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

Pamela Ellsworth; Eileen Kirshenbaum

Disclosures

Urol Nurs. 2010;30(1):29-39. 

In This Article

Pathophysiology of OAB

The exact cause(s) of idiopathic OAB is not well defined. Several theories regarding the etiology of OAB have been proposed, including neurogenic, myogenic, combined, and unknown etiologies. Factors such as decreased suprapontine inhibition, damaged axonal pathways in the spinal cord, increased lower urinary tract afferent input, loss of peripheral inhibition, and enhancement of excitatory neurotransmission in the micturition reflex pathways may account for neurogenic etiologies (de Groat, 1997).

The myogenic theory is based on the concept that partial denervation of the bladder, which may occur in individuals with bladder outlet obstruction and increased intravesical pressure, may alter the smooth muscle leading to increased excitability and an increased ability for activity to spread among the smooth muscle cells. This increased excitability and transmission among smooth muscle cells leads to "micromotions" of the detrusor smooth muscle, increasing intravesical pressure and stimulation of afferent receptors in the detrusor smooth muscle. These afferent receptors provide feedback to the central nervous system (CNS) and cause sensations associated with OAB Turner & Brading, 1997; Wein & Rackley, 2006).

More recently, the urothelium has been identified as a possible factor in the development of OAB. Acetylcholine may be released from the urothelium in greater quantities, or the sensory receptors in the urothelium may be more sensitive to the acetylcholine released, thus increasing afferent activity to the CNS, creating the sensation of urgency (de G roat, 2004; Wein & Rackley, 2006). Finally, there may be a combined etiology secondary to an abnormal leak of acetylcholine from the efferent nerve fibers that causes micromotions in the bladder smooth muscle, which in turn stimulates the CNS, leading to the sensation of urgency (Andersson, 2004).

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