Domitrz Izabela
Klinika Neurologii, Akademia Medyczna w Warszawie, Warszawa.
Neurol Neurochir Pol. 2007 Jan-Feb;41(1):70-5.
The pathogenesis of migraine aura, like migraine, remains unclear. The probable cause of migraine aura may be cortical spreading depression (CSD) and cerebral hypoperfusion. Ion changes, activation of the trigeminal nerve and release of neuropeptides seem to be secondary to CSD during an attack of migraine aura. There are many hypotheses of migraine pathogenesis. The focal symptoms during migraine aura may be due to transient constriction of a cerebral artery and headache can result from a sterile inflammatory reaction around the walls of dilated cranial vessels. The development of aura makes a vascular origin a remote possibility, while a primary disturbance of cortical neuron function, probably CSD and activation of the trigeminovascular system, is a more reasonable explanation.
与偏头痛一样，偏头痛先兆的发病机制仍不清楚。偏头痛先兆的可能病因或许是皮质扩散性抑制（CSD）和脑灌注不足。离子变化、三叉神经激活及神经肽释放似乎是偏头痛先兆发作时继发于CSD的表现。关于偏头痛的发病机制有许多假说。偏头痛先兆期间的局灶性症状可能是由于脑动脉短暂收缩所致，而头痛可能源于扩张的颅血管壁周围的无菌性炎症反应。先兆的出现使得血管源性病因可能性极小，而皮质神经元功能的原发性紊乱，可能是CSD和三叉神经血管系统激活，是一种更合理的解释。
