Neuroscience And Skilled Patient-Communication Are Essential When Dealing With Patients Suffering From Complex Pain Conditions
Patients with complex pain conditions, such as fibromyalgia, are now recognized as living with a chronic disease, according to the WHO (Nicholas M, 2019). While this is a huge step in terms of social recognition of the existence of pain in the absence of pathology, there’s still no cure or superior treatments available. Yet, it has become increasingly clear that self-management is essential and that patient education plays a pivotal role in self-management.
”Pain education, or PNE, has shown us a way forward in self-management of chronic pain. The next step is to embrace the narrative as a therapeutic intervention”
For more than 15 years patients have been educated to understand their pain as a result of hypersensitivity and/or reduced inhibition in the nervous system. However, in the same period only a minority of universities, colleges etc. world-wide meet the international recommendations for professional education on pain and neuroscience*. Consequently, many – even newly educated – healthcare professionals rely on their knowledge about anatomy and biomechanics to understand pain in the musculoskeletal system, despite obvious flaws in this theory (Palsson TS et al. 2019).
”Theories based on anatomy and biomechanics are inherently in conflict with a scientifically informed understanding of pain!”
As a skeptic, I’m comfortable with the concept of all theories being flawed (or ‘wrong’) and at the same time necessary for the clinician to make sense of the information (data) we get from our patients. Without theories, we would not be able to form a structure and make sense of experiences the patient shares. For the purpose of this blog, I choose to define a theory as any explanation that guide clinicians in their work (e.g. ‘hypersensitivity of the nervous system’ or ‘central sensitization’). Many theories are based on basic science (e.g. anatomy, physiology, and biochemistry) while others are not. My academic and research training has focussed on basic science, so this is where I will take my starting point, although I openly admit that my clinical aim is always to improve the disabilities and symptoms of the patient – not the underlying (theoretical) mechanism.
Neuroscience is to pain what biomechanics is to movement – not sufficient but essential and complex.
Traditionally, it was assumed that pain [insert your favourite body region] was related to structures in the anatomy, and brilliant thinkers such as Shirley Sarhman, Paul Hodges and Mark Laslett/Tom Petersen have provided (overlapping) theories that try to explain how ‘impaired’ biomechanics or anatomy can lead to painful experiences (Karayannis N et al. 2012).
Furthermore, these theories postulate a linear relationship between impairment-correction and pain-reduction, in other words; when impairments are corrected, the patient experiences pain relief. To many people (patients and professionals alike) this leads to the unfortunate and incorrect conclusion that if the patient experiences pain relief, then the theory must be correct. The unfortunate bit of this conclusion is that both parties tend to stick to such theories even when they are unlikely to help, and the theory is incorrect in assuming that if pain relief is observed after applying the theory, then they are causally related. In more scientific terms this has been called a correlation. A well-known example of this misunderstanding that degeneration of the spine could explain pain, while more recent evidence clearly shows this is not the case (see e.g. Brinjikji W et al. 2015) and a counter-recommendation that imaging should not be performed unless serious pathology is expected (Lin I et al. 2019).
However, the theories – flawed as they are – have provided many patients with both a novel understanding of their body and how it was related to pain relief. What has become increasingly clear over the last decades is that theories based on biomechanics or anatomy anywhere in the body cannot explain how movement causes pain, rather a neuroscience approach is necessary (Brumagne S et al. 2019).
The simplest version of the problem with anatomy/biomechanics as a model for pain seems to be that the link between consciousness and anatomy/biomechanics remains unexplored. The neuroscience approach, on the other hand, which tries to link the experience of pain to the transmission of signals from the body – including the brain – via neurons and non-neuronal cells, is a very well developed science, and even though our understanding of what consciousness is, remains theoretical, consensus is that signals in the body are the most likely measurable link between the objective (measurable), 3rdperson perspective and the experience, or 1stperson perspective, of pain.
“Neurobiology is not a core skill in most educations, but anatomy and biomechanics still is. This could be the reason for oversimplification of pain theories.”
The most famous neuroscience-based theory of how signals in the body relate to pain is arguably the Gate Control theory of Pain by Pat Wall and Ron Melzack, but there is a plethora of theories concerned with specific cell types (e.g. glia), neurobiological mechanisms (e.g. central sensitization), brain activity (e.g. Default Mode Network) and philosophy/cognitive neuroscience (e.g. predictive coding). Such theories are based on ‘sound, basic science’ and can be conceptualized as scaffolding systems on which clinicians can help patients understand their signs and symptoms, including pain, fear, behaviour, etc. Neither theory should be considered universal or ‘best’ for all patients, rather, a skilled clinician should understand the science behind and – perhaps most importantly – the boundaries of each theory.
How To Choose A Theory?
First of all, the theory must provide a good fit with the history of the patient. Luckily, most theories are adaptable and some even contain categories, which are open to interpretation and/or unable to be falsified clinically. E.g the theories of ‘overuse’ (biomechanics) and ‘central sensitization syndrome’ (neuroscience) are both based on clinical reasoning and could easily be applied to the same patient. They could even guide the patient to the same behaviour/action, albeit with different explanations:
|Overuse||Specific tissues are over-loaded (damaged) and pain is the response to an inflammatory response||graded exposure, education on [chosen theory]||Physical stress theory: Mueller MJ and Maluf KS, 2002|
|Central Sensitization Syndrome||The nervous system is overactive and the patient needs to calm it down||graded exposure, education on [chosen theory]||Nijs J et al. 2016|
To make things even more complicated, Artus and colleagues found that studies on the treatment effect in patients with non-specific low-back pain plateaus after 6-12 weeks in most people, indicating that neither of the existing treatments is superior nor specific.
So, when no one theory seems to explain everything, how do you choose? According to Sackett et al. (1996), we need to infer to best practice based on best available:
- basic and clinical science
However, since this is no guarantee for success it is insufficient to hope for improvement. Rather good, clinical practice implies the use of structured, patient-specific / functional and preferably validated, measurement tools to objectify when you’re wrong. In other words, once you have decided on an appropriate theory you should be able to predict a time-restricted and patient-specific outcome (i.e. a prognosis). These should be constructed in agreement with the beliefs, expectations, and priorities of the patient, and be specific and valid enough that improvements in your measurements reflect an improvement from the patient’s perspective. Since no causation can be established, relevant and consistent improvements can be considered sufficient to continue along with the same plan.
Unlike in the adventures of Sherlock Holmes or in matters of life-and-death, there is no binary (guilty/innocent or yes/no) answers when dealing with humans suffering from complex, non-specific pain. Thus, as clinicians, we must choose wisely and continuously monitor if the theory and accompanying interventions are benefitting the patient in ways that are meaningful to them.
Consequently, discarding a management plan based on the best available evidence can be the right choice if it leads to no change (or worsening). For obvious reasons, this necessitates a close and trustful collaboration between the patient and the practitioner.
How To Update Your Knowledge Of Science Without Becoming An Academic
As a clinician, you need clinical skills, such as communication skills, critical thinking/clinical reasoning and the ability to spot serious pathology. Ideally, you would also have to spend a few hundred hours studying aspects of neuroscience and philosophy. But chances are, the only basic science you’ve ever spend this long learning is anatomy and biomechanics. Consequently, it is very likely that you are strongly biased towards thinking that when it hurts during movement, movement is a likely cause or trigger of the pain. In other words, since most educations do not provide the knowledge necessary for complex reasoning based on neuroscience most clinicians still use anatomy and biomechanics to explain pain.
But answer this; how – if not via the neurons – should movement hurt?
To my knowledge, there is not a single theory that explains how movement generates consciousness and therefore also pain. The bias in my thinking is that I perceive pain as something we experience and not causally related to signaling in any part of our nervous system (rather they are correlated, and in the case of acute pain, this correlation is so strong that we perceive them as unified).
Coming back to the topic of this section; how to upgrade your knowledge without doing a university-based, post-graduate program? For most clinicians, the solution is weekend courses, in which they get in-depth knowledge about contemporary concepts of how to manage pain. Comparing these to international standards (e.g. IASP or EFIC curricula) clearly shows that there’s a bias towards some areas (e.g. patient education) and neglect of others (e.g. special groups, basic science and xxx). However, free information is available online and online educational initiatives are currently being developed by EFIC and IASP. I hope that, within the next few years, all aspects of the curricula will be covered and freely available. Furthermore, clinical exams – such as the EDPP – are already available to clinicians from all over the globe, providing a ‘peer-reviewed’ certification of the clinical skills.
If you prefer the lecture/classroom teaching style to online learning, or you just don’t want to wait, you can use the curricula most relevant for you to structure your own ‘port-folio’. I recommend looking for courses where the instructors themselves have qualifications within pain science (e.g. MSc’s in Pain or EDPx exams).
This was originally posted on The MTDC Blog. You can click here to read more blogs from them.
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Nicholas M, Vlaeyen JWS, Rief W, et al. The IASP classification of chronic pain for ICD-11.PAIN. 2019;160(1):28-37. doi:10.1097/j.pain.0000000000001390.
Palsson TS, Gibson W, Darlow B, Bunzli S, Lehman G, Rabey M, Moloney N, Vaegter HB, Bagg MK, Travers M. Changing the Narrative in Diagnosis and Management of Pain in the Sacroiliac Joint Area, Phys Ther. 2019 Jul 29.
Karayannis NV, Jull GA, Hodges PW. Physiotherapy movement based classification approaches to low back pain: comparison of subgroups through review and developer/expert survey. BMC Musculoskelet Disord. 2012;13:24. doi:10.1186/1471-2474-13-24.
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Brinjikji W, Luetmer PH, Comstock B, et al. Systematic Literature Review of Imaging Features of Spinal Degeneration in Asymptomatic Populations. AJNR Am J Neuroradiol. 2015;36(4):811-816. doi:10.3174/ajnr.A4173.
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Nijs J, Goubert D, Ickmans K. Recognition and Treatment of Central Sensitization in Chronic Pain Patients: Not Limited to Specialized Care. J Orthop Sports Phys Ther. 2016;46(12):1024-1028. doi:10.2519/jospt.2016.0612.
Artus M, van der Windt D, Jordan KP, Croft PR. The clinical course of low back pain: a meta-analysis comparing outcomes in randomised clinical trials (RCTs) and observational studies. BMC Musculoskelet Disord. 2014;15(1):68. doi:10.1186/1471-2474-15-68.
Artus M, van der Windt DA, Jordan KP, Hay EM. Low back pain symptoms show a similar pattern of improvement following a wide range of primary care treatments: a systematic review of randomized clinical trials. Rheumatology. 2010;49(12):2346-2356. doi:10.1093/rheumatology/keq245.
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