Neurogenic Bladder

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Pelvic Floor Exercises written for patients

Neurogenic bladder is bladder dysfunction that may be either flaccid or spastic. It is caused by neurological damage. The main symptom is overflow incontinence.

Any condition that impairs bladder and bladder outlet afferent and efferent signalling can cause neurogenic bladder. Causes may involve:

Central nervous system (CNS)

  • Cerebrovascular event.
  • Spinal injury.
  • Meningomyelocele.
  • Amyotrophic lateral sclerosis.

Peripheral nervous system (PNS)

  • Diabetes.
  • AIDS.
  • Alcohol.
  • Vitamin B12 deficiency neuropathies.
  • Herniated disc.
  • Damage due to pelvic surgery.

Mixed CNS and PNS

  • Parkinson's disease.
  • Multiple sclerosis.
  • Syphilis.
  • Tumours.

Bladder outlet obstruction often co-exists and may exacerbate symptoms.

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These include:

  • Reduced quality of life - with social isolation and embarrassment.
  • Increased frequency of urinary tract infections (UTIs) and urinary calculi.
  • Hydronephrosis with vesico-ureteral reflux may occur because the large urine volume puts pressure on the vesico-ureteral junction, causing dysfunction with reflux and, in severe cases, nephropathy.
  • Patients with high thoracic or cervical spinal cord lesions are at risk of autonomic dysreflexia (a life-threatening syndrome of malignant hypertension, bradycardia or tachycardia, headache, piloerection, and sweating due to unregulated sympathetic hyperactivity). This disorder may be triggered by acute bladder distention (due to urinary retention) or bowel distention (due to constipation or faecal impaction).
  • Bladder cancer.

Several classification systems are available based on neuro-urological criteria or bladder and urethral function.

A popular system based on urodynamic findings is as follows:

Flaccid (hypotonic) neurogenic bladder

In this condition, the bladder volume is large, pressure is low and contractions are absent. It may result from peripheral nerve damage or spinal cord damage at the S2 to S4 level. After acute cord damage, initial flaccidity may be followed by long-term flaccidity or spasticity, or bladder function may improve after days, weeks or months.

Spastic bladder

In spastic bladder, the volume is normal or small and involuntary contractions occur. It usually results from brain damage or spinal cord damage above T12. Precise symptoms vary by site and severity of the lesion. Bladder contraction and external urinary sphincter relaxation are typically unco-ordinated (detrusor-sphincter dyssynergia).

Mixed patterns

Mixed patterns (flaccid and spastic bladder) may be caused by many disorders, including syphilis, diabetes mellitus and brain or spinal cord tumours.

Overflow incontinence is the primary symptom in patients with a flaccid or spastic bladder. Patients retain urine and have constant overflow dribbling. Men typically also have erectile dysfunction. Patients with spastic bladder may have frequency, nocturia and urgency or spastic paralysis with sensory deficits.

A full clinical history and examination should be taken, including enquiry into other indirect problems - eg, bowel symptoms and sexual dysfunction. Also enquire about any dysfunction of mobility, cognition or hand and eye function from the underlying illness, as this may impact treatment options. Refer anyone with 'red flag' features - eg, haematuria, hydronephrosis or worsening renal impairment.

These may include:

  • Serum creatinine.
  • Post-void residual volume.
  • Renal ultrasonography.
  • Urodynamics - eg, cystometry and pressure-flow investigations (not indicated in those with low risk of renal complications but mandatory before any surgical intervention is considered).

Diagnosis is suspected clinically and large post-void residual volume confirms the diagnosis. Renal function is determined by measuring serum creatinine. Renal ultrasonography will rule out hydronephrosis.

Further studies are often not obtained in patients who are not able to self-catheterise or able to go to the bathroom - eg, severely debilitated elderly or post-stroke patients.

In patients with hydronephrosis or nephropathy who are not severely debilitated, cystography, cystoscopy, and cystometrography with urodynamic testing are usually recommended and may guide further therapy:

  • Cystography is used to evaluate bladder capacity and detect reflux.
  • Cystoscopy is used to evaluate duration and severity of retention (by detecting bladder trabeculations) and to check for bladder outlet obstruction.
  • Cystometrography can determine whether bladder volume and pressure are high or low; if done during the recovery phase of flaccid bladder after spinal cord injury, it can help evaluate detrusor functional capacity and predict rehabilitation prospects.
  • Urodynamic testing of voiding flow rates with sphincter electromyography can show whether bladder contraction and sphincter relaxation are co-ordinated.

Further specialised uro-neurogenic tests performed in secondary care may include:[2] 

  • 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.

Patients and carers need adequate support and education. Do not underestimate the effect on relationships and quality of life.

General measures

General treatment includes:

  • Monitoring of renal function - the National Institute for Health and Care Excellence (NICE) recommends lifelong 1- to 2-yearly ultrasound surveillance to high-risk patients - eg, those with vesico-ureteric reflux.
  • Monitor blood pressure if renal impairment is present.
  • Early ambulation/maintaining mobility.
  • Frequent changes of position.
  • Consideration of absorbent products to protect skin and clothing.[4] 
  • Urethral occlusive devices (artificial devices that may be inserted into the urethra or placed over the urethral meatus to prevent urinary leakage).

Specific treatment

A systematic review and meta-analysis found little evidence to inform best practice. A review of intermittent self-catheterisation regimens found that clean non-coated catheters were the most cost-effective. However, because they were designated as single-use devices, the authors recommended that a precautionary principle should be adopted and that patients should be offered a choice between hydrophilic and gel reservoir catheters.[5] 

UTIs[3] 

  • If UTI is suspected (based on symptoms and not only the dipstick), send sample for microscopy, culture and sensitivities. Be aware that bacterial colonisation of the catheter can also lead to abnormal urine dipstick and microbiological results, so treatment needs to be influenced by the symptoms.
  • High fluid intake to decrease risk of UTIs and urinary calculi (although this measure may exacerbate incontinence).
  • Antibiotic prophylaxis is not recommended routinely but can be used for frequent or severe UTIs. The need for prophylaxis should be reviewed regularly.
  • Catheter change - antibiotics are only indicated in those who have had a traumatic catheter change or previous UTI (with symptoms) following a previous change of catheter.

Immediate continuous or intermittent catheterisation

This is needed for a flaccid bladder, especially if the cause is an acute spinal cord injury. Intermittent self-catheterisation is preferable to indwelling urethral catheterisation, which has a high risk of recurrent UTIs and, in men, a high risk of urethritis, periurethritis, prostatic abscesses and urethral fistulas. Intermittent catheterisation has several advantages over other techniques, including fewer infections, reduced equipment needs and greater independence.[6] However, the patient (or carer) must be able and willing to perform the procedure, so it may not always be practical. Suprapubic catheterisation may be used if patients cannot self-catheterise.

Techniques to trigger voiding

For spastic bladder, treatment depends on the patient's ability to retain urine. Patients who can retain normal volumes can use techniques to trigger voiding - eg, applying suprapubic pressure, scratching the thighs; anticholinergics may be effective. For patients who cannot retain normal volumes, treatment is the same as that of urge incontinence and sacral nerve stimulation.

Improving bladder storage[3] 

Some patients - eg, in the presence of cognitive impairment - may be appropriate for behavioural management intervention. This may focus on timed voiding and habit training.

Injection of botulinum toxin type A into the bladder wall is recommended for adults and children who fulfil all three of the following criteria (unlicensed use):

  • Underlying spinal cord disease.
  • Overactive bladder.
  • Medical therapy with antimuscarinic drugs, which is either unsuccessful or not tolerated.

Repeat injections may be necessary. Catheterisation may be necessary after the procedure, as retention can occur. Residual volume and renal function may need to be monitored.

Antimuscarinics[3] 

Recommended for those with spinal cord pathology and symptoms of bladder overactivity. They should also be considered in the following:

  • Primary brain pathology and bladder overactivity.
  • Impaired bladder storage on urodynamic testing.

The following should be monitored in patients started on antimuscarinics:

  • Residual volume if not using catheterisation.
  • Adverse effects - eg, confusion and constipation.
  • UTIs - can be increased, as bladder emptying is affected.

NB: there is no role for alpha-blockers.

Neurogenic stress incontinence[3] 

  • Pelvic floor muscle strengthening can be useful for stress incontinence.
  • Biofeedback and electrical stimulation may also be options.
  • Synthetic tapes and slings are not recommended.
  • Surgery is usually a last resort (also see below):
    • Autologous fascial sling surgery - involves removal of fascial tissue from the abdomen and using it to support the urethra for the treatment of neurogenic stress incontinence.
    • Formation of artificial urinary sphincter - used if all other procedures have been ineffective and sling surgery is inappropriate. This is an option for patients who have adequate bladder capacity, good bladder emptying and upper extremity motor skills and who can comply with instructions for use of the device; if patients do not comply, life-threatening situations (eg, renal failure, urosepsis) can result. The possibility of repeat procedures and complications should be discussed with the patient and/or carers at the outset. It is important to monitor for renal impairment after the procedure.

Surgery[3] 

This is a last resort. It is usually indicated if patients have had, or are at risk of, severe acute or chronic sequelae, or if social circumstances, spasticity or quadriplegia prevent use of continuous or intermittent bladder drainage:

  • Sphincterotomy (for men) converts the bladder into an open draining conduit.[7] 
  • Sacral (S3 and S4) rhizotomy converts a spastic into a flaccid bladder.
  • Bladder augmentation - also called augmentation cystoplasty - involves enlarging the bladder storage capacity using intestinal sections. It is associated with a number of complications and requires adequate risk-benefit assessment before being undertaken.
  • Urinary diversion may involve an ileal conduit or ureterostomy. Cystectomy may also be recommended to prevent pyocystitis.

Prognosis is good if the disorder is diagnosed and treated before kidneys are damaged. But it will lead to a significant impact on the lives of patients and carers.

Further reading & references

  1. Dorsher PT, McIntosh PM; Neurogenic bladder. Adv Urol. 2012;2012:816274. doi: 10.1155/2012/816274. Epub 2012 Feb 8.
  2. Guidelines on Neuro-Urology; European Association of Urology (2015)
  3. Urinary incontinence in neurological disease: assessment and management; NICE Clinical Guideline (August 2012)
  4. Cameron AP, Jimbo M, Heidelbaugh JJ; Diagnosis and office-based treatment of urinary incontinence in adults. Part two: treatment. Ther Adv Urol. 2013 Aug;5(4):189-200. doi: 10.1177/1756287213495100.
  5. Bermingham SL, Hodgkinson S, Wright S, et al; Intermittent self catheterisation with hydrophilic, gel reservoir, and non-coated catheters: a systematic review and cost effectiveness analysis. BMJ. 2013 Jan 8;346:e8639. doi: 10.1136/bmj.e8639.
  6. Buckley B, Grant AM; What is the most effective management of neurogenic bladder dysfunction? BMJ. 2009 Mar 12;338:b659. doi: 10.1136/bmj.b659.
  7. Shamliyan TA, Wyman JF, Ping R, et al; Male urinary incontinence: prevalence, risk factors, and preventive interventions. Rev Urol. 2009 Summer;11(3):145-65.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Hayley Willacy
Current Version:
Peer Reviewer:
Dr Helen Huins
Document ID:
12249 (v4)
Last Checked:
23/03/2016
Next Review:
22/03/2021

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