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Schlafentzug und Schmerz

Ein Review der neuesten Literatur

Sleep deprivation and pain

A review of the newest literature

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Zusammenfassung

Es ist mittlerweile unstrittig, dass Schlafentzug bzw. -fragmentierung zu Hyperalgesien führt, die sich nicht als allgemeine Veränderung der Somatosensorik erklären lassen. Welche Schlafphasen für die Deprivationswirkung am relevantesten sind, ist nicht ausreichend geklärt. Teilweise paradox anmutende Befunde zur Deprivationswirkung auf schmerzevozierte Hirnpotenziale einerseits und subjektives Schmerzerleben andererseits lassen komplizierte Veränderungen von Gating-Mechanismen vermuten. Da die Wirkungen auf Affekt und Schmerz dissoziieren können, ist ein gemeinsamer Wirkungsmechanismus unwahrscheinlich. Daten aus Tierstudien lassen vermuten, dass schlafentzugsbedingte Hyperalgesien bei bestehenden Neuropathien besonders ausgeprägt sind. Einige tierexperimentelle Ergebnisse sowie der Befund, dass Schlafdeprivation die endogene Schmerzhemmung [“conditioned pain modulation“ (CPM)] stört, führten zu der Annahme, dass das serotoninerge System die Wirkung von Schlafentzug auf das Schmerzsystem vermittelt. Andere Neurotransmitter und -modulatoren müssen aber weiterhin berücksichtigt werden. Klinisch gilt es zu klären, warum bei bestimmten Personen schlafentzugsbedingte Hyperalgesien besonders leicht auftreten und länger persistieren.

Abstract

It has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?

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Danksagung

Wir danken der Dr. Robert-Pfleger-Stiftung (Bamberg) für die Förderung dieser Arbeit.

Einhaltung ethischer Richtlinien

Interessenkonflikt. A.J. Karmann, B. Kundermann und S. Lautenbacher geben an, dass kein Interessenkonflikt besteht. Dieser Beitrag beinhaltet keine Studien an Menschen oder Tieren.

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Authors and Affiliations

  1. Physiologische Psychologie, Otto-Friedrich-Universität Bamberg, Markusplatz 3, 96045, Bamberg, Deutschland

    A.J. Karmann & S. Lautenbacher

  2. Vitos Klinikum Gießen-Marburg, Gießen, Deutschland

    B. Kundermann

  3. Klinik für Psychiatrie und Psychotherapie, Philipps-Universität Marburg, Marburg, Deutschland

    B. Kundermann

Authors
  1. A.J. Karmann
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  2. B. Kundermann
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  3. S. Lautenbacher
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Correspondence to A.J. Karmann.

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Karmann, A., Kundermann, B. & Lautenbacher, S. Schlafentzug und Schmerz. Schmerz 28, 141–146 (2014). https://doi.org/10.1007/s00482-014-1394-6

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