Abstract
Intravesical botulinum toxin (BoNT) injection is effective in reducing urgency and urinary incontinence. It temporarily inhibits the detrusor muscle contraction by blocking the release of acetylcholine (Ach) from the preganglionic and postganglionic nerves in the efferent nerves. BoNT-A also blocks ATP release from purinergic efferent nerves in the detrusor muscle. In afferent nerves, BoNT-A injection markedly reduces the urothelial ATP release and increases nitric oxide (NO) release from the urothelium. BoNT-A injection in the urethra or bladder has been developed in the past few decades as the treatment method for detrusor sphincter dyssyndergia, incontinence due to neurogenic or idiopathic detrusor overactivity, sensory disorders, including bladder hypersensitivity, overactive bladder, and interstitial cystitis/chronic pelvic pain syndrome. Although the FDA only approved BoNT-A injection treatment for neurogenic detrusor overactivity and for refractory overactive bladder, emerging clinical trials have demonstrated the benefits of BoNT-A treatment in functional urological disorders. Cautious selection of patients and urodynamic evaluation for confirmation of diagnosis are crucial to maximize the successful outcomes of BoNT-A treatment.
Highlights
Botulinum toxin (BoNT), one of the most potent natural neurotoxins known for centuries, has been found with emerging medical efficacy in the past few decades [1,2]
The SV2 are expressed more abundantly in the cholinergic and parasympathetic fibers, as compared to the less than half expression to the sensory and sympathetic nerves. These findings suggest that the parasympathetic nerves are the main target of Botulinum toxin A (BoNT-A) action in the human urinary bladder [19]
BoNT-A injections are widely used in functional urology disorders, and therapeutic benefits have been noticed across a wide range of lower urinary tract diseases
Summary
Botulinum toxin (BoNT), one of the most potent natural neurotoxins known for centuries, has been found with emerging medical efficacy in the past few decades [1,2]. Acute BoNT poisoning was initially observed with vomiting, intestinal spasms, mydriasis, ptosis, dysphagia, and respiratory failure [4]. It may take 3–6 months to recover from botulinum intoxication [4]. Idiopathic DO and overactive bladder (OAB) patients were reported with successful treatment with intravesical BoNT-A injection [11,12]. The latest randomized controlled trial investigating the efficacy of BoNT-A injection for BPH-related lower urinary tract symptoms (LUTS) demonstrated no significant difference between the treatment group and the placebo [14]. BoNT-A intravesical injection treatment has been developed for interstitial cystitis/bladder pain syndrome (IC/BPS) because of its anti-inflammatory effects [15,16]. As the uses of BoNT-A expand in the field of urology, understanding its mechanisms and clinical effects is essential
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