Rationalisation of the pathology of migraine:

Two types of migraine:

1. “Classic” migraine - consists out of aura that leads to migraine – like nausea; vomiting; paraesthesias; visual scotomas or hemianopsia as well as speech abnormalities. It is often followed by a severe throbbing headache that can last for a few hours up to 2 days if left untreated.
2. The “common” migraine lacks aura, but it is similar. It is the most common type of migraine among people.

Pathophysiology:

The trigeminal nerve distribution to intracranial arteries is involved in migraine. Peptide neurotransmitters, especially calcitonin gene-related peptide, are released by these nerves. CGRP is a powerful vasodilator. Extravasation of plasma and plasma proteins into the perivascular space causes mechanical stretching which activates the pain nerve endings in the dura. The person will experience an amplitude of temporal artery pulsations.

 Treatments:

• 5-HT1D/1B agonists, also called triptans,  such as sumatriptan are almost exclusively used for the treatment of migraine. These drugs activate the 5-HT1D/1B receptors which are found on the presynaptic trigeminal nerve endings to inhibit vasodilating peptides→ vasoconstriction which may prevent the stretching of pain endings. (1^st line therapy for Acute migraine attacks) Contra-indicated for patients with coronary artery disease.  
• Ergot alkaloids:  Treatment of migraine e.g. Ergotamine & Ergonovine. These drugs act as mixed partial agonists at 5-HT2 and alpha-adrenergic receptors + it has a similar mechanism of action as triptans.
• Calcium channel blockers: Only for Prophylaxis. 
• Beta-Blockers: Just for prophylaxis and not for the acute attacks.
• Nonsteroidal anti-inflammatory analgesic agents e.g. aspirin & ibuprofen are used for the pain caused by the migraine.
• Parenteral Metoclopramide – patients experiencing severe nausea and vomiting.