Background: Spreading depression of Leao has been hypothesized as the basis
for the visual aura of the migraine attack, supported by cerebral blood fl
ow measurements of spreading hypoperfusion. The early depolarizing or activ
ation phase of experimental spreading depression, however, is associated wi
th a transient but pronounced cerebral blood flow increase that precedes sp
reading hypoperfusion.
Objective: To study this early phase of the migraine attack, we investigate
d visually triggered attacks of headache and visual symptoms using a red-gr
een checkerboard stimulus in patients with migraine.
Interventions: We studied occipital cortex activation during visual stimula
tion by measuring occipital cortex perfusion with functional magnetic reson
ance imaging-blood oxygenation level-dependent contrast in 10 patients with
migraine with aura and 2 patients with migraine without aura and 6 healthy
subjects.
Results: In 6 patients with migraine with aura and 2 patients with migraine
without aura, their typical headache with (n = 2) or without visual change
was visually triggered at 7.3 minutes (mean time) after visual stimulation
began. In 5 of these patients, the onset of headache or visual change, or
both, was preceded by suppression of initial activation (mean onset time, 4
.3 minutes; P<.001) The suppression slowly propagated into contiguous occip
ital cortex at a rate ranging from 3 to 6 mm/ min. This neuronal suppressio
n was accompanied by baseline contrast intensity increases that indicated v
asodilatation and tissue hyperoxygenation.
Conclusions: We conclude that visually triggered headache and visual change
in patients with migraine is accompanied by spreading suppression of initi
al neuronal activation and increased occipital cortex oxygenation. We postu
late that this spreading suppression may be associated with initial activat
ion of a migraine attack, independent of whether there are associated aura
symptoms. We further postulate that there may be an association between vas
odilation accompanying the initial stage of suppression and the induction o
f headache.