CGRP-mediated trigeminovascular reactivity in migraine patients treated with erenumab

Introduction

Migraine is a highly disabling disorder characterised by recurrent attacks of severe headache (https://ichd-3.org/). The trigeminovascular system and release of calcitonin gene-related peptide (CGRP), a neuromodulator and potent vasodilator, have a crucial role in the pathophysiology of migraine.1 Monoclonal antibodies targeting CGRP (eptinezumab, fremanezumab, galcanezumab) or its receptor (erenumab) are novel prophylactics. Unfortunately, it is currently unknown which mechanisms are underlying the variability in response rates.

In addition to spontaneous release during migraine, CGRP can be released from trigeminal nerve endings by external stimuli. Application of capsaicin on the forehead releases CGRP via activation of the transient receptor potential cation channel subfamily V member 1 of the trigeminal nerve and thereby increases forehead dermal blood flow (DBF).2 Forearm application of capsaicin also increases DBF and this effect can be inhibited by erenumab, but the dose–response relationship in this model does not seem to be…

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