Review Article

The Journal of Headache and Pain

, Volume 10, Issue 5, pp 317-325

First online:

Open Access This content is freely available online to anyone, anywhere at any time.

Migraine pain: reflections against vasodilatation

  • Alessandro PanconesiAffiliated with Email author 
  • , Maria Letizia BartolozziAffiliated with
  • , Leonello GuidiAffiliated with


The original Wolff’s vascular theory of migraine was supported by the discovery of a class of drugs, the triptans, developed as a selective cephalic vasoconstrictor agents. Even in the neurovascular hypothesis of Moskowitz, that is the neurogenic inflammation of meningeal vessels provoked by peptides released from trigeminal sensory neurons, the vasodilatation provoked by calcitonin gene-related peptide (CGRP) is considered today much more important than oedema. The role of cephalic vasodilatation as a cause of migraine pain was recently sustained by studies showing the therapeutic effect of CGRP receptor antagonists. We discuss the evidence against vasodilatation as migraine pain generator and some findings which we suggest in support of a central (brain) origin of pain.


Migraine Calcitonin gene-related peptide Triptans Vasodilatation Pain Migraine pathogenesis