Platelet activation and platelet–leucocyte interaction in patients with migraine. Subtype differences and influence of triptans
Corresponding Author
JA Zeller
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Dr Jörn A. Zeller, University Clinic Schleswig-Holstein, Campus Kiel, Department of Neurology, Schittenhelmstrasse 10, D-24105 Kiel, Germany. Tel. + 49 431 597 8708, fax + 49 431 597 8724, e-mail: [email protected]Search for more papers by this authorV Lindner
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Search for more papers by this authorK Frahm
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Search for more papers by this authorR Baron
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Search for more papers by this authorG Deuschl
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Search for more papers by this authorCorresponding Author
JA Zeller
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Dr Jörn A. Zeller, University Clinic Schleswig-Holstein, Campus Kiel, Department of Neurology, Schittenhelmstrasse 10, D-24105 Kiel, Germany. Tel. + 49 431 597 8708, fax + 49 431 597 8724, e-mail: [email protected]Search for more papers by this authorV Lindner
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Search for more papers by this authorK Frahm
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Search for more papers by this authorR Baron
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Search for more papers by this authorG Deuschl
Department of Neurology, Christian-Albrechts-University Kiel, Kiel, Germany
Search for more papers by this authorAbstract
As migraine is the result of an inflammatory mechanism with serotonergic signalling, leucocyte function, platelet function and intercellular communication between those cells is likely to be connected to the final pathway of the disease. We examined P-selectin expression on platelets (platelet activation) and leucocyte–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 migraine patients with aura. Patients who had taken a triptan within 3 days prior to the investigation showed platelet activation values similar to the control group. The variations in platelet activation patterns of migraine subgroups could indicate different pathomechanisms. Even outside an attack, migraine patients, particularly those without aura, show an increased level of platelet activation which seems to be down-regulated by triptans. This mechanism may account for the triptan-induced increases in headache frequency. The involvement of proinflammatory platelet–leucocyte cross-talk suggests a possible therapeutic strategy using anti-inflammatory drugs.
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