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The bladder, in concert with the urethra and the pelvic floor, is responsible for storage and periodic expulsion of urine. The integrated function of these components of the lower urinary tract (LUT) is dependent on a complex control system in the brain, spinal cord and peripheral ganglia, and on local regulatory factors (de Groat, 2006). Dysfunction of the central nervous control systems or of the components of the LUT can produce insufficient voiding and retention of urine, or different types of urinary incontinence (mainly urgency and stress incontinence), or the symptom complex of the “overactive bladder” (OAB), characterized by urgency, frequency with or without urgency incontinence, often with nocturia (Abrams et al, 2002).

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Pharmacologic treatment of urinary incontinence and LUT symptoms (LUTSs) including OAB is the main option, and several drugs with different modes and sites of action have been tried (Andersson, 2007; Andersson and Wein, 2004; Andersson et al, 2009a, 2009b; Ouslander, 2004; Zinner et al, 2004). However, to be able to optimize treatment, knowledge about the mechanisms of micturition and of the targets for treatment is necessary. Theoretically, failure to store urine can be improved by agents that decrease detrusor activity and increase bladder capacity, and/or increase outlet resistance.

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In this chapter, a brief review is given of the normal nervous control of the LUT and of some therapeutic principles used in the treatment of urinary incontinence.

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Normal micturition occurs in response to afferent signals from the LUT (Birder et al, 2010; de Groat, 2006; Fowler et al, 2008). Both bladder filling and voiding are controlled by neural circuits in the brain, spinal cord, and peripheral ganglia. These circuits coordinate the activity of the smooth muscle in the detrusor and urethra with that of the striated muscles in the urethral sphincter and pelvic floor. Suprapontine influences are believed to act as on–off switches to shift the LUT between the two modes of operation: storage and elimination. In adults, urine storage and voiding are under voluntary control and depend upon learned behavior. In infants, however, these switching mechanisms function in a reflex manner to produce involuntary voiding. In adults, injuries or diseases of the central nervous system (CNS) can disrupt the voluntary control of micturition and cause the reemergence of reflex micturition, resulting in OAB and detrusor overactivity (DO). Because of the complexity of the CNS control of the LUT, OAB and DO can occur as a result of a variety of neurological disorders as well as changes in the peripheral innervation and smooth and skeletal muscle components (Andersson and Arner 2004; Andersson and Wein, 2004).

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Filling of the bladder and voiding involve a complex pattern of afferent and efferent signaling in parasympathetic (pelvic nerves), sympathetic (hypogastric nerves), and somatic (pudendal nerves) pathways. These pathways constitute reflexes, which either keep the bladder in a relaxed ...

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