PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “overactive bladder”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,261 records · Page 70Linked to original sources

The role of corticotropin releasing factor and its antagonist, astressin, on micturition in the rat.

The purpose of this investigation was to evaluate the role of corticotropin releasing factor (CRF) on micturition. CRF is involved in the endocrine and central nervous system responses to stress and is also expressed in sites responsible for the control of micturition. In this investigation, cystometric experiments were performed in awake and unrestrained Wistar rats and on Spontaneous Hypertensive Rats, which are used as a rodent model of detrusor overactivity and anxiety. In vitro effects of CRF were evaluated using strips of detrusor muscle in an organ bath preparation. CRF (6.0 microg) administered via intrathecal and intraperitoneal routes, but not intracerebroventricularly, lowered the micturition threshold. CRF reduced the intercontraction interval by 28% and 26% after intrathecal or intraperitoneal administration, respectively, and reduced micturition volume by 34.7% and 30.2%, respectively. In Wistar-Kyoto rats, 6.0 microg intrathecal CRF significantly reduced intercontraction interval (423 +/- 79 vs. 669 +/- 59 s) and micturition volume (0.30 +/- 0.04 vs. 0.69 +/- 0.07 ml) compared to controls that received saline vehicle. These effects were blocked by pretreatment with 6.0 mug intrathecal astressin, a potent CRF antagonist, demonstrating that the effects are CRF receptor mediated. In Spontaneous Hypertensive Rats, 6.0 mug intrathecal CRF was found to have minimal stimulatory effects on the bladder, whereas astressin reduced baseline detrusor overactivity. CRF had no direct contractile effects on detrusor muscle strips. These results demonstrate that in the absence of detrusor overactivity, CRF stimulates micturition when administered via the intrathecal or intraperitoneal routes. Further studies are needed to explore the possibility whether CRF antagonists are effective for detrusor overactivity and the overactive bladder syndrome.

Animals↗

[Clinical manifestations of urinary disorders and their treatment in ageing men].

PROBLEMS OF THE PROSTATE: Benign hypertrophy of the prostate (BHP), when it occurs, is manifested by an obstruction or irritation related to overactivity of the bladder. The obstructive syndrome is defined by urodynamic tests. Urge incontinence and study of the pressure-flow ratio are the tests of choice. The functional handicap and impact on quality of life are assessed using the International Prostatism Symptoms Score (I-PSS). Efficient and fairly well tolerated medical treatment has reduced the indications for surgery. It relies on alpha-blockers, 5a-reductase inhibitors and phytotherapy. When indicated, the surgical treatment of choice is endoscopic resection of the prostate. Among the non-prostatic micturition disorders, urge micturition with, in extreme cases, incontinence are due to detrusor instability. This is of multifactor origin; enhanced by the local irritation or environmental factors, it usually occurs within a context of acute or chronic pathologies. Treatment is recommended with anticholinergic agents. New molecules have recently been launched, better tolerated than oxybutinine. Electrostimulation can be a good alternative in mentally normal patients. Micturition due to excess urine may be due to overactivity of the bladder, the major risk of which is acute urine retention. It can also be observed during neurological affections such as Parkinson's disease or during administration of certain drugs. Nocturnal polyuria is a frequent problem. However, simple hygiene and dietary measures and the control of certain concomitant diseases can usually relieve the symptoms. Medical treatment relies on desmopressine.

Adult↗

Endothelial nitric oxide synthase expression in neurogenic urinary bladders treated with intravesical resiniferatoxin.

OBJECTIVE: To investigate endothelial nitric oxide synthase (eNOS) immunoreactivity in bladder biopsies from patients with neurogenic detrusor overactivity (NDO) before and after treatment with intravesical resiniferatoxin, and compare this with control material; the distribution of two other vascular markers, von Willebrand Factor (vWF) and the vascular endothelial growth factor (VEGF), was also studied. PATIENTS AND METHODS: Flexible cystoscopic bladder biopsies from eight controls investigated for asymptomatic microhaematuria and 19 patients with refractory spinal NDO enrolled in a clinical trial of intravesical treatment with escalating doses of resiniferatoxin were immunostained with polyclonal rabbit antibodies for eNOS, vWF and VEGF. Fewer baseline NDO specimens (eight) were available for vWF and VEGF staining. Computerized image analysis was used to quantify immunoreactivity, and the Mann-Whitney test for statistical analysis. RESULTS: eNOS immunoreactivity was found in the suburothelium and less often in the urothelium, with a distribution indicating a location in small blood vessels at the urothelium-suburothelium junction. Immunostaining for vWF showed a similar location. There was a trend to higher eNOS values before treatment in those responding than in those not responding to resiniferatoxin (P = 0.059), and a significant reduction in eNOS immunoreactivity after successful treatment (P = 0.016). VEGF staining was weaker but there was a significant increase in pretreatment biopsies of responders to resiniferatoxin (P = 0.048). Clinical and histopathology features were similar in both groups. CONCLUSIONS: The trend for higher eNOS expression in patients with NDO who responded to resiniferatoxin suggests that increased vasculature or vasodilatation in the suburothelium may be necessary for successful intravesical treatment. Further studies with more patients are required to confirm this relationship and to examine the mechanisms underlying changes in vasculature with levels of bladder overactivity.

Administration, Intravesical↗

Lower urinary tract dysfunction in Machado-Joseph disease: a study of 11 clinical-urodynamic observations.

OBJECTIVES: Machado-Joseph disease (MJD), or hereditary spinocerebellar ataxia type 3, is the most common dominantly inherited ataxia. However, lower urinary tract (LUT) dysfunction in MJD has not been fully delineated. We investigated LUT dysfunction in MJD by clinical-urodynamic observations. METHODS: In 24 genetically diagnosed MJD, we recruited all 11 patients with LUT symptoms (six men, five women; age, 18-61 [mean 48] years; disease duration, 2-24 [mean 9] years; voiding difficulty, 7, urinary incontinence, 4). Urodynamic studies consisted of uroflowmetry, measurement of post-void residuals and electromyography (EMG)-cystometry. Neurophysiology tests consisted of motor unit potential (MUP) analysis of the sphincter and extremity muscles, tibial nerve somatosensory evoked potentials (SEP) and nerve conduction studies (NCS) of the extremities. RESULTS: Urodynamic abnormalities were seen in all 11 patients studied. Maximum or average flow rate was decreased in five. Post-void residual was noted in three but residual urine volume > 100 ml was noted in only one patient. Maximum urethral closure pressure was low in one and high in one of five patients studied. EMG-cystometry during filling showed detrusor overactivity in five, impaired bladder sensation in four, low compliance detrusor in one, uninhibited sphincter relaxation in one and incompetent urethra in one. Voiding phase abnormalities included detrusor areflexia in three and detrusor-sphincter dyssynergia in two. Bethanechol supersensitivity of the bladder was noted in one of three patients studied. Bulbocavernosus reflex was absent in two of five patients studied. MUP analysis showed neurogenic changes in six of nine sphincter muscles and in all six extremity muscles studied. Five patients had prolonged or absent cortical response in SEP and four had sensory axonal neuropathy in NCS, which were relevant to the impaired bladder sensation. CONCLUSION: In the present study, a half of MJD patients had LUT symptoms and they showed various urodynamic abnormalities. Detrusor overactivity, impaired bladder sensation, and neurogenic sphincter EMG were common findings, and large post-void residuals were rare. These findings are relevant to central and peripheral nervous system pathology of MJD.

Adolescent↗

Altered neurogenic and mechanical responses to acetylcholine, ATP and substance P in detrusor from rat with outlet obstruction.

The well-known side effects of anticholinergic compounds used to treat urinary incontinence caused by detrusor overactivity have addressed the interest on other pharmacological intervention. The purpose of the present work was to investigate the possible changes in purinergic and cholinergic components of parasympathetic neurotransmission in obstructed rat bladders with detrusor overactivity, and to examine the effect of the association of suramin, atropine and indomethacin on nerve-mediated responses to electrical field stimulation (EFS). Mechanical responses to exogenous acetylcholine, ATP and substance P were also evaluated. Altered sensitivities to acetylcholine and to the sensory neurotransmitter substance P, but unchanged sensitivity to the stable ATP analogue alpha,beta-methyleneATP were observed in bladders from obstructed rats. Suramin and atropine inhibited purinergic and cholinergic components of the neurogenic responses evoked by EFS in detrusor strips from control and obstructed rats. Interestingly, suramin enhanced the antagonistic effect of atropine on neurogenic responses of detrusor strips at all frequencies of stimulation tested. Our results suggest that the association between an antimuscarinic drug and an antagonist of P2X purinoceptors such as suramin might be helpful to reduce the therapeutic dosage of the antimuscarinic drug, along with its side effects. This approach may be of interest in the therapy of patients with bladder incontinence caused by detrusor overactivity, which do not even respond to a maximal dosage of antimuscarinic drug.

Acetylcholine↗

Overactivity and structural changes in the chronically ischemic bladder.

PURPOSE: Our aim was to study the effect of chronic ischemia on bladder contraction and detrusor smooth muscle reactivity. The relationship between structural damage and functional changes in the chronically ischemic bladder was also investigated. MATERIAL AND METHODS: Male New Zealand White rabbits were divided into arterial injury (AI), hypercholesterolemia (Hch) and control groups. The AI group (n = 18) underwent balloon endothelial injury of the iliac arteries and received a 0.5% cholesterol diet. The Hch group (n = 8) received a 0.5% cholesterol diet alone. The control group (n = 8) received a regular diet. After 16 weeks, iliac artery and bladder wall blood flows were recorded. Cystometrograms and arteriography were obtained and bladder tissues were processed for isometric tension measurement in the organ bath and for histological evaluation. RESULTS: At 16 weeks, blood flow through the iliac arteries was significantly reduced in the AI group compared with the Hch and control groups. In the AI group, 8 animals developed severe bladder ischemia (SBI) defined as greater than 60% decrease in bladder blood flow, 7 animals developed moderate bladder ischemia (MBI) defined as 40 to 60% decrease in bladder blood flow, and 3 animals failed to develop significant bladder ischemia (<40% decrease in bladder blood flow). In the control animals, bladder blood flow increased prior to contraction, decreased during contraction and rebounded to baseline levels after contraction. In animals with MBI and SBI, the increase in bladder blood flow prior to contraction and the rebound of blood flow after contraction, both seen in control animals, were diminished. Detrusor overactivity (significant increase in the frequency of spontaneous bladder contractions) was observed in the MBI group and impaired bladder contraction in the SBI group. In the organ bath, bladder strips from the MBI group demonstrated increased contractile response to carbachol and electrical field stimulation (EFS) while bladder strips from the SBI group showed impaired contractility. Hch alone produced only short-lived ischemia during bladder contraction and caused significantly lesser functional changes compared with those seen in MBI. Histological examination showed atherosclerotic occlusion in the iliac arteries and bladder microcirculation and marked disruption of urothelium in the MBI and SBI groups. Severe fibrosis was seen in bladder tissue from the SBI group, moderate fibrosis in tissue from the MBI group and mild fibrosis in tissue from the Hch group. CONCLUSIONS: Our studies show that chronic MBI is associated with detrusor overactivity and increased smooth muscle contractility to carbachol and EFS while chronic SBI is associated with impaired detrusor contraction. The mechanism of chronic ischemia-induced bladder dysfunction is not known and may involve multiple physiologic and structural changes in the bladder nerves, receptors and contractile components. Our studies suggest that ischemia-induced structural damage in the urothelium and possible chronic exposure of the underlying tissue and nerves to the urine may also play a role in MBI-induced detrusor overactivity. SBI-induced impairment of bladder contraction may involve, in part, extensive fibrosis and loss of bladder smooth muscle. Histopathophysiologic changes in bladder tissue from our MBI model are similar to those seen in patients with detrusor instability, suggesting that chronic ischemia may play a role in the development of idiopathic detrusor instability.

Animals↗

Is the short-term outcome of transurethral resection of the prostate affected by preoperative degree of bladder outlet obstruction, status of detrusor contractility or detrusor overactivity?

AIM: The aim of this study was to investigate whether the preoperative degree of bladder outlet obstruction (BOO), detrusor underactivity (DUA) or detrusor overactivity (DO) affected the short-term outcome of transurethral resection of the prostate (TURP) for patients with lower urinary tract symptoms suggestive of benign prostatic hyperplasia (LUTS/BPH). METHODS: Ninety-two patients with LUTS/BPH aged 50 years or older who were considered to be appropriate candidates for TURP were included in this study. Pressure-flow study and filling cystometry were performed to determine BOO, DUA and DO before TURP. The efficacy of TURP was determined at 3 months after surgery using the efficacy criteria for treatment of BPH assessed by the International Prostate Symptom Score, QOL index, maximum flow rate and postvoid residual urine volume. RESULTS: On preoperative urodynamics, 60%, 40% and 48% of patients showed BOO, DUA and DO, respectively. After TURP, 76% showed 'excellent' or 'good' overall efficacy, whereas only 13% fell into the 'poor/worse' category. The efficacy was higher as the preoperative degree of BOO worsened. In contrast, neither DO nor DUA influenced the outcome of TURP. However, the surgery likely provided unfavorable efficacy for patients having DO but not BOO. Only 20% of the patients who had both DO and DUA but did not have BOO achieved efficacy. CONCLUSIONS: Transurethral resection of the prostate is an effective surgical procedure for treatment of LUTS/BPH, especially for patients with BOO. DUA may not be a contraindication for TURP. The surgical indication should be circumspect for patients who do not have BOO but have DO.

Aged↗

Efficacy of the combination of an alpha1-blocker with an anticholinergic agent in the treatment of lower urinary tract symptoms associated with bladder outlet obstruction.

The combination of an alpha1-blocker with an anticholinergic is a new and promising therapeutic approach for bladder outlet obstruction and detrusor overactivity. Both placebo-controlled and comparative studies have demonstrated that the addition of an anticholinergic in the conventional treatment of patients with bladder outlet obstruction is safe, as the likelihood of acute urinary retention is low. Although the pathophysiology of detrusor overactivity is unknown and most probably multifactorial, it is not expected that the voiding phase is influenced by regular doses of anticholinergics, although high doses may affect detrusor contraction. However, safety issues must be studied further. The combination of tamsulosin with propiverine or tolterodine, and of doxasosin with tolterodine has been shown to cause a significant improvement of lower urinary tract symptoms when compared with alpha1-blocker monotherapy. Indisputably, the existing literature provides clear evidence that the combination of an alpha1-blocker with an anticholinergic extends physicians ability to manage lower urinary tract symptoms caused by bladder outlet obstruction and overactive bladder syndrome.

Adrenergic alpha-1 Receptor Antagonists↗

The role of capsaicin-sensitive afferent fibers in the lower urinary tract dysfunction induced by chronic spinal cord injury in rats.

The role of capsaicin-sensitive afferents in neurogenic voiding dysfunction was studied in chronic spinal cord injured rats (SCI). Cystometry and external urethral sphincter (EUS) electromyography were performed on 2 consecutive days after induction of urethane anesthesia in SCI rats 6-8 weeks after spinal cord injury. SCI rats exhibited voiding abnormalities including: non-voiding contractions (NVCs) before micturition, increased volume threshold (VT) for initiating voiding, increased amplitude and duration of voiding contractions, decreased voiding efficiency, increased residual urine, and changes in the pattern of the EUS-EMG. In SCI rats, the EUS electromyogram (EUS-EMG) consisted of more prominent tonic activity, shorter periods of bursting activity, and a reduction in the ratio of silent to active periods during bursting. These changes were more prominent during deeper levels of anesthesia on day 1. Capsaicin (125 mg/kg, s.c., 4 days before urodynamic examination) reduced VT and the number of NVCs, decreased the amplitude and duration of voiding contractions, partially normalized the pattern of EUS-EMG activity, and improved the voiding efficiency on day 1 after induction of anesthesia but not on day 2. Capsaicin treatment increased the percentage of animals (from 55% to 80%) that voided on day 1. The results indicate that capsaicin-sensitive C-fiber bladder afferents are not essential for reflex micturition in SCI rats. However, these afferents do contribute to overactivity of the bladder and detrusor sphincter dyssynergia in deeply anesthetized SCI rats.

Afferent Pathways↗

Decreased expression of G protein-coupled receptor kinases in the detrusor smooth muscle of human urinary bladder with outlet obstruction.

AIM: We examine the expression of mRNA of G protein-coupled receptor kinase (GRK) subtypes and muscarinic acetylcholine receptor (M) subtypes in the detrusor smooth muscle of the human urinary bladder. Furthermore, we confirm the presence and the localization of GRK proteins in the detrusor smooth muscle of the obstructed bladder in comparison with the control bladder. METHODS: Detrusor smooth muscle tissues of the human urinary bladder were obtained from 12 male patients; 6 patients did not have bladder outlet obstruction, and the other 6 patients had bladder outlet obstruction. Portions of the dome or anterior wall of the urinary bladder were used for the present study. Reverse transcription/polymerase chain reaction for GRK2, M2 and M3 was performed using total RNA extracted from human urinary bladder detrusor. Antibodies to GRK2, GRK3 and GRK4 were used to confirm the presence of the protein product in the human urinary bladder using immunohistochemical staining and the western blotting technique. RESULTS: All complementary DNA (cDNA) transcribed from three different mRNA (M2, M3 and GRK2) were successfully amplified and size-fractionated. The expression of GRK2 protein was strong in the human bladder detrusor, but was significantly weakened by western blotting in obstructed bladder in comparison with control bladder. CONCLUSIONS: Failure in desensitization mechanisms of muscarinic acetylcholine receptors might be related to storage symptom elicited by overactivity in obstructed bladder with benign prostatic hyperplasia.

Blotting, Western↗

Home uroflowmetry for the evaluation of boys with urinary incontinence.

PURPOSE: We recorded uroflowmetry at home in boys with urinary incontinence and correlated the results with videourodynamics. MATERIALS AND METHODS: Thirty-nine boys (mean age 8.4 +/- 2.0 years) with urinary incontinence underwent home uroflowmetry for 1 weekend. Artifactual spikes in 1 or more uroflow curves were present in 16 home uroflowmetry recordings. One patient, in whom none of the uroflow curves was interpretable, was excluded from the study. Of the remaining 38 boys 18 had monosymptomatic nocturnal enuresis, and 20 had nocturnal enuresis and diurnal voiding symptoms. Percentage expected bladder capacity is defined as functional/expected bladder capacity x 100%. Normal and obstructive home uroflowmetry levels are defined as functional bladder capacity at least 50% expected bladder capacity associated with multiple bell-shaped and obstructive uroflow curves, respectively. Small functional bladder capacity is defined as capacity less than 50% expected bladder capacity, regardless of uroflow patterns. Videourodynamics and cystoscopy were performed in 17 patients. RESULTS: Normal home uroflowmetry was noted in 5 patients (13%), obstructive uropathy in 8 (21%) and small functional bladder capacity in 25 (66%). Urodynamically 3 boys with normal home uroflowmetry had normal voiding, and 6 with obstructive home uroflowmetry had bladder outlet obstruction (of whom 1 also had detrusor overactivity). In addition, of 8 boys with small functional bladder capacity 4 had detrusor overactivity, 3 had bladder outlet obstruction and 1 had both findings. CONCLUSIONS: Normal home uroflowmetry predicted normal voiding, and abnormal recordings implied abnormal voiding function in boys with incontinence. Bladder outlet obstruction and detrusor overactivity were frequently disclosed by obstructive home uroflowmetry and small functional bladder capacity.

Child↗

Can bladder outflow obstruction be diagnosed from pressure flow analysis of voiding initiated by involuntary detrusor overactivity?

PURPOSE: We investigated whether a diagnosis of bladder outflow obstruction could be established from pressure flow analysis of a void initiated by involuntary detrusor overactivity. MATERIALS AND METHODS: A total of 79 men with lower urinary tract symptoms were identified prospectively. In each subject 2 sequential pressure flow studies were performed during the same session. Pressure flow data were recorded during a voluntary void and voiding initiated by involuntary detrusor overactivity. Pressure flow parameters were compared using the paired t test and differences in classification according to the International Continence Society nomogram were analyzed using the chi-square test. RESULTS: The maximum flow rate showed no significant difference between voluntary voiding and voiding initiated by involuntary detrusor overactivity. Detrusor pressure at maximum flow showed a slight, statistically significant but not clinically significant increase during voiding initiated by involuntary detrusor overactivity. However, the diagnostic classification remained unchanged in 64 of 79 men (80%). In no case was the diagnosis altered from bladder outflow obstruction to nonobstruction or vice versa when comparing the 2 pressure flow studies. There were significant increases in maximum detrusor pressure and detrusor pressure at the initiation of voiding during voiding initiated by involuntary detrusor overactivity. CONCLUSIONS: This study demonstrates that increased detrusor pressure observed during voiding subsequent to detrusor overactivity does not change the diagnostic classification in 80% of men. The results provide evidence that bladder outflow obstruction can be reliably diagnosed based on pressure flow parameters recorded during voiding initiated by involuntary detrusor overactivity.

Adult↗

Micturitional disturbance in patients with chronic inflammatory demyelinating polyneuropathy.

Eight of 32 patients (25%) with chronic inflammatory demyelinating polyneuropathy (CIDP) had micturitional disturbance, which consisted of voiding difficulty (n = 4), urgency (n = 4), or urgency incontinence (n = 1). Urodynamic studies on four symptomatic patients showed disturbed bladder sensation in two, bladder areflexia in one, and neurogenic changes of the external sphincter in one, indicative of peripheral parasympathetic and somatic nerve dysfunctions. Cystometry also showed detrusor overactivity in two patients but no evidence of CNS involvement, evidence that bladder overactivity occurs by probable pelvic nerve irritation.

Adolescent↗

[Physiopathology of BPH obstruction].

The underlying BPH related mechanisms of outlet obstruction are outlined (modification of the shape of the bladder neck, failure of funnel formation, geometric variations of the urethra, alpha 1 adrenoceptors mediated sympathetic hyperactivity at the level of the lower genito-urinary tract). Bladder voiding dysfunction in response to prostate obstruction is also discussed and correlated to ultrastructural patterns and clinical symptoms. Finally, a pathogenetic mechanism for detrusor overactivity in obstructed bladder is suggested.

Humans↗

Electromotive drug administration of lidocaine to anesthetize the bladder before botulinum-A toxin injections into the detrusor.

STUDY DESIGN: Prospective, open label, cross-over-designed clinical study. OBJECTIVE: To evaluate the effectiveness of an instillation of lidocaine into the bladder with versus without electromotive drug administration (EMDA) to anesthetize the bladder before botulinum-A toxin injections. SETTING: Neurourology, Swiss Paraplegic Center, Balgrist University Hospital, Zurich, Switzerland. METHODS: In all, 28 patients with severe neurogenic detrusor overactivity but preserved bladder sensibility were treated with botulinum-A toxin injections into the detrusor muscle. A measure of 300 u of botulinum-A toxin (Botox) was injected at 30 sites sparing the trigone. Prior to the injection, the bladder was anesthesized with conventional lidocaine instillation in a group of 10 patients and with lidocaine instillation enhanced by EMDA in 28 patients. The patients scored the injection pain on a 10-point rating scale. Pain rating scores with versus without EMDA enhancement of the lidocaine instillation were analyzed and the costs of the EMDA procedure were compared to general/spinal anesthesia. RESULTS: The mean pain score of the 10 patients who underwent the injections of Botox after conventional lidocaine instillation was 4.0 (SD 1.6). Following EMDA enhanced lidocaine instillation slight even or no pain occurred during the injections of Botox, and the mean pain score was 0.5 (SD 0.2). Compared to spinal or general anesthesia, the local anesthesia saved around 15% of the costs. CONCLUSIONS: EMDA enhanced instillation of lidocaine enables a sufficient anesthesia of the bladder wall that ensures a painless application of the botulinum-A toxin injections into the detrusor muscle. This method may avoid general or spinal anesthesia in patients with preserved bladder sensibility. It ensures considerable cost reduction, avoids anesthesia-related risks and complications and enables the procedure on an outpatient basis.

Administration, Intravesical↗

Surgical reconstruction of cloacal malformation can alter bladder function: a comparative study with anorectal anomalies.

PURPOSE: Patients with cloacal anomalies often suffer bladder dysfunction with recurrent urinary infections and incontinence. We examined the effect of surgical reconstruction by posterior sagittal approach and total urogenital mobilization in either causing or worsening bladder dysfunction. MATERIALS AND METHODS: Between August 2000 and December 2002 all new patients with cloacal anomalies were prospectively studied to assess the effect of surgical reconstruction by posterior sagittal approach and total urogenital mobilization on bladder function. A comparable group of patients with anorectal malformation (ARM) were studied as comparative controls to assess the effect of posterior sagittal approach without urogenital surgery. Structural anatomy was defined by radiology. Natural filling urodynamics via suprapubic catheter were performed in all infants at 0.2 to 9 months (mean 3) before surgical reconstruction. This assessment was repeated 6 to 24 months (mean 14.8) after surgery, and changes in bladder function were determined by comparative statistics. RESULTS: A total of 10 patients with cloacal anomalies (5 with short [less than 3 cm] and 5 with long common channel [greater than 3 cm]) and 20 patients with anorectal malformation were consecutively studied. At presentation bladder dysfunction was present in 9 of 10 patients with cloacal anomalies and in 12 of 20 patients with ARM. After surgery there was significant deterioration in bladder function in half of the cloacal group (5 of 10 patients, p = 0.04) and in 1 of 20 patients with ARM (p = 0.7). Of the 5 patients with cloacal anomalies who had deterioration of bladder function urodynamic pattern of detrusor overactivity changed to inadequate (atonic) bladder in 4, all of whom had a long common channel at presentation. CONCLUSIONS: Patients with cloacal malformation have a high incidence of innate bladder dysfunction. However, surgical reconstruction by total urogenital mobilization can cause further deterioration of bladder function, particularly in the group with a long common channel. Urodynamic assessment is necessary to detect bladder dysfunction in these patients.

Abnormalities, Multiple↗

Is the bladder a reliable witness for predicting detrusor overactivity?

PURPOSE: We determined how well the symptoms of OAB syndrome correlate with urodynamic DO using International Continence Society definitions. MATERIALS AND METHODS: The study included adult males and females 18 years or older who attended a tertiary referral center for urodynamics from February 2002 to February 2004. Patients were selected based on OAB syndrome symptoms (urgency, urgency urinary incontinence and frequency). The percent of patients who had symptoms alone or in combination and DO was calculated. RESULTS: There was a better correlation in results between OAB symptoms and the urodynamic diagnosis of DO in men than in women. Of men 69% and 44% of women with urgency (OAB dry) had DO, while 90% of men and 58% of women with urgency and urgency urinary incontinence (OAB wet) had DO. Stress urinary incontinence seems to have accounted for the decreased rates in women since 87% of women with urgency urinary incontinence also had the symptom of stress urinary incontinence. The ICS definition does not specify what constitutes abnormal voiding frequency. Analysis of results showed that increasing voiding frequency did not have any effect on increasing the accuracy of diagnosis of DO except in women with 10 or more daytime micturition episodes. CONCLUSIONS: The bladder is a better and more reliable witness in men than in women with a greater correlation between OAB symptoms and urodynamic DO, more so in the OAB wet than in OAB dry patients.

Female↗

Oral nitric oxide donors: a new pharmacological approach to detrusor-sphincter dyssynergia in spinal cord injured patients?

PURPOSE: Detrusor-sphincter dyssynergia is a common cause of bladder outlet obstruction in spinal cord injured patients and leads to poor bladder emptying and high bladder pressures, which if left untreated might cause renal failure. In this study, we tested the recently published hypothesis that oral administration of a nitric oxide donor could be a new pharmacological approach to treat detrusor-sphincter dyssynergia in humans with spinal cord injury. METHODS: 12 male spinal cord injured patients presenting with neurogenic detrusor overactivity and detrusor-sphincter dyssynergia were studied. 6 performed clean intermittent catheterisation and 6 used suprapubic tapping for bladder emptying. During cystometry the bladder was filled until the first overactive bladder contraction accompanied by detrusor-sphincter dyssynergia occurred while bladder and external urethral sphincter pressures were continuously recorded. Then the bladder was emptied and the patients received 10 mg of isosorbide dinitrate sublingually. Resting pressures were recorded and cystometry was repeated starting 15 min after drug administration. Maximal and mean values for bladder and external urethral sphincter pressures were calculated in both fillings and statistically compared by analysis of variance for repeated measurements (level of significance p < 0.05). RESULTS: Nitric oxide significantly reduced external urethral sphincter pressures at rest (p < 0.05) and during dyssynergic contraction (p < 0.05) while bladder pressures at rest and during contraction as well as the reflex volume remained unchanged. In the patients who used suprapubic tapping for bladder emptying the mean post triggering residual volume was significantly reduced (p < 0.05). CONCLUSIONS: Oral administration of nitric oxide donors significantly reduced bladder outlet obstruction due to detrusor-sphincter dyssynergia suggesting a role for nitric oxide in inhibitory neurotransmission to the urethral sphincter. This new approach could offer a potential pharmacological option to treat detrusor-sphincter dyssynergia in spinal cord injured patients.

Administration, Oral↗