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      Overactive bladder

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          Overactive bladder (OAB) is known to affect millions of people worldwide, with a subsequent deleterious impact on the quality of life. The clinical diagnosis of OAB requires, at a minimum, a meticulous history, physical examination, and urinalysis. The American Urological Association views OAB as a symptom complex, not a life-threatening disease, and recommends conservative measures and behavioral therapies as first-line treatment, including bladder training, bladder control strategies, pelvic floor muscle training, and fluid management. Current medical management approved by the US FDA include anti-muscarinics and beta3-agonists. Anti-muscarincs should be avoided in patients with narrow-angle glaucoma, and used with extreme caution in patients with impaired gastric emptying or a history of urinary retention. Surgical interventions may be offered, if second-line therapy using medications is not successful in obtaining adequate symptom control of OAB, and the patient is motivated and healthy. In uncomplicated patients, OAB may be clinically diagnosed and treated with conservative measures; however, the armamentarium for the diagnosis and treatment continues to expand for more complicated patients.

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          Most cited references 15

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          A neurologic basis for the overactive bladder.

          The functions of the lower urinary tract (LUT) to store and periodically release urine are dependent on neural circuits in the brain and spinal cord. This paper reviews the central neural control of micturition and how disruption of this control can lead to bladder overactivity and incontinence. Neuroanatomic, electrophysiologic, and pharmacologic techniques have provided information about the neural circuitry and the neurotransmitters involved in the central nervous control of voiding. Experimental models of neural injury, including spinal cord transection, cerebral infarction, and localized brain lesions, have been studied to identify the mechanisms contributing to the neurogenic overactive bladder. Normal storage of urine is dependent on 1) spinal reflex mechanisms that activate sympathetic and somatic pathways to the urethral outlet and 2) tonic inhibitory systems in the brain that suppress the parasympathetic excitatory outflow to the urinary bladder. Voiding is mediated by inhibition of sympathetic-somatic pathways and activation of a spinobulbospinal parasympathetic reflex pathway passing through a micturition center in the rostral pons. Damage to the brain can induce bladder overactivity by reducing suprapontine inhibition. Damage to axonal pathways in the spinal cord leads to the emergence of primitive spinal bladder reflexes triggered by C-fiber bladder afferent neurons. The C-fiber afferent neurotoxin capsaicin, administered intravesically, has been useful in treating certain types of neurogenic bladder overactivity. The central nervous mechanisms controlling the LUT are organized in the brain and spinal cord as simple on-off switching circuits that are under voluntary control. Damage to central inhibitory pathways or sensitization of peripheral afferent terminals in the bladder can unmask primitive voiding reflexes that trigger bladder overactivity.
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            A myogenic basis for the overactive bladder.

             A F Brading (1997)
            This article summarizes evidence supporting the conclusion that the spontaneous rises in pressure that occur in the overactive bladder, particularly in detrusor instability (DI), regardless of etiology, are myogenic. The evidence quoted has been obtained by several groups of investigators and includes electrophysiologic studies of detrusor myocytes, tension studies of strips of smooth muscle, in vivo experiments on animal models, and light and electron microscopic studies of the structure of the bladder wall. The results of these studies demonstrate changes in the properties, structure, and innervation of the detrusor. These changes are consistent with the hypothesis that partial denervation of the detrusor may be responsible for altering the properties of the smooth muscle, leading to increased excitability and increased ability of activity to spread between cells, resulting in coordinated myogenic contractions of the whole detrusor. It is suggested that alterations in the properties of the detrusor myocytes are a necessary prerequisite for the production of the unstable pressure rises seen in DI of any origin.
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              Prevalence and burden of overactive bladder in the United States


                Author and article information

                Family Medicine and Community Health
                Family Medicine and Community Health & American Chinese Medical Education Association (USA )
                December 2013
                December 2014
                : 1
                : 4
                : 36-39
                1Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, OH, USA
                Author notes
                CORRESPONDING AUTHOR: Elizabeth Ferry, Urology Institute, University Hospitals Case Medical Center and Department of Urology, Case Western Reserve University School of Medicine, Cleveland, OH, USA, E-mail: dmshah@ 123456wisc.edu
                Copyright © 2013 Family Medicine and Community Health

                This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 Unported License (CC BY-NC 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. See https://creativecommons.org/licenses/by-nc/4.0/.

                Self URI (journal page): http://fmch-journal.org/


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