Clinical Application of Botulinum Neurotoxin in Lower-Urinary-Tract Diseases and Dysfunctions: Where Are We Now and What More Can We Do?

Abstract

Botulinum toxin A (Botox) had been considered a promising drug that has an effect on functional disorders of the lower urinary tract. Because Botox exhibits anti-inflammatory and antispasmodic effects, Botox injection into the bladder can decrease detrusor contractility, reduce bladder hypersensitivity, and eliminate painful sensations. Injecting Botox into the bladder outlet can relax the hyperactivity of the bladder neck, and of the urethral smooth and striated muscles. Based on these therapeutic effects, Botox has been widely applied to treat lower-urinary-tract dysfunctions (LUTDs) such as overactive bladder and neurogenic detrusor overactivity. However, this treatment has not been licensed for use in other LUTDs such as interstitial cystitis, voiding dysfunction due to benign prostatic hyperplasia in men, and dysfunctional voiding in women. Botox has also not been approved for the treatment of children with overactive bladder and dysfunctional voiding; in patients with spinal cord injuries with detrusor sphincter dyssynergia and autonomic dysreflexia; or for poorly relaxed external sphincter in non-neurogenic patients. This article reviews the current knowledge regarding Botox treatment for LUTDs and discusses the potential clinical applications of Botox, as well as work that can be conducted in the future.

Intravesical Injection of Botulinum Toxin Type A in Patients with Refractory Overactive Bladder—Results between Young and Elderly Populations, and Factors Associated with Unfavorable Outcomes

“…UTI is another common but frustrating unfavorable outcome after intravesical BoNT-A injections [ 55 ]. A recent systemic review revealed that the prevalence rate of UTI after intravesical BoNT-A injection for treating OAB is approximately 29.8% [ 56 ].…”

Urogenital dysfunction following neurotrauma

“…Onabotulinumtoxin A (BoNT-A) injections into the detrusor have been licensed for the management of urinary incontinence due to neurogenic DO in several countries [30]. This is a potentially effective treatment in patients with DO following TBI not responding to oral medications, though there is a risk for developing urinary retention temporarily and therefore patients should be sufficiently counselled before proceeding with this treatment.…”

Role of Urological Botulinum Toxin-A Injection for Overactive Bladder and Voiding Dysfunction in Patients with Parkinson’s Disease or Post-Stroke

“…Botulinum toxin A (BoNT-A) is a neurotoxin derived from Clostridium botulinum . Its mechanism of action in treating overactive bladder (OAB) and urinary urgency incontinence (UUI) involves inducing flaccid paralysis via blockade of the acetylcholine release at the synaptic junction [ 1 ]. In addition, BoNT-A inhibits bladder afferent nerve firing and provides anti-inflammatory effects to manage bladder disorders.…”

“…The United States Food and Drug Administration (FDA) first approved BoNT-A in 2011 for the treatment of neurogenic detrusor overactivity (nDO) and then approved it later in 2013 for refractory OAB. The expectation for intradetrusor injection of BoNT-A for reducing urinary tract dysfunction (LUTD) would be to decrease detrusor contractility, reduce bladder hypersensitivity, and eliminate painful sensations [ 1 ]. Therefore, researchers investigated the application of BoNT-A to manage the detrusor hyperreflexia (i.e., nDO) and UUI, which both originated from upper motor neuron syndrome, as seen in patients with Parkinson’s disease (PD), post-stroke, and early dementia [ 2 ].…”