Delayed Hyperemia Following Hypoperfusion in Classic Migraine

Andersen, Andreas; Friberg, Lars; Olsen, Tom Skyhøj; Olesen, Jes

doi:10.1001/archneur.1988.00520260040017

Cited by 140 publications

(68 citation statements)

References 24 publications

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“…Our data confirmed previous reports that CSD-like phenomena can be seen with neuroimaging techniques (7,10,12,15,19,20,28). Like those previous studies, our data indicated a slowly spreading area of abnormal blood flow in the occipital lobe during migraine aura.…”

Section: Discussionsupporting

confidence: 92%

“…2C). The hyperemia is then followed by a mild hypoperfusion (6,18,19,(45)(46)(47)(48)(49)(50)(51)) lasting 1-2 h-not unlike what was described many minutes after the aura in human occipital cortex (7,10,15,20,21).…”

Section: Discussionmentioning

confidence: 92%

“…These include planar Xenon (6)(7)(8)(9), single photon emission tomography (8,(10)(11)(12)(13)(14), positron-emission tomography (15,16), magnetoencephalography (17,18), and MRI (19)(20)(21). Each demonstrated one or more aspects of CSD associated with migraine aura.…”

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confidence: 99%

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Mechanisms of migraine aura revealed by functional MRI in human visual cortex

Hadjikhani

Río

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

1,294

974

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Cortical spreading depression (CSD) has been suggested to underlie migraine visual aura. However, it has been challenging to test this hypothesis in human cerebral cortex. Using high-field functional MRI with near-continuous recording during visual aura in three subjects, we observed blood oxygenation level-dependent (BOLD) signal changes that demonstrated at least eight characteristics of CSD, time-locked to percept͞onset of the aura. Initially, a focal increase in BOLD signal (possibly reflecting vasodilation), developed within extrastriate cortex (area V3A). This BOLD change progressed contiguously and slowly (3.5 ؎ 1.1 mm͞min) over occipital cortex, congruent with the retinotopy of the visual percept. Following the same retinotopic progression, the BOLD signal then diminished (possibly reflecting vasoconstriction after the initial vasodilation), as did the BOLD response to visual activation. During periods with no visual stimulation, but while the subject was experiencing scintillations, BOLD signal followed the retinotopic progression of the visual percept. These data strongly suggest that an electrophysiological event such as CSD generates the aura in human visual cortex.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 92%

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Mechanisms of migraine aura revealed by functional MRI in human visual cortex

Hadjikhani

Río

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

1,294

974

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“…Migraine aura (Milner, 1958;Olesen et al, 1981Olesen et al, , 1990Andersen et al, 1988;Friberg et al, 1994;Lauritzen, 1994;Woods et al, 1994;Welch et al, 1998;Cao et al, 1999;Hadjikhani et al, 2001;James et al, 2001) may result from neocortical spreading depression (SD). Evidence of this potential interrelation stems from aspects of the classical defining characteristics of SD and how they might relate to the typical features of migraine aura through altered neocortical function.…”

Section: Introductionmentioning

confidence: 99%

Hippocampal spreading depression bilaterally activates the caudal trigeminal nucleus in rodents

Kunkler

Kraig

2003

Hippocampus

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Spreading depression (SD) and migraine aura involve transiently altered (i.e., increased followed by decreased) electrophysiological activity that propagates at the distinctive rate of millimeters per minute (mm/min), leading to the suggestion that they (and perhaps pain from migraine) are causally related via changes in the same brain structure. Neocortex is considered the anatomical zone associated with migraine aura and is the sole area known to induce caudal trigeminal nucleus (TNC) activation from SD in rodents. However, classical evidence of SD in human neocortex is reported only with severe brain disease, while migraine is a common and comparatively benign disorder. Because SD occurs in human hippocampus, and memory dysfunction referable to hippocampus is seen in migraineurs, we determined whether recurrent SD confined to hippocampus in rat could induce TNC activation. Our work shows that recurrent hippocampal SD evoked a significant (P < 0.05-0.001) increase in bilateral c-fos immunostaining within TNC superficial laminae compared with sham controls. Furthermore, hippocampal SD occurred with a correlated and transient change in spontaneous activity and blood flow in the ipsilateral neocortex without spread of SD to that area. Thus, hippocampal SD may be a previously unrecognized, potential trigger for nociceptive activation of TNC perhaps associated with migraine.

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“…A highly variable increase in the cerebral blood fl ow is often followed by oligemia [25,26] , but the periods of increased cerebral blood fl ow do not correlate temporally with the experience of migraine headache [8,23,27] , suggesting that the intracranial vasodilation is likely an epiphenomenon, rather than a cause of the migraine headache.…”

Section: Migraine Pathophysiologymentioning

confidence: 99%

Role of cortical spreading depression in the pathophysiology of migraine

2014

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A migraine is a recurring neurological disorder characterized by unilateral, intense, and pulsatile headaches. In one-third of migraine patients, the attacks are preceded by a visual aura, such as a slowly-propagating scintillating scotoma. Migraine aura is thought to be a result of the neurovascular phenomenon of cortical spreading depression (SD), a self-propagating wave of depolarization that spreads across the cerebral cortex. Several animal experiments have demonstrated that cortical SD causes intracranial neurogenic infl ammation around the meningeal blood vessels, such as plasma protein extravasation and pro-inflammatory peptide release. Cortical SD has also been reported to activate both peripheral and central trigeminal nociceptive pathways. Although several issues remain to be resolved, recent evidence suggests that cortical SD could be the initial trigger of intracranial neurogenic inflammation, which then contributes to migraine headaches via subsequent activation of trigeminal afferents.Keywords: cortical spreading depression; migraine; neurogenic inflammation; PET; trigeminal nociceptive pathway ·Review· IntroductionCortical spreading depression (SD), described first by Leao [1] , is a self-propagating wave of transient neuronal/ glial membrane depolarization that is accompanied by a transient negative shift of the direct current (DC) potential [2] and temporal elevation of cerebral blood flow (CBF) [3,4] throughout the cerebral hemisphere at a rate of 2-5 mm/ min [1, 5,6] . The rate of spreading correlates with the observed spread of the aura of a classical migraine [7] , which is characterized by a spot of fl ickering light that appears near the center of the visual field and then gradually expands outward [8][9][10] . Recently, cortical SD has been hypothesized to be the initial event involved in migraine headaches.Moskowitz et al. [11,12] proposed that pro-inflammatory peptides, such as substance P and calcitonin generelated peptide (CGRP), released from trigeminocervical nerve terminals in response to some unknown stimulation, probably cortical SD, induces vasodilation and plasma protein extravasation. Such neurogenic inflammation is thought to trigger a headache via stimulation of trigeminal afferents. Consistent with this hypothesis, cortical SD induced intracranial neurogenic inflammation around the meningeal blood vessels [13][14][15] , and subsequent activation of both peripheral [16] and central [17] trigeminal nociceptive pathways has been described. Here, we review the experimental evidence mainly from neurophysiological studies that has advanced the understanding of whether and how the neurovascular phenomenon of cortical SD causes intracranial neurogenic inflammation, and subsequently participates in triggering a migraine headache. Migraine PathophysiologyA migraine is a recurring neurological disorder characterized Yilong Cui, et al . Role of cortical spreading depression in the pathophysiology of migraine 813 by unilateral, intense, and pulsatile headaches lasting 4-72 h [18] , a...

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Delayed Hyperemia Following Hypoperfusion in Classic Migraine

Cited by 140 publications

References 24 publications

Mechanisms of migraine aura revealed by functional MRI in human visual cortex

Mechanisms of migraine aura revealed by functional MRI in human visual cortex

Hippocampal spreading depression bilaterally activates the caudal trigeminal nucleus in rodents

Role of cortical spreading depression in the pathophysiology of migraine

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