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

TY - JOUR

T1 - Timing and topography of cerebral blood flow, aura, and headache during migraine attacks

AU - Olesen, J

AU - Friberg, L

AU - Olsen, T S

AU - Iversen, Helle Klingenberg

AU - Lassen, N A

AU - Andersen, A R

AU - Karle, A

PY - 1990/12

Y1 - 1990/12

N2 - 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.

AB - 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.

KW - Adolescent

KW - Adult

KW - Aged

KW - Brain Mapping

KW - Cerebral Angiography

KW - Cerebral Cortex

KW - Cerebrovascular Circulation

KW - Female

KW - Functional Laterality

KW - Humans

KW - Male

KW - Middle Aged

KW - Migraine Disorders

KW - Time Factors

KW - Tomography, Emission-Computed, Single-Photon

U2 - 10.1002/ana.410280610

DO - 10.1002/ana.410280610

M3 - Journal article

C2 - 2285266

SN - 0364-5134

VL - 28

SP - 791

EP - 798

JO - Annals of Neurology

JF - Annals of Neurology

IS - 6

ER -