Rev Neurol France
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This review summarizes the history of migraine imaging and key findings of studies on functional neuroimaging in migraine and describes how these data have changed our view of the disorder. Functional neuroimaging during migraine attacks and also interictally has initiated the description of "the migraine brain". These studies have led to the demonstration of cortical spreading depression in migraine with aura, the crucial role for the brainstem during migraine attacks, and cortical hypersensitivity in migraineurs modulated by the trigeminal pathway, explaining sensory sensitization such as photophobia and osmophobia.
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The second edition of the International Classification of Headache Disorders revised in 2006 (ICHD-2R) gives a definition which requires 15 or more headache days per month over the past 3months with at least eight headache days per month that meet criteria for migraine without aura or that responds to migraine specific treatment. Approximately 2% of the global population suffers of chronic migraine (CM). ⋯ There is a high frequency of medication overuse. The treatment depends on evaluation with education, lifestyle modifications, and trigger management, behavioral and pharmacologic therapies.
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Migraine with aura is well known to be associated with an increased risk of ischemic stroke. This risk dramatically increases in smokers and uses of oral contraceptives. Brain MRI studies suggest that migraine is associated with silent brain infarcts. ⋯ A prothrombotic state in migraine is also another possible explanation due to genetic polymorphisms. Appropriate management for primary vascular prevention in migraineurs is not different from that proposed for the general population. Oral contraceptives should be avoided in migraineurs with aura, especially if they smoke.
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The aim of genetic studies in migraine is to identify key proteins in order to better understand the molecular mechanisms of this frequent but still incompletely understood condition. This review describes the current knowledge in the field of migraine genetics. Migraine genes have been, and still are, difficult to identify. ⋯ Three of the four polymorphisms are associated both with migraine without aura and migraine with aura, supporting the existence of molecular mechanisms shared by all varieties of migraine. The vast majority of the migraine genes are still to be identified. Future researches will rely on new GWAS on larger cohorts of patients and controls, with a better phenotypic assessment, and on extensive sequencing.
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Observational studies indicate an increased prevalence of patent foramen ovale (PFO) in migraineurs with aura and an increased prevalence of migraine and migraine with aura in patients with PFO but a recent stratified meta-analysis does not support pairwise association between PFO and migraine. There are conflicting data regarding causal relationship between these two conditions. According to recent studies, microembolization might provoke a decrease in cerebral oxygen saturation, thus triggering cortical spreading depression and, thereafter, migraine with aura attack. ⋯ The MIST study is the only prospective study available with a good design but this study gave a negative response about cure of migraine with aura and revealed a high morbidity for such a benign condition. Although PFO closure sometimes appears to affect migraine patterns favorably, the very low grade of available evidence to support this association precludes definitive conclusions. To date, PFO closure in migraineurs with aura is not recommended in daily practice.