Zusammenspiel von Schmerz, Entzündung und Nervensystem bei Arthritis

Zusammenfassung

Das Zusammenspiel von Entzündung und Nervensystem hat Bedeutung für die subjektiven Folgen der Arthritis, bestehend aus Schmerz und anderen subjektiven Symptomen, z. B. Schlafstörungen, Abgeschlagenheit, aber auch für die Ausprägung der Entzündung, da das Nervensystem über verschiedene neuronale Wege Entzündungsvorgänge modifizieren kann. Bei Entzündung wird das nozizeptive System für Reize sensibilisiert. Durch Veränderungen der zentralnervösen Verarbeitung kann der Schmerz in seinem Charakter verändert werden, und es können Komorbiditäten wie Depression und Angst auftreten. Sensibilisierungsvorgänge fördern auch die o.g. efferenten neuronalen Effekte. Bei der Induktion entzündungstypischer neuronaler Veränderungen spielen neben anderen Mechanismen auch proinflammatorische Zytokine eine Rolle, wobei verschiedene Zytokine an den Nervenzellen unterschiedlich wirken. Im experimentellen Modell der Antigen-induzierten Arthritis hat Tumornekrosefaktor-α eine funktionelle Bedeutung für die mechanische und thermische Hyperalgesie, Interleukin-6 und Interleukin-17 fördern vor allem die mechanische Hyperalgesie, während Interleukin-1β die thermische Hyper­algesie fördert. Als Folge der peripheren Entzündung wird Interleukin-6 auch im Rückenmark freigesetzt, und es wirkt dort als Schmerzverstärker. Ein Beitrag weiterer spinaler Zytokine ist wahrscheinlich. Zur Beurteilung der klinischen Relevanz von Entzündungen sollte nicht nur der Entzündungsprozess erfasst werden, sondern auch die subjektive Symptomatik als Ausdruck der begleitenden neuronalen Prozesse, wodurch sich therapeutische Ansätze möglicherweise optimieren lassen.

Abstract

The interaction between inflammation and the nervous system is important for the subjective consequences of arthritis such as pain and other symptoms, e. g., sleep disturbances, fatigue, and also for the expression of the inflammation because the nervous system can modify inflammatory processes through different neuronal pathways. In the course of inflammation the nociceptive system is sensitised for stimuli. Furthermore, the pain can be modified in its character by changes in the processing in the central nervous system, and co-morbidities such as depression and anxiety can occur. The processes of sensitisation also promote the efferent neuronal effects mentioned above. In the induction of inflammatory changes in the nervous system pro-inflammatory cytokines play a role, in addition to other mechanisms, and different cytokines seem to exert different actions on neurons. In the model of antigen-induced arthritis, tumour necrosis factor-α is functionally important for the induction of mechanical and thermal hyperalgesia, interleukin-6 and interleukin-17 promote mainly the generation of mechanical hyperalgesia whereas interleukin-1β mainly promotes thermal hyperalgesia. As a consequence of peripheral inflammation interleukin-6 is released in the spinal cord, and it acts as a pain amplifier. A contribution of other spinal cytokines is likely. In order to judge the clinical relevance of inflammation not only the inflammatory process should be monitored but also the subjective symtoms, as a readout parameter of arthritis-induced neuronal processes. This may help to optimise therapeutic approaches.

Schlüsselwörter

Arthritis - Schmerz - Zytokine

Key words

arthritis - pain - cytokines

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