第49回日本神経学会総会
＜教育講演4＞
片頭痛の病態生理―generatorを中心に―
濱田 潤一
北里大学神経内科学〔〒228-8555 相模原市北里1-15-1〕
Migraine is an episodic and popular headache disorder. Migraine arises from a primary cerebral dysfunction that leads to activation of trigeminovascualr system. In the 1940s cerebral arterial constriction and the following enhanced dilatation was considered to induce migraine attack. Next, the cortical neuronal change that is well linked to the migraine aura was considered to be primary mechanism of migraine attack. Recently, the trigeminovascular system has a main role in the pathophysiological mechanism of the migraine. From the animal studies, cortical spreading depression (CSD) may induce the activation of the trigeminovascular system and may be a trigger of the migraine pathological mechanism. Also the activation or the functional change of brainstem nuclei, involving periaqueductal grey matter, raphe nuclei, and locus ceruleus, may be a trigger of the migraine attack. We have showed that the level of plasma orexin-A in the migraine patients during headache free period is lower than that of control. From the animal experiments, we also showed that intracerebroventricular injection of orexin induces the increase in the cerebral cortical blood flow, and that the intraarterial application of orexin cannot increase the cerebral blood flow. We consider that orexinegic neurons in the lateral hypothalamus may be a generator of migraine.
Full Text of this Article in Japanese PDF (441K)
(臨床神経, 48：857−860, 2008)
key words：片頭痛, 三叉神経血管系, 脳幹, オレキシン, 視床下部
（受付日：2008年5月16日）
