Calcitonin Gene-Related Peptide Does Not Cause Migraine Attacks in Patients With Familial Hemiplegic Migraine

2011 ◽  
Vol 51 (4) ◽  
pp. 544-553 ◽  
Author(s):  
Jakob M. Hansen ◽  
Lise L. Thomsen ◽  
Jes Olesen ◽  
Messoud Ashina
Keyword(s):  
Familial Hemiplegic Migraine ◽  
Calcitonin Gene Related Peptide ◽  
Hemiplegic Migraine ◽  
Related Peptide ◽  
Calcitonin Gene

Immunohistochemical characterization of calcitonin gene-related peptide in the trigeminal system of the familial hemiplegic migraine 1 knock-in mouse

Cephalalgia ◽  
2011 ◽  
Vol 31 (13) ◽  
pp. 1368-1380 ◽  
Author(s):  
Rammya Mathew ◽  
Anna P Andreou ◽  
Linda Chami ◽  
Astrid Bergerot ◽  
Arn MJM van den Maagdenberg ◽  
...  
Keyword(s):  
Familial Hemiplegic Migraine ◽  
Calcitonin Gene Related Peptide ◽  
Control Group ◽  
Cell Diameter ◽  
Trigeminal Ganglia ◽  
Wild Type ◽  
Hemiplegic Migraine ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Significant Difference

Introduction: Familial hemiplegic migraine type 1 (FHM-1) is caused by mutations in the CACNA1A gene, with the R192Q mutation being the most common. Elevated calcitonin gene-related peptide (CGRP) levels in acute migraine and clinical trials using CGRP receptor antagonists suggest CGRP-related mechanisms are important in migraine. Methods: Wild-type and R192Q knock-in mice were anaesthetized and perfused. Using immunohistochemical staining, the expression of CGRP in the trigeminocervical complex (TCC) and in the trigeminal and dorsal root ganglia was characterized. Results: There was a 38% reduction in the percentage of CGRP-immunoreactive cells in the trigeminal ganglia ( p < 0.001) of R192Q knock-in mice compared to wild-type animals. The size distribution profile of CGRP-immunoreactive cells within the trigeminal ganglia demonstrated no significant difference in cell diameter between the two groups ( p ≥ 0.56). CGRP expression was also reduced in thoracic ganglia of R192Q knock-in mice (21% vs. 27% in wild-type group; p < 0.05), but not in other ganglia. In addition, decreased CGRP immunoreactivity was observed in the superficial laminae of the TCC in R192Q knock-in mice, when compared to the control group ( p < 0.005). Conclusion: The data demonstrates that the FHM-1 CACNA1A mutation alters CGRP expression in the trigeminal ganglion and TCC. This suggests further study of these animals is warranted to characterize better the role of these mutations in the neurobiology of migraine.

Calcitonin gene-related peptide triggers migraine-like attacks in patients with migraine with aura

Cephalalgia ◽  
2010 ◽  
Vol 30 (10) ◽  
pp. 1179-1186 ◽  
Author(s):  
Jakob Møller Hansen ◽  
Anne Werner Hauge ◽  
Jes Olesen ◽  
Messoud Ashina
Keyword(s):  
Migraine With Aura ◽  
Migraine Headache ◽  
Migraine Without Aura ◽  
Familial Hemiplegic Migraine ◽  
Calcitonin Gene Related Peptide ◽  
Hemiplegic Migraine ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Post Infusion ◽  
Migraine Pathogenesis

Introduction: Calcitonin gene-related peptide (CGRP) is a key molecule in migraine pathogenesis. Intravenous CGRP infusion triggers delayed migraine-like attacks in patients with migraine without aura (MO). In contrast to patients with MO, in prior studies patients with familial hemiplegic migraine (FHM) did not report more migraine-like attacks compared to controls. Whether CGRP triggers migraine in patients with typical (non-hemiplegic) migraine with aura is (MA) unknown. In the present study we examined the migraine inducing effect of CGRP infusion in patients suffering from MA and healthy controls. Methods: Fourteen patients suffering exclusively from migraine with typical aura (MA) and 11 healthy volunteers received a continuous intravenous infusion of 1.5 µg/min CGRP over 20 minutes. Headache and other migraine symptoms were scored every 10 minutes for one hour and self recorded hourly thereafter and until 13 hours post-infusion. Results: CGRP infusion induced significantly more delayed headaches in MA patients (12 out of 14) than in controls (2 out of 11) ( p = 0.001). Furthermore, significantly more MA patients (57%; 8 out of 14) fulfilled criteria for an experimentally induced migraine attack after CGRP than controls (0%; 0 out of 11) ( P = 0.003). Four patients (28%) reported aura symptoms after CGRP infusion. Conclusion: CGRP triggered migraine-like attacks without aura in patients suffering exclusively from MA. It also triggered a typical aura in 28% of the patients. These data indicate similar neurobiological pathways responsible for triggering migraine headache in MA and MO patients, and suggest differences between MA/MO and FHM.

Calcitonin gene-related peptide and migraine with aura: A systematic review

Cephalalgia ◽  
2014 ◽  
Vol 34 (9) ◽  
pp. 695-707 ◽  
Author(s):  
Jakob M Hansen ◽  
Messoud Ashina
Keyword(s):  
Systematic Review ◽  
Animal Studies ◽  
Literature Search ◽  
Randomized Clinical Trials ◽  
Original Data ◽  
Familial Hemiplegic Migraine ◽  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Calcitonin Gene

Background Calcitonin gene-related peptide (CGRP) is a key molecule in migraine pathophysiology. Most studies have focused on CGRP in relation to migraine without aura (MO). About one-third of migraine patients have attacks with aura (MA), and this is a systematic review of the current literature on CGRP and MA. Methods We performed a systematic literature search on MEDLINE for reports of CGRP and MA, covering basic science, animal and human studies as well as randomized clinical trials. Results The literature search identified 594 citations, of which 38 contained relevant, original data. Plasma levels of CGRP in MA patients are comparable to MO, but CGRP levels varied among studies. A number of animal studies, including knock-ins of familial hemiplegic migraine (FHM) genes, have examined the relationship between CGRP and cortical spreading depression. In patients, CGRP does not trigger migraine in FHM, but is a robust trigger of migraine-like headache both in MA and MO patients. The treatment effect of CGRP antagonists are well proven in the treatment of migraine, but no studies have studied the effect specifically in MA patients. Conclusion This systematic review indicates that the role of CGRP in MA is less studied than in MO. Further studies of the importance of CGRP for auras and migraine are needed.

Monoklonale Antikörper gegen CGRP oder den CGRP-Rezeptor in der Migräneprophylaxe

2020 ◽  
Vol 39 (07/08) ◽  
pp. 490-494
Author(s):  
Borries Kukowski
Keyword(s):  
Monoklonale Antikörper ◽  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Calcitonin Gene

ZUSAMMENFASSUNGDie Charakterisierung von calcitonin gene-related peptide (CGRP) als Schlüsselmolekül in der Pathophysiologie der Migräne hat nicht nur unser Verständnis der Erkrankung, sondern auch die Entwicklung neuer Therapien vorangetrieben. Seit kurzem steht mit den monoklonalen Antikörpern gegen CGRP oder den CGRP-Rezeptor eine spezifische und hoch selektive Option für die medikamentöse Prophylaxe der episodischen und chronischen Migräne zur Verfügung, die in zahlreichen klinischen Studien ihre Überlegenheit gegenüber Placebo belegt hat. Hier werden Erfahrungen aus dem praktischen Behandlungsalltag zur kurz- und mittelfristigen Wirksamkeit und Verträglichkeit mitgeteilt und weitere Aspekte wie Therapiewechsel bei Non-Response, Verlauf nach Therapieende und die Frage des Wirkungsortes unter Einbeziehung bereits publizierter Daten angesprochen.

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