD remain suboptimal due to a high incidence of side effects, relatively modest efficacy, poor patient compliance, and high long-term costs. Surgical procedures described to date do not work well for most cases of PFD featuring a prominent urge component; moreover, surgery may not be a suitable option for the many PFD patients who are elderly and faced with multiple medical comorbidities. Many studies using various measures have found that urge incontinence affects patients’ health-related quality of life (QOL) to a greater extent than does stress incontinence ⁶^–⁸; nevertheless, in part due to dissatisfaction with treatment alternatives and/or a public perception of unsatisfactory treatment outcomes, OAB often goes unrecognized and undermanaged. In the United States, only 25% of OAB patients surveyed (40% of those with incontinence) had seen a physician for management of bladder symptoms in the past year.⁴

Urologists have long recognized PFD as a root source of diverse voiding complaints, but many patients with concomitant constipation would seek referral for treatment of constipation before a definitive evaluation for voiding dysfunction. Gastroenterologists, in turn, might advise patients to have their urinary problems corrected before offering a definitive opinion and treatment for constipation. Gynecologists faced with a patient with chronic pelvic pain and urinary or fecal continence issues may refer the patient for management of these problems before addressing the pain itself. In many cases, these apparently disparate problems are in fact interrelated manifestations of the common functional problem of PFD.

Recent reports have provided additional evidence for epidemiologic associations among urinary incontinence and other PFD-related complaints such as incontinence of flatus and/or feces and prolapse symptoms.⁹ PFD probably also plays a significant role in the pathophysiology of female sexual disorders.¹⁰ In recent years, novel approaches for the treatment of both OAB and other manifestations of PFD have been the subject of growing interest; one of the most promising such approaches is percutaneous neurostimulation as a means of modulation of the sacral outflow tract to the pelvic floor.

PERCUTANEOUS NEUROMODULATION: RATIONALE AND THEORETICAL MECHANISM

Many groups over the past 20 years have focused efforts on stimulation of the S2 through S4 nerve roots at their origin from the sacral cord. Various techniques of central stimulation have been used successfully to treat OAB, pelvic pain, sphincteric incompetence, detrusor hyporeflexia, and idiopathic urinary retention.¹¹ Central sacral neuromodulation is successful for many patients with PFD¹² and has been shown to improve urinary function by both urodynamic and quality-of-life parameters.¹³ This modality, however, has significant drawbacks. Placement of the stimulator is invasive: the system requires trial runs with percutaneous needles placed through the sacral foramina to access the cord for up to 1 week and ultimately requires a general anesthesia for permanent stimulator implantation. Among patients with a successful response to initial lead placement, as many as 20% to 51% do not enjoy similar long-term success with permanent implantation. Moreover, the complication rate varies from 22% to 43%, and up to 50% of patients receiving sacral neurostimulators eventually require reoperation.¹⁴ Lead migration is a late complication that continues to limit the long-term efficacy of the central approach even in contemporary reports.¹⁵

Various approaches to minimally invasive neuromodulation have been tested, including perineal muscle stimulation for stress urinary incontinence; perineal nerve stimulation via the dorsal nerve of the penis for detrusor hyperreflexia; peripudendal percutaneous neural stimulation; and direct cutaneous stimulation of perineal, perianal, or perivaginal skin for the management of urge incontinence. The proliferation of these novel approaches to minimally invasive neuromodulation of the pelvic floor underscores the limitations of the more invasive central stimulation techniques. One of the most promising new approaches for multiple PFD-related complaints involves percutaneous posterior tibial nerve stimulation (PTNS).

The posterior tibial nerve is a mixed somatic/motor nerve containing fibers originating from spinal roots L4 through S3. These roots comprise the outflow of the sacral nerves, which modulate the somatic and autonomic nervous supply to the pelvic floor, innervating the bladder and urinary sphincter. Initial studies of potential approaches to peripheral neuromodulation of the sacral cord measured skin impedance at various points along the S2 and S3 dermatomes and identified a consistent area of high impedance above the medial malleolus. This area overlies the posterior tibial nerve and corresponds to the sanyinjiao, or Sp-6 (spleen-6) acupuncture point. In acupuncture practice, Sp-6 has been targeted for management of a variety of urinary complaints, as well as to stimulate labor and alleviate labor pain; traditional acupuncture at this point previously has been shown to produce transient improvements in urodynamic parameters.¹⁶

The precise mechanism by which neurostimulation, central or peripheral, exerts its influence on pelvic floor function remains unclear. In particular, conflicting data exist as to whether peripheral neurostimulation exerts a facilitative or inhibitory effect on urinary system neural pathways. Repetitive PTNS exerts a strong inhibitory effect on nociceptive spinothalamic tract neurons in primate studies, especially at high frequencies of stimulation, via activation of myelinated Aδ fibers.¹⁷ Primate data from the University of California at San Francisco (UCSF) demonstrated inhibition and even elimination of uninhibited bladder contractions during PTNS.¹⁸ In a feline model, on the other hand, S2 stimulation induced excitatory bladder effects at lower amperage and complete bladder inhibition at higher intensities.¹⁹ Peripheral afferent nerve stimulation in vivo abolished inappropriate detrusor contractions while leaving the normal micturition reflex intact. The therapeutic effect tended to increase with repetitive weekly treatments over 2 to 3 months.

One theory suggests that posterior PTNS results in improved blood flow to the pelvis. As yet unpublished data from UCSF, for example, found, among a cohort of five men with complete erectile dysfunction, that peripheral neurostimulation yielded an immediate doubling in cavernosal arterial diameter (from a mean of 3.8 mm to 7.5 mm) and velocity (from a mean 11 cm/sec to 20 cm/sec).

Another mechanistic hypothesis suggests that neurostimulation effects a change in the neurochemical environment along the sacral pathways. Chang and colleagues,²⁰ for example, studied expression of FOS protein, a marker for noxious stimulation of cell growth, in the rat spinal micturition center (L6-S2). Among normal animals, 0 to 4 cells per section at L6 were FOS-positive. After a standardized noxious insult to the rat bladder (1% acetic acid), FOS expression increased to a mean of 76 cells per section. A single 25-minute session of percutaneous neurostimulation at Sp-6 administered 1 hour before acetic acid infusion reduced FOS expression by 73%, to a mean of 20 cells per section.²⁰

EARLY EXPERIENCES WITH PERIPHERAL NEUROSTIMULATION

In 1983, McGuire and associates reported their “astonishingly good” results from transcutaneous tibial nerve stimulation (TTNS) applied via an adhesive electrode to 22 patients with a range of urologic diagnoses including detrusor instability, interstitial cystitis, radiation cystitis, and neurogenic bladder. Eight of 11 patients with detrusor instability were judged “dry” after TTNS, as assessed by urodynamics and cystography; two patients with multiple sclerosis were “improved,” four of five neurogenic bladder patients were likewise “dry” and one “improved,” and four of six cystitis patients experienced some degree of improvement.²¹ These early data, although not rigorously collected or reported, certainly indicated the potential utility of peripheral neurostimulation for bladder symptoms.

Based on experience with central neuromodulation both at UCSF ¹² and elsewhere, and in the hope of reaching a larger patient population, the Stoller Afferent Nerve Stimulator (SANS) was introduced 4 years later, offering a method for PTNS that would be minimally invasive and less expensive.

The application of PTNS, like that of other neuromodulatory strategies, requires a cooperative patient with a morphologically intact urinary tract, a preserved sacral spinal reflex center, a low degree of peripheral denervation of the pelvic floor striated musculature, and the ability to void spontaneously or via self-catheterization without electrical stimulus.¹¹ Pretreatment testing mirrors the standard workup for refractory OAB symptoms and includes urinalysis and urine culture, formal urodynamic profiling, and cystoscopy to rule out foreign bodies or anatomic or urothelial abnormalities explaining the symptoms.

For each PTNS session, the patient sits in a frog-leg position, and solid 34-gauge needles are placed bilaterally, three fingerbreadths (6 cm) superior to the medial malleolus. The needles are advanced to a depth of approximately 4 cm, angling posterior to the tibia and about 30 degrees cephalad. The trajectory points toward a potential needle exit anterior to the fibula. A grounding electrode (e.g., an adhesive electrocardiogram pad) is also applied on each side, ipsilaterally overlying the medial calcaneus. Electrical stimulation is typically administered from a battery-powered generator, at an amplitude just beneath the sensory threshold of 0.5 to 10 mA, with a fixed pulse width of 200 μsec and a fixed frequency of 20 Hz. Appropriate needle localization is verified by great toe plantar flexion or fanning of digits 2 through 5 in response to an initial higher amplitude stimulation. If the patient prefers, for increased comfort after the needles are applied, he or she may shift to a more comfortable position (i.e., out of frog-leg position), taking care not to dislodge the needles.

Continued stimulation is applied for 30 minutes, only on the side with the more pronounced response to the test pulse. However, both needles are left in situ during treatment. Sessions are repeated weekly for at least 10 to 12 weeks. Patients complete voiding and pain diaries; if they experience improvement in their symptoms, the frequency of therapy is tapered gradually to every 3 or 4 weeks. Some patients have been treated continuously for up to 10 years with sessions every 4 to 6 weeks, achieving sustained symptomatic relief but consistently experiencing relapse of symptoms when the SANS sessions are stopped for prolonged periods. Patients may experience transient discomfort at the initial skin puncture site, but there is minimal if any pain with needle advancement through the deeper tissues. No patient in our experience has complained of pain during the stimulation session.

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