Platelets and migraine

The pathogenesis of migraine, the third most frequent disease worldwide, is complex and multifaceted. Recentevidence suggests that this condition should be considered as a primary neurovascular disorder. The pathogenesisis sustained by a relative reduction of cerebral blood flow, which is then followed by reactive hyperaemia,sterile inflammation and hypersensitization of pain pathways. The leading triggers of the initial vasoconstrictionentail both hereditary or acquired cerebrovascular disorders, namely local endothelial or smooth muscledysfunction, arteriovenous malformations autoimmune and inflammatory disorders, along with cerebralmicroembolism.The existence of a potential relationship between platelet biology andmigraine has been hypothesizedmore than30 years ago, paving the way to a series of subsequent studies. Despite the clinical evidence that patients withessential thrombocythemia have a high frequency of headache symptoms, the epidemiological trials that haveinvestigated the platelet count in patients with an accurate diagnosis of migraine failed to report significant associations.Conversely, several lines of evidence attest that serotoninmetabolismis substantially impaired in migrainepatients, thus contributing to trigger or enhance vasoconstriction and hypersensitization of neuronalelements. Although abnormalities of nitric oxide metabolism should be confirmed in larger studies, publisheddata suggests that this compound may be effective to amplify the reactive vasodilatation that specifically followsthe initial reduction of cerebral blood flow. Another plausible link between platelet biology and migraine isrepresented by inflammation. Increased release of several proinflammatory cytokines, especially interleukins1, 6 and 8 and tumor necrosis factor-alpha, may occur after formation of platelet-leukocyte aggregates, andthesemediators can further contribute to increase sterile inflammation in the brain and facilitate pain signalling.