Jakob M Hansen1, Lise L Thomsen, Jes Olesen, Messoud Ashina. 1. Danish Headache Center, Departments of Neurology, Glostrup Hospital, Faculty of Health Sciences, University of Copenhagen, Glostrup, Copenhagen, Denmark.
Abstract
BACKGROUND: Calcitonin gene-related peptide (CGRP) is a key molecule in migraine pathogenesis. Intravenous CGRP triggers migraine-like attacks in patients with migraine with aura and without aura. In contrast, patients with familial hemiplegic migraine (FHM) with known mutations did not report more migraine-like attacks compared to controls. Whether CGRP triggers migraine-like attacks in FHM patients without known mutations is unknown. OBJECTIVE: In the present study we therefore examined the migraine-inducing effect of CGRP in FHM patients without known mutations and healthy controls. METHODS AND DESIGN: Eleven patients suffering from FHM without known mutations and 11 controls received an intravenous infusion of 1.5 µg/minute CGRP over 20 minutes. The study design was a balanced and controlled provocation study. Headache and other migraine symptoms were scored for 1 hour and self-recorded hourly thereafter until 13-hour postinfusion. RESULTS: We found no difference in the incidence of migraine-like attacks between the 2 groups, with 9% (1 of 11) of patients and 0% (0 of 10) of controls reporting migraine-like headache (P = 1.00). CGRP infusion did not induce aura symptoms in any of the participants. There was no difference in the incidence of CGRP-induced delayed headaches between the groups (P = .18). CONCLUSION: In contrast to patients suffering from migraine with aura and without aura, CGRP infusion did not induce more migraine-like attacks in FHM patients without known mutations compared to controls. It seems that the majority of FHM patients with and without known mutation display no sensitivity to CGRP signaling compared to common types of migraine.
BACKGROUND:Calcitonin gene-related peptide (CGRP) is a key molecule in migraine pathogenesis. Intravenous CGRP triggers migraine-like attacks in patients with migraine with aura and without aura. In contrast, patients with familial hemiplegic migraine (FHM) with known mutations did not report more migraine-like attacks compared to controls. Whether CGRP triggers migraine-like attacks in FHMpatients without known mutations is unknown. OBJECTIVE: In the present study we therefore examined the migraine-inducing effect of CGRP in FHMpatients without known mutations and healthy controls. METHODS AND DESIGN: Eleven patients suffering from FHM without known mutations and 11 controls received an intravenous infusion of 1.5 µg/minute CGRP over 20 minutes. The study design was a balanced and controlled provocation study. Headache and other migraine symptoms were scored for 1 hour and self-recorded hourly thereafter until 13-hour postinfusion. RESULTS: We found no difference in the incidence of migraine-like attacks between the 2 groups, with 9% (1 of 11) of patients and 0% (0 of 10) of controls reporting migraine-like headache (P = 1.00). CGRP infusion did not induce aura symptoms in any of the participants. There was no difference in the incidence of CGRP-induced delayed headaches between the groups (P = .18). CONCLUSION: In contrast to patients suffering from migraine with aura and without aura, CGRP infusion did not induce more migraine-like attacks in FHMpatients without known mutations compared to controls. It seems that the majority of FHMpatients with and without known mutation display no sensitivity to CGRP signaling compared to common types of migraine.
Authors: Peter J Goadsby; Philip R Holland; Margarida Martins-Oliveira; Jan Hoffmann; Christoph Schankin; Simon Akerman Journal: Physiol Rev Date: 2017-04 Impact factor: 37.312