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Could the New Anti-CGRP Monoclonal Antibodies Be Effective in Migraine Aura? Case Reports and Literature Review

Journal

JOURNAL OF CLINICAL MEDICINE
Volume 11, Issue 5, Pages -

Publisher

MDPI
DOI: 10.3390/jcm11051228

Keywords

migraine; headache; calcitonin gene-related peptide; monoclonal antibodies; migraine aura; cortical spreading depression; pain; triptans

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Recently, monoclonal antibodies (mAbs) targeting CGRP or its receptor have been approved for prophylactic use in migraine. While their efficacy in treating headache pain is well-documented, little is known about their effects on preventing migraine aura. This paper reports two cases of patients experiencing complete disappearance or reduction of aura symptoms when taking Galcanezumab or Erenumab, respectively. It also provides an overview of the controversial relationship between cerebral spreading depression and CGRP, as well as the potential central role of these mAbs in the pathophysiology of migraine aura.
Recently, monoclonal antibodies (mAbs) directed against calcitonin gene-related peptide (CGRP) (Eptinezumab, Fremanezumab, and Galcanezumab) or its receptor (Erenumab) have been approved for clinical use as prophylactic drugs for high-frequency episodic and chronic migraine. While their therapeutic effects on headache pain is well documented, there is scarce information on the usefulness of these medications in preventing migraine aura, which is believed to be associated with cortical spreading depression (CSD). Because of their large size, mAbs cannot easily cross the blood-brain barrier in high quantities, rendering the peripheral trigeminovascular system to likely be a major site of their action. In this paper, we report two cases of patients suffering from migraine with and without aura, who reported a complete disappearance of aura or reduced aura duration and intensity while taking Galcanezumab or Erenumab, respectively. Then, we present a brief overview of the literature about the controversial relationship between CSD and CGRP and about the potential additional central role of these mAbs in the pathophysiology of migraine aura.

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