Migraine pathophysiology and its clinical implications
Migraine pathophysiology and its clinical implications
复制标题
DOI：
10.1111/j.1468-2982.2004.00892.x
复制
发表时间：
2004-01-01
期刊：
影响因子：
4.9
通讯作者：
Silberstein, SD
中科院分区：
文献类型：
--
作者：
Silberstein, SD
偏头痛的血管假说现在已经被一种更综合的理论所取代，这种理论涉及血管和神经元成分。已经证明，一些偏头痛患者经历的视觉先兆是由皮质扩散性抑制引起的，并且这种神经元事件也可能激活血管周围神经传入，导致脑膜血管的血管舒张和神经源性炎症，从而引起搏动性疼痛。供应脑膜的副交感神经系统的参与也引起血管舒张和疼痛的增加。随着急性发作的进展，三叉神经核尾侧的感觉神经元变得敏感，导致皮肤异常性疼痛的现象。曲坦类药物可能在偏头痛发作过程中的几个点起作用。然而，中枢致敏的发展影响曲坦治疗的有效性。
The vascular hypothesis of migraine has now been superseded by a more integrated theory that involves both vascular and neuronal components. It has been demonstrated that the visual aura experienced by some migraineurs arises from cortical spreading depression, and that this neuronal event may also activate perivascular nerve afferents, leading to vasodilation and neurogenic inflammation of the meningeal blood vessels and, thus, throbbing pain. The involvement of the parasympathetic system supplying the meninges also causes increased vasodilation and pain. As an acute attack progresses, sensory neurones in the trigeminal nucleus caudalis become sensitized, resulting in the phenomenon of cutaneous allodynia. Triptans may act at several points during the progression of a migraine attack. However, the development of central sensitization impacts upon the effectiveness of triptan therapy.