BLADDER AND SEXUAL FUNCTION AND DYSFUNCTION

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CHAPTER 29 BLADDER AND SEXUAL FUNCTION AND DYSFUNCTION

The autonomic nervous system is sometimes perceived by neurologists as a somewhat mysterious, even miasmic, component of the nervous system. Consequently, when autonomic dysfunction accompanies a neurological disease process, neurologists often are reluctant to discuss the autonomic symptoms with their patients or to initiate specific evaluation or treatment, preferring to cede this to specialists in other disciplines such as cardiology, gastroenterology, and urology. However, autonomic dysfunction is an integral component of a number of neurological disease processes routinely managed by neurologists, and if attention to and assessment of autonomic dysfunction are inadequate, treatment of the disease and management of the patient may be inadequate. In this chapter, bladder and sexual dysfunction are addressed with the intent of providing practical information for the practicing neurologist.

BLADDER FUNCTION

At a basic level, the bladder has two primary functions. First, it serves as an expandable storage vessel, collecting urine produced by the kidneys. Most of its time is spent in this storage mode. The second function of the bladder is to actively contract and eliminate the stored urine, typically at socially acceptable times that are consciously determined by the individual. To achieve these functions, a fine-tuned and well-orchestrated symphony of actions involving the urethral sphincter, bladder, peripheral nerves, spinal cord, brainstem, and cerebral centers must take place. Damage to any portion of this interconnected system can result in urinary dysfunction.

Neuroanatomy and Neurophysiology

Cortex

There is a tendency to focus on the spinal cord and sacral nerves when bladder function is assessed, but cortical and brainstem centers play active and very important roles in the control of bladder function.^1,² Early information regarding cerebral control of voiding was collected in studies of individuals with structural brain lesions.³^–⁵ These studies demonstrated that lesions in the anterior frontal lobe may produce disturbances in bladder control. Affected individuals were noted to experience severe, precipitous urgency without prior sensation of bladder fullness, but coordination of detrusor and sphincter muscle function during micturition remained normal. Studies of individuals after stroke have also implicated the anteromedial frontal lobe and its descending pathway, along with the basal ganglia in the production of urinary dysfunction.⁶ More recent elegant neuroimaging studies with single photon emission computed tomography (SPECT), positron emission tomography, and functional magnetic resonance imaging have revealed a more detailed pattern of a complex array of cortical centers involved with voluntary regulation and control of bladder function, including not only frontal cortex but also the cingulate cortex, parietal cortex, basal ganglia, hypothalamus, and even the cerebellum.^2,⁷

Brainstem

Direct motor control of bladder function resides in the pons. The pontine micturition center, identified by Barrington in 1925 ^8,⁹ and now bearing his name, lies in the medial dorsal pons. Stimulation of this nucleus has the dual effect of producing both contraction of the detrusor muscle and relaxation of the urethral sphincter, the latter via inhibition of Onuf’s nucleus in the sacral spinal cord, with consequent micturition.¹⁰ A second, more lateral pontine region appears to tonically stimulate Onuf’s nucleus and to thus prevent micturition by inhibiting detrusor contraction and urethral relaxation.¹¹ Sensory information regarding the state of bladder filling does not appear to come directly to these two pontine centers; rather, its path is coordinated through neurons in the periaqueductal grey matter in the mesencephalon.^2,¹²

Spinal Cord and Peripheral Nerves

Control of bladder function at the spinal cord level is dependent on both autonomic and somatic mechanisms. Parasympathetic signals reach the bladder detrusor smooth muscle via pelvic nerves that originate in the intermediolateral column of the sacral cord at the S2-S4 levels, whereas sympathetic input arises from T11-L2 spinal cord levels and arrives at the smooth muscle of the bladder neck and urethra through the hypogastric nerves. The striated muscle of the urethral sphincter is innervated by a specialized group of anterior horn cells at the S2-S4 cord levels, first described by Onufrowicz in 1899 and now called Onuf’s nucleus.¹³ Their axons travel in the pudendal nerves to reach the sphincter.

Parasympathetic stimulation results in contraction of the detrusor muscle (mediated by acetylcholine) and relaxation of urethral smooth muscle (mediated by nitric oxide) with the net result of micturition.^14,¹⁵ Sympathetic stimulation has the opposite effect. Stimulation of Onuf’s nucleus produces contraction of the striated urethral sphincter.¹⁶

Sensory information from the bladder is transmitted by several different types of neurons.^16,¹⁷ Small, unmyelinated, mechanosensitive Aδ fibers have a low activation threshold and are the principal conduit for transmitting information regarding the degree of bladder filling. Nociceptive, unmyelinated C fibers respond primarily to noxious stimuli rather than bladder distension. Finally, somatic afferents from the urethra transmit information regarding imminence of micturition.

BLADDER DYSFUNCTION

A normally functioning bladder can expand to hold 400 to 500 mL of urine before detrusor contraction is triggered and bladder pressure increases, producing a sense of the need to void.¹⁴ Damage to the nervous system can produce three basic patterns of neurogenic bladder dysfunction, described in Table 29-1.

TABLE 29-1 Patterns of Neurogenic Bladder Dysfunction

Detrusor overactivity (detrusor hyperreflexia)

Detrusor underactivity (detrusor hyporeflexia)

Detrusor-sphincter dyssynergia

As already noted, lesions affecting cerebral centers, both cortical and subcortical, may remove inhibitory influences on bladder function with consequent development of detrusor contractions at bladder volumes smaller than normal but without disturbing the coordinated contraction and relaxation of the detrusor and sphincter muscles. This has been labeled detrusor hyperreflexia, or neurogenic detrusor overactivity,¹⁸ and may prompt urinary frequency, often accompanied by a sense of urgency, that can lead to incontinence.

In contrast, lesions involving neurons in the sacral cord or processes that damage the peripheral nerves emanating from this cord level result in reduced detrusor activity, with subsequent reduced urinary frequency and excessive bladder filling. The term hyporeflexic bladder is sometimes applied to this situation. This can also lead to incontinence, but of the overflow type.

Lesions of the suprasacral spinal cord, by severing communication between pontine and sacral centers, may result in a loss of the normal coordinated reciprocal actions of the detrusor and sphincter muscles so that they contract simultaneously, producing a combination of increased pressure within the bladder and increased resistance to urine outflow from the bladder. This is called detrusor-sphincter dyssynergia.

Obstruction of urine outflow from the bladder is usually caused by nonneurological processes (prostatic hypertrophy is an example), but on occasion, dystonic contractions of the urethral sphincter can cause similar difficulty in the setting of neurological disease. Symptoms of obstruction include hesitancy in initiating micturition, reduced urine flow, and dribbling.

Diagnostic Tests

Although diagnostic testing of bladder function is usually performed by a urologist, it is important for neurologists to be familiar with the types of testing employed and the significance of the findings. Therefore, several of the most frequently used tests are discussed briefly as follows (Table 29-2).

TABLE 29-2 Diagnostic Testing of Bladder Function

Urodynamic testing

Electromyography

Ultrasonography

Urodynamic Testing

Urodynamic testing actually entails a battery of tests, the exact complement of which can vary from urologist to urologist. Uroflowmetry is a screening study in which the patient urinates into a receptacle that measures the rate at which urine is voided. A urine flow curve is generated, and a variety of measurements, including mean and maximum flow rates, can be calculated. The normal flow curve has an unbroken bell shape, whereas obstructive lesions produce flattening and elongation of the curve. The flow curve in individuals with detrusor-sphincter dyssynergia is characterized by intermittent, discontinuous flow.¹⁹

Cystometry measures detrusor pressure during both bladder filling and voiding. After catheterization, the bladder is filled at a set rate, while intravesical pressure and rectal pressure (as a measure of abdominal pressure) are continuously recorded. This recording is called a cystometrogram. Detrusor pressure is calculated by subtracting the abdominal (rectal) pressure from the intravesical pressure. In a normally functioning bladder, detrusor compliance allows filling of the bladder without a significant rise in detrusor pressure. Hyperreflexic detrusor muscle contractions produce rises in pressure that occur suddenly and involuntarily as the bladder is filling. If the pressure produced by the hyperreflexic contraction is high enough, it can overcome the urethral sphincter muscles, and incontinence ensues. If the elastic properties of the detrusor muscle and bladder wall are decreased, compliance is reduced and detrusor pressure rises as the bladder fills, triggering the need for what might be called “premature urination” before bladder filling is complete. Detrusor hyperreflexia and diminished bladder compliance reflect suprasacral neurological injury.

Electromyography

Electromyography of the pelvic floor can be performed with either surface or needle electrodes. Surface electrodes are less invasive but record lower amplitude signals and are more prone to artifacts.²⁰ The normal electromyographic sphincter pattern consists of continuous activity that ceases before detrusor contraction initiates micturition. Failure of this coordinated sphincter relaxation and detrusor contraction to occur is what constitutes detrusor-sphincter dyssynergia.

Concentric needle electromyography of the urethral sphincter can also demonstrate a pattern of denervation and reinnervation. Evidence of this can be seen in structural lesions of the cauda equina and in degenerative processes that involve Onuf’s nucleus, such as multiple-system atrophy (MSA). Additional, more detailed, clinical neurophysiological testing can also be performed at specialized centers.²⁰

Bladder Ultrasonography

The measurement of the amount of urine remaining in the bladder after voiding can be accomplished noninvasively by means of ultrasonography. A postvoid residual amount of greater than 100 mL is considered abnormal.

Specific Neurological Diseases

Stroke

Bladder dysfunction after stroke is frequently described, although specific data about incidence are difficult to pinpoint.²¹ In a review of the topic of stroke and incontinence, Brittain and colleagues²² noted that in various studies, incontinence on hospital admission had been described in 32% to 79% of stroke patients and was still present in 25% to 28% at the time of discharge. Problems with incontinence persisted in 12% to 19% even months after discharge.

The pattern of urinary difficulty differs between patients with hemispheric stroke and those with lesions in the brainstem. In individuals with hemispheric stroke, Sakakibara and colleagues ⁶ documented nocturnal urinary frequency in 36%, urge incontinence in 29%, and difficulty voiding in 25%. Urinary symptoms were more frequent in persons with frontal lobe infarcts. Urodynamic testing in symptomatic patients demonstrated detrusor hyperreflexia in 68%, detrusor-sphincter dyssynergia in 14%, and uninhibited sphincter relaxation in 36%.

In a different group of patients after acute brainstem stroke, urodynamic studies showed detrusor hyperreflexia in 73%, low compliance bladder in 9%, atonic bladder in 27%, detrusor-sphincter dyssynergia in 45%, and uninhibited sphincter relaxation in 27%.²³ Lesions producing bladder dysfunction involved either the dorsolateral or medial pons.

Thus, as expected, patients with stroke, whether hemispheric or brainstem, experience predominantly overactive or irritable bladder symptoms, although obstructive symptoms, including urinary retention, may also develop.^23,²⁴ Large infarct size, aphasia, cognitive impairment, and functional disability are associated with increased risk of urinary incontinence after stroke.²⁵ Multiple infarcts, especially if bilateral, also predispose to urinary abnormalities after stroke.²⁶ Because of the variability in urinary dysfunction that may appear after a stroke, urodynamic testing is invaluable in documenting the specific nature of the dysfunction. Specific treatment can then be tailored to the documented deficit.

Parkinson’s Disease

Urinary symptoms are a frequent source of difficulty for individuals with Parkinson’s disease. Reported frequencies of urinary dysfunction in Parkinson’s disease show considerable variability, ranging from 36% to 90%.²⁷^–³⁰ Hobson and colleagues,²⁹ comparing a community-based sample of patients with Parkinson’s disease with a similar-aged healthy elderly control group, discovered that the relative risk for bladder symptoms in the group with Parkinson’s disease was more than twice that of the control group. Some^27,^28,³¹^–³³ but not all²⁹ studies have found a correlation between disease duration and severity and the presence of urinary symptoms. Irritative symptoms, such as frequency, urgency, and nocturia, are most common,^27,^28,^30,^34,³⁵ but obstructive symptoms may also be reported.

The most frequent finding on urodynamic testing in individuals with Parkinson’s disease is detrusor hyperreflexia. Studies have revealed detrusor hyperreflexia to be present in 45% to 100% of urologically symptomatic patients with Parkinson’s disease.³³^–³⁶ It is important to remember, however, that obstructive uropathies, such as prostatic hypertrophy, can be superimposed on detrusor hyperreflexia. In these instances, urodynamic testing can be especially helpful.

Urethral sphincter dysfunction may also develop in patients with Parkinson’s disease. Delayed relaxation of the sphincter on initiation of voiding, termed sphincter bradykinesia, has been reported in 11% to 42% of such patients.^32,^35,³⁷ This phenomenon may create an obstructive pattern, characterized by a reduced flow rate. Inability to relax the perineal muscles on initiation of micturition has also been identified in the setting of Parkinson’s disease.³⁸

The role of dopaminergic mechanisms in the production of urinary dysfunction in Parkinson’s disease has been the focus of research interest. In rats with unilateral 6-hydroxydopamine–induced lesions of the nigrostriatal pathway, bladder capacity was documented to be reduced and could be increased with administration of the dopamine D₁/D₅ receptor agonist SKF38393.³⁹ In contrast, a D₂/D₃/D₄ receptor agonist, quinpirole, reduced bladder capacity. In monkeys rendered parkinsonian by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) injection, the same pattern was evident in that the D₂ agonist bromocriptine excited the micturition reflex, whereas the mixed D₁/D₂ agonist pergolide inhibited the reflex.⁴⁰ Improvement in urinary symptoms has also been reported in humans whose treatment switched from bromocriptine to pergolide.⁴¹

Multiple-System Atrophy

Autonomic dysfunction is one of the basic clinical features of MSA. Orthostatic hypotension and genitourinary dysfunction are especially likely to develop. In contrast to Parkinson’s disease, urinary dysfunction in MSA tends to develop earlier in the course of the disease process, sometimes appearing even before the motor features ^31,⁴²; it is also more pervasively present. In a study by Stocchi and colleagues,³⁸ 100% of patients with MSA demonstrated some abnormality on urodynamic testing, whereas abnormalities were noted in only 63% of subjects with Parkinson’s disease.

Urodynamic studies can be very useful in characterizing the nature of bladder dysfunction in MSA.⁴³ A combination of detrusor hyperreflexia and impaired urethral sphincter function often produces a pattern of prominent urinary frequency and urgency, often accompanied by urge incontinence. Although this can also occur in Parkinson’s disease, it is typically a feature of only advanced Parkinson’s disease, whereas it can develop much earlier in the course of MSA. Urinary retention is also considerably more common in MSA than in Parkinson’s disease.^31,⁴⁴

Differentiating individuals with MSA from those with Parkinson’s disease is of very practical importance from the urological standpoint, because patients with MSA who undergo surgery for prostatic hypertrophy are at especially high risk for developing urinary incontinence as a complication of the procedure. Thus, medical management is preferable to surgical management of prostatic hypertrophy in individuals with MSA.³¹

Multiple Sclerosis

Symptoms of autonomic dysfunction may be present in almost 80% of patients with multiple sclerosis.⁴⁵ Urinary symptoms are the most common, present in 65% of the 63 patients evaluated by McDougall and McLeod. In their study, urgency and frequency were especially common, and urinary incontinence was reported by more than 30% of patients.

Detrusor-sphincter dyssynergia, as a consequence of spinal cord involvement, is the most common urodynamic finding in multiple sclerosis, reported in 15% to 20% of affected individuals.⁴⁶ However, because multiple sclerosis can affect all levels of the central nervous system, some patients show evidence of detrusor hyperreflexia as a result of involvement of suprapontine cerebral pathways.⁴⁶ Impaired voiding with hesitancy, interrupted urinary flow, and incomplete voiding can also be present.⁴⁷

Urinary symptoms increase in frequency and severity in tandem with disease severity and duration.⁴⁸^–⁵⁰ They are most evident in individuals with secondary progressive multiple sclerosis.⁴⁵