Neurogenic bladder dysfunction

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Neurogenic bladder
SpecialtyUrology, Neurology

Neurogenic bladder dysfunction, sometimes simply referred to as neurogenic bladder, is a dysfunction of the urinary bladder due to disease or injury of the central nervous system or peripheral nerves involved in the control of urination. There are multiple types of neurogenic bladder depending on the underlying cause and the symptoms. Symptoms include overactive bladder, urinary urgency, frequency, incontinence or difficulty passing urine. A range of diseases or conditions can cause neurogenic bladder including spinal cord injury, Multiple sclerosis, stroke, brain injury, spina bifida, peripheral nerve damage, Parkinson's disease, or other neurodegenerative diseases. Neurogenic bladder is diagnosed through a history and physical as well as imaging and more specialized testing. Treatment depends on underlying disease as well as symptoms and can be managed with behavioral changes, medications, surgeries, or other procedures. The symptoms of neurogenic bladder, especially incontinence, can have a significant impact on quality of life.


There are different types of neurogenic bladder depending on the underlying cause. There may be overlap between symptoms across these presentations.


Uninhibited bladder is usually due to damage to the brain from a stroke or brain tumor. This can cause reduced sensation of bladder fullness, low capacity bladder and urinary incontinence but does not lead to high bladder pressures that can cause kidney damage.[1]


In spastic neurogenic bladder (also known as upper motor neuron or hyper-reflexive bladder), the muscles of the bladder detrusor muscle and urethral sphincter do not work together and are usually tightly contracted at the same time. This phenomenon is also called detrusor external sphincter dyssynergia (DESD). This can cause urinary retention with high pressures in the bladder that could damage the kidneys. The bladder volume is usually smaller than normal due to increased muscle tone of the detrusor. Spastic neurogenic bladder is usually caused by damage to the spinal cord above the level of the 10th thoracic vertebrae (T10).[1][2]


In flaccid (also known as lower motor neuron or hypotonic) bladder, the muscles of the bladder lose ability to contract normally. This can cause the inability to void urine even if the bladder is full and cause a large bladder capacity. The internal urinary spincter is intact, however urinary incontinence is common. This is caused from damage to the peripheral nerves.[1]


Mixed type of neurogenic bladder can cause a combination of the above presentations. In mixed type A, the detrusor is flaccid but the spincter is overactive. This causes a large, low pressure bladder and inability to void although not as much risk for kidney damage as a spastic bladder. Mixed type B is characterized by a flaccid external sphincter and a spastic bladder causing problems with incontinence.[1]

Signs and symptoms[edit]

Neurogenic bladder can cause a range of urinary symptoms including sudden urges to urinary urgency, urinary incontinence or difficulty urinating (urinary retention.) The first sign of bladder dysfunction may be recurrent urinary tract infections.


Neurogenic bladder can be caused by damage or diseases of the central, peripheral or autonomic nervous systems. This includes any condition that impairs bladder signaling at any point along the tract from the micturition center in the brain to the spinal cord and peripheral nerves to the bladder.

Central nervous system[edit]

Damage to the brain or spinal cord is the most common cause of neurogenic bladder. Brain pathology can include stroke, brain tumors, multiple sclerosis, Parkinson's disease or other neurodegenerative conditions. Bladder involvement is more likely if the damage is in the area of the pons. Damage to the spinal cord from traumatic injury, demyelinating disease, syringomyelia, cauda equina syndrome, or spina bifida. Spinal cord compression from herniated disks, tumor, or spinal stenosis can also result in neurogenic bladder.[1]

Peripheral nervous system[edit]

Damage to the peripheral nerves of the bladder can cause neurogenic bladder, usually the flaccid type. Peripheral neuropathy can be caused by diabetes, alcoholism, and vitamin B12 deficiency. Peripheral nerves can also be damaged as a complication of major surgery of the pelvis, such as for removal of sacrococcygeal teratoma and other tumors.[1]


The diagnosis of neurogenic bladder is made based on a complete history and physical (including neurologic) examination, as well as use of imaging and specialized studies. History should include the onset, duration, triggers, severity, medical history and medications (especially anticholinergics, calcium channel blockers, diuretics, sedatives, alpha-agonists, alpha-antagonists).[2] Urinary symptoms include frequency, urgency, incontinence or any urinary tract infections (UTIs). Questionnaires can be helpful in quantifying symptom burden.[2] In children it is important to obtain an antenatal and developmental history.[3]

Ultrasound imaging is important to identify the shape of the bladder, post-void residual volume, and evidence of kidney damage such as kidney size, paranchymal thickness or ureteral dilation. A voiding cystourethrography study that uses contrast dye to obtain images of a full bladder as well as post-void residual volumes that can show changes in bladder shape consistent with neurogenic bladder.[3]

Urodynamic studies are an important component of the evaluation for neurogenic bladder. Urodynamics refers to the measurement of the pressure-volume relationship in the bladder. The bladder usually stores urine at low pressure and voiding can be completed without a dramatic pressure rise. Damage to the kidneys is imminent if the pressure rises above 40cm of water during filling. Bladder pressure can be measured by cystometry, during which the bladder is artificially filled with a catheter and bladder pressures and detrusor activity are monitored. Patterns of involuntary detrusor activity as well as bladder flexibility, or compliance, can be captured. The most valuable test to test for detrusor external sphincter dyssynergy (DESD) is to perform cystometry simultaneously with external sphincter electromyography (EMG). Uroflowmetry is a less-invasive study that can quantify the urine flow rate as an indicator of detrusor strength and sphincter resistance.[2] These studies can be repeated at regular intervals, especially if symptoms worsen or to measure response to therapies.[3]

Evaluation of kidney function through a serum creatinine should be obtained as well as a urine dipstick test to rule out infection.[2]

Imaging of the pelvis with CT scan or magnetic resonance imaging may be necessary, especially if there is concern for an obstruction such as a tumor. The inside of the bladder can be visualized by cystoscopy.


Treatment depends on the type of neurogenic bladder and co-morbidities and can include catherization, medications, surgeries or other procedures. The goals of treatment is to keep bladder pressures in a safe range and eliminate post-void residual volumes.


Emptying the bladder with the use of a catheter is the most common strategy for managing urinary retention from neurogenic bladder. For most patients, this can be accomplished with intermittent catherization which involves no surgery or permanently attached appliances. Intermittent catheterization involves using straight catheters (which are usually disposable or single-use products) several times a day to empty the bladder. This can be done independently by the patient or with help. For patients who are unable to tolerate disposable straight catheters, a Foley catheter allows continuous drainage of urine into a sterile drainage bag that is worn by the patient. The risk of urinary tract infections is higher with Foley catheters.


Oxybutynin is a common anti-cholinergic medication used to reduce spasmodic overactive contractions by blocking M3 muscarinic receptors in the detrusor. It's use is limited by side effects such as dry mouth, constipation and decreased sweating. Tolterodine is a longer acting anticholinergic that may be better tolerated.[3]

For urinary retention, cholinergics (muscarinic agonists) like bethanechol can improve the squeezing ability of the bladder. Alpha blockers can also reduce outlet resistance and allow complete emptying if there is adequate detrusor function.[3]

Botulinum Toxin[edit]

Botulinum toxin (botox) can be used through two different approaches. For spastic neurogenic bladder, the detrusor can be injected which will cause it to be flaccid for 6-9 months. This prevents high bladder pressures and intermittent catherization can be used during this time.[3]

Botox can also be injected into the external sphincter to paralyze a spastic sphincter in patients with detrusor sphincter dyssynergy.


Various strategies to modulate the interaction between the nerves and muscles of the bladder exist, including nonsurgical therapies (transurethral electrical bladder stimulation), minimally invasive procedures (sacral neuromodulation pacemaker), and operative (reconfiguration of sacral nerve root anatomy).[3]


Surgical interventions may be pursued if medical approaches have been trialed and maximized. This may include creation of a stoma that is continent and bypasses the urethra to empty the bladder directly. This conduit may be created from the appendix (Mitrofanoff stoma) or a portion of the ileum (‘Yang-Monti’ conduit).[3] The ileum and ascending colon can also be used to create a pouch accessible for catherization (Indiana pouch).


Neurogenic bladder can cause hydronephrosis, recurrent urinary tract infections, and recurrent kidney stones which may compromise kidney function. This is especially prominent in spastic neurogenic bladder that leads to high bladder pressures. Renal failure was previously a leading cause of mortality in patients with spinal cord injury.

See also[edit]


  1. ^ a b c d e f Dorsher PT, McIntosh PM (2012). "Neurogenic bladder". Advances in Urology. 2012: 816274. doi:10.1155/2012/816274. PMC 3287034. PMID 22400020.
  2. ^ a b c d e Amarenco, Gerard; Sheikh Ismaël, Samer; Chesnel, Camille; Charlanes, Audrey; LE Breton, Frederique (Dec 2017). "Diagnosis and clinical evaluation of neurogenic bladder". European Journal of Physical and Rehabilitation Medicine. 53 (6): 975–980. doi:10.23736/S1973-9087.17.04992-9. ISSN 1973-9095. PMID 29072046.
  3. ^ a b c d e f g h Sripathi, Venkataramani; Mitra, Aparajita (2017-07-01). "Management of Neurogenic Bladder". The Indian Journal of Pediatrics. 84 (7): 545–554. doi:10.1007/s12098-017-2356-7. ISSN 0973-7693.

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