As defined by the International Continence Society, overactive bladder (OAB) is the condition in which a patient has symptoms of urgency with or without urge incontinence, usually with frequency and nocturia, in the absence of infection, metabolic disturbance, or other pathologic factors that would account for these symptoms. It is a symptomatic diagnosis and therefore does not require the performance of urodynamic testing or cystometry for confirmation. Urgency is defined as the feeling that the patient must void immediately for fear of losing urine, and frequency is defined as greater than 10 micturitions in a 24-hour period. Urge incontinence describes involuntary loss of urine associated with an urgent, strong desire to void.

The term “detrusor overactivity” (unstable bladder) is more restrictive and describes an OAB caused by detrusor contractions documented by cystometrogram. Detrusor overactivity occurs when the bladder contracts spontaneously, or on provocation, during bladder filling while the patient is attempting to inhibit micturition. Detrusor overactivity is diagnosed during provocative cystometry when one of the following conditions occurs: a true detrusor pressure rise of 15 cmH₂O (motor urge incontinence) or a true detrusor pressure rise of less than 15 cmH₂O in the presence of urgency or urge incontinence (sensory urge incontinence) (1). Subthreshold detrusor contractions of less than 15 cm H₂O may have clinical significance and have been shown to cause urinary incontinence in 10% and urgency in 85% of patients (2).

Additionally, a urodynamic diagnosis associated with the symptom of urge incontinence in a frail elderly patient is detrusor hyperactivity with impaired contractility (DHIC). These patients have involuntary detrusor contractions causing incontinence but are unable to empty their bladders completely, leaving a large postvoid residual (3). A pressure rise during filling may represent decreased bladder compliance or insufficient time to accommodate the increase in volume because cystometry is time dependent (4), and this would not be considered as detrusor overactivity in this context.

Detrusor hyperreflexia is detrusor overactivity secondary to a known neurologic abnormality (1). The term “neurogenic bladder” is reserved for spinal cord injuries and other similar defects and their impact on bladder function.

Incorrect synonyms that have been applied to OAB include bladder dyssynergia and vesical instability. These terms should no longer be used.

The National Overactive Bladder Evaluation (NOBLE) program estimated the overall prevalence of OAB as 16.9% of women and 16.0% of men, a rate that corresponds to 33.3 million adult Americans, with an impact on quality of life equal to that of urinary incontinence (5,6). The occurrence of involuntary detrusor contractions in infancy is a normal state for bladder emptying and is later controlled by the development of cortical inhibition of reflex bladder activity. Farrar et al (7) described the prevalence of OAB as 8% to 50%, depending on age distribution. In more than 2,000 women studied by Abrams (8), OAB occurred in 38% of those 65 years of age or older and in 27% of those younger than 65 years of age. In institutionalized women, the incidence of urinary incontinence secondary to OAB is greater than 80% (9). Thus, the prevalence of OAB is greatest at the extremes of life; OAB has a 5% to 10% occurrence in premenopausal patients,
increasing to as much as 38% in elderly patients and perhaps to more than 80% in institutionalized incontinent elderly patients.

Although the severity of OAB has been measured by outcome variables such as micturition frequency or quantity of urine lost, the impact on quality of life must also be measured in terms of physical and psychological functioning. Psychosocial complications included disturbed sleep, impaired mobility and work productivity, isolation and depression, impaired domestic and sexual functioning, and diminished quality of life (10).

The symptoms of OAB include urgency, frequency (greater than 10 micturitions in a 24-hour period), urge incontinence, and nocturia (two times or more). There can also be a history of childhood nocturnal enuresis in some patients (11). OAB may coexist with genuine stress incontinence, and stressful activity may trigger a detrusor contraction causing urge incontinence. In 100 women with the urodynamic diagnosis of detrusor overactivity, Wiskind et al (12) reported that although 86% of patients had symptoms of urge incontinence, 76% also complained of stress incontinence. Sand et al (13) reported on 188 incontinent women, and of those reporting only stress incontinence, 34.9% had detrusor overactivity. Only 32.6% of patients reporting both urge and stress incontinence had detrusor overactivity.

Because the symptoms of OAB overlap with those of other lower urinary tract conditions, a number of other diagnoses must be entertained. Table 11.1 lists the differential diagnosis for these symptoms. A special word must be written about urethral instability, which tends to be rather poorly defined. Wise et al (14) investigated the prevalence and significance of urethral instability in a group of women with OAB. This occurred in 42% of patients with OAB and was strongly associated with the sequence of relaxation of the urethra before unprovoked detrusor contraction. Women with OAB and a stable urethra exhibited primary contraction of the detrusor, whereas the symptom of stress incontinence was more common in women with urethral instability. The investigators postulated that women with OAB should be divided into two groups: those with and those without urethral instability, the latter group possibly benefiting from α-agonist therapy. In addition, Petros and Ulmsten (15) found that provocative urethrocystometry revealed a rise in detrusor pressure followed by a fall in urethral pressure, both preceded by urge symptoms. They concluded that urethral instability, OAB, and urge incontinence were different manifestations of a prematurely activated micturition reflex. Urethral instability may not be a separate entity but a part of urine loss associated with urge.

Table 11.2 lists the etiologies of OAB. Neurologic diseases (multiple sclerosis, cerebrovascular disease, parkinsonism, Alzheimer’s disease), local bladder and urethral irritants (cystitis, foreign bodies, tumors), outflow obstruction (severe cystocele or vaginal vault prolapse), and medications (parasympathomimetics) must be considered as etiologies. Most cases, however, apart from those in very young or elderly patients, are idiopathic in nature. Del Carro et al (16) compared women with idiopathic OAB with age-matched controls using subtracted cystometry and anal sphincter electromyography sacral reflex analysis along with other neurologic tests using evoked potentials. All patients had normal neurophysiologic tests, and there was no significant difference between patients and controls. Because women with OAB do not appear to have either clinical or subclinical damage of central sensory or motor pathways, other investigators have put forth their theories regarding intrinsic bladder abnormalities. The pathophysiology of OAB may be principally neurogenic, myogenic, obstructive, or idiopathic.

All patients with OAB symptoms should undergo a basic evaluation, as outlined in the guidelines proposed by the Agency on Health Care Policy and Research (30), that includes a history, physical examination, measurement of postvoid residual volume, and urinalysis. Any risk factors that are associated with urinary incontinence should be identified and attempts made to modify them.

The classic history of OAB is that of a strong urge to void or a voiding frequency of greater than 10 micturitions in a 24-hour period that can be associated with sudden urine loss. The history should also include the following elements:

The physical examination should include the following: