Lower Urinary Tract Dysfunction Due to Neurologic Disease

Lower Urinary Tract Dysfunction Due to Neurologic Disease

Brendan Thomas Frainey

Howard B. Goldman


Neurogenic lower urinary tract dysfunction (NLUTD), or “neurogenic bladder” as it is commonly referred to, describes dysfunction of the bladder and urethra due to a clinically confirmed neurologic disorder.1,2 NLUTD is not a single entity but a variety of clinical signs and symptoms resulting in abnormal urinary storage and/or micturition.1 Similarly, NLUTD is due to a heterogenous group of neurologic diseases, which can be congenital (i.e., spina bifida [SB]) or acquired (i.e., stroke and spinal cord injury [SCI]) in nature and affect either the central (i.e., multiple sclerosis [MS]) and/or peripheral nervous system (i.e., pelvic plexus injury). As a result, NLUTD is quite common, with 40% to 90% of patients with MS, 37% to 72% with Parkinson disease (PD), 70% to 84% with spinal cord injuries, and 15% with stroke estimated to have some element of NLUTD.3,4 NLUTD can present in a variety of ways, but patients commonly note a change in baseline voiding function, reporting symptoms such as urinary urgency, frequency, incontinence, slow urinary stream, incomplete emptying, and recurrent urinary tract infection.

Although the clinical presentations and associated disease processes are diverse, the overarching goals of management for these patients are not. The main principles include protection of the upper urinary tract, prevention of urinary tract infections and sepsis, and maintenance of social continence and quality of life. To effectively do this, it is essential for the practicing urogynecologist to have a baseline understanding of normal micturition, the appropriate evaluation of patients with presumed NLUTD, and the main neurologic disease processes that can result in NLUTD so that these patients can be managed competently. In this chapter, we cover each of these topics and also provide a basic framework for categorizing patterns of NLUTD so that general treatment principles can be applied.


In order to understand how pathology in the nervous system may affect the lower urinary tract, it is critical to first understand normal micturition. At the most basic level, normal micturition involves a storage phase and emptying phase. Passive, low-pressure urinary storage requires relaxation of the smooth muscle within the bladder and an appropriate resting tone of both the internal urethral sphincter (IUS) and external urethral sphincter (EUS) to prevent incontinence. Emptying, or voiding, requires an adequate detrusor contraction coordinated with relaxation of the pelvic musculature and IUS and EUS.3,5,6,7

The neural control governing micturition requires synchronized input from the central nervous system (CNS), autonomic nervous system (both parasympathetic and sympathetic), and somatic nervous system.3,6 During bladder filling (storage phase), sympathetic and pudendal (somatic) nerves mediate tonic contraction of the IUS and EUS, respectively, via the sacral spinal cord and Onuf nucleus, creating a “guarding reflex” while the compliant bladder wall relaxes due to sympathetic inhibition of the detrusor muscle via the thoracolumbar spinal cord, preventing involuntary contractions during filling.5,7,8

Once the bladder reaches a critical volume (approximately 400 to 500 mL), stretch receptors within the detrusor illicit a spinal reflex, the “voiding reflex,” mediated by the pontine micturition center (PMC), or Barrington nucleus, within the brainstem.8,9 However, normal voiding is not initiated by a spinal reflex but is a voluntary decision primarily under cortical control. During bladder filling, the PMC is tonically inhibited, via the prefrontal cortex and periaqueductal gray in the midbrain. When it is socially acceptable to void, suppression of the voiding reflex ceases and micturition can occur.5,8,10 Voiding (emptying phase) is then primarily driven by parasympathetic stimulation of the detrusor muscle via the sacral spinal cord, resulting in a bladder contraction, but also relaxation of the pelvic musculature, bladder neck, and EUS, creating an open, unobstructed urinary channel.5,9

Therefore, for successful micturition to occur, there must be intact neural signaling between the cerebral cortex, brainstem, spinal cord, and peripheral nerves,
which is demonstrated in Figure 27.1. When diseases or injury to the nervous system occur, it can lead to differing forms of lower urinary tract dysfunction (LUTD), which is described later.


As with the assessment of any urogynecologic patient, evaluation of a patient with NLUTD requires a detailed history, physical examination, and appropriate laboratory and diagnostic studies. In this section, we review each of the major components of the history and physical, highlighting the unique aspects for patients with NLUTD.


The key components of the history include discussion of current symptoms (history of present illness) and characterization of the neurologic disease process while placing these items in the context of the patient’s overall lower urinary tract function. Other essential elements include assessment of bowel habits, sexual function, urinary tract infection and stone history, gynecologic history (if applicable), past medical and surgical history, current medications, family history, social history, functional status, and prior diagnostic studies performed (if applicable).2,3,11,12

Assessment of lower urinary tract function should involve questions regarding both storage and emptying symptoms. Storage symptoms include urinary urgency, frequency, nocturia, and urgency incontinence, whereas emptying symptoms include hesitancy, straining, intermittency, and reduced force of the urinary stream. The clinician should inquire if the patient self-catheterizes to empty the bladder. If so, document the frequency of catheterization, the type of catheter used, and if the patient is incontinent between catheterizations. A 2- to 3-day
voiding diary is also recommended and can provide objective data regarding voiding habits and urine volumes to support the reported history.12,13,14 Additionally, the frequency of symptomatic, culture-proven urinary tract infections must be evaluated because repeated infection can lead to long-term renal dysfunction.

When characterizing the neurologic disease or injury, several key components must be addressed2:

  • The location of the neurologic insult or “level of the lesion”—this aids the clinician in thinking about how normal micturition might be affected and predict patterns of LUTD (See “Classification” section for more details.)

  • The timing or onset of neurologic dysfunction—is the condition congenital or acquired? What is the time course from neurologic insult/disease to urologic symptomatology? Has there been a significant change from baseline?

  • The extent of the loss in function and the likelihood for progression—this will help determine appropriate management strategies and possible limitations for certain therapeutic options (i.e., manual dexterity and ability to self-catheterize)

The last several fundamental aspects of the history include assessment of bowel habits, presence of autonomic dysreflexia (AD), and functional status. Key questions regarding bowel function include Does the patient sense passage of flatus or stool? How frequently do they have a bowel movement? Are they on a bowel regimen, and what does this entail (laxatives, enemas, digital stimulation)? Are they incontinent of stool? These questions are critical as significant constipation can contribute to voiding dysfunction and must be managed aggressively. AD is a life-threatening clinical syndrome that can occur in patients with history of SCI. SCI patients, particularly those with lesions at thoracic level T6 or above, must be asked about a history of AD and associated signs and symptoms, which typically include severe hypertension, reflex bradycardia, sweating, flushing, and headache. Finally, the clinician must assess the patient’s functional status including mobility, dexterity, occupation, and support system at home because these will all impact management strategies.

Physical Exam

Essential elements of a focused neurourologic exam include assessment of gross motor function, abdominal exam, a brief skin exam, and genitourinary (GU) exam, including digital rectal exam, pelvic exam, reflex testing, and sacral sensitivity testing.13

When assessing gross motor function, the clinician is able gain most of the relevant information just on initial inspection. Does the patient use assistive devices or a wheelchair? Are the patient’s extremities contracted? Do they have manual dexterity? If the patient is able to stand or sit up, examine their back to assess for scoliosis, surgical scars, costovertebral angle tenderness, or lesions along the lower back such as a sacral dimple or hair tuft. If able to ambulate, assess the patient’s gait.

Next, the abdominal exam consists of inspection for surgical scars, hernias, stomas, or catheterizable channels. The abdomen can be palpated to assess for suprapubic discomfort or abdominal distention secondary to an overdistended bladder or severe constipation if there is concern for bowel dysfunction. A brief examination of the skin to assess for ulceration in dependent areas such as the sacrum, hips, and lower extremities is critical in patients who use a wheelchair or orthotics for ambulation.

The last major component consists of the GU exam, including a pelvic exam in females. Assess for traumatic hypospadias if the patient has a history of chronic indwelling catheter. The clinician can next proceed to sacral sensitivity and reflex testing. Sacral sensitivity testing consists of light touch, pinprick, and proprioceptive maneuvers to determine if there is decreased sensitivity in any of the sacral dermatomes.13 Abnormal findings can suggest lesions of the lumbosacral cord and their associated peripheral nerves. Reflex testing includes the bulbocavernosus reflex and anal reflex. The bulbocavernosus reflex is elicited by pinching the glans or applying pressure to the clitoris with a cotton swab while simultaneously assessing for anal sphincter contraction. In the female, one can often feel the bulbocavernosus contraction when two fingers are placed in the vagina. The anal reflex is performed by stroking the skin lateral to the anus and observing for anal contraction. For both, an absent reflex typically indicates a defect with the sacral reflex arc.12,13,15,16 However, in neurologically intact females, the bulbocavernosus reflex can be absent in 30% of women and is not considered pathologic.17 Finally, digital rectal exam should be performed to assess for prostatic enlargement in males and to assess for sphincter tone and fecal impaction in both males and females.

Laboratory and Diagnostic Studies

Relevant laboratory studies include urinalysis as well as urine culture if appropriate. Measurement of a postvoid residual urine volume (PVR), either via a portable bladder ultrasound device or straight catheterization, is also an essential component of the initial evaluation and provides important data regarding the patient’s ability to effectively empty their bladder.9,12,18,19 Although elevated residual volumes indicate voiding dysfunction, they unfortunately do not identify the etiology of incomplete emptying which can be secondary to poor
detrusor function or an obstructed outlet.9 Renal function panel and renal bladder ultrasound (RBUS) should also be considered, especially in patients with a history of chronic kidney disease or with elevated risk for upper tract deterioration.9,12,20 European Association of Urology guidelines recommend RBUS be performed every 6 months.12

Urodynamic testing is a cornerstone in the assessment of NLUTD. Per the International Continence Society, urodynamics (UDS) are recommended for the “initial and long-term surveillance” of NLUTD.21 However, it should always be used with a specific question in mind to help guide management.2 Patient presentation may also determine need for UDS. For example, all would agree that a recent SCI patient should have baseline UDS; yet, many would not require UDS for a very functional patient with MS who has overactive bladder symptoms but empties easily without a significant PVR.

Multichannel urodynamics consists of a filling cytometry phase and a voiding pressure flow study and provides the most objective assessment of the lower urinary tract. The addition of electromyography (EMG) provides a gross estimation of pelvic floor and EUS function. The use of fluoroscopy during urodynamics, or videourodynamics (VUDS), provides real-time assessment of anatomic and functional information during bladder filling and emptying.

UDS provides a great deal of clinical information on lower urinary tract mechanics. Specifically, during filling, it allows for determination of detrusor overactivity, compliance, bladder capacity, and incontinence. The pressure-flow portion provides information regarding voiding pressures, sphincter coordination, and the ability to empty effectively. As seen in Table 27.1, poor compliance, elevated detrusor leak point pressures (DLPP; >40 cm H2O), vesicoureteral reflux (VUR), and detrusor external sphincter dyssynergia (DESD) are key findings on VUDS suggestive of NLUTD and place the patient at risk for upper tract deterioration.1,22,23


Because of the heterogeneity in both clinical presentation and neurologic disease processes that can result in NLUTD, the authors believe that creating a classification system is useful to assist clinicians in predicting expected lower urinary tract symptoms (LUTS) and urodynamic findings. Although not absolute, we believe that categorization based on the location of the neurologic pathology or “level of the lesion” is the most intuitive way to recognize patterns of presentation for these patients, which is depicted in Figure 27.2 and Table 27.2.

Another method of characterizing patients with NLUTD uses a more functional classification system with urodynamic findings as an objective adjunct. With this system, the type of NLUTD can be categorized as a “failure to store” versus a “failure to empty” where either the bladder, the outlet (urinary sphincters), or both may be effected. The authors believe that this type of categorization may better assist clinicians in developing appropriate treatment and management strategies for these patients.


The principles of management for patients with NLUTD include protection of the upper urinary tract, prevention of urinary tract infections, and maintenance of social continence and quality of life.9,12 All treatment considerations should take into account the patient’s functional capability, level of social support, and goals of care. Urogynecologists should use a multidisciplinary approach with neurologists, physical medicine and rehabilitation specialists, and primary care physicians in order to provide this group of patients with appropriate, coordinated care.

Our method for determining the appropriate management strategy involves (1) identifying the location of the neurologic insult/lesion and (2) defining its effects on storage, emptying, or both. Treatment decisions should typically be based on objective urodynamic findings, but occasionally, therapies can be started prior to UDS if LUTS are straightforward and there is low risk for upper tract deterioration. Urodynamics can not only define whether there is a storage or emptying issue but also if it is a detrusor or outlet issue. Once these elements have been defined, the clinician can more easily determine the appropriate treatment approach. The various treatment approached based on functional assessment can be seen in Table 27.3. If the patient has abnormalities with both storage and emptying or both detrusor and outlet, the clinician should prioritize treatment of any high-risk features that place the patient at risk for upper tract deterioration and then consider level of symptomatic bother.

Storage Dysfunction: Detrusor

This is the most commonly encountered problem because many neurologic injuries lead to detrusor overactivity and occasionally poor compliance and decreased bladder capacity. First-line therapies include behavioral modifications such as bladder training, timed voiding, fluid management, and pelvic floor rehabilitation.2,9,24,25,26,27,28 Additional first-line therapy includes the use of anticholinergic agents such as oxybutynin, tolterodine, and trospium.12 However, adverse effects, specifically on cognition, must be factored, and if the risks outweigh the benefits, use of β3-agonists, mirabegron, or vibegron should be considered.

If these more conservative first-line options are unsuccessful, surgical options should be discussed. The intervention with the best evidence for neurogenic detrusor overactivity (NDO) is intravesical injection of botulinum toxin A (Botox).12,29,30,31,32,33,34,35 Of note, 200 units is the recommended dose for NDO as compared to 100 units in the nonneurogenic setting. Long-term data has demonstrated the efficacy of repeat injections and it can be done in the office without anesthesia.36,37 The most frequent complications include urinary tract infection and urinary retention, so the potential need for clean intermittent self-catheterization (CIC) in the postinjection period must be discussed with the patient.

Aside from Botox, other more minimally invasive surgical options include neuromodulation, specifically percutaneous tibial nerve stimulation (PTNS) and sacral neuromodulation (SNM). Although PTNS has shown some promise in MS and PD patients, it is limited by the fact that it requires frequent in-office treatments which may be difficult for this patient population.38,39 Implantable tibial nerve stimulation devices are currently being studied and may be of benefit to these patients in the future. SNM has also been studied in MS patients but overall has been limited by concerns over the need for regular magnetic resonance imaging (MRI) studies in this cohort and the progressive nature of many neurologic diseases.40 However, the concerns over MRI compatibility have now been obviated by the newest generation of MRI conditional SNM devices.41

More invasive surgical options include augmentation cystoplasty with or without concomitant continent catheterizable channel creation and urinary diversion. These options are only to be considered in appropriately selected patients where all other options have been exhausted. Augmentation cystoplasty incorporates an intestinal segment into the bladder to increase bladder capacity and lower storage pressures. Continent urinary diversions should be preferentially performed over incontinent diversions if feasible.12

Storage Dysfunction: Outlet

For patients with neurogenic stress urinary incontinence (SUI) due to an incompetent outlet and intrinsic sphincteric deficiency, surgical management provides the best outcomes. However, with any surgical procedure to correct SUI, there is a risk of creating obstruction. These risks and benefits must be weighed, especially in a neurogenic cohort. If the SUI is minor or the patient is a poor surgical candidate, conservative measures such as timed voiding, incontinence pessary, or use of external urinary collection devices can be considered. Conversely, if the SUI is severe, resulting in skin breakdown or significant decrement in patient quality of life, then surgical options should be discussed. Patients undergoing these procedures must be counseled on the risk for retention and possible need for CIC.

Urethral bulking agents are the least invasive option and can provide improvement in women. Urethral slings can be placed in both men and women but require different approaches. In females, slings are typically placed via a pubovaginal approach and can use mesh or autologous graft material such as rectus fascia or fascia lata. In males, slings can be placed either at the bladder neck via an abdominal approach or at the bulbar urethra via a perineal approach. Artificial urinary sphincters (AUS) can also be placed for severe incontinence but are typically only performed in males with NLUTD in the United States. In males, the cuff can be placed at either the bladder neck or the bulbar urethra with the pump located in the scrotum. An important consideration for AUS candidates is that they must have the manual dexterity to operate the pump. Finally, bladder
neck closure is a “last resort” option for the end-stage outlet and should be performed concomitantly with suprapubic tube (SPT) placement and/or some form of catheterizable channel.2,12,42

Emptying Dysfunction: Detrusor

CIC is the first-line treatment for patients who are unable to adequately empty their bladder.2,12 Occasionally, patients will require assistance from a caregiver or guardian if the patient does not have the manual dexterity or capability to perform CIC. The frequency of CIC is determined by urodynamic findings but is typically performed four to six times per day. Education of the patient and caregivers is essential for success.43 Silicone catheters are typically preferred because they are less susceptible to encrustation and many NLUTD patients are latex allergic.

SNM has been U.S. Food and Drug Administration approved for the treatment of nonobstructive urinary retention since 1999.44 It is thought to modulate the guarding reflex, facilitating voiding. However, currently, there is a dearth of evidence using SNM in patients with NLUTD.45

Emptying Dysfunction: Outlet

Emptying dysfunction due to the outlet in typically due to DESD. DESD refers to a detrusor contraction occurring concurrently with an involuntary contraction of the EUS and indicates inappropriate communication between the PMC and sacral spinal cord.1 This can be identified on fluoroscopy during VUDS or on a multichannel UDS tracing as depicted in Figure 27.3A,B. As earlier, CIC is the mainstay of treatment for patients who are unable to adequately empty their bladder, whether from an underactive detrusor or obstructed outlet. However, there are several additional therapeutic options that have been well studied in this realm and may be indicated if necessary to protect the upper tracts. First, botulinum toxin A injection into the EUS has been shown to lower detrusor pressures and improve voided volumes in patients with detrusor sphincter dyssynergia but requires repeated injections.46,47 Other endoscopic options include transurethral laser sphincterotomy which can be staged and repeated as needed so as not to totally lose sphincteric function.47,48,49 Finally, urinary diversion can be considered as a last option when the bladder and sphincter are too hostile and place the upper tracts at risk.


In this section, we address some of the most commonly seen neurologic disorders associated with NLUTD and briefly discuss prevalence, clinical presentation, urodynamic findings, and general treatment principles for each. Although this is not exhaustive, we encourage you to use our framework for categorizing various diseases and predicting the associated clinical presentation based on the location of neurologic insult.

Multiple Sclerosis

MS is an autoimmune demyelinating disorder of the CNS and is the most common nontraumatic disabling neurologic disease in young adults.50,51 The prevalence within the United States has been estimated at 150 per 100,000 individuals (˜400,000 individuals in the United States), with females 3 times as likely as males to develop MS.52 Demyelinating lesions can involve the cerebral cortex, spinal cord, and optic nerves, leading to a host of clinical manifestations.

LUTD is incredibly common in MS, with a reported 80% to 96% of patients pursuing urologic care.51,53 The incidence of NLUTD appears to increase with disease duration, with most MS patients having some element of LUTD within 6 to 10 years of diagnosis.9,54,55,56 Urinary urgency and frequency are the most commonly reported symptoms and are noted in 37% to 99% of MS patients. Obstructive symptoms such as incomplete emptying, hesitancy, and urinary retention are also common, occurring in 34% to 79% of patients. Urge incontinence has been reported in 19% to 80% of patients based on current series.51,55,57,58 Importantly, about 10% of patients will have LUTD as part of their initial presentation prior to a diagnosis of MS.53,59,60 Therefore, urogynecologist must have a high index of suspicion and refer to neurology if other findings of MS are noted on review of systems.

There are no standardized recommendations for the use of UDS in patients with MS. However, urodynamic abnormalities are abundant in MS patients and can be seen in 90% of individuals. The most common finding is detrusor overactivity (34% to 99%, mean occurrence 65%) followed by DESD (3% to 83%, mean 35%), detrusor underactivity (0% to 40%, mean 25%), and poor compliance (2% to 10%).51,55,61 UDS findings commonly do not correlate with clinical symptoms, with one study revealing 52% of patients without LUTS had “silent” UDS abnormalities.62 Despite this, the risk for upper tract deterioration in patients with MS is quite low, even in the presence of bladder outlet obstruction from DESD.63,64,65,66 Therefore, the universal use of UDS in patients with MS has come into question.53 However, UDS can be critical in determining the etiology of incomplete emptying in this group (hypocontractile detrusor vs. bladder outlet obstruction) so that the proper management strategies can be employed. Additionally, some studies have shown that neurologic symptom severity, defined by the Expanded Disability Status Scale (EDSS), positively correlates with pathologic UDS findings.53,67,68 Therefore, the authors believe that UDS are warranted in patients with severe neurologic symptoms or those with poor compliance or DESD on initial UDS because these patients may have higher risk for upper tract deterioration.66,69

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May 1, 2023 | Posted by in GYNECOLOGY | Comments Off on Lower Urinary Tract Dysfunction Due to Neurologic Disease

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