Pathology of migraine: During a migraine trigeminal nerve distribution to intracranial arteries are involved and the nerves release powerful vasodilators, like calcitonin gene-related peptide, and other peptide neurotransmitters. Migraine involves an ion channel in the aminergic brain stem nuclei. It consist of neural events resulting in the dilation of blood vessels that cause pain and result in further nerve activation. Substance P and neurokinin A may be involved and extravasation of plasma and plasma proteins into the perivascular space is a common, because of the action of the neuropeptides on the vessels. Mechanical stretching because of the perivascular edema may cause pain in the nerve endings of the dura.

Treatments: Sumatriptan, Naratriptan and Rizatriptan (triptans) are used in the treatment of acute migraine. Ergot alkaloids, non-steroidal anti-inflammatory analgesic agents, β-adrenoceptor blockers, calcium channel blockers, tricyclic antidepressants and SSRIs, and several anti-seizure agents are also used (some drugs for prophylaxis are also used). The 5-HT 1D/1B receptors on are activated by triptans, ergot alkaloids and antidepressants to inhibit the release of vasodilating peptides. Excessive firming of these nerve ends are suppressed by anti-seizure agents. Or the vasodilation and stretching of pain ends may be prevented by the vasoconstrictive effect of 5-HT agonists, like triptans and ergot alkaloids.