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Purpose of Review: In this review, we present the current literature on the diagnosis and management of stress urinary incontinence induced by sphincter deficiency associated with neurogenic lower urinary tract dysfunction. Recent Findings: Because sphincter deficiency stress urinary incontinence is not a common condition, there are no guidelines or large-scale clinical studies that focus on the diagnosis and management of this condition. Although there is consensus that urodynamic investigation is the only method to assess the function of the lower urinary tract, there is no established urodynamic criteria to diagnose neurogenic sphincter deficiency. As for the treatment of sphincter deficiency stress urinary incontinence in neurogenic patients, artificial urinary sphincter has a better success rate and a higher complication and reoperation rate than other methods including sling surgery and injection of bulking agents. Summary: Although there is a progress in the evaluation and management of neurogenic patients with sphincter deficiency stress urinary incontinence, a prospective multicenter clinical study on this condition should be highly recommended. [ABSTRACT FROM AUTHOR]

Objectives: To investigate bladder function in a model of nonbacterial prostatitis (NBP) induced in castrated rats by 17β-estradiol injection. Methods: Ten-month-old male Wistar rats were divided into two groups, sham and NBP (both N = 8). NBP was induced by castration followed by daily subcutaneous injection of 17β-estradiol for 30 days. On the 31st day after surgery, we investigated (1) voiding behavior, (2) bladder blood flow (BBF), (3) prostate and bladder weight, and proinflammatory cytokines (TNF-α and CXCL1) levels and (4) bladder contractile responses to electrical field stimulation (EFS), carbachol and KCl. Results: (1) Voiding behavior (average micturition volume, total urine volume and number of micturitions) and (2) BBF were not significantly different between the sham and NBP groups. (3) NBP led to a significant decrease in prostatic weight and increase in proinflammatory cytokine levels in the prostate, but NBP did not cause a significant change in bladder weight or proinflammatory cytokine levels in the bladder. (4) Bladder contractile forces in response to EFS, carbachol and KCl were not significantly affected by NBP. Conclusions: In this rat model, NBP did not cause a significant change in the level of proinflammatory cytokines in the bladder and affect bladder function. [ABSTRACT FROM AUTHOR]