Cao Y, Welch K M, Aurora S, Vikingstad E M
Headache Research Center, Department of Neurology, Henry Ford Health Sciences Center, Case Western Reserve University, Detroit, Mich. 48202-2689, USA.
Arch Neurol. 1999 May;56(5):548-54. doi: 10.1001/archneur.56.5.548.
Spreading depression of Leao has been hypothesized as the basis for the visual aura of the migraine attack, supported by cerebral blood flow measurements of spreading hypoperfusion. The early depolarizing or activation phase of experimental spreading depression, however, is associated with a transient but pronounced cerebral blood flow increase that precedes spreading hypoperfusion.
To study this early phase of the migraine attack, we investigated visually triggered attacks of headache and visual symptoms using a red-green checkerboard stimulus in patients with migraine.
We studied occipital cortex activation during visual stimulation by measuring occipital cortex perfusion with functional magnetic resonance imaging-blood oxygenation level-dependent contrast in 10 patients with migraine with aura and 2 patients with migraine without aura and 6 healthy subjects.
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 occipital cortex at a rate ranging from 3 to 6 mm/ min. This neuronal suppression was accompanied by baseline contrast intensity increases that indicated vasodilatation and tissue hyperoxygenation.
We conclude that visually triggered headache and visual change in patients with migraine is accompanied by spreading suppression of initial neuronal activation and increased occipital cortex oxygenation. We postulate that this spreading suppression may be associated with initial activation of a migraine attack, independent of whether there are associated aura symptoms. We further postulate that there may be an association between vasodilation accompanying the initial stage of suppression and the induction of headache.
莱奥的扩散性抑制被认为是偏头痛发作视觉先兆的基础，脑血流测量显示的扩散性低灌注支持了这一观点。然而，实验性扩散性抑制的早期去极化或激活阶段与扩散性低灌注之前短暂但明显的脑血流增加有关。
为了研究偏头痛发作的这个早期阶段，我们使用红-绿棋盘格刺激对偏头痛患者视觉诱发的头痛和视觉症状进行了调查。
我们通过功能磁共振成像-血氧水平依赖对比测量枕叶皮质灌注，研究了10例有先兆偏头痛患者、2例无先兆偏头痛患者和6名健康受试者在视觉刺激期间枕叶皮质的激活情况。
在6例有先兆偏头痛患者和2例无先兆偏头痛患者中，他们典型的伴有（n = 2）或不伴有视觉变化的头痛在视觉刺激开始后7.3分钟（平均时间）被视觉诱发。在这些患者中的5例中，头痛或视觉变化或两者的发作之前有初始激活的抑制（平均发作时间，4.3分钟；P<.001）。这种抑制以3至6毫米/分钟的速度缓慢扩散到相邻的枕叶皮质。这种神经元抑制伴随着基线对比强度增加，表明血管扩张和组织高氧。
我们得出结论，偏头痛患者视觉诱发的头痛和视觉变化伴随着初始神经元激活的扩散性抑制和枕叶皮质氧合增加。我们推测这种扩散性抑制可能与偏头痛发作的初始激活有关，无论是否伴有相关的先兆症状。我们进一步推测，抑制初始阶段伴随的血管扩张与头痛的诱发之间可能存在关联。
