Sacral Nerve Neuromodulation

Introduction

In 1982, the first sacral nerve neuromodulation (SNM) was performed by Tanagho and Schmidt at the University of California in San Francisco ( ). SNM, delivered by the InterStim system and developed by Medtronic (Minneapolis, MN, USA), was first introduced in Europe in 1994. In 2002, Medtronic released a new implantable tined lead (model #3889), making the procedure less invasive. In 2006, Medtronic released a smaller neuromodulator called InterStimII. The US Food and Drug Administration (FDA) approved SNM for three chronic, voiding dysfunction conditions: intractable urge incontinence in 1997, urgency/frequency syndrome, and nonobstructive urinary retention in 1999 for patients who had failed to respond or could not tolerate conservative treatments ( ). In 2011, the FDA approved SNM for chronic, fecal incontinence in patients who had failed or could not tolerate conservative treatment. The indications for SNM have expanded from intractable urge incontinence and urgency/frequency syndrome ( ; ) and idiopathic chronic urinary retention ( ; ), to include reestablishment of pelvic floor awareness, resolution of pelvic muscle tension and pain ( ), interstitial cystitis ( ), and neurogenic detrusor over activity ( ).

Mechanism of Action (MOA)

The mechanism of action (MOA) by which SNM works to alter bladder functions are not yet clearly understood; however, there are two proposed hypotheses:

• 1.

  SNM may restore balance between excitatory and inhibitory impulses to and from the pelvic organ at sacral and suprasacral levels.

• 2.

  Afferent and efferent pathways are modulated to provide a balance that results in improved bladder function ( ).

As reported by , the MOA of SNM is most likely multifactorial and impacts the neuroaxis at several different levels. One hypothesis for the MOA of SNM is that indirect stimulation of the pudendal nerve and direct inhibition of the preganglionic neurons suppresses detrusor over activity. Another hypothesis is that stimulation alters the transmission of sensory input from the bladder to the pontine micturition center by inhibiting involuntary, reflex voiding. Sacral neuromodulation most likely inhibits the guarding reflex, leading to a reduction in sphincter over activity and therefore a reduction in outlet resistance in cases of nonobstructive urinary retention. In fecal incontinence, Vitton et al. described evidence of a somatosympathetic reflex pathway, which might explain the reason why fecal incontinence treatment using SNM, leading to reduced colonic activity and increased tone of the anal sphincter complex, may be successful ( ). See the chapter by DeGroat in this book for a more detailed discussion of mechanisms of SNM.