Conference Update

Treatment strategies for neurogenic bladder

3 years ago, OP Editor

Various approaches to managing urinary disorders have been developed in recent years. Different therapies ranging from surgical interventions to pharmacological therapies, as well as catheterization or the endourethral prosthetic devices have become available. At the UAA Congress 2017, Dr. Hann-Chorng Kuo, The Tzu Chi General Hospital, Hualien, Taiwan, shared his insights into the management of neurogenic bladder.

In clinical practice, neurogenic bladder may induce bladder deformity, reduction of bladder capacity, hydronephrosis, and vesicoureteral reflux (VUR), potentially resulting in renal dysfunction, along with a decline in quality of life (QoL) and the progression of urinary incontinence (UI).1 Therefore, the principal goals of neurogenic bladder management are to preserve renal function and to maintain patient’s QoL by decreasing urological complications.1,2 Early diagnosis and treatment are important to prevent irreversible deterioration of the lower urinary tract (LUT) and upper urinary tract (UUT).

Intermittent catheterization (IC): The gold standard for neurogenic bladder management

Intermittent catheterization is the standard treatment for neuro-urological patients who cannot effectively empty their bladders (Table 1).3 Silicone catheters are preferred as they are less susceptible to encrustation and because of the high incidence of latex allergy in the neuro-urological patient population.3 To lower the risk of urological complications, such as bladder and renal stones, urinary infection, urethral fistulas, strictures and erosions, and bladder cancer,4 indwelling transurethral and suprapubic catheterization should only be used exceptionally with close control. Clean IC is highly recommended, but only 20% of patients initially on clean IC remained on this form of bladder management in a longitudinal study.4



Anticholinergics: Well-documented agents for neurogenic detrusor overactivity (NDO)

Anticholinergics, which increase bladder capacity and reduce episodes of UI secondary to NDO by the inhibition of parasympathetic pathways, are the first-line choice for treating NDO.3 Antimuscarinics have been used for many years to treat patients with NDO, and the responses of individual patients to antimuscarinic treatment are variable.3 Higher doses or a combination of antimuscarinic agents may be an option to maximize outcomes in neurological patients.3 Nonetheless, the high incidence of adverse events may lead to early discontinuation of antimuscarinics.3

ß3-adrenergic receptor agonist: Novel treatment for overactive bladder (OAB)

The mainstream treatment of patients with neurogenic bladder dysfunction is the use of anticholinergics and intermittent catheterization.1,3 However, these treatments are often insufficient, and different types of medication are sometimes needed.1 ß3-adrenergic receptor agonists have recently been introduced and evaluated in OAB, but clinical experience in neuro-urological patients is limited.3 Studies on safety and effectiveness of ß3-adrenergic receptor agonists in NDO are ongoing.3 Combination therapy with an antimuscarinic and a ß3-adrenergic receptor agonist may be an attractive option for NDO patients.1,3

Intravesical instillation of capsaicin or resiniferatoxin

Vanilloid receptor subtype 1 (VR1) is localized in the spinal cord, dorsal root ganglia, and visceral organs, including the bladder, urethra, and colon.5 Activation of VR1 results in spike-like currents that selectively excite and subsequently desensitize predominately the C fibers.5 The vanilloids, capsaicin and resiniferatoxin, desensitize the C-fibers and thereby decrease detrusor overactivity (DO), for a period of a few months, until the sensation of these fibers has been restored.3,5,6 The dosage is 1-2mMol capsaicin in 100mL 30% alcohol, or 10-100nMol resiniferatoxin in 100mL 10% alcohol for 30 minutes.3

Detrusor botulinum toxin A (BTX-A) injection

Treatment with botulinum toxin A (BTX-A) injected into the detrusor muscle for neurogenic detrusor overactivity has been reported to be effective.7 Detrusor BTX-A injection not only increases bladder capacity, but also decreases intravesical pressure. In a single-center, randomized, prospective study, 72 patients with neurogenic lower urinary tract dysfunction and UI secondary to spinal cord injury were randomized to receive either 200 or 300 units of onabotulinumtoxinA.8 Urodynamic parameters, incontinence severity, and QoL improved in both groups without any significant differences between groups (Figure 1).8 Uninhibited DO, defined as involuntary detrusor contractions (IDC) or increased detrusor tonicity during the filling phase, improved more in the 300 units group as compared to the 200 units group (Figure 2).8 The most common complication was urinary tract infection, which occurred in one third of patients.8





Urethral or detrusor BTX-A injections?

Detrusor injection of 200–300 units of onabotulinumtoxinA may reduce detrusor contractility, improve bladder compliance, and resume urinary continence, whereas urethral injection of onabotulinumtoxinA may reduce urethral resistance and facilitate bladder emptying.9 However, the former may induce detrusor underactivity and urinary retention, and the latter may cause undesired exacerbation of UI.9 In a prospective study investigating the therapeutic outcomes between urethral and detrusor injections of onabotulinumtoxinA in 55 patients with UI and/or difficult bladder emptying secondary to suprasacral cord injury, patients treated with detrusor onabotulinumtoxinA had greater QoL improvement than those treated with urethral injection (Table 2).9





1. Wada N, Shimizu T, Takai S, et al. Combinational effects of muscarinic receptor inhibition and beta3-adrenoceptor stimulation on neurogenic bladder dysfunction in rats with spinal cord injury. Neurourol Urodyn. 2017;36:1039-45.

2. Ku JH. The management of neurogenic bladder and quality of life in spinal cord injury. BJU Int. 2006;98:739-45.

3. Blok B, Pannek J, Castro-Diaz D, et al. European Association of Urology (EAU) Guidelines on Neuro-urology. 2017.

4. Cameron AP, Wallner LP, Tate DG, et al. Bladder management after spinal cord injury in the United States 1972 to 2005. J Urol. 2010;184:213-7.

5. Kim JH, Rivas DA, Shenot PJ, et al. Intravesical resiniferatoxin for refractory detrusor hyperreflexia: a multicenter, blinded, randomized, placebo-controlled trial. J Spinal Cord Med. 2003;26:358-63.

6. Igawa Y, Satoh T, Mizusawa H, et al. The role of capsaicin-sensitive afferents in autonomic dysreflexia in patients with spinal cord injury. BJU Int. 2003;91:637-41.

7. Ehren I, Volz D, Farrelly E, et al. Efficacy and impact of botulinum toxin A on quality of life in patients with neurogenic detrusor overactivity: a randomised, placebo-controlled, double-blind study. Scand J Urol Nephrol. 2007;41:335-40.

8. Chen YC, Kuo HC. The Therapeutic Effects of Repeated Detrusor Injections Between 200 or 300 Units of OnabotulinumtoxinA in Chronic Spinal Cord Injured Patients. Neurourol Urodyn. 2014;33:129-34.

9. Kuo HC. Therapeutic outcome and quality of life between urethral and detrusor botulinum toxin treatment for patients with spinal cord lesions and detrusor sphincter dyssynergia. Int J Clin Pract. 2013;67:1044-9.


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