Predictors of Response to Anti-CGRP Monoclonal Antibodies: A Retrospective Study
DOI:
https://doi.org/10.46531/sinapse/AO/214/2026Keywords:
Calcitonin Gene-Related Peptide, Calcitonin Gene-Related Peptide Receptor Antagonists/ therapeutic use, Migraine Disorders/drug therapy, Migraine Disorders/prevention & controlAbstract
Background: Anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies are effective and well-tolerated therapies for migraine prevention. However, up to 30–40% of patients do not respond. While some clinical features have been associated with treatment outcomes, evidence remains limited.
Methods: We conducted a retrospective study of patients with episodic or chronic migraine followed at a tertiary headache center who initiated anti-CGRP therapy for the first time between April 2021 and April 2024. Patients received either erenumab 70 mg or fremanezumab 225 mg. Demographic and clinical data were collected. Treatment response was defined as a ≥50% reduction in monthly headache days at 3 months. Patients were classified as responders or non-responders. Group comparisons were performed using chi-squared tests for categorical variables and Student’s t-test or Mann–Whitney test for continuous variables, according to data distribution.
Results: Sixty-eight patients were included (80.9% female; mean age 43.5 ± 11.5 years). Chronic migraine was present in 48.5%. Responders and non-responders did not differ significantly in age, sex, migraine type, baseline headache frequency, aura, unilateral pain, psychiatric comorbidities, medication overuse, prior preventive failures, or type of anti-CGRP antibody. Responders were more likely to report nausea and/or vomiting (76.6% vs. 52.4%, p = 0.008), whereas non-responders had a higher prevalence of vascular risk factors (33.3% vs. 12.8%, p = 0.046).
Conclusions: In our study, nausea/vomiting were associated with a favorable response to anti-CGRP therapy, replicating previous literature findings, while vascular risk factors were associated with non-response. These results suggest a potential interaction between vascular risk factors and CGRP-mediated mechanisms.
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Copyright (c) 2026 Vítor Mendes Ferreira, Miguel Serôdio, André Caetano, Miguel Viana-Baptista, Gonçalo Cabral

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