Migraine is associated with an aura that differs in duration which can involve visual scotomas, nausea, vomiting and is followed then with a severe throbbing one sided headache that can last for an few hours or 1-2 days. Migraine occurs because of the trigeminal nerve distribution to the intracranial arteries that release calcitonin gene-related peptide (CGRP), a potent vasodilator. a Common feature of migraine is the leakage of plasma and plasma proteins into the perivascular space probably because of the CGRP action on the vessels. The edema in perivascular space that occurs leads to mechanical stretching that cause an activation of pain nerve endings. Onset of an headache is usually characterized by the increase in amplitude of the temporal artery pulsations and the relief of pain is sometimes accompanied with the reduction of the pulsations.

There are a wide variety of drug groups used to treat a migraine. Examples are:

• Triptans, ergot alkaloids and antidepressants. These drugs may activate 5-HT 1D/1B receptors on the presynaptic trigeminal nerve endings to inhibit the release of vasodilating peptides. Direct acting 5-HT (triptans) agonist may prevent vasodilation thus stretching of the pain endings because of there vasoconstrictor action. Sumatriptan and ergotamine used for acute severe migraine.
• Anti-seizure agents may suppress the excessive firing of the trigeminal nerve endings.
• Anti-inflammatory analgesics are often helpful in controlling pain of the migraine.
• Beta blockers and calcium channel blockers are found to be effective for the prophylaxis of migraine in some patients. Anticonvulsants have some prophylactic efficacy in migraine.