s Reflex Urinary Incontinence: Management Options —Viquepedia

Reflex Incontinence

Pathology and Management of Reflex Incontinence/Neurogenic Bladder

There are several definitions for reflex urinary incontinence (UI) Opens in new window.

  • The International Continence Society (ICS) defines reflex UI as “uncontrolled urine loss occurring as a result of neurogenic disorders and caused by neurogenic detrusor overactivity;” they add that the leakage occurs in the absence of any desire to urinate.
  • The North American Nursing Diagnosis Association (NANDA) defines reflex UI as “urine loss occurring at somewhat predictable intervals of time when a specific bladder volume is reached;” their defining characteristics for this condition also include the absence of sensory awareness.

Despite subtle variations in these definitions, they share key elements that provide a broad but useful definition for reflex UI. For the purposes of this text,

Reflex UI is defined as involuntary urine loss caused by overactive detrusor contractions and occurring with diminished or absent sensory awareness of the urge to urinate.

The significance of detrusor-sphincter dyssynergia (DSD), which is typically associated with reflex UI, is also discussed.

Neurogenic detrusor overactivity is defined as the occurrence of uncontrolled bladder contractions in a patient with a neurologic lesion.

Among patients with reflex UI, overactive detrusor contractions may or may not produce urine loss, depending on the magnitude and duration of the contractions, and on the response of the urethral sphincter mechanism.

DSD is the loss of coordination between the striated sphincter and the detrusor muscle; that is, the sphincter does not consistently relax when the detrusor contracts. This condition is also known as vesicosphincter dyssynergia, and it is significant because contraction of the striated muscle components of the sphincter during bladder contraction causes a functional obstruction of the bladder outlet.


No epidemiologic data are available for the condition of reflex UI. However, some appreciation for its prevalence can be inferred from epidemiologic data for the principal neurologic conditions associated with reflex UI: spinal cord injury, spinal cord disease, multiple sclerosis (MS), and spina bifida.

In 2004, it was estimated that 247,000 Americans were living with a spinal cord injury. Estimates of the incidence of spinal cord injuries vary from 21.2 per million population to 60 per million; approximately 85% of these injuries affect the spinal segments located above the twelfth thoracic vertebra, and these lesions commonly produce reflex UI.

Reflex UI may also occur among persons with intervertebral disk disease, spinal stenosis, and cervical spondylosis. The prevalence of these conditions is not known, but the annual incidence of surgical intervention for these problems has been estimated at 52.3 per 100,000 population. Approximately 15% of these patients will experience clinically apparent voiding dysfunction, and reflex UI may occur if the nerve pathways innervating the lower urinary tract are compressed.

MS may also cause UI, and reflex UI occurs in persons with lesions of the thoracic or cervical spinal cord. The prevalence of MS in the United States is approximated 85 per 100,000 or 220,000. The incidence of MS varies according to age and geographic region; Hawaii’s annual estimated incidence is only 8.8 cases per 100,000 population, whereas Rochester, Minnesota, has an annual incidence of approximately 173 per 100,000 population. It has been estimated that as many as 96% of individuals with MS experience voiding dysfunction, 52% to 78% experience neurogenic detrusor overactivitiy, and approximately 50% experience vesicosphincter dyssynergia.

Reflex UI also occurs in certain children with spina bifida. The incidence of spina bifida is about 1 per 1000 live births. Fortunately, emphasis on primary prevention of neural tube defects via dietary supplementation of folic acid has led to a decline of this devastating defect over the past several decades.

Nevertheless, spina bifida continues to account for about 25% of the voiding dysfunction seen in pediatric urology practices in the United States. Approximately 54% of newborns with myelomeningoceles will have neurogenic detrusor overactivity and vesicosphincter dyssynergia. Among older children with spina bifida and neurologic deficits, 62% have neurogenic detrusor overactivity and 15% have vesicosphincter dyssynergia.

In addition to neurologic lesions, a small group of children without neurologic disease will experience both detrusor overactivity and vesicosphincter dyssynergia that adversely affects both lower and upper urinary tract function. This complex voiding dysfunction is called the nonneurogenic bladder of childhood, or the Hinman-Allen syndrome. The features of this disorder closely resemble the reflex UI associated with neurologic disease, and this disorder is therefore discussed.


Any neurologic lesion that affects the brain or the spinal cord above the sacral micturition center can cause neurogenic detrusor overactivity; however, only those conditions affecting spinal segments C2 to S1 result in reflex UI (see Box X1).

Box X1 | Etiology of Reflex Urinary Incontinence
Traumatic disorders
Spinal cord injury
Intervertebral disk disease
Congenital disorders
Familial hereditary spasticity
Cerebral palsy
Nontraumatic disorders
Multiple sclerosis
Acute disseminated encephalomyelitis
Landry-Guillain-Barré syndrome
Human immunodeficiency virus infection
Transverse myelitis
Systemic lupus erypthematosus

Neurologic disorders within or above the pons typically cause neurogenic detrusor overactivity with retention of sensory awareness and bladder-sphincter coordination; these patients are likely to experience urge incontinence Opens in new window rather than reflex UI. People do not usually survive lesions involving the medulla or C1 because of damage to the vital respiratory and cardiovascular centers.

Lesions affecting the lower spine (below S2) or the cauda equina cause loss of bladder contractility (detrusor areflexia) and may cause intrinsic sphincter deficiency; these patients typically experience overflow incontinence Opens in new window and may also have stress incontinence but do not experience reflex UI.

  1. Spinal Cord Injuries

Spinal cord injuries represent the most common spinal lesion, and these injuries frequently result in reflex UI. The likelihood that a specific spinal injury will lead to a neuropathic bladder and reflex UI is determined by its location, its completeness, and the occurrence and severity of vascular extension.

The level of a spinal cord injury can be described by the location of the affected vertebral body (the orthopedic level of injury) or by the level at which the spinal cord and nerve pathways are affected (the neurologic or functional level of injury). The orthopedic and neurologic levels are nearly identical in the high cervical region, but they do not correspond as closely in the remaining areas of the spinal column and spinal cord; therefore, it is important to determine whether the location of a spinal cord injury is being presented by orthopedic level or by functional level. To illustrate, injuries at the orthopedic level of C2-T12 (or L1) are associated with functional injuries at the level of C2-S1. These levels of injury are associated with detrusor hyperflexia, DSD, and reflex UI.

The effect of a specific neurologic lesion on bladder function is also influenced by the completeness of the injury. A complete injury produces both sensory and motor loss, whereas an incomplete injury is typically associated with loss of motor function but preservation of sensation. (In rare cases, an incomplete injury causes loss of sensation and preservation of motor function.)

Approximately 46% of all spinal injuries are incomplete; this statistic may be attributable in part to the use of steroids during the early postinjury period and the resultant reduction in edema and ischemia. Most patients with incomplete injuries experience reflex UI characterized by diminished awareness of bladder filling, neurogenic detrusor overactivity, and DSD; however, some patients retain bladder sensation, and a few patients with incomplete paralyzing lesions actually maintain continence.

The occurrence and severity of vascular extension comprise the third factor affecting a spinal cord injury’s effect on bladder function. Vascular extension is typically caused by ischemic injury to adjacent areas of the spinal cord, and the degree of vascular extension is influenced by the mechanism of injury and the immediacy of postinjury care.

Functional classification systems for spinal cord injury describe the lesion according to the highest level of neurologic involvement; however, vascular extension may cause damage to areas below the primary injury. This may be significant when one is considering the effect of an injury on bladder function; that is, inferior extension may account for the persistence of detrusor areflexia and intrinsic sphincter deficiency that sometimes occurs in patients with thoracic or even cervical-level injuries.

In addition to spinal cord injuries, spinal cord diseases (such as disk diseases or spinal stenosis) occasionally produce compression of the spine and damage to the associated nerve pathways; if the compression is at the level of the cervical or thoracic cord, it may produce reflex UI.

  1. Nontraumatic Spinal Disorders

The most common nontraumatic spinal disorders associated with reflex UI are spina bifida and MS; additional disorders include various autoimmune disorders and polyneuropathies.

Spina bifida Opens in new window is an umbrella term for congenital defects characterized by failure of the vertebral bodies to close and the associated spinal cord defects. In many cases, the defect is limited to the bony structures, but the meninges (meningocele) and the spinal cord itself (myelomeningocele) may herniate through the defect; if the spinal cord is involved, the child typically suffers significant neurologic deficits, that is, varying degrees of motor and sensory loss and possibly disorders of the cerebrospinal drainage system (Arnold-Chiari defect).

When the defect involves neurologic structures, it is termed myelodysplasia Opens in new window; this defect commonly involves multiple spinal segments, usually in the lumbar and sacral areas of the spine, although it may also involve the thoracic spine. Reflex UI is common among infants and children with myelodysplasia involving the thoracic and lumbar areas of the spine.

MS Opens in new window is a dymyelinating disease that affects multiple levels of the central nervous system. It typically strikes young adults between 16 and 50 years of age, peaking among those 23 or 24 years of age.

Persons who develop MS before 40 years of age commonly experience recurring episodes of neurologic impairment followed by spontaneous remission. This pattern continues even after the disease becomes clinically overt; there are periods of spontaneous exacerbations caused by demyelination within the nervous system, followed by remission or alleviation of symptoms as remyelination occurs. However, over a period of years, the repetitive scarring of the neurons and axons causes permanent dysfunction and progressive disability.

The symptoms of MS vary widely because of the wide distribution of the characteristic sclerotic plaques, but “typical” symptoms include sensory paresthesias in one or more extremities, weakness in one or more limbs, visual disturbances, and gait disturbances (or a slowly progressing weakness or spasticity of the lower extremities).

Approximately 10% of patients have voiding symptoms at the time of diagnosis, and voiding difficulties are the only symptom in 1% to 3% of all new cases. The most commonly reported voiding symptoms are urinary frequency, urgency, and urge incontinence; unfortunately, this symptom pattern is most commonly seen in women with urge Opens in new window or mixed stress-urge incontinence Opens in new window, and therefore the patient with only voiding symptoms and no neurologic deficit may be incorrectly diagnosed.

The clinician should be very thorough when assessing any young adult with apparent “urge” incontinence. If the symptoms of urge incontinence are associated with hesitancy, the recent onset of enuresis, or a urinary tract infection (UTI), the clinician should be suspicious of a neurologic deficit; these signs and symptoms indicate the possible presence of DSD, which is an ominous finding in any young adult with voiding dysfunction.

MS produces reflex UI when the lesion involve the spinal tracts that provide communication between the lower urinary tract and the modulatory areas in the spinal cord, pons, and cortex. The demyelinating plaques of MS affect the white matter of the dorsal columns of the spinal cord and especially the abundant white matter located in the cervical and thoracic areas of the cord. The plaques affect nerve structures below the level of the pons, and they compromise both sensory and motor function; therefore, reflex UI is common in patients with MS lesions involving the spinal cord.

Multiple other diseases cause progressive degeneration of the spinal cord and the development of reflex UI; these diseases are occasionally misdiagnosed as MS. For example, the human immunodeficiency virus is known to invade the central nervous system, and reflex UI sometimes occurs during the advanced stages of acquired immunodeficiency syndrome.

Other less common diseases that occasionally cause reflex UI include disseminated encephalomyelitis Opens in new window, arachnoiditis Opens in new window, cerebellar ataxia Opens in new window, Landry-Guillain-Barré syndrome Opens in new window, and transverse myelitis.

Transverse myelitis is characterized by inflammation of the spinal cord, which causes loss of motor and sensory activity below the involved segment(s). As in spinal cord injury, the bladder dysfunction associated with transverse myelitis is affected by the location of the area of inflammation; some patients develop urinary retention, whereas others develop reflex UI.

Systemic lupus erythematosus (SLE) is a well-known chronic autoimmune disorder characterized by formation of antibodies that attack the victim’s own tissues and serum factors; SLE is primarily known to affect the kidneys, skin, and hematologic system, but it can also affect the central nervous system, including the spine. Spinal involvement produces transverse myelopathy that results in motor and sensory deficits and in reflex UI when the lesion is located above S2.

  1. Nonneurogenic Neurogenic Bladder: Hinman-Allen Syndrome

Daytime UI (characterized by frequency, urgency, and urge incontinence) and nocturia or enuresis are not uncommon among school-aged children with apparently normal neurologic function. However, in as many as 20% of these children, and in approximately 0.5% of all patients with urge incontinence, detrusor overactivity is complicated by DSD.

In most cases, this dyssynergia does not lead to serious upper tract distress, and it can usually be resolved, either by elimination of the unstable bladder contractions or by a short course of biofeedback to eliminate the dyssynergic sphincter activity. However, a few of these children develop a nonneurogenic neurogenic bladder. This syndrome, also known as the Hinman-Allen syndrome, is a functional disorder that closely mimics reflex UI.

It is characterized by contraction of the striated muscle of the sphincter during voiding, which produces a functional obstruction of the bladder outlet. Children with nonneurogenic neurogenic bladders have profound changes in the radiographic appearance of the urinary tract. Hydroureteronephrosis, vesicoureteral reflux, scarring of the kidneys from febrile infections, and a trabeculated bladder are common findings. Renal insufficiency may occur, and renal failure with an elevated creatinine may already be present on initial evaluation.

The cause of the nonneurogenic neurogenic bladder is not known. It was originally postulated to represent an occult neurologic lesion; however, more recent research has not confirmed this hypothesis. Currently, the Hinman-Allen syndrome is attributed to persistence of the phase in toilet training when the child learns to contract the sphincter to delay voiding.

McGuire and Savastano have suggested that the dyssynergia associated with the Hinman-Allen syndrome may represent overutilization of “guarding behaviors” in response to unstable detrusor contractions. The guarding response is the contraction of the pelvic floor and periurethral striated muscles in an attempt to prevent or minimize leakage during an unstable detrusor contraction; in children, it is often accompanied by Vincent’s curtsy, that is, crossing the legs and bending the knees or placing one heel in the perineum, followed by the characteristic curtsy.

Bauer has studied children with nonneurogenic neurogenic bladders and their families, and he identifies several common psychogenic characteristics that may provide clues to its cause. For example, he notes that many of these families include a domineering, unyielding father who is tolerant of failure; divorce and alcoholism are also common. The child’s UI is frequently perceived as immature, defiant, and purposeful behavior and is commonly managed within the family by physical and mental punishment.

Gray reported on a series of 10 children who had been diagnosed with Hinman syndrome; he found that 90% had abnormalities noted on the Minnesota Multiphasic Personality Inventory, and 70% had a history of sexual abuse.


A discussion of the pathophysiology of reflex UI must focus on two primary aspects of this condition:

  1. the mechanism of leakage, and
  2. the effect on upper urinary tract function.

Because the potential effect of reflex UI on upper urinary tract health is so significant, the management of patients with this condition is often focused on the preservation of renal function, with little attention given to the problems caused by the urinary leakage. This section addresses each of these issues separately and also includes a discussion of the potential complications of reflex UI: UTI, renal calculi, and autonomic dysreflexia (AD).

  1. Urinary Incontinence

The primary mechanism for leakage in reflex UI is the occurrence of overactive detrusor contractions. These contractions occur at variable volumes, in response to bladder distension or other triggers (such as stroking the thigh or a sudden change in perineal skin temperature).

In some patients, overactive detrusor contractions are well sustained with good amplitude, leading to intermittent episodes of high-volume urinary leakage; in others, the contractions are low pressure and poorly sustained, resulting in frequent loss of small volumes of urine.

Because the sensation of bladder filling is diminished or absent in individuals with reflex UI, overactive detrusor contractions are associated with little or no urge to urinate. However, observations have shown that many patients with little or no bladder sensation usually experience some identifiable sensation of impending micturition, however “atypical.”

For example, many patients with complete spinal cord injuries experience a tingling in the arms, hands, or face before micturition, whereas other report a “rushing” sensation that may represent a mild sympathetic discharge. Unfortunately, a literature search of the MEDLINE and CINAHL databases up to January 2004 yielded no research in this area, and it is not known whether these warnings of impending micturition can be successfully exploited in the clinical management of this complex form of incontinence.

Although neurogenic detrusor overactivity is clearly the primary cause of incontinence in patients with reflex UI, other factors may also contribute to urine loss. For example, persons with reflex UI may also experience stress UI caused by inadequate urethral sphincter resistance. This is particularly common among women who may have had preexisting stress UI before a spinal cord injury or the development of MS.

Patients with lesions affecting the lower spinal segments and those with long-standing obstruction and severe trabeculation of the bladder are also at risk for low bladder wall compliance and overflow incontinence. In addition, some patients with reflex UI may develop continuous or extraurethral urinary leakage as a result of fistula development.

  1. Upper Urinary Tract Damage

The relationship between upper urinary tract function and reflex UI is illustrated by the history of spinal cord injury management, with particular emphasis on morbidity and mortality. During the midtwentieth century, urinary tract complications were the leading cause of death after spinal cord injury. Urosepsis and renal failure accounted for 43% of the spinal cord injury deaths reported among World War II and Korean War soldiers and veterans. Fortunately, since that time, we have gained a keener appreciation and understanding of the relationship between UI and renal function. As a result, the life expectancy after a spinal cord injury has improved dramatically, and the proportion of deaths attributable to urinary tract complications has fallen to a range of 3% to 16%.

Some individuals with reflex UI are at much greater risk for upper tract distress and compromised renal function than others; factors determining the risk for any one person include the presence of DSD, the severity of obstruction caused by this dyssynergia, and bladder wall compliance. The presence of these characteristics may be said to represent “hostile bladder function,” a term sometimes used to describe the potential for dysfunction in the lower urinary tract to cause distress in the upper tracts.

Two factors contribute to low detrusor filling pressures, which allow the ureters to overcome ureterovesical junction resistance and to fill the bladder:

  1. normal detrusor tonus; and
  2. normal viscoelastic properties of the bladder wall; that is, sufficient elasticity to allow the bladder to stretch and fill at low pressures.

This distensibility of the bladder wall is measured during urodynamic testing and is expressed as bladder wall compliance. Low bladder wall compliance refers to the loss of normal distensibility and results in higher intravesical filling pressures. Poor or low bladder wall compliance increases the risk of upper tract distress because the elevated intravesical filling pressures functionally obstruct the ureters and ultimately the kidneys.

Several factors associated with reflex UI may lead to low bladder wall compliance. Long-term use of an indwelling catheter is one of these factors, possibly because of the chronic infection that frequently occurs with this management approach. In children with voiding dysfunction, chronic bacteriuria has been associated with increased urine levels of fibroblast growth factor; this could lead to the disposition of fibrous tissue in the bladder wall, which would be expected to reduce distensibility and thus to lower compliance.

In addition to the effects of infection and inflammation, prolonged bladder drainage may itself contribute to reduced compliance and thus diminish the bladder’s ability to function as an effective storage vesicle.

Another factor that may contribute to reduced compliance in the patient with reflex UI is denervation of the lumbosacral spinal segments, as occurs in children with myelodysplasia. This denervation contributes to low bladder wall compliance because it seems to promote collagen deposition within the bladder wall, which is seen on radiographic imaging as trabeculation.

Among individuals with reflex UI, trabeculation is often seen after a prolonged period of “reflex” voiding with condom catheter containment; the reason may be that reflex voiding requires the detrusor to mount contractile pressures high enough to overcome any bladder outlet obstruction and to achieve bladder evacuation.

  1. Urinary Tract Infection

Chronic bacteriuria and symptomatic UTIs are common among patients with reflex UI. The long-term sequelae of UTI relate to progressive damage to the renal parenchyma and ultimate renal insufficiency. The patient with DSD and bladder outlet obstruction is at particular risk for UTI because elevated residual volumes and urinary stasis increase the risk that bacteriuria will evolve from an asymptomatic to a symptomatic state.

Any UTI in the individual with reflex UI carries the risk of upper tract involvement, leading to pyelonephritis and bacteremia, unless both the infection and the voiding dysfunction are aggressively managed. The risk for pyelonephritis is increased further in the patient with low bladder wall compliance, vesicoureteral reflux, or ureterohydronephrosis.

Pyelonephritis is a very significant complication from the long-term perspective because of its negative effect on the renal parenchyma; pyelonephritis may cause renal scarring, which involves the replacement of functioning nephrons with fibrotic tissue. When recurrent episodes of pyelonephritis occur, the number of scars and the volume of nonfunctioning renal parenchyma increase, ultimately leading to a poorly functioning or nonfunctioning kidney. Infants and children are at greatest risk for this complication, but it also occurs among adults, especially when the infection is complicated by obstruction.

In the short-term, pyelonephritis causes significant morbidity (fever, pain, and possibly nausea, vomiting, and dehydration) and can lead to bacteremia and urosepsis unless it is promptly and effectively treated. Urosepsis is defined as the presence of tachypnea, tachycardia, and fever or chills in combination with hypoxemia, elevated plasma lactate concentration, or oliguria in the patient with clinical or definitive laboratory evidence of a UTI. Septic shock occurs when urosepsis results in hypotension, characterized by a sustained decrease in systolic blood pressure to 90 mm Hg or less or a drop of 40 mm Hg that lasts for at least I hour.

  1. Urinary Calculi

Another complication of reflex UI is urinary stone disease. Urinary stasis and immobility, both common among patients with paralyzing spinal disorders, are known to increase the risk for urinary calculus formation. In addition, some of the pathogens commonly associated with UTI, such as the Proteus and other urease-producing bacteria, predispose the individual to calculus formation. This association is explained by the finding that these bacteria can split urea to form ammonia, which raises the urinary pH as well as the concentration of ammonia; the result may be precipitation of ammonium phosphate and the formation of magnesium-ammonium phosphate stones. Urinary calculi are a significant complication for the individual with reflex UI because they create or exacerbate obstruction, increase the risk of bacteremia and sepsis, and compromise renal function.

  1. Autonomic Dysreflexia

AD, sometimes called “autonomic hyperreflexia,” is a syndrome characterized by sweating, headache Opens in new window, and hypertension and caused by extreme stimulation of the autonomic nervous system. The condition is peculiar to spinal cord injury, and it primarily affects patients with functional injury levels of T6 and above, although cases of AD have been reported with injuries at T7 and T8.

It is the hypertension associated with AD that carries the greatest risk for mortality; the systolic blood pressure during an episode of dysreflexia can reach 300 mm Hg, and the diastolic pressure can climb to 220 mm Hg.

Several conditions are known to precipitate episodes of AD, such as overdistension of the rectal vault or the presence of an infected pressure ulcer, but the most common stimuli for these life-threatening episodes are associated with the urinary bladder.

The relationship between the urinary bladder and AD was first observed in 1947. Specific events that may produce AD include bladder filling and overdistension; this effect is particularly pronounced during filling cystometry.

AD may also be precipitated by a hyperreflexic detrusor contraction in the presence of DSD; it is not known whether it is the presence of DSD itself, or the magnitude of detrusor stimulation produced by contraction against the obstructed outlet, that causes the episode of AD. However, it is known that elimination of the bladder outlet obstruction (by transurethral sphincterotomy or placement of a urethral stent) alleviates the AD, even though it does not reverse the underlying neurologic abnormality that produces the dyssynergic sphincter activity.


  1. History

The voiding history should emphasize the current bladder management program.

Unlike persons with stress, urge, or mixed stress-urge UI, most persons with reflex UI do not manage their bladder by spontaneous voiding. In contrast, a common management approach is by intermittent catheterization (IC). In this case, it is particularly important to determine the typical frequency of catheterization and the presence of leakage between catheterizations.

Some patients manage their bladders with indwelling catheters, and it is important to determine why the catheter was inserted, the length of time a catheter has remained in place, the size of the catheter and retention balloon, the material of construction (latex, silicone, etc.), and the presence of any leakage around the catheter (bypassing) or blockage. Still other patients manage their reflex UI with spontaneous voiding and urinary containment; many men contain their leakage with a condom catheter, but women and some men use adult incontinent briefs.

The review of systems must include a careful history of the neurologic disorder leading to the reflex UI and its effect on the patient’s general health and functional abilities. Adults with reflex UI and no known neurologic lesion require prompt referral to a neurologist for a thorough evaluation.

The urologic history includes any history of UTI, especially febrile infections, and any urinary problem requiring hospitalization. It is helpful to query the patient about symptoms leading to suspicion of UTI.

Because sensations of bladder filling are diminished or absent, dysuria and suprapubic discomfort are infrequent and unreliable indicators of infection.

The appearance and odor of the urine are also unreliable indicators; cloudy urine may simply reflect phosphaturia from consumption of meat, and changes in urinary odor may be caused by the diet or the medications rather than by bacteriuria.

Nonetheless, clinical experience has shown that even patients with complete spinal injuries often notice changes that are indicative of UTI. Common “indicators” among this population include increased spasticity, a change in the pattern of reflex voiding, or new onset of leakage between catheterizations; new-onset incontinence and changes in the pattern of reflex voiding are probably attributable to the effect of baceriuria on detrusor contractility.

Many patients with reflex UI are very well informed about their UTI history, and it is worthwhile to query the patient and to review available medical records to determine whether the patient’s UTIs are caused by a Proteus species or another urease-producing organism. It is also important to ask the patient about any previous history of urinary calculi, because the risk of recurrent stones is about 50% in the general population, and it is probably even higher among those with reflex UI and a neurologic disorder.

  1. Physical Examination

The general examination should focus on the patient’s functional status, including sensory level, mobility, and dexterity. The patient’s living environment should also be assessed in terms of support for the patient’s efforts to maintain continence or adequate urinary containment. The patient with reflex UI and a paralyzing neurologic condition should be assessed for seating (that is, type and design of wheelchair), assistive devices used for ambulation (if applicable), and choice of clothing.

McDowell has suggested assessing the time required for an elderly person with UI to move to the bathroom and prepare for urination by removing necessary clothing and sitting on the toilet. This assessment strategy is also appropriate for the individual with impaired mobility and dexterity because of a neurologic disorder. Similarly, the person who manages his or her bladder with IC should be assessed for the ability to wash his or her hands, prepare the catheter, remove or adjust clothing, and complete the catheterization procedure. If the patient relies on family members or other caregivers to assist with or perform the catheterization procedure, the assessment should include the ability of the involved individuals to perform the procedure appropriately.

In addition to routine evaluation of the genitalia and the perineal skin, a focused but thorough neurologic examination must be included in assessment of the patient with reflex UI; this should include testing for perineal sensation, bulbocarvernosus reflex, and pelvic floor muscle strength.

  1. Diagnostic Testing

A urinalysis is completed as a routine portion of any incontinence evaluation, and it is particularly important in the assessment of a patient with reflex UI because of the risk for UTI. Because of this risk, some clinicians routinely obtain urine cultures for these patients; however, this practice has not been shown to improve patient outcomes or to be cost-effective.

Current recommendations are to limit cultures and treatment for UTI to patients with symptomatic infections (that is, infections associated with fever or hematuria) and patients with reflex UI who have both bacteriuria and pyuria on microscopic examination of the urine. Treatment of asymptomatic bacteriuria is discouraged because it has not been shown to benefit patients. Instead, it may harm patients by favoring colonization with bacterial strains that are resistant to oral or parenteral antibiotics.

Although urodynamic testing is reserved for complex or complicated cases of urge, stress, or mixed stress-urge UI, it should be routinely performed for patients with reflex UI. Urodynamic testing for the with reflex UI must answer two essential questions:

  1. what is the mechanism underlying urinary leakage, and
  2. is this bladder likely to produce upper tract distress?

In evaluating the mechanism(s) of leakage, the examiner must be aware that the leakage may be of mixed cause. Although overactive detrusor contractions are characteristic of reflex UI, patients must also be evaluated for stress incontinence and for evidence of extraurethral UI.

When evaluating for neurogenic detrusor overactivity, it is important to observe both the magnitude and duration of the contraction and the pressure at which urinary leakage occurs.

  • The detrusor LPP is the detrusor pressure at which urinary leakage first occurs; an elevated detrusor LPP (particularly values greater than 80 cm H2O) is associated with severe obstruction and upper urinary tract distress.
  • The abdominal LPP is the abdominal force required to produce urinary leakage. Any measurable abdominal LPP indicates the presence of stress UI.

When assessing abdominal LPP in a patient with reflex UI, it is important to remember that many patients will be unable to perform Valsalva’s maneuver effectively. Therefore, it may be necessary for the examiner to apply external pressure over the bladder to elicit stress leakage. Extraurethral UI should be suspected when urine loss is observed that is not associated with detrusor overactivity or increased abdominal pressure. However, urodynamic studies lack sensitivity in the evaluation of extraurethral UI; additional evaluation may be required if the fistula is subtle.

An evaluation of the potential of the bladder to cause upper tract distress is based on measurement of bladder wall compliance, maximum detrusor contraction pressure, the maximum urethral pressure gradient, and/or the detrusor LPP.

Bladder wall compliance is a measurement of the distensibility of the bladder wall during bladder filling and storage. The compliance of the bladder wall can be calculated by dividing the change in pressure that occurs during bladder filling by the corresponding change in bladder volume.

Persons with normal bladder function have high bladder wall compliance (with values exceeding 30 mL/cm H2O); normal compliance allows the bladder to fill to high volumes (300 to –600 mL) while maintaining how detrusor pressures (usually less than 15 cm H2O).

Low bladder wall compliance indicates excessive detrusor pressure acting on the bladder wall, intravesical urinary contents, the bladder outlet (urethrovesical junction), and the paired inlets (ureterovesical junctions). Values of 10 mL/cm H2O or lower are associated with a high risk for upper urinary tract distress and/or overflow UI.

Treatment and Management

The treatment of reflex UI is based on the results of the incontinence evaluation, knowledge of the underlying neurologic disorder and its natural history, assessment of the patient’s neurologic status and functional ability, and the patient’s preferences. Because of the complexity of these considerations and the profound effect of the bladder management program on the lives of the patient, family, and caregivers, this decision should be made in collaboration with an interdisciplinary team, such as the rehabilitation team; at a minimum, the decision should be made in close consultation with the patient, family or significant others, primary care provider, continence care clinician, and neurologist or psychiatrist. Table 1.1 provides a listing of management options and the potential for incontinence and upper tract distress with each.

Table 1.1 | Bladder Management Programs
Spontaneous voidingNone30%
Reflex voiding program29% to 30%70%*
Intermittent catheterization7%45%
Indwelling catheter75%†29%
*Urinary incontinence rate based on reported frequency of failure of condom catheter to contain urine (“wet continence”). †Risk is correlated with number of years indwelling catheter is used to manage reflex urinary incontinence. Data from Anson C, Gray M: Secondary urologic complications of spinal injury, Urol Nurs 13:107-112, 1993, and Killorin WK, Gray M, Bennett JK, Green BG: Evaluative urodynamics and bladder management in predicting upper urinary tract infection in male spinal cord injury, Paraplegia 30:437-441, 1992.
  1. Spontaneous Voiding

A few patients (17% to 20%) with spinal cord injuries or other neurologic conditions associated with reflex UI experience neurogenic detrusor oveactivity and vesicosphincter dyssynergia but retain sensory awareness of bladder filling. Within this small group of patients, some retain reasonable continence. Technically, because these patients retain sensation, their UI can be classified as urge; however their management is cited here because they have DSD, and their neurologic condition is indentical to those conditions that typically lead to reflex UI.

The patient who is managed with a spontaneous voiding program typically perceived the urge to urinate, followed by a brief period of hesitancy. The initial desire to urinate is usually produced by an overactive detrusor contraction, and the gap between this sensation and the onset of urination can be attributed to the presence of DSD. This brief period of hesitancy is usually followed by micturition (or by urinary leakage if the patient cannot reach the toilet within a brief period of time).

Because the patient is likely to have compromised mobility or dexterity caused by the underlying neurologic disorder, it is particularly important to maximize access to the toilet and to warn the patient that it will not be feasible to postpone urination for a prolonged period. Issues of mobility, dexterity, and toilet access should be addressed by a rehabilitation-oriented interdisciplinary team. The patient may benefit from a referral to a psychiatrist or rehabilitation nurse practitioner.

Because most patients with reflex UI have DSD as well as neurogenic detrusor overactivity, antimuscarinic agents such as oxybutynin or tolterodine must be used with care. Given in larger dosages, these drugs may produce urinary retention, particularly if detrusor muscle contraction strength is also compromised. However, alpha-adrenergic antagonists, such as terazosin, doxazosin, alfuzosin, or tamsulosin, may be beneficial because they reduce urethral resistance; several of these agents (such as terazosin and doxazosin) also exert a mild anticholinergic effect through their actions on the central nervous system.

Patients managing their bladders with spontaneous voiding programs must be counseled regarding their risk for UTI. They should be taught the signs and symptoms of UTI: dysuria, suprapubic discomfort, and lower back pain. They also should be advised that a UTI is likely to produce an acute exacerbation of their UI. This information is particularly important because many patients with a UTI fail to recognize the significance of their worsening incontinence and respond by altering their fluid intake or their prescribed medication until the UTI escalates into a febrile infection.

Table 1.2 provides the recommended dosage, administration, side effects, and precautions associated with administration of alpha-adrenegic blocking agents. The patients should also be taught the principles of fluid management to include avoidance of high-volume fluid intake over a short period of time and limitation of bladder irritants.

Table 1.2 | Alpha-Adrenergic Antagonists
AgentDosage (Applies to all agents listed)AdministrationPotential side effects (Applies to all agents listed)Nursing considerations
Terazosin (Hytrin)Initial dosage, 1 mgTitrate slowly to maximum of 5 to 10 mg HSOrthostatic hypotension (exacerbated by dehydration)Orthostatic hypotension can be significant.

Advised the patient to take the drug at HS, arise slowly and dangle the legs briefly before getting out of bed. Missing more than two doses may cause severe orthostatic hypotension (when medications taken again); it may be necessary to retitrate the drug to a therapeutic dose.
Doxazosin (Cardura)Initial dosage, 1 mgTitrate slowly to maximum of 4 to 8 mg HS
Tamsulosin (Flomax)0.4 to 0.8 mgAdminister at HSDrowsinessTitration is not required; one may start patients at either 0.4 or 0.8 mg.
Headache (uncommon)
Profound fatigue (uncommon)
This is rare, but it may necessitate discontinuation of the alpha-adrenergic antagonists.
RhinitisAdvise the patient to avoid taking a decongestant for rhinitis.
Decongestants contain an alpha-adrenergic agonist, which interferes with the intended action of the alpha-adrenergic antagonists.
Alfuzosin10 mgAdminister 1 hour after a mealDizzinessNo initial dose titration is needed.
This is associated with reduced risk for retrograde ejaculation as compared with other agents.
  1. Reflex Voiding

Some patients with reflex UI may be managed by a “reflex,” or “trigger,” voiding program. In this program, the bladder empties by means of overactive contractions, and urinary leakage is contained by a condom catheter attached to a drainage bag. Because there is no adequate external collection device for women, the reflex voiding program is currently limited to men.

chiasmus diagram showing abba pattern
Figure X1 | Condom Catheter

If a strict definition of continence is applied, a reflex voiding program does not provide for continence. Rather, the goal of management is to contain the urine and to maintain skin integrity. Joseph and colleagues have defined a goal of “wet continence” for the management of these patients; rather than seeking to prevent urinary leakage, the nurse seeks to enable the patient to contain urine within a drainage system, to prevent soiling of clothing, and to eliminate odor.

Urinary containment relies on the successful application of a condom catheter (Figure X1). The selection of the condom catheter is particularly important as it represents the most likely point of containment failure. The ideal catheter should contain all urinary leakage while maintaining the integrity of the penile skin. It should fit snugly over the penile shaft but should provide sufficient distensibility to accommodate changes in penile circumference associated with erection.

Many condom catheters are manufactured of latex, and these work well for many patients; however, other patients with reflex UI, especially those with myelodysplasia or allegies to latex, are unable to tolerate natural latex in contact with the skin. For these patients, there are condom catheters made of alternative materials such as silicone.

The condom catheter must be sized correctly to fit the penis. Various sizes are available, and most companies provide measuring guides. The clinician should consider both the length and the circumference of the catheter; the condom should generally cover most or all of the shaft of the penis and should fit snugly but not tightly. The catheter should have a reinforced end that resists twisting and kinking and that drains freely so urine does not pool.

A watertight seal is critical and may be obtained either through adhesive or by a constrictive band or balloon. Self-adhesive catheters are available and are simple for the patient or caregiver to apply; however, the patient must be monitored for any sensitivity to the adhesive. The drainage bag must also be carefully selected. For the patient with reflex UI, the drainage mechanism deserves special attention; the drain port must provide security from leakage but should allow the patient with reduced dexterity and hand strength to open and close the mechanism with a sweeping motion of the thumb or hand.

Once the external containment device and drainage system are selected, the patient or caregiver must be taught how to change the device and how to manage the system. Most patients with reflex UI being managed with condom drainage are taught to change the device daily; although some patients can “keep the condom on” for longer periods, this is generally discouraged because of the increased risk for UTI.

Although many patients find the concept of a reflex voiding program attractive, the clinician should be aware that this management approach is associated with significant risk of upper urinary tract distress (29% to 32%). This is primarily attributable to the outlet obstruction created by DSD. Theoretically, skeletal muscle relaxants such as baclofen or diazepam could be used to reduce the activity of the striated sphincter muscle; unfortunately, the dosages required to relieve DSD are so high that the side effects and toxicities outweigh any potential therapeutic benefit.

Although oral skeletal muscle relaxants have not proved beneficial in the management of DSD, intrathecal administration of baclofen has been found to relieve skeletal muscle spasticity and pain related to a variety of spinal disorders. This treatment has also been found to relieve the obstruction produced by DSD in some patients; however, it carries significant risks and is therefore reserved for generalized and disabling skeletal muscle spasticity.

In contrast to skeletal muscle relaxants, alpha-adrenergic blocking agents have proved beneficial in the management of patient with reflex UI. Alpha-adrenergic agents exert several beneficial effects:

  1. they reduce the magnitude of obstruction caused by DSD,
  2. they reduce urethral smooth muscle tone,
  3. they reduce maximum detrusor contraction pressure, and
  4. they lower residual urinary volumes and improve quality of life.

Terazosin and doxazosin must be titrated to reach optimal therapeutic dosages, whereas alfuzosin and tamsulosin require no titration. The spinal cord-injured patient with reflex UI should be evaluated for dehydration or a low serum sodium level before treatment with one of these drug is begun; any abnormalities should be corrected before the initiation of therapy to minimize the risk for dizziness or postural hypotension. The risk for these side effects is also minimized by instructing the patient to take the drug immediately before sleep and to consult a health care provider if more than one dose is inadvertently missed.

  1. Intermittent Catheterization

Intermittent cauterization (IC) provides regular evacuation of the bladder by in-and-out catheterization. The patient is typically taught to self-catheterize using clean technique; care providers or family members may also be taught the procedure. IC is effective because it provides regular, complete bladder evacuation for the patient with a neurologic disorder resulting in reflex UI.

Most patients who maintain at least partial dexterity of the upper extremities are candidates for this procedure. IC as a management program may initially appear undesirable; however, it has advantages that make it an attractive when considered carefully by the patient and caregiver. From the patient’s perspective, the benefits of IC also include reduced effect on body image (as compared with indwelling catheter or reflex voiding with condom containment, both of which require externally obvious drainage systems) and reduced risk for skin damage. The unaltered appearance of the perineum and genitalia my also promote sexual adjustment.

Despite its advantages, an IC program is associated with certain risks. In addition to the potential for upper tract distress among a small group of patients, there is an 18% risk of bladder calculi and a 9% risk of epididymitis among men. The risk for bacteriuria approaches 100%; however, this statistic must be interpreted in light of the relatively low risk for symptomatic UTI, particularly when compared with patients managed with an indwelling catheter.

Some unique issues must be addressed when an IC program is initiated for the patient with reflex UI. These patients typically have limited mobility affecting the lower and possibly the upper extremities; it is frequently advantageous to involve the occupational therapist or physical therapist in developing assistive devices and in maximizing wheelchair mobility. These strategies can prove invaluable in helping the individual to compensate for limitations in strength or dexterity.

There is at least one device available to assist the female patient who has limited sight or compromised upper extremity function to locate the urethra and perform self-catheterization. This lightweight L-shaped plastic device has two “arms”; one arm is inserted into the vagina, and the other arm extends over the urethra with openings that align with the urethra and facilitate catheter insertion.

If the patient is unable to perform self-catheterization even with the use of assistive devices, it may be necessary to teach one or more caregivers the procedure. Instruction of a family member or caregiver is also beneficial for the patient who is “routinely” independent with catheterization, so backup is available when needed (as during periods of illness). The patient is also taught how to direct another person through the procedure. In teaching patients and caregivers, it is important to keep the procedure simple and to emphasize a clean as opposed to sterile approach.

  1. Medications in Conjunction with Intermittent Catheterization

IC as a single strategy is typically inadequate for management of the patient with reflex UI; overactive detrusor contractions occurring between catheterizations in response to various stimuli may cause frequent episodes of leakage. Therefore, antimuscarinic medications are commonly used to control neurogenic detrusor overactivity.

Multiple anticholinergic or antimuscarinic drugs are available and appropriate for these patients; typically, these medications must be administered in significant does, and multiple agents may be required (as shown in Table 1.3).

Table 1.3 | Anticholinergic Drugs Used to Treat Reflex Urinary Incontinence
Agent and usual dosage (adults)Common side effectsNursing considerations
Immediate-release oxybutynin (Ditropan IR: 5 mg 2–3 times daily)Dry mouthThis side effect can be significant and can interfere with speaking, singing, or eating.
Extended-release oxybutynin (Ditropan XL: 5 to –15 mg once daily)Encourage the patient to drink adequate amounts of fluids, chew gum, or suck on hard candy to stimulate salivation.
Extended-release tolterodine (Detrol LA: 4 mg once daily)Intolerance to heatHeat intolerance with flushing, fatigue, or fever when patients are exposed to heat is particularly significant for children, for the elderly, and for some individuals with a spinal cord injury or disorder that interferes with normal mechanisms for managing body temperature.
Trospium (Sanctura: 20 mg twice daily)Advise the patient of the potential for heat intolerance. Dosage may require adjustment during warmer weather.
Transdermal oxybutynin (Oxytrol: 3.9–mg/day; patch applied twice weekly)Blurred visionThis condition is typically limited to fine print and dissipates after the first 5 to 7 days of administration. Significant, persistent blurred vision requires adjustment of the dose or discontinuation of the anticholinergic drug.
Confusion, altered mentationThis condition indicates drug toxicity and necessitates discontinuation or dose adjustment. Elderly patients are particularly susceptible to this side effect.
ConstipationThis may be significant, particularly for the patient with reflex urinary incontinence and limited mobility or impaired abdominal muscle tone. A change in the patient’s bowel management program may be required.
Increased intraocular pressureThis is significant for patients with narrow-angle glaucoma. It is essential to consult with an ophthalmologist before prescribing an anticholinergic medication for a patient with narrow-angle glaucoma.

It is usually advisable to begin with a single agent (such as oxybutynin, tolterodine, or trospium). If a second agent is needed, it is best to select one with slightly different pharmacologic properties (such as imipramine) or a different route of administration (such as adding transdermal oxybutynin to oral tolterodine or trospium).

In teaching the patient with reflex UI about the principles and specifics of his or her bladder management program, it is important to include strategies for management of recurrent leakage.

Patients should be instructed to avoid significant restrictions of fluid intake unless specifically directed to do so by their health care provider. They should be taught to recognize recurrent leakage as a potential sign of UTI and should know that they should return to the clinic for urinalysis and microscopic urine examination should this develop. If the urinalysis and microscopic examination reveal UTI, the patient is treated appropriately. If the examination is negative for UTI, it may be necessary to alter the patient’s antispasmodic medications or fluid intake program.

  1. Indwelling Catheter

On initial consideration, the indwelling catheter appears to be an attractive bladder management option for the patient with reflex UI; it provides continuous urinary drainage, which prevents complications associated with high-pressure detrusor contractions and DSD, and it eliminates the necessity for chronic IC.

A urethral catheter presents a barrier to sexual function, but this can be minimized by use of a suprapubic catheter. However, when viewed from a long-term perspective, an indwelling catheter represents the greatest risk for upper tract distress, significant risk for urinary leakage, and the highest rate of patient dissatisfaction (when compared with all other bladder management programs outlined above).

Indwelling catheterization is also associated with an increased risk of bladder cancer; chronically catheterized paraplegic patients have been found to have a 2% to 10% risk of tumor development, typically squamous cell carcinoma. This risk is attributed to chronic inflammation, but the precise mechanisms resulting in cellular mutation in these patients remain unknown. The risk for cancer is greater among patients with bladder stones, which justifies annual monitoring with urine cytology, and possibly endoscopy.

Despite these risks, it is unrealistic to state than an indwelling catheter should be avoided at all costs among patients with reflex UI. Short-term catheterization may be required for the treatment of pressure ulcers or for monitoring of urine output during acute illnesses. However, long-term catheterization should be used only when it represents the best management option for that patient, that is, in situations in which other strategies are not feasible. Examples of appropriate use include the terminally ill patient, the patient with altered mentation who is unable to cooperate with alternative programs, or a patient with a high cervical lesion for whom an indwelling catheter permits home management with limited assistance (as from family members who work during the day) as opposed to institutionalization.

When an indwelling catheter is selected as the best management option for an individual patient, it is important to select the catheterization site thoughtfully and then to select a catheter that best meets that patient’s needs. For many patients with a paralyzing neurologic disorder and reflex UI, a suprapubic cystostomy site offers significant advantages as compared with urethral catheterization.

The suprapubic site eliminates the risk for urethral erosion, removes the catheter from the bacteria-laden perineum, and facilitates sexual adjustment. However, there are potential disadvantages; initial placement of the catheter requires minor surgery, and patients with stress UI may leak from the urethra despite the presence of the catheter. The decision regarding placement should be made in close consultation with the patient, urologist, and primary care provider.

  1. Reflex Voiding and Intermittent Catheterization

Some male patients with reflex UI manage their bladders with a combination of reflex voiding and IC; the combined strategy provides for complete bladder evacuation on a regular basis and also provides for containment of leakage between catheterizations. Nevertheless, this approach is associated with a relatively high risk of serious urinary complications, including UTI.

One factor that increases the risk for UTI is the abundance of bacteria on the penile skin of patients managed with condom catheters. In their study, Anson and Gray found that the combination of reflex voiding and IC was associated with more serious urinary tract complications than any other management program, except for an indwelling catheter. Therefore, this combination is recommended only when it represents the sole alternative to place of an indwelling catheter.


Reflex UI is one of the most difficult types of incontinence to manage because it involves loss of normal innervations to the bladder or the sphincter, or to both, and is typically associated with devastating injuries or illnesses that produce significant loss of sensory and motor function in addition to the disturbances in bowel and bladder function.

In addition, the pathologic changes in bladder and sphincter function associated with reflex UI create a potentially “hostile” bladder that is likely to cause upper tract distress and eventual renal insufficiency.

Management for any patient must be individualized and based on a comprehensive and thorough assessment; any management plan must address preservation of renal function as well as the control of urinary leakage.

Major treatment options include voluntary voiding, reflex voiding with condom containment, IC, medications to reduce bladder or sphincter contractility, indwelling catheters, and surgical intervention to create a low-pressure reservoir for urine. Effective implementation of any bladder management plan requires a team approach in which the patient and caregiver or caregivers are integral members of the team; the continence nurse is also a critical member of the team and typically assumes primary responsibility for ongoing patient assessment, education, and counseling.

    Adapted from: Urinary & Fecal Incontinence: Current Management Concepts Authored by Dorothy B. Doughty. References as cited include:Ackely BJ, Ladwig GB: Nursing diagnosis handbook, ed 6, St. Louis, 2002, Mosby.
  1. Kim MJ, McFarland GK, McLane AM: Pocket guide to nursing diagnoses, St. Louis, 1995, Mosby.
  2. Abrams P, Cardozo L, Fall M, et al: The standardization of terminology of lower urinary tract function: report from the Standardization Sub-Committee of the International Continence Society, Neurourol Urodyn 21: 167-178, 2002.
  3. Clifton GL: Spinal cord injury in the Houston-Galveston area, Tex Med 79:55-57, 1983.
  4. Fine PT, DeVivo MJ, McEachran AB: Incidence of acute traumatic hospitalized spinal cord injury in the United States, Am J Epidemiol 115:475-479, 1982.
  5. Griffin MR, Opitz JL, Kurland LT, et al: Traumatic spinal cord injury in Olmstead County, Minnesota, 1935-1981, Am J Epidemiol 121:884-895, 1985.
  6. Stover SL: Epidemiology of neurogenic bladder, Rehabil Clin North Am 4:211-220, 1993.
  7. Noonan CW, Kathman SJ, White MC: Prevalence estimates for MS in the United States and evidence of an increasing trend for women, Neurology 58(1):136-138, 2002.
  8. Anderson DS, Ellebery JH, Leventhal CM, et al: Revised estimate of the prevalence of multiple sclerosis in the United States, Ann Neurol 31:333-336, 1992.
  9. Sadovnick AD, Ebers GC: Epidemiology of multiple sclerosis: a critical overview, Can J Neurol Sci 20:17-29, 1993.
  10. Bauer SB: Neuropathic dysfunction of the lower urinary tract. In: Walsh PC, Retik A, Vaughan ED, Wein AJ, editors: Campbell’s urology, ed 8, Philadelphia, 2002, WB Saunders, pp 2231-2261.
  11. Bauer SB: Management of the obstructed urinary tract associated with neurogenic bladder dysfunction, Urol Clin North Am 17(2):395-406, 1990.
  12. Webster GD, El-Mahrouky A, Stone AR, Zakrzewski C: The urological evaluation and management of patients with myelodysplasia, Br J Urol 58:261-265, 1986.
  13. Allen TD: Forty years experience with voiding dysfunction, BJU Int 92(suppl 1):15-22, 2003.
  14. Barrinton FJF: The nervous control of micturition, Queens J Exp Physiol 8:33, 1915.
  15. deGroat WC, Ryall W: Reflexes to the sacral parasympathetic neurons concerned with micturition in the cat, J Physiol (Lond) 200:87-108, 1969.
  16. Chancellor MB, Blaivas JG: Detrusor-external sphincter dyssynergia, Ciba Found Symp Neurobiol Incontinence 151:195-205, 1990.
  17. Yarkony GM: Spinal cord injury: medical management and rehabilitation, Gaithersburg, Md., 1994, Aspen.
  18. Kennelly MJ, Rudy DC: Incontinence caused by neurologic disease. In: O’Donnell PD, editor: Urinary incontinence, St. Louis, 1997, Mosby.
  19. Gray M: Nursing planning, intervention, and evaluation for altered urinary function. In: Broadwell Jackson D, Saunders RB, editors: Child health nursing, Philadelphia, 1993, JB Lippincott.
  20. Thielen KR, Miller GM: Multiple sclerosis of the spinal cord: magnetic resonance appearance, J Comput Assist Tomogr 20:434-438, 1996.
  21. Hermieu JF, Delmas V, Boccon-Gibod L: Micturition disturbances and human immunodeficiency virus infection, J Urol 156:157-159, 1996.
  22. Leach GD, Farsaii A, Kark P, Raz S: Urodynamic manifestations of cerebellar ataxia, J Urol 128:348-350, 1982.
  23. Bannister R: Brain and Bannister’s clinical neurology, Oxford, UK, 1991, Oxford University Press.
  24. Grbavac Z, Gilja I, Gubarev N, Bozicevic D: Neurologic and urodynamic characteristics of patients with Guillain-Barré syndrome, Lijec Vjesn 111:17-20, 1989.
  25. Singh NK, Jaiswal AK, Misra S, Srivastava PK: Assessment of autonomic dysfunction in Guillain-Barré syndrome and its prognostic implications, Acta Neurol Scand 75:101-105, 1987.
  26. Berger Y, Blaivas JG, Oliver L: Urinary dysfunction in transverse myelitis, J Urol 144(1):103-105, 1990.
  27. Hald TG, Bradley WE: The urinary bladder: neurology and dynamics, Baltimore, 1982, Williams & Wilkins.
  28. Sakakibara R, Hattori T, Yasuda K, Yamanishi T: Micturition disturbance in acute transverse myelitis, Spinal Cord 24:481-485, 1996.
  29. Miakowski C: Immunologic system. In: Thompson JM, McFarland GK, Hirsch JE, Tucker SM, editors: Clinical nursing, St. Louis, 1997, Mosby.
  30. Bauer SB: The unstable bladder in childhood, Urol Clin North Am 7(2):321-326, 1980.
  31. Webster GD, Koefoot RB Jr, Sihelnick S: Urodynamic abnormalities in neurologically normal children with micturition dysfunction, J Urol 132(1):74-77, 1984.
  32. J’rgensen TM, Djurhuus JC, Schrᴓder HD: Idiopathic detrusor sphincter dyssynergia in neurologically normal patients with voiding abnormalities, Eur Urol 8(2): 107-110, 1982.
  33. Hinman F Jr: Nonneurogenic neurogenic bladder (the Hinman syndrome): 15 years later, J Urol 36(4):769-777, 1986.
  34. Mix LW: Occult neuropathic bladder, Urology 10(1):1-9, 1977.
  35. Hinman F: Urinary tract damage in children who wet, Pediatrics 54(2): 143-150, 1974.
  36. Rudy DC, Woodside JR: Non-neurogenic neurogenic bladder: its relationship between intravesical pressure and the external sphincter EMG, Neurourol Urodyn 10:169-176, 1991.
  37. McGuire EJ, Savastano JA: Urodynamic studies in enuresis and nonneurogenic bladder, J Urol 132:299-302, 1984.
  38. Vincent SA: Postural control of urinary incontinence: the curtsy sign, Lancet 2:631, 1996.
  39. Gray M: Sphincter reeducation for pediatric voiding dysfunction complicated by dyssynergia, Association for Continence Advice International Conference, Bournemouth, UK, April 1993.
  40. Killorin WK, Gray M, Bennett JK, Green BG: Evaluative urodynamics and bladder management in predicting upper urinary tract infection in male spinal cord injury, Paraplegia 30:437-441, 1992.
  41. Walter JS, Wheeler JS Jr, Dunn RB: Dynamic bulbocavernous reflex: dyssynergia evaluation following spinal cord injury, J Am Paraplegia Soc 17(3):140-145, 1994
  42. Le CT, Price M: Survival from spinal cord injury, J Chronic Dis 35:487-489, 1982.
  43. Hackler RH: A 24-year prospective mortality study in the spinal cord injured patient: comparison with the long term living paraplegic, J Urol 117:486-489, 1977.
  44. DeVivo MJ, Kartus PL, Stover SL, et al: Cause of death for patients with spinal cord injuries, Arch Intern Med 149:1761-1766, 1989.
  45. Wein AJ, Van Arsdalen K, Levin RM: Pharmacologic therapy. In: Krane RJ, Siroky MB, editors: Clinical neurourology, Boston, 1991, Little, Brown.
  46. Anson C, Gray M: Secondary urologic complications of spinal injury, Urol Nurs 13:107-112, 1993.
  47. McGuire EJ, Cespedes RD, O’Connell HE: Leak point pressures, Urol Clin North Am 23:253-262, 1996.
  48. Kieswetter H: Neurogenic bladder as a cause of urinary tract infection, Wien Med Wochenschr 141:560-563, 1991.
  49. Petersen T, Jensen PB: Evaluation of the urinary tract in children with myelodysplasia, Acta Neurol Scand 75:46-51, 1987.
  50. Galloway NT, Mekras JA, Helms M, Webster GD: An objective score to predict upper urinary tract deterioration in myelodysplasia, J Urol 145:535-537, 1991.
  51. Griffiths DJ: Hydrodynamics of the bladder and urethra. In: Mundy AR, Stephenson TP, Wein AJ, editors: Urodynamics: principles, practice, and application, London, 1994, Churchill Livingstone.
  52. Ogawa T, Yoshida T, Fujinaga T: Bladder deformity in traumatic spinal cord injury patients. Hinyokika Kiyo 34:1173-1178, 1988.
  53. Schecter H, Leonard CD, Scribner CH: Chronic pyelonephritis as a cause of renal failure in dialysis candidates: analysis of 173 patients, JAMA 216:514-517, 1971.
  54. McDowell BJ: Basic elements of continence assessment, Urol Nurs 14:120-124, 1994.
  55. Seki N, Masuda K, Tanaka M, et al: Relationship between febrile urinary tract infection and urodynamics in myelodysplastic children with vesicoureteral reflux, Urol Int 71(3):280-284, 2003.
  56. Weld KJ, Dmochowski RR: Effect of bladder management on urological complications in spinal cord injured patients, J Urol 163(3):768-772, 2000.
  57. Joseph AC, Giroux J, Briggs DS, et al: Clinical guidelines for bladder management in the spinal cord injured patient, Jackson Heights, N.Y., 1998, American Association of Spinal Cord Injury Nurses.
  58. Bang RL: Penile edema induced by continuous condom catheter use and mimicking keloid scar, Scand J Urol Nephrol 28:333-335, 1994.
  59. Pidde TJ, Little TW: Hydronephrosis due to improper condom catheter use, J Am Paraplegia Soc 17:168-170, 1994.
  60. Taylor TA, Waites KB: A quantitative study of genital skin flora in male spinal cord injured outpatiens, Am J Phys Med Rehabil 72(3):117-121, 1993.
  61. Loubser PG, Narayan RK, Sandin KJ, et al: Continuous infusion of intrathecal baclofen: long-term effects on spasticity in spinal cord injury, Paraplegia 29:48-64, 1991.
  62. Perkash I: Efficacy and safety of terazosin administration to improve voiding in spinal cord injury, J Spinal Cord Med 18:236-339, 1995.
  63. Perrigot M, Delauche-Cavallier MC, Amarenco G, et al: Effect of intravenous alfuzosin on urethral pressure in patients with neurogenic bladder dysfunction: DORALI study group, Neurourol Urodyn 15:119-131, 1996.
  64. Swierzewski SJ III, Gormley EA, Belville WD, et al: The effect of terazosin on bladder function in the spinal cord injured patient, J Urol 151:951-954, 1994.
  65. Catz A, Luttwak ZP, Agranov E, et al: The role of external sphincterotomy for patients with a spinal cord lesion, Spinal Cord 35:48-52, 1997.
  66. Lockhart JL, Vorstmann B, Weinstein D, Politano VA: Sphincterotomy failure in neurogenic bladder disease, J Urol 135:86-89, 1986.
  67. Beleggia F, Beccia E, Imbriani E, et al: The use of type A botulin toxin in the treatment of detrusor-sphincter dyssynergia, Arch Ital Urol Androl 69 (Suppl 1):61-63, 1997.
  68. Chai T, Chung AK, Belville WD, Faerber GJ: Compliance and complications of clean intermittent catheterization in the spinal cord injured patient, Paraplegia 33:161-163, 1995.
  69. Louis DT, Joseph AC: Providing a self-catheterization prosthesis for a handicapped patient, J Wound Ostomy Continence Nurs 25(2):107-110, 1998.
  70. Hirsch DD, Fainstein V, Musher DM: Do condom catheter collecting systems cause urinary tract infection? JAMA 242:340-341, 1979.
  71. Johnson ET: The condom catheter: urinary tract infection and other complications, South Med J 76:579-582, 1983.
  72. Trop CS, Bennett CJ: Autonomic dysreflexia and its urologic complications: a review, J Urol 146:1461-1469, 1991.
  73. Hofseth LJ, Dunn BP, Rosin MP: Micronucleus frequencies in urothelial cells of catheterized patients with chronic bladder inflammation, Mutat Res 352: 65-72, 1996.
  74. Johnson JR, Roberts PL, Olsen RJ, et al: Prevention of catheter-associated urinary tract infection with a silver oxide-coated urinary catheter: clinical and microbiologic correlates, J Infect Dis 162:1145-1150, 1990.
  75. Murakami S, Igarashi T, Tanaka M, et al: Adherence of bacteria to various urethral catheters and occurrence of catheter-induced urethritis, Hinyokika Kiyo 39:107-111, 1993.
  76. Riley DK, Classes DC, Steens LE, Burke JP: A large randomized trial of a silver impregnated urinary catheter: lack of efficacy and staphylococcal superinfection, Am J Med 98:349-356, 1995.