Overactive bladder syndrome (OAB) is characterized by urgency, usually associated with increased daytime frequency and nocturia, with or without urgency urinary incontinence. In France, its prevalence is estimated at 14%, with approximately one-third of patients presenting a "wet" form, i.e. with urinary leakage. Diagnosis relies on medical history, clinical examination, bladder diaries, symptom scores and, when needed, a pad test. Management should be individualized and starts with lifestyle and behavioral measures, possibly combined with pelvic floor muscle training, local estrogen therapy and transcutaneous tibial nerve stimulation when indicated. Pharmacological treatment includes anticholinergics and β3-agonists (mirabegron and vibegron), and refractory cases may benefit from intradetrusor botulinum toxin injections or sacral neuromodulation. Invasive surgical procedures remain exceptional and are reserved for severe cases, most often in patients with neurological disorders.

While not uncommon, urinary incontinence is less common in men than in women incidence increases, reaching up to 32% at age 80. There are several mechanisms of UI, with urgency being the most common, accounting for 40 to 80% of cases.UI due to chronic retention secondary to benign prostatic hypertrophy is not the only cause, and symptoms of bladder hyperactivity with incontinence should be treated with caution. Incontinence due to sphincter insufficiency is mainly secondary to prostate surgery (hypertrophy or cancer).While the patient's request for treatment of this UI should be paramount, co-morbidities, the severity of symptoms, and the presence of nocturia must be investigated. Complementary tests include PSA, urinalysis, creatinine, and reno vesical-prostatic ultrasound.Treatment options are chosen according to the type of incontinence and the patient's preferences. If the patient wishes, a referral to a urologist is also recommended.

Nuclear medicine neuroimaging is becoming increasingly important for the diagnosis and differential diagnosis of Parkinson's disease, atypical parkinsonian syndromes and more rare neurological (movement) disorders. We report on a 46-year-old woman presented with frequent falls, a gradually progressive bipyramidal syndrome with gait ataxia, dysphagia, urinary urgency and -incontinence, low mood with disturbed emotional regulation and a mild asymmetric hypokinetic rigid syndrome. Additionally, she had a blurry vision, asymmetrical ptosis and abnormal vertical saccades. [18F]FDG PET/CT of the brain showed unspecific pattern of regional cortical hypometabolism and, more pronounced, striatal hypometabolism. [123I]FP-CIT SPECT showed a complete absence of on-target binding. Subsequent genetic testing revealed two variants in SPG7. The patient showed a modest favourable response on levodopa. This case illustrates profound neurodegeneration of the presynaptic dopaminergic nigrostriatal neurons in SPG7.

Background/Objectives: Mesh-related complications after surgery for stress urinary incontinence (SUI) and pelvic organ prolapse (POP) remain a clinical challenge, and surgical revision is often required. However, its impact on functional outcomes and continence status is incompletely defined. This study aimed to evaluate voiding and continence outcomes after surgical revision of vaginal synthetic mesh. Methods: This retrospective multicenter study included 55 consecutive women undergoing surgical revision of synthetic mesh for symptomatic complications after SUI or POP procedures between March 2021 and April 2025. Preoperative evaluation included clinical assessment, uroflowmetry, and selective imaging or urodynamic studies. Surgical management included mesh section, partial removal, or total removal via vaginal, abdominal, or combined approaches. The primary outcome was change in Qmax and post-void residual (PVR). Secondary outcomes included symptom resolution, changes in urgency urinary incontinence (UUI) and SUI, and postoperative complications. Results: Obstructive voiding dysfunction was the leading indication for revision (47.3%). Median Qmax increased from 13.0 to 18.0 mL/s (p = 0.0013), and median PVR decreased from 55.0 to 5.0 mL (p < 0.001). UUI improved from 56.4% to 34.5% (p = 0.017, McNemar's exact test). Conversely, SUI increased from 20.0% to 56.4% (p < 0.001), although only 16 patients (29.1%) had clinically significant postoperative SUI, of whom 7 underwent a secondary anti-incontinence procedure. Intraoperative complications were infrequent (5.5%), while postoperative urinary tract infections occurred in 16.4%. Conclusions: Mesh revision surgery improves voiding function and reduces storage symptoms in selected patients but carries a substantial risk of recurrent or de novo SUI, underscoring the need for careful patient selection and counseling, with an acceptable safety profile in experienced centers.

Background/Objective: Intradetrusor onabotulinumtoxinA is an established treatment for refractory idiopathic overactive bladder (OAB); however, data on predictors of treatment response and patient management after the initial injection are limited. This study evaluated the clinical outcomes, safety, factors associated with treatment failure, and retreatment pathways following intradetrusor onabotulinumtoxinA in women with refractory idiopathic OAB. Methods: This retrospective cohort study included 41 women with refractory idiopathic OAB treated with 100 U intradetrusor onabotulinumtoxinA between November 2022 and January 2026. Efficacy was assessed using 3-day bladder diaries, validated patient-reported outcome measures (UDI-6, IIQ-7, and OAB-V8), and the Treatment Benefit Scale (TBS). Safety outcomes, factors associated with treatment failure, retreatment preferences, and subsequent management strategies were analyzed. Results: Significant improvements were observed in daytime frequency, urgency episodes, urgency urinary incontinence episodes, and validated patient-reported outcome measures (all p < 0.001). Treatment success according to the TBS was achieved in 68.3% and 46.3% of patients at 12 and 24 weeks, respectively. Diffuse bladder trabeculation was independently associated with treatment failure at 12 weeks (aOR 11.90, 95% CI 1.99-71.14; p = 0.007), whereas no significant independent association was observed at 24 weeks. Urinary tract infection occurred in 19.5% of patients, and temporary clean intermittent catheterization was required in one patient (2.4%). By postoperative week 24, 53.7% of patients declined repeat treatment, most commonly because of inadequate symptom improvement (77.3%). Among those declining reinjection, 59.1% resumed or continued pharmacological therapy. Conclusions: Intradetrusor injection of 100 U onabotulinumtoxinA was associated with significant improvement and acceptable safety in women with refractory idiopathic OAB. Diffuse bladder trabeculation may help identify patients at risk of poor treatment response, warranting further validation in larger patient cohorts. Documenting retreatment decisions and management provides real-world evidence that may support long-term counseling and decision-making.

Lower urinary tract symptoms that significantly impair quality of life in men may result from benign prostatic hyperplasia, overactive bladder, or a combination of both conditions. The diagnosis of benign prostatic hyperplasia, a voiding dysfunction due to outlet obstruction, can be made with a thorough history and physical examination. A validated questionnaire should be used to make an accurate initial diagnosis and to monitor treatment effect over time. Selective alpha-1 blockers are an appropriate first-line drug choice for most patients; however, 5-alpha reductase inhibitors and phosphodiesterase type 5 inhibitors may also be used, alone or in combination with each other, depending on symptom severity and if alternative treatment options are needed. If medical therapy is ineffective, surgical and interventional procedures aimed at opening the prostatic urethra are available to ameliorate symptoms. Overactive bladder manifests with urinary urgency, frequency, and nocturia with or without incontinence. The diagnosis of this storage dysfunction due to detrusor overactivity can be made with a thorough history, physical examination, urinalysis, and assessment of the residual volume of urine in the bladder after voiding. First-line treatment for overactive bladder includes beta-3 agonists as well as pelvic floor physical therapy and behavioral interventions. If left untreated, benign prostatic hyperplasia and overactive bladder can result in significant social isolation and relationship strain.

Bladder sensory neurons are essential components of lower urinary tract sensory encoding and micturition reflex control. They detect bladder filling, stretch, inflammatory mediators, and pathogen-associated stimuli, and they communicate with urothelial cells, immune cells, and stromal cells through neuropeptides such as calcitonin gene-related peptide (CGRP), substance P (SP), and vasoactive intestinal peptide (VIP). Under physiological conditions, this neuro-immune-urothelial axis contributes to bladder homeostasis. Under pathological conditions, including neural injury, infection, inflammation, or epithelial barrier disruption, TRP channels, purinergic signaling, neurotrophic factors, chemokines, and voltage-gated ion channels can induce peripheral sensitization, increased excitability of dorsal root ganglion (DRG) neurons, spinal plasticity, and central sensitization, thereby contributing to urinary frequency, urgency, bladder pain, and detrusor overactivity in neurogenic bladder and interstitial cystitis/bladder pain syndrome (IC/BPS). This review summarizes the anatomical and functional organization of bladder sensory afferents, sensory neuron-associated molecular signaling, neuro-immune-urothelial interactions, disease-specific mechanisms, and targeted therapeutic strategies. We also discuss the translational potential and limitations of interventions targeting TRPV1/TRPV4/TRPA1, P2X3, CGRP, SP/neurokinin receptors, NGF, ion channels, botulinum toxin, and neuromodulation. These mechanisms provide a framework for understanding neurogenic mechanisms in bladder disorders and for developing targeted interventions.

Overactive bladder (OAB) is a prevalent condition characterized by urinary urgency, frequency, and nocturia, with or without urge urinary incontinence. It significantly affects quality of life and is associated with increased rates of depression and sexual dysfunction. Lower urinary tract (LUT) control relies on coordinated activity across peripheral, spinal, and supraspinal networks. Individuals with OAB exhibit abnormal supraspinal network activity. Current treatments primarily target peripheral pathways and have limited efficacy. Repetitive transcranial magnetic stimulation (rTMS) offers a non-invasive approach to modulate networks involved in LUT control.