Update on the Pharmacologic Management of Overactive Bladder: The Present and the Future

Pamela Ellsworth; Eileen Kirshenbaum


Urol Nurs. 2010;30(1):29-39. 

In This Article

Management of Refractory OAB

Despite the many antimuscarinic agents currently available and the use of behavioral therapy, some individuals will remain refractory to therapy and/or will not tolerate antimuscarinic therapy. Currently, neuromodulation is the only FDA-approved second-line therapy for the management OAB. Detrusor injection of botulinum toxin remains investigational in the treatment of OAB.

Neuromodulation is thought to treat OAB symptoms by restoring the balance between the inhibitory and excitatory control systems at various sites in both the peripheral and central nervous systems (Craggs & McFarlane, 1999; Schmidt, 1986; Van der Pal, Heesakkers, & Bemelmans, 2006). A variety of forms of neuro modulation have been used, including intravesical stimulation, pudendal nerve stimulation, sacral nerve stimulation, and tibial nerve stimulation (Fandel & Tanagho, 2005; van Balken, Vergunst, & Bemelmans, 2004). Urgent® PC (Uroplasty, Inc., Minnetonka, MN) is a percutaneous tibial nerve stimulation therapy that is FDA-approved for OAB. Sacral nerve stimulation (InterStim® Therapy Sacral Nerve Stimulation, Medtronic, Minneapolis, MN) is approved by the FDA and is the most common form of neuromodulation used in the treatment of OAB symptoms refractory to pharm acologic and behavioral therapy. The technique of sacral nerve modulation involves the initial placement of an external lead that allows for test stimulation. Individuals who respond favorably to the test stimulation undergo placement of the surgically implanted system. Additional information on this treatment modality can be found at www.seekwellness.com/incontinence/interstim.htm and www.medtronic.com/your-health/overactive-bladder/

Although not currently a p p roved by the FDA, injection of botulinum toxin into the bladder is being used off label in the management of OAB refractory to standard therapies (Sahai, Khan, & Dasgupta, 2007). Botulinum toxin is a very potent neurotoxin derived from the anaerobic bacterium clostridium botulinum. Botulinum toxin A and B are currently marketed under the trade names of Botox® ( Allergan, Irvine, CA) and Dysport® ( The Center for Applied Microbiology and Research [CAMR], Ipsen Biopharm, Ltd.), respectively. Botulinum toxin selectively blocks the release of acetylcholine from the nerve endings.

A review of the literature to compare intravesical botulinum toxin injection with other tre a tments for OAB (Duthie, Wilson, Herbison, & Wilson, 2007) concluded that for the most part, botulinum toxin was superior to placebo in outcomes, such as UI episodes, bladder capacity, maximum detrusor pressure, and QOL. Low doses of botulinum toxin (100 U to 150 U) appeare d to have beneficial effects, but higher doses (300 U) may have been more effective. Moreover, effects of botulinum toxin exceeded those of intravesical resiniferatoxin (an investigational agent) (Duthie et al., 2007).


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