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Review
. 2021 Jun 29;10(13):2898.
doi: 10.3390/jcm10132898.

OnabotulinumtoxinA in Migraine: A Review of the Literature and Factors Associated with Efficacy

Affiliations
Review

OnabotulinumtoxinA in Migraine: A Review of the Literature and Factors Associated with Efficacy

Jason C Ray et al. J Clin Med. .

Abstract

The efficacy of onabotulinumtoxinA (OnaB-A) as a preventative treatment for chronic migraine, emerging fortuitously from clinical observation is now supported by class one evidence and over two decades of real-world clinical data. There is still limited ability to predict a clinically meaningful response to OnaB-A for individual patients, however. This review summarises briefly the proposed mechanism of OnaB-A in chronic migraine, the literature of predictors of clinical response, and recent developments in the field.

Keywords: botulinum toxin; migraine; predictors of efficacy.

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Conflict of interest statement

J.C.R. has received compensation from the Pharmaceutical Society of Australia, sponsored by Viatris for educational material. E.J.H. has served on advisory boards for Sanofi-Genzyme, Novartis, Teva, Eli Lilly, Allergan, Lundbeck, been involved in clinical trials sponsored by Novartis, Teva, Xalud, Daewong and Novotech, and has received payment for educational presenta-tions from Allergan, Teva, Eli Lilly and Novartis. M.M. has served on advisory boards for Allergan, Autonomic Technologies Inc, Eli Lilly Novartis, Pfizer, Salvia and TEVA; has received payment for educational presen-tations from Allergan, electroCore, Eli Lilly, Novartis and TEVA; has received grants from Abbott, Medtronic and electroCore; and has a patent on system and method for diagnosing and treating headaches (WO2018051103A1, issued).

Figures

Figure 1
Figure 1
The PREEMPT protocol for injection of onabotulinumtoxinA (stylised)—green dots represent injection sites [12].
Figure 2
Figure 2
Mechanism of action of botulinum toxin [12]. (a) Normal synaptic transmission; arriving active channel opens voltage-gated calcium channels, allowing influx of calcium. Calcium allows synaptic vesicle docking via SNARE proteins, neurotransmitter release, and activation of post-synaptic potential. (b) Neuronal uptake of onabotulinumtoxinA, internalisation of botulinum toxin via synaptic vesicle, and cleavage of SNAP-25 protein causing inhibition of neurotransmitter release.

References

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    1. The International Classification of Headache Disorders 3rd edition. [(accessed on 12 August 2019)]; Available online: https://ichd-3.org/
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