Migraine involves neurovascular, functional, and anatomical alterations. Migraine sufferers experience an intense unilateral and pulsatile headache frequently accompanied with vomiting, nausea, photophobia, etc. Although there is no ideal preventive medication, frequency in migraine days may be partially decreased by some prophylactics, including antihypertensives, antidepressants, antiepileptics and CGRPergic inhibitors. However, the mechanisms of action involved in antimigraine prophylaxis remain elusive.
This review recaps some of the main neurovascular phenomena related to migraine and currently available preventive medications. Moreover, it discusses the major mechanisms of action of the recommended prophylactic medications.
In the last three years, migraine prophylaxis has evolved from purely non-specific to specific antimigraine treatments. Overall, non-specific treatments involve neural actions, whereas specific pharmacotherapy (represented by CGRP receptor antagonists and CGRPergic monoclonal antibodies) is predominantly mediated by neurovascular mechanisms that may include, to a greater or lesser extent: (i) reduction in the frequency of cortical spreading depression (CSD) events; (ii) inhibition of pain sensitization; (iii) blockade of neurogenic inflammation; and/or (iv) increase in cranial vascular tone. Accordingly, the novel antimigraine prophylaxis promises to be more effective, devoid of significant adverse effects (unlike non-specific treatments), and more beneficial to the quality of life of migraine patients.