Pain Neuroscience Education (PNE)

Original Editor - David Greaves, Lynette Fox, and Katie White as part of the Nottingham University Spinal Rehabilitation Project

Top Contributors -  
Page Owner - Ina Diener as part of the One Page Project

Introduction[edit | edit source]

Low back pain (LBP) is currently considered to be the most common cause of disability and time off work in the over 45 age group, with it being reported that 84% people will experience LBP at some point during their life.[1] Whilst LBP is generally considered a self-limiting condition it can have severe implications to the patient’s psychological and physical health. Results from a UK survey, analysing the consultation prevalence for LBP showed that 417 per 10 000 registered patients sought medical help for their LBP, with the highest numbers being seen in the 45- 64 age group (536 per 10 000).[2] However study data was only drawn from one area of the United Kingdom, including 100,000 patients, thus this area may not be generalisable to the United Kingdom as a whole. Furthermore the study only considered patients reporting their pain to a General Practitioner, so only measured patients who seeking health care advice thus failed to consider the whole population suffering LBP.[2] Further to this, an Australian cohort study discovered whilst most patient’s recovered 1/3 had not fully recovered after 1 year.[3] LBP is clearly a substantial problem for both the health system and the socioeconomic environment, thus effective management is critical.

Updated NICE guidelines for Chronic LBP states that information and self-care advice should be provided to patients to promote self-management by fostering a positive attitude and providing realistic expectations to patients. However, the type, duration, frequency and content of this advice was not reported on.[4]

What is Pain Neuroscience Education?[edit | edit source]

Pain neuroscience education (PNE), also known as therapeutic neuroscience education (TNE), consists of educational sessions for patients describing in detail the neurobiology and neurophysiology of pain and pain processing by the nervous system.[5]
This educational approach has been used by physiotherapists therapeutically since 2002 in various countries including the UK, US and Australia and differs considerably from traditional education strategies such as back school and biomechanical models.[6] This is due to how likelihood of pain chronicity (e.g. for an MSK condition) may not likely be caused by unhealthy or dysfunctional tissues but brain plasticity leading to hyper-excitability of the central nervous system, known as central sensitisation.[7] Therefore, a deeper level reasoning and treatments beyond a medical model is required.

Initially, PNE changes a patient’s perception of pain. For example, a patient may have believed that damaged tissues were the main cause for their pain, and by receiving education about pain neurophysiology the patient understands that pain may not correctly represent the health of the tissue, but may be due to extra-sensitive nerves. As a result, patients have been found to have a reduction in fear avoidance behaviours and are more able and willing to move. PNE can be used with a combination of treatments, including exercise therapy that can be used to break down movement-related pain memories with graded exposure to exercise and decrease sensitivity of the nervous system.[7]

What is Central Sensitisation?[edit | edit source]

Central sensitisation is a neural condition developing from plastic changes that occur within the central nervous system (spinal cord), causing the manifestation of chronic pain.[8] Theory of central sensitisation explains that spinal neurons are in state of hyperexcitability with lower nociceptive threshold.[9] Additionally, peripheral inputs from not only A δ and C fibres but also innocuous Aβ mechanoreceptor fibres of injured and adjacent non-injured tissues, increase summation of action potentials at the dorsal root ganglion as pictured below:

Figure 3: normal neural activity vs spinal neurones in a state of hyper-excitability (Sciable and Richter, 2004)

Effects of central sensatisation.png

Figure 4:Systemic effects of central sensitisation[8]

These plastic changes cause a state of persistent hyper-sensitivity to develop, even after tissue healing has occurred. Thus the patient continues to experience pain, even with less provocation[8]. The theory of central sensitisation was highlighted in the 1960’s, when the pain gate theory advocated that the sensory relay system could be modulated by inhibitory controls (pressure).[10]
Central sensitization also involves changes in the brain at cellular level[8]. However other research has suggested that sensitization may develop from: activity-dependent synaptic plasticity, gap junctions, astrocytes, membrane excitability and gene transcription.[10]
Whilst it has long been recognised that Strokes and Spinal Cord injuries can cause central sensitization, it is not fully understood why it may develop following musculoskeletal injury[8]. However it has been proposed that there may be one of two reasons for its development, although there is no conclusive evidence to support this:[8]
Pre-existing factors (genetics) that may predispose an individual to have altered central nervous system functioning following injury
Factors (environmental) that may cause altered central nervous system functioning once injury has occurred. i.e. (anxiety, stress, depression, fear-avoidance and poor sleep)
Figure 4:Systemic effects of central sensitisation (McAllister, 2012)

Figure 5: Pain behaviours caused by central sensitisation

History of Pain Models and Development of PNE[edit | edit source]

The biomedical model is most commonly used by physiotherapists and other medical health professionals for the management of pain.[11][12] The model follows that pain and injury interrelated, thus an increase in pain means further tissue damage have occurred and vice-versa.[12] This model, called the Cartesian model, is over 450 years old, and many argue inaccurate and significantly outdated.[12]

The Cartesian ‘mid-body’ was first proposed in the early 16th Century by the French Philosopher, Mathematician and Scientist Rene Descartes, in an attempt to show that humans were a mechanical body controlled by a rational soul.[11] Descartes model proposed that the brain was the centre of senses, receiving hollow nerve tubes through which free spirits flowed. Nerves were connected to the brain as a piece of rope may be connected to an alarm; thus as pulling of the rope would cause

Why is the Model Considered Outdated?[edit | edit source]

Descartes model continues to be used in current medical practice and influences the perception that all pain is a result of injury and tissue damage.[11] Clinicians frequently use the biological model to explain patient’s pain, describing pain as being due to either disc, joint or abnormal movement pattern.[12] The resulting treatment is therefore focused on addressing the abnormal movement pattern or faulty tissue, and the pain goes away. However research has shown that education using words such as “bulging”, “herniated” and “ruptured” actually increases patient's levels of fear and anxiety, resulting in protected movements and lack of exercise compliance.[12]

However Descartes biomedical model has been questioned in recent years, with critics arguing that it fails to consider the perception of pain from the nervous system, as well as the psychological and social factors that may influence recovery.[11] Furthermore both psychiatrists and behavioural scientists have highlighted specific medical examples to further question the validity of Descartes model. The examples below suggest that pain may potentially be a phenomenon more than just nociception, and may have a neurological element:

  • Pain was not expressed by a soldier injured in war until reaching the hospital[13]
  • Similar injuries in different patients caused substantially different pain responses[13]
  • An incision to the skin twice as deep as that of another, does not hurt twice as much[13]
  • Why 40% of people with horrific injuries felt either no or a low intensity of pain[14]
  • Why up to 70% of people's do not report pain or associated symptoms consistent with their X-ray/ MRI finding [15][16]
  • Why 51% of amputees reported phantom pain and 76% phantom sensations including: cold, electric sensations and movement in the phantom limb.[17]

Furthermore in Beecher’s[18] comparison study of 150 male civilian patients in contrast to wartime casualties, it was discovered that 83% in the civilian group requested narcotics, whilst only 32% of military patients with the same extent of tissue damage asked for them; thereby suggesting the level of pain experienced is patient dependent. This example therefore proposes that the patient's beliefs emotions and past experiences of pain can alter the brains interpretation of the pain. However the validity of study findings must be questioned, as investigations were conducted 60 years ago, thus may be significantly outdated. Furthermore the study did not consider the effect of shock or adrenaline, which has been proposed to influence immediate pain responses.

The Pain-Neuroscience Education Model[edit | edit source]

In the last century Descartes biomedical model has been replaced by the biopsychosocial model of chronic pain[13], in which pain is classified as being due to increased sensitivity of the nervous system rather than further injury.[11] In layman’s terms, pain persists after tissue healing, due to the fact that the body’s alarm system remains activated, and are stimulated by a much lower intensity of stimulus[12]; i.e. a much lower degree of movement provocation causes pain.

Investigations by the Therapeutic Neuroscience research team at the ‘International Spine and Pain Institute’ has discovered that people in pain are interested in pain and more specifically the mechanisms of pain.[19]Thus, current treatment for patients with chronic pain should have a greater focus on educating patients about the neuroscience of their pain, rather than classifying their pain as being due to faulty movement patterns or damaged tissues.                                                            

Video of Alarm Systems[edit | edit source]

What Does PNE Involve?[edit | edit source]

PNE first of all puts the complex process of describing the nerves and brain into a format that is easy to understand for everyone; no matter whether the target audience is of a particular age, educational level or ethnic group.[5]

This is made possible by using simplified scientific language used with additional methods of presenting information that may include the use of:
• Simple pictures
• Examples
• Booklets
• Metaphors
• Drawings
• Workbook with reading/question-answer assignments
• Neurophysiology Pain Questionnaires

Methods of PNE delivery vary but can typically involve around 4 hours of teaching that is provided to a group or individually, either in single or multiple sessions.[6]

Figure 6. showing the content of PNE education sessions with patients[5]

Figure showing the content of PNE education sessions

How is PNE Used in Clinical Practice?[edit | edit source]

A metaphor/story that can be found here: ( is used by Louw et al.[20] in clinical practice to teach patients about complex pain physiology including extra-sensitive nerves, inflammation, injury and how pain is created in the brain. It is such an example that helps patient to break away from a view of a particular tissue being the issue (e.g. generative disc) and helps the patient think towards the problem being related to pain and a sensitive nervous system.[20] Therefore, Instead of pain following spinal surgery being seen as the ‘problem has not resolved’ or ‘there is something still wrong with the disc’, PNE would explain pain is sensitive to act as a protector which is perfectly normal after surgery.

Video Interview of Low Back Pain From a Patient's Point of View[edit | edit source]

Indicators For the Use of PNE[edit | edit source]

Chronic Musculoskeletal Conditions[21][edit | edit source]

Chronic MSK conditions.jpg

These conditions are often characterised by brain plasticity that leads to hyperexcitability of the central nervous system (central sensitisation). 

  • PNE is recommended in
    central sensitisation conditions like these,
    as the patient may present with maladaptive
    cognitions, behaviour, or coping
    strategies in response to pain.
  • Typically they acquire a protective (movement-related) pain memory, which causes a barrier to adhere to therapeutic treatment such as exercise, decreasing the likelihood of a good outcome.
  • Therefore these maladaptive behaviours, central sensitisation and previous failed treatments are all indicators for PNE 
  • Evidence showing benefits for pre op MSK patients.[20][22]

Figure 7. (right): showing chronic MSK conditions with positive PNE results from current evidence.[21]

The Benefits and Drawbacks of PNE[edit | edit source]

Table 1:showing the benefits and drawbacks of PNE[20][23][24] [edit | edit source]

Benefits Drawbacks
RCT's have shown a reduction in fear and catastrophizing, due to the immediate effect of PNE on improving attitudes and beliefs about pain. Evidence suggests PNE alone is not a viable intervention for pain and disability
Positive effect on disability and physical performance Provides concerns regarding healthcare cost
Increased pain thresholds during physical tasks Less availability of such specialized education to patients in remote regions
Improved adherence and outcomes of therapeutic exercises "in clinic" attendance issues arise for patients with time and financial constraints
May reconceptualise the patients' beliefs on physiotherapy Clinicians need to be trained in PNE competencies
Improved passive and active range of motion Long term effects are not as significant as short term
No harmful effects Future research required on the notion of individual and group curricula; e.g. what is taught, how it is taught and measured

Brain Activity Clinical Imaging of PNE Effect[edit | edit source]

Types of Brain Activity Imaging[edit | edit source]

There are various types of brain imaging to show brain activity in pain states, some scans of which are pictured below:

PET, MRS and fMRI.png

Figures 8 - 10: left to right are Positron emission tomography (PET), magnetic resonance spectroscopy (MRS) and functional magnetic resonance imaging (fMRI) of pain.[25][26][27]

Effects of PNE Imaged[edit | edit source]

By teaching a patient more about how pain works with reassurance that pain doesn’t always mean tissue damage, their pain eases considerably and they experience other benefits including increased movement, better function and reduced fear avoidance. The effects of decreased pain related brain activity are measurable via brain imaging as demonstrated in the example below:

A high-level dancer who was scheduled for back surgery in two days due to experiencing significant back pain for almost two years, was scanned using fMRI. Areas of brain activity related to pain were demarcated in red.

Figure 11: row 1 - patient relaxing. Note no red areas.
FMRI row 1.png

Figure 12: row 2 - patient was asked her to move her painful back while in the scanner. These images demonstrated brain activity related to pain whereby larger areas of red signifies more pain related activity, hence more pain.

FMRI row 2.png

Figure 13: row 3 - after initial scans the patient was taken out of the scanner and provided with a teaching session about pain for 20-25 minutes. Following this, the scan of the patient was immediately repeated doing the same painful task as performed in Row 2. Note this time however, there was significantly less activity (fewer red areas) despite performing the same movement.[20]

FMRI row 3.png

There is an obvious link with patient catastrophising thoughts and pain related brain activity, shown by the immediate reduction in brain activity following PNE provision in the above example. Furthermore, there is a link in attention to pain that when negatively perceived, impacts on the experience of pain being greater. One study[26] demonstrated that pain related brain activity was greater in patients with Alzheimer’s, than age matched healthy controls. However, in this population there is less reporting of pain and analgesic use. Is this due to difficulty to communicate pain or due to reduced attention to pain?

Critical Appraisal of the Evidence[edit | edit source]

Paper 1:The Effect of Neuroscience Education on Pain, Disability, Anxiety, and Stress in Chronic Musculoskeletal Pain[5][edit | edit source]

A recent systematic review investigating the benefits of pain neuroscience education (PNE), discovered that PNE significantly decreased pain, pain catastrophisation and perceived disability compared to the control group (ongoing medical care), in both the short and long-term. Although the review searched all major databases, only 8 studies were included in the review, with all included studies having either good, very good or excellent methodological quality. Nevertheless results from the review failed to discover the most effective frequency and duration of PNE sessions, with RCT’s reporting sessions lasting for 30minutes to 4 hours, with no consensus to the number of required sessions. Moreover the review considered all types of chronic musculoskeletal pain including: Whiplash, Chronic Fatigue syndrome, widespread pain and Chronic Low Back Pain (LBP), thus may lack the generalisability to the treatment of LBP.

Becky mead table of evidence.png

Paper 2: Preoperative Pain Neuroscience Education for Lumbar Radiculopathy[20][edit | edit source]

Compared to the previous systematic review’s poor generalisability of PNE for a range of chronic pain conditions, researchers in this multi-centred randomised control trial focused solely on preoperative PNE for lumbar radiculopathy.

Louw et al., 2014 table 1.jpg

The internal validity of the study is positive with measures in place to reduce risk of bias where possible. Methodological quality could have only improved through blinding but is not appropriate for the groups. Sample size powered. The study scored a Pedro scale of 8/11. The secondary outcomes improving patient experiences after surgery and health utilisation are hugely clinically relevant, especially in relation to the financial challenges of National Health Service (NHS) in the UK. Any reduction in services post-surgery and thus reducing costs, whilst additionally improving patient experiences with minimal cost to implement cannot be overlooked.

However, the UK’s NHS and health insurance systems in the US will differ dramatically in relation to resources available and how often treatments can be accessed. Subsequently, this study did not control the amount of rehabilitation patients were allowed to access, which could further skew results of outcomes, especially compared to the UK where amount of rehabilitation will be determined by post-operative protocol. Finally, the generalisability of the findings to another type of surgery, e.g. spinal fusion, or a patient with non-specific low back pain must be applied with caution despite promising outcomes due to the specificity of the results to surgery for radiculopathy.

Paper 3: Pain neurophysiology education for the management of individuals with chronic low back pain: A systematic review and meta-analysis'[edit | edit source]

With regard to the concerns of generalising the results from the previous RCT to non-specific low back pain patients, a systematic review and meta-analysis by Clarke, Ryan and Martin[6], investigated the impact of PNE, specifically on that management of patients with chronic low back pain.

SR on PNE 1.jpg

The limitations of this review, as critically appraised using the JBI checklist, were the small number of studies included in the review and furthermore, both studies included were published by one of the co-authors of the PNE manual, so there is a potential conflict of interest. There also could have been a wider range of resources used to search for studies as only 3 databases were observed.

However, the critical appraisal of the papers selected was independently assessed by 2 reviewers, minimising bias and each RCT was assessed using the Cochrane back review group (CBRG) guidelines.Contrary to the previous systematic review by Louw et al.[5] which focused on a range of chronic conditions, this review is specific to CLBP which make it more generalizable. Lastly the implications for practice and research were based primarily on the reported data.

Paper 4: Use of therapeutic neuroscience education to address psychosocial factors associated with acute low back pain: a case report[22][edit | edit source]

Despite some research being done for chronic pain, scant evidence exists in PNE as a treatment in acute pain as a method of preventing chronic pain. This case study attempts to address this issue to guide the way for further research.

PNE data extraction table Lynette. pic2.png

Although case reports aren’t generalisable or robust they do provide a unique opportunity to present pilot evidence to inform the direction of RCT’s, reviews and guidelines. As a case report the limitations are that use of controls are not a necessity, thus the outcomes for this patient may purely be spontaneous recovery, furthermore other Rx provided in addition to PNE may be credited.

Clinical Bottom Line[edit | edit source]

Due to the limited numbers of studies, study specificity and relatively poor level of methodological quality; currently it is difficult to draw solid conclusions to the specific clinical benefits of PNE for reducing LBP, perceived disability and function.

Resources[edit | edit source]

  2. How to Explain Pain to Patients
  3. A Practical guide for Therapeutic Neuroscience Education

References[edit | edit source]

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  3. Henschke N, Maher CG, Refshauge KM, Herbert RD, Cumming RG, Bleasel J. et al. Prognosis in patients with recent onset low back pain in Australian primary care: inception cohort study. BMJ. 2008; 337 (a171).
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  15. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation.. Journal of Bone and Joint Surgery American 1990; 72 (3): 403-8.
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  18. Beecher HK. The Relationship to the Significance of Wound to Pain Experienced. Journal of the American Medical Association. 1956;161 (17):1609-13.
  19. Louw A, Louw Q, Crous LC. Preoperative education for lumbar surgery for radiculopathy. South African Journal of Physiotherapy. 2009; 65(2):3-8.
  20. 20.0 20.1 20.2 20.3 20.4 20.5 Louw A, Diener I, Landers MR, Puentedura EJ. Preoperative pain neuroscience education for lumbar radiculopathy: a multicenter randomized controlled trial with 1-year follow-up. Spine. 2014; 39(18):1449-1457.
  21. 21.0 21.1 Moseley GL, Butler DS. Fifteen years of explaining pain: the past, present, and future. The Journal of Pain. 2015;16(9):807-813.
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  23. Moseley GL. Joining forces–combining cognition-targeted motor control training with group or individual pain physiology education: a successful treatment for chronic low back pain. Journal of Manual & Manipulative Therapy. 2003; 11(2):88-94. .
  24. Moseley GL. Evidence for a direct relationship between cognitive and physical change during an education intervention in people with chronic low back pain. European Journal of Pain. 2004; 8(1):39-45. .
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  27. Casey KL, Morrow TJ, Lorenz J, Minoshima S. Temporal and spatial dynamics of human forebrain activity during heat pain: analysis by positron emission tomography. Journal of Neurophysiology. 2001;85(2):951-959.

Keller T and Krames ES. (2009). “On the Shoulders of Giants”: A History of the Understandings of Pain, Leading to the Understandings of Neuromodulation. Neuromodulation. 12 (2), 77-84.