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As migraine is the result of an inflammatory mechanism with serotonergic sign alling, leucocyte function, platelet function and intercellular communication be tween those cells is likely to be connected to the final pathway of the disease. We examined P- selectin expression on platelets (platelet activation) and leuc ocyte- platelet aggregate formation in 72 migraine patients during their attack - free interval and controls using a flow cytometric assay. Patients suffering from migraine without aura had a significantly increased platelet activation and leucocyte- platelet aggregation compared with the control group, unlike the mi graine patients with aura. Patients who had taken a triptan within 3 days prior to the investigation showed platelet activation values similar to the control gr oup. The variations in platelet activation patterns of migraine subgroups could indicate different pathomechanisms. Even outside an attack, migraine patients, p articularly those without aura, show an increased level of platelet activation w hich seems to be down- regulated by triptans. This mechanism may account for th e triptan- induced increases in headache frequency. The involvement of proinfla mmatory platelet- leucocyte cross- talk suggests a possible therapeutic strate gy using anti- inflammatory drugs.
As migraine is the result of an inflammatory mechanism with serotonergic sign alling, leucocyte function, platelet function and intercellular communication be tween those cells is likely to be connected to the final pathway of the disease. We examined P-selectin expression on platelets (platelet activation ) and leuc ocyte-platelet aggregate formation in 72 migraine patients during their attack - free interval and controls using a flow cytometric assay. Patients suffering from migraine without aura had a significant increased platelet activation and leucocyte-platelet aggregation compared with the control group, unlike the mi graine patients with aura. Patients who had taken a triptan within 3 days prior to the investigation show platelet activation values similar to the control gr oup. The variations in platelet activation patterns of migraine subgroups could indicate different pathomechanisms. Even outside an attack, migraine patients, p articularly those without aura, show an increased level of platelet activation w hich seems to be down-regulated by triptans. This mechanism may account for th e triptan- induced increases in headache frequency. The involvement of proinfla mmatory platelet- leucocyte cross- talk suggests a possible therapeutic strate gy using anti - inflammatory drugs.