The primary functions of the urinary bladder are storage of urine and coordinated emptying. Incontinence and urinary retention are common presenting symptoms of bladder dysfunction in patients with neurologic disorders cared for by physiatrists. Optimal management of the neurogenic bladder requires an understanding of the neuroanatomy, physiology, and classification of neurogenic bladder types. Clinical evaluation and individualized management, including behavioral, pharmacologic, and surgical techniques, are outlined and common complications are reviewed.
Neuroanatomy and Physiology
Detrusor and Sphincter Muscle Characteristics
Previously, the detrusor muscle in humans was said to have no gap junctions and a one-to-one innervation ratio. Although this is not likely to be correct, innervation of the bladder is nevertheless dense and complex. Contraction of the detrusor muscle is initiated by phosphorylation of the light myosin chain and terminated by dephosphorylation. Contraction is initiated by an increase in intracellular calcium released from intracellular sources and an influx of extracellular calcium. This influx is controlled by as many as four calcium channels (three voltage-sensitive and one receptor-sensitive), which probably explains why calcium channel blockers are not effective inhibitors of detrusor activity in the clinical setting. Relaxation of the detrusor is associated with an influx of potassium into the cell. In addition to smooth muscle, collagen forms nearly 50% of the bladder wall in healthy individuals. This proportion increases considerably in disease states. In the striated muscle of the distal sphincter, the majority of fibers are slow twitch, whereas those in the pelvic floor are a mixture of fast and slow twitch. Maintenance of sphincter tone facilitates continence, but not a fast contractile response, which probably explains why suddenly stopping a urine stream is difficult.
Lower Urinary Tract Pharmacology: Receptors and Neurotransmitters
The bladder contains cholinergic muscarinic and nicotinic receptors and α- and β-adrenergic receptors.
Muscarinic Receptors and Transmitters
The receptors active during bladder contraction are cholinergic muscarinic (M 2 and M 3 ) receptors widely distributed in the body of the bladder, trigone, bladder neck, and urethra. The M 2 receptors predominate structurally in normal bladders, but the M 3 receptors might be more important functionally. This distribution of M 3 receptors explains the widespread use of antimuscarinic agents for the treatment of overactive bladder (OAB) and the relatively recent rush by pharmaceutical companies to develop more M 3 -selective compounds.
Cholinergic nicotinic receptors are primarily located in the striated sphincter.
Adrenergic Receptors and Transmitters
Adrenergic receptors are concentrated in the trigone, bladder neck, and urethra and are predominantly α 1 . These have recently been subdivided into α 1a , α 1b , and α 1d . Identification of these α 1 subgroups allows increased specificity with regard to therapeutic agents. For example, α 1a -selective antagonists (i.e., tamsulosin and silodosin) are widely used in the treatment of benign prostatic hyperplasia and disorders of bladder neck dysfunction. Likewise, α 1d receptors may be more important in the symptom of bladder urgency, and naftopidil, a combined α 1a /α 1d drug, is being studied in the treatment of benign prostatic hyperplasia and OAB, and is approved for clinical use in Japan.
Norepinephrine-containing nerve cells are also found in the paravesical and intramural ganglia. Some authors describe norepinephrine terminals in the striated muscle of the distal sphincter, although most would dispute this. When these cells are active, they have excitatory effects and maintain continence by contraction of the bladder neck and urethral smooth muscle. β 2 -Adrenergic and β 3 -adrenergic receptors are found in the bladder neck and also in the body of the bladder. These receptors are inhibitory when activated and can produce relaxation at the bladder neck on initiation of voiding and relax the bladder body to enhance storage ( Figure 20-1 ). In fact, a β 3 -antagonist, mirabegron, the first new drug for the treatment of OAB that is not an antimuscarinic, was approved by the U.S. Food and Drug Administration (FDA) in 2012, and studies demonstrate similar efficacy to standard antimuscarinic agents.
Other Receptors and Transmitters
Other lower tract transmitters have been considered, but much of the evidence for their presence and activity is from preclinical animal models. The role of these other transmitters in normal and disease states in humans is uncertain. Many lower tract transmitters have opposing effects on lower tract function, depending on their site of action. Purine receptors (P 1 , stimulated by adenosine, and P 2 , stimulated by adenosine triphosphate [ATP]) have their effects at the pelvic ganglia and the neuroeffector junction. They have inhibitory and facilitative effects, respectively, on the detrusor muscle. Vasointestinal polypeptide, by contrast, enhances transmission of acetylcholine in pelvic ganglia and inhibits acetylcholine-mediated contraction in the detrusor. Neuropeptide Y has excitatory functions on the detrusor muscle and indirect facilitative effects by inhibiting norepinephrine release. This transmitter also has inhibitory effects by blocking acetylcholine release and blocks the atropine-resistant bladder contraction. Tachykinins are found mostly in afferent nerves, where their effects are to augment the micturition reflex and also transmit pain sensation. Tachykinins augment the contractile and vascular response in inflammatory states. Prostaglandins cause the slow onset of contractions of the detrusor, whereas parathyroid hormone–related peptide causes relaxation. ATP is heavily involved in urothelial to detrusor signaling and is likely to represent the nonadrenergic noncholinergic transmitter that mediates bladder contraction.
The main effector transmitter for contraction of the urethra is norepinephrine, via the α 1 receptors. Smooth muscle relaxation is mediated by the effects of acetylcholine in the pelvic ganglia. This releases nitric oxide (NO) in the urethral wall, resulting in relaxation of urethral smooth muscle. NO has been studied as a potential treatment for detrusor sphincter dyssynergia. However, systemic effects have limited its utility.
Prostaglandins, in contrast to their effects on the detrusor, cause a relaxation of the urethral muscle. Prostaglandins have been tried in various clinical states of urinary retention but without consistent results and may be important in the generation of low-amplitude spontaneous rhythmic contractions during the filling phase of micturition. Because of its stimulatory effect on the detrusor smooth muscle, prostaglandin E 2 has been used as a preclinical model of detrusor overactivity.
Serotonin appears to be an antagonist that causes urethral muscle contraction. It might be important in the production of irritative urethral symptoms and in bladder neck and sphincteric contraction. The combined norepinephrine and serotonin reuptake inhibitor, duloxetine, has been used for the treatment of stress urinary incontinence in Europe but is not approved for this indication in the United States. It may also have uses in the treatment of some forms of neurogenic voiding dysfunction.
Estrogens
The role of estrogens on the lower urinary tract in women is confined to secondary effects on tissues and receptors because they do not appear to have direct transmitter effects.
Transmitter Function Depends on Location
In the brainstem and spinal cord the various transmitters described earlier can have a variety of inhibitory and facilitative actions, depending on their site of action. Serotonin might have inhibitory detrusor effects at the midbrain level, and uptake of serotonin might be blocked by tricyclics (used in the treatment of nocturnal enuresis). Activation of opiate receptors in the brainstem and sacral spinal cord inhibits voiding. This might partly explain the retention of urine seen with the use of these agents. The pudendal motor neuron bodies are situated in the lateral border of the ventral horn of the sacral cord (Onuf nucleus). Serotonin and norepinephrine reuptake inhibitors prolong the effect of these agents in the synaptic cleft of Onuf nucleus and increase the activity of the external sphincter.
A complete discussion of the pharmacology of the lower urinary tract can be found in Steers.
Lower Urinary Tract Innervation
Peripheral Innervation
The afferent and efferent peripheral pathways include autonomic fibers that are carried in the pelvic (parasympathetic) and hypogastric (sympathetic) nerves, and somatic fibers that are carried in the pudendal nerves ( Figure 20-2 and Table 20-1 ). In healthy individuals, the micturition reflex is triggered by sensory information regarding bladder filling volume. Once a threshold filling volume is reached, afferent Aδ fibers relay information back to the central nervous system. In pathologic states, stimulation of capsaicin or vanilloid receptor subtype 1 (VR1) (receptors expressed by unmyelinated afferents in the bladder) lead to excitation of C-afferent fibers, possibly mediating bladder dysfunction as a result of inflammatory reactions. These receptors are cation channels, expressed almost exclusively by the primary sensory neurons involved in nociception and neurogenic inflammation, which can also be activated by noxious heat and changes in pH. In suprasacral neurogenic bladder disease, these capsaicin-sensitive vanilloid receptors and C-afferent fibers have a major role in the pathogenesis of detrusor overactivity. Intravesical capsaicin and resiniferatoxin, which block transmission through C-afferent fibers for several months, have been used experimentally to treat detrusor overactivity when it does not respond to the usual pharmacologic agents. Larger studies are needed to clarify the clinical role of these agents.
| Receptor | Pelvic (Parasympathetic) | Hypogastric (Sympathetic) | Pudendal (Somatic) |
|---|---|---|---|
| Bladder wall tension | + | — | — |
| Bladder mucosal nociception (pain, temperature, chemical irritation) | + | + | — |
| Urethral mucosal sensation (pain, temperature, passage of urine) | — | — | + |
Micturition Reflex
The reflex center for the coordination and control of lower urinary tract function, referred to as the pontine micturition center (PMC), lies in the pons along with the other autonomic centers ( Figure 20-3 ). Coordination of bladder and sphincter activity is dependent on intact connections to the PMC. For the micturition reflex to be successfully completed, timing is crucial. In this regard, the sphincter must relax just before the onset of a bladder contraction to achieve unobstructed voiding. Thus, disruptions in pathways between the PMC and the sacral outflow to the bladder can lead to detrusor sphincter dyssynergia, a leading cause of obstruction in individuals with suprasacral spinal cord injury (SCI).
Other Lower Urinary Tract Reflexes
Not shown in Figure 20-3 is a facilitatory reflex with afferent axons originating from the bladder and synapsing on the pudendal nerve nucleus at S2, S3, and S4 (Onuf nucleus). This allows inhibition of pelvic floor activity during voiding. Another important reflex uses the local segmental innervation of the external sphincter with afferents from the urethra, sphincter, and pelvic floor, and efferents in the pudendal nerve. Higher (voluntary) control over the pelvic floor is achieved through afferents that ascend to the sensory cortex. Descending fibers from the motor cortex synapse with the pudendal motor nucleus.
Lower Urinary Tract Function
Urodynamic studies in both healthy individuals and those with neurologic disease have yielded clinical insights into the normal and abnormal function of the lower urinary tract that occur with development and aging ( Figure 20-4 ).
Voiding Function in Infants and Young Children
Neonates and infants have involuntary reflex voiding that occurs at approximately 50 to 100 mL volumes. Sometime after the first year of life, the child begins to show some awareness of bladder evacuation and can begin to delay urination for a brief period by contracting the voluntary sphincter. For normal control, the detrusor reflex has to be inhibited by the higher centers above the level of the PMC. By 5 years of age, approximately 90% of children have volitional control of voiding. The remaining 10% have a more infantile or immature pattern, with involuntary detrusor activity that occurs between voluntary voids producing frequency, urgency, and occasionally urge incontinence and nocturnal enuresis. Most of these children gradually have inhibition of the detrusor reflex and resolution of enuresis by the onset of puberty. Treatment is almost always with reassurance and observation.
Voiding Function in Adults
With bladder filling, there is only a minimal increase in intravesical pressure (known as accommodation) together with an increase in recruitment of activity in the pelvic floor and voluntary sphincter. Normal voiding is initiated by voluntary relaxation of the pelvic floor with subsequent release of inhibition of the detrusor reflex at the pontine level, resulting in detrusor contraction. Detrusor contraction is maintained steadily throughout voiding, and the pelvic floor remains quiescent.
Voiding Function in Older Adults
OAB is a symptom syndrome identified as elevated urinary urgency usually with increased daytime frequency and nocturia in the absence of identifiable causes. The prevalence of OAB in the adult U.S. population is estimated at nearly 20% and increases with age, making it a common and bothersome geriatric condition. Lower urinary tract symptoms including frequency, urgency, and incontinence with incomplete emptying are common in older adults. Urodynamic studies show that many older adults have involuntary bladder contractions during filling that may explain these symptoms. These contractions may be poorly sustained and result in incomplete emptying. This condition, now called detrusor underactivity by the International Continence Society, is poorly understood and may be neurogenic or myogenic in origin.
Older adult men can have prostatic obstruction caused by benign prostatic hyperplasia, and women can have incontinence related to impaired sphincter activity or stress incontinence. However, in the absence of these well-defined mechanical factors, changes in bladder function in older adults have been ascribed to loss of cerebral inhibition resulting from minor strokes as well as changes in the bladder wall caused by collagen deposition. Changes in bladder function can also result from polyuria secondary to reduced renal concentrating ability, diuretic use, lack of normal increase in antidiuretic hormone secretion at night, and mobilization of lower extremity edema during sleep. In this regard, the American Urological Association now recommends completion of a frequency-volume chart in the workup of all men with benign prostatic hyperplasia and as a consideration in patients with OAB. Patients with more than 3 L of total urine production in 24 hours can be diagnosed with polyuria and can often be treated with behavioral modifications. Likewise, patients with more than 33% of their total 24-hour urine production occurring in the overnight period are diagnosed as having nocturnal polyuria and may have underlying medical conditions rather than primary bladder dysfunction.
Classification of Neurogenic Bladder Dysfunction
The neurogenic bladder has been classified in a variety of ways, beginning with the anatomic classification of Bors and Comarr. The first functional classification was based on cystometric findings, and five basic groups were described: (1) reflex, (2) uninhibited, (3) autonomous, (4) motor paralytic, and (5) sensory neurogenic bladders. Later, a more anatomic classification system was proposed, in which the neurogenic bladder was subdivided into types including supraspinal, suprasacral spinal, infrasacral, peripheral autonomic, and muscular lesions ( Figure 20-5 ). At the same time, others developed functional classifications, all of which were based on conventional urodynamic evaluations. This was an attempt to categorize the lower urinary tract according to the passive storage ability of the bladder and the activities and coordination of the detrusor and sphincter mechanisms ( Table 20-2 ). In practice, it is common to use a combination of both anatomic and functional classifications. Clinical management is based on functional changes demonstrated by urodynamic testing.
| Type of Failure | Bladder Factors | Outlet Factors |
|---|---|---|
| Failure to store | Hyperactivity | |
| Decreased compliance | Denervated pelvic floor | |
| Bladder neck descent | ||
| Intrinsic bladder neck sphincter failure | ||
| Failure to empty | Areflexia | |
| Hypocontractility | Detrusor sphincter dyssynergia (striated sphincter and bladder neck) | |
| Nonrelaxing voluntary sphincter | ||
| Mechanical obstruction (benign prostatic hypertrophy or stricture) |
Evaluation of Neurogenic Bladder Dysfunction
History and Physical Examination
Although the symptoms associated with neurogenic bladder dysfunction are often misleading and correlate poorly with objective findings, relief of symptoms is often the patient’s main concern. It is often helpful to have the patient or attendant complete a standardized “void diary” to record fluid intake, output, and incontinence episodes over several 24-hour periods. A history of recurrent urinary tract infection (UTI) can be directly associated with acute changes in voiding function. The patient’s ability to sense bladder fullness and notice incontinence can also be useful. The history should help determine whether there were voiding symptoms before the causative neurologic event or any premorbid conditions such as diabetes, stroke, and previous urologic or pelvic surgery. The neurologic diagnosis, especially the level of the lesion and its completeness, is important in predicting the type of lower urinary tract dysfunction that might be expected.
The physical examination should assess mental status and confirm the level of the neurologic deficit (if present). Perineal sensation and pelvic floor muscle and rectal tone are particularly important. Reflexes are also important, but the bulbocavernosus, cremasteric, and anal reflexes are sometimes difficult to elicit. The skin of the perineum and the amount of bladder support should be assessed. In women, a pelvic examination is warranted to assess for adequate estrogenization and any evidence of vaginal wall support defects. Good estrogenization is evidenced by a pink and moist vaginal mucosa with good rugae, whereas lack of estrogenization reveals a pale, dry, and smooth vaginal mucosa. In this regard, evidence now supports the use of topical vaginal estrogen for the prevention of recurrent UTIs in postmenopausal women. Physical examination findings of cystocele or pelvic organ prolapse can indicate vaginal wall support defects. The evaluation of voiding dysfunction in men should include a prostate examination. Prostate size or consistency alone is not a good indicator of obstruction, which can only be established with formal pressure-flow urodynamic studies. However, prostate size has clearly been associated with the development of urinary retention in randomized trials. It is also important to assess the patient’s motivation, lifestyle, body habitus, and physical impairments including upper limb function, lower limb function, and spine range of motion.
Diagnostic Testing for Neurogenic Bladder Dysfunction
Indications for Diagnostic Testing
The extent of upper and lower urinary tract testing has to be individualized for each patient and each neurologic condition. The upper tract needs evaluation if there are symptoms suggestive of pyelonephritis or history of renal disease. Some neurologic conditions such as stroke, Parkinson’s disease, and multiple sclerosis infrequently cause upper tract involvement. For these conditions, a simple baseline screening test such as renal ultrasonography (US) is sufficient. Persons with spinal cord lesions and myelodysplasia need more extensive and regular upper tract surveillance with both structural and functional tests. The lower urinary tract evaluation can be simple, from urinalysis to urine culture to measurement of postvoid residual (PVR). A full urodynamic evaluation might be necessary, however, especially if incomplete bladder emptying, incontinence, recurrent bacteriuria, or upper tract changes are present.
Bladder findings on urodynamic studies cannot be used alone to determine the level of neurologic lesion. For example, a suprasacral neurogenic bladder from a complete SCI can remain areflexic, and a conal or cauda equina bladder can exhibit high pressures from poor compliance ( Table 20-3 ). Although the anatomic level of the neurologic lesion can suggest to the clinician the most likely pattern of bladder dysfunction, urodynamic testing should be performed to confirm this. Functional bladder studies in traumatic SCI are best deferred until spinal shock has resolved.
| Term | Definition |
|---|---|
| Bladder | |
| Hyperactivity | Contractions of the detrusor during filling |
| Hypocontractility | Unsustained contractions causing failure to empty |
| Areflexia | Absent contractions with attempt to void |
| Compliance | Change in volume divided by change in baseline pressure with filling (<10 mL/cm H 2 O abnormal; 10 to 20 mL/cm H 2 O borderline if capacity reduced) |
| Outlet | |
| Detrusor sphincter dyssynergia | |
| At bladder neck | Usually in patients with tetraplegia and autonomic hyperactivity |
| At striated sphincter | Uncoordinated pelvic floor and striated sphincter contraction with detrusor contraction during attempts to void |
| Nonrelaxing sphincter | Poor voluntary relaxation of voluntary sphincter in patients with areflexia attempting to void by the Valsalva maneuver |
| Decreased outlet resistance | Incontinence caused by damage to the bladder neck or striated sphincter, pelvic floor descent, or denervation |
Upper Tract Tests
Ultrasonography
US is a low-risk and relatively low-cost test for routine evaluation of the upper urinary tract, and is also easy for the patient. It is not sensitive enough to evaluate acute ureteral obstruction, and in this clinical setting non–contrast-enhanced computed tomography (CT) should be performed. US is adequate for imaging chronic obstruction and dilation, scarring, renal masses (both cystic and solid), and renal stones. The ureter is seen on US imaging only if dilated. The bladder, unless empty, can be evaluated for wall thickness, irregularity, and the presence of bladder stones.
Plain Radiography of the Urinary Tract: Kidneys, Ureter, and Bladder
A kidney, ureter, and bladder (KUB) study is often combined with US to identify any possible radiopaque calculi in the ureter or bladder stones not seen on US.
Computed Tomography
CT is often performed without contrast enhancement, and this study has replaced KUB, US, and excretory urography in the evaluation of the upper tracts when acute obstruction from stones is a possibility. It is also the most sensitive study for detecting small bladder stones in patients with an indwelling catheter in whom the bladder is collapsed around the catheter.
Excretory Urography or Computed Tomography/Intravenous Pyelogram
A CT without and then with intravenous contrast, with a delayed phase, has largely replaced the excretory urogram. The delayed phase can be used to reconstruct a complete urogram and, hence, the study is now called a “CT-Urogram” or CTU. If the serum creatinine concentration is greater than 1.5 mg/dL, or if the patient has insulin-dependent diabetes, intravenous contrast agent administration increases the risk of contrast-related nephropathy. In these cases, alternative studies include US, radioisotope renography, and possibly cystoscopy with retrograde pyelography. The “gold standard” for the workup of patients with asymptomatic microscopic hematuria (defined as greater than three red blood cells per high powered field in the absence of identifiable causes) is the CTU. Imaging choices should be made in the context of results of a formal microscopic urine analysis.
Creatinine Clearance Time
This has been the gold standard for assessing renal function and is said to approximate the glomerular filtration rate (GFR). Its accuracy depends on meticulous urine collection, and it can be misleading in some clinical situations. For example, in patients with low muscle mass and a 24-hour creatinine excretion of less than 1000 mg, the calculated creatinine clearance time can be too inaccurate to be clinically useful. Because of such limitations, more endogenous markers of GFR are being increasingly studied. Chief among these has been serum cystatin C, which is a low-molecular-weight protein filtered at the glomerulus. It is produced by all nucleated cells, and unlike creatinine, it is not secreted by the renal tubule and is not affected by muscle mass. Cystatin C is, however, increased in inflammation. Efforts are under way to improve agreement among commercially available assays.
Isotope Studies
The technetium-99m dimercaptosuccinic acid (DMSA) scan is still the best study for both differential function and evaluation of the functioning areas of the renal cortex. The renogram obtained with technetium-99m mertiatide (MAG-3) also gives information on urinary tract drainage, as well as a good assessment of differential function. In patients who might have ureteral reflux, these studies should be done only after the bladder has been drained with an indwelling catheter. Iothalamate is another contrast medium used in excretory urography. It is of low molecular weight and is handled by the kidney in a manner identical to inulin. Both unlabeled and radioisotopic iothalamate have been used to measure GFR.
Lower Tract Tests
Urinalysis, Culture, and Sensitivity Testing
These tests are done routinely for all patients with neurogenic bladder disease and should be repeated as often as necessary or at the very least at routine follow-up annually. These would also be recommended before invasive procedures in cases of suspected UTI (i.e., with cloudy, foul-smelling, or bloody urine) or with new lower urinary tract symptoms such as incontinence, frequency, or dysuria. In persons with SCI who lack sensation, UTI symptoms may also include increased spasticity or autonomic dysreflexia. Bacteriuria should be treated before any invasive urologic procedure or test is performed.
Postvoid Residual
The PVR is simple to determine and clinically useful, especially when compared with previous recordings and considered in conjunction with the bladder pressure, clinical symptoms, and the appearance of the bladder wall. PVRs can vary throughout the day. A catheter insertion has been used for PVR in the past, but there are now simple US machines that noninvasively obtain the PVR. A low (less than 20% of bladder capacity) PVR is not by itself indicative of a “balanced” bladder, as it was once defined, because high intravesical pressures can be present despite low PVR values.
Cystography
This study is usually performed to test for the presence or absence of ureteral reflux, and it also shows the outline and shape of the bladder. Findings suggestive of increased bladder pressure, such as diverticuli or an irregular bladder contour due to trabeculation, can be observed. However, it does not provide information about bladder pressure corresponding to reflux; for this, urodynamic testing is needed (discussed later).
Significant bacteriuria should be treated before the test is performed. Blood pressure should be monitored in persons with SCI at risk for, or with a history of, autonomic dysreflexia. In many cases urodynamic studies, which include fluoroscopy of the bladder and monitoring of the intravesical pressure, are more clinically useful.
Urodynamics
Urodynamics, a pressure-flow study of lower urinary tract function, remains the gold standard for the evaluation of lower urinary tract function and dysfunction. The study involves insertion of a catheter into the bladder and a second catheter to measure abdominal pressures into the rectum, ostomy, or vagina. The catheter in the bladder serves as a filling catheter and is also used for real-time pressure monitoring. An abdominal pressure tracing is helpful to distinguish intravesical pressure variations (resulting from intraabdominal transmission) from contractions of the detrusor itself. Reported filling rates vary, but usually range from 25 to 60 mL/min and should be reported as physiologic (≤weight [kg]/4 in mL/min) or nonphysiologic for rates above this threshold.
During filling, patients are asked to suppress voiding. Normal values include a capacity of 300 to 600 mL, with an initial sensation of filling at approximately 50% of capacity. In children younger than 2 years, the formula 2 × age (years) + 2 will give the expected bladder capacity in ounces. For children aged 2 years and older, the appropriate formula to calculate the bladder capacity in ounces is age (years)/2 + 6. To convert to mL, multiply the ounces by 30. The sensation of normal fullness is said to be appreciated in the lower abdomen with a sense of urgency in the perineum. Bladder compliance is the change in volume divided by the increase in baseline pressure during filling (i.e., before a detrusor contraction). This value should be greater than 30 mL/cm H 2 O, with 10 to 20 mL/cm H 2 O usually defined as borderline and less than 10 mL/cm H 2 O defined as poor compliance. The patient is asked to suppress detrusor contractions during this test. Any detrusor contraction during the filling phase of the test, usually defined as a phasic pressure change of more than 15 cm H 2 O, is abnormal and is labeled as an involuntary detrusor contraction. Individuals with involuntary detrusor contractions are classified as having “detrusor overactivity” in the absence of an identifiable cause or “neurogenic detrusor overactivity” when the voiding dysfunction is clearly associated with a neurogenic etiology. It is important to distinguish “detrusor overactivity,” which is reserved purely for urodynamic findings, from the term OAB, which is a purely clinical term.
Although patients can be instructed to try to void at capacity, many are unable to generate a detrusor contraction. The presence of an easily obtainable involuntary detrusor contraction confirms the presence of detrusor overactivity in a patient with a suprasacral or supraspinal lesion. However, the absence of a contraction does not necessarily imply true acontractility in a patient with an infrasacral lesion.
Urethral Pressure Profiles
Urethral pressure profiles are obtained by withdrawing a measuring device (microtip transducer or perfused side-hole catheter) gradually down the urethra and measuring centrally oriented forces. It has limited value except in determining whether a sphincter-active area is still present after a sphincterotomy, which can also be evaluated by fluorourodynamics.
Sphincter Electromyography
Sphincter electromyography (EMG) can be combined with the cystometrogram (CMG) or preferably with a full multichannel videourodynamic study. Recordings have been made with a variety of electrodes (monopolar, coaxial needle, and surface electrodes) from the levator, perianal, or periurethral muscles. Because some authors claim there is a functional dissociation between these muscle groups, periurethral recordings are preferred. The integrated EMG is displayed on the same trace as the bladder pressure. Normally, EMG activity gradually increases as bladder capacity is reached during bladder filling, and then becomes silent just before voiding. Low levels of EMG activity with no recruitment during filling are a common pattern in complete SCI. When a reflex detrusor contraction occurs in these patients, the EMG activity in the sphincter can increase rather than decrease. With this detrusor sphincter dyssynergia, voiding often occurs toward the end of the detrusor contraction because the striated sphincter relaxes more quickly than the smooth muscle of the bladder. This type of sphincter EMG does not display individual motor units and cannot be used for the evaluation of infrasacral denervation of the pelvic floor musculature (for which standard needle EMG is needed). Diagnostic integrated EMG recordings from the external urethral sphincter are difficult to obtain, invasive, and painful in patients who are sensate. The fluoroscopic appearance of the urethra is an alternative method of determining sphincter dysfunction and is preferred after distal sphincterotomy if recurrent distal sphincter dyssynergia is suspected ( Figure 20-6 ).
Videourodynamics/Fluorourodynamics
This study is designed to give the maximum information about the filling and voiding phases of lower urinary tract function, and every effort is made to make it as physiologic as possible. A videourodynamic study is indicated in the following patients: those with incomplete spinal cord lesions with incontinence who have some ability to void and inhibit voiding voluntarily but empty incompletely; persons with mechanical obstruction (e.g., benign prostatic hyperplasia) with neuropathy; candidates for sphincterotomy, to assess detrusor contraction and the presence or absence of bladder neck obstruction in addition to striated sphincter dyssynergia; those who fail to respond to pharmacotherapy; those who may be candidates for surgical procedures such as augmentation, continent diversion, or placement of an artificial sphincter or a suprapubic catheter; patients who have deterioration of the upper tracts; and patients who relapse frequently with symptomatic bacteriuria. The procedure requires placement of a seven-French two-channel catheter in the bladder and an eight-French balloon catheter in the rectum. EMG of the sphincter can be recorded along with bladder, rectal, and detrusor (bladder minus rectal) pressures. A contrast solution delivered at physiologic or supraphysiologic rates (i.e., ≥ weight [kg]/4 in mL/min) is used to fill the bladder, with the patient sitting or lying as appropriate. The blood pressure is recorded in patients with spinal cord lesions above T6 to monitor for autonomic dysreflexia. The bladder image is monitored intermittently with fluoroscopy, and the combined radiographic and urodynamic image is mixed on the same screen and can be recorded on videotape (see Figure 20-6 ). If the patient can sit and void during the study, a flow rate can also be recorded. A videourodynamic study in children with myelodysplasia or SCI might have to be modified, and adequate clinical information can often be obtained by recording bladder pressure combined with fluoroscopy. Table 20-3 lists urodynamic terms used to categorize bladder and outlet abnormalities.
Cystoscopy
The only routine indication for cystoscopy is the presence of a long-term indwelling suprapubic or urethral catheter because the presence of the catheter increases the risk for bladder tumor development. Cystoscopy is recommended after 5 years in high-risk patients, such as smokers, or after 10 years in those with no risk factors. Cystoscopy should also be performed after CTU in patients who have gross or microscopic hematuria that cannot be attributed to UTI, stones, or trauma. Often a noncontrast CT is the only study that will pick up small bladder stones, especially if the bladder is collapsed around an indwelling catheter. Repeated lower tract infections can be an indication for cystoscopy and can reveal nonopaque foreign bodies, such as hairs, that have been introduced by catheterization.
Nonpharmacologic Treatment of Neurogenic Bladder Dysfunction
General Principles
Bladder management should be undertaken in the context of the whole person. Patient goals are to empty the bladder not more than every 3 to 4 hours, remain continent, sleep without interference from incontinence or a urinary drainage system, and avoid recurrent UTI or other complications. Less than optimal bladder management decreases the person’s social, vocational, and avocational potential. The following discussion describes specific management approaches ( Table 20-4 ).
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