Zusammenfassung
Die Entwicklung von Sumatriptan basierte ganz wesendich auf der Hypothese einer vaskulären Genese der Migräne, wie sie in den klassischen Untersuchungen von Graham u. Wolff [26] postuliert wurde. Zentraler Punkt in der Auslösung einer Migräneattacke ist nach dieser Theorie die Dilatadon großer meningealer Gefäße, die zur Stimulation afferenter Fasern des N. trigeminus führt. Dicht innervierte Gefäßwände finden sich intrakraniell besonders in der Dura mater, die demnach der Ort der schmerzhaften Dilatation sein müßte. Daß eine Reizung solcher Gefäße Schmerzen erzeugen kann, ist seit langem bekannt [41, 46]. Darüber hinaus konnte kürzlich gezeigt werden, daß die experimentelle Ballondilatadon intrakranieller Gefäße in der Tat schmerzhaft ist [38]. Schließlich wiesen Friberg et al. [22] mit transkranier Dopplersonographie und Single-photon-emissions-Computertomographie nach, daß große intrakra nielle Gefäße während einer Migräneattacke dilatiert sind und daß die erfolgreiche Therapie der Attacke mit einem Verschwinden der Dilatation einhergeht (vgl. Tabelle 13.1).
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Lohse, M.J., Ensink, F.B.M. (1994). Pharmakologie von Sumatriptan. In: Ensink, F.B.M., Soyka, D. (eds) Migräne. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-93522-0_16
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