Pathology:

Migraine involves the trigeminal nerves distribution to intracranial and highly possibly extracranial arteries. These nerves release peptide neurotransmitters, whereas calcitonin gene-related peptide (CGRP) is an extreme powerful vasodilator. These neurotransmitters cause vasodilatory effects. The above-mentioned neurotransmitters also cause the extravasation of plasma and plasma proteins in to the perivascular space, which leads to mechanical stretching. The mechanical stretching is the cause of activation of the pain nerve endings in the dura. Migraine involve nausea, vomiting, paresthesias, visual scotomas, hemianopsia and speech abnormalities.

Current treatment and mechanism of action:

Triptans e.g. Sumatriptan: The first line drug therapy for acute severe migraines. These drugs are selective agonist for 5-HT 1D and 5-HT 1B receptors. They activate these receptors on the presynaptic trigeminal nerve ends to inhibit the release of the vasodilating peptides. Triptans should not be used in patients with coronary artery disease because they have the ability to cause coronary vasospasms.

Lasmiditan: Is a highly selective 5-HT 1F receptor agonist and is effective in treating migraines. The agent lacks vasoconstriction actions and is a much more cardiovascular save than the triptans. The drug reduces trigeminal nerve stimulation-induced plasma and plasma protein extravasation in dura vessels. Lasmiditan is used in acute migraines.

Ergot alkaloids e.g. Ergotamine and Ergonovine: The ergot derivates have mixed partial agonist effects at 5-HT2 and at alpha adrenoceptors. These drugs cause a marked smooth muscle contraction but they also block alpha agonist vasoconstriction. The effects mentioned above helps to reduce the vasodilation which causes the migraine.

Anti-inflammatory analgesics e.g. aspirin: These drugs are only helpful in controlling the pain of the migraine and not resolving the migraine itself.