Sleep and Chronic Pain – Research Update – March 2014

The association between poor sleep and chronic pain is an interesting subject.

For those interested, I previously posted on Sleep and Chronic Pain back in September 2012.

I had the following fantastic article forwarded to me by a colleague, and I thought it apt to provide a research update on this topic.

Finan PH, Goodin BR, Smith MT. The association of sleep and pain: an update and a path forward. J Pain. 2013 Dec;14(12):1539-52.

For those of you just wanting the key abstract info…….

A key trend emerging from population-based longitudinal studies is that sleep impairments reliably predict new incidents and exacerbations of chronic pain.

Microlongitudinal studies employing deep subjective and objective assessments of pain and sleep support the notion that sleep impairments are a stronger, more reliable predictor of pain than pain is of sleep impairments.

Recent experimental studies suggest that sleep disturbance may impair key processes that contribute to the development and maintenance of chronic pain, including endogenous pain inhibition and joint pain.

For those wanting more detail…….

The paper was designated as a “Critical Review”. Its purpose, according to the authors, was to “critically examine the recent prospective and experimental literature (2005-present) in an attempt to update the field on emergent themes pertaining to the directionality and mechanisms of the association of sleep and pain”.

It is a very extensive article that I would encourage you all to read if you can access it. Given the extensive nature of it, I have tried to pull out some of the key conclusions that the authors reached from their synthesis/review of the data. Here we go:

On Sleep Disturbance and Development of Pain:

  • Elevated insomnia symptoms increase the risk of exacerbating existing headache and developing new incident headache.
  • Insomnia symptoms at baseline significantly increased the risk of developing chronic musculoskeletal pain (both widespread and regional).
  • Prospective studies indicate that sleep disturbance:
    • Increases the risk for new-onset cases of chronic pain in pain-free individuals.
    • Worsens the long-term prognosis of existing headache and chronic musculoskeletal pain
    • Influences daily fluctuations in clinical pain.
  • Insomnia symptoms significantly increase the risk of developing future chronic pain disorders in previously pain-free individuals.
  • Existing pain is not a strong predictor of new incident cases of insomnia.
  • Deeper assessments of sleep disturbance tend to suggest that sleep disturbance is a stronger predictor of future pain than pain of sleep disturbance.
  • In a series of analyses involving associations between depression, fatigue, sleep, and pain, the best-fitting structural equation model included a path in which sleep predicted pain.

On Quality/Good Sleep. It has been shown to:

  • Predict chronic widespread pain symptom resolution over 15 months.
  • Improve the long-term prognosis of individuals with tension-type headache, migraine, and chronic musculo-skeletal pain.

On Poor Sleep and Increased Pain Sensitivity:

  • Tentative support for the notion that sleep deprivation increases pain sensitivity.
    • Healthy subjects report spontaneous bodily pain after 2 nights of partial (4 hours) sleep deprivation, and this effect increases as the number of nights of partial sleep deprivation increases.
    • Partial sleep deprivation may produce hyperalgesia.
    • Continuous 4-hour sleep restriction for only 1 night resulted in elevations in self-reported pain, fatigue, depression, and anxiety in rheumatoid arthritis patients but not controls. In addition:
      • Disease-specific measures of pain severity and painful joint counts were elevated in the rheumatoid arthritis patients following partial sleep deprivation.
      • Partial sleep deprivation altered both psychosocial symptoms and disease-specific markers of rheumatoid arthritis.

On Impact of Sleep Disturbance on Pain Inhibition:

  • Conditioned Pain Modulation (CPM) is a measure of endogenous opioid-mediated pain inhibition. Reduced CPM efficacy results in impaired pain inhibition.
    • Sleep disturbance and/or poor sleep efficiency were significantly associated with diminished CPM efficacy in Temporomandibular disorder, fibromyalgia and rheumatoid arthritis patients (relative to healthy controls).
  • Research suggests that total sleep deprivation selectively augments the activity of nociceptive pathways without altering the perception of non-nociceptive somatosensory stimuli.
    • Patients have demonstrated reductions in heat pain threshold following total sleep deprivation, whereas detection thresholds (e.g. touch) remained unchanged.
  • Sleep deprivation appears to dysregulate endogenous opioid systems. This may increase vulnerability to central sensitization and persistent pain.

Other Conclusions:

  • It remains to be determined if the association of sleep and pain varies across different chronic pain disorders. The present review synthesizes findings from a wide range of disorders, including neuropathic, musculoskeletal, headache/migraine, and idiopathic pain disorders.
  • Efforts to prevent and treat chronic pain may be well served to target sleep disturbance as a point of primary prevention and intervention.
  • The biopsychosocial model provides an excellent framework through which to integrate these and other potential mechanisms of the association of sleep and pain, such as inflammation and neuroendocrine factors.
  • The past decade of research has allowed us to move past the question of whether sleep and pain are related.

Fascinating stuff!

Just before I throw in my musings on the above I thought I would highlight a couple of other recent sleep related studies I found when further looking into this research update.

Haack et al (2007) conducted a study to investigate the effects of reduced sleep duration on peripherally circulating inflammatory mediators (e.g. plasma interleukin levels). The study involved 18 volunteers who were randomly assigned to either 12 days of sleeping 8 hours per night or 4 hours per night. The patients sleeping 4 hours per night demonstrated elevated Interleukin levels versus the 8 hour per night sleepers.  Key conclusions being:

  • Insufficient sleep quantity may facilitate and/or exacerbate pain through elevations of interleukin.
  • In disorders where sleep disturbances are common, insufficient sleep quantity itself may establish and maintain its co-occurrence with pain and increased inflammation.

Tang et al (2012) aimed to compare the characteristics of patients who have pain-related insomnia with those reporting primary insomnia and to identify psychological factors that predict pain-related insomnia. This was due to the thoughts/assumptions that the 2 types of insomnia share the same presentation and maintaining mechanisms. The authors  had chronic pain patients with concomitant insomnia complete a selection of questionnaires that measured sleep patterns, psychological attributes, and cognitive-behavioral processes associated with the persistence of insomnia. Their responses were compared with those of primary insomnia patients. Interestingly the results showed that the Pain-related Insomnia Group did not differ from the Primary Insomnia Group in their pattern and severity of sleep disturbance. The only one area of difference was that the Primary Insomnia Group was distinguishable from the Pain-related Insomnia Group by their greater tendency to worry. The conclusions reached by the study were:

  • There are more similarities than differences between the 2 types of insomnia. Besides pain, mood, and presleep, thought processes also seem to have a role in the manifestation of pain-related insomnia.
  • It is suggested that hybrid treatments that seek to simultaneously address factors across these domains may represent more effective treatments than 1-dimensional interventions.

A study by Haack et al (2012) aimed to assess the role of chronic sleep disturbances in pain processing.  The authors compared both participants with insomnia and healthy controls. Results showed:

  • Primary insomnia subjects reported experiencing spontaneous pain on twice as many days as healthy controls.
  • Primary insomnia subjects had lower pain thresholds than healthy controls.
  • Unexpectedly, pain facilitation, as assessed with temporal summation of pain responses, was reduced in primary insomnia compared to healthy controls.
  • Pain inhibition, as assessed with the diffuse noxious inhibitory control paradigm (DNIC), was attenuated in insomnia subjects when compared to controls.
  • Conclusions:
    • The authors proposed that pain-inhibitory circuits in patients with insomnia are in a “state of constant activation to compensate for ongoing subclinical pain, and that this constant activation ultimately may result in a ceiling effect of pain-inhibitory efforts”.

Mullington et al (2010) investigated the research relating to sleep loss and inflammation. The abstract from their article summarised the findings well:

Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss. Elevations in these mediators have been found to occur in healthy, rigorously screened individuals undergoing experimental vigils of more than 24h, and have also been seen in response to various durations of sleep restricted to between 25 and 50% of a normal 8h sleep amount.

While these altered profiles represent small changes, such sub-clinical shifts in basal inflammatory cytokines are known to be associated with the future development of metabolic syndrome disease in healthy, asymptomatic individuals.

Although the mechanism of this altered inflammatory status in humans undergoing experimental sleep loss is unknown, it is likely that autonomic activation and metabolic changes play key roles.

My thoughts?

So I hope we can all see how critical sleep is, not only in the treatment of pain, but also the prevention of pain. Poor sleep has the potential to interfere with descending pain inhibitory pathways, increase levels of biological markers that contribute to inflammation, and has a direct effect on creating/causing pain in previously pain free individuals. It also has been shown to be predictive of future pain, and development of pain states/conditions.

So sleep quality should be something that we routinely screen our patients for. Whilst I am not saying that we screen all of our patients for sleep issues it would certainly seem imperative to do so for those patients who are:

  • Experiencing recurrent-episodic problems where poor sleep might be a contributing factor.
  • Not getting better!
  • Getting worse!

How can we assess sleep quality?

  1. Ask the patient directly
    1. How many hours of sleep do they get a night?
    2. Do they feel like they get a restful/restorative amount of sleep?
    3. Does a night(s) of poor sleep seem to increase their pain?
  2. Screen them:
    1. Pittsburgh Sleep Quality Index is a nice starting point. Plenty of other information is also available through this link to the University of Pittsburgh Sleep Medicine Unit.

How it can be treated is another post on its own, but good starting points might be:

  • Encouraging regular exercise.
  • Meditation/mindfulness.
  • Finding time to relax before bed.
  • Medication via their General Practitioner or Pharmacist.
  • Promoting good sleep hygiene e.g. getting to bed earlier!

Thanks for reading.


Finan PH, Goodin BR, Smith MT. The association of sleep and pain: an update and a path forward. J Pain. 2013 Dec;14(12):1539-52.

Haack M, Scott-Sutherland J, Santangelo G, Simpson NS, Sethna N, Mullington JM. Pain sensitivity and modulation in primary insomnia. Eur J Pain. 2012 Apr;16(4):522-33.

Haack M, Sanchez E, Mullington JM. Elevated inflammatory markers in response to prolonged sleep restriction are associated with increased pain experience in healthy volunteers. Sleep. 2007 Sep;30(9):1145-52.

Mullington JM, Simpson NS, Meier-Ewert HK, Haack M. Sleep loss and inflammation. Best Pract Res Clin Endocrinol Metab. 2010 Oct;24(5):775-84.

Tang NK, Goodchild CE, Hester J, Salkovskis PM. Pain-related insomnia versus primary insomnia: a comparison study of sleep pattern, psychological characteristics, and cognitive-behavioral processes. Clin J Pain. 2012 Jun;28(5):428-36.

About the Author:

Mark is a Specialist Musculoskeletal Physiotherapist who consults at both Insight Physiotherapy and Pain Options, in Perth, Western Australia. He specialises in the assessment and management of persistent/chronic musculoskeletal pain. In addition to his clinical role he maintains regular involvement in education of the profession having held a Teaching Fellow position at the University of Western Australia for 10 years and regularly presenting at courses and seminars through the Australian Physiotherapy Association and private education sector. Mark is also a Facilitator for the Australian College of Physiotherapists Specialisation Training Program and a Sessional Academic at Curtin University. The views expressed on this blog are his own.

3 Comments on "Sleep and Chronic Pain – Research Update – March 2014"

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  1. Ian Rubin says:

    Thanks Mark for a well researched/sourced article on an important topic. In my work as a wellness coach I always appreciate a greater understanding of how the body works so I can empower my clients to greater health. If my approach appeals to you and I can be of any assistance, please let me know. Or if you just want to connect I’m happy to make time to chat via skype/email.

    Your friend in wellness,

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