The pathophysiology of migraine: year 2005

Abstract

IntroductionDespite the high frequency of migraineurs in the general population, the pathogenesis of this disorder is still unclear.There is a great need for a better understanding of the mechanisms underlying the pain, the accompanying symptoms, as well as the premonitory symptoms and the aura. Progress in translational research is impeded by the lack of a validated experimental model and by the lack of tools to J Headache Pain (2005) M. Gabriella Buzzi Michael A. MoskowitzAbstract Migraine is a complex pathophysiology 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, it is possible that visual, motor or sensory aura might be responsible for the generation of the pain through the above mechanisms

Personality in patients with migraine evaluated with the "Temperament and Character Inventory"

“…Using other research strategies, other authors have supported the serotoninergic aetiological link with HA [38][39][40][41][42][43]. The results of the present study indirectly support serotoninergic involvement in the physiopathology of migraine, as has been shown extensively in the literature [44,45].…”

Migraine and motion sickness: What is the link?

“…As noted in Section 2.2, vasodilatation during attacks of migraine may be driven in a vicious circle by an interaction between nociceptive trigeminal-parasympathetic vasodilatation and painful neurogenic inflammation (Moskowitz, 1993;Buzzi and Moskowitz, 2005). Extracranial blood vessels dilate more readily in migraine sufferers than controls during psychological stress (Drummond, 1982), head pain (Drummond, 1997;Drummond and Granston, 2005) and optokinetic stimulation (Drummond and Granston, 2004;Cuomo-Granston, 2008).…”

Migraine disease: evolution and progression

“…Among NO donors, nitroglycerin (NTG) has undergone extensive experimental investigation in the neurological field, because typical headaches develop in migraineurs (but not normals) with a 4-6 h latency after its administration [8]. In experimental animal models, NTG administration induces an up-regulation of proinflammatory genes (iNOS, interleukin-6, interleukin-1), mast cell and macrophage activation, with a subsequent, delayed inflammatory reaction in the dura mater of the rat (4-6 h) [9].…”