Regional Cerebral Blood Flow and Oxygen Metabolism during Migraine with and Without Aura

Andersson, Jacob; Muhr, Carin; Lilja, Anders; Valind, Sven; Lundberg, P. O.; Långström, Bengt

doi:10.1046/j.1468-2982.1997.1705570.x

Cited by 54 publications

(42 citation statements)

References 36 publications

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“…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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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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“…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.

1,314

999

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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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“…Only one study using PositronEmission-Tomography (PET) performed during human migraine aura documented cortical regions corresponding to the visual cortex with significant reduction in CBF (-23% :oligaemia) and Cerebral Metabolic Rate of Oxygen (CMRO 2 ) (-22%) but no change in Oxygen Extraction Fraction (OEF) compared to baseline. These data suggest that cerebral ischemia is not the primary cause of the attacks in these cases [3].…”

Section: Introductionmentioning

confidence: 64%

“…In this study, a clear temporal and spatial correlation is established between the visual symptoms of the aura and the BOLD signal change [2]. During migraine aura some neuroimaging studies demonstrated reduction in cerebral blood flow (CBF) that is not sufficient magnitude to cause ischemia and is termed "oligaemia" [3][4][5]. The oligaemia starts before the onset of aura and extends into the headache phase outlasting the aura symptoms [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

“Prolonged” migraine aura: New information on underlying mechanisms

Viola¹,

Viola

Litterio³

et al. 2011

Translational Neuroscience

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The aim of this study is to identify the pathophysiology of "prolonged" migraine aura not clearly understood. We studied cortical cerebral microcirculation by Near Infrared Spectroscopy system (NIRS) and cerebral macrocirculation by transcranial Doppler (TCD) in 8 subjects (3 M and 5 F, age range 21-41 years) during spontaneous "prolonged" migraine aura in according to ICHD-II criteria 2004 (code 1.6.2.) up to 24 hours after the end of aura and compared the results with the headache-free periods. During aura NIRS showed a significant decrease of the Arterial Pulse Wave of Cerebral Microcirculation (APWCM) amplitude (-33 % ± 5.7), p<0.001, and a significant increase of Cerebral Tissue Oxygen Saturation (SctO 2 ) (+15.5 % ± 5.1), p<0.001 contralateral to the symptoms of aura compared with the headache-free periods; TCD showed a significant increase of Pulsatility Index (+36.5 % ± 6.5), p<0.001 and a significant decrease of the diastolic velocity in the posterior and middle cerebral artery contralateral to the symptoms of aura compared with the headache-free periods. In conclusion during "prolonged" migraine aura we find areas of cortical hypoperfusion corresponding to the topography of aura symptoms that are the result of a decreased metabolic demand rather than an ischemic mechanism.

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Regional Cerebral Blood Flow and Oxygen Metabolism during Migraine with and Without Aura

Cited by 54 publications

References 36 publications

The pathophysiology of migraine: year 2005

The pathophysiology of migraine: year 2005

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

“Prolonged” migraine aura: New information on underlying mechanisms

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