Personal view: Modelling pain mechanisms of migraine without aura

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Standard

Personal view : Modelling pain mechanisms of migraine without aura. / Olesen, Jes.

I: Cephalalgia, Bind 42, Nr. 13, 2022, s. 1425-1435.

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Harvard

Olesen, J 2022, 'Personal view: Modelling pain mechanisms of migraine without aura', Cephalalgia, bind 42, nr. 13, s. 1425-1435. https://doi.org/10.1177/03331024221111529

APA

Olesen, J. (2022). Personal view: Modelling pain mechanisms of migraine without aura. Cephalalgia, 42(13), 1425-1435. https://doi.org/10.1177/03331024221111529

Vancouver

Olesen J. Personal view: Modelling pain mechanisms of migraine without aura. Cephalalgia. 2022;42(13):1425-1435. https://doi.org/10.1177/03331024221111529

Author

Olesen, Jes. / Personal view : Modelling pain mechanisms of migraine without aura. I: Cephalalgia. 2022 ; Bind 42, Nr. 13. s. 1425-1435.

Bibtex

@article{12cfc3c624754f6ca3045961b0e17e07,
title = "Personal view: Modelling pain mechanisms of migraine without aura",
abstract = "Introduction: This review aims to model migraine nociception. Methods: Personal experience and litterature. Results: Genetic and environmental factors in combination decide whether a person suffers from migraine. Endogenous and/or exogenous factors precipitate the individual attacks. Nociception takes place around blood vessels. There is a growing understanding of the molecular pathophysiological mechanisms of migraine from human provocation studies. Rodent models of migraine are necessary to understand the complex interrelation between the many putatively involved molecules and tissues but their relevance for human migraine is uncertain. The crucial element in migraine nociception is a unit consisting of endothelial cells, vascular smooth muscle cells, perivascular nerve fibers (trigeminal, parasympathetic and sympathetic) and mast cells. Attacks may start outside the brain by humoral or neurogenic activity releasing nociceptive substances around blood vessels. They may also (perhaps more often) start by the brain generating efferent activity in autonomic and somatic nerves. Conclusion: Human and rodent studies can quickly uncover the {"}mystery of migraine{"}.",
keywords = "Headache, arteries, CGRP, NO, PACAP, trigeminovascular system, NITRIC-OXIDE, MUSCLE TENDERNESS, HEADACHE, ATTACKS, PATHOPHYSIOLOGY, BLOOD, PHOSPHODIESTERASE-3, HEMODYNAMICS, INHIBITOR, DISORDER",
author = "Jes Olesen",
year = "2022",
doi = "10.1177/03331024221111529",
language = "English",
volume = "42",
pages = "1425--1435",
journal = "Cephalalgia",
issn = "0800-1952",
publisher = "SAGE Publications",
number = "13",

}

RIS

TY - JOUR

T1 - Personal view

T2 - Modelling pain mechanisms of migraine without aura

AU - Olesen, Jes

PY - 2022

Y1 - 2022

N2 - Introduction: This review aims to model migraine nociception. Methods: Personal experience and litterature. Results: Genetic and environmental factors in combination decide whether a person suffers from migraine. Endogenous and/or exogenous factors precipitate the individual attacks. Nociception takes place around blood vessels. There is a growing understanding of the molecular pathophysiological mechanisms of migraine from human provocation studies. Rodent models of migraine are necessary to understand the complex interrelation between the many putatively involved molecules and tissues but their relevance for human migraine is uncertain. The crucial element in migraine nociception is a unit consisting of endothelial cells, vascular smooth muscle cells, perivascular nerve fibers (trigeminal, parasympathetic and sympathetic) and mast cells. Attacks may start outside the brain by humoral or neurogenic activity releasing nociceptive substances around blood vessels. They may also (perhaps more often) start by the brain generating efferent activity in autonomic and somatic nerves. Conclusion: Human and rodent studies can quickly uncover the "mystery of migraine".

AB - Introduction: This review aims to model migraine nociception. Methods: Personal experience and litterature. Results: Genetic and environmental factors in combination decide whether a person suffers from migraine. Endogenous and/or exogenous factors precipitate the individual attacks. Nociception takes place around blood vessels. There is a growing understanding of the molecular pathophysiological mechanisms of migraine from human provocation studies. Rodent models of migraine are necessary to understand the complex interrelation between the many putatively involved molecules and tissues but their relevance for human migraine is uncertain. The crucial element in migraine nociception is a unit consisting of endothelial cells, vascular smooth muscle cells, perivascular nerve fibers (trigeminal, parasympathetic and sympathetic) and mast cells. Attacks may start outside the brain by humoral or neurogenic activity releasing nociceptive substances around blood vessels. They may also (perhaps more often) start by the brain generating efferent activity in autonomic and somatic nerves. Conclusion: Human and rodent studies can quickly uncover the "mystery of migraine".

KW - Headache

KW - arteries

KW - CGRP

KW - NO

KW - PACAP

KW - trigeminovascular system

KW - NITRIC-OXIDE

KW - MUSCLE TENDERNESS

KW - HEADACHE

KW - ATTACKS

KW - PATHOPHYSIOLOGY

KW - BLOOD

KW - PHOSPHODIESTERASE-3

KW - HEMODYNAMICS

KW - INHIBITOR

KW - DISORDER

U2 - 10.1177/03331024221111529

DO - 10.1177/03331024221111529

M3 - Review

C2 - 35796522

VL - 42

SP - 1425

EP - 1435

JO - Cephalalgia

JF - Cephalalgia

SN - 0800-1952

IS - 13

ER -

ID: 344811762