Abstract

Introduction: Sensitisation of the nervous system in a patient with migraine is supposed to be associated with calcitonin gene-related peptide (CGRP) activity. Therefore, the vascular response to human αCGRP (hαCGRP) could be a surrogate marker for the sensitization. We hypothesize that vascular response to hαCGRP is augmented in a patient with migraine.Methods: Twenty healthy subjects and 20 patients with migraine participated in our study. TCD was used to monitor mean arterial velocity in the middle cerebral artery (vm MCA). Simultaneously, end-tidal CO2 (Et-CO2), mean arterial pressure (MAP), and heart rate (HR) were measured. The reconstruction of the signals was made for basal conditions, during and after CGRP infusion which were compared using statistics.Results: In both groups, we found significant decrease between measurement points of vm MCA and Et-CO2 during and after hαCGRP infusion. MAP did not show significant trends during the infusion, but it was significantly increased after the infusion in migraine patients only. Responses to hαCGRP, defined as differences between two measurement points, were significantly higher for vm MCA and Et-CO2 in patients with migraine. A significant difference between groups was found in MAP response. Significant relationships were found between migraine and vm MCA, Et-CO2, and MAP.Conclusion: In patients with migraine, vm MCA responses to hαCGRP are significantly higher and are associated with CGRP-induced headache which indicates that patients with migraine are more prone to sensitization.

Highlights

  • Sensitisation of the nervous system in a patient with migraine is supposed to be associated with calcitonin gene-related peptide (CGRP) activity

  • An immediate headache was found in seven migraine patients (35%) and in three healthy participants (15%) with a statistically significant difference between the groups (p = 0.010) while delayed headaches appeared in 13 migraine patients (65%) and one healthy person (5%) (p < 0.01)

  • Migraine was significantly related to immediate CGRP-induced headaches (OR = 3.05, 95%CI 1.25–7.39; p = 0.014) and delayed CGRP-induced headaches (OR = 35.26; 95%CI 9.84–126.45; p < 0.001) as well

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Summary

Introduction

Sensitisation of the nervous system in a patient with migraine is supposed to be associated with calcitonin gene-related peptide (CGRP) activity. We hypothesize that vascular response to hαCGRP is augmented in a patient with migraine. Migraine is recognized as an episodic or chronic state of nervous system sensitization involving a CGRP-dependent process [1]. It is well-known that CGRP induces vasodilatation and enhances neuronal transmission [2]. The level of brain sensitization could be reflected in CGRP induced cerebral hemodynamic changes detected by transcranial Doppler sonography (TCD). Only a few studies have investigated exogenous hαCGRP response of cerebral circulation.

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