The bladder serves two main functions, to store and expel urine. Control of the voiding mechanism requires an intact neuromuscular system, from higher cortical centres to the detrusor and sphincter muscles.

Structurally, the bladder muscle or detrusor consists of a network of interdigitating smooth muscle fibres which converge into three layers at the bladder neck. This muscle network, accompanied by the musculature derived from the ureters and trigone, forms the autonomic internal sphincter. The external sphincter, located just distal to the prostate gland in the male and at the level of the mid-urethra in the female, is a striated somatic muscle supplied by the pudendal nerve (S2–4). The motor supply of the bladder is largely autonomic, with the sympathetic fibres (T8–L4) producing relaxation of the detrusor and contraction of the internal sphincter (by way of &agr;-adrenergic receptors located at the bladder neck). The parasympathetic nerves (S2–4) supply the detrusor and initiate contraction. The hypogastric and pelvic nerves are sensory to both the bladder mucosa and the detrusor muscle spindles, which detect bladder distension (Fig. 1) 1541.

As the bladder fills, sensory fibres in the bladder wall send impulses to the sacral nerve roots. These discharges travel up the spinal column to the detrusor nucleus in the brain-stem (dorsolateral tegmental nucleus of the pons). Modifying inhibitory influences from the cortex, basal nuclei, and cerebellum determine the timing of voiding. When urination is initiated, the detrusor nucleus co-ordinates micturition by causing synchronized inhibitory sympathetic discharge via the thoracolumbar outflow to the internal sphincter, inhibitory somatic discharge via the pudendal nerve to the external sphincter, and excitatory discharge via the sacral parasympathetic nerves to the detrusor muscle. This sequence results in relaxation of the sphincters with simultaneous bladder contraction, which should allow free flow of urine through a normal urethra.

Disease anywhere between the cerebral cortex and the distal urethra can give rise to voiding problems. Such diversity of site and type of pathology should be borne in mind when taking a history from these patients.

General questioning about the desire to void, frequency, urgency, hesitancy, dribbling, incontinence, nocturia, control, and quality of the stream is important. The past medical history may show evidence of prior urological surgery or neurological disease. A careful review of all organ systems, with special attention to neurological and bowel dysfunction, should be performed.

The abdomen should be examined and bladder distension assessed. The lower back should be inspected for evidence of spina bifida occult and perineal sensory function should be noted. Rectal and vaginal examinations will reveal the presence of masses and sphincter tone. The bulbocavernosus reflex (S2–4), a contraction of the anal sphincter upon squeezing the glans penis or the clitoris, is elicited; a lower extremity neurological examination is also required.

All parts of the urinary tract are dependent on one another for optimal function. Evaluation of bladder pathology requires knowledge of kidneys, ureters, bladder, prostate, and urethra. Although the results of the history and physical examination will direct the course and sequence of the evaluation, most patients will require some combination of the following tests.

High pressure within the bladder can produce breakdown of the valvular ureterovesical junction, with subsequent transmission of this pressure to the kidney. This may result in hydronephrosis, pyelonephritis, and renal dysfunction. Renal ultrasound or intravenous urography may delineate hydronephrosis and serum creatinine may reflect a deterioration in renal function.

The bladder is filled with radiographic contrast material via a catheter and the patient is observed fluoroscopically while voiding. This study provides information about the ability of the internal urethral sphincter to relax, the degree of trabeculation of the bladder wall (a reflection of intravesical pressure), and the presence of an anatomical obstruction such as a urethral stricture.

These attempt to reproduce the patient's symptoms while measuring various physiological parameters of bladder function, thereby identifying the pathological process. There are four components to simple urodynamics: flowmetry, postvoid residual, cystometry, and electromyography. While the patient voids, the rate and pattern of the stream are recorded (flowmetry). This reflects the strength of the detrusor muscle and any outflow obstruction (Fig. 2) 1542. After the patient has voided, a catheter is passed and the postvoid residual urine volume is recorded. This part of the study provides a quantitative estimate of a patient's ability to empty his bladder; however it provides no information about causative pathology.

Cystometry involves filling of the bladder with water or carbon dioxide through a catheter. The patient then reports the symptoms that he experiences as his bladder fills. Simultaneous measurement of bladder and abdominal pressure allows assessment of bladder sensation, capacity, and the ability to generate and suppress a detrusor contraction (Fig. 3) 1543. The electrical activity of the external sphincter may also be monitored during cystometry and voiding (electromyography). This allows evaluation of the co-ordination of the voiding mechanism.

Information about the prostate and urethra obtained from the voiding cystourethrogram may be supplemented by cystoscopy. Cystoscopic visualization of the lower urinary tract is also important to rule out other bladder disease, such as tumours or stones, that may have given rise to the patient's symptoms.

Although many classification systems for bladder dysfunction have been proposed, none is entirely satisfactory. The simplest and most convenient is the functional classification, since it depends on observable bladder characteristics rather than theoretical and often controversial mechanisms of bladder pathology. This system divides bladder dysfunction into failure to store and failure to empty. It is based on the following concepts. First, for a bladder to store urine it must have a normal compliance, no involuntary contractions, and a closed outlet at rest and during periods of increased intra-abdominal pressure. Second, for a bladder to empty it must have a sufficient detrusor contraction, sphincteric relaxation, and an unobstructed urethra. Patients often have problems with more than one component of bladder function and therefore fall into more than one category. However a combination of terms that will allow a rational approach to treatment can usually be derived.

The most common cause of detrusor instability (involuntary, unsuppressible detrusor contraction) is decreased inhibition of the detrusor nucleus due to cortical atrophy. This problem is seen in conditions such as stroke, dementia, or Parkinson's disease (Fig. 3(b)) 1543. Before making this diagnosis, it is important to rule out other bladder pathology, such as infection, tumours, or stones, which may cause increased detrusor irritability and mimic a hyper-reflexic bladder. Treatment is directed towards decreasing bladder contractility with anticholinergics (propantheline) and smooth muscle relaxants (oxybutynin). In severe cases which are intractable to medication, bladder augmentation with a bowel patch may be indicated.

Stress incontinence is the involuntary loss of urine associated with an elevation of intra-abdominal pressure, caused by events such as coughing, sneezing, or lifting heavy objects. This is found most commonly in females and is due to hypermobility of the proximal urethra and urethrovesical junction. Such hypermobililty results in the failure to transmit equally increases in intra-abdominal pressure to both the bladder and urethra, leading to leakage of urine. It is most common in females. The most probable cause of stress incontinence is hypermobility of the urethrovesical junction, which results in failure of transmission of increases in intra-abdominal pressure equally to both the urethra and bladder. Treatment consists of either transabdominal or transvaginal suspension of the urethrovesical junction.

Failure to store urine due to outlet pathology is unusual in males. The most common, albeit rare cause is injury to the external sphincter at the time of transurethral or open surgical resection of the prostate. The most effective treatment is placement of an artificial sphincter.

The most common causes of a large capacity flaccid hypotonic bladder are spinal shock after a cord injury, sacral cord pathology, subacute combined degeneration of the cord, tabes dorsalis, peripheral neuropathy (as in diabetes mellitus), and bladder decompensation secondary to chronic distension (Fig. 3(c)) 1543. Therapy is directed towards decreasing the postvoid residual volume by frequent timed voiding or intermittent catheterization. Detrusor contraction may be augmented by administration of a cholinergic agent such as betanechol, although such treatment is frequently unsuccessful.

Patients with complex neurological dysfunction occasionally demonstrate signs of both failure to store urine and failure to empty the bladder. This problem is common in patients with detrusor sphincter dys-synergia following suprasacral spinal cord injuries, in patients with certain types of myelodysplasia, and in multiple sclerosis. The usual problem is an unstable detrusor (failure to store) combined with a dysco-ordinate non-relaxation of the external sphincter (failure to empty) when voiding is initiated. Detrusor sphincter dys-synergia is a result of interruption of neural pathways from the sacral cord to the detrusor nucleus, interfering with the co-ordination of the somatic and autonomic components of micturition. This lack of co-ordination can result in high pressure voiding against an intermittently closed external sphincter. If the condition is not treated it may lead to vesicoureteric reflux, hydronephrosis, pyelonephritis, and renal damage. Initial therapy consists of decreasing bladder contractility with anticholinergics such as propanthyline and smooth muscle relaxants (oxybutynin). Where such treatment proves insufficient bladder outlet resistence may be reduced by a combination of bladder neck relaxants (&agr;-blockers such as phenoxybenzamine or prazosin) and intermittent catheterization. External sphincterotomy (destruction of the external sphincter) with condom catheter drainage is an option in males with irreversible neurological defects. This procedure would not be performed in females, since it results in uncontrollable incontinence.

Patients with bladder outlet obstruction (failure to empty) such as those with benign prostatic hyperplasia or urethral strictures, often develop detrusor instability (failure to store). Seventy-five per cent of patients experience an improvement in their symptoms when the obstruction is relieved. Bladder relaxants should not be used prior to treatment of the obstruction as they may precipitate urinary retention.

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