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      Detrusor sphincter dyssynergia: a review of physiology, diagnosis, and treatment strategies

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          Abstract

          Detrusor sphincter dyssynergia (DSD) is the urodynamic description of bladder outlet obstruction from detrusor muscle contraction with concomitant involuntary urethral sphincter activation. DSD is associated with neurologic conditions such as spinal cord injury, multiple sclerosis, and spina bifida and some of these neurogenic bladder patients with DSD may be at risk for autonomic dysreflexia, recurrent urinary tract infections, or upper tract compromise if the condition is not followed and treated appropriately. It is diagnosed most commonly during the voiding phase of urodynamic studies using EMG recordings and voiding cystourethrograms, although urethral pressure monitoring could also potentially be used. DSD can be sub-classified as either continuous or intermittent, although adoption of this terminology is not widespread. There are few validated oral pharmacologic treatment options for this condition but transurethral botulinum toxin injection have shown temporary efficacy in reducing bladder outlet obstruction. Urinary sphincterotomy has also demonstrated reproducible long term benefits in several studies, but the morbidity associated with this procedure can be high.

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          Most cited references43

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          Functional anatomy of the female pelvic floor.

          The anatomic structures in the female that prevent incontinence and genital organ prolapse on increases in abdominal pressure during daily activities include sphincteric and supportive systems. In the urethra, the action of the vesical neck and urethral sphincteric mechanisms maintains urethral closure pressure above bladder pressure. Decreases in the number of striated muscle fibers of the sphincter occur with age and parity. A supportive hammock under the urethra and vesical neck provides a firm backstop against which the urethra is compressed during increases in abdominal pressure to maintain urethral closure pressures above the rapidly increasing bladder pressure. This supporting layer consists of the anterior vaginal wall and the connective tissue that attaches it to the pelvic bones through the pubovaginal portion of the levator ani muscle, and the uterosacral and cardinal ligaments comprising the tendinous arch of the pelvic fascia. At rest the levator ani maintains closure of the urogenital hiatus. They are additionally recruited to maintain hiatal closure in the face of inertial loads related to visceral accelerations as well as abdominal pressurization in daily activities involving recruitment of the abdominal wall musculature and diaphragm. Vaginal birth is associated with an increased risk of levator ani defects, as well as genital organ prolapse and urinary incontinence. Computer models indicate that vaginal birth places the levator ani under tissue stretch ratios of up to 3.3 and the pudendal nerve under strains of up to 33%, respectively. Research is needed to better identify the pathomechanics of these conditions.
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            Prognostic value of urodynamic testing in myelodysplastic patients.

            We herein describe the clinical progress of 42 myelodysplastic patients studied urodynamically and followed for a mean of 7.1 years. Urodynamic evaluation included urethral pressure profilometry, simultaneous determination of urethral pressure, intravesical pressure and external anal or external urethral sphincter electromyography with fluoroscopic voiding cystourethrography. Assessment of urethral function showed 36 patients (86 per cent) with an open vesical outlet and nonfunctional proximal urethral. Cystometrography revealed that 7 of 42 patients (17 per cent) had reflex detrusor activity: 4 with coordinated micturition and 3 with detrusor-sphincter dyssynergia. Thirty-five patients (83 per cent) had areflexic detrusor dysfunction: 5 with atomic detrusor response and 30 with a progressive increase in pressure with increasing volume. The intravesical pressure at the time of urethral leakage was 40 cm. water or less in 20 patients and at pressures greater than this value in 22 patients. No patient in the low pressure group had vesicoureteral reflux and only 2 showed ureteral dilatation on excretory urography. In contrast, of the patients in the higher pressure group 15 (68 per cent) showed vesicoureteral reflux and 18 (81 per cent) showed ureteral dilatation on excretory urography. Thus, a striking relationship between the urethral closure pressure and intravesical pressure at the time of urethral leakage and the clinical course in this group of myelodysplastic patients is demonstrated. Every patient with a normally closed vesical outlet was continent on intermittent catheterization and an anticholinergic agent, while only 60 per cent of patients with open bladder outlets similarly treated achieved good urinary control and none was dry. An artificial sphincter device would seem to be a reasonable method to achieve urinary control in the latter patients but the detrusor response to filling also must be considered. Detrusor hypertonia should be controlled or controllable before a sphincter augmenting device can be used safely. Treatment options for patients with high urethral closure pressures include intermittent catheterization and anticholinergic medications or a sphincter ablative procedure to decrease the outlet resistance combined with anticholinergic therapy and implantation of an artificial sphincter. However, only longer followup will determine if these therapeutic regimens will prevent upper urinary tract deterioration.
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              Effects of botulinum A toxin on detrusor-sphincter dyssynergia in spinal cord injury patients.

              We evaluated the ability of low doses of botulinum A toxin, an inhibitor of acetylcholine release at the neuromuscular junction, to denervate and relax the spastic rhabdosphincter in 11 men with spinal cord injury and detrusor-sphincter dyssynergia. Toxin concentration, injection volume, percutaneous versus cystoscopic injection of the sphincter and number of injections were evaluated in 3 treatment protocols. All 10 patients evaluated by electromyography after injection showed signs of sphincter denervation. Bulbosphincteric reflexes in the 10 patients evaluated after injection were more difficult to obtain, and they showed a decreased amplitude and normal latency. The urethral pressure profile in the 7 patients in whom it was measured before and after treatment decreased an average of 27 cm. water after toxin injections. Post-void residual urine volume decreased by an average of 146 cc after the toxin injections in 8 patients. In the 8 patients for whom it could be determined toxin effects lasted an average of 50 days. The toxin also decreased autonomic dysreflexia in 5 patients.
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                Author and article information

                Journal
                Transl Androl Urol
                Transl Androl Urol
                TAU
                Translational Andrology and Urology
                AME Publishing Company
                2223-4691
                February 2016
                February 2016
                : 5
                : 1
                : 127-135
                Affiliations
                [1]Department of Urology, University of Michigan, Ann Arbor, MI, USA
                Author notes
                Correspondence to: John T. Stoffel, MD. Department of Urology, University of Michigan, Ann Arbor, MI, USA. Email: jstoffel@ 123456med.umich.edu .
                Article
                tau-05-01-127
                10.3978/j.issn.2223-4683.2016.01.08
                4739973
                26904418
                5440a9e3-48b2-4833-a3ac-783f8bf843da
                2016 Translational Andrology and Urology. All rights reserved.
                History
                : 30 November 2015
                : 05 January 2016
                Categories
                Review Article

                detrusor sphincter dyssynergia (dsd),neurogenic bladder,urodynamics,external urinary sphincter (eus)

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