Urinary and Sexual Dysfunction


9	Urinary and Sexual Dysfunction

The complex neural mechanisms involved in bladder regulation make this process sensitive to a wide variety of neurologic diseases affecting the central and peripheral nervous systems, including but not limited to stroke, dementia, Parkinson disease, multiple sclerosis (MS), and diabetes. Understanding the anatomy and physiology of the normal bladder is important for both diagnosis and management of impaired bladder control.

BLADDER CONTINENCE

ANATOMY AND PHYSIOLOGY

Bladder control is maintained at different levels of the nervous system and involves sensory pathways as well as voluntary and involuntary motor pathways. Several neuroanatomic connections important for bladder control create “circuits” with key components located in the brain, spinal cord, and peripheral nerve ganglia. These neural circuits coordinate the activity of smooth muscle (involuntary control of the bladder and urethra) and striated muscle (voluntary control of the external urethral sphincter) leading to urinary storage or micturition (voiding) (Fig. 9-1).

Voluntary micturition is controlled by a circuit connecting the dorsomedial frontal lobes to the medial (M) region of the pontine micturition center (PMC). Through learned behavior, the frontal lobes provide volitional control of micturition by initiating a decrease in urethral pressure. This is followed by increased contraction of the detrusor muscle, leading to voiding. The nearby lateral (L) region of the PMC, on the other hand, produces a powerful contraction of the urethral sphincter (promoting storage).

Urinary storage and voiding is also controlled by reflexes at the spinal level, which affect the PMC signaling. For example, afferent signals of bladder distention trigger sympathetic outflow in the hypogastric and pudendal nerves to promote urethral constriction and continence. During elimination of urine, efferent firing in the pelvic nerves triggers the spinobulbospinal reflex that passes through the PMC and promotes parasympathetic outflow to the bladder and urethra, allowing for bladder emptying (Fig. 9-1).

Lesions affecting the coordinated effort of the PMC produce a loss of inhibitory control over spinal reflexes. Then, when the bladder becomes distended, the micturition reflex is automatically activated at the spinal level, without the patient’s awareness or control, and detrusor hyperreflexia (DH) and incontinence occur. Likewise, lesions affecting the peripheral input and spinal reflexes can lead to a variety of urinary symptoms including urinary retention, incontinence, hesitancy, and overflow urinary incontinence.

DIAGNOSTIC EVALUATION

The first objective in the evaluation of bladder dysfunction is to determine if the problem is neurologic or not and, if it is, localize the lesion causing the urinary difficulties. A detailed history is essential. It is important to obtain information about initiation; voiding problems such as frequency, stream characteristics, urine volume, fullness, and urgency; effects of posture, cough, Valsalva maneuver, and medications; and associated bowel and sexual dysfunction.

Thorough physical and neurologic examinations are necessary. The examiner seeks signs of frontal lobe dysfunction, parkinsonian features, a sensory level, myelopathy, and so forth. Laboratory evaluation includes urinalysis to rule out infection. Measurement of the post-void residual (PVR) by bladder ultrasound or catheterization is important in the characterization of bladder dysfunction. The PVR is the residual volume in the bladder after voiding. A normal PVR is less than 50 mL. Urodynamic studies can clarify the characteristics of incontinence, determine the underlying neurologic abnormality, categorize vesicourethral dysfunction, and provide a basis for appropriate therapy.

Some urodynamic studies include the following:

•Cystometry: Provides information about bladder compliance, capacity, and volume at first sensation and at urge to void; voiding pressure; and the presence of uninhibited detrusor contractions.

•Cystourethroscopy: Assesses the integrity of the lower urinary system and identifies important urethral and bladder lesions.

•Neurophysiologic studies: These include electromyography (EMG) of the sphincter and pelvic floor muscles. Urodynamic findings in various types of neurogenic bladder dysfunctions are listed in Table 9-1.

KEY POINTS

●The M region in the pons is the site of activation of micturition.

●History and a complete neurologic examination are important in the evaluation of bladder incontinence.

●PVR should be less than 50 mL. Increased PVR implies poor bladder emptying. Sphincter dyssynergia and atonic bladder are common neurogenic causes of elevated PVR.

TABLE 9-1. Urodynamic Findings in Neurogenic Bladder
Type	Capacity	Compliance	Others
Spastic bladder	Decreased	Reduced	Uninhibited detrusor contractions
Atonic bladder	Increased	Increased	Low voiding pressure and flow rate

CLASSIFICATION

Based on the patient’s symptoms, urinary incontinence can be classified as follows:

Urge incontinence is an involuntary loss of urine associated with a strong desire to void (urgency), usually associated with detrusor instability (DI). When the DI is the result of a neurologic problem, the term detrusor hyperreflexia is used and its clinical expression is a spastic bladder. DH is common in patients with strokes, frontal lobe dysfunction, suprasacral spinal cord lesions, and MS. It is usually accompanied by detrusor-sphincter dyssynergia (DSD), which is inappropriate contraction of the external sphincter with detrusor contraction. This can result in urinary retention, vesicoureteral reflux, and subsequent renal damage.

Stress incontinence is an involuntary loss of urine during coughing, sneezing, laughing, or other physical activities that increase intraabdominal pressure (in the absence of detrusor contraction or an overdistended bladder). This is common in multiparous women who have cystoceles or weakened muscles of the pelvic floor. Other causes include urethral hypermobility, significant displacement of the urethra and bladder neck, and intrinsic urethral sphincter deficiency caused by congenital weakness in patients with myelomeningocele or epispadias. This can also be seen in patients who have had prostatectomy, local trauma, or radiation.

Mixed incontinence is a combination of urge and stress incontinence.

Overflow incontinence is an involuntary loss of urine associated with overdistention of the bladder, typically reflecting a lower motor neuron problem. Patients report constant dribbling and urge or stress incontinence symptoms. Causes of overflow incontinence include an underactive or acontractile (atonic) detrusor because of drugs, diabetic neuropathy, lower spinal cord injury or radical pelvic surgery (interrupting innervation to the detrusor muscle), or urethral or bladder outlet obstruction, leading to overdistention and overflow.

KEY POINTS

●Spastic bladder implies an upper motor neuron problem caused by lesions involving the frontal lobes, pons, or suprasacral spinal cord. Symptoms include incontinence with urgency and frequency. Urodynamics show decreased capacity and reduced compliance.

●Stress incontinence is rarely a neurologic problem.

●Atonic bladder implies a lower motor neuron lesion at the level of the conus medullaris, cauda equina, or sacral plexus; or it may reflect peripheral nerve dysfunction. It is characterized by overflow incontinence and increased capacity and compliance.

●Sphincter dyssynergia produces an increased PVR, with fluctuating voiding pressures and varying flow rate.

●A small PVR is good; a large PVR with a spastic or atonic bladder is not. It can cause increased intrabladder pressure with deleterious effects on the ureters and kidneys.

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