Bladder-sphincter dysfunction in myelomeningocele

 Pediatric urodynamics taught us that detrusor-sphincter dyssynergia creates a bladder outlet obstruction in about 50% of any population of children with myelomeningocele. This functional obstruction causes renal damage due to obstructive uropathy, exactly the same way as a congenital anatomical urethral obstruction does. Pediatric urodynamics also taught us that in children with myelomeningocele pelvic floor activity and detrusor activity can be abnormal (hyperactive or inactive) completely independent from each other. These insights have changed the management of myelomeningocele. Children with overactivity of the pelvic floor can be singled out at infant age, and started on clean intermittent catherization, to prevent obstructive uropathy and preserve renal function. Children with detrusor overactivity can be singled out too at very early age, and treated with anticholinergics, to prevent irreversible structural damage to the detrusor and preserve normal bladder capacity and compliance. Received: 20 July 1999 / Accepted: 24 January 2001     

An update on the treatment of detrusor-sphincter dyssynergia with botulinum toxin type A

The aim of this study was to evaluate the relaxant effect of two preparations (BOTOX® versus Dysport®) of botulinum toxin type A (BTX-A) on the external urethral sphincter in patients with neurogenic voiding disorders. Ten male spinal cord injury patients with detrusor- external urethral sphincter dyssynergia (DSD) were clinically assessed before, and 4–6 weeks after, transurethral or transperineal BTX-A injections (BOTOX® 100 U or Dysport® 250 U) into the external urethral sphincter. Patients with persistent difficulties in voiding or high post-void residual volumes were re-injected with the same product up to three times. All patients were urodynamically examined within 120 days of injection. In total, 30 BTX-A injection cycles (one to three injections) were administered. Significant ( P < 0.05) reductions in the DSD duration post-injection, the time interval between the start of bladder contractions and voiding, and DSD seventy post-treatment were observed. All patients who presented with a residual volume pre-treatment showed a marked decrease post-treatment. These effects lasted 6 months. Improvements in urodynamic parameters were significantly better following BOTOX® than DysporP treatment ( P < 0.05), although the Dysport® dose used is now considered less potent than that of BOTOX®. Thus, injections of BTX-A into the external urethral sphincter are a valuable treatment option for DSD in spinal cord injury patients. Treatment success appears to depend on the seventy of DSD before treatment.     

BTXA治疗脊髓损伤后神经原性膀胱的临床研究

目的：观察尿道括约肌内注射A型肉毒毒素BTXA对脊髓损伤后神经原性膀胱逼尿肌-尿道括约肌不协同的疗效。比较两种注射途径的优劣。方法：选择存在逼尿肌-括约肌不协同的17例脊髓损伤患者进行尿道外括约肌BTXA注射，分为经尿道（TU）注射组和经会阴（TP）注射组，TU组采用膀胱镜定位4点注射法，TP组采用肛门指检定位1点尿道周围注射法，每病例注射100U。结果：两组治疗前后排尿障碍情况均有显著性改善，注射后3天-2周开始出现漏尿次数及间断导尿次数减少，残余尿量减少，每次排尿量增加；治疗后1个月的统计结果显示，间断导尿次数、残余尿量减少，每次排尿量增加（P〈0．05），注射后1个月尿动力学检查提示第一次无抑制性收缩时膀胱容量及最大膀胱容量增加（P〈0．05），最大尿道压降低（P〈0．05）；注射后3个月上述指标虽有所回升，但并未回到注射前；两种注射途径在排尿日记及尿动力学参数的变化上差异无显著性意义。结论：尿道外括约肌的BTXA注射治疗可明显改善脊髓损伤后神经原性膀胱的逼尿肌-括约肌不协同，改善排尿功能，降低残余尿量及漏尿的发生，减少尿路感染及自主神经反射的发生：经会阴注射和经膀胱镜注射对神经原性膀胱的疗效无明显差异。     

Midodrine: Insidious development of urologic adverse effects in patients with spinal cord injury: A report of 2 cases

Midodrine, a prodrug, is converted after oral administration into its active drug, desglymidodrine, which acts as an α₁-adrenoceptor stimulant. Midodrine is prescribed for the treatment of neurogenic orthostatic hypotension in patients with spinal cord injury. By virtue of its α₁-adrenergic effects, midodrine causes an increase in the tone of the vesical sphincter, which may silently lead to progressive retention of urine, particularly in patients with spinal cord injury who void urine spontaneously. Further, midodrine may aggravate detrusor-sphincter dyssynergia, which can lead to hydroureteronephrosis. A 68-year-old man with C-4 tetraplegia was voiding urine satisfactorily through reflex detrusor contractions. He was prescribed midodrine (5 mg at 8:00am, 5 mg at 1:00pm, and 2.5 mg at 10:00pm) for postural hypotension. During the next 7 wk, this patient experienced severe leg spasms while passing urine, and the flow of urine became very slow. Intravenous urography showed bilateral hydroureteronephrosis, although an earlier study had revealed normal kidneys. Midodrine therapy was stopped, and intermittent catheterization 4 times a day, along with oral oxybutynin, was started. After midodrine was discontinued, the leg spasms during passage of urine and slowing of the urine stream coincident with the spasms disappeared completely. The patient was able to pursue activities of daily living without taking midodrine. A 40-year-old man with C-7 tetraplegia was passing urine spontaneously with no problem. For postural hypotension, he was prescribed midodrine (5 mg in the morning and 2.5 mg at lunchtime), fludrocortisone (100 μg daily), and ephedrine (15 mg by mouth, taken 10 min before getting up in the morning). Three months later, the patient presented with sweating. During the day, he would pass only small amounts of urine, but from evening onward, he would void large volumes of urine, and the sweating would diminish. Intravenous urography showed vesical diverticula; a postmicturition film revealed moderate residual urine. This patient was able to stop taking the second dose of midodrine, but he required midodrine and ephedrine in the morning to enable him to get up without feeling dizzy. After the noon midodrine dose was stopped, the patient’s sweating diminished by late afternoon. During the morning hours, however, he continued to sweat and had difficulty passing urine. Intermittent catheterization was not possible in the community setting, and the patient remains under close follow-up. These cases illustrate that patients with cervical spinal cord injury who void spontaneously may develop insidious urologic adverse effects after taking midodrine for postural hypotension. When patients with spinal cord injury develop urologic adverse effects while taking midodrine, the drug should be stopped, and other pharmacologic agents (eg, fludrocortisone) and nonpharmacologic methods should be prescribed for management of orthostatic hypotension. If a patient continues to require midodrine to control postural hypotension, intermittent catheterization combined with antimuscarinic therapy (eg, oxybutynin) should be recommended instead of spontaneous voiding.     

Applications of Botulinum toxin in urogynaecology

Botulinum toxin (BTX) is a neurotoxin produced by bacterium clostridium. It is the most poisonous naturally occurring substance known to mankind. The neurotoxin binds to the peripheral cholinergic terminals and inhibits acetylcholine release at that junction leading to flaccid paralysis. This process appears to offer an attractive therapeutic option, filling the void between anticholinergics and surgery in cases of neurogenic and idiopathic detrusor overactivity, detrusor sphincter dyssynergia (DSD), interstitial cystitis and pelvic pain. This article reviews the application of Botulinum toxin A in these conditions.     

The development of reflex bladder activity following spinal cord injury in cats and a method to control it

Spinal cord transection is associated with the development of detrusor external sphincter dyssynergia in cats. These findings indicate that the cat is a suitable model for the study of lower urinary tract dysfunction after spinal cord injury. Inhibition of reflex detrusor activity was achieved by activation of a sacral inhibitory pathway by electrical stimulation of the sacral roots or anal sphincter in normal and spinal—injured animals, indicating presence of a sacral inhibitory pathway.     

A型肉毒毒素治疗神经源性尿潴留21例临床观察

目的：观察A型肉毒毒素治疗神经源性尿潴留的疗效,不良反应和有效时间。方法：收集21例神经疾病后尿潴留患者,A型肉毒毒素尿道外括约肌注射,记录治疗前后症状,尿流动力学指标,综合评估A型肉毒毒素治疗神经源性尿潴留的疗效,并记录不良反应和有效时间。结果：A型肉毒毒素治疗神经源性尿潴留,患者症状可明显改善,生存质量评分和国际下尿路综合征症状评分明显改善,尿流动力学指标明显改善,未见明显不良反应,疗效可维持（34-1）（1～5）个月。结论：A型肉毒毒素尿道外括约肌注射是一种治疗神经源性尿潴留的有效方法,短期内对部分患者能够显著改善排尿症状,提高生存质量,且未见不良反应。     

原发性膀胱颈梗阻/原发性膀胱颈协同失调的诊断与治疗现状

原发性膀胱颈梗阻(primary bladder neck obstruction,PBNO)/原发性膀胱颈协同失调(primary bladder neck dyssynergia,PBND)是一组病因不明的膀胱颈梗阻综合征,临床表现为排尿期症状(排尿费力、尿踌躇、尿流变细、排空不全等)、储尿期症状(尿频、尿急、尿失禁、夜尿等)或两者同时存在。影像尿动力检查(video-urodynamic study,VUDS)是诊断PBNO/PBND的金标准,PBNO/PBND特征为高压低流的排尿模式,在影像透视下可见膀胱颈未开放或开放不全。轻症患者可采取观察、药物治疗及间歇清洁自家导尿等措施进行保守治疗,保守治疗无效的患者应行经尿道膀胱颈电切术。为进一步了解PBNO/PBND及其进展,本文就相关研究进展进行综述。     

Non-pharmacologic options for the management of voiding dysfunction in multiple sclerosis

Multiple sclerosis is a neuroinflammatory condition that can cause significant bladder dysfunction manifesting either as overactive bladder or impaired bladder emptying.Patients will often complain of urgency,frequency,nocturia,urgency incontinence,hesitancy,straining to void,and incomplete bladder emptying.While these symptoms can be treated with pharmacologic agents,often patients will require more significant treatments.Patients should first be evaluated with urodynamics in order to adequately diagnose the pathologic condition causing their symptoms.These interventions include catheter use,injection of botulinum toxin,neuromodulation,urethral stenting,sphincterotomy,suprapubic catheter with bladder neck closure,bladder augmentation and urinary diversion.The purpose of this review is to examine the evidence supporting each of these treatment options so urologic providers can better provide for this unique and complex patient population.