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      Sleep, Experimental Pain and Clinical Pain in Patients with Chronic Musculoskeletal Pain and Healthy Controls

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          Everyday variations in night sleep in healthy pain-free subjects are at most weakly associated with pain, whereas strong alterations (eg, sleep deprivation, insomnia) lead to hyperalgesic pain changes. Since it remains unclear how substantial sleep alterations need to be in order to affect the pain system and lead to a coupling of both functions, the present study aimed at providing sufficient variance for co-variance analyses by examining a sample consisting of both healthy subjects and chronic pain patients.


          A sample of 20 chronic musculoskeletal pain patients and 20 healthy controls was examined. This sample was assumed to show high inter-individual variability in sleep and pain, as pain patients frequently report sleep disturbances, whereas healthy subjects were required to be pain-free and normal sleepers. Sleep of two non-consecutive nights was measured using portable polysomnography and questionnaires. Experimental pain parameters (pressure pain thresholds (PPT), temporal summation of pain (TSP), conditioned pain modulation (CPM)) and situational pain catastrophizing (SCQ) were assessed in laboratory sessions before and after sleep. Pain patients’ clinical pain was assessed via questionnaire.


          As expected, both groups differed in several sleep parameters (reduced total sleep time and sleep efficiency, more time awake after sleep onset, lower subjective sleep quality in the patients) and in a few pain parameters (lower PPTs in the patients). In contrast, no differences were found in TSP, CPM, and SCQ. Contrary to our expectations, regression analyses indicated no prediction of overnight pain changes by sleep parameters.


          Since sleep parameters were hardly apt to predict overnight pain changes, this leaves the association of both systems mainly unproven when using between-subject variance for verification.

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          Most cited references 36

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          Sleep deprivation and pain perception.

          Chronically painful conditions are frequently associated with sleep disturbances, i.e. changes in sleep continuity and sleep architecture as well as increased sleepiness during daytime. A new hypothesis, which has attracted more and more attention, is that disturbances of sleep cause or modulate acute and chronic pain. Since it is well-known that pain disturbs sleep the relationship between the two has since recently been seen as reciprocal. To fathom the causal direction from sleep to pain we have reviewed experimental human and animal studies on the effects of sleep deprivation on pain processing. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can interfere with analgesic treatments involving opioidergic and serotoninergic mechanisms of action. The still existing inconsistency of the human data and the exclusive focus on REM sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity.
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            Self-reported sleep and mood disturbance in chronic pain patients.

            To evaluate the prevalence of self-reported sleep disturbance and its relationship to mood disturbance in chronic pain patients. Survey of patients referred to a multidisciplinary outpatient pain clinic. The sample consisted of 105 consecutive patients (59 men and 46 women), with an average age of 41.5 (SD +/-13.4) years. Self-report measures of sleep disturbance and visual analog scales of mood disturbance (anxiety and depression) and pain experience (intensity and unpleasantness). Patients were grouped according to whether they considered themselves "poor" (n = 68) or "good" (n = 37) sleepers. Poor sleepers reported more difficulties initiating and maintaining sleep and greater pain intensity and pain unpleasantness than did good sleepers. The two groups did not differ on measures of depressive or anxious mood. The results suggest that sleep disturbance is a prevalent complaint in chronic pain patients, but it is not always associated with an underlying mood disturbance.
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              Enhanced temporal summation of second pain and its central modulation in fibromyalgia patients.

              We have previously shown that fibromyalgia (FMS) patients have enhanced temporal summation (windup) and prolonged decay of heat-induced second pain in comparison to control subjects, consistent with central sensitization. It has been hypothesized that sensory abnormalities of FMS patients are related to deficient pain modulatory mechanisms. Therefore, we conducted several analyses to further characterize enhanced windup in FMS patients and to determine whether it can be centrally modulated by placebo, naloxone, or fentanyl. Pre-drug baseline ratings of FMS and normal control (NC) groups were compared with determine whether FMS had higher pain sensitivity in response to several types of thermal tests used to predominantly activate A-delta heat, C heat, or cold nociceptors. Our results confirmed and extended our earlier study in showing that FMS patients had larger magnitudes of heat tap as well as cold tap-induced windup when compared with age- and sex-matched NC subjects. The groups differed less in their ratings of sensory tests that rely predominantly on A-delta-nociceptive afferent input. Heat and cold-induced windup were attenuated by saline placebo injections and by fentanyl (0.75 and 1.5 microg/kg). However, naloxone injection had the same magnitudes of effect on first or second pain as that produced by placebo injection. Hypoalgesic effects of saline placebo and fentanyl on windup were at least as large in FMS as compared to NC subjects and therefore do not support the hypothesis that pain modulatory mechanisms are deficient in FMS. To the extent that temporal summation of second pain (windup) contributes to processes underlying hyperalgesia and persistent pain states, these results indirectly suggest that these processes can be centrally modulated in FMS patients by endogenous and exogenous analgesic manipulations. Copyright 2002 International Association for the Study of Pain

                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                19 December 2019
                : 12
                : 3381-3393
                [1 ]Physiological Psychology, University of Bamberg , Bamberg, Germany
                [2 ]Department of Anesthesiology and Pain Therapy, Kantonsspital Baden , Baden, Switzerland
                [3 ]Center for Pain Medicine, Regiomed Klinikum Lichtenfels , Lichtenfels, Germany
                [4 ]Department of Anesthesiology and Pain Therapy, Sozialstiftung Bamberg , Bamberg, Germany
                Author notes
                Correspondence: Cindy Stroemel-Scheder Department of Physiological Psychology, University of Bamberg , Markusplatz 3, Bamberg96045, GermanyTel +49 951 863 2056 Email cindy.stroemel@uni-bamberg.de
                © 2019 Stroemel-Scheder et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 1, Tables: 5, References: 48, Pages: 13
                This study was financially supported by Dr. Robert-Pfleger-Stiftung Bamberg.
                Original Research

                Anesthesiology & Pain management

                clinical pain, sleep, experimental pain, chronic pain


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