Can Pain Neuroscience Education Improve Endogenous Pain Inhibition?

Many chronic musculoskeletal pain disorders are characterized by the presence of central sensitization, which implies that the central nervous system is in a hypersensitive state in those who suffer from these disorders. Sensitivity to pain results from the outcome of the battle between pathways which facilitate the passage of nociceptive information, and pathways which suppress nociceptive messages [1]. The important ability of our body to modulate pain, is termed endogenous pain modulation, and is affected in those who suffer from chronic musculoskeletal pain and central sensitization [2,3]. Specifically endogenous pain facilitation is enhanced, while endogenous pain inhibition is impaired, and this misbalance may result in a potentiation of the perceived pain. If sensitization of the central nervous system is in some part responsible for the persistent chronic pain complaints experienced by these patients, then treatment strategies should perhaps focus on trying to “desensitize” the central nervous system and improving endogenous pain modulation.

One of the strategies which can be used to “desensitize” the central nervous system is the use of pain neuroscience education. Pain neuroscience education relies on deep learning, aimed at reconceptualising pain, based on the assumption that appropriate cognitive and behavioural responses will follow when pain is appraised as less dangerous [4]. Although most of the educational models have limited efficacy in increasing pain and disability in patients with chronic musculoskeletal pain, and may even increase patients’ fears [5], it seems that education concerning pain neuroscience in one of the strategies that can be used to improve the balance between endogenous pain facilitation and inhibition.

As descending facilitatory pathways depart from brain areas that are involved in the regulation of cognitive and emotional reactions, negative thoughts, emotions and behaviors regarding pain can modulate activity in the pathways facilitating nociception, and thus contribute to the persistence of pain and presence of central sensitization [6]. Previous studies have shown that pain neuroscience education can be used to alter how patients think, feel and behave when they are suffering pain (reviewed in [5]). These studies have also shown that pain neuroscience education reduces self-reported pain levels and improves pain-free movement performance in chronic musculoskeletal pain disorders such as chronic whiplash, chronic low back pain and chronic fatigue syndrome. In a recent double blind randomized controlled trial we examined the efficacy of pain neuroscience education in fibromyalgia, by randomly allocating 30 patients to either pain neuroscience education or activity management education [7]. Each patient received individual education during a one on-one session, a written brochure to read at home, and a session over the telephone. Fibromyalgia patients were able to comprehend the complex material about the neurophysiology of pain and were able to reproduce the content up to 3 months after the initial session as was expressed by the Neurophysiology of Pain Test scores and resulted in a large effect size. In the short-term fibromyalgia patients worried less about their pain complaints after they received this type of education. In the long term, improvements in vitality, physical functioning, mental health and general health perceptions were established using the Medical Outcomes Short Form 36 Health Status Survey. A small effect size was established for increases in vitality and physical functioning, while large effect sizes were established regarding improved mental health and general health perceptions.

In a case study Moseley has shown that brain activity in cortical regions involved in pain processing reduced after pain neuroscience education [8]. Although these results need to be confirmed in a larger sample, the question arises if pain neuroscience education is capable of improving descending nociceptive processing orchestrated by the brain? The results of our recent study suggest that this is in fact the case, as pain neuroscience education was able to improve endogenous pain inhibition in Fibromyalgia [7]. Using a spatial summation procedure which consisted of gradual immersion of the dominant arm into noxious hot water (46°C) we examined the influence of pain neuroscience education on the efficacy of endogenous pain inhibition in fibromyalgia. In healthy pain-free people, the perceived pain during this procedure is not related to the surface area which is stimulated, as the inhibitory efferents efficiently counterbalance the facilitatory afferents, while in fibromyalgia is has been shown that the pain inhibitory systems are not optimally recruited [9,10]. In our study, fibromyalgia patients from both educational groups showed similar results at the start of the study and one week after they received the educational intervention. But changes in the pain inhibitory systems could be detected after 3 months [7]. The fibromyalgia patients which received pain neuroscience education showed lower pain scores during the spatial summation procedure then patients who received activity management education. Furthermore the pain scores form the fibromyalgia patients which received the control intervention consisting of activity management tended to augment as the immersed surface increased, which indicates a deficit of the endogenous pain inhibitory systems, while in the pain neuroscience group pain perception was no longer related to the stimulated surface area after 3 months, indicating an efficient activation of the endogenous pain inhibitory systems. The fact that these observations were not present one week after the educational intervention was finalized but were established during the follow-up could indicate that changes of the central nervous in those who experience chronic musculoskeletal pain and central sensitization need time to occur. Thus when examining the influence of an intervention on descending nociceptive processing, a sufficient long follow-up is required. The observations made by Mosley, together with the current findings regarding the positive effects on descending nociceptive inhibition, suggests that neuroscience education has an influence on central pain processing. Although more research is necessary to provide us with insights on how pain neuroscience education exactly influences central pain processing, this type of education has shown to be a useful component in the treatment of various chronic musculoskeletal pain disorders and is easily implemented into the rehabilitation programs used by clinicians.

And I can hear you thinking; “Ok, but how should I exactly apply pain neuroscience education?”. Well, pain neuroscience education can take place in a number of ways. It can be provided to subjects during individual or group session(s), in a written or oral form. We know that relying on written education regarding pain neuroscience is insufficient [11]. Oral education has been shown to be more effective [12]. Our recent study showed that the combination of oral education and written information to read at home in addition to a one-on-one session is a valuable part of pain neuroscience education, as patients their knowledge regarding  pain neurophysiology further increased after the initial session by afterwards reading the written information at home and by implementing the new insights into their daily life [7]. We feel that providing written information is especially important for those patients with memory or concentration problems, as they get the chance to read the information which was provided during the oral session once again after the session. In our study patients were encouraged to apply what was learned during therapy in their daily life, and patients had the chance to discuss questions and experiences with the therapist. The best effects of pain neuroscience education are achieved during an individual session [12]. In this way the therapist can adapt the content of the education to the individual illness perceptions and emotions of the patient. Although education can consist of one or more sessions with a duration of 30 minutes to 4 hours, recent studies increasingly use one or two sessions with a duration between 30 and 45 minutes [5,12]. These shorter sessions allow an easy implementation of pain neuroscience education into the clinical practice, where it can be combined with other therapeutic strategies.

Those who want more information about the content of pain neuroscience education can consult the book “Explain Pain” by David Butler and Lorimer Moseley [13], which is available in different languages. Guidelines for giving pain neuroscience education have been published by the Pain In Motion research group [12].

About Jessica Van Oosterwijck

Jessica Van OosterwijckJessica loves to travel not only foreign countries but also her own country (Belgium). In 2006 she obtained her degree as a physiotherapist at the University College based in Antwerp (Belgium). She continued her studies at the Vrije Univeristeit Brussel in order to obtain a Phd in Rehabilitation Sciences and Physiotherapy. During her years as a Phd student she got to know all about central sensitization, chronic pain and what the Belgian capital city, Brussels, has to offer. Is 2011 she went on to discover the city of Ghent where she works at present as a postdoctoral fellow of Ghent University (Belgium). She is also a member of the Pain In Motion research group. Her main research topics of interest are central nervous system mechanisms of pain and fatigue, exercise pathophysiology, pain-motor interactions, and rehabilitation in chronic pain populations like those suffering from chronic fatigue syndrome, fibromyalgia, chronic whiplash associated disorders, chronic and recurrent low back pain, osteoarthritis and cancer survivors. When she is not studying chronic pain mechanisms and interventions you can usually find her in a bar exploring the complex tastes of Belgian Beers.

References

[1] Millan MJ. Descending control of pain. Prog Neurobiol 2002;66:355-474.

[2] Nijs J, Kosek E, Van Oosterwijck J, & Meeus M (2012). Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise? Pain Physician, 15 (3 Suppl) PMID: 22786458

[3] Yunus MB (2007). Fibromyalgia and overlapping disorders: the unifying concept of central sensitivity syndromes. Sem Arthritis Rheumatol, 36 (6), 339-56 PMID: 17350675

[4] Moseley GL. Joining forces e combining cognition-targeted motor control training with group or individual pain physiology education: a successful treatment for chronic low back pain. J Man Manip Ther 2003a;11:88e94.

[5] Louw A, Diener I, Butler DS, & Puentedura EJ (2011). The effect of neuroscience education on pain, disability, anxiety, and stress in chronic musculoskeletal pain. Arch Phys Med Rehabil., 92 (12), 2041-56 PMID: 22133255

[6] Zusman M. Forebrain-mediated sensitization of central pain pathways: “non-specific” pain and a new image for MT. Man Ther 2002;7:80-88.

[7] Van Oosterwijck J, Meeus M, Paul L, De Schryver M, Pascal A, Lambrecht L, & Nijs J (2013). Pain physiology education improves health status and endogenous pain inhibition in fibromyalgia: a double-blind randomized controlled trial. Clin J Pain, 29 (10), 873-82 PMID: 23370076

[8] Moseley GL (2005). Widespread brain activity during an abdominal task markedly reduced after pain physiology education: fMRI evaluation of a single patient with chronic low back pain. Aust J Physiother, 51 (1), 49-52 PMID: 15748125

[9] Julien N, Goffaux P, Arsenault P, et al. Widespread pain in fibromyalgia is related to a deficit of endogenous pain inhibition. Pain 2005;114:295-302.

[10] de Souza JB, Potvin S, Goffaux P, Charest J, Marchand S. The deficit of pain inhibition in fibromyalgia is more pronounced in patients with comorbid depressive symptoms. Clin J Pain 2009;25:123-127.

[11] van Ittersum MW, van Wilgen CP, Groothoff JW, & van der Schans CP (2011). Is appreciation of written education about pain neurophysiology related to changes in illness perceptions and health status in patients with fibromyalgia? Patient Educ Couns, 85 (2), 269-74 PMID: 20880654

[12] Nijs J, Paul van Wilgen C, Van Oosterwijck J, van Ittersum M, & Meeus M (2011). How to explain central sensitization to patients with ‘unexplained’ chronic musculoskeletal pain: practice guidelines. Man Ther, 16 (5), 413-8 PMID: 21632273

[13] Butler D, Moseley GL. Explain Pain. Adelaide: NOI Group Publishing; 2003.

Comments

  1. Great summary article and great piece of research. Thank you for the post.

  2. John Quintner says:

    Hi Jessica. May I be so rude as to make some comments on your opening sentences?

    1. In my opinion, your first sentence employs a circular argument. Can you spot it?

    Here is a clue. Yunus employs circular arguments in support of his concept of “central sensitivity syndromes (CSS)”. For example, he states: “Central and common to CSS are CS.” [Yunus MB. The prevalence of fibromyalgia in other chronic pain conditions. Pain Research and Treatment 2012; (2012): 584573. Epub 2011 Nov 17.]

    2. Can you please explain what you mean by the phrase “sensitivity to pain”?

    3. Neural pathways can appear to compete with each other at the electro-physiological level but do they really “go into battle”?

  3. Hi John,
    Thanks for your questions. I guess I had my ‘clinician hat’ on when I was writing this article, but then again I really feel this type of research is meant to be read by clinicians in the first place, as we hope that will see the benefits pain neuroscience education and implement it into their evidence based treatment programs for chronic pain patients. On the other hand we often share these type of summary blogs through social media (such as BIM, http://www.paininmotion.be) to inform patients about the research we are conducting and the related findings. Although researchers and clinicians usually know what central sensitization entails, many patients have never hear about the term central sensitization. Therefore I wanted to briefly and in a simple way clarify that the term central sensitization in the first sentence, rather than argue it. A more biological explanation of central sensitization is that central pain processing pathways localized in the spinal cord and the brain sensitize, which entails altered sensory processing in the brain, long-term potentiation of brain synapses, impaired functioning of top-down anti-nociceptive mechanisms, and (over)activation of top-down pain facilatory pathways which augment nociceptive transmission. One of aspects we explain to our patients during the pain neuroscience education is that when noxious external stimuli are applied to our body or when there is tissue damage, this does not automatically result in a pain sensation. Nociceptive information processing and consequent pain perception is subject to significant pro- and anti-nociceptive modulations. An altered interaction of these pro- and anti-nociceptive mechanisms will contribute to chronic pain states. For instance dysfunctions of descending modulatory pathways will resulting in reduced inhibition/enhanced facilitation, which in turn can result in an enhanced pain sensation. Although there is no real physiological battle between the inhibitory and faciltatory pathways, we use such expressions to explain how these mechanisms work or fail and the related outcome to our patients during the pain neuroscience education. Those who want to know more about the endogenous pro- and anti-nociceptive modulatory mechanisms I would like to refer to the article of Bingel and Tracey (Physiology 2008;23:371-380).

  4. John Quintner says:

    Jessica, thanks for your prompt response. This raises yet another issue – “central pain processing pathways” do not exist.

    We all have to be very careful with our use of language, both in communications that take place between clinicians, and those between clinicians and their patients.

    If it is any consolation, circular arguments abound in the Pain Medicine literature. The rules of logical argument sometimes go unheeded.

  5. John Quintner says:

    Jessica, I know that the accusation of being pedantic may be leveled at me. But conceptual confusion is reflected by our use of such terms as “pain fibres,” “pain pathways, “pain processing,” “pain sensitivity,” and “pain centres”. The ridiculous “maldynia/eudynia” dichotomy is the most recent example of confused thinking. Finally, in my opinion, the well intentioned attempt to promote chronic pain from symptom to disease status is another example of taxonomic confusion.

    If we are confused in our thinking it comes as no surprise that pain sufferers are in the same boat. I am all for neuroscience education being used as a powerful tool in pain management, but we first need to make sure that we are using language that is unambiguous and scientifically accurate, and that we are not reliant upon circular argument.

  6. Jeff Lee says:

    I read the full text paper this was based on, and the blog is good summary of the main ideas and findings. Like the addition of the practical tips. Cheers

  7. stuart miller says:

    John, from my understanding, there are certain patterns of brain activity that occur prior to insight (Kounios and Beeman 2009). Would it be important to try to work towards setting up an environment conducive to this in neurophysiology education ? – the suggested parameters in the last 2 paragraphs of Jessica’s blog were helpful to me. Creating a state in which people are receptive to information would be important – the challenge I have in education, from my understanding, is that the so-called pain processing networks are also lit up with any salient input that requires attention – when everything is threatening it is hard to process anything. Where do you think a discussion on sensitization should start ? What would be the basic framework to begin a discussion ?- I feel it starts with empathy and a beginner’s mind and hopefully with non-violent communication that doesn’t espouse right or wrong in terms of judgements but what do you feel is important ? Thanks for this site and its insight.

  8. John Quintner says:

    Stuart, I use a simple motif that is applicable to sensitization, whether it be peripheral and/or central. This provides a basic framework for the conversation.

    It features a “conversation” taking place (via signaling molecules) in the periphery between an injured cell, nearby cells, the nerves in the locality, and alerted immuno-competent cells.

    Much the same conversations are also taking place within the central nervous system between the neural and glial elements.

    The various clinical correlates of these conversations can then be outlined and explained.

    This framework was inspired by the work of Polly Matzinger (as an aside, the story of how she was first attracted to immunology is worth a read).

    Does this answer your question?

    Ref: Matzinger P. Tolerance, danger, and the extended family. Ann Rev Immunol 1994;12: 991-1045.

  9. stuart miller says:

    John, thanks for this – very helpful – in the case of persistent pain – do you still start the conversation with an injured cell in every case ? – I will read and try to understand Matzinger’s work. Have you read ‘The Other Brain’ by R Douglas Fields on glial function? I have read some of Freeman’s work – nonlinear dynamics is hard to conceptualize – any help on a beginner’s guide or article ?

  10. John Quintner says:

    Stuart, my response was a guide to explaining sensitization to a person in pain who is seeking an explanation for such complex phenomena as allodynia, hyperalgesia, spread of pain, etc.

    I endorse your recommendations on how to commence a clinical conversation.

    No, I have not read the book you mention. Andrew Koob’s The Root of Thought (2009) provides a readable account of glial function.

    As for non-linear dynamics, I am sure a web search will turn up many suitable articles.

  11. I am interested what others think of this statement: “Well delivered Explain Pain education currently has the best outcomes of any intervention for pain”

    It is mentioned on the NOI website.

  12. I have read this as well. I am curious to see the evidence that has led them to this conclusion.

  13. I’ve asked them for references. They replied with the reference list of the Explain Pain book.
    However is that enough to justify the conclusion?