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Chronischer Schmerz und Stressachse: autonomes Nervensystem und Hypothalamus-Hypophysen-adrenokortikale Achse (HPA)

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Zusammenfassung

Der Sympathikotonus ist konsistent bei chronisch myofaszial-skelettalen Schmerzen infolge Arthrosen, rheumatischer Arthritis und zentral bedingter Schmerzen (Fibromyalgie) gesteigert. Zusätzlich zur Dekonditionierung der Mikrozirkulation bestehen pathophysiologische Verhältnisse der Gewebeversorgung und im interstitiellen Raum. Die defizitäre Sympatholyse ist ein weiterer Faktor. Alle Faktoren schränken die physische Leistungsfähigkeit ein. Die Sympathikotonie und die Alterungsprozesse triggern gemeinsam regionale Ischämien. Triggerpunkte sind ein Merkmal myofaszial-skelettaler Schmerzsyndrome und ebenso autonome Regulationsstörungen. Der CLBP, die Fibromyalgie und die Osteoarthrose weisen einen erhöhten Sympathikotonus auf. Bei der Fibromyalgie bestimmt die hyperreaktive sympathische vaskuläre Reaktion bei physischen wie psychischen Belastungen das Geschehen. Das sympathische und sensorische Nervensystem scheint entscheidend an den pathogenetischen Vorgängen der Arthrose beteiligt zu sein.

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  1. Department für Orthopädie, Unfall- und Wiederherstellungschirurgie, Martin-Luther-Universität Halle-Wittenberg, Halle-Wittenberg, Deutschland

    Wolfgang Laube

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Laube, W. (2022). Chronischer Schmerz und Stressachse: autonomes Nervensystem und Hypothalamus-Hypophysen-adrenokortikale Achse (HPA). In: Schmerztherapie ohne Medikamente. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-63846-0_4

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