Open Access

The pathophysiology of migraine: year 2005

The Journal of Headache and Pain20056:165

DOI: 10.1007/s10194-005-0165-2

Received: 15 April 2005

Accepted: 15 April 2005

Published: 13 May 2005


Migraine is a complex patholophysiology in which both central and peripheral components of the trigeminal pain pathway probably play a significant role, both in the symptoms and signs of the attack and in the mechanisms of action of antimigraine compounds, such as triptans, which constitute the most important therapy for aborting migraine pain and posses several mechanisms on 5–HT receptor–mediated actions. The experimental neurogenic inflammation model represents a simple procedure to obtain preliminary information on well characterized receptortargeted drugs. The apparent paradox observed with certain drugs that are shown to be effective in this model but not in clinical trials offers the opportunity to better manipulate structure–activity to obtain the best pharmacological profile using an array of experimental models. The observation that nitric oxide donors induce migraine–like pain in migraineours and that nitric oxide plays a pivotal role in the control of several functions in the central nervous system, has prompted the use of such molecules for better understanding the pathophysiology of migraine attacks. A link between central and peripheral components of the trigeminal pain pathway is provided by the observation that cortical spreading depression in the rat activates trigeminovascular afferents and induces a series of cortical meningeal and brainstem events consistent with the development of headache. Studies in humans support the hypothesis that cortical spreading depression underlies migraine.aura. Therefore, tt is possible that visual, motor or sensory aura might be responsible for the generation of the pain through the above mechanisms

Key words

Trigeminovascular system Neurogenic inflammation Nitric oxide Cortical Spreading depression Migraine aura