Open-label study evaluating outpatient urethral sphincter injections of onabotulinumtoxinA to treat women with urinary retention due to a primary disorder of sphincter relaxation (Fowler's syndrome).

OBJECTIVES: To assess the efficacy (defined as improvements in maximum urinary flow rate [Qmax ] of ≥50%, post-void residual urine volume [PVR] and scores on the International Prostate Symptom Score [IPSS] questionnaire) and safety of urethral sphincter injections of onabotulinumtoxinA in women with a primary disorder of urethral sphincter relaxation, characterised by an elevated urethral pressure profile (UPP) and specific findings at urethral sphincter electromyography (EMG), i.e. Fowler's syndrome. PATIENTS AND METHODS: In this open-label pilot Institutional Review Board-approved study, 10 women with a primary disorder of urethral sphincter relaxation (elevated UPP, sphincter volume, and abnormal EMG) presenting with obstructed voiding (five) or in complete urinary retention (five) were recruited from a single tertiary referral centre. Baseline symptoms were assessed using the IPSS, and Qmax and PVR were measured. After 2% lidocaine injection, 100 U of onabotulinumtoxinA was injected into the striated urethral sphincter, divided on either side, under EMG guidance. Patients were reviewed at 1, 4 and 10 weeks after injection, and assessed using the IPSS, Qmax and PVR measurements. The UPP was repeated at week 4. RESULTS: The mean (range) patient age was 40 (25-65) years, and the mean symptom scores on the IPSS improved from 25.6 to 14.1, and the mean 'bother' score reduced from 6.1 to 3.5 at week 10. As compared with a baseline mean Qmax of 8.12 mL/s in the women who could void, the Qmax improved to 15.8 mL/s at week 10. Four of the five women in complete retention could void spontaneously, with a mean Qmax of 14.3 mL/s at week 10. The mean PVR decreased from 260 to 89 mL and the mean static UPP improved from 113 cmH2 O at baseline to 90 cmH2 O. No serious side-effects were reported. Three women with a history of recurrent urinary tract infections developed a urinary tract infection. There were no reports of stress urinary incontinence. Seven of the 10 women opted to return for repeat injections. CONCLUSIONS: This pilot study shows an improvement in patient-reported lower urinary tract symptoms, and the objective parameters of Qmax , PVR and UPP, at 10 weeks after urethral sphincter injections of onabotulinumtoxinA. No serious side-effects were reported. This treatment could represent a safe outpatient treatment for young women in retention due to a primary disorder of urethral sphincter relaxation. However, a larger study is required to confirm the findings of this pilot study.

Is overactive bladder a brain disease? The pathophysiological role of cerebral white matter in the elderly.

Small-vessel disease of the brain affecting the deep white matter characteristically manifests with neurological syndromes, such as vascular dementia and vascular parkinsonism. There is, however, compelling evidence to suggest that white matter disease can cause overactive bladder and incontinence, and in some patients these might be the initial manifestation. As white matter disease increases significantly with age, and preferentially affects the prefrontal deep white matter, white matter disease becomes an anatomical substrate in the brain etiology of overactive bladder. Treatment entails the management of small-vessel disease risk factors and anticholinergic drugs that do not easily penetrate the blood-brain barrier, to improve bladder control. In short, when caring for elderly overactive-bladder patients, we should look at both the brain and the bladder.

The neural control of micturition.

Micturition, or urination, occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. The neural circuitry that controls this process is complex and highly distributed: it involves pathways at many levels of the brain, the spinal cord and the peripheral nervous system and is mediated by multiple neurotransmitters. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary or reflex micturition, leading to urinary incontinence. This is a major health problem, especially in those with neurological impairment. Here we review the neural control of micturition and how disruption of this control leads to abnormal storage and release of urine.

Bladder dysfunction in a transgenic mouse model of multiple system atrophy.

Multiple system atrophy (MSA) is an adult-onset neurodegenerative disorder presenting with motor impairment and autonomic dysfunction. Urological function is altered in the majority of MSA patients, and urological symptoms often precede the motor syndrome. To date, bladder function and structure have never been investigated in MSA models. We aimed to test bladder function in a transgenic MSA mouse featuring oligodendroglial α-synucleinopathy and define its applicability as a preclinical model to study urological failure in MSA. Experiments were performed in proteolipid protein (PLP)-human α-synuclein (hαSyn) transgenic and control wild-type mice. Diuresis, urodynamics, and detrusor strip contractility were assessed to characterize the urological phenotype. Bladder morphology and neuropathology of the lumbosacral intermediolateral column and the pontine micturition center (PMC) were analyzed in young and aged mice. Urodynamic analysis revealed a less efficient and unstable bladder in MSA mice with increased voiding contraction amplitude, higher frequency of nonvoiding contractions, and increased postvoid residual volume. MSA mice bladder walls showed early detrusor hypertrophy and age-related urothelium hypertrophy. Transgenic hαSyn expression was detected in Schwann cells ensheathing the local nerve fibers in the lamina propria and muscularis of MSA bladders. Early loss of parasympathetic outflow neurons and delayed degeneration of the PMC accompanied the urological deficits in MSA mice. PLP-hαSyn mice recapitulate major urological symptoms of human MSA that may be linked to αSyn-related central and peripheral neuropathology and can be further used as a preclinical model to decipher pathomechanisms of MSA.

Nerve growth factor (NGF): a potential urinary biomarker for overactive bladder syndrome (OAB)?

UNLABELLED: WHAT'S KNOWN ON THE SUBJECT? AND WHAT DOES THE STUDY ADD?: The search for a biomarker in overactive bladder syndrome (OAB) is an emerging field of interest, as bladder dysfunction is a common complaint that causes significant morbidity. A biomarker may give us insight as a diagnostic tool, and also inform us about how severe the condition is, how it may progress and how it may best be treated. The protein of interest here is nerve growth factor (NGF) and it has been shown to be a dynamic molecule in the bladder of patients with OAB. Urinary levels have been seen to rise in patients with OAB and fall in those who respond to treatment. However, there have also been many studies that examine this trend in numerous other conditions, e.g. interstitial cystitis, bladder outflow obstruction, renal stone disease and patients with neurological impairment after stroke. As a result the specificity of this as a potential urinary biomarker for OAB is questioned. This is a review of published studies, which discusses the pros and cons of NGF as a potential urinary biomarker. The evidence is examined and the studies are summarised together in a Table. Questions remain about the reliability, practicality and specificity of NGF as a biomarker for OAB. These questions need to be addressed by further studies that could clarify the points raised. OBJECTIVE: To review the current literature on the use of urinary nerve growth factor (NGF) as a potential biomarker for overactive bladder syndrome (OAB). METHOD: A comprehensive electronic literature search was conducted using the PubMed database to identify publications relating to urinary NGF. RESULTS: There are a growing number of publications that have measured urinary NGF levels in different types of bladder dysfunction. These range from OAB, bladder pain syndrome, idiopathic and neurogenic detrusor overactivity, bladder oversensitivity and bladder outflow obstruction. Urinary NGF levels do appear to be raised in these pathological states when compared with healthy control samples. In patients with OAB, these raised urinary NGF levels appear to also reduce after successful treatment with antimuscarinics and botulinum toxin A, which indicates a potential use in monitoring responses to treatment. However, raised levels are not limited to OAB, which questions its specificity. Urinary NGF measurements are performed with an enzyme-linked immunosorbent assay using polyclonal antibodies to NGF. The technique requires standardisation, and the different antibodies to NGF require validating. Also a definition of what is the 'normal' range of NGF in urine is still required before it can be used as a diagnostic and prognostic tool. CONCLUSIONS: Whilst the evidence for an increased urinary NGF in OAB appears convincing, many questions about its validity remain including: specificity, sensitivity, cost- and time-effectiveness. Many criteria for what constitutes a biomarker still need to be evaluated and met before this molecule can be considered for this role.

Inhibitory control task is decreased in vascular incontinence patients.

OBJECTIVE: 'Vascular incontinence' is a part of elderly incontinence due to cerebral white matter change (WMC). We studied the relationship between performance on several cognitive tasks and urodynamic detrusor overactivity (DO) in patients with vascular incontinence. METHODS: We recruited 40 patients with lower urinary tract symptoms due to WMC [20 male, 20 female; mean age 77 years (60-89 years)]. Other neurologic, urologic, and systemic causes of LUT dysfunction were excluded. All patients underwent urodynamics tests and two sets of cognitive tasks, i.e., the Mini-Mental State Examination (MMSE) (general cognitive tasks), and the Frontal Assessment Battery (FAB) (frontal lobe tasks). RESULTS: The most common urinary symptom was urinary urgency (27 patients), followed by urinary incontinence (26) and nocturnal urinary frequency (25). The urodynamic testing revealed DO in 22 patients. The cognitive testing revealed that the patients' mean MMSE score was 25.8 (range 15-30), and their mean FAB score was 13.6 (4-18). There was no relationship between DO and the total MMSE or FAB score, but our analysis of the relationship between DO and the six subdomains of the FAB (conceptualization, mental flexibility, programming, sensitivity to interference, inhibitory control, and environmental autonomy) revealed a significant relationship between DO and the inhibitory control task (p < 0.005). CONCLUSIONS: The results of the present study showed that performance on an inhibitory control task is decreased in vascular incontinence patients with DO.

Urinary retention for the neurologist.

Urinary retention is a common problem, most often due to an anatomical lesion in the urinary tract causing obstruction, such as a urethral stricture or prostate enlargement. However, a subset of patients have no structural urological lesion, and so require neurological evaluation. We present a patient with acute urinary retention who was found to have chronic meningitis, and review the neurological causes for urinary retention.

Development and Validation of a Prognostic Model to Predict Overall Survival in Multiple System Atrophy.

Background: Multiple system atrophy (MSA) is a devastating disease characterized by a variable combination of motor and autonomic symptoms. Previous studies identified numerous clinical factors to be associated with shorter survival. Objective: To enable personalized patient counseling, we aimed at developing a risk model of survival based on baseline clinical symptoms. Methods: MSA patients referred to the Movement Disorders Unit in Innsbruck, Austria, between 1999 and 2016 were retrospectively analyzed. Kaplan-Meier curves and multivariate Cox regression analysis with least absolute shrinkage and selection operator penalty for variable selection were performed to identify prognostic factors. A nomogram was developed to estimate the 7 years overall survival probability. The performance of the predictive model was validated and calibrated internally using bootstrap resampling and externally using data from the prospective European MSA Study Group Natural History Study. Results: A total of 210 MSA patients were included in this analysis, of which 124 patients died. The median survival was 7 years. The following clinical variables were found to significantly affect overall survival and were included in the nomogram: age at symptom onset, falls within 3 years of onset, early autonomic failure including orthostatic hypotension and urogenital failure, and lacking levodopa response. The time-dependent area under curve for internal and external validation was >0.7 within the first 7 years of the disease course. The model was well calibrated showing good overlap between predicted and actual survival probability at 7 years. Conclusion: The nomogram is a simple tool to predict survival on an individual basis and may help to improve counseling and treatment of MSA patients.

The possible role of opiates in women with chronic urinary retention: observations from a prospective clinical study.

PURPOSE: Urinary retention in women often presents a diagnostic difficulty, and the etiology may remain unidentified even after excluding structural and neurological causes. We evaluated a group of women referred to a specialist center with unexplained urinary retention. MATERIALS AND METHODS: A total of 61 consecutive women with complete urinary retention were evaluated. Urological and neurological investigations locally had failed to identify a cause. Urethral pressure profile, sphincter volume measurement and in some cases urethral sphincter electromyography were performed to diagnose a primary disorder of sphincter relaxation (Fowler's syndrome). RESULTS: Mean patient age was 39 years (range 18 to 88). Following investigations, a probable etiology was identified in 25 (41%) women, the most common being Fowler's syndrome. Of the women 24 (39%) were being treated with opiates for various pain syndromes and in 13 no other cause of retention was identified. Opiates could be discontinued in only 2 patients, and both demonstrated improved sensations and voiding. CONCLUSIONS: The cause of urinary retention may remain unknown in spite of extensive investigations. Young women regularly using prescription opiates for various undiagnosed pain syndromes present a challenging clinical problem and this study suggests that iatrogenic causes should be considered if voiding difficulties emerge. An association between opiate use and constipation is well-known and, although urinary retention is a listed adverse event, it appears to be often overlooked in clinical practice. It is hypothesized that Fowler's syndrome is due to an up-regulation of spinal cord enkephalins and that exogenous opiates may compound any functional abnormalities predisposing young women to urinary retention.

Long-term effect on quality of life of repeat detrusor injections of botulinum neurotoxin-A for detrusor overactivity in patients with multiple sclerosis.

PURPOSE: We studied the effect of repeat detrusor botulinum neurotoxin type A injections on urinary symptoms, health and quality of life in patients with refractory neurogenic detrusor overactivity secondary to multiple sclerosis. MATERIALS AND METHODS: This was a prospective, open label, single center study in 137 patients with multiple sclerosis treated with detrusor injections of botulinum neurotoxin type A with observations made from 2002 to 2009. A minimally invasive outpatient technique was used for injection. Patients were asked to contact the department if and when they required repeat treatment. Recurrent detrusor overactivity was then identified on urodynamics. The primary outcomes measured were the change in symptoms and quality of life, as assessed by the Urogenital Distress Inventory, Incontinence Impact Questionnaire and EuroQol-5 Dimensions questionnaires (www.ion.ucl.ac.uk/departments/repair/themes/uroneurology) before and 4 weeks after botulinum treatment. Continence status, the need for clean intermittent self-catheterization before and after injections, and interinjection intervals were also analyzed. RESULTS: Mean Urogenital Distress Inventory and Incontinence Impact Questionnaire 7 scores showed considerable improvement 4 weeks after each treatment even when repeated 6 times. Almost all patients relied on clean intermittent self-catheterization after treatment. Before the first treatment 83% of patients were incontinent but 4 weeks after the first treatment 76% (104 of 137) became completely dry. This efficacy was sustained with repeat injections. The median interval between re-treatments remained constant at 12 to 13 months. CONCLUSIONS: Repeated detrusor botulinum neurotoxin type A injections for refractory neurogenic detrusor overactivity in patients with multiple sclerosis have a consistent effect on bladder control, resulting in sustained improvement in quality of life.

Comparison of the impact on health-related quality of life of repeated detrusor injections of botulinum toxin in patients with idiopathic or neurogenic detrusor overactivity.

STUDY TYPE: Therapy (case series). LEVEL OF EVIDENCE: 4. What's known on the subject? and What does the study add? We know that repeated injections of botulinum toxin A are effective in treating refractory detrusor overactivity particularly in NDO. This study shows that in both NDO and IDO repeated injections of the toxin improve quality of life as assessed by three validated questionnaires. The effect is most marked after the first injection in NDO patients but thereafter similar in both groups. OBJECTIVE: To compare the effect of repeated detrusor injections of botulinum toxin (BoNT-A) on health-related quality of life (HRQL) in patients with idiopathic (IDO) or neurogenic detrusor overactivity (NDO). PATIENTS AND METHODS: Between 2003 and 2009, 151 patients (109 with NDO and 42 with IDO) were treated by BoNT-A (Botox®, Allergan Inc., Irvine, CA, USA). Changes in HRQL were assessed using the validated short forms of Urogenital Distress Inventory (UDI-6), the Incontinence Impact Questionnaire (IIQ-7) and EuroQOL-5D (EQ-5D) before and 4 weeks after BoNT-A. RESULTS: The maximum number of repeated injections was five (mean±sd, 2.8±1.05). Mean±sd follow-up was 27.49±17.01 months. The UDI-6 and IIQ-7 questionnaires showed a consistent improvement after repeated injections in both groups with detrusor overactivity. The EQ-5D was not statistically different before and after each injection in either the NDO or IDO population. After repeated injections, no statistical differences in the change on the UDI-6 and IIQ-7 scores were found between NDO and IDO, except after the first treatment, when the decrease in UDI-6 was higher in NDO than in IDO. The EQ-5D anxiety and depression subscore improved in both groups after each injection and with the number of injections. In IDO, after the second injection, no patient reported extreme anxiety or depression and, after the fourth injection, none had anxiety or depression. The inter-injection interval was shorter after the first injection in those with NDO than in IDO but was similar thereafter. CONCLUSIONS: Intradetrusor injections of BoNT-A improved the HRQL of both NDO and IDO patients. Although improvement in HRQL was greater and the duration of efficacy shorter in NDO patients after the first injection, there was no significant difference after subsequent injections. Mean inter-injection interval in IDO and in NDO patients was similar from the second injection onwards and improvements in HRQL score were the same.

Bowel biofeedback treatment in patients with multiple sclerosis and bowel symptoms.

BACKGROUND: Bowel symptoms are common in patients with multiple sclerosis, but current treatment is empirical. OBJECTIVE: This study aimed to identify effect of biofeedback on bowel symptoms, mood, and anorectal physiology in patients with multiple sclerosis. DESIGN: This was a prospective observational study: the amount of change between pre- and posttreatment values of outcome measures was compared and analyzed. Responders were considered to be patients who demonstrated an improvement greater than or equal to the 25th percentile of the change in bowel score. Comparison between responders and nonresponders was performed. SETTINGS: This investigation was conducted at a neurogastroenterology clinic, tertiary referrals center. PATIENTS: Thirty-nine patients with multiple sclerosis and constipation and/or fecal incontinence were included in the study. INTERVENTION: Patients were given bowel biofeedback therapy. MAIN OUTCOME MEASURES: The primary outcome measures were the Wexner Constipation and Wexner Incontinence scores. The secondary outcome measures were hospital anxiety and depression scores and anorectal physiology parameters. RESULTS: Data are reported as median and interquartile ranges. After biofeedback there was significant improvement in Wexner Constipation (12 (5-19) pretreatment vs 8 (4-14) posttreatment, P = .001), Wexner Incontinence (12 (3-15) pretreatment vs 4 (2-10) posttreatment, P < .001) and hospital depression scores (7 (3-11) pretreatment vs 5 (3-10) posttreatment, P = .015). The 5-second endurance squeeze pressure was also improved (21 (11-54) mmHg pretreatment vs 43 (26-59) mmHg posttreatment, P = .001). Posttreatment change of Wexner Constipation was -2(-5/0), and of Wexner Incontinence was -3(-9/0) ("-" indicates improvement). Therefore, those patients who had a reduction of at least 5 points in the Wexner Constipation score and/or of at least 9 points in the Wexner Incontinence score were considered responders (18 patients, 46%). They showed a greater improvement of only 5-second endurance squeeze pressure (23.5 (7.5/32.75) mmHg responders vs 4 (-6/20) mmHg nonresponders, P = .008); no difference was observed in the comparison of baseline variables with nonresponders. Significant negative relationship existed between the change in the Wexner Constipation score (-2 (-5/0)) and the pretreatment Wexner Constipation score (12 (5/19), ß = -0.463, P < .001), and the change in the Wexner Incontinence score (-3 (-9/0)) with the pretreatment Wexner Incontinence score (12 (3/15), ß = -0.590, P < .001). So, the higher the initial bowel symptom score, the greater the improvement. LIMITATIONS: This study was limited by the lack of a control group. CONCLUSIONS: Biofeedback improves bowel symptoms, depression, and 5-second endurance squeeze pressure in patients with multiple sclerosis.

Neurogenic detrusor overactivity in patients with spinal cord injury: evaluation and management.

Lower urinary tract dysfunction can have a significant impact on patients with spinal cord injury. Over the years, many treatment options have become available. This article reviews the assessment and management of neurogenic detrusor overactivity, with a particular focus on articles from the recent literature. Recent guidelines on the subject will be discussed. Management options include antimuscarinics and bladder emptying measures, botulinum toxin A, and neuromodulation in refractory cases and surgery for intractable cases. Recent and relevant publications in these areas will be summarized and discussed.

Urinary incontinence following deep brain stimulation of the pedunculopontine nucleus.

Low-frequency deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) has been reported to improve akinesia and gait difficulties in patients with Parkinson's disease (PD). We report on a patient with PD and L: -dopa refractory gait symptoms who developed detrusor over-activity immediately after right PPN DBS. Proximity between caudal PPN and brainstem structures implicated in control of micturition is a possible explanation.

Immunohistochemical expression of muscarinic receptors in the urothelium and suburothelium of neurogenic and idiopathic overactive human bladders, and changes with botulinum neurotoxin administration.

PURPOSE: To investigate the possible associations of urothelial and suburothelial muscarinic receptors with human bladder pathophysiology we examined the immunohistochemical expression of muscarinic receptors types 1, 2 and 3 in the bladder urothelium and suburothelium of patients with neurogenic or idiopathic detrusor overactivity compared with that in controls. We also examined associations with patient quantified symptoms and the effect of intradetrusor botulinum neurotoxin type A treatment. MATERIALS AND METHODS: We obtained bladder biopsies from 36 patients with detrusor overactivity before, and 4 and 16 weeks after treatment with intradetrusor botulinum neurotoxin type A via flexible cystoscopy. Patients with neurogenic detrusor overactivity were injected with 300 U botulinum neurotoxin type A and those with idiopathic detrusor overactivity received 200 U. Control biopsies were taken from 7 patients during investigation for asymptomatic microscopic hematuria. We studied muscarinic receptor immunohistochemical expression using commercial antibodies to muscarinic receptors 1, 2 and 3 with results quantified by image analysis. RESULTS: We noted decreased suburothelial muscarinic receptor immunoreactivity in detrusor overactivity biopsies vs controls, which were significant for muscarinic receptors 1 and 3. After successful botulinum neurotoxin treatment we noted only increased muscarinic receptor 1 and 2 immunoreactivity. Urothelial muscarinic receptor 1 and 3 immunoreactivity was increased after treatment. We identified no substantial urothelial muscarinic receptor 2 immunoreactivity. Receptor levels showed inverse correlations with patient urgency and frequency. CONCLUSIONS: Decreased muscarinic receptor levels in the urothelium and suburothelium of patients with detrusor overactivity were largely restored to control levels after successful treatment with botulinum neurotoxin type A. Correlations of receptor levels with patient symptoms further support a role for urothelial and suburothelial muscarinic receptors in detrusor overactivity in humans.

A decade of functional brain imaging applied to bladder control.

Over the last 10 years functional brain imaging has emerged as the most powerful technique for studying human brain function. Although the literature is now vast, including studies of every imaginable aspect of cortical function, the number of studies that have been carried out examining brain control of bladder function is relatively limited. Nevertheless those that have been reported have transformed our thinking. This article reviews that development in the context of emerging ideas of interoception and a working model of brain activity during bladder filling and emptying is proposed. Some studies have also been carried out using functional imaging methods to examine pathophysiological bladder conditions or the effect of treatments and these are reviewed and future work anticipated.

Lower urinary tract symptoms following neurological illness may be influenced by multiple factors: observations from a neurorehabilitation service in a developing country.

AIMS: To evaluate the pattern of lower urinary tract dysfunction (LUTD) in patients with neurological disease in the setting of a rehabilitation service in a developing country, and analyze causes for unexpected lower urinary tract symptoms (LUTS). METHODS: Patients with neurological disorders and having significant LUTS were prospectively evaluated. Level of neurological lesion was localized by neurological examination and investigations. LUTD was evaluated by symptom analysis, bladder diaries and ultrasonography. Storage symptoms were managed using antimuscarinic medications and voiding dysfunction, when significant, was managed by catheterization and patients were regularly followed up. Patients with symptoms that had not been expected based upon their level of neurological lesion were further evaluated. RESULTS: Fifty patients (mean age 43.5 +/- 18.3 years) were included and according to neurological localization, were categorized into suprapontine (n = 9; 18%), infrapontine/suprasacral (n = 25; 50%) or infrasacral (n = 16; 32%) groups. Incontinence was more common in patients with suprapontine and infrapontine/suprasacral lesions (n = 20) (P < 0.03), hesitancy more common with infrapontine/suprasacral lesions (n = 20) (P = 0.004) and retention more with infrasacral lesions (n = 13) (P < 0.001). Patients belonging to suprapontine and infrapontine/suprasacral groups more likely showed improvement at follow up (P = 0.008). Fourteen patients (28%) had unexpected LUTS and this was due to urological causes (n = 6) or multiaxial neurological involvement (n = 8). Potentially treatable factors were managed, resulting in symptom relief. CONCLUSION: LUTS in neurological disease may be at variance with the pattern expected based upon level of neurological lesion. Such patients may require further evaluation and consideration should be given to concomitant urological conditions and multiaxial neurological involvement.

Rehabilitation in practice: neurogenic lower urinary tract dysfunction and its management.

This series of articles for rehabilitation in practice aims to cover a knowledge element of the rehabilitation medicine curriculum. Nevertheless they are intended to be of interest to a multidisciplinary audience. The competency addressed in this article is 'the trainee consistent demonstrates a knowledge of the pathophysiology of various specific impairments including bladder dysfunction' and 'management approaches for specific impairments including bladder dysfunction'. The lower urinary tract (bladder and urethra) has two roles: storage of urine and emptying at appropriate times. The optimal and coordinated activity of the lower urinary tract is subject to a complex neural control which involves all levels of the nervous system, from cortex to peripheral innervation. The complexity of the neural control of lower urinary tract explains the high prevalence of urinary disturbances in neurologic disease. Information obtained from history taking and supplemented by use of a bladder diary forms the cornerstone of evaluation. Ultrasonography is used to assess the degree of incomplete bladder emptying, and for assessing the upper tracts. Urodynamic tests, with or without simultaneous fluoroscopic monitoring, assess detrusor and bladder outlet function and give fundamental information about detrusor pressure and thus the risk factor for upper tract damage. Impaired emptying is most often managed by clean intermittent self-catheterization and this should be initiated if the post-void residual urine is greater than 100 mL or exceeds one third of bladder capacity, or rarely if spontaneous voiding is dangerous due to high detrusor pressure. Storage symptoms are most often managed using antimuscarinic medications. Other options include desmopressin to reduce urine output or intra-detrusor injection of botulinum toxin type A to reduce detrusor overactivity. Understanding of the underlying mechanism of lower urinary tract dysfunction is crucial for effective management.

Benign prostatic obstruction and parkinson's disease--should transurethral resection of the prostate be avoided?

PURPOSE: According to the literature transurethral resection of the prostate in patients with Parkinson's disease has an increased risk of postoperative urinary incontinence. However, this conclusion might have been reached because some patients with multiple system atrophy incorrectly diagnosed as Parkinson's disease were included in these reports. Therefore, we investigated the outcome of transurethral prostate resection in patients with a secure neurological diagnosis of Parkinson's disease. MATERIALS AND METHODS: A total of 23 patients with Parkinson's disease who underwent transurethral prostate resection for benign prostatic obstruction were evaluated retrospectively. Subsequent neurological developments in patients were followed, ensuring that those with multiple system atrophy had not been included in analysis. RESULTS: At transurethral prostate resection median patient age was 73 years, median duration of Parkinson's disease before the resection was 3 years, and median Hoehn and Yahr scale was 2. Of the 14 patients with a preoperative indwelling urinary catheter transurethral prostate resection restored voiding in 9 (64%) and only 5 (36%) required catheterization postoperatively. Of the 10 patients with preoperative urge urinary incontinence, continence was restored in 5 and improved in 3 following transurethral prostate resection. There were no cases of de novo urinary incontinence after transurethral prostate resection. At a median postoperative followup of 3 years transurethral prostate resection was successful in 16 of the 23 patients (70%). CONCLUSIONS: Transurethral prostate resection for benign prostatic obstruction in patients with Parkinson's disease may be successful in up to 70% and the risk of de novo urinary incontinence seems minimal. Thus, Parkinson's disease should no longer be considered a contraindication for transurethral prostate resection provided that preoperative investigations including urodynamic assessment indicate prostatic bladder outlet obstruction.