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DOI: 10.1055/s-0035-1569275
Schlaf und Schmerz
Sleep and PainPublication History
Publication Date:
10 February 2016 (online)
Zusammenfassung
Schlaf, Schlafstörung und Schmerz stehen in einem vielfältigen (patho)physiologischen Zusammenhang. Besonders gut bekannt ist die Rolle von Schlaf im Kontext mit chronobiologischen Schmerzerkrankungen, zu deren prominentesten Vertretern der Clusterkopfschmerz sowie der „Hypnic Headache“ gehören. Schlafstörungen können sich aber auch – wie jüngste experimentelle Studien an Gesunden zeigen – negativ auf Schmerzempfindlichkeit und Spontanschmerz auswirken. Schon eine Nacht Schlafentzug führt zu einer gesteigerten Schmerzempfindlichkeit für mechanische und thermische Reize, nach mehrtägiger Schlafrestriktion klagen selbst Gesunde über Spontanschmerzen. Erste klinische Patientenstudien unterstützen die Hypothese, nach der Schlafstörungen für Schmerzpatienten das Potenzial eines eigenständigen „Aggravationsfaktors“ haben. Dies hat erheblich pathophysiologische Relevanz, da Schlafstörungen – unabhängig von der Schmerzpathogenese – zu den häufigsten Begleitbeschwerden von Schmerzpatienten zählen. Studien zufolge haben schlafmedizinische Maßnahmen durchaus das Potenzial, chronische Schmerzsyndrome positiv zu beeinflussen. Der Beitrag von Schlafstörungen am Schmerzsyndrom kann jedoch stark variieren, weshalb er im klinischen Patientenalltag letztlich individuell erfasst werden muss. Pathophysiologische Erklärungsansätze beruhen derzeit auf 2 Grundbeobachtungen. So legen tierexperimentelle Studien nahe, dass Schlafmangel/Schlafentzug durch hierdurch induzierte Veränderungen in der Neurotransmitter-Balance zu einer funktionellen Störung des endogenen schmerzmodulierenden Systems führt. Ein weiterer pathophysiologischer Ansatz, der bisher jedoch noch wenig erforscht ist, bezieht sich auf die Interaktion zwischen Schlafmangel und Immunsystem. So können die chronobiologisch fein abgestimmten pro- und antiinflammatorischen Immunvorgänge durch chronischen Schlafmangel aus dem Gleichgewicht geraten. Das hieraus resultierende proinflammatorische Übergewicht kann – z. B. in Form einer verstärkten Freisetzung proinflammatorischer/pronozizeptiver Zytokine – negativen Einfluss auf das nozizeptive System ausüben. Die klinische Bedeutung des pathophysiologischen Zusammenhangs zwischen Schlafstörung und Schmerz wird im schmerztherapeutischen Alltag bisher eher unterschätzt. Für die Zukunft wäre es daher wünschenswert, eine standardisierte Schlafdiagnostik und –therapie im schmerztherapeutischen Alltag fest zu implementieren.
Abstract
Sleep, sleep deprivation and pain are closely intertwined. It is well established that sleep plays an important role in chronobiological pain disorders. Cluster and hypnic headaches are prominent examples of pain disorders with circadian rhythmicity. More recently, the impact of disturbed sleep on both spontaneous pain and pain sensitivity has been recognized. Experimental studies have shown that one night of total sleep deprivation can induce generalized, mechanical and thermal pain hypersensitivity. Sleep restriction over several days results in spontaneous pain. Several clinical studies suggest that sleep deprivation/disruption acts as an independent „pain aggravating“ factor. Insomnia in pain patients is of therapeutic relevance since disturbed sleep is one of the most frequently reported complaints of pain patients. Clinical studies have shown that improved sleep (either by cognitive behavioral insomnia therapy or by the use of hypnotics) alleviates the (chronic) pain condition. However, the contribution of disturbed sleep to pain intensity may vary considerably and needs to be determined individually. The mechanism by which disturbed sleep affects nociception is currently unknown. There is some evidence of sleep deprivation causing imbalance of the endogenous pain modulatory system by reinforcing pro-nociceptive whilst attenuating the anti-nociceptive system. The interplay between sleep and the immune system may play an important role. Sleep deprivation induces release of pro-inflammatory cytokines. Due to their pro-nociceptive properties, they may impact on pain sensitivity, resulting in hypersensitivity to evoked pain.
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