Abstract
This systematic review summarizes the clinical manifestations and the existing knowledge about the pathophysiology of migraine. In the pathophysiology of migraine the activation of trigeminovascular system and the release of calcitonin gene-related peptide (CGRP), substance P and neurokinin A plays the most important role.
These mediators lead to the sterile perivascular neurogenic inflammation in meninges. The attention is targeted especially to the CGRP, which seems to be the key mediator in the pathophysiology of migraine.
In trigeminovascular system activation of certain subtypes of transient receptor potential (TRP) channels, so called TRPV1 and TRPA1 is responsible for the release of CGRP and other mediators from trigeminal nociceptive neurons. The most promising new approach in the prophylactic treatment are monoclonal antibodies able to block either CGRP or its receptor, such as erenumab, fremanezumab, galcanezumab, and eptinezumab.
Recently attention has focused on pituitary adenylate cyclase-activating peptide 38 (PACAP38), which seemed to be an interesting molecule in migraine. However preventative effect of monoclonal antibodies against this peptide was not confirmed.