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Therapeutic Neuroscience Education: Evidence and Application

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Cameron Yuen

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Transcript of Therapeutic Neuroscience Education: Evidence and Application

A Brief History of Pain
Therapeutic Neuroscience Education: Evidence and Application

Objectives
Outline a brief history of the theories of pain.
Describe the Therapeutic Neuroscience Education (TNE) model for pain treatment.
Review literature for evidence of efficacy.
Describe how to implement TNE in an outpatient orthopedic setting.
Case Studies?

Cameron Yuen SPT, CSCS
For a more comprehensive look at pain from a neuroimmunoendocrine perspective, see Corinne Cooley's lecture series.
Cartesian Model
Early Biomedical
Gate Control
Neuromatrix
Biopsychosocial
Cognitions
Perceptions

Simply stated, this model proposed that pain is a stimulus produced at the site of irritation. This pain message is then transmitted to the brain.
1 unit of pain is equal to 1 unit of tissue damage.
Descartes model continues to be the driving force in the delivery of medicine today (Goldberg, 2008).
Cartesian Model of Pain
Pain Problem #1

Instruct the patient to remove their foot from the fire, and avoid the fire altogether.
Logical and appropriate response in threatening acute setting, but is less likely to help in persistent pain state.
Analogous to fear avoidance model, which is shown to lead to increased pain and disability (Vlaeyen & Linton, 2000).

Pain Problem #2
Put out the fire with bucket of water thereby getting rid of the source of pain.
Analogous to prescription medications and injections aiming to ‘put out the fire’ of inflammation.
Despite the steady increase in steroid injections, the prevalence of chronic pain continues to increase (Wall & Melzack, 2005), not to mention the opioid epidemic.
Dousing the fire seems to not always work for chronic pain (Louw, 2013).


Pain Problem #3
Remove the pain signal to the brain by cutting the wire, and no pain will be experienced.
Analogous to various surgeries to ‘cut out’ or alter the source of pain (Louw, 2013).
Unfortunately, for example, 20% of lumbar discectomies result in same or increased levels of pain (Ostelo, Costa et al, 2004).

Early Biomedical Models
Several broad perspectives: Specificity, Intensity, Pattern Response.
Unique and specialized nerve endings involved in the transmission of painful information.
Distinct sensations operate within identical neural circuitry by way of intensity.
Nociceptive information due to the pattern of responses in afferent systems (Gatchel & Peng, 2007).
Gate Control Theory
Perception of pain is modulated by excitatory and inhibitory effect on interneurons.

Ascending modulation: Increased mechanoreceptor activity causes pre-synaptic inhibitory effect on interneurons in dorsal horn, leading to decreased perception of pain.

Descending modulation: There is also an intrinsic analgesia system which serves as inhibitory mediator on interneurons.

While helpful, the explanation is only partially correct. Does not account for, among other phenomena, phantom pain.
Ramachandran, 1998; Butler, 2000
Model continues to exert influences on how therapists view pain:
Direct link between tissue damage and pain experience.
Pain as an input driven system.
In cases of chronic pain, tissues are not healing and damage is ongoing.
Ronald Melzack himself has urged healthcare providers to recognize the shortcomings of the pain gate and embrace the current, more updated view of pain, the brain and the
neuromatrix
(Melzack, 1996; Melzack, 1999; Melzack, 2001; Louw, 2013).
Pain is a multidimensional experience produced by characteristic “neurosignature” patterns of nerve impulses generated by a widely distributed neural network.
These neurosignature patterns may be triggered by sensory inputs, but they may also be generated independently of them.
Acute pains evoked by brief noxious inputs have been meticulously investigated by neuroscientists, and their sensory
transmission mechanisms are generally well understood.
However, chronic pain syndromes, which are often characterized by severe pain associated with little or no discernible injury or pathology, remain a mystery.
Pain, then, is produced by the output of a widely distributed neural network in the brain rather than directly by sensory input evoked by injury, inflammation, or other pathology.
The Biopsychosocial Model
Sought to combine theories in order to generate the more inclusive theory of pain.

Recognized that there was a certain degree of specificity for peripheral nerve function.

Also realized that there was a certain degree of pattern recognition that was responsible for peripheral and central processing of noxious information (Gatchel & Peng, 2007).
Correcting all PSB factors is not clinically attainable and is unlikely to change the future course of a lower back condition.
The Biopsychosocial Model
Cognition
Bottom-up approach
Top-down approach
Therapy aimed at decreasing nociceptive signals. This is generally targeting tissues and joints.
Therapy aimed at educating patients about their pain and reducing perceived threats.
"We have randomized controlled trials that produce the highest quality of evidence. They strongly suggest that the procedure is next to useless. If there is any benefit, it is very small and there are downsides, expense and potential complications."
We need both!
At the heart of a true biopsychosocial approach is cognition.

What a patient thinks, feels, and believes about his or her condition will significantly impact their examination, treatment, and prognosis.
Vlaeyen, Kole-Snijders, Boeren, & van Eek, 1995
Exam:
Therapist determines stiff joint is associated with pain and disability
Treatment:
Joint mobilization
Exam:
Therapist determines that altered muscle recruitment is associated with pain and disability.
Treatment:
Motor control approach
Exam:
Therapist determines that their limited function is due to altered beliefs about their pain.
Treatment:
TNE approach
To treat patients with chronic pain, we need to change cognitions.

Two particular cognitions which need to be addressed before engaging in movement or manual based approach are fear and catastrophizing.
Fear
Fear within the general population is often associated with belief that movement will not only increase pain, but futher damage tissues.
Fear Avoidance
Early intervention, especially education, may have significant impact in the path chosen after injury.
Olveira, Gevirtz, & Hubbard, 2006
Pain is more prevalent in patients with lower education levels, and healthcare providers who experience a similar injury to non-medically trained persons report significantly less pain.
Schmidt et al., 2007; Virani, Ferrari, & Russel, 2001

Threatening and provocative terminology is likely to induce some level of fear and increase pain experience.
Sloan & Walsh, 2010
Catastrophizing
Clinicians should watch for phrases such as:
Now that I have a bulging disc, I will never walk again.
I've got arthritis. I will never run again.
Beliefs
Maladaptive beliefs need to change to allow for normal movement, exercise, and function.
Kendall & Watson, 2000; Louw 2013
Cognitions and Beliefs
Placebo = Perception + Expectation
Placebo is often viewed as a "fake" or sham treatment. Placebo should be seen more as the endogenous mechanism of pain experience modulation.
Louw, 2013
Fake treatment + psychosocial context surrounding pain experience
Dr. Fabrizio Benedetti
Placebo And Nocebo: Different Contexts, Different Pains
Introduction to TNE
Two forms of education
Goals and content of TNE
Delievery methods

What type of education to deliver? Would viewing these images help a patient recover faster, or help ease pain, fear, and anxiety?
Might increase fear in patients, which in turn may increase pain!
Morr, Shanti et al, 2010
Evidence of Efficacy
A new model to educate patients as a means to modulate pain and disability is needed.
Patients in pain want to know more about pain, not anatomy.
Louw et al., 2009
Goal: Top-down approach to threat desensitization with the aim of altering cognitions surrounding pain experience.
TNE Sessions Contain:

Neurophysiology of pain
No reference to anatomical or pathoanatomical aspects of pain
No discussion of emotional or behavioral aspects of pain
Nociception and nociceptive pathways
Neurons, action potentials, and synapses
Spinal inhibition and facilitation
Peripheral sensitization
Central sensitization
Plasticity of the nervous system
Just education?
Therapists need not worry about becoming de-facto psychologists. The value is in adding TNE to your practice, not replacing it with an education-only approach.
"All concepts are in play, all the time."
Anatomy
Physiology

Pain Science
Biomechanics
Psychology
Kinesiology

Nerve Function
Exercise Science
Tissue Healing
Dr. Jason Silvernail
Delivery Methods
Duration and frequency of TNE sessions quite varied in literature.
Some lasted as long as four hours (Moseley, 2003)
More recent studies reported sessions of 30 minutes (Meeus, Nijs et al., 2010; Van Oosterwijck, Nijs et al., 2011).
Varied between single sessions and multiple sessions (Moseley, Hodges et al., 2004; Moseley, 2004)
Most common frequency between multiple sessions was one week (Van Oosterwijck, Nijs et al., 2011).
What is important is that the patient truly understands it.
"But facts are not everything - at least half the business lies in how you interpret them!"
- Dostoevsky
Lots of variation...
Format and Tools
Education was primarily performed during one-on-one sessions.
Only two studies utilized group sessions.
One-on-one sessions tended to result in superior outcomes.
TNE sessions should be accompanied with pictures, examples, metaphors, hand drawings, workbooks with reading/quesion-answer assignments, and the Neurophysiology Pain Questionnaire. (Van Oosterwijck, Nijs et al., 2011)
Sample workbook by Dr. Greg Lehman
Adjunct Treatment
TNE can be preceded by, combined with, or followed by any therapeutic activity. Various adjuncts in the literature include:
Manual therapy, include mobilization and manipulation
Soft tissue, massage
Neurodynamics
Spinal stabilization exercise
Home exercises
Circuit training
Aerobic exercise
TNE only
Therapists should educate in one-on-one sessions using various examples, metaphors, and pictures explaining the neurophysiology of their pain experience.

The education approach should include physical movement, especially aerobic exercise. (Louw, Diener et al., 2011)
With all the attention surrounding TNE, the question must be posed: Does it work?
Two Systematic Reviews
The Effect of Neuroscience Education on Pain, Disability, Anxiety, and Stress in Chronic Musculoskeletal Pain, 2011
The Efficacy of Pain Neuroscience Education on Musculoskeletal Pain: A Systematic Review of the Literature, 2016
The Effect of Neuroscience Education on Pain, Disability, Anxiety, and Stress in Chronic Musculoskeletal Pain

Louw A, Diener I, Butler DS, Puentedura EJ, 2011

Objective: To evaluate the evidence for the effectiveness of neuroscience education for pain, disability, anxiety, and stress in chronic musculoskeletal pain.
Search Strategy
neuroscience
neurobiology
neuro-physiology
pain
pain education
pain science education
stress
anxiety.
Keywords:
Critical Appraisal
6 high quality RCTs, 1 pseudo RCT, 1 comparative study
Quality ranged from 11 (good) to 15 (excellent)
Outcomes: 4 categories related to pain, function and disability, psychosocial issues, and movement.
Pain
Pain ratings (numeric pain rating scale [NPRS] and visual analog scale [VAS])
Pain knowledge (Neurophysiology of Pain Test)
Pressure pain thresholds (PPTs)
Self-report symptoms (WAD symptom list)
Roland Morris Disability Questionnaire (RMDQ)
Neck Disability Index (NDI)

Function and Disability

Tampa Scale of Kinesiophobia (TSK)
Pain Catastrophization Scale (PCS)
Pain Coping Inventory (PCI)
Survey of Pain Attitudes (Revised) (SOPA[R])
Pain Self-Efficacy Questionnaire (PSEQ)
Psychosocial
Neurodynamic tests: Straight leg raise (SLR) and brachial plexus provocation test (BPPT)
Trunk forward flexion and neck extension
Abdominal draw-in maneuver
Endurance: Sit-to-stand, 50-foot walk test, 5-minute walk test, and step count
Movement
Limitations
Number of studies included.
Heterogenous nature of studies precludes meta-analysis.
inconsistent control groupings impacts causality.
Influence of NE content vs individual attention and acknowledgement that pain is real?
Conclusions
For chronic MSK pain disorders, there is compelling evidence that an education strategy addressing the neurophysiology and neurobiology of pain can have a postive effect on pain, disability, catastrophizing, and physical performance.
The Efficacy of Pain Neuroscience Education on Musculoskeletal Pain: A Systematic Review of the Literature, 2016
Louw A, Zimney K, Puentedura EJ, Diener I, 2016
Since the publication of the last systematic review, various studies utilizing PNE have been published:

Gallagher, McAuley, and Moseley, 2013
Ittersum et al., 2014
Louw, Diener, Landers, and Puentedura, 2014
Robinson and King, 2011
Van Ittersum, van Wilgen, Groothoff, and Van der Schans, 2011.
This growth of additional PNE studies, along with the reflection by Moseley and Butler (2015) on 15 years of teaching people about pain begs the question if the increased research activity in PNE has resulted in any increased evidence for this educational approach?

The original review was also handicapped in assessing efficacy by including lower level papers and the inability to evaluate methodologically each study in comparative fashion.
Objective:
Update and explore the efficacy of PNE as a treatment approach for people suffering MSK pain.
Search and Inclusion:
Employed same methodology reported by Louw, Diener, Butler, and Puentedura (2011) in order to add to and combine the cumulative evidence for PNE.

The end result would be an expansion of the research results ranging from 2002 (Moseley, 2002) to the present (2016).

Additionally, the new review only included RCTs.
Outcomes
● Pain rating (Numeric Pain Rating Scales or Visual Analog Scale) (Gallagher, McAuley, and Moseley, 2013; Louw, Diener, Landers, and Puentedura, 2014; Moseley, 2002; Pires, Cruz, and Caeiro, 2015; Ryan, Gray, Newton, and Granat, 2010; Vibe Fersum et al., 2013)

● Pain knowledge (Neurophysiology of Pain Questionnaire or Pain Biology Questionnaire) (Meeus et al., 2010; Van Oosterwijck et al., 2013)

● Pain Vigilance and Awareness Questionnaire (Van Oosterwijck et al., 2013)

● Pressure Pain Threshold (Meeus et al., 2010; Téllez-García et al., 2014; Van Oosterwijck et al., 2013)

● Spatial summation procedure (Van Oosterwijck et al., 2013)
Outcomes related to pain
● Roland Morris Disability Questionnaire (Moseley, 2002, 2003c; Ryan, Gray, Newton, and Granat, 2010; Téllez-García et al., 2014)

● Oswestry Disability Index (Louw, Diener, Landers, and Puentedura, 2014; Téllez-García et al., 2014; Vibe Fersum et al., 2013)

● Neck Disability Index (Beltran-Alacreu, Lopez-de-Uralde-Villanueva, Fernandez-Carnero, and La Touche, 2015)

● Fibromyalgia Impact Questionnaire (Ittersum et al., 2014; Van Oosterwijck et al., 2013)

● Revised Illness Perception Questionnaire for Fibromyalgia (Ittersum et al., 2014)

● Short Form 36 Health Status Survey (Van Oosterwijck et al., 2013)

● Quebec Back Pain Disability (Pires, Cruz, and Caeiro, 2015)

● Patient-Specific Functional Scale (Gallagher, McAuley, and Moseley, 2013)
Outcomes related to function and disability
● Tampa Scale of Kinesiophobia (Beltran-Alacreu, Lopez-de-Uralde-Villanueva, Fernandez-Carnero, and La Touche, 2015; Meeus et al., 2010; Pires, Cruz, and Caeiro, 2015; Van Oosterwijck et al., 2013)

● Pain Catastrophization Scale (Gallagher, McAuley, and Moseley, 2013; Ittersum et al., 2014; Moseley, Nicholas, and Hodges, 2004)

● Pain Coping Inventory (Meeus et al., 2010; Van Oosterwijck et al., 2013)

● Survey of Pain Attitudes (revised) (Moseley, Nicholas, and Hodges, 2004)

● Pain Self-Efficacy Questionnaire (Ryan, Gray, Newton, and Granat, 2010)

● Hopkins Symptoms Checklist (Vibe Fersum et al., 2013)

● Fear Avoidance Beliefs Questionnaire (Beltran-Alacreu, Lopez-de-Uralde-Villanueva, Fernandez-Carnero, and La Touche, 2015; Vibe Fersum et al., 2013)

● Beliefs about surgery (Louw, Diener, Landers, and Puentedura, 2014)
Outcomes related to function and disability
● Straight leg range of motion (Moseley, Nicholas, and Hodges, 2004)

● Lumbar range of motion (Moseley, Nicholas, and Hodges, 2004; Vibe Fersum et al., 2013)

● Abdominal draw in task (Moseley, Nicholas, and Hodges, 2004)

● Repeated sit to stand test (Ryan, Gray, Newton, and Granat, 2010)

● 50-foot walk test (Ryan, Gray, Newton, and Granat, 2010)

● 5-minute walk test (Ryan, Gray, Newton, and Granat, 2010)

● Step count (Ryan, Gray, Newton, and Granat, 2010)

● Neck flexor muscle endurance test (Beltran-Alacreu, Lopez-de-Uralde-Villanueva, Fernandez-Carnero, and La Touche, 2015)

● Visual Analog Fatigue Scale (Beltran-Alacreu, Lopez-de-Uralde-Villanueva, Fernandez-Carnero, and La Touche, 2015)
Outcomes related to movement
The results of this updated systematic review of PNE for MSK pain provide supporting evidence for PNE improving pain ratings, pain knowledge, disability, pain catastrophization, fear-avoidance, attitudes and behaviors regarding pain, physical movement, and healthcare utilization.
Need to be consider the heterogeneous nature of the studies included in this systematic review.

Also important to recognize that no PNE study showed any outcome to be worse than the control groups, thus implying a significant risk–benefit ratio in favor of PNE.

In comparison with the previous systematic review, the quality of the studies, number of studies, and total number of patients (n = 734) are substantially increased.

This increase not only reflects the increased activity in this field of study, but also impacts the conclusions that can be made in regards to the efficacy of PNE.
Conclusions
Strong evidence supports the use of PNE for MSK disorders in reducing pain ratings, limited knowledge of pain, disability, pain catastrophization, fear-avoidance, unhealthy attitudes and behaviors regarding pain, limited physical movement and healthcare utilization.
TNE Implementation
Cut to the chase!
Contents
Neurophysiology of pain
No reference to anatomical or pathoanatomical models
No discussion of emotional or behavioral aspects of pain
Nociception and nociceptive pathways
Neurons, synapses, action potentials
Spinal inhibition and facilitation
Peripheral and central sensitization
Plasticity of nervous system
"My greatest strength as a consultant is to be ignorant and ask a few questions." - Peter Drucker
How to Present to Patients?
Precise starting point will vary from patient to patient depending on current understanding.
Needs to be understandable - simple terms; no jargon.
Alarms and Nails
Aim: Educate about nerves.

Nerves work like alarm system.
Depending on many different factors, such as stress, movement, temperature, etc., electrical activity can go up or down.
Alarm is triggered when activity reaches threshold.
Waking up the Alarm System
Aim: Understand that tissue heals, and pain may be result of increased nerve sensitivity.

Depending on contextual factors, alarm system might stay resting just below firing level instead of returning to resting level.
Now that nerves are more sensitive, it requires less activity before pain level is reached.
Nerve Sensors
Aim: Understand how nontraditional stimuli increase pain.

Various sensors designed to protect and inform you.
These sensors are constantly updated based on environment, and therefore can be changed for the better.
Take the stimulus away from sensor by gentle movement, relaxation, and knowledge.
Pain and Injury
Aim: develop an understanding that injury and pain are not synonymous, and that pain is an output.

Would it hurt to sprain your ankle?
Would it hurt to sprain your ankle if a speeding bus was coming right at you?
Phantom pain vs. soldiers in battle.
Central Sensitization
Aim: Explain concept of central sensitization and CNS plasticity.

Persistant pain causes many worries, and brain will alter incoming messages if deemed important.
Pressing 'X' on keyboard but seeing 'XXXX' on screen.
Perceived importance of information makes CNS hypervigilant.
Driving the Same Road Over and Over
Aim: Understand processing of pain and strengthening of pathways leading to heightened sensitivity.

Your brain has a map of your body, and as tissues heal, certain maps (neurotags) fade away.
If pain continues, and map is used often, changes occur, and travel becomes faster.
Wet and Dry Brains
Aim: Understand how brain can modulate pain, and how they can engage the endogenous mechanisms.

Brain produces chemicals to ease danger messages.
Wet brains are full of chemicals to ease pain.
As we get more worried about your pain, the brain slows the pour of medicine in order to protect the perceived threat.
We can change the flow of medicine through knowledge, aerobic exercise, and certain medicines.
Understanding Context
Aim: Understand that injuries do not occur in a vacuum, and environmental issues influence pain.

Countless reasons for different pain experiences with similar injuries.
Important to understand that injuries occur in different evironments.
if hurt in a stressful environment, there are likely to be a lot of stress chemicals floating through body, which will increase sensitivity.
In the end, altering cognitions and perceptions around pain is what is important. You get to choose how to present it.

The following list is provided only as a sample, as there are many ways to get the same message across.
Inflammatory Soup
Aim: Explain persistant inflammation, antridromic impulses, and thoughts. (helpful for post-op)

Explanation of normal swelling after sprained ankle - soup.
After initial injury, extra sensitive nerves cause persistent swelling. Nerves send messages both ways, and will signal the release of chemicals if needed.
When Lions Attack
Aim: Understand acute and chronic stress response.

Stress response as a protective system, with pain being only one defense mechanism.
Chronic stress response visualized as a lion, which serves as a constant threat.
List of threats is long: no one knows why you still have pain, life is miserable, job issues, failed treatments, movement hurts, nothing helps, family issues.
Practical Considerations
Several studies had education sessions lasting hours - not practical, but luckily not necessary.
Not all strategies can be absored by every healthcare system, and every therapist has their own unique clinical environement.
Time
The more time devoted to TNE, the greater the chance for success.
Begin during first visit.
One strategy: Designate specific days of week for such patients.
Utilize email, homework, discuss only 2-3 questions at a time.
Cost Effectiveness
Should not be extensive, stand-alone treament.
More cost effective in context of PT (exercise and manual therapy).
one-on-one is superior, but group sessions work as well.
Billing
Changing beliefs and cognitions direct impacts movement, function, and motor control. It is therefore suggested to bill as neuromuscular re-education.
Could also bill as therapeutic exercise or therapeutic activites.
Case Studies
FInal Words...
Strong evidence supports the use of PNE for MSK disorders in reducing pain ratings, limited knowledge of pain, disability, pain catastrophization, fear-avoidance, unhealthy attitudes and behaviors regarding pain, limited physical movement and healthcare utilization.
Questions?
Discussion.
“Simplicity is the ultimate sophistication.” Leonardo da Vinci
Louw, 2016
image: http://www.rosslab.neurobio.pitt.edu/specificitytheory/
image: http://www.rosslab.neurobio.pitt.edu/intensitytheory/
image: http://www.rosslab.neurobio.pitt.edu/patterntheory/
Melzack, 2001
Melzack, 2001
Melzack, 2001
Melzack, 2001
Melzack, 2001
Louw, 2013
Melzack, 2001
Louw, 2013
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Louw. 2013
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Louw, 2013
Louw, 2013
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Louw, 2013
References
Butler DS, Matheson J. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000.

Carlino E, Benedetti F. Placebo and Nocebo Effects. The Handbook of Behavioral Medicine. 2014:36-57.

Gatchel RJ, Peng YB, Peters ML, Fuchs PN, Turk DC. The biopsychosocial approach to chronic pain: Scientific advances and future directions.Psychological Bulletin. 2007;133(4):581-624.

Gifford L. Topical Issues in Pain. Falmouth: CNS Press; 2002.
Identifying psychosocial yellow flags and modifying management

Goldberg JS. Revisiting the Cartesian model of pain. Medical Hypotheses. 2008;70(5):1029-1033.

Louw A, Louw L, Crous C. Preoperative education for lumbar surgery for radiculopathy. South African Journal of Physiotherapy. 65(2):3-8.

Louw A, Diener I, Butler DS, Puentedura EJ. The Effect of Neuroscience Education on Pain, Disability, Anxiety, and Stress in Chronic Musculoskeletal Pain. Archives of Physical Medicine and Rehabilitation. 2011;92(12):2041-2056.

Louw A, Puentedura E. Therapeutic Neuroscience Education: Teaching Patients about Pain: a Guide for Clinicians. Story City, IA: International Spine and Pain Institute; 2013.

Louw A, Diener I, Fernández-De-Las-Peñas C, Puentedura EJ. Sham Surgery in Orthopedics: A Systematic Review of the Literature. Pain Med Pain Medicine. November 2016.

Louw A, Zimney K, Puentedura EJ, Diener I. The efficacy of pain neuroscience education on musculoskeletal pain: A systematic review of the literature.Physiotherapy Theory and Practice. 2016;32(5):332-355.

Meeus M, Nijs J, Oosterwijck JV, Alsenoy VV, Truijen S. Pain Physiology Education Improves Pain Beliefs in Patients With Chronic Fatigue Syndrome Compared With Pacing and Self-Management Education: A Double-Blind Randomized Controlled Trial. Archives of Physical Medicine and Rehabilitation. 2010;91(8):1153-1159.

Melzack R. Gate control theory: on the evolution of pain. Pain Forum. 1996;5(2):128-138.

Melzack R. From the gate to the neuromatrix. Pain. 1999;82.

Melzack R. Pain and the neuromatrix in the brain. Journal of Dental Education. 2001;65(12):1378-1382.

Morr S, Shanti N, Carrer A, Kubeck J, Gerling MC. Quality of information concerning cervical disc herniation on the Internet. The Spine Journal. 2010;10(4):350-354.

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.

Moseley GL, Nicholas MK, Hodges PW. A Randomized Controlled Trial of Intensive Neurophysiology Education in Chronic Low Back Pain. The Clinical Journal of Pain. 2004;20(5):324-330.

Moseley G. 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.

Oliveira A, Gevirtz R, Hubbard D. A Psycho-Educational Video Used in the Emergency Department Provides Effective Treatment for Whiplash Injuries.Spine. 2006;31(15):1652-1657.

Oosterwijck JV, Nijs J, Meeus M, et al. Pain neurophysiology education improves cognitions, pain thresholds, and movement performance in people with chronic whiplash: A pilot study. The Journal of Rehabilitation Research and Development JRRD. 2011;48(1):43.

Ostelo RW, Costa LOP, Maher CG, Vet HCD, Tulder MWV. Rehabilitation after lumbar disc surgery. Cochrane Database of Systematic Reviews Reviews. August 2008.

Ramachandran VS, Blakeslee S. Phantoms in the Brain: Probing the Mysteries of the Human Mind. New York: William Morrow; 1998.

Schmidt CO, Raspe H, Pfingsten M, et al. Back Pain in the German Adult Population. Spine. 2007;32(18):2005-2011.

Sloan TJ, Walsh DA. Explanatory and Diagnostic Labels and Perceived Prognosis in Chronic Low Back Pain. Spine. 2010;35(21).

Sloan TJ, Walsh DA. Explanatory and Diagnostic Labels and Perceived Prognosis in Chronic Low Back Pain. Spine. 2010;35(21).

Virani SN, Ferrari R, Russell AS. Physician resistance to the late whiplash syndrome. J Rheumatol. 2001;28(9):2096-2099.

Vlaeyen JW, Kole-Snijders AM, Boeren RG, Eek HV. Fear of movement/(re)injury in chronic low back pain and its relation to behavioral performance. Pain. 1995;62(3):363-372.

Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain. 2000;85(3):317-332.

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Louw, 2013
Alarms At Home
A normal alarm at home is not designed to go off with normal activity. It is set up to go off when a door or window is broken.
Your alarm is set so high, that even knocking on the door sets it off.
Common Questions
How do you know my alarm system is extra sensitive?
Why do nerves stay extra sensitive?
What can be done to calm these nerves to a normal level?
How do we know it's extra sensitive
Common question when medical tests show up as normal.
But, this is good news as medical tests are designed to detect serious issues which need attention.
You probably notice that familiar movements are now more painful, and areas which were previously nonpainful are now painful.
Why do nerves stay sensitive?
It is normal for nerves to increase in sensitivity following injury.
Continued sensitivity will be determined by various factors going on in life at the time of the pain including:
Failed treatments
Family issues
Levels of fear
Concerns about your job
Different explanations for your pain
If your brain does not know the cause of the pain, it will decide that there is still a threat and defenses will stay up.
What can be done to calm the nerves?
Most patients want to know right off the bat.
Simply by beginning to understand why nerves stay sensitive will actually help decrease the sensitivity of the alarm system.
The alarm system remains on high alert when there are more questions than answers.
Once you have a better understanding, incorporating movement and aerobic exercises help release calming chemicals.
Treatment Options
As patient gains understanding, they will be curious how to treat.
Explanation of pain - Studies show that the more you understand your pain, the better you will do. Invite the patient to ask more questions.
Aerobic exercise - helps pump blood and oxygen throughout body, calms nerves, and helps with depression, mood, and sleep.
Medication - your physician will assist with medications which help calm nerves such as anti-seizure and anti-depressants.
Take Home Messages for Patients
There are many ways to help make your tissues healthier and less sensitive. Since they are not injured, they do not need to be "fixed."
You will likely experience pain as part of your therapy. It will take time to calm them down, but understand that you are not hurt, and your nerves are simply making you aware that they are sensitive.
Over time, these messages will become dampened, and you will be able to increase your activity.
Louw, 2013
Louw, 2013
Louw, 2013
Louw, 2013
Louw, 2013
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