Home About us Contact
|
Home About us Contact | ||
|
|
||
External Urethral Sphincter (external + urethral_sphincter)
Selected AbstractsUrodynamic findings in children with cerebral palsyINTERNATIONAL JOURNAL OF UROLOGY, Issue 8 2005M IHSAN KARAMAN Abstract Aim: More than one-third of children with cerebral palsy are expected to present with dysfunctional voiding symptoms. The voiding dysfunction symptoms of the cerebral palsy patients in the present study were documented. Methods: Of the study group, 16 were girls and 20 were boys (mean age: 8.2 years). Children with cerebral palsy were evaluated with urodynamics consisting of flow rate, filling and voiding cystometry, and electromyography findings of the external urethral sphincter to determine lower urinary tract functions. Treatment protocols were based on the urodynamic findings. Anticholinergic agents to reduce uninhibited contractions and to increase bladder capacity were used as a treatment. Clean intermittent catheterization and behavioral modification were used for incomplete emptying. Results: Of the children, 24 (66.6%) were found to have dysfunctional voiding symptoms. Daytime urinary incontinence (47.2%) and difficulty urinating (44.4%) were the most common symptoms. Urodynamic findings showed that neurogenic detrusor overactivity (involuntary contractions during bladder filling) with a low bladder capacity was present in 17 (47.2%) children, whereas detrusor,sphincter dyssynergia was present in four patients (11%). The mean bladder capacity of patients with a neurogenic bladder was 52.2% of the expected capacity. Conclusions: The present study concluded that voiding dysfunction was seen in more than half of the children with cerebral palsy, which is a similar result to other published studies. We propose that a rational plan of management of these patients depends on the evaluation of the lower urinary tract dysfunction with urodynamic studies. These children benefit from earlier referral for assessment and treatment. [source] External urethral sphincter activity in diabetic ratsNEUROUROLOGY AND URODYNAMICS, Issue 5 2008Guiming Liu Abstract Aim To examine the temporal effects of diabetes on the bladder and the external urethral sphincter (EUS) activity in rats. Methods Female Sprague-Dawley rats (n,=,24) were divided into two groups: streptozotocin-induced diabetic rats and age-matched controls. Cystometrograms (CMGs) were taken under urethane anesthesia and electromyograms (EMG) of the EUS were evaluated in all rats at 6 and 20 weeks after diabetes induction. After EMG assessment, the tissues of the urethra were harvested for morphological examination. Results Diabetes caused reduction of body weight, but an increase in bladder weight. CMG measurements showed diabetes increased threshold volume, contraction duration, high-frequency oscillations (HFO), and residual volume. Peak contraction amplitude increased in 6-week but not 20-week diabetic rats. EUS-EMG measurements showed increased frequency of EUS-EMG bursting discharge during voiding in 6-week diabetic rats (8.1,±,0.2 vs. 6.9,±,0.6/sec) but not in 20-week (5.8,±,0.3 vs. 6.0,±,0.2/sec) diabetic rats compared with controls. EUS-EMG bursting periods were also increased in both 6-week and 20-week diabetic rats compared with controls. EUS-EMG silent periods were reduced in 6-week diabetic rats, but were not changed in 20-week diabetic rats compared with controls. Active periods did not change in 20-week diabetic rats, but increased in 6-week diabetic rats compared with controls. Morphometric analysis showed atrophy of the EUS after 20 week but not 6 weeks of DM induction. Conclusions Our data indicates diabetes causes functional and anatomical abnormalities of the EUS. These abnormalities may contribute to the time-dependent bladder dysfunction in diabetic rats. Neurourol. Urodynam. 27:429,434, 2008. © 2008 Wiley-Liss, Inc. [source] Voiding reflex in chronic spinal cord injured cats induced by stimulating and blocking pudendal nerves,,NEUROUROLOGY AND URODYNAMICS, Issue 6 2007Changfeng Tai Abstract Aims To induce efficient voiding in chronic spinal cord injured (SCI) cats. Methods Voiding reflexes induced by bladder distension or by electrical stimulation and block of pudendal nerves were investigated in chronic SCI cats under ,-chloralose anesthesia. Results The voiding efficiency in chronic SCI cats induced by bladder distension was very poor compared to that in spinal intact cats (7.3,±,0.9% vs. 93.6,±,2.0%, P,<,0.05). In chronic SCI cats continuous stimulation of the pudendal nerve on one side at 20 Hz induced large amplitude bladder contractions, but failed to induce voiding. However, continuous pudendal nerve stimulation (20 Hz) combined with high-frequency (10 kHz) distal blockade of the ipsilateral pudendal nerve elicited efficient (73.2,±,10.7%) voiding. Blocking the pudendal nerves bilaterally produced voiding efficiency (82.5,±,4.8%) comparable to the efficiency during voidings induced by bladder distension in spinal intact cats, indicating that the external urethral sphincter (EUS) contraction was caused not only by direct activation of the pudendal efferent fibers, but also by spinal reflex activation of the EUS through the contralateral pudendal nerve. The maximal bladder pressure and average flow rate induced by stimulation and bilateral pudendal nerve block in chronic SCI cats were also comparable to those in spinal intact cats. Conclusions This study shows that after the spinal cord is chronically isolated from the pontine micturition center, bladder distension evokes a transient, inefficient voiding reflex, whereas stimulation of somatic afferent fibers evokes a strong, long duration, spinal bladder reflex that elicits efficient voiding when combined with blockade of somatic efferent fibers in the pudendal nerves. Neurourol. Urodynam. 26:879,886, 2007. © 2007 Wiley-Liss, Inc. [source] Selective activation of the sacral anterior roots for induction of bladder voidingNEUROUROLOGY AND URODYNAMICS, Issue 2 2006Narendra Bhadra Abstract Aim We investigated the efficacy of selective activation of the smaller diameter axons in the sacral anterior roots for electrically induced bladder voiding. Materials and Methods Acute experiments were conducted in five adult dogs. The anterior sacral roots S2 and S3 were implanted bilaterally with tripolar electrodes. Pressures were recorded from the bladder and from the proximal urethra and the external urethral sphincter. A detector and flow meter monitored fluid flow. A complete sacral dorsal rhizotomy was carried out. The effects of two types of pulse trains at 20 Hz were compared; quasitrapezoidal pulses (500 µsec with 500 µsec exponential decay) and interrupted rectangular (100 µsec, 2 sec on/2 sec off). Before rhizotomy, rectangular pulse trains (100 µsec) to activate all fibers were also applied. The experimental design was block randomized before and after rhizotomy. Results Quasitrapezoidal pulses showed block of sphincter activation with average minimum current for maximum suppression of 1.37 mA. All pulse types evoked average bladder pressures above the basal sphincter closure pressure. The pressure patterns in the proximal urethra closely followed the bladder pressures. Before dorsal rhizotomy, stimulation evoked a superadded increase in sphincter pressures with slow rise time. After rhizotomy, the sphincter pressure patterns followed the bladder pressures during selective activation and voiding occurred during stimulation with quasitrapezoidal trains and in between bursts with interrupted rectangular stimulation. Conclusions Selective activation of sacral ventral roots combined with dorsal rhizotomy may provide a viable means of low-pressure continuous voiding in neurological impairment. Neurourol. Urdynam. © 2005 Wiley-Liss, Inc. [source] Botulinum toxin for the treatment of lower urinary tract symptoms: A reviewNEUROUROLOGY AND URODYNAMICS, Issue 1 2005A. Sahai Abstract Aims To review the available literature on the application of botulinum toxin in the urinary tract, with particular reference to its use in treating detrusor overactivity (DO). Methods Botulinum toxin, overactive bladder (OAB), detrusor instability, DO, detrusor sphincter dyssynergia (DSD), and lower urinary tract dysfunction were used on Medline Services as a source of articles for the review process. Results DO poses a significant burden on patients and their quality of life. Traditionally patients have been treated with anti-cholinergic drugs if symptomatic, however, a significant number find this treatment either ineffective or intolerable due to side effects. Recent developments in this field have instigated new treatment options, including botulinum toxin, for patients' refractory to first line medication. Botulinum toxin, one of the most poisonous substances known to man, is a neurotoxin produced by the bacterium Clostridium botulinum. Botulinum toxin injections into the external urethral sphincter to treat detrusor sphincter dyssynergia has been successfully used for some years but recently its use has expanded to include voiding dysfunction. Intradetrusal injections of botulinum toxin into patients with detrusor overactivity and symptons of the overactive bladder have resulted in significant increases in mean maximum cystometric capacity and detrusor compliance with a reduction in mean maximum detrusor pressures. Subjective and objective assessments in these patients has shown significant improvements that last for 9,12 months. Repeated injections have had the same sustained benefits. Conclusions Application of botulinum toxin in the lower urinary tract has produced promising results in treating lower urinary tract dysfunction, which needs further evaluation with randomised, placebo-controlled trials. © 2004 Wiley-Liss, Inc. [source] Striated muscle and nerve fascicle distribution in the female raturethral sphincterTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 2 2007Ronald J. Kim Abstract The anatomical basis for urinary continence depends on a thorough understanding of the tissues in the urethra. The objective of this study was to evaluate the morphology and neuroanatomy of urethral striated muscle, called the rhabdosphincter or external urethral sphincter, in normal female rats. Urethras from 12 female rats were dissected from the bladder, fixed, embedded in paraffin or epon, and sectioned every 1 mm. Striated muscle content was taken as the ratio of the striated muscle area to net urethral area. Nerve fascicles containing myelinated axons near the rhabdosphincter were counted and mapped. Both striated muscle content and number of nerve fascicles peak in the proximal third of the urethra, with a secondary peak at the distal end of the urethra. This secondary peak may correspond to an analog of the combined compressor urethrae/urethrovaginal sphincter located in the distal urethra in human. The rhabdosphincter has a variable distribution along the length of the urethra. In the middle and distal thirds of the urethra, the dorsal striated muscle fibers between the urethra and vagina become more sparse. The majority of nerve fascicles are contained in the lateral quadrants of the urethra, similar to the lateral distribution of somatic nerves in humans. In conclusion, this study demonstrates the normal distribution of the striated musculature and neuroanatomy in the urethra, with similarities to the human. It thus supports and extends the usefulness of the rat as an experimental model for studying urinary incontinence. Anat Rec 290:145,154, 2007. © 2007 Wiley-Liss, Inc. [source] Neural control of the urethra and development of pharmacotherapy for stress urinary incontinenceBJU INTERNATIONAL, Issue 8 2003M.O. Fraser SUMMARY This review discusses the control of the urethra by the central nervous system, emphasizing the importance of nervous system control and the role of serotonin and noradrenaline in storage, micturition and sphincter reflexes. The concept of pharmacological neuromodulation and the use of pharmacological therapy as first-line therapy for stress urinary incontinence (SUI) is presented. Coordination between the urinary bladder and urethra is mediated by many reflex pathways organized in the brain and spinal cord. During bladder filling, activation of mechanoreceptor afferent nerves in the bladder wall triggers firing in the cholinergic efferent pathways to the external urethral sphincter and in sympathetic adrenergic pathways to the urethral smooth muscle. These storage reflexes depend on interneuronal circuitry in the spinal cord and are modulated by descending pathways. It would therefore seem that neurotransmission in the central nervous system and periphery may be important in SUI, and moreover that pharmacological agents affecting these neurotransmitter pathways may be used to treat SUI. The central and peripheral mechanisms of action of duloxetine affect serotonin and noradrenaline neurotransmission in ways that may ameliorate the symptoms of SUI. [source] | ||||||||||