Pain sensitivity in sleepy pain-free normals

Sleep Disorders & Research Center, Henry Ford Health System, Detroit, MI 48202, USA.
Sleep (Impact Factor: 4.59). 09/2009; 32(8):1011-7.
Source: PubMed


Past studies have shown that acute experimental reduction of time in bed in otherwise healthy, non-sleepy people leads to hyperalgesia. We hypothesized that otherwise healthy, sleepy people may also exhibit hyperalgesia relative to their non-sleepy counterparts.
Between-groups sleep laboratory study.
Hospital-based sleep disorders center.
Twenty-seven, healthy, normal participants (age 18-35 years) were recruited and categorized into sleepy and non-sleepy groups based on their average sleep latencies on a screening multiple sleep latency test (MSLT).
Both groups were then allowed 8 hours time in bed, following which they underwent pain sensitivity testing (10:30 and 14:30) and sleepiness assessments by the MSLT (10:00, 12:00, 14:00, and 16:00). Pain sensitivity assessments were made by measuring finger withdrawal latencies to a radiant heat source delivering 5 different heat intensities.
This study showed that after only one night of 8 hours time in bed, the sleepy participants continued to be sleepy and exhibited a more rapid finger withdrawal response (i.e., increased pain sensitivity) to radiant heat than non-sleepy participants.
This suggests that sleepy individuals experience hyperalgesia in response to a painful stimulus when compared with non-sleepy individuals.

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Available from: Timothy A Roehrs, Jul 22, 2014
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    • "Based on the presumed evidence that inadequate or fragmented sleep could promote systemic inflammation [21], [24], [30], [57], [71], another reason for the lack of an effect of sleep disruption on pain behavior and/or analgesia might have been the adjustment of the model for the presence of systemic inflammation, using IL-6, IL-1β, and TNF-α; however, the unadjusted model did not reveal any effect neither. Another potential confounder for the hyperalgesic effect of sleep disruption may be inquired in the evidence that physiological sleepiness (i.e., determined objectively by the Multiple Sleep Latency Test, MSLT) in otherwise healthy pain-free volunteers has been associated with an enhanced sensitivity to experimental heat pain [72] and decreased opioid potency for analgesia [73]. In the present experiment, we employed the Epworth sleepiness scale (ESS), a subjective instrument with a nonetheless excellent correlation with MSLT [74], to evaluate habitual sleepiness in our subjects. "
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    ABSTRACT: Obstructive sleep apnea (OSA) is characterized by recurrent nocturnal hypoxia and sleep disruption. Sleep fragmentation caused hyperalgesia in volunteers, while nocturnal hypoxemia enhanced morphine analgesic potency in children with OSA. This evidence directly relates to surgical OSA patients who are at risk for airway compromise due to postoperative use of opioids. Using accepted experimental pain models, we characterized pain processing and opioid analgesia in male volunteers recruited based on their risk for OSA. After approval from the Intitutional Review Board and informed consent, we assessed heat and cold pain thresholds and tolerances in volunteers after overnight polysomnography (PSG). Three pro-inflammatory and 3 hypoxia markers were determined in the serum. Pain tests were performed at baseline, placebo, and two effect site concentrations of remifentanil (1 and 2 µg/ml), an μ-opioid agonist. Linear mixed effects regression models were employed to evaluate the association of 3 PSG descriptors [wake after sleep onset, number of sleep stage shifts, and lowest oxyhemoglobin saturation (SaO(2)) during sleep] and all serum markers with pain thresholds and tolerances at baseline, as well as their changes under remifentanil. Forty-three volunteers (12 normal and 31 with a PSG-based diagnosis of OSA) were included in the analysis. The lower nadir SaO(2) and higher insulin growth factor binding protein-1 (IGFBP-1) were associated with higher analgesic sensitivity to remifentanil (SaO(2), P = 0.0440; IGFBP-1, P = 0.0013). Other pro-inflammatory mediators like interleukin-1β and tumor necrosis factor-α (TNF-α) were associated with an enhanced sensitivity to the opioid analgesic effect (IL-1β, P = 0.0218; TNF-α, P = 0.0276). Nocturnal hypoxemia in subjects at high risk for OSA was associated with an increased potency of opioid analgesia. A serum hypoxia marker (IGFBP-1) was associated with hypoalgesia and increased potency to opioid analgesia; other pro-inflammatory mediators also predicted an enhanced opioid potency. CLINICALTRIALS.GOV NCT00672737.
    PLoS ONE 01/2013; 8(1):e54807. DOI:10.1371/journal.pone.0054807 · 3.23 Impact Factor
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    • "The current study findings support that, beyond the experimental manipulation of sleep duration and continuity, the type of sleep disturbances experienced in primary insomnia contribute to an increase in pain sensitivity. At this point, it is not clear which aspects of sleep in primary insomnia are predictive of changes in pain sensitivity, such as duration, fragmentation, or even effects on daytime functioning (e.g., subjective sleepiness, which has been recently found related to pain sensitivity (Chhangani et al., 2009)). "
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    ABSTRACT: Sleep of good quantity and quality is considered a biologically important resource necessary to maintain homeostasis of pain-regulatory processes. To assess the role of chronic sleep disturbances in pain processing, we conducted laboratory pain testing in subjects with primary insomnia. Seventeen participants with primary insomnia (mean ± SEM 22.6 ± 0.9 yrs, 11 women) were individually matched with 17 healthy participants. All participants wore an actigraph device over a 2-week period and completed daily sleep and pain diaries. Laboratory pain testing was conducted in a controlled environment and included (1) warmth detection threshold testing, (2) pain sensitivity testing (threshold detection for heat and pressure pain), and (3) tests to access pain modulatory mechanisms (pain facilitation and inhibition). Primary insomnia subjects reported experiencing spontaneous pain on twice as many days as healthy controls during the at-home recording phase (p < 0.05). During laboratory testing, primary insomnia subjects had lower pain thresholds than healthy controls (p < 0.05 for heat pain detection threshold, p < 0.08 for pressure pain detection threshold). Unexpectedly, pain facilitation, as assessed with temporal summation of pain responses, was reduced in primary insomnia compared to healthy controls (p < 0.05). Pain inhibition, as assessed with the diffuse noxious inhibitory control paradigm (DNIC), was attenuated in insomnia subjects when compared to controls (p < 0.05). Based on these findings, we propose that pain-inhibitory circuits in patients with insomnia are in a state of constant activation to compensate for ongoing subclinical pain. This constant activation ultimately may result in a ceiling effect of pain-inhibitory efforts, as indicated by the inability of the system to adequately function during challenge.
    European journal of pain (London, England) 04/2012; 16(4):522-33. DOI:10.1016/j.ejpain.2011.07.007 · 2.93 Impact Factor
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    • "Inadequate sleep has been recognized as associated with and contributing to a poorer quality of life, an increase in morbidity/mortality and heightened pain perception [Cappuccio et al. 2010; Moldofsky, 2010; Chhangani et al. 2009]. There is a growing recognition among clinicians of the importance of sleep in global patient care. "
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    ABSTRACT: Poor sleep health is increasingly recognized as contributing to decreased quality of life, increased morbidity/mortality and heightened pain perception. Our purpose in this study was to observe the effect on sleep parameters, specifically sleep efficiency, in rheumatoid arthritis (RA) patients treated with anti-tumor necrosis factor alpha (anti-TNF-α) therapy. This was a prospective observational study of RA patients with hypersomnolence/poor sleep quality as defined by the Epworth Sleepiness Scale (ESS) and Pittsburgh Sleep Quality Index (PSQI). Study patients underwent overnight polysomnograms and completed questionnaire instruments assessing sleep prior to starting anti-TNF-α therapy and again after being established on therapy. The questionnaire included the ESS, PSQI, the Berlin instrument for assessment of obstructive sleep apnea (OSA) risk, restless legs syndrome (RLS) diagnostic criteria, and measures of disease activity/impact. A total of 12 RA patients met inclusion criteria, of which 10 initiated anti-TNF-α therapy and underwent repeat polysomnograms and questionnaire studies approximately 2 months later. Polysomnographic criteria for OSA were met by 60% of patients. Following anti-TNF-α therapy initiation, significant improvements were observed by polysomnography (PSG) for sleep efficiency, increasing from 73.9% (SD 13.5) to 85.4% (SD 9.6) (p = 0.031), and 'awakening after sleep onset' time, decreasing from 84.1 minutes (SD 43.2) to 50.7 minutes (SD 36.5) (p = 0.048). Questionnaire instrument improvements were apparent in pain, fatigue, modified Health Assessment Questionnaire (mHAQ), and Rheumatoid Arthritis Disease Activity Index (RADAI) scores. Improved sleep efficiency and 'awakening after sleep onset' time were observed in RA patients treated with anti-TNF-α therapy.
    Therapeutic advances in musculoskeletal disease 10/2011; 3(5):227-33. DOI:10.1177/1759720X11416862
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