Perfusion‐weighted imaging defects during spontaneous migrainous aura

Cutrer, F. Michael; Sorensen, A. Gregory; Weisskoff, Robert M.; Østergaard, Leif; Río, Margarita Sánchez del; Lee, E. John; Rosen, Bruce R.; Moskowitz, Michael A.

doi:10.1002/ana.410430108

Cited by 328 publications

(228 citation statements)

References 21 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%

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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.

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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%

“…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.…”

mentioning

confidence: 99%

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

Hadjikhani

Río

et al. 2001

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

Self Cite

1,330

999

View full text Add to dashboard Cite

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“…High-field strength functional MRI to map progression of the BOLD events during migraine aura confirmed previous reports that CSD-like phenomena can be seen with neuroimaging techniques [80]. A slowly spreading area of perturbed BOLD signal has also been described in the occipital lobe during migraine aura.…”

Section: The Migraine Aura: Ascending To the Central Origin Of Migrainesupporting

confidence: 82%

“…CSD is a wave of neuronal and glial depolarisation, followed by long-lasting suppression of neural activity, and it can be evoked in mammals with lissencephalic [63,64] or folded cortex [65]. Human neuroimaging such as planar Xenon [66][67][68][69], single photon emission tomography [68,[70][71][72][73][74] positron-emission tomography [75,76], magnetoencephalography [77,78] and MRI [79][80][81] support the hypothesis that CSD underlies migraine [82]. However many subjects never experience symptoms of typical visual auras in studies showing spreading hypoperfusion [75] or blood oxygenation level-dependent (BOLD) signal changes [79], and the initial hyperaemia characteristics of CSD were not directly demonstrated in human cortex.…”

Section: The Migraine Aura: Ascending To the Central Origin Of Migrainementioning

confidence: 99%

The pathophysiology of migraine: year 2005

Buzzi

Moskowitz

2005

J Headache Pain

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IntroductionDespite the high frequency of migraineurs in the general population, the pathogenesis of this disorder is still unclear.There is a great need for a better understanding of the mechanisms underlying the pain, the accompanying symptoms, as well as the premonitory symptoms and the aura. Progress in translational research is impeded by the lack of a validated experimental model and by the lack of tools to J Headache Pain (2005) M. Gabriella Buzzi Michael A. MoskowitzAbstract Migraine is a complex pathophysiology in which both central and peripheral components of the trigeminal pain pathway probably play a significant role, both in the symptoms and signs of the attack and in the mechanisms of action of antimigraine compounds, such as triptans, which constitute the most important therapy for aborting migraine pain and posses several mechanisms on 5-HT receptor-mediated actions. The experimental neurogenic inflammation model represents a simple procedure to obtain preliminary information on well characterized receptortargeted drugs. The apparent paradox observed with certain drugs that are shown to be effective in this model but not in clinical trials offers the opportunity to better manipulate structure-activity to obtain the best pharmacological profile using an array of experimental models. The observation that nitric oxide donors induce migraine-like pain in migraineours and that nitric oxide plays a pivotal role in the control of several functions in the central nervous system, has prompted the use of such molecules for better understanding the pathophysiology of migraine attacks. A link between central and peripheral components of the trigeminal pain pathway is provided by the observation that cortical spreading depression in the rat activates trigeminovascular afferents and induces a series of cortical meningeal and brainstem events consistent with the development of headache. Studies in humans support the hypothesis that cortical spreading depression underlies migraine aura. Therefore, it is possible that visual, motor or sensory aura might be responsible for the generation of the pain through the above mechanisms

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“…All such ionic unbalance is believed to depolarize adjacent neurons and glia, thereby facilitating its spread. An advancing wave of brief excitation would then be followed by a longerlasting inhibition of spontaneous and evoked neuronal activity that traverses the cortex (Somjen 2001, Goadsby 2007, Lauritzen 1994, Cutrer et al 1998, Hadjikhani et al 2001and Bowyer et al 2001. In humans, evidence for a causal role of CSD in the aura comes from functional magnetic resonance imaging (fMRI) performed during migraine attacks with aura (Hadjikhani et al 2001) The nature and mechanisms of the primary brain dysfunction leading to the activation of the meningeal trigeminal nociceptors remain incompletely understood (for reviews see Charles 2009, Goadsby et al 2009a, Levy et al 2009 and it is controversial whether CSD can initiate the migraine headache cascade by itself.…”

Section: Migraine and Familial Hemiplegic Migraine (Fhm)mentioning

confidence: 99%