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What is the exact working mechanism of botulinum toxin A and sacral nerve stimulation in the treatment of overactive bladder/detrusor overactivity? ICI-RS 2017

Research output: Contribution to journalReview article

Sachin Malde, Christopher Fry, Brigitte Schurch, Tom Marcelissen, Marcio Averbeck, Alex Digesu, Arun Sahai

Original languageEnglish
Pages (from-to)S108-S116
JournalNeurourology and Urodynamics
Volume37
Issue numberS4
DOIs
PublishedJun 2018

Bibliographical note

© 2018 Wiley Periodicals, Inc.

King's Authors

Abstract

AIMS: Botulinum toxin A (BTX-A) and sacral nerve stimulation (SNS) are established treatments for overactive bladder (OAB) and are standard of care in refractory cases in international guidelines. Despite long term use over decades their "exact" working mechanisms are not entirely clear. At the ICI-RS meeting in Bristol in 2017 a think tank was convened to address the question.

METHODS: The think tank conducted a literature review and an expert consensus meeting focusing on current mechanisms and what could be learned from clinical experience and objective urodynamic data.

RESULTS: BTX-A results suggests effects on both filling and voiding parts of the micturition cycle. The salient data in this regard is presented as well as additional studies related to the urothelium and evidence for central effects. Urodynamics have consistently shown increases in bladder capacity, compliance, and reductions in detrusor pressures during filling, however post void residuals also increase in a dose-dependent fashion. During SNS activation of somatic afferents inhibits bladder sensory pathways and reflex bladder hyperactivity. Evidence in cats suggest the inhibition of bladder activity occurs primarily in the CNS by inhibition of the ascending or descending pathways of the spinobulbospinal micturition reflex. Urodynamics have suggested improvement in bladder capacity and reduction in detrusor pressures during filling with little observed effects on voiding parameters.

CONCLUSIONS: The working mechanism of BTX-A and SNS is complex. The exact mechanisms are still unknown, although considerable progress has been made in our understanding. Further research proposals are suggested to help further elucidate these mechanisms.

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