Percutaneous tibial nerve stimulation can be considered an effective treatment for detrusor overactivity incontinence with 71% of patients considered responders, while none of those treated with placebo was considered a responder. The relevance of a placebo effect seems to be negligible in this patient population.

Parkinson's disease (PD) is a common neurodegenerative disorder, and lower urinary tract (LUT) dysfunction is one of the most common autonomic disorders with an estimated incidence rate of 27-80%. Studies have shown that bladder dysfunction significantly influences quality-of-life (QOL) measures, early institutionalisation, and health economics. We review the pathophysiology of bladder dysfunction in PD, lower urinary tract symptoms (LUTS), objective assessment, and treatment options. In patients with PD, disruption of the dopamine D1-GABAergic direct pathway may lead to LUTS. Overactive bladder (OAB) is the most common LUT symptom in PD patients, and an objective assessment using urodynamics commonly shows detrusor overactivity (DO) in these patients. The post-void residual (PVR) volume is minimal in PD, which differs significantly from multiple system atrophy (MSA) patients who have a more progressive disease that leads to urinary retention. However, subclinical detrusor weakness during voiding may also occur in PD. Regarding bladder management, there are no large, double-blind, prospective studies in this area. It is well recognised that dopaminergic drugs can improve or worsen LUTS in PD patients. Therefore, an add-on therapy with anticholinergics is required. Beta-3 adrenergic agonists are a potential treatment option because there are little to no central cognitive events. Newer interventions, such as deep brain stimulation (DBS), are expected to improve bladder dysfunction in PD. Botulinum toxin injections can be used to treat intractable urinary incontinence in PD. Transurethral resection of the prostate gland (TURP) for comorbid BPH in PD is now recognised to be not contraindicated if MSA is excluded. Collaboration of urologists with neurologists is highly recommended to maximise a patients' bladder-associated QOL. Neurourol. Urodynam. 35:551-563, 2016. © 2015 Wiley Periodicals, Inc.

BackgroundPercutaneous Tibial Nerve Stimulation (PTNS) has been proposed for the treatment of overactive bladder syndrome (OAB), non-obstructive urinary retention (NOUR), neurogenic bladder, paediatric voiding dysfunction and chronic pelvic pain/painful bladder syndrome (CPP/PBS). Despite a number of publications produced in the last ten years, the role of PTNS in urinary tract dysfunctions remains unclear. A systematic review of the papers on PTNS has been performed with the aim to better clarify potentialities and limits of this technique in the treatment of OAB syndrome and in other above mentioned urological conditions.MethodsA literature search using MEDLINE and ISI web was performed. Search terms used were “tibial nerve” and each of the already mentioned conditions, with no time limits. An evaluation of level of evidence for each paper was performed.ResultsPTNS was found to be effective in 37-100% of patients with OAB, in 41-100% of patients with NOUR and in up to 100% of patients with CPP/PBS, children with OAB/dysfunctional voiding and patients with neurogenic pathologies. No major complications have been reported.Randomized controlled trials are available only for OAB (4 studies) and CPP/PBS (2 studies). Level 1 evidence of PTNS efficacy for OAB is available. Promising results, to be confirmed by randomized controlled studies, have been obtained in the remaining indications considered.ConclusionsPTNS is an effective and safe option to treat OAB patients. Further studies are needed to assess the role of PTNS in the remaining indications and to evaluate the long term durability of the treatment. Further research is needed to address several unanswered questions about PTNS.

Silencing of microRNAs (miRNAs) by promoter CpG island methylation may be an important mechanism in prostate carcinogenesis. To screen for epigenetically silenced miRNAs in prostate cancer (PCa), we treated prostate normal epithelial and carcinoma cells with 5-aza-2'-deoxycytidine (AZA) and subsequently examined expression changes of 650 miRNAs by megaplex stemloop reverse transcription-quantitative PCR. After applying a selection strategy, we analyzed the methylation status of CpG islands upstream to a subset of miRNAs by methylation-specific PCR. The CpG islands of miR-18b, miR-132, miR-34b/c, miR-148a, miR-450a and miR-542-3p showed methylation patterns congruent with their expression modulations in response to AZA. Methylation analysis of these CpG islands in a panel of 50 human prostate carcinoma specimens and 24 normal controls revealed miR-132 to be methylated in 42% of human cancer cases in a manner positively correlated to total Gleason score and tumor stage. Expression analysis of miR-132 in our tissue panel confirmed its downregulation in methylated tumors. Re-expression of miR-132 in PC3 cells induced cell detachment followed by cell death (anoikis). Two pro-survival proteins-heparin-binding epidermal growth factor and TALIN2-were confirmed as direct targets of miR-132. The results of this study point to miR-132 as a methylation-silenced miRNA with an antimetastatic role in PCa controlling cellular adhesion.