[THE IRRITABLE BLADDER IN WOMEN].
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Autonomic Nervous System Diseases↗
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Prolonged bladder distension: experience in the treatment of detrusor overactivity and interstitial cystitis.
Prolonged bladder distension continues to be recommended for the treatment of detrusor instability and other bladder conditions. We have reviewed our experience of the technique. A total of 45 patients have undergone 50 procedures. Only 1 of 29 patients with detrusor instability had sustained improvement. 6 of 7 patients with interstitial cystitis noted improvement, sustained in 3. All the other patients noted some improvement. There was a 20% complication rate. 33 (75%) of the living patients returned questionnaires with 27% feeling that the operation was worthwhile. We feel that prolonged distension of the bladder is unhelpful in the treatment of patients with detrusor instability. Its place in the management of patients with interstitial cystitis and irritative symptoms remains controversial. The place of simple bladder distension should be considered.
Adolescent↗
[Incontinence of the urine and the irritable bladder in the female].
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Androgens↗
Localization of M2 and M3 muscarinic receptors in human bladder disorders and their clinical correlations.
PURPOSE: We studied the cellular localization of muscarinic receptor subtypes 2 and 3 in the human bladder and related any changes in overactive and painful bladder syndromes to measures of clinical dysfunction. MATERIALS AND METHODS: Bladder specimens obtained from patients with painful bladder syndrome (11), idiopathic detrusor overactivity (12) and from controls with asymptomatic microscopic hematuria (16) were immunostained using specific antibodies to muscarinic receptor subtypes 2 and 3, and to vimentin, which is a marker for myofibroblasts. Immunostaining results were quantified with computerized image analysis and correlated with clinical dysfunction using frequency and urgency scores. RESULTS: Muscarinic receptor subtype 2 and 3 immunoreactivity was observed in the urothelium, nerve fibers and detrusor layers. In addition, strong myofibroblast-like cell staining, similar to vimentin, was present in the suburothelial region and detrusor muscle. A significant increase in suburothelial myofibroblast-like muscarinic receptor subtype 2 immunoreactivity was seen in patients with painful bladder syndrome (p = 0.0062) and idiopathic detrusor overactivity (p = 0.0002), and in muscarinic receptor subtype 3 immunoreactivity in those with idiopathic detrusor overactivity (p = 0.0122) with a trend in painful bladder syndrome. Muscarinic receptor subtype 2 and 3 immunoreactivity significantly correlated with the urgency score (p = 0.0002 and 0.0206, respectively) and muscarinic receptor subtype 2 immunoreactivity correlated with the frequency score (p = 0.0029). No significant difference was seen in urothelial and detrusor muscarinic receptor subtypes 2 and 3 or vimentin immunostaining. CONCLUSIONS: To our knowledge this is the first study to show the cellular localization of muscarinic receptor subtypes 2 and 3 in the human bladder. The increase in muscarinic receptor subtypes 2 and 3 immunostaining in myofibroblast-like cells in clinical bladder syndromes and its correlation with clinical scores suggests a potential role in pathophysiological mechanisms and the therapeutic effect of anti-muscarinic agents.
Adult↗
Depressed contractile responses to neurokinin A in idiopathic but not neurogenic overactive human detrusor muscle.
OBJECTIVE: The role of tachykinins such as neurokinin A in regulating bladder function is unclear, but NK2 receptors seem to mediate contraction in the human bladder and it has been suggested that these peptides may have a role in the pathophysiology of bladder dysfunction. The present study investigates neurokinin receptor-mediated contractility of detrusor muscle in the idiopathic overactive and neurogenic overactive bladder and investigates the neurokinin receptor subtypes involved. METHODS: Human bladder was obtained from patients undergoing cystectomy (normal) or clam cystoplasty (idiopathic overactive) and from patients with spinal injuries (neurogenic overactive). Strips of isolated detrusor muscle were mounted in physiological Krebs-bicarbonate solution and cumulative concentration-response curves to 1 nM to 300 microM neurokinin A (NKA) were obtained in the absence and presence of neurokinin receptor antagonists, either the NK2 receptor-selective antagonist SR 48968 or the NK3 receptor-selective antagonist SB 223412. RESULTS: NKA evoked concentration-dependent contraction of normal, idiopathic, and neurogenic overactive detrusor strips. In idiopathic overactive detrusor muscle, NKA-induced contraction was significantly reduced relative to normal detrusor (0.031 +/- 0.005 mg/g, n = 11 versus 0.193 +/- 0.039 mg/g, n = 7). Sensitivity to the peptide was also significantly (p < 0.01) reduced in idiopathic overactive detrusor, with mean pEC50 values (concentration producing 50% maximal response) of 6.62+/-0.16 (n = 11) compared to 7.47+/-0.19 (n = 7) in normal detrusor. In contrast, NKA-induced responses of neurogenic overactive detrusor were similar to those in normal detrusor, with a mean maximum contraction of 0.199 +/- 0.036 mg/g (n = 10) and mean pEC50 value of 7.85+/-0.16 (n = 10). NKA curves in all groups were shifted to the right by the NK2 receptor-selective antagonist SR 48968 with high affinity, pK(B) values being similar in normal, idiopathic, and neurogenic overactive detrusor (8.85 + 0.08, n = 14; 8.97 +/- 0.13, n = 12; 8.73 +/- 0.12, n = 8, respectively). In contrast the NK3 receptor-selective antagonist SB 223412 had a minimal effect on NKA responses and affinity values were low (pK(B) 5.81 +/- 0.11, n = 12 in normal; 5.75 +/- 0.08, n = 12 in idiopathic overactive, and 5.77 +/- 0.13, n = 11 in neurogenic overactive). CONCLUSION: These data indicate that NKA-induced responses are impaired in detrusor muscle from idiopathic overactive human bladder, but not in detrusor muscle from neurogenic overactive bladder. The NK2 receptor subtype appears to mediate NKA responses in the normal, idiopathic overactive, and neurogenic overactive detrusor. This is important evidence suggesting a difference between the bladder pathophysiology observed in idiopathic versus neurogenic overactive detrusor.
Benzamides↗
The pathophysiology of lower urinary tract symptoms after brachytherapy for prostate cancer.
OBJECTIVES: To determine the spectrum of pathophysiology underlying the lower urinary tract symptoms (LUTS) persisting for > or = 6 months after brachytherapy for localized prostate cancer. PATIENTS AND METHODS: A database of men from two practice settings was searched for men who developed LUTS persisting for > or = 6 months after completing brachytherapy for localized prostate cancer. Patients were evaluated with a structured history and physical examination, International Prostate Symptom Score (IPSS), 24-h voiding diary, noninvasive free-flow uroflowmetry, postvoid residual urine volume (PVR), cystoscopy and a video-urodynamic study. Specific data collected included symptoms, elapsed time since brachytherapy, Gleason score, IPSS, total number of voids/24 h, maximum voided volume, cystoscopic findings, and urodynamics findings (PVR, maximum urinary flow rate, Schaefer obstruction grade, Watts factor, incidence of detrusor overactivity (DO) urethral obstruction and low bladder compliance). These data were compared with those from a previous study of men with LUTS who did not have prostate cancer. RESULTS: The study included 47 men (aged 54-88 years); the median (range) interval between brachytherapy and evaluation was 1.5 (0.5-13) years. Thirty-seven men complained of overactive bladder symptoms (79%), and 31 of incontinence (71%), 21 of obstructive symptoms (44%), and persistent dysuria in 12 (26%). Comparison of urodynamic findings in men with unselected causes of LUTS vs LUTS due to brachytherapy revealed the following comparisons: DO in 252 of 541 (47%) unselected vs 28 of 33 (85%) brachytherapy, (P < 0.001); and urethral obstruction in 374 of 541 (69%) unselected vs 24 of 33 (73%) brachytherapy (P = 0.85). CONCLUSION: The pathophysiology and severity of persistent LUTS in men after brachytherapy differs from that of men with LUTS in the general population. Men after brachytherapy have a much higher incidence of DO, prostatic and urethral strictures and prostatic urethral stones.
Aged↗
Detrusor hyperactivity with impaired contractile function. An unrecognized but common cause of incontinence in elderly patients.
Little is known about the causes of urinary incontinence in institutionalized elderly people, despite the fact that $8 billion is annually devoted to diapering those afflicted. We have identified a specific physiological abnormality--detrusor hyperactivity with impaired contractile function (DHIC)--that, although previously unrecognized, is the second most common (33%) cause of incontinence in this setting. Detrusor hyperactivity with impaired contractile function is a distinct physiological subset of detrusor hyperreflexia and presents with a seemingly paradoxical set of findings: the bladder is overactive but empties ineffectively. This imparied emptying is due to diminished detrusor contractile function and is associated with bladder trabeculation, a slow velocity of bladder contraction, little detrusor reserve power, and a significant amount of residual urine. Aside from its high prevalence, the importance of DHIC is that it may present as urinary retention, may closely mimic prostatic outlet obstruction, may explain why past therapeutic trials for detrusor hyperreflexia have failed, and may necessitate a change in the current nosology of bladder dysfunction. Furthermore, DHIC may represent a more advanced stage in the natural history of detrusor hyperreflexia, a stage characterized by deterioration of detrusor contractile efficiency. Thus, this previously unrecognized cause of incontinence in the elderly is common and raises several important issues.
Aged↗
Refractory neurogenic detrusor overactivity.
Refractory neurogenic detrusor overactivity refers to the clinical condition that is no longer manageable by anticholinergic therapy. This condition represents a formidable task to caregivers because the treatment of urinary incontinence and adequate protection of the upper urinary tract become extremely difficult. Treatment options for refractory neurogenic detrusor overactivity include detrusor injections of botulinum toxin and intravesical instillation of vanilloid compounds, mainly resiniferatoxin, or anticholinergic drugs. If these options fail, bladder augmentation or sacral anterior root stimulation offers excellent outcomes, although at much higher costs and risks to the patients.
Botulinum Toxins, Type A↗
Treating neurogenic detrusor overactivity in order to manage autonomic dysreflexia - A systematic review.
INTRODUCTION: Autonomic dysreflexia (AD) is a severe and potentially life-threatening complication of a spinal cord injury (SCI), particularly in patients with lesions at or above the sixth thoracic level. Neurogenic detrusor overactivity (NDO) is one of the main triggering factors. The impact of NDO treatment on AD remains insufficiently clarified. METHODS: We conducted a systematic review of the literature in PubMed and Cochrane Database between January 1990 and May 2025. Eligible studies included patients with SCI and AD undergoing treatment for NDO, including antimuscarinics, botulinum toxin (BTX) or augmentation cystoplasty. The primary outcome was the assessment of systolic blood pressure (SBP) parameters in patients undergoing cystomanometry. RESULTS: Of the thirteen eligible studies, only five were included. No study evaluated augmentation cystoplasty. One study (12 patients) evaluating fesoterodine and four studies (95 patients) evaluating BTX injection demonstrated improved urodynamic parameters and a decrease in severity of AD during urodynamic studies and in daily life. Improvements in AD-HR-QoL and I-QoL scores were also demonstrated. DISCUSSION: Controlling NDO with fesoterodine or BTX injection reduces the prevalence and severity of AD, likely by limiting abnormal C-fiber recruitment and reducing neurogenic inflammation. BTX additionally modulates TRPV1-expressing afferents, which further reduces AD risk. Although hypertensive peaks improve, submaximal parameters remain unchanged, highlighting the need for additional complementary strategies. CONCLUSION: The use of BTX and fesoterodine for NDO treatment effectively reduces AD episodes in patients with SCI. Further long-term studies are needed to confirm the cardiovascular benefits and inform future therapeutic strategies.
Humans↗
Obstructive urodynamic findings in idiopathic detrusor overactivity.
PURPOSE: To investigate the obstructive findings urodynamically in idiopathic detrusor overactivity and compare them (maximum flow rate 'Q max' detrusor pressure at maximum flow 'PQ max') with control group. MATERIALS AND METHODS: Cystometric evaluation and pressure flow studies were performed in 25 women with symptoms of idiopathic detrusor overactivity and control group comprised 40 women with anatomic incontinence without cystocele. Patients with pelvic floor prolapse, motor urgency and poor compliance were excluded from the study. Q max less than 15 ml/s and PQ max more than 40 cm water were accepted as obstruction. RESULTS: After cystometric evaluation, obstruction was found in 36% of patients with idiopathic detrusor overactivity and 15% in control group. The range of maximum flow rate and PQ max values were 2-43.7 ml/s (mean 14.47 +/- 10.22) and 10-143 cm water (mean 58.97 +/- 35.13) in idiopathic urge syndrome group. These values were 6.6-51.8 ml/s (mean 23.24 +/- 12.43) and 9.7-61 cm water (mean 25.56 +/- 12.43) respectively in control group. Q max and PQ max parameters were compared statistically between the two groups. Idiopathic detrusor overactivity group had lower mean Q max and higher mean PQ max values than control group (P < 0.001) Table 1. CONCLUSION: Obstruction percentage was found to be more in idiopathic detrusor overactivity group than the control group.
Adult↗
[Vesical neuropathy in systemic vasculitis: 3 cases].
Bladder neuropathy was diagnosed in 3 patients with systemic vasculitis (temporal arteritis: 1 case; periarteritis nodosa: 2 cases). Clinical characteristics were: dysuria, diminished or abolished bladder sensation leading to indolent bladder retention. Urodynamic investigation showed hypotonic and underactive detrusor, increased detrusor compliance, hyposensitive bladder, and/or overactive urethral closure. Needle electrode examination showed signs of denervation of periurethral muscles; sacral evoked latencies were increased, favouring pudenal nerve alterations. Symptoms and urodynamic abnormalities resolved following corticosteroid therapy. Clinical and therapeutic implications of bladder neuropathy in necrotizing vasculitis are emphasized.
Adult↗
[Surgery with ileum segment for enlargement of bladder in the treatment of overactive neurogenic urinary incontinence: follow-up studies].
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Adolescent↗
The contribution of cholinergic detrusor excitation in a pig model of bladder hypocompliance.
OBJECTIVE: To investigate the role of cholinergic excitation in mediating changes in detrusor compliance (manifested on conventional cystometry as an incremental rise in detrusor pressure as bladder volume increases) under conditions of propofol-sedation in the pig. Materials and methods Consecutive cystometrograms (CMGs) were obtained from eight female Large White pigs at a bladder filling rate of 50 mL/min. The first CMG was obtained while the pig was awake and unsedated. Two subsequent CMGs were obtained after light to moderate sedation with propofol (2-8 mg/kg/h) before and after the administration of intravenous atropine (0.02 mg/kg). RESULTS: All bladders were highly compliant over the volumes instilled (before sedation) with a maximum pressure during the filling phase of 0.9 cmH2O and a compliance of 943 mL/cmH2O. After sedation with propofol, the maximum pressure during the filling phase increased to 14 cmH2O with a compliance of 69 mL/cmH2O. Atropine antagonized this change in compliance; after sedation and atropine, the maximum pressure during the filling phase decreased to 4 cmH2O (P < 0.05) and the compliance increased to 337 mL/cmH2O (P < 0.05). CONCLUSION: The decrease in compliance seen in the pig bladder after sedation with propofol is mediated via muscarinic excitation. This probably occurs as a result of low-level tonic release of acetylcholine by the efferent parasympathetic nerves. The existence of such efferent excitatory activity during the storage phase in the overactive human bladder might explain the efficacy of bladder-selective muscarinic antagonists in a proportion of patients with detrusor hyper-reflexia and instability.
Animals↗
Detrusor overactivity and urge urinary incontinence [corrected] following midurethral versus bladder sling procedures.
OBJECTIVE: The objective of the study was to compare detrusor overactivity and urge urinary incontinence rates after midurethral slings versus bladder neck slings. STUDY DESIGN: Three hundred forty subjects underwent midurethral slings or bladder neck slings. Comparisons were made using Student's t test and chi2 test. Multivariate analysis was performed to detect confounding factors. RESULTS: More patients in the midurethral sling group resolved detrusor overactivity than in the bladder neck sling group (38% versus 15%, P < .001). In addition, subjects in the midurethral sling group had significantly lower rates of de novo detrusor overactivity than subjects in the bladder neck sling group (29% versus 62%, P = .002). The only significant predictors of postoperative detrusor overactivity were preoperative detrusor overactivity (P < .001) and sling type (P < .001). After adjusting for preoperative detrusor overactivity, bladder neck slings significantly increased the risk for persistent detrusor overactivity (odds ratio 3.9). CONCLUSION: Midurethral slings have increased rates of resolution of detrusor overactivity and lower rates of de novo detrusor overactivity than transvaginal bladder neck sling procedures.
Aged↗
The spontaneously hypertensive rat: insight into the pathogenesis of irritative symptoms in benign prostatic hyperplasia and young anxious males.
Recent epidemiological studies have shown that hypertensive men are more likely to undergo surgical intervention for irritative voiding symptoms from BPH than age-matched controls. Indeed, noradrenergic nerves which regulate vascular tone also participate in the functional component of bladder outlet obstruction due to BPH. Newer, less invasive therapies for BPH such as thermal therapy can relieve symptoms yet do not eliminate obstruction based on urodynamic studies. Coincidentally, drugs such as alpha-adrenoceptor antagonists, which have been thought to relieve obstruction due to a peripheral effect, can be given intrathecally in animals to relieve urinary frequency due to obstruction. Taken together these observations implicate both peripheral and central sympathetic pathways in the motor control of the urinary bladder especially with disease states. We have used the hypertensive and behaviourally hyperactive spontaneously hypertensive rat (SHR), to investigate the roles sympathetic pathways or micturition. Elevated nerve growth factor (NGF) derived from vascular and bladder smooth muscle cells of the SHR appears to direct morphological, biochemical, and functional changes. The increase in NGF can apparently be explained by stabilization of its mRNA leading to increased synthesis in NGF. Bladders from SHRs develop a profuse noradrenergic hyperinnervation compared with the control WKY strain. Since afferents supplying the SHR bladder are hypertrophied, changes in afferent pathways are also likely. These differences in innervation and NGF in the SHR may explain changes in function. SHRs void 3 times as frequently as their genetic controls. Urinary frequency can be reduced by alpha-adrenoceptor antagonists. Cystometrograms performed in SHRs reveal lower bladder capacities and micturition volumes and the presence of unstable contractions compared with the WKY rat. Intrathecal, rather than intra-arterial administration of the alpha-adrenoceptor antagonist doxazosin reduces unstable contractions in the SHR. In vitro muscle bath studies have shown enhanced responses of SHR bladder smooth muscle to alpha-adrenoceptor agonists. It is likely that upregulation of NGF production causes sensory and possibly noradrenergic pathways to elicit hyperactive voiding. Increase in NGF in the adult bladder due to pathological conditions yields similar, yet distinct, consequences for voiding behaviour and innervation. Likewise, increased NGF in adult bladders following obstruction or inflammation triggers neuronal hypertrophy, enhanced reflex activity and urinary frequency. In contrast to the SHR, hyper-innervation is not observed. Moreover, peripheral or spinal alpha-adrenoceptor blockade eliminates urinary frequency following obstruction. These observations support the role for sympathetic pathways in the motor function of the bladder, especially in congenital or adult disease states. A similar process may underlie the neuroplasticity involved in alterations after obstruction or inflammation of the lower urinary tract in humans. The SHR strain raises the possibility that a common genetic defect exists capable of predisposing to both hypertension and overactivity of the urinary bladder. Whether a genetic predisposition to sustained bladder overactivity in response to inflammatory stimuli in obstruction exists in humans is an intriguing prospect.
Animals↗
Botulinum toxin type A injections for treating neurogenic detrusor overactivity combined with low-compliance bladder in patients with spinal cord lesions.
OBJECTIVE: To evaluate botulinum toxin type A (BTX-A) for treating neurogenic detrusor overactivity in patients with spinal cord lesions, including those with abnormally low bladder compliance. DESIGN: Nonrandomized, before-after trial (9-mo follow-up). SETTING: Hospitalized care. PARTICIPANTS: Ten patients with high detrusor contraction pressure and/or poor response to oxyphencyclimine with incontinence selected as a consecutive sample. INTERVENTION: BTX-A (Botox; 300U) was injected into the detrusor muscle. MAIN OUTCOME MEASURES: Urinary continence, functional bladder capacity, bladder compliance, detrusor contraction pressure, and volume at first reflex voiding. Measurements were taken before and 6, 16, and 36 weeks posttreatment. RESULTS: Six weeks after treatment, complete continence was restored in 7 patients without oxyphencyclimine. Mean functional bladder capacity (P=.008), compliance (P=.012), and reflex volume (P=.045) significantly increased, whereas maximal detrusor contraction pressure significantly decreased (P<.001). Urodynamic variables remained significantly improved at 16 weeks, but values were returning toward baseline levels by 36 weeks. The procedure was generally uneventful, without any serious side effects. CONCLUSIONS: BTX-A injections are an effective, well-tolerated treatment for neurogenic detrusor overactivity in patients with spinal cord lesions, even in patients with abnormally low bladder compliance. Patients may require repeat injections after 16 weeks to remain continent.
Adolescent↗
Clinical relevance of urodynamic investigation tests prior to surgical correction of genital prolapse: a literature review.
Urodynamic investigations have been advocated to be incorporated in the standard diagnostic workup of patients undergoing surgical correction of genital prolapse. Stress incontinence is reported by 40% of patients with genital prolapse. Urodynamic stress incontinence (USI) is diagnosed in 70-75% of these patients. Occult urodynamic stress incontinence (OUSI) is diagnosed in about 50% of the patients with genital prolapse not reporting stress incontinence before surgery. Performing urodynamic investigation in patients undergoing prolapse surgery may be valuable if diagnosing USI or OUSI results in the selection of the optimal treatment strategy. This treatment strategy is either a combination of prolapse and stress incontinence surgery or prolapse surgery at the beginning and re-evaluation of possible stress incontinence afterwards. The combination of prolapse and stress incontinence surgery has the advantage of attempting to solve two problems at the same moment, but carries an increased risk on unwanted side-effects, of which, voiding dysfunction and detrusor overactivity are the most important. This review presents a literature overview of what has been proven about the diagnostic and therapeutic value of urodynamic investigations in patients undergoing prolapse surgery.
Female↗
Anterior vaginal wall prolapse and voiding dysfunction in urogynecology patients.
We investigated whether women with and without anterior vaginal wall prolapse have voiding differences. Women (n=109) who presented to a urogynecology practice were categorized into two groups based on anterior vaginal wall prolapse: stages 0 and 1 and stages 2, 3, and 4. Women with prolapse were older than the women without prolapse but the groups were otherwise similar demographically. There was a higher rate of activity-related urine loss and use of wetness protection amongst women without prolapse. There was no significant difference for urgency symptoms or urge incontinence. Urodynamic testing found no significant differences for maximal flow rate or maximal urethral closing pressures. Postvoid residual volume and detrusor overactivity were not different but approached significance. Anterior vaginal wall prolapse of stage 2 or greater was not associated with urge incontinence or voiding function in this population. Women without prolapse were more likely to report stress incontinence.
Adult↗