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Journal ArticleDOI

Neuropeptides in Migraine and Cluster Headache

Lars Edvinsson, +1 more
- 01 Oct 1994 - 
- Vol. 14, Iss: 5, pp 320-327
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TLDR
Treatment with sumatriptan aborts headache in migraine and cluster headache as well as the concomitant peptide release and subjects with spontaneous attacks of migraine show release of CGRP in parallel with headache.
Abstract
The cerebral circulation is invested by a rich network of neuropeptide Y (NPY) and noradrenaline containing sympathetic nerve fibers in arteries, arterioles and veins. However, the nerve supply of vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) containing fibers is sparse. While noradrenaline and NPY cause vasoconstriction, VIP, SP and CGRP are potent vasodilators. Stimulation of the trigeminal ganglion in cat and man elicits release of SP and CGRP. Subjects with spontaneous attacks of migraine show release of CGRP in parallel with headache. Cluster headache patients have release of CGRP and VIP during bouts. Treatment with sumatriptan aborts headache in migraine and cluster headache as well as the concomitant peptide release.

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Citations
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Journal ArticleDOI

CGRP as the target of new migraine therapies — successful translation from bench to clinic

TL;DR: Treatments that target calcitonin gene-related peptide (CGRP) and its receptor are proving effective for migraine treatment, and the hypothesis that CGRP has a major role in migraine pathophysiology is strongly supported.
Journal ArticleDOI

Regulation of Calcitonin Gene‐Related Peptide Secretion From Trigeminal Nerve Cells by Botulinum Toxin Type A: Implications for Migraine Therapy

TL;DR: The objective is to determine the effect of botulinum toxin type A on calcitonin gene‐related peptide secretion from cultured trigeminal ganglia neurons.
Journal ArticleDOI

Calcitonin Gene‐Related Peptide (CGRP) and Migraine

TL;DR: Results suggest that, in migraine, activation of trigeminal nerves release CGRP and other peptides that cause the release of proinflammatory mediators, which might be mediated by activation of mitogen‐activated protein kinase pathways.
Journal ArticleDOI

The role of mast cells in migraine pathophysiology.

TL;DR: A better understanding of brain mast cell activation in migraines would be useful and could lead to several points of prophylactic intervention.
References
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Journal ArticleDOI

Flunarizine in Prophylaxis of Childhood Migraine: A Double-Blind, Placebo-Controlled, Crossover Study

TL;DR: It is concluded that flunarizine is an effective drug for the treatment of childhood migraine and in a study of this length no serious side effects were discovered.
Journal ArticleDOI

Vasoactive peptide release in the extracerebral circulation of humans during migraine headache

TL;DR: A substantial elevation of the calcitonin gene‐related peptide level in the external jugular but not the cubital fossa blood was seen in both classic and common migraine, and may have importance in the pathophysiology of migraine.
Journal ArticleDOI

The trigeminovascular system and migraine: Studies characterizing cerebrovascular and neuropeptide changes seen in humans and cats

TL;DR: These data characterize some aspects of the cerebrovascular physiology of the trigeminovascular system and demonstrate important interactions between this system and the effective antimigraine agents sumatriptan and dihydroergotamine and that such interactions can be represented in animal models.
Book

Headache and Other Head Pain

TL;DR: The second edition of Harold Wolff's monograph on headache possesses many features not included in the original monograph, and contains an account of studies concerning the phenomena of vasoconstriction and the later painful vasodilation and lowered pain threshold which characterize the migraine attack.
Journal ArticleDOI

Focal hyperemia followed by spreading oligemia and impaired activation of rcbf in classic migraine

TL;DR: The results indicate that the vasospastic model of the migraine attack is too simplistic and the normal rCBF increase during cortical activity was impaired in 6 patients.
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