Timing and topography of cerebral blood flow, aura, and headache during migraine attacks

Abstract

Ten years of study has resulted in considerable but fragmented knowledge about regional cerebral blood flow in migraine with aura (classic migraine). In the present study, the number of repeatedly studied patients (n = 63) was large enough to determine statistically significant sequences of events and statistically significant spatial relations. The first observable event was a decrease of regional cerebral blood flow posteriorly in one cerebral hemisphere. Further development of this pathological process was accompanied by the aura symptoms. Thereafter headache occurred while regional cerebral blood flow remained decreased. During the headache phase, regional cerebral blood flow gradually changed from abnormally low to abnormally high without apparent change in headache. In some patients headache disappeared while regional cerebral blood flow remained increased. Although regional cerebral blood flow reduction and aura symptoms in the great majority of patients were unilateral, one-third had bilateral headache. Unilateral headache usually localized to the side on which regional cerebral blood flow was reduced and from which the aura symptoms originated (i.e., aura symptoms were perceived to occur contralaterally but presumably originated in the hypoperfused hemisphere). Our results suggest a simple model for migraine attacks: A pathological disturbance in one cerebral hemisphere causes the aura symptoms and after a time delay, it also causes the headache by stimulating local vascular nociceptors. Bilateral headache caused by a unilateral cerebral disturbance may be explained by recent neuroanatomical and neurophysiological findings.

Migraine and motion sickness: What is the link?

“…For example, the headache of migraine with aura frequently begins while regional cerebral blood flow is diminished (Olesen, Friberg, Skyhøj Olsen, Iversen, Lassen, Andersen and Karle, 1990). Furthermore, the presence of severe headache during the vasoconstrictive state that follows subarachnoid haemorrhage suggests that vasodilatation is an 'epiphenomenon' to nociceptive discharge rather than the cause of it (Macfarlane, 1993).…”

The pathophysiology of migraine: year 2005

“…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.…”

Eficácia de três drogas sobre a aura migranosa: um estudo randomizado placebo controlado

“…Há, ainda, experimentos que correlacionam disfunções em canais de cálcio voltagem-dependentes, que regulam a liberação de serotonina, com o desencadeamento da aura. Funcionamento inadequado desses canais com diminuição da transmissão serotoninérgica poderia ser um dos eventos importantes 13 . Pela fisiopatologia presumida da aura, que implica baixos níveis de magnésio como importante deflagrador do processo, a eficácia do sulfato de magnésio é um achado coerente 14 .…”