Migraine
A primary headache disorder driven by transient neuronal and vascular dysfunction (cortical spreading depression generates the aura, trigeminovascular activation generates the pain), producing a stereotyped, self-limiting attack rather than a structural lesion.
First principles
Migraine is a primary disorder of brain excitability, not simply a vascular event
Migraine begins with a slow wave of neuronal and glial depolarisation spreading across the cortex, called cortical spreading depression, which is the physiological correlate of aura when it crosses sensory or visual cortex. This wave activates trigeminal sensory afferents that innervate the meninges and their vessels, releasing vasoactive neuropeptides such as CGRP that cause sterile neurogenic inflammation and vasodilation of meningeal vessels (the trigeminovascular system), which is perceived as pulsating pain and explains why the pain is typically unilateral and throbbing.
Educational content pending clinical review. Not medical advice.