Dual Therapy With Anti-CGRP Monoclonal Antibodies and Botulinum Toxin for Migraine Prevention: Is There a Rationale?
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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Dual Therapy With Anti-CGRP Monoclonal Antibodies and Botulinum Toxin for Migraine Prevention : Is There a Rationale? / Pellesi, Lanfranco; Do, Thien P.; Ashina, Håkan; Ashina, Messoud; Burstein, Rami.
I: Headache, Bind 60, Nr. 6, 2020, s. 1056-1065.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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TY - JOUR
T1 - Dual Therapy With Anti-CGRP Monoclonal Antibodies and Botulinum Toxin for Migraine Prevention
T2 - Is There a Rationale?
AU - Pellesi, Lanfranco
AU - Do, Thien P.
AU - Ashina, Håkan
AU - Ashina, Messoud
AU - Burstein, Rami
PY - 2020
Y1 - 2020
N2 - Objective: To narratively review the pathophysiological rationale of dual therapy with anti-calcitonin gene-related peptide monoclonal antibodies and botulinum toxin type A in treatment-resistant chronic migraine prevention. Background: For the prevention of chronic migraine, several pharmacological therapies are available, including oral medications, botulinum toxin type A, and the newly approved monoclonal antibodies targeting calcitonin gene-related peptide or its receptor. However, monotherapy does not yield benefits in some affected individuals, which raises the question of whether dual therapy with monoclonal antibodies and botulinum toxin type A hold promise in patients with treatment-resistant chronic migraine. Method: We searched MEDLINE for articles published from database inception to December 31st, 2019. Publications were largely selected from the past 10 years but commonly referenced and highly regarded older publications were not excluded. Results: Preclinical data suggest that anti-calcitonin gene-related peptide monoclonal antibodies and botulinum toxin type A have synergistic effects within the trigeminovascular system. Of note, findings indicate that fremanezumab – an antibody targeting the calcitonin gene-related peptide – mainly prevents the activation of Aδ-fibers, whereas botulinum toxin type A prevents the activation of C-fibers. Conclusion: There is currently only indirect preclinical evidence to support a rationale for dual therapy with anti-calcitonin gene-related peptide monoclonal antibodies and botulinum toxin type A for chronic migraine prevention. Rigorous studies evaluating clinical efficacy, safety, and cost-effectiveness are needed.
AB - Objective: To narratively review the pathophysiological rationale of dual therapy with anti-calcitonin gene-related peptide monoclonal antibodies and botulinum toxin type A in treatment-resistant chronic migraine prevention. Background: For the prevention of chronic migraine, several pharmacological therapies are available, including oral medications, botulinum toxin type A, and the newly approved monoclonal antibodies targeting calcitonin gene-related peptide or its receptor. However, monotherapy does not yield benefits in some affected individuals, which raises the question of whether dual therapy with monoclonal antibodies and botulinum toxin type A hold promise in patients with treatment-resistant chronic migraine. Method: We searched MEDLINE for articles published from database inception to December 31st, 2019. Publications were largely selected from the past 10 years but commonly referenced and highly regarded older publications were not excluded. Results: Preclinical data suggest that anti-calcitonin gene-related peptide monoclonal antibodies and botulinum toxin type A have synergistic effects within the trigeminovascular system. Of note, findings indicate that fremanezumab – an antibody targeting the calcitonin gene-related peptide – mainly prevents the activation of Aδ-fibers, whereas botulinum toxin type A prevents the activation of C-fibers. Conclusion: There is currently only indirect preclinical evidence to support a rationale for dual therapy with anti-calcitonin gene-related peptide monoclonal antibodies and botulinum toxin type A for chronic migraine prevention. Rigorous studies evaluating clinical efficacy, safety, and cost-effectiveness are needed.
KW - antagonism
KW - combined therapy
KW - headache
KW - neurotransmission
KW - pain
KW - pathophysiology
U2 - 10.1111/head.13843
DO - 10.1111/head.13843
M3 - Review
C2 - 32437038
AN - SCOPUS:85085052085
VL - 60
SP - 1056
EP - 1065
JO - Headache
JF - Headache
SN - 0017-8748
IS - 6
ER -
ID: 254463682