Pathophysiology of migraine
Pathophysiology of migraine
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DOI：
10.1007/s10072-004-0295-3
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发表时间：
2004-10-01
影响因子：
3.3
通讯作者：
Bussone, G
中科院分区：
文献类型：
--
作者：
Bussone, G
偏头痛的确切发病机制仍有待确定。特别是有越来越多的证据偏头痛的神经基础。我们现在有大量的数据支持中枢神经元过度兴奋作为诱发偏头痛的关键生理障碍的概念。神经元兴奋性增加的原因可能是多方面的。最近，钙通道异常已被引入作为一个潜在的机制发作间期神经元兴奋性。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氨基酸系统。因此，可以假设遗传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，镁在偏头痛中含量低。我们目前认为偏头痛发作起源于大脑。发作的触发器启动去极化神经电和代谢事件，类似于Leao的扩散性抑郁症。该事件激活头痛和相关的发作特征，其机制尚待确定，但似乎涉及外周三叉神经血管或脑干通路，或两者兼而有之。细胞膜的兴奋性，也许部分是由基因决定的，是大脑对攻击敏感的途径。增加或减少神经元兴奋性的因素构成触发攻击的阈值。
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.