Calcitonin gene-related peptide does not cause the familial hemiplegic migraine phenotype

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Calcitonin gene-related peptide does not cause the familial hemiplegic migraine phenotype. / Hansen, J.M.; Thomsen, L.L.; Olesen, J.; Ashina, M.

I: Neurology, Bind 71, Nr. 11, 2008, s. 841-847.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Hansen, JM, Thomsen, LL, Olesen, J & Ashina, M 2008, 'Calcitonin gene-related peptide does not cause the familial hemiplegic migraine phenotype', Neurology, bind 71, nr. 11, s. 841-847.

APA

Hansen, J. M., Thomsen, L. L., Olesen, J., & Ashina, M. (2008). Calcitonin gene-related peptide does not cause the familial hemiplegic migraine phenotype. Neurology, 71(11), 841-847.

Vancouver

Hansen JM, Thomsen LL, Olesen J, Ashina M. Calcitonin gene-related peptide does not cause the familial hemiplegic migraine phenotype. Neurology. 2008;71(11):841-847.

Author

Hansen, J.M. ; Thomsen, L.L. ; Olesen, J. ; Ashina, M. / Calcitonin gene-related peptide does not cause the familial hemiplegic migraine phenotype. I: Neurology. 2008 ; Bind 71, Nr. 11. s. 841-847.

Bibtex

@article{ce288aa004c711deb05e000ea68e967b,
title = "Calcitonin gene-related peptide does not cause the familial hemiplegic migraine phenotype",
abstract = "Objective: The neuropeptide calcitonin gene-related peptide (CGRP) is a migraine trigger that plays a crucial role in migraine pathophysiology, and CGRP antagonism is efficient in the treatment of migraine attacks. Familial hemiplegic migraine (FHM) is a dominantly inherited subtype of migraine with aura associated with several gene mutations. FHM shares many phenotypical similarities with common types of migraine, indicating common neurobiological pathways. We tested the hypothesis that the FHM genotype confers a CGRP hypersensitive phenotype. Methods: We included 9 FHM patients with known mutations in the CACNA1A and ATP1A2 genes and 10 healthy controls. All subjects received IV infusion of CGRP (1.5 mu g/min). We recorded headache intensity on a verbal rating scale and vascular changes in the middle cerebral artery and the superficial temporal artery. Results: CGRP infusion did not induce an aura in any of the participants. The incidences of reported migraine and migraine-like headache were not different in the two groups, with 22% (2 of 9) reporting migraine in the patient group and 10% (1 of 10) reporting migraine-like headache in the control group (95% CI -0.31 to 0.55; p = 0.58). Headache severity and intensity were not different between the groups. Conclusions: Familial hemiplegic migraine ( FHM) patients do not show hypersensitivity of the calcitonin gene-related peptide (CGRP)-cyclic adenosine 3 ', 5 '-monophosphate pathway, as characteristically seen in migraine patients without aura. This indicates that the pathophysiologic pathways underlying migraine headache in FHM may be different from the common types of migraine and questions whether CGRP antagonists would be effective in the treatment of FHM patients Udgivelsesdato: 2008/9/9",
author = "J.M. Hansen and L.L. Thomsen and J. Olesen and M. Ashina",
note = "Times Cited: 0ArticleEnglishHansen, J. MUniv Copenhagen, Glostrup Hosp, Fac Hlth Sci, Danish Headache Ctr, Nordre Ringvej 57,Bolig 23-24, DK-2600 Glostrup, DenmarkCited References Count: 38345ZULIPPINCOTT WILLIAMS & WILKINS530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USAPHILADELPHIA",
year = "2008",
language = "English",
volume = "71",
pages = "841--847",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams & Wilkins",
number = "11",

}

RIS

TY - JOUR

T1 - Calcitonin gene-related peptide does not cause the familial hemiplegic migraine phenotype

AU - Hansen, J.M.

AU - Thomsen, L.L.

AU - Olesen, J.

AU - Ashina, M.

N1 - Times Cited: 0ArticleEnglishHansen, J. MUniv Copenhagen, Glostrup Hosp, Fac Hlth Sci, Danish Headache Ctr, Nordre Ringvej 57,Bolig 23-24, DK-2600 Glostrup, DenmarkCited References Count: 38345ZULIPPINCOTT WILLIAMS & WILKINS530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USAPHILADELPHIA

PY - 2008

Y1 - 2008

N2 - Objective: The neuropeptide calcitonin gene-related peptide (CGRP) is a migraine trigger that plays a crucial role in migraine pathophysiology, and CGRP antagonism is efficient in the treatment of migraine attacks. Familial hemiplegic migraine (FHM) is a dominantly inherited subtype of migraine with aura associated with several gene mutations. FHM shares many phenotypical similarities with common types of migraine, indicating common neurobiological pathways. We tested the hypothesis that the FHM genotype confers a CGRP hypersensitive phenotype. Methods: We included 9 FHM patients with known mutations in the CACNA1A and ATP1A2 genes and 10 healthy controls. All subjects received IV infusion of CGRP (1.5 mu g/min). We recorded headache intensity on a verbal rating scale and vascular changes in the middle cerebral artery and the superficial temporal artery. Results: CGRP infusion did not induce an aura in any of the participants. The incidences of reported migraine and migraine-like headache were not different in the two groups, with 22% (2 of 9) reporting migraine in the patient group and 10% (1 of 10) reporting migraine-like headache in the control group (95% CI -0.31 to 0.55; p = 0.58). Headache severity and intensity were not different between the groups. Conclusions: Familial hemiplegic migraine ( FHM) patients do not show hypersensitivity of the calcitonin gene-related peptide (CGRP)-cyclic adenosine 3 ', 5 '-monophosphate pathway, as characteristically seen in migraine patients without aura. This indicates that the pathophysiologic pathways underlying migraine headache in FHM may be different from the common types of migraine and questions whether CGRP antagonists would be effective in the treatment of FHM patients Udgivelsesdato: 2008/9/9

AB - Objective: The neuropeptide calcitonin gene-related peptide (CGRP) is a migraine trigger that plays a crucial role in migraine pathophysiology, and CGRP antagonism is efficient in the treatment of migraine attacks. Familial hemiplegic migraine (FHM) is a dominantly inherited subtype of migraine with aura associated with several gene mutations. FHM shares many phenotypical similarities with common types of migraine, indicating common neurobiological pathways. We tested the hypothesis that the FHM genotype confers a CGRP hypersensitive phenotype. Methods: We included 9 FHM patients with known mutations in the CACNA1A and ATP1A2 genes and 10 healthy controls. All subjects received IV infusion of CGRP (1.5 mu g/min). We recorded headache intensity on a verbal rating scale and vascular changes in the middle cerebral artery and the superficial temporal artery. Results: CGRP infusion did not induce an aura in any of the participants. The incidences of reported migraine and migraine-like headache were not different in the two groups, with 22% (2 of 9) reporting migraine in the patient group and 10% (1 of 10) reporting migraine-like headache in the control group (95% CI -0.31 to 0.55; p = 0.58). Headache severity and intensity were not different between the groups. Conclusions: Familial hemiplegic migraine ( FHM) patients do not show hypersensitivity of the calcitonin gene-related peptide (CGRP)-cyclic adenosine 3 ', 5 '-monophosphate pathway, as characteristically seen in migraine patients without aura. This indicates that the pathophysiologic pathways underlying migraine headache in FHM may be different from the common types of migraine and questions whether CGRP antagonists would be effective in the treatment of FHM patients Udgivelsesdato: 2008/9/9

M3 - Journal article

VL - 71

SP - 841

EP - 847

JO - Neurology

JF - Neurology

SN - 0028-3878

IS - 11

ER -

ID: 10870367