Sleep mediates the relationship between central sensitization and clinical pain
PainSci summary of Burton 2016?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focussed on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible. ★★★☆☆?3-star ratings are for average studies, with no more (or less) than the usual common problems. Ratings are a highly subjective opinion, and subject to revision at any time. If you think this paper has been incorrectly rated, please let me know.
A major driver of chronic pain is “central sensitization” (basically turning up the “volume” on all pain). The phenomenon is well-known, but how it works is still a mystery, and its relationship with sleep has barely been studied. This study looked carefully 133 patients with knee arthritis, comparing those who slept well versus those who did not. They found, with a high degree of certainty, that “sleep fragmentation may strongly affect the pain and CS relationship; consequently, these results underscore the importance of considering and treating sleep in patients with chronic pain.”
Knee osteoarthritis (KOA), a chronic degenerative joint disorder, is characterized by knee joint pain. Emerging research demonstrates that a significant number of patients evidence central sensitization (CS), a hyperexcitability in nociceptive pathways, which is known to increase and maintain clinical pain. The clinical correlates of CS in KOA, however, are poorly understood. Sleep disturbance is prevalent in older adults with KOA, and well known to have a bi-directional effect on pain. Recent studies suggest associations between poor sleep and measures of CS. Clinical pain and CS are overlapping concepts and are believed to also have a bidirectional relationship. While an area of expanding interest, few studies have investigated possible interactions between clinical pain, sleep, and CS. We conducted secondary data analyses on a case–control study of KOA patients with and without insomnia to examine the impact of sleep on the relationship between CS and clinical pain. A total of 133 participants were included in the current analyses (73% Female, 59% non-Hispanic white, mean age=61, SD=9.8). They completed daily diaries to evaluate sleep and clinical pain and underwent extensive quantitative sensory testing (thermal & mechanical temporal summation, after sensations and conditioned pain modulation were used to create a composite CS index). Hayes’ PROCESS macro was used to examine the effects of sleep fragmentation on the relationship between CS and clinical pain, as recorded by self-reported pain diaries. Sleep fragmentation (wake after sleep onset reported via daily diaries) mediated the relationship between CS and clinical pain (total effect p<0.001; direct and indirect effects p<0.001), even when controlling for sex and race (variables known to influence both pain and sleep). These results indicate that greater sleep fragmentation may strongly affect the pain and CS relationship; consequently, these results underscore the importance of considering and treating sleep in patients with chronic pain.
- PS Central Sensitization in Chronic Pain — Pain itself can change how pain works, resulting in more pain with less provocation
These two articles on PainScience.com cite Burton 2016 as a source: