| Abstract: |
AbstractOveractive bladder disease is defined by the Standardization Subcommittee of the (ICS) as urinary urgency, with or without urinary incontinence, usually with frequency and nocturia, with no proven infection or other obvious pathology (NOBLE) program: 16.5% of the USA population (16% of men and 16.9% of women) over 18 years of age had symptoms consistent with overactive bladder. Urgency and urge incontinence usually result from an involuntary increase in bladder pressure due to bladder smooth muscle over-activity during the filling phase of the micturition cycle. The pathophysiology of overactive bladder remains unclear, but there are two widely accepted explanations. First, partial denervation of the detrusor muscle is believed to increase excitability secondary to changes in central nervous system pathways that inhibit bladder activity. Second, increased sensitivity of the sensory nerve endings in the bladder results in increased excitability of the detrusor muscleors. All cases often underwent a complete history and physical examination, multichannel video urodynamics, and completed a 3 day voiding diary for evaluation. Baseline laboratory evaluation included a basic metabolic panel, urinalysis, and urine culture. urinary tract infections are treated and sterile urine cultures are documented prior to evaluation of the patients . Options for the treatment of OAB include behavioural interventions, which are collectively considered first-line treatments for OAB symptoms with or without urinary incontinence (UI). Behavioural interventions are aimed at changing patient lifestyle and behaviour and at teaching techniques to suppress urgency and improve continence skills. Behavioural interventions can be readily prescribed in the primary care setting, either before or concomitantly with pharmacotherapy .Antimuscarinics, including darifenacin, fesoterodine, oxybutynin, solifenacin, tolterodine and trospium chloride, are pharmacological treatments for OAB. Treatment options available for patients with refractory OAB symptoms include botulinum neurotoxin-A injections into the detrusor muscle; surgical procedures (e.g. augmentation and urinary diversion); neuromodulation, which involves stimulation of the sacral nerves using implanted electrical devices and more recently, posterior tibial nerve stimulation .
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