Migraine: the platelet hypothesis after 10 years
Hanington, E.
Biomedicine and PharmacoTherapy 43(10): 719-726
1989
ISSN/ISBN: 0753-3322 PMID: 2701286 DOI: 10.1016/0753-3322(89)90160-1Document Number: 379165
The hypotheses that defective platelet structure and function is the basis for migraines is presented, with evidence explaining the biochemical, clinical, pathological, and pharmacological aspects of migraine. Platelets undergo 2 types of reaction, a shape change and a granule release reaction, releasing adenosine diphosphate (ADP) serotonin 5-hydroxy-tryptamine (5-HT), and thromboglobulin in response to collagen and thrombin. Platelets from migraine suffers contain more ADP, have more dense granules, and show some qualitative differences in their release reaction. Their platelets aggregate more readily when exposed to 5-HT, their platelet fibrinogen receptors have greater affinity, and their platelet membranes show altered viscosity. Some drugs that inhibit platelet aggregation, such as methysergide, aspirin, and amitryptylline, are beneficial in cases of migraine. Some migraine triggers, such as tyramine and catecholamines, are known to be vasoactive. The release by platelets of 5-HT may account for the visual aura or prodrome that migraine patients experience. Some migraine precipitating factors, such as stress, fatigue, hunger, certain foods, and hormones, may stimulate 5-HT release by platelets. Alterations in hormones, notably puberty, menstruation, oral contraceptive use, and menopause, are characterized by altered platelet aggregation and by onset of migraine in previously healthy people. Other arguments in favor of the platelet hypothesis involve prostacyclin deficit during menstruation and migraine associated with sudden decline in platelet numbers in cases of thrombocytopenic purpura and essential thrombocythemia.