Bussone G
National Neurological Institute C Besta, Via Celoria 11, I-20133 Milan, Italy.
Neurol Sci. 2004 Oct;25 Suppl 3:S239-41. doi: 10.1007/s10072-004-0295-3.
The exact pathogenesis of migraine remains to be determined. In particular there is increasing evidence for the neural basis of migraine. We now have a body of data supporting the concept of central neuronal hyperexcitability as a pivotal physiological disturbance predisposing to migraine. The reasons for increased neuronal excitability may be multifactorial. Most recently, abnormality of calcium channels has been introduced as a potential mechanism of interictal neuronal excitability. Mutant voltage gated P/Q type calcium channel genes likely influence presynaptic neurotransmitter release, possibly of excitatory amino-acid systems or inhibitory. It could therefore be hypothesised that genetic abnormalities result in a lowered threshold of response to trigger factors. There is also evidence from spectroscopic studies that magnesium is low in migraine. We currently conceive of a migraine attack as originating in the brain. Triggers of an attack initiate a depolarising neuroelectric and metabolic event likened to the spreading depression of Leao. This event activates the headache and associated features of the attack by mechanisms that remain to be determined, but appear to involve either peripheral trigeminovascular or brain stem pathways, or both. Excitability of cell membranes, perhaps in part genetically determined, is the brain's route of susceptibility to attacks. Factors that increase or decrease neuronal excitability constitute the threshold for triggering attacks.
偏头痛的确切发病机制尚待确定。尤其是，越来越多的证据表明偏头痛存在神经学基础。目前我们有大量数据支持中枢神经元兴奋性过高这一概念，它是偏头痛易感性的关键生理紊乱因素。神经元兴奋性增加的原因可能是多方面的。最近，钙通道异常被认为是发作间期神经元兴奋性的潜在机制。突变的电压门控P/Q型钙通道基因可能影响突触前神经递质的释放，可能是兴奋性氨基酸系统或抑制性系统。因此可以推测，基因异常导致对触发因素的反应阈值降低。光谱研究也有证据表明偏头痛患者体内镁含量较低。目前我们认为偏头痛发作始于大脑。发作的触发因素引发一种去极化的神经电和代谢事件，类似于利奥的扩散性抑制。这一事件通过尚未确定的机制激活头痛及发作的相关症状，但似乎涉及外周三叉神经血管通路或脑干通路，或两者皆有。细胞膜的兴奋性，可能部分由基因决定，是大脑对发作易感性的途径。增加或降低神经元兴奋性的因素构成了触发发作的阈值。
