Borgdorff P et al. – New strategies for migraine medication and risk reduction of stroke are suggested.

• A role for platelet aggregation in a number of migraineurs is indicated by reports of an increased platelet activity during attacks and favorable effects of antiplatelet medication.
• Authors hypothesize that in those patients, a migraine attack with or without aura may both be caused by a rise in platelet–released plasma serotonin, albeit at different concentration.
• At high concentrations, serotonin may cause vasoconstriction and, consequently, the neuronal signs of aura, whereas at low concentrations, it may already stimulate perivascular pain fibers and cause vasodilation via local formation of nitric oxide, prostaglandins, and neuropeptides.
• Platelet aggregation may be unilaterally evoked by elevated shear stress in a stenotic cervico–cranial artery, by reversible vasoconstriction or by other cardiovascular abnormality, eg, a symptomatic patent foramen ovale.
• This most likely occurs when a migraine trigger has further enhanced platelet aggregability; literature shows that many triggers either stimulate platelets directly or reduce endogenous platelet antagonists like prostacyclin.