|Full Text Guidelines||Summary of Changes||Scientific Publications & Appendices||Pocket Guidelines||Archive||Panel|
The European Association of Urology (EAU) Neuro-Urology Guidelines aim to provide information for clinical practitioners on the incidence, definitions, diagnosis, therapy, and follow-up of neuro-urological disorders. These Guidelines reflect the current opinion of experts in this specific pathology and represent a state-of-the art reference for all clinicians, as of the publication date.
The terminology used and the diagnostic procedures advised throughout these Guidelines follow the recommendations for investigations of the lower urinary tract (LUT) as published by the International Continence Society (ICS) [1-3]. Readers are advised to consult other EAU Guidelines that may address different aspects of the topics discussed in this document.
It must be emphasised that clinical guidelines present the best evidence available to the experts but following guideline recommendations will not necessarily result in the best outcome. Guidelines can never replace clinical expertise when making treatment decisions for individual patients, but rather help to focus decisions - also taking personal values and preferences/individual circumstances of patients into account. Guidelines are not mandates and do not purport to be a legal standard of care.
The EAU Neuro-Urology Guidelines Panel consists of an international multidisciplinary group of neuro-urological experts. All experts involved in the production of this document have submitted potential conflict of interest statements which can be viewed on the EAU website: http://www.uroweb.org/guideline/neuro-urology/.
A quick reference document, the Pocket Guidelines, is available in print and as an app for iOS and Android devices. These are abridged versions which may require consultation with the full text version. A guideline summary has also been published in European Urology . All are available through the EAU website: http://www.uroweb.org/guideline/neuro-urology/.
The EAU published the first Neuro-Urology Guidelines in 2003 with updates in 2008, 2014, and 2017. This 2020 document represents a limited update of the 2019 publication. The literature was assessed for all chapters.
The function of the LUT is mainly storage and voiding of urine, which is regulated by the nervous system that coordinates the activity of the urinary bladder and bladder outlet. The part of the nervous system that regulates LUT function is disseminated from the peripheral nerves in the pelvis to highly specialised cortical areas. Any disturbance of the nervous system involved, can result in neuro-urological symptoms. The extent and location of the disturbance will determine the type of LUT dysfunction, which can be symptomatic or asymptomatic. Neuro-urological symptoms can cause a variety of long-term complications; the most significant being deterioration of renal function. Since symptoms and long-term complications do not correlate , it is important to identify patients with neuro-urological symptoms, and establish if they have a low or high risk of subsequent complications. The risk of developing upper urinary tract (UUT) damage and renal failure is much lower in patients with slowly progressive non-traumatic neurological disorders than in those with spinal cord injury or spina bifida . In summary, treatment and intensity of follow-up examinations are based on the type of neuro-urological disorder and the underlying cause.
For the 2020 Neuro-Urology Guidelines, new and relevant evidence has been identified, collated and appraised through a structured assessment of the literature. A broad and comprehensive literature search, covering all sections of the Neuro-Urology Guidelines was performed. Databases searched included Medline, EMBASE, and the Cochrane Libraries, covering a time frame between May 31st 2018 and 1st April 2019. A total of 754 unique records were identified, retrieved and screened for relevance. A detailed search strategy is available online: http://uroweb.org/guideline/neuro-urology/?type=appendices-publications.
For each recommendation within the guidelines there is an accompanying online strength rating form, the bases of which is a modified GRADE methodology [7,8]. Each strength rating form addresses a number of key elements namely:
- the overall quality of the evidence which exists for the recommendation, references used in this text are graded according to a classification system modified from the Oxford Centre for Evidence-Based Medicine Levels of Evidence ;
- the magnitude of the effect (individual or combined effects);
- the certainty of the results (precision, consistency, heterogeneity and other statistical or study related factors);
- the balance between desirable and undesirable outcomes;
- the impact of patient values and preferences on the intervention;
- the certainty of those patient values and preferences.
These key elements are the basis which panels use to define the strength rating of each recommendation. The strength of each recommendation is represented by the words ‘strong’ or ‘weak’ . The strength of each recommendation is determined by the balance between desirable and undesirable consequences of alternative management strategies, the quality of the evidence (including certainty of estimates), and nature and variability of patient values and preferences.
Additional information can be found in the general Methodology section of this print, and online at the EAU website; http://www.uroweb.org/guideline/. A list of associations endorsing the EAU Guidelines can also be viewed online at the above address.
Publications ensuing from panel-led systematic reviews have all been peer-reviewed. The 2015 Neuro-Urology Guidelines were subject to peer review prior to publication.
Neuro-urological symptoms may be caused by a variety of diseases and events affecting the nervous system controlling the LUT. The resulting neuro-urological symptoms depend predominantly on the location and the extent of the neurological lesion. There are no exact figures on the overall prevalence of neuro-urological disorders in the general population, but data are available on the prevalence of the underlying conditions and the relative risk of these for the development of neuro-urological symptoms. It is important to note that the majority of the data shows a very wide range of prevalence/incidence. This reflects the variability in the cohort (e.g. early or late stage disease) and the frequently small sample sizes, resulting in a low level of evidence in most published data (summarised in Table 1).
Table 1: Epidemiology of Neuro-Urological Disorders
Suprapontine and pontine lesions and diseases
Frequency in General Population
Type and Frequency of Neuro-Urological Symptoms
450 cases/100,000/yr (Europe) , 10% of cardiovascular mortality.
Nocturia - overactive bladder (OAB) - urgency urinary incontinence (UUI) - detrusor overactivity (DO), other patterns less frequent . 57-83% of neuro-urological symptoms at 1 month post-stroke, 71-80% spontaneous recovery at 6 months . Persistence of urinary incontinence (UI) correlates with poor prognosis .
Alzheimer’s disease (80%),
Vascular (10%), Other (10%).
6.4% of adults > 65 yrs .
OAB - UUI – DO 25% of incontinence in Alzheimer’s
Parkinsonian syndrome (PS)
Idiopathic Parkinson’s disease (IPD): 75-80% of PS.
Non-IPD: Parkinson’s-plus (18%):
- Multiple system atrophy (MSA),
- Progressive supranuclear palsy,
- Corticobasal degeneration,
- Dementia with Lewy bodies.
Secondary Parkinson’s (2%)
Second most prevalent neurodegenerative disease after Alzheimer’s disease.
Rising prevalence of IPD with age .
MSA is the most frequent non-IPD PS.
Urinary symptoms affect 50% at onset, with urgency and nocturia being the most common. Patients with urinary symptoms at presentation have worse disease progression in Parkinson’s disease .
Infections account for a major cause of mortality in MSA .
Impaired detrusor contractility with post-void residual (PVR) > 150 mL seems to be the urodynamic finding distinguishing MSA from IPD [21-23].
26.8/100,000/yr in adults (> 19 yrs), (17.9 benign, 8.9 malignant) .
Incontinence occurs mainly in frontal location (part of frontal syndrome or isolated in frontal location) .
Cerebral palsy: 3.1-3.6/1,000 in children aged 8 yrs .
46% of patients with cerebral palsy suffer from UI, with 85% of patients having abnormal urodynamic studies (NDO most common 59%). Upper tract deterioration is rare (2.5%) .
Traumatic brain injury
44% storage dysfunction,
38% voiding dysfunction,
60% urodynamic abnormalities .
Normal pressure hydrocephalus
0.5% of the population > 60, up to 2.9% of those > 65 .
Classic triad of gait and cognitive disturbance along with UI. Incontinence affects 98-100% of patients .
Lesions and diseases between caudal brainstem and sacral spinal cord
Spinal cord injury (SCI)
Prevalence of traumatic SCI in
developed countries ranges from 280 to 906/million .
Neurogenic detrusor overactivity (NDO) and detrusor sphincter dyssynergia (DSD) (up to 95%) and detrusor underactivity (up to 83%) depending on the level of the lesion .
Spina bifida (SB)
Spina bifida 3-4/10,000
Lumbar and lumbosacral form are the most common (60%) .
Bladder function is impaired in up to 96% of SB patients . Over 50% of patients are incontinent . Patients with open and closed defects can have equally as severe neurogenic lower urinary tract dysfunction .
Lesions and diseases of the peripheral nervous system
Lumbar canal stenosis
Male (5%) and female (3%) > 35 yr have had a lumbosciatic
episode related to disc prolapse.
Incidence: approx. 5/100,000/yr
More common in females > 45 yr.
26% difficulty to void and acontractile detrusor .
Detrusor underactivity (up to 83%) .
Tarlov cysts: early sensation of filling (70%), NDO (33%), urethral instability (33%) and stress urinary incontinence (SUI) (33%) .
Iatrogenic pelvic nerve lesions
Cervical cancer (multimodal
therapy, radiotherapy and surgery).
After abdomino-perineal resection: 50% urinary retention.
After total mesorectal excision: 10-30% voiding dysfunction .
Other causes of peripheral
neuropathy causing neuro-urological symptoms: alcohol abuse; lumbosacral zona and genital herpes; Guillain Barré syndrome.
Worldwide, prevalence of
pharmacologically treated diabetes 8.3% .
Urgency/frequency +/- incontinence .
Hyposensitive and detrusor
underactivity at later phase .
Disseminated central diseases
Multiple sclerosis (MS)
Prevalence: 83/100,000 in Europe .
10% of MS patients present with
voiding dysfunction at disease onset, 75% of patients will develop it after 10 yrs of MS .
DO: 86% .
DSD: 35% .
Detrusor underactivity: 25% .
Relevant definitions can be found in the general ICS standardisation reports [2,3,44]. Supplementary online Tables S1 and S2 list the definitions from these references, partly adapted, and other definitions considered useful for clinical practice: https://uroweb.org/guideline/neuro-urology/?type=appendices-publications.
The normal physiological function of the LUT depends on an intricate interplay between the sensory and motor nervous systems. When diagnosing neuro-urological symptoms, the aim is to describe the type of dysfunction involved. A thorough medical history, physical examination and bladder diary are mandatory before any additional diagnostic investigations can be planned. Results of the initial evaluation are used to decide the patient’s long-term treatment and follow-up.
The pattern of LUT dysfunction following neurological disease is determined by the site and nature of the lesion. A very simple classification system for use in daily clinical practice to decide on the appropriate therapeutic approach is provided in Figure 1 .
Figure 1: Patterns of lower urinary tract dysfunction following neurological disease
The pattern of LUT dysfunction following neurological disease is determined by the site and nature of the lesion. Panel (A) denotes the region above the pons, panel (B) the region between the pons and the sacral cord and panel (C) the sacral cord and infrasacral region. Figures on the right show the expected dysfunctional states of the detrusor-sphincter system. Figure adapted from Panicker et al.  with permission from Elsevier.
PVR = post-void residual.
Early diagnosis and treatment are essential in both congenital and acquired neuro-urological disorders . This helps to prevent irreversible changes within the LUT, even in the presence of normal reflexes [46,47]. Furthermore, urological symptoms can be the presenting feature of neurological pathology [48,49]. Early intervention can prevent irreversible deterioration of the LUT and UUT . Long term follow up (life-long) is mandatory to assess risk of UUT damage, renal failure and bladder cancer [51-53].
History taking should include past and present symptoms and disorders (Table 4). It is the cornerstone of evaluation, as the answers will aid selection of diagnostic investigations and treatment options.
- In non-traumatic neuro-urological patients with an insidious onset, a detailed history may find that the condition started in childhood or adolescence .
- Urinary history consists of symptoms associated with both urine storage and voiding.
- Bowel history is important because patients with neuro-urological symptoms may also have related neurogenic bowel dysfunction .
- Sexual function may be impaired because of the neuro-urological condition .
- Special attention should be paid to possible warning signs and symptoms (e.g. pain, infection, haematuria and fever) requiring further investigation.
- Patients with SCI usually find it difficult to report urinary tract infection (UTI)-related symptoms accurately [57,58].
- The presence of urinary, bowel and sexual symptoms without neurological symptoms could be suggestive of an underlying neurological disease or condition.
- Ambulatory status after acute SCI does not predict presence or absence of unfavourable urodynamic parameters .
Table 4: History taking in patients with suspected neuro-urological disorder
Childhood through to adolescence and into adulthood
Hereditary or familial risk factors
Specific female: menarche (age); this may suggest a metabolic disorder
History of diabetes
Diseases, e.g. multiple sclerosis, parkinsonism, encephalitis, syphilis
Accidents and operations, especially those involving the spine and central nervous system
Lifestyle (smoking, alcohol and drugs); may influence urinary, sexual and bowel function
Quality of life
Specific urinary history
Onset of urological history
Relief after voiding; to detect the extent of a neurological lesion in the absence of obstructive uropathy
Initiation of micturition (normal, precipitate, reflex, strain, Credé)
Interruption of micturition (normal, paradoxical, passive)
Mode and type of voiding (catheterisation)
Frequency, voided volume, incontinence, urgency episodes
Genital or sexual dysfunction symptoms
Sensation in genital area
Specific male: erection, (lack of) orgasm, ejaculation
Specific female: dyspareunia, (lack of) orgasm
Frequency and faecal incontinence
Desire to defecate
Initiation of defecation (digitation)
Acquired or congenital neurological condition
Mental status and comprehension
Neurological symptoms (somatic and sensory), with onset, evolution and any treatment
Spasticity or autonomic dysreflexia (especially in lesions at or above level Th 6)
Mobility and hand function
Bladder diaries provide data on the number of voids, voided volume, pad weight and incontinence and urgency episodes [3,60]. Although a 24-hour bladder diary (recording should be done for three consecutive days) is reliable in women with UI [61,62], no research has been done on bladder diaries in neuro-urological patients. Nevertheless, bladder diaries are considered a valuable diagnostic tool.
An assessment of the patient’s present and expected future quality of life (QoL) is important to evaluate the effect of any therapy. Quality of life is an essential aspect of the overall management of neuro-urological patients, for example when evaluating treatment related changes on a patient’s QoL . The type of bladder management has been shown to affect health-related QoL (HRQoL) in patients with SCI [64,65] and MS , as does the presence or absence of urinary and faecal incontinence . Other research has also highlighted the importance of urological treatment and its impact on the urodynamic functionality of the neuro-urological patient in determining patient QoL .
In recent years a proliferation in the number of questionnaires to evaluate symptoms and QoL has been seen. Condition-specific questionnaires can be used to assess symptom severity and the impact of symptoms on QoL. A patient’s overall QoL can be assessed using generic questionnaires. It is important that the questionnaire of choice has been validated in the neuro-urological population, and that it is available in the language that it is to be used in.
Three condition-specific questionnaires for urinary or bowel dysfunction and QoL have been developed specifically for adult neuro-urological patients . In MS and SCI patients the Qualiveen [70,71] is validated and can be used for urinary symptoms. A short form of the Qualiveen is available [70,71] and it has been translated into various languages [72-77]. Although several objective and subjective tools have been used to assess the influence of neurogenic bladder on QoL in SCI, the Quality life index-SCI and Qualiveen are the only validated condition-specific outcomes that have shown consistent sensitivity to neurogenic bladder . The Neurogenic Bladder Symptom Score (NBSS) has been validated in neurological patients to measure urinary symptoms and their consequences [79,80]. The QoL scoring tool related to Bowel Management (QoL-BM)  can be used to assess bowel dysfunction in MS and SCI patients.
In addition, sixteen validated questionnaires that evaluate QoL and asses urinary symptoms as a subscale or question in neuro-urological patients have been identified [82,83] (Table 5). The condition-specific Incontinence-Quality of Life (I-QoL) questionnaire which was initially developed for the non-neurological population has now also been validated for neuro-urological patients .
A patient’s overall QoL can be assessed by generic HRQoL questionnaires, the most commonly used being the I-QOL, King’s Health Questionnaire (KHQ), or the Short Form 36-item and 12-item Health Survey Questionnaires (SF-36, SF-12) . In addition, the quality-adjusted life year (QALY), quantifies outcomes, by weighing years of life spent in a specified health state, adjusted by a factor representing the value placed by society or patients on their specific health state .
No evidence was found for which validated questionnaires are the most appropriate for use, since no quality criteria for validated questionnaires have been assessed .
Table 5: Patient questionnaires
Underlying neurological disorder
MS, SCI, Congenital neurogenic bladder
In addition to a detailed patient history, attention should be paid to possible physical and intellectual disabilities with respect to the planned investigations [99,100]. Neuro-urological status should be described as completely as possible (Figure 2) . Patients with a high spinal cord lesion or supraspinal neurological lesions may suffer from a significant drop in blood pressure when moved into a sitting or standing position. All sensations and reflexes in the urogenital area must be tested . Furthermore, detailed testing of the anal sphincter and pelvic floor functions must be performed (Figure 2) [6,101]. It is essential to have this clinical information to reliably interpret later diagnostic investigations.
Additionally, urinalysis, blood chemistry, ultrasonography, residual and free flowmetry and incontinence quantification should be performed as part of the routine assessment of neuro-urological patients [6,102].
Autonomic dysreflexia (AD) is a sudden and exaggerated autonomic response to various stimuli in patients with SCI or spinal dysfunction. It generally manifests at or above level Th 6. The stimulus can be distended bladder or bowel. For example, iatrogenic stimuli during cystoscopy or urodynamics can trigger AD . It can also be secondary to sexual stimulation or a noxious stimulus, e.g. infected toe nail or pressure sore. Autonomic dysreflexia is defined by an increase in systolic blood pressure > 20 mmHg from baseline  and can have life-threatening consequences if not properly managed.
Figure 2: Lumbosacral dermatomes, cutaneous nerves, and reflexes
The physical examination includes testing sensations and reflexes mediated through the lower spinal cord. Abnormal findings would suggest a lesion affecting the lumbosacral segments; mapping out distinct areas of sensory impairment helps to further localise the site of the lesion. Distribution of dermatomes (areas of skin mainly supplied by a single spinal nerve) and cutaneous nerves over the perianal region and back of the upper thigh (A), the perineum  (B), male external genitalia  (C) and root values of lower spinal cord reflexes (D). Figure adapted from Panicker et al.  with parts A-C adapted from Standring , both with permission from Elsevier.
Table 6: Neurological items to be specified
Sensation S2-S5 (both sides)
Type (light touch/pin prick)
Knee and ankle reflexes
Plantar responses (Babinski)
Anal sphincter tone
Voluntary contractions of anal sphincter and pelvic muscles (increased/normal/reduced/absent)
Descensus (prolapse) of pelvic organs
Summary of evidence
Early diagnosis and treatment are essential in both congenital and acquired neuro-urological disorders to prevent irreversible changes within the LUT.
An extensive general history is the basis of evaluation focusing on past and present symptoms including urinary, sexual, bowel and neurological functions.
Assessment of present and expected future QoL is an essential aspect of the overall management of neuro-urological patients and is important to evaluate the effect of any therapy.
Quality of life assessment should be completed with validated QoL questionnaires for neuro-urological patients.
Bladder diaries provide data on the number of voids, voided volume, pad weight and incontinence and urgency episodes.
Take an extensive general history, concentrating on past and present symptoms.
Take a specific history for each of the four mentioned functions - urinary, bowel, sexual and neurological.
Pay special attention to the possible existence of alarm signs (e.g. pain, infection, haematuria, fever) that warrant further specific diagnosis.
Assess quality of life when evaluating and treating the neuro-urological patient.
Use available validated tools including the Qualiveen and I-QoL for urinary symptoms and the QoL-BM for bowel dysfunction in multiple sclerosis and spinal cord injury patients. In addition, generic (SF-36 or KHQ) questionnaires can be used.
Use MSISQ-15 and MSISQ-19 to evaluate sexual function in multiple sclerosis patients.
Acknowledge individual patient disabilities when planning further investigations.
Describe the neurological status as completely as possible, sensations and reflexes in the urogenital area must all be tested.
Test the anal sphincter and pelvic floor functions.
Perform urinalysis, blood chemistry, bladder diary, residual and free flowmetry, incontinence quantification and urinary tract imaging.
I-QoL = Incontinence Quality of Life Instrument; QoL-BM = Quality of Life Bowel Management scoring tool; KHQ = King’s Health Questionnaire; SF-36 = Short Form 36-item Health Survey Questionnaires; MSISQ 15/19 = Multiple Sclerosis Intimacy and Sexuality Questionnaire 15/19 question version.
Urodynamic investigation is the only method that can objectively assess the function and dysfunction of the LUT. In neuro-urological patients, invasive urodynamic investigation is even more challenging than in general patients. Any technical source of artefacts must be critically considered. It is essential to maintain the quality of the urodynamic recording and its interpretation . Same session repeat urodynamic investigations are crucial in clinical decision making, since repeat measurements may yield completely different results .
In patients at risk of AD, it is advisable to measure blood pressure during the urodynamic study [109,110]. The rectal ampulla should be empty of stool before the start of the investigation. All urodynamic findings must be reported in detail and performed, according to the ICS technical recommendations and standards [1,111].
Free uroflowmetry and assessment of residual urine: Provides a first impression of the voiding function and is compulsory prior to planning any invasive urodynamics in patients able to void. For reliable information, it should be repeated at least two to three times . Possible pathological findings include a low flow rate, low voided volume, intermittent flow, hesitancy and residual urine. Care must be taken when assessing the results in patients unable to void in a normal position, as both flow pattern and rate may be modified by inappropriate positions.
Filling cystometry: This test is the only method for quantifying the patient’s filling function. The status of LUT function must be documented during the filling phase. However, this technique has limited use as a solitary procedure. It is much more effective combined with bladder pressure measurement during micturition and is even more effective in video-urodynamics.
The bladder should be empty at the start of filling. A physiological filling rate should be used with body-warm saline. Possible pathological findings include DO, low bladder compliance, abnormal bladder sensations, incontinence, and an incompetent or relaxing urethra. There is some evidence that a bladder capacity < 200 mL and detrusor pressures over 75 cm H2O are independent risk factors for UUT damage in patients with SCI .
Detrusor leak point pressure : Appears to have no use as a diagnostic tool. Some positive findings have been reported [113-115], but sensitivity is too low to estimate the risk to the UUT or for secondary bladder damage [116,117].
Pressure flow study: Reflects the coordination between detrusor and urethra or pelvic floor during the voiding phase. It is even more effective if combined with filling cystometry and video-urodynamics. Lower urinary tract function must be recorded during the voiding phase. Possible pathological findings include detrusor underactivity, bladder outlet obstruction (BOO), DSD, a high urethral resistance, and residual urine.
Most types of obstruction caused by neuro-urological disorders are due to DSD [118,119], non-relaxing urethra, or non-relaxing bladder neck [120,121]. Pressure-flow analysis mainly assesses the amount of mechanical obstruction caused by the urethra’s inherent mechanical and anatomical properties and has limited value in patients with neuro-urological disorders.
Electromyography (EMG): Reflects the activity of the external urethral sphincter, the peri-urethral striated musculature, the anal sphincter and the striated pelvic floor muscles. Correct interpretation may be difficult due to artefacts introduced by other equipment. In the urodynamic setting, an EMG is useful as a gross indication of the patient’s ability to control the pelvic floor. Possible pathological findings include inadequate recruitment upon specific stimuli (e.g. bladder filling, involuntary detrusor contractions, onset of voiding, coughing, Valsalva manoeuvre) suggesting a diagnosis of DSD .
Urethral pressure measurement: Has a very limited role in neuro-urological disorders. There is no consensus on parameters indicating pathological findings .
Video-urodynamics: Is the combination of filling cystometry and pressure flow studies with imaging. It is the optimum procedure for urodynamic investigation in neuro-urological disorders . Possible pathological findings include all those described in the cystometry and the pressure flow study sections, and any morphological pathology of the LUT and reflux to the UUT .
Ambulatory urodynamics: This is the functional investigation of the urinary tract, which predominantly uses the natural filling of the urinary tract to reproduce the patient’s normal activity. Although this type of study might be considered when conventional urodynamics does not reproduce the patient’s symptoms, its role in the neuro-urological patient still needs to be determined [125,126].
Triggered tests during urodynamics: Lower urinary tract function can be provoked by coughing, triggered voiding, or anal stretch. Fast-filling cystometry with cooled saline (the ‘ice water test’) will discriminate between upper and lower motor neuron lesions [127,128]. Patients with upper motor neuron lesions develop a detrusor contraction if the detrusor is intact, while patients with lower motor neuron lesions do not. However, the test does not seem to be fully discriminative in other types of patients .
Previously, a positive bethanechol test  (detrusor contraction > 25 cm H2O) was thought to indicate detrusor denervation hypersensitivity and the muscular integrity of an acontractile detrusor. However, in practice, the test has given equivocal results. A variation of this method was reported using intravesical electromotive administration of the bethanechol , but there was no published follow-up. Currently, there is no indication for this test.
The following tests are advised as part of the neurological work-up :
- electromyography (in a neurophysiological setting) of pelvic floor muscles, urethral sphincter and/or anal sphincter;
- nerve conduction studies of pudendal nerve;
- reflex latency measurements of bulbocavernosus and anal reflex arcs;
- evoked responses from clitoris or glans penis;
- sensory testing on bladder and urethra.
Other elective tests, for specific conditions, may become obvious during the work-up and urodynamic investigations.
Summary of evidence
Urodynamic investigation is the only method that can objectively assess the (dys-)function of the LUT.
Video-urodynamics is the optimum procedure for urodynamic investigation in neuro-urological disorders.
Specific uro-neurophysiological tests are elective procedures and should only be carried out in specialised settings.
Perform a urodynamic investigation to detect and specify lower urinary tract (dys-)function, use same session repeat measurement as it is crucial in clinical decision making.
Non-invasive testing is mandatory before invasive urodynamics is planned.
Use video-urodynamics for invasive urodynamics in neuro-urological patients. If this is not available, then perform a filling cystometry continuing into a pressure flow study.
Use a physiological filling rate and body-warm saline.
In many patients with neuro-urological disorders, the UUT is at risk, particularly in patients who develop high detrusor pressure during the filling phase. Although effective treatment can reduce this risk, there is still a relatively high incidence of renal morbidity [133,134]. Patients with SCI or SB have a higher risk of developing renal failure compared with patients with slowly progressive non-traumatic neurological disorders, such as MS and Parkinson’s disease (PD) .
Caregivers must be informed of this risk and instructed to watch carefully for any signs or symptoms of a possible deterioration in the patient’s renal function. In patients with poor muscle mass cystatin C based glomerular filtration rate (GFR) is more accurate in detecting chronic kidney disease than serum creatinine estimated GFR [136,137]. There are no high level evidence publications available which show the optimal management to preserve renal function in these patients .
- protection of the UUT;
- achievement (or maintenance) of urinary continence;
- restoration of LUT function;
- improvement of the patient’s QoL.
Further considerations are the patient’s disability, cost-effectiveness, technical complexity and possible complications .
Renal failure is the main mortality factor in SCI patients who survive the trauma [141,142]. Keeping the detrusor pressure during both the filling and voiding phases within safe limits significantly reduces the mortality from urological causes in these patients [143-145] and has consequently become the top priority in the treatment of patients with neuro-urological symptoms [139,140].
In patients with high detrusor pressure during the filling phase (DO, low bladder compliance), treatment is aimed primarily at conversion of an overactive, high-pressure bladder into a low-pressure reservoir despite the resulting residual urine . Reduction of the detrusor pressure contributes to urinary continence, and consequently to social rehabilitation and QoL. It is also pivotal in preventing UTIs [146,147]. However, complete continence cannot always be obtained.
Incomplete bladder emptying is a serious risk factor for UTI, high intravesical pressure and incontinence. Methods to improve the voiding process should therefore be practiced.
Bladder expression: The downwards movement of the lower abdomen by suprapubic compression (Credé) or by abdominal straining (Valsalva) leads to an increase in intravesical pressure, and generally also causes a reflex sphincter contraction [148,149]. The latter may increase bladder outlet resistance and lead to inefficient emptying. The high pressures created during these procedures are hazardous for the urinary tract [150,151]. Therefore, their use should be discouraged unless urodynamics show that the intravesical pressure remains within safe limits .
Long-term complications are unavoidable for both methods of bladder emptying . The already weak pelvic floor function may be further impaired, thus introducing or exacerbating already existing stress urinary incontinence .
Triggered reflex voiding: Stimulation of the sacral or lumbar dermatomes in patients with a upper motor neuron lesion can elicit a reflex detrusor contraction . The risk of high pressure voiding is present and interventions to decrease outlet resistance may be necessary . Triggering can induce AD, especially in patients with high level SCI (at or above Th 6) . All assisted bladder emptying techniques require low outlet resistance. Even then, high detrusor pressures may still be present. Hence, patients need dedicated education and close urodynamic and urological surveillance [151,154,155].
Note: In the literature, including some of the references cited here, the concept "reflex voiding" is sometimes used to cover all three assisted voiding techniques described in this section.
External appliances: Social continence may be achieved by collecting urine during incontinence, for instance using pads. Condom catheters with urine collection devices are a practical method for men . The penile clamp is absolutely contraindicated in case of NDO or low bladder compliance because of the risk of developing high intravesical pressure and pressure sores/necrosis in cases of altered/absent sensations.
The term bladder rehabilitation summarises treatment options that aim to re-establish bladder function in patients with neuro-urological symptoms. Strong contraction of the urethral sphincter and/or pelvic floor, as well as anal dilatation, manipulation of the genital region, and physical activity inhibit micturition in a reflex manner [140,156]. The first mechanism is affected by activation of efferent nerve fibres, and the latter ones are produced by activation of afferent fibres . Electrical stimulation of the pudendal nerve afferents strongly inhibits the micturition reflex and detrusor contraction . This stimulation might then support the restoration of the balance between excitatory and inhibitory inputs at the spinal or supraspinal level [140,158]. Evidence for bladder rehabilitation using electrical stimulation in neurological patients is mainly based on small non-comparative studies with high risk of bias.
Peripheral temporary electrostimulation: Tibial nerve stimulation and transcutaneous electrical nerve stimulation (TENS) might be effective and safe for treating neurogenic LUT dysfunction, but more reliable evidence from well-designed randomised controlled trials (RCTs) is required to reach definitive conclusions [158-160]. In post-stroke patients TENS has been shown to effectively improve urodynamic findings and QoL [161-163].
Peripheral temporary electrostimulation combined with pelvic floor muscle training and biofeedback: In MS patients, combining active neuromuscular electrical stimulation with pelvic floor muscle training and EMG biofeedback can achieve a substantial reduction of neuro-urological symptoms [164,165]. This treatment combination seems to be more effective than either therapy alone [166,167]. However, the combination of intravaginal electrostimulation and pelvic floor muscle training was not superior to pelvic floor muscle training alone in reducing urinary incontinence in women with incomplete spinal cord injury .
Intravesical electrostimulation: Intravesical electrostimulation can increase bladder capacity and improve bladder filling sensation in patients with incomplete SCI or myelomeningocele (MMC) . In patients with neurogenic detrusor underactivity, intravesical electrostimulation may also improve voiding and reduce residual volume [170,171].
Summary: To date, bladder rehabilitation techniques are mainly based on electrical or magnetic stimulation; however, there is a lack of well-designed studies.
A single, optimal, medical therapy for neuro-urological symptoms is not always available. Commonly, a combination of different therapies (e.g. intermittent catheterisation and antimuscarinic drugs) is advised to prevent urinary tract damage and improve long-term outcomes, particularly in patients with a suprasacral SCI or MS [151,174-176].
Antimuscarinic drugs: Are the first-line choice for treating NDO, increasing bladder capacity and reducing episodes of UI secondary to NDO by the inhibition of parasympathetic pathways [140,177-183]. Antimuscarinic drugs have been used for many years to treat patients with NDO [181,182,184], and the responses of individual patients to antimuscarinic treatment are variable. Despite a meta-analysis confirming the clinical and urodynamic efficacy of antimuscarinic therapy compared to placebo in adult NDO, a more recent integrative review has indicated that the information provided is still too limited for clinicians to be able to match trial data to the needs of individual patients with SCI, mainly due to the lack of use of standardised clinical evaluation tools such as the American Spinal Injury Association bladder diary and validated symptoms score [182,185].
Higher doses or a combination of antimuscarinic agents may be an option to maximise outcomes in neurological patients [178,179,186-189]. However, these drugs have a high incidence of adverse events, which may lead to early discontinuation of therapy. Despite this, NDO patients have generally shown better treatment adherence compared to idiopathic DO patients .
Choice of antimuscarinic agent: Oxybutynin [140,178,179,181,182,191], trospium [182,188,192], tolterodine  and propiverine [182,194] are established, effective and well tolerated treatments even in long-term use [181,182,195,196]. Darifenacin [197,198] and solifenacin  have been evaluated in NDO secondary to SCI and MS [182,197-199] with results similar to other antimuscarinic drugs. A pilot study using solifenacin in NDO due to PD showed an improvement in UI . Fesoterodine, an active metabolite of tolterodine, has also been introduced; to date there has been no published clinical evidence for its use in the treatment of neuro-urological disorders. Favourable results with the new drug imidafenacin have been reported in suprapontine as well as SCI patients [201,202].
Side effects: Controlled-release antimuscarinics have some minor side effects, e.g. dry mouth . It has been suggested that different ways of administration may help to reduce side effects . Imidafenacine has been safely used in neurological patients with no worsening of cognitive function .
Beta-3-adrenergic receptor agonists
The role of mirabegron in neuro-urological patients is still unclear. In MS and SCI patients, with very short follow up, mirabegron has not demonstrated any significant effect on detrusor pressure or cystometric capacity despite the reported improvement in LUTS [205,206]. A significant subjective improvement in OAB symptoms has also been reported using lower dosages of mirabegron in patients affected by CNS lesions without any negative effects on voiding function . A standard dosage of 50 mg has been found effective with no worsening of cognitive function in patients with PD . Combination therapy with mirabegron and desmopressin in MS patients has shown promising results; however, clinical experience is still very limited in neuro-urological populations .
In preliminary studies, improvements in daily incontinence rates, nocturia, daytime and 24 hour voids, as well as the low risk of adverse events, suggest that cannabinoids may be effective and safe in MS patients . A concomitant improvement in OAB symptoms has been reported in male MS patients using daily tadalafil to treat neurogenic erectile dysfunction (ED) . A systematic review found that desmopressin may be effective for treating nocturia in MS patients; however, adverse events were common, with the included studies being heterogeneous and of low quality .
Detrusor underactivity: Cholinergic drugs, such as bethanechol and distigmine, have been considered to enhance detrusor contractility and promote bladder emptying, but are not frequently used in clinical practice . Only preclinical studies have documented the potential benefits of cannabinoid agonists for improving detrusor contractility when administered intravesically [214,215].
Decreasing bladder outlet resistance: α-blockers (e.g. tamsulosin, naftopidil and silodosin) seem to be effective for decreasing bladder outlet resistance, PVR and AD [216-218].
Increasing bladder outlet resistance: Several drugs have shown efficacy in selected cases of mild SUI, but there are no high-level evidence studies in neurological patients .
Summary of evidence
Long-term efficacy and safety of antimuscarinic therapy for NDO is well documented.
Mirabegron does not improve urodynamic outcomes in NDO patients.
Maximise outcomes for neurogenic detrusor overactivity by considering a combination therapy.
Use antimuscarinic therapy as the first-line medical treatment for neurogenic detrusor overactivity.
Prescribe α-blockers to decrease bladder outlet resistance.
Do not prescribe parasympathomimetics for underactive detrusor.
Intermittent self- or third-party catheterisation [219,220] is the preferred management for neuro-urological patients who cannot effectively empty their bladders . Sterile IC, as originally proposed by Guttmann and Frankel , significantly reduces the risk of UTI and bacteriuria [140,221,222], compared with clean IC introduced by Lapides et al. . However, it has not yet been established whether or not the incidence of UTI, other complications and user satisfaction are affected by either sterile or clean IC, coated or uncoated catheters or by any other strategy .
Contributing factors to contamination are insufficient patient education and the inherently greater risk of UTI in neuro-urological patients [140,226-230]. The average frequency of catheterisations per day is four to six times  and the catheter size most often used is between 12-16 Fr. In aseptic IC, an optimum frequency of five times showed a reduction of UTI . Ideally, bladder volume at catheterisation should, as a rule, not exceed 400-500 mL.
Indwelling transurethral catheterisation and, to a lesser extent, suprapubic cystostomy are associated with a range of complications as well as an enhanced risk for UTI [140,232-239]; therefore, both procedures should be avoided, when possible. Silicone catheters are preferred as they are less susceptible to encrustation and because of the high incidence of latex allergy in the neuro-urological patient population .
Summary of evidence
Intermittent catheterisation is the standard treatment for patients who are unable to empty their bladder.
Indwelling transurethral catheterisation and suprapubic cystostomy are associated with a range of complications as well as an enhanced risk for UTI.
Use intermittent catheterisation, whenever possible aseptic technique, as a standard treatment for patients who are unable to empty their bladder.
Thoroughly instruct patients in the technique and risks of intermittent catheterisation.
Avoid indwelling transurethral and suprapubic catheterisation whenever possible.
To reduce DO, antimuscarinics can also be administered intravesically [204,241-244]. The efficacy, safety and tolerability of intravesical administration of 0.1% oxybutynin hydrochloride compared to its oral administration for treatment of NDO has been demonstrated in a recent randomised controlled study . This approach may reduce adverse effects due to the fact that the antimuscarinic drug is metabolised differently  and a greater amount is sequestered in the bladder, even more than with electromotive administration .
The vanilloids, capsaicin and resiniferatoxin, desensitise the C-fibres for a period of a few months [245,246]. Clinical studies have shown that resiniferatoxin has limited clinical efficacy compared to botulinum toxin A injections in the detrusor .
Although preliminary data suggest that intravesical vanilloids might be effective for treating neurogenic LUT dysfunction, their safety profile appears to be unfavourable . Currently, there is no indication for the use of these substances, which are not licensed for intravesical treatment.
Summary of evidence
A significant reduction in adverse events was observed for intravesical administration of oxybutynine compared to oral administration.
Offer intravesical oxybutynin to neurogenic detrusor overactivity patients with poor tolerance to the oral route.
Botulinum toxin A causes a long-lasting but reversible chemical denervation that lasts for about nine months [248,249]. The toxin injections are mapped over the detrusor in a dosage that depends on the preparation used. Botulinum toxin A has been proven effective in patients with neuro-urological disorders due to MS, SCI and PD in multiple RCTs and meta-analyses [250-252]. Urodynamic studies might be necessary after treatment in patients with maximal filling pressure of > 40 cm H2O cm in order to monitor the effect of the injections on bladder pressure . Repeated injections seem to be possible without loss of efficacy, even after initial low response rates, based on years of follow up [248,254-257]. The clinical efficacy of botulinum toxin A injection in patients with low morbidity after failure of augmentation enterocystoplasty has been demonstrated . A switch between different toxin variations may improve responsiveness . The most frequent side effects are UTIs, urinary retention and haematuria . Intermittent catheterisation may become necessary, this is especially relevant in MS patients as they do not often perform IC prior to intravesical botulinum toxin injections. However, a lower dose of botulinum toxin A (100 U) may reduce the rate of clean IC in MS patients . Rare complications include generalised muscle weakness and AD . Current research focuses on different delivery approaches to injection such as liposome encapsulated botulinum toxin to decrease side effects . Neuro-urological patients with an indwelling catheter and concomitant bladder pain and/or catheter bypass leakage could benefit from intravesical botulinum injections .
Reduction of the bladder outlet resistance may be necessary to protect the UUT. This can be achieved by chemical denervation of the sphincter or by surgical interventions (bladder neck or sphincter incision or urethral stent – Section 22.214.171.124). Incontinence may result and can be managed by external devices (Section 126.96.36.199).
Botulinum toxin A: This can be used to treat DSD effectively by injecting the sphincter at a dose that depends on the preparation used. The dyssynergia is abolished only for a few months, necessitating repeat injections. The efficacy of this treatment has been reported to be high with few adverse effects [264-266]. However, a recent Cochrane report concluded that, because of limited evidence, future RCTs assessing the effectiveness of botulinum toxin A injections also need to address the uncertainty about the optimal dose and mode of injection . In addition, this therapy is not licensed.
Balloon dilatation: Favourable immediate results were reported , but there have been no further reports since 1994; therefore, this method is no longer recommended.
Increasing bladder outlet resistance: This can improve the continence condition. Despite early positive results with urethral bulking agents, a relative early loss of continence is reported in patients with neuro-urological disorders [140,269,270].
Urethral inserts: Urethral plugs or valves for the management of (female) stress incontinence have not been applied in neuro-urological patients. The experience with active pumping urethral prosthesis for treatment of the underactive or acontractile detrusor were disappointing .
188.8.131.52.7.Summary of evidence and recommendations for botulinum toxin A injections and bladder neck procedures
Summary of evidence
Botulinum toxin A has been proven effective in patients with neuro-urological disorders due to MS or SCI in multiple RCTs and meta-analyses.
Bladder neck incision is indicated only for secondary changes (fibrosis) at the bladder neck.
Use botulinum toxin injection in the detrusor to reduce neurogenic detrusor overactivity in multiple sclerosis or spinal cord injury patients if antimuscarinic therapy is ineffective.
Bladder neck incision is effective in a fibrotic bladder neck.
There is considerable heterogeneity in outcome parameters and definitions of cure used to report on outcome of surgical interventions for SUI in neuro-urological patients . The heterogeneity of outcome reporting makes it difficult to interpret and compare different studies and therapies. A consistent comparison of the outcomes of therapy can only be made after standardisation of outcome parameters and definitions of cure or success; therefore, it would seem prudent to develop a core outcome set (COS) for use in UI research in neuro-urological patients . Until such a COS is developed it would seem feasible to use both a subjective and objective outcome parameter and the combination of both to define cure . Due to the importance of QoL for neuro-urological patients a disease-specific QoL questionnaire or a bother questionnaire validated for neuro-urological patients should be used as the subjective outcome parameter .
Increasing the bladder outlet resistance has the inherent risk of causing high intravesical pressure. Procedures to treat sphincteric incontinence are therefore suitable only when the detrusor activity can be controlled and when no significant reflux is present. A simultaneous bladder augmentation and IC may be necessary .
Urethral sling: Various materials have been used for this procedure with enduring positive results. The procedure is established in women with the ability to self-catheterise [140,273-276]. There is growing evidence that synthetic slings can be used effectively with acceptable medium to long-term results and minimal morbidity in neurological patients [277,278]. Besides the pubovaginal sling, which has been considered the procedure of choice in this subgroup of patients, recent reports suggest that both the transobturator and the retropubic approaches may also be considered, with similar failure rates and a reduction in the need for IC. However, for both approaches a higher incidence of de novo urgency was reported [278,279]. In men, both autologous and synthetic slings may also be an alternative [280-284].
Artificial urinary sphincter (AUS): This device was introduced by Light and Scott for patients with neuro-urological disorders . It has stood the test of time and acceptable long-term outcomes can be obtained . However, the complication rates and re-operation rates are higher than in non-neurogenic patient groups (up to 60%), so it is advisable that patients are conscientiously informed about the success rates as well as the complications that may occur after the procedure [287,288]. In a case series with 25 years follow up only 7.1% of patients were revision free at 20 years . Re-interventions are commonly due to infection, urethral atrophy or erosion and mechanical failure.
There is growing interest in the use of this device in women with development of laparoscopic and robot-assisted approaches which appear to reduce infection and erosion rates [290-293]. Long-term surgical and patient-reported outcomes are needed to determine the role of AUS placement in female patients with neurogenic SUI .
Adjustable continence device - ProACT/ACT®: The efficacy of this device has been reported mainly in post-prostatectomy incontinence. A marginally lower cure rate has been reported in neurological patients when compared to non-neurological patients . A retrospective study in neuro-urological patients reported a low rate of efficacy and high complication rate for this device .
Functional sphincter augmentation: Transposing the gracilis muscle to the bladder neck  or proximal urethra , can enable the possible creation of a functional autologous sphincter by electrical stimulation [297-299]; therefore, raising the prospect of restoring control over the urethral closure.
Bladder neck and urethra reconstruction: The classical Young-Dees-Leadbetter procedure  for bladder neck reconstruction in children with bladder exstrophy, and Kropp urethra lengthening  improved by Salle , are established methods to restore continence provided that IC is practiced and/or bladder augmentation is performed [140,303].
Endoscopic techniques for treating anatomic bladder outlet obstruction :
- Transurethral resection of the prostate is indicated in male patients with refractory LUT symptoms due to benign prostatic obstruction. Special consideration should be given to pre-operative abnormal sphincter function which can lead to de novo or persistent UI [305,306].
- Bladder neck resection is indicated in patients with high PVR and when a prominent obstruction of the sclerotic ring in the bladder neck is identified during cystoscopy. The resection can be performed between the three or nine o’clock position or full circle .
- Urethrotomy is indicated in patients with urethral strictures. Cold knife or neodymium:YAG contact laser urethrotomy at the twelve o’clock position can be performed [308,309]. In recurrent strictures, open surgery should be considered.
- Sphincterotomy has been shown to be an efficient technique for the resolution of AD, hydronephrosis and recurrent UTI, and for decreasing detrusor pressures, PVR and vesicoureteral reflux. It is irreversible and should be limited to men who are able to wear a condom catheter. By staged incision, bladder outlet resistance can be reduced without completely losing the closure function of the urethra [139,140,310]. The incision with less complications is the twelve o’clock sphincterotomy with cold knife  or neodymium:YAG laser . Sphincterotomy needs to be repeated at regular intervals in many patients , but it is efficient and does not cause severe adverse effects [139,268]. Secondary narrowing of the bladder neck may occur, for which combined bladder neck incision might be considered .
Bladder neck incision: This is indicated only for secondary changes at the bladder neck (fibrosis) [139,315]. This procedure is not recommended in patients with detrusor hypertrophy, which causes thickening of the bladder neck .
Stents: Implantation of urethral stents results in continence being dependent on adequate closure of the bladder neck . The results are comparable with sphincterotomy and the stenting procedure has a shorter duration of surgery and hospital stay [316,317]. However, the costs , possible complications and re-interventions [318,319] are limiting factors in their use [320-323].
Sacral anterior root stimulation (SARS) is aimed at producing detrusor contraction. The technique was developed by Brindley  and is only applicable to complete lesions above the implant location, as its stimulation amplitude is over the pain threshold. The urethral sphincter efferents are also stimulated, but because the striated muscle relaxes faster than the smooth muscle of the detrusor, so-called "post-stimulus voiding" occurs. This approach has been successful in highly selected patients [325-327]. Although it has been shown that detrusor pressure during SARS decreases over time, the changes do not seem to be clinically relevant during the first decade after surgery . By changing the stimulation parameters, this method can also induce defecation or erection. A recent study reported that Charcot spinal arthropathy should be considered as a potential long-term complication of SARS, leading to spinal instability and to SARS dysfunction .
Sacral rhizotomy, also known as sacral deafferentation, has achieved some success in reducing DO [330-332], but nowadays, it is used mostly as an adjuvant to SARS [325,333-336]. Alternatives to rhizotomy are sought in this treatment combination [337-339].
When the bladder is covered by striated muscle, that can be stimulated electrically, or ideally that can be contracted voluntarily, voiding function can be restored to an acontractile bladder. The rectus abdominis  and latissimus dorsi  have been used successfully in patients with neuro-urological symptoms [347,348].
The aim of auto-augmentation (detrusor myectomy) is to reduce DO or improve low bladder compliance. The advantages are: low surgical burden, low rate of long-term adverse effects, positive effect on patient QoL, and it does not preclude further interventions [139,140,349-352].
Replacing or expanding the bladder by intestine or other passive expandable coverage will improve bladder compliance and at least reduce the pressure effect of DO [353,354]. Improved QoL and stable renal function has been reported during long-term follow-up . Patients performing IC with augmentation cystoplasty had better urinary function and satisfaction with their urinary symptoms compared to patients performing IC with or without botulinum toxin treatment . Long-term complications included bladder perforation (1.9%), mucus production (12.5%), metabolic abnormalities (3.35%), bowel dysfunction (15%), and stone formation (10%) .
The procedure should be used with caution in patients with neuro-urological symptoms, but may become necessary if all less-invasive treatment methods have failed. Special attention should be paid to patients with pre-operative renal scars since metabolic acidosis can develop . Bladder substitution with bowel after performing a supratrigonal cystectomy , to create a low-pressure reservoir, is indicated in patients with a severely thick and fibrotic bladder wall . Intermittent catheterisation may become necessary after this procedure. The long-term scientific evidence shows that bladder augmentation is a highly successful procedure that stabilises renal function and prevents anatomical deterioration; however, lifelong follow-up is essential in this patient group given the significant morbidity associated with this procedure [355,358].
When no other therapy is successful, urinary diversion must be considered for the protection of the UUT and for the patient’s QoL .
Continent diversion: This should be the first choice for urinary diversion. Patients with limited dexterity may prefer a stoma instead of using the urethra for catheterisation. For cosmetic reasons, the umbilicus is often used for the stoma site [359-364]. A systematic review of the literature concluded that continent catheterisable tubes/stomas are an effective treatment option in neuro-urological patients unable to perform intermittent self-catheterisation through the urethra . However, the complication rates were significant with 85/213 post-operative events requiring re-operation . Tube stenosis occurred in 4-32% of the cases. Complications related to concomitant procedures (augmentation cystoplasty, pouch) included neovesicocutaneous fistulae (3.4%), bladder stones (20-25%), and bladder perforations (40%). In addition, data comparing HRQoL before and after surgery were not reported .
Incontinent diversion: If catheterisation is impossible, incontinent diversion with a urine-collecting device is indicated. Ultimately, it could be considered in patients who are wheelchair bound or bed-ridden with intractable and untreatable incontinence, in patients with LUT destruction, when the UUT is severely compromised, and in patients who refuse other therapy . An ileal segment is used for the deviation in most cases [140,366-369]. Patients gain better functional status and QoL after surgery .
Undiversion: Long-standing diversions may be successfully undiverted or an incontinent diversion changed to a continent one with the emergence of new and better techniques for control of detrusor pressure and incontinence . The patient must be carefully counselled and must comply meticulously with the instructions . Successful undiversion can then be performed .
Summary of evidence
Bladder augmentation is an effective option to decrease detrusor pressure and increase bladder capacity, when all less-invasive treatment methods have failed.
Urethral sling placement is an established procedure, with acceptable medium- to long-term results, in women with the ability to self-catheterise.
Artificial urinary sphincter insertion is a viable option, with acceptable long-term outcomes, in males. The complication and re-operation rates are higher in neuro-urological patients; therefore, patients must be adequately informed regarding the success rates as well as the complications that may occur following the procedure.
Perform bladder augmentation in order to treat refractory neurogenic detrusor overactivity.
Place an autologous urethral sling in female patients with neurogenic stress urinary incontinence who are able to self-catheterise.
Insert an artificial urinary sphincter in male patients with neurogenic stress urinary incontinence.
Urinary tract infection is the onset of signs and/or symptoms accompanied by laboratory findings of a UTI (bacteriuria, leukocyturia and positive urine culture) . There are no evidence-based cut-off values for the quantification of these findings. The published consensus is that a significant bacteriuria in persons performing IC is present with > 102 cfu/mL, > 104 cfu/mL in clean-void specimens and any detectable concentration in suprapubic aspirates. Regarding leukocyturia, ten or more leukocytes in centrifuged urine samples per microscopic field (400x) are regarded as significant .
The pathogenesis of UTI in neuro-urological patients is multifactorial. Male gender seems to be a risk factor for febrile UTI . Several etiological factors have been described: altered intrinsic defence mechanisms, impaired washout and catheterisation . Poor glycemic control has been established as a risk factor for UTI in women with type 1 diabetes . However, the exact working mechanisms remain unknown. The presence of asymptomatic bacteriuria in SCI patients is higher than in the general population, and varies depending on bladder management. Prevalence of bacteriuria in those performing clean IC varies from 23-89% . Sphincterotomy and condom catheter drainage has a 57% prevalence . Asymptomatic bacteria should not be routinely screened for in this population .
Individuals with neuro-urological symptoms, especially those with SCI, may have other signs and symptoms in addition to or instead of traditional signs and symptoms of a UTI in able-bodied individuals. Other problems, such as AD, may develop or worsen due to a UTI . The most common signs and symptoms suspicious of a UTI in those with neuro-urological disorders are fever, new onset or increase in incontinence, including leaking around an indwelling catheter, increased spasticity, malaise, lethargy or sense of unease, cloudy urine with increased urine odour, discomfort or pain over the kidney or bladder, dysuria, or AD [225,378]. New incontinence is the most specific symptom, whereas cloudy and foul smelling urine has the highest positive predictive value for UTI diagnosis .
Urine culture and urinalysis are the optimum tests for the diagnosis of UTI in neuro-urological patients. A dipstick test may be more useful to exclude than to prove UTI [380,381]. As bacterial strains and resistance patterns in persons with neuro-urological disorders may differ from those of able-bodied patients, microbiologic testing is mandatory .
Bacteriuria in patients with neuro-urological disorders should not be treated. Treatment of asymptomatic bacteriuria results in significantly more resistant bacterial strains without improving the outcome . Urinary tract infections in persons with neuro-urological disorders are by definition a complicated UTI; therefore, single-dose treatment is not advised. There is no consensus in the literature about the duration of treatment as it depends on the severity of the UTI and the involvement of kidneys and the prostate. Generally, a five to seven day course of antibiotic treatment is advised, which can be extended up to fourteen days according to the extent of the infection . The choice of antibiotic therapy should be based on the results of the microbiologic testing. If immediate treatment is mandatory (e.g. fever, septicaemia, intolerable clinical symptoms, extensive AD), the choice of treatment should be based on local and individual resistance profiles . In patients with afebrile UTI, an initial non-antibiotic treatment may be justified [385,386].
Recurrent UTI in patients with neuro-urological disorders may indicate suboptimal management of the underlying functional problem, e.g. high bladder pressure during storage and voiding, incomplete voiding or bladder stones. The improvement of bladder function, by treating DO by botulinum toxin A injection in the detrusor , and the removal of bladder stones or other direct supporting factors, especially indwelling catheters, as early as possible, are mandatory .
If the improvement of bladder function and removal of foreign bodies/stones is not successful, additional UTI prevention strategies should be utilised. In a meta-analysis the use of hydrophilic catheters was associated with a lower rate of UTI . Bladder irrigation has not been proven effective .
Various medical approaches have been tested for UTI prophylaxis in patients with neuro-urological disorders. The benefit of cranberry juice or probiotics for the prevention of UTI could not be demonstrated in RCTs [389,390]. Methenamine hippurate is not effective in individuals with neuro-urological symptoms . There is no sufficient evidence to support the use of L-methionine for urine acidification to prevent recurrent UTI . There is only weak evidence that oral immunotherapy reduces bacteriuria in patients with SCI  and that recurrent UTIs are reduced . Low-dose, long-term, antibiotic prophylaxis can reduce UTI frequency, but increases bacterial resistance and is therefore not recommended .
Weekly cycling of antibiotic prophylaxis provided long-term positive results, but the results of this trial need to be confirmed in further studies . Another possible future option, the inoculation of apathogenic Escherichia coli strains into the bladder, has provided positive results in initial studies, but because of the paucity of data , cannot be recommended as a treatment option. There is initial evidence that homeopathic treatment can decrease UTI frequency . In addition, intravesical gentamycin instillations can reduce UTI frequency without increasing the number of multi-resistant bacteria .
In summary, based on the criteria of evidence-based medicine, there is currently no preventive measure for recurrent UTI in patients with neuro-urological disorders that can be recommended without limitations. Therefore, individualised concepts should be taken into consideration, including immunostimulation, phytotherapy and complementary medicine . Prophylaxis in patients with neuro-urological disorders is important to pursue, but since there are no data favouring one approach over another, prophylaxis is essentially a trial and error approach.
Summary of evidence
Treatment of asymptomatic bacteriuria results in significantly more resistant bacterial strains without improving patient outcome.
Low-dose, long-term, antibiotic prophylaxis does not reduce UTI frequency, but increases bacterial resistance.
Recurrent UTI in patients with neuro-urological disorders may indicate suboptimal management of the underlying functional problem. Improvement of bladder function as early as possible is mandatory.
There is currently no preventive measure for recurrent UTI in patients with neuro-urological disorders that can be recommended without limitations.
Do not screen for or treat asymptomatic bacteriuria in patients with neuro-urological disorders.
Avoid the use of long-term antibiotics for recurrent urinary tract infections (UTIs).
In patients with recurrent UTI, optimise treatment of neuro-urological symptoms and remove foreign bodies (e.g. stones, indwelling catheters) from the urinary tract.
Individualise UTI prophylaxis in patients with neuro-urological disorders as there is no optimal prophylactic measure available.
These Guidelines specifically focus on sexual dysfunction and infertility in patients with a neurological disease [400,401]. Non-neurogenic, male sexual dysfunction and infertility are covered in separate EAU Guidelines [402,403]. In neuro-urological patients sexual problems can be identified at three levels: primary (direct neurological damage), secondary (general physical disabilities) and tertiary (psychosocial and emotional issues) sexual dysfunction . Adopting a systematic approach, such as the PLISSIT model (Permission, Limited Information, Specific Suggestions and Intensive Therapy) , provides a framework for counselling and treatment involving a stepwise approach to the management of neurogenic sexual dysfunction. Sexual dysfunction is associated with neurogenic LUT dysfunction in patients with MS  and SB . Although various patient reported outcome measures (PROMs) are available to evaluate sexual function, the evidence for good PROMs is limited and studies with high methodological quality are needed .
Phosphodiesterase type 5 inhibitors (PDE5Is) are recommended as first-line treatment in neurogenic ED [400,401]. In SCI patients, tadalafil, vardenafil and sildenafil have all improved retrograde ejaculation and improved erectile function and satisfaction on IIEF-15. Tadalafil 10 mg was shown to be more effective than sildenafil 50 mg. All currently available PDE5Is appear to be effective and safe, although there are no high level evidence studies in neuro-urological patients investigating the efficacy and side effects across different PDE5Is, dosages and formulations .
For MS patients two studies reported significant improvement in ED when using sildenafil and tadalafil. One study; however, showed no improvement in ED with sildenafil.
In PD normal erectile function was described in over half of the patients using sildenafil 100 mg and a significant improvement in IIEF-15 score was found compared to placebo. While most neuro-urological patients require long-term therapy for ED some have a low compliance rate or stop therapy because of side effects [410,411], most commonly headache and flushing . In addition, PDE5Is may induce relevant hypotension in patients with tetraplegia/high-level paraplegia and multiple system atrophy [410,411]. As a prerequisite for successful PDE5I-therapy, some residual nerve function is required to induce erection. Since many patients with SCI use on-demand nitrates for the treatment of AD, they must be counselled that PDE5Is are contraindicated when using nitrate medication.
Fampridine to treat neurogenic spasticity has been shown to be beneficial in improving ED in two domains of the IIEF-15 in SCI and MS patients, however, with a significant discontinuation rate due to severe adverse events . Sublingual apomorfine was shown to have poor results on ED in SCI patients and side-effects in half of the patients . In PD pergolide mesylate showed a significant improvement in IIEF-15 scores up to twelve months follow-up .
Mechanical devices (vacuum tumescence devices and penile rings) may be effective but are less popular [415-419].
Patients not responding to oral drugs may be offered intracavernous injections (alprostadil, papaverine and phentolamine) that have been shown to be effective in a number of neurological conditions, including SCI, MS, and diabetes mellitus [420-426], but their use requires careful dose titration and some precautions. Complications of intracavernous drugs include pain, priapism and corpora cavernosa fibrosis.
Intracavernous vasoactive drug injection is the first-line therapeutic option in patients taking nitrate medications, as well as those with concerns about drug interactions with PDE5Is, or in whom PDE5Is are ineffective. The impact of intracavernous injections on ejaculation and orgasmic function, their early use for increasing the recovery rate of a spontaneous erection, and their effectiveness and tolerability in the long-term are unclear . Intra-urethral alprostadil application is an alternative, but a less effective, route of administration [422,427].
Sacral neuromodulation for LUT dysfunction may improve sexual function; however, high level evidence studies are lacking.
Penile prostheses may be considered for treatment of neurogenic ED when all conservative treatments have failed. At a mean follow-up of seven years 83.7% of patients with SCI were able to have sexual intercourse . Serious complications, including infection and prosthesis perforation, may occur in about 10% of patients, depending on implant type [428-430].
Summary of evidence
The long-term efficacy and safety of oral PDE5Is for the treatment of ED is well documented.
Intracavernous vasoactive drug injections have been shown to be effective in a number of neurological conditions, including SCI and MS; however, their use requires careful dose titration and precautions.
Mechanical devices (vacuum tumescence devices and penile rings) may be effective but are less popular.
Reserve penile prostheses for selected patients, those in which all conservative treatments have failed, with neurogenic ED.
Prescribe oral phosphodiesterase type 5 inhibitors as first-line medical treatment in neurogenic erectile dysfunction (ED).
Give intracavernous injections of vasoactive drugs (alone or in combination) as second-line medical treatment in neurogenic ED.
Offer mechanical devices such as vacuum devices and rings to patients with neurogenic ED.
Male fertility can be compromised in the neurological patient by ED, ejaculation disorder, impaired sperm quality or various combinations of these three disorders. Among the major conditions contributing to neurogenic infertility are pelvic and retroperitoneal surgery, diabetes mellitus, SB, MS and SCI . Erectile dysfunction is managed as described previously. Retrograde ejaculation may be reversed by sympathomimetic agents contracting the bladder neck, including imipramine, ephedrine, pseudoephedrine, and phenylpropanolamine . The use of a balloon catheter to obstruct the bladder neck may be effective in obtaining antegrade ejaculation . If antegrade ejaculation is not achieved, the harvest of semen from the urine may be considered .
Prostatic massage is safe and easy to use for obtaining semen in men with lesions above Th 10 . In several patients, vibrostimulation or transrectal electroejaculation are needed for sperm retrieval [431,435,436]. Semen retrieval is more likely with vibrostimulation in men with lesions above Th 10 [437-439]. In men with SCI, especially at or above Th 6, AD might occur during sexual activity and ejaculation [440,441]; patients at risk and fertility clinics must be informed and aware of this potentially life-threatening condition. In SCI patients the use of oral midodrine can improve sperm retrieval at vibrostimulation .
In men with MS, use of disease modifying drugs during the conception phase, has not been associated with altered pregnancy outcomes . Surgical procedures, such as, microsurgical epididymal sperm aspiration (MESA) or testicular sperm extraction (TESE), may be used if vibrostimulation and electroejaculation are not successful [444,445]. Pregnancy rates in patients with SCI are lower than in the general population, but since the introduction of intracytoplasmic sperm injection (ICSI), men with SCI now have a good chance of becoming biological fathers [446-448].
The following has been reported on sperm quality and motility:
- bladder management with clean IC may improve semen quality compared to indwelling catheterisation, reflex voiding or bladder expression ;
- in SCI patients sperm quality decreases at the early post traumatic phase demonstrating lower spermatozoid vitality (necrospermia), reduced motility (asthenospermia) and leucospermia ;
- long-term valproate treatment for epilepsy negatively influences sperm count and motility ;
- vibrostimulation produces samples with better sperm motility than electrostimulation [451,452];
- electroejaculation with interrupted current produces better sperm motility than continuous current ;
- freezing of sperm is unlikely to improve fertility rates in men with SCI .
Summary of evidence
Vibrostimulation and transrectal electroejaculation have been shown to be effective for sperm retrieval in neuro-urological patients.
Surgical procedures, such as, microsurgical epididymal sperm aspiration or testicular sperm extraction, may be used if vibrostimulation and electroejaculation are not successful.
In men with SCI at or above Th 6, AD might occur during sexual activity and ejaculation.
Perform vibrostimulation and transrectal electroejaculation for sperm retrieval in men with spinal cord injury.
Perform microsurgical epididymal sperm aspiration, testicular sperm extraction and intracytoplasmic sperm injection after failed vibrostimulation and/or transrectal electroejaculation in men with spinal cord injury.
Counsel men with spinal cord injury at or above Th 6 and fertility clinics about the potentially life-threatening condition of autonomic dysreflexia.
The most relevant publications on neurogenic female sexual dysfunction are in women with SCI and MS. After SCI, about 65-80% of women continue to be sexually active, but to a much lesser extent than before the injury, and about 25% report a decreased satisfaction with their sexual life [455-458]. Although sexual dysfunction is very common in women with MS, it is still often overlooked by medical professionals [459,460].
The greatest physical barrier to sexual activity is UI. A correlation has been found between the urodynamic outcomes of low bladder capacity, compliance and high maximum detrusor pressure and sexual dysfunction in MS patients. Problems with positioning and spasticity affect mainly tetraplegic patients. Peer support may help to optimise the sexual adjustment of women with SCI in achieving a more positive self-image, self-esteem and feelings of being attractive to themselves and others [455,461-463].
The use of specific drugs for sexual dysfunction is indicated to treat inadequate lubrication. Data on sildenafil for treating female sexual dysfunction are poor and controversial . Although good evidence exists that psychological interventions are effective in the treatment of female hypoactive sexual desire disorder and female orgasmic disorder , there is a lack of high-level evidence studies in the neurological population.
Neurophysiological studies have shown that women with the ability to perceive Th 11-L2 pin-prick sensations may have psychogenic genital vasocongestion. Reflex lubrication and orgasm is more prevalent in women with SCI who have preserved the sacral reflex arc (S2-S5), even when it has not been shown in an individual woman that a specific level and degree of lesion is the cause of a particular sexual dysfunction. In SCI women with a complete lesion of the sacral reflex, arousal and orgasm may be evoked through stimulation of other erogenous zones above the level of lesions [465-467].
Sacral neuromodulation for LUT dysfunction may improve sexual function but high-evidence studies are lacking . Women with SCI reported dissatisfaction with the quality and quantity of sexuality-related rehabilitation services and were less likely to receive sexual information than men [465,468,469].
There are few studies on female fertility in neurological patients. More than a third (38%) of women with epilepsy had infertility and the relevant predictors were exposure to multiple (three or more) antiepileptic drugs, older age and lower education .
Although it seems that the reproductive capacity of women with SCI is only temporarily affected by SCI with cessation of menstruation for approximately six months after SCI , there are no high-level evidence studies. About 70% of sexually active women use some form of contraception after injury, but fewer women use the birth control pill compared to before their injury .
Women with SCI are more likely to suffer complications during pregnancy, labour and delivery compared to able-bodied women. Complications of labour and delivery include bladder problems, spasticity, pressure sores, anaemia, and AD [473-477]. Obstetric outcomes include higher rates of Caesarean sections and an increased incidence of low birth-weight babies [472,475-477].
There is very little published data on women’s experience of the menopause following SCI . Women with MS who plan a pregnancy should evaluate their current drug treatment with their treating physician [481-483]. Clinical management should be individualised to optimise both the mother’s reproductive outcomes and MS course [482-484].
Summary of evidence
Data on specific drugs for treating female sexual dysfunction are poor and controversial.
There are limited numbers of studies on female fertility in neurological patients, clinical management should be individualised to optimise both the mother’s reproductive outcomes and medical condition.
Do not offer medical therapy for the treatment of neurogenic sexual dysfunction in women.
Take a multidisciplinary approach, tailored to individual patient’s needs and preferences, in the management of fertility, pregnancy and delivery in women with neurological diseases.
Neuro-urological disorders are often unstable and the symptoms may vary considerably, even within a relatively short period. Regular follow-up is therefore necessary to assess the UUT .
Depending on the type of the underlying neurological pathology and the current stability of the neuro-urological symptoms, the interval between initial investigations and control diagnostics may vary and in many cases should not exceed one to two years. In high-risk neuro-urological patients this interval should be much shorter. Urinalysis should be performed only when patients present with symptoms . The UUT should be checked by ultrasonography at regular intervals in high-risk patients; about once every six months [6,486]. In these patients, physical examination and urine laboratory should take place every year [6,486]. In MS patients higher scores on the Expanded Disability Status Scale (EDSS) are associated with risk factors for UUT deterioration . A urodynamic investigation should be performed as a diagnostic baseline, and repeated during follow-up, more frequently in high-risk patients [6,486]. In addition, bladder wall thickness can be measured on ultrasonography as an additional risk assessment for upper tract damage , although a ‘safe’ cut-off threshold for this has not been agreed . The utility of DMSA for follow-up of neuro-urological patients has not been fully evaluated . Any significant clinical change warrants further, specialised, investigation [6,486]. However, there is a lack of high level evidence studies on this topic and every recommendation must be viewed critically in each individual neuro-urological patient .
The increased prevalence of muscle invasive bladder cancer in neuro-urological patients also warrants long-term follow-up . The exact frequency of cystoscopy with or without cytology remains unknown, but presence of risk factors similar to the general population should trigger further investigation .
Adolescent patients with neurological pathology are at risk of being lost to follow-up during the transition to adulthood. It is important that a standardised approach during this transition is adopted to improve follow-up and specific treatment during adult life .
Summary of evidence
Neuro-urological disorders are often unstable and the symptoms may vary considerably, therefore, regular follow-up is necessary.
Assess the upper urinary tract at regular intervals in high-risk patients.
Perform a physical examination and urine laboratory every year in high-risk patients.
Any significant clinical changes should instigate further, specialised, investigation.
Perform urodynamic investigation as a mandatory baseline diagnostic intervention in high-risk patients at regular intervals.
Neuro-urological disorders have a multi-faceted pathology. They require an extensive and specific diagnosis before one can embark on an individualised therapy, which takes into account the medical and physical condition of the patient and the patient’s expectations about their future. The urologist can select from a wealth of therapeutic options, each with its own pros and cons. Notwithstanding the success of any therapy embarked upon, close surveillance is necessary for the patient’s entire life.
These Guidelines offer you expert advice on how to define the patient’s neuro-urological symptoms as precisely as possible and how to select, together with the patient, the appropriate therapy. This last choice, as always, is governed by the golden rule: as effective as needed, as non-invasive as possible.
1. Schafer, W., et al. Good urodynamic practices: uroflowmetry, filling cystometry, and pressure-flow studies. Neurourol Urodyn, 2002. 21: 261.
2. Abrams, P., et al. Reviewing the ICS 2002 terminology report: the ongoing debate. Neurourol Urodyn, 2009. 28: 287.
3. Abrams, P., et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn, 2002. 21: 167.
4. Groen, J., et al. Summary of European Association of Urology (EAU) Guidelines on Neuro-Urology. Eur Urol, 2015.
5. Nosseir, M., et al. Clinical usefulness of urodynamic assessment for maintenance of bladder function in patients with spinal cord injury. Neurourol Urodyn, 2007. 26: 228.
6. Panicker, J.N., et al. Lower urinary tract dysfunction in the neurological patient: clinical assessment and management. Lancet Neurol, 2015. 14: 720.
7. Guyatt, G.H., et al. GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. BMJ, 2008. 336: 924.
8. Guyatt, G.H., et al. What is "quality of evidence" and why is it important to clinicians? BMJ, 2008. 336: 995.
9. Phillips B, et al. Oxford Centre for Evidence-based Medicine Levels of Evidence. Updated by Jeremy Howick March 2009. 1998.
10. Guyatt, G.H., et al. Going from evidence to recommendations. BMJ, 2008. 336: 1049.
11. Townsend, N., et al. Cardiovascular disease in Europe - epidemiological update 2015. Eur Heart J, 2015.
12. Tibaek, S., et al. Prevalence of lower urinary tract symptoms (LUTS) in stroke patients: a cross-sectional, clinical survey. Neurourol Urodyn, 2008. 27: 763.
13. Marinkovic, S.P., et al. Voiding and sexual dysfunction after cerebrovascular accidents. J Urol, 2001. 165: 359.
14. Rotar, M., et al. Stroke patients who regain urinary continence in the first week after acute first-ever stroke have better prognosis than patients with persistent lower urinary tract dysfunction. Neurourol Urodyn, 2011. 30: 1315.
15. Lobo, A., et al. Prevalence of dementia and major subtypes in Europe: A collaborative study of population-based cohorts. Neurologic Diseases in the Elderly Research Group. Neurology, 2000. 54: S4.
16. Na, H.R., et al. Urinary incontinence in Alzheimer’s disease is associated with Clinical Dementia Rating-Sum of Boxes and Barthel Activities of Daily Living. Asia Pac Psychiatry, 2015. 7: 113.
17. Grant, R.L., et al. First diagnosis and management of incontinence in older people with and without dementia in primary care: a cohort study using The Health Improvement Network primary care database. PLoS Med, 2013. 10: e1001505.
18. Pringsheim, T., et al. The prevalence of Parkinson’s disease: a systematic review and meta-analysis. Mov Disord, 2014. 29: 1583.
19. Picillo, M., et al. The PRIAMO study: urinary dysfunction as a marker of disease progression in early Parkinson’s disease. Eur J Neurol, 2017. 24: 788.
20. Papatsoris, A.G., et al. Urinary and erectile dysfunction in multiple system atrophy (MSA). Neurourol Urodyn, 2008. 27: 22.
21. Kim, M., et al. Impaired detrusor contractility is the pathognomonic urodynamic finding of multiple system atrophy compared to idiopathic Parkinson’s disease. Parkinsonism Relat Disord, 2015. 21: 205.
22. Sakakibara, R., et al. A guideline for the management of bladder dysfunction in Parkinson’s disease and other gait disorders. Neurourol Urodyn, 2015.
23. Yamamoto, T., et al. Postvoid residual predicts the diagnosis of multiple system atrophy in Parkinsonian syndrome. J Neurol Sci, 2017. 381: 230.
24. Dolecek, T.A., et al. CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the United States in 2005-2009. Neuro Oncol, 2012. 14 Suppl 5: v1.
25. Maurice-Williams, R.S. Micturition symptoms in frontal tumours. J Neurol Neurosurg Psychiatry, 1974. 37: 431.
26. Christensen, D., et al. Prevalence of cerebral palsy, co-occurring autism spectrum disorders, and motor functioning - Autism and Developmental Disabilities Monitoring Network, USA, 2008. Dev Med Child Neurol, 2014. 56: 59.
27. Samijn, B., et al. Lower urinary tract symptoms and urodynamic findings in children and adults with cerebral palsy: A systematic review. Neurourol Urodyn, 2017. 36: 541.
28. Tagliaferri, F., et al. A systematic review of brain injury epidemiology in Europe. Acta Neurochir (Wien), 2006. 148: 255.
29. Kulakli, F., et al. Relationship between urinary dysfunction and clinical factors in patients with traumatic brain injury. Brain Inj, 2014. 28: 323.
30. Aruga, S., et al. Effect of cerebrospinal fluid shunt surgery on lower urinary tract dysfunction in idiopathic normal pressure hydrocephalus. Neurourol Urodyn, 2018. 37: 1053.
31. Singh, A., et al. Global prevalence and incidence of traumatic spinal cord injury. Clin Epidemiol, 2014. 6: 309.
32. Weld, K.J., et al. Association of level of injury and bladder behavior in patients with post-traumatic spinal cord injury. Urology, 2000. 55: 490.
33. Kondo, A., et al. Neural tube defects: prevalence, etiology and prevention. Int J Urol, 2009. 16: 49.
34. Sawin, K.J., et al. The National Spina Bifida Patient Registry: profile of a large cohort of participants from the first 10 clinics. J Pediatr, 2015. 166: 444.
35. Wiener, J.S., et al. Bladder Management and Continence Outcomes in Adults with Spina Bifida: Results from the National Spina Bifida Patient Registry, 2009 to 2015. J Urol, 2018. 200: 187.
36. Peyronnet, B., et al. Comparison of neurogenic lower urinary tract dysfunctions in open versus closed spinal dysraphism: A prospective cross-sectional study of 318 patients. Neurourol Urodyn, 2018. 37: 2818.
37. Bartolin, Z., et al. Relationship between clinical data and urodynamic findings in patients with lumbar intervertebral disk protrusion. Urol Res, 2002. 30: 219.
38. Baker, M., et al. Urogenital symptoms in women with Tarlov cysts. J Obstet Gynaecol Res, 2018. 44: 1817.
39. Lange, M.M., et al. Urinary and sexual dysfunction after rectal cancer treatment. Nat Rev Urol, 2011. 8: 51.
40. Federation, I.D., IDF Diabetes Atlas, 6th edn. 2013, International Diabetes Federation: Brussels, Belgium.
41. Yuan, Z., et al. Diabetic cystopathy: A review. J Diabetes, 2015. 7: 442.
42. Pugliatti, M., et al. The epidemiology of multiple sclerosis in Europe. Eur J Neurol, 2006. 13: 700.
43. de Seze, M., et al. The neurogenic bladder in multiple sclerosis: review of the literature and proposal of management guidelines. Mult Scler, 2007. 13: 915.
44. Gajewski, J.B., et al. An International Continence Society (ICS) report on the terminology for adult neurogenic lower urinary tract dysfunction (ANLUTD). Neurourol Urodyn, 2018. 37: 1152.
45. Del Popolo, G., et al. Diagnosis and therapy for neurogenic bladder dysfunctions in multiple sclerosis patients. Neurol Sci, 2008. 29 Suppl 4: S352.
46. Satar, N., et al. The effects of delayed diagnosis and treatment in patients with an occult spinal dysraphism. J Urol, 1995. 154: 754.
47. Watanabe, T., et al. High incidence of occult neurogenic bladder dysfunction in neurologically intact patients with thoracolumbar spinal injuries. J Urol, 1998. 159: 965.
48. Ahlberg, J., et al. Neurological signs are common in patients with urodynamically verified "idiopathic" bladder overactivity. Neurourol Urodyn, 2002. 21: 65.
49. Bemelmans, B.L., et al. Evidence for early lower urinary tract dysfunction in clinically silent multiple sclerosis. J Urol, 1991. 145: 1219.
50. Klausner, A.P., et al. The neurogenic bladder: an update with management strategies for primary care physicians. Med Clin North Am, 2011. 95: 111.
51. Cetinel, B., et al. Risk factors predicting upper urinary tract deterioration in patients with spinal cord injury: A retrospective study. Neurourol Urodyn, 2017. 36: 653.
52. Elmelund, M., et al. Renal deterioration after spinal cord injury is associated with length of detrusor contractions during cystometry-A study with a median of 41 years follow-up. Neurourol Urodyn, 2016.
53. Ineichen, B.V., et al. High EDSS can predict risk for upper urinary tract damage in patients with multiple sclerosis. Multiple Sclerosis, 2017. 1352458517703801: 01.
54. Bors, E., et al. History and physical examination in neurological urology. J Urol, 1960. 83: 759.
55. Cameron, A.P., et al. The Severity of Bowel Dysfunction in Patients with Neurogenic Bladder. J Urol, 2015.
56. Vodusek, D.B. Lower urinary tract and sexual dysfunction in neurological patients. Eur Neurol, 2014. 72: 109.
57. Linsenmeyer, T.A., et al. Accuracy of individuals with spinal cord injury at predicting urinary tract infections based on their symptoms. J Spinal Cord Med, 2003. 26: 352.
58. Massa, L.M., et al. Validity, accuracy, and predictive value of urinary tract infection signs and symptoms in individuals with spinal cord injury on intermittent catheterization. J Spinal Cord Med, 2009. 32: 568.
59. Bellucci, C.H.S., et al. Acute spinal cord injury - Do ambulatory patients need urodynamic investigations? J Urol, 2013. 189: 1369.
60. Kessler, T.M. Diagnosis of urinary incontinence. JAMA, 2008. 300: 283; author reply 283.
61. Honjo, H., et al. Impact of convenience void in a bladder diary with urinary perception grade to assess overactive bladder symptoms: a community-based study. Neurourol Urodyn, 2010. 29: 1286.
62. Naoemova, I., et al. Reliability of the 24-h sensation-related bladder diary in women with urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct, 2008. 19: 955.
63. Henze, T. Managing specific symptoms in people with multiple sclerosis. Int MS J, 2005. 12: 60.
64. Liu, C.W., et al. The relationship between bladder management and health-related quality of life in patients with spinal cord injury in the UK. Spinal Cord, 2010. 48: 319.
65. Myers, J.B., et al. Patient reported bladder-related symptoms and quality of life after spinal cord injury with different bladder management strategies. J Urol, 2019: 202: 574.
66. Khalaf, K.M., et al. The impact of lower urinary tract symptoms on health-related quality of life among patients with multiple sclerosis. Neurourol Urodyn, 2016. 35: 48.
67. Szymanski, K.M., et al. All Incontinence is Not Created Equal: Impact of Urinary and Fecal Incontinence on Quality of Life in Adults with Spina Bifida. J Urol, 2017. Part 2. 197: 885.
68. Pannek, J., et al. Does optimizing bladder management equal optimizing quality of life? Correlation between health-related quality of life and urodynamic parameters in patients with spinal cord lesions. Urology, 2009. 74: 263.
69. Patel, D.P., et al. Patient reported outcomes measures in neurogenic bladder and bowel: A systematic review of the current literature. Neurourol Urodyn, 2016. 35: 8.
70. Bonniaud, V., et al. Qualiveen, a urinary-disorder specific instrument: 0.5 corresponds to the minimal important difference. J Clin Epidemiol, 2008. 61: 505.
71. Bonniaud, V., et al. Development and validation of the short form of a urinary quality of life questionnaire: SF-Qualiveen. J Urol, 2008. 180: 2592.
72. Bonniaud, V., et al. Italian version of Qualiveen-30: cultural adaptation of a neurogenic urinary disorder-specific instrument. Neurourol Urodyn, 2011. 30: 354.
73. Ciudin, A., et al. Quality of life of multiple sclerosis patients: translation and validation of the Spanish version of Qualiveen. Neurourol Urodyn, 2012. 31: 517.
74. D’Ancona, C.A., et al. Quality of life of neurogenic patients: translation and validation of the Portuguese version of Qualiveen. Int Urol Nephrol, 2009. 41: 29.
75. Pannek, J., et al. [Quality of life in German-speaking patients with spinal cord injuries and bladder dysfunctions. Validation of the German version of the Qualiveen questionnaire]. Urologe A, 2007. 46: 1416.
76. Reuvers, S.H.M., et al. The urinary-specific quality of life of multiple sclerosis patients: Dutch translation and validation of the SF-Qualiveen. Neurourol Urodyn, 2017. 36: 1629.
77. Reuvers, S.H.M., et al. The validation of the Dutch SF-Qualiveen, a questionnaire on urinary-specific quality of life, in spinal cord injury patients. BMC Urology, 2017. 17: 88.
78. Best, K.L., et al. Identifying and classifying quality of life tools for neurogenic bladder function after spinal cord injury: A systematic review. J Spinal Cord Med, 2017. 40: 505.
79. Welk, B., et al. The conceptualization and development of a patient-reported neurogenic bladder symptom score. Res Rep Urol, 2013. 5: 129.
80. Welk, B., et al. The Neurogenic Bladder Symptom Score (NBSS): A secondary assessment of its validity, reliability among people with a spinal cord injury. Spinal Cord, 2018. 56: 259.
81. Gulick, E.E. Bowel management related quality of life in people with multiple sclerosis: psychometric evaluation of the QoL-BM measure. Int J Nurs Stud, 2011. 48: 1066.
82. Tsang, B., et al. A systematic review and comparison of questionnaires in the management of spinal cord injury, multiple sclerosis and the neurogenic bladder. Neurourol Urodyn, 2015.
83. Akkoc, Y., et al. Assessment of voiding dysfunction in Parkinson’s disease: Reliability and validity of the Turkish version of the Danish Prostate Symptom Score. Neurourol Urodyn, 2017. 36: 1903.
84. Schurch, B., et al. Reliability and validity of the Incontinence Quality of Life questionnaire in patients with neurogenic urinary incontinence. Arch Phys Med Rehabil, 2007. 88: 646.
85. Hollingworth, W., et al. Exploring the impact of changes in neurogenic urinary incontinence frequency and condition-specific quality of life on preference-based outcomes. Qual Life Res, 2010. 19: 323.
86. Cella, D.F., et al. Validation of the functional assessment of multiple sclerosis quality of life instrument. Neurology, 1996. 47: 129.
87. Wesson, J.M., et al. The functional index for living with multiple sclerosis: development and validation of a new quality of life questionnaire. Mult Scler, 2009. 15: 1239.
88. Gold, S.M., et al. Disease specific quality of life instruments in multiple sclerosis: validation of the Hamburg Quality of Life Questionnaire in Multiple Sclerosis (HAQUAMS). Mult Scler, 2001. 7: 119.
89. Goodin, D.S. A questionnaire to assess neurological impairment in multiple sclerosis. Mult Scler, 1998. 4: 444.
90. Foley, F.W., et al. The Multiple Sclerosis Intimacy and Sexuality Questionnaire -- re-validation and development of a 15-item version with a large US sample. Mult Scler, 2013. 19: 1197.
91. Sanders, A.S., et al. The Multiple Sclerosis Intimacy and Sexuality Questionnaire-19 (MSISQ-19). Sex Disabil, 2000. 18: 3.
92. Marrie, R.A., et al. Validity and reliability of the MSQLI in cognitively impaired patients with multiple sclerosis. Mult Scler, 2003. 9: 621.
93. Vickrey, B.G., et al. A health-related quality of life measure for multiple sclerosis. Qual Life Res, 1995. 4: 187.
94. Honan, C.A., et al. The multiple sclerosis work difficulties questionnaire (MSWDQ): development of a shortened scale. Disabil Rehabil, 2014. 36: 635.
95. Welk, B., et al. The validity and reliability of the neurogenic bladder symptom score. J Urol, 2014. 192: 452.
96. Bonniaud, V., et al. Measuring quality of life in multiple sclerosis patients with urinary disorders using the Qualiveen questionnaire. Arch Phys Med Rehabil, 2004. 85: 1317.
97. Franceschini, M., et al. Follow-up in persons with traumatic spinal cord injury: questionnaire reliability. Eura Medicophys, 2006. 42: 211.
98. Noreau, L., et al. Development and assessment of a community follow-up questionnaire for the Rick Hansen spinal cord injury registry. Arch Phys Med Rehabil, 2013. 94: 1753.
99. Husmann, D.A. Mortality following augmentation cystoplasty: A transitional urologist’s viewpoint. J Pediatr Urol, 2017.
100. Yang, C.C., et al. Bladder management in women with neurologic disabilities. Phys Med Rehabil Clin N Am, 2001. 12: 91.
101. Podnar, S., et al. Protocol for clinical neurophysiologic examination of the pelvic floor. Neurourol Urodyn, 2001. 20: 669.
102. Harrison, S., et al. Urinary incontinence in neurological disease: assessment and management. NICE Clinical Guideline 2012. [CG148].
103. Liu, N., et al. Autonomic dysreflexia severity during urodynamics and cystoscopy in individuals with spinal cord injury. Spinal Cord, 2013. 51: 863.
104. Krassioukov, A., et al. International standards to document remaining autonomic function after spinal cord injury. J Spinal Cord Med, 2012. 35: 201.
105. Labat, J.J., et al. Diagnostic criteria for pudendal neuralgia by pudendal nerve entrapment (Nantes criteria). Neurourol Urodyn, 2008. 27: 306.
106. Brown, D., Atlas of regional anesthesia. 3rd. ed. 2006, Philadelphia
107. Standring, S., Gray’s anatomy, . 40th ed. 2008.
108. Bellucci, C.H., et al. Neurogenic lower urinary tract dysfunction--do we need same session repeat urodynamic investigations? J Urol, 2012. 187: 1318.
109. Walter, M., et al. Autonomic dysreflexia and repeatability of cardiovascular changes during same session repeat urodynamic investigation in women with spinal cord injury. World J Urol, 2015.
110. Walter, M., et al. Prediction of autonomic dysreflexia during urodynamics: A prospective cohort study. BMC Med, 2018. 16: 53.
111. Gammie, A., et al. International Continence Society guidelines on urodynamic equipment performance. Neurourol Urodyn, 2014. 33: 370.
112. McGuire, E.J., et al. Leak-point pressures. Urol Clin North Am, 1996. 23: 253.
113. Ozkan, B., et al. Which factors predict upper urinary tract deterioration in overactive neurogenic bladder dysfunction? Urology, 2005. 66: 99.
114. Wang, Q.W., et al. Is it possible to use urodynamic variables to predict upper urinary tract dilatation in children with neurogenic bladder-sphincter dysfunction? BJU Int, 2006. 98: 1295.
115. Musco, S., et al. Value of urodynamic findings in predicting upper urinary tract damage in neuro-urological patients: A systematic review. Neurourol Urodyn, 2018.
116. Linsenmeyer, T.A., et al. The impact of urodynamic parameters on the upper tracts of spinal cord injured men who void reflexly. J Spinal Cord Med, 1998. 21: 15.
117. McGuire, E.J., et al. Prognostic value of urodynamic testing in myelodysplastic patients. J Urol, 1981. 126: 205.
118. Krongrad, A., et al. Bladder neck dysynergia in spinal cord injury. Am J Phys Med Rehabil, 1996. 75: 204.
119. Weld, K.J., et al. Clinical significance of detrusor sphincter dyssynergia type in patients with post-traumatic spinal cord injury. Urology, 2000. 56: 565.
120. Rossier, A.B., et al. 5-microtransducer catheter in evaluation of neurogenic bladder function. Urology, 1986. 27: 371.
121. Al-Ali, M., et al. A 10 year review of the endoscopic treatment of 125 spinal cord injured patients with vesical outlet obstruction: does bladder neck dyssynergia exist? Paraplegia, 1996. 34: 34.
122. Bacsu, C.D., et al. Diagnosing detrusor sphincter dyssynergia in the neurological patient. BJU Int, 2012. 109 Suppl 3: 31.
123. Lose, G., et al. Standardisation of urethral pressure measurement: report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn, 2002. 21: 258.
124. Marks, B.K., et al. Videourodynamics: indications and technique. Urol Clin North Am, 2014. 41: 383.
125. Virseda, M., et al. Reliability of ambulatory urodynamics in patients with spinal cord injuries. Neurourol Urodyn, 2013. 32: 387.
126. Virseda-Chamorro, M., et al. Comparison of ambulatory versus video urodynamics in patients with spinal cord injury. Spinal Cord, 2014. 52: 551.
127. Geirsson, G., et al. The ice-water test--a simple and valuable supplement to routine cystometry. Br J Urol, 1993. 71: 681.
128. Geirsson, G., et al. Pressure, volume and infusion speed criteria for the ice-water test. Br J Urol, 1994. 73: 498.
129. Al-Hayek, S., et al. The 50-year history of the ice water test in urology. J Urol, 2010. 183: 1686.
130. Lapides, J. Neurogenic bladder. Principles of treatment. Urol Clin North Am, 1974. 1: 81.
131. Riedl, C.R., et al. Electromotive administration of intravesical bethanechol and the clinical impact on acontractile detrusor management: introduction of a new test. J Urol, 2000. 164: 2108.
132. Podnar, S., et al. Lower urinary tract dysfunction in patients with peripheral nervous system lesions. Handb Clin Neurol, 2015. 130: 203.
133. Ouyang, L., et al. Characteristics and survival of patients with end stage renal disease and spina bifida in the United States renal data system. J Urol, 2015. 193: 558.
134. Lane, G.I., et al. Clinical outcomes of non-surgical management of detrusor leak point pressures above 40 cm water in adults with congenital neurogenic bladder. Neurourol Urodyn, 2018. 37: 1943.
135. Lawrenson, R., et al. Renal failure in patients with neurogenic lower urinary tract dysfunction. Neuroepidemiology, 2001. 20: 138.
136. Dangle, P.P., et al. Cystatin C-calculated Glomerular Filtration Rate-A Marker of Early Renal Dysfunction in Patients With Neuropathic Bladder. Urology, 2017. 100: 213.
137. Mingat, N., et al. Prospective study of methods of renal function evaluation in patients with neurogenic bladder dysfunction. Urology, 2013. 82: 1032.
138. Averbeck, M.A., et al. Follow-up of the neuro-urological patient: a systematic review. BJU Int, 2015. 115 Suppl 6: 39.
139. Stöhrer, M., et al. Diagnosis and treatment of bladder dysfunction in spinal cord injury patients. Eur Urol Update Series 1994. 3: 170. [No abstract available].
140. Apostolidis, A., et al., Neurologic Urinary and Faecal Incontinence, In: Incontinence 6th Edition, P. Abrams, L. Cardozo, S. Khoury & A. Wein, Editors. 2017.
141. Chamberlain, J.D., et al. Mortality and longevity after a spinal cord injury: systematic review and meta-analysis. Neuroepidemiology, 2015. 44: 182.
142. Game, X., et al. Botulinum toxin A detrusor injections in patients with neurogenic detrusor overactivity significantly decrease the incidence of symptomatic urinary tract infections. Eur Urol, 2008. 53: 613.
143. Frankel, H.L., et al. Long-term survival in spinal cord injury: a fifty year investigation. Spinal Cord, 1998. 36: 266.
144. Jamil, F. Towards a catheter free status in neurogenic bladder dysfunction: a review of bladder management options in spinal cord injury (SCI). Spinal Cord, 2001. 39: 355.
145. Thietje, R., et al. Mortality in patients with traumatic spinal cord injury: descriptive analysis of 62 deceased subjects. J Spinal Cord Med, 2011. 34: 482.
146. Hackler, R.H. A 25-year prospective mortality study in the spinal cord injured patient: comparison with the long-term living paraplegic. J Urol, 1977. 117: 486.
147. Rodrigues, P., et al. Involuntary detrusor contraction is a frequent finding in patients with recurrent urinary tract infections. Urol Int, 2014. 93: 67.
148. Bauer, S.B. Neurogenic bladder: etiology and assessment. Pediatr Nephrol, 2008. 23: 541.
149. Barbalias, G.A., et al. Critical evaluation of the Crede maneuver: a urodynamic study of 207 patients. J Urol, 1983. 130: 720.
150. Reinberg, Y., et al. Renal rupture after the Crede maneuver. J Pediatr, 1994. 124: 279.
151. Wyndaele, J.J., et al. Neurologic urinary incontinence. Neurourol Urodyn, 2010. 29: 159.
152. Menon, E.B., et al. Bladder training in patients with spinal cord injury. Urology, 1992. 40: 425.
153. Furusawa, K., et al. Incidence of symptomatic autonomic dysreflexia varies according to the bowel and bladder management techniques in patients with spinal cord injury. Spinal Cord, 2011. 49: 49.
154. Outcomes following traumatic spinal cord injury: clinical practice guidelines for health-care professionals. J Spinal Cord Med, 2000. 23: 289.
155. El-Masri, W.S., et al. Long-term follow-up study of outcomes of bladder management in spinal cord injury patients under the care of the Midlands Centre for Spinal Injuries in Oswestry. Spinal Cord, 2012. 50: 14.
156. Fall, M., et al. Electrical stimulation. A physiologic approach to the treatment of urinary incontinence. Urol Clin North Am, 1991. 18: 393.
157. Vodusek, D.B., et al. Detrusor inhibition induced by stimulation of pudendal nerve afferents. Neurourol Urodyn, 1986. 5: 381.
158. Gross, T., et al. Transcutaneous Electrical Nerve Stimulation for Treating Neurogenic Lower Urinary Tract Dysfunction: A Systematic Review. Eur Urol, 2016. 69: 1102.
159. Schneider, M.P., et al. Tibial Nerve Stimulation for Treating Neurogenic Lower Urinary Tract Dysfunction: A Systematic Review. Eur Urol, 2015.
160. Booth, J., et al. The effectiveness of transcutaneous tibial nerve stimulation (TTNS) for adults with overactive bladder syndrome: A systematic review. Neurourol Urodyn, 2018. 37: 528.
161. Liu, Y., et al. Effects of Transcutaneous Electrical Nerve Stimulation at Two Frequencies on Urinary Incontinence in Poststroke Patients: A Randomized Controlled Trial. Am J Phys Med Rehabil, 2016. 95: 183.
162. Guo, G.Y., et al. Effectiveness of neuromuscular electrical stimulation therapy in patients with urinary incontinence after stroke: A randomized sham controlled trial. Medicine, 2018. 97: e13702.
163. Shen, S.X., et al. A retrospective study of neuromuscular electrical stimulation for treating women with post-stroke incontinence. Medicine (United States), 2018. 97: e11264.
164. McClurg, D., et al. Neuromuscular electrical stimulation and the treatment of lower urinary tract dysfunction in multiple sclerosis--a double blind, placebo controlled, randomised clinical trial. Neurourol Urodyn, 2008. 27: 231.
165. Ferreira, A.P.S., et al. A Controlled Clinical Trial On The Effects Of Exercise On Lower Urinary Tract Symptoms In Women With Multiple Sclerosis. Am J Phys Med Rehabil, 2019.
166. McClurg, D., et al. Comparison of pelvic floor muscle training, electromyography biofeedback, and neuromuscular electrical stimulation for bladder dysfunction in people with multiple sclerosis: a randomized pilot study. Neurourol Urodyn, 2006. 25: 337.
167. Ferreira, A.P., et al. Impact of a Pelvic Floor Training Program Among Women with Multiple Sclerosis: A Controlled Clinical Trial. Am J Phys Med Rehabil, 2016. 95: 1.
168. Elmelund, M., et al. The effect of pelvic floor muscle training and intravaginal electrical stimulation on urinary incontinence in women with incomplete spinal cord injury: an investigator-blinded parallel randomized clinical trial. Int Urogynecol J, 2018. 29: 1597.
169. Hagerty, J.A., et al. Intravesical electrotherapy for neurogenic bladder dysfunction: a 22-year experience. J Urol, 2007. 178: 1680.
170. Primus, G., et al. Restoration of micturition in patients with acontractile and hypocontractile detrusor by transurethral electrical bladder stimulation. Neurourol Urodyn, 1996. 15: 489.
171. Lombardi, G., et al. Clinical efficacy of intravesical electrostimulation on incomplete spinal cord patients suffering from chronic neurogenic non-obstructive retention: a 15-year single centre retrospective study. Spinal Cord, 2013. 51: 232.
172. Brusa, L., et al. Effects of inhibitory rTMS on bladder function in Parkinson’s disease patients. Mov Disord, 2009. 24: 445.
173. Centonze, D., et al. Effects of motor cortex rTMS on lower urinary tract dysfunction in multiple sclerosis. Mult Scler, 2007. 13: 269.
174. Thomas, L.H., et al. Treatment of urinary incontinence after stroke in adults. Cochrane Database Syst Rev, 2008: CD004462.
175. Yeo, L., et al. Urinary tract dysfunction in Parkinson’s disease: a review. Int Urol Nephrol, 2012. 44: 415.
176. Phe, V., et al. Management of neurogenic bladder in patients with multiple sclerosis. Nature Reviews Urology, 2016. 13: 275.
177. Andersson, K.E. Antimuscarinic mechanisms and the overactive detrusor: an update. Eur Urol, 2011. 59: 377.
178. Bennett, N., et al. Can higher doses of oxybutynin improve efficacy in neurogenic bladder? J Urol, 2004. 171: 749.
179. Horstmann, M., et al. Neurogenic bladder treatment by doubling the recommended antimuscarinic dosage. Neurourol Urodyn, 2006. 25: 441.
180. Kennelly, M.J., et al. Overactive bladder: pharmacologic treatments in the neurogenic population. Rev Urol, 2008. 10: 182.
181. Madersbacher, H., et al. Neurogenic detrusor overactivity in adults: a review on efficacy, tolerability and safety of oral antimuscarinics. Spinal Cord, 2013. 51: 432.
182. Madhuvrata, P., et al. Anticholinergic drugs for adult neurogenic detrusor overactivity: a systematic review and meta-analysis. Eur Urol, 2012. 62: 816.
183. Stohrer, M., et al. EAU guidelines on neurogenic lower urinary tract dysfunction. Eur Urol, 2009. 56: 81.
184. Mehnert, U., et al. The management of urinary incontinence in the male neurological patient. Curr Opin Urol, 2014. 24: 586.
185. Stothers, L., et al. An integrative review of standardized clinical evaluation tool utilization in anticholinergic drug trials for neurogenic lower urinary tract dysfunction. Spinal Cord, 2016. 31: 31.
186. Amend, B., et al. Effective treatment of neurogenic detrusor dysfunction by combined high-dosed antimuscarinics without increased side-effects. Eur Urol, 2008. 53: 1021.
187. Cameron, A.P. Pharmacologic therapy for the neurogenic bladder. Urol Clin North Am, 2010. 37: 495.
188. Menarini, M., et al. Trospium chloride in patients with neurogenic detrusor overactivity: is dose titration of benefit to the patients? Int J Clin Pharmacol Ther, 2006. 44: 623.
189. Nardulli, R., et al. Combined antimuscarinics for treatment of neurogenic overactive bladder. Int J Immunopathol Pharmacol, 2012. 25: 35s.
190. Tijnagel, M.J., et al. Real life persistence rate with antimuscarinic treatment in patients with idiopathic or neurogenic overactive bladder: a prospective cohort study with solifenacin. BMC Urology, 2017. 17: 13.
191. Cameron, A.P., et al. Combination drug therapy improves compliance of the neurogenic bladder. J Urol, 2009. 182: 1062.
192. Isik, A.T., et al. Trospium and cognition in patients with late onset Alzheimer disease. J Nutr Health Aging, 2009. 13: 672.
193. Ethans, K.D., et al. Efficacy and safety of tolterodine in people with neurogenic detrusor overactivity. J Spinal Cord Med, 2004. 27: 214.
194. McKeage, K. Propiverine: A review of its use in the treatment of adults and children with overactive bladder associated with idiopathic or neurogenic detrusor overactivity, and in men with lower urinary tract symptoms. Clin Drug Invest, 2013. 33: 71.
195. Nicholas, R.S., et al. Anticholinergics for urinary symptoms in multiple sclerosis. Cochrane Database Syst Rev, 2009: CD004193.
196. van Rey, F., et al. Solifenacin in multiple sclerosis patients with overactive bladder: a prospective study. Adv Urol, 2011. 2011: 834753.
197. Bycroft, J., et al. The effect of darifenacin on neurogenic detrusor overactivity in patients with spinal cord injury. Neurourol Urodyn 2003. 22: A190.
198. Carl, S., et al. Darifenacin is also effective in neurogenic bladder dysfunction (multiple sclerosis). Urology, 2006. 68 250. [No abstract available].
199. Amarenco, G., et al. Solifenacin is effective and well tolerated in patients with neurogenic detrusor overactivity: Results from the double-blind, randomized, active- and placebo-controlled SONIC urodynamic study. Neurourol Urodyn, 2015. 29: 29.
200. Zesiewicz, T.A., et al. Randomized, controlled pilot trial of solifenacin succinate for overactive bladder in Parkinson’s disease. Parkinsonism Rel Disord, 2015. 21: 514.
201. Sakakibara, R., et al. Imidafenacin on bladder and cognitive function in neurologic OAB patients. Clin Auton Res, 2013. 23: 189.
202. Sugiyama, H., et al. Effect of imidafenacin on the urodynamic parameters of patients with indwelling bladder catheters due to spinal cord injury. Spinal Cord, 2017. 55: 187.
203. Stohrer, M., et al. Efficacy and tolerability of propiverine hydrochloride extended-release compared with immediate-release in patients with neurogenic detrusor overactivity. Spinal Cord, 2013. 51: 419.
204. Schroder, A., et al. Efficacy, safety, and tolerability of intravesically administered 0.1% oxybutynin hydrochloride solution in adult patients with neurogenic bladder: A randomized, prospective, controlled multi-center trial. Neurourol Urodyn, 2016. 35: 582.
205. Krhut, J., et al. Efficacy and safety of mirabegron for the treatment of neurogenic detrusor overactivity-Prospective, randomized, double-blind, placebo-controlled study. Neurourol Urodyn, 2018. 37: 2226.
206. Welk, B., et al. A pilot randomized-controlled trial of the urodynamic efficacy of mirabegron for patients with neurogenic lower urinary tract dysfunction. Neurourol Urodyn, 2018. 37: 2810.
207. Chen, S.F., et al. Therapeutic efficacy of low-dose (25mg) mirabegron therapy for patients with mild to moderate overactive bladder symptoms due to central nervous system diseases. LUTS: Lower Urinary Tract Symptoms, 2018.
208. Peyronnet, B., et al. Mirabegron in patients with Parkinson disease and overactive bladder symptoms: A retrospective cohort. Parkinsonism Rel Disord, 2018. 57: 22.
209. Zachariou, A., et al. Effective treatment of neurogenic detrusor overactivity in multiple sclerosis patients using desmopressin and mirabegron. Can J Urol, 2017. 24: 9107.
210. Abo Youssef, N., et al. Cannabinoids for treating neurogenic lower urinary tract dysfunction in patients with multiple sclerosis: a systematic review and meta-analysis. BJU Int, 2017. 119: 515.
211. Francomano, D., et al. Effects of daily tadalafil on lower urinary tract symptoms in young men with multiple sclerosis and erectile dysfunction: a pilot study. J Endocrinol Invest, 2017. 40: 275.
212. Phe, V., et al. Desmopressin for treating nocturia in patients with multiple sclerosis: A systematic review: A report from the Neuro-Urology Promotion Committee of the International Continence Society (ICS). Neurourol Urodyn, 2019. 38: 563.
213. Barendrecht, M.M., et al. Is the use of parasympathomimetics for treating an underactive urinary bladder evidence-based? BJU Int, 2007. 99: 749.
214. Apostolidis, A. Taming the cannabinoids: new potential in the pharmacologic control of lower urinary tract dysfunction. Eur Urol, 2012. 61: 107.
215. Gratzke, C., et al. Effects of cannabinor, a novel selective cannabinoid 2 receptor agonist, on bladder function in normal rats. Eur Urol, 2010. 57: 1093.
216. Abrams, P., et al. Tamsulosin: efficacy and safety in patients with neurogenic lower urinary tract dysfunction due to suprasacral spinal cord injury. J Urol, 2003. 170: 1242.
217. Gomes, C.M., et al. Neurological status predicts response to alpha-blockers in men with voiding dysfunction and Parkinson’s disease. Clinics, 2014. 69: 817.
218. Moon, K.H., et al. A 12-week, open label, multi-center study to evaluate the clinical efficacy and safety of silodosin on voiding dysfunction in patients with neurogenic bladder. LUTS: Lower Urinary Tract Symptoms, 2015. 7: 27.
219. Guttmann, L., et al. The value of intermittent catheterisation in the early management of traumatic paraplegia and tetraplegia. Paraplegia, 1966. 4: 63.
220. Lapides, J., et al. Clean, intermittent self-catheterization in the treatment of urinary tract disease. J Urol, 1972. 107: 458.
221. Wyndaele, J.J. Intermittent catheterization: which is the optimal technique? Spinal Cord, 2002. 40: 432.
222. Prieto-Fingerhut, T., et al. A study comparing sterile and nonsterile urethral catheterization in patients with spinal cord injury. Rehabil Nurs, 1997. 22: 299.
223. Prieto, J., et al. Intermittent catheterisation for long-term bladder management. Cochrane Database Syst Rev, 2014: CD006008.
224. Kiddoo, D., et al. Randomized Crossover Trial of Single Use Hydrophilic Coated vs Multiple Use Polyvinylchloride Catheters for Intermittent Catheterization to Determine Incidence of Urinary Infection. J Urol, 2015. 194: 174.
225. Goetz, L.L., et al. International Spinal Cord Injury Urinary Tract Infection Basic Data Set. Spinal Cord, 2013. 51: 700.
226. Bakke, A., et al. Physical predictors of infection in patients treated with clean intermittent catheterization: a prospective 7-year study. Br J Urol, 1997. 79: 85.
227. Günther, M., et al. Auswirkungen des aseptischen intermittierenden Katheterismus auf die männliche Harnröhre. Der Urologe B, 2001. 41: 359.
228. Kurze, I., et al. Intermittent Catheterisation and Prevention of Urinary Tract Infections in Patients with Neurogenic Lower Urinary Tract Dysfunction - Best PracticeAn Overview. [German]. Aktuelle Neurologie, 2015. 42: 515. [No abstract available].
229. Waller, L., et al. Clean intermittent catheterization in spinal cord injury patients: long-term followup of a hydrophilic low friction technique. J Urol, 1995. 153: 345.
230. Wyndaele, J.J. Complications of intermittent catheterization: their prevention and treatment. Spinal Cord, 2002. 40: 536.
231. Woodbury, M.G., et al. Intermittent catheterization practices following spinal cord injury: a national survey. Can J Urol, 2008. 15: 4065.
232. Bennett, C.J., et al. Comparison of bladder management complication outcomes in female spinal cord injury patients. J Urol, 1995. 153: 1458.
233. Chao, R., et al. Fate of upper urinary tracts in patients with indwelling catheters after spinal cord injury. Urology, 1993. 42: 259.
234. Larsen, L.D., et al. Retrospective analysis of urologic complications in male patients with spinal cord injury managed with and without indwelling urinary catheters. Urology, 1997. 50: 418.
235. Mitsui, T., et al. Is suprapubic cystostomy an optimal urinary management in high quadriplegics?. A comparative study of suprapubic cystostomy and clean intermittent catheterization. Eur Urol, 2000. 38: 434.
236. Weld, K.J., et al. Effect of bladder management on urological complications in spinal cord injured patients. J Urol, 2000. 163: 768.
237. Weld, K.J., et al. Influences on renal function in chronic spinal cord injured patients. J Urol, 2000. 164: 1490.
238. West, D.A., et al. Role of chronic catheterization in the development of bladder cancer in patients with spinal cord injury. Urology, 1999. 53: 292.
239. Lavelle, R.S., et al. Quality of life after suprapubic catheter placement in patients with neurogenic bladder conditions. Neurourol Urodyn, 2016. 35: 831.
240. Hollingsworth, J.M., et al. Determining the noninfectious complications of indwelling urethral catheters: a systematic review and meta-analysis. Ann Intern Med, 2013. 159: 401.
241. Buyse, G., et al. Intravesical oxybutynin for neurogenic bladder dysfunction: less systemic side effects due to reduced first pass metabolism. J Urol, 1998. 160: 892.
242. Di Stasi, S.M., et al. Intravesical oxybutynin: mode of action assessed by passive diffusion and electromotive administration with pharmacokinetics of oxybutynin and N-desethyl oxybutynin. J Urol, 2001. 166: 2232.
243. Haferkamp, A., et al. Dosage escalation of intravesical oxybutynin in the treatment of neurogenic bladder patients. Spinal Cord, 2000. 38: 250.
244. Pannek, J., et al. Combined intravesical and oral oxybutynin chloride in adult patients with spinal cord injury. Urology, 2000. 55: 358.
245. Giannantoni, A., et al. Intravesical resiniferatoxin versus botulinum-A toxin injections for neurogenic detrusor overactivity: a prospective randomized study. J Urol, 2004. 172: 240.
246. Kim, J.H., et al. Intravesical resiniferatoxin for refractory detrusor hyperreflexia: a multicenter, blinded, randomized, placebo-controlled trial. J Spinal Cord Med, 2003. 26: 358.
247. Phe, V., et al. Intravesical vanilloids for treating neurogenic lower urinary tract dysfunction in patients with multiple sclerosis: A systematic review and meta-analysis. A report from the Neuro-Urology Promotion Committee of the International Continence Society (ICS). Neurourol Urodyn, 2018. 37: 67.
248. Del Popolo, G., et al. Neurogenic detrusor overactivity treated with english botulinum toxin a: 8-year experience of one single centre. Eur Urol, 2008. 53: 1013.
249. Reitz, A., et al. European experience of 200 cases treated with botulinum-A toxin injections into the detrusor muscle for urinary incontinence due to neurogenic detrusor overactivity. Eur Urol, 2004. 45: 510.
250. Yuan, H., et al. Efficacy and Adverse Events Associated With Use of OnabotulinumtoxinA for Treatment of Neurogenic Detrusor Overactivity: A Meta-Analysis. Int Neurourol J, 2017. 21: 53.
251. Cheng, T., et al. Efficacy and Safety of OnabotulinumtoxinA in Patients with Neurogenic Detrusor Overactivity: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. PLoS One, 2016. 11: e0159307.
252. Wagle Shukla, A., et al. Botulinum Toxin Therapy for Parkinson’s Disease. Seminars in Neurology, 2017. 37: 193.
253. Koschorke, M., et al. Intradetrusor onabotulinumtoxinA injections for refractory neurogenic detrusor overactivity incontinence: do we need urodynamic investigation for outcome assessment? BJU International, 2017. 120: 848.
254. Ginsberg, D., et al. Phase 3 efficacy and tolerability study of onabotulinumtoxinA for urinary incontinence from neurogenic detrusor overactivity. J Urol, 2012. 187: 2131.
255. Grosse, J., et al. Success of repeat detrusor injections of botulinum a toxin in patients with severe neurogenic detrusor overactivity and incontinence. Eur Urol, 2005. 47: 653.
256. Rovner, E., et al. Long-Term Efficacy and Safety of OnabotulinumtoxinA in Patients with Neurogenic Detrusor Overactivity Who Completed 4 Years of Treatment. J Urol, 2016.
257. Ni, J., et al. Is repeat Botulinum Toxin A injection valuable for neurogenic detrusor overactivity-A systematic review and meta-analysis. Neurourol Urodyn, 2018. 37: 542.
258. Michel, F., et al. Botulinum toxin type A injection after failure of augmentation enterocystoplasty performed for neurogenic detrusor overactivity: preliminary results of a salvage strategy. The ENTEROTOX study. Urology, 2019.
259. Bottet, F., et al. Switch to Abobotulinum toxin A may be useful in the treatment of neurogenic detrusor overactivity when intradetrusor injections of Onabotulinum toxin A failed. Neurourol Urodyn, 2017. 21: 21.
260. Leu, R., et al. Complications of Botox and their Management. Curr Urol Rep, 2018. 19: 90.
261. Tullman, M., et al. Low-dose onabotulinumtoxinA improves urinary symptoms in noncatheterizing patients with MS. Neurology, 2018. 91: e657.
262. Tyagi, P., et al. Past, Present and Future of Chemodenervation with Botulinum Toxin in the Treatment of Overactive Bladder. J Urol, 2017. 197: 982.
263. Young, M.J., et al. Another Therapeutic Role for Intravesical Botulinum Toxin: Patients with Long-stay Catheters and Refractory Bladder Pain and Catheter Bypass Leakage. Eur Urol Focus, 2018.
264. Dykstra, D.D., et al. Treatment of detrusor-sphincter dyssynergia with botulinum A toxin: a double-blind study. Arch Phys Med Rehabil, 1990. 71: 24.
265. Schurch, B., et al. Botulinum-A toxin as a treatment of detrusor-sphincter dyssynergia: a prospective study in 24 spinal cord injury patients. J Urol, 1996. 155: 1023.
266. Huang, M., et al. Effects of botulinum toxin A injections in spinal cord injury patients with detrusor overactivity and detrusor sphincter dyssynergia. J Rehabil Med, 2016. 48: 683.
267. Utomo, E., et al. Surgical management of functional bladder outlet obstruction in adults with neurogenic bladder dysfunction. Cochrane Database Syst Rev, 2014. 5: CD004927.
268. Chancellor, M.B., et al. Prospective comparison of external sphincter balloon dilatation and prosthesis placement with external sphincterotomy in spinal cord injured men. Arch Phys Med Rehabil, 1994. 75: 297.
269. Bennett, J.K., et al. Collagen injections for intrinsic sphincter deficiency in the neuropathic urethra. Paraplegia, 1995. 33: 697.
270. Block, C.A., et al. Long-term efficacy of periurethral collagen injection for the treatment of urinary incontinence secondary to myelomeningocele. J Urol, 2003. 169: 327.
271. Schurch, B., et al. Intraurethral sphincter prosthesis to treat hyporeflexic bladders in women: does it work? BJU Int, 1999. 84: 789.
272. Reuvers, S.H.M., et al. Heterogeneity in reporting on urinary outcome and cure after surgical interventions for stress urinary incontinence in adult neuro-urological patients: A systematic review. Neurourol Urodyn, 2018. 37: 554.
273. Barthold, J.S., et al. Results of the rectus fascial sling and wrap procedures for the treatment of neurogenic sphincteric incontinence. J Urol, 1999. 161: 272.
274. Gormley, E.A., et al. Pubovaginal slings for the management of urinary incontinence in female adolescents. J Urol, 1994. 152: 822.
275. Kakizaki, H., et al. Fascial sling for the management of urinary incontinence due to sphincter incompetence. J Urol, 1995. 153: 644.
276. Mingin, G.C., et al. The rectus myofascial wrap in the management of urethral sphincter incompetence. BJU Int, 2002. 90: 550.
277. Abdul-Rahman, A., et al. Long-term outcome of tension-free vaginal tape for treating stress incontinence in women with neuropathic bladders. BJU Int, 2010. 106: 827.
278. Losco, G.S., et al. Long-term outcome of transobturator tape (TOT) for treatment of stress urinary incontinence in females with neuropathic bladders. Spinal Cord, 2015. 53: 544.
279. El-Azab, A.S., et al. Midurethral slings versus the standard pubovaginal slings for women with neurogenic stress urinary incontinence. Int Urogynecol J, 2015. 26: 427.
280. Athanasopoulos, A., et al. Treating stress urinary incontinence in female patients with neuropathic bladder: the value of the autologous fascia rectus sling. Int Urol Nephrol, 2012. 44: 1363.
281. Groen, L.A., et al. The AdVance male sling as a minimally invasive treatment for intrinsic sphincter deficiency in patients with neurogenic bladder sphincter dysfunction: a pilot study. Neurourol Urodyn, 2012. 31: 1284.
282. Mehnert, U., et al. Treatment of neurogenic stress urinary incontinence using an adjustable continence device: 4-year followup. J Urol, 2012. 188: 2274.
283. Daneshmand, S., et al. Puboprostatic sling repair for treatment of urethral incompetence in adult neurogenic incontinence. J Urol, 2003. 169: 199.
284. Herschorn, S., et al. Fascial slings and bladder neck tapering in the treatment of male neurogenic incontinence. J Urol, 1992. 147: 1073.
285. Light, J.K., et al. Use of the artificial urinary sphincter in spinal cord injury patients. J Urol, 1983. 130: 1127.
286. Farag, F., et al. Surgical treatment of neurogenic stress urinary incontinence: A systematic review of quality assessment and surgical outcomes. Neurourol Urodyn, 2016. 35: 21.
287. Kim, S.P., et al. Long-term durability and functional outcomes among patients with artificial urinary sphincters: a 10-year retrospective review from the University of Michigan. J Urol, 2008. 179: 1912.
288. Wang, R., et al. Long-term outcomes after primary failures of artificial urinary sphincter implantation. Urology, 2012. 79: 922.
289. Guillot-Tantay, C., et al. [Male neurogenic stress urinary incontinence treated by artificial urinary sphincter AMS 800TM (Boston Scientific, Boston, USA): Very long-term results (>25 years)]. Traitement de l’incontinence urinaire masculine neurologique par le sphincter urinaire artificiel AMS 800TM (Boston Scientific, Boston, Etats-Unis) : resultats a tres long terme (>25 ans). 2018. 28: 39.
290. Fournier, G., et al. Robotic-assisted laparoscopic implantation of artificial urinary sphincter in women with intrinsic sphincter deficiency incontinence: initial results. Urology, 2014. 84: 1094.
291. Biardeau, X., et al. Robot-assisted laparoscopic approach for artificial urinary sphincter implantation in 11 women with urinary stress incontinence: surgical technique and initial experience. Eur Urol, 2015. 67: 937.
292. Peyronnet, B., et al. Artificial urinary sphincter implantation in women with stress urinary incontinence: preliminary comparison of robot-assisted and open approaches. Int Urogynecol J, 2016. 27: 475.
293. Phe, V., et al. Stress urinary incontinence in female neurological patients: long-term functional outcomes after artificial urinary sphincter (AMS 800(TM) ) implantation. Neurourol Urodyn, 2017. 36: 764.
294. Scott, K.A., et al. Use of Artificial Urinary Sphincter and Slings to Manage Neurogenic Bladder Following Spinal Cord Injury-Is It Safe? Curr Bladder Dysf Rep, 2017. 12: 311.
295. Ammirati, E., et al. Management of male and female neurogenic stress urinary incontinence in spinal cord injured (SCI) patients using adjustable continence therapy. Urologia, 2017. 0: 16.
296. Ronzi, Y., et al. Neurogenic stress urinary incontinence: is there a place for Adjustable Continence Therapy (ACTTM and ProACTTM, Uromedica, Plymouth, MN, USA)? A retrospective multicenter study. Spinal Cord, 2019.
297. Janknegt, R.A., et al. Electrically stimulated gracilis sphincter for treatment of bladder sphincter incontinence. Lancet, 1992. 340: 1129.
298. Chancellor, M.B., et al. Gracilis muscle transposition with electrical stimulation for sphincteric incontinence: a new approach. World J Urol, 1997. 15: 320.
299. Chancellor, M.B., et al. Gracilis urethromyoplasty--an autologous urinary sphincter for neurologically impaired patients with stress incontinence. Spinal Cord, 1997. 35: 546.
300. Donnahoo, K.K., et al. The Young-Dees-Leadbetter bladder neck repair for neurogenic incontinence. J Urol, 1999. 161: 1946.
301. Kropp, K.A., et al. Urethral lengthening and reimplantation for neurogenic incontinence in children. J Urol, 1986. 135: 533.
302. Salle, J.L., et al. Urethral lengthening with anterior bladder wall flap (Pippi Salle procedure): modifications and extended indications of the technique. J Urol, 1997. 158: 585.
303. Rawashdeh, Y.F., et al. International Children’s Continence Society’s recommendations for therapeutic intervention in congenital neuropathic bladder and bowel dysfunction in children. Neurourol Urodyn, 2012. 31: 615.
304. Wyndaele, J.-J., et al. Surgical management of the neurogenic bladder after spinal cord injury. World J Urol, 2018.
305. Moisey, C.U., et al. Results of transurethral resection of prostate in patients with cerebrovascular disease. Br J Urol, 1978. 50: 539.
306. Roth, B., et al. Benign prostatic obstruction and parkinson’s disease--should transurethral resection of the prostate be avoided? J Urol, 2009. 181: 2209.
307. Elsaesser, E., et al. Urological operations for improvement of bladder voiding in paraplegic patients. Paraplegia, 1972. 10: 68.
308. Cornejo-Davila, V., et al. Incidence of Urethral Stricture in Patients With Spinal Cord Injury Treated With Clean Intermittent Self-Catheterization. Urology, 2017. 99: 260.
309. Perkash, I. Ablation of urethral strictures using contact chisel crystal firing neodymium:YAG laser. J Urol, 1997. 157: 809.
310. Schurch, B., et al. Botulinum toxin type a is a safe and effective treatment for neurogenic urinary incontinence: results of a single treatment, randomized, placebo controlled 6-month study. J Urol, 2005. 174: 196.
311. Madersbacher, H., et al. Twelve o’clock sphincterotomy: technique, indications, results. (Abbreviated report). Urol Int, 1975. 30: 75.
312. Perkash, I. Laser sphincterotomy and ablation of the prostate using a sapphire chisel contact tip firing neodymium:YAG laser. J Urol, 1994. 152: 2020.
313. Noll, F., et al. Transurethral sphincterotomy in quadriplegic patients: long-term-follow-up. Neurourol Urodyn, 1995. 14: 351.
314. Derry, F., et al. Audit of bladder neck resection in spinal cord injured patients. Spinal Cord, 1998. 36: 345.
315. Perkash, I. Use of contact laser crystal tip firing Nd:YAG to relieve urinary outflow obstruction in male neurogenic bladder patients. J Clin Laser Med Surg, 1998. 16: 33.
316. Chancellor, M.B., et al. Long-term followup of the North American multicenter UroLume trial for the treatment of external detrusor-sphincter dyssynergia. J Urol, 1999. 161: 1545.
317. Seoane-Rodriguez, S., et al. Long-term follow-up study of intraurethral stents in spinal cord injured patients with detrusor-sphincter dyssynergia. Spinal Cord, 2007. 45: 621.
318. Gajewski, J.B., et al. Removal of UroLume endoprosthesis: experience of the North American Study Group for detrusor-sphincter dyssynergia application. J Urol, 2000. 163: 773.
319. Wilson, T.S., et al. UroLume stents: lessons learned. J Urol, 2002. 167: 2477.
320. Abdul-Rahman, A., et al. A 20-year follow-up of the mesh wallstent in the treatment of detrusor external sphincter dyssynergia in patients with spinal cord injury. BJU Int, 2010. 106: 1510.
321. Pannek, J., et al. Clinical usefulness of the memokath stent as a second-line procedure after sphincterotomy failure. J Endourol, 2011. 25: 335.
322. Polguer, T., et al. [Treatment of detrusor-striated sphincter dyssynergia with permanent nitinol urethral stent: results after a minimum follow-up of 2 years]. Prog Urol, 2012. 22: 1058.
323. van der Merwe, A., et al. Outcome of dual flange metallic urethral stents in the treatment of neuropathic bladder dysfunction after spinal cord injury. J Endourol, 2012. 26: 1210.
324. Brindley, G.S. An implant to empty the bladder or close the urethra. J Neurol Neurosurg Psychiatry, 1977. 40: 358.
325. Krasmik, D., et al. Urodynamic results, clinical efficacy, and complication rates of sacral intradural deafferentation and sacral anterior root stimulation in patients with neurogenic lower urinary tract dysfunction resulting from complete spinal cord injury. Neurourol Urodyn, 2014. 33: 1202.
326. Benard, A., et al. Comparative cost-effectiveness analysis of sacral anterior root stimulation for rehabilitation of bladder dysfunction in spinal cord injured patients. Neurosurgery, 2013. 73: 600.
327. Martens, F.M., et al. Quality of life in complete spinal cord injury patients with a Brindley bladder stimulator compared to a matched control group. Neurourol Urodyn, 2011. 30: 551.
328. Krebs, J., et al. Long-term course of sacral anterior root stimulation in spinal cord injured individuals: The fate of the detrusor. Neurourol Urodyn, 2017. 36: 1596.
329. Krebs, J., et al. Charcot arthropathy of the spine in spinal cord injured individuals with sacral deafferentation and anterior root stimulator implantation. Neurourol Urodyn, 2016. 35: 241.
330. Nagib, A., et al. Successful control of selective anterior sacral rhizotomy for treatment of spastic bladder and ureteric reflux in paraplegics. Med Serv J Can, 1966. 22: 576.
331. Schneidau, T., et al. Selective sacral rhizotomy for the management of neurogenic bladders in spina bifida patients: long-term followup. J Urol, 1995. 154: 766.
332. Young, B., et al. Percutaneous sacral rhizotomy for neurogenic detrusor hyperreflexia. J Neurosurg, 1980. 53: 85.
333. Koldewijn, E.L., et al. Bladder compliance after posterior sacral root rhizotomies and anterior sacral root stimulation. J Urol, 1994. 151: 955.
334. Singh, G., et al. Intravesical oxybutynin in patients with posterior rhizotomies and sacral anterior root stimulators. Neurourol Urodyn, 1995. 14: 65.
335. Van Kerrebroeck, P.E., et al. Results of the treatment of neurogenic bladder dysfunction in spinal cord injury by sacral posterior root rhizotomy and anterior sacral root stimulation. J Urol, 1996. 155: 1378.
336. Kutzenberger, J.S. Surgical therapy of neurogenic detrusor overactivity (hyperreflexia) in paraplegic patients by sacral deafferentation and implant driven micturition by sacral anterior root stimulation: methods, indications, results, complications, and future prospects. Acta Neurochir, 2007. 97: 333.
337. Bhadra, N., et al. Selective suppression of sphincter activation during sacral anterior nerve root stimulation. Neurourol Urodyn, 2002. 21: 55.
338. Kirkham, A.P., et al. Neuromodulation through sacral nerve roots 2 to 4 with a Finetech-Brindley sacral posterior and anterior root stimulator. Spinal Cord, 2002. 40: 272.
339. Schumacher, S., et al. Extradural cold block for selective neurostimulation of the bladder: development of a new technique. J Urol, 1999. 161: 950.
340. Wollner, J., et al. Surgery Illustrated - surgical atlas sacral neuromodulation. BJU Int, 2012. 110: 146.
341. Kessler, T.M., et al. Sacral neuromodulation for neurogenic lower urinary tract dysfunction: systematic review and meta-analysis. Eur Urol, 2010. 58: 865.
342. Lombardi, G., et al. Sacral neuromodulation for neurogenic non-obstructive urinary retention in incomplete spinal cord patients: a ten-year follow-up single-centre experience. Spinal Cord, 2014. 52: 241.
343. Lay, A.H., et al. The role of neuromodulation in patients with neurogenic overactive bladder. Curr Urol Rep, 2012. 13: 343.
344. Puccini, F., et al. Sacral neuromodulation: an effective treatment for lower urinary tract symptoms in multiple sclerosis. Int Urogynecol J Pelvic Floor Dysf, 2016. 27: 347.
345. Zhang, Y.H., et al. Enveloping the bladder with displacement of flap of the rectus abdominis muscle for the treatment of neurogenic bladder. J Urol, 1990. 144: 1194.
346. Stenzl, A., et al. Restoration of voluntary emptying of the bladder by transplantation of innervated free skeletal muscle. Lancet, 1998. 351: 1483.
347. Gakis, G., et al. Functional detrusor myoplasty for bladder acontractility: long-term results. J Urol, 2011. 185: 593.
348. Ninkovic, M., et al. The latissimus dorsi detrusor myoplasty for functional treatment of bladder acontractility. Clin Plast Surg, 2012. 39: 507.
349. Duel, B.P., et al. Alternative techniques for augmentation cystoplasty. J Urol, 1998. 159: 998.
350. Snow, B.W., et al. Bladder autoaugmentation. Urol Clin North Am, 1996. 23: 323.
351. Stohrer, M., et al. Bladder auto-augmentation--an alternative for enterocystoplasty: preliminary results. Neurourol Urodyn, 1995. 14: 11.
352. Stohrer, M., et al. Bladder autoaugmentation in adult patients with neurogenic voiding dysfunction. Spinal Cord, 1997. 35: 456.
353. Vainrib, M., et al. Differences in urodynamic study variables in adult patients with neurogenic bladder and myelomeningocele before and after augmentation enterocystoplasty. Neurourol Urodyn, 2013. 32: 250.
354. Krebs, J., et al. Functional outcome of supratrigonal cystectomy and augmentation ileocystoplasty in adult patients with refractory neurogenic lower urinary tract dysfunction. Neurourol Urodyn, 2016. 35.
355. Hoen, L., et al. Long-term effectiveness and complication rates of bladder augmentation in patients with neurogenic bladder dysfunction: A systematic review. Neurourol Urodyn, 2017. 07: 07.
356. Myers, J.B., et al. The effects of augmentation cystoplasty and botulinum toxin injection on patient-reported bladder function and quality of life among individuals with spinal cord injury performing clean intermittent catheterization. Neurourol Urodyn, 2019. 38: 285.
357. Mitsui, T., et al. Preoperative renal scar as a risk factor of postoperative metabolic acidosis following ileocystoplasty in patients with neurogenic bladder. Spinal Cord, 2014. 52: 292.
358. Perrouin-Verbe, M.A., et al. Long-term functional outcomes of augmentation cystoplasty in adult spina bifida patients: A single-center experience in a multidisciplinary team. Neurourol Urodyn, 2019. 38: 330.
359. Moreno, J.G., et al. Improved quality of life and sexuality with continent urinary diversion in quadriplegic women with umbilical stoma. Arch Phys Med Rehabil, 1995. 76: 758.
360. Peterson, A.C., et al. Urinary diversion in patients with spinal cord injury in the United States. Urology, 2012. 80: 1247.
361. Sylora, J.A., et al. Intermittent self-catheterization by quadriplegic patients via a catheterizable Mitrofanoff channel. J Urol, 1997. 157: 48.
362. Van Savage, J.G., et al. Transverse retubularized sigmoidovesicostomy continent urinary diversion to the umbilicus. J Urol, 2001. 166: 644.
363. Vanni, A.J., et al. Ileovesicostomy for the neurogenic bladder patient: outcome and cost comparison of open and robotic assisted techniques. Urology, 2011. 77: 1375.
364. Wiener, J.S., et al. Bladder augmentation versus urinary diversion in patients with spina bifida in the United States. J Urol, 2011. 186: 161.
365. Phe, V., et al. Continent catheterizable tubes/stomas in adult neuro-urological patients: A systematic review. Neurourol Urodyn, 2017.
366. Atan, A., et al. Advantages and risks of ileovesicostomy for the management of neuropathic bladder. Urology, 1999. 54: 636.
367. Cass, A.S., et al. A 22-year followup of ileal conduits in children with a neurogenic bladder. J Urol, 1984. 132: 529.
368. Hald, T., et al. Vesicostomy--an alternative urine diversion operation. Long term results. Scand J Urol Nephrol, 1978. 12: 227.
369. Schwartz, S.L., et al. Incontinent ileo-vesicostomy urinary diversion in the treatment of lower urinary tract dysfunction. J Urol, 1994. 152: 99.
370. Sakhri, R., et al. [Laparoscopic cystectomy and ileal conduit urinary diversion for neurogenic bladders and related conditions. Morbidity and better quality of life]. Prog Urol, 2015. 25: 342.
371. Herschorn, S., et al. Urinary undiversion in adults with myelodysplasia: long-term followup. J Urol, 1994. 152: 329.
372. Mukai, S., et al. Retrospective study for risk factors for febrile UTI in spinal cord injury patients with routine concomitant intermittent catheterization in outpatient settings. Spinal Cord, 2016. 54: 69.
373. Vasudeva, P., et al. Factors implicated in pathogenesis of urinary tract infections in neurogenic bladders: some revered, few forgotten, others ignored. Neurourol Urodyn, 2014. 33: 95.
374. Lenherr, S.M., et al. Glycemic Control and Urinary Tract Infections in Women with Type 1 Diabetes: Results from the DCCT/EDIC. J Urol, 2016. 196: 1129.
375. Bakke, A., et al. Bacteriuria in patients treated with clean intermittent catheterization. Scand J Infect Dis, 1991. 23: 577.
376. Waites, K.B., et al. Epidemiology and risk factors for urinary tract infection following spinal cord injury. Arch Phys Med Rehabil, 1993. 74: 691.
377. Nicolle, L.E., et al. Infectious Diseases Society of America guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults. Clin Infect Dis, 2005. 40: 643.
378. Pannek, J. Treatment of urinary tract infection in persons with spinal cord injury: guidelines, evidence, and clinical practice. A questionnaire-based survey and review of the literature. J Spinal Cord Med, 2011. 34: 11.
379. Alavinia, S.M., et al. Enhancing quality practice for prevention and diagnosis of urinary tract infection during inpatient spinal cord rehabilitation. J Spinal Cord Med, 2017. 40: 803.
380. Deville, W.L., et al. The urine dipstick test useful to rule out infections. A meta-analysis of the accuracy. BMC Urol, 2004. 4: 4.
381. Hoffman, J.M., et al. Nitrite and leukocyte dipstick testing for urinary tract infection in individuals with spinal cord injury. J Spinal Cord Med, 2004. 27: 128.
382. Biering-Sorensen, F., et al. Urinary tract infections in patients with spinal cord lesions: treatment and prevention. Drugs, 2001. 61: 1275.
383. Everaert, K., et al. Urinary tract infections in spinal cord injury: prevention and treatment guidelines. Acta Clin Belg, 2009. 64: 335.
384. Clark, R., et al. The ability of prior urinary cultures results to predict future culture results in neurogenic bladder patients. Neurourol Urodyn, 2018. 37: 2645.
385. Pannek, J., et al. Treatment of Complicated Urinary Tract Infections in Individuals with Chronic Neurogenic Lower Urinary Tract Dysfunction: Are Antibiotics Mandatory? Urologia Int, 2018.
386. Del Popolo, G., et al. Recurrent bacterial symptomatic cystitis: A pilot study on a new natural option for treatment. Arch Ital Urol Androl, 2018. 9: 101.
387. Jia, C., et al. Detrusor botulinum toxin A injection significantly decreased urinary tract infection in patients with traumatic spinal cord injury. Spinal Cord, 2013. 51: 487.
388. Waites, K.B., et al. Evaluation of 3 methods of bladder irrigation to treat bacteriuria in persons with neurogenic bladder. J Spinal Cord Med, 2006. 29: 217.
389. Gallien, P., et al. Cranberry versus placebo in the prevention of urinary infections in multiple sclerosis: a multicenter, randomized, placebo-controlled, double-blind trial. Mult Scler, 2014. 20: 1252.
390. Toh, S.L., et al. Probiotics [LGG-BB12 or RC14-GR1] versus placebo as prophylaxis for urinary tract infection in persons with spinal cord injury [ProSCIUTTU]: a randomised controlled trial. Spinal Cord, 2019. 57: 550.
391. Lee, B.S., et al. Methenamine hippurate for preventing urinary tract infections. Cochrane Database Syst Rev, 2012. 10: CD003265.
392. Günther, M., et al. Harnwegsinfektprophylaxe. Urinansäuerung mittels L-Methionin bei neurogener Blasenfunktionsstörung. Urologe B, 2002. 42: 218.
393. Hachen, H.J. Oral immunotherapy in paraplegic patients with chronic urinary tract infections: a double-blind, placebo-controlled trial. J Urol, 1990. 143: 759.
394. Krebs, J., et al. Effects of oral immunomodulation therapy on urinary tract infections in individuals with chronic spinal cord injury-A retrospective cohort study. Neurourol Urodyn, 2018.
395. Poirier, C., et al. Prevention of urinary tract infections by antibiotic cycling in spinal cord injury patients and low emergence of multidrug resistant bacteria. Medecine et Maladies Infectieuses, 2016. 16: 16.
396. Darouiche, R.O., et al. Multicenter randomized controlled trial of bacterial interference for prevention of urinary tract infection in patients with neurogenic bladder. Urology, 2011. 78: 341.
397. Pannek, J., et al. Usefulness of classical homeopathy for the prophylaxis of recurrent urinary tract infections in individuals with chronic neurogenic lower urinary tract dysfunction. J Spinal Cord Med, 2018: 1.
398. Cox, L., et al. Gentamicin bladder instillations decrease symptomatic urinary tract infections in neurogenic bladder patients on intermittent catheterization. Can Urol Assoc J, 2017. 11: E350.
399. Pannek, J., et al. Usefulness of classical homoeopathy for the prevention of urinary tract infections in patients with neurogenic bladder dysfunction: A case series. Indian J Res Homoeopathy, 2014. 8: 31.
400. Rees, P.M., et al. Sexual function in men and women with neurological disorders. Lancet, 2007. 369: 512.
401. Lombardi, G., et al. Management of sexual dysfunction due to central nervous system disorders: a systematic review. BJU Int, 2015. 115 Suppl 6: 47.
402. Jungwirth, A., et al., EAU Guidelines on Male Infertility, in Presented at the 30th Annual Congress in Madrid. 2015.
403. Hatzimouratidis, K., et al., EAU guidelines on Male Sexual Dysfunction and Premature Ejaculation., in Presented at the 30th Annual Congress in Madrid. 2014.
404. Foley, F.W., Sexuality, In: Multiple Sclerosis: A Guide for Families. Kalb. RC., Editor. 2006, Demos Medical Publishing: New York, USA.
405. Annon, J.S., PLISSIT Therapy, In: Handbook of Innovative Psychotherapies. R. Corsini, Editor. 1981, Wiley & Sons: New York.
406. Fragala, E., et al. Relationship between urodynamic findings and sexual function in multiple sclerosis patients with lower urinary tract dysfunction. Eur J Neurol, 2015. 22: 485.
407. Game, X., et al. Sexual function of young women with myelomeningocele. J Pediatr Urol, 2014. 10: 418.
408. ‘t Hoen, A., et al. A Quality Assessment of Patient-Reported Outcome Measures for Sexual Function in Neurologic Patients Using the Consensus-based Standards for the Selection of Health Measurement Instruments Checklist: A Systematic Review. Eur Urol Focus, 2016.
409. Chen, L., et al. Phosphodiesterase 5 Inhibitors for the Treatment of Erectile Dysfunction: A Trade-off Network Meta-analysis. Eur Urol, 2015. 68: 674.
410. Lombardi, G., et al. Ten years of phosphodiesterase type 5 inhibitors in spinal cord injured patients. J Sex Med, 2009. 6: 1248.
411. Lombardi, G., et al. Treating erectile dysfunction and central neurological diseases with oral phosphodiesterase type 5 inhibitors. Review of the literature. J Sex Med, 2012. 9: 970.
412. Cardenas, D.D., et al. Two phase 3, multicenter, randomized, placebo-controlled clinical trials of fampridine-SR for treatment of spasticity in chronic spinal cord injury. Spinal Cord, 2014. 52: 70.
413. Strebel, R.T., et al. Apomorphine sublingual as primary or secondary treatment for erectile dysfunction in patients with spinal cord injury. BJU Int, 2004. 93: 100.
414. Pohanka, M., et al. The long-lasting improvement of sexual dysfunction in patients with advanced, fluctuating Parkinson’s disease induced by pergolide: evidence from the results of an open, prospective, one-year trial. Parkinsonism Relat Disord, 2005. 11: 509.
415. Chancellor, M.B., et al. Prospective comparison of topical minoxidil to vacuum constriction device and intracorporeal papaverine injection in treatment of erectile dysfunction due to spinal cord injury. Urology, 1994. 43: 365.
416. Cookson, M.S., et al. Long-term results with vacuum constriction device. J Urol, 1993. 149: 290.
417. Denil, J., et al. Vacuum erection device in spinal cord injured men: patient and partner satisfaction. Arch Phys Med Rehabil, 1996. 77: 750.
418. Levine, L.A. External devices for treatment of erectile dysfunction. Endocrine, 2004. 23: 157.
419. Levine, L.A., et al. Vacuum constriction and external erection devices in erectile dysfunction. Urol Clin North Am, 2001. 28: 335.
420. Bella, A.J., et al. Intracavernous pharmacotherapy for erectile dysfunction. Endocrine, 2004. 23: 149.
421. Bodner, D.R., et al. The application of intracavernous injection of vasoactive medications for erection in men with spinal cord injury. J Urol, 1987. 138: 310.
422. Deforge, D., et al. Male erectile dysfunction following spinal cord injury: a systematic review. Spinal Cord, 2006. 44: 465.
423. Dinsmore, W.W., et al. Treating men with predominantly nonpsychogenic erectile dysfunction with intracavernosal vasoactive intestinal polypeptide and phentolamine mesylate in a novel auto-injector system: a multicentre double-blind placebo-controlled study. BJU Int, 1999. 83: 274.
424. Hirsch, I.H., et al. Use of intracavernous injection of prostaglandin E1 for neuropathic erectile dysfunction. Paraplegia, 1994. 32: 661.
425. Kapoor, V.K., et al. Intracavernous papaverine for impotence in spinal cord injured patients. Paraplegia, 1993. 31: 675.
426. Vidal, J., et al. Intracavernous pharmacotherapy for management of erectile dysfunction in multiple sclerosis patients. Rev Neurol, 1995. 23: 269.
427. Bodner, D.R., et al. Intraurethral alprostadil for treatment of erectile dysfunction in patients with spinal cord injury. Urology, 1999. 53: 199.
428. Gross, A.J., et al. Penile prostheses in paraplegic men. Br J Urol, 1996. 78: 262.
429. Kimoto, Y., et al. Penile prostheses for the management of the neuropathic bladder and sexual dysfunction in spinal cord injury patients: long term follow up. Paraplegia, 1994. 32: 336.
430. Zermann, D.H., et al. Penile prosthetic surgery in neurologically impaired patients: long-term followup. J Urol, 2006. 175: 1041.
431. Fode, M., et al. Male sexual dysfunction and infertility associated with neurological disorders. Asian J Androl, 2012. 14: 61.
432. Lim, T.C., et al. A simple technique to prevent retrograde ejaculation during assisted ejaculation. Paraplegia, 1994. 32: 142.
433. Philippon, M., et al. Successful pregnancies and healthy live births using frozen-thawed sperm retrieved by a new modified Hotchkiss procedure in males with retrograde ejaculation: first case series. Basic Clin Androl, 2015. 25: 5.
434. Arafa, M.M., et al. Prostatic massage: a simple method of semen retrieval in men with spinal cord injury. Int J Androl, 2007. 30: 170.
435. Kolettis, P.N., et al. Fertility outcomes after electroejaculation in men with spinal cord injury. Fertil Steril, 2002. 78: 429.
436. Chehensse, C., et al. The spinal control of ejaculation revisited: a systematic review and meta-analysis of anejaculation in spinal cord injured patients. Hum Reprod Update, 2013. 19: 507.
437. Beretta, G., et al. Reproductive aspects in spinal cord injured males. Paraplegia, 1989. 27: 113.
438. Brackett, N.L., et al. Application of 2 vibrators salvages ejaculatory failures to 1 vibrator during penile vibratory stimulation in men with spinal cord injuries. J Urol, 2007. 177: 660.
439. Sonksen, J., et al. Ejaculation induced by penile vibratory stimulation in men with spinal cord injuries. The importance of the vibratory amplitude. Paraplegia, 1994. 32: 651.
440. Claydon, V.E., et al. Cardiovascular responses to vibrostimulation for sperm retrieval in men with spinal cord injury. J Spinal Cord Med, 2006. 29: 207.
441. Ekland, M.B., et al. Incidence of autonomic dysreflexia and silent autonomic dysreflexia in men with spinal cord injury undergoing sperm retrieval: implications for clinical practice. J Spinal Cord Med, 2008. 31: 33.
442. Soler, J.M., et al. Midodrine improves ejaculation in spinal cord injured men. J Urol, 2007. 178: 2082.
443. Pecori, C., et al. Paternal therapy with disease modifying drugs in multiple sclerosis and pregnancy outcomes: a prospective observational multicentric study. BMC Neurol, 2014. 14: 114.
444. Brackett, N.L., et al. Treatment of infertility in men with spinal cord injury. Nat Rev Urol, 2010. 7: 162.
445. Raviv, G., et al. Testicular sperm retrieval and intra cytoplasmic sperm injection provide favorable outcome in spinal cord injury patients, failing conservative reproductive treatment. Spinal Cord, 2013. 51: 642.
446. Schatte, E.C., et al. Treatment of infertility due to anejaculation in the male with electroejaculation and intracytoplasmic sperm injection. J Urol, 2000. 163: 1717.
447. Shieh, J.Y., et al. A protocol of electroejaculation and systematic assisted reproductive technology achieved high efficiency and efficacy for pregnancy for anejaculatory men with spinal cord injury. Arch Phys Med Rehabil, 2003. 84: 535.
448. Taylor, Z., et al. Contribution of the assisted reproductive technologies to fertility in males suffering spinal cord injury. Aust N Z J Obstet Gynaecol, 1999. 39: 84.
449. Rutkowski, S.B., et al. The influence of bladder management on fertility in spinal cord injured males. Paraplegia, 1995. 33: 263.
450. Hamed, S.A., et al. Seminal fluid analysis and testicular volume in adults with epilepsy receiving valproate. J Clin Neurosci, 2015. 22: 508.
451. Ohl, D.A., et al. Electroejaculation versus vibratory stimulation in spinal cord injured men: sperm quality and patient preference. J Urol, 1997. 157: 2147.
452. Brackett, N.L., et al. Semen quality of spinal cord injured men is better when obtained by vibratory stimulation versus electroejaculation. J Urol, 1997. 157: 151.
453. Brackett, N.L., et al. Semen retrieval in men with spinal cord injury is improved by interrupting current delivery during electroejaculation. J Urol, 2002. 167: 201.
454. DeForge, D., et al. Fertility following spinal cord injury: a systematic review. Spinal Cord, 2005. 43: 693.
455. Ferreiro-Velasco, M.E., et al. Sexual issues in a sample of women with spinal cord injury. Spinal Cord, 2005. 43: 51.
456. Kreuter, M., et al. Sexuality and sexual life in women with spinal cord injury: a controlled study. J Rehabil Med, 2008. 40: 61.
457. Kreuter, M., et al. Sexual adjustment and quality of relationship in spinal paraplegia: a controlled study. Arch Phys Med Rehabil, 1996. 77: 541.
458. Szymanski, K.M., et al. Sexual identity and orientation in adult men and women with spina bifida. J Pediatr Rehabil Med, 2017. 10: 313.
459. Kessler, T.M., et al. Sexual dysfunction in multiple sclerosis. Expert Rev Neurother, 2009. 9: 341.
460. Lew-Starowicz, M., et al. Prevalence of Sexual Dysfunctions Among Women with Multiple Sclerosis. Sex Disabil, 2013. 31: 141.
461. Reitz, A., et al. Impact of spinal cord injury on sexual health and quality of life. Int J Impot Res, 2004. 16: 167.
462. Harrison, J., et al. Factors associated with sexual functioning in women following spinal cord injury. Paraplegia, 1995. 33: 687.
463. Westgren, N., et al. Sexuality in women with traumatic spinal cord injury. Acta Obstet Gynecol Scand, 1997. 76: 977.
464. Fruhauf, S., et al. Efficacy of psychological interventions for sexual dysfunction: a systematic review and meta-analysis. Arch Sex Behav, 2013. 42: 915.
465. Alexander, M., et al. Spinal cord injuries and orgasm: a review. J Sex Marital Ther, 2008. 34: 308.
466. Sipski, M.L., et al. Physiologic parameters associated with sexual arousal in women with incomplete spinal cord injuries. Arch Phys Med Rehabil, 1997. 78: 305.
467. Sipski, M.L., et al. Sexual arousal and orgasm in women: effects of spinal cord injury. Ann Neurol, 2001. 49: 35.
468. McAlonan, S. Improving sexual rehabilitation services: the patient’s perspective. Am J Occup Ther, 1996. 50: 826.
469. Schopp, L.H., et al. Impact of comprehensive gynecologic services on health maintenance behaviours among women with spinal cord injury. Disabil Rehabil, 2002. 24: 899.
470. Sukumaran, S.C., et al. Polytherapy increases the risk of infertility in women with epilepsy. Neurology, 2010. 75: 1351.
471. Axel, S.J. Spinal cord injured women’s concerns: menstruation and pregnancy. Rehabil Nurs, 1982. 7: 10.
472. Jackson, A.B., et al. A multicenter study of women’s self-reported reproductive health after spinal cord injury. Arch Phys Med Rehabil, 1999. 80: 1420.
473. Baker, E.R., et al. Pregnancy in spinal cord injured women. Arch Phys Med Rehabil, 1996. 77: 501.
474. Baker, E.R., et al. Risks associated with pregnancy in spinal cord-injured women. Obstet Gynecol, 1992. 80: 425.
475. Bertschy, S., et al. Delivering care under uncertainty: Swiss providers’ experiences in caring for women with spinal cord injury during pregnancy and childbirth - an expert interview study. BMC Pregnancy Childbirth, 2016. 16: 181.
476. Le Liepvre, H., et al. Pregnancy in spinal cord-injured women, a cohort study of 37 pregnancies in 25 women. Spinal Cord, 2017. 55: 167.
477. Skowronski, E., et al. Obstetric management following traumatic tetraplegia: case series and literature review. Aust N Z J Obstet Gynaecol, 2008. 48: 485.
478. Cross, L.L., et al. Pregnancy, labor and delivery post spinal cord injury. Paraplegia, 1992. 30: 890.
479. Hughes, S.J., et al. Management of the pregnant woman with spinal cord injuries. Br J Obstet Gynaecol, 1991. 98: 513.
480. Dannels, A., et al. The perimenopause experience for women with spinal cord injuries. SCI Nurs, 2004. 21: 9.
481. Vukusic, S., et al. Multiple sclerosis and pregnancy in the ‘treatment era’. Nat Rev Neurol, 2015. 11: 280.
482. Amato, M.P., et al. Management of pregnancy-related issues in multiple sclerosis patients: the need for an interdisciplinary approach. Neurol Sci, 2017. 38: 1849.
483. Delaney, K.E., et al. Multiple sclerosis and sexual dysfunction: A need for further education and interdisciplinary care. NeuroRehabilitation, 2017. 41: 317.
484. Bove, R., et al. Management of multiple sclerosis during pregnancy and the reproductive years: a systematic review. Obstet Gynecol, 2014. 124: 1157.
485. Przydacz, M., et al. Recommendations for urological follow-up of patients with neurogenic bladder secondary to spinal cord injury. Int Urol Nephrol, 2018. 50: 1005.
486. Abrams, P., et al. A proposed guideline for the urological management of patients with spinal cord injury. BJU Int, 2008. 101: 989.
487. Pannek, J., et al. Clinical usefulness of ultrasound assessment of detrusor wall thickness in patients with neurogenic lower urinary tract dysfunction due to spinal cord injury: Urodynamics made easy? World J Urol, 2013. 31: 659.
488. Silva, J.A., et al. Association between the bladder wall thickness and urodynamic findings in patients with spinal cord injury. World J Urol, 2015. 33: 131.
489. Veenboer, P.W., et al. Diagnostic accuracy of Tc-99m DMSA scintigraphy and renal ultrasonography for detecting renal scarring and relative function in patients with spinal dysraphism. Neurourol Urodyn, 2015. 34: 513.
490. Ismail, S., et al. Prevalence, management, and prognosis of bladder cancer in patients with neurogenic bladder: A systematic review. Neurourol Urodyn, 2018. 37: 1386.
491. Lewis, J., et al. A framework for transitioning patients from pediatric to adult health settings for patients with neurogenic bladder. Neurourol Urodyn, 2017. 36: 973.
All members of the Neuro-urology working group have provided disclosure statements of all relationships that they have that might be perceived as a potential source of a conflict of interest. This information is publically accessible through the European Association of Urology website: http://uroweb.org/guideline. This guidelines document was developed with the financial support of the European Association of Urology. No external sources of funding and support have been involved. The EAU is a non-profit organisation and funding is limited to administrative and travel and meeting expenses. No honoraria or other reimbursements have been provided.
The format in which to cite the EAU Guidelines will vary depending on the style guide of the journal in which the citation appears. Accordingly, the number of authors or whether, for instance, to include the publisher, location, or an ISBN number may vary.
The compilation of the complete Guidelines should be referenced as:
EAU Guidelines. Edn. presented at the EAU Annual Congress Amsterdam 2020. ISBN 978-94-92671-07-3.
If a publisher and/or location is required, include:
EAU Guidelines Office, Arnhem, The Netherlands. http://uroweb.org/guidelines/compilations-of-all-guidelines/
References to individual guidelines should be structured in the following way:
Contributors’ names. Title of resource. Publication type. ISBN. Publisher and publisher location, year.