Many diseases or conditions involving the brain, spinal cord, and peripheral nerve can affect the function and structure of the bladder and sphincter as well as the synergic action of the two structures. Although complete lesions at different levels of the nervous system may produce typical urodynamic findings, the symptoms of patients suffering from the same lesion may vary due to nerve plasticity, secondary changes from infection, fibrosis, etc. Many diseases can also involve both peripheral and central nervous system to varying degrees. Incontinence can also be due to patient's inability to respond to sensory cue from bladder or having no perception of bladder fullness at all.
Failure of Bladder Storage Function
Loss of reservoir function in a contracted bladder can be caused by poor compliance in the detrusor muscle. Intravesical pressure rises with minimal bladder filling, exceeding the outlet resistance and causing urinary leakage. Failure of reservoir function may be found in patients who have meningomyelocele or exhibit other upper motor neuron lesions. Although these patients may have partial lesions with significant striated sphincteric activity offering some degree of resistance, early loss of bladder compliance increases intravesical pressure with minimal bladder filling and overcomes remaining outlet resistance (Figure 30–20). These patients, once recognized, must be managed aggressively because they often have a significant risk to the upper urinary tract, which can lead to possible vesicoureteral reflux, early renal deterioration, or lower ureteral obstruction.
Urodynamic recording in a patient with evidence of detrusor/sphincter dyssynergia, showing spontaneous activity in the bladder associated with a burst of activity in the external sphincter interrupting voiding. This represents a classic demonstration of upper motor neuron dysfunction leading to urinary incontinence as a result of detrusor hyperactivity or hyperreflexia. R, rectal pressure; B, bladder pressure; U2, distal urethral pressure.
Failure of Sphincter Function
Complete lesions of the sacral segment or the cauda equina result in a total loss of smooth and striated sphincteric activity. The external sphincter offers minimal resistance. Most patients experiencing such failure can retain some volume, because the bladder musculature becomes atonic and intravesical pressure remains low, but any increase in intravesical pressure can cause leakage and the bladder never reaches full capacity. Consequently, the integrity of the upper urinary tract is not endangered, as in cases of reservoir failure.
Diagnostic evaluation of neuropathic urinary incontinence determines whether the condition arises from detrusor or sphincteric dysfunction, or from a combination of the two. In many patients with multiple sclerosis, spinal stenosis, herniated disk, or partial traumatic damage to the spinal cord, the contribution of neural deficit to urinary incontinence can be difficult to determine.
A complete urologic and neurologic history, physical examination, and urodynamics (cystometry, urethral pressure recordings, uroflowmetry) should be performed. Ultrasound evaluation, which can accurately measure renal size and identify scarring, calculi, and hydronephrosis (obstruction or vesicoureteral reflux), is an appropriate baseline study for all patients with neuropathic lesions. Other radiologic studies (voiding cystourethrography, excretory urography, computed tomography scanning, MRI) and neurologic studies (electromyography, evoked potentials) are performed as indicated. Cystourethroscopy is not recommended as part of the routine screening evaluation; if clinically indicated, it is used to assess the integrity of the urethra and identify stricture sites, diverticula, calculi, or other anatomic abnormalities.
The following are valuable in determining the underlying cause of incontinence:
Bladder responses to progressive filling.
Sphincteric pressure profile and its response to progressive filling and the initiation of voiding.
The presence of detrusor overactivity.
Electromyographic studies of the striated urinary sphincter.
In selected patients, response to neurostimulation of the sacral roots and pudendal nerve and measurement of latencies.
Differentiation among incontinence caused by neurogenic detrusor overactivity and poor bladder compliance is a straightforward process. Significant findings include sphincteric weakness, precipitous sphincteric relaxation, and decrease in pressure, as well as a lack of electromyographic activity of the pelvic floor musculature and external sphincter.
The proper diagnosis can be achieved by establishing the integrity of the sacral root reflex arc by neurostimulation of the sacral roots, with simultaneous recording of intravesical and intraurethral pressures at the levels of the internal and the external sphincter. The extent of one cause relative to another (eg, sphincteric weakness versus detrusor overactivity) should be taken into consideration, and management should be directed toward the predominating cause of incontinence.
The management of neurogenic urinary incontinence can be challenging. The rehabilitation of the neuropathic condition and the alleviation of potentially damaging sequelae must be the guiding principles of management (see also Chapter 28—Neuropathic Bladder Disorders). Choices must be made according to the severity and potential progression of the lesion and the integrity of the system, with great care taken to prevent deterioration of the upper tracts. In patients with spinal cord injury and meningomyelocele, early treatment provides the best chance of preserving the integrity of the entire urinary system.
Failure of Storage Function
Anticholinergic agents are commonly used to treat detrusor overactivity. These medications inhibit the binding of acetylcholine to muscarinic receptors in the detrusor muscle, increasing bladder capacity and inhibiting involuntary contractions. Treatment with oxybutynin chloride (Ditropan) 5 mg three times daily, tolterodine tartrate (Detrol) 2 mg twice daily, and single-dose extended release daily formulations (Ditropan XL 10 mg and Detrol ER 4 mg) has proven to be highly effective and well tolerated. Fesoterodine fumarate (Toviaz), propiverine hydrochloride (Detrunorm), trospium chloride (Sanctura), and the more selective M3 receptor antagonists (darifenacin hydrochloride [Enablex] and solifenacin succinate [Vesicare]) are newer anticholinergic options (Andersson et al, 2009). Dosages can be increased above these levels in some patients, dependent on tolerance of adverse effects and treatment response. Common side effects include dry mouth, palpitations, constipation, nausea, or drowsiness, although newer extended-release formulations provide a reduced incidence versus immediate-release anticholinergics.
Propantheline bromide (Pro-Banthine) and imipramine hydrochloride (Tofranil) are considered second-line treatments for some patients, while the efficacy of flavoxate hydrochloride (Urispas) is unclear (Corcos et al, 2006).
Injection of botulinum-A toxin into the detrusor muscle for both children and adults who have failure of reservoir function is a promising new treatment that has demonstrated a significant increase in bladder capacity and compliance as well as symptomatic improvement for several weeks after cystoscopic injection (Chancellor, 2010). This neurotoxin binds to the presynaptic nerve endings of cholinergic neurons and leads to a temporary chemodenervation and the reduction of neural activity, as well as changes the muscarinic receptors in the bladder (Datta et al, 2010).
Failure of Sphincter Mechanism
CIC is the first line of conservative management in this group. Although such patients have very low outlet resistance, atonic bladder function may result in some retention. Most of the time, CIC every 4–6 hours avoids leakage. When CIC is not possible and the increase in intravesical pressure becomes excessive, the patient can wear pads or diapers. Pharmacotherapy has proven unsuccessful to date.
For spastic hyperreflexive male patients, this procedure can eliminate outlet resistance so that, with an external appliance or condom catheter, the bladder will remain empty (Perkash, 2007). Although many consider this procedure the easiest way to preserve the upper urinary tract, it is clearly not rehabilitative and might interfere with other treatments.
In patients with poor compliance owing to bladder wall hypertrophy or fibrosis, augmentation improves reservoir function. If the sphincteric mechanism is adequate, detubularized bowel segments can be used to expand a small contracted bladder. Usually, patients will be required to perform CIC to empty the bladder postoperatively.
Artificial Urinary Sphincter (AUS)
For patients with severe sphincteric damage and a low-pressure, large-capacity bladder, the AUS is a useful option. In males, it is applied around the bulbous urethra. When the device is deflated, the patient can void either by detrusor contraction (if some capability is preserved) or by straining and the Valsalva maneuver. A complete sphincterotomy can be performed first.
Continent Urinary Diversion
This method should be considered only with progressively deteriorating upper urinary tract function, and even then, a simple conduit is often preferable.
In selected patients with detrusor overactivity, stimulation of the sacral roots can be used to suppress the overactive detrusor. If such patients with spinal cord injury, meningomyelocele, multiple sclerosis, and other neuropathies show significant improvement after temporary testing, a permanent electrode can be placed over the most responsive root, usually S3.
Complete dorsal rhizotomy of S2–S4 extra- or intradurally effectively eliminates detrusor hyperreflexia and increases bladder capacity. Increases have been seen from a capacity of 150 or 200 mL to 600–800 mL. In patients with suprasegmental lesions and spastic upper motor neuron lesions, sacral root electrode (bladder pacemaker) implantation promotes detrusor contraction and bladder evacuation.