It is very interesting to look back to 1988 and realize how little was known regarding electrical stimulation or neuromodulation in the management of voiding dysfunction and pelvic pain. The original chapter had sparse data on the use of transcutaneous electrical nerve stimulation (TENS) as a means to improve symptoms of interstitial cystitis. It was suggested that other sites of stimulation such as intravaginal or posterior tibial nerve may improve clinical outcomes. The author commented that the ideal site of stimulation was unknown and research was needed to identify the best stimulation parameters to achieve good clinical outcomes. Since that time, cutaneous stimulation is routinely used, but still with little evidence. It is often physical therapists who use TENS and inferential stimulation units as a multimodal approach to managing chronic pelvic pain. There has been broadened interest in the impact of the pelvic floor and neuromuscular dysfunction as an underlying trigger for pain associated with interstitial cystitis. Thus, neuromodulation is a reasonable modality to offer patients with interstitial cystitis symptoms.

The author was insightful in proposing inhibition of bladder afferents, modulation of bladder efferents, an impact on opioid/endorphin release and perhaps a local influence on the detrusor inflammatory cell aggregates as potential mechanisms of action of electrical stimulation. Interestingly, despite years of research on neuromodulation since the book was published in 1988, we still do not have a clear understanding as to how neuromodulation works. A significant amount of research has focused on the effect of sacral neuromodulation (SNM) on afferent sensory nerve fibers, with the dominant theory being that electrical stimulation of these somatic afferent fibers modulates voiding and continence reflex pathways in the central nervous system (CNS).

The control of sensory input to the CNS is thought to work through a gate control mechanism.

The gate control theory states that noxious stimuli perception does not entirely depend on the A-delta and C-fiber sensory nerves transmitting information to the CNS, but on the pattern of peripheral nerve activity. A-delta bladder afferent nerve fibers project to the pontine nuclei to provide inhibitory and excitatory input to reflexes controlling bladder and sphincter function. Afferent C-fibers within the bladder are normally thought to be mechano-insensitive and unresponsive and thus referred to as silent C-fibers. These normally inactive C-fibers may be sensitized by inflammation or infection, thus causing activation of involuntary micturition reflexes and detrusor overactivity. Sensory input from large myelinated pudendal nerve fibers may modulate erroneous bladder input conveyed by A-delta or C-fiber afferents at the gate control level of the spinal cord. Detrusor hyperreflexia then may be attributed to a deficiency of the inhibitory control systems involving pudendal afferent nerves. The success of electrical neuromodulation for detrusor hyperreflexia may result from the restoration of the balance between bladder inhibitory and excitatory control systems. The stimulation of urethral afferents to facilitate the micturition reflex and stimulation of the dorsal nerve of the clitoris to inhibit bladder activity have been demonstrated in animal models for SNM.