Migraine pathophysiology and its clinical implications


Dr Stephen D. Silberstein, Jefferson Headache Center, 111 South 11th Street, Suite 8130 Gibbon, Philadelphia, PA 19107, USA. Tel. +1-215-955-2072, fax. +1-215-955-6682, e-mail. stephen.silberstein@jefferson.edu


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The vascular hypothesis of migraine has now been superseded by a more integrated theory that involves both vascular and neuronal components. It has been demonstrated that the visual aura experienced by some migraineurs arises from cortical spreading depression, and that this neuronal event may also activate perivascular nerve afferents, leading to vasodilation and neurogenic inflammation of the meningeal blood vessels and, thus, throbbing pain. The involvement of the parasympathetic system supplying the meninges also causes increased vasodilation and pain. As an acute attack progresses, sensory neurones in the trigeminal nucleus caudalis become sensitized, resulting in the phenomenon of cutaneous allodynia. Triptans may act at several points during the progression of a migraine attack. However, the development of central sensitization impacts upon the effectiveness of triptan therapy.