Fanciullacci M, Alessandri M, Bandini E B
Istituto di Clinica Medica Generale e Terapia Medica IV, Università degli Studi di Firenze.
Ann Ital Med Int. 1992 Jul-Sep;7(3 Suppl):41S-45S.
Studies of regional cerebral blood flow in migraine with aura have shown that the aura phase is associated with hypoperfusion in the cortical area which relates topographically to the clinical symptoms. Thus, the previously hypoperfused area becomes hyperperfused. However, there is no strict association between hyperperfusion and headache. The mode of hypoperfusion propagation recalls the circulatory manifestations of experimental cortical spreading depression. In addition, there are no focal cerebral blood flow abnormalities in migraine without aura. During the headache phase of migraine, dilation of both the large extra- and intracranial arteries takes place. A bulk of biochemical evidence has suggested that the pain in migraine is caused by blood vessels which are dilated and sensitized by circulating pain-producing substances e.g. bradykinin, serotonin and histamine (sterile inflammation). Recently, perivascular trigeminal fibres (trigeminovascular system) which, when stimulated, release sensory peptides (substance P and the calcitonin gene-related peptide) capable of provoking marked vasodilation and plasma extravasation (neurogenic inflammation) have been identified. Thus, the activation of the trigeminovascular system is probably involved in the vasodilatative and nociceptive phenomena of the migraine attack. The finding of a reduced endorphinergic brain tonus in migraine patients supports the hypothesis of a central nociceptive derangement in migraine. Nonetheless, the exact relationship between vasodilation and headache remains to be defined. However, the potent antimigraine effectiveness of sumatriptan--an agonist of the serotonin receptors which selectively constricts dilated arteries during the migraine attack--once again stresses the fact that serotonin is probably the crucial factor in the link between vasodilation and headache.
对伴先兆偏头痛患者的局部脑血流研究表明，先兆期与皮质区域灌注不足相关，该区域在地形学上与临床症状相关。因此，先前灌注不足的区域会出现灌注过度。然而，灌注过度与头痛之间并无严格关联。灌注不足的传播方式让人联想到实验性皮质扩散性抑制的循环表现。此外，无先兆偏头痛患者不存在局部脑血流异常。在偏头痛的头痛期，颅内和颅外的大血管都会扩张。大量生化证据表明，偏头痛中的疼痛是由血管扩张引起的，这些血管因循环中的致痛物质（如缓激肽、血清素和组胺）而变得敏感（无菌性炎症）。最近，已确定了血管周围的三叉神经纤维（三叉神经血管系统），受到刺激时，该系统会释放能够引发显著血管扩张和血浆外渗的感觉肽（P物质和降钙素基因相关肽）（神经源性炎症）。因此，三叉神经血管系统的激活可能参与了偏头痛发作时的血管扩张和伤害感受现象。偏头痛患者脑内内啡肽能张力降低的发现支持了偏头痛中枢伤害感受紊乱的假说。尽管如此，血管扩张与头痛的确切关系仍有待确定。然而，舒马曲坦（一种血清素受体激动剂，在偏头痛发作时能选择性收缩扩张的动脉）强大的抗偏头痛效果再次强调了血清素可能是血管扩张与头痛之间联系的关键因素这一事实。
