NSD should be suspected based on a careful medical history followed by a precise physical examination. Whereas neurogenic detrusor overactivity presents as urge urinary incontinence, NSD usually appears as stress incontinence. Stress urinary incontinence (SUI) is a condition of involuntary loss of urine on effort, physical exertion, sneezing, or coughing that is often bothersome to the patient and frequently affects quality of life [4]. Patients with SUI related to NSD usually report severe incontinence, often occurring with minimal changes in position [5]. Nevertheless, total incontinence should also raise the suspicion of other concomitant pathology, e.g., urinary-vaginal fistula or an ectopic ureter [6]. Patients should be asked about precipitating events, because any activity with an increase in intra-abdominal pressure can lead to involuntary loss of urine. Incontinence can occur with minimal activity such as walking or rising from a chair. Clinicians should be aware that the amount of urine loss may be out of proportion to the stress [7]. Severity of urinary incontinence, frequency of occurrence, and volume of urine lost should be carefully evaluated. This can be assessed by asking about pad usage, including pad weight, size, number of pads used, and number of urinary incontinence episodes per day. Onset and duration of reported complaints need to be documented. Fluid intake habits should be investigated and patients should be asked how much fluid they drink each day, what type of fluids they prefer, and how many times they void over a 24 h period. Patients should also be questioned about other urological complaints, including storage symptoms (urgency, frequency, nocturia); voiding problems (hesitancy, straining, poor and intermittent flow); post-micturition symptoms (sensation of incomplete emptying, post-micturition dribble); and impaired bladder sensation. Thus, negative responses to queries regarding symptoms of predominant urgency, incomplete emptying, incontinence associated with chronic urinary retention (referred to as overflow incontinence), functional impairment, and continuous leakage in patients with underlying neurological disorder may indicate NSD. Careful assessment of symptoms indicating possible complications (hematuria, dysuria, fever) should be conducted to rule out comorbid pathology such as malignancy, urolithiasis, or urinary tract infection.

After the urologic history, thorough neurologic and medical histories should be obtained. Neurological symptoms related to the underlying neurological pathology should be documented with onset, evolution, and any treatment. Storage symptoms including incontinence may be aggravated by different comorbidities. Furthermore, intrinsic sphincter deficiency may also be caused by non-neurogenic damage to structures that constitute the urethral sphincter mechanism (direct sphincter injury resulting from urethral catheter trauma or previous surgical interventions related to non-neurogenic causes). Stress incontinence may also result from weakness in the supporting tissues of the urethra and leads to urethral hypermobility [8]. Therefore, a carefully conducted medical history should elicit information regarding endocrine disorders (i.e., complicated and poorly uncontrolled diabetes, diabetes insipidus); cardiovascular diseases (volume status or diuretic therapy can increase urine flow and cause incontinence); urological conditions (i.e., urolithiasis, bladder/prostate cancer); respiratory dysfunctions with chronic cough (i.e., chronic obstructive pulmonary disease, chronic bronchitis); fecal motility disorders (constipation or fecal incontinence); chronic pelvic pain; mobility deficits; pelvic cancers; pelvic radiation; mental health disorders; dementia; inability to ambulate; and cognitive impairment. Special attention should be paid to previous extensive or radical pelvic surgery (e.g., radical hysterectomy or prostatectomy), as well as anti-incontinence surgery or complex urethral procedures (e.g., urethral diverticulectomy or urethrovaginal fistula repair). In women, a thorough obstetric and gynecological history must be obtained to exclude other potential causes of SUI. A general obstetric history with labor duration, mode of delivery, birth weights of children, year of delivery, intrapartum complications (e.g., childbirth-related injuries, obstetric anal sphincter injury, peri-urethral lacerations, wound breakdown), as well as de novo post-partum urinary symptoms (e.g., urinary retention requiring prolonged catheterization or SUI) that may be precipitated by cesarean section, epidural block, or prolonged labur may be necessary for evaluation [9–12]. Pelvic organ prolapse or previous surgery may influence the success of future treatment [13]. Factors that suggest a history of prolapse include prior use of a pessary, dyspareunia, and sensation of vaginal pressure or fullness.

As patients with neurourological symptoms may also suffer from neurogenic bowel and sexual dysfunctions, bowel and sexual histories are important [14, 15]. Bowel history should elicit information regarding pattern and frequency of defecation; length of time to evacuate; rectal sensation; desire to defecate; and possible episodes of fecal incontinence, constipation or defecation initiation (digitation, suppository use) [16]. Sexual history should investigate symptoms of genital or sexual dysfunction, presence of sensation in genital area, lack of desire (loss of libido), difficulty in achieving orgasm, possible dyspareunia in females and erectile dysfunction or ejaculation problems (premature, delayed, retrograde, anejaculation) in males.

In addition, a complete list of the patient’s medications (including over-the-counter drugs) should be obtained to determine whether individual drugs might influence the function of the bladder or urethra leading to urinary incontinence. Agents that can exacerbate incontinence include diuretics, alpha-adrenergic blockers, caffeine, and alcohol [7]. Angiotensin-converting enzyme inhibitors (ACEI) may increase coughing, leading to more frequent episodes of incontinence [17]. When appropriate, these agents should be stopped or changed to help manage the patient’s incontinence.

A well-conducted medical history should be completed with an assessment of the patient’s social situation. Accessibility to care, toileting, and supplies may be limited by financial constraints or other social factors. Family or caregiver support should be determined and the patient’s independence should be evaluated.

A proper history should aim not only to diagnose the cause and nature of bladder dysfunction but also to identify associated complications (Chaps. 10–15).

Although medical history is important and useful in screening for those with NSD, it has been shown that patient history is strongly limited in diagnosing this specific pathology [18].

A comprehensive medical history should be followed by thorough examination. It should begin with a general evaluation of mental status, cognitive impairment, obesity, physical dexterity, mobility, balance, and coordination. Special attention should be paid for mobility, as patients with impaired mobility may not have enough time to reach the toilet before incontinence occurs. Abdominal examination should be carefully and routinely performed. It should rule out diastasis recti, masses, ascites, and organomegaly, which can influence intra-abdominal pressure leading to incontinence [19]. Examination of the back may reveal skin dimples, scar, or hair tuft indicative of spinal dysraphism or the tethered cord syndrome [5]. Pelvic examination should include an evaluation for inflammation, infection, and atrophy, as chemical irritation from urinary or fecal incontinence as well as impaired sensation may substantially contribute to skin damage. Because the urethra and trigone are estrogen-dependent tissues, estrogen deficiency may also contribute to sphincter dysfunction [5]. The most common finding in patients with inadequate estrogen levels is atrophic vaginitis presented as thinning and paleness of the vaginal epithelium, loss of rugae, disappearance of the labia minora, and presence of a urethral caruncle [19]. Pelvic organ prolapse (with cystocele, urethral polyps, or rectocele) often accompanies atrophic vaginitis [17, 20–22]. The prolapse can also produce a relative obstruction of the urethra that can impair bladder emptying, thus masking or reducing the severity of symptoms. This is referred to as occult, potential, masked, or hidden SUI [23]. With reduced prolapse, SUI may become apparent or worsen [24]. When organ prolapse occurs, it should be documented with recommended methods and standards. In day-to-day clinical practice, it is currently recommended to employ the simplified pelvic organ prolapse quantification system (S-POP-Q) [25, 26]. Sensation within the genitourinary area should be assessed and documented (see Chap. 4, “Medical History and Physical Examination,” Fig. 4.​1). Digital examination of the rectum with assessment of anal sphincter tone and voluntary contraction should be performed. Evaluation of bulbocavernosal (and other spinal cord-mediated, see Chap. 4, Table 4.​4) reflexes is also important. Fecal loading of the large intestine and rectum should be described. Examination of the urethra may reveal diverticula, usually identified as a distal bulge under the urethra. Gentle massage of the area frequently produces a purulent discharge from the urethral opening. In patients with chronic indwelling catheters any abnormalities should be documented. These include traumatic hypospadias in men and bladder neck erosion in women.

As NSD patients typically complain of SUI , this condition should be carefully investigated and documented. Cough stress test objectively demonstrates leakage from the urethra simultaneously with a cough and it is diagnostic of SUI [25, 27]. Of note, negative result of the test (absence of leakage) does not exclude presence of stress incontinence [25, 27]. Delayed fluid loss is considered a negative cough stress test result and should elicit attention of cough-induced detrusor overactivity (see Chap. 7) [23]. The cough stress test is usually performed when the patient has a comfortably full bladder or following retrograde filling to a volume of at least 300 mL [28, 29]. The test can be performed in the supine or standing position. However, if done supinely and the result is negative, the test must be repeated in the standing position with the bladder filled to at least 300 mL [30]. The patient stands while wearing a pad or with his or her legs shoulder-width apart over a cloth or paper sheet on the floor to see the leakage [17]. If no leakage is observed despite patient symptoms of stress incontinence, the health care provider needs to ensure that the patient had a full bladder by measurement of voided urine volume and post-void residual [23]. Moreover, false-negative results may occur if the cough is not forceful enough, if the pelvic floor muscles contract to override urethral sphincter incompetence, or if severe prolapse masks the leakage [25, 31]. In patients with prolapse, the reduction of the prolapse should be performed [24, 27]. Nowadays, it is recommended to perform a cough stress test in all patients initially suspected for stress incontinence [30]. A modification of the cough stress test is the supine empty stress test. After voiding, the patient is placed in the supine position and asked to perform cough and Valsalva straining maneuvers. A positive test is recorded if urethral leakage is observed from the meatus coincident during any maneuver [32]. Although this test has not been found to be reliable nor validated in neurogenic patients, available data suggest that when the result is negative (no leakage), intrinsic sphincter deficiency is less likely to exist [30, 33].

Although NSD has been associated with a fixed, well-supported urethra, in some patients NSD can be present in association with urethral hypermobility. Thus, SUI due to NSD may be additionally aggravated. Urethral hypermobility refers to the excessive downward displacement of the urethra during Valsalva [25]. The Q-tip (cotton swab) test has been proposed to quantitate objectively the degree of urethral hypermobility. It is performed by inserting a lubricated cotton tipped swab into the urethra to the level of the urethrovesical junction of a patient in the lithotomy position (Fig. 9.1) [34]. Then, the angle of the swab compared with horizontal is assessed. Next, the patient coughs or strains, and the change in the angle of the swab is noted [25, 35]. Hypermobility is defined as a Q-tip angle of more than 30° from horizontal [35]. Clinicians should be aware that Q-tip test is not standardized or reproducible, since there is no control of the amount of pressure generated when the patient strains [5].

Manual urethral support may help to distinguish between intrinsic sphincter deficiency and urethral hypermobility (descent of the bladder neck). The test, known as the Bonney test , manually supports the anterior vaginal wall, correcting urethral hypermobility (Fig. 9.2) [5]. The goal of the test should not be to elevate the anterior vaginal wall but to prevent its descent. The index and middle fingers are placed on both sides of the urethra to support the bladder neck. If no urine leaks on stress, incontinence seems to be caused by descent of the bladder neck. If urine still leaks, incontinence due to intrinsic sphincter deficiency is highly suspected. However, there is a tendency to occlude the urethra simultaneously with correction of urethral hypermobility. The use of a ring forceps instead of fingers may lower the risk of this occlusion. Similarly to the Q-tip test, the Bonney test is not standardized or reproducible, and absence of urine leakage does not exclude intrinsic sphincter deficiency.

More recently, Thubert et al. have described a simple clinical test that involves gentle downward traction of the posterior vaginal wall provided by a split speculum performed with the bladder filled with 400 mL of saline in a supine position [36]. A positive test (leakage demonstrated during the procedure) was shown to correlate with intrinsic sphincter deficiency (defined as maximal urethral closure pressure <20 cm H₂O) with a positive predictive value of 94.67%. Note that the test has not yet been validated in neurological patients.

In neurologically impaired patients who present with SUI, assessment of pelvic floor muscle strength should also be conducted. It can easily be performed by instructing the patient to squeeze (contract) their pelvic floor muscles and then vaginally palpating the effect [30, 33].

Clinicians should not forget about pulmonary and cardiovascular assessment in patients suspected of SUI due to NSD. The pulmonary examination should rule out any possible cause of chronic cough. The cardiovascular examination should look for evidence of volume overload (edema) that might lead to increased urine flow and aggravate incontinence.

A bladder diary can provide an accurate record of urinary output, average voided volume, frequency of voiding, frequency and nature (precipitating events) of incontinent episodes, as well as type and volume of fluid intake. Evaluation of symptoms and assessment of impact on quality of life can be facilitated by the use of validated questionnaires, both condition-specific instruments and general validated questionnaires. Urinalysis and/or urine culture are vital to assessing the incontinent patient with neurogenic lower urinary tract dysfunction and should be obtained to rule out urinary tract infection, hematuria, proteinuria, and glycosuria. Blood chemistry, including assessment of serum creatinine level, helps to evaluate the patient’s overall condition. The pad-weighing test helps to assess the severity of incontinence. Upper tract studies must also be considered in high-risk patients, specifically those with spinal cord injuries and spina bifida. Post-voiding residual volume, free flowmetry, bladder ultrasound, cystoscopy, computed tomography, magnetic resonance imaging, nuclear renogram, and voiding cystourethrography should be performed when clinically indicated, based on patient history as well as relevant symptoms and signs. Details regarding discussed tests are presented in Chap. 7.

Urodynamic testing provides objective data of NSD. Low maximal urethral closure pressure (MUCP) (<20 cm H₂O) and low abdominal leak point pressure (ALPP) (<60 cm H₂O) are commonly used as indicators of intrinsic sphincter deficiency [8, 37–40]. Physicians should bear in mind that it is difficult to make these values absolute cutoffs, thus discrepancies in the literature do exist [38]. Furthermore, there is a lack of true consensus on methodologies for measuring MUCP and ALPP [40]. The value of MUCP depends on the type, size, and rigidity of the urethral catheter, patient position, bladder volume, withdrawal speed, and rate of infusion if fluid-perfused catheters are used, and orientation of urethral sensor(s) if micro tip catheters are used [41]. The measurement of ALPP depends on patient position, bladder volume, size of any catheter in the urethra used to measure intravesical pressure, baseline pressure used, speed of response in detecting leakage from the meatus, and how the patient increases abdominal pressure [42].

The high-pressure zone of the mid-urethra produces MUCP. If this area is deficient, incontinence may occur. MUCP is the maximum difference between the maximum urethral pressure and the intravesical pressure [4]. Typically, MUCP is measured at rest, as opposed to ALPP, which is measured during an increase in intra-abdominal pressure and simulates the real world scenario that leads to leakage [38].

ALPP is the intravesical pressure at which urine leakage occurs due to increased abdominal pressure in the absence of a detrusor contraction [4]. ALPP can be induced either by cough (cough leak point pressure) or by Valsalva (Valsalva leak point pressure). It has been shown that cough leak point pressure is typically larger than the Valsalva leak point pressure, and the latter parameter demonstrates less variability in provoking SUI [43, 44]. Therefore, some experts suggest that Valsalva maneuver is more reliable for assessing intrinsic sphincter deficiency than cough [8]. Of note, a recently published update of Good Urodynamic Practices and Terms by the International Continence Society introduced the single term “leak point pressure” [45]. The leak point pressure (LPP) is the pressure (spontaneous or provoked) that has caused fluid to be expelled from the bladder at the moment that it is visible outside the urethra (may also be used for extra-urethral urine loss or stoma). This may refer to abdominal, cough or Valsalva leak point pressure. Provocation and pressure recording site (“type of LPP”) should be reported. Intravesical volume can affect the LPP measurement if it is either too high or too low. It is recommended to assess the LPP for the first time at a bladder volume of 150 mL and then re-test at volumes of 200–300 mL [39, 46]. Re-testing can be performed every 50–100 mL until SUI is elicited and a combination of cough and Valsalva can be used to reproduce signs of urinary leakage [47].

As SUI can also be caused by urethral hypermobility, urodynamics may help to distinguish between intrinsic sphincter deficiency and urethral hypermobility. It has been proposed that ALPP of 60 cm H₂O or less indicates a significant degree of intrinsic sphincter deficiency , whereas ALPP of 90 cm H₂O or more is usually associated with pure urethral hypermobility. ALPP values between 60 and 90 cm H₂O form a gray area in which hypermobility and intrinsic sphincter deficiency usually coexist [48].

Video-urodynamics gives a more precise view of the bladder neck during filling and voiding. Many authors consider video-urodynamics as an optimum method for the diagnosis of intrinsic sphincter deficiency (leakage without urethral hypermobility), particularly in neurological patients [8]. Observation of an open bladder neck and proximal urethra seen on video imaging may be of value for proper diagnosis of NSD [40, 49]. Fluoroscopy can also be used to capture images during urinary leakage of small amounts, undetectable with conventional urodynamics. However, additional costs and the requirements of radiological equipment make this test impractical or even unavailable at some centers.

Figure 9.3 presents an example of urodynamics in a patient with NSD [47].

Pelvic floor muscle therapy aims to strengthen and to improve the functional activity of the pelvic floor muscles, which ameliorates the symptoms of SUI [51]. A recently published study on standardized pelvic floor exercises (12-week course) for improvement of SUI in women with intrinsic sphincter deficiency has shown that this specific group of patients benefits subjectively and objectively from this modality [52]. However, authors of this paper did not reveal the underlying causes of intrinsic sphincter deficiency . A study by McClurg et al. demonstrated concurrent results in patients with multiple sclerosis suffering from SUI [53]. It is clear that physiotherapy cannot be universally applied but may be taken into account in willing patients with an ability to contract the pelvic floor muscles since it has no deleterious side effects . Individual therapy in pelvic floor rehabilitation is a necessity and should be tailored to the patient’s capabilities.

The surgical approach for NSD aims to increase the bladder outlet resistance but may also cause high intravesical pressure. Therefore, surgery is recommended when the detrusor activity can be controlled and when no significant vesicoureteral reflux is present [16]. Regardless of the type of procedure, simultaneous or delayed bladder augmentation and intermittent catheterization may sometimes be necessary. A recent meta-analysis, evaluating all surgical treatment options for neurogenic SUI, demonstrated that in neurogenic individuals complication rates and reoperation rates are higher and success rates are lower compared to non-neurogenic patients [54]. Artificial urinary sphincter (AUS) had the highest percentage of success, followed by urethral sling procedures, compared to the urethral bulking agents, which reported the highest rate of failure.

AUS should be considered in particular for NSD patients with good bladder capacity, proper bladder compliance, no indications for augmentation cystoplasty , spontaneous voiding without the assistance of a catheter, adequate manual efficiency and dexterity, as well as intellectual ability and adequate cognitive function to operate the device [3, 68]. Pre-operative endoscopic evaluation is highly recommended, as unrecognized urethral pathology can complicate surgical implantation and possibly affect expectations of long-term outcomes.

Nowadays, the most frequently implanted AUS worldwide is the AMS800 device (Boston Scientific, Marlborough MA, USA) (Fig. 9.6) [69]. A recently conducted consensus conference on AUS developed the recommendations regarding indications, management/implantation, and follow-up/revision of AMS800^™ [70]. Report of this conference with well-developed guidelines undoubtedly constitute a reference document and can substantially help urologists in their day-to-day clinical practice.

Authors of this comprehensive document reported that pre-operative prophylactic antibiotics should be administered within 60 min of the incision. Moreover, all efforts should be made to ensure low bacterial counts at the time of AUS placement. All infection sites, including the urinary tract, should be treated before the procedure, to protect the operative field from potential bacterial contamination [71]. Skin bacterial counts should also be lowered with immediate pre-operative skin preparation. Surgery for AUS implantation may be performed either in lithotomy or supine position. Surgeons should be permitted their choice of razors or clippers for pre-operative preparation of the male genitalia. Then, skin preparation with chlorhexidine-alcohol (superior to povidone-iodine) needs to be performed. Furthermore, 5-min pre-operative, topical antimicrobial scrub is recommended. The perineal incision is preferred for AUS cuff placement but in some patients with spine or limb deformities or neuro-motor conditions, the transscrotal incision may be a useful alternative to perineal cuff placement. Urethral dissection should be performed sharply with direct visualization, confirming the integrity of the urethra. There are two implantation approaches, peri-urethral and trans-corporal. Whereas the first is considered as the standard approach, the second may be considered under certain circumstances, such as patients presenting with a history of previous urethral surgery or in those with urethral abnormalities. After dissection, the surgeon determines the proper cuff size to be used by measuring the circumference of the tissue around the urethra or bladder neck. If the measurement is between sizes, the larger size should be chosen. In neurological patients, the majority of available studies prefer placement at the bladder neck (in male around the prostate) rather than bulbar urethra [3]. Bladder neck placement can reduce the risk of AUS damage when rigid cystoscopy has to be performed due to complications of neurogenic bladder. As neurological patients frequently need additional intermittent catheterization, AUS location at the bladder neck has been reported to limit the risk of urethral erosion in the context of long-term intermittent catheterization [72]. Moreover, in wheelchair-bound individuals, extended sitting may produce elevated pressure on the bulbar urethra, increasing the risk of erosion due to decubitus ulcers when the cuff is placed in this area. A study of 51 males with NSD who underwent AUS implantation with cuff placement at the bladder neck reported satisfying results in the majority of patients [66]. After implantation, prosthesis may be filled with either sterile saline or contrast filling solution. A pressure-regulating balloon of 61–70 cm H₂O is most often used but in patients with bladder neck cuff, the 71–80 cm H₂O pressure-regulating balloon may be preferred, depending on surgeon preference. The pressure-regulating balloon should be filled with 22–27 cc fluid while the cuff is empty. After filling, the pressure-regulating balloon must be placed under the abdominal wall fascia and may be inserted into the retro-pubic space or into a space created between the abdominal musculature and the transversalis fascia. The next step involves pump placement in the dependent portion of the scrotum, anterior to the testicle, to ensure that patients can access it postoperatively. When all components have been implanted, the required connections need to be made. Use of the AMS Quick Connect (Boston Scientific, Marlborough MA, USA) in all AUS placement is recommended. The final stage of AUS implantation involves inspection of the urethra for potential injury and intra-operative assessment of efficacy. The device should be cycled several times under direct visualization to ensure adequate function of the hydraulic mechanism. Postoperative care includes short-term catheterization (less than 14 Fr, removed after a brief period, usually overnight), oral analgesia, and/or stool softener, as well as proper education of physical activity and lifting (limited physical activity during the 6-week postoperative period). Standard administration of postoperative antibiotics is not currently recommended. AUS should be activated at 4–6 weeks post-implantation. Physical long-term follow-up should be ensured between 3 and 6 months postoperatively and periodically thereafter, at least yearly. Mandatory evaluation should include assessment of symptoms consistent with device malfunction, infection, and/or erosion.

For neurologically impaired patients, modified implantation techniques have been proposed. One proposal, investigated in patients after spinal cord injury, suggested that pump replacement with a subcutaneous port enables adjustment of the cuff pressure also postoperatively and omits the necessity to repetitively activate the pump. During 8-year follow-up, this modification proved to be successful, reliable, safe, and cost-effective [73]. Nevertheless, this technique remains a single center experience on 51 patients. The second proposal, with the AUS cuff placement at the bladder neck without implantation of both the reservoir and the pump, achieved only 31% continence rate [74]. Recent studies also report the feasibility of implanting the AUS using the da Vinci robot [72]. Although these modifications may help to achieve better results, they cannot be recommended for daily clinical practice.

It has been shown that individuals with neurogenic lower urinary tract dysfunction have higher numerical complication rate vs. post-prostatectomy patients [75]. Possible complications include erosion (cuff erosion into the urethra and pump erosion into the scrotum/labia), urethral atrophy, infection, and mechanical/device-related failure leading to reoperation with revision, replacement, or removal in 7–100% of implanted cases [67]. Specific complications of AUS placement in a group of neurogenic patients, mainly because of retro-pubic and bladder neck dissections, may also include bladder neck, urethral, and rectal perforations [60, 65]. The mean reoperation rate for the AUS has been estimated as 51%, which is a relatively high percentage in comparison to the reoperation rate of 27% in non-neurogenic patients [54]. AUS erosion is the major cause of AUS removal in a contemporary neurogenic bladder series, with a reported rate from 6 to 31% [61, 76]. AUS removal resulting from sphincter infection has been found to be more frequent (up to 8%) in neurogenic than in non-neurogenic persons [73]. If AUS infection is suspected, cystourethroscopy should be undertaken to evaluate the urethra for cuff erosion. In gross or persistent infections, the entire device should be explanted as soon as it is clinically safe [70]. Note that the AUS infection rate does not appear to increase in patients who catheterize compared to those who void spontaneously or who empty their bladders with the Credé maneuver [77]. However, intermittent catheterization frequently leads to high-level erosion due to repeated urethral traumas [60, 78]. This emphasizes the importance of proper patient education with the catheterization technique preceded by the AUS deactivation procedure. In some patients, simultaneous augmentation cystoplasty should be considered and can be done safely at the time of AUS implantation [3].

It is currently recommended that neurogenic patients who receive AUS must undergo long-term urological follow-up with UDS monitoring and upper tract imaging to detect upper urinary tract deterioration [70]. A potential risk of AUS placement in patients with NSD is the new onset of detrusor overactivity. This complication occurs frequently, in about 30% of patients after AUS insertion, and the onset may be delayed by several years [79]. Studies reported that 4–42% of AUS recipients with neurogenic lower urinary tract dysfunction may eventually require augmentation cystoplasty [60, 76, 80]. This stresses the need for lifelong surveillance with urodynamic control after AUS placement in patients with NSD [80].

A median AUS lifespan is about 5–7 years [81–83]. Since people with neurogenic lower urinary tract dysfunction are often comparatively young, AUS should be considered with caution in young individuals, as it is highly probable that AUS replacement will be needed [49]. Because each revision requires replacement of the AUS cuff to a different location along the urethra, lifetime management with the AUS may not be possible if implemented in relatively young patients [3].