The sacral nerve stimulation (SNS) device (InterStim, Medtronic, Minneapolis, MN) has approval from the US Food and Drug Administration for the indications of refractory urge incontinence, refractory urgency, and frequency, and approved indications include urinary urge incontinence, urgency–frequency, nonobstructive urinary retention, and fecal incontinence. As a minimally invasive urologic procedure, it has demonstrated long-term efficacy and safety.

Electrical stimulation of the sacral nerve can paradoxically inhibit urge incontinence in overactive bladder-wet patients and yet restore spontaneous urination in underactive bladder patients with idiopathic urinary retention. The effects of sacral neuromodulation depend on electrical stimulation of the afferent axons in the spinal roots that in turn modulate voiding and continence reflex pathways in the central nervous system (Leng and Chancellor 2005). The stimulation effect is afferent mediated because the intensities of stimulation do not activate movements of striated muscles.

How does neuromodulation treat nonobstructive urinary retention? I believe that SNS activates the somatic afferent inputs that modulate sensory processing and micturition reflex pathways in the sacral spinal cord (Yoshimura and Chancellor 2011). In cases of UAB and dysfunctional voiding, SNS can inhibit the aberrant guarding reflexes.

Most visceral organs such as the blood vessels, heart, and gastrointestinal tract receive a tonic autonomic regulation and are “turned on” most of the time. The urinary bladder is different because it is functionally “turned off” most of the time except for the six to eight times a day when a person voluntarily urinates.

The bladder is turned on in an “all-or-none” manner to eliminate urine (Fig. 8.1). The ability to “turn on,” in switch-like fashion, to urinate is facilitated by positive feedback loops in the micturition reflex pathway. Amplification of bladder afferent activity can activate sufficient efferent excitatory signals to the bladder to initiate micturition. This positive feedback is effective for promoting sustained bladder contraction until the bladder is emptied (Yoshimura and Chancellor 2011).

Bladder afferent nerves send signals of bladder fullness and discomfort to the brain in order to initiate the micturition reflex (Yoshimura and de Groat 1997; de Groat 1997). The bladder afferent pathways are composed mostly of two types of axons: small myelinated A-delta fibers and unmyelinated C-fibers. A-delta fibers transmit signals mainly from mechanoreceptors that detect bladder fullness. The C-fibers mainly detect noxious signals and initiate painful sensations. The bladder C-fiber nociceptors perform a similar function and signal the central nervous system during urinary tract infection, inflammation after radiation, or intravesical chemotherapy. C-fiber bladder afferents can also trigger voiding in abnormal conditions such as neurogenic detrusor overactivity (Yoshimura and de Groat 1997).

The urethra and urinary sphincter are on a “turned-on” state except for short periods when we urinate and voluntarily relax our sphincter muscle. There is an important bladder to urethral reflex that is mediated by sympathetic efferent pathways to the urethra. This excitatory reflex promotes urethral smooth muscle contraction during the bladder storage phase and thus is called the guarding reflex (de Groat et al. 1997).

The guarding reflex is not activated during micturition, but rather, when bladder pressure is momentarily increased during events such as a sneeze or cough. A second guarding reflex is triggered and amplified by bladder afferent signaling, which then synapses with sacral interneurons that in turn activate urethral external sphincter efferent neurons via the pudendal nerve (Shaker and Hassouna 1998; Yoshimura and Chancellor 2011). The activation of pudendal urethral efferent pathways contracts the external urinary sphincter and prevents stress urinary incontinence (Fig. 8.2).

Brain pathways are necessary to turn off sphincter and urethral guarding reflexes to allow efficient bladder emptying. Thus, spinal cord injury produces bladder–external sphincter dyssynergia and inefficient bladder emptying by eliminating the brain mechanisms. This may also occur after more subtle neurologic lesions in patients with idiopathic urinary retention. Before the development of brain control of micturition, at least in animals, the stimulation of somatic afferent pathways passing through the pudendal nerve from the perineum can initiate efficient voiding by activating bladder efferent pathways and turning off the excitatory pathways to the urethral outlet (de Groat 1997). Sacral nerve stimulation may elicit similar responses in patients with urinary retention and turn off excitatory outflow to the urethral outlet and promote bladder emptying. Because sphincter activity can generate afferent input to the spinal cord that can in turn inhibit reflex bladder activity, an additional benefit of suppressing sphincter reflexes would be a facilitation of bladder activity.

The voiding and guarding reflexes discussed are activated at different and opposite times. When we urinate, the voiding reflex is turned on and the guarding reflex is turned off. When we are sleeping, the voiding reflex is turned off while the guarding reflex is turned on. Anatomically the neuronal wiring of the voiding and guarding reflexes is located in close proximity to each other in the S2–S4 levels of the human spinal cord (Table 8.2). For patients with UAB, neuromodulation’s benefit is believed to activate the pudendal nerve afferents originating from the pelvic organs into the spinal cord and restore the inhibited voiding reflexes by suppressing exaggerated guarding reflexes (Leng and Chancellor 2005; Yoshimura and Chancellor 2011) (Fig. 8.3). In patients with overactive bladder, pudendal afferents may activate the afferent limb of inhibitory reflexes that promote bladder storage. This blocks input to the pontine micturition center, thereby restricting involuntary detrusor contractions without interfering with normal voiding patterns. In patients with fecal incontinence, the pudendal afferent somatic fibers are believed to be working by inhibiting colonic propulsive activity and activating the internal anal sphincter.

Current approved indications for sacral neuromodulation include urinary urge incontinence, urgency–frequency, nonobstructive urinary retention, and fecal incontinence (Noblett and Cadish 2014). SNS involves a two-stage procedure. The initial phase is considered the test stimulation period where the patient is allowed to evaluate whether the therapy is effective. There are two techniques that exist to perform the test stimulation.