Author(s): Philippines Cabahug, MD, Jing Chen, MD
Originally published: November 10, 2011 Last updated: April 18, 2024
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Disease/Disorder

Definition

Neurogenic lower urinary tract dysfunction (NLUTD), previously termed neurogenic bladder dysfunction, is defined as abnormal function of either the bladder, bladder neck, and/or its sphincters related to a neurologic disorder. Common symptoms include urinary incontinence, urgency, nocturia, straining, incomplete voiding, and urinary retention. NLUTD is the preferred term to emphasize that the voiding issue is not confined to the bladder alone.1 

Etiology

Neurogenic bladder can arise from a spectrum of neurological disorders. The location and extent of the neurologic lesion determines the pattern of dysfunction. Based on the anatomic location, the etiologies can be categorized as suprapontine, spinal (infrapontine-suprasacral), and sacral/infrasacral lesions.2,3

Suprapontine causes include stroke, traumatic brain injury, multiple sclerosis (MS), multiple systems atrophy, Alzheimer’s disease, and hydrocephalus.

Spinal (infrapontine-suprasacral) causes include spinal cord injury/disease of various etiologies. Traumatic SCI is the most common spinal lesion affecting voiding. Other spinal etiologies include demyelination (multiple sclerosis, transverse myelitis), vascular (arteriovenous malformations, spinal cord infarct), neoplasm, hereditary (hereditary spastic paraplegia), infectious (tropical spastic paraplegia), or degenerative causes (cervical spondylosis).

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).

Epidemiology including risk factors and primary prevention

The prevalence of neurogenic bladder varies based on the underlying neurological condition, the duration of disease, and the severity of underlying neurological diagnoses. For instance, more than half of stroke patients report urinary incontinence during the acute phase of stroke. The prevalence of neurogenic bladder in Parkinson’s disease ranges between 38 and 71%. Lower urinary tract symptoms are reported in 32 to 96% of patients with multiple sclerosis (MS). SCI leads to neurogenic bladder in about 70–84% of patients.4 Lower urinary tract dysfunction is common in spina bifida, reported in more than 90% of children.5

Patho-anatomy/physiology

Control of micturition is coordinated between 3 main centers6

  • 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.
  • Pontine micturition center ‑ Coordinates relaxation of the urinary sphincter when the bladder contracts.
  • 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 lesion2,6

  • Suprapontine lesions (e.g., cerebrovascular accident CVA): Patients present predominantly with storage symptoms.  Spontaneous involuntary detrusor contractions occur due to removal of the tonic inhibition of the PMC. Urodynamic studies (UDS) show detrusor overactivity without detrusor sphincter dyssynergia.
  • Suprasacral lesions (e.g., spinal cord lesions and disorders): Patients may present with both storage and voiding symptoms. 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.
  • Sacral/Infrasacral lesions (e.g.  injuries to the conus, sacral nerve roots):  This results in predominantly voiding symptoms. Patients may present with a highly compliant and acontractile bladder with high bladder volumes. Postvoid residuals (PVR) are more than 100 mL. UDS may show hypocontractile or acontractile detrusor.

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.7  

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.6

Infrasacral lesions: In cauda equina syndrome (CES), early symptoms of bladder dysfunction can be subtle, such as difficulty in initiating the urinary stream.8 Early stage bladder dysfunction in diabetes may present with bladder hypertrophy, remodeling and increased contractility.9

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.7

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.10

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.9

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.12

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.12,13 Patients with SCI are prone to upper tract damage and renal disease.12

Genitourinary tract infections, such as cystitis or pyelonephritis, are common. Bladder stones may develop.12

Essentials of Assessment

History

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). Important factors to elicit also include cognitive ability, upper and lower extremity function, spasticity and dexterity, mobility, supportive environment, medication history, and lifestyle factors such as smoking, alcohol, or addictive drugs. A bladder diary is a simple, noninvasive, and inexpensive method of collecting information regarding urinary symptoms and bladder patterns. A voiding diary should include day-time and night-time voiding frequency, volumes voided, incontinence, and urge episodes.1,2

Physical examination

A detailed physical exam is warranted, including examination of the abdomen, pelvic and genital organs. Full neurologic exam should include mental status and comprehension, sensation in S2 through S5 dermatomes, sacral reflexes (e.g., bulbocavernosus reflex), anal sphincter tone and volitional contraction, and pelvic floor function.2,14

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.14

Laboratory studies

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

Basic metabolic panel is obtained at baseline. Follow blood urea nitrogen and creatinine concentrations.In patients with reduced muscle mass, changes in creatinine may not accurately reflect changes in renal function. Cystatin C measurements can be a better marker of renal function in patients with significantly diminished muscle mass. The above laboratory studies form part of a basic neuro-urological assessment.2

Imaging

A post-void residual (PVR) should be performed at the time of diagnosis and may be checked periodically thereafter to monitor for changes in bladder emptying ability, regardless of symptoms, or at the discretion of the physician following management changes.1   

In patients known to be at high risk of upper urinary tract disease, surveillance ultrasonography should be undertaken periodically to detect upper urinary tract dilatation or renal scarring. Ultrasound can also be used to demonstrate urinary tract stones, which might develop in patients with neurogenic LUT dysfunction.1 Surveillance strategies differ between various organizations but are usually performed yearly or biennially.

Supplemental assessment tools

Uroflowmetry is a valuable non-invasive investigation, especially when combined with a measurement of the PVR volume, to detect voiding dysfunction. It should be done before any treatment and can be used to monitor treatment outcomes. However, flow rate and PVR volume depend on both detrusor function and bladder outlet resistance. Thus, uroflowmetry is unable to discriminate between the underlying mechanisms, which would require the use of invasive urodynamics.2

Invasive urodynamics, generally a combination of cystometry and pressure-flow study in those who are able to void, with or without simultaneous fluoroscopic monitoring (i.e., video-urodynamics), assesses detrusor and bladder outlet function and provides information about detrusor pressure and compliance, and thus the risk factors for upper urinary tract damage. Urodynamics is not only prognostic but also valuable for guidance of appropriate treatment, especially if initial symptom- based therapy has failed.2

Cystoscopy may be indicated in the setting of unexplained hematuria or pyuria; suspected urethral pathology such as stricture or false passage; bladder stones; or known or suspected bladder cancer.1 

The American Urological Association and Society of Urodynamics, Female Pelvic Medicine & Uro- genital Reconstruction (AUA/SUFU) guideline was developed to inform clinicians on the proper evaluation, diagnosis, and risk stratification of patients with neurogenic bladder and the non-surgical and surgical treatment options available. Patients with neurogenic bladder should be risk-stratified as either low-, moderate-, high-, or unknown-risk. After diagnosis and stratification, patients should be monitored according to their level of risk at regular intervals. Patients who experience new or worsening signs and symptoms should be reevaluated and risk stratification should be repeated.1

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.14

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). Antibiotic prophylaxis has been shown to reduce the rate of UTI in patients with neurogenic bladder who perform clean intermittent catheterization (CIC). Concerns regarding the use of antimicrobial prophylaxis include the development of antimicrobial resistance and the potential side effects of the medication.15 Shared decision-making and full discussion regarding the potential harms related to acquiring an antibiotic resistant infection should be factored into the decision for antibiotic prophylaxis for UTI prevention.16

Antimuscarinics reliably increase maximum cystometric capacity (MCC) and voided/catheterized volumes, decrease detrusor pressure, and may improve urgency and incontinence across diverse neurogenic bladder pathologies. There is no evidence for the superiority of any particular medication.16

Emerging evidence exists for use of the more recently approved beta-3 agonist in the neurogenic bladder population. Additional evidence suggests that the use of alpha-blockers combined with antimuscarinics can ameliorate symptoms across several etiologies of neurogenic bladder.16

After shared decision-making with the patient regarding risks and benefits, concomitant therapy with beta-3 adrenergic receptor agonists and antimuscarinics presents a reasonable treatment option. 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 Bladder13,17,18

Neurogenic-Bladder-Table-1

Table 2. Non-pharmacologic Treatment of Neurogenic Bladder 6,18,19 

Neurogenic-Bladder-Table-2

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.19

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).20 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.

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. It is reported to improve incontinence and increase functional bladder capacity in SCI patients. Evidence for patients with Parkinson’s disease, CVA, and myelomeningocele were not as strong.16

A standardized dose and injection protocol remains to be established.10 For NDO, effective doses were intradetrusor injections of 200-300 units of (A/Ona) into 20-30 sites.21 In DSD, injections to the external sphincter range from 50-200 units (many studies use 100 units). 22

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.13

Neurostimulation Techniques: Neuromodulation and neurostimulation techniques continue to advance. 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). 23

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.24

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.25

Sacral posterior root rhizotomy with sacral anterior root stimulation can be done to manage refractory involuntary detrusor contractions and underactive detrusor.10,14

Regenerative medicine and stem cell therapy: Research into stem cell therapy for neurogenic bladder is ongoing. The main mechanisms of stem cells to reconstitute or restore bladder dysfunction are migration, differentiation, and paracrine effects. Stem cell transplantation may offer potential benefits in regenerating nerve tissue and restoring bladder function in some cases. However, higher quality of study is still needed to prove its effectiveness.26

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.

References

  1. Ginsberg DA, Boone TB, Cameron AP, Gousse A, Kaufman MR, Keays E, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Diagnosis and Evaluation. J Urol. 2021;206(5):1097-105. Epub 20210908. doi: 10.1097/ju.0000000000002235. PubMed PMID: 34495687.
  2. Panicker JN, Fowler CJ, Kessler TM. Lower urinary tract dysfunction in the neurological patient: clinical assessment and management. The Lancet Neurology. 2015;14(7):720-32. doi: 10.1016/s1474-4422(15)00070-8. PubMed PMID: 26067125.
  3. Linsenmeyer TA. Neurogenic bladder following spinal cord injury. In: Kirshblum S, & Lin, V. W. , editor. Spinal cord medicine: Springer Publishing Company; 2018.
  4. Hamid R, Averbeck MA, Chiang H, Garcia A, Al Mousa RT, Oh SJ, et al. Epidemiology and pathophysiology of neurogenic bladder after spinal cord injury. World J Urol. 2018;36(10):1517-27. Epub 20180511. doi: 10.1007/s00345-018-2301-z. PubMed PMID: 29752515.
  5. Panicker JN. Neurogenic Bladder: Epidemiology, Diagnosis, and Management. Semin Neurol. 2020;40(5):569-79. Epub 20201016. doi: 10.1055/s-0040-1713876. PubMed PMID: 33065745; PubMed Central PMCID: PMC9715349.
  6. Bladder management for adults with spinal cord injury: a clinical practice guideline for health-care providers. J Spinal Cord Med. 2006;29(5):527-73. PubMed PMID: 17274492; PubMed Central PMCID: PMC1949036.
  7. 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
  8. Spector L, Madigan L, Rhyne A, Darden B, Kim D. Cauda Equina Syndrome. J Am Acad Orthop Surg 2008;16:471-479.
  9. 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
  10. Jeong SJ, Cho SY, Oh SJ. Spinal cord/brain injury and the neurogenic bladder. Urol Clin North Am. 2010;37(4):537-46. doi: 10.1016/j.ucl.2010.06.005. PubMed PMID: 20955905.
  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. Panicker JN, Fowler CJ. The bare essentials: uro-neurology. Pract Neurol. 2010;10(3):178-85. doi: 10.1136/jnnp.2010.213892. PubMed PMID: 20498196.
  13. Cameron AP. Pharmacologic therapy for the neurogenic bladder. Urol Clin North Am. 2010;37(4):495-506. Epub 20100811. doi: 10.1016/j.ucl.2010.06.004. PubMed PMID: 20955901.
  14. Stöhrer M, Blok B, Castro-Diaz D, Chartier-Kastler E, Del Popolo G, Kramer G, et al. EAU guidelines on neurogenic lower urinary tract dysfunction. Eur Urol. 2009;56(1):81-8. Epub 20090421. doi: 10.1016/j.eururo.2009.04.028. PubMed PMID: 19403235.
  15. Fisher H, Oluboyede Y, Chadwick T, Abdel-Fattah M, Brennand C, Fader M, et al. Continuous low-dose antibiotic prophylaxis for adults with repeated urinary tract infections (AnTIC): a randomised, open-label trial. Lancet Infect Dis. 2018;18(9):957-68. Epub 20180628. doi: 10.1016/s1473-3099(18)30279-2. PubMed PMID: 30037647; PubMed Central PMCID: PMC6105581.
  16. Ginsberg DA, Boone TB, Cameron AP, Gousse A, Kaufman MR, Keays E, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Treatment and Follow-up. J Urol. 2021;206(5):1106-13. Epub 20210908. doi: 10.1097/ju.0000000000002239. PubMed PMID: 34495688.
  17. Wyndaele JJ, Kovindha A, Madersbacher H, Radziszewski P, Ruffion A, Schurch B, et al. Neurologic urinary incontinence. Neurourol Urodyn. 2010;29(1):159-64. doi: 10.1002/nau.20852. PubMed PMID: 20025021.
  18. Lamin E, Smith AL. Urologic agents for treatment of bladder dysfunction in neurologic disease. Curr Treat Options Neurol. 2014;16(3):280. doi: 10.1007/s11940-013-0280-3. PubMed PMID: 24464489.
  19. Panicker JN, de Sèze M, Fowler CJ. Rehabilitation in practice: neurogenic lower urinary tract dysfunction and its management. Clinical rehabilitation. 2010;24(7):579-89. doi: 10.1177/0269215509353252. PubMed PMID: 20584864.
  20. Dinh A, Davido B, Duran C, Bouchand F, Gaillard JL, Even A, et al. Urinary tract infections in patients with neurogenic bladder. Med Mal Infect. 2019;49(7):495-504. Epub 20190315. doi: 10.1016/j.medmal.2019.02.006. PubMed PMID: 30885540.
  21. Chancellor MB, Elovic E, Esquenazi A, Naumann M, Segal KR, Schiavo G, et al. Evidence-based review and assessment of botulinum neurotoxin for the treatment of urologic conditions. Toxicon. 2013;67:129-40. Epub 20130213. doi: 10.1016/j.toxicon.2013.01.020. PubMed PMID: 23415704.
  22. Peyronnet B, Gamé X, Vurture G, Nitti VW, Brucker BM. Botulinum Toxin Use in Neurourology. Rev Urol. 2018;20(2):84-93. doi: 10.3903/riu0792. PubMed PMID: 30288145; PubMed Central PMCID: PMC6168325.
  23. Bhide AA, Tailor V, Fernando R, Khullar V, Digesu GA. Posterior tibial nerve stimulation for overactive bladder-techniques and efficacy. Int Urogynecol J. 2020;31(5):865-70. Epub 20191218. doi: 10.1007/s00192-019-04186-3. PubMed PMID: 31853597; PubMed Central PMCID: PMC7210232.
  24. Kreydin E, Zhong H, Latack K, Ye S, Edgerton VR, Gad P. Transcutaneous Electrical Spinal Cord Neuromodulator (TESCoN) Improves Symptoms of Overactive Bladder. Front Syst Neurosci. 2020;14:1. Epub 20200206. doi: 10.3389/fnsys.2020.00001. PubMed PMID: 32116576; PubMed Central PMCID: PMC7017715.
  25. Barboglio Romo PG, Gupta P. Peripheral and Sacral Neuromodulation in the Treatment of Neurogenic Lower Urinary Tract Dysfunction. Urol Clin North Am. 2017;44(3):453-61. doi: 10.1016/j.ucl.2017.04.011. PubMed PMID: 28716325.
  26. Salehi-Pourmehr H, Nouri O, Naseri A, Roshangar L, Rahbarghazi R, Sadigh-Eteghad S, et al. Clinical application of stem cell therapy in neurogenic bladder: a systematic review and meta-analysis. Int Urogynecol J. 2022;33(8):2081-97. Epub 20211112. doi: 10.1007/s00192-021-04986-6. PubMed PMID: 34767058.

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

Philippines Cabahug, MD, Junghoon Choi, MD. Neurogenic Bladder. 12/15/2020

Author Disclosure

Philippines Cabahug, MD
Nothing to Disclose

Jing Chen, MD
Nothing to Disclose