Originally, SNM was not considered an option for neurogenic LUTD; however, some studies have suggested that SNM is also effective in these patients [14, 15]. Taking into account that SNM is minimally invasive and completely reversible, it is of great interest whether this treatment option is valuable for patients with neurogenic LUTD before resorting to more invasive procedures.

Chartier-Kastler et al. [14] studied nine women treated for refractory neurogenic urge incontinence with SNM. Neurological spinal diseases included viral and vascular myelitis in one patient each, multiple sclerosis in five, and traumatic spinal cord injury in two. All patients had clinically significant improvement of incontinence, and five were completely dry. Average number of voids per day decreased from 16.1 to 8.2. Urodynamic parameters at 6 months after implant improved significantly from baseline, including maximum bladder capacity from 244 to 377 ml and volume at first uninhibited contraction from 214 to 340 ml. Maximum detrusor pressure at first uninhibited contraction increased in three, stabilized in two, and decreased in four patients. Urodynamic results returned to baseline when stimulation was inactivated. All patients subjectively reported improved visual analog scale results by at least 75 % at last follow-up.

In the study of Lombardi and Del Popolo [16], 24 SCI patients, tested using mini-invasive approach with percutaneous technique and tined lead, were enrolled and divided into two groups: 13 individuals in the urinary retention category and 11 suffering from overactive bladder syndrome. All the subjects underwent definitive SNM implantation and maintained a clinical improvement of more than 50 % compared with baseline. Four subjects with urinary retention needed a new implant in the contralateral S3 sacral root because of loss of efficacy. The authors concluded that SNM is a therapy to consider in the treatment of NLUTS for partial SCI patients, even if the loss of clinical benefits for patients with retentive NLUTS must be taken into account.

Also in the experience of Hohenfellner and colleagues [17], SNM has been reported to be effective in the treatment of neurogenic bladder dysfunction. Their patient population consisted of 27 patients with bladder storage failure due to detrusor hyperreflexia and/or bladder hypersensitivity (15), failure to empty due to detrusor areflexia (11), and combined bladder hypersensitivity and detrusor areflexia (1). Twelve patients underwent chronic sacral neuromodulation with unilateral electrode implantation into one of the dorsal S3 foramina. However, they reported a high loss of efficacy rate after 54 months of follow-up, suggesting that the treatment could be temporary.

These results were confirmed by Chaabane et al. [18] in 62 patients (detrusor overactivity in 34 cases and chronic urinary retention in 28 cases). Out of the 62 patients, 41 patients (66.1 %) had more than 50 % improvement on urodynamic evaluation and bladder diary and 37 were implanted. With a mean follow-up of 4.3 years, results remained similar to the evaluation phase in 28 cases (75.7 %), were partially altered in three cases (8.1 %), and lost in six cases (16.2 %), suggesting that results depend on the type of the underlying neurologic disease and in particular whether it may progress or not.

In patients suffering from chronic neurogenic nonobstructive urinary retention (N-NOR), SNM is highly efficacious in the medium follow-up. Thirty-six/85 patients (42 %) responded to percutaneous first stage of SNM. Eleven out of 34 patients at follow-ups were “inconstant responders” because they returned to similar baseline voiding symptoms, but responded again with an implant on the contralateral S3 sacral root. Two failed twice and responded once again after an S4 sacral root implant [19].

The inherent course of the neurologic disease or injury (i.e., stable or progressive disorder) certainly greatly influences the LUTD and consequently the effect of SNM.

Moreover, SNM may be initially successful in a patient with MS but may stop working after MS relapses. In addition, early SNM in patients with complete spinal cord injury during spinal shock (i.e., the bladder areflexia phase) could prevent detrusor overactivity and urinary incontinence [20], whereas SNM has been attempted without success in complete chronic spinal cord injury patients [21], emphasizing the significance of the time point of SNM. In the case that the benefits of early SNM in patients with complete spinal cord injury may be reproduced in randomized trials and if these findings can be conveyed to patients with other neurologic diseases or injuries, this will completely revolutionize the management of neurogenic LUTD.

However, a pooled success rate of 68 % for the test phase and of 92 % for permanent SNM indicates that SNM may be effective and safe for the treatment of patients with neurogenic LUTD [5].

Discussing the efficacy and safety of SNM for neurogenic LUTD, it is important to be aware of the fact that these patients usually have undergone multiple failed previous treatments. Thus, a pooled success rate of 68 % for the test phase is more than just some benefit. After failed conservative treatment, SNM testing seems worthwhile in patients with neurogenic LUTD before more invasive treatments are considered. In addition, patients with neurologic disease or injury often suffer not only from LUTD but also from bowel dysfunction; because SNM may be beneficial for both conditions, patients with combined dysfunctions appear to be good candidates for SNM, with a high impact on the associated QoL.

Moreover, the overall results in patients with neurogenic LUTD are in line with the findings in patients with non-neurogenic LUTD and success rates are probably not lower than for established indications of SNM in non-neurogenic voiding dysfunction. This is also consistent with the fact that in some patients, non-neurogenic LUTD may actually be neurogenic but not yet be discovered.

Sacral neuromodulation (SNM) represents a promising option for managing treatment-refractory neurogenic bladder dysfunction. It remains to be seen, however, which types of neurogenic bladder dysfunction and which underlying neurological disorders best respond to SNM. However, it should be noted that high frequency diathermy and unipolar electrocauterization are contraindicated in patients with neuromodulators, that during extracorporeal shock wave lithotripsy the focal point should not be in the direct vicinity of the neuromodulator or the electrode, that ultrasound and radiotherapy in the region of the implanted components should be avoided, that the neuromodulation should be discontinued in pregnancy, and that MRI examinations should only be conducted when urgently indicated and the neuromodulator is turned off.

The pudendal nerve is a major contributor to bladder afferent regulation and bladder function. Because the pudendal nerve carries such a large percentage of afferent fibers, neuromodulation of the pudendal nerve is an attractive option for refractory detrusor hyperreflexia.

Dorsal genital nerve (DGN) stimulation has shown to be able to suppress undesired detrusor bladder contractions in patients with both neurogenic detrusor overactivity (NDO) and detrusor sphincter dyssynergia (DSD) [22] and repeated conditional short duration electrical stimulation significantly increased cystometric capacity in patients with spinal cord injury [23]. The increase was mainly caused by an inhibition of detrusor contractions.

Opisso et al. [24] investigated whether patients with neurogenic detrusor overactivity can sense the onset of bladder contraction and in turn suppress the contraction by electrical stimulation of the dorsal penile–clitoral nerve. A total of 17 patients with neurogenic detrusor overactivity underwent three cystometric filling trials. The first cystometry was used to determine bladder capacity. The second cystometry was done with automatic electrical stimulation of the pudendal nerve when the bladder reached a threshold pressure of 10 cm H₂O above the mean detrusor pressure. The third filling cystometry was done with patients controlling the pudendal stimulation and asked to begin stimulation when they could sense the onset of an uninhibited bladder contraction. Compared to peak pressure for cystometry, 1 average peak pressure during suppressed contractions for cystometries 2 and 3 was 49 and 26 % lower, respectively. The average delay of the onset of stimulation during cystometry 3 with respect to cystometry 2 was 5.7 s. They concluded that patient-controlled genital nerve stimulation is as effective as automatic controlled stimulation to treat neurogenic detrusor overactivity, increase bladder capacity, and prevent uninhibited detrusor contractions, although patients must be trained in the technique.

Spinelli and colleagues [25] described their experience with pudendal nerve stimulation using a device with a quadripolar tined lead placed at Alcock canal in 15 patients with neurogenic bladder. In this study, the average number of incontinent episodes among this group of patients decreased from seven to three episodes per day. Eight patients became continent during the screening phase of the study, and four patients had a greater than 50 % improvement in the number of incontinent episodes experienced per day. Urodynamic evaluation in seven patients revealed a significant increase in detrusor capacity and a decrease in maximum detrusor pressure. The authors suggest that based on these preliminary data, pudendal nerve stimulation is an effective therapeutic alternative for neurogenic overactive bladder particularly in nonresponder patients to antimuscarinic drugs and in whom traditional sacral neuromodulation failed, before to consider more invasive procedures such as bladder augmentation.

Posterior tibial nerve stimulation (PTNS) was found to be effective in 37–100 % of patients with overactive bladder (OAB), in 41–100 % of patients with nonobstructive urinary retention, and in up to 100 % of patients with chronic pelvic pain/painful bladder syndrome (CPP/PBS), children with OAB/dysfunctional voiding, and patients with neurogenic pathologies [26]. Moreover, there is evidence that the improvement in OAB symptoms using PTNS is comparable to the effect of antimuscarinics but with a better side effect profile [27]. Acute urodynamic effects of PTNS were observed in a mixed population of OAB patients, most of whom neurologically impaired (multiple sclerosis, spinal cord injury, Parkinson’s disease).

During stimulation, an increase of first involuntary detrusor contraction volume and of cystometric capacity was found [28]. In this study, a total of 44 consecutive patients with urge incontinence, frequency, and urgency secondary to overactive bladder were studied. Of the patients, 37 had detrusor hyperreflexia due to multiple sclerosis (13), spinal cord injury (15), or Parkinson’s disease (9), and 7 had idiopathic detrusor instability. Routine cystometry at 50 ml/min was done to select the patients with involuntary detrusor contractions appearing before 400 ml maximum filling volume. Repeat cystometry was performed immediately after the first study during left posterior tibial nerve stimulation using a surface self-adhesive electrode on the ankle skin behind the internal malleolus with shocks in continuous mode at 10 Hz. frequency and 200 ms wide. Volume comparison was done at the first involuntary detrusor contraction and at maximum cystometric capacity. The test was considered positive if the volume at the first involuntary detrusor contraction and/or at maximum cystometric capacity increased 100 ml or 50 % during stimulation compared with standard cystometry volumes.

Mean first involuntary detrusor contraction volume on standard cystometry was 162.9 ± 96.4 ml, and it was 232.1 ± 115.3 ml during posterior tibial nerve stimulation. Mean maximum cystometric capacity on standard cystometry was 221 ± 129.5 ml, and it was 277.4 ± 117.9 ml during stimulation. Posterior tibial nerve stimulation was associated with significant improvement in first involuntary detrusor contraction volume (p < 0.0001) and significant improvement in maximum cystometric capacity (p < 0.0001). The test was considered positive in 22 of the 44 patients.

Although some studies suggested that PTNS could be effective in the management of severe OAB in multiple sclerosis (MS), without compromising bladder emptying or inducing side effect and even in the absence of an acute cystometric effect [29–32], these results were not confirmed by other authors [33] that failed to obtain acute urodynamic reductions of detrusor overactivity.

Other studies suggested that PTNS could also be effective to suppress detrusor overactivity in patients with Parkinson’s disease [34].

However, low evidence studies (only prospective nonrandomized trials are available), short study periods, heterogeneous indications, and treatment modality make it difficult to draw any definitive conclusions, and in order to recommend PTNS as a practical treatment option, randomized controlled trials, long-term data, and health economic analysis are needed.

In 1969, Brindley developed a device to stimulate sacral roots at the level of the cauda equina. The first Brindley stimulator was implanted in a patient in 1978. Although the first implants did not involve posterior sacral rhizotomy, lesions to these nerves during surgery led to the advantage of leaving the patient’s bladder completely areflexic and restoring normal bladder compliance and curing reflex incontinence. Subsequently, placement of the Brindley stimulator was combined with sacral posterior rhizotomy [35]. The denervation step is skipped in cases of genital sensation and reflex erections.

The objective of the Brindley technique is to improve both voiding and effective continence. Any patient with a stable supra-sacral spinal cord lesion (paraplegia, tetraplegia) with a reflex bladder (incontinence, vesico-sphincter dyssynergia resistant to medical treatment with the risk of upper urinary tract involvement) can benefit from the Brindley technique. The electrodes are placed on the anterior sacral roots in order to obtain the desired micturition. Posterior sacral rhizotomies are indispensable to the technique as they suppress detrusor and sphincter hyperreflexia and improve continence, thereby protecting the upper urinary tract.

Ninety percent of patients gain satisfactory continence and no longer require an incontinence appliance, with a significant improvement of the quality of life. Bladder capacity and compliance increase dramatically. As a consequence, urinary infection rate decreases. The majority of patients remain dry, and more than 80 % have a complete voiding or a post-void residue of less than 50 ml and do not require any catheterization [36]. Over a retrospective review of 500 patients with a Brindley stimulator, 411 were still in use with the patients pleased [37].

Ergon and colleagues [35] reviewed their experience with 93 SCI patients with sacral anterior root stimulators combined with posterior sacral rhizotomy. They reported that 83 patients used their stimulators for micturition, and 82 were fully continent.

Van Kerrebroeck et al. [38] reported that complete continence during daytime was achieved in 73 % of patients and in 86 % at night in 52 patients in which complete posterior sacral root rhizotomies were performed and a Finetech–Brindley sacral anterior root stimulator implanted. Significant increase in bladder capacity and bladder compliance was achieved in all patients. Residual urine was reduced significantly, resulting in a decrease of the incidence of urinary tract infections.

However, the major limitation to this form of neuromodulation is that it requires an intact neural pathway between the sacral cord nuclei of the pelvic nerve and the bladder. Furthermore, the irreversibility of the sacral deafferentation may limit future treatment options.

Since 1975 intravesical electrical stimulation (IVES) has been used as a rehabilitative technique for children with myelodysplasia [39, 40]. Worldwide, several other investigators have used IVES to treat neurogenic bladder dysfunction secondary to a variety of factors, including SCI, myelodysplasia, and other neurologic diseases [41]. Impressive results from IVES have been reported, including the restoration of bladder sensation with filling and stimulation of the detrusor contraction, conscious urinary control, and a significant increase in bladder capacity. These benefits have been achieved without harmful effects on the upper urinary tract.