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Pathophysiologie der Migräne im klinischen Kontext

Pathophysiology of migraine and clinical implications

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Zusammenfassung

Die Pathophysiologie der Migräne wird durch genetische und Umweltfaktoren bestimmt. Basierend auf einer zerebralen Dyshabituation und einer niedrigen Serotoninkonzentration kann durch Trigger eine Attacke ausgelöst werden. Initial werden oft unspezifische Vorboten geklagt, die häufig von einer Aura gefolgt sind, meist in Form visueller Reizsymptome. Das elektrophysiologische Korrelat der Aura ist die „cortical spreading depression“. Diese kann das trigeminovaskuläre System aktivieren und stellt einen möglichen Auslöser der Schmerzphase dar. Der typische halbseitige pulsierende Kopfschmerz wird durch eine neurogene Entzündung im Bereich der Meningen hervorgerufen. Der manchmal geklagte Nackenschmerz ist migränespezifisch und anatomisch durch den trigeminozervikalen Komplex zu erklären. Es treten funktionelle Veränderungen ein, die den Kopfschmerz aufrechterhalten. Hierzu gehören eine Sensitisierung von Neuronen des trigeminalen Nucleus caudalis und eine vom periaquäduktalen Grau (PAG) absteigende veränderte Antinozizeption. Triptane greifen sowohl peripher an Neuronen des N. trigeminus als auch zentral im Bereich des PAG an. Nach Auftreten einer zentralen Sensitisierung verlieren sie ihre Wirksamkeit.

Abstract

Migraine pathophysiology is determined by genetic and environmental factors. Based on altered cerebral habituation and low serotonin levels, certain triggers can elicit a migraine attack. Following initial unspecific prodromi, an aura follows in many patients which most often consists of visual symptoms. Cortical spreading depression is the electrophysiological correlate of the aura and can activate the trigemino-vascular system. This is one potential mechanism initiating the pain process. The characteristic unilateral pulsating headache is caused by a neurogenic inflammation in the meninges. Neck pain as reported by some patients is a migraine-specific feature, the anatomical basis being the trigemino-cervical complex. Functional changes in the pain processing system maintain the headache. Among these are sensitization of trigeminal nucleus caudalis neurons and an altered antinociception descending from the periaquaductal grey. Triptans have a peripheral and central mode of action, but they are no longer effective once central sensitization has occurred.

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Interessenkonflikt

Prof. Dr. Hans-Christoph Diener hat Honorare für die Teilnahme an klinischen Tests, die Mitwirkung an Beratungsgremien und Vortragstätigkeiten erhalten von: Addex Pharma, Allergan, Almirall, Astra-Zeneca, Bayer Vital, Berlin Chemie, CoLucid, Böhringer Ingelheim, Bristol-Myers Squibb, GlaxoSmithKline, Grünenthal, Janssen-Cilag, Lilly, La Roche, 3 M Media, MSD, Novartis, Johnson & Johnson, Pierre Fabre, Pfizer, Schaper and Brümmer, Sanofi Aventis, Weber & Weber.

Finanzielle Untersützung für Forschungsprojekte wurde zur Verfügung gestellt von Allergan, Almirali, Astra-Zeneca, Bayer, GlaxoSmithKline, Janssen-Cilag, Pfizer.

Die Kopfschmerzforschung an der Abteilung für Neurologie in Essen erhält Förderungsmittel von der Deutschen Forschungsgemeinschaft (DFG), dem Bundesministerium für Bildung und Forschung (BMBF) und der Europäischen Union.

Dr. Markus Schürks ist Forschungsstipendiat der Deutschen Forschungsgemeinschaft (DFG).

Dr. Markus Schürks und Prof. Dr. Hans-Christoph Diener haben keine Eigentümerinteressen und halten keine Anteile an einem Pharmaunternehmen.

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Authors and Affiliations

  1. Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, 900 Commonwealth Avenue East, 3rd fl, Boston, MA 02215-1204, USA

    M. Schürks

  2. Klinik für Neurologie, Universitätsklinikum Essen, Essen, Deutschland

    M. Schürks & H.-C. Diener

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Correspondence to M. Schürks.

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Schürks, M., Diener, HC. Pathophysiologie der Migräne im klinischen Kontext. Schmerz 22, 523–530 (2008). https://doi.org/10.1007/s00482-008-0693-1

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