• J Headache Pain · Oct 2009

    Review

    Migraine pain: reflections against vasodilatation.

    • Alessandro Panconesi, Maria Letizia Bartolozzi, and Leonello Guidi.
    • Health Authority 11, Empoli (Florence), Italy. a.panconesi@virgilio.it
    • J Headache Pain. 2009 Oct 1; 10 (5): 317-25.

    AbstractThe 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.

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