Neurogenic Bladder: Neuroanatomy, Physiology, Pathophysiology, Types, Laboratory Studies, Medications Used and Complications


The normal function of the urinary bladder is to store and expel urine in a coordinated and controlled manner.

Medical Definition: This coordinated activity is regulated by the central and peripheral nervous systems. Neurogenic bladder is a term that is applied to the malfunctioning of the urinary bladder due to a neurological dysfunction that arises from traumas, illnesses, or internal or external injuries.

Symptoms of neurogenic bladder vary from lack of detrusor activity to hyperactivity, depending on the site of the neurological lesion. The urinary sphincter can also be affected, resulting in a lack of training or hyperactivity and loss of sphincter coordination with bladder function.

Appropriate therapy for neurogenic bladder and a successful treatment outcome is based on accurate diagnosis through careful medical and voiding history, along with various clinical examinations, including urodynamics and selective studies of radiographic images.


Normal urination is essentially a spinal reflex modulated by the central nervous system (brain and spinal cord), which coordinates the function of the bladder and urethra. Three peripheral nerves innervate the bladder and urethra from the autonomic nervous system (ANS) and the somatic nervous system.

The central nervous system is composed of the brain, the brainstem, and the spinal cord.


The brain is the master control of the entire urinary system.


Cognitive control of urination is achieved by communicating several cerebral structures to the periaqueductal gray matter, which controls the pontine urination center to suppress or trigger avoiding reflex.

The brain receives information through afferent pathways that ascend from the bladder and provide information about how full the bladder is. The higher brain centers determine whether it is socially acceptable to annul and trigger structures downstream to allow or suppress the voiding reflex.

As a result of dependence on higher brain centers, specific brain injuries or diseases (e.g., stroke, cancer, dementia) can cause loss of voluntary control of the normal micturition reflex and symptoms such as urinary urgency.

The signal transmitted by the brain is routed through 2 intermediate segments (the brainstem and the sacral spinal cord) before reaching the bladder.


The brainstem is at the base of the skull. The lump is located within the brainstem, a specialized area that serves as an important relay center between the brain and the bladder (see image below). The lump is responsible for coordinating the urinary sphincters and the bladder activities.

The mechanical process of urination is coordinated in an area of ​​the protuberance known as the pontine center of urination (CPM). The CPM coordinates the relaxation of the urethral sphincter and the detrusor contraction to facilitate urination.

The bridge transmits afferent information from the bladder to higher brain centers, which communicate with the periaqueductal gray matter. This repeating station collects brain input and factor inputs from this center to signal the CPM to activate or suppress the micturition reflex.

The conscious sensations associated with the activity of the bladder are transmitted to the protrusion of the cerebral cortex. The interaction of various excitatory and inhibitory neuronal systems influences PMC activity, which attempts to activate the voiding reflex by default.

This voiding reflex causes the urethral sphincters to open while allowing the detrusor to contract and expel urine.

Emotions experienced in the higher brain centers can later affect the CPM, so some may experience excitement or fear incontinence.

The brain’s ability to control CPM is part of the social skills children experience during growth and development. In general, the brain takes control of the swell through the periaqueductal gray substance when the children undergo toilet training.

When the bladder fills up, the detrusor muscle stretch receptors send a signal to the lump, which notifies the brain. People perceive this signal (fullness of the bladder) as a sudden urge to urinate or a urinary need.

In everyday situations, the brain sends an inhibitory signal to the protrusion through the periaqueductal gray substance to inhibit the contraction of the bladder until a bath is found.

When the CPM is deactivated, the desire to urinate disappears, which allows the patient to delay urination until finding a socially acceptable place and time. When urination is appropriate, the brain eliminates its suppression of the CPM through the periaqueductal gray matter, allowing the urinary sphincter to open and the detrusor to contract and empty the bladder.

Spinal cord

The spinal cord extends from the brainstem to the lumbosacral spine. It is found in the spinal canal and is protected by cerebrospinal fluid, meninges, and the spine—the spinal cord functions as a long path of communication between the brainstem and the sacral spinal cord.

When the sacral cord receives sensory information from the bladder, this signal travels through the spinal cord to the pons and then to the brain’s higher centers.

The brain interprets this signal and sends a response through the swell that travels through the spinal cord to the sacral cord and, later, to the bladder. The periaqueductal gray substance that inhibits the pons can suppress this signal of “response,” part of the micturition reflex, which the periaqueductal gray importance can stop inhibits the pons.

The spinal cord is an essential intermediary between the pons and the sacral medulla in the normal cycle of filling and emptying the bladder. An intact spinal cord is critical for normal urination.

Depending on the level of injury, a spinal cord injury can lead to urinary frequency, urgency, and urge incontinence, which the difficulty in emptying the bladder can complicate.

This occurs because the urinary bladder and the sphincter are no longer coordinated and both exercise hyperactivity, a condition called detrusor-sphincter dyssynergia (DDE).

The sacral spinal cord is the terminal portion of the spinal cord, located in the lower back in the lumbar area. This is a specialized portion of the spinal cord known as the sacral reflex center. It is responsible for the contractions of the bladder. The sacral reflex center is the primitive voiding center.

In babies, the upper center of micturition control (the brain) is not mature enough to control the bladder, so the power of micturition comes from signals sent from the sacral cord. When the urine fills the infant’s bladder, a sign of excitement is forwarded to the sacrum cord.

When the sacral cord receives this signal, the spinal reflex center automatically activates the detrusor so that it contracts. The result is involuntary detrusor contractions with coordinated urination.

There is a continuous cycle of filling and emptying the bladder, so infants and young children depend on diapers until they enter the toilet. As the child’s brain matures and develops, he gradually gains control of the bladder and urinary sphincters to inhibit involuntary urination.

The control of the transitions of the micturition process from the sacral reflex center to the pontine urination center is further modulated by the higher cerebral centers that process the emotions and the social context.

Severe sacral cord injury results in loss of bladder function. Affected patients may develop urinary retention, called detrusor areflexia. The detrusor can not be contracted, so the patient will not be able to urinate, and urinary retention will occur.

Peripheral nerves

Peripheral nerves form a network of ways to send and receive information throughout the body. The nerves enter and exit the spinal cord, transmitting nerve information to and from the brain. Related but separate neural pathways influence the urethral bladder and sphincters.

The autonomic nervous system is outside the central nervous system. Regulates the actions of internal organs under involuntary control. The autonomic nervous system is divided into the sympathetic and parasympathetic systems.

When the sympathetic nervous system is active, it causes the bladder to increase its capacity without increasing the resting pressure of the detrusor (accommodation) and stimulates the internal urinary sphincter to remain well closed.

The sympathetic activity also inhibits parasympathetic stimulation, preventing contractions of the bladder. When the sympathetic nervous system is active, urinary accommodation occurs, and the voiding reflex is suppressed.

The parasympathetic nervous system works opposite to that of the sympathetic nervous system. In terms of urinary function, the parasympathetic nerves stimulate the detrusor contract. Immediately before parasympathetic stimulation, the sympathetic influence on the internal urethral sphincter is suppressed so that the internal sphincter relaxes and opens.

In addition, the activity of the pudendal nerve, a somatic nerve, is inhibited from causing the opening of the external sphincter. The result is the facilitation of voluntary voiding.

The somatic nervous system regulates the actions of the muscles under voluntary control. Examples of these muscles are the external urinary sphincter and the pelvic diaphragm. The pudendal nerve originates in the Onuf nucleus and regulates the voluntary actions of the external urinary sphincter and the pelvic diaphragm.

The activation of the pudendal nerve causes contraction of the external sphincter, which occurs with activities such as Kegel exercises (which also target the large muscles of the pelvic floor). Some reflex activities can also happen through the pudendal nerve, such as sphincter contractions during sneezing, coughing, and laughter, the so-called continence reflex.

Physiology and physiopathology


The average person will lose approximately 4-8 times during a day. The urinary bladder is in storage mode most of the day, which allows the individual to participate in activities more critical than urination.

The bladder’s normal function consists of 2 phases: filling and emptying. The normal urination cycle requires that the urinary bladder and urethral sphincter work together as a coordinated unit to store and empty urine.

During urinary storage, the bladder acts as a low-pressure receptacle. In contrast, the urinary sphincter maintains a high resistance to urinary flow to keep the exit of the bladder closed.

During the elimination of urine, the bladder contracts to expel urine while opening the urinary sphincter (low resistance) to allow urinary flow without obstructions and emptying the bladder.

Filling phase

During the filling phase, the bladder accumulates increasing volumes of urine while the pressure inside the bladder remains low. The pressure inside the bladder should be less than the urethral pressure during the filling phase. The urine will leak if the bladder pressure exceeds the urethral pressure (resistance).

The filling of the urinary bladder depends on the intrinsic viscoelastic properties of the bladder and the inhibition of the parasympathetic nerves. Therefore, the filling of the bladder is mainly a passive event.

The sympathetic nerves also facilitate the storage of urine in the following ways:

  • The sympathetic nerves inhibit the parasympathetic nerves from causing contractions of the bladder.
  • The sympathetic nerves directly cause relaxation and expansion of the detrusor muscle.
  • The sympathetic nerves close the neck of the bladder by narrowing the internal urethral sphincter. This sympathetic entrance in the lower urinary tract is constantly active during the filling of the bladder.

As the bladder fills up, the pudendal nerve becomes excited—stimulation of the pudendal nerve results in the external urethral sphincter contraction.

The contraction of the external sphincter, together with that of the internal sphincter, maintains the urethral pressure (resistance) higher than the normal pressure of the bladder. This increase in urethral pressure with filling is the reflection of continence.

Pressure gradients within the bladder and urethra play an essential functional role in normal urination. As long as the urethral pressure is greater than that of the bladder, the person will remain on the continent. Urinary incontinence will occur if the urethral pressure is abnormally low or the intravesical pressure is unusually high.

During some physical activities and with coughing, sneezing, or laughter, the pressure inside the abdomen increases sharply. This increase is transmitted to the bladder and, in response, the urethra, both anatomically and functionally, is designed to increase its pressure and maintain continence.

When the pressure transmitted to the bladder is more significant than inside the urethra, the urine is filtered, which results in stress incontinence.

Emptying phase

The storage phase of the urinary bladder can be changed to the emptying degree either involuntarily (by reflex) or voluntarily. Involuntary reflex emptying occurs in a baby when the volume of urine exceeds the threshold of urination.

When the bladder is complete, the stretch receptors inside the bladder wall signal the sacral cord. The sacral cord, in turn, sends a message to the bladder to initiate urination.

At this point, the pudendal nerve causes relaxation of the urethral sphincter, also accompanied by a broader relaxation of the pelvic floor. The sympathetic nerves send a message to the internal sphincter to relax and open, resulting in less urethral resistance.

The parasympathetic nerves trigger the detrusor contraction when the urethral sphincters relax and open. When the bladder contracts, the pressure generated by the bladder overcomes the urethral pressure, which produces a urinary flow.

These coordinated series of events allow the unhindered automatic release of stored urine. While conscious control of this reflex develops after infancy, the primitive voiding reflex may reappear with spinal cord injuries.

Delay in cancellation or voluntary cancellation

The bladder’s function is automatic, but it is entirely governed by the brain, which makes the final decision about the cancellation or not. The normal urination function means that an individual can stop and start urinating at the command.

In addition, the individual can delay urination until a socially acceptable time and place. The healthy adult is aware of the filling of the bladder and can voluntarily initiate or delay urination.

In a healthy adult, the CPM functions as an on-off switch signaled by stretch receptors in the wall of the bladder and, in turn, is modulated by inhibitory and excitatory neurological influences of the brain.

When the bladder is complete, the stretch receptors are activated. The individual perceives the activation of the stretch receptors when the bladder is complete, which indicates the need to evacuate or the sensation of urinary urgency.

When an individual can not find a bath nearby, the brain bombards the CPM with many inhibitory signals through the periaqueductal gray substance to prevent detrusor contractions. At the same time, an individual can actively contract the levator muscles to keep the external sphincter closed or initiate distraction techniques to suppress urination.


If a problem occurs within the nervous system, the entire urination cycle is affected. Any part of the nervous system can be affected, including the brain, the pons, the spinal cord, the sacral medulla, and the peripheral nerves. A dysfunctional voiding condition results in different symptoms, ranging from acute urinary retention to an overactive bladder.

Urinary incontinence results from a dysfunction of the bladder, the sphincter, or both. Overactive bladder is associated with the symptoms of urge incontinence, while lack of sphincter activity (decreased resistance) produces symptomatic stress incontinence. A combination of detrusor overactivity and lack of sphincter activity can lead to mixed symptoms.

Brain injuries

Brain injuries above the bridge interrupt the higher conscious control of urination. The urinary reflexes of the lower urinary tract, the primitive voiding reflex, remain intact. Affected people show signs of urge incontinence and experience symptoms of overactive bladder.

The bladder empties too quickly and too often, with relatively low volumes of urine, and deferring urination or storing a large volume becomes difficult. Waking up frequently at night to cancel is also common in such situations.

Typical examples of a brain injury are stroke, brain tumor, and head trauma. Hydrocephalus, cerebral palsy, and Shy-Drager syndrome are central nervous system pathologies affecting voiding function. Dementia can also affect the socially appropriate control of urination.

Spinal cord injuries

Diseases or injuries of the spinal cord between the protrusion and the sacral spinal cord also cause overactive bladder, often accompanied by urge incontinence. The bladder empties too frequently, and the public image can be similar to a brain injury, except that the external sphincter can paradoxically contract.

Suppose both the bladder and the external sphincter become spastic simultaneously. The affected person will feel an overwhelming desire to urinate, but only a tiny amount of urine can leak out. This is called detrusor-sphincter dyssynergia since the bladder, and the external sphincter is not in synergy.

The causes of spinal cord injuries include physical trauma, tumors, ischemia, multiple sclerosis (MS), and other neurodegenerative conditions. Children born with myelomeningocele may have neurogenic bladder from birth or may develop it later as they grow up due to anchoring of the spinal cord.

Sacral cord injury

Selected lesions of the sacrum cord and corresponding nerve roots arising from the sacrum can prevent the bladder from emptying and the patient from sensing a full bladder.

Persons that can not feel a full bladder may be at risk of urinary retention and damage to the kidneys due to the high pressure of storing large volumes of urine.

If the bladder can not contract, there is a condition called detrusion of areflexia, which also leads to the storage of large volumes of urine and may be accompanied by overflow incontinence. Typical causes are a sacral cord tumor, a herniated disc, and lesions that crush the pelvis.

This condition can also occur after a lumbar laminectomy, radical hysterectomy, or abdominoperineal resection. Rapid growth in childhood can also lead to the detrusor areflexia of a spinal cord tied in patients with previous trauma or congenital malformations such as spina bifida.

Peripheral nerve injury

Diabetes mellitus, AIDS, and iatrogenic injury can cause peripheral neuropathy that causes urinary retention. These disorders interrupt the bladder’s nerves and lead to a silent and painless distension of the bladder.

Patients with long-standing diabetes also often have an altered feeling of bladder filling, further complicating the situation. As with the injury to the sacral medulla, affected persons will have difficulty urinating and may develop a hypocontractile bladder.

Other diseases that cause this condition are poliomyelitis, Guillain-Barré syndrome, severe genital herpes infection, pernicious anemia, and neurosyphilis (tabes dorsalis).

Types of neurogenic bladders

Supraspinal lesions

Supraspinal lesions involve the central nervous system above the pons. They include stroke, brain tumor, Parkinson’s disease, and Shy-Drager syndrome.


After a stroke, the brain can enter a temporary phase of acute cerebral shock. During this time, the urinary bladder will be in retention-detrusion of areflexia. Almost 25% of affected people develop acute urinary retention after a stroke.

After the shock phase disappears, the bladder shows detrusor hyperreflexia with the coordinated activity of the urethral sphincter. This occurs because the PMC is released from the cerebral inhibitory center. Patients with detrusor hyperreflexia complain of urinary frequency, urgency, and urge incontinence.

The treatment for the cerebral shock phase is permanent Foley catheter placement or clean intermittent catheterization (CIL). Detrusor hyperreflexia is treated with anticholinergic medications to facilitate the filling and storage of the bladder.

Tumor cerebral

Detrusor hyperreflexia with coordinated urethral sphincter is the most common observed urodynamic pattern associated with a brain tumor. These patients complain of urinary frequency and urgency and urge incontinence. The first-line treatment for detrusor hyperreflexia includes anticholinergic medication.

Parkinson’s disease

This is a degenerative disorder of pigmented neurons of substantia nigra. It produces dopamine deficiency and increased cholinergic activity in the striatum. Specific urinary bladder symptoms include frequency, urgency, nocturia, and urge incontinence.

The urodynamic findings of Parkinson’s disease are more consistent with detrusor hyperreflexia and urethral sphincter bradykinesia. The striated urethral sphincter often shows a poorly sustained contraction.

As with other supraspinal lesions, the treatment for Parkinson’s disease is to facilitate filling the bladder and promote urinary storage with anticholinergic agents.

In men with Parkinson’s disease who show symptoms of bladder outlet obstruction (OSV) due to benign prostatic hypertrophy (BPH), the diagnosis of OSV should be confirmed by multichannel urodynamic studies.

The most common cause of postprostatectomy incontinence in a patient with Parkinson’s disease is detrusor hyperreflexia. If transurethral resection of the prostate (RTP) is performed without urodynamic confirmation of the obstruction, the patient may become incontinent after the RTP procedure.

Shy-Drager’s syndrome

Shy-Drager syndrome is a rare, progressive, degenerative disease that affects the autonomic nervous system with multisystem organ atrophy. In addition to parkinsonian symptoms, patients often have cerebellar ataxia and autonomic dysfunction. Clinical manifestations include orthostatic hypotension, anhidrosis, and urinary incontinence.

The degeneration of the Onuf nucleus produces the denervation of the external striated sphincter. Sympathetic atrophy of the nerve causes a nonfunctional bladder and an open bladder neck.

Urodynamic evaluation often reveals detrusor hyperreflexia, although some patients may have detrusor areflexia or poorly sustained bladder contractions. Usually, the neck of the bladder (internal sphincter) will be open at rest, with denervation of the striated sphincter.

The treatment for Shy-Drager syndrome is to facilitate urinary storage with anticholinergic agents coupled with CIL or a permanent catheter. Patients with Shy-Drager syndrome should avoid having an RTP because the risk of total incontinence is high.

Spinal cord injuries

Neurogenic bladder from spinal cord injuries can take various forms, depending on the mechanism and site of the damage.

Spinal cord trauma

When an individual suffers a spinal cord injury (for example, a diving accident or damage to a motor vehicle), the initial neurological response is a spinal shock. During this spinal shock phase, the affected individual experiences flaccid paralysis below the lesion level, and somatic reflex activity is depressed or absent.

The anal and bulbocavernosus reflex is typically absent. The autonomic activity is depressed, and the individual experiences urinary retention and constipation. The urodynamic findings are consistent with the Aretrlexic detrusor and rectum. However, the internal and external activities of the urethral sphincter are normal.

The spinal shock phase usually lasts 6 to 12 weeks but may persist longer in some cases. The urinary bladder should be drained with CIL or a permanent urethral catheter.

When the spinal shock phase disappears, the bladder function returns, but the detrusor activity increases in reflex excitability to a hyperactive state (i.e., detrusor hyperreflexia). Depending on the level of the lesion, hyperreflexia of the detrusor-detrusor of the sphincter-detrusor (HDD-ED) may develop.

Therefore, these patients should be monitored for leaks between the CIL, and periodic urodynamic tests should be performed for this alteration in detrusor behavior. During urodynamic studies, intravesical instillation of cold saline may indicate the return of reflex activity or help characterize the lesion better.

Realizing that the supra-aural lesions exhibit a detrusor areflexia in the initial lesion but progress to a hyperreflexia state over time is essential. In contrast, lesions of the sacral medulla are associated with areflexia bladders that may become hypertonic over time.

Spinal cord injuries on the sixth thoracic vertebra

Individuals who sustain a complete section of the umbilical cord above the sixth thoracic vertebra (T6) most often will have urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia. A unique complication of the T6 lesion is autonomic dysreflexia.

Autonomic dysreflexia is an exaggerated sympathetic response to any stimulus below the lesion level. This most commonly occurs with cervical cord injuries. Often, the inciting event is the instrumentation of the urinary bladder or the rectum, causing visceral distension.

The symptoms of autonomic dysreflexia include sweating, headache, hypertension, and reflex bradycardia. The acute treatment of autonomic dysreflexia is to decompress the rectum or the bladder.

Decompression will usually reverse the effects of sympathetic flow without opposition. If additional measures are required, parenteral ganglionic or adrenergic blocking agents, such as chlorpromazine, can be used.

Oral blockers, including terazosin, can be used to prevent patients with autonomic dysreflexia. Alternatively, spinal anesthesia can be used as a prophylactic measure whenever bladder instrumentation is performed.

Spinal cord injuries below T6

People suffering spinal cord injuries below the T6 level will have urodynamic findings of detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia, but not autonomic dysreflexia.

The neurological evaluation will reveal skeletal muscle spasticity with hyper reflexive deep tendon reflexes. Affected patients will demonstrate an extensor plantar response and a positive Babinski sign.

These individuals will experience incomplete bladder emptying secondary to detrusor sphincter dyssynergia or the loss of facilitatory input from higher centers. The cornerstones of the treatment are CIL and anticholinergic medications.

Multiple sclerosis

MS is caused by focal demyelinating lesions of the central nervous system. It commonly involves the posterior and lateral columns of the cervical spinal cord. There is a poor correlation between clinical symptoms and urodynamic findings. Therefore, using urodynamic studies to evaluate patients with MS is critical.

The most common urodynamic finding is detrusor hyperreflexia, which occurs in 50-90% of patients with MS. Up to 50% of patients will demonstrate HDD-ED. Detrusor areflexia occurs in 20-30% of cases. The optimal therapy for a patient with MS and incontinence should be individualized and based on the urodynamic findings.

Injuries of the peripheral nerve

Peripheral nerve injuries that cause detrusor areflexia may be due to any of the following:

  • Diabetes mellitus
  • Tabes dorsalis (neurosífilis)
  • Herpes infection
  • Lumbar disc herniation
  • Radical pelvic surgery
Diabetic cystopathy

Neurogenic bladder dysfunction occurs ten or more years after diabetes mellitus. Neurogenic bladder occurs due to autonomic and peripheral neuropathy. A metabolic alteration of the Schwann cell produces segmental demyelination and altered nerve conduction.

The first symptoms of diabetic cytopathic are loss of bladder filling sensation and loss of motor function.

The classical urodynamic findings associated with this condition are elevation of residual urine level, decreased bladder sensitivity, impaired detrusor contractility, and, eventually, detrusor areflexia.

Paradoxically, detrusor overactivity with impaired contractile function (DHIC) has also been observed. The treatment of diabetic cystopathy is CIL, permanent long-term catheterization, or urinary diversion.

Tabes dorsal

In dorsal tabes, central and peripheral nerve conduction is affected. Affected patients experience a decrease in bladder sensation and increased urination intervals. The most common urodynamic finding associated with neurosyphilis is detrusor areflexia with normal sphincter function.

Herpes infection

Herpes zoster is a neuropathy associated with painful vesicular eruptions in the affected nerve distribution. The herpes virus remains inactive in the dorsal root ganglia or sacral nerves.

The sacral nerve involvement leads to a deterioration of the detrusor function. The early stages of herpes infection are associated with lower urinary tract symptoms of urinary frequency, urgency, and urge incontinence.

Later stages include a decreased bladder sensation, increased residual urine, and urinary retention. Urinary retention is self-limited and will resolve spontaneously by eliminating herpes infection.

Lumbar disc herniation

The slow and progressive hernia of the lumbar disc can irritate the sacral nerves and cause hyperreflexia of the detrusor. Conversely, acute compression of the sacral roots associated with deceleration trauma will prevent nerve conduction and lead to detrusor areflexia.

A typical urodynamic finding in the sacral nerve lesion is detrusor areflexia with intact bladder sensation. Denervation of the associated internal sphincter may occur.

If the peripheral sympathetic nerves are damaged, the internal sphincter will be open and will not work. Peripheral sympathetic nerve damage often occurs in association with detrusor denervation. The striated sphincter, however, is preserved.

Pelvic surgery

Patients undergoing major pelvic surgery, such as radical hysterectomy, abdominoperineal resection, proctocolectomy, or total exenteration, will experience postoperative bladder dysfunction. The most common is that postoperative patients manifest symptoms of areflexia of the detrusor.

However, up to 80% of affected patients will experience a spontaneous recovery of function within six months after surgery.

Laboratory studies

These include the following:

  • Urinalysis and urine culture: Urinary tract infection can cause irritative urination and urge incontinence symptoms.
  • Urinary cytology: symptoms of irritative urination disproportionate to the general clinical picture and haematuria justify urinary cytology and cystoscopy, as they may indicate carcinoma in situ of the urinary bladder
  • Studies of renal function: blood urea nitrogen (NUS) and creatinine (Cr) are controlled if a compromise of renal function is suspected.

Other tests

An evacuation diary is a daily record of the bladder activity of the patient. It is objective documentation of the patient’s voiding pattern, episodes of incontinence, and the inciting events associated with urinary incontinence.

The pad test is an objective test that documents and can quantify the loss of urine. It can be helpful to assess the severity of incontinence.

Diagnostic procedures

The procedures used to investigate a possible neurogenic bladder include the following:

  • Post-void residual bladder volume
  • Rate of uroflow
  • Fill cystometrogram
  • Evacuation cystometrogram (pressure-flow study)
  • Study of Histogram
  • Electromyography (EMG)
  • Cystoscopy
  • Videodinamica
Post-void residual bladder volume

Measurement of postvoid residual urine (ORP) is a part of the essential evaluation for urinary incontinence. If the ORP is high, the bladder may be poorly contractile, or the bladder outlet may be obstructed. Both conditions can cause urinary retention with overflow incontinence.

Rate of uroflow

The uroflow rate is a valuable screening test used primarily to evaluate bladder outlet obstruction and identify detrusor weakness. The uroflow rate is the volume of voided urine per unit of time.

The low uroflow rate may reflect urethral obstruction, a weak detrusor, or both. This test alone can not distinguish a block from a contractile detrusor.

Fill cystometrogram

A filling cystometrogram (CMG) evaluates the bladder’s capacity, compliance, and the presence of phasic contractions (detrusor instability). More commonly, a liquid filling medium is used.

An average adult bladder contains approximately 50-500 ml of urine. During the test, provocative maneuvers help reveal the instability of the bladder.

Cystometrograma miccional

The pressure-flow study records the voiding detrusor pressure and the urinary flow rate simultaneously. This is the only test capable of evaluating the contractility of the bladder and the extension of a bladder outlet obstruction.

Pressure flow studies can be combined with an evacuation cystogram and a video urodynamic study for complicated cases of incontinence.


A static cystogram (anteroposterior and lateral) helps confirm the presence of stress incontinence, the degree of movement of the urethra, and the presence of a cystocele. Intrinsic sphincter deficiency will be evident from an open bladder neck. A vesicovaginal fistula or a bladder diverticulum can also be observed.

An evacuation cystogram can evaluate the functioning of the bladder neck and urethral function (internal and external sphincter) during the filling and emptying phases. Avoiding a cystogram can identify a urethral diverticulum, urethral obstruction, and vesicoureteral reflux.


EMG helps determine if urination is coordinated or uncoordinated. The failure of urethral relaxation during contraction of the bladder results in uncoordinated urination (detrusor sphincter dyssynergia). EMG allows an accurate diagnosis of detrusor sphincter dyssynergia common in spinal cord injuries.


The role of cystoscopy in the evaluation of neurogenic bladder is to allow the discovery of bladder lesions (e.g., bladder cancer, bladder stones) that would not be diagnosed only with urodynamics.

The general agreement is that cystoscopy is indicated for patients with persistent symptoms of irritative urination or hematuria. The doctor can quickly diagnose obvious causes of overactivity of the bladder, such as cystitis, stones, and tumors. This information is essential in determining the etiology of incontinence and can influence treatment decisions.


The videodinámica is the criterion standard for evaluating a patient with incontinence. The video urodynamics combines the radiographic findings of the voiding cystourethrogram (CUGM) and the multichannel urodynamics.

The video urodynamics allows the documentation of the lower urinary tract anatomy, such as vesicoureteral reflux and bladder diverticulum, and the functional flow-pressure relationship between the bladder and the urethra.

Treatment and management

Medical care

The treatment of urinary incontinence varies depending on the type, as follows:

  • Stress incontinence can be treated with surgical methods and some non-surgical methods.
  • Urinary incontinence can be treated with behavioral modification, pharmacotherapy, or third-line procedures.
  • Mixed incontinence may require medications and surgery.
  • Overflow incontinence is usually treated by emptying the bladder with a catheter.
  • Another incontinence can be resolved by treating the underlying cause, such as urinary tract infection or constipation.

Do not consider anti-incontinence products a panacea for urinary incontinence; however, the judicious use of pads and devices to contain urine loss and maintain skin integrity is extremely useful in selected cases.

Absorbent pads and internal and external collecting devices have an essential role in treating chronic incontinence. The criteria for using these products are pretty simple and are beneficial in certain situations:

  • Failure of all other treatments and persistent incontinence
  • Illness or disability that prevents participation in care
  • Inability to benefit from medications
  • Incontinence disorders that can not be corrected with surgery
  • Waiting for surgery

Absorbent products

Absorbent products are pads or garments designed to absorb urine to protect skin and clothing. Available in both disposable and reusable forms, they are a temporary means of keeping the patient dry until a more permanent solution is available.

By reducing humidity and odor, they help maintain patient comfort and allow them to function in everyday activities. They can be used temporarily until a definitive treatment comes into force or if the therapy produces less than perfect results.

The absorbent products are helpful during the initial evaluation and the study of urinary incontinence. As a complement to behavioral and pharmacological therapies, they play an essential role in caring for people with intractable incontinence.

Instead of definitive interventions, do not use absorbent products to reduce or eliminate urinary incontinence. Early dependence on absorbent pads can impede continence, providing the user with a false sense of security.

The misuse of absorbent products can contribute to the breakdown of the skin and urinary tract infections. Therefore, proper use, meticulous care, and frequent pads or garment changes when using absorbent products are necessary.


The urinary diversion, using several catheters, has been one of the pillars of the therapy against incontinence. The use of catheters for bladder drainage has withstood the test of time.

Bladder catheterization can be a temporary measure or a permanent solution for urinary incontinence. Different types of bladder catheterization include permanent urethral catheters, suprapubic tubes, and self-intermittent catheterization.

Permanent urethral catheters

Commonly known as Foley catheters, permanent urethral catheters have historically been the mainstay of treatment for bladder dysfunction. If urethral catheters are used for a long-term condition, they should be changed monthly.

A visiting nurse can change these catheters in offices, clinics, or homes. The standard catheter size for urinary retention is 16 ° F or 18 ° F, with a balloon filled with 10 ml of sterile water.

Larger catheters (e.g., 22F, 24F) with more enormous balloons treat the extremely bloody urine found in other urological conditions or diseases. The proper management of permanent urethral catheters varies by individual.

The usual practice is to replace permanent catheters and collection bags at least once a month. However, catheters that develop incrustations and problems with urine drainage should be changed more frequently.

All permanent catheters that remain in the urinary bladder for more than two weeks are colonized with bacteria. Bacterial colonization does not mean that the patient has a clinical infection of the bladder. Symptoms of a bladder infection include foul odor, purulent urine, and hematuria.

Fever with flank pain is often present if it involves upper tracts. If a bladder infection occurs, change the entire catheter and drainage system. The urinary drainage bag does not need to be disinfected to prevent disease.

Routine irrigation of catheters is not necessary. However, some authors favor using irrigation with 0.25% acetic acid because it is bacteriostatic, minimizes the incrustation of the catheter, and decreases the odor. When this method is used, 30 ml are instilled into the bladder and allowed to drain freely twice a day.

Continuous antibiotic prophylaxis is not only unnecessary for patients with permanent catheters but is contraindicated because it promotes the generation of bacteria resistant to common antibiotics. Using a permanent Foley catheter in people who can not leave home requires close supervision of a visiting nurse and additional personal hygiene care.

Despite its apparent advantages, using a Foley catheter for a prolonged period (e.g., months or years) is strongly discouraged. Long-term urethral catheters present significant health risks.

Permanent urethral catheters are an important cause of urinary tract infections that affect the urethra, bladder, and kidneys. Within 2-4 weeks after catheter insertion, bacteria will be present in the bladder of most women. Asymptomatic bacterial colonization is common and does not represent a health hazard.

However, symptomatic urinary tract infections can lead to urosepsis and death without treatment.

It has been found that the mortality rate of residents of nursing homes with urethral catheters is three times higher than that of residents without catheters; this may be more a reflection of the severity of the comorbid conditions that lead to the clinical decision to use chronic bladder drainage than the causality of the use of chronic bladder drainage.

The use of a urethral catheter is contraindicated in treating urge incontinence. Other problems associated with permanent urethral catheters include incrustation of the catheter, spasms of the bladder that produce urinary leakage, hematuria, and urethritis. More severe complications include:

  • Stone formation in the bladder.
  • Development of a periurethral abscess.
  • Kidney damage.
  • Urethral erosion.

Another problem with long-term catheterization is bladder contracture, which occurs with urethral catheters and suprapubic tubes. It has been reported that anticholinergic therapy and intermittent clamping of the catheter in combination are beneficial in preserving the integrity of the bladder with prolonged use of the catheter.

People who did not use the medication and the daily clamping regimen experienced decreased bladder capacity. For this reason, some doctors recommend using anticholinergic drugs with intermittent catheter impingement if a reconstruction of the lower urinary tract is anticipated in the future.

Restrict the use of permanent catheters in the following situations:

  • As for comfort measures for the terminally ill
  • To avoid contamination or to promote the healing of severe pressure ulcers
  • In cases of inoperable urethral obstruction that prevents the emptying of the bladder
  • In people with severe problems and for whom alternative interventions are not an option
  • When a person lives alone and a caregiver is not available to provide other support measures
  • For patients with acute diseases that require accurate monitoring of the water balance
  • For severely disabled people for whom changes in clothing and bedding are painful or damaging

Suprapubic catheters

A suprapubic tube is an attractive alternative to using a long-term urethral catheter. The most common use of a suprapubic catheter is in individuals with spinal cord injuries and a bladder that does not work well. Both paraplegic and quadriplegic individuals have benefited from this form of urinary diversion.

Smaller catheters are usually placed when suprapubic tubes are needed (e.g., 14F, 16F). Like the urethral catheter, the suprapubic lines should regularly be changed once a month.

Suprapubic catheters have many advantages. With a suprapubic catheter, the risk of urethral damage is eliminated. Multiple emptying tests can be performed without having to remove the catheter. A suprapubic tube is more patient-friendly because the catheter exits the lower abdomen instead of the genital area.

Bladder spasms occur less frequently because the suprapubic catheter does not irritate the trigone or urethral catheter. In addition, suprapubic tubes are more hygienic for the individual, and bladder infections are minimized because the line is removed from the perineum.

A nurse or a doctor quickly changes the suprapubic catheters. A suprapubic tube is less likely to be dislodged than a urethral catheter because the exit site is tiny. When the line is removed, the hole in the abdomen is quickly sealed with scarring.

Indications for suprapubic catheters include short-term use after gynecological, urologic, and other surgery.

Suprapubic catheters can be used whenever the clinical situation requires a bladder drainage device; however, suprapubic catheters are contraindicated in people with chronically unstable bladders or intrinsic sphincter deficiency because of the involuntary loss of urine is not prevented.

A suprapubic tube does not prevent spasms of the bladder in unstable bladders or improve the mechanism of urethral closure in an incompetent urethra.

The potential complications of long-term suprapubic catheterization are similar to those associated with permanent urethral catheters, including leakage around the catheter, urinary bladder stone formation, urinary tract infection, and catheter obstruction.

There is a possibility of intestinal injury during the initial placement of a suprapubic tube. Although it is uncommon, it is known that intestinal perforation occurs with the order of suprapubic lines for the first time. Other possible complications include cellulitis around the tube site and hematoma.

If the suprapubic tube falls inadvertently, the tube outlet will close quickly within 24 hours if the line is not replaced with a new one. If the displacement of the box is recognized immediately, a new TV can be reinserted quickly and painlessly, provided that the tube site remains intact.

A suprapubic catheter is an alternative solution to a permanent urethral catheter in patients who require long-term bladder drainage. Possible exclusive problems of suprapubic catheters include skin infection, bruising, bowel injury, and issues with the reattachment of the catheter.

The long-term management of a suprapubic tube can also be problematic if the health care provider does not have the knowledge and experience of suprapubic catheter management or if the individual confined to their home does not have quick access to a medical center in case of an emergency.

However, the suprapubic catheter offers many advantages over long-term urethral catheters in the appropriate situation.

Intermittent Catheterization

Intermittent catheterization or self-catheterization is a way of draining the bladder at regular intervals instead of continuous bladder drainage.

A prerequisite for self-catheterization is the ability of patients to use their hands and arms; however, in a situation where a patient has a physical or mental disability, a caregiver or a health professional can perform an intermittent catheterization for the patient.

Of the three possible options (i.e., urethral catheter, suprapubic tube, intermittent catheterization), intermittent catheterization is the best solution for the bladder decompression of motivated people who can participate physically and cognitively in their care.

Many studies of young patients with spinal cord injuries have shown that intermittent catheterization is preferable to permanent catheters (i.e., the urethral catheter, the suprapubic tube) for both men and women.

Intermittent catheterization has become a healthy alternative to permanent catheters for people with chronic urinary retention due to a clogged, weak, or non-functioning bladder. Young children with myelomeningocele have also benefited from the use of intermittent catheterization.

For those children, antibiotic prophylaxis (chemoprophylaxis at low doses) has been commonly prescribed for urinary tract infections. A study by Zegers et al. found that this practice can be safely suspended, especially in children, patients with low urinary tract infection rates, and patients without vesicoureteral reflux.

Intermittent catheterization can be performed using a soft red rubber catheter or a short rigid plastic catheter. Plastic catheters are preferable to red rubber catheters because they are easier to clean and last longer.

The bladder should be drained regularly, either based on a time interval (for example, upon awakening, every 3-6 hours during the day, and before bedtime) or according to the volume of the bladder. Remember that the average adult bladder contains approximately 400-500 ml of urine.

Ideally, the quantity drained should not exceed 400-500 mL each time. This drainage limit may require a decrease in the patient’s fluid intake or an increase in the frequency of catheterizations. For example, if the catheterization is done every 6 hours and the drained amount is 700 ml, increase the catheterization frequency to perhaps, every 4 hours to keep the volume drained to 400-500 ml.

Intermittent catheterization is designed to simulate normal urination. The average adult empties the bladder four to five times a day. Therefore, catheterization should be done four to five times a day; however, individual catheterization programs may vary, depending on the amount of fluid ingested.

Candidates for intermittent catheterization must have intact motivation and physical and cognitive abilities. Anyone with good manual dexterity and an accessible urethra can perform self-catheterization. Young children and the older population can do this every day without problems.

A home caregiver or visiting nurse can be instructed to perform an intermittent catheterization for people who cannot self-catheterize. Self-catheterization can be done almost anywhere, including at home and work.

Intermittent catheterization can be performed using a sterile catheter or a clean, non-sterile catheter. Intermittent catheterization, using a neat technique, is recommended for young individuals with a bladder that can not be emptied without any other option available. Patients should wash their hands with soap and water.

Sterile gloves are not necessary. Clean intermittent catheterization results in lower infection rates than the rates seen with permanent catheters.

Studies show that in patients with spinal cord injuries, bacteria in the bladder is 1-3% per catheterization, and one to four episodes of bacteriuria occurs per 100 days of intermittent catheterization performed four times a day. In addition, the infections that occur are generally handled without complications.

In general, the systematic use of long-term suppressive therapy with antibiotics in patients with chronic clean intermittent catheterization is not recommended. The use of regular suppressive antibiotic treatment in people who regularly use a clean intermittent catheterization is undesirable because it can cause the emergence of resistant bacterial strains.

A study of patients with acute spinal cord injury in 15 centers across North America revealed that using a hydrophilic coated catheter for intermittent catheterization delayed the onset of the first symptomatic urinary tract infections treated with antibiotics.

In addition, a reduction in the incidence of symptomatic infection of the urinary tract during hospital rehabilitation was observed for these patients.

A sterile technique for intermittent catheterization has been recommended for older adults and those with a weak immune system. Older people have a higher risk than younger people of developing bacteriuria and other complications of intermittent catheterization because they do not have a robust defense system against infection.

Although the incidence of infection and other complications in elderly patients who use sterile versus clean intermittent catheterization is not well established, sterile intermittent catheterization seems to be the safest method for this high-risk population.

The potential advantages of performing an intermittent catheterization include the patient’s autonomy, the absence of permanent catheters and bags, and unimpeded sexual relations. Possible complications of intermittent catheterization include bladder infection, urethral trauma, urethral inflammation, and stenosis.

The concomitant use of anticholinergic therapy will maintain acceptable intravesical pressures and prevent contracture of the bladder.

Studies have shown that long-term use of intermittent catheterization appears to be preferable to permanent catheterization (i.e., urethral catheter, suprapubic tube) concerning urinary tract infections and the development of stones within the bladder or kidneys.

In general, the management of infections in the environment of catheters and drainage tubes is a challenge. The practical use of bacterial interference represents a novel and perhaps effective method in the prevention of infections; however, at this time, it is difficult to do it clinically outside of the research setting.

Other studies can show that this modality is more advantageous from a clinical point of view in practice settings.

Surgical Care

Surgical care for stress incontinence involves procedures that increase resistance to urethral leakage, which include the following:

  • Periurethral loading therapy
  • Honda procedures
  • Artificial urinary sphincter

Surgical care for urge incontinence involves procedures that improve bladder compliance or bladder capacity, which include the following:

  • Sacral neuromodulation
  • Botulinum toxin injections
  • Increase in the bladder

A Cochrane review that included four randomized controlled trials of botulinum toxin A injection as a treatment for detrusor-sphincter dyssynergia (DDE) found that intraurethral injections could improve some urodynamic measures after 30 days.

However, the studies had a high risk of bias, the quality of the evidence was limited, and the need for reinjection was a significant drawback. The authors advised that more study of effectiveness is needed; The optimal dose and mode of injection have not yet been determined, and sphincterotomy may be a more practical option for long-term treatment.

Fluid intake

The quantity and quality of the liquids consumed will influence urinary symptoms. Fluids refer to all beverages consumed daily, including water, soft drinks, and milk. The human body receives water from the consumed beverages and the consumed foods.

The recommended amount of liquids consumed (all types) in 24 hours adds up to 6 to 8 glasses. The benefits of adequate fluid intake include the prevention of dehydration, constipation, urinary tract infections, and the formation of kidney stones.

Some patients tend to drink water excessively. Others take medications that dry their mouths, so they drink more water. Some patients who try to lose weight follow a diet that requires consuming large amounts of water.

Excessive water intake worsens the irritative symptoms of the bladder. The amount of fluid needed per day is calculated based on the patient’s lean body mass. Therefore, the amount of fluid requirement will vary per individual.

Some older patients do not drink enough fluids to stay well hydrated. They minimize their fluid intake to unacceptable levels, thinking that they will experience minor incontinence if they drink less.

Trying to prevent incontinence by excessively restricting fluids can irritate the bladder and worsen urgency incontinence. In addition, dehydration contributes to constipation. If a patient has a constipation problem, recommend eating a fiber-rich diet, receiving adequate hydration, and administering laxatives.

Many drinks contain caffeine. Caffeine is a natural diuretic and has a direct excitatory effect on the bladder’s smooth muscle. Therefore, caffeine products produce an excessive amount of urine and exacerbate the symptoms of urinary frequency and urgency.

Products that contain caffeine include coffee, tea, hot chocolate, and soda. Even chocolate milk and many over-the-counter medications contain caffeine.

Of the caffeine products, coffee contains the highest amount of caffeine. Drip coffee has the highest caffeine, followed by filtered coffee and instant coffee. Even decaffeinated coffee contains a small amount of caffeine.

Decaffeinated coffee contains an amount of caffeine similar to the amount in chocolate milk. People who consume a large amount of caffeine should slowly decrease the amount consumed to avoid significant withdrawal responses, such as headaches and depression.

Studies have shown that carbonated drinking drinks, citrus fruit drinks, and acidic juices can worsen irritative urination or urgency symptoms. The consumption of artificial sweeteners has also been theorized to contribute to urge incontinence.

Nighttime urination and incontinence are fundamental problems in the elderly population. Women who have nocturia more than twice a night or who experience nocturnal enuresis may benefit from fluid restriction and the elimination of caffeine-containing beverages from their diet at night.

Patients should restrict liquids after dinner to sleep uninterruptedly during the night.

Pelvic floor exercise

Incontinence exercises emphasize rehabilitation and strengthening the pelvic floor muscles critical to maintaining urinary continence. The pelvic floor muscles are also known as levator ani muscles because they work to elevate levitation or elevate the pelvic organs to their proper place.

Pelvic prolapse and stress incontinence occur when the lifting muscles weaken and fail. An anatomical defect of the levator ani muscles requires physical rehabilitation. If aggressive physical therapy does not work, surgery is justified.

Pelvic floor exercises, sometimes called Kegel exercises, are a rehabilitation technique used to tighten and tone the pelvic floor muscles. Kegel exercises can be performed to eliminate urge incontinence.

The contraction of the external urinary sphincter induces reflex relaxation of the bladder. The rehabilitation of the pelvic floor muscles can be used to reprogram the urinary bladder and decrease the frequency of incontinence episodes.

People who benefit most from pelvic floor exercises tend to be young, healthy, and able to identify lifting muscles accurately. These rehabilitation exercises can be used for urge incontinence and mixed incontinence.

For urge incontinence, pelvic floor muscle exercises are used to retrain the bladder. When the patient contracts the external urethral sphincter, the bladder relaxes automatically so that the urge to urinate finally disappears. Severe contractions of the pelvic floor muscles will suppress bladder contractions.

Every time patients feel urinary urgency, they can try to stop the sensation by contracting the pelvic floor muscles. These steps will give the patient more time to stroll to the bathroom with urinary control.

By regularly training the external sphincter, patients can gradually increase the time between micturition by 1 to 3 hours. Patients should begin to see improvement in 3-4 weeks. Therefore, this technique can be used for symptoms of urgency, urge incontinence, and mixed incontinence (stress and urgency incontinence).

Patients should practice contraction of the levator ani muscles immediately before and during situations where leakage may occur. This will condition the external sphincter to contract with increases in abdominal pressure or when the need to urinate is imminent. This is known as the protection reflex.

When the patient tightens the external urinary sphincter just as sneezing approaches, the involuntary loss of urine is frustrating. By pulling the levator muscles of the anus when the sense of urgency arises, the sensation of impending contraction of the bladder will dissipate.

By making this maneuver a habit, patients will develop a protective mechanism against stress and urge incontinence.

The beneficial effects of pelvic floor muscle exercises alone have been well documented in the medical literature. It has been reported that the successful reduction of urinary incontinence ranges from 56-to 95%. Pelvic floor exercises are practical, even after multiple surgeries against incontinence.

Electrical stimulation

Electrical stimulation is an area of ​​active research in treating neurogenic bladder. It has been successfully applied to the genital nerve with an overactive bladder and has decreased detrusor contractions and improved bladder capacity.

In addition, this treatment was considered adequate and tolerable by the patients who participated in the study. It is not clear if sacral neuromodulation has a role in treating neurogenic detrusor overactivity, but this is an area of ​​ongoing research.

In general, electrical stimulation has remarkable potential as a treatment for neurogenic bladder.

Medications are used to treat neurogenic bladder.

Pharmacological therapy for overactive bladder may be more effective when combined with a pelvic exercise regimen. The three main medications used to treat urge incontinence include anticholinergic drugs, antispasmodics, and tricyclic antidepressants.

All medications with adverse anticholinergic effects are contraindicated if patients have documented narrow-angle glaucoma. Wide-angle glaucoma is not a contraindication to its use. Urinary retention, intestinal obstruction, ulcerative colitis, myasthenia gravis, and severe heart disease are contraindications of anticholinergics.

These agents can impair the patient’s ability to perform dangerous activities, such as driving or operating heavy machinery, due to the possibility of drowsiness. Anticholinergic medications should not be combined with alcohol, sedatives, or hypnotics.

However, anticholinergics in urinary retention with a catheterization regimen can help improve bladder capacity.

When treatment with a single drug does not work, combination therapy can be used. In general, agents with different mechanisms of action must be combined to improve urge incontinence; for example, the combination of a beta-3 agonist with an anticholinergic can be used to treat detrusor overactivity.

Together, these medications produce a synergistic effect to relax the unstable bladder, retain it in the urine, and prevent urge incontinence. However, the anticholinergic side effects may be additive because both drugs have similar adverse reactions.

Anticholinergic and antispasmodic medications

Anticholinergic medications are the first-line pharmacological therapy in urge incontinence. They effectively treat urge incontinence because they inhibit involuntary contractions of the bladder.

They are also helpful in treating urinary incontinence associated with frequency, urgency, and nocturnal enuresis. All anticholinergic drugs have similar performance and toxicity profiles.

Potential adverse effects of all anticholinergic agents include blurred vision, dry mouth, heart palpitations, drowsiness, and facial flushing. When anticholinergic medications are used in excess, acute urinary retention may occur.

Antispasmodic medications

Antispasmodic medications relax the smooth muscles of the urinary bladder. By exerting a direct spasmolytic action on the bladder’s smooth muscle, it has been reported that antispasmodic drugs increase the bladder’s capacity and effectively reduce or eliminate urge incontinence.

The profile of adverse effects of antispasmodic drugs is similar to that of anticholinergic agents. These drugs can impair the patient’s ability to perform mental attention and physical coordination activities. Drinking alcohol and using sedatives in combination with these antispasmodic medications is contraindicated.

Solifenacin Succinate (VESIcare)

Solifenacin succinate causes a competitive activity of the muscarinic receptor antagonist, which produces an anticholinergic effect and inhibition of smooth muscle contraction of the bladder. It is indicated for overactive bladder with urgency, frequency, and urge incontinence symptoms.

Darifenacina (Enablex)

Darifenacin is a prolonged-release product that causes competitive muscarinic receptor antagonist activity. Reduces contractions of the smooth muscle of the bladder.

It has a high affinity for M3 receptors involved in the contraction of the smooth muscle of the bladder and gastrointestinal (GI), the production of saliva, and the function of the iris sphincter. Darifenacin is indicated for overactive bladder with urgency, urgency, and frequency incontinence symptoms. The product must be swallowed whole; do not chew, divide or crush.

Oxybutynin Chloride (Ditropan IR, Ditropan XL)

Oxybutynin chloride has anticholinergic effects and direct muscle relaxants on the urinary bladder. It provides a local anesthetic effect on the irritable bladder. Urodynamic studies have shown that oxybutynin increases the size of the bladder, decreases the frequency of symptoms, and delays the initial desire to empty.

Ditropan XL has an innovative drug delivery system, the oral osmotic delivery system (SAOO). The Ditropan XL tablet has a bilayer core containing a drug layer and a pusher layer containing osmotic components.

The outer tablet comprises a semipermeable membrane with a precision laser-perforated hole that allows the drug to be released at a constant rate.

When the drug is ingested, the aqueous environment in the GI tract causes the water to enter the tablet through the semipermeable membrane at a constant speed. The introduction of water into the tablet liquefies the drug and causes the pusher layer to swell osmotically.

As the thrust layer swells, force the drug suspension out of the orifice at a constant rate for 24 h.

Ditropan XL reaches steady-state levels for 24 hours. Avoid first-pass metabolism of the liver and upper gastrointestinal tract to avoid cytochrome P450 enzymes. It has excellent efficacy with minimal adverse effects.

Medical studies have shown that oxybutynin chloride reduces incontinence episodes by 83-90%. It is reported that the total continence rate is 41-50%. The average reduction in urinary frequency was 23%. In clinical trials, only 1% stopped taking Ditropan XL due to dry mouth, and less than 1% stopped taking Ditropan XL due to the adverse effects of the CNS.

Tolterodine L-tartrate (Detrol and Detrol LA)

Tolterodine L-tartrate is a competitive muscarinic receptor antagonist for overactive bladder. It differs from other anticholinergic types in that it has selectivity for the urinary bladder over the salivary glands.

It has a high specificity for muscarinic receptors and has minimal activity or affinity for other neurotransmitter receptors and potential targets, such as calcium channels. In clinical studies, the average decrease in urge incontinence episodes was 50%, and the average reduction in urinary frequency was 17%.

Trospium (Sanctura)

Trospium is a quaternary ammonium compound that causes antispasmodic and antimuscarinic effects. Antagonizes the effect of acetylcholine on muscarinic receptors. The parasympathetic effect reduces the tone of the smooth muscle in the bladder. Trospium is indicated to treat the symptoms of overactive bladder (e.g., urinary incontinence, urgency, frequency).

Fesoterodine (Toviaz)

Fesoterodine is a competitive muscarinic receptor antagonist. The antagonistic effect decreases contractions of the bladder’s smooth muscle. It is indicated for the symptoms of overactive bladder (e.g., urinary incontinence or urgency, urgency, and frequency). Fesoterodine is available as a 4 or 8 mg prolonged-release tab.

Tricyclic antidepressants

The treatment of bladder dysfunction is an inappropriate use of tricyclic antidepressants. These medications work to increase the levels of norepinephrine and serotonin. In addition, they exhibit anticholinergic effects and direct muscle relaxants on the urinary bladder.

Imipramine (Tofranil)

Imipramine is a typical tricyclic antidepressant. It facilitates urine storage by decreasing bladder contractility and increasing output resistance. It has an alpha-adrenergic effect in the neck of the bladder and an antispasmodic effect in the detrusor muscle.

Imipramine hydrochloride has a local anesthetic effect on the bladder mucosa.

Amitriptyline (Elavil)

Amitriptyline is a tricyclic antidepressant with sedative properties. It increases circulating levels of norepinephrine and serotonin by blocking its reuptake into nerve endings and is not practical for use in urge incontinence.

However, it is highly effective in decreasing the symptoms of urinary frequency in women with pelvic floor muscle dysfunction. Amitriptyline restores serotonin levels and helps break the cycle of pelvic floor muscle spasms. It is well tolerated and effective in most women with urinary frequency.

Beta-3 adrenergic receptor

Mirabegron was approved in 2012 by the United States Food and Drug Administration (FDA) to treat overactive bladder.

In an initial study of its efficacy for the treatment of neurogenic detrusor overactivity in 15 patients with spinal cord injury, a significant reduction in bladder evacuation frequency by 24 h (8.1 vs. 6.4, P = 0.003) and by episodes of incontinence for 24 h (2.9 vs. 1.3, P = 0.027) was observed. However, due to the limited size of the study, more research is needed.


Prolonged contact of urine with unprotected skin causes contact dermatitis and skin degradation. These skin disorders can cause pressure ulcers and ulcers if left untreated, leading to secondary infections.

For people with a decompensated bladder that does not empty well, postvoid residual urine can cause an overgrowth of bacteria and a subsequent urinary tract infection (UTI).

In patients with neurogenic bladder, UTIs often do not produce classic symptoms; In contrast, these patients may have abdominal or back pain, increased spasticity, and urinary incontinence.

Untreated UTIs can quickly lead to potentially fatal autonomic dysreflexia or sepsis, while overtreatment promotes antibiotic resistance. However, there are few evidence-based practices to prevent UTIs in this population.

Complications of specific interventions include the following:

  • Long-term permanent catheters can cause recurrent bladder infection, bladder stones, ascending pyelonephritis, and urethral erosion
  • Intermittent catheterization can cause bladder infections or urethral injury
  • Long-term suprapubic tubes can cause spasms in the bladder, bladder stones, and bladder infection
  • Possible exclusive problems of suprapubic catheters include skin infection, bruising, bowel injury, and issues with reattachment of the catheter


The prognosis of patients with incontinence due to the neurogenic bladder is excellent with modern medical care. With improved information technology, well-trained medical personnel, and advances in medical knowledge, patients with incontinence should not experience the morbidity and mortality of the past.

Although the final well-being of the patient depends on the underlying condition that has precipitated urinary incontinence, urinary incontinence is easily treated and prevented by adequately trained health personnel.

Patient education

For information on patient education, see Bladder Control Problems, Bladder Control Medications, Inability to Urinate, and Foley Catheter.

Patients can conduct Internet searches to obtain information about their condition. Using the search terms “intermittent neurogenic bladder catheter” and “intermittent spinal cord injury catheter,” Ho et al. found 71 online videos.

However, most of the videos provided low-quality information, and some offered conflicting information about the guidelines of the European Association of Urology for intermittent catheterization.

Videos that the authors considered to be of good quality were not ranked prominently according to the YouTube search algorithm, suggesting that users would be less likely to access them.