|Year : 2017 | Volume
| Issue : 4 | Page : 187-191
Current pharmacological and surgical treatment of underactive bladder
Yuan-Hong Jiang, Cheng-Ling Lee, Jia-Fong Jhang, Hann-Chorng Kuo
Department of Urology, Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, Taiwan
|Date of Submission||18-May-2017|
|Date of Decision||14-Jun-2017|
|Date of Acceptance||15-Jun-2017|
|Date of Web Publication||4-Dec-2017|
Department of Urology, Buddhist Tzu Chi General Hospital, 707, Section 3, Chung-Yang Road, Hualien
Source of Support: None, Conflict of Interest: None
Underactive bladder (UAB) or detrusor underactivity (DU) is a common yet still poorly understood urological problem. In addition to true detrusor failure and neuropathy, the inhibitory effects of detrusor contraction by the striated urethral sphincter and the bladder neck through alpha-adrenergic activity may also play a role in the development of UAB or DU. Treatment of UAB or DU aims to reduce the postvoid residual (PVR) urine volume and increase voiding efficiency, either by spontaneous voiding or abdominal straining. Pharmacotherapy with parasympathomimetics or cholinesterase inhibitors might be tried, and benefits can be achieved in combination with alpha-blockers. Bladder outlet surgeries, including urethral onabotulinumtoxinA injection, transurethral incision of the bladder neck, and transurethral incision or resection of the prostate can effectively improve voiding efficiency and decrease the PVR in most patients with DU. The mechanisms have not been well elucidated. It is likely that ablation of the bladder neck or prostatic urethra might not only decrease bladder outlet resistance but also abolish the sympathetic hyperactivity which inhibits detrusor contractility in patients with idiopathic UAB or DU.
Keywords: Bladder function, Detrusor underactivity, Medical treatment, Urinary retention
|How to cite this article:|
Jiang YH, Lee CL, Jhang JF, Kuo HC. Current pharmacological and surgical treatment of underactive bladder. Tzu Chi Med J 2017;29:187-91
|How to cite this URL:|
Jiang YH, Lee CL, Jhang JF, Kuo HC. Current pharmacological and surgical treatment of underactive bladder. Tzu Chi Med J [serial online] 2017 [cited 2019 Jun 26];29:187-91. Available from: http://www.tcmjmed.com/text.asp?2017/29/4/187/219744
| Introduction|| |
Underactive bladder (UAB) or detrusor underactivity (DU) is a common urological problem in the elderly resulting in incomplete bladder emptying or chronic urinary retention. It causes impaired quality of life and is a threat to health as well . The pathophysiology of UAB or DU may involve aging, bladder outlet obstruction, diabetes mellitus, and neurogenic etiology . Patients with UAB or DU usually void with abdominal straining and large postvoid residual (PVR) urine is noted. Bladder sensation might also be impaired . DU is also commonly seen in elderly patients with a weak general condition and multiple medical diseases, or after major surgery . Some possible underlying pathogeneses for the development of transient DU have been postulated, including detrusor muscle damage, increased urethral afferent activity and neurological inhibition, and defective mucosal mechanoreceptors and chemoreceptors ,,. This article reviews the current treatment modalities for DU [Table 1].
| Current Management of Underactive Bladder|| |
In clinical practice, patients with UAB or DU might have improvement of symptoms or regain spontaneous voiding after an indwelling catheter or after transurethral resection of the prostate (TURP). During the recovery period of one to 3 months, clean intermittent catheterization (CIC) or an indwelling Foley catheter or cystostomy for voiding training is usually recommended. However, not all patients with UAB or DU can recover from difficult urination or chronic urinary retention in the short term. Patients who need CIC or an indwelling Foley catheter may have a low quality of life and emotional distress .
| Pharmacotherapy for Underactive Bladder or Detrusor Underactivity|| |
The treatment goal for UAB or DU is to relieve voiding difficulty, reduce PVR and prevent urinary tract infection or upper urinary tract deterioration. If possible, recovery of detrusor contractility to efficiently empty the bladder should be achieved. Otherwise, a decrease in bladder outlet resistance or increased cortical perception of bladder sensation may also improve voiding efficiency after treatment. However, medical treatment for UAB or DU has usually been disappointing. A recent review of systemic literature research failed to find effective treatment strategies for DU .
The efficacy of cholinergic drugs for reduction of the PVR in patients with UAB or DU is still controversial. Parasympathomimetic agents, such as bethanechol, have been found to reduce the PVR at a dose of 50 mg four times daily in combination with intravesical instillation of prostaglandin E2 1.5 mg. However, the improvement was limited (PVR decreased from 426 mL to 325 L, P = 0.015) compared with placebo . Recent research does not support the clinical efficacy of bethanechol for DU ,. Acetylcholinesterase inhibitors, such as distigmine bromide, have also been found to improve the maximum flow rate and detrusor pressure . A combination of bethanechol chloride (60 mg/day) or distigmine bromide (15 mg/day) and an alpha-blocker is more effective than monotherapy for the treatment of voiding difficulty in patients with UAB . Cholinesterase inhibitors might inhibit degradation of acetylcholine and provide beneficial effects for patients with UAB or DU. However, adverse events such as frequent defecation, fecal incontinence, diarrhea and frequent urination might bother patients . Furthermore, these pharmacological treatments might not be suitable for patients with detrusor hyperactivity and inadequate contractility, in whom overactive symptoms are exacerbated after pharmacological treatment.
Decrease of bladder outlet resistance by medication has been considered effective to reduce the PVR and improve voiding efficiency and is widely prescribed for patients with UAB or DU. However, there have been few randomized control trials to prove the efficacy. One recent study demonstrated women with DU could have significant improvement in the International Prostate Symptom Score (IPSS), maximum flow rate (Qmax), PVR, and voiding efficiency after taking tamsulosin 0.2 mg daily . Combination of an alpha-blocker with distigmine 5 mg daily was also found to improve the IPSS and quality of life index as well as reduce the PVR . Combined silodosin and distigmine could increase voiding efficiency in Zucker diabetic fatty rats, a model of DU-like syndrome. Adding an alpha-blocker to an acetylcholinesterase inhibitor might result in additive efficacy . In addition to pharmacological treatment, percutaneous tibial nerve stimulation and intravesical electrical stimulation have been shown effective for nonneurogenic, refractory lower urinary tract dysfunction in children ,.
| Botulinum Toxin a Urethral Injection for Underactive Bladder or Detrusor Underactivity|| |
The pathomechanism of UAB or DU is complex, including detrusor failure and a poorly relaxed or nonrelaxed urethral sphincter . A spastic or poorly relaxed urethral sphincter is the main pathophysiology of dysfunctional voiding. It results in incomplete bladder emptying and might be one of the causes of DU ,. Therefore, the urethra is an important therapeutic target in patients with DU.
Botulinum toxin A has been used for more than 10 years to treat adults with neurogenic or nonneurogenic voiding dysfunction due to a spastic or nonrelaxing urethral sphincter ,,,. In patients with voiding dysfunction and urinary retention, indwelling catheters can be removed after urethral onabtulinumtoxinA injection . Urethral onabotulinumtoxinA injection had been used to treat patients with DU and nonrelaxing urethral sphincter after radical hysterectomy . In patients with DU due to cauda equina lesions, dysfunctional voiding, peripheral neuropathy and idiopathic etiologies, onabotulinumtxinA at a dose of 50 U was effective in reducing the median voiding pressure (56.5 ± 41.2 vs. 39.0 ± 38.4 cmH2O), maximal urethral closure pressure (65.5 ± 38.1 vs. 50 ± 32.1 cmH2O), and PVR volume (300 ± 189.1 vs. 50 ± 153.6 mL) at 2 weeks after treatment and the efficacy remained for 3 months . In a study involving patients with low detrusor contractility, 48% (13 of 27) of patients who received an injection of onabotulinumtoxinA 50–100 U into the urethral sphincter showed improvement in detrusor contractility, indicating the neuromodulation effects between the urethral sphincter and bladder . The therapeutic effects of botulinum toxin A on voiding dysfunction not only decrease urethral resistance by paralyzing the striated urethral sphincter but modulate detrusor contractility by eliminating the inhibitory effect of urethral afferent nerves on detrusor nucleus. For patients with DU, urethral sphincter onabltulinumtoxinA injection might result in a reduction in urethral resistance, which allows patients to void more easily with the aid of abdominal pressure . However, if the patient is weak and cannot generate adequate abdominal pressure to void, voiding difficulty, and a large PVR volume might persist.
Other causes of failed urethral botulinum toxin A treatment besides low abdominal pressure in patients with DU include a tight urethral sphincter, bladder neck obstruction, and psychological inhibition of voiding . An open bladder neck is an important factor in patients who use abdominal pressure to passively overcome urethral resistance. If patients with DU cannot open the bladder neck by abdominal straining, urethral sphincter onabotulinumtoxinA injection might not be successful. Furthermore, as in patients with dysfunctional voiding, repeat urethral sphincter onabtulinumtoxinA 100 U injections in patients with DU might be necessary to achieve greater reduction of urethral resistance and facilitate abdominal straining to void .
| Transurethral Incision of the Bladder Neck for Women With Detrusor Underactivity|| |
Endoscopic bladder neck incision for patients with bladder neck dysfunction was first reported by Turner-Warwick in 1973 . In Choudhury's study of the therapeutic effectiveness of transurethral incision of the bladder neck (TUI-BN) for women with bladder neck obstruction, the mean PVR decreased from 143 to 27 ml . Jhang and Kuo had previously reported the short-term results in women with DU who received TUI-BN . After the procedure, the PVR decreased by 56.3%, and 20 of 27 (74.1%) patients were free of CIC. Excellent results were reported in 14 (45.2%), moderate results in 11 (35.5%), and poor results in six (19.3%) patients after TUI-BN. A recent report of long-term follow-up after TUI-BN for women with DU showed an improved mean voiding efficiency and reduced PVR during a mean follow-up of 61.8 months. Multivariate analysis revealed that baseline intravesical pressure (Pves) was a significant predictor of successful results (OR = 1.024, P = 0.038) . Adequate deep incision of the bladder neck to the serosa layer is postulated to allow the bladder neck to remain wide open and reduce bladder outlet resistance during a long-term follow-up. A higher Pves at baseline predicted a satisfactory outcome, suggesting these patients can generate more powerful abdominal pressure to overcome decreased urethral resistance after TUI-BN compared with patients with a lower baseline Pves.
In normal micturition, the bladder neck can open to a funnel shape which facilitates urine flow through a nonobstructed outlet. Some women with DU can still urinate efficiently by abdominal straining because they can effectively open the bladder neck and relax the pelvic floor muscles during voiding. A nonopening bladder neck results in functional outlet obstruction during abdominal straining to urinate in women with DU. Therefore, ablating the anatomical structure of the bladder neck and reducing bladder outlet resistance are helpful in facilitating spontaneous urination by abdominal straining in these DU patients. After TUI-BN for women with DU, the mean voiding detrusor pressure significantly improved in some patients, especially in those with nonneurogenic DU. Fifteen of 19 male patients (78.9%) with nonneurogenic noncontractile bladders also had significant return of detrusor contractility after holmium laser enucleation of the prostate . Contractions of the urethral sphincter stimulate proprioceptive nerves in the bladder muscle, which then activate inhibitory neural control of bladder contraction ,. The bladder neck and proximal urethra also play roles in the guarding reflex of the micturition cycle . The greatest concentrations of nerves in the bladder neck are at the 4 and 8-o'clock positions . TUI-BN can not only destroy the bladder neck structure but also damage neural innervation. Some patients with nonneurogenic DU may regain detrusor contractility after TUI-BN through disruption of the guarding reflex. For the other patients, TUI-BN reduces bladder outlet resistance and allows them to void using a lower abdominal straining force .
The adverse effects of TUI-BN in women include stress urinary incontinence in the daytime and overflow urinary incontinence during sleep. Preoperative urodyamic study to detect a low compliant bladder might alert the surgeon to the need for a less invasive TUI-BN. Augmentation enterocystoplasty might be needed to increase bladder volume before TUI-BN in patients with small, contracted bladders. Surgical complications include postoperative hemorrhage and inadvertent vesicovaginal fistula. The former can be avoided by meticulous hemostasis, the latter by careful inspection of tissue properties during TUI-BN, especially in women who have had radiotherapy for pelvic cancer.
| Transurethral Resection of the Prostate for Men With Detrusor Underactivity|| |
Bladder function and voiding efficiency may differ between patients with DU. According to the classification of Cucchi et al., UAB/DU can be divided into: (1) low detrusor contraction velocity, low isovolumetric detrusor pressure, and voiding efficiency >67%, (2) low detrusor contraction velocity, low isovolumetric detrusor pressure and voiding efficiency 67% or greater, and (3) low maximum contraction velocity, normal isovolumetric detrusor pressure and voiding efficiency 67% or greater . In men with UAB/DU with or without outlet obstruction, prostatic resistance may play an important role in voiding efficiency. A long-term follow-up urodynamic study reported that TURP may not always be effective in male patients with low detrusor contractility . However, one study found that after TUR-P, the IPSS, quality of life index, and PVR were significantly improved in patients with nonobstructed and weak bladder contractility and all parameters improved in patients with obstructed and/or normal bladder contractility . Another study also suggested that men with DU may still have a significantly improved Qmax and PVR after TURP .
Clinical experience also reveals that patients with chronic urinary retention may resume spontaneous voiding and normal detrusor contractility with time after appropriate treatment and bladder management. Therefore, various medical and surgical treatments including bladder outlet surgeries and urethral sphincter botulinum toxin A injection have been used to improve voiding efficiency based on clinical and urodynamic findings. Between 1998 and 2015, a total of 86 men with DU were treated in our department. Among the 86 men, 38 of the 44 who had TURP (86.4%) and 9 of the 16 (56.2%) who had transurethral incision of the prostate (TUIP) regained spontaneous voiding without an indwelling catheter or CIC. Patients with bladder function recovery had significantly greater bladder compliance (79.1 ± 108.8 vs. 38.3 ± 51.5, P = 0.024) and higher detrusor pressure (6.44 ± 7.59 v 3.65 ± 3.3, P = 0.02) than those without recovery .
| Recovery of Bladder Function After Bladder Outlet Surgery|| |
The bladder neck and prostatic urethra are innervated by the sympathetic adrenergic nerves. Ablation of the bladder neck and prostatic urethra might abolish the sympathetic hyperactivity which inhibits detrusor contractility. It is also possible that the inhibitory effect of adrenergic hyperactivity on detrusor contractility can be modulated after TUIP or TURP, resulting in a recovery of detrusor function that has been inhibited. We have previously performed TUI-BN to decrease the bladder outlet resistance in patients with UAB/DU . Patients with idiopathic DU may regain adequate detrusor contractility and resume spontaneous voiding ,. This phenomenon was observed not only in idiopathic DU but also in neurogenic DU, suggesting a micturition facilitating reflex might be triggered after TUI-BN . TUI-BN was performed in 22 spinal cord injured patients with voiding dysfunction due to bladder neck dysfunction and detrusor sphincter dyssynergia. Detrusor pressure decreased significantly in 9 who had a high baseline voiding pressure and increased significantly in 13 who had impaired detrusor contractility . Recent study also revealed that improved bladder voiding function can be achieved by TUI-BN in patients with bladder neck dysfunction and impaired detrusor contractility. Even in the patients with persistent DU, 67% could void adequately with the aid of abdominal straining .
Transurethral bladder outlet surgery, including TUI-BN, TUIP, and TURP, not only relieve bladder outlet resistance but also might reduce the inhibitory effect of detrusor contractility caused by alpha-adrenergic hyperactivity in the bladder neck and prostatic urethra , thus facilitating urination in male patients with idiopathic DU, either by spontaneous voiding or abdominal straining . If DU remains after transurethral surgery, the lower urethral resistance provides a chance for patients to urinate by abdominal straining and most of them can resume spontaneous voiding without a catheter.
| Conclusion|| |
UAB or DU is a common yet still poorly understood the urological problem. Treatment of UAB or DU aims to reduce the PVR and increase voiding efficiency. Pharmacotherapy with parasympathomimetics or cholinesterase inhibitors with or without alpha-blockers is the first line treatment. In failed cases, bladder outlet surgeries, including urethral onabotulinumtoxinA injection, TUI-BN, TUIP or TURP can effectively improve voiding efficiency and decrease the PVR in most patients with DU.
Financial Support and Sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Resnick NM, Yalla SV, Laurino E. The pathophysiology of urinary incontinence among institutionalized elderly persons. N Engl J Med 1989;320:1-7.
Andersson KE. The many faces of impaired bladder emptying. Curr Opin Urol 2014;24:363-9.
Smith PP. Aging and the underactive detrusor: A failure of activity or activation? Neurourol Urodyn 2010;29:408-12.
Ueda T, Yoshimura N, Yoshida O. Diabetic cystopathy: Relationship to autonomic neuropathy detected by sympathetic skin response. J Urol 1997;157:580-4.
Andersson KE. Detrusor underactivity/underactive bladder: New research initiatives needed. J Urol 2010;184:1829-30.
Miyazato M, Yoshimura N, Chancellor MB. The other bladder syndrome: Underactive bladder. Rev Urol 2013;15:11-22.
Osman NI, Chapple CR. Fowler's syndrome – A cause of unexplained urinary retention in young women? Nat Rev Urol 2014;11:87-98.
Taylor JA 3rd
, Kuchel GA. Detrusor underactivity: Clinical features and pathogenesis of an underdiagnosed geriatric condition. J Am Geriatr Soc 2006;54:1920-32.
Juszczak K, Drewa T. Pharmacotherapy in detrusor underactivity: A new challenge for urologists and pharmacologists (from lab to clinic). Pharmacol Rep 2016;68:703-6.
Hindley RG, Brierly RD, Thomas PJ. Prostaglandin E2 and bethanechol in combination for treating detrusor underactivity. BJU Int 2004;93:89-92.
Krishnamoorthy S, Kekre NS. Detrusor underactivity: To tone or not to tone the bladder? Indian J Urol 2009;25:407-8.
] [Full text]
Bougas DA, Mitsogiannis IC, Mitropoulos DN, Kollaitis GC, Serafetinides EN, Giannopoulos AM, et al. Clinical efficacy of distigmine bromide in the treatment of patients with underactive detrusor. Int Urol Nephrol 2004;36:507-12.
Barendrecht MM, Oelke M, Laguna MP, Michel MC. Is the use of parasympathomimetics for treating an underactive urinary bladder evidence-based? BJU Int 2007;99:749-52.
Yamanishi T, Yasuda K, Kamai T, Tsujii T, Sakakibara R, Uchiyama T, et al. Combination of a cholinergic drug and an alpha-blocker is more effective than monotherapy for the treatment of voiding difficulty in patients with underactive detrusor. Int J Urol 2004;11:88-96.
Sugaya K, Kadekawa K, Onaga T, Ashitomi K, Mukouyama H, Nakasone K, et al. Effect of distigmine at 5 mg daily in patients with detrusor underactivity. Nihon Hinyokika Gakkai Zasshi 2014;105:10-6.
Chang SJ, Chiang IN, Yu HJ. The effectiveness of tamsulosin in treating women with voiding difficulty. Int J Urol 2008;15:981-5.
Tatemichi S, Tsuchioka K, Yonekubo S, Maruyama K, Kobayashi M. Effects of silodosin, an α1A-adrenoceptor antagonist, and distigmine, an acetylcholinesterase inhibitor, and their combined effects on impaired voiding function in Zucker diabetic fatty rats. Pharmacology 2015;95:285-92.
Capitanucci ML, Camanni D, Demelas F, Mosiello G, Zaccara A, De Gennaro M, et al. Long-term efficacy of percutaneous tibial nerve stimulation for different types of lower urinary tract dysfunction in children. J Urol 2009; 182(Suppl 4): 2056-61.
Gladh G, Mattsson S, Lindström S. Intravesical electrical stimulation in the treatment of micturition dysfunction in children. Neurourol Urodyn 2003;22:233-42.
de Groat WC, Fraser MO, Yoshiyama M, Smerin S, Tai C, Chancellor MB, et al. Neural control of the urethra. Scand J Urol Nephrol Suppl 2001;207:35-43.
Smith CP, Chancellor MB. Emerging role of botulinum toxin in the management of voiding dysfunction. J Urol 2004;171:2128-37.
de Sèze M, Petit H, Gallien P, de Sèze MP, Joseph PA, Mazaux JM, et al. Botulinum a toxin and detrusor sphincter dyssynergia: A double-blind lidocaine-controlled study in 13 patients with spinal cord disease. Eur Urol 2002;42:56-62.
Mehta S, Hill D, Foley N, Hsieh J, Ethans K, Potter P, et al. A meta-analysis of botulinum toxin sphincteric injections in the treatment of incomplete voiding after spinal cord injury. Arch Phys Med Rehabil 2012;93:597-603.
Kuo HC. Botulinum A toxin urethral injection for the treatment of lower urinary tract dysfunction. J Urol 2003;170:1908-12.
Kuo HC. Effectiveness of urethral injection of botulinum A toxin in the treatment of voiding dysfunction after radical hysterectomy. Urol Int 2005;75:247-51.
Kuo HC. Effect of botulinum a toxin in the treatment of voiding dysfunction due to detrusor underactivity. Urology 2003;61:550-4.
Kuo HC. Recovery of detrusor function after urethral botulinum A toxin injection in patients with idiopathic low detrusor contractility and voiding dysfunction. Urology 2007;69:57-61.
Liao YM, Kuo HC. Causes of failed urethral botulinum toxin A treatment for emptying failure. Urology 2007;70:763-6.
Jiang YH, Wang CC, Kuo HC. OnabotulinumtoxinA urethral sphincter injection as treatment for non-neurogenic voiding dysfunction – A randomized, double-blind, placebo-controlled study. Sci Rep 2016;6:38905.
Turner-Warwick R, Whiteside CG, Worth PH, Milroy EJ, Bates CP. A urodynamic view of the clinical problems associated with bladder neck dysfunction and its treatment by endoscopic incision and trans-trigonal posterior prostatectomy. Br J Urol 1973;45:44-59.
Choudhury A. Incisional treatment of obstruction of the female bladder neck. Ann R Coll Surg Engl 1978;60:404-7.
Jhang JF, Jiang YH, Kuo HC. Transurethral incision of the bladder neck improves voiding efficiency in female patients with detrusor underactivity. Int Urogynecol J 2014;25:671-6.
Jhang JF, Jiang YH, Lee CL, Kuo HC. Long-term follow up and predictive factors for successful outcome of transurethral incision of the bladder neck in women with detrusor underactivity. J Formos Med Assoc 2016;115:807-13.
Mitchell CR, Mynderse LA, Lightner DJ, Husmann DA, Krambeck AE. Efficacy of holmium laser enucleation of the prostate in patients with non-neurogenic impaired bladder contractility: Results of a prospective trial. Urology 2014;83:428-32.
Thor KB, de Groat WC. Neural control of the female urethral and anal rhabdosphincters and pelvic floor muscles. Am J Physiol Regul Integr Comp Physiol 2010;299:R416-38.
Junginger B, Baessler K, Sapsford R, Hodges PW. Effect of abdominal and pelvic floor tasks on muscle activity, abdominal pressure and bladder neck. Int Urogynecol J 2010;21:69-77.
Ball TP Jr., Teichman JM, Sharkey FE, Rogenes VJ, Adrian EK Jr. Terminal nerve distribution to the urethra and bladder neck: Considerations in the management of stress urinary incontinence. J Urol 1997;158:827-9.
Cucchi A, Quaglini S, Rovereto B. Proposal for a urodynamic redefinition of detrusor underactivity. J Urol 2009;181:225-9.
Thomas AW, Cannon A, Bartlett E, Ellis-Jones J, Abrams P. The natural history of lower urinary tract dysfunction in men: The influence of detrusor underactivity on the outcome after transurethral resection of the prostate with a minimum 10-year urodynamic follow-up. BJU Int 2004;93:745-50.
Han DH, Jeong YS, Choo MS, Lee KS. The efficacy of transurethral resection of the prostate in the patients with weak bladder contractility index. Urology 2008;71:657-61.
Ou R, Pan C, Chen H, Wu S, Wei X, Deng X, et al. Urodynamically diagnosed detrusor hypocontractility: Should transurethral resection of the prostate be contraindicated? Int Urol Nephrol 2012;44:35-9.
Lee KH, Kuo HC. Bladder function recovery after treatment in male patients with detrusor underactivity – Clinical results and predictive factors. J Urol 2017; 197(Suppl 4S): e748.
Peng CH, Kuo HC. Transurethral incision of bladder neck in treatment of bladder neck obstruction in women. Urology 2005;65:275-8.
Ke QS, Kuo HC. Transurethral incision of the bladder neck to treat bladder neck dysfunction and voiding dysfunction in patients with high-level spinal cord injuries. Neurourol Urodyn 2010;29:748-52.
Chen YC, Wang CC, Kuo HC. Therapeutic effects of transurethral incision of the bladder neck on primary bladder neck dysfunction refractory to alpha-adrenergic blockade in men. Formos J Surg 2012;45:78-82.
Reitz A, Schmid DM, Curt A, Knapp PA, Schurch B. Afferent fibers of the pudendal nerve modulate sympathetic neurons controlling the bladder neck. Neurourol Urodyn 2003;22:597-601.
Masumori N, Furuya R, Tanaka Y, Furuya S, Ogura H, Tsukamoto T, et al. The 12-year symptomatic outcome of transurethral resection of the prostate for patients with lower urinary tract symptoms suggestive of benign prostatic obstruction compared to the urodynamic findings before surgery. BJU Int 2010;105:1429-33.