It Hurts: Chronic Pain and the Architecture of Sleep
—These researchers found that daytime pain sensitivity was associated with reduced REM sleep percentage in women with TMD and insomnia. Understanding the mechanisms behind the link between sleep and pain could lead to more effective sleep treatments for patients with pain disorders.
According to a new study, pain sensitivity is associated with reduced time spent in the rapid-eye-movement (REM) stage in subsequent sleep in women with temporomandibular disorders (TMDs) and insomnia.1
Longitudinal studies have demonstrated that poor sleep is associated with an increased risk of the subsequent development of a pain condition.2
The reverse seems obvious: pain would interfere with sleep. However, “this topic has received surprisingly limited attention, and as such the underlying mechanism linking pain and sleep architectural disturbances remains unresolved,” wrote researchers from Johns Hopkins, the University of Maryland, the University of Virginia, and the University of California, Irvine, who assessed whether daytime pain was associated with altered sleep architecture and EEG waveforms the following night in women with TMD.
“[I]t is not yet known whether heightened daytime pain in chronic pain conditions feeds forward to disrupt specific components of sleep physiology.”
Study design
The study was an exploratory analysis of pre-randomization data from a larger 5-year study.3 Women with TMD aged 18-60 years, an average pain severity score ≥3 over the previous week on a scale of 0-10, a pain catastrophizing scale score >8, and an insomnia severity index score >8 were included.
Quantitative sensory testing was used to derive a general pain sensitivity index, which was a composite of scores from heat pain threshold and tolerance, masseter pressure pain threshold, conditioned pain modulation, thermal and mechanical temporal summation, an average pain sensitivity from cold pressor testing, and after sensations from these tests. A central sensitization index to analyze dynamic pain was derived from averaging scores for conditioned pain modulation, thermal and mechanical temporal summation, and after sensations from these tests.
Participants used an ambulatory polysomnography device at home on the night following the quantitative sensory testing to measure the percentage of time in stages N1, N2, slow-wave, and REM sleep, and the relative power in alpha, beta, delta, sigma, and theta bands.
Pain and sleep associations
Study participants had a mean age of 36.02 ± 11.10 years and a mean pain severity score of 4.25 ± 1.67. The mean pain catastrophizing scale score was 20.37 ± 11.15, and the mean insomnia severity index score was 15.69 ± 3.98.
The researchers found no association between the masseter pain pressure threshold, central sensitization index, and general pain sensitivity index with the percentage of time spent in stage N1, N2, or slow-wave sleep. The percentage of time spent in REM sleep, however, was significantly associated with masseter pressure pain threshold (P = .043), central sensitization (P = .033), and general pain sensitivity (P = .037).
They also found no association between the pain sensitivity indexes and relative power in any of the power bands.
“Tentative interpretation”
Although exploratory, the study suggested that chronic pain may affect sleep via the REM stage.
The researchers wrote that understanding the mechanisms behind the link between sleep and pain could lead to more effective sleep treatments for patients with pain disorders. “Sleep is modifiable through pharmacological, and non-pharmacological interventions that can be targeted in a clinical setting for those with chronic pain,” they wrote.
The study's limitations included the absence of male participants and a single night for sleep analysis. Furthermore, the researchers did not correct for multiple comparisons in their statistical analysis to reduce false negatives. “Accordingly, we recommend tentative interpretation of these findings,” they wrote.
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