Intradetrusor botulinum toxin injection

Mechanism of action

Your browser needs to be JavaScript capable to view this video

Try reloading this page, or reviewing your browser settings

This segment will explain the concept and mechanism of action of Intradetrusor injection of Botulinum toxin with overall success rate and need of repeat dosing with tips to avoid resistance.

Keywords

  • Neuromuscular blockade
  • Sympathetic nerves
  • acetylcholine
  • reversal
  • resiistance

Conflict of Interest

The author declares no conflict of interest.

About this video

Author(s)
Amita Jain
First online
28 April 2021
DOI
https://doi.org/10.1007/978-981-33-6650-3_1
Online ISBN
978-981-33-6650-3
Publisher
Springer, Singapore
Copyright information
© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2020

Video Transcript

Mechanism of action. Following intradetrusor injection, botulinum toxin affects the different pathways of the detrusor activity via inhibition of acetylcholine release. In addition, it inhibits afferent neurotransmitters and sensory pathways as well. It blocks neuromuscular transmission by binding to receptor sights on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine.

Clinical signs usually manifest within two to three days. And peak effects seen within five to six weeks of injection. Recovery after intramuscular injection takes place normally within 12 weeks as new nerve terminals sprout and allow for reconnection of the neuron with the end plates.

However, the sprouts are partially effective, and subsequently regress while the primary neuromuscular junction reactivates. As a result, most patients require repeat dosing every six to 12 months.

Unfortunately, a four to 10% of patients undergoing repetitive treatment with botulinum toxin will eventually become resistant to toxin, probably via antibody-mediated resistance. Shorter dosing intervals, more booster doses, and higher overall treatment doses are significantly associated with increased antibody-mediated toxin resistance.