Vasoactive Peptide Levels in The Plasma of Young Migraine Patients With and Without Aura Assessed Both Interictally and Ictally

Gallai, Virgilio; Sarchielli, Paola; Floridi, A; Franceschini, Maristella; Codini, Michela; Glioti, G; Trequattrini, Alberto; Palumbo, Renato

doi:10.1046/j.1468-2982.1995.1505384.x

Cited by 179 publications

(103 citation statements)

References 22 publications

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“…Goadsby et al 14 were the first to document increased CGRP levels in the external jugular venous blood of patients during migraine attack, a finding that has since been replicated in cubital venous 15 and internal jugular venous 16 blood. Furthermore, CGRP infusion causes migraine-like head- ache, 17 and antagonism with BIBN 4096 BS provides effective prophylaxis.…”

Section: Discussionmentioning

confidence: 96%

Transcerebral Exchange Kinetics of Nitrite and Calcitonin Gene-Related Peptide in Acute Mountain Sickness

Bailey

Taudorf

Berg

et al. 2009

Stroke

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Background and Purpose-High-altitude headache is the primary symptom associated with acute mountain sickness, which may be caused by nitric oxide-mediated activation of the trigeminovascular system. Therefore, the present study examined the effects of inspiratory hypoxia on the transcerebral exchange kinetics of the vasoactive molecules, nitrite (NO 2 • ), and calcitonin gene-related peptide (CGRP). Methods-Ten males were examined in normoxia and after 9-hour exposure to hypoxia (12.9% O 2 ). Global cerebral blood flow was measured by the Kety-Schmidt technique with paired samples obtained from the radial artery and jugular venous bulb. Plasma CGRP and NO 2 • were analyzed via radioimmunoassay and ozone-based chemiluminescence. Net cerebral exchange was calculated by the Fick principle and acute mountain sickness/headache scores assessed via clinically validated questionnaires. Results-Hypoxia increased cerebral blood flow with a corresponding increase in acute mountain sickness and headache scores (PϽ0.05 vs normoxia). Hypoxia blunted the cerebral uptake of NO 2 • , whereas CGRP exchange remained unaltered. No relationships were observed between the change (hypoxia-normoxia) in cerebral NO 2• or CGRP exchange and acute mountain sickness/headache scores (PϾ0.05). Conclusion-These

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Section: Discussionmentioning

confidence: 96%

Transcerebral Exchange Kinetics of Nitrite and Calcitonin Gene-Related Peptide in Acute Mountain Sickness

Bailey

Taudorf

Berg

et al. 2009

Stroke

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“…CGRP levels are elevated during spontaneous and nitroglycerin-induced migraine (Goadsby et al, 1990;Gallai et al, 1995;Juhasz et al, 2003) and reduced by triptan antimigraine drugs (Goadsby et al, 2002). A causal role for CGRP in migraine has been revealed by induction of migrainelike headache after peripheral injection of CGRP (Lassen et al, 2002) and by the effectiveness of the CGRP receptor antagonist 1-piperidinecarboxamide, N-[2-[[5-amino-L-[[4-(4-pyridinyl)-lpiperazinyl]carbonyl]pentyl]amino]-1-[(3,5-dibromo-4-hydroxyphenyl)methyl]-2-oxoethyl]-4-(1,4-dihydro-2-oxo-3(2 H)-quinazolinyl) (BIBN4096BS) as an antimigraine drug (Olesen et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Sensitization of Calcitonin Gene-Related Peptide Receptors by Receptor Activity-Modifying Protein-1 in the Trigeminal Ganglion

Zhang

Winborn²,

Prado³

et al. 2007

J. Neurosci.

224

256

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The neuropeptide calcitonin gene-related peptide (CGRP) from the trigeminal ganglion has been established as a key player in the pathogenesis of migraine. In this study, we provide evidence that the responsiveness of neuronal CGRP receptors is strongly enhanced in vitro and in vivo by expression of human receptor activity-modifying protein-1 (hRAMP1), an obligatory subunit of the CGRP receptor. We first demonstrated that activation of CGRP receptors on cultured trigeminal ganglion neurons increased endogenous CGRP mRNA levels and promoter activity. To establish whether RAMP1 is limiting in vivo as indicated from the culture studies, a transgenic mouse expressing hRAMP1 in the nervous system was generated. After CGRP injection into the whiskerpad, the hRAMP1 transgenic mice displayed 2.2 Ϯ 0.2-fold greater plasma extravasation, which is a measure of neurogenic inflammation. These results demonstrate that RAMP1 is functionally rate limiting for CGRP receptor activity in the trigeminal ganglion, which raises the possibility that elevated RAMP1 might sensitize some individuals to CGRP actions in migraine.

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“…It is, therefore, inevitable that CGRP plays a major role in nociception. The clinical observations of a release of CGRP during migraine has been confirmed in subsequent studies by others [47]. In addition, following sumatriptan administration, CGRP levels returned to control levels with successful amelioration of the headache [46].…”

Section: Migraine Attacksmentioning

confidence: 58%

“…4) [45,46]. There was no difference between migraine with aura or without aura; both resulted in substantial increases in venous CGRP levels [46,47]. In addition, a somewhat higher basal level of CGRP was noted in the cubital fossa vein blood also outside the attack [48].…”

Section: Migraine Attacksmentioning

confidence: 96%

Sensory nerves in the human cerebral circulation and trigeminal ganglion: role in primary headaches

Edvinsson

2002

J Headache Pain

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IntroductionWith the advances in the understanding of cranial pain processing that have been made over the last few years it has become clear that cranial vessels have an important role in the expression of vascular pain syndromes such as migraine and cluster headache. Recent data show that specific populations of cerebrovascular sensory nerves are involved in the pathophysiology of these pain syndromes. The present review provides an account of my interpretation of available data on perivascular peptides in the pathogenesis of primary headaches. This includes a detailed description of the human cerebrovascular sensory innervation, the origin, immunocytochemical distribution and ultrastructural features of perivascular nerves and their role in primary headaches. A general view of the pathophysiologyCurrent data provide a model in which a central "generator", different in migraine ( Fig. 1) and in cluster headache, is activated. This may initiate a wave of "spreading depression" or vasoconstriction via amine-containing fibers originating in the brain stem [1]. Following alteration of cerebral blood vessel tone, the trigeminovascular reflex [2] is initiated to counter-balance cerebrovascular constriction, in part via release of calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP). The study of neuropeptide levels in migraine and cluster headache is now providing a link between clinical and basic research that is so crucial if the pathophysiology is to be understood (for more details see [3]). In migraine (with and without aura), marked Lars EdvinssonAbstract Our knowledge of the nervous control of the cerebral circulation has increased by the use of denervations and retrograde tracing in combination with immunohistochemical techniques. We have demonstrated that cerebral vessels are supplied with sensory nerve fibers containing a multiplicity of transmitter substances originating in the trigeminal ganglion. The majority of these transmitters are neuropeptides, but the gaseous signal substance, nitric oxide (NO), is also included. In primary headaches, calcitonin generelated peptide (CGRP) is released in parallel with the headache, while the parasympathetic nerve transmitter vasoactive intestinal peptide (VIP) is released in parallel with facial symtoms. Thus, the perivascular nerves participate in the pathogenesis of primary headaches. Current migraine drugs, e.g. triptans, act in part by inhibiting the release of CGRP from the sensory nerves.

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Vasoactive Peptide Levels in The Plasma of Young Migraine Patients With and Without Aura Assessed Both Interictally and Ictally

Cited by 179 publications

References 22 publications

Transcerebral Exchange Kinetics of Nitrite and Calcitonin Gene-Related Peptide in Acute Mountain Sickness

Transcerebral Exchange Kinetics of Nitrite and Calcitonin Gene-Related Peptide in Acute Mountain Sickness

Sensitization of Calcitonin Gene-Related Peptide Receptors by Receptor Activity-Modifying Protein-1 in the Trigeminal Ganglion

Sensory nerves in the human cerebral circulation and trigeminal ganglion: role in primary headaches

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