Clinical Neuroscience, Merck Research Laboratories, North Wales, PA 19454-1099, USA.
Nat Rev Neurol. 2010 Oct;6(10):573-82. doi: 10.1038/nrneurol.2010.127. Epub 2010 Sep 7.
Over the past 300 years, the migraine field has been dominated by two main theories-the vascular theory and the central neuronal theory. The success of vasoconstrictors such as ergotamine and the triptans in treating acute migraine bolstered the vascular theory, but evidence is now emerging that vasodilatation is neither necessary nor sufficient to induce a migraine attack. Attention is now turning to the core migraine circuits in the brain, which include the trigeminal ganglia, trigeminal nucleus, medullary modulatory regions, pons, periaqueductal gray matter, hypothalamus and thalamus. Migraine triggers are likely to reflect a disturbance in overall balance of the circuits involved in the modulation of sensory activity, particularly those with relevance to the head. In this Review, we consider the evidence pointing towards a neuronal mechanism in migraine development, highlighting the role of calcitonin gene-related peptide (CGRP), which is found in small to medium-sized neurons in the trigeminal ganglion. CGRP is released during migraine attacks and can trigger migraine in patients, and CGRP receptor antagonists can abort migraine. We also examine whether other drugs, such as triptans, might exert their antimigraine effects via their actions on the neuronal circuit as opposed to the intracranial vasculature.
在过去的 300 年里，偏头痛领域一直由两种主要理论主导——血管理论和中枢神经元理论。麦角胺和曲坦类等血管收缩剂在治疗急性偏头痛方面的成功支持了血管理论，但现在有证据表明，血管扩张既不是引发偏头痛发作的必要条件，也不是充分条件。人们现在开始关注大脑中的偏头痛核心回路，包括三叉神经节、三叉神经核、髓质调节区域、脑桥、导水管周围灰质、下丘脑和丘脑。偏头痛的诱因可能反映了参与感觉活动调节的回路整体平衡的紊乱，特别是那些与头部相关的回路。在这篇综述中，我们考虑了指向偏头痛发展中神经元机制的证据，强调了降钙素基因相关肽（CGRP）的作用，CGRP 存在于三叉神经节中的小到中型神经元中。CGRP 在偏头痛发作期间释放，并可在患者中引发偏头痛，CGRP 受体拮抗剂可中止偏头痛。我们还研究了其他药物，如曲坦类，是否可能通过其对神经元回路的作用而不是颅内血管来发挥其抗偏头痛作用。
