Torsten Liem
Laut Untersuchungen von Levy et al. wird eine weitläufige Berührungs- bzw. Schmerzüberempfindlichkeit von trigeminozervikale und lumbosakrale Schmerzbahnen verursacht, die durch die Degranulation von Mastzellen aktiviert werden [28]. Es war aber weiterhin unklar, welcher Mechanismus die Berührungsüberempfindlichkeit der Hinterpfoten von Ratten verursachte. Die gängige Hypothese erklärte z.B. nicht den zeitlichen Ablauf der beobachteten Veränderungen. Die Hypothese der peripheren LCS-Ausstrombahn soll zu diesen Beobachtungen beitragen.
• Generell läuft die Signalübertragung im LCS über gelöste Substanzen, insbesondere Proteine, Zellen, Exosome, Mikrovesikel oder Mikropartikel, die einflussreiche Signalmoleküle enthalten [29, 30].
• LCS läuft vom Subarachnoidalraum entlang der peripheren LCS-Ausstrombahn zwischen das Epineurium und das Perineurium. Der LCS verteilt sich in den Nerven in deren gesamtem Verlauf und ist auch in Kontakt mit den neuronalen Ganglien. Der LCS gelangt schließlich in das peripherere Gewebe, dort, wo die Nerven enden. Dort geht der LCS in die extrazelluläre Gewebeflüssigkeit über.
• Jede Form von pathogenen LCS-Bestandteilen kann potenziell dort mit den Nerven der peripheren LCS-Ausstrombahn interagieren, wo eine Interaktion möglich ist. Das hat pathogene Konsequenzen, und zwar an verschiedenen Stellen, vom Subarachnoidalraum bis hin zu den Nervenendigungen und dem angrenzenden Gewebe.
• Pathogene LCS-Bestandteile im Subarachnoidalraum können z.B. durch Mastzellen innerhalb der Meningen nahe des Subarachnoidalraums freigesetzt werden. Durch die Degranulation von Mastzellen freigesetzte Moleküle und Partikel könnten dann über den LCS alle Teile der peripheren LCS-Ausstrombahn erreichen und so lokale Auswirkungen hervorrufen.
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