was included in the ICI 5 edition PFMT (24) vs PFMT + resistance device (28) 52 Women with SUI or MUI (stress predominant) PFMT: As below without device PFMT +resistance; 5 quick and 5 slow (sustained), high-intensity contractions daily. Advised to hold contractions as long as possible, relaxing their PFM for an equivalent time before repeating the process. Intravaginal resistance: instructions to use the Pelvic-Toner Device concurrently whilst exercising. Two clinic visits and one phone call Reported cure (based on the Q11 of the ICIQFluts) PFMT 0/13 PFMT+resistance 1/15 Non-sign. difference btw groups (p=0.429) Improvement (post-Tx) PFMT 10/19 PFMT+resistance 11/21 Non-sign. difference btw groups 16 weeks of treatment, outcomes assessed at post-Tx and at 6 month follow-up Dropouts (at 6 month) PFMT 9/24 PFMT + resistance 15/28

/pdf/adult-conservative-management-23g1y2j6gw.pdf

Adult conservative management

Botulinum toxin A, brain and pain.

Lower urinary tract (LUT) dysfunction is common in patients with multiple sclerosis and is a major negative influence on the quality of life of these patients. The most commonly reported symptoms are those of the storage phase, of which detrusor overactivity is the most frequently reported urodynamic abnormality. The clinical evaluation of patients' LUT symptoms should include a bladder diary, uroflowmetry followed by measurement of post-void residual urine volume, urinalysis, ultrasonography, assessment of renal function, quality-of-life assessments and sometimes urodynamic investigations and/or cystoscopy. The management of these patients requires a multidisciplinary approach. Intermittent self-catheterization is the preferred option for management of incomplete bladder emptying and urinary retention. Antimuscarinics are the first-line treatment for patients with storage symptoms. If antimuscarinics are ineffective, or poorly tolerated, a range of other approaches, such as intradetrusor botulinum toxin A injections, tibial nerve stimulation and sacral neuromodulation are available, with varying levels of evidence in patients with multiple sclerosis. Surgical procedures should be performed only after careful selection of patients. Stress urinary incontinence owing to sphincter deficiency remains a therapeutic challenge, and is only managed surgically if conservative measures have failed. Multiple sclerosis has a progressive course, therefore, patients' LUT symptoms require regular, long-term follow-up monitoring.

Management of neurogenic bladder in patients with multiple sclerosis

Understanding of the role of urothelium in regulating bladder function is continuing to evolve. While the urothelium is thought to function primarily as a barrier for preventing injurious substances and microorganisms from gaining access to bladder stroma and upper urinary tract, studies indicate it may also function in cell signaling events relating to voiding function. This review highlights urothelial abnormalities in bladder pain syndrome/interstitial cystitis (BPS/IC), feline interstitial cystitis (FIC), and nonneurogenic idiopathic overactive bladder (OAB). These bladder conditions are typified by lower urinary tract symptoms including urinary frequency, urgency, urgency incontinence, nocturia, and bladder discomfort or pain. Urothelial tissues and cells from affected clinical subjects and asymptomatic controls have been compared for expression of proteins and mRNA. Animal models have also been used to probe urothelial responses to injuries of the urothelium, urethra, or central nervous system, and transgenic techniques are being used to test specific urothelial abnormalities on bladder function. BPS/IC, FIC, and OAB appear to share some common pathophysiology including increased purinergic, TRPV1, and muscarinic signaling, increased urothelial permeability, and aberrant urothelial differentiation. One challenge is to determine which of several abnormally regulated signaling pathways is most important for mediating bladder dysfunction in these syndromes, with a goal of treating these conditions by targeting specific pathophysiology.

/pdf/evidence-for-bladder-urothelial-pathophysiology-in-5atxvn7w50.pdf

Evidence for Bladder Urothelial Pathophysiology in Functional Bladder Disorders

Overactive bladder affects millions of adults, with profound personal and economic costs. Although antimuscarinic drugs can cause a reduction in voiding symptoms, the effect is modest, and many patients are intolerant of the side effects, or do not experience sufficient relief. For these patients, the modulation of bladder reflex pathways via percutaneous tibial nerve stimulation (PTNS) or via implanted sacral nerve stimulation (SNS) has been acknowledged as a logical next step in the algorithm of care. This review examines the mechanism of action, the relative benefits, adverse effects, and costs of percutaneous nerve stimulation compared to other treatment modalities.

/pdf/percutaneous-tibial-nerve-stimulation-a-clinically-and-cost-ivf8xmfrf7.pdf

Percutaneous Tibial Nerve Stimulation: A Clinically and Cost Effective Addition to the Overactive Bladder Algorithm of Care

Ureteric injury is rarer than previously reported in association with developed world vesico-vaginal fistulae

Study design, materials and methods This is a prospective evaluation over 18 months of patients who found first line treatments intolerable or ineffective. PTNS treatment was administered in a weekly course of 30minute stimulations, using UrgentPC, from Uroplasty, for a total of 12 weeks. Symptoms were objectively assessed using the ICIQOAB and ICIQLUTS-QoL questionnaires and bladder diaries at baseline and after 12 weeks of treatment. Patients opting to continue treatment after 12 weeks returned for top-up session.

Percutaneous tibial nerve stimulation for the management of the idiopathic and neurogenic overactive bladder: A safe and effective treatment

INTRODUCTION
Intravesical botulinum toxin A (BTX-A) has been long established as treatment for overactive bladder and neurogenic bladder dysfunction. However, most published data are reported among a female cohort. Adverse events such as intermittent self-catheterization (ISC) and urinary tract infections (UTIs) play a large role in discontinuation of therapy. There is currently limited information regarding predictive factors to appropriately counsel male patients.


MATERIALS AND METHODS
We retrospectively collected data on male patients undergoing their first intravesical BTX-A therapy from January 2016 to July 2021 in two high-volume centers. Data included demographics, past medical and surgical history, and urodynamic parameters. Patients were excluded if they had a long-term catheter or ISC before initiation of therapy.


RESULTS
A total of 69 men were included in the study with a median age of 66 years. There were 18 patients with neurogenic bladder dysfunction. Thirty men had urge incontinence secondary to radical prostatectomy or bladder outflow surgery. Overall rates of ISC were 43.5%. Predictors for ISC included a baseline postvoid residual (PVR) ≥ 50 mL (odds ratio [OR]: 4.2, 95% confidence interval [CI]: 1.36-13.03, p = 0.01), BTX-A dose >100 units (OR: 4.2, 95% CI: 1.36-13.0, p = 0.01). Stress urinary incontinence was protective against ISC (OR: 0.20, 95% CI: 0.04-1.00, p = 0.049) as well as history of prostatectomy/bladder outflow obstruction (BOO) surgery (OR: 0.16, 95% CI: 0.05-0.47, p < 0.001). A multivariable logistic regression model with these factors yielded a c-statistic of 0.80 (optimism-adjusted = 0.75). An enlarged prostate was the only predictor for UTI among our male cohort (OR: 8.0, 95% CI: 2.03-31.5, p = 0.003).


CONCLUSIONS
This is the first study assessing risk factors of adverse events among men following BTX-A injection. High PVR and BTX-A dose of >100U were predictors of requiring ISC after BTX-A. Stress incontinence, previous radical prostatectomy, and BOO surgery were all protective against needing ISC post-BTX-A. An enlarged prostate was associated with development of UTI. These factors can be used to assist in counseling male patients regarding their risk of ISC and UTI.

Predictors for adverse events following intravesical botulinum toxin injections in men.

Neurofibromatosis type I is a common autosomal dominant inherited disorder of neural crest origin, affecting 1 in 3000 people.1 Plexiform neurofibromas, benign peripheral nerve sheath tumours, are considered pathognomonic of neurofibromatosis type I. Pelvic involvement is uncommon and is associated with considerable morbidity.1 

A 29-year-old man reported 8 years of progressively increasing left hemiscrotal and gluteal swelling. He had noticed numbness over the penis and scrotum, difficulties with ejaculation and experiencing an orgasm, and perineal pain particularly when trying to ejaculate. He could achieve an erection and had preserved sexual drive, and no bladder or bowel symptoms. He took gabapentin and had never used serotonin-selective reuptake inhibitors. There was no family history of neurofibromatosis type I.

General examination was normal with no other cutaneous manifestations of neurofibromatosis type I, suggesting a …

https://pn.bmj.com/content/practneurol/early/2019/12/09/practneurol-2019-002375.full.pdf

Jai Seth

Papers

Ureteric injury is rarer than previously reported in association with developed world vesico-vaginal fistulae

Percutaneous tibial nerve stimulation for the management of the idiopathic and neurogenic overactive bladder: A safe and effective treatment

Predictors for adverse events following intravesical botulinum toxin injections in men.

Pelvic plexiform neurofibromatosis presenting with genital numbness.

presenting complaint of benign joint hypermobility syndrome