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INTRODUCTION

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Overactive bladder is an umbrella term that collectively covers several lower urinary tract conditions including urgency incontinence. The International Continence Society defines overactive bladder as “urgency, with or without urgency incontinence, usually with frequency and nocturia, in the absence of pathologic or metabolic factors that would explain these symptoms.”1 Specific definitions of the various presentations are listed as follows:

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  • Urgency—a sudden, compelling desire to pass urine, which is difficult to defer

  • Frequency—complaint by the patient that she voids too often by day (generally considered normal to void ≤8 times per day)

  • Nocturia—complaint that individual has to wake up ≥1 time per night to void

  • Urgency incontinence—the complaint of involuntary leakage accompanied by or immediately preceded by urgency

  • Detrusor overactivity incontinence—incontinence due to an involuntary detrusor contraction

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Overactive bladder is estimated to affect approximately 42.2 million adults in the United States resulting in a $24.9 billion annual cost for treatment.2 Typically overactive bladder and urgency incontinence are treated with behavioral and/or pharmacological interventions. Currently there are nine commercially available anticholinergic medications on the market specifically targeted at treating overactive bladder. Newer medications such as beta-3 agonists are an alternative pharmacological intervention. Unfortunately, anticholinergics have a high discontinuation rate due to a variety of factors including, most importantly, lack of efficacy and high side effect profile.3 For those who are refractory to conservative measures, or who have contraindications to pharmacological intervention, there are several surgical alternatives available for treatment including sacral neuromodulation and intravesical botulinum injection. There are also other more invasive, nonreversible surgical interventions such as denervation procedures and augmentation cystoplasty that are briefly included in this chapter.

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SACRAL NEUROMODULATION

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Sacral nerve stimulation (SNS) delivers nonpainful, mild electrical pulses to the sacral nerves to modulate the reflexes that influence the bladder, sphincter, and pelvic floor to improve or restore normal voiding function. It has been available in the United States as a treatment option for refractory voiding dysfunction since 1997 and in Europe since 1994. Currently over 80,000 implants have been performed worldwide, with recent exponential growth occurring in the United States. Since its inception, the therapy has evolved to a minimally invasive procedure that can be performed as an outpatient under local anesthesia. Current FDA-approved indications for SNS include urinary urgency incontinence, urgency–frequency, and nonobstructive urinary retention. With the performance of more implants worldwide, data suggest a benefit of SNS on other types of pelvic floor dysfunction such as chronic constipation and fecal incontinence.4

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Mechanism of Action

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The exact mechanism of action of SNS in the treatment of voiding dysfunction is not completely understood; however, several theories exist. de Groat demonstrated that sacral preganglionic outflow to the bladder receives inhibitory input from both somatic and visceral afferents.5-7 In addition to providing important insight into the organization of these inhibitory pathways, de ...

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