Mechanisms underlying migraine chronification

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Chronification of migraine occurs in approximately 3% of entire cases annually. Some risk factors, like obesity and affective disorder, exacerbate the migraine disease conditions. The incidence of migraine chronification is dependent on the baseline frequency of migraine attacks. Functional MRI data support that dysfunction of the descending anti-nociceptive systems plays an important role in the development of migraine chronification. Moreover, several studies employing voxel-based morphometry have revealed morphological alterations of gray matter density in various brain regions, some of which are irrelevant to the sensory or limbic systems. It remains to be determined whether such organic changes are either causative of or attributable to migraine chronification. A preclinical study showed that cortical spreading depression can activate matrix metalloproteinase-9, potentially leading to disruption of blood-brain barrier and subsequent parenchymal damage. We demonstrated that TRPV1 (transient receptor potential vanilloid subfamily, member 1) stimulation in the trigeminal nociceptors induces morphological changes of microglia and astrocytes in the trigeminal nucleus caudalis. Recently, botulinum neurotoxin type-A (BoNT-A) has been approved for patients with chronic migraine. The primary action of BoNT-A is inhibition of regulated exocytosis at the peripheral nerve terminals, raising the possibility that certain peripheral factors are implicated in the development of migraine chronification.

Original languageEnglish
Pages (from-to)1012-1013
Number of pages2
JournalClinical Neurology
Volume52
Issue number11
DOIs
Publication statusPublished - 2012

Fingerprint

Migraine Disorders
Type A Botulinum Toxins
Cortical Spreading Depression
Trigeminal Nuclei
TRPV Cation Channels
Limbic System
Nociceptors
Matrix Metalloproteinase 9
Exocytosis
Microglia
Blood-Brain Barrier
Mood Disorders
Peripheral Nerves
Astrocytes
Obesity
Magnetic Resonance Imaging
Incidence
Brain

Keywords

  • Botulinum neurotoxin type-A (BoNT-A)
  • Chronic migraine
  • Descending anti-nociceptive system
  • Member 1)
  • Migraine chronification
  • TRPV1 (transient receptor potential vanilloid subfamily

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Mechanisms underlying migraine chronification. / Shibata, Mamoru.

In: Clinical Neurology, Vol. 52, No. 11, 2012, p. 1012-1013.

Research output: Contribution to journalArticle

@article{1ff4604f10c64fa4857616bbd00ae47f,
title = "Mechanisms underlying migraine chronification",
abstract = "Chronification of migraine occurs in approximately 3{\%} of entire cases annually. Some risk factors, like obesity and affective disorder, exacerbate the migraine disease conditions. The incidence of migraine chronification is dependent on the baseline frequency of migraine attacks. Functional MRI data support that dysfunction of the descending anti-nociceptive systems plays an important role in the development of migraine chronification. Moreover, several studies employing voxel-based morphometry have revealed morphological alterations of gray matter density in various brain regions, some of which are irrelevant to the sensory or limbic systems. It remains to be determined whether such organic changes are either causative of or attributable to migraine chronification. A preclinical study showed that cortical spreading depression can activate matrix metalloproteinase-9, potentially leading to disruption of blood-brain barrier and subsequent parenchymal damage. We demonstrated that TRPV1 (transient receptor potential vanilloid subfamily, member 1) stimulation in the trigeminal nociceptors induces morphological changes of microglia and astrocytes in the trigeminal nucleus caudalis. Recently, botulinum neurotoxin type-A (BoNT-A) has been approved for patients with chronic migraine. The primary action of BoNT-A is inhibition of regulated exocytosis at the peripheral nerve terminals, raising the possibility that certain peripheral factors are implicated in the development of migraine chronification.",
keywords = "Botulinum neurotoxin type-A (BoNT-A), Chronic migraine, Descending anti-nociceptive system, Member 1), Migraine chronification, TRPV1 (transient receptor potential vanilloid subfamily",
author = "Mamoru Shibata",
year = "2012",
doi = "10.5692/clinicalneurol.52.1012",
language = "English",
volume = "52",
pages = "1012--1013",
journal = "Clinical Neurology",
issn = "0009-918X",
publisher = "Societas Neurologica Japonica",
number = "11",

}

TY - JOUR

T1 - Mechanisms underlying migraine chronification

AU - Shibata, Mamoru

PY - 2012

Y1 - 2012

N2 - Chronification of migraine occurs in approximately 3% of entire cases annually. Some risk factors, like obesity and affective disorder, exacerbate the migraine disease conditions. The incidence of migraine chronification is dependent on the baseline frequency of migraine attacks. Functional MRI data support that dysfunction of the descending anti-nociceptive systems plays an important role in the development of migraine chronification. Moreover, several studies employing voxel-based morphometry have revealed morphological alterations of gray matter density in various brain regions, some of which are irrelevant to the sensory or limbic systems. It remains to be determined whether such organic changes are either causative of or attributable to migraine chronification. A preclinical study showed that cortical spreading depression can activate matrix metalloproteinase-9, potentially leading to disruption of blood-brain barrier and subsequent parenchymal damage. We demonstrated that TRPV1 (transient receptor potential vanilloid subfamily, member 1) stimulation in the trigeminal nociceptors induces morphological changes of microglia and astrocytes in the trigeminal nucleus caudalis. Recently, botulinum neurotoxin type-A (BoNT-A) has been approved for patients with chronic migraine. The primary action of BoNT-A is inhibition of regulated exocytosis at the peripheral nerve terminals, raising the possibility that certain peripheral factors are implicated in the development of migraine chronification.

AB - Chronification of migraine occurs in approximately 3% of entire cases annually. Some risk factors, like obesity and affective disorder, exacerbate the migraine disease conditions. The incidence of migraine chronification is dependent on the baseline frequency of migraine attacks. Functional MRI data support that dysfunction of the descending anti-nociceptive systems plays an important role in the development of migraine chronification. Moreover, several studies employing voxel-based morphometry have revealed morphological alterations of gray matter density in various brain regions, some of which are irrelevant to the sensory or limbic systems. It remains to be determined whether such organic changes are either causative of or attributable to migraine chronification. A preclinical study showed that cortical spreading depression can activate matrix metalloproteinase-9, potentially leading to disruption of blood-brain barrier and subsequent parenchymal damage. We demonstrated that TRPV1 (transient receptor potential vanilloid subfamily, member 1) stimulation in the trigeminal nociceptors induces morphological changes of microglia and astrocytes in the trigeminal nucleus caudalis. Recently, botulinum neurotoxin type-A (BoNT-A) has been approved for patients with chronic migraine. The primary action of BoNT-A is inhibition of regulated exocytosis at the peripheral nerve terminals, raising the possibility that certain peripheral factors are implicated in the development of migraine chronification.

KW - Botulinum neurotoxin type-A (BoNT-A)

KW - Chronic migraine

KW - Descending anti-nociceptive system

KW - Member 1)

KW - Migraine chronification

KW - TRPV1 (transient receptor potential vanilloid subfamily

UR - http://www.scopus.com/inward/record.url?scp=84880522166&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84880522166&partnerID=8YFLogxK

U2 - 10.5692/clinicalneurol.52.1012

DO - 10.5692/clinicalneurol.52.1012

M3 - Article

C2 - 23196500

AN - SCOPUS:84880522166

VL - 52

SP - 1012

EP - 1013

JO - Clinical Neurology

JF - Clinical Neurology

SN - 0009-918X

IS - 11

ER -