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Context Detrusor underactivity (DUA) is a common but relatively under-researched bladder dysfunction. Underactive bladder (UAB) is the symptom-based correlate of DUA. Recently, there has been renewed interest in this topic. Objective To systematically review and summarise the most recent literature and discuss this in the context of what is already known. Evidence acquisition A systematic review of the literature was performed in December 2017 using Medline and Scopus databases. Separate searches of each database used a complex search strategy including “free text” protocols. Search terms included “underactive bladder”, “detrusor underactivity”, “acontractile bladder”, “detrusor failure”, “detrusor areflexia”, “atonic bladder”, “chronic retention”, and “impaired bladder contractility”. Evidence synthesis The initial search retrieved a total of 1690 studies; of these 44 were included in the final analyses. Conclusions Although there has been an expansion in the literature concerning all aspects of DUA and UAB, knowledge on its epidemiology and aetiopathogenesis is still lacking; there remains a need to develop accurate reproducible diagnostic criteria and effective treatments, in particular drug therapies. Patient summary Recently, there has been renewed interest in underactive bladder with expanding research in this area. The lack of simple, reproducible, noninvasive diagnostic criteria has precluded an accurate estimation of the magnitude of the problem. Recent studies have highlighted the potential role of impaired bladder blood supply in causing bladder underactivity.

The acontractile bladder (AcB) is a urodynamic-based diagnosis wherein the bladder is unable to demonstrate any contraction during a pressure flow study. Although it is often grouped with underactive bladder, it is a unique phenomenon and should be investigated independently. The purpose of the present review was to examine the current literature on AcB regarding its pathology, diagnosis, current management guidelines, and future developments. We performed a review of the PubMed database, classifying the evidence for AcB pathology, diagnosis, treatment, and potential future treatments. Over the 67 years covered in our review period, 42 studies were identified that met our criteria. Studies were largely poor quality and mainly consisted of retrospective review or animal models. The underlying pathology of AcB is variable with both neurological and myogenic aetiologies. Treatment is largely tailored for renal preservation and reduction of infection. Although future developments may allow more functional restorative treatments, current treatments mainly focus on bladder drainage. AcB is a unique and understudied bladder phenomenon. Treatment is largely based on symptoms and presentation. While cellular therapy and neuromodulation may hold promise, further research is needed into the underlying neuro-urological pathophysiology of this disease so that we may better develop future treatments.

Kedi ve kopeklerde detrusor arefleksisi norojenik ya da nonnorojenik nedenlerle sekillenmektedir. Mekanik ya da fonksiyonel uriner obstruksiyondan kaynaklanan idrar kesesinin uzun sureli asiri dolgunlugu detrusor kas atonisini de beraberinde getirmektedir. Kolinerjik bir agonist olan Betanekol, parasempatomimetik etkiyle idrar kesesi duvarini saran detrusor kasinin kontraksiyon ve gerilimini arttirmaktadir. 2 kedi ve 1 kopegi iceren olgu serisinde; detrusor arefleksili kopek ve kedilerde Betanekol kullaniminin kese tonusu uzerine klinik etkisi vurgulanmistir.

The pathophysiologic mechanisms of female voiding dysfunction are poorly understood, and there are neither standard definitions nor guidelines for diagnosis and treatment. Conceptually, voiding phase dysfunction may be due to bladder and/or outlet causes. Bladder causes include detrusor contraction of inadequate magnitude and/or duration to effect bladder emptying (detrusor underactivity) or the absence of detrusor contraction (detrusor areflexia). Outlet causes consist of bladder outlet obstruction due to urethral sphincter over activity (functional obstruction) or anatomical pathologies (mechanical obstruction). Etiology of female voiding dysfunction is multifactorial and several different pathophysiologic mechanisms and clinical entities, including overactive pelvic floor (OPF) are suggested. Accurate diagnosis and optimal management of these clinical entities are yet to be defined.

A literature search in PubMed using the search terms underactive bladder, detrusor underactivity, bladder underactivity, impaired detrusor contractility, acontractile detrusor, detrusor failure, hypotonic failure, detrusor areflexia, post-void residual, and chronic retention in combination with children resulted in only ten papers directly discussing underactive bladder and detrusor underactivity with the exclusion of papers on posterior urethral valve papers that discussed detrusor underactivity in some form. With such a paucity of information on a problem that is so difficult to treat, we seem to be ignoring an important problem in pediatric urology. This chapter will review the epidemiology, causes, diagnosis, and treatment of pediatric underactive bladder.

The current study aims to explore the possible correlations between detrusor excitability and the expression of C-kit and connexin-43 (Cx43). Fifty-two adult female Sprague Dawley (SD) rats were randomly divided into the normal control (NC), supra-sacral cord injury (SSCI) and sacral cord injury (SCI) groups. Neurogenic bladder models were established. Urodynamic examination, bladder pathological observation and detrusor muscle excitability detection were performed. Meanwhile, the expression of C-kit and Cx43 was detected using immunohistochemistry and Western blot analysis. The detrusor leak point pressure of the SSCI group increased significantly compared to the NC group, whereas that of the SCI group decreased significantly. The spontaneous detrusor muscle contraction frequency of the SSCI group increased significantly compared to the NC group, whereas that of the SCI decreased significantly. The C-kit and Cx43 positive expression in the SSCI was significantly higher than that in the control group, whereas that in the SCI group was significantly lower (P < 0.01) The C-kit and Cx43 protein content in the SSCI group was significantly higher compared to the NC group, whereas that in the SCI group was significantly lower (P < 0.01). Changes in excitability and the expression of C-kit and Cx43 expression contribute to the occurrence of detrusor hyperreflexia and areflexia. Key words: Spinal cord injuries, detrusor hyperreflexia, detrusor areflexia, urodynamics, C-kit, connexin-43.

This chapter introduces the anatomical structure and physiology of the bladder together with a description of bladder disorders such as detrusor hyperreflexia, detrusor areflexia, overactive bladder syndrome, and urine retention. Sacral root stimulation as used by the Finetech-Brindley SARS (Finetech Medical Ltd.) and Sacral Neuromodulation as used by the InterStim system (Medtronic) are presented.

A significant proportion of women with lumbar disc prolapse experience voiding dysfunction. The most common finding is detrusor areflexia, frequently associated with impaired sensation. The pertinent neuropathophysiologic findings, clinical features and methods of evaluation and treatment are reviewed.

To study the correlation between neurological level of spinal injury and bladder functions as detected by urodynamic study.Analytical study.Seventy individuals with traumatic spinal cord injury (SCI) admitted to the Department of Physical Medicine and Rehabilitation, S.M.S. Medical College and Hospital, Jaipur. Detailed clinical, neurological evaluation as per American Spinal Injury Association Classification and radiological assessment were done along with clinical examination of bladder and urodynamic study.Out of 65 patients with suprasacral injuries, 53 (81.5%) demonstrated hyperreflexia with or without detrusor sphincter dyssynergia, 6 (9.2%) detrusor areflexia, and 6 (9.2%) had normal bladders, 41 (59.4%) low compliance (20 ml/cmH2O), and 47 (72.30%) had high detrusor leak pint pressures (40 cmH2O). Of the five patients with sacral injuries, one (20%) showed detrusor hyperreflexia, four (80%) detrusor areflexia, and one (20%) had low bladder compliance; all five (100%) had high detrusor leak point pressures.The correlation between somatic neurologic findings, spinal imaging studies, and urodynamic findings in patients with SCI is not exact. Therefore, bladder management should not completely rely only on clinical bladder evaluation or neurological examination alone, but should always include urodynamic studies.

Female urinary retention is a common urological problem with many possible etiologies. Prior treatments attempted to decrease urethral resistance, but current neurourologic investigation has shown that this is rarely needed. Intermittent catheterization, along with diagnosing appropriate etiologic factors is the best management. If the workup reveals no organic etiology, psychological investigation may be needed because many of the patients have a significant psychosocial history. A multidisciplinary approach between the urologist, the psychiatrist and the neurologist usually provides the best management for females with urinary retention.

Myasthenia gravis (MG) is a common neuromuscular disorder, however, voiding dysfunction in conjunction with MG is rare. A review of the literature yielded only 7 prior reports of such a combination. Most of the reported cases involved incontinence in males which developed after a transurethral resection of the prostate. Only 3 cases described de novo voiding dysfunction. We report a fourth patient. In all 4 cases of de novo dysfunction, the voiding problem either heralded a new diagnosis of MG or an exacerbation of the disease process. It is hypothesized that autonomic dysfunction in patients with MG might indicate a unique subset with a worse prognosis.

Blackwell Publishing, HIDEHIRO, KAKIZAKI ; KANAME, AMEDA ; SHINYA, KOBAYASHI ; HIROSHI, TANAKA ; TAKASHI, SHIBATA ; TOMOHIKO, KOYANAGI, International journal of urology, 10(11), 2003, 576-581., Backgroud: The therapeutic role of α-blockers in the treatment of voiding disorders due to benign prostatic hyperplasia has been extensively examined. To investigate a possible effect of α1-blocker on urodynamic voiding parameters in patients with neurogenic bladder, we conducted a clinical trial using tamsulosin. Methods: Twenty-four patients (14 men and 10 women) ranging from 24 to 82 years of age (mean age 61 years) with neurogenic bladder were analyzed. Urodynamic studies were performed before and after treatment with 0.4 mg tamsulosin daily for 4 weeks. Results: On uroflowmetry, the average flow rate (from 4.6 ± 3.3 to 6.7 ± 3.0 mL/s, P = 0.04), maximum flow rate (from 9.4 ± 6.8 to 14.1 ± 7.0 mL/s, P = 0.016) and residual urine rate (from 46 ± 29 to 32 ± 21%, P = 0.02) improved significantly. In patients with detrusor contraction during voiding, detrusor opening pressure and detrusor pressure at maximum flow decreased significantly from 69.0 ± 36.2 to 49.2 ± 26.4 cmH2O (P = 0.046) and from 66.7 ± 34.6 to 53.6 ± 26.5 cmH2O (P = 0.007), respectively. On the other hand, in patients with detrusor areflexia, vesical opening pressure (from 78.2 ± 23.4 to 61.6 ± 25.2 cmH2O), or vesical pressure at maximum flow (from 68.6 ± 23.2 to 62.9 ± 25.2 cmH2O) did not change significantly after treatment. Conclusion: Tamsulosin reduces functional urethral resistance during voiding and improves flow rate in patients with neurogenic bladder. It has more beneficial urodynamic effects in patients with detrusor contraction during voiding than in patients with detrusor areflexia.

This test is similar to urethral denervation testing in that it relies on Cannon’s hypothesis that a denervated end organ will give an exaggerated response when re-exposed to its neural transmit-ter. The test is performed to identify detrusor areflexia in cases of decentralization of the bladder. The test is performed by first obtaining a baseline cystometrogram. This is followed by the administration of 0.03 mg/kg of bethanecol chloride subcutaneously. The usual dose is 2.5 mg. Bethanecol should not be used in patients with asthma, cardiac disease or hyperthyroidism as it may induce bronchospasm, hypotension and atrial fibrillation in these patients. A second postadministration cystometrogram is done 30 min later. Alternatively, the intravesical pressure can be measured continuously after the introduction of a known amount of fluid into the bladder. Recording continues until an increase of 15 cmH2O occurs or 30 min has passed.

When all medical therapies for detrusor instability have failed partial denervation of the detrusor by surgical hypogastric nerve resection may be indicated for some patients. Although good results may be obtained in up to 90% of selected patients initially, recurrences are frequent in these and other nerve resections or neurologic procedures. If hypogastric nerve resection or phenol injection is to be considered, preliminary evaluation of the patient with unilateral and bilateral hypogastric nerve blocks is indicated to determine the anticipated response of the detrusor muscle to surgical resection or phenol injection of these nerves. Assessment of detrusor function during filling and micturition is accomplished after anesthetic nerve block to look for resolution of detrusor overactivity and to rule out detrusor areflexia.

A total of 48 consecutive spina bifida patients undergoing routine urodynamic studies was classified into 2 groups depending upon whether they demonstrated uninhibited bladder contractions. Of the patients 34 demonstrated detrusor hyperreflexia and 14 had detrusor areflexia. These 2 groups were then subdivided depending on the continence status. Of the areflexic and hyperreflexic groups, 6 and 7 patients, respectively, were wet despite at least 2 years of conservative medical management. Leak point pressure and leak point volume were determined in all patients and results were compared in both subgroups. In the hyperreflexic groups leak point volume but not leak point pressure was significantly different between the wet and dry patients. The areflexic group demonstrated the opposite finding, that is the leak point pressure but not the leak point volume was significantly different between wet and dry patients. From these studies we determined that in the areflexic group leak point pressure was useful to predict incontinence, whereas in the hyperreflexic group leak point volume was more useful. The addition of the measurement of leak point pressure and leak point volume during routine urodynamic studies in myelodysplastic patients enhances accurate diagnosis and may select those who will best benefit from bladder augmentation and/or a procedure to increase outlet resistance.

Summary Bladder dysfunction is a major complication of human T-lymphotrophic virus type I associated myelopathy (HAM). Four patients (3 females and 1 male, aged between 23 and 44 years), who had suffered from HAM for an average of 6 years complained variously of difficulty in micturition, frequency, bed wetting and/or urge incontinence. They were investigated urodynamically. A significant amount of urine was retained in the bladder of 3 patients. During the storage phase, bladder sensation was well preserved in all 4 patients but severe uninhibited detrusor contractions were observed in 3. At micturition, detrusor contractility was present in 3 and completely lost in 1. Of the 4 patients with HAM, 3 suffered from detrusor hyper-reflexia and 1 from detrusor areflexia.

A group of 21 mentally retarded patients with severe, long-standing urinary symptoms underwent urodynamical investigation. The most common abnormalities were detrusor areflexia and detrusor hyper-reflexia. Of 11 patients treated surgically, 10 derived marked benefit. Drugs were successful in reducing micturition problems in 3/6 patients. Severely retarded patients with spastic quadriplegia are difficult to investigate and if this is associated with detrusor hyper-reflexia it is impossible to treat them in any way. Severely retarded patients with detrusor areflexia and infrequent voiding can benefit from bladder outlet surgery. Patients with moderate (especially mild) retardation can be investigated and treated in the same way as non-retarded people.

To determine the effect of back closure on the detrusor-external sphincter coordination, we reviewed the medical records of 40 neonates with myelodysplasia studied prospectively with urodynamic assessment and renal ultrasonography before closure of the spinal defect, within 7 days of closure and at 3-month intervals thereafter. Only 31 of the 40 neonates met all criteria for inclusion. All renal sonograms were normal before and after closure. Urodynamic evaluation demonstrated coordinated detrusor-sphincter activity in 18 neonates before and after closure. During prolonged followup 1 patient had detrusor areflexia and 4 had detrusor-sphincter dyssynergia. Of 11 neonates who demonstrated detrusor areflexia and no external sphincter activity before closure 10 were unchanged on initial post-closure evaluation (4 had detrusor-sphincter dyssynergia during followup), while 1 demonstrated detrusor areflexia with external sphincter overactivity and vesicoureteral reflux after closure. The latter patient subsequently had detrusor hyperreflexia, more severe reflux and upper tract deterioration. She was temporized with a cutaneous vesicostomy. One patient demonstrated detrusor-sphincter dyssynergia before closure and detrusor areflexia with no external sphincter activity after closure, the consequence of surgical division of the neural placode during back closure. The remaining patient demonstrated detrusor-sphincter dyssynergia before and after closure. This patient had coordinated detrusor-sphincter activity during followup. Those neonates who presented with or later had detrusor-sphincter dyssynergia were managed initially with neuropharmacological agents and clean intermittent catheterization. An unsuccessful outcome was managed by cutaneous vesicostomy. Our study demonstrates that neonatal closure of the spinal cord defect does not appear to affect detrusor-sphincter coordination adversely, and re-emphasizes the need for careful and regular followup in children with myelodysplasia to detect deterioration of the urinary tract.

Among 60 spinal cord injury patients who underwent external urethral sphincterotomy 45 experienced success and 15 failed. Failure was established when symptomatic urinary tract infections and high vesical residuals persisted. Urodynamic findings demonstrated detrusor areflexia in 10 patients (66 per cent), detrusor-sphincter dyssynergia in 2 (13.2 per cent), detrusor hyperreflexia with unsustained bladder contractions in 1 (6.6 per cent), and detrusor hyperreflexia and bladder neck obstruction in 2 (13.2 per cent). Among these failures poor detrusor contractility predominated. Detrusor-sphincter dyssynergia may indicate an inadequate surgical relief of obstruction. Bladder neck obstruction may indicate that a bladder neck incision should be considered when an external sphincterotomy is performed.

38 patients with severe urge or urge incontinence, who did not respond to conservative therapy, were treated with selective sacral nerve blockade using a local anesthetic (bupivacaine). 6 patients of this group had definite selective sacral denervation with phenol. In 31 patients a urodynamic study was done previous to the sacral nerve block as well as 10 and 90 min after the injection. Within the first 2-7 weeks the success rate was about 70% in regard to bladder capacity and mean volume at first desire to void. On long-term follow-up (greater than 7 months), the success rate decreased to about 16%. Only 1 patient of the phenol group still has complete detrusor areflexia for now more than 2 years. 4 male patients with advanced or locally recurrent bladder tumors had the sacral block because of severe perineal or suprapubic pain. Subjectively their response seemed to be better. According to our experience nonoperative central bladder denervation with selective sacral nerve blockade using local anesthetics or phenol shows no convincing results on long-term follow-up. Since it is a minimal invasive technique, which can be repeated several times, it may be helpful for some patients and offers a chance to bypass major surgical denervation procedures.

The urological aspects of the tethered cord syndrome were investigated in 15 adults. Impaired detrusor contractility was the most common among the urological symptoms and signs (73 per cent of the patients). Bladder dysfunction was confirmed urodynamically in 93 per cent of the patients and detrusor areflexia was predominant in 60 per cent. Pathological grades were proposed to classify the severity of the tethered cord syndrome. While restoration of bladder function was satisfactory in 67 per cent of the patients postoperatively, the over-all result was less (60 per cent). Patients with sensory motor paralysis of the bladder, symptoms more than 3 years in duration, cutaneous stigmas or a high pathological grade of the syndrome will not benefit from an operation. We conclude that neurogenic bladder secondary to the tethered cord syndrome is curable provided that the underlying pathological condition is recognized properly and an operation is performed early.

A total of 7 patients with the Guillain-Barre syndrome and voiding dysfunction, large post-voiding residuals or urinary retention underwent urodynamic evaluation. Of the patients 4 had detrusor areflexia with a positive bethanechol supersensitivity test, including 3 with electromyographic evidence suggestive of neuropathy. This is the expected pattern in the Guillain-Barre syndrome. However, 3 patients had detrusor hyperreflexia with appropriate sphincteric relaxation, which was associated with Babinskys sign in 2. The presence of detrusor hyperreflexia suggests the possibility of Guillain-Barre pathological conditions involving the central nervous system, although the Guillain-Barre syndrome typically is a disease of the peripheral nervous system. Long-term urodynamic studies may help clarify such issues in future patients.

A total of 26 patients with symptomatic voiding dysfunction underwent cystometrography concomitant with simultaneous perineal floor and rectus abdominis electromyography. Of the patients 20 had well defined neurological pathological conditions. Cystometrography/perineal electromyography revealed detrusor hyperreflexia with appropriate sphincter relaxation in 8 patients, with vesicosphincter dyssynergia in 10 and with pseudo-dyssynergia in 2. Rectus electromyography in these patients did not reveal electromyographic activity during the filling and expulsion phases of the cystometrogram. However, the 6 neurologically normal patients were noted to have detrusor areflexia with nonrelaxation of the sphincter on urodynamic examination. These patients characteristically attempted to void by abdominal straining, resulting in a concomitant increase in rectus and perineal electromyography activity. We conclude that the addition of rectus electromyography to the standard urodynamic methodology can improve significantly the recognition of intravesical pressure elevation owing to voluntary contraction of the abdominal musculature.

The changing clinical course of multiple sclerosis is a hallmark of the disease. The neurourologic findings in this disorder have been well documented in the literature but the occurrence of urodynamic changes with time has been mentioned only briefly. Ten men and 8 women had 2 or more urodynamic evaluations, consisting of cystometrography and perineal floor needle electromyography during 2 months to 6 years (mean 25 months). The initial urodynamic patterns included a normal study in 1 patient, detrusor areflexia in 7 and detrusor hyperreflexia in 10 (5 with vesicosphincter dyssynergia). Re-examinations were done for persistent or new symptoms. The urodynamic pattern changed in 10 patients (55 per cent), including cystometrographic changes in 7, newly developed neuropathic changes on electromyography in 5 and changes in detrusor-sphincter interaction in 9 (with 5 new cases of vesicosphincter dyssynergia). Of the 8 patients who did not demonstrate a urodynamic change 5 had vesicosphincter dyssynergia that persisted on followup. Vesicosphincter dyssynergia was the predominant pattern noted on re-evaluation, acting as a urodynamic indicator of progressive multiple sclerosis. Careful neurourologic assessment should be performed routinely in the followup of multiple sclerosis patients who are unresponsive to treatment or who manifest new symptoms.

Neurosyphilis today is a rare problem. We describe a man who presented with organic brain syndrome, psychosis and incontinence, and diagnosis was neurosyphilis with resultant bladder dysfunction. Urodynamic studies defined the voiding dysfunction as detrusor areflexia with a positive bethanechol test. This case reminds us of the necessity of obtaining a test for venereal disease to rule out neurosyphilis in patients with idiopathic voiding dysfunction.

We investigated 63 patients with detrusor areflexia by cystometrography, perineal floor electromyography and bethanechol chloride supersensitivity testing. Of the patients 48 had unequivocal evidence of neuropathy, while 15 were neurologically normal and served as controls. The bethanechol chloride supersensitivity test was positive in 98 per cent of the patients and none of the controls, whereas neuropathic changes by electromyography were found in 67 per cent of the patients and 7 per cent of the controls. These findings suggest that the bethanechol chloride supersensitivity test is more sensitive and more specific than perineal floor electromyography in corroborating bladder neuropathy.

A total of 33 patients who demonstrated detrusor areflexia during cystometry underwent the bethanechol denervation supersensitivity test. In each instance the presence or absence of a neurologic lesion was documented carefully by complete neurologic evaluation. Of the 21 patients with a neurogenic bladder there was a falsely negative rate of 24 per cent. Of the 12 patients without a neurogenic bladder the falsely positive rate was 50 per cent. It is concluded that a positive bethanechol test is not by itself indicative of neurogenic bladder nor does a negative test exclude this diagnosis.

A positive bethanechol supersensitivity test (BST) usually indicates neuropathic detrusor areflexia and warrants neurologic correlation. Seven females, average age thirty-three years, with straining to void and high residual urines, had detrusor areflexia, with a borderline or positive BST, ranging from 19 cm water to 55 cm H2O change in intravesical pressure after 5 mg of subcutaneous bethanechol. However, all patients had a normal neurologic workup, even though 2 patients had insignificant spina bifida occulta. Two of the patients also had prior pelvic surgery, 1 of whom was azotemic, and 4 of the patients had psychosocial problems; factors reported to be associated with a false positive BST. The positive BST is not diagnostic of neurogenic detrusor areflexia because of the many variables that can influence the test. Therefore, the bethanechol supersensitivity test should be interrupted in light of the complete neurourologic evaluation.

Electrophysiologic evaluation of the neural pathways involved in bladder and urethral function is described in 30 patients with diabetes mellitus. The study showed decreased conduction velocities in patients with the detrusor reflex as well as in detrusor areflexia. The findings indicated that diabetic vesical dysfunction is principally the result of segmental demyelination in the peripheral nerve supply to the detrusor muscle and urethra.

A total of 57 patients with neuropathic or nonneuropathic detrusor areflexia was studied with the bethanechol supersensitivity test, electromyography of the urethral rhabdosphincter and bulbocavernosus reflex latency. The sensitivity of these tests in detecting neuropathic areflexia was 90, 87.5 and 78.1 per cent, respectively, and the specificity was 95.6, 76 and 80 per cent, respectively. When all 3 tests were performed together the combined accuracy approached 100 per cent. These combined tests are useful in the diagnosis of patients with equivocal bladder neuropathic conditions and in those with subtle neurological lesions.

Twenty-three patients who previously demonstrated no detrusor contraction during cystometry were evaluated using a combined uroflowmetry and abdominal wall electromyography. Ten patients voided without abdominal straining (normal detrusor reflexia), 11 could not void without abdominal straining (detrusor areflexia, detrusor weakness, or bladder outlet obstruction), and 2 had equivocal findings with the method.

A young woman fell onto her low back and sustained a transverse sacral fracture associated with urinary complaints consistent with detrusor areflexia. She was treated with intermittent bladder catheterization and was able to void normally within six days.

Urodynamic evaluation was done 45 times on 41 consecutive patients with multiple sclerosis. Bladder symptoms correlated poorly with any single urodynamic finding and, accordingly, a comprehensive evaluation was necessary to define the underlying pathophysiology. Only 63 per cent of the patients with symptoms of urgency, frequency and urge incontinence actually were found to have uninhibited bladder contractions, while 73 per cent of the patients with obstructive symptoms had detrusor areflexia. Six patients (15 per cent) had a marked change in urodynamic findings upon repeat examination either because of a change in symptomatology or poor response to treatment. An additional 6 patients had vesicoureteral reflux. Bladder symptoms in multiple sclerosis patients should serve more to alert the clinician to the need for urodynamic testing than to mandate specific treatment.

The relationship between neurological urinary symptoms and urodynamic findings in patients with multiple sclerosis was examined. The duration of multiple sclerosis was significantly longer in patients with urinary symptoms. The presence of urinary symptoms correlated with the severity of the pyramidal or sensory lesions and the total disability score. Cystometrograms revealed detrusor hyperreflexia in 67 per cent of the patients, areflexia in 21 per cent and a normal detrusor in 12 per cent. Somatic dyssynergia was found in 20 of the 39 patients whose examination revealed clear-cut results. Positive correlation was found between urge incontinence and detrusor hyperreflexia, and between hesitancy and detrusor areflexia but no relationship was found between urological symptoms and sphincter function. Analysis of the neurological lesions in relation to the cystometric findings revealed a positive correlation among pyramidal lesions, detrusor hyperreflexia and detrusor areflexia, and between cerebellar lesions and detrusor areflexia. The correlation between detrusor dysfunction and high total disability score disappeared when patients with high pyramidal scores were excluded. No correlation could be detected between somatic dyssynergia and the various neurological lesions.

We report a case of detrusor areflexia caused by vincristine neurotoxicity and documented by urodynamic testing. Vincristine commonly induces peripheral neuropathy but rarely causes voiding dysfunction. Neurourological evaluation aided in monitoring and understanding this problem.