Treatment Of Neurogenic Detrusor Overactivity Research Articles

Efficacy of Peripheral Lidocaine Application (Neural Therapy) in the treatment of neurogenic detrusor overactivity in multiple sclerosis patients (P3.366)

Efficacy of Peripheral Lidocaine Application (Neural Therapy) in the treatment of neurogenic detrusor overactivity in multiple sclerosis patients (P3.366)

Efficacy and Adverse Events Associated With Use of OnabotulinumtoxinA for Treatment of Neurogenic Detrusor Overactivity: A Meta-Analysis.

PurposeOnabotulinumtoxinA is used widely for the treatment of neurogenic detrusor overactivity. We conducted a systematic review and meta-analysis to assess its efficacy and safety for neurogenic detrusor overactivity treatment.MethodsA systematic literature review was performed to identify all published randomized double-blind, placebo-controlled trials of onabotulinumtoxinA for neurogenic detrusor overactivity treatment. MEDLINE, Embase, and the CENTRAL were employed. Reference lists of retrieved studies were reviewed carefully.ResultsSix publications involving 871 patients, which compared onabotulinumtoxinA with a placebo were analyzed. Efficacy of onabotulinumtoxinA treatment was shown as a reduction of the mean number of urinary incontinence episodes per day (mean difference, -1.41; 95% confidence interval [CI], -1.70 to -1.12; P<0.00001), maximum cystometric capacity (135.48; 95% CI, 118.22–152.75; P<0.00001), and maximum detrusor pressure (-32.98; 95% CI, -37.33 to -28.62; P<0.00001). Assessment of adverse events revealed that complications due to onabotulinumtoxinA injection were localized primarily to the urinary tract.ConclusionsThis meta-analysis suggests that onabotulinumtoxinA is an effective treatment for neurogenic detrusor overactivity with localized advent events.

Šlapinimosi sutrikimai po stuburo traumų ir jų gydymas botulino toksino A endovezikinėmis injekcijomis

Neurogeninės kilmės šlapinimosi sutrikimai, atsiradę dėl stuburo traumos, yra aktuali problema. Sunkus stuburo pažeidimas gali sukelti padidėjusį šlapimo pūslės jautrumą, tuštinamojo pūslės raumens (detruzoriaus) hiperaktyvumą, o dėl to šlapimo nelaikymą kaupimo fazės metu. Praradus spinalinę kontrolę, kuri normaliai koordinuoja detruzoriaus susitraukimą ir šlaplės sfinkterio atsipalaidavimą šlapinantis, vystosi detruzoriaus ir sfinkterio sinerginis susitraukinėjimas arba, atvirkščiai – vezikosfinkterinė dissinergija, sukelianti fiziologiškai nenormalų šlapimo pasišalinimą. Šie pokyčiai gali pakenkti paciento gyvenimo kokybei, todėl taikomi įvairūs gydymo būdai. Pirmo pasirinkimo medikamentai yra anticholinerginiai vaistai. Jiems tapus nebeveiksmingais ir norint išvengti chirurginio gydymo, naudojamos botulino toksino A inkekcijos į šlapimo pūslės raumenį arba šlaplės sfinkterį. Botulino toksino A injekcijos – tai naujas gydymo metodas šlapinimosi sutrikimams gydyti. Jis yra veiks­mingas ir sukelia mažai nepageidaujamų reiškinių, todėl ši procedūra vis dažniau atliekama klinikinėje praktikoje. Injekcijomis siekiama sumažinti slėgį pūslėje ir retinti šlapimo nelaikymo epizodų skaičių, be to, galima atlikti kartotines injekcijas.

476 - The value of urinary BDNF levels on assessment of the botulinum toxin type A treatment for neurogenic detrusor overactivity in children with myelodysplasia

Abstract Purpose Urinary cytokines are proposed to predict the urodynamic findings and outcome of intradetrusor botulinum neurotoxin type A injection (iBoNT-Ai) in children with myelodysplasia. The relationship between urinary brain-derived neurotrophic factor (BDNF) and neurogenic and non-neurogenic detrusor overactivity (NDOA) has been shown, as well. In this prospective study, we aimed to investigate the effect of iBoNT-Ai on urine BDNF levels in children with NDOA due to myelodysplasia. Material and Methods Urine samples of children with NDOA due to myelodysplasia were collected and analyzed, before and after iBoNT-Ai (first and third months) along with urodynamics before and 6 week after iBoNT-Ai. BDNF levels and urodynamic findings were analyzed and statistical comparisons were done. Results Mean age was 100.0 ± 34.5 months. Rate of girls/boys was 2.8 in 23 children. BDNF levels significantly declined (p 2 O or less at the postoperative urodynamics had statistically high urine BDNF levels compared to the ones above 5 mL/cmH 2 O, suggesting high urine BDNF to predict treatment failure. Conclusions Present study can hardly suggest urine BDNF to be a follow-up marker in children with NDOA due to myelodysplasia. However, it has an obscure role in treatment planning which needs to be revealed with large-numbered future prospective studies.

166 - Combined treatment of DDAVP and mirabegron represents an effective treatment of neurogenic detrusor overactivity in patients with multiple sclerosis

166 - Combined treatment of DDAVP and mirabegron represents an effective treatment of neurogenic detrusor overactivity in patients with multiple sclerosis

Efficacy of peripheral lidocaine application (neural therapy) in the treatment of neurogenic detrusor overactivity in multiple sclerosis patients.

Many agents and treatments are used in the treatment of neurogenic detrusor overactivity (NDO) in MS patients, but no study has been conducted on the use of peripheric lidocaine (neural therapy-NT) on MS patients. We evaluated the effects of local administration of lidocaine on NDO in Multiple Sclerosis (MS) patients. For each patient local anesthetic lidocaine was injected at each session. Sessions were held once a week for 5 weeks. At each session, Th 10-L1, urogenital segment intradermal injections, Frankenhauser, and sacral epidural injections were given. The patients had clinical and urodynamic assessment 1 month before and 3, 9, and 12 months after NT. In addition, multiple sclerosis quality of life inventory (MSQL-54) and bladder control scale (BLCS) was performed for patients. Twenty-eight patients were included in the study (8 males, 20 females). The patients' average age was 31.7 ± 8.1 years. The injection therapy significantly improved volume at first involuntary bladder contraction (FCV), maximal detrusor pression during filling (P det. max.), maximal cystometric bladder capacity (MCC) after 3 months. Also, the MSQL-54 and BLCS scores were improved with treatment. However, these improvements reached a maximum 3 months after treatment, but from the 9 month a regression was seen in the parameters, and after 12 months the findings were seen to be slightly above their basal levels. These results suggest that NDO treatment in MS patients could be an effective treatment which is easy and has very few side effects, and is cost effective.

Botulinum toxin in spinal cord injury patients with neurogenic detrusor overactivity.

Evidence for the efficacy and safety of intravesical onabotulinum toxin A (onabotA) injections has led to them being licensed in many countries, including Korea, for the treatment of patients with urinary incontinence due to neurogenic detrusor overactivity (NDO) resulting from spinal cord injury or multiple sclerosis who are refractory or intolerant to anticholinergic medications. OnabotA injections have an inhibitory effect on acetylcholine release for up to 10 months, with a recommended dose of 200 U. OnabotA treatment has a beneficial effect not only on urinary symptoms, but also on quality of life. Several clinical studies have shown onabotA to have better effects than placebo in achieving continence, reducing incontinence episodes, improving urodynamic parameters, and improving health-related quality of life. Urinary tract infections and postvoid residual volume are the most prevalent side effects. In patients with residual volume, clean intermittent catheterization may be necessary. In patients with spinal cord injury or multiple sclerosis, it is recommended to evaluate physical and cognitive function before intravesical onabotA injection to ensure that the patient and caregiver are able to perform catheterization if necessary. Further controlled trials should assess the optimal dose, injection technique, long-term safety of repeated injections, and optimal timing of onabotA treatment in the treatment of NDO.

Does the Technique or Pattern Matter When Injecting OnabotulinumtoxinA?

OnabotulinumtoxinA (BTX-A) is a treatment option for patients with neurogenic detrusor overactivity (NDO) or idiopathic overactive bladder (OAB) inadequately controlled with or intolerant to oral medications. The currently approved dosing is 100 U for OAB and 200 U for NDO which is commonly injected into the detrusor muscle via 20–30 trigone-sparing sites. Growing evidence suggests that the efficacy of BTX-A may be maintained with fewer injection sites, varying injection depth, and differing injection locations. This review focuses on the recent literature regarding various BTX-A injection techniques for the treatment of NDO and OAB.

V06 - “Clam” bladder augmentation: An effective third line treatment for neurogenic detrusor overactivity

V06 - “Clam” bladder augmentation: An effective third line treatment for neurogenic detrusor overactivity

Long-term real life efficacy of onabotulinum toxin A for the treatment of neurogenic detrusor overactivity in a population using intermittent self-catheterization

Intradetrusor injection of onabotulinum toxin A (IDIBA) is the third-line therapy for patients with neurogenic detrusor overactivity (NDO). There is few evidence of long-term efficacy but no study assessed reasons for failure or abandonment of IDIBA and CISC (clean intermittent self-catheterization) combined strategy. We aimed to assess its long-term outcome in NDO management, and analyze failure and discontinuation. We retrospectively reviewed medical records of patients admitted in our neurourology department between 2001 and 2013. Inclusion criteria were: age > 18, NDO secondary to spinal cord injury (SCI), multiple sclerosis (MS) or myelomeningocele, NDO management associating IDIBA and CISC, failure of a 3-month combination of two anticholinergics and a 3 year follow-up minimum. Patients with bladder surgery were excluded. Clinical, urodynamic and radiologic data before the first injection, six weeks after the first and last injections were analyzed. Primary endpoints were failure (defined by clinical or urodynamic criteria) and abandonment rates at 3, 5 and 7 years. We secondarily analyzed risk factors for failure and discontinuation. During selected period, 292 patients were included, with mean age 40 ± 13.6 years, 58.2% males and mean duration of NDO 10.8 years. Etiologies for NDO were SCI (84.6%), MS (10.6%) and myelomeningocele (3.4%). After 3 years, 219 patients (80.6%) were still treated, 128 (71.1%) and 58 (60.8%) after 5 and 7 years respectively. Failure rates were 12.6%, 22.2% and 28.9% after 3, 5 and 7 years respectively. Discontinuation rate after 7 years was 11.3%. Reasons were: difficulties related to CISC (3.8%), personal convenience (2.7%), pseudobotulism (2.4%), pregnancy (1.03%), pain (1.03%) and prostatic cancer (0.3%). Clinical, urodynamic and radiologic severity criteria of NDO before IDIBA initiation were major risk factors for treatment failure. This is the first long-term follow-up study of patients with NDO treated by IDIBA and CISC. Less than two third of patients were still treated after 7 years. The main reason for abandonment was difficulties with CISC. Choosing the best time for IDIBA initiation could improve the management of these patients. Further studies are needed to determine the impact of initiation timing, and prior oral anti-muscarinics use on long-term efficiency.

Use of Botulinum Toxin A in the Treatment of Lower Urinary Tract Disorders: A Review of the Literature.

Botulinum neurotoxin (BoNT) is used to treat a variety of ailments, and its therapeutic application in lower urinary tract disorders (LUTDs) is well studied. Robust evidence supporting the efficacy and tolerability of BoNT in the treatment of neurogenic detrusor overactivity (NDO) and non-neurogenic overactive bladder (OAB) has led to regulatory approval for these conditions. Use of BoNT in the treatment of interstitial cystitis/bladder pain syndrome, chronic pelvic pain, and detrusor sphincter dyssynergia has demonstrated some promise, but is still evolving and off-label for these indications. Trials to date do not support the use of BoNT for benign prostatic hyperplasia. This comprehensive review outlines the mechanisms of BoNT in the treatment of LUTDs in adults and presents background and updated data examining the efficacy and adverse events associated with the use of BoNT in common urologic applications.

Indications for Augmentation Cystoplasty in the Era of OnabotulinumtoxinA.

Overactive bladder (OAB) with or without a neurogenic etiology that is refractory to conventional first-, second-, and third-line therapies is a challenging condition that typically leaves the physician and the patient with few options. Historically, treatment for patients who did not respond to any of the few pharmacologic choices focused on more invasive surgical options--specifically, augmentation cystoplasty (AC). In 2011 and 2013, the Food and Drug Administration (FDA) approved intradetrusor injection of onabotulinumtoxinA for the treatment of neurogenic detrusor overactivity (NDO) and idiopathic detrusor overactivity (IDO), respectively. Since then, a dramatic decline in the use of AC has called into question its utility in the treatment algorithm of this difficult patient population. The purpose of this paper is to review the current body of literature in order to outline the circumstances in which AC is still a relevant therapeutic option.

How botulinum toxin in neurogenic detrusor overactivity can reduce upper urinary tract damage?

Intradetrusor injections of botulinum toxin are the cornerstone of medical treatment of neurogenic detrusor overactivity. The primary aim of this treatment is to ensure a low pressure regimen in the urinary bladder, but the mechanisms leading to long-term protection of the urinary tract remain poorly understood. In this paper, we highlight the potential benefits of intradetrusor injections of botulinum toxin regarding local effects on the bladder structures, urinary tract infections, stone disease, vesico ureteral reflux, hydronephrosis, renal function based on a comprehensive literature review.

Initial experience with the treatment of neurogenic detrusor overactivity with a new β-3 agonist (mirabegron) in patients with spinal cord injury

It is a retrospective chart analysis. In patients with neurogenic lower urinary tract dysfunction (NLUTD) due to spinal cord injury (SCI), neurogenic detrusor overactivity (NDO) can cause both deterioration of the upper urinary tract and urinary incontinence. Antimuscarinic treatment is frequently discontinued due to side effects or lack of efficacy, whereas injection of onabotulinumtoxin into the detrusor is a minimally invasive procedure with risks of urinary retention, infection and haematuria. Mirabegron, a new β-3 agonist, is a potential new agent for treatment of NDO. Aim of the study was to evaluate the efficacy of mirabegron in SCI patients with NLUTD. Swiss Paraplegic Center, Nottwil, Switzerland. A retrospective chart analysis of SCI patient treated with mirabegron. Fifteen patients with NDO were treated with mirabegron for a period of at least 6 weeks. Significant reduction of the frequency of bladder evacuation per 24 h (8.1 vs 6.4, P=0.003), and of incontinence episodes per 24 h (2.9 vs 1.3, P=0.027) was observed. Furthermore, we observed improvements in bladder capacity (from 365 to 419 ml), compliance (from 28 to 45 ml cm(-1) H(2)0) and detrusor pressure during storage phase (45.8 vs 30 cm H(2)0). At follow-up, 9/15 patients were satisfied with the therapy, 4/15 reported side effects (3 × aggravation of urinary incontinence, 1 × constipation). Mirabegron may evolve as an alternative in the treatment of NDO. We observed improvements in urodynamic and clinical parameters. Due to the limited number of patients and the retrospective nature of the study, prospective, placebo-controlled studies are necessary.

Efficacy of 200 IU versus 300 IU botulinum toxin intradetrusor injections in the treatment of neurogenic detrusor overactivity

Botulinum toxin is a second-line treatment for neurogenic detrusor overactivity [1] . The primary objective of this study was to compare the duration of efficacy of botulinum toxin intradetrusor injections (BTI) at a dose of 200 IU (only dosage approved by marketing authorisation (MA) in 2011) versus a dose of 300 IU (dose previously used). Retrospective review of a prospective cohort of all patients receiving BTI between 24 August 2011 (date of MA) and 1st March 2014 in Nantes, divided into 2 groups. Group 1 had already received BTI at a dose of 300 IU before the MA and group 2 initiated treatment at a dose of 200 IU. One hundred and thirty-four patients were followed for a mean of 4.7 years. In group 1 ( n = 83), the duration of efficacy was decreased in 49.7% of patients ( n = 41) at the 200 IU dose and the dose was subsequently increased to 300 IU in these patients. In group 2 ( n = 51), 37.3% of patients ( n = 19) failed to respond to a dose of 200 IU and the dose was increased to 300 IU. The mean duration of efficacy of BTI was significantly lower at 200 IU (7.7 months) compared to 300 IU (10.0 months) ( P = 0.001598). In group 1, a shorter previous duration of efficacy at 300 IU was a prognostic factor for failure of the 200 IU dose ( P = 0.0004421). In this study, the duration of efficacy of BTI was longer at a dose of 300 IU than at a dose of 200 IU. In other studies this result was not identified [2] , but is worthing discussing because of the benefit to the patient.

Current and potential urological applications of botulinum toxin A.

Botulinum toxin subtype A (BoNT-A) is a potent neurotoxin that can selectively modulate neurotransmitter release from nerve endings, resulting in muscular paralysis. BoNT-A might also act on sensory nerves, and have an anti-inflammatory effect. In the first urological use of BoNT-A, injection into the urethral sphincters of patients with detrusor-sphincter dyssynergia resulted in a reduction of urethral resistance and improved voiding efficiency. Subsequently, intravesical BoNT-A injections have received regulatory approval for treatment of neurogenic detrusor overactivity owing to spinal cord lesions or multiple sclerosis, and idiopathic overactive bladder in adults. BoNT-A has also been widely used to treat patients with the off-label indications of neurogenic or non-neurogenic voiding dysfunction and male lower urinary tract symptoms owing to BPH and bladder-neck dysfunction. Other indications for which urologists have applied BoNT-A injections include interstitial cystitis/bladder pain syndrome, bladder oversensitivity and chronic pelvic pain syndrome. BoNT-A is currently delivered as an intravesical injection; however, use of liposome encapsulated formulations is also beginning to show some therapeutic potential.

Transient receptor potential channel modulators as pharmacological treatments for lower urinary tract symptoms (LUTS): myth or reality?

Transient receptor potential (TRP) channels belong to the most intensely pursued drug targets of the last decade. These ion channels are considered promising targets for the treatment of pain, hypersensitivity disorders and lower urinary tract symptoms (LUTS). The aim of the present review is to discuss to what extent TRP channels have adhered to their promise as new pharmacological targets in the lower urinary tract (LUT) and to outline the challenges that lie ahead. TRP vanilloid 1 (TRPV1) agonists have proven their efficacy in the treatment of neurogenic detrusor overactivity (DO), albeit at the expense of prolonged adverse effects as pelvic 'burning' pain, sensory urgency and haematuria. TRPV1 antagonists have been very successful in preclinical studies to treat pain and DO. However, clinical trials with the first generation TRPV1 antagonists were terminated early due to hyperthermia, a serious, on-target, side-effect. TRP vanilloid 4 (TRPV4), TRP ankyrin 1 (TRPA1) and TRP melastatin 8 (TRPM8) have important sensory functions in the LUT. Antagonists of these channels have shown their potential in pre-clinical studies of LUT dysfunction and are awaiting clinical validation.

Effect of intravesical botulinum neurotoxin-A injection on detrusor hyperreflexia in spinal cord injured patients.

To evaluate the effects of Botulinum Toxin A injection into the detrusor muscle on various voiding parameters in spinal cord injured patients with neurogenic detrusor hyperreflexia Materials and methods: 24 patients with spinal cord injuries who had detrusor overactivity and urinary incontinence and were refractory to oral medications, were injected 300 IU of BTX-A into the detrusor muscle. The pre-and post-treatment evaluations included determination of bladder urinary continence status, frequency/volume chart of CIC, Incontinence Quality of Life questionnaire (I-QOL) and patient satisfaction. The urodynamic parameters measured included maximum cystometric capacity (MCC), reflex detrusor volume (RDV) and maximum detrusor pressure during bladder contraction (MDP) were analyzed at the outset and during the follow-up (2, 6, and 24 weeks) examinations. The evaluation of urodynamic parameters during follow-up examinations (2, 6 and 24 weeks) revealed significant increase in mean reflex volume (p<0.05) and cystometric capacity (p<0.05), on the other detrusor pressure decreased significantly (p<0.05). In majority of patients there was considerable reduction in incontinence episodes and no complications or side effects were reported. Most of the patents were satisfied with the treatment. The use of Botulinum toxin type A for treatment of neurogenic detrusor overactivity in spinal cord injured patients is safe and efficacious. In our 24-week study period, there was significant improvement in most urodynamic parameters with consistence and subjective satisfaction indicated by the treated patients.

Current and future drugs for treatment of MS-associated bladder dysfunction

A majority of patients diagnosed with multiple sclerosis (MS) will develop lower urinary tract symptoms (LUTS) during the course of the disease. Even if antimuscarinic (anticholinergic) treatment is currently the mainstay of conservative treatment of neurogenic detrusor overactivity (NDO), including MS-induced NDO, extensive data regarding their effectiveness and safeness are lacking. When antimuscarinic medications fail to prove efficacious, a further option is intradetrusor injections of onabotulinumtoxin A. In several studies, more than half (and up 76%) of the patients treated with onabotulinumtoxin A experienced significant improvement in symptoms or even achieved complete continence. Cannabis extracts have shown some promise but has still not gained wide acceptance as an effective treatment. Over the last few years many new disease-modifying drugs that have been approved and introduced for treatment of MS. These drugs may have effects not only on the MS disease process, but also on the disease symptoms, including LUTS. However, MS is not primarily a bladder disease and treatment of the underlying pathophysiology should be the main goal of treatment. Since most of the urology drugs are targeting LUTS, these drugs should be regarded as “adds on” to treatments modifying the underlying disorder. Considering that most of these drugs have not been studied specifically with respect to efficacy on LUTS, and since they are not without significant side effects, it seems important that if and when they are going to be used for treatment of bladder symptoms should be a joint decision between the neurologist and urologist taking care of the patient.

Effectiveness of botulinum toxin (300 UI) in the treatment of neurogenic detrusor overactivity (NDO) on the occurence of symptomatic urinary tract infections

Effectiveness of botulinum toxin (300 UI) in the treatment of neurogenic detrusor overactivity (NDO) on the occurence of symptomatic urinary tract infections