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Disease/ Disorder


Neurogenic bladder is defined as bladder dysfunction resulting from a central or peripheral neurologic insult. Possible symptoms include urinary incontinence, urgency, nocturia, straining, incomplete voiding, and urinary retention.1

Initially, a functional classification was used based on cystometric findings: (1) reflex, (2) uninhibited, (3) autonomous, (4) motor paralytic, and (5) sensory. Presently, a combination of both functional and anatomic classification (based on lesion level) is used (Discussed further under Patho-anatomy/physiology).2


Neurogenic bladder can result from nervous system disease. The location and extent of neurologic lesion will affect presentation.

Suprapontine causes include stroke, traumatic brain injury, multiple systems atrophy, Alzheimer’s disease, and hydrocephalus.3

Suprasacral causes include demyelination (multiple sclerosis, transverse myelitis), spinal cord injury (SCI), vascular (arteriovenous malformations, spinal cord infarct), neoplasm, hereditary (hereditary spastic paraplegia), infectious (tropical spastic paraplegia), cervical spondylosis, and other disorders affecting the suprasacral spinal cord.3

Infrasacral (spinal root and peripheral) causes include spinal dysraphism, arachnoiditis, intervertebral disk prolapse, cauda equina lesions, diabetes mellitus, hereditary (hereditary motor sensory neuropathy), and iatrogenic (pelvic or retroperitoneal surgery).3

Epidemiology including risk factors and primary prevention

Cerebrovascular pathology, most commonly the lesions in the anteromedial frontal lobe and putamen, can cause neurogenic bladder in 20% to 50% of patients.4-6 If untreated, 20% to 30% of patients will suffer from incontinence 6-months poststroke.4

Most patients with spinal cord lesions and some patients with peripheral neuropathy will develop neurogenic bladder. Fifty percent of diabetics will develop neuropathy, with 75% to 100% of these patients developing lower urinary tract dysfunction.4


Control of micturition is coordinated between 3 main centers:7

  1. Sacral micturition center (S2-4 reflex center) – Afferent impulses from the bladder enter the S2-S4 sacral segments and trigger efferent parasympathetic impulses to the bladder causing bladder contraction. This reflex is usually triggered by bladder distention.
  2. Pontine micturition center ‑ Coordinates relaxation of the urinary sphincter when the bladder contracts.
  3. Cerebral cortex ‑ Inhibitory control of to the sacral micturition center. It allows for voluntary control of micturition

Voiding dysfunction can be classified according to the level of the lesion:7

  1. Suprapontine lesions (e.g. cerebrovascular accident CVA): These cause involuntary spontaneous or induced contractions of the detrusor muscle. Urodynamic studies (UDS) show detrusor overactivity without detrusor sphincter dyssynergia.
  2. Suprasacral lesions (e.g. spinal cord lesions and disorders):  Loss of coordinated activity results in detrusor-sphincter dyssynergia (DSD), which is the simultaneous contraction of the detrusor and external urinary sphincter. This leads to incomplete bladder emptying and abnormally high bladder pressures. UDS may show detrusor overactivity and DSD.
  3. Infrasacral lesions (e.g.  injuries to the conus, sacral nerve roots):  This results in a highly compliant and acontractile bladder with high bladder volumes. Postvoid residuals (PVR) are more than 100 mL. UDS may show detrusor underactivity and sphincter insufficiency.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

New onset/acute:

Many central neurologic disorders temporarily result in an areflexic bladder.

Suprapontine lesions: Detrusor areflexia often develops immediately post-stroke. Urinary incontinence is common.  Uninhibited detrusor overactivity and urge incontinence may develop.8  

Suprasacral lesions: During the spinal shock period (6- to 12-weeks post injury), patients with SCI have a competent bladder neck, but there is detrusor acontractility/underactivity. Urinary retention is common, and incontinence occurs when there is overflow. The return of the bulbocavernosus reflex marks the recovery from spinal shock, at which  time detrusor activity gradually returns.7

Infrasacral lesions: In cauda equina syndrome (CES), early symptoms of bladder dysfunction can be subtle, such as difficulty in initiating the urinary stream.9 Early stage bladder dysfunction in diabetes may present with bladder hypertrophy, remodeling and increased contractility.10

Subacute and chronic: 

Suprapontine lesions: Post-stroke incontinence is multifactorial.  Detrusor overactivity is the most common UDS finding in stroke patients.  Urinary incontinence is more prevalent in post-stroke patients with impaired awareness and cognition, poor lower limb motor function and depression. Many patients show improvement in voiding dysfunction by one year post-stroke. Persistence of urinary incontinence at 1 year is a poor prognostic factor for mortality, functional recovery and institutionalization.8

Suprasacral lesions:Once there is recovery from spinal shock, patients with SCI develop incontinence because of involuntary detrusor contractions. Suprasacral lesions can present with high bladder pressures and PVR because of the coexistence of detrusor overactivity with dyssynergia.5

Infrasacral lesions:  Most patients with CES develop an areflexic or acontractile detrusor and present with urinary retention and/or overflow incontinence. Detrusor overactivity has been reported in 15-31% of patients with CES.11  In late stage diabetes, decreased peak voiding pressures are seen, and patients may present with atonic bladder, decreased sensation and poor emptying.10

Specific secondary or associated conditions and complications

Both supraspinal and suprapontine injuries result in detrusor overactivity and incontinence. In spinal cord pathologies the simultaneous presence of reduced bladder wall compliance and DSD cause increased bladder pressure, which leads to structural bladder wall changes such as trabeculations and diverticuli.6

Vesicoureteral reflux (VUR) and hydronephrosis may develop with increased bladder pressures (> 40 cm H2O).1 This can lead to renal impairment and even end stage renal disease.1,6 Patients with SCI are prone to upper tract damage and renal disease.6

Genitourinary tract infections, such as cystitis or pyelonephritis, are common. Bladder stones may develop.6

Essentials of Assessment


History should include the following: symptoms of urinary, bowel, sexual, and neurologic dysfunction and episodes of urinary tract infections (UTI) or autonomic dysreflexia (AD). In obtaining the urinary history, determine voiding pattern, bladder sensation, urinary incontinence, mode, and type of voiding (catheterization). A bladder diary should include day-time and night-time voiding frequency, volumes voided, incontinence, and urge episodes.3,6,12

Physical examination

A detailed physical exam is warranted. Inspection of the abdominal wall, prostate palpation, and observation of pelvic organ prolapse is recommended.12

Full neurologic exam should include mental status and comprehension, sensation in S2 through S5 dermatomes, reflexes, anal sphincter tone and volitional contraction, and pelvic floor function.4

Functional assessment

Assess for physical and mental conditions that could impact mobility and function. Spasticity, for example, impacts ease of care, while cognitive deficits can affect the ability to self-catheterize.12

Laboratory studies

Urinalysis is obtained when symptoms or signs of infection are present.6  UTI symptoms may be different in individuals with neurogenic bladder.

Basic metabolic panel ‑ obtain baseline and follow blood urea nitrogen and creatinine concentrations.4 In patients with reduced muscle mass, changes in creatinine may not accurately reflect changes in renal function.


Ultrasonography ‑ a portable bladder scanner can be used to determine PVR. Periodic ultrasound should be performed to assess for renal parenchymal loss, hydronephrosis, hydroureters, or stones.5,13

Surveillance strategies differ between various organizations but are usually performed yearly or biennially.

Voiding cystourethrography ‑ performed if vesicoureteral reflux or urethral strictures is suspected.12

Renal scan ‑ technetium Tc 99m mertiatide nuclear renal scan provides a qualitative assessment of renal function.9,13

Supplemental assessment tools

UDS assess detrusor and bladder outlet function. Uroflowmetry is a noninvasive assessment of voiding. Filling cystometry and pressure-flow studies are more invasive and measure pressure-volume relationships during bladder filling and voiding.3,4

Video-urodynamics provides the most comprehensive information for evaluating neurogenic bladder. It combines filling cystometry and pressure-flow studies with radiologic imaging.12

Electromyography of the pelvic floor muscles, urethral, and/or anal sphincters is a semi-quantitative measure used to detect DSD and pelvic-floor relaxation disorders.12

Social role and social support system

Identify the patient’s goals, motivation, and available social support system since those may impact the method of bladder management selected.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Goals of treatment are to protect the upper urinary tract, prevent urinary tract infection (UTI), achieve continence, and improve quality of life. Patients with neurogenic bladder are prone to develop UTI.  Screening for infection is only indicated in symptomatic patients. Asymptomatic bacteriuria is not an indication for antibiotics unless stone-forming bacteria are present (Proteus, Klebsiella, and Serratia species).14 While long-term use of prophylactic antibiotics is typically not indicated, it may sometimes be used for patients with recurrent UTI in the presence of VUR and hydropnephrosis.3

Antimuscarinics are widely used for neurogenic detrusor overactivity. They decrease bladder activity and filling pressures, increase bladder capacity, and compliance. Selective and nonselective alpha-blockers are partially successful in decreasing bladder-outlet resistance. Aside from being used in the treatment of benign prostatic hypertrophy, they can relieve both voiding and bladder storage symptoms. Combination therapy of alpha-blockers with antimuscarinics may be of benefit.15 There is no evidence of effective drug treatment for neurogenic detrusor underactivity.12.

Prolonged use of anticholinergic medications is associated with increased risk for delirium and dementia in elderly patients. A study suggests that risk for dementia is lower with beta-3 agonists vs. more traditional anticholinergics.16

Current pharmacologic agents for bladder management are summarized in table 1 and non-pharmacologic modalities in table 2.

Table 1. Pharmacologic Therapy for Neurogenic Bladder1,15,17

Table 2. Non-pharmacologic Treatment of Neurogenic Bladder3,7,15

Coordination of care

Multidisciplinary: adopt a comprehensive approach to managing the patient’s urologic, neurologic, functional, and social issues. Maintain regular interaction and consultation between the patient, caregivers, physicians (general practitioner and/or a specialist experienced in neuro-urology, e.g. a physiatrist/urologist/neurologist), nurses, and members of the rehabilitation team (physical and occupational therapy). Nurses can evaluate continence needs, trial and adaptation of catheters, and ensure education and follow-up. The therapist can evaluate for barriers to following a catheterization program, such as spasticity, sensory-motor deficits, and cognitive/behavioral issues. They can assess the need for appliances to facilitate catheterization and home modifications.3

Patient and family education

Patients and caregivers have an active role in the management of bladder dysfunction. Specifics have been described earlier.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

A detailed history and physical examination, bladder diary, and PVR measurements are essential in evaluation of neurogenic bladder. Urodynamics are useful in initial evaluation and follow-up.

Urine is not routinely tested unless patients are symptomatic (e.g., fever, malaise, increased tone/spasms).18

Clean intermittent self-catheterization is the preferred method to facilitate bladder emptying when feasible.

Cutting Edge/ Emerging and Unique Concepts and Practice

Botulinum neurotoxin (BoNT) injections: An alternative treatment for detrusor/bladder overactivity and DSD. Injections can be performed either to the detrusor muscle (for detrusor overactivity) or the outlet (for increased outlet resistance, DSD).  BoNT causes a reversible chemical denervation that lasts approximately 9 months. Loss of efficacy is not reported with repeated injections. No ultrastructural changes are seen on histologic studies.19

 There is level I evidence that intradetrusor injection of onabotulinumtoxinA (A/Ona) is beneficial for treatment of refractory neurogenic detrusor overactivity (NDO) in patients with MS and SCI. In patients with SCI, BoNT can reduce the frequency and severity of autonomic dysreflexia.20  It is reported to improve incontinence and increase functional bladder capacity in SCI patients.15  Evidence for patients with Parkinson’s disease, CVA, and myelomeningocele were not as strong.20 

A standardized dose and injection protocol remains to be established.5 For NDO, effective doses were intradetrusor injections of 200-300 units of (A/Ona) into 20-30 sites.19  In DSD, injections to the external sphincter range from 50-200 units (many studies use 100 units).21

Most common adverse events reported are urinary tract infections (especially for patients with diabetes or multiple sclerosis) and increased post void residual. It should be avoided in patients with neuromuscular disorders such as myasthenia gravis.20 An occasional adverse effect is generalized muscle weakness.4  BoNT A is classified as pregnancy category C (no adequate/well-controlled studies).20

Intravesical therapies with capsaicin (CAP) and resiniferatoxin (RTX) are used to decrease detrusor overactivity. CAP and RTX act on vanilloid receptors, which desensitizes C-fibers. However, these agents have limited clinical efficacy compared with BTX injections.1

Neuromodulation: Various stimulation/neuromodulation techniques are being studied for patients who do not respond to other treatment methods.

  • Percutaneous and transcutaneous tibial nerve stimulation (PTNS/TTNS): Neuromodulation involves stimulating the tibial nerve at the medial malleolus using a needle (PTNS) or a surface electrode pads (TTNS). Studies have shown that PTNS improves overactive bladder better than antimuscarinics or placebo and has additive benefits when used with antimuscarinics. TTNS also reported to improve symptoms of overactive bladder (urgency, incontinence, and frequency).22
  • Transcutaneous electrical spinal cord neuromodulator (TESCoN): A non-invasive neuromodulation technique to better control overactive bladder. Uses adhesive electrodes over the interspinous ligaments of T11 and L1 (cathode) and over the iliac crests (anode). A study showed that TESCoN reduced detrusor overactivity, increase bladder capacity, and reduced incontinence episodes in patients with various etiologies.23
  • Sacral neuromodulation (SNM): A device with electrode is placed through the S3 foramen to target the S3 nerve percutaneously, which is responsible for innervation to the bladder, pelvic floor muscles, and external urethral sphincter. Not eligible for patients who would require future MRI scans. Studies have shown promising results, especially for patients with multiple sclerosis and spinal cord injury. Adverse events include lead migration, infection, pain at the site of implantation, and need for revision of the implanted pulse generator. Infection rates are higher for patients with diabetes.24
  • Sacral posterior root rhizotomy with sacral anterior root stimulation can be done to manage refractory involuntary detrusor contractions and underactive detrusor.5,12

Gaps in the Evidence- Based Knowledge

Additional research is needed to identify optimal measures to prevent complications of neurogenic bladder, including prospective studies to compare the benefits, risks, and complications of different bladder management methods.


  1. Cameron AP. Pharmacologic therapy for the neurogenic bladder. Urol Clin North Am. 2010;37:495-506.
  2. Cardenas D, Chiodo A, Samson G. Management of bladder dysfunction. In: Braddom RL, Chan l, Harrast MA, et al, eds. Physical Medicine & Rehabilitation. 4th ed. Philadelphia, Pa: Saunders Elsevier; 2011:604.
  3. Panicker JN, de Seze M, Fowler CJ. Rehabilitation in practice: neurogenic lower urinary tract dysfunction and its management. Clin Rehabil. 2010;24:579-589.
  4. Stohrer M, Blok B, Castro-Diaz D, et al. Guidelines on neurogenic lower urinary tract dysfunction. March 2008. Available at: http://www.uroweb.org/gls/pdf/Neurogenic%20LUTS%202010.pdf. Accessed April 19, 2011.
  5. Jeong SJ, Cho SY, Oh SJ. Spinal cord/brain injury and the neurogenic bladder. Urol Clin North Am. 2010;37:537-546.
  6. Panicker JN, Fowler CJ. The bare essentials: uro-neurology. Pract Neurol. 2010;10:178-185.
  7. Consortium for Spinal Cord Medicine. Bladder management for adults with spinal cord injury: a clinical practice guideline for health-care providers. J Spinal Cord Med. 2006;29:527-573.
  8. Panfili Z, Metcalf M, Griebling T.  Contemporary evaluation and treatment of poststroke lower urinary tract dysfunction. Urologic Clinics of North America. 2017; 44 (403-414). doi: 10.1016/j.ucl.2017.04.007
  9. Spector L, Madigan L, Rhyne A, Darden B, Kim D. Cauda Equina Syndrome. J Am Acad Orthop Surg 2008;16:471-479.
  10. Daneshgari F, Liu G, Birder L, Hanna0Mitchell A, Chacko S.  Diabetic Bladder Dysfucntion: Current Translational Knowledge. The Journal of Urology. 2009;182 s18-s26, doi: 10.1016/JURO.2009.08.070
  11. Kim S, Kwon H, Hyun J.  Detrusor overactivity in patients with cauda equine syndrome. Spine. 2014: 39 (16):E955-961. doi: 10.1097/BRS.0000000000000410
  12. Stohrer M, Blok B, Castro-Diaz D, et al. EAU guidelines on neurogenic lower urinary tract dysfunction. Eur Urol. 2009;56:81-88.
  13. Kaynan AM, Perkash I. Neurogenic bladder. In: Frontera WR, Silver JK, Rizzo TDJ, eds. Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain, and Rehabilitation. 2nd ed. Philadelphia, Pa: Saunders Elsevier; 2008:736.
  14. Favazza T, Midha M, Martin J, Grob BM. Factors influencing bladder stone formation in patients with spinal cord injury. J Spinal Cord Med. 2004;27:252-254.
  15. Lamin E, Smith AL. Urologic agents for treatment of bladder dysfunction in neurologic disease. Curt Treat Options Neurol. 2014; 16:280
  16. Blayne Welk, Eric McArthur. Increased risk of dementia among overactive bladder patients treated with an anticholinergic medication compared to a beta-3 agonist: a population-based cohort study. BJU Int. 2020 Mar 13. doi: 10.1111/bju.15040.
  17. Wyndaele JJ, Kovindha A, Madersbacher H, et al. Neurologic urinary incontinence. Neurourol Urodyn. 2010;29:159-164.
  18. Dinh A, Davido B, Duran C, et al. Urinary tract infections in patients with neurogenic bladder. Médecine et Maladies Infectieuses. 2019;49 (7):495 – 504.  http://dx.doi.org/10.1016/j.medmal.2019.02.006.  doi: 10.1016/j.medmal.2019.02.006.
  19. Chancellor MB, Elovic E, Esquenazi A, Naumann M. Evidence-based review and assessment of botulinum neurotoxin for the treatment of urologic conditions. Toxicon. 2013; 67: 129-140.
  20. Kaviani A, Khavari R. Disease-specific outcomes of botulinum toxin injections for neurogenic detrusor overactivity. Urologic Clinics of North America. 2017;44(3):463-474. http://dx.doi.org/10.1016/j.ucl.2017.04.012. doi: 10.1016/j.ucl.2017.04.012.
  21. Peyronnet B, Gamé X, Vurture G, Nitti V, Brucker B. Botulinum toxin use in neurourology. Rev Urol. 2018;20(2):84–93 doi: 10.3909/riu0792
  22. Bhide AA, Tailor V, Fernando R, Khullar V, Digesu GA. Posterior tibial nerve stimulation for overactive bladder-techniques and efficacy. International urogynecology journal. 2019. https://www.ncbi.nlm.nih.gov/pubmed/31853597. doi: 10.1007/s00192-019-04186-3.
  23. Kreydin E, Zhong H, Latack K, Ye S, Edgerton VR, Gad P. Transcutaneous electrical spinal cord neuromodulator (TESCoN) improves symptoms of overactive bladder. Frontiers in systems neuroscience. 2020;14:1. https://www.ncbi.nlm.nih.gov/pubmed/32116576. doi: 10.3389/fnsys.2020.00001.
  24. Barboglio Romo PG, Gupta P. Peripheral and sacral neuromodulation in the treatment of neurogenic lower urinary tract dysfunction. Urologic Clinics of North America. 2017;44(3):453-461. http://dx.doi.org/10.1016/j.ucl.2017.04.011. doi:10.1016/j.ucl.2017.04.011.

Original Version of the Topic

Philippines Cabahug, MD, Shawn Murphy, DO. Neurogenic Bladder. 11/10/2011

Previous Revision(s) of the Topic

Philippines Cabahug, MD, Shawn Murphy, DO. Neurogenic Bladder. 9/18/2020

Author Disclosure

Philippines Cabahug, MD
Nothing to Disclose

Junghoon Choi, MD
Nothing to Disclose