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[Physiopathology of the migraine attack and mechanisms of action of anti-migraine agents: recent findings in animals].
Pathol Biol (Paris). 2000 Sep; 48(7):593-607.PB

Abstract

No current experimental model on migraine is fully satisfactory, and constructing a single model which takes into account all the various clinical and pharmacological aspects does not seem feasible. A critical review of the large number of experimental approaches developed over the past 20 years to investigate migraine attacks and an examination of recent research in the various fields of animal biology seems to be more pertinent in this context. A neurovascular cortical spreading depression could be one of the mechanisms involved in aura formation, but its association with headache is enigmatic, and the implication of hypoxia in its etiopathogenesis remains controversial. Intercritical neuronal hyperexcitability, which has been proposed as a possible biological basis for the onset of migraine, may trigger the development of aura, but also the activation of the trigeminovascular system. An independent but concomitant activation of both phenomena could be driven by a mesencephalic noradrenergic or cortical limbic generator. The trigemino-vascular model of perivascular neurogenic inflammation does not explain certain experimental and pharmacological properties of anti-migraine drugs. The clinical efficacy of the 5-HT1B/D agonists is based on a vasoconstrictive effect and on their inhibition of neurogenic inflammation, while calcitonin gene-related peptide (CGRP) plays a major role in vasodilatation and substance P in neurogenic inflammation. The initiation and initial development of migraine probably involve a prior peripheral sensitization of the trigeminal nociceptors, while the susceptibility to onset of an attack, maintenance of the migrainous state and the clinical variability must certainly rely on central sensitization within the trigeminal caudate nucleus. The numerous experimental approaches to the physiopathology of migraine developed over recent years, each of which provides a basis for the development of new classes of anti-migraine drugs, are not exclusive of one another. Rather, they contribute to providing various specific aspects of a physiopathogenic theory of migraine, which at the present time has to be both wide-ranging and adaptive.

Authors+Show Affiliations

Centre d'évaluation et traitement de la douleur, CHU de Lyon, hôpital neurologique GRECA, Lyon, France.

Pub Type(s)

English Abstract
Journal Article
Review

Language

fre

PubMed ID

11072637

Citation

Mick, G. "[Physiopathology of the Migraine Attack and Mechanisms of Action of Anti-migraine Agents: Recent Findings in Animals]." Pathologie-biologie, vol. 48, no. 7, 2000, pp. 593-607.
Mick G. [Physiopathology of the migraine attack and mechanisms of action of anti-migraine agents: recent findings in animals]. Pathol Biol. 2000;48(7):593-607.
Mick, G. (2000). [Physiopathology of the migraine attack and mechanisms of action of anti-migraine agents: recent findings in animals]. Pathologie-biologie, 48(7), 593-607.
Mick G. [Physiopathology of the Migraine Attack and Mechanisms of Action of Anti-migraine Agents: Recent Findings in Animals]. Pathol Biol. 2000;48(7):593-607. PubMed PMID: 11072637.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Physiopathology of the migraine attack and mechanisms of action of anti-migraine agents: recent findings in animals]. A1 - Mick,G, PY - 2000/11/10/pubmed PY - 2001/2/28/medline PY - 2000/11/10/entrez SP - 593 EP - 607 JF - Pathologie-biologie JO - Pathol. Biol. VL - 48 IS - 7 N2 - No current experimental model on migraine is fully satisfactory, and constructing a single model which takes into account all the various clinical and pharmacological aspects does not seem feasible. A critical review of the large number of experimental approaches developed over the past 20 years to investigate migraine attacks and an examination of recent research in the various fields of animal biology seems to be more pertinent in this context. A neurovascular cortical spreading depression could be one of the mechanisms involved in aura formation, but its association with headache is enigmatic, and the implication of hypoxia in its etiopathogenesis remains controversial. Intercritical neuronal hyperexcitability, which has been proposed as a possible biological basis for the onset of migraine, may trigger the development of aura, but also the activation of the trigeminovascular system. An independent but concomitant activation of both phenomena could be driven by a mesencephalic noradrenergic or cortical limbic generator. The trigemino-vascular model of perivascular neurogenic inflammation does not explain certain experimental and pharmacological properties of anti-migraine drugs. The clinical efficacy of the 5-HT1B/D agonists is based on a vasoconstrictive effect and on their inhibition of neurogenic inflammation, while calcitonin gene-related peptide (CGRP) plays a major role in vasodilatation and substance P in neurogenic inflammation. The initiation and initial development of migraine probably involve a prior peripheral sensitization of the trigeminal nociceptors, while the susceptibility to onset of an attack, maintenance of the migrainous state and the clinical variability must certainly rely on central sensitization within the trigeminal caudate nucleus. The numerous experimental approaches to the physiopathology of migraine developed over recent years, each of which provides a basis for the development of new classes of anti-migraine drugs, are not exclusive of one another. Rather, they contribute to providing various specific aspects of a physiopathogenic theory of migraine, which at the present time has to be both wide-ranging and adaptive. SN - 0369-8114 UR - https://www.unboundmedicine.com/medline/citation/11072637/[Physiopathology_of_the_migraine_attack_and_mechanisms_of_action_of_anti_migraine_agents:_recent_findings_in_animals]_ L2 - http://www.diseaseinfosearch.org/result/4811 DB - PRIME DP - Unbound Medicine ER -