On the possible relation of spreading cortical depression to classical migraine.

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On the possible relation of spreading cortical depression to classical migraine. / Lauritzen, M.

In: Cephalalgia : an international journal of headache, Vol. 5 Suppl 2, 01.01.1985, p. 47-51.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Lauritzen, M 1985, 'On the possible relation of spreading cortical depression to classical migraine.', Cephalalgia : an international journal of headache, vol. 5 Suppl 2, pp. 47-51. https://doi.org/10.1177/03331024850050S208

APA

Lauritzen, M. (1985). On the possible relation of spreading cortical depression to classical migraine. Cephalalgia : an international journal of headache, 5 Suppl 2, 47-51. https://doi.org/10.1177/03331024850050S208

Vancouver

Lauritzen M. On the possible relation of spreading cortical depression to classical migraine. Cephalalgia : an international journal of headache. 1985 Jan 1;5 Suppl 2:47-51. https://doi.org/10.1177/03331024850050S208

Author

Lauritzen, M. / On the possible relation of spreading cortical depression to classical migraine. In: Cephalalgia : an international journal of headache. 1985 ; Vol. 5 Suppl 2. pp. 47-51.

Bibtex

@article{dac0749a78f443ed9d1261bf8e3cdf64,
title = "On the possible relation of spreading cortical depression to classical migraine.",
abstract = "During the first 1 to 2 h of the classical migraine attack a hypoperfusion develops which starts in the posterior part of the brain and progresses anteriorly at a rate of 2-3 mm/min. The hypoperfusion stops at primary sulci outlining major cortical macro- and microstructural changes, but seems not to be inhibited by other changes of the cortical architecture. The low flow regions are cortical and the low flow persists for 4-6 h, until the attack abates. Regions of hyperperfusion are either minor or non-existent. A similar behavior characterizes the velocity and mode of evolution of a cortical spreading depression, a transient perturbation of cortical neuronal function which has profound and long-lasting influence on the cortical blood flow. This paper briefly summarizes the arguments which have been put forward in recent years suggesting that spreading depression is a pathogenetic mechanism of migraine.",
author = "M. Lauritzen",
year = "1985",
month = jan,
day = "1",
doi = "10.1177/03331024850050S208",
language = "English",
volume = "5 Suppl 2",
pages = "47--51",
journal = "Cephalalgia",
issn = "0800-1952",
publisher = "SAGE Publications",

}

RIS

TY - JOUR

T1 - On the possible relation of spreading cortical depression to classical migraine.

AU - Lauritzen, M.

PY - 1985/1/1

Y1 - 1985/1/1

N2 - During the first 1 to 2 h of the classical migraine attack a hypoperfusion develops which starts in the posterior part of the brain and progresses anteriorly at a rate of 2-3 mm/min. The hypoperfusion stops at primary sulci outlining major cortical macro- and microstructural changes, but seems not to be inhibited by other changes of the cortical architecture. The low flow regions are cortical and the low flow persists for 4-6 h, until the attack abates. Regions of hyperperfusion are either minor or non-existent. A similar behavior characterizes the velocity and mode of evolution of a cortical spreading depression, a transient perturbation of cortical neuronal function which has profound and long-lasting influence on the cortical blood flow. This paper briefly summarizes the arguments which have been put forward in recent years suggesting that spreading depression is a pathogenetic mechanism of migraine.

AB - During the first 1 to 2 h of the classical migraine attack a hypoperfusion develops which starts in the posterior part of the brain and progresses anteriorly at a rate of 2-3 mm/min. The hypoperfusion stops at primary sulci outlining major cortical macro- and microstructural changes, but seems not to be inhibited by other changes of the cortical architecture. The low flow regions are cortical and the low flow persists for 4-6 h, until the attack abates. Regions of hyperperfusion are either minor or non-existent. A similar behavior characterizes the velocity and mode of evolution of a cortical spreading depression, a transient perturbation of cortical neuronal function which has profound and long-lasting influence on the cortical blood flow. This paper briefly summarizes the arguments which have been put forward in recent years suggesting that spreading depression is a pathogenetic mechanism of migraine.

UR - http://www.scopus.com/inward/record.url?scp=0022065776&partnerID=8YFLogxK

U2 - 10.1177/03331024850050S208

DO - 10.1177/03331024850050S208

M3 - Journal article

C2 - 4016941

AN - SCOPUS:0022065776

VL - 5 Suppl 2

SP - 47

EP - 51

JO - Cephalalgia

JF - Cephalalgia

SN - 0800-1952

ER -

ID: 201457932