Casucci Gerardo, Villani Veronica, Frediani Fabio
Casa di Cura S. Francesco, Viale Europa 21, 82036 Telese Terme (BN), Italy.
Neurol Sci. 2008 May;29 Suppl 1:S123-6. doi: 10.1007/s10072-008-0902-9.
The pathogenesis of migraine is obscure. A hyperexcitable brain state has been postulated. Cortical spreading depression (CSD) is the most suggestive argument for the brain hyperexcitability. It has been showed that valproate, topiramate, amitriptyline and propranolol inhibit CSD in rats, which suggests that most preventative treatments of migraine act by normalising neuronal firing and increasing a genetically lowered and environmentally modified threshold for neuronal discharge. It has also been suggested that some antimigraine prophylactic drugs (i.e., amitriptyline, candesartan and magnesium) may act by restoring central nociceptive dysmodulation.
偏头痛的发病机制尚不清楚。有人提出存在一种大脑过度兴奋状态。皮质扩散性抑制(CSD)是支持大脑过度兴奋的最具说服力的证据。研究表明,丙戊酸盐、托吡酯、阿米替林和普萘洛尔可抑制大鼠的CSD,这表明大多数偏头痛预防性治疗是通过使神经元放电正常化以及提高因遗传因素降低和环境因素改变的神经元放电阈值来发挥作用的。也有人提出,一些抗偏头痛预防性药物(即阿米替林、坎地沙坦和镁)可能通过恢复中枢伤害性感觉失调来发挥作用。