Migraine is a prevalent disabling neurologic disease with attacks that can vary in intensity of pain and in associated symptoms, such as aura, nausea and photophobia and phonophobia.2,3 Previous theories on the underlying cause of migraine have evolved with recent research and we now know more than ever about its pathophysiology.
Regardless of the initial trigger of migraine, the headache is generally thought to involve the activation of the trigeminovascular system (TGVS), a catalyst for the release of vasoactive neuropeptides, such as calcitonin gene-related peptide (CGRP), that cause inflammation and vasodilation that leads to head pain.4
Migraine aura has been attributed to cortical spreading depression (CSD), characterized by changes in blood flow and brain activity. Recent evidence also demonstrates CSD plays a role in activation of the TGVS. Activation of the TGVS leads to peripheral sensitization of the trigeminal nerve, followed later by central sensitization.4