ABSTRACT
Overactive bladder (OAB) is defined as a symptom syndrome characterized by urgency, with or without urge incontinence, usually with frequency and nocturia. Other descriptors for this symptom complex are the urge syndrome or urgency-frequency syndrome.1 Patients with OAB represent a substantial proportion of patients with urinary symptomatology. One-third of them suffer from incontinence.2 As compared with women with effort-related urinary incontinence, women with urgency-related incontinence have a poor overall quality of life, perhaps related to both the volume of urine lost as well as the unpredictable nature of the leakage.3-5
Multiple classes of pharmacologic agents are potentially useful (meaning that they have a mechanism which is plausible on paper) to clinically decrease bladder activation and contractility or decrease sensation and thereby treat OAB. In the United States, at least, only the antimuscarinics have been “approved” for use in the treatment of OAB, implying that a proof of principle has been satisfied with respect to therapeutic response. Some6 have argued that, although statistically significant, the differences between antimuscarinic drugs and placebo in terms of treatment results are small, and may be of questionable clinical significance, especially in view
of the fact that the differences between active drugs and placebo in terms of tolerability seem to be greater. The Committee on Pharmacology at the International Consultation on Incontinence (ICI), utilizing somewhat different methodology to assess clinical effectiveness7 has made recommendations for the treatment of overactive bladder, finding the antimuscarinic drugs to be clinically useful. The ICI committee did have the advantage, in its latest report, of more contemporary data than were available to Herbison et al.,6
and data which assessed not only individual symptoms and urodynamic findings but also quality of life instruments and global impression scales. Antimuscarinic drugs remain the first line pharmacological treatment for overactive bladder. There is no reason to expect these agents to cure the underlying disturbance, the pathophysiology of which, though widely discussed, has not been firmly established, except in the case of certain neurologic injuries or diseases, and, even then, the sensory activators, neural paths, and efferent mechanisms are still somewhat disputed.8
