I n t eg r a t i n g

Manual Therapy
a nd

Pain Neuroscience

Twelve principles for treating

the body and the brain

Adriaan Louw
PT, PhD

Emilio Puentedura
PT, DPT, PhD, OCS, GDMT, FAAOMPT

Stephen Schmidt
PT, MPhysio, OCS, FAAOMPT

Kory Zimney
PT, DPT
 I nt e gr at i ng

Manual Therapy
a nd

Pain Neuroscience

Twelve principles for treating

the body and the brain

Adriaan Louw
PT, PhD

Emilio Puentedura
PT, DPT, PhD, OCS, GDMT, FAAOMPT

Stephen Schmidt
PT, MPhysio, OCS, FAAOMPT

Kory Zimney
PT, DPT
© Copyright 2019 Adriaan Louw

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in
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The procedures and practices described in this book should be implemented in a manner consistent with
professional standards set for the circumstances that apply in each situation. Every effort has been made to
confirm accuracy of the information presented and to correctly relate generally accepted practices.

The authors, editor and publisher cannot accept responsibility for errors or exclusions or for the outcome of
the application of the material presented herein. There is no expressed or implied warranty of this book or
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Foreword
Michael Shacklock
DipPT, MAppSc, FACP

In the last 30 years, manual therapy has come under considerable scrutiny, particularly from the
scientific community. In the 1990s, Prof. Gwendolen Jull aptly put it by saying, “Prove it or lose it.”
Challenged is the idea that the therapist’s hand can detect and cure mechanical or structural problems.
This has resulted in a variety of statements such as, “Manual therapy techniques are not specific so
you can’t make a diagnosis with it.” “It’s only placebo, so stop doing it.” “It doesn’t produce long-term
changes, so it’s a waste of time.”

Much of the challenge to manual therapy has come from the nervous system, ultimately from Robert
Elvey’s seminal work on the brachial plexus; David Butler’s book, Mobilisation of the Nervous System;
Louis Gifford’s treatise Clinical Biology of Aches and Pains and Prof. Clifford Woolf’s work on central
sensitization, then brain plasticity and a connection to the psychosocial. It seemed logical to follow the
afferent impulse from the tissues, along the nerves to the central nervous system, through to perception
and experience. A step in this direction came in 1991 when David Butler, Helen Slater and I came
away from a physiotherapy conference in which only a small number of presentations included neural
mechanisms. So, in 1995 we held an international multidisciplinary pain conference entitled Moving in
on Pain. Included as speakers were physical therapists, psychologists, psychiatrists, pain physiologists,
rheumatologists and pain physicians—many luminaries in the pain field. Not the least of these was Prof.
Patrick Wall who, at that time, was the doyen of research into central pain mechanisms and the creator
of the gate control theory of pain with Prof. Ronald Melzack.

Prof. Wall had been studying smashing the nociceptor with vigor for quite some time and it was not
surprising that he did this beautifully again at the conference. As usual, he pointed out the inaccuracy of
Descartes’ illustration of a person with a pain center in the brain connected to a linear neural pathway
leading from the foot, which is positioned near a fire. Historically, it is probably the most common
depiction of noci-nihilism by illustrating the failure of this linear model of pain. In another contribution with
Noordenbos, Prof. Wall presented a patient with a knife wound in their back in which their spinal cord
was partially cut. Even though the alleged pain pathways had been incised, the patient could still localize
noxious stimuli in their lower limbs—enter idiosyncratic nociceptive pathways and neuroplasticity.

What supports the statement that pain and nociception are not directly linked is that people with
tissue damage, pathology or mechanical dysfunction do not always hurt. This is further supported by
countless daily observations and many studies, the most widely discussed being asymptomatic disc
herniation. This has produced the generalization that pathology doesn’t produce pain which, in light of
a growing body of recent research, is often incorrect. Being the anarchist that he was, Prof. Wall gave a
presentation to pain scientists in which he cogently argued for the statement:

“Pain and nociception have nothing to do with each other.”

He was then asked, “Do you actually believe what you just said?”

Prof. Wall replied, “Of course not, but what if it were true!”

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE i

In my personal communications with him, my understanding was that he never believed that nociception
is unimportant. But he rightfully wanted us to move away from our dependence on pathology and
nociception as a single linear cause of pain and instead stimulate interest in the experiential and
personal aspects of pain for reasons of compassion and humanitarianism, let alone disrupt inappropriate
pathology-based treatments. It was a tremendous step forward, but there are times when this is taken
too far.

When one follows science and clinical practice, pendular effects occur, many notable failures of which
serve as models for caution when reading research on a subject that is early in its development. A
significant one was the gastric ulcer. It was initially thought to be caused by stress, so the world treated it
with psychology. It has since been found to be caused by helicobacter pylori infection and antibacterial
treatment can cure it. Here, our understanding of relationships between pain, pathology and dysfunction
(aka nociception) is still embryonic. It is more complex than Einstein’s theory of relativity, so naturally it
is going to take time to find causes and solutions. In the physical health professions, there has been a
huge pendular effect in the direction of “Nociception is unimportant,” which takes too much simplicity
from noci-nihilism.

A poignant example is the single level disc herniation and degenerative spondylolisthesis. Instead of
selecting asymptomatic or symptomatic subjects and looking for pathologies, the study was done in a
different direction. Data were collected in people with this pathology and tested for a factor that might
differentiate those with and without pain. The presence or absence of segmental instability was what
differentiated whether people had pain.1 Furthermore, there is now systematic review and meta-analysis
evidence of close associations between disc herniation and low back pain.2,3 It now appears that some
of our rejections of pathology and nociception have been premature.

In the neurodynamics area, another example of how things change is when early studies showed a
lack of impairment of median nerve movement in people with carpal tunnel syndrome. From this it
was logically advised: “There is no impairment of nerve movement, so stop mobilizing the nerve.”
After much more study, nerve sensitivity is an important aspect of nerve pain and there is systematic
review evidence of lack of nerve movement in this common clinical problem.4 Massive reductions (up
to 90%) in nerve root excursion occur in people with lumbar radiculopathy from disc herniation.5 Our
group has shown that this is also expressed in reduced spinal cord movement and those who recover
show a return of cord movement to normal.6 Evidence that manual neural mobilization of certain neural
problems can have beneficial effects has also reached the systematic review level.7 As we learn more
about how to study something, some of it sticks and some of it is found to be wrong. The pendulum
often heads back to the middle and a balance in clinical practice returns. It has now become incumbent
upon the clinician to investigate, more proficiently than ever, whether nociception does or does not hurt
in each individual.

A good question to ask of manual therapy is whether it produces changes in tissue structure, nociception
and pain. At its entry into health practice, repetitive strain injury was dismissed by many. Now there
is experimental evidence that repetitive movement not only produces tissue pathology, but it also
produces increased nociception and pain-related behavior. Manual therapy can produce reductions in
nociception, pain behavior and pathology, including scar tissue formation.8,9 Manual therapy produces
a torrent of mechanisms that we are still only learning about. It is fascinating that we believe pain is
an experience influenced by psychosocial factors (true) yet, until recently, we have paid little attention

ii INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE

to the psychosocial, cognitive, conceptual and other central nervous system (and tissue) aspects of
manual therapy. We are told on a psychological basis, “Meet the patient where they are, establish a good
therapeutic relationship, and facilitate them to a better place.” Physically, this is exactly what manual
therapy can be used to do and this book shows the way.

Manual therapy influences many desirable aspects of patient care; Empathy, connection and
communication with the patient; Investigation, “Where is your pain? Is it here, or here?”; Reassurance. It
also helps with visualization, conceptualization and the practice of appropriate movement and exercise.
It provides rapid pain relief and is safer than opioids. It can also be used to educate people on how to
move, which is a cornerstone of self-efficacy and independence. The problem was not so much manual
therapy, but the way it was applied. It clearly can be an aspect of some patient care and integrated with
other interventions; perceptual and behavioral change, self-management and exercise. I see that the
current challenge to manual therapy is great, but it should not cause it to stop. Instead it should change
the way it is done—be specific, or general, or omit it, where the evidence suggests—and this ought to
include both the brain and the body.

This book is a wonderful illustration of how manual therapy can be done in a way that is more in touch
with contemporary musculoskeletal medicine, rehabilitation and pain science. I highly recommend
this book as it is about time someone put it all together. I wholeheartedly congratulate the authors on
this initiative.

References
1. Dombrowski ME, Rynearson B, LeVasseur C, et al. ISSLS PRIZE IN BIOENGINEERING SCIENCE 2018:
dynamic imaging of degenerative spondylolisthesis reveals mid-range dynamic lumbar instability not evident
on static clinical radiographs. Eur Spine J. Apr 2018;27(4):752-762.
2. Brinjikji W, Luetmer PH, Comstock B, et al. Systematic literature review of imaging features of spinal
degeneration in asymptomatic populations. AJNR. American journal of neuroradiology. Apr 2015;36(4):
811-816.
3. Chun SW, Lim CY, Kim K, Hwang J, Chung SG. The relationships between low back pain and lumbar
lordosis: a systematic review and meta-analysis. The spine journal: official journal of the North American
Spine Society. Aug 2017;17(8):1180-1191.
4. Ellis R, Blyth R, Arnold N, Miner-Williams W. Is there a relationship between impaired median nerve
excursion and carpal tunnel syndrome? A systematic review. J Hand Ther. Jan - Mar 2017;30(1):3-12.
5. Kobayashi S, Suzuki Y, Takahiro A, Yoshizawa H. Changes in nerve root motion and intraradicular blood flow
during intraoperative femoral nerve stretch test. Journal of Neurosurgery (Spine). 2003;99:298-305.
6. Rade M, Pesonen J, Kononen M, et al. Reduced Spinal Cord Movement With the Straight Leg Raise
Test in Patients With Lumbar Intervertebral Disc Herniation. Spine (Phila Pa 1976). Aug 1 2017;42(15):
1117-1124.
7. Basson A, Olivier B, Ellis R, Coppieters M, Stewart A, Mudzi W. The Effectiveness of Neural Mobilization for
Neuromusculoskeletal Conditions: A Systematic Review and Meta-analysis. J Orthop Sports Phys Ther. Sep
2017;47(9):593-615.
8. Bove GM, Delany SP, Hobson L, et al. Manual therapy prevents onset of nociceptor activity, sensorimotor
dysfunction, and neural fibrosis induced by a volitional repetitive task. Pain. Mar 2019;160(3):632-644.
9. Bove GM, Chapelle SL, Hanlon KE, Diamond MP, Mokler DJ. Attenuation of postoperative adhesions using
a modeled manual therapy. PLoS One. 2017;12(6):e0178407.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE iii

Preface
The effectiveness of manual therapy treatments and whether or not to use them has been an ongoing
debate among therapists for some time. The debate has intensified in recent years as our understanding
of pain science has evolved and the results of more studies have come out refuting some of the traditional
theories behind the efficacy of manual therapy. The idea to write this book began with a typical bar
napkin brainstorming session and discussion around our point of view: We need not focus on “manual
therapy OR pain science,” but instead, “manual therapy AND pain science.” Just as all knowledge and
clinical practice evolve over time, manual therapy and pain science are both evolving and the clinician
needs to evolve, too. That is where the 12 Principles in this book come in.

As the authors, we each have a physical therapy origin story which includes being initially trained to
utilize manual therapy as part of our clinical practice. As we have come to know each other and work
closely together—teaching and conducting research into pain science— none of us has abandoned the
foundation of our clinical experience. That’s why we continue to use and conduct research into manual
therapy, as well. As each of us has come to understand pain and neuroscience better, we have shifted
the way we use manual therapy based on the pain neuroscience principles shared in this book. Now,
we want to share these principles with you.

Principle 1: Effectiveness of Manual Therapy, “It Works,” discusses some of the many ways the
neurophysiological and biopsychosocial aspects of manual therapy can effectively help people in pain.

Principle 2: Clinical Reasoning Is a Cornerstone of Manual Therapy, “Think Big,” looks at how the
clinician’s clinical reasoning needs to evolve with the updated science regarding pain and manual
therapy. As a cornerstone of clinical practice, it’s important for manual therapists to utilize sound clinical
reasoning based on current evidence and emerging models of pain.

Principle 3: Reshaping Beliefs and Attitudes about Pain, “Know Pain; Know Gain,” covers various
models of pain. How do we as humans, and manual therapists, learn about pain? What models have
shaped our beliefs and led us to where we are now? This principle aims to draw manual therapists “out”
of the tissues, to some extent, and have them explore bigger, broader concepts around pain.

Principle 4: Nociception and Pain Are Not the Same Construct, “Nociception ≠ Pain,” reminds us that
tissues do matter. Nociceptive information is relevant, but pain and nociception are different constructs.
We cover in more detail how the pain type classifications can reconceptualize how we use manual
therapy depending on what pain type the patient presents with.

Principle 5: Language Matters, “Sticks and Stones,” is about the words we use and how they make a
difference. We dive into the research around words and language and the effect communication can
have on the therapeutic alliance and the patient outcome. Manual therapy is usually thought of as being
“all about your hands,” but a therapist’s words matter, too.

Principle 6: Nerves Are Sensitive for a Reason, “Don’t Be So Sensitive,” delves into the clinical complexity
of allodynia, hyperalgesia and central sensitization (nociplastic pain). Some level of sensitization is
present in every patient presenting for treatment and ranges from local sensitization to extreme pain—all
impacting the physical examination and treatment offered by manual therapists. This section provides
a clinical, working knowledge of sensitization for clinicians.

iv INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE

Principle 7: The Brain Has a Body Map, “Use it or Lose it,” gets into a deeper understanding of
neuroplasticity. Functional and structural changes in the brain can powerfully influence a pain
experience. For manual therapists especially, the dynamic health of the cortical maps may powerfully
influence pain. We show how manual palpation (examination and treatment) may indeed be a form of
sensory integration and discrimination, which may ease pain.

Principle 8: The Importance of Hands-On Therapy, “We Are Physical Beings,” makes sure we do
not swing the neuroscience pendulum too far by discussing only the mind. We need to make sure we
don’t forget about the physical body. We discuss how a physical examination should be seen from a
neuroscience perspective.

Principle 9: Trust Is the Foundation of Therapeutic Alliance, “Trust Me,” looks into how the relationship
between the therapist and patient is part of the healing process. Building a better therapeutic alliance
with your patient has been shown to improve outcomes. We explore the primary components of
therapeutic alliance and how we can become intentional about this during a clinical visit.

Principle 10: The Importance of Assessing for Yellow Flags, “Caution Ahead,” opens the door to a
discussion about the psychosocial issues that are a part of every patient we treat. Just as we mentioned,
we can’t swing the pendulum too far away from the bio of the physical person. We need to keep the
balance and realize that psychosocial factors can also shape our patients. We walk through how to
assess for yellow flags and what to do upon finding them.

Principle 11: Additional Treatments Complement Manual Therapy, “One for All and All for One,”
discusses how no one treatment is ever going to “fix” something as complex as persistent pain. There
are lots of different treatments that can be helpful, and it is a skilled manual therapist/clinician who can
find the right combination to help the patient in front of them. We touch on many different interventions
that can be helpful in treating people in pain. Gone are the days of the “one-trick pony” when it comes
to manual therapy.

Principle 12: Putting More Thought into Treatment Choices, “Right Treatment, Right Time, Right
Patient,” reviews how the principles fit into a sound evidence-based practice treatment plan that is
created around each individual patient. We walk through the process of putting the various principles in
the book into clinical practice based on the needs of the patient in front of you.

This is not meant to be a definitive “be-all and end-all” book on manual therapy, or pain science. As
new knowledge comes to light, new principles will have to be added and old principles changed and
modified. Some of the principles may be argued differently than how we are presenting them now,
which is great. Our hope is that these important topics continue to spark lively discussion and debate to
improve our understanding, and ultimately, improve the lives of the patients we care for.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE v

Acknowledgements
Writing a book is never an easy task. This book is a culmination of thoughts and ideas from many people
who have influenced us throughout our careers.

We would be remiss if we did not acknowledge the many influential therapists and researchers who
we have learned so much from and who have helped develop our views on these principles of manual
therapy and pain science. From those forming the foundations of our manual therapy knowledge, like
James Cyriax, Gregory Grieve and Geoff Maitland, to those blazing a trail into the realm of neurodynamics
and mobility of the nervous system, like David Butler, Michael Shacklock and Michel Coppitiers, and of
course, those whose ideas are expanding our horizons to include the brain, like Louis Gifford, Clifford
Woolf and Lorimer Moseley. We have been lucky to meet and rub shoulders with some of the greatest
minds in manual therapy and pain science. For that we are truly thankful.

To every student and clinician who has taken classes from us throughout the years, you have challenged
us to stay current with the evidence while keeping the day-to-day clinical practice practicality in mind,
which has motivated us tremendously.

We MUST thank our patients over the years for teaching us—often before the books or studies could get
it right—about compassion, empathy, the importance of listening and touch, and that they must remain
the focus of this equation—not us.

Most of all, we want to thank our families for the immense support they have provided us through the
years. Without their understanding and encouragement, none of this would be possible. The pain and
manual therapy world may know our names; Adriaan, Louie, Kory and Steve, but they should also know
these names; Colleen, Danielle, Janet and Tina.

Adriaan Louw
Emilio “Louie” Puentedura
Steve Schmidt
Kory Zimney

vi INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE

Table of Contents

INTRODUCTION:
The Current State of Manual Therapy.................................................................... 1

PRINCIPLE 1:
Effectiveness of Manual Therapy ........................................................................... 21

PRINCIPLE 2:
Clinical Reasoning Is a Cornerstone of Manual Therapy .................... 41

PRINCIPLE 3:
Reshaping Beliefs and Attitudes About Pain ................................................. 67

PRINCIPLE 4:
Nociception and Pain Are Not the Same Construct................................. 95

PRINCIPLE 5:
Language Matters............................................................................................................. 111

PRINCIPLE 6:
Nerves Are Sensitive for a Reason .....................................................................125

PRINCIPLE 7:
The Brain Has a Body Map..........................................................................................153

PRINCIPLE 8:
The Importance of Hands-On Therapy ............................................................175

PRINCIPLE 9:
Trust Is the Foundation of Therapeutic Alliance ....................................195

PRINCIPLE 10:
The Importance of Assessing for Yellow Flags ........................................ 209

PRINCIPLE 11:
Additional Treatments Complement Manual Therapy ......................... 221

PRINCIPLE 12:
Putting More Thought into Treatment Choices ........................................ 239

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE vii

List of Abbreviations
CBT Cognitive Behavioral Therapy
CLBP Chronic Low Back Pain
CNS Central Nervous System
CPR Clinical Prediction Rule
CRPS Complex Regional Pain Syndrome
CS Central Sensitization
CSI Central Sensitization Inventory
DRG Dorsal Root Ganglion
EBM Evidence Based Medicine
EBP Evidence Based Practice
FABQ Fear-Avoidance Beliefs Questionnaire
fMRI Functional Magnetic Resonance Imaging
GMI Graded Motor Imagery
HPA Hypothalamus-Pituitary Axis
IASP International Association for the Study of Pain
IFOMPT International Federation of Orthopaedic Manipulative Physical Therapists
KeeleSBT Keele StartBack Tool
LBP Low Back Pain
MOM Mature Organism Model
MCID Minimal Clinical Important Difference
MDC Minimal Detectable Change
NPRS Numeric Pain Rating Scale
ODI Oswestry Disability Index
PAG Periaqueductal Grey
PCS Pain Catastrophization Scale
PET Positron Emission Tomography
PNE Pain Neuroscience Education
PPT Pressure Pain Threshold
PT Physical Therapy
RCT Randomized Clinical Trial
ROM Range of Motion
RSD Reflex Sympathetic Dystrophy
SLR Straight Leg Raise
SPECT Single-Photon Emission Computerized Tomography
TA Therapeutic Alliance
TENS Transcutaneous Electrical Neuromuscular Stimulation
TPD Two-point Discrimination
TSK Tampa Scale of Kinesiophobia
US United States (of America)
WAD Whiplash Associated Disorder

viii INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE

 INTRODUCTION

The Current State of Manual Therapy

Close your eyes for a moment and imagine you’re a clinician in the 1970s or 1980s. You’re
surrounded by manual therapy pioneers such as Cyriax, Grieve, Maitland, Kaltenborn,
McKenzie, Mulligan and more.1 Manual therapy conferences are buzzing with excitement,
heated discussions, live patient demonstrations by various “gurus” and the inevitable turf
battles.2 Manual therapy seminars are overflowing with attendees. Clinicians who are investing
significant time and money to learn the latest techniques, become fixated on one approach to
become a “Maitland therapist” or a “McKenzie therapist,” etc.

The clinical side is even more idyllic; patients flock to manual therapy clinics and seemingly
present with 100% mechanical, nociceptive-based pain states, in need of skilled manual
therapy treatments. For the pure manual therapist, time is not to be wasted on exercise; find
the problem and fix the problem. The skilled manual therapist seemingly “finds” the main
problem effortlessly, “fixes it” and the pain is gone! This is the heyday of manual therapy.
Fibromyalgia does not even exist in these clinics. If patients do not respond to the treatment
it’s either the skill, or lack of skill, of the clinician (more classes are needed), or the patient
is at fault because they “undid” the treatment through their activities outside the clinic. The
best part? The documentation. Subjective: patient is better. Objective: movement is better.
Treatment: same as the last time. Done. Next patient. At this time, we’ll pause for the “old
timers” to reminisce and think back to the glory days. In some regions of the world, the
patient’s “chart” existed on a 3” x 5” index card that you carried in your back pocket. For
young clinicians, this is something so unbelievable it’s worthy of an episode or two on the
History channel!

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 1

Fast forward nearly 50 years. The world
has changed so much for the modern
manual therapist:

• There is a global epidemic of pain,

especially chronic pain.3,4

• The Institute of Medicine estimates that, in the United States (US) alone, 126.1 million
adults experience pain over a three-month period, with 25.3 million suffering from daily
chronic pain.5,6

• The chronic pain epidemic seems to be increasing—an alarming fact backed by

epidemiological data from the early 1990s showing one in seven people were struggling
with chronic pain whereas, recent data indicate it is now closer to one in four.4,5,7

The challenges for the manual therapist do not stop with chronic, widespread pain, but are
also present with the most ubiquitous of “musculoskeletal” complaints; chronic spinal pain.
Even though billions of dollars have been spent on it annually,8 9 low back pain (LBP), is still the
most widely reported musculoskeletal disorder and accounts for 25% of outpatient physical
therapy (PT) visits.10-12

• The rates of chronic low back pain (CLBP) are increasing, as well as associated disability
and healthcare-seeking behaviors.13-16

BACK PAIN

DISABILITY

TIME

Rates of low back pain and disability over time.

2 INTRODUCTION
• Studies show that people still struggle with back issues months to years after treatment.17,18

• At least two out of three people struggle with neck pain during their lifetime and 50% of
people reported having difficulty with neck pain during the last year.10,11,19-22

• As with LBP, neck pain accounts for 25% of outpatient PT visits in the US,11 thus implying
that 50% of outpatient PT case volumes consist of neck and back pain, many of which
progress to chronicity.19

• Although few studies are available on the topic, it is estimated that one in four people
experience some type of thoracic pain annually,23-27 which is prone to progress toward
chronic pain.28 By adding thoracic pain into the mix, it can easily be estimated that nearly two
out of three patients who attend outpatient PT do so because of problems with spinal pain.

Don’t think manual therapy has become challenging enough? Beyond the prevalence of
chronic pain and high rates of spinal pain, consider the following:

• In many industrialized countries, the proportion of the older population is increasing

rapidly.29 This creates additional challenges for manual therapists treating aging
populations, including multiple co-morbidities and complex health conditions.30-33

• With the call for evidence-based medicine (EBM), there is a constant need to present
the “evidence” for manual therapy.34-40 The evidence for thrust joint manipulation is
moderate at best, though possibly stronger when patients are sub-grouped.1,41-45 For other
manual therapy interventions such as spinal mobilization and neural tissue mobilization
(neurodynamics), the evidence is even less compelling.46-50

• A push toward a biopsychosocial framework has led some to question the tenets of a
manual therapy approach. For example, use of a hands-on approach may result in a risk
of patients becoming dependent upon the therapist and not shifting the locus of control
to the patient.50,51

• There is compelling evidence that palpation, a traditional cornerstone of assessment for the
manual therapist, has limited efficacy, especially when considering reliability of segmental
mobility assessment and bony landmarks.52,53

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 3

• Documentation. This is not unique to
manual therapists, but it surely impacts
the modern manual therapist more than
in the past. The push toward standardized
electronic medical records has negated or
minimized the “hieroglyphics” of old school
manual therapy documentation, which
allowed for an abbreviated (shorthand)
and consistent form of communication
(within the profession of manual therapy).

• Current best evidence contained in

various practice guidelines requires the
addition and increased use of exercise by
the modern manual therapist.54-56

• Advances in various fields of therapy, such as psychosocial constructs of pain, patient

expectations, etc., require the modern therapist to become a “jack of all trades” versus
the specialized manual therapist, even within manual therapy. Long gone are the days of
only following one approach. The modern manual therapist surely must be able to perform
manual therapy techniques (including thrust joint manipulation, mobilization, muscle-
energy, neural mobilization, soft tissue mobilization, etc.), but also teach various forms of
exercise, possibly utilize dry needling, teach a patient more about pain, etc.

4 INTRODUCTION
• The regulatory and economic climate, including pay-for-performance, ever-increasing
deductibles and copays, creates a practice environment in which clinicians are required
to demonstrate value in their treatments (and show it fast).63

• Continued dominance of biomedical models has shown an inability to explain a human’s

pain experience,57-60 and may increase a pain experience via constructs such as fear-
avoidance61,62 and pain catastrophization.63,64

• There is an expanding scope of interest, both inside and outside of manual therapy. To be
a skilled and well-rounded clinician, there is no longer only one “guru” to follow. Outside of
the manual therapy world, expanding interests, driven by current social issues (i.e., opioid
epidemic, concussions in sport and combat, etc.) have led to increased areas of practice
expertise including dry needling, pain science, pelvic health, concussion management,
post-traumatic stress disorders, etc.

• Lower reimbursement and increased productivity demands drive delegation of various

treatments to support personnel who are not allowed, trained, able or willing to perform
manual therapy.65

The list goes on and on. The reality is that the

modern manual therapist faces significantly
more (and possibly different) challenges in
the current practice environment than in the
past. This book is about those challenges,
especially when it comes to the understanding
and treatment of pain from a neuroscience
perspective. We strongly believe that the same
skill sets that make manual therapists great
in a biomedical and orthopedic domain can
become their greatest assets when it comes
to taking on these various challenges, but only
if they’re open-minded and willing to embrace
change.50,66,67 Pain science did not emerge as a
means to replace manual therapy, but rather to
enhance it. But it’s only for the bravest manual
therapists who are willing to shift their paradigm.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 5

Emerging Pain Science…Out of Manual Therapy
Utilizing pain science within the context of physical therapy care is seen through various
treatments specifically aimed at treating pain, especially chronic pain. This includes pain
neuroscience education (PNE), neural tissue mobilization, graded motor imagery (GMI),
sensory discrimination training, etc. What is interesting is that much of our understanding of
pain science has emerged out of manual therapy, thus implying that these two approaches
are not mutually exclusive.

Neural Tissue Mobilization

Neural tissue mobilization, as we currently understand it, has a rich history from our current
manual therapy perspective.

• James Cyriax: Dr. James Cyriax (1904-1985), the author of the 1954 classic Textbook of
Orthopaedic Medicine, was likely the most influential and iconic “manual therapist.” Apart
from his exceptional high-velocity thrust skills, descriptions of capsular patterns, cross
friction and end-feel assessments, he also had an interest in, and published writings,
related to neural tissue irritation and movement.68 Cyriax studied and wrote about various
aspects of “dural pain” including the use of passive neck flexion “pulling the dura upward”
and straight leg raise “pulling the dura down,” thus assessing its sensitivity to movement.68

• Geoff Maitland: Australian manual therapy icon Geoff Maitland (1924-2010) was known
for his meticulous examinations, clinical reasoning, “comparative signs” and use of gentle
oscillatory mobilization techniques. However, Maitland also had an interest in neural tissue
movement. In the late 1970s and subsequent 1980s, Maitland took the Cyriax concept of
“dural pain” further with his interest in and writings on the slump test.69-71

• Bob Elvey: Bob Elvey (1943-2013) was a gifted educator, clinician and manual therapist,
serving as the president of Musculoskeletal Physiotherapy Australia from 1981 to 1985 and
president of the International Federation of Orthopaedic Manipulative Physical Therapists
(IFOMPT) from 1984 to 1992.72 Elvey, however, is best remembered for his clinical and
cadaveric studies into the development and now widespread use of the various upper limb
neurodynamic tests.73-75

• David Butler: One of the most noteworthy therapists that emerged from Geoff Maitland’s
postgraduate diploma in manipulative therapy at the University of South Australia was
David Butler. During and immediately following his manual therapy training, Butler, along
with various other manual therapy classmates (Gifford, Shacklock, etc.), published a series
of thought-provoking papers and book chapters (in manual therapy textbooks) on neural
tissue mobilization.76-81 In 1991, Butler’s now iconic book, Mobilisation of the Nervous
System, became a “must read” for all manual therapists with an interest in mobilizing
neural tissue.82 From within these teachings of manual therapy for the nervous system,
additional pain science emerged, culminating in PNE.83,84

6 INTRODUCTION
 Shacklock Coppieters Neurodynamics
Butler
nsion
r a l Te
Elvey Neu
Cyriax McKenzie
Maitland
Manual Therapy
Mennell Kaltenborn Mulligan
Grieve

TIME

Emergence of neurodynamics out of manual therapy.

The aforementioned manual therapists who played a significant role in the evolution of neural
tissue mobilization were by no means the first, or only, manual therapists to explore active
and/or passive movement of the nervous system. The history of neural tissue movement
is far more extensive and historical than portrayed here. For example, it could be argued
Imhotep (2800 BC) described the slump test: “When he extends (both legs), he contracts
them both immediately, because of the pain he causes in the vertebra of his spinal column.”85
The intent of this book is not to delve into a historically accurate description of neural tissue
mobilization, but rather make the case that neural tissue mobilization emerged, in part, out
of traditional orthopedic approaches featuring many of the revered manual therapy “gurus.”
Many neurodynamic tests and neural mobilization techniques are described in various manual
therapy textbooks by these pioneers.71,82,86,87 Although a modern neurodynamics approach
now includes advanced pain science concepts such as glial cell activity, central sensitization,
neuroplasticity, neuroimmune responses, etc.,88-91 the manual handling skills (tests and
treatments) still resemble and build upon some of the original manual therapy concepts.2,82,85

Pain Neuroscience Education

In the literature, PNE as we currently view it began approximately 20 years ago thanks
to the late Louis Gifford.57,92 PNE started as a blend of basic science, clinical experience,
collaboration with other professionals and PTs’ newfound interest in neurodynamics in the
mid-to-late 1980s.58,93,94 The early neural tissue mobilization, however, was more likely
Pain
“another tissue to mobilize,” using similar manual therapy principles and Nijs vantage points.93 To
Neuroscience
Education
its credit, neural tissue mobilization did move us out of the jointsMoseley and muscles (biomedical
Butler
model), inching us closer to the brain, the nervous system and viewing our patients through
Gifford
a multisystem approach (biopsychosocial model).93 As our understanding of pain grew, it
sprouted PNE. This newfound interest culminated inShacklock early pain Coppieters
science papers, 84,94
along with
Neurodynamics
the first documented presentation of PNE, Butler
“Explaining Pain to Patients” at the International
l Te n s i o n
Association for the Study of Pain e u r a in Austria in 1999 by Louis Gifford and
(IASP) conference
Elvey N
Heather Muncey.95 By virtue of explaining a pain experience to a patient with this newfound
knowledge of pain,Cyriax
PNE was developed. McKenzie
Maitland
Manual Therapy
Mennell Kaltenborn Mulligan
Grieve

TIME
INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 7
 Pain
Nijs Neuroscience
Education
Moseley
Butler
Gifford
Shacklock Coppieters Neurodynamics
Butler
nsion
r a l Te
Elvey Neu
Cyriax McKenzie
Maitland
Manual Therapy
Mennell Kaltenborn Mulligan
Grieve

TIME

Emergence of pain neuroscience education out of neurodynamics, out of manual therapy.

The first study involving PNE was published by Moseley in 2002.96 Since then, research into
PNE has expanded to include published case studies, case series, randomized controlled trials
and various systematic reviews.97 Recent PNE research has shown that PNE combined with
movement (including manual therapy) is superior to PNE only,97-99 once again underscoring
the fact that manual therapy and PNE may indeed be mutually inclusive versus exclusive.67

Graded Motor Imagery (GMI)

Of the three pain science approaches currently surrounding manual therapy, GMI is the most
recent in the orthopedic/manual therapy realm. GMI is a collective term describing various
therapeutic strategies aimed at targeting cortical reorganization associated with chronic
pain states. GMI commonly includes normalizing laterality (left/right discrimination of body
parts), motor imagery (a form of visualization), mirror therapy, sensory discrimination and
emerging virtual reality applications.100-102 Given GMI is a collective term incorporating various
techniques, the history of GMI is less clear and evolves from multiple different perspectives
Psy
and disciplines. For example, mirror therapy as it is currently used and understood can be
cho
lo g y
traced back to Ramachandran’s “virtual reality box” in 1995.103 It could obviously be argued
that mirrors, since being invented (6000 BC), have likely influenced movement
Sports Science
and
Graded human
Motor
performance since the start. Left/right judgment studies from the worldMoseley Imagerystarted
of psychology
emerging in the mid-1970sienand ce then progressed from there with increasing interest from other
sc Butler
uro
disciplines.104-107 Motor
Ne imagery may be traced back to philosopher Aristotle (384-322 BC)
with his concept of “phantasia” or mental imagery in cognition.108 Given the vastPain amount of
Nijs Neuroscience
information available on motor imagery, it could be argued that it culminated from a blend of
Education
Moseley
education, medicine, music, psychology and sports. 109
Butler
Gifford
Shacklock Coppieters Neurodynamics
Butler
n
ra l Te n s i o
Elvey Neu
8 INTRODUCTION
Cyriax McKenzie
Maitland
 Psy
cho
lo gy

Sports Science Graded Motor

Imagery
Moseley
e
scienc Butler
uro
Ne
Pain
Nijs Neuroscience
Education
Moseley
Butler
Gifford
Shacklock Coppieters Neurodynamics
Butler
n
ra l Te n s i o
Elvey Neu

Cyriax McKenzie
Maitland
Manual Therapy
Mennell Kaltenborn Mulligan
Grieve

TIME

Emergence of graded motor imagery.

So, where does manual therapy fit in? Even though not directly “from” manual therapy, current
pain science approaches around manual therapy utilize various components of GMI.66,110,111
The end result? If the modern manual therapist wants to develop a pain science approach in
their manual therapy practice, then knowledge and application of neurodynamics, PNE and
GMI is required.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 9

The Body Has a Brain
The end result of the emergence of pain
science in the last two decades was a “brain-
centric” perspective of the nature of pain and
interventions targeting pain relief. The paradigm
shift around pain that was beginning to occur
in manual therapy also coincided with the
publication of Ron Melzack’s revolutionary
pain neuromatrix concept in 2001.112 The
neuromatrix theory of pain proposed that pain
is a multidimensional experience produced
by a characteristic pattern of nerve impulses
generated by a widely distributed neural network in the brain. This pattern of brain activity is
also referred to as a “neurosignature.” It is thus believed that pain is produced as an output of
a widely distributed neural network in the brain rather than directly by sensory input evoked
by injury, inflammation or other pathology.

Pain is a multiple-system output, activated by an

individual’s specific pain neural signature. The neural
signature is activated whenever the brain concludes that
the body tissues are in danger and action is required.113

The evolution of the neuromatrix concept can likely be traced to the development of advanced
brain scanning technologies in the early 1990s.114,115 Scientists using positron emission
tomography (PET) and single-photon emission computed tomography (SPECT) scans showed
that, with the application of painful superficial cutaneous heat stimulation, multiple cortical
and subcortical brain areas were activated.116,117 This technology shifted attention toward the
human brain and its role in a pain experience, ultimately culminating in the conceptualization
of the pain neuromatrix concept.112,118

10 INTRODUCTION
fMRI of a patient with lower back pain during painful tasks (image from Louw, et al.).119

This “brain-shift” led to various positive outcomes. For example, it can be argued it catapulted
the biopsychosocial constructs of pain, allowing modern manual therapists to become
increasingly aware of issues such as emotions and pain, cognitions and pain, the influence of
fear-avoidance and pain catastrophization, yellow flags, etc. In fact, over the last two decades,
many PT and manual therapy conferences regularly featured keynote and breakout sessions
on these various concepts. An apt quote coined on social media during a recent American
Academy of Orthopaedic Manual Physical Therapists Conference sums up the state of affairs:

“I showed up at a manual therapy conference

only to have a pain conference break out!”

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 11

The one pain science area that has
blossomed during this “brain-centric”
period is PNE. If pain is 100% produced
by the brain, then education must be
the only way to help, right? It is argued
the increased use and teaching of PNE
might have had clinicians question the
use and importance of manual therapy
Tissues Brain
skills, including manual handling of the
neural tissue (neurodynamics).50 This
shift toward a brain-centric perspective
culminated in some cynical and overly
simplified ideas such as:

• “No need for skilled manipulation and localized techniques because it’s all non-specific
effects anyway; no need to be detailed in treating the tissues.”

• “It’s not important to address problems with body tissues related to pain problems; it’s all
about the brain—no need to treat the various tissues of the body.’”

What are the potential consequences to a brain-biased perspective on pain? It is clear that
the shift toward the brain is largely to blame for clinicians questioning the importance of
manual therapy.

But…the Brain Has a Body, Too

Hindsight is 20/20. With the brain being the focus,
the biopsychosocial model of pain likely shifted to the
psychosocial model of pain, leaving behind “the bio.”
The bio, or biological aspects of care, pertains heavily
to manual therapy and it’s time to re-establish the
bio component of a true biopsychosocial approach.
Why bio? Modern pain science has demonstrated that
chronic pain causes functional and structural changes in the brain. Additionally, peripheral
biological and physiological processes (which can be altered with manual therapy) play a
powerful role in a human being’s pain experience. For example:

• It has been shown that injury to peripheral nerve or noxious electrical stimulation produce
activation of C-fibers within peripheral nerves. The resultant barrage of nociceptive impulses
into the central nervous system (CNS) cause an increase in the permeability of the blood-
spinal cord barrier as well as the blood-brain barriers.120 Both of these barriers are critical
in the CNS’s ability to extract and receive correct information from the periphery, including
location, side of the body, etc. These studies demonstrated heightened microglial activity
in the dorsal horn of the spinal cord, on the affected side, which triggers a cascade of

12 INTRODUCTION
 widespread immune changes.120,121 The end result is that a biological peripheral process
results in central and cortical changes critical in the development and maintenance of a
human’s pain experience. What is even more intriguing, and likely clinically relevant, is
the fact that the blood-spinal cord and blood-brain barrier changes occur after only a few
hours of nerve compression,120,121 whereas clinicians often see patients with peripheral
neurogenic contributions (i.e., radiculopathy) that have been present for weeks, months
and even years.

• The neuropeptide oxytocin is known to have anti-nociceptive and analgesic, as well

as anxiolytic and antidepressant effects; all very important in easing a human’s pain
experience.122 The intriguing part is that oxytocin is not only increased with the establishment
of trust as part of the therapeutic alliance (TA), but oxytocin levels are powerfully influenced
with hands-on skillsets including massage and manual therapy.123-125

• A plethora of qualitative studies have shown that patients want to be physically examined
and touched, including the use of manual therapy.126,127 Additionally, it has been shown
that patients’ beliefs regarding manual therapy enhance treatment outcomes.45

• In neurodynamics, current research has focused on neuro-inflammation and the effect

of active and passive movement.88 For example, passive neural mobilization induces
dispersion of intraneural fluid, which is associated with peripheral neuropathic pain;
constant barrage into the CNS and potential development of central sensitization (CS).128,129

• Neural mobilization reverses behavioral and cellular changes that characterize neuropathic
pain and also decreases neuroimmune activity, specifically glial cell activity.130

• Spinal mobilization changes inflammation around the nerve root and dorsal root ganglion,
which ultimately reduces the pain experience.131

Want more evidence that the brain has an interdependent relationship with the body? It has
been shown that immobilization of body parts results in a rapid alteration in sensorimotor
representation and is powerfully linked to neuroplastic changes associated with development
and maintenance of a pain experience.132-135 The opposite of immobilization? Movement, active
and/or passive. It could be argued that modern pain science clinicians who follow a “brain-
centric-only” approach (such as a PNE-only, hands-off approach) are limiting their efficacy
and definitely not practicing a true biopsychosocial approach. Sure, the anti-manual therapy
critic can argue there are many “non-manual” styles of movement such as aerobic exercise
which can be combined with cognitive behavioral therapy (CBT), but we argue (and explore
in later principles) that there is a definite place for skilled passive movement, deliberate touch
and other forms of movement applied by a manual therapist. However, to do this effectively, it
is critical that the modern manual therapist update their pain science knowledge.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 13

Pain Science: Hands-On or Hands-Off?
A review of the previous sections hopefully has the manual
therapist and “pain clinician” starting to reconceptualize the
notion of pain science and manual therapy cohabitating. Is
a pain science approach hands-on or hands-off?51 Is this
just “another excuse” to force a square peg into a round
hole? We argue no, not even close! Neuroscience has given
us an amazing opportunity to embrace the future, but only
for those open and brave enough to change:

• The manual therapist must carefully reconsider the underlying mechanisms of what
manual therapy exactly does. This includes letting go of archaic ideas of manual therapy.
They must change their language and let go of provocative biomedical, fear-inducing
explanations of pain and pain experiences.136 They must become more aware of the non-
specific effects of manual therapy and realize placebo is real, can be measured, plays
a huge role in patient outcomes and has shown some of the most robust effects on
reducing pain.137

• For the anti-manual therapy (hands-off conceptualization) or the “pain-science-is-the-

only-way” practitioner, the time is also now. Now is the time to recognize the brain has
a body and many biological, peripheral “tissue issues” powerfully drive both cortical re-
organization and a human’s pain experience. With that appreciation, the clinician can
utilize movement, including passive movement, as a significant vehicle to alter brain
processes and positively change a patient’s pain experience.

The end result? Louis Gifford, who pioneered much of the current pain science from a manual
therapy perspective, is famous for proposing (and will be emphasized in this book):

“Top-down before bottom-up and top-down

while bottom-up.”93

14 INTRODUCTION
Gifford implied that clinicians (especially manual therapists) teach, educate and alleviate
psychological distress (i.e., fear-avoidance and pain catastrophization) before embarking on
a bottom-up (tissue) treatment, i.e., manual therapy. Anecdotally, good manual therapists
do this very well. Gifford also implied educating while doing physical/tissue (bottom-up)
treatments, which is in line with current best-evidence for PNE.97 Notice, there’s no mention
of “only top-down” or “only bottom-up.” As modern manual therapists, embracing current
pain neuroscience revelations, it is critical to avoid splitting the body and the brain. They
both reside together in symbiosis, and one cannot thrive without the other. In the same way,
our treatment cannot be directed in only a physical domain but must integrate the whole of
our systems.

Sample
Tissues Tissues

Environment Environment

Conclusion
We hope, after reading the introduction, you’re excited to explore the interdependence of
manual therapy and pain science; we are. That’s why, instead of rewriting a manual therapy
book that “painificates” every aspect of traditional manual therapy (subjective examination,
physical examination, treatment, etc.) we opted to explore the most poignant pain issues as
they pertain to manual therapy. What follows are 12 thought-provoking principles manual
therapists and pain specialists could use to explore the merger of pain science and manual
therapy—each on their own as a stand-alone thought—or combined into an overall shift.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 15

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Miller T, Mintken PE. Immediate Effects of Mirror
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112. Melzack R. Pain and the neuromatrix in the
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113. Moseley GL. A pain neuromatrix approach to
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114. Flor H. The functional organization of the brain
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19
115. Flor H, Braun C, Elbert T, Birbaumer N. Extensive
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116. Talbot JD, Marrett S, Evans AC, Meyer E, Bushnell
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118. Melzack R. From the gate to the neuromatrix.
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20 INTRODUCTION
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 PRINCIPLE 1

Effectiveness of Manual Therapy

1.1: Hypoalgesic Effect ........................................ 23

1.2: Psychosocial Effect ...................................... 25

1.3: Mechanical Effect ......................................... 28

1.4: Autonomic Effect ........................................... 29

1.5: Neuromuscular Effect ................................ 30

1.6: Chemical Effect............................................... 30

1.7: Neuroplastic Effect....................................... 32

1.8: Socioeconomic Effect ................................ 34

Conclusion......................................................................... 35

Principle 1 References ............................................ 36

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 21

It Works
Every day thousands of patients experiencing
low back pain, neck pain, etc., receive
manual therapy treatments. A number of
these patients leave “significantly better,” be
it with decreased pain, improved movement
or decreased disability.1 Assuming for one
second that manual therapy techniques occur
in a vacuum and we can negate the various
outside factors (non-specific effects),2 the use
of manual techniques often results in positive
outcomes. What exactly are the effects of manual therapy? This question, and its answers,
powerfully demonstrate how strongly pain science and manual therapy are correlated.

In 1992, Lance Twomey published a paper in the Physical Therapy journal entitled “A rationale
for the treatment of back pain and joint pain by manual therapy.”3 The paper was a breath
of fresh air, since there was little interest at that time in understanding the effects of manual
therapy apart from “decreasing pain, increasing movement and making people better.”
The introduction of evidence-based practice (EBM) in the latter part of the 1990s focused
attention on the efficacy and effectiveness of treatments, including manual therapy.4 This led
to an explosion of various studies aiming to prove manual therapy works, even though the
exact underlying mechanisms remained speculative and unknown. For example, in the journal
Manual Therapy in 2009, Bialosky and colleagues published an iconic paper that examined
the current thoughts on the underlying mechanisms behind manual therapy.2 In their paper,
the authors cite just 18 references prior to the year 2000 and only eight of those papers include
research that directly studied the potential mechanisms underlying manual therapy. Sure,
EBM focused on clinical effectiveness, but the increased research activity soon boiled over
into basic science studies, including studies exploring the underlying mechanisms of manual
therapy. In line with the evolution of manual therapy, early manual therapy mechanism studies
focused heavily on mechanical reasons for its proposed success, including “movement of
vertebrae,” “changing bony alignment,” “direct effects on collagen and cartilage,” etc.3,8,9 Fast
forward 20 years, and we realize the mechanical aspects of manual therapy are likely not the
main mechanisms behind patient improvement following manual therapy.2

22 PRINCIPLE 1 | EFFECTIVENESS OF MANUAL THERAPY

Back to the question: What are the effects of manual therapy? In line with the original model
Bialosky and colleagues introduced, we propose eight broad categories for the underlying
mechanisms for manual therapy:

• Hypoalgesic effect • Neuromuscular effect

• Psychosocial effect • Chemical effect

• Mechanical effect • Neuroplastic effect

• Autonomic effect • Socioeconomic effect

Please realize, this is not a complete or authoritative list of manual therapy mechanisms,
but rather a list that can help you recognize some possible mechanisms underlying manual
therapy efficacy. These mechanisms incorporate a lot of current pain science concepts into
manual therapy. Furthermore, please realize these mechanisms do not work in isolation, and
there is a powerful interplay between all the various mechanisms.

1.1: Hypoalgesic Effect

When a patient seeks treatment one of the primary
goals is the reduction of pain.10 One mechanism
that contributes to reduced pain is hypoalgesia,
or a decreased sensitivity to nociceptive stimuli
associated with pain.2 It is argued that the analgesic
response to manual therapy is likely due to stimulation
of afferent nociceptors into the CNS, which in turn
triggers descending inhibitory pathways originating
primarily from the periaqueductal grey area (PAG)
of the midbrain.2,11-13 This theory of a centrally
mediated hypoalgesic mechanism is underscored
by various studies showing immediate local and
remote effects following manual therapy, especially
thrust joint manipulation.14-16 Of clinical note is the ability of a manual technique to facilitate a
hypoalgesic effect in a remote area. For example, Cleland et al., showed that thoracic thrust
joint manipulation resulted in immediate analgesic effects in patients with mechanical neck
pain.15 Fernandez-Carnero et al., showed that cervical spine thrust joint manipulation produced
an immediate bilateral increase in pressure pain thresholds and pain-free grip strength in
patients with lateral epicondylalgia.17

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 23

 SMALL NERVE
If hypoalgesia is aFIBERS
decreased sensitivity to nociceptive stimuli associated with pain,2 Gate
Control should also be considered as a possible mechanism of manual therapy, especially
18

rhythmic, graded oscillatory mobilization techniques.19 Even though Gate Control has come
under scrutiny with the evolution of the pain neuromatrix, biopsychosocial model, etc.,20-22 it is
still a valid model to explain modulation of nociception from the periphery and a human pain
experience. Melzack and Wall proposed that a gating mechanism exists in the dorsal horn
ofINHIBITORY cord.18 Small nerve fibers (“noxious sensory
the spinalNEURON receptors”) and large nerve fibers
PROJECTION
(“normal sensory receptors”) synapse on projection cells, CELLSwhich travel up the spinothalamic
tract to the brain, and inhibitory interneurons within the dorsal horn. The interplay between
these connections was thought to determine when “potentially painful” stimuli would proceed
NO INPUT=
to the brain. Many treatments such as large amplitude passive range of motion, transcutaneous
electrical neuromuscular stimulation (TENS) or massage are thought toGATE control pain, in part,
CLOSED
by activating low-threshold, large-diameter, non-nociceptive sensory nerve fibers dealing with
touch,LARGE
pressure
NERVEand vibration, which inhibit “pain transmission” by closing the gate to “pain
FIBERS
transmission” at the spinal cord level.

SMALL NERVE FIBERS

INHIBITORY NEURON PROJECTION

CELLS

LARGE FIBER INPUT=

GATE CLOSED
LARGE NERVE FIBERS

SMALL NERVE FIBERS

INHIBITORY NEURON PROJECTION

CELLS
24 PRINCIPLE 1 | EFFECTIVENESS OF MANUAL THERAPY

SMALL FIBER INPUT=

1.2: Psychosocial Effect
How can a manual physical treatment result in a psychosocial benefit? It is argued that various
psychosocial processes are involved including placebo, patient expectations, graded exposure,
TA, trust and more.2 As we delve further into pain science it becomes increasingly clear that
there’s a powerful interplay between the physical body and the brain and vice versa.23

With the emergence of pain science, there has been

increased interest in and discussion of “placebo.”23
Obviously, placebo does not only pertain to
medications, but also therapeutic interventions,
including manual therapy. Unfortunately, placebo
is often viewed as a “fake” or sham treatment.
However, the word placebo originated from the
Latin phrase for I shall please. Placebo should be
seen more as the endogenous mechanisms of pain
experience modulation—tapping into the brain’s
internal pharmacy; beliefs and expectations are at
the heart of this. Expecting and believing a treatment
will work allows for an enhanced endogenous
mechanism and, even if the actual, physical treatment is supposed to “do nothing,” it is hard
to consider the treatment fake.24 Patients carry expectations and beliefs with them, which can
modulate their pain experiences.25-27 For example, Puentedura and colleagues showed that
positive patient expectations that cervical spine thrust joint manipulation would help neck
pain, was a key factor in successful outcomes following manipulation for neck pain.27 This
implies that a patient who believes manual therapy will work for them (positive expectation),
will experience a better outcome. On the flipside, a patient who believes a treatment will not
work, including manual therapy (nocebo), may powerfully negate the potential benefit of the
actual treatment.23,28 Placebo effects have shown biological changes in dopamine production,
opioid pathways and CNS activation and on a psychological level. Placebo effects have shown
to be powerfully intertwined with expectations of benefit, conditioning and learning as well
as negative affect.2,23,28 If patient expectations modulate a pain experience then it is argued
that clinicians who meet or exceed patient expectations would impact pain. What are those
expectations? Various studies have shown that patients attending PT for LBP expect education
and information on diagnosis, prognosis and the plan of care, but also physical needs including
being physically examined and physically treated.10,29,30 Can you see how manual therapy,
including skilled physical tests and treatment, may in fact—beyond mechanical reasons—
impact a person’s pain experience?

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 25

In recent years, especially with the interest in pain
neuroscience, attention has shifted to TA.31,32 TA is defined
as the working rapport or positive social connection
between the patient and the clinician and consists of a
complex blend of clinician technical skill, verbal and non-
verbal communication, sense of warmth, collaboration and
trust.33 Increasing evidence supports the notion that TA,
especially trust, is shown to influence pain.31,34-36 How do
we build clinical trust? There are several strategies (active
listening, being present, etc.), but also through touch via
the neuropeptide oxytocin.37,38 Oxytocin facilitates a range
of sensory and psychological processes essential for
adaptive social behavior such as bonding and attachment
formation.39 It is believed oxytocin plays a significant role
in acute pain relief and is released during physical touch
including physical tests and manual treatments.34,37,40

In 1993, the late Gordon Waddell coined the iconic phrase: “The fear of pain is worse than
pain itself.”41 Fear can be a powerful psychosocial barrier to recovery, especially from spinal
pain.42,43 Fear constitutes a threat and when the brain is presented with a threat, it produces
pain to protect.44 Fear may also be related to a physical issue, i.e., being touched or physically
palpated or treated, especially in the presence of allodynia. It is now well established that a
significant part of a person’s pain experience is correlated with the vigilance of the central
and peripheral nervous system.45,46 In a subgroup of patients seeking care from a manual
therapist, the CNS becomes hypervigilant and poses significant clinical challenges to the use
of active and passive movement strategies to normalize impairments, including techniques
such as manual therapy.47-49 In a normal control state, when pressure is applied to tissues,
i.e., a mobilization technique to a spinal level, there is a normal tolerance.50 In the early phase
of pressure, light pressure is sensed as innocuous and easily tolerated by the patient. As
pressure is increased, innocuous sensations progress to noxious, with a gradual increase
in pain sensitivity, in line with the added noxious exposure. This model closely resembles
Maitland’s movement diagrams and grades of movement. The Maitland model often focused on
resistance, starting with the beginning of resistance (R1), progressing to the end of resistance
(R2).51 Although much refined, the original graded mobilizations differentiated between small
(Grade I) and large (Grade II) movements short of resistance, and large (Grade III) and small
(Grade IV) movements into resistance.51 Anecdotally, in line with the sensitization model,
clinicians and patients often encounter increased discomfort in these ranges of movement,
as innocuous pressure progresses to noxious.50,52 Patients often report that the pressure
“hurts good,” with various studies showing such mechanical pressure being associated with
increased endogenous analgesia.2,53

26 PRINCIPLE 1 | EFFECTIVENESS OF MANUAL THERAPY

PAIN SENSATION
Hyperalgesia

PAIN SENSATION
Normal Normal

Allodynia

INNOCUOUS NOXIOUS STIMULUS INTENSITY INNOCUOUS NOXIOUS STIMULUS INTENSITY

Figure 1.1: Pain sensation and stimulus intensity in a normal and sensitized state of allodynia and hyperalgesia.

Pain, especially chronic pain, is associated with an increased vigilance of the CNS, referred
to as CS.46,50 CS is defined as an increased responsiveness ofHyperalgesia nociceptive neurons in the
CNS to normal and subthreshold afferent input. Normal, healthy, non-threatening touch is
50

then perceived as a threat and may increase an individual’s pain experience. CS, however, is
PAIN SENSATION

PAIN SENSATION
Normal Normal
often used as a blanket term and contains two clinically important aspects of a hypervigilant
nervous system: hyperalgesia and allodynia. It has been proposed that CS, over time, moves
a hyperalgesic stage towards an allodynic stage.50 Clinically, this increased sensitization
fromProposed
Hyperalgesia FIRING
over space
timeforis well described and poses a significant challenge to manual therapists.45,54 In the
LEVEL
PAIN SENSATION

Manual Allodynia
allodynic Normal
Therapystate, light innocuous manual techniques are then perceived as pain, limiting the
application of manual therapy to the patient. It is withinLots of room
this model that it could be argued that
for activities
a strategy
INNOCUOUS can be employed whereby
NOXIOUS CS can be “shifted”
STIMULUS INTENSITY INNOCUOUSalong the innocuous
NOXIOUS scaleINTENSITY
Graded STIMULUS further to
Allodynia
the right towards the noxious, lowering the threat value. This, in turn, may potentially create a
mobilization
“window” for the application of manual therapy via gradually exposing patients to (hands-on) NORMAL
Alarm Activates ELECTRICAL
stimuli/sensory input, thus demonstrating again how the combination of manual therapy LEVELand
painINNOCUOUS
science canNOXIOUS
achieve more positive results.
STIMULUS INTENSITY
55
BEFORE PAIN AFTER PAIN

Proposed
space for Hyperalgesia FIRING
LEVEL
PAIN SENSATION

Manual
Therapy
Normal
Lots of room
for activities
Allodynia Graded
mobilization
NORMAL
Alarm Activates ELECTRICAL
LEVEL
INNOCUOUS NOXIOUS STIMULUS INTENSITY BEFORE PAIN AFTER PAIN

Figure 1.2: Proposed potential PNE shift of the stimulus intensity and a metaphorical alarm system depiction
of central sensitization before and after a painful experience.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 27

1.3: Mechanical Effect
In addition to the “bio” aspect of the biopsychosocial approach, it’s important to acknowledge
and explore mechanical effects of manual therapy. Irritation of the neuromeningeal structures
of the spine is often cited as a cause of pain, i.e., radiculopathy.56,57 Although the vast
amount of current research in this field pertains to chemical irritation, evidence also points
to mechanical issues whereby space around the neuromeningeal structures is compromised,
resulting in swelling, increased immune responses, demyelination, exposure of axons, ion
channel proliferation, etc.58 This mechanical stimulation may result in a powerful nociceptive
input to the CNS and possible resulting pain experience and in this model, addressing the
mechanical source of nociception, i.e., reduction in space, is seen as a possible mechanism to
alleviate pain.58,59 For example, various studies have shown that lateral glides of the neck result
in immediate reduction of neck and/or arm pain,60,61 and it has been proposed that techniques
such as lateral glides and distraction in fact do produce increased “space,” which may be one
of the mechanisms underpinning the immediate reduction in pain.62-64 Likewise, these lateral
glides of the neck have shown to facilitate median nerve movement in the carpal tunnel using
diagnostic ultrasound imaging.60

In the original Twomey article, another mechanical model for manual therapy was proposed,
tied to collagen deformation during sitting and forward flexion— referred to as flexion creep.3
In this model, the author proposed that diurnal fluid changes in the lumbar disc, loadbearing
of the spine and collagen deformation put the posterior annulus fibers at risk for annulus
tears and techniques such as extension exercises, prone-on-elbow positions and/or central
posterior-anterior mobilization techniques may in fact delay or reduce creep, thus in essence
protecting the lumbar discs.12

In the mid-1990s, there were a significant amount of cadaveric studies done on whiplash-
associated disorders (WAD).65,66 In groundbreaking research, Twomey, Taylor and colleagues
dissected cervical spines of deceased individuals from motor vehicle collisions showing
significant damage to cervical discs and zygapophyseal joints.65,66 It was shown that
zygapophyseal (facet) joints often following trauma ended up with cartilage damage similar
to a meniscus injury in the knee, resulting in a loose fragment of cartilage which may impede
movement by “locking” the joint. In this model, the authors argued that manual techniques,
especially thrust techniques, aimed at “opening” the joint may in fact dislodge the cartilaginous
fragment, restore movement and ease pain.3

In 1964, the now-iconic “Nachemson positions” were published and since then have
been validated by other studies, whereby the pressure in lumbar discs was measured in
various positions, culminating in a series of positions where disc pressure was increased
or decreased.67,68

28 PRINCIPLE 1 | EFFECTIVENESS OF MANUAL THERAPY

Figure 1.3: Disc pressure in various positions and during different tasks.

Increased disc pressure was attributed to and used to explain why “discogenic” pain was
worse in certain positions, while decreased disc pressure positions were used to ease pain—
by patients and clinicians alike. From a purely mechanical vantage point, if a patient was
experiencing acute LBP, a manual therapist could position them in a supine, hook lying
position, apply manual traction techniques and in essence “ease the pain,”51 thus taking
advantage of positional/load attenuation of nociception.

Again, the various mechanisms underpinning manual therapy are complex and don’t work in
isolation, but numerous studies show immediate changes in range of motion (ROM) following
manual therapy techniques, often implying a potential mechanical effect.62,69-73

1.4: Autonomic Effect

Another mechanism that may contribute to the positive effects of manual therapy is the
interplay between the autonomic nervous system and manual therapy. This is especially
true in osteopathy and chiropractic. For example, in a placebo-controlled study on healthy
subjects it was shown that grade III mobilization techniques applied to the T4 vertebra resulted
in a sympatho-excitatory effect in the hand, implicating a potential link between manual
treatments of the thorax and the autonomic nervous system.74 In fact, a plethora of studies
show that spinal manual therapy techniques result in immediate autonomic changes including
blood flow into the extremities, blood pressure, heart rate variability, venous insufficiency,
respiratory and cardiovascular function and more.75-81 This is intriguing since we know, from a
pain science perspective, how important factors including blood flow and respiration are when
it comes to a pain experience— all of which can potentially be positively impacted by manual
therapy. For example, it has been shown that increased blood flow can powerfully influence
neuropathic pain.82-84

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 29

1.5: Neuromuscular Effect
Another area that has garnered
interest in manual therapy is the
effect of manual techniques on a
person’s ability to facilitate improved
motor control. In this model it’s
often proposed that pain influences
local or innervated muscles and
by applying a manual technique the manual therapist can, in essence, “reboot” the system
allowing muscles to contract more efficiently or allow for increased movement. A great example
comes from Raney and colleagues, who investigated the immediate effect of lumbar thrust
joint manipulation on the contraction of transversus abdominus and internal oblique in nine
patients experiencing LBP.85 The study showed an immediate increase in muscle contraction
thickness using diagnostic ultrasound for the transversus abdominus (primary stabilizer), but
not the internal oblique. In a powerful follow-up study, Puentedura et al., showed that the
same approach, applied to healthy pain-free individuals (college students needing money),
did not result in these immediate changes, thus implicating the powerful connection between
pain, motor control and spinal manipulation.86 To date, this immediate change in motor control
following spinal manual therapy has been found in the cervical spine with changes in shoulder
movement and biceps contraction,87-89 and in the lumbar spine, with changes in quadriceps
contraction.90 Even with the recent interest in sensorimotor integration (head positioning) it has
been shown that cervical spine manipulation positively influences sensory motor function.91

1.6: Chemical Effect

As will be stated in Principle 2.3, irritation of the neuromeningeal structures of the spine is
often cited as a cause of pain, i.e., radiculopathy.56,57 From a medical perspective, especially
interventional medicine, a lot of interest has been placed on chemical irritation of innervated
structures as means to explain the underlying pain mechanism and proposed treatment.92 In
manual therapy, traditional models often focused on mechanical reasons for improvement,
but they have now also spilled over to the possibility of manual therapy resulting in a chemical/
circulatory effect as a means to ease a painful experience. For example, scientists have shown
that passive neural mobilization can actually induce dispersion of intraneural fluid, which in
turn has been associated with neuropathic pain.58,93-95 Specific to manual therapy of the spine,

30 PRINCIPLE 1 | EFFECTIVENESS OF MANUAL THERAPY

scientists recently conducted an amazing study whereby they induced an “inflammatory soup”
to the L5 intervertebral foramen of a rat mimicking lumbar radiculopathy and activation of the
dorsal root ganglion (DRG) and then treated the spine with manual therapy.96 In this study, the
application of a spinal manipulation via a pencil eraser to the affected level resulted in thermal
and mechanical hypoalgesia and decreased excitability of the DRG. More impressive was the
fact that the application of the manual treatment resulted in changes still evident two to three
weeks later. The idea of fluid dispersion via active and/or passive movement should not be
all that surprising. Fluid dynamics is likely a main principle of any and all rehabilitation from
ankle sprains to knee replacements. In fact, it has been shown that extension exercises of the
spine result in the largest fluid transfer in and around lumbar discs, which may be a potential
mechanism behind the directional preference model used by manual therapists to alleviate
pain and improve movement.97

Current pain science research has a strong focus on the interplay between the nervous system,
immune system and endocrine system.98 For example, proliferation of pro-inflammatory
immune molecules such as interleukin-1 (IL-1), interleukin 6 (IL-6) and tumor necrosis factor
alpha (TNF- ) have been shown to powerfully contribute to increased pain states.98 In line
with this, it is not surprising that current pain programs focus on various immune-buffering
behaviors including sleep hygiene, nutrition, exercise, meditation, etc., as a means to affect
the immune system and decrease pain. What’s interesting, is that manual therapy—compared
to control, has been shown to powerfully drive IL-1 and TNF- down, which may, once again,
be an underlying mechanism contributing to manual therapy’s ability to decrease pain.99

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 31

1.7: Neuroplastic Effect
Advances in brain scanning technology
in recent years100 have provided a greater
understanding of the structural and
functional changes in the brain of an
individual suffering from pain.101 It is now
well established that a person’s physical
body is represented in the brain by a network
of neurons.102-105 This representation
refers to the pattern of activity that is
evoked when a particular body part is
stimulated. The area of the brain most
commonly associated with representation
is the primary somatosensory cortex
(S1).102-105 Interestingly, these neuronal
representations of body parts are dynamically maintained and studies have shown that
patients with chronic pain display different S1 representations than people with no pain.101,106-
110
The interesting phenomenon associated with cortical restructuring is the fact that the body
maps expand or contract, in essence increasing or decreasing the body map representation
in the brain. Furthermore, these changes in shape and size of body maps seem to correlate
to increased pain and disability.101,111 Various factors have been linked to the development of
this altered cortical representation of body maps in S1 including neglect and decreased use
of the painful body part.112 This reorganization of body maps occurs quickly. Studies have
shown that when four fingers are webbed together for 30 minutes, cortical maps associated
with the fingers change.105 This finding has significant clinical importance as it underscores
the importance of strategies such as movement, tactile and visual stimulation of the CNS and
brain as a means to help maintain S1 representation.48,49

In recent years, scientists began exploring the notion that manual therapy, as a form of sensory
integration and/or sensory discrimination, may also be a powerful mechanism in alleviating
pain. In studies on LBP it has been shown that sensory discrimination via tactile stimulation
results in immediate changes in pain, movement and sensitivity of the nervous system.48,49
These results have since been replicated in patients experiencing knee and shoulder
pain.113 More specific to the S1, a recent manual therapy study randomized 62 patients with
CLBP showed that a neuroplasticity explanation, compared to a traditional biomechanical
explanation, resulted in a measurable difference in straight leg raise (SLR).114 In line with this
research, Louw et al., (submitted for publication 2019) examined cortical representation of

32 PRINCIPLE 1 | EFFECTIVENESS OF MANUAL THERAPY

LBP before and after manual therapy using body charts and pain drawings. In this study,
patients drew body charts indicating the location of their pain before, immediately after, and
at follow-up after receiving a manual therapy intervention. Results demonstrated a reduction
in pain area of 35% with manual therapy, which in turn correlated to decreased pain ratings
and movement. This emerging research may furthermore underscore the notion that manual
therapy may indeed be seen as a form of sensory integration and/or sensory discrimination.

Before Immediately Upon

After Return

Figure 1.4: Body chart drawings before, immediately after and at follow-up after manual therapy interventions.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 33

1.8: Socioeconomic Effect
A common argument against manual therapy interventions is the fact that when we compare
two groups of patients, one receiving a manual therapy intervention and the other not, i.e.,
exercise only, the outcomes pertaining to pain and disability are similar one year later.115 To
add fuel to the fire, it is also proposed that long-term outcomes should be the only metric
applied to determine the effect of a treatment. In contrast, it can be argued that short-term,
immediate results from an intervention may also yield valuable gains, potentially underscoring
the notion of ensuring scientists measure appropriate outcomes.

One measurement of outcomes is socioeconomic improvement. In the validation study of the

lumbar spinal manipulation clinical prediction rule (CPR) study, Childs et al., examined the
impact on healthcare utilization between patients receiving lumbar manipulation and those
receiving exercise only.116 At six-month follow-up, 9.6% of the manipulation group and 25% of
the exercise group reported similar time missed at work. This data, along with growing evidence
that spinal manipulation is a powerful treatment to ease acute pain and disability,116,117 may
help a patient return to work, which can powerfully boost self-efficacy. From a pain science
perspective, self-efficacy has been shown to powerfully influence pain and psychological well-
being.118 Time away from work has been shown to be the single biggest predictor of recovery
from a work injury.119,120 All of these factors may be positively influenced by manual therapy.
This potential socioeconomic advantage only strengthens the argument that patients with LBP
should seek non-pharmacological approaches first as a means do “de-medicalize” acute and
sub-acute LBP, steering patients away from harmful exposure to opioids, medical imaging and
surgical interventions. A good example of this is the “Virginia Mason” study for LBP, which
showed significant benefit in directing patients to a non-medical route for LBP early on.121

Figure 1.5: Virginia Mason example for a pathway for low back pain management.

34 PRINCIPLE 1 | EFFECTIVENESS OF MANUAL THERAPY

Conclusion
This principle will likely elicit different responses from different readers. For those truly
interested in seeing inside the “black box” of manual therapy and its effects, this expansion
of the original Bialosky paper is a welcome discussion. In between, we’ve woven in specific
pain science to demonstrate how pain science and manual therapy are interrelated. For the
naysayers, this principle may add fuel to the fire, spewing out the notion that we’re trying to fit
square pegs into round holes. We acknowledge we’ve taken liberty with some concepts and
even created very fragile frameworks, but that’s exactly the purpose of this book—pushing
the envelope; thinking outside the box. We know manual therapy works and it works on
many levels.

One final comment, which emerged from writing this principle. It used to irk us when we read
papers comparing two groups of patients. One group received “physical therapy” and the
other group received medication, surgery or injections. We would scream: “Physical therapy is
a profession; not a treatment!” Could it be that such a description (patients receiving physical
therapy) may be more accurate, given the numerous interplaying factors to a successful
outcome, including explanations, touch, therapeutic alliance, etc.? We realize this question
is in contrast to a call to delineate manual therapy as either mobilization or manipulation,122
but it’s worth pondering, considering the totality of what we do during a manual therapy
intervention and the fact that it does not occur in isolation.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 35

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changes in posteroanterior stiffness and active
range of movement of the cervical spine
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2008;33(19):E673-679.
70. Nansel D, Jansen R, Cremata E, Dhami MS,
Holley D. Effects of cervical adjustments on
lateral-flexion passive end-range asymmetry
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71. Martinez-Segura R, Fernandez-de-las-Penas
C, Ruiz-Saez M, Lopez-Jimenez C, Rodriguez-
Blanco C. Immediate effects on neck pain and
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subjects presenting with mechanical neck pain:
a randomized controlled trial. J Manipulative
Physiol Ther. 2006;29(7):511-517.
72. Cassidy JD, Lopes AA, Yong-Hing K. The
immediate effect of manipulation versus
mobilization on pain and range of motion in
the cervical spine: a randomized controlled
trial. J Manipulative Physiol Ther. 1992;15(9):
570-575.
73. Klein P, Broers C, Feipel V, et al. Global 3D
head-trunk kinematics during cervical spine
manipulation at different levels. Clin Biomech
(Bristol, Avon). 2003;18(9):827-831.
74. Jowsey P, Perry J. Sympathetic nervous system
effects in the hands following a grade III postero-
anterior rotatory mobilisation technique applied
to T4: a randomised, placebo-controlled trial.
Man Ther. 2010;15(3):248-253.
75. Donovan JS, Kerber CW, Donovan WH, Marshall
LF. Development of spontaneous intracranial
hypotension concurrent with grade IV
mobilization of the cervical and thoracic spine:
a case report. Archives of physical medicine and
rehabilitation. 2007;88(11):1472-1473.
76. Karason AB, Drysdale IP. Somatovisceral
response following osteopathic HVLAT: a pilot
study on the effect of unilateral lumbosacral
high-velocity low-amplitude thrust technique
on the cutaneous blood flow in the lower limb.
J Manipulative Physiol Ther. 2003;26(4):
220-225.
77. Win NN, Jorgensen AM, Chen YS, Haneline
MT. Effects of Upper and Lower Cervical Spinal
Manipulative Therapy on Blood Pressure and
Heart Rate Variability in Volunteers and Patients
With Neck Pain: A Randomized Controlled,
Cross-Over, Preliminary Study. J Chiropr Med.
2015;14(1):1-9.
78. Bakhtadze MA, Vernon H, Karalkin AV, Pasha SP,
Tomashevskiy IO, Soave D. Cerebral perfusion in
patients with chronic neck and upper back pain:
preliminary observations. J Manipulative Physiol
Ther. 2012;35(2):76-85.
79. de Araujo FX, Macagnan FE, Della Mea Plentz
R, Silva MF. Autonomic effects after anterior-to-
posterior cervical mobilization. J Orthop Sports
Phys Ther. 2015;45(1):46-47.
80. Yung E, Wong M, Williams H, Mache K. Blood
pressure and heart rate response to posteriorly
directed pressure applied to the cervical spine
in young, pain-free individuals: a randomized,
repeated-measures, double-blind, placebo-
controlled study. J Orthop Sports Phys Ther.
2014;44(8):622-626.
81. McGuiness J, Vicenzino B, Wright A. Influence
of a cervical mobilization technique on
respiratory and cardiovascular function. Man
Ther. 1997;2(4):216-220.
82. Shen J, Fox LE, Cheng J. Swim therapy reduces
mechanical allodynia and thermal hyperalgesia
induced by chronic constriction nerve injury in
rats. Pain Medicine. 2013;14(4):516-525.
83. Kuphal KE, Fibuch EE, Taylor BK. Extended
swimming exercise reduces inflammatory and
peripheral neuropathic pain in rodents. J Pain.
2007;8(12):989-997.
84. Chen YW, Li YT, Chen YC, Li ZY, Hung CH.
Exercise training attenuates neuropathic
pain and cytokine expression after chronic
constriction injury of rat sciatic nerve. Anesth
Analg. 2012;114(6):1330-1337.
85. Raney NH, Teyhen DS, Childs JD. Observed
changes in lateral abdominal muscle thickness
after spinal manipulation: a case series using
rehabilitative ultrasound imaging. J Orthop
Sports Phys Ther. 2007;37(8):472-479.
86. Puentedura EJ, Landers MR, Hurt K, Meissner
M, Mills J, Young D. Immediate effects of
lumbar spine manipulation on the resting and
contraction thickness of transversus abdominis
in asymptomatic individuals. J Orthop Sports
Phys Ther. 2011;41(1):13-21.
87. McClatchie L, Laprade J, Martin S, Jaglal SB,
Richardson D, Agur A. Mobilizations of the
asymptomatic cervical spine can reduce signs
of shoulder dysfunction in adults. Man Ther.
2009;14(4):369-374.
88. Dunning J, Rushton A. The effects of
cervical high-velocity low-amplitude thrust
manipulation on resting electromyographic
activity of the biceps brachii muscle. Man Ther.
2009;14(5):508-513.
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89. Boyles RE, Ritland BM, Miracle BM, et
al. The short-term effects of thoracic
spine thrust manipulation on patients with
shoulder impingement syndrome. Man Ther.
2009;14(4):375-380.
90. Grindstaff TL, Hertel J, Beazell JR, Magrum
EM, Ingersoll CD. Effects of lumbopelvic joint
manipulation on quadriceps activation and
strength in healthy individuals. Man Ther.
2009;14(4):415-420.
91. Haavik-Taylor H, Murphy B. Cervical spine
manipulation alters sensorimotor integration:
a somatosensory evoked potential study. Clin
Neurophysiol. 2007;118(2):391-402.
92. Bogduk N. A narrative review of intra-articular
corticosteroid injections for low back pain. Pain
Med. 2005;6(4):287-296.
93. Brown CL, Gilbert KK, Brismee JM, Sizer
PS, Roger James C, Smith MP. The effects of
neurodynamic mobilization on fluid dispersion
within the tibial nerve at the ankle: an
unembalmed cadaveric study. J Man Manip
Ther. 2011;19(1):26-34.
94. Gilbert KK, Smith MP, Sobczak S, James CR,
Sizer PS, Brismee JM. Effects of lower limb
neurodynamic mobilization on intraneural fluid
dispersion of the fourth lumbar nerve root: an
unembalmed cadaveric investigation. J Man
Manip Ther. 2015;23(5):239-245.
95. Lundborg G, Dahlin LB. The Pathophysiology of
Nerve Compression. Hand Clinics. 1992;8(No
2):215-227.
96. Song XJ, Gan Q, Cao JL, Wang ZB, Rupert
RL. Spinal manipulation reduces pain and
hyperalgesia after lumbar intervertebral foramen
inflammation in the rat. J Manipulative Physiol
Ther. 2006;29(1):5-13.
97. Adams MA, May S, Freeman BJ, Morrison HP,
Dolan P. Effects of backward bending on lumbar
intervertebral discs. Relevance to physical
therapy treatments for low back pain. Spine.
2000;25(4):431-437; discussion 438.
98. Chapman CR, Tuckett RP, Song CW. Pain and
stress in a systems perspective: reciprocal
neural, endocrine, and immune interactions.
The journal of pain: official journal of the
American Pain Society. 2008;9(2):122-145.
99. Teodorczyk-Injeyan JA, Injeyan HS, Ruegg
R. Spinal manipulative therapy reduces
inflammatory cytokines but not substance P
production in normal subjects. J Manipulative
Physiol Ther. 2006;29(1):14-21.
100. Flor H. The functional organization of the brain
in chronic pain. Prog Brain Res. 2000;129:
313-322.
101. Flor H, Braun C, Elbert T, Birmbaumer
N. Extensive reorganisation of primary
somatosensory cortex in chronic back pain
patients. Neuroscience Letters. 1997;244:5-8.
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102. Wand BM, Parkitny L, O’Connell NE, et al.
Cortical changes in chronic low back pain:
current state of the art and implications for
clinical practice. Man Ther. 2011;16(1):15-20.
103. Penfield W, Boldrey E. Somatic, motor and
sensory representation in the cerebral cortex of
man as studied by electrical stimulation. Brain:
a journal of neurology. 1937;60:389-448.
104. Flor H. The functional organization of the brain
in chronic pain. In: Sandkühler J, Bromm B,
Gebhart GF, eds. Progress in Brain Research,
Vol 129. Amsterdam: Elsevier; 2000.
105. Stavrinou ML, Della Penna S, Pizzella V, et
al. Temporal dynamics of plastic changes in
human primary somatosensory cortex after
finger webbing. Cerebral cortex. 2007;17(9):
2134-2142.
106. Maihofner C, Handwerker HO, Neundorfer B,
Birklein F. Patterns of cortical reorganization in
complex regional pain syndrome. Neurology.
2003;61(12):1707-1715.
107. Moseley GL. I can’t find it! Distorted body image
and tactile dysfunction in patients with chronic
back pain. Pain. 2008;140(1):239-243.
108. Lotze M, Moseley GL. Role of distorted
body image in pain. Curr Rheumatol Rep.
2007;9(6):488-496.
109. Moseley GL. Distorted body image in
complex regional pain syndrome. Neurology.
2005;65(5):773.
110. Flor H, Elbert T, Muhnickel W, Pantev C. Cortical
reorganisation and phantom phenomena in
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1998;119:205-212.
111. Lloyd D, Findlay G, Roberts N, Nurmikko
T. Differences in low back pain behavior
are reflected in the cerebral response to
tactile stimulation of the lower back. Spine.
2008;33(12):1372-1377.
112. Marinus J, Moseley GL, Birklein F, et al. Clinical
features and pathophysiology of complex
regional pain syndrome. Lancet Neurol.
2011;10(7):637-648.
113. Louw A, Farrell K, Zimney K, et al. Pain
and Decreased Range of Motion in Knees
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Intervention. Pain and Rehabilitation.
2017;Summer(43):20-30.
40 PRINCIPLE 1 | EFFECTIVENESS OF MANUAL THERAPY
114. Louw A, Farrell K, Landers M, et al. The effect
of manual therapy and neuroplasticity education
on chronic low back pain: a randomized clinical
trial. Journal of Manual & Manipulative Therapy.
2016:1-8.
115. Hoving JL, de Vet HC, Koes BW, et al. Manual
therapy, physical therapy, or continued
care by the general practitioner for patients
with neck pain: long-term results from a
pragmatic randomized clinical trial. Clin J Pain.
2006;22(4):370-377.
116. Childs JD, Fritz JM, Flynn TW, et al. A clinical
prediction rule to identify patients with low
back pain most likely to benefit from spinal
manipulation: a validation study. Ann Intern
Med. 2004;141(12):920-928.
117. Flynn T, Fritz J, Whitman J, et al. A clinical
prediction rule for classifying patients with
low back pain who demonstrate short-term
improvement with spinal manipulation. Spine.
2002;27(24):2835-2843.
118. Costa LdCM, Maher CG. Self-efficacy is more
important than fear of movement in mediating
the relationship between pain and disability in
chronic low back pain. European journal of pain
(London, England). 2011;15(2):213-219.
119. Horsley R. Factors that affect the occurrence and
chronicity of occupation-related musculoskeletal
disorders. Best Pract Res Clin Rheumatol.
2011;25(1):103-115.
120. Kapoor S, Shaw WS, Pransky G, Patterson W.
Initial patient and clinician expectations of return
to work after acute onset of work-related low
back pain. J Occup Environ Med. 2006;48(11):
1173-1180.
121. Flynn TW, Smith B, Chou R. Appropriate use of
diagnostic imaging in low back pain: a reminder
that unnecessary imaging may do as much
harm as good. J Orthop Sports Phys Ther.
2011;41(11):838-846.
122. Mintken PE, DeRosa C, Little T, Smith B.
AAOMPT clinical guidelines: A model for
standardizing manipulation terminology in
physical therapy practice. J Orthop Sports Phys
Ther. 2008;38(3):A1-6.
 PRINCIPLE 2

Clinical Reasoning Is a
Cornerstone of Manual Therapy

2.1: Health Condition (Disorder, Disease

State, Pathology) .............................................47

2.2: Body Structure or

Function Impairments.................................47

2.3: Sources of Symptoms ................................ 48

2.4: Activity and Participation

Restriction ........................................................... 48

2.5: Personal Factors (Pain Beliefs,

Coping Style, Self-Efficacy) ................... 49

2.6: Environmental Factors (Social

Influences, Economic, Political,
Home or Work Status, etc.) ................... 53

2.7: Pain Mechanisms.......................................... 53

2.8: Contributing and Perpetuating

Factors ....................................................................57

2.9: Precautions/Contraindications ............ 58

2.10: Management Approach............................ 59

2.11: Prognosis ............................................................. 60

Conclusion......................................................................... 63

Principle 2 References ............................................ 64

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 41

Think Big
Principle 1 demonstrates that manual therapy
works on many levels. However, in order for it
to work, there are a lot of choices the manual
therapist needs to make when interacting
with patients. What questions to ask? What
assessment procedures to choose? Which
techniques to administer? To better appreciate the importance of these questions, we need
to dive deeper and consider how a manual therapist makes clinical decisions. In other
words, we need to understand what many consider to be the cornerstone of manual therapy:
clinical reasoning.

Most manual therapists have some understanding of clinical reasoning theory, which was likely
shaped by their professors during professional training. Surveys of health care professional
programs show considerable differences in clinical reasoning content, pedagogical approaches,
hours of instruction and theory.1-3 As most programs have a biomedically-focused curriculum,
it is understandable that many clinicians approach clinical decisions using a biomedical
reasoning strategy. However, faced with the multidimensional challenge of chronic pain it
is critical for the modern therapist to think beyond muscles and joints and expand their
reasoning strategy to include biopsychosocial concepts.4 This is easier said than done (or
done well); we all feel comfortable in our own silos of expertise.

42 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

The intersection of clinical reasoning with evidence-based
practice (EBP) is an additional issue. As described by Sackett
and colleagues in the mid-1990s, EBP is the process of applying
patient-centered care while “integrating individual clinical
expertise with the best available external evidence.”5 Although
EBP is an important and continually growing movement within
all healthcare disciplines, it is not without its critics. However,
some of the criticism likely originates from misrepresentations
of the EBP concept, such as: “Only systematic reviews or meta-
analyses ‘count’ as evidence;” “EBP = Empathy, a Belief of the
Past (loss of clinical empathy);” “Clinical decisions are data-driven only;” “EBP is a cookbook
approach.”6-8 Additionally, there is some concern that too much emphasis has been placed
on the randomized trial with linear cause-and-effect assumptions.9

Because many medical conditions (including chronic pain

states) emerge in a non-linear fashion, with contributions
from multiple body systems and psychosocial domains, some
feel that current research models are inadequate to inform
the complexity of patient care.9 However, clinicians who have
embraced EBP as a framework (which balances patient-
centered collaboration with the best available evidence
and the experience of the clinician) will recognize the error
of overemphasizing any one of its three core components.
Additionally, it is critical that EBP concepts should represent
part of a sound reasoning strategy within a broader
biopsychosocial approach.10

Two of the most commonly cited definitions for clinical

reasoning are:

1. Clinical reasoning is a context-dependent way of thinking

and decision making in professional practice.11

2. Clinical reasoning refers to the thinking and decision

making processes that are used in clinical practice.12

However, as healthcare practice has been slowly evolving from a biomedical approach
toward a biopsychosocial approach, clinical reasoning also needs to evolve. Clinical reasoning
principles must expand beyond merely seeking potential tissue-based sources of pain and
relevant contributing factors. While these factors continue to play an important role in informing
clinical decisions, the modern manual therapist should consider other critical components in
patient-centered care.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 43

Recognizing the need for a broader reasoning construct,
some have suggested it is more appropriate to consider
clinical reasoning on the conceptual level versus trying
to narrow its description down to a brief statement. For
example, the Clinical Reasoning Curricula and Assessment
Research Consortium (CRCARC) of the American Council
of Academic Physical Therapy developed the following
operational definition for the various layers in the clinical reasoning process: Clinical reasoning
is a nonlinear, recursive cognitive process in which the clinician synthesizes information
collaboratively with the patient, caregivers, and the health care team in the context of the
task and the setting. The clinician reflectively integrates information with previous knowledge
and best available evidence in order to take deliberate action.2 This captures the complexity
of the reasoning process, incorporates EBP terms, and recognizes the collaborative nature
of the relationship between the patient and healthcare professionals. However, perhaps
it misses the point that the patient undergoes an internal reasoning process during each
healthcare encounter. It can be difficult for the clinician to appreciate the reasoning process
from the patient’s perspective. A pain model which addresses this challenge is the onion-skin
model, which will be described further in the next principle. Using the metaphor of an onion,
Loeser13 attempted to represent multiple
domains of a pain experience from the
perspective of the clinician observer.
During the initial encounter the clinician
is only able to listen to the patient’s
story and observe their pain behaviors,
while other details remain veiled within
deeper layers of the figurative onion.
However, as a TA is formed, additional
layers of the onion may be revealed
through a collaborative effort. If
successful, additional information may
begin to emerge, allowing the clinician
to appreciate the patient’s suffering,
emotions, thoughts, and beliefs related
to the pain experience.

Although the onion metaphor addresses hidden layers of pain and the importance of trust and
collaboration (Principle 9), it does this from the perspective of the clinician. But what about
the patient? As the patient shares their story and listens to the therapist’s response, a complex
reasoning process helps them determine whether the therapist’s proposed plan is a plausible
solution. If the therapist does not gain the patient’s trust, or their proposed plan of care fails to
meet the patient’s expectations and conceptualization of what course of action should occur,
there will likely be little meaningful engagement in the rehabilitation process on the part of the
patient. Therefore, it is important to have an ongoing dialogue during the episode of care to
gain a better understanding of the patient’s evolving beliefs and expectations in the context of
the rehabilitation process.

44 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

As mentioned previously, clinical reasoning goes far beyond considering the diagnostic process
and deciding which treatments to choose. In fact, clinical reasoning research literature cites
many different reasoning strategies involved in the reasoning process, including diagnostic,
narrative, procedural, interactive/collaborative, intuitive, dialectical, pattern-recognition,
predictive/prognostic, ethical, and teaching as a form of reasoning (see Table 2.1. for a brief
description of each).4,12,14-18 This list of strategies points to the iterative nature of clinical
reasoning, which describes how a therapist integrates many different reasoning strategies,
weighing information from multiple domains, discerning a wise course of action, executing the
plan, measuring results, and then reflecting on the process.3

Table 2.1. Reasoning strategies.

Reasoning and problem solving during the diagnostic process.

Diagnostic Traditionally this has been more biomedical in scope, seeking to identify
reasoning the problematic process or tissue pathology and potential contributing
or perpetuating factors.12

Gaining a better appreciation of the patient’s pain experience (multiple

domains) using active listening strategies as the patient reveals their “story.”
Narrative
The clinician attempts to understand the problem from the perspective of
reasoning
the patient including pain beliefs, expectations, emotions, coping, hope
and values.12

Procedural Reasoning about the decisions on which assessment tests or treatment

reasoning interventions are selected.12

Interactive/ The reasoning process during development of the therapeutic alliance as

collaborative well as the collaborative nature of decision making during the progression
reasoning of the episode of care.12

Intuitive This strategy could also include recognition of emotion or “gut feelings”
reasoning and the role of intuition in the reasoning process.15-17

Dialectical This form of reasoning refers to the interaction between multiple

reasoning reasoning strategies.12

Recognition of clinical patterns has been described as a common

reasoning strategy used by experts. This form of reasoning relates to
Pattern
extensive clinical experience and ability to diagnose, treat and develop a
recognition
prognosis based on prior experiences and background understanding of
the clinical problem.12,14,18

Predictive/ This form of reasoning recognizes both the therapist and patient’s
prognostic impression of the expected outcome as well as the anticipated timeframe
reasoning to achieve the results.12

Ethical Recognition of potential ethical dilemmas which may impact treatment

reasoning decisions or goals for the therapy.12

The cognitions of the therapist focused on assessment and delivery

Teaching as
of patient education, whether the information was understood by the
a form of
patient, and how to modify the content or delivery style to achieve
reasoning
better comprehension.12, 15

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 45

While it may seem obvious that multiple reasoning strategies come
into play during patient care, it is prudent for the clinician-scholar
to reflect on these processes in order to maximize the potential
benefit for the patient in need. In 2001, during a conference
presentation on critical thinking during the diagnostic process,
the radiologist Charles Aprill commented that, “We seldom think
about what we don’t think about.”19 Dr. Aprill’s observation is
likely correct; without making a conscious effort to reflect on our
cognitions, biases, and preconceptions it would be easy to slip
into a state of clinical obliviousness, ignorant of ongoing reasoning
errors, stagnant in professional growth, and disserving our patients.
Hence, the idea of metacognition (taking time to think about the thinking/reasoning process)
is one which could serve all clinicians well.11 An example of a type of metacognitive exercise
could be to spend time individually or during a staff meeting to discuss challenging cases not
only for solutions, but also to dissect the complex cognitive processes and reasoning involved.

Because chronic pain is so complex—impacting the individual, their family, social network,
work setting and society—it is important for the therapist to consider different reasoning
strategies, and various categories of information while using these strategies. Often referred to as
hypothesis categories, they help the therapist to thoroughly investigate the problem from a more
comprehensive biopsychosocial perspective. Hypothesis categories, initially proposed by Mark
Jones20 in 1987, represent various lines of inquiry which can inform clinical decisions. Although
other categories could certainly be added, he recommended the following as a minimum:

1. Consideration of health condition (disorder, disease state, pathology)

2. Body structure or function impairments
3. Sources of symptoms
4. Activity and participation restriction
5. Environmental factors (social influences, economic,
political, home or work status, etc.)
6. Personal factors (pain beliefs, coping style, self-efficacy)
7. Type of pain/pain mechanism
8. Contributing/perpetuating factors
9. Precautions/contraindications
10. Management selections, and
11. Prognosis20,21

Within this framework, clinical reasoning can be seen as a means to fill in a puzzle. As patients
present with their symptoms, reasoning categories such as the above allow the clinicians
to systematically and methodically complete the whole picture—within a biopsychosocial
construct which is especially important for chronic pain.

46 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

2.1: Health Condition (Disorder, Disease State, Pathology)
Owing to the complexity of one of the most (perhaps the most)
expensive health care conditions, chronic pain continues to
evade attempts to narrow it down to a simple cause and effect.22
In fact, Patrick Wall, one of the great pain scientists of our age
and co-developer of the Gate-Control Theory of pain, stated, “It
is inherently ridiculous to consider pain as an isolated entity.”23
Despite this, pain is often portrayed in the media, advertising and
fictional works as something related to a problematic structure
or pathologic process which, once identified, is quickly ameliorated when the single solution
is administered (thus restoring health). Unfortunately, such reductive conceptualizations are
often closer to myth than reality.24 In some cases there may be an identifiable lesion or disease
state which resulted in a chronic pain state, in some there are multiple findings which may
not be relevant to the pain complaint, and others can present with disabling pain and yet no
identifiable structural flaws.25-27

Regardless of the challenges with identifying the relevant pathology, the hypothesis category
of health condition shares relevant links with other hypothesis categories such as personal
factors (e.g. pain beliefs, prior experiences, family history), pain mechanisms, management
decisions, precautions/contraindications, and prognosis. For example, an individual with
restricted motion from apparent mechanical back pain, but who was diagnosed with prostate
cancer nine months ago and who has recently been experiencing pain which does not ease
with rest, and unexplained weight loss, should immediately raise suspicion that there is
potentially much more at stake than managing a movement restriction. Understanding the
pathology, whether suspected, emerging or already identified, should provide the clinician
with a potential intervention plan, but also inform multiple other categories and lines of inquiry.

2.2: Body Structure or Function Impairments

As was the case with the health condition category, decisions related
to body structure/function may have implications for multiple other
categories. The patient with chronic pain will often present with
restricted motion and generalized tenderness, have a poor exercise
capacity, will probably be deconditioned, exhibit motor performance
dysfunctions, report problems with fatigue, and may have additional
cognitive or psychosocial complaints. The challenge for the modern
manual therapist is to discern which of these many problems are most relevant! When the
patient hurts everywhere, reports that nothing makes it better, and everything makes it worse,
there will undoubtedly be plenty of “positive” findings on examination. It is our opinion that in
patients like these who have severe pain states, may have had multiple treatment failures and
conflicting diagnoses that a “low-tech but highly skilled” examination is a good way to begin.
Instead of focusing on the minutiae of high-level manual examination, such as passive mobility
testing at each spinal segment and detailed palpation in all areas of pain (difficult when the
entire body chart is filled in as symptomatic), the assessment takes a broader perspective.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 47

Using this method, the therapist can glean a tremendous amount of meaningful information,
begin to build a TA and avoid flaring-up the patient’s symptoms on the initial evaluation.
Suggestions for the initial consult may include steps such as: screening for red and yellow
flags (yellow flags are in the psychosocial domain), abbreviated palpation exam (possibly
including pressure pain threshold testing), neurological screening, basic functional assessment
(balance, gait speed, range of motion, etc.), and use of relevant functional questionnaires.

2.3: Sources of Symptoms

Although this hypothesis category may have some overlap with body
structure/function, in this case “sources” indicate body tissues that
may be culpable contributors to nociceptive input and, therefore, play
a role in the pain experience. Lest this sound like an encouragement to
investigate potential nociceptive sources using a biomedical paradigm,
it is important for the reader to recognize that pain states do not exist in isolation.23 Peripheral
sources from the body tissues nearly always play some role in chronic pain states, and
likewise, there are always central contributions; the key is to determine the relative proportion
for each (more on this later).28 When considering potential nociceptive sources, the clinician
should consider any of the local body structures under or adjacent to the area of symptoms,
but also potential sources for referred pain (somatic, neurogenic, vascular, visceral).

2.4: Activity and Participation Restriction

Activity restrictions refer to the impaired ability for the patient
to perform desired functional tasks whereas a participation
impairment describes the capacity for the person to engage in
life situations (home, work, recreational, leisure). Most clinicians
are required to measure activity impairments, set goals at the
activity level and demonstrate a meaningful change in order
to justify the need for therapy. Various objective measures,
questionnaires and clinical scales can be used to quantify
changes at the activity level, and they are very important in helping the patient with chronic
pain toward their goals. While regulatory agencies do not yet place the same level of importance
on participation-level goals and measures, these may be the most important to the patient.
If goals have any pull to motivate a person to seek help and actively engage in rehabilitation,
participation-level goals may reign supreme. For example, which goal do you think might
motivate a patient to actively engage in the plan of care: a goal to walk independently for up to
150 feet without a device or a goal to improve walking ability to be able to go fishing with his
grandson for his 10th birthday? The 10th birthday fishing trip will win every time! Participation-
level goals involve activities that we value the most; they get us out of bed in the morning, and
they provide a sense of identity, responsibility and purpose. The participation domain aligns
with our life values and should be recognized as an important hypothesis category when
making clinical decisions.

48 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

2.5: Personal Factors (Pain Beliefs, Coping Style, Self-Efficacy)
Related to the broad concept of personal factors as a hypothesis
category, it is first important to spend a little time reviewing
general conceptualizations of pain before considering a topic like
“pain beliefs.” To do this, we will begin by reflecting on the word
“biopsychosocial.” It is easy to break the concept into three different
silos (the bio, the psycho and the social). On the biological side,
manual therapists are experts at identifying and recognizing the
relevant biologic factors and dysfunctional body tissues involved
in pain states via skilled assessment. However, in recent years
there has been an explosion of neuroscience research using imaging technologies such as
Functional Magnetic Resonance Imaging (fMRI), Diffusion Tensor Imaging (DTI), Positron
Emission Tomography (PET scan), Magnetoencephalography (MEG), transcranial magnetic
stimulation (TMS), and others. These techniques accelerated the understanding about
how neural networks function during normal brain activity, but also with problems such as
depression, Alzheimer’s disease, autism, and many other conditions including, of course,
pain. Functional neuroimaging of various pain states (either induced experimentally or related
to health conditions) appears to have corroborated the hypothesis that pain is a brain output
constructed through complex processing in multiple systems to ascertain the level of threat
facing the individual.28,29 An example, which is perhaps an oversimplification of this idea,
would be that if no relevant threat is perceived in the brain’s protection systems, then no
pain would be produced. Another way to say this would be if no harm to the organism was
recognized/computed, then there is no need for protection by pain. Conceivably, this could
explain instances when there are substantial nociceptive inputs from a bodily injury/damage,
and yet the individual experiences no pain. Think of all the stories you may have heard of
someone performing a heroic act despite significant injury (military and sports stories come to
mind) or the numerous studies of people who are pain-free and yet demonstrate considerable
pathology on imaging.30 It can easily be said that more than half of asymptomatic people show
structural problems on imaging (torn rotator cuffs, herniated discs, arthritis, bone spurs and
more). Of course, the opposite is also true: some may experience horrific pain even with no
significant nociceptive inputs due to the brain’s appraisal of danger.

A story that illustrates this point is the construction

worker who jumped off some scaffolding and
landed on a large nail, which impaled his foot.31
The nail came through, proximal to the steel
toe-box surrounding his toes and forefoot and
penetrated through the top of his work boot.
He was in agony while being transported to the
emergency department and required strong pain
medication and sedation before the nail could
be pulled out for even the slightest touch or
movement caused excruciating pain. However,
once the boot was removed, (perhaps you have
already guessed what happened next) it became
apparent that the nail went up between the toes,
with no tissue injury whatsoever!31,32

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 49

Stories like this and contemporary theories of pain have helped many to reconceptualize pain
from a bottom-up, pain-as-input, Cartesian-perspective and into the complexities of the brain.
However, we must be cautious to not fall into a reverse Cartesian paradox where clinicians
place too much focus on central processes and abandon the periphery.33 Despite amazing pain
neuroscience research, there is still much to be learned about the biology of many common
pain states. One example is the large majority of patients with “non-specific” back pain; no
significant finding on diagnostic tests, and yet plenty of pain.33 We also need to understand
more about the dynamic relationship between peripheral and central contributions to a pain
experience. Has the clinical pendulum swung too far toward the supremacy of the brain to
explain all things pain? Perhaps we have become too “neuro-centric” and are not placing
enough emphasis on exploration of the non-neural biologic systems relevant to pain (both in
the body tissues, but also immune, endocrine and other systems).34-36

Now that we have reviewed some of the challenges to the understanding of pain, what about
pain beliefs? Some hints at what the patient believes about the nature of pain could emerge
during the interview. In many cases their true thoughts may remain hidden without specifically
targeted questions. Some questions to consider could include:

• What do you think is the real cause of your pain problem?

• Why do you think you are still hurting?
• What worries you the most about your pain?
• What do you think needs to be done to help your pain?
• What do you think it will take to get you better?
• Where do you see yourself in three years, in respect to this pain problem?

To explore pain beliefs in more detail, there

are many different questionnaires which may
assist the clinician, such as the Fear Avoidance
Beliefs Questionnaire (FABQ),37 Pain Beliefs
Questionnaire,38 Back Beliefs Questionnaire39
and many others. These questionnaires
provide a deeper understanding related to
patient pain beliefs and could be used to
establish a baseline or measure change over
time. However, we recommend not only using
the raw numeric score and recording it in the
medical record, but also following up with
related questions based on patient responses.

50 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

For example, one of the questions on the FABQ is, “Physical activity might harm my back.”
A reasonable follow up would be to ask the patient why they think physical activity might
hurt their back. Many people have an inaccurate belief that the back is a fragile, vulnerable
structure which, once injured, may lead to an inability to work or do activities which might
cause further injuries.40,41 These conceptualizations would likely need to be addressed during
the episode of care to improve chances for success.

Within the broad hypothesis category of personal factors, it is also important for the clinician
to get an appreciation of the patient’s coping style as well as an understanding of their self-
efficacy. Patients with a passive coping style will tend to place more of an emphasis on the
manual therapist as the responsible party for whether the treatment is a success or failure.
Additionally, a passive coping style tends to be associated with worse outcomes, more pain
and greater disability than individuals with a more active approach.42 Coping refers to the
ability of the patient to use emotional, physical, cognitive or behavioral strategies to address
the factors associated with their disease or pain state. Indications of a more passive style might
include a lack of active engagement in the treatment
plan, poor compliance with self-management
instructions, unwillingness to perform exercise,
withdrawal from social engagement, preference
for passively applied treatment modalities (heat,
electrical stimulation, ice, traction, etc.), and
indicators of helplessness or relinquishing control
over a situation.

Although a thorough patient interview will likely provide the manual therapist with an indication
of the patient’s coping style, questionnaires such as the Coping Strategies Questionnaire (CSQ)
and the Pain Coping Questionnaire (PCQ) could be utilized for deeper appraisal.43,44 Closely
associated with concepts of coping, self-efficacy was defined by Bandura as “the belief in
one’s capabilities to organize and execute the sources of action required to manage prospective
situations.”45 As is common with patients who exhibit a passive coping style, individuals with
poor self-efficacy may feel that the locus of control has shifted away from themselves to the
therapist (or healthcare system). The Pain Self-Efficacy Questionnaire (PSEQ) is one of several
survey-based tools to help the clinician identify problems with self-efficacy which could be
addressed during the course of therapy.46 By actively engaging the patient throughout the
episode of care, helping them identify meaningful goals, and utilizing shared decision-making
throughout the episode of care may enhance self-efficacy, and provide the encouragement
they need to actively pursue solutions.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 51

Regarding the psychological domain, there appears to be increased public awareness and
decreased stigma regarding mental health issues like depression. These days people seem to
be a little more willing to share their mental health concerns and seek help. This cultural shift
is important because it has been demonstrated that depression is far more common in people
with chronic pain than most realize. Why wouldn’t it be? When you consider the definition of
pain, it should be clear that emotions are involved in any pain experience:

Pain is a sensory and emotional experience

associated with actual or potential tissue damage
or described in terms of such damage.47

In other words, pain will always involve emotion. This also means that pain can influence
emotions, and in a similar way, emotions can influence pain. This bi-directionality between
pain and emotions may be part of the reason why a majority of patients with chronic pain will
experience symptoms of depression.48,49 If ignored, unrecognized or left untreated, depression
may become a significant factor leading to treatment failure for patients with chronic pain.50
To improve identification of depression there are now many easy-to-use, valid and reliable
screening questionnaires such as the Patient Health Questionnaire 9 (which also has shorter
forms available) or the Beck Depression Inventory.51

52 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

2.6: Environmental Factors (Social Influences, Economic,
Political, Home or Work Status, etc.)
Among the three domains of the term biopsychosocial, the social
domain may be the most neglected. This is somewhat surprising
considering that, generally speaking, people are social by nature.
Therefore, pain will most certainly have an effect upon the person at
an individual level (obviously) but also on their social environment,
their relationships at home or at work, and how they interact with
other people. Pain could also impact their relationship to healthcare
providers. Consider the time a patient spends with their clinician
during a treatment session compared to the amount of time spent in the patient’s own social
environment. If the therapist worked with the patient for an hour, once per week, that is
only 1/168th of the time in a supportive, healing, clinical environment! What if the patient’s
social environment is one where pain has led to unemployment, frequent sleep disruptions, a
spouse who is fed up with having to do all of the work, financial struggles, disrupted normal
roles/responsibilities, and increasing life stress? Other common factors known as the social
determinants of health include educational status, financial standing, type of employment,
work environment, whether they are happy at work, experience with pain problems in other
family members, cultural pain beliefs, health literacy, political environment, health policy, and
much more. Furthermore, if the clinician is primarily grounded in a biomedically dominant
paradigm, such social factors could seem irrelevant to the treatment plan. In other cases,
clinicians with a strong biomedical perspective may even
stigmatize patients who have too much psychosocial
“baggage.”52 If the patient’s presentation doesn’t fit the
therapist’s model of how they think pain is supposed to
behave, the patient may get shifted to another clinician,
referred to another practice or discharged with the phrase,
“I’m sorry, I don’t think therapy can help you with this type
of problem.”

2.7: Pain Mechanisms

Most manual therapy systems use the patient’s “SINS” as
critical factor in problem solving. An understanding of this
tool provides an excellent framework for planning the physical
examination and can be highly useful in guiding treatment
selection. For those not familiar with the acronym:

• S = Severity
• I = Irritability
• N = Nature
• S = Stage
• (Sometimes an additional S is added as a cue for the Stability of the symptoms [SINSS])

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 53

Severity refers to the level of pain intensity but also describes the extent which pain interferes
with daily activities. Irritability is comprised of three elements which include: how easily
symptoms are provoked, how painful or severe they become, how long the symptoms take to
settle back to baseline. The Nature of the problem represents the manual therapist’s hypothesis
for the etiology of the problem, which could include additional psychosocial factors. Stage
refers to the status of the problem or process of recovery (e.g. acute, sub-acute, chronic,
stages of tissue healing, etc.).56

However useful appreciating the SINS may be, an additional letter might endow them with
superpowers. The letter “P” for Pain mechanisms… thus converting SINS to SPINS is the
linchpin for this concept. Just as the SINS can help provide clues for the manual therapist
on how to proceed, understanding the pain mechanisms guides the clinician toward a much
deeper understanding of the physiology of how pain works, the qualities of its behavior, and
a different appreciation for what can be done to improve the situation. It is hard to imagine
appropriate medical treatment for an infection without understanding the nature of the
pathogen. If the intervention did not address the specific mechanistic problem, the treatment
would fail. Antibiotics do not work for viral conditions nor would a statin drug effectively address
cancer. In other words, treatments need to be based upon the mechanisms of the condition
for the best chances of success. We feel that when clinicians recognize and understand the
neurophysiological processes which underpin various pain states, we move a step closer to
developing well informed and more effective treatment plans.

The topic of pain mechanisms will be

discussed in more detail in Principle
3. However, for the purposes of
understanding pain mechanisms
related to hypothesis categories it is
important to have a basic understanding
of the concept, based in Gifford’s
Mature Organism Model.53 Although
there is much debate as to how pain
mechanisms should be defined, several
broad categories can be considered. In
general, most clinicians might say there
are two types of pain, nociceptive and
neuropathic. However, research into this
topic has described different subtypes.
From the PT literature, Keith Smart and colleagues did some amazing work consolidating
patterns of characteristic behaviors and symptoms into the mechanism-based classifications
including: nociceptive, peripheral neuropathic and central sensitization.54-60 For simplicity,
these classifications will be presented in table format (see Table 2.2.) with further explanation
in the next principle.

54 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

Table 2.2. Clinical characteristics of the three main pain mechanisms.

Peripheral Central Sensitization/

Nociceptive60 Neuropathic59 Nociplastic58
• Pain localized to area of • Pain referred in • Disproportionate,
injury or dysfunction (± a dermatomal or non-mechanical,
somatic referral) cutaneous distribution unpredictable pattern
of pain provocation
• Clear, proportionate • Pain/symptom in response to
mechanical or provocation with multiple non-
anatomical nature to mechanical tests which specific aggravating
aggravating or easing move, load or compress or easing factors
factors neural tissue (active or
Classification Characteristics

passive, neurodynamic, • Diffuse non-anatomic

• Pain usually SLR, etc.) areas of pain and
intermittent and sharp tenderness on
with movement or • History of nerve palpation
mechanical provocation injury, pathology
or mechanical • Pain disproportionate to
• May have dull constant compromise the nature and extent of
ache or throb at rest the injury or pathology

• Pain not associated • Strong association

with dysesthesias, night with maladaptive
pain, burning, shooting, psychosocial factors
electric shock-like (negative emotions,
poor self-efficacy,
maladaptive pain
beliefs, altered family/
work/social life,
medical conflict)

After reviewing the information in Table 2.2, we hope the manual therapist will recognize these
very familiar qualities in their patients. It is likely that countless patients around the world,
with features characteristic of centrally sensitized pain, are being treated using techniques,
surgeries and drugs which are more suited to nociceptive pain problems. The inevitable failure
is frustrating to both patient and clinician. However, the manual therapist should also be
thinking, “YES! I recognize these patterns!” Per Smart and colleague’s analysis, the patterns
are a simple and quite a robust way to categorize dominant pain mechanisms. Although they
did not further divide each classification, the clinician should also appreciate that subcategories
could easily be added. For example, in the nociceptive classification, nociceptive pain could
be stemming from somatic (muscles, tissues, bones) or from visceral sources. Nociceptive
pain could also have a pattern suggesting more of an inflammatory process, or an ischemic
process. An additional concept should also be considered… it is unlikely there is only one type
of pain in operation in most of our patients.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 55

Do you remember back to the purity of your training? Where
common, classic syndromes were presented? Perhaps you
learned about the common features with discogenic pain,
tennis elbow, shoulder impingement, and so on. And then
you finally got to the clinic and rarely saw the “pure” pattern?
When you had a patient come in for their “tennis elbow”
they did indeed have a sore elbow… but also with a bit of
cervical radiculopathy, end-stage renal disease, on dialysis,
some herpes zoster and “triple fibromyalgia.” Life is always
a bit of a mixed picture, and likewise with pain mechanisms.
An excellent way to contemplate categories is by using a pie
chart to visualize what proportion of each of the different types
of mechanism that are in operation. Using your subjective
interview and physical examination you can further clarify
which of the pain mechanisms are the most dominant. Review the pie charts below from three
different patient interviews. Based on the proportions represented in the pie charts, consider
how you might examine each patient differently as well as how this classification tool would
impact treatment decisions.

Nociceptive Nociceptive Nociceptive

Peripheral Neurogenic Peripheral Neurogenic Peripheral Neurogenic
Central/Nociplastic Central/Nociplastic Central/Nociplastic

Figure 2.1: Varying degrees of the clinical presentation of the three main pain mechanisms used in
clinical reasoning.

These are obviously three very different pie charts, from three very different patients. As data
begins to emerge during the patient’s narrative, the clinician should begin to estimate which
pain mechanisms are in operation. These estimates should then prompt further inquiry to help
further discriminate between suspected pain mechanisms. This should also assist in decisions
about the type and extent of physical examination procedures as well as treatment plans.

56 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

2.8: Contributing and Perpetuating Factors
The hypothesis category for contributing and perpetuating
factors refers to the many potential elements which could play a
role in the origin or maintenance of the pain problem (Principle
10). These factors could be related to body structure or function
such as a muscle imbalance, obesity, a hooked type 3 acromion,
diabetes, contracture, poor eyesight leading to forward head
posture, motor control dysfunction, or many other issues.
Contributing or perpetuating factors could also be environmental
or related to activities or participation in life roles. Some examples
might include: a physically demanding job with poor workplace ergonomics, spending most of
the day standing on a concrete floor, running with improper footwear, sitting in a wheelchair
which does not provide correct support, or using improperly sized equipment. Prior activities
could also play an important role as a factor which led to the onset of a pain problem. For
example, perhaps the seemingly trivial incident of turning to back up the car was the moment
severe neck pain started. However, upon further questioning you discovered that three weeks
prior to the incident the patient moved to a new house, spent hours removing wallpaper
and painting most of the ceilings. Psychosocial factors such as pain beliefs, stress events,
depression, and other issues were discussed previously in the section describing personal
factors. Sleep impairment is another important factor which has implications for multiple
categories and is often not discussed during routine therapy sessions. Recently however,
the importance of sleep as a factor in overall health has received more attention, with some
calling for sleep to be regarded as a vital sign.61 Sleep has been implicated as a risk factor for
cognitive dysfunction, cardiovascular disease, metabolic syndrome, increased mortality and
(you guessed it) chronic pain.62 Sleep and pain are thought to have a bidirectional relationship
in that increased pain leads to worse sleep, and sleep problems lead to more pain.63,64 This
goes far beyond the notion that pain just wakes you up and then causes disrupted sleep. Pain
interferes with the entire sleep mechanism, which increases sensitivity, amplifies pain and can
decrease the likelihood for improvement in pain conditions.65 Due to the fact that impaired
sleep has such profound effects upon pain, as well as multiple other body systems, evaluation
of sleep should become a routine element in all manual therapy assessments.66

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 57

2.9: Precautions/Contraindications
All healthcare providers share the common principle of primum
non nocere (first, do no harm). One method for reducing the risk of
a harmful event is to recognize preexisting or emerging precautions
or contraindications to manual therapy. From the moment the
patient enters the clinic, and throughout the episode of care, the
clinician should be assessing for indicators which could radically
shift the care plan. For example, perhaps you have a 1:30pm
patient scheduled for a new evaluation. All you know about the patient is that he is 36 years
old and has complaints of chronic, but worsening neck pain. He has seen several different
physicians and has a working diagnosis of “chronic neck strain.” When you call his name,
the patient rises with minor difficulty from the chair, and then seems to have an odd, clumsy
gait pattern. At first you are not sure, but then as you watch him more closely you see a
somewhat uncoordinated walking quality, once needing to balance himself using his hand on
the doorframe. You walk toward the treatment room thinking to yourself, “Hang on… that’s
not normal… that… is an ataxic gait pattern!” A brief history, a few special questions, and a
neurological exam investigating a suspected upper-motor neuron condition leads to a phone
call where you describe your concerns and request further medical workup. Two weeks later
you get a note in the mail which starts with, “Thank you for saving my life.” It turns out that
you were the only one to recognize the subtle ataxic gait pattern, ask the right questions and
do the limited neuro exam which demonstrated long-tract signs, which lead to the call, which
prompted the MRI, which identified the cervical tumor, and the next-day surgery.

Every day we have the opportunity to serve our patients, guide

them toward their goals, and help them get back to doing the
things they want to do. But every day, there is also potential to
identify serious, and sometimes unidentified or emerging health
conditions. There is also the likelihood that you will need to
manage patients with a host of existing conditions which could
be a precaution for some interventions, or a contraindication
to others. In general, the list of contraindications/precautions
for manual therapists should be familiar: conditions resulting in skeletal compromise (e.g.
tumors or metastatic disease, infections, recent surgery, fracture, severe osteoporosis, spinal
fusion, instability, dislocation, congenital dysplasia, inflammatory disease, etc.), neurological
conditions (e.g. myelopathy, cauda equina, neurological deficit from compression, sudden
emesis/nausea/vertigo), signs/symptoms indicating vascular compromise (e.g. cervical arterial
dysfunction, aortic aneurysm, bleeding disorders, compartment syndrome, anticoagulation),
signs/symptoms indicating visceral disorders (e.g. angina pectoris, urinary tract infections,
acute abdominal pain with guarding, kidney stones, etc.), psychological/psychiatric issues
(also known as orange flags), psychosocial issues (also known as yellow flags), adverse
reactions to prior manipulation, or worsening signs/symptoms.67 Of course, one of the most
important on the list should likely be “a failure of diagnosis, or incorrect diagnosis.”68

In daily practice, the hypothesis category of precautions/contraindications aims to ensure

patient safety (to the best of one’s ability). As alluded to above, the concerns about precautions/
contraindications extend to the evaluation and not only to treatment decisions. For example,
there are cases in which no physical examination should be conducted, and immediate referral

58 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

initiated (in some cases via emergency services). In other cases, as with the example above
of the cervical tumor, a limited examination with referral for additional medical workup. A
further challenge facing the clinician can be to determine to what extent or vigor to examine or
treat the patient in the spectrum of features which range between “OK for all exam/treatment
options” to strictly contraindicated. To assist in identifying potential “red flags” (signs of serious
pathology) it is typically recommended to use a body-systems screening review or a list of
special questions thought to identify such problems.69-71 Furthermore, it does appear that
manual therapists with specialty training are better equipped to identify red flags and make
appropriate management decisions.72 However, recently there has been increasing debate
about whether special questions intended to identify red flags are valid. While a positive
response to a red flag question may indicate the presence of a red flag diagnosis, a negative
response does not always indicate the absence of disease.73 For example, in many cases
patients with spinal malignancy may not present with any red flags. On the other hand, the use
of red-flag screening questions appears to reduce the chance of missing serious pathology
in primary care clinics.74 Some of the discrepancies reported in the literature may be due to
inconsistencies between different lists of red flags.75,76 However, until consensus is reached
as to which questions demonstrate the best diagnostic value it is important to remember that
most guidelines continue to endorse their practice.

2.10: Management Approach

Earlier in this principle, you may recall the quote from Patrick
Wall, “It is inherently ridiculous to consider pain as an isolated
entity.”23 When presented with a complex problem such as
chronic pain, the manual therapist should consider having this
quote tattooed on their forearm as a readily accessible reminder.
Chronic pain is not really isolated in any way. It is a complex, multi-dimensional body protection
system. It is adaptive, reflective, dynamic, proactive, reactive and bioplastic. It is coupled to
many other body systems (motor, immune, endocrine, behavioral, memory, emotions, stress,
etc.) and thus cannot be treated in an isolated fashion. In other words, it’s more complex.
The modern manual therapist must address the complexity of the problem with a more
comprehensive approach than only manipulating body tissues. We need to move beyond only
managing the physical and include the intellect and the emotions. We cannot only address
one piece of the pie but help find the untapped potential within each individual and treat
the whole person. We must recognize the need to become better biopsychosocial clinicians.
On the biological domain, as mentioned previously, there is still much to be learned about
the biology and physiology of many pain conditions. However, an underappreciated factor for
many manual therapists is the concept of pain mechanisms. It is our opinion that recognition
of the dominant pain mechanisms should be fundamental to inform the direction of care for
every patient complaining of pain. This includes not just the hands-on portion of care, but also
what the patient needs to understand about their pain in order to move forward. They need to
be equipped with an appropriate explanation for why they still hurt, what to do about it, and it
must be in a way which is easy to understand, plausible and compelling. We feel this is one of
the key pieces to integrating modern neuroscience into manual therapy.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 59

2.11: Prognosis
Predicting the path of recovery is sometimes relatively easy. Everyone
has probably cut their finger at some point in their life, but once the
bleeding stopped… what happened next? In almost every case the
cut healed. If it didn’t heal, there was probably a good reason as
to why it didn’t: severe diabetes, a blood clotting disorder, severe
malnutrition, an infection, vascular insufficiency or some other
disease process which disrupted the healing process. The fact is that most body tissues
heal as well as they can in a period of about three to six months. Sure, there may be some
scarring and yes, the tissue may not be back to its previous state… but the structure of the
body tissues repaired itself as well as possible during that time period. So, what happens with
chronic pain? It is important to recall
that tissue healing (or the health status
of the tissues) does not always relate to
ongoing pain. In many pain states, even
where all red flags have been ruled Tissue Pain
out and body tissues have structurally Problem Problem
healed there can be continued pain.
In this case, most people report “it still
feels like there is something wrong” with
their body tissues. However, symptoms
persisting beyond this time frame
are more likely to be related to a pain
problem rather than only an issue with
the tissues.

Based on our understanding of how tissues heal (the stages of tissue healing) it is fairly easy
to predict how long some types of injuries take to improve. For example, consider these rough
time frames for healing:

• How long for that finger cut to heal and symptoms settle? A few days to a week?

• How long for a finger cut which needed a few stitches? Ten days to two weeks?

• How long for a finger that was nearly amputated, but successfully reattached? Perhaps
three months?

• What about a Grade I ankle sprain? Two to four weeks?

• Grade 2 knee MCL sprain? Four to eight weeks?

These are relatively easy to predict because we have a frame of reference based on the stages
of tissue healing and we are trained to recognize the pattern.

60 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

 Stages of Tissue Healing

Hemostasis Inflammation

Pain Proliferation/Repair Phase

Maturation/Remodeling Phase
RESPONSE INTENSITY

Days Weeks Stages of Tissue Healing

Months

ACUTE SUB-ACUTE CHRONIC

Hemostasis Inflammation
Figure 2.2: Stages of tissue healing.
Pain Proliferation/Repair Phase
Maturation/Remodeling Phase
Some other pain problems prove much more difficult to provide a confident prognosis. Some
examples could include fibromyalgia, complex regional painvs.
syndrome,
a tissue failed
issue back surgery,
RESPONSE INTENSITY

Pattern indicating a problem with pain systems

chronic fatigue syndrome, irritable bowel syndrome, phantom limb pain, chronic migraine
headaches, post-shingles neuralgia, etc. In some cases, there may not have been an “injury”
at its onset. Perhaps the pain problem started insidiously one day. The patient thought it would
go away, but it progressed, grew, expanded, and developed a mind of its own over time. In
Pain
cases like this where pain levels do not correlate with the status of the body tissues or phases
Days Weeks Months
of healing, and it has persisted beyond expected healing times, and any red flags have been
ruledACUTE
out it is likely that SUB-ACUTE
the body tissues are not the primaryCHRONIC
drivers to ongoing pain. In this
case the responsibility falls to the nociplastic processes occurring within the body’s protection
RESPONSE INTENSITY

systems. This pattern is easily recognizable (once the manual therapist is trained) and is
illustrated below.

Pattern indicating a problem with pain systems vs. a tissue issue

Days Weeks Months

ACUTE SUB-ACUTE CHRONIC

Pain
RESPONSE INTENSITY

Days Weeks Months

ACUTE SUB-ACUTE CHRONIC

Figure 2.3: Pattern associated more with an aberrant pain system than tissue issues.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 61

This is challenging for many reasons, but mostly because this pattern is not at all familiar
to most of the public (nor many healthcare providers who attempt a cure by continually
addressing the peripheral tissue issues). In addition, we probably don’t yet know enough
about the biology, the psychology or the social determinants for these types of pain puzzles.

Sometimes once a treatment plan has been initiated, the response may provide an early
indicator at how far and how fast someone will progress. It is often helpful to refer to a graph
to represent expected changes, explain how progress will occur, and to emphasize the aim to
make steady progress toward activity and participation goals. There will clearly be situations
in which you can’t give a reliable prediction if (or when) they will be able to get rid of their pain.

Function

Pain

TIME

Figure 2.4: The progression of pain versus function over time with proper pain management.

However, with good confidence you can often predict how soon a patient will be able to do
more of the things they want to do. On the graph above, the reader should notice that the
plotted lines are not straight. The lines go up and down with a daily variation in function and
in pain levels. It is important to reassure that it is normal for pain levels or functional ability
to go up and down on any given day. Some days can be good, while others bad. Sometimes
the patient might know why the pain was worse on a particular day, but sometimes they can’t
identify a specific reason. This is a normal pattern for most patients, and they should be
encouraged not to worry over this cycle. The key is to keep moving forward toward their goals,
and even on a “bad day” the most important thing is usually to keep moving.

62 PRINCIPLE 2 | CLINICAL REASONING IS A CORNERSTONE OF MANUAL THERAPY

Conclusion
This principle reviewed some of the challenges the
modern manual therapist faces when making clinical
decisions. Yet the nature of clinical decisions and manual
therapy practice seems to have changed over time. Things
which seemed to have “worked” just 25 years ago are not
always reliable fixes for the clinical problems of today. Was
it just a simpler time? Or, perhaps our understanding of
pain was simpler? Or, maybe we knew less? Based on
pain research, things clearly have changed over the years
and we need to change to adapt to new challenges. Rates
of disability from pain are climbing, the opioid problem
continues to claim many lives, obesity rates continue to
climb, and public understanding about the nature of pain
remains sorely lacking. In our world of quick fixes and
instant gratification, pain is regarded as something which
should not occur and is not a normal part of life. When pain does manifest, an easy structural/
mechanical, surgical or pharmacological cure should be readily available. And why not? It’s
how we think about discomfort these days. When it’s too hot, turn on the air conditioner. Too
cold, crank up the heater. Feeling hungry, open the refrigerator. People are getting used to
having it their way, conveniently and quickly. Why shouldn’t getting rid of pain be the same?
After all, billions of dollars in pharmaceutic advertising promotes the idea of a simple solution
to medical woes.77 Information about pain, sometimes good, but often inaccurate, is instantly
available and may be part of the problem.78 The modern manual therapist needs to wrestle with
all of this complexity, and one of the primary tools to do this is with sound clinical reasoning.

In this principle we examined some of the contemporary definitions for clinical reasoning and
outlined the many forms of clinical reasoning (e.g. diagnostic, narrative, procedural, interactive/
collaborative, intuitive, dialectical, pattern-recognition, predictive/prognostic, ethical, and
teaching as a form of reasoning). Each of these strategies permit the clinician to assess the
breadth of information gathered in the context of the patient evaluation and subsequent care.
We would argue that through the process of clinical mentorship, peer review, and ongoing
metacognitive exercises there is a tremendous potential to cultivate one’s reasoning expertise.
The utility of organizing clinical information using hypothesis categories is a method to help
thoroughly investigate the patient’s problem and collaboratively decide upon a plan of care.
In addition, this degree of scrutiny applied to the patient’s problem will undoubtedly build the
foundation for a strong alliance between the manual therapist and clinician.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 63

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 PRINCIPLE 3

Reshaping Beliefs and

Attitudes About Pain

3.1: The Framing of Pain Beliefs .................. 69

3.2: Descartes and the Specificity

Theory of Pain................................................... 74

3.3: Other Pain Theories—

Pattern and Intensity ...................................76

3.4: The Gate Control Theory ......................... 77

3.5: The Biopsychosocial

Model of Illness ............................................... 80

3.6: Pain and the Neuromatrix .......................81

3.7: The Mature Organism Model ............... 84

3.8: Pain Mechanisms.......................................... 85

3.9: Pain Phenotypes ............................................ 88

3.10: Biopsychosocial Phenotypes ............... 90

Conclusion.......................................................................... 91

Principle 3 References ............................................ 92

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 67

Know Pain; Know Gain
In the last principle, we presented a refreshed overview
of clinical reasoning concepts. While this should be a
familiar subject for manual therapists, we hope this
overview of emerging concepts was helpful. Traditional
clinical reasoning content is primarily focused on the
diagnostic process, identifying sources of symptoms,
application of appropriate manual techniques, and
reflection on the response. Contemporary clinical
reasoning theories suggest the need to conceptualize
this process with a much broader scope. In theory,
it’s easy to say that a biopsychosocial approach is
the most suitable for multidimensional problems
such as chronic pain, but in actual clinical practice
where theoretical constructs meet the rigors of real
patient care, substantial challenges arise. Held to the
demands of life in the clinical trenches, where patients demand your time and expect hands-
on care, things like regulatory compliance mandates, productivity standards, and constantly
shifting reimbursement models demand your full attention. In real world environments,
sometimes it can feel easier to stick with a straightforward biomedical approach. That way,
you don’t need to slog through the boggy edges of the clinical fairway or address maladaptive
cognitions or ride a rollercoaster of patient emotions. You would just need to address the stiff,
painful motion segment, provide some motor control training, wrap it up with a bit of home
program packaging, and move to your next client. This seemed to have worked just fine 20
or 30 years ago… but the times have changed, and so have our patients. Hopefully, you are
able to recognize this, and hopefully you have not made it to this point in the book without
realizing this relatively simplistic approach won’t work for many chronic pain states… it’s just
too unidimensional.

In this principle, we’ll address the process of

reconceptualizing pain by taking a tour of past
and present pain models. Why discuss the past in
a book on modern pain neuroscience and manual
therapy perspectives? The reason is simple—in order
to understand the pain epidemic we’re currently
experiencing, we need to appreciate where the
problem started. One aspect of the pain epidemic
stems from the beliefs people have about pain. In
this principle, we will review how many common
beliefs about pain were shaped. When you consider
how these concepts originated, you will see that for most of the public, and many healthcare
providers, we are stuck in the past. Unfortunately, outdated beliefs about pain may be one of
the impediments toward better treatment of pain problems in the future. To change the course
of the pain epidemic we need to understand more about how pain works from a modern,
neuroscience perspective while gaining a better grasp of contemporary pain models.

68 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

3.1: The Framing of Pain Beliefs
Pain is a normal part of the human experience. Throughout history, people have struggled to
find the right words to describe pain. There have been many attempts to define pain, describe
its nature, and shifting viewpoints over time. The fact that pain is characteristically subjective
may be what gives rise to its elusive nature. Although everyone experiences pain (except
the very few unfortunate folks with a congenital insensitivity to pain1), we all experience it
differently. A painful sensation that might feel excruciating for one person could be relatively
benign for another. To explore how this can occur, let’s examine the ways in which context
can alter a pain experience.

The environment, or context, in which someone

encounters a potentially painful stimulus is a variable
which can determine whether pain is experienced or
not. A commonly cited example is neck or back pain
following a motor vehicle collision (MVC). It has been
reported that even in low velocity MVCs up to 50% of
individuals report pain.2 However, other research has
demonstrated there is more to post-MVC pain than
velocity. Simotas et al. followed a group of demolition
derby drivers and observed some interesting results.3
Each of the 40 drivers surveyed had an average of
more than 50 MVCs for each of their 30 demolition
derbies during their careers. Of these, the mean and
maximum speeds were 26 and 45 mph, with 55%
being rear-end collisions. It would seem that this
group (with an average of 1,500 MVCs) should have
ample biomedical rationale for ongoing whiplash or
other spine-related pain, but that’s not what was
reported. For those who experienced pain following a
demolition derby event, it typically went away within a
few weeks. Of the 40 drivers, 37 reported no ongoing
neck pain! The remaining three reported mild chronic neck pain (which didn’t stop them
from continuing with their demolition derby driving aspirations). Those who did admit to some
chronic neck pain actually felt it had nothing to do with the demolition derby driving! Maybe
they thought it was the way they sat at their computer desk?

This is clearly an example of a change in environment or context affecting the amount of

pain and disability. What’s the difference between a whiplash-sufferer who had one, low-
velocity MVC, and a derby driver with no pain despite repeated high-velocity MVCs? Context
certainly is one of the chief differences (unexpected vs. expected, innocent victim vs. willing
participant, negative emotions vs. positive emotions, etc.). To explore additional examples,
review the following list of how context can alter a pain experience:

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 69

• Love as an analgesic: In an experiment with romantic couples,
a painful heat stimulus was applied to the arm of the female in
several conditions: in a room alone, in a room with a romantic
partner, and holding hands with the romantic partner. Although
the same heat stimulus was applied in each of the different
conditions, the level of pain reported was highest when alone,
less when the romantic partner was in the same room, and
least when holding hands with the romantic partner. In fact, the pain levels experienced
when alone in the room were more than double the pain reported when holding hands!4

• Seeking attractive pain researchers: In this project, attractive subjects

were recruited to observe a test of cold pain thresholds in either male
or female subjects. When male participants were subjected to cold
pain stimuli, they reported significantly less pain when it was applied in
front of an attractive female observer than a male observer. The effect
wasn’t quite as extreme with the female subjects, but the results were
opposite! The female subjects tended to report higher pain levels with
the attractive male observer than with an attractive female observer.5

• Using the word “pain” can create pain: Hall and Stride described an experiment where
they used electric stimulation to investigate the word “pain” used in the instructions.
They found that if subjects were informed that they would receive an electric stimulus,
which is usually painful, the subjects reported pain during the stimulation (no surprise
here, they expected it to be painful). However, when subjects were informed they would
receive electric stimulation but the word “pain” was omitted, the same intensity of electric
stimulation was not reported to be painful.6

• Music to tame the painful beast: A painfully hot stimulus

was applied to the arms of subjects in several conditions: in
silence, while listening to non-musical noise, while listening
to music, or while listening to their favorite music. Although
the heat stimulus was the same in all conditions, it hurt the
most during silence, a bit less with non-musical noise, and
even less when listening to music. However, when listening
to self-selected favorite music, pain was “robustly” relieved!7

70 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

• The color of pain: The subjects in this
study watched for either a red or green
light which was followed by a painful
electric shock. Before the experiment
began, one group was instructed that
a green light would cause an analgesic
stimulation to occur during the electric shock and thus produce less pain. When shown a
red light, they were told it would not include the analgesic stimulation which would result
in more pain. No surprises here—in all subjects the red light produced far more pain than
the green light despite the fact that there was no “analgesic stimulation” and the electric
shock intensity was the same irrespective of the color of light. In a different phase of the
same project, the subjects were not told the meaning of the colored lights. Instead, they
observed a demonstration of the color of light, plus painful stimulation and the effects of
the red (more painful) or green (less painful) lights. After observing the demonstration
these subjects went through the experiment and reported the same relationship as was
modeled during the demonstration (red light = painful, green light = minimal or no pain).
The results of these experiments illustrated a type of placebo analgesia based on the
subject’s belief that red light = more pain and green light = less pain. However, it also
demonstrated that social observational learning can alter beliefs and expectations—i.e.,
the context of beliefs about the color of light altered experimental pain.8

These quirky examples from the dusty fringes of the pain research library are evidence that
there is much more going on during the pain process than a simple transmission of a “pain
impulse” to the brain. If that were the case, red lights wouldn’t hurt more than green, an
attractive observer wouldn’t change a pain response, a painful stimulus would feel the same
whether or not you are holding hands with your sweetheart, and a car crash would feel the
same in the mall parking lot as it does in a demolition derby. All of these examples show
that there is more to pain than “painful input” to the brain. Where did the idea that pain
originates from the body’s tissues develop? A few hypotheses involve personal experience,
our social network, our discipline-specific training about pain, the use of language, and a 17th
century philosopher.

Let’s begin with our personal experiences. Each of us is an expert on our own pain experiences,
and yet this occurs in relative isolation as we cannot fully share our true experience with
others. Of course, others can witness our pain behaviors, emotions, antalgic movements, and
pain related disability; but pain itself cannot be visualized in a biomedical sense. Likewise,
because we lack words with enough descriptive potential to convey our emotions, we are
constrained in our attempts to communicate this experience to others. Instead, as explored by
Scarry in The body in pain: the making and unmaking of the world, a person’s description of
their pain is often limited to the use of metaphor in an attempt to approximate the experience.9
However, these attempts often fall short as evidenced by a lack of understanding by healthcare
providers and ongoing frustration of patients.10,11, 12-14

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 71

On an individual level, pain can be a cruel teacher. It provides an immediate, highly
unpleasant, yet very persuasive lesson to determine which activities and situations we should
avoid. These lessons provide everyday correlations between tissue damage and pain. You
don’t need to repeatedly grab something extremely hot to learn that it is not a wise decision.
Once is quite sufficient, which should highlight the connection between pain and learning/
memory processes. Think about it—in order for pain to be a good body protection system it
must be reactive, but also needs to reflect on past events while projecting to future potential
threats. Early pain learning experiences could include a scraped knee, a cut finger, stepping
on a Lego™, a bee sting, or getting a shot at the doctor’s office. These familiar experiences, or
versions of them, are all instances where you did something to damage your body’s tissues,
and it hurt in the exact place the damage occurred. These are all bits of implicit learning
through a cause and effect relationship; injure your body tissues and pain is the result.

In addition to personal experiences, we’ve all had plenty of social learning experiences with
pain. From Uncle Eddie’s gout attacks, to Dad’s “trick” knee, to brother Jimmie’s bad “rotary
cup” you’ve probably seen people in your life grab their gouty toe, trick knee or bad shoulder,
and complain about the pain. You’ve observed how it changed their behavior and how they
tried to ease the pain, and you may even have participated in rituals to try and help. Perhaps,
as a result you were required to do more than your share of household chores or take on a
second job to help with financial obligations, or maybe you were the “chosen one” who had to
rub liniment on Granny’s bunions.15

72 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

Simply watching television can result in additional pain-
related social learning. Although each has a slightly
different spin, pharmaceutical advertisements provide
a general message that goes something like this: “Pain
is not normal, and it’s wrecking your life. Take this pill,
feel the pain ease away, and get back to what you like
to do.” It sounds so simple, so easy and compelling—
just take the pill! From a very early age, we have been
conditioned to believe that medication is the way to
manage pain. Many of us learned through our parents that a little pain meant a Band-Aid™
or icepack was in order. But for more severe pain, the question was likely asked, “Do you
need some medication?” If so, perhaps it was provided with a little unintentional placebo and
positive affirmation, “Here, take this, it will help ease your pain.”

Even healthcare providers contribute to the social learning that takes place around pain. A
medical appointment for a pain-related problem might include an assessment, management
process, and pain education from a healthcare provider who most likely has a biomedically-
based diagnostic and treatment perspective. A typical appointment involves a brief search for
painful tissues, a bit of poking and prodding, some extreme language describing the problem:
“torn,” “unstable,” “herniated,” “bone-on-bone,” “degenerated” and treatment advice to
address the damaged structure. Because most training programs for healthcare providers
tend to be more biomedically oriented this pattern of interaction should not be surprising. In
addition, most of the training clinicians received in school was likely outdated and, in most
cases, provided with insufficient depth to give providers an adequate foundation for addressing
a complex problem like chronic pain.16-19 For example, in 2011 it was reported that only one-
third of physicians felt comfortable managing patients with chronic pain, and only 1% felt
that the work was satisfying.20 In fact, it has been reported that despite recommendations in
practice guidelines, clinicians often provide patient management advice in line with their own
pain beliefs. If clinicians are more fear-avoidant about their own pain, management advice to
their patients will reflect these beliefs.21-23

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 73

In summary, our pain beliefs are constantly being shaped
by our personal experiences and social learning about
pain (e.g. social environment, media coverage about
pain, learning about pain from our healthcare system).
Unfortunately, our beliefs about pain are influenced by
a rather narrow perspective; most of our pain knowledge
comes from learning about acute pain. A growing concern
is the lack of accurate information about pain (especially chronic pain). It has been reported
that the majority of freely available internet-based information on back pain is of low credibility
and provides mostly inaccurate information.24 An additional concern is the low percentage
of health literacy, which is the ability for a person to understand and act on health-related
information. The U.S. Department of Education reported that only 12% of Americans are
proficient in health literacy for basic health related topics!25 This startling perspective is even
more concerning when you consider that pain literacy is likely much worse.

The language we use to describe pain may also play a role in cultivating particular pain beliefs.
For example, when we say “back pain” it stands to reason this means pain originating from
the back. Likewise, for knee pain or tooth pain or a headache. It’s just much easier to say
“wrist pain” than “a nociceptive experience referencing the wrist in the body’s representation.”
While our use of these terms is perhaps efficient, the semantics of this language may be
misleading. The term “back pain” means pain coming from the back, which subtly suggests
pain originates from the body, or that pain is an input. To frame this concept further, we
must step back in time and turn our attention to a much beloved 17th century philosopher,
Rene Descartes.

3.2: Descartes and the Specificity Theory of Pain

Descartes provided the philosophical framework for a
pain model which continues to influence us (or haunt us)
hundreds of years later. In 1664, he described the nature
of pain as being akin to a type of messaging system to
convey the pain message to the brain. The figure shows a
familiar illustration which depicts a boy kneeling with his
foot too close to a fire. Descartes proposed that the fire
would cause particles in the skin to become active, which
would pull a very thin thread to ring the pain bell on the
other end.26,27 The idea of pain as an input, exemplified
by Descartes, continues to influence how most of us think
about pain. Over time, this Cartesian conceptualization
was likely influential in the development of the Specificity Theory of pain which described pain
as a specific sensory modality.28 This may also be why most students will finish neuroanatomy
with the idea that “pain” travels up the spinothalamic tract. Patrick Wall, one of the greatest
pain scientists of our time, felt strongly that such ideas perpetuated a false understanding of
pain physiology. In 1986 he stated along with Steve McMahon:

74 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

 “The labeling of nociceptors as pain fibers was not an
admirable simplification, but an unfortunate trivialization
under the guise of simplification.”29

As discussed above, if “pain” were traveling up the spinothalamic tract, pain would be an
input arising from the body tissues. Thus, it is more accurate to describe the spinothalamic
tract as a nociceptive messaging pathway or use the term nociceptor rather than pain sensor.
Biologically speaking, “there is no such thing as a pain sensor!”30

In addition to accuracy, the philosophical issue with the notion of pain as an input is in the
absence of an identifiable “pain driver.” If your patient had an x-ray, blood work, diagnostic
ultrasound, nerve conduction test, MRI, and CT scan, all with negative results, many clinicians
might proclaim that it is not “real” pain. As Qunitner and colleagues mentioned, in these cases
the patient’s reports of pain are, “at best doubted and at worst disbelieved.”31 For further
review of this fascinating tale of pain models, see the excellent chapter Evolution of Pain
Theories in Melzack and Wall’s classic book, The Challenge of Pain.32

Descartes also contributed another piece to our current understanding of pain: the concept
of a split between mind and body (mind-body dualism). Although there are some who feel
that Cartesian dualism has been misinterpreted, it is commonly considered that Descartes
suggested the mechanistic physical self was separate to that of the immaterial mind which
is both indivisible and sentient.26,33,34 In essence, this is another thread in the tapestry of our
perpetual misunderstandings about the nature of pain. As mentioned above, in the absence of
imaging findings or other features to validate that there is something structurally or biologically
wrong to cause pain, the conclusion that would often be reached is that the pain is “all in their
head” (aka: not real pain). If most of the public and many clinicians share such beliefs, it is no
wonder that patients with non-specific back pain, fibromyalgia, chronic fatigue, Lyme disease,
irritable bowel syndrome, headache, and other functional pain syndromes feel like they have
been let down, stigmatized, patronized, underserved, over-medicated, and mismanaged by
the medical system.10,11,13,14,35,36 Indeed, the notion that it is hard to get well if you must prove
you are ill is completely understandable.37

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 75

3.3: Other Pain Theories—Pattern and Intensity
The theoretical underpinnings of the Specificity Theory had been evolving for centuries and
include contributions from Herophilus in the 3rd century BCE, the 2nd century AD Greek
physician Galen, Descartes in the 17th century AD, and more modern additions from the likes
of Johannes Müller, Max Von Frey, and Charles Sherrington.28,32 However, this was by no means
the only theory about pain. Two other theories about pain also emerged during this timeframe
including the Pattern Theory and the Intensity Theory of Pain. Goldscheider, in the late 1800s,
and his contemporaries in the early to mid-1900s proposed that the characteristics of pain
were too complex to be determined only by specific nerve types. Instead these scientists
hypothesized that the patterns of nerve firing and/or the intensity of the nerve impulses
were responsible for some of the pathological features of pain. Contributors to these ideas
described observations of increased frequency of peripheral nerve firing as well as central
summation. In the 1940s Livingston began to describe features of neuropathic pain (such as
causalgia, phantom pain, etc.) and postulated that summation likely altered central reactivity
via reverberating circuits.32 This added increased clarity for the pathogenesis of these severe
pain syndromes which previously defied concrete explanation. His ideas also began to lay
the foundation for some of our current conceptualizations of central sensitization (CS). As
models of central modulation of pain began to arise, one additional neurophysiological theory
emerged, the Sensory Interaction Theory. In 1959 Noordenbos advanced the concept of
central control in which large diameter nerve fibers could interact with smaller afferent nerves
with the spinal cord in a way to dampen peripheral neural inputs to the brain.32 Up until this
point, most models considered nociceptive pathways to be direct links to the brain without
opportunity for signaling adjustment. To the casual reader, these seemingly disparate theories
served as critical developments for contemporary pain theories yet to be developed.

Before moving to the current era of pain models, there is one last theory which needs to be
discussed—the idea that pain has an emotional component. While this would seem obvious
now, in the heyday of the specificity theory when all the rage surrounded research on pain as a
sensory modality, the thought of pain having an emotional domain seemed antiquated. Isn’t it
interesting how beliefs and popular understanding shift over time? During the Classical period of
Greek philosophy in the 3rd and 4th centuries BC, where thinkers like Plato, Aristotle, Epicurus
and Socrates were at the pinnacle of intellectual theorizing, pain was not considered to have
anything to do with sensation. Although there was ongoing debate (that is what philosophers
do) pain was mainly considered to be an emotion, more like the opposite of pleasure than a
type of sensation.38 So, in the late 1800s when the philosopher and psychologist H.R. Marshall
proposed that pain has an emotional quality which occurs alongside the sensory experience 32
he observed that painful events rapidly produce very persuasive negative emotional responses
to the event to take action. It would seem this was one of the last of the missing elements
needed to catapult us toward a modern conceptualization of pain.

76 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

3.4: The Gate Control Theory
The next stop on this historical tour of pain models took place in 1965. The two principal
characters in this significant contribution to the understanding of pain were Patrick Wall
and Ronald Melzack. In 1959, Melzack joined the faculty of the Massachusetts Institute of
Technology (MIT) in Boston where he quickly became acquainted with Patrick Wall because
he needed space to conduct research. This meeting cultivated an amazing partnership
seeking an alternative to current thinking about pain as well as a way to reconcile disparities
between the specificity and pattern theories. Based on the foundations described previously
in this principle, Melzack and Wall recognized the need to integrate brain processes to existing
pain models, as well as the idea of spinal cord neural signal modulation. Although Melzack left
MIT in 1963 to join the faculty at McGill University, their collaboration continued. According to
Melzack’s account, their efforts toward developing a new pain model were fueled by numerous
trips to Boston, the consumption of large amounts of duty-free Canadian whisky and vigorous
debate.39 What resulted was the monumental publication of their newly developed Gate
Control Theory of pain in the November 1965 issue of Science.40 They were both surprised
by the reception of the new theory. Probably because their theory was so different from the
prevailing beliefs at the time, there was a surge in pain research trying to prove or disprove
their new concept. However, within a decade, their theory had been included in standard
curricula of most medical schools and physiology textbooks.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 77

As you are likely aware, because gate control remains a standard part of the core pain
curriculum in most health-related programs, the theory hypothesized that both small-fiber
nociceptors and large-fiber sensory afferent nerves synapse in the dorsal horn of the spinal
cord. The “gate” of the system is the substantia gelatinosa which can effectively prevent
nociceptive information from being transmitted to higher centers when inhibited by inputs
from large-fiber sensory afferents. If nociceptive input exceeds the inhibitory controls, the gate
is opened to allow nociceptive information to ascend. Although lost to many clinicians who
consider gate control to relate only to spinal cord filtering of nociceptive inputs, many have
forgotten that the theory also included the concept of central control over the system. Central
control, as shown in the original 1965 paper, could permit further modulation of nociceptive
inputs through feedforward and feedback mechanisms. In fact, when describing the impact
of the Gate Control Theory, Melzack stated:

“Never again, after 1965, could anyone try to explain

pain exclusively in terms of peripheral factors. The theory
forced the medical and biological sciences to accept
the brain as an active system that filters, selects and
modulates inputs.”40

78 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

 SMALL NERVE FIBERS

INHIBITORY NEURON PROJECTION

CELLS

NO INPUT=
GATE CLOSED

LARGE NERVE FIBERS

SMALL NERVE FIBERS

INHIBITORY NEURON PROJECTION

CELLS

LARGE FIBER INPUT=

GATE CLOSED
LARGE NERVE FIBERS

SMALL NERVE FIBERS

INHIBITORY NEURON PROJECTION

CELLS

SMALL FIBER INPUT=

GATE OPEN
LARGE NERVE FIBERS

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 79

3.5: The Biopsychosocial Model of Illness
In 1977, George Engel proposed the Biopsychosocial Model of illness which suggests that
no biological system exists in isolation.41 In contrast to the cause-and-effect relationship of
the biomedical model, biopsychosocialism acknowledges that illness could arise and cause
an impact, not solely through biology, but also through psychological or sociocultural factors.
Engle considered these relationships paramount to the understanding of illness as part of
the human experience. Soon after its publication, the biopsychosocial model was recognized
as a way to better understand and address the complexities of chronic pain. Although now,
decades later, the biomedical model of disease still seems to be the prevailing paradigm for
managing pain, there is growing recognition that a more comprehensive model is needed to
address the ongoing pain epidemic. See the table below to compare differences between
biomedical and biopsychosocial concepts. After reviewing the table, consider differences in
outcome between a biomedical and biopsychosocial approach for a patient with chronic back
pain who has arrived at your manual therapy practice.

Table 3.1. Comparison between a biomedical and biopsychosocial approach.

Biomedical
Focus on disease/illness
Search for single factor biological/
physical cause and effect relationship
Treat symptoms to alter the
disease process
More reductionist
More clinician centered
Patient’s role is passive
If you can identify the single cause and
treat it correctly, health will be restored
People are not responsible for illness
(bacteria, viruses, chemical imbalances
are the cause)
Pain is caused by tissue damage
Pain should be avoided during activity or
exercise to avoid causing more damage
Pain reduction must precede
functional gain
Biopsychosocial
Focus is on health/wellness, recognizes
continuum between health and illness
Multiple factors of biological,
psychological, social and behavioral
factors interact
Treat the disease to alter the symptoms
More holistic
More patient centered
Patient’s role is as an active participant
Multiple factors of biological, psychological
and social factors interact, cannot treat
one in isolation
People’s behavior influences health;
combinations of bio, psycho &
social factors
Pain is complex and multifactorial
Pain can be related to altered sensitivity,
isn’t the only factor to determine
exercise status
Functional gain can occur even with pain

80 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

When a new patient comes to see you, it is very likely they have been on the medical merry-
go-round for quite some time and have seen many different providers. In some cases, they
may also have had numerous imaging consults with little definitive biologic rationale for why
they still hurt. In such a situation, a biomedically-based clinician might be suspicious of a
psychogenic, non-organic or functional pain condition. In some cases, this could result in
dismissal (“Sorry, therapy can’t help you.”) or referral to another expert. If the patient was
to be treated, perhaps the chronic back pain could be rationalized by poor posture, bad
biomechanics or a muscle imbalance. Areas of tenderness could be addressed with manual
therapy, but to what end? In many cases, patients like these may experience temporary relief,
only to return later with similar complaints—or move on to the next provider in search of the
structural-mechanical cause of their pain. Perhaps this cycle, repeated thousands of times
every day around the world, is a reason why the costs for back pain continue to rise?42

Now consider the same problems from a biopsychosocial perspective. From the biological
end, much of the examination might be similar, however, the modern manual therapist might
look with more depth to ascertain which pain mechanisms are most involved (more on this
later in the next principle). From a psychological perspective, it would be important to screen
for psychosocial yellow flags—depression, anxiety and substance abuse, but also assess
coping strategies and readiness to change. From a social perspective—factors related to the
home, family, work or cultural environment. All of these interrelated factors could easily be
missed if the clinician remains overly focused on the back pain.

3.6: Pain and the Neuromatrix

The late 1990s brought many changes to the understanding of pain. With an exponential
rise in pain neuroscience research we knew more about pain and its neurobiology than ever
before. However, there was much more to understand about how pain worked. One of the key
figures in the modern understanding of pain, Ronald Melzack, began to think more about his
contribution of the Gate Control Theory. Although this idea revolutionized our understanding
of pain, led to an explosion of pain-related research, and helped to explain the theoretical
basis for many types of pain interventions, something was still missing. In other words—there
were problems at the pain gate. Some of the factors which continued to bother Melzack about
the gate, particularly in light of the new research on pain, biopsychosocialism, and functional
brain imaging studies, included:

• Limited explanation for central factors in the pain experience

• It did not include the immune system or inflammation, and the endocrine system was
not mentioned

• It couldn’t explain persistent pain, explanations for some pain conditions remained elusive
(most notably phantom limb pain)

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 81

His conclusion? A new pain model was needed which could incorporate all that had occurred
in the pain neuroscience world since 1965, and in particular address contemporary aspects
of brain function. For the second time in his life, Melzack developed a new model which would
change how pain was to be understood by the scientific community—the Neuromatrix. In
1999, he proposed that, “a genetically built-in matrix of neurons for the whole body produces
characteristic nerve-impulse patterns for the body and myriad somatosensory qualities we
feel. I have termed the network, whose spatial distribution and synaptic links are initially
determined genetically and are later sculpted by sensory inputs, a neuromatrix.”39 He argued
that inputs to the neuromatrix included cognitive features (such as memories, experiences and
beliefs), sensory inputs and emotional inputs. Patterns of activity within the neuromatrix would
then be generated within sensory, cognitive and affective neuromodules to make sense of the
inputs. Outputs from the neuromatrix could be pain perception (with sensory, affective and
cognitive dimensions), action programs, and stress-regulation programs (cortisol, endorphins,
immune, norepinephrine).43

Inputs to Body-Self Neuromatrix From: Outputs to Brain Areas that Produce:

Body-Self Matrix
Cognitive Related Brain Areas Pain Perception
Memories of past experience, Sensory, affective, and
attention, meaning, anxiety C cognitive dimensions

Sensory Signaling Systems S Action Programs

Cutaneous, visceral, Involuntary and voluntary
musculoskeletal inputs A action programs

Emotion Related Brain Areas Stress Regulation Programs

Limbic system and associated Cortisol, norepinephrine, and
homeostatic/stress mechanisms endorphin levels as well as
immune system activity

TIME

In the years since Melzack proposed the Neuromatrix model, brain imaging has continued to
improve, providing better fidelity in which to study the implications of this model. Presently,
there are numerous imaging studies which have helped to describe the patterns of neural
activation within the pain matrix proposed by Melzack. Some of the key brain areas activated
during a pain experience include the primary and secondary somatosensory, insula, anterior
cingulate cortex, prefrontal cortices and thalamus.44 Other areas activated within the central
nervous system include the spinal cord, premotor and motor cortices, basal ganglia, amygdala,
hypothalamus, hippocampus, cerebellum and many other areas.45,46 Taken together, this
matrix serves to identify and localize nociceptive threats, determine salience and, if deemed
necessary, formulate an action plan.

82 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

However, something different appears to occur in the transition to chronic pain. As compared
to the acute pain neuromatrix, chronic pain displays a characteristically different activation
pattern and was described by Hashmi and colleagues as a type of “shapeshifting” pain.47
During the transition from acute to chronic pain, a change in the brain activation matrix occurs
with a “shift” from nociceptive-salience circuits toward emotional circuitry. This process
change appears to begin at about three months and continues to the one-year mark, at which
point the new pattern is relatively established. Think back to patients you have seen over a
longer period of time and you may have even recognized when this shift occurred. Research
into this transition has shown that, over time, there is increased connectivity in regions such as
the prefrontal cortex (executive functions, complex behavior, decision making), limbic system
(emotional regulation), nucleus accumbens (reinforcement learning, reward processing).47-49
Doesn’t this match your observations of individuals who have been suffering with persistent
pain? Many of these patients have been failed by the medical system, so they often present
as more complex in general.

SMA M1 S1 PPC

ACC PCC
S2
Insula

BG Thalamus
PFC Hypth
Amygdala
PAG
SMA M1 S1
PPC
PB Cerebellum

ACC PCC
S2
Insula

BG Thalamus
PFC Hippo
NA Hypth
Amygdala PAG

PB Cerebellum

However, they are often resistant to change, have difficulty making decisions and learning new
concepts, become easily frustrated, and have difficulty managing emotions. This research
helps us understand why we may recognize some of these features in our patients, but more
importantly this suggests we should be managing them differently! Clearly a unidimensional
approach will be insufficient to address the multiplex of problems.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 83

3.7: The Mature Organism Model
Around the same time that Melzack was developing his neuromatrix paradigm, a PT in the
U.K. named Louis Gifford was also struggling with how to best manage his patients who were
in pain. During his early years of practice, he found that patient care was often not quite like
what was written in his PT books (or what his teachers said). He had traveled to Australia to
study in Adelaide with Geoff Maitland in the mid 1980s and learned a great deal about how to
communicate with patients and became a proficient manual therapist. However, he didn’t feel
that his questions about chronic pain were fully addressed so he began devouring articles and
textbooks on the topics of pain, stress neuroimmunology, psychology and more—anything
that could help explain the complexities of his patients in pain. One of the concepts which
seemed to consistently emerge from his readings was that all organisms seek to survive.
From a complex organism such as a mature adult human, down to a single-celled amoeba,
all creatures seem to share an innate survival mechanism. Gifford considered this to be a
basic concept of evolutionary biology. To ensure survival, they must constantly sample their
environment (both internal and external), scrutinize whether there is any threat, and determine
an appropriate response. Sample Scrutinize Respond. From this premise, along with
other pieces of existing and emerging pain science research, he began to formulate a model
which could be used to explain how mature organisms respond to threats. Not surprisingly, he
called this new concept the Mature Organism Model (MOM).50,51

Shown in the figure, the model demonstrates how the nervous system continually samples the
body tissues as well as the environment for potential threats. The sampled information then is
sent to the brain to be scrutinized to determine whether any action should be taken. Depending
on the processing that occurs, the system may construct either a behavioral or physiological
output. Although it bears some similarity to Melzack’s Neuromatrix, the illustration is elegantly
simple in its visual representation of a complex, multidimensional process like pain. In contrast
to many previous models with straight-through tracts, the diagram of the MOM easily conveys
the circular pattern of feedforward and feedback built into the system.

84 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

Gifford organized the MOM into three components: inputs to the system, processing of the
inputs, and outputs. Inputs to the system would, of course, include sensory afferents but also
a sampling of the environmental context of the sensory inputs. Earlier in this principle, there
was a comparison between demolition derby drivers and people who had a whiplash injury
following a low velocity MVC. This is an example of the MOM in action, sampling not just
the body tissues after an MVC, but also the context of the experience. Inputs to the system
involve nociceptive contributions from the body tissues which may result in mechanical pain,
ischemic pain or inflammatory pain. Nociceptive inputs from peripheral nerve tissue may result
in pain with different features than other body tissues. This includes a pattern of symptoms
represented by a familiar nerve distribution, mechanosensitive to nerve loading, and a different
quality of symptoms (burning, stinging, paresthesia, deep aching or cramping).52,53

For pain problems which involved the processing/scrutinizing of inputs (from the dorsal horn of
the spinal cord upward to cortical centers) Gifford described central pain mechanisms which
could involve a sensory, cognitive or affective dimension. Aspects such as past experiences,
social situation, culture, pain beliefs, knowledge about pain, expectations, fear, and other
psychosocial factors could impact processing/scrutinizing to alter the appraisal of threat to the
body system. As a response, the CNS could orchestrate an action plan it deemed appropriate
for the situation. The outputs from the CNS could include construction of a pain experience.
However, other outputs include respiration, autonomic nervous system, stress systems (fight/
flight), neuroendocrine outputs (cortisol or other stress hormones), altered motor planning
(antalgic movement), or altered descending modulation. These outputs could be exercised
in isolation, or act in combination depending on the biologic need as computed by the CNS.

3.8: Pain Mechanisms

In 2009, Deyo and colleagues wrote a paper describing the skyrocketing costs for the treatment
of LBP. One of the recommendations to improve care for pain and reduce overall costs was for
clinicians to get “a better understanding of the basic science of pain mechanisms.”54

Building on the work started by Louis Gifford, Keith Smart and colleagues worked to adapt
the MOM into a more concrete method to determine which pain mechanisms contribute to a
given pain problem. Their initial effort included a Delphi study that included over 100 content
experts in the pain field, in order to define key clinical indicators to the pain categories:
nociceptive pain, peripheral neuropathic pain and central mechanisms.55 In the studies which
followed, their team was able to narrow the results into clusters which demonstrated robust
utility and were simple to apply in a clinical environment.56-60 This mechanism model is further
explored and explained in other principles as well.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 85

Table 3.2. Classification of nociceptive, peripheral neuropathic and central (nociplastic)
pain mechanisms

Peripheral Central Mechanisms

Nociceptive55-57,60
• Pain localized to the area
of injury or dysfunction,
+/- somatic referral
• Clear, proportionate
mechanical or
anatomical nature to
aggravations and eases
• Usually intermittent and
sharp with movement or
mechanical provocation;
may be a more constant
dull ache or throb at rest
Absence of:
• Pain with other
dysesthesias
• Night pain or
disturbed sleep
• Antalgic postures or
movement
• Pain variously described
as burning, shooting or
electric-shock-like
Neuropathic55,56,58,60 (Nociplastic) 55,56,59,60
• Pain referred in • Disproportionate,
a dermatomal or non-mechanical,
cutaneous nerve unpredictable pattern
distribution of pain provocation in
response to multiple or
• History of nerve injury, non-specific aggravating/
pathology or mechanical easing factors
compromise
• Pain disproportionate to
• Pain/symptom the nature and extent of
provocation with injury or pathology
mechanical testing
which move, load or • Diffuse/non-anatomic
compress neural tissue areas of pain/tenderness
(e.g. active, passive or on palpation
neurodynamic tests)
• Strong association
with maladaptive
psychosocial factors
(e.g. negative emotions,
poor self-efficacy,
maladaptive beliefs and
pain behaviors)

• Sensitivity 90.9% • Sensitivity 86.3% • Sensitivity 91.8%

• Specificity 91.0% • Specificity 96.0%, • Specificity 97.7%
• Dx odds ratio 100.67 • Dx odds ratio 150.9 • Dx Odds Ratio 486.56

One of the most impressive elements the

team reported was the diagnostic odds
ratio (DOR). By their calculations the
DOR for the cluster of clinical indicators
for nociceptive pain mechanisms was
approximately 100. Essentially, what
this means is that patients who meet
the clinical indicators for the nociceptive
category are 100x more likely to be in the nociceptive category than another. When you look
at the DOR for central mechanisms you should notice that when these clinical indicators
are present, that patient is nearly 500x more likely to have central contributions to their pain
experience than another category. We feel that these clusters that Smart and colleagues put
together are indeed very smart! Even the novice clinician could easily apply this categorization
process without much difficulty.

86 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

We also would like to highlight the importance of understanding pain mechanisms. If someone
were to ask you what the point of having a diagnosis is, hopefully your response would be
something like, “To know what the problem is and how to treat it.” But what about for pain
mechanisms—what’s the point? We hope you will recognize and agree with us, that the point
in being able to identify the mechanism behind the pain problem is to determine the best
course of treatment from a physiological perspective, but also to inform potential educational
interventions. For example, if you are working with an individual with central sensitized pain
as the predominant factor, choosing interventions which are intended to help nociceptive
inflammatory pain would likely fail. Without understanding pain mechanisms, in some ways
we are throwing therapeutic darts blindly, somehow hoping that our therapy will find the target.

The final point about understanding pain mechanisms is that nothing in biology exists in
complete isolation, and everything is dynamic. So, when considering pain mechanisms, it
is generally a good practice to estimate the proportion for each of the different mechanisms
rather than only one. For example, even in a pain state like chronic lateral epicondylitis/
epicondylalgia, there will frequently be multiple mechanisms involved. Perhaps the majority
of the problem is related to nociceptive inflammatory
mechanisms, however, it is not uncommon for the radial
nerve to become sensitized or have central mechanisms
contributing to the problem.61-63 Due to the likelihood
of multiple mechanisms in operation, one method of
depicting this is to use a pie chart. In the example shown,
the majority of the problem was estimated to be from
central mechanisms, although other mechanisms were
also suspected. It should be noted that although Smart
and colleagues initially considered defining an “output
mechanisms” cluster, there was insufficient evidence
to identify a clear pattern with such a broad systems- Nociceptive
based category (autonomic, motor, stress, immune, Peripheral Neurogenic
endocrine, etc.).64 That being said, sometimes clinicians Central/Nociplastic
find it is useful to consider output systems as factors Output
when estimating relevant contributions to a patient’s pain
experience. Once you feel like you have a good estimate Figure 3.1: Pie chart depicting
of the relative proportion of pain mechanisms, don’t forget presence of various pain
mechanisms including dominant
that pain mechanisms will likely shift over time! mechanism

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 87

3.9: Pain Phenotypes
While having a basic understanding of patient categorization
using pain mechanisms is extremely helpful, it is too simple
to cover all of the complexities of chronic pain. Have you ever
wondered why some people with knee osteoarthritis, who
appear to have the same pain mechanisms respond really well
to exercise and others don’t? Or why some folks find a steroid
injection to be a miracle and others find it a curse? Or why some
hate the cold while others love it? Or why some respond better to one medication than another?
Of course, such variable responses drive therapists (and patients) nuts, because many
decisions made in the clinic are grounded in past successes with similar patient problems.
“Okay, last time I treated someone who had this problem, a little warm-up exercise and a
joint mobilization worked like magic! I’ll start out with that and see how it goes…” Experiential
learning, developing clinical patterns, prognostication, and pragmatic guidelines for treatment
prioritizing are some of the fundamentals that help us better determine what direction the plan
of care should head. Unfortunately, when none of these approaches work and your patient
reacts differently than you anticipate, it can get pretty frustrating. Don’t blame your patient
for not fitting into your own model of how pain should work! There must be something else
which could explain such drastic differences in intervention response. One of the ideas about
what could be happening is an extension of the concept of classifying pain states using pain
mechanisms. The concept, which perhaps is a bit like a pain-related biological fingerprint is
known as pain phenotypes.

Initially this concept was to determine if we could be

entering the era of truly individualized pharmaceuticals
based on precise categorization of pain mechanisms.
This emerging field has generated lots of interest and
hope in other areas of medicine, such as in some types
of cancer immunotherapies and genetic profiles,65
so why not with pain interventions? Although the bulk of the research on pain phenotypes
has focused on pharmacological management, this concept could also have implications
for nonpharmacological methods. For example, based on a particular pain phenotype the
therapist of the future could have better tools to know how the patient should respond to
manual therapy, exercise or neurodynamics.

One of the most common means for defining pain phonotypes is with sensory profiling. This
type of assessment goes beyond the standard light touch and proprioception screening to
more thoroughly account for pain-associated sensory perturbations. Two methods commonly
used to establish the sensory profiles of pain phenotypes include neuropathic pain screening
questionnaires (e.g. painDETECT, LANSS, StEP, NPQ, DN4, ID Pain66) or specific sensory
testing during the physical examination. This type of sensory testing is more formally known
as Quantitative Sensory Testing (QST) in which there are a range of standardized, well-
validated and reliable protocols.67 Baron and colleagues reviewed this topic with an example
of an abbreviated QST protocol as well as questions from neuropathic pain questionnaires to
determine pain phenotypes of patients with neuropathic pain. The concept was to understand
more about why some patients with neuropathic pain demonstrate variable responses to
pharmacological management. They recruited subjects with either radicular pain, post-shingles

88 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

3x more likely in post-shingles neuralgia (PHN) Subgroup RAD DPN PHN
n=2094 n=1623 n=498
2
1
0 1. 18% 13% 34%
-1
-2
Burning

Prickling

Allodynia

Shooting

Thermal

Numbness

Light Pressure
2. 22% 26% 5%

Only occurred with lumbar radiculopathy (RAD) 3. 29% 37% 25%

2
1
0 4. 16% 16% 11%
-1
-2
Burning

Prickling

Allodynia

Shooting

Thermal

Numbness

Light Pressure

5. 15% 0% 0%

Figure 3.2: Pain phenotypes for radiculopathy, diabetic neuropathy and post-herpetic neuralgia.

neuropathic pain or painful diabetic neuropathy; all cases of peripheral neuropathic pain.
The sensory modalities tested, and neuropathic questionnaire items included: complaints of
burning, pins/needles (prickling), shooting pain, tests for allodynia (pain from a non-noxious
stimuli, usually light brushing), thermal pain thresholds, numbness and pain from gentle blunt
pressure. When the data was plotted, it became very clear that although all of these patients
met the diagnostic classification criteria for “neuropathic pain” they demonstrated substantial
differences in sensory profile.68-70 The authors surmised that the different pain phenotypes
identified provide evidence explaining why patients with seemingly the same type of pain
(neuropathic pain in this case) respond differently to pharmaceutical intervention: in actuality,
the underlying pain mechanism is different!

Perhaps you are thinking, “Okay, interesting enough—but I don’t really see many people
with post-herpetic neuralgia in my clinic.” Fair statement—but how about knee osteoarthritis?
Carduso and colleagues did a similar study with almost 300 subjects with knee osteoarthritis.
Care to guess what they found? That’s right—despite the same diagnosis and same type
of clinical condition, they identified multiple different sensory profiles (implicating different
pain mechanisms). Some of the patients had a low pain sensitivity to pressure pain, others
demonstrated temporal summation of punctate pain, some hated cold (it actually caused
more pain), others exhibited a high sensitivity to heat pain and temporal summation of
heat pain, and one last group had an average pain sensitivity across most modalities.71
As mentioned previously, this should get you excited about contemplating effectiveness
of nonpharmacological treatment. Up until this point, assessing for pain phenotypes has
probably not been part of your diagnostic or treatment-centered clinical reasoning schema!

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 89

3.10: Biopsychosocial Phenotypes
Before this principle is wrapped up, there is one final point to discuss. Up to this point, we have
reviewed the history and development of pain models across the centuries, considered how
these models have shaped our pain beliefs, discussed classification using pain mechanisms,
and then refined the idea a bit further with pain phenotypes. That was a lot of territory to cover,
and we hope you now have a better appreciation for the current state of pain neuroscience
models. However, the longer you are in clinical practice the more you will begin to notice
the trends in therapeutic management. Sometimes a particular method seems to rise from
nowhere to become the “it” thing to try with your patients. In the past 15 years, it seems that
the clinical pendulum has been swinging in the direction of all things brain and neuroscience.
Some have even coined the swing as the “seductive allure of neuroscience explanations.”72-74
Sure, it is very impressive to see some of the amazing neuroscience images of brain function,
but we must also ground ourselves in a comprehensive reality without abandoning what we
know about the physicality of the body. It was never only about the body tissues, just as it
should never be solely about what is happening in the cortex—it is always about both. We
must not become too neurocentric in our thinking and we must remember to embrace the
enormous complexity of the inseparable relationship between mind and body lest we fall into
a brain-centric Cartesian dualism.75

In considering this concept, the modern manual therapist should not only consider pain
phenotypes, but in light of our bioplasticity (not just plastic processes in nerves, but all other
biologic systems), appraise the notion of a biopsychosocial phenotype. What would this look
like? Although this paradigm has not been fully explored, perhaps this is an appropriate venue
(with an appropriate audience). The table below includes key indicators that represent a
potential biopsychosocial phenotype.

Table 3.3. Key indicators that represent a potential biopsychosocial phenotype.

Biological Psychological Social

Pain mechanisms Depression Socioenvironmental
Family
Pain phenotype Pain beliefs
Work
Measures of physical Coping
functioning (e.g. gait speed, Community
standardized measures) Emotional functioning
Relationships
Sleep Stress
Cultural
Pain intensity Self-efficacy
Productivity
Pain frequency Health-related life quality
Satisfaction with social roles
Perception of goal status

90 PRINCIPLE 3 | RESHAPING BELIEFS AND ATTITUDES ABOUT PAIN

 Socioenvironmental Socioenvironmental
Cognitive Sensorimotor Cognitive Sensorimotor
Belief Disintegration Belief Disintegration

Emotional LOW
Nociceptive Emotional LOW
Nociceptive
Affective MODERATE
Physiological Affective MODERATE
Physiological
HIGH HIGH
VERY HIGH VERY HIGH
Central Peripheral Central Peripheral
Nociplastic Neuropathic Nociplastic Neuropathic

Figure 3.3: Radar plots showcasing various biopsychosocial pain phenotypes.

The indicators listed in the table are a collection of proposals from the authors, but also
suggested domains from the VAPAIN consensus statement of core outcome domains, the
Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials (IMMPACT) as
well as patient preference suggestions.76-78 But to be able to visualize these in a useful way
in the clinic, one graphical method would be to use a radar plot. For example, given the
selected measures from the table above, the data could be plotted to rapidly visualize domains
to prioritize during therapy. This method for representing multidimensional pain profiles has
been proposed as a means to improve pattern recognition in clinical reasoning and to visualize
outcomes in LBP, but not previously described as a biopsychosocial phenotype.79,80

Conclusion
As we continue our pain neuroscience journey for manual therapists, our hope is that you
continue to place high value on your manual skills, expertise, clinical wisdom, and patient
experiences while at the same time balancing this emerging knowledge. As time passes, we
will continue to discover more about the intricacies of how our amazing system operates to
detect and manage bodily threats. As Chapman and colleagues so elegantly stated: “Through
a common chemical language comprising neurotransmitters, peptides, endocannabinoids,
cytokines, and hormones, an ensemble of interdependent nervous, endocrine, and immune
processes operates in concert to cope with the injury. These processes act as a single agent
and comprise a super-system.”81 The information in this principle was presented to help the
reader appreciate, recognize, and characterize aspects of this super-system in an effort to
better understand pain and help patients who are suffering.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 91

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 PRINCIPLE 4

Nociception and Pain Are Not

the Same Construct

4.1: What is Nociception? .................................. 96

4.2: The Biomedical Model of Pain ........... 98

4.3: Nociception and Pain Are

Not Directly Linked.................................... 102

4.4: It Has to Be More Than Just

Nociception ..................................................... 104

4.5: PNE Is Not Meant to Be

“Hands-Off” ................................................... 106

4.6: Do We Need to Reconceptualize

Manual Therapy? ........................................ 107

Conclusion...................................................................... 107

Principle 4 References ......................................... 108

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 95

Nociception ≠ Pain
As discussed in the introduction, pain science
emerged out of manual therapy. To truly understand
and appreciate this, let’s travel back in time to the
heyday of the manual therapy profession. Imagine
for a moment it’s the late 1970s and you are a fly
on the wall in Geoff Maitland’s clinic in Adelaide,
Australia. He is conducting a very thorough subjective
examination of a new patient with recent onset left-
sided neck pain with occasional radiation into the
left lateral shoulder area. Maitland is asking where
the patient feels pain (and where they don’t); what
the pain is like (sharp, dull, aching, gnawing, etc.);
whether the pain is there all the time or if it comes
and goes (constant versus intermittent); whether they
feel pain in one, or separate areas (if separate, can the pain occur independently, or must one
pain be present before the other). Maitland asks what makes the pain worse and what makes
it better (aggravating and easing factors); when the pain is aggravated, how severe is it and
how long does it take to settle back down to normal once the aggravating activity is stopped
(severity and irritability). He asks how the pain is at night, first thing in the morning, and at the
end of the day (24-hour behavior pattern). He then asks what brought the pain on (mechanism
of injury) and follows up with more questions to build a complete picture of the patient’s
experience since the onset of neck pain. By the end of the subjective examination, Maitland
has a very good idea what he will need to test during the objective examination. He already
has a working hypothesis of what is likely causing the patient’s pain; the objective examination
will simply confirm or refute his hypothesis. Of course, this is assuming the patient was able
to accurately answer all of Maitland’s questions. In other words, assuming the patient has a
nociceptive dominant pain condition.

4.1: What is Nociception?

Nociception is defined as the neural process of encoding and processing noxious stimuli.1 In
other words, it is an input (encoding) into the nervous system that warns us of damaging or
potentially damaging events (stimuli) which might include extreme temperature (touching a
hot stove) or mechanical stimulation (spraining an ankle). Nociception is simply the signal or
input to the brain that tissue injury or potential tissue injury has occurred. It is important, from
a pain perspective, to realize and recognize that nociception may not necessarily cause pain.2

96 PRINCIPLE 4 | NOCICEPTION AND PAIN ARE NOT THE SAME CONSTRUCT

Since we now know that pain can be classified into various potential categories (i.e., nociceptive,
peripheral neurogenic or nociplastic [CS]), Keith Smart and colleagues undertook a study to
identify symptoms and signs associated with a clinical classification of nociceptive dominant
pain in patients with LBP, with or without leg pain.3 They found a cluster of seven clinical
criteria predictive of nociceptive dominant pain:

1. Pain localized to the area of injury/dysfunction

2. Clear, proportionate mechanical/anatomical nature to aggravating and easing factors

3. Usually intermittent and sharp with movement/mechanical provocation; may be

a more constant dull ache or throb at rest

4. No pain in association with other dysesthesias

5. No night pain/disturbed sleep

6. No antalgic postures/movement patterns

7. No pain descriptors of burning, shooting, sharp or electric shock-like

Smart and colleagues found the likelihood of a patient having a dominance of nociceptive pain
if they experience this cluster of clinical criteria is high (92.7%, 95% CI: 88.7 – 95.6%).3 They
reported a diagnostic odds ratio of 100.7 which indicated that the cluster was 100 times more
likely to accurately predict a clinical classification of nociceptive pain.3

Returning to Maitland’s clinic, if the

patient met all seven of the criteria
listed above, then the decision to
use manual therapy would be pretty
straightforward. If the patient had
localized left-sided neck pain with
occasional radiation into the left lateral
shoulder area, and turning the head to
the left or side-bending to the left made
the pain worse, while turning to the
right, side-bending to the right and looking down made the pain better, then most of us would
reason that the primary nociceptive driver (input) would likely be the facet joints on the left
side of the cervical spine. We could imagine Maitland testing active range of motion, with slight
overpressure (as irritability was established as low) and finding limited motion into extension,
left rotation and left lateral flexion. He might then test central posterior-to-anterior pressures
in the middle cervical spine as well as unilateral posterior-to-anterior pressures on the left.
He might find positive reproduction of the patient’s pain with central posterior-to-anterior
pressures and left unilateral posterior-to-anterior at C2-3 and C3-4.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 97

At this point we’ll pause a little for (i) the “experienced” manual therapist
to reminisce and (ii) younger manual therapists to re-read the step-by-
step beauty of these manual systems, passed down over time and still
helpful today to millions of people!

Next, we could imagine seeing Maitland reassess the patient’s active

range of motion into left rotation and lateral flexion. What might we expect
to happen? The patient would likely report less pain and demonstrate
greater range of motion into those movement directions. This is the kind of scenario that would
take place more often than not in the manual therapy world during the late 1970s and early
1980s. We could argue that the patient likely had an injury or some kind of tissue damage
to the left C2-3 and C3-4 facet joints. Perhaps an overstretching of the joint capsule during
prolonged positioning in right rotation and right lateral flexion (sleeping half on and half off a
pillow) then moved into left rotation and left lateral flexion, entrapping the synovial fat pad. This
clinical reasoning is based on the biomedical model of pain, which is still valid.

4.2: The Biomedical Model of Pain

Manual therapy is deeply rooted in a biomedical model of pain through its strong focus on
nociceptive input from tissues and tissue injury.4-6 When focusing on this biomedical model,
manual therapists like Maitland, Cyriax, Kaltenborn, etc., would seek to find the anatomy
or biomechanics at fault, or the nociceptive driver. In our example, the left C2-3 and C3-4
facet joints. If the faulty biomechanics or pathoanatomy could be “corrected,”* and noting
improved pain and range of motion into the provocative directions after central posterior to
anterior and left unilateral posterior to anterior would suggest it could be, then it would be
expected that pain and disability would be recovered.4-6 The manual therapist would simply
need to continue with the mobilization interventions, and if appropriate, perhaps introduce a
thrust joint manipulation to the affected cervical spine levels.

*We need to acknowledge that we don’t really “correct” (change) anatomy. Anatomical structures are not
moved or displaced with manual treatments. Rather, manual therapy affects processes. Per Principle 1,
in the facet joint example, mobilizations to the cervical spine likely affected various physiological and
biological processes such as inflammation, irritations of nociceptors, etc., versus correcting an anatomical
structure. Sure, you may think of it “correcting” (restoring) homeostasis on a chemical, mechanical
or even thermal level, but realize again we don’t correct structures, as much as we affect underlying
processes associated with nociception.

98 PRINCIPLE 4 | NOCICEPTION AND PAIN ARE NOT THE SAME CONSTRUCT

 But how well do these biomedical models work when
explaining a patient’s pain? How might a patient react to an
explanation that their facet joints on the left side of the neck
got “stuck” and they have a “locked neck” because they may
have slept with their neck in an awkward position overnight?
We could argue that if the manual therapy treatment relieves
the pain completely and relatively quickly, that the patient
might be okay with such an explanation. But what if that
same pain comes back in a few days, a few weeks, or a few
months? What would the patient think and feel about his or her facet joints repeatedly “getting
stuck?” There is evidence to suggest that these biomedical models (if used without care) show
limited efficacy in decreasing pain and disability, and that they may in fact increase fear in
patients, which in turn can increase their pain.7,8

If clinicians use only a biomedical model to teach patients about pain, could they be
indoctrinating patients into believing all pain must have an anatomical or biomechanical
explanation? To highlight this idea, let’s look at an interesting study from 2009.9 Patients who
were scheduled to have lumbar discectomy for low back and leg pain (confirmed lumbar
radiculopathy) were randomized into two groups. They all underwent the same discectomy
surgery procedures, except one group was given the “damaged disc” material (apologies
for the term—direct quote from the paper) that had been removed
during surgery. The other group was not given (nor shown) their
removed disc material. What were the results? The group that was
given their disc material recovered significantly better in terms of:

• Leg pain (91.5 vs 80.4%; p<0.05)9

• Back pain (86.1 vs 75.0%; p<0.05)9

• Limb weakness (90.5 vs 56.3%; p<0.02)9

• Paresthesia (88.0 vs 61.9%; p<0.05)9

• Reduced analgesic use (92.1 vs 69.4%; p<0.02)9

What could account for the different outcomes of these two groups when the exact same
surgical technique was used on all the patients? Was the continued pain following surgery
viewed differently by members of the two groups? Imagine you were in the group given the
damaged disc material in a small sterile container. Experiencing pain following surgery might
be rationalized as pain from the surgery, or pain from healing after the surgery: “It can’t be
from the disc because I can see it right here in this container.” Now imagine you were in
the group that was not given the disc material following surgery. Experiencing pain after the
surgery might be rationalized very differently: “It still hurts, maybe they didn’t take out enough
of the bad disc material. Maybe they took out the wrong disc, or maybe they damaged the
nerve as they took the disc out.”

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 99

The biomedical model of pain is one of the traditional
or “old” pain models. Our knowledge of pain and pain
processing has evolved considerably.10 It is persistence of
the Cartesian model of pain (Rene Descartes, 1664) that
is most likely to blame for many of the misconceptions
about pain. Despite this, it continues to be a driving force
in the delivery of medicine today.11,12 The Cartesian model
proposed that if you placed your foot into or too close to
a fire, then a message would be sent to the brain via a
pathway/wire (nerve). So far so good. But Descartes
actually believed that nerves were hollow tubes through
which spirits flowed in a mechanical manner. The message was sent to the brain, which was
the center of all the senses. The injury to the foot, caused by the fire, had a mechanical input
which resulted in the ringing of a bell at the other end of the pathway or tube in the brain,
producing pain. We now know that this is not only incorrect, but also an overly simplistic view
of pain, which often leads to equally incorrect and overly simplistic treatment options.

One option might be for the person to take their foot out of the fire and then avoid the fire from
thereon. This is analogous to telling someone to do whatever it takes to stop the pain (get away
from the fire) and avoid doing anything that brings on the pain (back into the fire). Although
this might seem like a logical response in an acute, threatening scenario, it is much less likely
to help in the long run. In persistent pain states, the modern analogy of such an approach is
the fear avoidance model, which has been shown to lead to increased pain and disability.13

A second option might be to douse the fire with a bucket of water. The modern medical
analogy of a “bucket of water” would be prescription medications or injections which aim
to “put out the fires” of local inflammation. In the last five years, there has been a 629%
increase in Medicare expenditures in the U.S. for
epidural steroid injections and a 423% increase
in expenditures for LBP,14 and yet pain rates are
increasing, not decreasing. A PT analogy might be
the application of modalities such as moist heat,
ultrasound, or electrical stimulation. These might
help temporarily, but in the long run, dousing the
fire does not always work. Yes, manual therapy
should also be mentioned here as a means to
“put out the fire,” which may explain its efficacy in
acute and sub-acute pain, but lack in its ability to
extinguish chronic pain.

100 PRINCIPLE 4 | NOCICEPTION AND PAIN ARE NOT THE SAME CONSTRUCT
A third and perhaps the most drastic option to the
Cartesian model of relieving pain would be “cutting
the wire.” Cutting the wire means that the message
to the brain is severed. Therefore, if the brain cannot
receive “pain messages,” no pain will be experienced.
The modern analogy for this would be surgery. Of course, the idea that pain only occurs
because a body part that is injured sends “pain messages” to the brain is a fallacy. If this were
true, then surgery would be 100% successful. This is obviously not the case, which is proven
by the fact that 20% of patients have the same (or worse) pain following a lumbar discectomy15
and there is only a 50% success rate in decreasing pain following a lumbar fusion.16,17

Cartesian thinking has persisted within the Biomedical model of pain despite the fact that
many healthcare providers acknowledge there are many incorrect assumptions that have to
be made, namely:18

• There is a direct link between the amount of tissue damage and the level of pain
experienced—patients and society truly believe this.

• All pain is caused by injury and increased pain means more damage.

• There is a division of mind and body, where pain is either physical or psychological or mental
illness versus physical illness; this may have fueled the social stigma of psychological
issues or even psychological pain.

• In cases of chronic pan, according to the Cartesian model, tissues are not healing and
damage is ongoing.

• Nociception and pain are synonymous.

• Pain is an input driven system.

• The nervous system is simply built for conduction (a wire).18

Pain is obviously much more complex than a simple input driven system of protection, and
the biomedical model or explanation of pain is totally inadequate. But how did we realize this?
We noticed that sometimes nociception did not result in pain and vice versa: people with lots
of pain sometimes display little/no nociception.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 101

4.3: Nociception and Pain Are Not Directly Linked
The biomedical model of pain suggests that whenever you are injured, or have tissue damage,
you will feel pain. This is how you know you have been injured and the tissue will need time
to repair. But this is simply not so. One of the most pivotal shifts in the understanding of
pain emerged in the late 1990s with studies scanning pain-free individuals. There are many
normative studies on asymptomatic subjects which demonstrate there is poor correlation
between the health of the tissues and a pain experience. Here are some examples:

Low Back:

• It is estimated that 40% of asymptomatic people will

have a “bulging disc” on magnetic resonance imaging
(MRI).19,20

• Disc “bulges” have been shown to reabsorb within weeks

or months.21-23

• In 40-year-old asymptomatic people, between 25-50%

will demonstrate disc degeneration and signs of previous
injury, endplate changes, foraminal stenosis and facet joint degeneration on spinal
imaging.24

• Lumbar spine degeneration starts in a person’s early 20s and there is little correlation
between arthritis and LBP later in life.24-27

• In asymptomatic elite tennis players, 33% had spondylolisthesis when scanned, with
several demonstrating pars fractures, stress fractures, etc., yet no pain.20

• Despite presenting with the same LBP, patients received completely different MRI results
when visiting different imaging centers and were given different interpretations of the
results by radiologists.28

Neck:

• Among people with significant degenerative changes

noted on their imaging, only 10% experience pain.29

• 90% of asymptomatic people undergoing cervical MRI

scan have a “bulging” disc (including people in their early
20s).30

• Demolition derby drivers crash over 1,500 times during

their career; averaging over 24 mph, and yet almost all
report no chronic whiplash-associated neck pain.31

102 PRINCIPLE 4 | NOCICEPTION AND PAIN ARE NOT THE SAME CONSTRUCT
Shoulder:

• One in three people over the age of 30 and two out of three
people over the age of 70 have abnormal MRI findings
related to their shoulder, including complete rotator cuff
tears.32-34

• After successful rotator cuff surgery and postoperative

rehabilitation to regain full range of motion, strength and
function, 90% of patients’ MRI reports show “abnormal
findings” and 20% still have a complete rotator cuff tear.35

Knee:

• In asymptomatic individuals, 20-50% of MRIs reveal

significant “degenerative” changes, highlighting the poor
correlation between knee OA, pain and disability.36,37

• In active collegiate basketball players with no knee pain

35% of MRI scans show significant abnormalities.38

• It is currently estimated that one in three knee

replacements are unnecessary.39

Hip:

• MRI of asymptomatic people show abnormalities in 73%

of hips and labral tears in 69% of the asymptomatic
group.40

• Hip MRI studies show that femoroacetabular impingement

and labral injuries are common in asymptomatic
individuals.41

• In hockey players with no hip pain, two out of three have

scans that show significant degenerative changes.42

Wow! Did you get that? What we see on scans and tests pertaining to the health of the tissues
does not necessarily correlate to the experience of pain and disability! So, we can observe that
injury and/or degenerative processes can be present in an individual, yet they may experience
little to no pain. The opposite is also true. Many people suffer from significant and debilitating
pain, yet no injury has occurred, and no disease process can be identified. It is important to
acknowledge that injury/tissue damage and pain are not synonymous. While often present
together, you can have one without the other.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 103

4.4: It Has to Be More Than Just Nociception
Manual therapy seemed to work quite well for the majority of
patients in the heyday of the profession, and we may even
assume it was simply because the majority of our patients had
nociceptive dominant pain presentations. We simply don’t have
epidemiological data to know for certain, but we do know we had
limited insight into other pain mechanisms and likely viewed many
patients through “nociceptive” glasses. If patients responded well
to manual therapy, we were correct. If they did not respond well, it
was often thought these patients “undid” the treatments at home.
Furthermore, if the patient did not return (likely in many nociplastic
cases), it must be because they were “fixed.” Manual therapists,
however, started noticing a slowly growing minority of patients
who didn’t respond as well to the manual therapy interventions.
These patients described more severe pain that involved the
extremities, with descriptors such as “prickling, tingling, pins
and needles, electric shocks or shooting, hot or burning, numb
feeling, and radiating pain.” These were patients with peripheral
neurogenic pain, which is pain thought to be attributable to a lesion or dysfunction in a peripheral
nerve, dorsal root ganglion, or dorsal root arising from trauma, compression or ischemia.43-45
New clinical thinking and intervention approaches were required for these patients, and it
spawned the concept of the mobility and health of the peripheral nervous system. Of course,
the straight leg raise test (SLR) (Lasègue’s sign) had been around since Charles Lasègue,
a French clinician who described two cases of sciatica aggravated by weight bearing and
hip and knee flexion in his 1864 article Thoughts of Sciatica.46 It was primarily used as a
diagnostic test for lumbar radiculopathy strongly suggestive of an underlying disc herniation,
but it was often misinterpreted. A positive
SLR test had to reproduce radiating leg
pain and not merely back pain.47 Using
this criterion, a meta-analysis reported its
diagnostic accuracy as 91% sensitivity and
26% specificity,48 which made it a valid
measure to rule out disc herniation.

Much of the early challenge to only the “joint” and “joint tissue” as the main target of manual
therapy can be attributed to Maitland’s early work on examination of movement of the
pain sensitive structures in the vertebral canal (the dura mater and nerve root sleeves),49
which ultimately led to the development of the slump test.50 Then Robert Elvey’s seminal
work51 on the brachial plexus tension test spawned a wave of cadaveric and clinical studies
on the movement properties of the major nerves in the extremities. This was the dawn of
neurodynamics, and an introduction to the concept that nerves need three things to stay
healthy and function normally: space, movement and blood.52

104 PRINCIPLE 4 | NOCICEPTION AND PAIN ARE NOT THE SAME CONSTRUCT
Keith Smart and colleagues undertook a second study to identify symptoms and signs
associated with a clinical classification of peripheral neuropathic dominant pain in patients
with low back pain, with or without leg pain.53 They found a cluster of three clinical criteria
predictive of peripheral neuropathic dominant pain:

1. Pain referred in a dermatomal or cutaneous distribution

2. History of nerve injury, pathology or mechanical compromise

3. Pain/symptom provocation with mechanical/movement tests (e.g. Active/Passive,

Neurodynamic) that move/load/compress neural tissue

Smart and colleagues found that the likelihood that a patient has a dominance of peripheral
neuropathic pain if they experience this cluster of clinical criteria is high (86.3%, 95% CI: 78.0
– 92.3%).53 They reported a diagnostic odds ratio of 150.86 which indicated that the cluster
was 150 times more likely to accurately than inaccurately predict a clinical classification of
peripheral neuropathic pain.53

This meant that now the manual therapy world had some treatment approaches for joints
and major peripheral nerve pathways. Mobilize and manipulate joints or mobilize the nervous
system, then keep things moving with therapeutic exercise. You’d think the life of a manual
therapist in the late 1980s was great! But no, there was still an ever-increasing number of patients
who did not seem to have a nociceptive dominant, or peripheral neuropathic dominant pain
presentation. These were the patients who said their pain had been bothering them forever;
many could not remember when or how their pain had started and, in most cases, it had been
present for years. These patients would say they hurt everywhere; many could not accurately
locate where they hurt, stating that the pain was all over their body. They said everything
they did made them feel worse, and that nothing made them feel better. Unfortunately,
they attracted labels such as “malingerers,” “non-responders,” or “chronic pain patients.”
Through Louis Gifford’s early work on pain and the Mature Organism Model, and Clifford Woolf’s
work,54-56 we soon started to hear more about CS as a cause of persistent pain states.57,58 CS
pain is now operationally defined as “an amplification of neural signaling within the CNS that
elicits pain hypersensitivity.”56 Much of the work on CS focused on brain plasticity and the
connection to the psychosocial, and this is when pain science pioneers like Gifford, Butler and
Moseley began ushering in the concepts of PNE.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 105

Keith Smart and colleagues undertook a third study to identify symptoms and signs associated
with a clinical classification of CS dominant pain in patients with LBP, with or without leg
pain.59 They found a cluster of four clinical criteria predictive of CS (nociplastic) dominant pain:

1. Disproportionate, non-mechanical, unpredictable pattern of pain provocation in response

to multiple/non-specific aggravating/easing factors

2. Pain disproportionate to the nature and extent of injury or pathology

3. Strong association with maladaptive psychosocial factors (e.g. negative emotions, poor
self-efficacy, maladaptive beliefs and pain behaviors)

4. Diffuse/nonanatomic areas of pain/tenderness on palpation

Smart and colleagues found that the likelihood that a patient has a dominance of CS pain if
they experience this cluster of clinical criteria is high (91.8%, 95% CI: 84.5 – 96.4%). They
reported a diagnostic odds ratio of 486.56 which indicated that the cluster was around 480
times more likely to accurately than inaccurately predict a clinical classification of central
sensitization pain.

4.5: PNE Is Not Meant to Be “Hands-Off”

As manual therapists in the 21st century we are learning how pain works at the biological,
physiological and psychological levels. We now have a handle on things, don’t we? If our patient
presents with a nociceptive dominant pain mechanism, we take the traditional manual therapy
route. If our patient presents with a peripheral neuropathic dominant pain mechanism, we turn
to the neurodynamic approaches of PNE for neuropathic pain. But what if the patient presents
with a CS dominant (nociplastic) pain mechanism? Do we avoid using any hands-on manual
therapy techniques and merely talk to our patients?

Many manual therapists who started using the PNE approach on patients with a CS dominant
pain mechanism were immediately reluctant to “touch” their patients. If nociception is not the
primary driver for the patient’s pain experience, then why attempt to change or eliminate that
nociceptive input? Furthermore, these patients were often “too hot to handle” and demonstrated
allodynia and hyperalgesia as part of their centrally sensitized state. Part and parcel of the
presentation was the perceived presence of maladaptive illness perceptions and maladaptive
pain cognitions.60 It was reasoned that the most important thing was to reconceptualize pain for
these patients. The PNE message was that their pain was no longer an accurate reflection of the
health or status of their tissues or tissue injury. Clinicians would reason that attempting to localize
a tissue source (joint, intervertebral foramen, nerve pathway, etc.) in such a patient would merely
serve to subvert that important message. You are telling them that their pain likely has nothing to
do with their “bulging disc,” or the “arthritic/stiff joint” in their spine, so how can it make sense
for you to mobilize that spine passively with a manual therapy technique? Such thinking sets
off a debate about whether musculoskeletal practice should be “hands-on” or “hands-off.”61,62

106 PRINCIPLE 4 | NOCICEPTION AND PAIN ARE NOT THE SAME CONSTRUCT
4.6: Do We Need to Reconceptualize Manual Therapy?
Thinking that manual therapy interventions should be avoided for patients who present with
CS dominant pain may reflect the questions we have about the effects of manual therapy. If we
limit those effects to mechanical changes in the tissues, it would make sense to steer clear of
manual therapy for these patients. But is that all manual therapy can achieve? Is it only passive
movement at the joint that occurs? There is good evidence showing that manual therapy can
result in reduction in nociception, pain behavior and local pathology, including scar tissue
formation.63,64 Despite years of research and a wealth of published evidence, exactly how
manual therapy works remains a bit of a mystery. Bialosky et al.65 proposed a comprehensive
model of the mechanisms through which manual therapy might exert its effects (Principle 1).
They proposed the effects were likely a combination of mechanical, neurophysiological, and
psychological (expectation of benefit) effects. The truth is that manual therapy produces a
cascade of mechanisms we are only just discovering.

Conclusion
Following the principle on pain models, this principle describes how those models can
influence the view (positive or negative) of the tissues (nociception) as the focus of pain. It is
important to understand and appreciate the complex relationship between nociception and
pain. The fact that people with tissue damage, pathology or mechanical dysfunction do not
always experience any pain supports the idea that the two are not always directly linked. But
this does not mean that nociception is not important to consider in patients presenting with
pain complaints. We have a classification system that can be used to determine which pain
mechanism might be the dominating factor affecting the patient’s pain, and that can help us
target treatment appropriately.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 107

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van Tulder MW. Rehabilitation after lumbar
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16. Deyo RA, Nachemson A, Mirza SK. Spinal-
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17. Deyo RA, Gray DT, Kreuter W, Mirza S, Martin
BI. United States trends in lumbar fusion
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Jun 15 2005;30(12):1441-1445; discussion
1446-1447.
18. Louw A, Puentedura E. Therapeutic
Neuroscience Education: Teaching patients
about pain. Minneapolis, MN: OPTP; 2013.
19. Videman T, Battie MC, Ripatti S, Gill K, Manninen
H, Kaprio J. Determinants of the progression in
lumbar degeneration: a 5-year follow-up study
of adult male monozygotic twins. Spine. Mar 15
2006;31(6):671-678.
20. Alyas F, Turner M, Connell D. MRI findings in the
lumbar spines of asymptomatic, adolescent, elite
tennis players. British journal of sports medicine.
Nov 2007;41(11):836-841; discussion 841.
21. Yukawa Y, Kato F, Matsubara Y, Kajino G,
Nakamura S, Nitta H. Serial magnetic resonance
imaging follow-up study of lumbar disc
herniation conservatively treated for average 30
months: relation between reduction of herniation
and degeneration of disc. J Spinal Disord. Jun
1996;9(3):251-256.
22. Masui T, Yukawa Y, Nakamura S, et al. Natural
history of patients with lumbar disc herniation
observed by magnetic resonance imaging for
minimum 7 years. J Spinal Disord Tech. Apr
2005;18(2):121-126.
23. Komori H, Shinomiya K, Nakai O, Yamaura
I, Takeda S, Furuya K. The natural history of
herniated nucleus pulposus with radiculopathy.
Spine. Jan 15 1996;21(2):225-229.
24. Kjaer P, Leboeuf-Yde C, Korsholm L, Sorensen
JS, Bendix T. Magnetic resonance imaging and
low back pain in adults: a diagnostic imaging
study of 40-year-old men and women. Spine.
May 15 2005;30(10):1173-1180.
25. Gignac MA, Davis AM, Hawker G, et al. “What
do you expect? You’re just getting older”: A
comparison of perceived osteoarthritis-related
and aging-related health experiences in middle-
and older-age adults. Arthritis Rheum. Dec 15
2006;55(6):905-912.
26. Thielke S, Sale J, Reid MC. Aging: are these 4
pain myths complicating care? J Fam Pract. Nov
2012;61(11):666-670.
27. DePalma MJ, Ketchum JM, Saullo TR, Laplante
BL. Is the history of a surgical discectomy
related to the source of chronic low back pain?
Pain Physician. Jan-Feb 2012;15(1):E53-58.
28. Herzog R, Elgort DR, Flanders AE, Moley
PJ. Variability in diagnostic error rates of 10
MRI centers performing lumbar spine MRI
examinations on the same patient within a
3-week period. The spine journal: official journal
of the North American Spine Society. Apr
2017;17(4):554-561.
29. Okada E, Matsumoto M, Fujiwara H, Toyama Y.
Disc degeneration of cervical spine on MRI in
patients with lumbar disc herniation: comparison
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J. Apr 2011;20(4):585-591.
30. Nakashima H, Yukawa Y, Suda K, Yamagata M,
Ueta T, Kato F. Abnormal findings on magnetic
resonance images of the cervical spines in 1211
asymptomatic subjects. Spine (Phila Pa 1976).
Mar 15 2015;40(6):392-398.
31. Simotas AC, Shen T. Neck pain in demolition
derby drivers. Arch Phys Med Rehabil. Apr
2005;86(4):693-696.
32. Sher JS, Uribe JW, Posada A, Murphy BJ, Zlatkin
MB. Abnormal findings on magnetic resonance
images of asymptomatic shoulders. The Journal
of bone and joint surgery. American volume. Jan
1995;77(1):10-15.
33. Reilly P, Macleod I, Macfarlane R, Windley J,
Emery RJ. Dead men and radiologists don’t lie:
a review of cadaveric and radiological studies
of rotator cuff tear prevalence. Annals of the
Royal College of Surgeons of England. Mar
2006;88(2):116-121.
34. Milgrom C, Schaffler M, Gilbert S, van Holsbeeck
M. Rotator-cuff changes in asymptomatic adults.
The effect of age, hand dominance and gender.
J Bone Joint Surg Br. Mar 1995;77(2):296-298.
35. Spielmann AL, Forster BB, Kokan P, Hawkins
RH, Janzen DL. Shoulder after rotator cuff
repair: MR imaging findings in asymptomatic
individuals--initial experience. Radiology. Dec
1999;213(3):705-708.
36. Munk B, Lundorf E, Jensen J. Long-term
outcome of meniscal degeneration in the knee:
poor association between MRI and symptoms
in 45 patients followed more than 4 years. Acta
Orthop Scand. Feb 2004;75(1):89-92.
37. Bedson J, Croft PR. The discordance between
clinical and radiographic knee osteoarthritis: a
systematic search and summary of the literature.
BMC musculoskeletal disorders. 2008;9:116.
38. Major NM, Helms CA. MR imaging of the
knee: findings in asymptomatic collegiate
basketball players. AJR Am J Roentgenol. Sep
2002;179(3):641-644.
39. Riddle DL, Jiranek WA, Hayes CW. Use of a
validated algorithm to judge the appropriateness
of total knee arthroplasty in the United States:
a multicenter longitudinal cohort study. Arthritis
Rheumatol. Aug 2014;66(8):2134-2143.
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40. Register B, Pennock AT, Ho CP, Strickland CD,
Lawand A, Philippon MJ. Prevalence of abnormal
hip findings in asymptomatic participants: a
prospective, blinded study. Am J Sports Med.
Dec 2012;40(12):2720-2724.
41. Frank JM, Harris JD, Erickson BJ, et al.
Prevalence of Femoroacetabular Impingement
Imaging Findings in Asymptomatic Volunteers:
A Systematic Review. Arthroscopy. Jun
2015;31(6):1199-1204.
42. Silvis ML, Mosher TJ, Smetana BS, et al. High
prevalence of pelvic and hip magnetic resonance
imaging findings in asymptomatic collegiate and
professional hockey players. Am J Sports Med.
Apr 2011;39(4):715-721.
43. Woolf CJ. Dissecting out mechanisms
responsible for peripheral neuropathic pain:
implications for diagnosis and therapy. Life Sci.
Apr 9 2004;74(21):2605-2610.
44. Devor M. Sodium channels and mechanisms
of neuropathic pain. The journal of pain: official
journal of the American Pain Society. Jan
2006;7(1 Suppl 1):S3-S12.
45. Devor M. Responses of nerves to injury in
relation to neuropathic pain. In: McMahon SB,
Koltzenburg M, eds. Textbook of pain. 5th ed:
Elsevier: Churchill Livingstone; 2006:905 - 927.
46. Camino Willhuber GO, Piuzzi NS. Straight Leg
Raise Test. StatPearls. Treasure Island (FL)2019.
47. Rabin A, Gerszten PC, Karausky P, Bunker CH,
Potter DM, Welch WC. The sensitivity of the
seated straight-leg raise test compared with
the supine straight-leg raise test in patients
presenting with magnetic resonance imaging
evidence of lumbar nerve root compression.
Arch Phys Med Rehabil. Jul 2007;88(7):
840-843.
48. Deville WL, van der Windt DA, Dzaferagic A,
Bezemer PD, Bouter LM. The test of Lasegue:
systematic review of the accuracy in diagnosing
herniated discs. Spine (Phila Pa 1976). May 1
2000;25(9):1140-1147.
49. Maitland GD. Negative disc exploration: positive
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50. Maitland G. The slump test: examination and
treatment. Australian Journal of Physiotherapy.
1985;31:215-219.
51. Hall T, Jull G. Obituary: Robert Elvey 1943 -
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52. Louw A, Mintken P, Puentedura L.
Neurophysiologic Effects of Neural Mobilization
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Arendt-Nielsen L, Gerwin RD, eds. Tension-type
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53. Smart KM, Blake C, Staines A, Thacker M,
Doody C. Mechanisms-based classifications of
musculoskeletal pain: Part 2 of 3: Symptoms
and signs of peripheral neuropathic pain in
patients with low back (+/-leg) pain. Manual
therapy. Aug 2012;17(4):345-351.
54. Scholz J, Woolf CJ. Can we conquer pain? Nat
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55. Ji RR, Kohno T, Moore KA, Woolf CJ. Central
sensitization and LTP: do pain and memory
share similar mechanisms? Trends Neurosci.
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56. Woolf CJ. Central sensitization: implications for
the diagnosis and treatment of pain. Pain. Mar
2011;152(3 Suppl):S2-15.
57. Coderre TJ, Melzack R. The contribution of
excitatory amino acids to central sensitization and
persistent nociception after formalin-induced
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58. Woolf CJ, Shortland P, Sivilotti LG. Sensitization
of high mechanothreshold superficial dorsal
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chemosensitive primary afferent activation.
Pain. Aug 1994;58(2):141-155.
59. Smart KM, Blake C, Staines A, Thacker M,
Doody C. Mechanisms-based classifications of
musculoskeletal pain: Part 1 of 3: Symptoms
and signs of central sensitisation in patients with
low back (+/-leg) pain. Manual therapy. Aug
2012;17(4):336-344.
110 PRINCIPLE 4 | NOCICEPTION AND PAIN ARE NOT THE SAME CONSTRUCT
60. Nijs J, Paul van Wilgen C, Van Oosterwijck
J, van Ittersum M, Meeus M. How to
explain central sensitization to patients with
‘unexplained’ chronic musculoskeletal pain:
practice guidelines. Manual therapy. Oct
2011;16(5):413-418.
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swings in musculoskeletal physiotherapy
practice. Manual therapy. Jun 2012;17(3):
199-200.
62. Zusman M. Hands on, hands off? The swings in
musculoskeletal physiotherapy practice. Manual
therapy. Jun 2013;18(3):e13.
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MP, Mokler DJ. Attenuation of postoperative
adhesions using a modeled manual therapy.
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therapy prevents onset of nociceptor activity,
sensorimotor dysfunction, and neural fibrosis
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2019;160(3):632-644.
65. Bialosky JE, Bishop MD, Price DD, Robinson
ME, George SZ. The mechanisms of manual
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pain: a comprehensive model. Man Ther.
2009;14(5):531-538.
 PRINCIPLE 5

Language Matters

5.1: Language Shapes Perception............112

5.2: Choosing Our Language ........................114

5.3: Words That Can Harm ............................117

5.4: Words That Can Heal .............................. 120

5.5: Reassurance .................................................. 122

Conclusion...................................................................... 122

Principle 5 References ......................................... 123

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 111

Sticks and Stones
Most of us are familiar with the common childhood phrase: “Sticks and stones may break my
bones, but words will never hurt me.” While we can agree that words do not have the ability to
inflict physical harm like sticks and stones, they can produce pain.1 Understanding that pain
is based on a perception of threat, it’s important that we gain greater appreciation for the role
our language has when it comes to healing (and not hurting) our patients. Although manual
therapy is primarily based on what we do with our hands, our words are important, too.
That’s because words can be helpful or harmful and can affect the patient’s pain response
and recovery.2

5.1: Language Shapes Perception

The brain is a prediction machine that is constantly trying to make sense of the world based
on its predictions. Try reading this if you do not believe it:

It deosn’t mttaer waht oredr the ltteers in a

wrod are, the olny iprmoetnt tihng is taht the frist
and lsat ltteer be in the rghit pclae. The rset can
be a toatl mses and you can sitll raed it wouthit
porbelm. Tihs is bcuseae the huamn mnid deos not
raed ervey lteter by istlef, but the wrod as a wlohe.3

By using the first and last letter and reading the word as a whole, the brain predicts what the
real word is, allowing you to read it. Still not convinced your brain is a predictor?

112 PRINCIPLE 5 | LANGUAGE MATTERS

Is the middle character the number 13 or the letter B?4 Your brain uses its ability to predict,
creating the illusion of a “13” or a “B” based on the surrounding information it takes in. These
two examples demonstrate the way visual clues and reading prediction create our reality. This
process takes place during every clinical encounter. The patient’s brain is taking in all sorts
of information and predicting the reality of whether it should protect with pain or not, and the
words we use are part of that patient’s prediction model.

Other evidence of the ways in which words can shape or create our perception further
emphasizes the importance of words. Research out of UC San Diego investigated how
metaphors can shape how we see the world.5 If your city’s crime rate was described as
a “beast” versus a “virus,” would it make a difference in what action you think should be
taken? Research says yes, 71% of people thought more police enforcement was needed if the
crime rate was described as a “beast,” but when the crime rate was described as a “virus”
only 54% thought more enforcement was needed. Beasts are things to be tamed through
enforcement—a virus would require a much different approach. More specific to the medical
world—a study examined a simple phrase used during a needle stick procedure to see how
it altered the patients’ pain perception.6 One group was told, “this will sting” while the other
group was told, “beware, I’m about to start.” The “sting” group reported an average pain of 2.7
on the NPRS compared to only 1.6 in the “beware” group. Using different words influenced
the pain perception of these patients during the procedure, proving that the words we choose
can change the patient experience. The words we use can also affect how the patient
ultimately chooses to manage their condition.7 Patients have been found to choose more
aggressive management for low-risk conditions
when presented with a diagnostic explanation that
had more medical terminology in it.8 So we may
want to be careful throwing out a diagnosis of a
“counter nutated sacrum that is tilted on a left-on-
right axis with a left ilia upslip.”

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 113

The challenges we face when our worldly
perception is affected by words is complicated
even further by the fact that our natural inclination
is to hold on to negative messages more than
positive ones. Alison Ledgerwood9 and colleagues
conducted some interesting studies that
investigated how loss frames are stickier than gain frames, based on the framing principles of
Tversky & Kahneman.10 People tend to hold on to messages framed in a negative light (or the
loss of something) more than messages framed in a positive light (that demonstrate the gains).
The following study is an example. A group of people were told that a new surgical procedure
provides a survival rate of 70% (gain frame) and another group was told that the mortality
rate is 30% (loss frame). When both groups were asked to evaluate the performance of the
new procedure, the gain group rated the procedure significantly higher than the loss group.
The “sticky” part of holding on to the loss perspective came when the statistics were flipped.
This time, the gain group was given the information framed as a loss—that the mortality
rate is 30% while the initial loss frame group was presented the information framed as a
gain—that the survival rate is 70%. When this occurred, the original gain framing group lost
confidence in the procedure and rated it much lower; however, the original loss framing group
did not significantly change their evaluation of the procedure when given the new information
framed as a gain. This group held onto the loss perspective even when presented with the
gain perspective. This is because people tend to hold on to the negative, and it takes more
than one positive to get them to shift. Hopefully, these examples help the manual therapist
understand more deeply how positive words about a treatment—“We can get that joint moving
again after we manipulate it,” or “We will get those tender points worked out so you can move
better”—contribute to the patient doing better.

5.2: Choosing Our Language

Why do we say the things we do? Have you ever considered
where you picked up various phrases you use during
day-to-day clinical appointments? “Your core is weak.”
“You have a crooked spine.” “Your muscles are as tight
as a drum.” Many phrases used by manual therapists
were picked up from various instructors and professors
during training or from other colleagues once working
in the field. The goal of language is to communicate
meaning and understanding to others. Unfortunately,
many common phrases are repeated with little reflection
about how they may affect patients.11,12 As we will explore
later in this principle, there are phrases that can provide
comfort and encourage healing, while others may induce
fear, which can inadvertently cause harm.

114 PRINCIPLE 5 | LANGUAGE MATTERS

Most medical language is bogged down by
technical jargon that is often beyond the
understanding of the patient. To help improve
communication with patients, it is time to follow
the lead of other professions by replacing
fancy medical speak with plain language that
patients understand.13,14 This does not mean
we need to dumb down our message, but we
do need to be clear and concise. The ability
to simplify complex messages is what makes
a skilled medical communicator. Also, remember that no single word is helpful or harmful in
isolation; what’s important is how words are put together and used within the context of the
entire conversation.

We know that manual therapists don’t purposefully choose language that

could negatively affect a patient—so why might we choose words that
communicate the wrong message? Let’s explore some of the reasons.15

Limited time

In today’s fast-paced medical environment time is often limited. This can make it difficult to
craft a thoughtful explanation for a patient’s problem and sometimes makes it easier to use a
simple metaphor to explain a treatment. When stressed and rushed, we often fail to create the
open, reflective, and self-aware atmosphere needed for mindful practice.16

The element of uncertainty

No matter how diligent you are in evaluating a patient, there is still an element of uncertainty
behind most medical conditions. This can make a manual therapist uncomfortable, since they
don’t want to inaccurately diagnose a patient, or cause additional uncertainty. Not to mention
the fear of legal repercussions due to the litigious nature of healthcare. This fear could cause
a practitioner to muddle their message and avoid being as succinct as they could.

Wanting to provide comfort and reassurance

In an age when patients have instant access to answers from Siri and Google, we may want
to provide the short, simple explanations patients can find online. “This is your problem, and
we can fix it” can be comforting and reassuring, as long as it does not backfire on us later if
it turns out that our explanation is not so accurate, and we ultimately can’t “fix” the problem.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 115

Wanting to create a sense of urgency

As clinicians, there are times when we want to use stronger language to generate a sense
of urgency in the patient to encourage them to be compliant with a home program or help
them fully grasp the significance of their condition. The use of extreme/negative language
such as “If you don’t do this, you are certain to get worse,” to shame and guilt a patient into
compliance is not the most effective approach. The use of this kind of language can induce
increased fear and anxiety for the patient.17 We know that patient-centered care and shared
decision making is a much better way to initiate positive behavior change.18-21

Habit

Through lectures, conferences, and communication with professors and experts in the field
we can become comfortable using terms and language heard often during our training. As this
language becomes second nature to us we may begin using terms and phrases without giving
second thought to their meaning.

Common vernacular

Lastly, many phrases have become part of the

vernacular used commonly despite evidence that
they may be inaccurate.20,22 Your back gets “thrown
out” when you lift improperly; the joint gets “wear
and tear” if used too much; “bad posture” causes
back or neck pain; and the list goes on. Because
they provide simple and easy explanations, and
because they have been used for so long, these
phrases become ingrained in the lexicon. Changing
them can be a challenge—making it seem easier to
continue using them.

No matter what the reasons are for using terms

and phrases that may not be helpful (and could
potentially be harmful) there’s always an opportunity
to change the language we use. It’s important for
the manual therapist to be as attentive and mindful
of their choice of words as they are to the skill in
which they use their hands.

116 PRINCIPLE 5 | LANGUAGE MATTERS

5.3: Words That Can Harm
Pain is based on the perception of threat and words can shape our
perception based on expectations from the predictive brain. When
we use words that create a negative expectation, we can elicit a
nocebo response (the opposite of the placebo response). Studies
using brain imaging techniques have shown that various portions of
the brain (anterior cingulate cortex, parietal operculum, and posterior
insula) become more active when people have negative expectations
compared to positive ones.23 These brain regions have an effect
on the perceived pain that individuals feel along with altering the
stress response system through the HPA axis.23,24 This evidence
indicates that the use of harmful language can create negative
biological consequences.

The changes that take place are evident when we use these negatively framed words and
induce a nocebo effect, which can alter a person’s biology and their psychology, as well.
Growing evidence shows that the psychosocial factors a patient presents with are better
predictors of pain and disability than pathoanatomical factors, especially as the problem
persists.25-28 Historically, manual therapists were focused on the pathoanatomical state of
the patient and created every evaluative attempt possible to palpate abnormal structures.
Knowing the reliability of some of these attempts is questionable,29-31 the modern manual
therapist needs to consider the psychosocial components and the effects of their language.
The words we use during evaluation and treatment can have a profound impact on the way a
patient views their body and the potential outcome of their treatment.7,32 When telling a patient
they have “degenerative disc disease” or “instability of their spine,” consider how this could
affect them. Each patient may have a different understanding of these terms, and the fact that
health literacy is low for many individuals is an additional factor.14,33 This is highlighted in the
qualitative study done by Barker and colleagues that examines responses from patients being
treated for LBP.34 One example from the study shows that very few patients were familiar with
the term “instability,” interpreting it to mean the back could “go out” at any time.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 117

• Even if they get you back to working order
your back is still unstable because the least
little thing can throw it off again.

• Something’s a bit loose: it’s liable to

pop out.

Each patient may understand common

medical terminology differently than others.
Terms can be misconstrued, meaning can
be misunderstood, and some messages
have a negative connotation attached to
them. Barker’s study found that clinicians
were generally aware of the challenges they
had communicating with patients with back
pain—and used strategies to address those
challenges. Despite these efforts, patients
reported feeling that the healthcare provider
was unable to explain the problem in a way
that was understandable.

Hafner35 found similar themes when she studied the explanations a group of patients were
given regarding their back pain and whether or not they understood the explanations. The
results support the biomedical model by showing that even in chronic conditions the source of
back pain was attributed to a structural fault in the spine. Ongoing support of the biomedical
model, even in chronic conditions, persisted with focus directed at the sole source of back
pain arising from some structural fault within the spine. This made the patient feel their
back was vulnerable—which was unnecessary since the belief was based on inaccurate
and inappropriate information and a pessimistic prognosis. This disempowered the patient,
leading them into a passive role within the therapeutic process. These results show why it’s so
important to improve communication with patients by using plain language and explanations
that patients can understand in order to reduce fear and anxiety. The table on the following
page is from an orthopedic manual therapy publication and is an example of how clinicians
are slowly but surely beginning to think about the language they use.1

118 PRINCIPLE 5 | LANGUAGE MATTERS

Table 5.1. Typical words to avoid and alternatives for patients.

Words to avoid Alternatives

• Chronic degenerative changes • Normal age changes

• Negative test results • Everything appears to be normal

• Instability • Needs more strength and control

• Wear and tear • Normal age changes

• Neurological • Nervous system

• Don’t worry • Everything will be okay

• Bone on bone • Narrowing and tightness

• Tear • Pull

• Damage • Reparable harm

• Paresthesia • Altered sensations

• Trapped nerve • Tight but can be stretched

• Lordosis • The normal curve in your back

• Kyphosis • The normal curve in your back

• Bulge/herniation • Bump/swelling

• Disease • Condition

• Effusion • Swelling

• Chronic • It may persist, but you can overcome it

• Diagnostics • X-ray or scan

• You are going to have to live with this • You may need to make some
adjustments

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 119

5.4: Words That Can Heal
Good communication is important for all social connections, and the patient-provider
relationship is no different. Effective communication between patient and provider results
in various improved outcomes including higher patient satisfaction, increased patient
activation and involvement in care, higher quality of life, decreased anxiety, reduced pain
and improved health markers.32,36 These improved outcomes are due to various pathways.32
Patients with better understanding and knowledge of their condition make more informed
decisions about their medical care.37 Improved communication between therapist and patient
can help the patient by providing the needed information to navigate the complex medical
system effectively. It also improves self-efficacy, providing the information and knowledge to
enhance their self-care skills—another pathway where communication has shown to enhance
outcomes.38,39 Improving the patient’s ability to manage and cope with their emotions can
help reduce their suffering, which is especially important if a condition persists.40 Positive,
constructive communication can also help in the development of TA and trust—another
pathway for communication to aid in improved outcomes, as discussed in more detail
in Principle 9.21,41,42

The use of effective communication to aid in the healing process is part of the development of
a more patient-centered care approach.43,44 This approach entails: taking on a biopsychosocial
perspective and understanding the multidimensionality of the individual illness experience,
sharing power and responsibility, and showing sensitivity and empathy for the patient. In the
healthcare field, it is sometimes best to utilize the technique the late Oliver Wendell Holmes,
Sr., shared with his medical students when he would remind them that:

“The sharp edges of science need some rounding off

with a touch of humanity.”45

Clinicians often try to convey a message through the

use of metaphors. The patient then has to unpack that
message and take out what they see as important.12
Consider the common use of the metaphor comparing
the body to a machine, like a car, and various injuries
or conditions compared to the wear and tear that can
occur if a car is not properly maintained. Although
the objective may be to convey a positive message to
the patient—the importance of maintenance through
an exercise program, that may not be what the patient takes away from the message. In fact,
the patient might take the following from this metaphor: because of wear and tear, my back
may blow out, leaving me stranded on the roadside, especially if I put more wear and tear on
my body through exercise. In addition, the patient may take away that there is nothing that can
be done except maybe replace the broken or worn-out parts. What if we change this metaphor
to one that represents the body as a living, changing, growing, adaptable organism that needs
new challenges to adapt and respond. This could encourage the patient to add new exercises
that could help with adaption and growth.

120 PRINCIPLE 5 | LANGUAGE MATTERS

Positively framed messages that create positive expectations are often
at the heart of placebo effects we see with various interventions.46
It’s important for clinicians to remember that placebo effects are
present in all treatments (real and sham) and are part of the normal
patient-clinician interaction.47,48 The use of supportive language
providing reassurance and support from a trusted clinician can have
significant effects on the benefits of the treatment.41,49,50 We know
that patients with higher positive expectations for their treatment
outcomes show greater functional improvements and have better
outcomes.51 Supportive language can include positive framing. As
mentioned earlier, messages can be framed in a positive light (benefits focused), or in a
negative light (listing side effects the patient might experience). In a clinical example, O’Conner
et al.52 told people receiving a flu shot that 60% of the people did not get a sore arm as a side
effect (positive framing) and the other group that 40% of the people did get a sore arm after
the shot (negative framing). The group receiving a positively framed message had fewer side
effects and actually had less absence from work three days later. Interestingly, another study
showed that when patients were told the side effect was indicative of the treatment working,
the patients reported more side effects than a control group, but the intensity of the side
effects was less severe.53 As a manual therapist, think about the times you may have used a
phrase like this after a thrust technique: “You will probably be sore later today or tomorrow, but
that is a good sign that we mobilized the right spot.” Hopefully you can see how this positively
framed message, along with a properly delivered manual technique, may have helped elicit
a positive response from your intervention. To be perfectly straight forward, there is nothing
wrong with enhancing placebo effects to improve treatment outcomes; it simply needs to be
done in an ethical manner.54,55

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 121

5.5: Reassurance
Reassurance, positive framing, and improved
communication can add to the healing response
of patients, which is why we advocate for the
ethical and judicious use of these types of
messaging. Reassurance is meant to remove
fear and doubt the patient might have about
their condition, while providing comfort. This
can be accomplished by providing information,
instruction, and persuasion.56 The information and
instruction provided (as we have shown), can be
helpful or harmful depending on the framing of the
message, the anxiety level of the patient, and the
patient’s knowledge base. Assessing the patient’s
understanding of the message, along with their
anxiety level, is paramount for the manual therapist to consider when delivering information
about the patient’s condition and the proposed treatment plan. Patients with greater anxiety
typically will have a resurgence of fear and anxiety, even after reassurance is provided.57 When
providing information, a topic of concern is the use of imaging, especially for many acute
non-traumatic problems such as acute LBP.58 Currently, the evidence does not support the
use of imaging, and many case presentations show the overuse of imaging to be a common
practice. The skilled clinician will need to delicately balance the patient’s desire to know what is
happening with their back, with the value early imaging findings may provide. Evidence shows
that being too dismissive of a patient‘s concerns can also be problematic, so it’s important
to consider an empathetic discussion that could lead toward shared understanding.59 While
the vast majority of research into reassurance provided improved outcomes, one study
shows that reassurance could have some adverse effects when provided by parents to their
children.60 The authors of the study suggest several possible reasons for this. First: providing
reassurance conveyed a message that there was indeed something to worry about. Second:
the parental reassurance possibly triggered a release of negative emotions. This is why it’s
important for clinicians to be mindful when delivering reassurance, as it could possibly have
negative consequences.

Conclusion
Hopefully, this principle has helped improve your understanding of why words do matter;
manual therapy is not just about the therapist’s hands. The words used to explain a patient’s
condition, the reassurance the patient is given, and the framing of our messages and the
patient’s prognosis, all play a role in how effective treatment is, and in the outcomes of our
manual treatments. Enhancing our communication skills is just as important as improving our
handling skills as we provide manual therapy interventions. While words alone may be neutral,
the context in which they are delivered can have substantial biological and psychosocial
effects on the patient and their healing response. Being mindful of the words we use can add
to the effective outcomes we all desire for our patients.

122 PRINCIPLE 5 | LANGUAGE MATTERS

Principle 5 References
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the impact of language in musculoskeletal
rehabilitation. journal of orthopaedic & sports
physical therapy. 2018;48(7):519-522.
2. J B. In the Beginning was the Word. Journal of
Bone and Joint Surgery. 2006;88A(2):442-445.
3. Rayner K, White SJ, Liversedge S. Raeding wrods
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Predictive coding and the language-perception-
cognition interface. Current Directions in
Psychological Science. 2015;24(4):279-284.
5. Moxley M. Can Language Influence Our
Perception of Reality? Slate. 2014. http://
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6. Ott J AS, Nouri K, Promberger R. An Everyday
Phrase May Harm Your Patients: The influence
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McCaffery K. Words do matter: a systematic
review on how different terminology for the same
condition influences management preferences.
BMJ Open. 2017;7(7):e014129.
9. Ledgerwood A, Boydstun AE. Sticky prospects:
loss frames are cognitively stickier than gain
frames. Journal of experimental psychology
General. 2014;143(1):376-385.
10. Kahneman D. Thinking, fast and slow.
Macmillan; 2011.
11. Lang EV, Hatsiopoulou O, Koch T, et al. Can
words hurt? Patient–provider interactions during
invasive procedures. Pain. 2005;114(1-2):
303-309.
12. Loftus S. Pain and its metaphors: A dialogical
approach. Journal of Medical Humanities.
2011;32(3):213-230.
13. Kimble J. Writing for dollars, writing to please.
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14. Stableford S, Mettger W. Plain language:
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challenge. Journal of public health policy.
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15. Bedell SE, Graboys TB, Bedell E, Lown B. Words
that harm, words that heal. Archives of Internal
Medicine. 2004;164(13):1365-1368.
16. Epstein RM. Mindful Practice. JAMA: The
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17. Louw A, Diener I, Puentedura E. Comparison of
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18. Légaré F, Ratté S, Gravel K, Graham ID.
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decision-making in clinical practice: update
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perceptions. Patient education and counseling.
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19. Barry MJ, Edgman-Levitan S. Shared decision
making—the pinnacle of patient-centered
care. New England Journal of Medicine.
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20. Darlow B, Dean S, Perry M, Mathieson F, Baxter GD,
Dowell A. Easy to harm, hard to heal: patient views
about the back. Spine. 2015;40(11):842-850.
21. Pinto RZ, Ferreira ML, Oliveira VC, et al. Patient-
centered communication is associated with
positive therapeutic alliance: a systematic review.
Journal of physiotherapy. 2012;58:77-87.
22. Darlow B, Dowell A, Baxter GD, Mathieson F,
Perry M, Dean S. The Enduring Impact of What
Clinicians Say to People With Low Back Pain.
Annals of Family Medicine. 2013;11(6):527-534.
23. Benedetti F, Lanotte M, Lopiano L, Colloca
L. When words are painful: unraveling the
mechanisms of the nocebo effect. Neuroscience.
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24. Fabbro F, Crescentini C. Facing the experience
of pain: A neuropsychological perspective.
Physics of life reviews. 2013.
25. Hancock MJ, Maher CG, Latimer J, et al.
Systematic review of tests to identify the disc,
SIJ or facet joint as the source of low back pain.
Eur Spine J. 2007;16(10):1539-1550.
26. Pincus T, Vogel S, Burton AK, Santos R, Field
AP. Fear avoidance and prognosis in back pain:
a systematic review and synthesis of current
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27. Thomas E, Silman AJ, Croft PR, Papageorgiou
AC, Jayson MI, Macfarlane GJ. Predicting who
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28. Moore JE. Chronic low back pain and
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and rehabilitation clinics of North America.
2010;21(4):801-815.
29. Alqarni AM, Schneiders AG, Hendrick PA.
Clinical tests to diagnose lumbar segmental
instability: a systematic review. J Orthop Sports
Phys Ther. 2011;41(3):130-140.
30. Kmita A, Lucas NP. Reliability of physical
examination to assess asymmetry of anatomical
landmarks indicative of pelvic somatic
dysfunction in subjects with and without low
back pain. International Journal of Osteopathic
Medicine. 2008;11(1):16-25.
31. Ferreira ML, Ferreira PH, Latimer J, Herbert
RD, Maher C, Refshauge K. Relationship
between spinal stiffness and outcome in
patients with chronic low back pain. Man Ther.
2009;14(1):61-67.
32. Street RL, Jr., Makoul G, Arora NK, Epstein
RM. How does communication heal? Pathways
linking clinician-patient communication to health
outcomes. Patient education and counseling.
2009;74(3):295-301.
33. Rudd RE. Health literacy skills of US adults.
American Journal of Health Behavior.
2007;31(1):S8-S18.
34. Barker KL, Reid M, Minns Lowe CJ. Divided
by a lack of common language? A qualitative
study exploring the use of language by
health professionals treating back pain. BMC
Musculoskelet Disord. 2009;10:123.
35. Hafner C. The information we give may be
detrimental. In: Gifford L, ed. Topical Issues in
Pain 4. Bloomington, IN: AuthorHouse UK Ltd.;
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36. Griffin SJ, Kinmonth A-L, Veltman MW, Gillard
S, Grant J, Stewart M. Effect on health-related
outcomes of interventions to alter the interaction
between patients and practitioners: a systematic
review of trials. The Annals of Family Medicine.
2004;2(6):595-608.
37. Sanders Thompson VL. Making decisions in a
complex information environment: evidential
preference and information we trust. BMC
medical informatics and decision making.
2013;13 Suppl 3:S7.
38. Altmaier E, Russell D, Kao C, Lehmann
T, Weinstein JN. Role of Self-Efficacy in
Rehabilitation Outcome Among Chronic Low
Back Pain Patients. Journal of Counseling
Psychology. 1993;40(3):335-339.
39. Keedy NH. Health locus of control, self-efficacy,
and multidisciplinary intervention for chronic
back pain. 2009.
40. Arora NK, Gustafson DH. Perceived Helpfulness
of Physicians’ Communication Behavior and
Breast Cancer Patients’ Level of Trust Over
Time. Journal of General Internal Medicine.
2009;24(2):252-255.
41. Fuentes J, Armijo-Olivo S, Funabashi M, et al.
Enhanced therapeutic alliance modulates pain
intensity and muscle pain sensitivity in patients
with chronic low back pain: an experimental
controlled study. Phys Ther. 2014;94(4):477-489.
42. Hall AM, Ferreira PH, Maher CG, Latimer J,
Ferreira ML. The influence of the therapist-
patient relationship on treatment outcome in
physical rehabilitation: a systematic review. Phys
Ther. 2010;90(8):1099-1110.
43. Mead N, Bower P. Patient-centred consultations
and outcomes in primary care: a review of the
literature. Patient education and counseling.
2002;48(1):51-61.
44. Mead N, Bower P. Patient-centredness: a
conceptual framework and review of the
empirical literature. Social science & medicine.
2000;51(7):1087-1110.
45. Frank JD, Frank JB. Persuasion and healing:
A comparative study of psychotherapy. JHU
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46. Barnes K, Faasse K, Geers A, et al. Can
positive framing reduce nocebo side effects?
Current evidence and recommendation for
future research. Frontiers in pharmacology.
2019;10:167.
47. Bystad M, Bystad C, Wynn R. How can placebo
effects best be applied in clinical practice?
A narrative review. Psychology research and
behavior management. 2015;8:41.
48. Benedetti F. The Patient’s Brain - The
neuroscience behind the doctor-patient
relationship. Oxford, NY: Oxford University
Press; 2011.
49. Kaptchuk TJ, Kelley JM, Conboy LA, et al.
Components of placebo effect: randomised
controlled trial in patients with irritable bowel
syndrome. Bmj. 2008;336(7651):999-1003.
50. Louw A, Zimney K, Landers MR, Luttrell M,
Clair B, Mills J. A randomised controlled trial
of ‘clockwise’ultrasound for low back pain.
The South African journal of physiotherapy.
2016;72(1).
51. Myers SS, Phillips RS, Davis RB, et al. Patient
expectations as predictors of outcome in
patients with acute low back pain. J Gen Intern
Med. 2008;23(2):148-153.
52. O’Connor AM, Pennie RA, Dales RE. Framing
effects on expectations, decisions, and side
effects experienced: the case of influenza
immunization. Journal of clinical epidemiology.
1996;49(11):1271-1276.
53. Fernandez A, Kirsch I, Noël L, et al. A test of
positive suggestions about side effects as a way
of enhancing the analgesic response to NSAIDs.
PloS one. 2019;14(1):e0209851.
54. Simmons B. Problems in deceptive medical
procedures: an ethical and legal analysis of the
administration of placebos. Journal of medical
ethics. 1978;4(4):172-181.
55. Simmonds MJ. Pain and the placebo in
physiotherapy: A benevolent lie? Physiotherapy.
2000;86(12):631-637.
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Reassurance: help or hinder in the treatment of
pain. Pain. 2008;134(1-2):5-8.
57. Lucock M, Morley S, White C, Peake M.
Responses of consecutive patients to
reassurance after gastroscopy: results of
self-administered questionnaire survey. Bmj.
1997;315(7108):572-575.
58. Modic MT, Obuchowski NA, Ross JS, et al. Acute
low back pain and radiculopathy: MR imaging
findings and their prognostic role and effect on
outcome. Radiology. 2005;237(2):597-604.
59. Dowrick CF, Ring A, Humphris GM, Salmon
P. Normalisation of unexplained symptoms by
general practitioners: a functional typology. Br J
Gen Pract. 2004;54(500):165-170.
60. McMurtry CM, McGrath PJ, Chambers CT.
Reassurance can hurt: Parental behavior and
painful medical procedures. The Journal of
Pediatrics. 2006;148(4):560-561.
 PRINCIPLE 6

Nerves Are Sensitive for a Reason

6.1: Starting at the Nociceptor (and

Following It Up to the Brain) .............. 127

6.2: Ion Channels .................................................. 129

6.3: Dorsal Root Ganglion............................... 136

6.4: Dorsal Horn..................................................... 138

6.5: Manual Therapy and Sensitivity...... 148

Conclusion...................................................................... 149

Principle 6 References ......................................... 150

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 125

Don’t Be So Sensitive
How do you write a book about pain without a clinical discussion of allodynia, hyperalgesia and
central sensitization? You don’t! How do you write a book about pain without mentioning the
flawed model by Rene Descartes? You don’t! As many students of pain science are aware, it
is inconceivable to attend a pain conference today without the Cartesian model being blamed,
in part, for the pain epidemic.1 In that model, various flaws are often highlighted including the
fallacy that avoidance will help decrease pain in the long run; the concept that cutting cords
(nerve ablation and surgery) will result in pain-free patient populations; and the disastrous
modern-day practice of dousing “fires” with pharmaceuticals, which has resulted in a global
pain epidemic.2 These are all flaws associated with the Cartesian model and unfortunately,
we’re not done with Rene. Often overlooked in the Cartesian model of pain is the notion that
information is passed to the brain (from the fire) via a tube, acting as a passive, neutral conduit
for information. We obviously know that this pathway is the nervous system, and it’s far from
being a passive conductor or bystander.3

In fact, various biological and physiological processes along the pathway have the ability
to increase or decrease information, which impacts the pain experience considerably. This
section will focus on the various processes along the pathway of the peripheral and CNS,
ultimately influencing sensitization of the nervous system. It’s this sensitization that poses a
significant challenge to the manual therapist. What follows is not an in-depth discussion of the
various biological and/or physiological processes associated with peripheral and CS. Many
comprehensive academic and clinical books cover this in detail.4-8 What follows, is a clinical,
working knowledge (summary and clinical importance) of these various processes.

126 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

6.1: Starting at the Nociceptor
(and Following It Up to the Brain)
The late professor Patrick Wall’s mandate to Towards the CNS

follow information from nociceptors, up the

afferent neuron, via the CNS and ultimately to
the brain, likely contributed to the explosion of
the interest in pain science, culminating in the
current excitement centering on the brain and Mechanical
its production of pain. Often forgotten in this
mandate, are the nociceptors and what happens,
in terms of peripheral sensitization. Yes, Principle Immune
4 discussed nociception, but from a clinical
perspective. In this section, the goal is to ensure Temperature
understanding of nociception from the biological Neurogenic
perspective to allow us to follow the afferent Inflammation
neuron to the CNS and beyond. Nociception is Tissue
Inflammation
critical for detecting damage or potential damage,
and it requires specialized sensory neurons,
referred to as nociceptors. At its most basic level nociceptors can be stimulated in three
ways: mechanically, thermally and chemically. Changes in the environment are sensed by the
nociceptor with the intent to inform the CNS and brain for a potential behavioral response/
action.9 Nociceptors pass along information about the intensity, duration and location of
peripheral noxious stimulation.10

Here’s the important (clinical) part: nociceptive primary afferents are capable of modifying input
before it is ever transmitted to the CNS.3 Inflammation produces a long-lasting neuroplastic
change in the signaling pathway mediating pro-inflammatory cytokine-induced sensitization
and mechanical hyperalgesia,11 which is referred to as hyperalgesic priming. With injury, the
peripheral and CNS undergo profound but reversible hypersensitivity in the injured/inflamed
and surrounding tissues.12 This is normal, and part of the protection process our bodies use
to defend against danger. A number of different forms of functional, chemical, and structural
plasticity can sensitize the central nociceptive system to produce pain hypersensitivity under
both normal and pathological circumstances, some of which may become persistent.13 All
of this pertains to peripheral sensitization, which represents a reduction in threshold and an
amplification in the responsiveness of nociceptors. This occurs when the peripheral terminals
of these high-threshold primary sensory neurons are exposed to inflammatory mediators (e.g.,
cytokines) at the site of tissue injury.13 This causes a sensitization of the injury site, which again
is normal and protective. These changes can arise quickly or develop over time in response to
“peripheral” or “central” processes that increase neuronal excitability within the CNS. For the
manual therapist, this means that by the time you touch a person presenting with pain from
an injury, the nervous system in and around the injury site will already be sensitized.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 127

As we will discuss later (and throughout the book), centrally, increased responsiveness of
spinal nociceptive neurons and their cortical projections can outlast the tissue-based input
or be maintained by a normally subthreshold tissue-based input, a situation known as CS.14
Peripheral sensitization thus has an effect on the CNS. Inflammatory agents in damaged tissue
increase the excitability of nociceptor terminals (peripheral sensitization) causing enhanced
sensitivity to noxious and non-noxious stimuli at the injured site (primary hyperalgesia). The
ensuing barrage of peripheral input can soon trigger changes within the spinal cord that
contribute to segmental (central) sensitization by enhancing excitatory inputs and reducing
inhibitory inputs.14

Time out! Are you seeing what we’re seeing? Consider this:

• Tissue health is critically important when it comes to sensitization

• Inflammation is a powerful driver of sensitization

• Acute pain and the various biological cohabitants

(inflammation, inflammatory responses, etc.) are
powerful drivers of pain

• Manual therapy has shown efficacy in acute, non-

radicular pain; immediate hypoalgesia and movement
is being explored as a means to modulate inflammation
and immune responses in patients

• All of this underscores the premise of the book: Don’t forget about the tissues and the
various ways manual therapy interventions can influence these biological processes that
underpin a pain experience!

To make things even worse, many of the same inflammatory agents (e.g., cytokines) can spill
over into the circulation and cause a systemic inflammatory response. Systemically, cytokines
can reach or signal the CNS via a number of routes and activate spinal and brain glial cells,
which produce a range of substances that are instrumental to setting the stimulus−response
profile in nociceptive pathways and adaptive behavior.14 See Principle 7 on neuroplasticity.

128 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

6.2: Ion Channels
It is imperative to understand the difference between normal sensitization (when no changes to
the system have occurred), adaptive (protective) sensitization, and pathological (maladaptive)
sensitization. Woolf describes “good pain” (adaptive sensitization) as a useful response of the
organism; it provides early warning and protection. Contrast that with “bad” pain (maladaptive
sensitization), which is an expression of pathological changes in the nervous system.15 In the
peripheral nervous system this is often referred to as neuropathic pain—which is associated
with pathological changes along the nervous system, and serves no biological advantage,
while causing significant stress and suffering.12,15 Neuropathic pain may be one of the most
acute and painful conditions encountered by the manual therapist, i.e., acute “hot” lumbar or
cervical radiculopathy. To give you an idea of the severity of neuropathy—narcotics, such as
morphine, have no effect on neuropathic pain.12,15 There is no treatment available to prevent
the development of neuropathic pain.12 What does all of this mean? Manual therapists that
routinely encounter neuropathic pain conditions such as lumbar and cervical radiculopathy,
CRPS, post-herpetic neuralgia, etc., need a working knowledge of neuropathic pain. One such
change is often associated with injured nerves that become hyperexcitable due to abnormal
expression of ion channels.15 What do ion channels have to do with a manual therapist? A lot.
Raise your hand (yes, we can see through the book) if you have had a patient tell you that their
pain gets worse when it’s cold outside? How about increased pain when they experience more
stress? How many patients are “better than the local weatherman” at predicting cold fronts?
These are common patient statements in manual therapy and until a working knowledge of ion
channels is instilled, may cause significant frustration for both the patient and the therapist.7,16
Ion channels are described in detail in various complex papers, mostly by Devor,17-20 and other
clinical textbooks and chapters.2,6,7,16 Refer to these for additional background and detailed
information. What follows is a summary and working clinical understanding of ion channels:6

• Ion channels are proteins clumped together to form a channel. Ion channels are mainly
synthesized in the Dorsal Root Ganglion (DRG) based on genetic coding (DNA). Once
built, they are transported along the axon via axoplasmic transport to their destination site.

• Ion channels insert into the outer wall of the axon (axolemma) and provide a channel
(gate) between the external and internal axonal environment.

• Ion channels allow electrically

charged (positive and/or
negative) ions to flow in or
out of the axon, which in turn
alters the electrical current/
gradient within the axon.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 129

• Inside the axon there is a resting membrane potential of about -70 millivolts, which means
that the inside of the neuron is 70 millivolts less than the outside. At rest, there are relatively
more sodium ions outside the neuron and more potassium ions inside that neuron.

• Depending on the number and kind of ions flowing in/out of the axon via ion channels,
an action potential may ensue. Once a resting membrane potential of -55 millivolts is
achieved, an action potential (electrical spike/message) ensues.

ACTION
POTENTIAL

Repolariza
tion
lariza
Depo
VOLTAGE

tion

THRESHOLD

STIMULUS
REFRACTORY
PERIOD

TIME

• There are many different kinds of ion channels, most of which are very important for the
manual therapist:

Voltage channels –Mainly open/close due to electrical activity of the ions

Chemical channels–Open the channel with circulating fluid in the area, such as
adrenaline
Temperature channels–Open and close with changes in temperature
Mechanical channels–Open due to mechanical stimuli, such as pressure or tension
Immune channels–Open due to immune molecules, such as cytokines
Spontaneous channels–Some transient receptor potential channels seem to open for
no reason
Hydrogen channels–Voltage-gated proton channels open with depolarization, but in a
strongly pH-sensitive manner
Light-gated channels–Open with changes in light

130 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

TEMPERATURE STRESS MOVEMENT IMMUNE BLOOD FLOW

Here is a visual example of various ion channels:

• Blue: Voltage channels pre- and post-opening.

When voltage changes, it opens the channel.

• Red: Chemical channels, serving as an example of

adrenaline docking into the ion channel, acting as a
key (triangle) and opening the ion channel.

• Green: Mechanical channel with a cytoskeleton of

collagen that is mechanically acted upon (i.e., pulled
or touched) and opening the channel.
(Image adapted from Devor).19

• Depending on the concentration and total number of ion channels present, an axon may
develop an action potential (“fire”) via stimuli such as stress, fear, movement, pressure,
immune changes (flu), temperature changes, etc. If enough ion channels open during a
stressful time (e.g., MVC), a patient may indeed present clinically and state: “I feel my neck
more when I’m stressed,” or “My pain gets worse when I’m stressed.” The underpinned
biology of ion channel expression explains this clinical phenomenon.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 131

• Most ion channels open for a fraction of a second. In chronic pain, various channels may
be replaced with G-protein channels that may stay open for minutes. This replacement
(plasticity) is a part of the shift in peripheral gating and the CNS’s need for more information
from the periphery.

• Ion channels continually change. It has been reported that the half-life of a typical ion
channel is approximately 48 hours, thus allowing for continued plasticity in the sensitivity
of the nervous system.18,20 What’s truly important, is to realize that the expression of ion
channels is dynamic and continually changing (e.g., an immune-mediated ion channel
drops out of the axolemma, but a stress channel inserts in its place).

Even though significantly more complicated, clinically it is important to understand the concept of ion
channel deposition. It is estimated that a single axon contains approximately 1 million ion channels,
thus the human body has trillions upon trillions of ion channels. The typical half-life of an ion channel
is estimated to be around 48 hours. Therefore (and the important clinical part), if we could freeze
time and count the number of ion channels and the distribution (ratios) of the various ion channels in
a person at any given time, it would be a representation of:

1. Genetic coding – Based on genetic coding each person has a different expression of ion channels.
For example, in any large gathering, such as a seminar, there are some people who are “cold” and
need to wear a sweater or coat, yet the person next to them is fine with only a shirt. The genetic coding
behind ion channels creates some level of difference between people, at least to a small extent.
Furthermore, given epigenetics (environmental influence of gene expression), differences will also
develop as we adapt to our environments, i.e., move and live in environments with different climates.

2. What the brain thinks we need for survival – If we consider the fact that ion channels play a
significant role in protection and survival, and humans face various stressors (a cold front coming
in, looming medical test, surgery, etc.) ion channels adapt accordingly to “monitor and inform” the
brain of impending threats. It would make sense as weather changes and temperatures plummet,
that we become aware of it (beyond regular senses), so we can protect ourselves—by putting on
a coat, for example. Similarly, if we do not monitor our stress (levels of circulating adrenaline and
cortisol), we may become susceptible to a stroke or cardiac event. In this model, the brain uses its
available information and adapts the sensitivity of the nervous system via ion channel expression for
survival purposes.

132 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

• Ion channels are typically found in certain places. Myelinated axons create a natural
barrier to ion channel insertion with the presence of the myelin sheath. Therefore, it is well
documented that ion channels typically are found in higher concentrations in areas where
there is less myelin, including the DRG, Nodes of Ranvier and where myelin is pathologically
removed from the axon (injury, disease, etc.).18,19,21,22 Myelin can be removed via:

Mechanical force: Myelin can be physically “peeled” away from an axon. For example,
during an injury, such as an inversion ankle sprain, axons (sural nerve) may have
myelin removed via the sudden inversion sprain.
Immune processes: There are several immune-based disease states that demyelinate
axons, such as multiple sclerosis, human immunodeficiency virus (HIV), etc.23
Chemical stripping: Inflammatory substances released at the time of an injury may
dissolve the myelin surrounding the axon. Various inflammatory and immune cells are
known to be part of this “chemical stripping” of the axon, e.g., inflammation process
in disc herniation24-27 or chemotherapy.28,29

What does all of this mean? We humbly suggest a few “take home” messages for the
manual therapist:

• Odd symptoms are real, and patients are not “making them up.” They CAN become
sensitive to various odd (non-mechanical) stimuli such as stress and cold temperatures.

• The system is plastic and just as it can become more sensitive to certain stimuli, it can
become less sensitive as well. This can provide hope for people in pain.

• Ion channels underscore the premise of biopsychosocialism since stress management,

relaxation, sleep hygiene, etc., should also be part of the modern manual therapist’s
repertoire to help calm down the sensitized nervous system.

• The nervous system is not a fixed constant in the transmission of impulses (see paragraph
one of this principle). The conduit (axon) can in fact alter (increase or decrease) the
message sent to the CNS and thus play a significant role in pain.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 133

 TEMPERATURE STRESS MOVEMENT IMMUNE BLOOD FLOW

In line with the last point, we must finish with this critical clinical aspect when it comes to ion
channels. In school, we are taught that nerves are pathways or conductors of messages; not
originators of impulses. Theory dictates that impulses are generated at the terminal endings
and then fired via the axons. In lieu of the ion channel discussion, we know this cannot be
entirely true. It is now well established that when an abnormal concentration of ion channels
is found in the axolemma, the axon develops an ability to generate its own impulses and
thus not merely impulse conducting. These areas are referred to as ectopic nerve pacemakers
or abnormal impulse generating sites (AIGS). Depending on the concentration of the specific
type of ion channels in the area, the axon can depolarize in response to opening of those ion
channels and an action potential can ensue with higher levels of adrenaline (fear, anxiety, stress
or anger), movement and/or mechanical pressure, temperature shifts in the environment, etc.
The demyelination of axons and resultant upregulation of ion channels into the bare axolemma
can help clinicians explain some of the pain that patients may experience after surgery or
injury. These impulse generating sites have been demonstrated in:

134 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

• Knee arthroscopy: Myelin stripping of the infrapatellar branches of the saphenous nerve on
the medial aspect of the knee.30 The resultant nerve sprouting, as the nerve regenerates to
reconnect with its distal segments, leaves a series of un-myelinated axons with a resulting
upregulation of ion channels.31-34 Clinically, if a patient experiences disproportionate
pain following a knee arthroscopy, even though range of motion or stability appear to be
unaffected, it may have more to do with nerve sensitivity than actual structural issues in
and around the knee.

• Lumbar disc herniation and radiculopathy: There is growing evidence that lumbar
radiculopathy is associated with a chemical activation of the DRG and adjacent axons.
Following a disc herniation, powerful chemicals including phospholipase A2, thrombaxin,
interleukins, etc., leak from the disc and not only chemically stimulate the DRG, but
start a demyelination process in the proximal nerve root.24-27 With demyelination, there is
increased availability for upregulation of ion channel deposition, development of AIGS and
persistent and high-level pain, despite the fact that the original disc injury has healed.28,29

• Medial scapular border pain mimicking Cloward referral patterns: It is now well established
that the cervical discs, as well as cervical zygapophyseal joints, are known to refer pain to
the upper thoracic spine and medial border of the scapula.35-41 Cervical disc lesions, as an
example, are quite common and associated with a MVC.42-44 With the chemical activation
of the DRG, referred pain is often felt in the upper thoracic spine, clinically known as
Cloward areas.35,36,45 From a pain science perspective, though, clinicians are also urged
to consider another possible pain pattern which may mimic Cloward and zygapophyseal
pain referral: posterior primary rami nerves. Anatomically, the posterior primary rami of
the spinal nerves arise in T2 spinal level through T6 spinal level and pursue a right-angled
course through the multifidus muscle and local fascia.46 It is proposed that with sudden
hyperflexion of the neck, upper thoracic spine and ribs during an MVC, the sudden
movement and mechanical stretch may cause local demyelination, resulting in a bare
axolemma. The bare axolemma will in turn allow for an abnormal upregulation of ion
channels locally, which may become a major source of persistent thoracic pain, which
should be differentially diagnosed in relation to other referral patterns.47

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 135

6.3: Dorsal Root Ganglion

Cervical zygapophyseal
joint pain referrals

Cervical disc pain referrals

Posterior (dorsal) primary

rami nerves

Before we delve into the complexity of the dorsal horn, which pioneers such as Patrick Wall
and Clifford Woolf spent considerable time studying, we must discuss the DRG, since it plays
a significant role in neuropathic pain. The DRG is a cluster of cell bodies of the sensory
(afferent) neurons and in essence “outside the dorsal
horn of the spinal cord.” The DRG is non-myelinated,
thus contains a very high number of ion channels. This
high concentration of ion channels in and around the DRG
leads to a heightened sensitivity of the DRG to various
stimuli associated with ion channel activation.17,48,49 The
DRG is extremely mechanosensitive and it’s postulated
that it has a high affinity for adrenaline channels, making it
more susceptible to circulating adrenaline.17,50,51 A few key
clinical issues:

136 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

• The DRG has been reported as “the most sensitive structure in the human body” and
clinically it’s associated with extreme pain, especially neuropathic pain.10,12,15,17,52 Following
inflammation, sensory neurons in the DRG can be sensitized to sub-threshold mechanical
stimuli causing significant mechanical hyperalgesia53

• The DRG may display periods of extreme latency after injury, with reported after-discharge
occurring two to three weeks after insult. For example, mechanical stimulus of the DRG in
a MVC54 may “compress” the DRG, but the axon may not fire for two to three weeks. It is
believed that this after-discharge may be due to a delayed immune and stress response.55,56
Pain onset days after injury or “flares” days after manual treatment can easily be explained,
expected and should be understood by the clinician and patient alike.

• In recent years, with the increased amount of research associated with complex regional
pain syndrome (CRPS), a lot of attention has shifted to the DRG. Following injury, it has
been shown that post-ganglionic sympathetic fibers grow toward the DRG and form a
basket weaving around the DRG.12,57 This is important, as the sympathetic nervous system,
an efferent system, releases adrenaline around the already heavily ion-channel-populated
DRG and may easily cause the firing of an action potential with the release of adrenaline
(fear, anxiety, stress, etc.).57,58 This resultant action potential fires bi-directionally:

With orthodromic impulses (the orthodox way), there is a barrage into the CNS which
may result in the development of CS.
Antidromic or retrograde depolarization in turn may fire action potentials towards
the target tissues resulting in release of substance P, histamine and other vasoactive
substances. This results in the target tissue redness, warmth and swelling with
spreading pain and additional changes within the CNS.59

Can you see up to this point, how the peripheral nervous system does not act as a passive
conduit of information—a passive and neutral bystander? No, it is a living, breathing, inquisitive
system that can amplify or dampen information from the periphery and its sensitivity can
make manual handling extremely difficult or impossible. Treatments to “only the target tissue”
(joint) may be inadequate and should thus entail various strategies to ease the sensitization of
the nervous system. For example, PNE has shown an ability to calm down mechanosensitivity
of the nervous system via neurodynamic tests and/or pressure pain thresholds.60 Pumping
blood and oxygen around a sensitized nervous system through activities like aerobic exercise
has been shown to dampen sensitization of the nervous system.61-63 Once again, through
simple neurobiology we make the case for pain science and manual/physical therapy to co-
exist and the modern manual therapist to add to their Swiss Army knife of skills!

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 137

6.4: Dorsal Horn
Clifford Woolf, one of the most noteworthy students from Patrick Wall’s lab “discovered” the
phenomenon of CS in the early 1980s.10 He demonstrated that neurons change as a result
of repeated input and in essence undergo a functional neuroplasticity. This was published in
1983 in the journal Nature.52 In Woolf’s own words, a powerful statement:

“I was able to demonstrate that a very brief (10-20

seconds) period of low-frequency stimulation of a nerve at
C-fiber strength could trigger CS for up to an hour.”10,52

In contrast to peripheral sensitization (primary hyperalgesia—local sensitization at the target

area), CS is responsible for secondary hyperalgesia—the spread of tenderness or enhanced
pain sensitivity outside of an area of injury. It’s also responsible for tactile allodynia—pain in
response to light touch, and is a common component of both inflammatory and neuropathic
pain.11 CS results from changes in the properties of neurons in the CNS—the pain is no longer
coupled (as acute nociceptive pain is), to the presence, intensity, or duration of particular
peripheral stimuli.13 CS represents a major functional shift in the somatosensory system
from high-threshold nociception to low-threshold pain hypersensitivity.13 These changes can
arise quickly or develop over time in response to “peripheral” or “central” processes that
increase neuronal excitability within the central nervous system. CS is complex and even
“beyond” tissue issues. For example, CS can be moderated or triggered by psychological or
behavioral aspects via shared neural circuitries and interconnected neuroimmune pathways.
Both psychological stressors (e.g., depression) and behavioral stressors (e.g., poor sleep)
have been associated with measures of CS, and frequently occur together in chronic pain
conditions, including chronic LBP.14 Clinically, CS is a challenge since there are no laboratory
tests or imaging for it; sensory tests alone might lack sensitivity to consistently detect the
various manifestations of CS.14

At this point, the manual therapist might ask, “So what?” Why does all of this matter on a
Monday morning in a busy clinic? Let’s determine whether you’ve experienced any of these
clinical presentations. If you feel compelled to do so, mark the examples below that you’ve
seen or heard about in the clinic:

Persistent, ongoing pain (pain getting worse over time; not better)

Allodynia (pain from stimuli that should not hurt, i.e., light touch or Grade 1 minus,
minus mobilizations)

Hyperalgesia (more pain that should be expected from the stimuli)

Spreading pain (pain spreading to adjacent areas)

138 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

 Mirror pains (pain is felt in the same area as the affected part, but on other side of
the body)

Widespread tenderness (pain with palpation all over the body)

All examination movements hurt (not just rotation left, or side-bend left)

Most manual therapists see and hear about these types of presentations on a regular basis.
The good news: We can explain it; it DOES happen, and we can help it (neuroplasticity). The
bad news? When patients present with these signs and symptoms, they often find themselves
in the unfortunate position of having to defend themselves. These patterns do not readily fit
into the orthopedic domain or textbooks and some clinicians may even question the validity
of this type of pain presentation. What follows is a brief and very basic description of the
development of CS. It is our hope that this will help the manual therapist understand what
happens in CS and why patients can (and do) show up with these signs and symptoms.

In mathematics, one plus one equals two. In pain neuroscience, one plus one may end up
being five, five thousand or even five million. For a manual therapist to develop a working
knowledge of CS, a basic knowledge of the dorsal horn and the various processes is needed.
In its simplest form, the dorsal horn receives nociceptive information from the target tissue via
a variety of nociceptive fibers.10 The incoming information of the various nociceptors is met by
interneurons, which can either block the information or allow the information to be passed onto
second-order neurons. The second-order neurons then take the information from spinal level to
the brain for interpretation and potential action.10,12,64 Various second-order neurons exist, with
the majority of current pain research focusing on two: wide dynamic ranging (WDR) neurons
and nociceptive specific (NS) neurons. It is believed that most “day-to-day” information is
passed onto the brain via the WDR neurons. However, NS neurons require a certain threshold
to activate and are often more associated with “if needed in case of severe threat.”10,12,64

Other From
dermatomes the brain
Endogenous
ns

ron
eu
ro

eu
gn
ngin
Intern

ra
namic
C Fiber (danger) e dy
Wid

cific
A-Beta Fiber (light touch) N o c i c e p tive s p e

Mo
the body to
e of
r sid
r

Othe

Figure 6.1: The various “players” in the dorsal horn involved in processing of nociceptive information and
ultimately, a pain experience.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 139

However, at each spinal level it’s far more complicated with adjacent spinal levels trying to
send information in (convergence theory), sympathetic actions, immune processes, motor
neurons, information from the other side of the body, etc. In a healthy, normal individual,
gating via various processes only allows for selected information (exact location; side of the
body; type of nociceptive information, etc.) to enter the dorsal horn, get passed onto the brain
and processed accordingly. In this case, the patient knows exactly where the information
came from (i.e., dermatome), what type of stimulus (light touch versus danger) and what side
of the body.10,12,64 Additionally, when the information is sent to the brain for processing and
interpretation, it has endogenous mechanisms to increase incoming information (facilitation)
or suppress incoming information (inhibition).65

The following is an example that illustrates the process of suppressing (inhibiting) incoming
information which occurs on a daily basis. The medial aspect of the knee contains various
sensory receptors and fibers. A-beta fibers constantly send sensory information to the spinal
cord for interpretation in the form of light touch. As your pants touch the medial aspect
of the knee, this sensory information is passed through the spinal cord via the L3 dorsal
horn, hoping to inform the brain of the pants touching the medial aspect of the knee.
These interneurons are sometimes referred to as relay neurons, association neurons,
connector neurons or local circuit neurons, and are best defined as a neuron that forms
a connection between other neurons. In the CNS, the term interneuron is used for small,
locally acting neurons, in contrast to larger projection neurons with long-distance connections.
CNS interneurons are typically inhibitory and use the neurotransmitter gamma-Aminobutyric
Acid (GABA) or glycine. However, excitatory interneurons using glutamate also exist, as do
interneurons that release neuromodulators like acetylcholine. Following input from A-beta
fibers, the interneuron may block the message with a release of GABA. In this case, the
message terminates and the sensation of light touch from the pants is not registered cortically
and you are, thus, not aware of the pants rubbing your leg.10

140 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

 Other From Other From
dermatomes the brain dermatomes the brain
Endogenous Endogenous

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eu n ron

eu
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Intern

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namic namic
C Fiber (danger) e dy C Fiber (danger) e dy
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Following an acute injury, A-delta and C fibers send nociceptive information to the spinal cord
with the intent to pass the message to the brain for interpretation and action. For an injury to
the medial aspect of the knee, the sensory afferent input will be received into the dorsal horn
of the spinal cord (L3) from the affected side (left or right). The nociceptive messages from
the A-delta fibers chemically activate -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid
(AMPA) receptors on the second-order neurons via glutamate.10,12,64,66 Second-order neurons
will then relay messages from the spinal cord to the brain. The nociceptive information is
passed onto the brain for interpretation and action. Although intense, pain will not usually last
in this acute stage. Part of the reason is because of inhibition via the endogenous mechanisms
of the brain, spinal cord, and descending pathways. Descending pathways—usually from the
periaqueductal gray (PAG) area, produce serotonin, endorphins, opioids and enkephalins,
which inhibit the nociception and, ultimately, the pain experience.65 If stimulation of the medial
knee persists (e.g., excessive valgus with prolonged walking, or sensitive nerves around the
knee after surgery or injury) then nociceptive fibers will continue firing, in this case longer
lasting C fibers play a greater role.

Other From
dermatomes the brain From
Endogenous Other
dermatomes the brain
s

Endogenous
ro n

ron
s
eu

eu n
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Intern

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C Fiber (danger) e dy rang
Intern

Wid namic
C Fiber (danger) e dy
Wid
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A-Beta Fiber (light touch) N o c i c e p t iv e s p c
e ci fi
A-Beta Fiber (light touch) N o c i c e p t iv e s p

Mo
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INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 141

Nociceptive input that passes the interneuron blockade needs to be sent on to the brain via
second-order neurons. Basic neuroscience dictates that, for a nerve impulse to continue,
specific receptors are needed for specific neurotransmitters. If A-delta fibers release glutamate
and there are no AMPA receptors available on the second-order neurons, the electrochemical
message stops. This availability of receptors is part of the plasticity of the nervous system
and may therefore modulate a pain experience. Receptors are continually replaced, and the
expression of receptor types is variable. The ability to feel the pants touch the medial part
of the knee or threatening stimulus from the knee is modulated by receptors on the second-
order neurons and neurotransmitters. Although centrally mediated endogenous processes
are important and well described in severe and acute injuries, the descending fibers from the
brain are likely active in day-to-day stimuli, as well.65

In an injury or degenerative process, nociceptive fibers send repeated messages to the dorsal
horn of the spinal cord. In the spinal cord, repeated stimulation at constant strength of dorsal
root afferents, including nociceptive C fibers, can elicit a progressive increase in the number
of action potentials generated by motor neurons and interneurons.13,67 This process, referred
to as “action potential windup,” is the consequence of a cumulative membrane depolarization,
resulting from the temporal summation of slow synaptic potentials. Simply stated: With persistent
input from the periphery, changes to the spinal cord second-order neurons and, ultimately,
brain pathways, lead to a heightened sensitization.176,177 With persistent nociception via C
fibers from the knee, permanent neuroplastic changes may occur. It is now well established
that after a constant barrage from the C fibers, some of the interneurons may die due to high
levels of amino acids.10,66,68,69 With a persistent toxic environment, it is unlikely the interneuron
will regenerate. The result is a decreased ability to modulate nociception and ultimately a pain
experience. With less ability to modulate the incoming information, thresholds are easily met
for nociceptive specific second-order neurons, increasing firing to the brain. Notice how “one
impulse” results in “two impulses” being sent to the brain. This amplification of input is an
essential part of the development of CS, hence the idea that in neuroscience one plus one is
not necessarily two.

Other From
dermatomes the brain Other From
Endogenous dermatomes the brain
Endogenous
ns

ron
eu eu
ro

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Intern

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namic
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Wid namic
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A-Beta Fiber (light touch) N o c i c ep t i ve sp e

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side the b to
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Endogenous
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142 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

Second-order receptors change, as well. From a primitive survival viewpoint, the brain will
want to know about danger in order to protect. Pain is a signal that protection is necessary.
To facilitate this process, receptors in the second-order neurons are replaced with receptors
that will facilitate an increase of danger messages to the brain for analysis. During day-to-
day normal activity, receptors open and close in milliseconds.19 In response to this threat,
receptors—which usually open and close fast—can be replaced with receptors that stay open
longer (up to several minutes) such as the G-protein receptors, which are commonly found
in the central nervous system. The end result is an “open gate.” The second-order neuron is
therefore more easily stimulated and fires faster, creating increased sensitivity. In the spinal
cord, repeated stimulation (at constant strength) of dorsal root afferents including nociceptive
C-fibers can elicit a progressive increase in the number of action potentials generated by
motoneurons and interneurons.13,67

This description of what happens in the central nervous system is extremely simplified; One
nerve fiber carries a message to the dorsal horn of the spinal cord, which interacts with the
interneuron, followed by the second-order neuron, and the message is sent to the brain.
Obviously, the real process is a lot more complex:10,12,64,68

• A-delta, A-beta, C fibers and many more enter the dorsal horn.

• There are numerous interneurons.

• Each neuron connects with upwards of 5,000–10,000 other neurons, so there is

convergence of multiple neurons onto a single neuron and divergence of that neuron onto
multiple neurons.

• There are descending fibers from the brain supplying endogenous chemicals such as
opioids, enkephalins, endorphins and serotonin, which allows for a cortical modulation of
nociception and the pain experience.

• Convergence of adjacent spinal levels (for example, L2 and L4) also access the
L3 spinal level.

• Other fibers are also present—motor, sympathetic, etc.

• There are many immune processes, e.g., glial cell activation, etc.

• Input to the dorsal horn is also received from the other side of the body.

• There are numerous second-order neurons from the L3 spinal level aimed at relaying the
nociceptive information to the brain for interpretation.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 143

 Other From
dermatomes the brain
Endogenous

ns
eu

ro
n
ing
rang
C Fiber (danger) dynamic
e
Wid

cific
A-Beta Fiber (light touch) N o c i c e p tive s p e

Mo
ody to
the b
e of

r
r sid
Othe

With the loss of the interneuron, and thus a primary gating property, various spinal levels,
other neurons, neurons from the other side of the body, etc., have access to second-order
neurons, ultimately increasing the information the brain receives. However, the information is
no longer as precise (ability to feature extract) because the brain now receives both C fiber
and A-beta fiber information; information from various levels; information from the other side
of the body, etc. Collectively, these processes will likely increase the threat level of the brain.
Additionally, in these advanced stages, there is a reduction (or possible inability) of the brain to
engage to descending endogenous mechanisms to alter the pain experience, thus in essence
allowing for an increased pain experience.

Other From
dermatomes the brain
Endogenous
ns

eu
ro

gn
ra ngin
namic
C Fiber (danger)
ide dy
W

cific
A-Beta Fiber (light touch) N o c i c e p tive s p e

Mo
ody to
the b
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r

r sid
Othe

Another consequence of the constant barrage into the spinal cord is a plastic shift in the
organization of neurons within dorsal horn laminae. In neuroscience, it is well understood that
various nociceptors (A-beta, C, etc.) enter the dorsal horn in various layers or lamina. With the
constant barrage into the CNS C fibers actually “pull back” out of certain lamina and A-beta
grows in. This allows normally innocuous light touch information to access the nociceptive
system, which clinically may result in light touch allodynia.12,64

144 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

Even though it’s very basic, this description clearly shows that many of the clinical features are
real and not psychosomatic. Spreading pain, bilateral pain, pain due to light touch, etc., are
biological and are consequences of the various processes described in this section.

Table 6.1. Key indicators that represent a potential biopsychosocial phenotype.

Process Clinical consequence

Death of the inhibitory neurons Decreased ability to inhibit peripheral
nociception
C fibers pull back; A -fibers grow in Allodynia

Upregulation of second-order neurons Increased firing towards the brain

Upregulation of second-order neurons Functional shifts in the brain – pain

neuromatrix
Inappropriate synapsing – other levels Spreading pain

Inappropriate synapsing – other fibers Sympathetic, immune, motor contributions

Inappropriate synapsing – other side Bilateral “mirror” pains

Decreased endogenous mechanisms Allodynia and hyperalgesia

Altered information from the periphery Structural shifts in the brain – homuncular
smudging
Alterations of immune function – glial cells Opening of the spinal-cord-blood-barrier

Even when considering the simplistic description of CS, there are some key elements that may
go unnoticed:

• Acute pain predicts chronic pain. There is a growing body of evidence that the intensity
and duration of acute pain predicts chronic pain.10,12,64,68,70 With a constant barrage
into the CNS, especially C fibers, there is an increased chance of inter-neuronal death,
receptor field changes, loss of inhibitory gating, etc. (This may be good news for manual
therapists since manual therapy has a robust, fast-acting hypoalgesic effect on acute and
sub-acute pain).

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 145

• In all people, the dorsal horn is quite resilient and deals with nociceptive bombardment on
a regular basis. If you mildly sprain your ankle, there will be a short-term barrage increase
to the CNS, but as the endogenous inhibitory mechanisms help and nociception eases
from the periphery, the various systems and processes return to normal, ready for the next
assault. It is the prolonged barrage and intensity of the barrage that likely predicts inter-
neuronal death. It is also important to realize that it is only nociception and the brain’s
interpretation and the value it places on the information likely also plays a role in the
plasticity changes in the dorsal horn, thus bringing the environmental factors in again.

• With the loss of the interneuron, expansion of receptors fields

and decrease in endogenous mechanisms, the clinical question
will usually arise: If the interneuron does not grow back, what
do we do?

If you review the various images related to this section, what

is the most powerful tool you can turn on? The brain. The
essence of PNE is to activate the brain, and to improve
knowledge and understanding about the pain experience.
PNE has been shown to have a significant positive impact on pain catastrophization,
and this, in turn, has been shown to activate the naturally occurring opioids and
cannabinoids in the brain, which can powerfully alter a pain experience.71 This
activation and the ability to get the brain to downregulate the incoming nociception is
referred to as a “top-down” approach.7

Clinicians should also consider the “bottom-up” approach. Even though the world
of pain science has moved heavily toward the pain neuromatrix (plasticity changes,
glial cell activation, PNE, etc.) it is imperative to understand that various traditional
approaches can also help modulate the pain experience. Gate control is still relevant
and using any and all possible means to alter input to the CNS (especially C-fiber
activity), can help modulate the threat appraisal of the brain. For example:

– Cryotherapy has been shown to slow C-fiber activity down, thus decreasing the
nociception being sent into the dorsal horn of the spinal cord and ultimately
decreasing the threat appraisal of the brain.72 Additionally, via its vasoactive
properties, ice has been shown to decrease pro-inflammatory chemicals in injured
and diseased tissues, which further decreases nociception.

– Electrical stimulation, including transcutaneous electrical stimulation (TENS), has

been shown to be effective in altering pain experiences via Gate Control and the
endogenous opioid system.73,74 By altering the amount and duration of peripheral
input to the central nervous system, it alters information passed onto the brain and
the threat appraisal of the brain.

A foundational aspect of PNE, however, is the PNE+ concept of teaching a patient about
pain while “doing something physical” as well.75 The clinical manifestation, per Gifford, is
“top-down while bottom-up,” which involves educating while doing physical treatment.7

146 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

 Additionally, it is well understood that many times cognitions, such as fear avoidance,
need to be addressed prior to physical treatment as a means to get some endogenous
mechanisms to start: “top-down before bottom-up.”7

Sample

Tissues Tissues

Environment Environment

With persistent input from the periphery, there is likely to be a change in the descending
modulation of the brain and the endogenous chemical release of opioids, enkephalins,
endorphins and serotonin.76,77 This endogenous process is very powerful and essential for
survival.78,79 Endogenous chemicals, which are needed to modulate the incoming nociception
and ultimately the pain experience, are reduced in chronic pain states.76,77,80 In chronic pain,
from an evolutionary survival perspective, the brain needs more information from the tissues
(nociception) to best determine the most appropriate course of action. By reducing the normal
endogenous chemicals, the brain allows more information to ascend for further interpretation.

Did you get all that? Can you see how complex CS is? Can you see how patients may indeed
show up with “non-traditional” symptoms? Can you see the importance of the health of
the physical tissues? Can you see them as a potential target for manual treatment such
as neurodynamics?

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 147

6.5: Manual Therapy and Sensitivity
Let’s end with the beginning (of the principle). Rene started to send us in the right direction
with his depiction of information moving from the foot to the brain. Although being “blamed”
for the poor modern pain models, we don’t often give him enough credit for “taking us to the
brain.” In a perfect world, even though it might be graphically hard to illustrate, he would have
told us (if he knew) that the messenger system (nervous system) can further influence the
message before it reaches the all-important brain. The clinical presence of sensitization—be
it allodynia, primary hyperalgesia, and/or secondary hyperalgesia creates problems for both
patients and clinicians. Patients experience odd, poorly understood and poorly explained
symptoms and often find themselves in the unfortunate position of having to “prove” they
(really) hurt. Manual therapists who are dogmatically trained, indoctrinated with pain referral
patterns, instructed in absolute black and white clinical scenarios, and yet have limited pain
science knowledge often “don’t know what to do with these patients.” In cases like these,
patient responses to manual treatment and examination do not follow expected traditional
patterns and then there’s the dreadful, inevitable “flare” after manual treatment, which takes a
lot of fun out of manual therapy. Sensitization is real, complex, and a part of every patient. One
last clinical thought: The nervous system, and the various processes we describe here, are
plastic and intertwined with “(neural) memory.” During the course of various episodes of LBP,
as an example, the nervous system will ramp up to protect, hopefully dampen down during
recovery and “life is good.” As this happens repeatedly, primary and secondary hyperalgesia
will likely cause a system to become sensitized over time.

FIRING
LEVEL

PATIENT’S
NORMAL
ELECTRICAL
LEVEL

NORMAL
ELECTRICAL
LEVEL

1987 1994 2002 2011 2015 2019

Figure 6.1: Increased sensitization of the nervous system over time

148 PRINCIPLE 6 | NERVES ARE SENSITIVE FOR A REASON

Conclusion
Principle 6 embodies professor Patrick Wall’s mandate to follow the nociceptor from the target
tissue to the brain. It clearly showcases how the nervous system is not merely a passive
conduit but modulates the information along its path. Information is modulated via ion
channel expression, dorsal horn neuroplastic changes, inhibition, facilitation, expansion of
receptor fields, immune changes, etc. The clinical correlate is clear: The nervous system can
become increasingly sensitive over time, which alters clinical presentations, physical tests
and treatments the manual therapist must consider. Sensitization is normal and part of the
protective system in patients. On the flipside, sensitization can be positively influenced by
various treatments and interactions by clinicians, ultimately easing pain and providing hope
for those struggling with persistent pain.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 149

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 PRINCIPLE 7

The Brain Has a Body Map

7.1: Self Versus Non-Self ................................ 154

7.2: Recognizing Changes.............................. 158

7.2.1: Central Sensitization

(Nociplastic) ................................. 158

7.2.2: Plasticity .......................................... 160

7.3: Treatment ......................................................... 164

7.3.1: GMI ..................................................... 164

7.3.2: Manual Therapy ........................ 166

Conclusion...................................................................... 171

Principle 7 References ......................................... 172

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 153

Use It or Lose It
In Principle 1, we discussed the various potential mechanisms behind the efficacy of manual
therapy, including structural changes in the brain. In the world of pain science, this area
is getting a lot of attention and could potentially lead to significant advances in helping
people who experience pain. It’s this body of work that has shown significant potential to
help some of the most complicated pain states in the world, including phantom limb pain,
CLBP, and complex regional pain syndrome (CRPS), which was previously referred to as
reflex sympathetic dystrophy (RSD).1,2 Emerging from this work, clinicians now readily use
treatments such as mirror therapy, motor imagery, virtual reality, sensory discrimination,
laterality reconstruction and more.1-3 More impressive is that these “advanced” treatments
are now front and center at various conferences (including manual therapy conferences), in
journals and in clinical practice. If the intent of this book is to get manual therapists to “take
on” pain science, it would make sense that the modern, biopsychosocial manual therapist
develop a working knowledge of neuroplasticity.

High
eat Thr
Thr
7.1: Self Versus Non-Self L ow
e at

It is now well understood that pain is 100% produced

by the brain when it faces a threat: No brain, no pain.4,5
Threats come in a variety of forms, spanning various
biological, psychological and social factors.6,7 On the
biological level, threats include injury to tissues, surgery,
accidents, disease, aging of the various bodily tissues and
more. Psychological constructs such as elevated levels of
depression, fear-avoidance, or pain catastrophization are now recognized as significant threats,
powerfully impacting a pain experience.8,9 Additionally, various social factors have been shown
to drive a pain experience, including socioeconomic factors, relationships, employment, etc.10
In this principle, we will explore the biological threat of body schema, or body maps in the
brain. It is within this exploration that we will develop a working knowledge of neuroplasticity:
What it is; what it means; how to assess for it; and how to address it (if necessary).

Injury Injury Injury

Other Surgery Other Surgery Other Surgery

Social Accident Social Accident Social Accident

Cata Cata Cata

stroph Disease stroph Disease stroph Disease
ization ization ization
Fear Aging Fear Aging Fear Aging
Brain Brain Brain
Maps Maps Maps

154 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

It is now well established that a person’s physical
body is represented in the brain by a network
of neurons.11-14 This representation refers to the
pattern of activity that is evoked when a particular
body part is stimulated. The most famous area
of the brain associated with representation is the
primary somatosensory cortex (S1).11-14 These
maps are genetically coded when we are born.
More importantly, especially clinically, is that
these neuronal representations of body parts
(maps) are dynamically maintained and it has been shown that patients with pain (especially
chronic pain) display different S1 representations than people with no pain.15-20 The interesting
phenomenon associated with cortical restructuring is the fact that the body maps expand
or contract, in essence increasing or decreasing the body map representation in the brain
(size).15,16 These changes in shape and size of body maps powerfully correlate to increased
pain and disability.15,21 Various factors have been linked to the development of this altered
cortical representation of body maps in S1 including neglect, bracing/casting, decreased use
of the painful body part, etc.22 This reorganization of body maps occurs quickly. It has been
shown that when four fingers are webbed together for 30 minutes, cortical maps associated
with the fingers change.14 These maps are environmentally sculpted and it is this sculpting,
“use it or lose it” that may play a significant role in the development of pain. It is argued that
when the maps are cortically healthy (sharp), the brain’s threat level is likely low. The body
part is easily recognized; appears to be normal size and the ability to recognize left and right
(laterality) is highly accurate and fast.19,23,24 When the body part is not moved regularly or
optimally; due to pain, being in a cast or brace, high levels of fear, or the body part does not
exist (amputation), the cortical map is not “exercised” leading to various changes that impact
a pain experience. Emerging neuroscience research has shown that when the body part isn’t
used there are several “neuroplastic consequences,” including:13,16,19,23-26

• Cortical “smudging” whereby the ability to

clearly identify the body part is decreased
by the patient experiencing pain. It is
argued that clinical tests such as two-point
discrimination (TPD) may help determine
the health of the cortical map in people
with pain.17,27,28

• Difficulty with left-right discrimination. A series of studies have shown that pain, and
even the anticipation of pain, leads to decreased ability to accurately identify left and right
body parts as well as left and right movements of the spine, and even facial expressions,
in patients with headaches.29-33 Additionally, along with decreased accuracy, patients
with pain also experience decreased speed in their ability to identify left or right, often
significantly beyond values for normal healthy volunteers.29-33

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 155

• Size changes: The cortical maps have the capacity to expand or contract, thus
impacting the perceived size of the body part, which in turn significantly influences the
pain experience.16,24

It is thought that these various alterations in body recognition increase threat, resulting in an
increased pain experience. Furthermore, it is important to realize that pain can be initiated
when a cortical map is altered, thus implying pain can be initiated due to immobilization, fear
of movement, limited movement, etc.34-36

at High
hre Th
wT re

Lo

at
It is currently believed that the threat appraisal of the brain in regard to the neuroplastic
changes is triggered by various immune responses as a means to protect the individual. The
altered body part is a threat as it’s not readily perceived as part of the person’s normal body. It
has even been proposed (Butler: personal communication) that the brain struggles to identify
“self” from “non-self.” The theory that pain may alter a patient’s ability to recognize certain
body parts is underscored by studies showing that people with advanced pain states develop
a form of “neglect” similar to patients who have suffered a stroke.17,37,38

There are likely numerous biological and physiological causes behind the alterations in
body maps. One area of particular interest for clinicians is emerging research regarding
neuroimmune responses and tying the health of the peripheral nervous system to cortical
maps and pain. In recent years, there has been increased interest in the interplay between
the nervous system and immune system, specifically via glial cell activation.39 Glial cells
outnumber neurons 10 to 1 and play a critical part in immune function.40 Scientists have
shown that both injury to peripheral nerve and electrical stimulation of C fibers (barrage into
the CNS) cause an increase in the permeability of the blood-spinal cord barrier as well as
the blood-brain barrier.39 Both of these barriers are critical in the CNS’s ability to extract and
receive correct information from the periphery, including location, side of the body, etc. These
studies have shown heightened microglial activity in the dorsal horn of the spinal cord, on the
affected side, which in turn triggers a cascade of immune changes.39,41

156 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

The importance of these aggressive immune responses to nerve compression and peripheral
input into the CNS by C fibers should show manual therapists that peripheral processes (i.e.,
cervical and lumbar radiculopathy) have significant consequences not only at the triggering
site, but along the axon, dorsal root ganglion (DRG), dorsal horn, spinal cord blood-barrier,
second-order neuron activation, pain neuromatrix, blood-brain barrier and plasticity.39,41 What
is even more intriguing, and likely clinically relevant, is the fact that the blood-spinal cord and
blood-brain changes occur after only a few hours of nerve compression,39,41 whereas clinicians
often see patients with peripheral neurogenic contributions (i.e., radiculopathy) that have been
present for weeks, months and even years. This connection of the various bodily systems
underscores that many pain states seen by manual therapists are complex, intertwined and
more widespread than what was previously believed. Many traditional manual therapists may
falsely believe that these “advanced” neuroplastic changes occur rarely, and only in very
complex conditions such as CRPS (which they don’t treat). Below is a list of diagnoses and
clinical issues that have been correlated with changes in the body maps. How many of these
conditions or issues do you see on a daily basis?

Table 7.1. Various conditions in which altered body maps (schema) have been documented

Altered body maps (schema) have been documented in the following

situations17,19,29,33,36,37,42-44
Radiculopathy Obesity Aging
CRPS Pregnancy Chronic LBP
Carpal Tunnel Syndrome Knee Osteoarthritis Arm and Hand Pain
Expectation of Pain Immobilization Surgery
Amputees Anesthesia Headaches
Dystonia Post-Stroke Facial Pain

What does all of this mean to the modern (pain science) manual therapist? We suggest
contemplating and answering the following questions for every patient you treat:

• Have these changes occurred in my patient?

• How do I test for this suspected condition?

• If I find an impairment, what do I do about it?

• Could manual therapy help and if so, how?

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 157

7.2: Recognizing Changes
One of the primary reasons patients seek care is for pain relief.45,46 Consequently, the attending
clinician will seek to develop an understanding of the underlying mechanism/s of the patient’s
pain experience, including treatment.7 If, from a neuroplastic perspective, pain is powerfully
driven by the health of the cortical maps,15-20 it would imply that clinicians (including manual
therapists) should be able to recognize cortical changes in order to determine their potential
involvement in a pain experience and potential treatment. In research, advanced scans and
tests such as functional magnetic resonance imaging (fMRI), positron emission tomography
(PET), trans-magnetic stimulation (TMS) and magnetoencephalography (MEG) are often used
to assess for changes in the brain. How, then, should a clinician in a busy clinic assess
changes in brain maps?

7.2.1: Central Sensitization (Nociplastic)

Some good news first: Most clinicians already have the skillset to screen for neuroplastic
changes. We know that neuroplastic changes are associated with increased pain states,
especially the prevalence of allodynia and hyperalgesia.11,13,25,26 In its simplest form, if a
patient presents with a heightened sensitized nervous system, it is highly probable that altered
plasticity may be present. The easiest place to start is the clinical presentation of CS (nociplastic
changes).47 In Principle 3 (pain models), Gifford’s mature organism model (MOM), introduced
and familiarized clinicians with pain mechanisms—nociceptive, peripheral neurogenic and
CS (nociplastic).48 Smart and his colleagues have examined the various subjective (and some

Musculoskeletal Pain?

Disproportionate?

No Central Diffuse
Sensitization Pain?

Central
Yes = Central
Sensitization
Sensitization
Inventory ≥ 40

No = No Central Yes = Central

Sensitization Sensitization

158 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

objective) clues to determine which pain mechanism may be dominant.47,49-51 Based on this
classification, it is now well documented, and accepted, that if patients display the following
cluster of signs and symptoms it’s 486 times more likely a patient is in the “CS” category
(versus nociceptive or peripheral neurogenic): Disproportionate pain; disproportionate
aggravating and easing factors; diffuse palpation tenderness and psychosocial issues (i.e.,
depression, fear-avoidance and pain catastrophization).47 Additionally, clinicians may choose
to use the central sensitization inventory (CSI). The 25-question CSI survey scores answers
for each question ranging from 0-4 points, with the CSI potential score ranging from 0-100
points.52 The CSI has proven to have high reliability and validity, and it is proposed that a score
of 40 or above is indicative of central sensitization.53 If we combine the cluster from Smart and
colleagues, along with the emerging CSI data, a clinician can work through an algorithm to
determine the possible clinical presence of CS.

Manual therapy classes commonly teach that a diagnosis is derived mainly from the subjective
interview; information derived during the physical examination helps with confirmation or
rejection of the hypothesis.54,55 In the above paragraph, we detail the subjective process
(Smart and CSI), to develop an initial diagnosis pertaining to the presence of CS. Objectively,
Nijs and colleagues describe a series of physical tests that may help establish the clinical
presence of CS:53

Assessment of pressure pain thresholds (PPT) at sites remote from

the symptomatic area
Peripheral Sensitization

Assessment of sensitivity to
touch during manual palpation
at sites remote from the
symptomatic area56

Assessment of sensitivity to
Central Sensitization
vibration at sites remote from
the symptomatic area57,58

Assessment of sensitivity to
heat and/or cold at sites remote
from the symptomatic area

Assessment of pressure pain

thresholds during and following
exercise

Assessment of joint end feel

Positive neurodynamic tests

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 159

7.2.2: Plasticity

The aforementioned discussion of CS does not verify the presence of structural changes in
the brain but may provide an initial clue of potential underlying plasticity changes. Similar to
any/all manual therapy processes, including Smart’s classification, a series of common signs
and symptoms may help establish the presence of altered body schema. Subjectively, patients
may report spreading pain; bilateral (mirror) pain;
pain “outside of the body”; problems with left/right WARM
discrimination (especially after the pain started);
“missing” body parts; perceived alterations in shape
and size of the body part; temperature changes,
etc. These various subjective clues, along with the
clinical presence of CS can be used to develop a
hypothesis regarding the health of the cortical maps. COOL
An additional subjective clue that is gaining interest
is the use of body charts. It has been proposed that the way a patient colors in a body chart
may be a powerful clinical clue as to the health of the brain’s map, since the S1 map is used
to connect a sensation to a specific area of the body,59 (along with various processes and
pathways in the peripheral and central nervous system and dorsal horn). For example, two
patients with forearm and hand pain present at a clinic for treatment. One colors in a very
discrete area focusing on the thumb and index finger with the map well defined, while the
other “similar” patient with forearm and hand pain colors in the whole forearm and hand.
Which of these two patients may potentially have an issue with their body map? In addition to
using body charts to determine the site of pain, we suggest clinicians use them to screen for
neuroplastic changes. As with CS, we need objective tests to rule up or rule down a hypothesis
that an altered body map may be contributing to a patient’s pain experience. Various sensory
tests are used in advanced neurological conditions such as spinal cord injuries, stroke, brain
injuries, etc., but we will focus on three specific tests that manual therapists may want to
become familiar with and start using in their daily practice. Why these three tests? They are
well described, have normative data, and have been used to help diagnose increasingly more
musculoskeletal conditions within the manual therapy realm.

160 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

• Laterality (left/right discrimination): Laterality or left/right judgment tasks help determine
an individual’s ability to accurately identify left from right while performing these tasks.23,29
It is well established that people in pain experience a delay in their ability to correctly
identify body parts. The good news? Normative data is available for various body parts,
which allows clinicians to judge the health of the cortical maps. For hands and feet, as an
example, a “healthy” person can correctly identify more than 80% of left/right judgement
tasks and average between 1.5 and 2.5 seconds per image.60,61 For the spine, which is
used to recognize which direction the back or neck is moving, normative data points to
80% accuracy and a speed of 1.1 to 2.1 seconds per image.61,62 For clinicians specializing
in headaches and/or facial pain, Von Piekartz and Mohr showed a deficit in a patients
ability to identify basic facial expressions including happiness, sadness, surprise, anger,
disgust and fear.32,33 For these reasons,
it is recommended that clinicians
utilize laterality testing for patients who
show the signs of altered mapping.
On a practical level, clinicians can
use various applications (noigroup’s
recognise™ or orientatefree™) or flash
cards (noigroup) and compare results
to the normative data.

• Two-point discrimination (TPD): Another test manual

therapists can consider using is TPD. It is now well
established that tactile acuity is distorted in people
struggling with pain.17,27,43,63 Again, as with laterality, there
are normative data that allow a manual therapist to test
for TPD and make a judgment call about the health of the
body map being tested.27

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 161

 Neck
Avg. = 45.9 mm
SD = 18.4 mm

Inferior Angle Interior Hand

of the Scapula Avg. = 10.4 mm
Avg. = 52.2 mm SD = 4.2 mm

Upper Lateral Arm

Avg. = 42.4 mm

Mid Medial Forearm Finger Pad

Avg. = 31.5 mm Avg. = 2.5 mm
Back
Avg. = 55.5 mm
SC = 12.7 mm First Dorsal
Mid Posterior Thigh Interosseous
Avg. = 42.2 mm Avg. = 21.0 mm
Distal Lateral Leg
Avg. = 41.6 mm
Foot
Avg. = 20.9 mm
SD = 8.9mm 1-2 Metacarpal Interspace
Tip Great Toe Avg. = 23.9 mm
Avg. = 6.6 mm

During TPD testing, clinicians are encouraged to use the normative data chart as a guide. As
an example: For a patient with LBP, the calipers are opened to the normative data (55.5mm)
and then a patient’s ability to discriminate one or two points is assessed. If they are able to do
so, TPD acuity testing is intact. If not, the calipers are opened wider, say 65mm. If the patient
is able to discriminate one or two points, this is still within normal values given the standard
deviation of 12.7mm. Once the caliper exceeds 68.2mm, the value is deemed abnormal.
These results will be compared to the other side, or adjacent areas. Typically, these values
are significantly altered, clearly indicating an issue with acuity. For example, Moseley showed
in a case series of patients with CLBP that calipers sometimes had to exceed 100mm before
patients could correctly report being touched by one or two points.17

• Localization: A third sensory test that’s gaining interest is localization.64 In its simplest form,
it tests the patient’s ability to correctly identify where they are being touched. For example,
a 9-block grid is designed, and the patient is taught to use it to identify a tactile stimulus
using a pencil eraser. After instruction, the patient’s ability
to correctly identify the area of stimulation is calculated.11,28
Typically, 20 areas are stimulated and a score (percentage
correct) is calculated to determine localization accuracy. No
data is available on the normative values for localization,
minimal detectable change,11,28 but it’s suggested (in line
with laterality) that a score over 80% may indicate sufficient
1 2 3
localization.65 To date, this method has been described in
patients with LBP, postoperative lumbar surgery, shoulder 4 5 6
pain and knee pain—all common conditions that manual 7 8 9
therapists treat. 28,64-66

162 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

Back to our initial questions: Have these changes occurred in my patient and how do I test for
it? In the preceding narrative we described various procedures to screen and test the health
of a patient’s cortical maps. At the conclusion of these tests, a clinician should be able to
determine if the cortical maps are healthy, or better yet, whether or not they are contributing to
the patient’s pain experience. If so, treatment must include a series of strategies to normalize
the map/s. Once again, it is worth noting: Not all patients have issues with their cortical maps,
nor do all patients need a “neuroplastic” approach to their treatment. In a sub-group of patients,
however, these neuroplastic events can powerfully drive pain states and by being unaware of
them (or not specifically normalizing these maps) treatment may be limited. This is a key
process to evaluate and treat chronic pain. The end result is a potential sequence of screening:

New Patient

Screen for Red Flags Refer

Clear

CSI Smart Body chart

Score ≥ 40 Disproportionate pain Localized
Score < 40 Disproportionate Diffuse
aggravating and
easing factors
Diffuse palpation tenderness
Psychosocial issues

Plasticity Issue? No

Possibly

Central Sensitization Plasticity

Pressure pain thresholds Laterality
Palpation Two Point
Heat/Cold Discrimination
Vibration Localization
End-feel
Neurodynamic tests

Plasticity Issue?

Yes No

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 163

7.3: Treatment
Graded Motor Imagery (GMI) is an approach to restoring
altered body maps that is gaining a lot of attention.1,2,67,68
GMI is a collective term describing various “synaptic
exercises” and includes normalizing laterality (left/right
discrimination of body parts), motor imagery (visualization),
mirror therapy, sensory discrimination and more.2,67,68 In
essence, many of the tests described above (laterality,
TPD and localization) become the treatment. Various studies have shown that GMI strategies
influence pain and movement,1,2,67,68 with most research focusing on CRPS and LBP.2,64,66-68
It has been proposed that GMI follows a sequential progression of treatments starting with
laterality reconstruction, followed by motor imagery and then mirror therapy.68 It has also been
shown that individual remapping techniques such as mirror therapy, localization and sensory
discrimination might yield clinical benefits without a sequential delivery of GMI.64,66,69-72 The
intent of this section is not to provide a thorough description of GMI but to show that there
are various clinical ways to restore these maps. Books specific to GMI have been written and
clinicians are encouraged to consult such resources.61,73 In the next section, we will provide
practical examples of GMI for the modern manual therapist embracing neuroplasticity.

7.3.1: GMI

Rather than systematically going through the stages of GMI, we will describe a series of studies
incorporating GMI principles applied to patients with primarily musculoskeletal conditions.
These principles were applied by manual therapists as a means to explore the use of GMI in
general orthopedic-based practices. We believe this will highlight the blend of pain science and
orthopedic practice, and provide clinical ideas for ways to start implementing GMI treatments:

• Localization post-lumbar surgery for chronic LBP and shoulder/knee pain:64 Following
lumbar surgery, it’s not uncommon for doctors to choose not to send patients to
rehabilitation, and one plausible reason might be the surgeon’s concerns about “undoing”
the results of the surgical procedure.74 From a neuroplastic perspective, authors argued
that the limited movement and pain may facilitate changes in cortical maps. In a case
study, a 56-year-old patient who underwent lumbar surgery for CLBP and radiculopathy
attended rehabilitation prior to, and immediately after, surgery. In the postoperative period,
treatment consisted only of localization—identifying where she was being touched (for five
minutes). Measurements of PPT, active trunk flexion, and SLR were taken upon her arrival,
and before her departure from therapy, after the localization treatment. In the six sessions
(twice a week for three weeks), her active lumbar flexion and SLR improved following
therapy, with SLR exceeding minimal clinical important differences (MCID). Interestingly,
PPT measures showed a local calming of the nervous system around the surgical site (the
back) as well as the affected (radiculopathy) leg, but not the thoracic spine or hand. So,
what does this mean? Although this is a case study, it may open the door to investigate
how mapping issues can help restore movement and facilitate recovery after surgery,
especially when there are precautions. One important note about the study: The laterality
and localization were negatively affected from before surgery to after surgery, indicating
the surgery may have had an effect on brain maps.

164 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

 1 2 3
• Localization case series on patients with CLBP:66 In a follow-up
study to the lumbar surgery localization, the same research team 4 5 6
examined the immediate effect of localization on a series of 16
patients with CLBP for a mean duration of 11.9 years; mean pain
rating 5.6/10; mean Oswestry Disability Index of 34.38% and high
7 8 9
levels of fear-avoidance regarding physical activity. Similarly, this
group of patients received a brief five-minute, 9-grid localization treatment. After only
five minutes of localization, mean pain scores for LBP decreased by 1.91/10, exceeding
MCID for chronic LBP. Active forward flexion improved a mean of 4.8 centimeters, again
exceeding MCID. Although this was only a case series, with no controls and no long-
term follow-up, it’s impressive that such a novel (and likely non-threatening) intervention
produced such powerful, immediate results. In patients with high levels of fear, including
fear of being touched, could this be a potential step towards hands-on treatment? Could
patients benefit from incorporating such an activity into their home program? Could the
clinician focus their limited clinic time with patients on manual treatments and exercise,
while teaching a spouse or family member the localization exercise for home use in-
between actual clinical sessions?

• Localization for knee and shoulder pain:71 You may be able to guess the results of this study.
The same group of scientists was asked if localization would work on other joints, such as
knees and/or shoulders. The patients in this study experienced knee and/or shoulder pain
with limited movement. They received a 9-block shoulder or knee grid treatment for five
minutes. In 55 patients with limited ROM and a mean duration of 32.9 months of shoulder
pain, active shoulder flexion was significantly improved after the intervention, with 50%
of the patients exceeding the minimal detectable change (MDC) for shoulder ROM. In 25
patients with knee pain (mean duration 11.2 months) significant improvements in knee
flexion occurred and again 50% of the patients exceeded MDC.

• Mirror therapy for shoulder pain:65 In a recent case series of 69 consecutive patients with
shoulder pain and limited ROM, scientists used a stand-up mirror commonly found in
rehabilitation departments and had each patient hold their affected arm (pain and limited
range of motion) behind the mirror, and then watched them raise the unaffected arm 10
times—moving it slowly up and down through the normal range of the joint in flexion.
Immediately following this very brief intervention, there was significant improvement in
self-reported pain (p = 0.014), pain catastrophization (p < 0.001) and kinesiophobia
(p = 0.012). Additionally, active ROM improved significantly (p < 0.001) with a mean
increase of 14.5 degrees, exceeding MCID. It is also interesting to note that nearly half
(49.3%) of these patients were postoperative. Once
again, this is only a case series, with no controls
and no long-term follow-up. Still, this information
may be clinically valuable as these exercises could
yield immediate changes in pain, kinesiophobia,
pain catastrophization and limited ROM. Again,
this exercise can be performed before, during, or
after manual therapy, and can be added to a home
exercise program.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 165

7.3.2: Manual Therapy

Could it be that manual therapy results in similar neuroplastic changes? Could manual therapy
be a form of sensory integration and/or sensory discrimination? In line with the previous GMI
studies, scientists recently started a series of exploratory studies in this direction. These
studies, plus the overall concept, yield some potential avenues for manual therapists interested
in blending pain science with manual therapy:

• A neuroscience description for spinal mobilization:75 In line with the various

aforementioned GMI studies, scientists have since embarked on more manual-specific
studies, trying to link manual therapy to neuroplasticity. In a randomized controlled trial
(RCT) 62 patients with CLBP (mean duration of 9.3 years) were given the same manual
treatment (Grade II mobilization) to their lumbar spine but received either a mechanical
(traditional) or neuroscience explanation of the treatment.

Table 7.2. Neuroplastic and biomechanical explanations for manual therapy

Neuroplasticity Biomechanical (CG)

Explanation
• Take a look at this picture—it’s a picture
of a brain map of a human body.
• In your brain there is a map telling you
where your body parts are. For example,
if we had you close your eyes and touch
your nose with your right index finger,
you’d have no problem doing it.
Explanation
• Here is a picture of your low back.
• There are five bones in your lower back.
• When life is good and we move, for
example bending forward, each level
takes part in the movement and in
essence shares the load.

• When life is good and we move during
daily tasks, these maps are “exercised”
and they stay healthy—sharp and crisp,
so we know where the body parts are.
• When we have pain, move less and do
less, the brain areas are not exercised
and in essence become blurred.
• When we develop back pain, some levels
stiffen up due to swelling and muscle
spasms, as a means to protect you.
• I am going to do some treatment on
your back using my hands to loosen the
joints, with the aim to make each level
move better.

• Scientists have proven that this happens

very fast and the more “blurred” the area
is, the more pain we have.

• We can retrain the brain maps.

• Today I am going to perform some

manual treatments on your back as
a means to help your brain sharpen
its maps.

166 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

Table 7.2. Continued

Neuroplasticity Biomechanical (CG)

Explanation Explanation

Words during the treatment Words during the treatment

• Let the patient know which level you’re
on (i.e., L5) and have them verbalize it.
• When moving to another level, repeat
the process.
• No mention of what is found, but rather
a “general” stiffness and manual loosing
up of each level.

The study failed to show any significant changes in LBP, leg pain, and active trunk flexion,
but SLR showed a significant difference in favor of the neuroplasticity explanation (p = .041).
Additionally, participants in the neuroplasticity group were 7.2 times more likely to improve
beyond the MDC on the SLR than participants in the mechanical group. As an exploratory
study, the results showed that a neuroplasticity explanation, compared to a traditional
biomechanical explanation, resulted in a measurable difference in SLR in patients with CLBP
when receiving manual therapy. It also showed that patients are indeed able to understand
and use information presented to them from a neuroplasticity perspective.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 167

• Body charts following spinal mobilization: As stated previously; body charts and, more
specifically, how patients color a body chart in, may indicate potential issues with the
S1 representation of the affected body part.59 In an exploratory study (Louw, et al. – in
preparation) patients with LBP were asked to color in the affected area on a body chart
before, immediately after, and at a follow-up visit after receiving a standardized series of
graded mobilization techniques to the lumbar spine. Using a grid system to quantify the
affected body area, scientists were able to show an average shrinking of the affected area
by 33.7%, which correlated to a reduction in LBP and leg pain. Below are two examples
showing the body drawings before, immediately after and upon follow-up.

Immediately Upon
Before After Return

Immediately Upon
Before After Return

Figure 7.1: Body charts of two patients before, immediately after and at follow-up after manual therapy

168 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

Again, this study is a case series, which needs controls and a longer follow-up, but it’s still
intriguing to see manual therapy from this plasticity perspective.

• Sensory discrimination options for mobilization: In line with these studies, it may be
suggested that we include the brain as a more important factor in manual therapy. Instead
of “face in the hole” (on the treatment table), and manual therapy being passive, we suggest
clinicians use manual techniques as a form of sensory integration and/or discrimination.
For example, while doing manual mobilization techniques on the lumbar spine, a patient
is asked to close their eyes while the clinician provides information about the technique,
requiring the patient to pay attention to what’s taking place through their sense of touch.
For example, a technique can be performed lightly (Grade II) or stronger (Grade III), but
as the clinician delivers the treatment, instead of passively receiving the treatment, the
patient is encouraged to discriminate and verbalize the different techniques. With no visual
cues, other senses are needed, which requires use (exercise) of the S1 map. Examples
may be light versus strong techniques; directional (“am I pushing towards the left or the
right?”) or location (upper, mid or low back). The techniques don’t change, but the brain
is introduced into the treatment.

Left or Right?
Light or Strong?
High or Low?

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 169

• Pre-manipulative sensory cueing: What about manipulation? Sensory discrimination may
seem helpful during oscillatory mobilization techniques, but what about a thrust technique
that is typically a relatively brief intervention? A clue may come from our experts: When
watching them, you will often notice they don’t “just thrust” someone, but carefully use
various “pre-thrust” skills to assess and prepare the patient for the actual thrust technique.76
This preparation may include soft tissue work, pre-thrust movements in the direction of
the intended thrust, “mini-thrusts,” and asking for feedback about the patient’s level of
comfort (i.e., more or less side flexion). It could be argued that various pre-manipulative
procedures such as positioning, or having a patient close their eyes to “feel” and “assess”
movements pre-thrust, could be considered a motor-imagery version of manipulation.

• Directional preference via motor imagery: Motor imagery uses powerful premotor cortex
mirror neurons to activate movement pathways without moving, or simply stated: moving
without moving. This has incredible potential for individuals suffering from significant
pain and/or fear of movement. Using this powerful intervention, an ongoing clinical trial is
being conducted to explore the use of motor imagery for the delivery of extension-based-
directional preference treatments (Louw, et al. – in progress). In this study, patients are
screened to be extension-based in terms of directional preference. Patients receive either
actual extension exercises, or “imagined” (motor imagery) extension exercises, followed
by actual exercises. Even though the study is in its early phase it may indicate a need for
physical movement; imagined movement may also be effective, while the combination
may prove to be even more powerful—especially for people with high levels of fear who
might benefit from a motor imagery version prior to actual movement.

170 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP

• Sensorimotor retraining: The focus of this principle has been the alteration of sensory
maps as they pertain to the pain experience. It is important to acknowledge that studies are
being done that include the motor map area, specific to manual therapy interventions. For
example, Paul Hodges’ team has completed a series of studies examining reorganization
of the motor cortex in patients experiencing LBP through spinal stabilization exercises.77
Furthermore, Luomajoki, et al., showed altered body maps associated with pelvic and
postural positioning and movement.28 Therapeutically speaking, tactile input (touching
while doing spinal stabilization exercises) or sensorimotor retraining with head lasers, can
also be tied back to neuroplastic changes, but aimed towards the motor cortex.

Conclusion
This principle is not definitively about neuroplasticity, GMI or manual therapy. Instead it
introduces what we believe is an amazing next frontier in the field of manual therapy: Exploring
a brain-assisted form of manual therapy by integrating the body and the brain. For too long,
manual therapy has been passive, and the brain has been excluded from the equation. GMI
is an exciting new frontier in pain science. Manual therapy works and patients demand it; why
not combine the two for even better results? We’ll leave you with this:

If the brain is the ultimate representational device,

then perhaps our ultimate target should be directed
towards the representation…in the brain.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 171

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Annual scientific meeting of The Pain Society
(Britain)2003; Glasgow, Scotland.
26. Flor H, Braun C, Elbert T, Birbaumer N. Extensive
reorganization of primary somatosensory cortex
in chronic back pain patients. Neurosci Lett.
1997;224(1):5-8.
27. Catley MJ, Tabor A, Wand BM, Moseley GL.
Assessing tactile acuity in rheumatology and
musculoskeletal medicine--how reliable are
two-point discrimination tests at the neck,
hand, back and foot? Rheumatology (Oxford).
2013;52(8):1454-1461.
28. Luomajoki H, Moseley GL. Tactile acuity and
lumbopelvic motor control in patients with back
pain and healthy controls. British journal of
sports medicine. 2011;45(5):437-440.
29. Moseley GL. Why do people with complex regional
pain syndrome take longer to recognize their
affected hand? Neurology. 2004;62(12):2182-
2186.
30. Moseley GL, Sim DF, Henry ML, Souvlis T.
Experimental hand pain delays recognition of
the contralateral hand--evidence that acute
and chronic pain have opposite effects on
information processing? Brain Res Cogn Brain
Res. 2005;25(1):188-194.
31. Bray H, Moseley GL. Disrupted working body
schema of the trunk in people with back
pain. British journal of sports medicine.
2011;45(3):168-173.
32. von Piekartz H, Mohr G. Reduction of head and
face pain by challenging lateralization and basic
emotions: a proposal for future assessment and
rehabilitation strategies. The Journal of manual
& manipulative therapy. 2014;22(1):24-35.
33. von Piekartz H, Wallwork SB, Mohr G, Butler
DS, Moseley GL. People with chronic facial pain
perform worse than controls at a facial emotion
recognition task, but it is not all about the
emotion. J Oral Rehabil. 2015;42(4):243-250.
34. Louw A. Treating the brain in chronic pain. In: C
FdlP, J C, Dommerholt J, eds. Manual Therapy
for Musculoskeletal Pain Syndromes. Vol 1.
London: Churchill Livingston; 2015.
35. Meugnot A, Almecija Y, Toussaint L. The
embodied nature of motor imagery processes
highlighted by short-term limb immobilization.
Experimental psychology. 2014;61(3):180-186.
36. Meugnot A, Agbangla NF, Toussaint L. Selective
impairment of sensorimotor representations
following short-term upper-limb immobilization.
Quarterly journal of experimental psychology.
2016;69(9):1842-1850.
37. Moseley GL, Gallagher L, Gallace A. Neglect-
like tactile dysfunction in chronic back pain.
Neurology. 2012;79(4):327-332.
38. Moseley GL, Olthof N, Venema A, et al.
Psychologically induced cooling of a specific
body part caused by the illusory ownership of an
artificial counterpart. Proc Natl Acad Sci U S A.
2008;105(35):13169-13173.
39. Beggs S, Liu XJ, Kwan C, Salter MW. Peripheral
nerve injury and TRPV1-expressing primary
afferent C-fibers cause opening of the blood-
brain barrier. Mol Pain. 2010;6:74.
40. Watkins LR, Hutchinson MR, Milligan ED,
Maier SF. “Listening” and “talking” to neurons:
implications of immune activation for pain
control and increasing the efficacy of opioids.
Brain Res Rev. 2007;56(1):148-169.
INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 173
41. Hu P, McLachlan EM. Macrophage and
lymphocyte invasion of dorsal root ganglia after
peripheral nerve lesions in the rat. Neuroscience.
2002;112(1):23-38.
42. Beales D, Lutz A, Thompson J, Wand BM,
O’Sullivan P. Disturbed body perception,
reduced sleep, and kinesiophobia in subjects
with pregnancy-related persistent lumbopelvic
pain and moderate levels of disability: An
exploratory study. Manual therapy. 2016;21:69-
75.
43. Falling C, Mani R. Ageing and obesity indices
influences the tactile acuity of the low back
regions: A cross-sectional study. Manual
therapy. 2016;23:25-31.
44. Stenekes MW, Geertzen JH, Nicolai JP, De
Jong BM, Mulder T. Effects of motor imagery
on hand function during immobilization after
flexor tendon repair. Arch Phys Med Rehabil.
2009;90(4):553-559.
45. McRae M, Hancock MJ. Adults attending
private physiotherapy practices seek diagnosis,
pain relief, improved function, education
and prevention: a survey. J Physiother.
2017;63(4):250-256.
46. Verbeek J, Sengers MJ, Riemens L, Haafkens
J. Patient expectations of treatment for back
pain: a systematic review of qualitative and
quantitative studies. Spine. 2004;29(20):2309-
2318.
47. Smart KM, Blake C, Staines A, Thacker M,
Doody C. Mechanisms-based classifications of
musculoskeletal pain: Part 1 of 3: Symptoms
and signs of central sensitisation in patients
with low back (+/-leg) pain. Manual therapy.
2012;17(4):336-344.
48. Gifford LS. Pain, the tissues and the nervous
system. Physiotherapy. 1998;84:27-33.
49. Smart KM, Blake C, Staines A, Thacker M,
Doody C. Mechanisms-based classifications of
musculoskeletal pain: Part 3 of 3: Symptoms
and signs of nociceptive pain in patients
with low back (+/-leg) pain. Manual therapy.
2012;17(4):352-357.
50. Smart KM, Blake C, Staines A, Thacker M,
Doody C. Mechanisms-based classifications of
musculoskeletal pain: Part 2 of 3: Symptoms
and signs of peripheral neuropathic pain in
patients with low back (+/-leg) pain. Manual
therapy. 2012;17(4):345-351.
51. Smart KM, Blake C, Staines A, Doody C.
Clinical indicators of ‘nociceptive’, ‘peripheral
neuropathic’ and ‘central’ mechanisms of
musculoskeletal pain. A Delphi survey of expert
clinicians. Man Ther. 2009;15(1):80-87.
52. Mayer TG, Neblett R, Cohen H, et al. The
development and psychometric validation of
the central sensitization inventory. Pain Pract.
2012;12(4):276-285.
53. Nijs J, Van Houdenhove B, Oostendorp RA.
Recognition of central sensitization in patients
with musculoskeletal pain: Application of pain
neurophysiology in manual therapy practice.
Manual therapy. 2010;15(2):135-141.
54. Jones MA, Rivett DA. Clinical Reasoning for
Manual Therapists. Edinburgh: Butterworth
Heinemann; 2004.
55. Jones MA. Clinical reasoning: the foundation of
clinical practice. Part 1. Australian Journal of
Physiotherapy. 1997;43:167-170.
56. Walsh J, Hall T. Reliability, validity and diagnostic
accuracy of palpation of the sciatic, tibial and
common peroneal nerves in the examination
of low back related leg pain. Manual therapy.
2009;14(6):623-629.
57. Greening J, Lynn B, Leary R. Sensory and
autonomic function in the hands of patients with
non-specific arm pain (NSAP) and asymptomatic
office workers. Pain. 2003;104(1-2):275-281.
58. Tyros I, Soundy A, Heneghan NR. Vibration
sensibility of the median nerve in a population
with chronic whiplash associated disorder: Intra-
and inter-rater reliability study. Manual therapy.
2016;25:81-86.
59. Wand BM, Keeves J, Bourgoin C, et al.
Mislocalization of sensory information in people
with chronic low back pain: a preliminary
investigation. The Clinical journal of pain.
2013;29(8):737-743.
60. Breckenridge JD, McAuley JH, Butler DS,
Stewart H, Moseley GL, KA. G. Shoulder left/right
judgement task: development and establishment
of a normative dataset.. Physiotherapy.
2015;101(5):e169-170.
61. Moseley GL, Butler DS, Beames TB, Giles TJ.
The Graded Motor Imagery Handbook. Adelaide
Noigroup Publications; 2012.
62. Wallwork SB, Butler DS, Fulton I, Stewart
H, Darmawan I, Moseley GL. Left/right neck
rotation judgments are affected by age, gender,
handedness and image rotation. Manual
therapy. 2013.
63. Elsig S, Luomajoki H, Sattelmayer M, Taeymans
J, Tal-Akabi A, Hilfiker R. Sensorimotor tests,
such as movement control and laterality
judgment accuracy, in persons with recurrent
neck pain and controls. A case-control study.
Man Ther. 2014;19(6):555-561.
64. Louw A, Schmidt SG, Louw C, Puentedura EJ.
Moving without moving: immediate management
following lumbar spine surgery using a graded
motor imagery approach: a case report.
Physiother Theory Pract. 2015;31(7):509-517.
174 PRINCIPLE 7 | THE BRAIN HAS A BODY MAP
65. Louw A, Puentedura EJ, Reese D, Parker P,
Miller T, Mintken PE. Immediate Effects of Mirror
Therapy in Patients With Shoulder Pain and
Decreased Range of Motion. Arch Phys Med
Rehabil. 2017;98(10):1941-1947.
66. Louw A, Farrell K, Wettach L, Uhl J, Majkowski
K, Wedling M. Immediate effects of sensory
discrimination for chronic low back pain: a case
series. New Zealand Journal of Physiotherapy.
2015;43(2):58-63.
67. Moseley GL. Graded motor imagery is effective
for long-standing complex regional pain
syndrome: a randomised controlled trial. Pain.
2004;108(1-2):192-198.
68. Moseley GL. Graded motor imagery for
pathologic pain: a randomized controlled trial.
Neurology. 2006;67(12):2129-2134.
69. Wand BM, Tulloch VM, George PJ, et al. Seeing It
Helps: Movement-related Back Pain Is Reduced
by Visualization of the Back During Movement.
The Clinical journal of pain. 2012;28(7):602-
608.
70. Moseley GL. Using visual illusion to reduce
at-level neuropathic pain in paraplegia. Pain.
2007;130(3):294-298.
71. Louw A, Farrell K, Zimney K, et al. Pain
and Decreased Range of Motion in Knees
and Shoulders: A Brief Sensory Remapping
Intervention. Pain and Rehabilitation.
2017;Summer(43):20-30.
72. Louw A, Puentedura EJ, Reese D, Parker P,
Miller T, Mintken PE. Immediate Effects of Mirror
Therapy in Patients With Shoulder Pain and
Decreased Range of Motion. Arch Phys Med
Rehabil. 2017.
73. Louw A, Louw C, Zimney K. Why Are My Nerves
So Sensitive? Minneapolis, MN: OPTP; 2014.
74. Louw A, Louw Q, Crous L. Preoperative education
for lumbar surgery for radiculopathy. SA Journal
of Physiotherapy. 2009;65(2):3-8.
75. Louw A, Farrell K, Landers M, et al. The effect
of manual therapy and neuroplasticity education
on chronic low back pain: a randomized clinical
trial. J Man Manip Ther. 2017;25(5):227-234.
76. Puentedura EJ, O’Grady WH. Thrust Joint
Manipulation Skills for the Spine. 1 ed.
Minneapolis, MN: OPTP; 2018.
77. Tsao H, Galea MP, Hodges PW. Reorganization
of the motor cortex is associated with postural
control deficits in recurrent low back pain. Brain:
a journal of neurology. 2008;131(Pt 8):2161-
2171.
 PRINCIPLE 8

The Importance of
Hands-On Therapy

8.1: Why a Physical Examination?............ 176

8.2: It’s All About…Sensitivity ..................... 179

8.3: Words That Sensitize and

Words That Desensitize ......................... 180

8.4: Are You Okay? ............................................... 182

8.5: Neurodynamics............................................ 186

8.6: Neuroplasticity .............................................. 189

8.7: How Many Tests Do You Need? ..... 190

8.8: Manual Physical Treatment ................ 191

Conclusion...................................................................... 191

Principle 8 References ......................................... 192

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 175

We Are Physical Beings
The main question this book aims to answer: Should pain
science be hands-on or hands-off? The answer to this
question is important to both manual therapists and pain
neuroscientists. Some pain science experts argue hands-
on treatment lacks evidence of effectiveness for patients
experiencing chronic pain. Some experts feel it creates a
dependence on the clinician by minimizing the internal locus of control. Because chronic pain
is so complex, some feel that tissue-issues are not that important.1 Through the principles in
this book, we aim to show how pain science and manual therapy can, and should, coexist.
In this section, we will delve into aspects of the physical examination and physical (manual)
treatments, from a pain science perspective. After all, manual therapists are physical therapists!

8.1: Why a Physical Examination?

Ask a manual therapist at a continuing education event why they do physical examinations and
the response is surprising; the inquiry is often met with a blank stare and sometimes even a
bit of anger. This underscores the common answer, “Because we do.” Yes, in clinical practice,
just like at religious events, there are rituals.2 The typical ritual for a new patient includes the
completion of paperwork (patient information, review of systems and standardized outcome
measures), a patient interview, a physical examination, treatment and reassessment. So, back
to the question: Why do we do physical examinations? Maybe, from a ritual perspective, partly
because it’s “what we do.” Obviously, this is not a good answer, but there is evidence that
rituals are comforting for patients.3 There are several reasons (in no particular order) why a
physical examination is important:

• To confirm the subjective hypothesis/diagnosis: In order to deliver optimal care a

clinician must establish a diagnosis.4 In manual therapy, the diagnosis is based primarily
on information gained from the subjective interview.5 The information gained from the
physical examination is designed to help the clinician confirm or negate certain hypotheses
and fine-tune the clinical diagnosis. This merger of subjective and objective information
improves a clinician’s ability to recognize clinical patterns and often distinguishes expert
clinicians from novices.6

• To find “comparative” signs to use as assessment for progress: The ultimate goal of
any treatment interaction is to address a patient’s needs based on what they’re typically
experiencing: pain, decreased function and physical limitations
in movement.7,8 Pain as a subjective experience is often
assessed with a numeric pain rating scale (NPRS) while function
is assessed with various standardized outcome measures. For
physical (movement) limitations, physical measures are needed,
i.e., ROM with a goniometer, tape measure or inclinometer. The
physical examination provides an opportunity to establish baseline
measures and to re-measure movements at subsequent visits in
order to plan treatments and determine their effectiveness.

176 PRINCIPLE 8 | THE IMPORTANCE OF HANDS-ON THERAPY

• To find physical clues for treatment: It is only logical that if physical
movement (an exercise program) is going to be part of the treatment
plan, then physical movement should be assessed. Movement and
movement restrictions are often an important factor when developing
a manual therapy plan of care,9 which means a physical examination
is an integral part of designing the treatment plan.

• To determine a patient’s movement/safety limitations: People in pain move differently

than those who aren’t in pain for various reasons, including fear of movement, physical
tissue limitations, postoperative limitations imposed by the surgeon, etc.10 The physical
examination, prior to treating/exercising a patient, is necessary to ensure safety from a
movement perspective by establishing limitations that need to be adhered to for safe and
effective treatment.

• To screen for red flags: In every area of medicine, it is

imperative to screen for red flags or medical etiologies
underlying a pain experience.11 With the increased
push towards direct access care in rehabilitation, it is as
important as ever that manual therapists screen for red
flags. Although a review of systems, along with various
questions, may help uncover the presence of red flags,
a physical examination can be extremely helpful. For
example: a test could determine the absence of reflexes, loss of motor control, or a positive
Babinski sign. Any seasoned clinician will recall at least one patient interaction when there
was no mention of a past surgery during the interview, yet when a garment is removed a
huge scar is revealed from L1 to S1. When questioned, the patient replies: “Oh, yes, I had
a fusion last year!”

• To determine a patient’s willingness to move: In recent years, there has been increased
awareness, testing of, and clinical importance assigned to fear of movement, i.e.,
kinesiophobia.12 That’s because fear of movement powerfully influences pain, a patient’s
willingness to move, prognosis and treatment options.12-14 Apart from a survey, the physical
examination is the most powerful method to establish a patient’s fear of movement and
willingness to move, in addition to any fear of being touched.

• To meet patient needs and expectations: Patient surveys always include the word
“physical” when identifying patient expectations for PT or chiropractic appointments for
musculoskeletal pain.7,8 It’s true—patients expect to be physically examined. Many manual
therapists are familiar with this clinical scenario: A patient returns from the surgeon’s office
quite upset because the surgeon never even looked at, or moved, the affected body part.
The origin of the word “placebo,” is “I shall please.” Since the placebo effect has the most
robust effect on pain ever recorded in research,15 why not give patients what they want
and expect?3,15

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 177

• To treat patients: Physical examinations are a form of treatment. Many astute clinicians
have noticed that during the course of a skilled and careful examination some patients
“get better,” even before starting the actual treatment plan. This is illustrated in a study
currently being prepared for publication. In the study, 34 patients with LBP attended
PT. Measures were taken of back and leg pain; pain catastrophization; fear avoidance;
active lumbar flexion in standing; and PPT at the low back, upper trapezius and dominant
hand. These measures were taken three times: prior to the interview, immediately after the
interview, and immediately after the physical examination. The objective of the study was
to determine if the subjective interview, and/or the physical examination, yielded a positive
therapeutic effect even before actual (formal) treatment started. All patients, from entering
the clinic to completion of the examination, were overall 25% improved in all measures.
Specific to physical examination, there was a significant (p < 0.001) improvement in PPT
at the low back and active lumbar flexion. What does this mean? Examinations are also
treatments, or—at a minimum—they influence outcomes.

Measurements Measurements Measurements

25% Improvement

There are likely more reasons for performing physical examinations, but it’s quite clear
already—physical tests and treatments are important when it comes to helping people in pain.
We would argue that nobody does this better than manual therapists. During postgraduate pain
certification classes and pain fellowship programs we often hear from non-manual therapy
trained clinicians; they are often impressed by the skills of manual therapy-trained students
when it comes to performing systematic, thorough, and deliberate physical examinations, and
then connecting the results to a sound clinical reasoning model.

178 PRINCIPLE 8 | THE IMPORTANCE OF HANDS-ON THERAPY

8.2: It’s All About…Sensitivity
In Principle 3, we delved into various pain mechanisms that we believe to be foundational
to blending pain science and manual therapy. At minimum, knowing the basic three
classifications of nociceptive dominant, peripheral neurogenic dominant, or CS (nociplastic)
dominant,16-18 should help us realize that a physical test and its outcome are only part of the
puzzle. The underlying pain mechanism powerfully dictates the results and interpretation
of the findings. For example, in a peripheral neurogenic dominant pain state an upper limb
neurodynamic test may be a powerful tool to help rule in (specificity) or out (sensitivity)
cervical radiculopathy.19 However, if a similar upper limb neurodynamic test produces pain
in a patient with widespread and long-lasting pain from fibromyalgia, with a CS dominant
mechanism, it provides little therapeutic insight.20 That’s just it; input, often normal input via
a physical examination, into a hypervigilant nervous system may yield “false positives,” unless
the attending clinician is aware of underlying pain mechanisms. It’s important to remember
this key aspect when you consider any/all tests used in manual therapy. For example, in
the current sacroiliac (SI) joint dysfunction literature it is believed that a single test is not
powerful enough to determine the presence of SI joint dysfunction and that the presence of
several “positive” tests is necessary.21,22 If we analyze, for example, the criteria from Laslett, it
would be the test’s ability to reproduce “the patient’s pain.”21 What if, under these anatomical
structures, lies a hypersensitive nervous system? Surely, if typical normal stresses of nutation,
compression, distraction, etc., are applied to the lumbopelvic region a patient will likely
complain of pain; even “their pain” on every test, which may falsely make the clinician believe
the underlying mechanism is an SI joint dysfunction. In this book, it isn’t necessary to review
all physical tests known. Instead, we want clinicians to understand that their current tests may
show high sensitivity or specificity. However, they are likely only applicable orthopedically to
nociceptive dominant pain states or neurologically for peripheral neurogenic pain states, and
not for central sensitized (nociplastic) pain states. Keeping this in mind, can you reflect on
patients, or tests you use regularly, and see how this may have played a role in the test results?

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 179

8.3: Words That Sensitize and Words That Desensitize
In Principle 5, we stressed the importance of language; showing that a clinician’s words can
harm or heal. It’s not surprising that words can also influence the execution, results and validity
of physical examinations. This manual therapy study is a powerful example:23 participants with
low back and leg pain were asked to participate in a study. One at a time, each participant
was placed supine on a plinth, and sensors were placed on the affected leg. The attending
clinician performed a straight leg raise test. Before the test, patients were told, “This is a test to
see how tight your hamstrings are.” Measurements were taken. The subjects then underwent
a second SLR test, but this time the clinician informed them, “This is a test to see how well
your sciatic nerve moves.” The end result? The second test, using the “nerve” explanation
resulted in a significant decrease in straight leg raise. It was the same test, using different
language—that resulted in different outcomes.

“Muscle” “Nerve”

Unfortunately, clinicians in the orthopedic/manual therapy field use many common

words that can be harmful (Principle 5). Potentially harmful language is often used when
explaining conditions, while diagnosing a patient, and even while performing tests. Here are
a few examples:

• Pain: In the 1990s, pain was added as the fifth vital sign due to the rise of chronic
pain and the ensuing opioid epidemic. With the advent of pain science and the use of
advanced brain imaging, we now know that asking pain ratings repeatedly may in fact
increase a pain experience.24 In the Maitland approach, as an example, patients are often
bombarded with the question, “What’s your pain level?” This is asked during various
stages of the evaluation. For a patient with LBP, the therapist (often standing behind
the patient and out of sight) may ask a patient: “What’s your current (resting) pain?”

180 PRINCIPLE 8 | THE IMPORTANCE OF HANDS-ON THERAPY

 Once the patient executes active forward flexion, they are asked their pain at the end of
flexion; pain on return to neutral. Was the pain “their pain”— the pain that brought them
in for treatment? No – that’s just flexion! We do not suggest that clinicians skip assessing
pain, or even pain with movement. We simply caution the overuse of pain assessment as
it may induce fear or heighten a pain experience.25,26 Could we instead ask patients during
or after movements, “How did that feel?”

Manual therapists should be aware that in 2016 the American Medical Association
recommended pain ratings be dropped as the “fifth vital sign,”27 as it might be part of the
opioid epidemic overly focusing on pain. In fact, the Joint Commission (JACHO), which
oversees 21,000 healthcare organizations and programs in the U.S., has stated one of the
biggest misconceptions is that pain ratings are required for all patients.28 Also realize it’s
not just the word “pain” that may be an issue, but even the pain scales using various facial
expressions (Wong Baker scales). For example, in some cultures smiling does not suggest
feeling “good,” but is often interpreted as embarrassment or anger.29

• Test names: Imagine you’re a patient who’s experiencing excruciating LBP. You’re sitting
on a treatment table behind a curtain and from the other side of the curtain the therapist
tells you: “In order to examine your crippling back pain, we are going to do an instability
test in an effort to reproduce your pain!” How do you feel about seeing your therapist
now? Not only does an “instability test” sound intimidating but the idea of reproducing
pain doesn’t sound so pleasant, either. How about the brachial plexus tension test? The SI
joint provocation test, Distraction test…the list goes on and on. Yes, we realize these tests
are worded this way in the literature, but this terminology does not need to be used when
talking to patients. These tests are valuable and should be used whenever necessary but,
as covered in Principle 5, we suggest softening the language you use when discussing
such tests. Unfortunately, some clinicians are more interested in showing their knowledge,
versus providing the information a patient needs without inducing fear.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 181

• Framing: Another critical element of the
physical examination is the way language
is used to frame a situation while conveying
information to a patient. It’s not uncommon
during a clinical rotation for a student
examining a patient to provide a synopsis
such as this: “Mrs. Jones is in Room 2. She
has back and leg pain and cannot sit, cannot
sleep, and cannot drive for more than 30
minutes.” Although the information may be
accurate, it begs the question: “What CAN Mrs. Jones do?” We tend to focus on the
negatives, even during physical examinations. Once a physical examination is complete
it’s suggested (and customary) to share information that’s been gathered with the patient.
Think about it: Do you focus only on the negative, or do you also discuss the positive to
help ease fears? Psychologists have studied the “framing effect,” which is the principle
that our beliefs, interpretations and choices are influenced by the way information is
framed through different words, settings and situations. Studies have shown that once
a situation is framed negatively, the patient’s thoughts shift negative and it’s extremely
hard to shift them back to positive.30 More importantly, this shift towards the negative has
a powerful negative effect on endogenous opioid and cannabinoid production, ultimately
decreasing production of these natural painkillers, increasing the pain experience.31
Furthermore, negative framing may induce fear—a powerful driver of chronicity—which
causes increased brain activity in emotional areas such as the amygdala,32 which has been
shown to increase distrust of healthcare providers.31 It’s important to think about how you
convey information and test results to patients. Do you present them with a glass that’s half
empty, or a glass that’s half full?

8.4: Are You Okay?

It is imperative that a patient be, and feel, safe when they
visit any healthcare clinic. Not only does this pertain to
serious issues like verbal, physical, or sexual abuse; it
also means they should feel safe emotionally. When a patient arrives at the clinic with an illness,
injury or dysfunction, they should never leave feeling worse after being treated by the clinician.
Safety has been shown to be a key element when patients are asked to rate the quality of an
office visit.33 As stated in Principle 8.3, examination findings should be shared with patients to
inform them of the diagnosis, prognosis, plan of care, and self-help strategies, without the use
of threating words and descriptions. Unfortunately, many patients who attend rehabilitation
for LBP receive this message upon leaving the clinic: “The low back is vulnerable, susceptible
to injury and needs protecting.”34 How sad, especially since this message is the opposite of
what we know to be true! Since we’re on this topic, it’s a great time to remind you of the most
powerful words in medicine: “You’re going to be okay.”35 It’s that simple. You can help patients
feel emotionally safe by sharing honest details about test results, the diagnosis, and plan of
care, interspersed with these important words: “It’s going to be okay.”

182 PRINCIPLE 8 | THE IMPORTANCE OF HANDS-ON THERAPY

This point in the book is a good time to share some good
news that applies to most manual therapists: If you were
to lose your job, you are already qualified for another
one—working for the CIA or the FBI! In lieu of modern
pain science, it is quite comical that we often “hide” from
our patients. LBP is the most common disorder treated
by manual therapists, and where do we position ourselves
during the majority of the physical examination? Behind
the patient! It is believed that certain types of pain, like
LBP, are enhanced by the fact that the body part is “out of
sight.” Then we add the clinical “FBI agent” who stands
out of sight and provides verbal cues when the patient
moves: “Oooooh…” “Aaaaah…” “That’s not good…” If
you think we’re exaggerating, pay attention to clinicians
who often park themselves behind the patient and utter
phrases that could increase fear and anxiety.

Then there’s the hole of shame in the plinth. Same thing—we poke and push and prod on
the low back, thoracic spine and/or neck, expressing our concerns, while the patient (now
immobilized in the hole) is left to wonder: “Am I okay? What’s going on back there?”

While it’s unavoidable that some tests must be done from behind, a concerted effort must be
made to stay within the visual field of the patient. That means stepping forward after each test
to ask the patient for the next movement or explain findings. And the plinth? Turn the patient’s
neck towards you while you examine the back!

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 183

Manual therapy approaches often differ when it
comes to demonstrating a test for a patient. One
approach is to have the clinician describe what
they want the patient to do (i.e., forward flexion),
without demonstrating how to do it, in order to
observe spontaneous movement.36 Another
approach is to have the clinician describe and
demonstrate a specific test to clarify exactly
what the clinician wants the patient to do. There is an argument for each approach, however,
a pain science gem may come into play: Mirror neurons. In 1996, a scientist accidently
discovered mirror neurons in monkeys while observing them eating. The same neuronal
networks they activated during actual eating (feeding themselves) were activated when they
observed others (the scientist) eating. This finding has a lot of potential to help people in
pain, especially those struggling with severe pain. Additionally, it is now known that a high
concentration of these mirror neurons are present in the premotor cortex, where movement
is planned prior to execution. What does this mean? A patient who raises their arm to full,
end-range-of-motion flexion may cause a mechanical irritation (i.e., sub-acromial mechanical
stimulus of a tendon), resulting in a painful experience, which may cause the patient to move
less. In Principle 7, we described the process of “smudging” and with limited use of a painful
body part followed by smudging, a painful experience can be maintained or exacerbated. How
do we keep the cortical map healthy, while avoiding nociceptive input from the sub-acromial
innervated structures? Mirror neurons. In an example such as this, mirror therapy (tricking
the brain), or motor imagery (imagining flexion or positions of the arm in various aspects of
flexion) may “exercise” the map without moving the arm, possibly while the inflammatory
phase eases. So, let’s return to the physical examination: Demonstrating a physical test for a
patient will definitely activate premotor cortex mirror neurons, which could be good or bad.
Given the close association between fear, fear-avoidance, pain catastrophization, and pain,
clinicians may choose to demonstrate a movement (showing that movement is good, easy and
comfortable), while addressing fears, before asking the patient to move. Current pain science
research shows that patients with LBP who are able to “see” their back move (via mirrors),
versus not see their back move, had significantly decreased LBP.37 This research is in line
with current evidence supporting the notion that people with chronic musculoskeletal pain
report more sensory disturbances and pain during the experimental conditions, indicating
that visual manipulation influences pain outcomes in this population.38 A newer version of this
phenomenon is the projection of the patient’s back to a video screen in front of them.

184 PRINCIPLE 8 | THE IMPORTANCE OF HANDS-ON THERAPY

Although this work is still in the early stages, it is believed that sensorimotor incongruence
(opposite of what’s expected) may play a role in chronic LBP.38,39 All this means is that we
need to realize vision powerfully influences pain (good and bad). Could it be that we carefully
demonstrate pain-free, normal movement in a safe clinical environment for fearful patients,
versus those with lower levels of fear?

In contrast to Principle 8.3 (Words That Sensitize and Words That

Desensitize), loss to gain has a tremendously powerful effect. By ensuring
a physical examination has an optimistic tone, and includes less fear-
driven language and more reassurance, we can frame a patient’s clinical
presentation to be more positive than negative.30 In direct comparison
to the negative spin, this allows for enhanced naturally occurring opioids
and cannabinoids to increase, resulting in a hypoalgesic effect.3,15,31 Add
to this the neuroscience finding that emotions (hopefully positive), are
contagious. In fact, optimism has been shown to:40-43

• Protect against anxiety

• Be associated with reduced pain intensity and physical symptoms related to

open heart surgery

• Improve pain-induced impairments in executive function tasks; brief intervention:

imagine your future best possible self

• Predict positive physical health outcomes

The last thing we want to do (or you need us to do) is describe all
physical tests used in manual therapy and then dissect each from
a pain perspective. Our goal is to remind you that any physical test
you perform is not done in a sterile lab on a “normal” individual.
In fact, numerous factors influence the outcome of a test, which
is powerfully driven by senses, and the brain’s interpretation of
the information it receives. A commonly used phrase is: “All’s
well that ends well.” It is important to note that this is not just a
saying—researchers have proven it to be true clinically. Patients
typically recall two key aspects of a clinical interaction, including
key events, which are often physical tests or treatments—good
or bad. Include this with the fact that long-term follow-up studies
show patients attending PT for LBP do not remember what was
done to them in terms of treatment or tests, but DO remember how
the clinician made them feel.44,45 This only further emphasizes the
importance of providing patients assurance during the physical
treatment that indeed, they are okay.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 185

8.5: Neurodynamics
As we delve into the merger of pain science
and manual therapy it is absolutely necessary
to discuss the physical tests and treatments of
the nervous system—neurodynamics. In the
manual therapy field, neurodynamics (formerly
neural tension) became popular in the late 1970s
(Bob Elvey), followed by Butler, Shacklock, and
Coppieters (see the Introduction).46-50 Now,
with the advent of pain science and a better
understanding of nerve movement, sensitization
of the nervous system, glial cell activation, neuroinflammation, ion channel expression, etc.,51
we realize neurodynamics is a series of tests developed to ascertain the ability to move, and
the sensitivity to movement of the nervous system.52 Neurodynamic tests have come a long
way in terms of research and are now referenced in literature and considered a powerful
strategy to rule in/out cervical radiculopathy.19 They play a role in the clinical presentation of
peripheral neurogenic pain17 and central sensitization pain mechanisms,20 etc. Again, the aim
is not to describe all the available neurodynamic tests as some textbooks do,53,54 but rather
introduce and shed light on some new ideas as we merge pain science and manual therapy.

• “Neural tension” reconceptualized: In the original manual therapy studies about neural
movement, the name “neural tension” became commonplace.48 Tension, however, was
(is) a poor word choice to describe the movement properties of the nervous system as
it is very provocative from a linguistic perspective and led to very aggressive tests and
treatments in the mid-to-late 1990s.53 Shacklock introduced the concept of neurodynamics
partly in lieu of the various physiological, fluid properties (neural inflammation, fluid
dynamics, axoplasmic flow, etc.) versus a mechanical “stretch” but also representing a
less provocative terminology associated with normal nerve movements.52

• Active or passive: Many manual therapists are familiar with the painstaking process of
applying an upper limb neurodynamic test. In several of the tests, especially on the upper
limbs, the tests take quite some time to execute and can clinically slow down the physical
examination. We may even contemplate the unimaginable fact that some clinicians do
not readily perform these tests, since they “take too long.” In contrast, in recent years
it has been prosed (where possible), neurodynamic tests are performed actively by the
patient prior to a passive clinician test or passively tested at all.53 Active tests allow for
quick screening. If a patient can actively perform the various upper limb neurodynamic
tests, with no symptoms or limitations, it allows for a quick screen and no additional need
to perform the passive (more time consuming) tests. Additionally, having a patient actively
perform the test themselves gives them more control, which is key when it comes to pain
and sensitivity. This reduces threat of poorly performed tests, aggressive tests or sensitivity
to touch.

186 PRINCIPLE 8 | THE IMPORTANCE OF HANDS-ON THERAPY

• Order of movement: Neurodynamics, a sequential loading via addition of various
movements, aims to add mechanical loading/testing of a specific nerve, based on
its anatomical location.53,54 Nerves, however, can be loaded in a variety of sequences,
providing numerous ways to perform a certain neurodynamic test.55 For example, a study
by Nee and colleagues demonstrates that to load the median nerve, a clinician may start
proximal with neck side flexion; this is followed by shoulder abduction, external rotation
of the arm, extension of the elbow, forearm supination and wrist and finger extension. In
reverse, a clinician may start with wrist and finger extension, forearm supination, elbow
extension, whole arm external rotation, shoulder abduction and finally neck side flexion.
In the end, the clinician “ends up in the same final position,” but movements were “from
proximal” or “from distal.” What does this mean clinically?

8
Standard
CHANGE IN STRAIN (%)
6

Distal- 4
Proximal
2

Proximal- 0
Distal -2
Start Stage 1 Stage 2 Stage 3
Figure 8.1: Different amounts of strain on the median nerve during different sequences of the neurodynamic test

There are options when it comes to handling people in pain (i.e., move less painful areas
first) and slowly, carefully and incrementally add movements “towards” a sensitive area,
versus: “This is the way the book describes this process, and it’s how we do it—take it or
leave it!” For example: Let’s say there is a patient with severe neck pain following a motor
vehicle accident and they are afraid to move. The clinician is interested in assessing the
sensitivity of the nervous system via a slump test. Typically, the slump test starts with
neck flexion, followed by trunk flexion, knee extension and dorsiflexion. However, for this
particular patient, a better (more patient friendly) version of the test may be “bottom-up”—
starting with dorsiflexion, knee extension, trunk flexion and lastly, slight neck flexion, thus
“slowly moving upward towards the neck.”

• “Positive” neurodynamic test: What constitutes a “positive” neurodynamic test? In

older manual therapy paradigms, this started with “reproducing the pain the patient is
complaining of.”36 As we’re into Principle 8, by now it should be easy to reason why this
may not always be the best strategy—and it may not even be possible. Do we really want
to “reproduce” a high level of pain, or severe latency, which then might linger for the
remainder of the session, the rest of the day, or even for days and weeks going forward? In
some cases, it may not even be possible to reproduce a patient’s pain—think of the runner
who only experiences pain 22 miles into a marathon. It’s highly unlikely that a quick test
in a clinic will “reproduce” their pain. So, let’s return to the question: What constitutes a
positive test? We suggest the following:

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 187

 No single test can stand by itself. It’s true that research has shown that neurodynamic
tests are improving in reliability, sensitivity and specificity, but just like any orthopedic
test, more data is needed.

Remember the pain mechanisms—all tests “become positive” in central sensitized

(nociplastic) pain states.

Differences in ROM may give clues but be careful with symmetry or thinking “only” of
ROM differences. For example, a patient may have normal range of motion of a joint,
but the neurodynamic test results in “more sensitivity” on one arm versus the other.
This may indicate a potential issue, yet range was comparable to the other side.

Normative data. There is normative data pertaining to neurodynamic tests, specifically

for symptomatic and asymptomatic individuals, and a test may be compared to the
normative data available.

Structural differentiation. A key aspect of neurodynamic

tests is the addition or subtraction of load on the nervous
system by moving a remote body part. For example,
a common test for someone with LBP is active trunk
flexion. In many cases, when patients reach their limit,
they may complain of “tight hamstrings.” This may be
true, but what happens to the “hamstring symptoms”
when neck flexion is added? If neck flexion alters leg
symptoms, it’s less likely to be from the local tissue
(hamstring) influences, since the origin and insertion of the hamstrings are limited
to the lower extremity. This crude, yet helpful process may help increase or decrease
suspicion of a sensitized nervous system. Note again, it does not specifically say it’s
the neural structures (single tests cannot do this) but it does add valuable information.

Common signs and symptoms. Neural tissue has some typical, familiar symptoms in familiar
places. In Smart’s classification, pain in dermatomes or cutaneous distributions is cited as
a key factor in determining a peripheral neurogenic mechanism. Numbness and pins and
needles are common in neuropathic pain, but not nociceptive, etc. So, if a neurodynamic test
evokes such known symptoms, again, the likelihood of a positive test increases.

Finally, and most importantly, is function. If, through sound clinical reasoning, a
clinician performs a neurodynamic test and “finds something” (range of motion deficit,
pain, neurological symptoms, asymmetry, etc.) and is able to improve the symptoms
so the patient functions better, the test becomes “positive” because it indicates a
symptom needed to be addressed in treatment.

188 PRINCIPLE 8 | THE IMPORTANCE OF HANDS-ON THERAPY

• Neuroimmune responses, pain and neurodynamics: In Principle 7 we described how the
immune responses following nerve irritation result in a cascade of events, including glial
cell activation, neuroinflammation, changes in blood flow, changes in the blood-spinal-
cord barrier and blood-brain barrier—which is now being linked to altered cortical maps
and persistent pain.51,56 The key issue here is that these changes occur fast (within hours
or days) and given the high incidence of radiculopathy, manual therapists need to “find
it” and begin treating it immediately. Current neurodynamic treatments have shown that
some of the main mechanisms behind neural tissue mobilization is fluid dispersion and
decrease in neuroimmune activity,57-60 which positively influences the aforementioned
central changes. The “so what” is that it’s imperative that a clinician develop skilled
neurodynamic handling in order to test a sensitized nervous system to find these issues
early in order to influence change as soon as possible.

8.6: Neuroplasticity
Principle 7 describes the concept of neuroplasticity in detail,
pointing to the structural changes of the brain due to pain,
fear of pain, immobilization, amputation, bracing, etc.61
Additionally, the principle describes a series of tests that have
become increasingly common in musculoskeletal medicine, including TPD, localization and
left/right discrimination. In conjunction with neuroplastic changes, we also discussed the
cohabitation of CS with these plastic changes and, once again, described a series of tests
that can be used to test sensitivity of the nervous system. One such test is PPT, which uses
a pressure algometer and steadily applies pressure to common body areas, often comparing
left to right or local versus remote areas.62,63 The goal here is not to explain each test in detail,
but to point out how current orthopedic manual therapy should add these tests if altered
plasticity and/or sensitivity is suspected (Principle 7 flow diagram).

It’s also important to note the inclusion

of motor control. To date, the majority
of “neuroplastic” manual therapy
treatments have been performed
to treat pain. In the last 20 years
manual therapy has made advances
in treatments including motor control
(spinal stabilization) and recently
sensory motor retraining (deep neck
flexors) for neck pain.64-67 These tests
(and subsequent treatments) should be
seen from a tactile input (touch, laser targeting) and visual cues or feedback. To reiterate the
point that “evaluation is treatment,” it’s apparent when we see a patient trying to engage motor
control strategies during a “test of stabilization” (anterior draw test), palpation and guidance
(i.e., pelvic movement) which often improves the activity, since it’s providing sensorimotor
feedback. Which once again, underscores the importance of touch.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 189

8.7: How Many Tests Do You Need?
Observing a master clinician compared to a novice is very revealing. Recent research has
shown that experts are faster than novices at performing skills and solving problems, with
little error.6,68 The same can be said of physical examinations. Novice clinicians often use
a multitude of tests to ensure they test everything to avoid “missing anything.” In contrast,
the skilled clinician quickly zooms in, using only a handful of tests during the diagnostic
process. The question then arises: How many tests are necessary? How many tests should
be performed? Should all tests be performed on the first visit? Third-party payer (insurance),
government or institutional rules often imply that all tests need to be performed at the first visit,
but clinically this is not the case. So, how many tests are necessary? The answer is complex,
patient and condition dependent, and pain mechanism dependent.69 As a general rule, in
nociceptive dominant mechanisms more tests can be tolerated, while in allodynic states fewer
tests (sometimes none) should be performed.20 In fact, as we describe various tests and the
interplay of the brain and nervous system, the modern manual therapist might feel a sense
of relief. It’s possible to test various anomalies without being in/around the affected area! In
the case of a raging cervical radiculopathy, laterality testing (using the opposite arm) can be
very valuable. An upper limb neurodynamic test of the other arm, the neck, trunk, or even
the leg, may be informative, without moving the affected limb. It is, however, imperative that
the clinician has a clear (or, as clear as possible) understanding of the various underlying
mechanisms before starting the physical examination. Unfortunately, clinicians are creatures
of habit often performing the same tests, in the same order, for the same type of patient. For
example: In the case of LBP we always start with active trunk flexion, followed by extension,
side-flexion and then rotation, right? Wrong. The clinical presentation (pain mechanism,
plasticity issues, fear-avoidance, etc.) will determine the choice, sequence, number and
intensity of tests.

The algorithm in Principle 7 may be quite helpful, as well as information provided in Principle 12:
Putting More Thought into Treatment Choices.

190 PRINCIPLE 8 | THE IMPORTANCE OF HANDS-ON THERAPY

One last point regarding physical examinations and the necessary
number of tests comes from the late Louis Gifford—call it a clinical
nugget.70 Upon completion of any physical tests, it is highly
recommended that you ask the patient: “Is there anything else you’d like
me to check?” This classic and very useful strategy includes the patient,
which can have a positive effect on their beliefs and expectations. For
example, after a few physical tests for LBP, a patient may ask you to
check their leg length. Sure, you’re aware that leg length and LBP are poorly correlated,10 but
if you perform the tests you show the patient that you listened and are open to their ideas and
beliefs. Plus, you may actually discover pertinent information, while fostering TA and gaining
further insight into the patient’s beliefs, which powerfully drive a pain experience.

8.8: Manual Physical Treatment

The main focus of this section is the importance of physical touch during the physical
examination. There are various reasons why the physical examination is so important, including
the opportunity to form a bond between the clinician and patient, who is injured and may feel
scared and vulnerable. In addition, the potential mechanisms (which are described in detail in
Principle 1) are additional reasons for physical treatment. These mechanisms include:

• Hypoalgesic effect • Neuromuscular effect

• Psychosocial effect • Chemical effect

• Mechanical effect • Neuroplastic effect

• Autonomic effect • Socioeconomic effect

The book as a whole supports the notion that (when applicable) treatment should include
varying types of hands-on approaches.

Conclusion
Movement is the biggest painkiller on the planet. If movement is being considered for
treatment, surely it must be assessed. This includes accessing the ability to move; fear of
movement; sensitivity to movement, etc. Physical examinations are the cornerstone of the
manual therapy assessment process and they take practice, skill and discipline. The pain
science paradigm mandates expansion of current orthopedic tests including reevaluation of
the manual therapist’s rituals pertaining to these tests to include concepts of therapeutic
alliance, sensitization of the nervous system, etc.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 191

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2010;15(4):376-381.
56. Beggs S, Liu XJ, Kwan C, Salter MW. Peripheral
nerve injury and TRPV1-expressing primary
afferent C-fibers cause opening of the blood-
brain barrier. Mol Pain. 2010;6:74.
57. Brown CL, Gilbert KK, Brismee JM, Sizer
PS, Roger James C, Smith MP. The effects of
neurodynamic mobilization on fluid dispersion
within the tibial nerve at the ankle: an
unembalmed cadaveric study. J Man Manip
Ther. 2011;19(1):26-34.
58. Gilbert KK, Smith MP, Sobczak S, James CR,
Sizer PS, Brismee JM. Effects of lower limb
neurodynamic mobilization on intraneural fluid
dispersion of the fourth lumbar nerve root: an
unembalmed cadaveric investigation. J Man
Manip Ther. 2015;23(5):239-245.
59. Song XJ, Gan Q, Cao JL, Wang ZB, Rupert
RL. Spinal manipulation reduces pain and
hyperalgesia after lumbar intervertebral foramen
inflammation in the rat. Journal of manipulative
and physiological therapeutics. 2006;29(1):
5-13.
60. Santos FM, Silva JT, Giardini AC, et al. Neural
mobilization reverses behavioral and cellular
changes that characterize neuropathic pain in
rats. Mol Pain. 2012;8:57.
61. Louw A. Treating the brain in chronic pain. In: C
FdlP, J C, Dommerholt J, eds. Manual Therapy
for Musculoskeletal Pain Syndromes. Vol 1.
London: Churchill Livingston; 2015.
62. Fernandez-de-Las-Penas C, Madeleine P,
Caminero A, Cuadrado M, Arendt-Nielsen
L, Pareja J. Generalized neck-shoulder
hyperalgesia in chronic tension-type headache
and unilateral migraine assessed by pressure
pain sensitivity topographical maps of the
trapezius muscle. Cephalalgia. 2009.
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63. Fernandez-de-las-Penas C, de la Llave-Rincon
AI, Fernandez-Carnero J, Cuadrado ML, Arendt-
Nielsen L, Pareja JA. Bilateral widespread
mechanical pain sensitivity in carpal tunnel
syndrome: evidence of central processing in
unilateral neuropathy. Brain. 2009;132(Pt
6):1472-1479.
64. Hodges PW, Richardson CA. Inefficient
muscular stabilization of the lumbar spine
associated with low back pain. A motor control
evaluation of transversus abdominis. Spine.
1996;21(22):2640-2650.
65. Hodges PW, Richardson CA. Feedforward
contraction of transversus abdominis is not
influenced by the direction of arm movement.
Exp Brain Res. 1997;114(2):362-370.
66. Falla D, Jull G, Hodges PW. Feedforward activity
of the cervical flexor muscles during voluntary
arm movements is delayed in chronic neck pain.
Exp Brain Res. 2004;157(1):43-48.
67. Jull GA, Falla D, Vicenzino B, Hodges PW. The
effect of therapeutic exercise on activation of
the deep cervical flexor muscles in people with
chronic neck pain. Man Ther. 2009;14(6):
696-701.
68. Jensen GM, Gwyer J, Hack LM. Expertise in
Physical Therapy Practice. St. Louis, MO:
Saunders-Elsevier; 2007.
69. Gifford LS. Pain, the tissues and the nervous
system. Physiotherapy. 1998;84:27-33.
70. Gifford L. Aches and Pain. Cornwall: Wordpress;
2014.
 PRINCIPLE 9

Trust Is the Foundation of

Therapeutic Alliance

9.1: Therapeutic Alliance ................................ 197

9.2: Therapeutic Alliance and

Outcomes ......................................................... 199

9.3: Trust ...................................................................... 200

9.4: Predictors of Trust in the Patient-

Provider Relationship............................... 203

9.4.1: Age ...................................................... 203

9.4.2: Race ................................................... 204

9.4.3: Provider Personality and

Behavior .......................................... 204

9.4.4: Patient Characteristics ......... 204

9.4.5: Relational and

Contextual Factors .................. 205

Conclusion...................................................................... 205

Principle 9 References ......................................... 206

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 195

Trust Me
Many aspiring manual therapists watch their preceptors intently to learn, through observation,
how these experienced practitioners use their “magic” hands so skillfully. Less experienced
manual therapists often focus solely on the physical handling while learning manual technique
after manual technique in hopes of achieving the outcomes the masters of the trade consistently
accomplish. After feeling like they’ve achieved some level of “magic” in their hands after a
weekend course, these new clinicians often experience some initial frustration when they
return to the clinic, apply manual techniques, and don’t achieve the same outcomes as
explained during training. The new manual therapist may attribute this to the fact that they
don’t have the same skillful hands as the expert and may focus more narrowly on their hands
in future seminars. However, we are beginning to appreciate that the skill of master manual
therapists is not solely based on their hands, requiring us to take a much broader view of the
clinic encounter. This allows us to recognize that the skilled therapist’s ability to create and be
part of a strong therapeutic alliance (TA) is often an important factor in the positive outcomes
that are achieved. The importance of trusting caregivers can be traced back more than
1.77 million years.1 Although society has progressed and medical practices have evolved,
this basic tenant remains: patients are putting their trust in the hands of their caregivers. This
relationship based on trust between patient and healthcare provider has come to be known as
the therapeutic alliance (also called working alliance or therapeutic relationship).

196 PRINCIPLE 9 | TRUST IS THE FOUNDATION OF THERAPEUTIC ALLIANCE

9.1: Therapeutic Alliance
Much of the theoretical groundwork around the concept of TA can be traced back to work
done in the field of psychology,2-5 but has expanded to include medical practitioners including
physicians,6,7 nurses,8,9 chiropractors,10 occupational therapists,11 and physical therapists.12-15
In the early 1900s Sigmund Freud described the relationship that develops between patient
and provider as a clinical phenomenon which could not be accounted for in normal interactions
between individuals.16 He coined the term “transference” to convey the idea of the transfer
of traits, emotions, and expectations from therapist to patient. As manual therapists, we need
to appreciate that it’s a whole lot more than just manual techniques we are transferring to
patients during the clinical encounter.

Bordin’s 1979 essay17 further developed these

ideas into the current concept known as TA.
He proposed that the therapeutic relationship
between the patient (the one seeking change)
and the therapist (the change agent) is one of
the keys, if not the most important key, in the
change process. Bordin argued that the “magic,”
or experience of change, that occurs during
manual therapy may not be solely due to the
hands of the therapist and he proposed three
key features within the TA: an agreement on
goals, an assigned task or series of tasks, and
the development of the bond.

Many manual therapists who train alongside master manual therapists will observe these key
features displayed during clinical encounters with patients. If you have an opportunity to watch
old video footage from sessions conducted by Maitland (known for doing only manual therapy
and very little exercise) you will appreciate the strong presence he had with patients as he
questioned them and clinically reasoned through their problems. It’s important to recognize
that these actions helped build TA through agreement on goals, assignment of tasks, and
development of a bond with one another. The master manual therapist takes cues from the
patient to set mutually agreed upon goals and set the direction for the plan of care in order to
help the patient return to their normal activities. Often, master manual therapists were masters
at creating TA before we even had a name for this skill—and in many cases they were fully
aware of how it contributed to treatment outcomes. These clinicians would put together a plan
of care that included distinct homework and follow-up treatments to maintain and advance
the manual work that was done during the treatment session; all of which was contributing
to a strong therapeutic alliance. This strong relationship between the patient and therapist
often grew in strength to the point that the patient would only see “their” manual therapist
for treatment.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 197

The literature shows that the ability to build TA is based on a variety of characteristics,
including the therapist being nonjudgmental,18,19 exhibiting strong communication and
listening skills (verbal and non-verbal),7,19-23 demonstrating empathy,18,19,24-27 showing high
levels of provider competency,18,19,28 demonstrating trust,7,13,18,21,22,26,29 collaborating with the
patient successfully,18,19,22,27-29 being respectful, validating the patient’s feelings,21,22,24,26 and
developing rapport/connection.18,19,21,26,27

Unfortunately, while the aspiring manual therapist focuses on the hands of the master
clinician, many of these important characteristics (which were probably not taught directly)
go unnoticed. Fortunately, many aspiring manual therapists pick up on these skills and traits
intuitively over time, ultimately becoming excellent clinicians. It’s likely that these clinicians
are able to avoid some of the characteristics and techniques that have proven to negatively
impact the therapeutic alliance, which can prevent some clinicians with talented hands from
achieving maximal outcomes.4 These characteristics include: Being too rigid (my way or the
highway), being self-focused (I’m the reason the patient got better), sharing personal conflicts
(you think you have it bad—listen to what I have going on), being critical of the patient (if you
just did what I tell you then you would get better), lacking involvement in the process (I don’t
have time for all of the emotional talk—just lie on the table and let me fix you). Unsurprisingly,
these characteristics cause patients to perceive the clinician as lacking compassion and
understanding and can ultimately have a negative effect on the therapeutic relationship.5,30,31

Research has shown that when a provider

experiences stress caused by organizational
aspects of work, it negatively effects the TA
between patient and provider.15 We all get it:
Our healthcare system is messed up. Insurance
companies want to make money and avoid
paying for patient services, and other providers
do not know what they are doing. But spreading
these frustrations to our patients does not help;

198 PRINCIPLE 9 | TRUST IS THE FOUNDATION OF THERAPEUTIC ALLIANCE

it’s not their fault. Consider this when you reflect on the stress associated with your current
employment and the effect it may have on patient outcomes. It’s also important to recognize
that creating a strong, healthy TA is not just up to you. Patients need to do the following: have
trust in the therapist,13,18,32 actively engage in treatment,6,18,21,32-35 have some perceived utility
of treatment,6,18,27,34,36,37 and speak and act authentically.18 These multiple components can
enhance or take away from the TA between therapist and patient, which could affect the
relationship and outcomes. The importance of TA is summed up in this key statement made by
Bill Boissonnault at the 2018 American Academy of Orthopaedic Manual Therapy Conference:

“We need to stop referring to ‘non-specific’ effects

and TA as ‘soft skills.’ They are ESSENTIAL skills!”

9.2: Therapeutic Alliance and Outcomes

Pain is complex and multidimensional, and the process
of helping relieve people from pain is multidimensional in
nature, too. It would be great if we could point to one aspect
of treatment and say it was the “one factor” that caused a
good outcome but in reality it is a combination of elements that leads to a positive outcome.
All manual techniques and therapeutic interventions are performed within the context of the
TA, which has an effect on outcomes. We caution therapists to steer away from the idea that
it was “this or that” intervention that caused the optimal outcome. Instead we encourage
therapists to recognize that it may have been “this and that” intervention that caused an
optimal outcome. That’s because a positive outcome is not the result of a manual technique
alone, and it’s not achieved by therapeutic alliance alone; both are needed.

Research shows that a strong TA is one factor that usually has a positive effect on patient
outcomes.38 Results of a strong TA include increased adherence to the treatment program,7,39
improved overall satisfaction with the provider’s care,40 and positive influence on health status.41
Similarly improved outcomes have been shown in studies more specific to PT care. Hall et al.,13
did a systematic review of 13 studies focused on TA and outcomes in physical rehabilitation.
They found a positive correlation between TA and outcomes related to treatment adherence,
pain, function, mental health, and satisfaction with treatment. Lakke and Meerman14 studied
individuals with chronic musculoskeletal pain and found strong evidence that TA had an
influence on therapy outcomes, including decreased pain and improved physical function. A
specific study that was done as part of Lakke and Meerman’s systematic review was published
by Fuentes and his colleagues,12 taken from his dissertation project.42 They found a large
effect size for changes in pain intensity and muscle pain sensitivity with an enhanced TA over
the groups with limited therapeutic delivery of care. Interestingly, the group that received sham
treatments with an enhanced TA outperformed the group that received active treatments and
limited TA. These results all support the most important point: The relationship matters.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 199

9.3: Trust
Complex social and psychological
interactions take place during the
building of TA between the clinician
and patient. Core emotions
including liking and disliking,
gratitude, sympathy, empathy, honesty, respect, guilt, trust, and suspicion all play a role in the
development of the bond that occurs during TA.4,43 Miciak found four key characteristics of a
strong and healthy bond that develops during TA in PT:26

• Nature of rapport • Trust

• Respect • Care/attachment

As a primary characteristic that helps build the foundation of TA, trust has been studied
substantially.44-47 Miciak’s research highlights the following three overlapping aspects of trust
within the TA:

1. Patient trust in the clinician (interpersonal trust)

2. Overlap of professional trust and personal trust (interpersonal and social trust)

3. Clinician trust in the patient (interpersonal trust)26

The importance of these interactions demonstrates the bidirectional component of trust that
occurs between the patient and therapist.

Trust is foundational to any relationship when altruistic behavior is involved.48 We now

understand that there are certain critical elements that are vital for the development of trust.44

• First, trust evolves out of past experiences,

which is why it is developing and changing as a
relationship develops over time. This is how trust
can grow between a patient and their health care
provider over time.

• Second, individual motives need to be perceived

as altruistic and a person’s actions need to
consistently show reliability and dependability.

• Trust is associated with the feelings of confidence

and security, knowing that a caring response
from the other person in the relationship can be
expected. This is why confidence on the side of
both the clinician and patient can have significant
benefits to the manual therapy experience.

200 PRINCIPLE 9 | TRUST IS THE FOUNDATION OF THERAPEUTIC ALLIANCE

Trust is a dynamic versus a fixed trait; it changes and develops over time.49,50 Trust grows
based on past experiences, making every interaction and positive outcome a component of
future success as trust builds.44 Think of the Maitland test/retest process and how showing
improvement of the asterisk sign builds trust for the next session and implementation of the
manual technique. Each individual in a relationship is learning about the trustworthiness of
the other as the relationship evolves over time. While the initial trust measurement can occur
rapidly (less than one hundredth of a second),51 it takes time to develop and deepen that trust,
which is why follow-up visits often help build trust within the TA.49 However, it should be noted
that additional time with the patient does not guarantee improved trust; other mechanisms
that can positively or negatively affect the level of trust are in play. It should be obvious
that scheduling patients who aren’t seeing improvement cannot be justified as a means to
build trust.

Trust is more than a feeling; it can be linked to

oxytocin, with chemistry and biology at its root.52,53
You may remember learning in physiology class that
oxytocin plays a role in lactation and childbirth. In
addition, this neuropeptide hormone has significant
neurobiological effects on the central nervous
system, especially in the area of attachment and
trust.54 Zak and colleagues52,53 seminal work
demonstrated that oxytocin plays a key role in the
development of trust between individuals. More
specifically, oxytocin has been shown to reduce
the release of stress hormones and works as an
anxiolytic by decreasing the stress response system.54 Some of this functioning takes place by
suppressing the activity of the amygdala (our primary fear center), which decreases feelings
of untrustworthiness and restores trustworthiness.55 Strong evidence shows that oxytocin
changes people’s affect; lower levels of oxytocin correlate with depression, whereas increased
levels are associated with elevated mood and decreased anxiety.54 This provides insight as
to why we often observe improved mood in patients following treatment. An improvement in
mood could be traced back to potential boosts in oxytocin to the patient’s system through
the development of trust within the therapeutic alliance. The benefits of oxytocin do not stop
there—it has also been shown to provide modulation of nociception and pain perception.54,56,57
There is also evidence that oxytocin is elevated through physical touch, which should be of
interest to manual therapists.54,58

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 201

There are five overlapping domains involved
in trust between the patient and their
healthcare provider. These are: fidelity,
competence, honesty, confidentiality, and
global trust.46,47,59,60

• Fidelity is caring and advocating for

the patient’s best interest. When we
step back and see the entire treatment
encounter outside of the “magic” hands,
we see the care that the manual therapist puts into their patients.

• Competence is providing quality care without error. We’ve heard the argument that skill
may not matter in manual therapy because we “cannot be specific” on isolating segments
with our techniques. We would argue the opposite; skill and competence are vital to
the execution of manual therapy techniques—not so much for the physical segments
handled, but for the development of trust with the patient as they perceive competence
and confidence in the hands of their manual therapist.

• Honesty is telling the truth without misrepresenting facts. This is key for the modern manual
therapist as they continue to redefine what they are doing. We know we are not putting
joints back in or out of place, so being more honest with patients about the mechanisms
(See Principle 1) can only build trust and enhance the TA.

• Confidentiality is the secure use and sharing of a patient’s personal information. This
also includes the use of a private, enclosed space for one-on-one sessions, to create an
environment where patients feel safe sharing private information.

• Global trust is harder to define but has been described as the irreducible soul of trust,
which combines elements of some, or all, of the other domains.61 This is a part of the
treatment that we all recognize when it’s there, although it’s hard to nail down specifically
what it is; you just know when it’s there. In health care, trust has been shown to be
more of a one-dimensional construct.59 This means patients tend not to distinguish trust
toward healthcare providers in the basic domains of fidelity, competence, honesty, and
confidentiality; instead, patients are more likely to use a global trust measurement. They
know what trust feels like when they experience it.

Another interesting point about trust in healthcare is that there are two types: social trust
and interpersonal trust.46,47,62 Social trust is the general trust in the collective institutions and
healthcare professions. The media and personal experiences can influence a person’s level of
general social trust. That’s why interactions with past healthcare providers will affect the level
of trust a patient has in you. Whereas, interpersonal trust is the trust developed with a specific
therapist through repeated interactions over time. The good news for a therapist treating a
patient who has had a negative experience with a previous therapist is that individual trust, on
average, is one-fourth higher than global social trust in the same populations.59

202 PRINCIPLE 9 | TRUST IS THE FOUNDATION OF THERAPEUTIC ALLIANCE

9.4: Predictors of Trust in the Patient-Provider Relationship
Hopefully, by now you agree that TA and trust are key components (in addition to manual
techniques) to successful patient treatment outcomes. You may be thinking, wouldn’t it
be great to just use a “trust-o-meter” to measure a patient’s level of trust? Unfortunately,
this technology has not been developed yet. Besides being a silly idea, there is a reason
this device doesn’t exist—there simply are not many strong or consistent predictors of trust
development in the patient-therapist relationship. The good news:
this suggests that most patients enter into the relationship with
the ability to develop trust.47 The bad news: we have our work cut
out for us as we try to develop trust. As we all know, relationships
are complex. Personal and cultural factors (along with trust types)
affect how the various characteristics involved in a trust equation
interact, compound, and modify each other.63 The following
study, performed in India, demonstrates the complexity of inter-
relatedness across spectrums, by finding that different groups had
different levels of trust.63

• One group in the study was labeled “comfort-based” because they were comfortable
talking with their physicians. The older females, living in rural communities, who had low
education levels, demonstrated the highest levels of trust in this group.

• Another group was labeled the “personal” trust group because they felt a personal
connection with the physician. Those in the group who were younger, lived in urban areas,
and had high education levels had the highest levels of trust.

This study demonstrates the unique individuality that every patient, and provider, brings to the
therapeutic relationship and is a reminder that we have to be careful not to stereotype patients
or place them in any particular category. That being said, there are markers that can provide
insights as we assess and develop trust with our patients.

9.4.1: Age

In most studies, age has a modest positive

correlation with trust, showing that the older the
individual the more they tend to trust their healthcare
provider.7,64-67 One study demonstrates that age has
more of a “U” shape pattern in regards to trust;
middle age individuals having the lowest levels of
trust, and younger and older patients having higher
levels of trust.68

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 203

9.4.2: Race

Race is another predictor of trust levels. Various

studies have demonstrated that African American
and Hispanic patients show lower levels of trust on
multiple levels regarding their health care, including
trust in their providers.64,66,69-71 These lower levels of
trust are found mostly when there is a discordance
between the provider and the patient.72 Recognize
that, even with a racial difference between provider
and patient, the trust levels are still relatively high.70 Just be aware that as providers, we may
need to work a bit more to gain trust in those of a different race.

9.4.3: Provider Personality and Behavior

The strongest predictors of trust are therapist personality and behavior, which is promising
since this is something we as clinicians can work to improve upon. The personality and behavior
traits with the highest correlation to improved trust scores are all related to communication
and interpersonal skills.7,50,61,73-75 The ability to explore the patient experience is a key factor
in developing trust with a patient.7,60 Simply allowing a patient the time to tell their story and
skillfully exploring their history is fundamental to building trust and TA. Another key factor in
the development of trust over time is providing emotional support to the patient.76 Studies have
shown that early on in the relationship, patients receiving informational and decision-making
support along with emotional support was important. However, as time progressed, it was
only the emotional support that continued to be important for building trust with the patient.
This is important to consider when working with a patient with a chronic pain condition who
you see over an extended period of time. Lastly, an additional key interpersonal trait and
communication skill is the ability to enter into shared decision making with the patient and
take a patient-centered approach to delivery of care.60,77

9.4.4: Patient Characteristics

When it comes to patient characteristics across the spectrum, there is little to no consistent
relationship to trust levels with providers. Education level is all over the board with some
research showing negative correlation,63,66,67,69 some research showing positive correlation,63,65
and no correlation in others.67,78 Patient reported health status has also shown variable results
with some positive relationships with improved trust levels in patients with better reported
health status toward their physicians,7,66,69,78 but this was not found in all studies.65,67,73,79
Socioeconomic class does not show any significant connection with trust levels of a patient
toward their provider.65-67,78,79 One patient characteristic that has some correlation to trust is
medical skepticism. The patients with higher levels of medical skepticism had lower levels of
trust in physicians;69 this makes perfect sense—if your patient is skeptical about what you
say they are less likely to agree with your treatment plan, and probably won’t trust you all
that much.

204 PRINCIPLE 9 | TRUST IS THE FOUNDATION OF THERAPEUTIC ALLIANCE

9.4.5: Relational and Contextual Factors

Relational and contextual factors are important and can help improve trust in the patient-
provider relationship. Typically, the longer the relationship with the provider and the
more frequent the interactions, the higher the trust levels compared to those with short
relationships.7,61,65,67,68,71-73,75 Interestingly, evidence has shown that during the relationship the
correlation between the length of the relationship and trust is weak. This potentially means
that patients form their trust impression early with their providers and do not alter much
from their initial trust assessment.47 Patients who are able to independently choose their
providers seem to have higher trust levels with providers.59,61,72-75,78,80 This can be a challenge
in the current U.S. healthcare market with preferred provider lists and less choice when it
comes to selecting providers. Higher levels of social trust also tend to lead to higher levels
of interpersonal trust in one’s therapist.59 Longer wait times, prior disputes with a provider,
planning to switch providers, or seeking a second opinion have also been associated with
lower levels of trust, which makes sense.61,72,78

Conclusion
We hope you take the information in this principle in stride. TA and trust alone are not the
only elements leading to improved outcomes, but we can’t focus only on what our hands are
doing or what patient exercises are doing to help improve outcomes. We need to appreciate
the complexity of the clinical encounter between therapist and patient, and how TA can have
a positive effect on treatment outcomes. We need to continually consider how psychological
states can influence biology and how these biological factors can influence psychological
states. By being more mindful of the various traits and components that can enhance trust
and TA, we can use these alongside our interventions to help maximize our outcomes. There
is more though: an underlying theme of the book, treatments, healthcare and the current
state of affairs. It is somewhat sad that time and effort has to now (overtly) be spent on
teaching clinicians, including manual therapists, to create trust and thus build a TA. A lot of
attention has been given to perfecting skills and techniques and “sharpening” the tool, be
it manual therapy, PNE, exercise, etc., but as this principle and the book show, there are
powerful underlying issues we need to keep in front of us, none more than a true interest in
helping people that present for treatment. Best place to end this principle? The timely quote
by Theodore Roosevelt.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 205

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208 PRINCIPLE 9 | TRUST IS THE FOUNDATION OF THERAPEUTIC ALLIANCE
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Trust and satisfaction with physicians, insurers,
and the medical profession. Medical care.
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 PRINCIPLE 10

The Importance of Assessing

for Yellow Flags

10.1: Assessing for Yellow Flags ................211

10.2: Attitudes and Beliefs about Pain 212

10.3: Behaviors ...................................................... 212

10.4: Compensation Issues .......................... 213

10.5: Diagnosis and Treatment Issues. 213

10.6: Emotions ........................................................ 214

10.7: Family ............................................................... 214

10.8: Work .................................................................. 214

10.9: Patient Questionnaires........................ 215

10.10: Social .................................................................217

Conclusion...................................................................... 218

Principle 10 References ...................................... 219

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 209

Caution Ahead
Anyone who has treated at least one patient with chronic pain can attest: pain is complex.
We have discussed the amazing complexity of pain and how it relates to manual therapy in
previous principles in this book. Not only is pain complex, especially when it becomes chronic,
so are the people who suffer from it. Let’s face it, people are amazingly complex—especially
when we consider them from a biopsychosocial perspective.1 We each have unique biology
based on the various interactions of our genes, which results in individuality from a biological
perspective.2 But, as discussed in the Pain Models principle, psychology and sociology also
shape us. These aspects are just as complex (if not more complex) and unique, than our
biology. Adding these three components (bio, psycho, and social) together truly makes us
human.3 Simply viewing pain as a basic cause and effect equation (injury + tissue damage
= pain) is a thing of the past. We now know that pain is a complex interaction of multiple
dynamic systems in a multi-causal equation (injury2 /tissue damage x psychological factors
+ social environment ≈ pain). While this multi-causal equation is hard to solve, the better we
understand some of the variables involved, the better we can help our patients.

Most manual therapy training is focused more on biological

components and less on psychosocial components. We often hear
manual therapists baulk at the idea of dealing with these psychosocial
components, “I’m a manual therapist not a psychologist!” This is true,
and unless a clinician is professionally trained in psychology or sociology they need to be
careful not to overstep boundaries. However, this does not mean we cannot be informed by
these areas of study to help deepen our understanding of each patient we come in contact
with.4 It is well known that a patient’s reaction to pain is one of the most important factors
in the development of disability and suffering.5-8 Psychological and social variables play a
significant role in how an individual reacts to pain.9,10 This principle will provide an overview
to help the manual therapist identify those at risk, based on known predictors. We will also
talk about how to modify patient management based on these psychosocial variables. The
work of Nicholas Kendall, Steve Linton, Chris Main, Paul Watson and others will be reviewed.
The reader is encouraged to search and review their work in more detail for a more complete
understanding of these psychosocial variables, which have been labeled “yellow flags.”11-15

210 PRINCIPLE 10 | THE IMPORTANCE OF ASSESSING FOR YELLOW FLAGS

10.1: Assessing for Yellow Flags
Historically, a manual therapist would not explicitly
assess psychosocial variables when a patient
presented to therapy with an injury or illness. Many
experienced manual therapists would, however,
intuitively identify these factors, which can ultimately
effect outcomes. When the clinician more fully
understands these factors, it will help them to better VS
predict outcomes and identify if there’s a need to
refer the patient to other healthcare providers who
are more qualified to help the patient work through
these variables. In addition, a deeper appreciation
of these factors often makes the clinician more
empathetic toward the patient; seeing them as a
complete person dealing with a complex challenge with multiple variants. This is one reason
we now use patient-first language: We refer to a “patient with low back pain,” not a “low back
pain patient.” We need to remember that the patient as a person is the primary focus, and the
anatomical location or biomedical problem is secondary.

A thorough and efficient history-taking process is one of the most important steps to help the
therapist better understand the patient and their needs. This history-taking process can be
broken into two components of information: utilization of standardized patient questionnaire
measurement tools and the subjective interview. This process is essential to help the clinician
discover important patient information, including: Why did the patient come to therapy? What
caused the injury or illness? What is the patient’s medical history? What level of discomfort are
they feeling? These are important starting questions, but the therapist may need to dig deeper
to reveal potential yellow flags that could be barriers to achieving a positive outcome. In their
research, Linton and Hallden16 showed that the following factors most consistently predict
poor outcomes:

1 The presence of a belief that pain is harmful and potentially disabling

2 Fear-avoidance behaviors with reduced activity levels

3 Low mood and withdrawal from social interaction

4 An expectation that passive treatments, and not active participation in therapy, would help

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 211

First, let’s explore some topics that are important to cover
during the interview process; then we will cover various tools
a therapist can use to augment the interview process. Kendall
and Watson developed a mnemonic to help remember the
variables to be explored in the clinical interview (ABCDEFW).15
These are not listed in order of importance, but should all be
explored during the interview process as the clinician looks for factors that may predict poor
outcomes or potential need for referral to other healthcare professionals.

10.2: Attitudes and Beliefs about Pain

One of the top predictors of poor outcomes that Linton and Hallden found was the patient’s
belief that his or her condition was harmful and/or disabling. This can lead to catastrophic
thinking and fearing the worst, which often leads to the second factor of a poor outcome—fear
avoidance behaviors. The patient may think that all pain must be gone before they can return
to any activity, because of the maladaptive belief that pain always signals more injury. This
kind of inaccurate thinking probably comes from the old belief: “if it hurts don’t do it.” This
is commonly seen in patients who equate all pain with tissue injury and think the more pain
they experience the more tissue damage there must be. This discovery gives the therapist an
opportunity to change the patient’s perception by providing them with accurate information
about their condition and recovery. When a therapist can build up positive thoughts of
resiliency and recovery over negative views of disablement and damage, it can go a long way
to assist in changing the patient’s attitudes and beliefs about pain and aiding in their recovery.

10.3: Behaviors
During the exploration of behaviors, the therapist is learning
what the patient is (or is not) doing because of the pain. This
provides insight into the patient’s coping strategies. Passive
coping strategies (bed rest, excessive reliance on external aids
such as braces or taping; self-medication through smoking,
alcohol intake, or other street drugs; and little to no physical
activity) have been demonstrated to be highly predictive of poor
outcomes.13,17 How often do we see the patient wearing multiple
braces, which are no longer serving the original purpose? It’s
important to be aware of these avoidance type behaviors, as well as the reverse behavior—
endurance. Many patients try to endure the pain without pacing themselves.18 We often refer
to patients with an endurance-related response to pain as the “boom-busters,” which are the
individuals who endure the pain as long as they can until they bust and have to spend a week
in bed, disabled by the excruciating pain they worked so hard to ignore. Recognizing these
two types of behaviors is important, so the perceptive clinician can encourage and support a
patient in overcoming fear avoidance behaviors and help modify the boom-buster behaviors
with more appropriate pacing.

212 PRINCIPLE 10 | THE IMPORTANCE OF ASSESSING FOR YELLOW FLAGS

10.4: Compensation Issues
Basic psychology based on Maslow’s Hierarchy of Needs
shows that when you endanger someone’s basic survival
needs, it is all they can focus on. Patients often have to deal
with compensation issues that can affect their basic need
for food and housing. We know that the association between
financial compensation and disability is complex and linked
with our messy healthcare system. Two-thirds of the people that file for bankruptcy say medical
bills or other health-related issues contributed to their financial difficulties.19 Gaining insight
into a patient’s financial incentives to return (or not return) to work will provide information that
the therapist can use to better understand the patient’s motivations.

10.5: Diagnosis and Treatment Issues

Never underestimate the power of the healthcare system to make some patients worse. The
patient entering into the healthcare system may be given various diagnoses from different
providers for the same ailment.20 They may even be given new care instructions that conflict
with old recommendations for the same long-standing problem. The use of research and
evidence is great for clinical practice but can leave a patient scratching their head. Not to
mention the loss of trust when they are told to do (or not to do) something, only to be told a
few years later to do the exact opposite.21 How does the patient navigate conflicting directions
from different healthcare providers? One PT uses hot packs, an ultrasound and massage;
another puts the patient on the table and uses thrust techniques; a third PT never touches the
patient and only uses exercise; and another may use a completely different form of exercise.
Unfortunately, the more clinicians a patient sees the more diagnoses they might be given—
along with a plethora of treatments and explanations that may be conflicting. During the
interview process, we gain understanding about the messages the patient has been given
about their condition, along with what they understand about all the various diagnoses and
treatments delivered. This will provide insight into thoughts and misconceptions they may
have regarding their diagnosis and treatment.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 213

10.6: Emotions
Just saying the word “emotions” to an analytical manual
therapist who is more comfortable with the biomedical
approach can create an adverse response. Isn’t it interesting
that we avoid talking about emotions with our patients, yet
everything that makes us human revolves around emotions?
There is no escaping it. Many of us have heard the famous
saying: “The fear of pain is worse than pain itself.”22 Evidence
shows that emotional states such as fear, anxiety and sadness are related to chronic pain
states.5,23-25 While these emotional states are not the responsibility of the manual therapist, the
therapist should give the patient the time and space to express their feelings, and then provide
empathetic responses, before helping the patient seek any necessary additional healthcare
services if they show an interest in doing so.

10.7: Family
Family dynamics can be interesting to say the least—as we all can attest based on experiences
with our own families. When a family member is experiencing chronic pain, it can place a great
deal of stress on other family members, and the family unit as a whole. There are two common
responses to people with chronic pain. Some family members take on an over-protective role.
While the intent may be to show care and support, it can be counter-productive by reinforcing
fear of harm and reducing active participation in daily tasks. The opposite path is the overly-
punitive response of the family member as seen through guilt, ignoring, and/or shamming the
person who is experiencing pain. This can lead to further detrimental psychosocial issues. As
we’ve addressed before, these types of issues are outside of the direct influence of the manual
therapist, but recognizing the potential impact on pain and offering support can be helpful.

10.8: Work
The last yellow flag variable is work related. Remember, work does
not have to be an occupation that a person receives a paycheck for.
Most people do some form of meaningful work, whether it is paid
employment, volunteer activities, and/or household duties. Much of
our sense of self-worth is tied to our occupation.26 The level of job
satisfaction has been shown to have a strong correlation to reports
of pain while at work.27 Factors such as poor supervisor relations,
manual or menial related tasks, belief that work is harmful, extended
time in static positions, lower educational backgrounds, and minimal
return to work options are all important to explore with a patient.
Each of these variables has been linked to potential delay in return
to work and prolonged disability.

214 PRINCIPLE 10 | THE IMPORTANCE OF ASSESSING FOR YELLOW FLAGS

10.9: Patient Questionnaires
Various patient questionnaire tools have been developed and validated through the years to help
with assessment of potential yellow flags that may lead to poor outcomes. Many of these tools
have been shown to successfully predict whether a patient should be placed into a category
such as high, moderate, or low risk for progression into chronicity. It is not the intent of this
principle to provide a comprehensive list or cover all the psychometric properties of each test,
but to make the clinician aware of common tools that could be used in clinical practice and
for research. It’s important to keep in mind that many of the constructs these scales are used
to capture are multidimensional in nature; any scale
used or developed will have limitations in capturing
all the details of the patient’s lived experience. These
tools should not be used as a substitute for history-
taking, but instead as an adjunct to it.

• Fear Avoidance Belief Questionnaire (FABQ):

The FABQ was developed by Gordon Waddell and
colleagues in 1993.28 It was used in one of the first
studies that showed very little correlation between
pain intensity and disability. The FABQ is a series
of 16 questions broken into two subgroups of
fear around physical activity (FABQ-PA) and work
(FABQ-W). The questions are answered by the patient using a 7 point Likert scale from 0
= completely disagree to 6 = completely agree. Research has shown that FABQ-PA scores
greater than 14 and FABQ-W scores greater than 34 have an increased likelihood of not
returning to work.29

Their analysis showed that the severity of pain could only explain 14% of the variance of
disability in activities of daily living. In addition, of all the biomedical measures combined it
could only explain 5% of the variance with work loss. The FABQ was much more predictive
as it could help explain 32% of the variance of disability in activities of daily living, and 28%
for work loss.29 Using this tool can give the clinician insight into potential prognosis based
on fear as a psychosocial variable.

• Pain Catastrophizing Scale (PCS): Michael Sullivan and colleagues introduced the PCS in
1995 to help facilitate research on how catastrophization influences the pain experience.30
Since then, it has been used in both clinical practice and research settings.31 The PCS is
a 13-item instrument using a 5 point Likert scale that patients rate from 0 = not at all, to 4
= all the time. The instrument questions are further broken down into three subscales of
rumination, magnification, and helplessness. A total PCS score greater than 30 represents
clinically relevant levels of catastrophization.31

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 215

• Tampa Scale of Kinesiophobia (TSK): The TSK was developed in 1991 by Miller, Kori, and
Todd to look into how kinesiophobia played into chronic pain behaviors.32,33 The original
scale had 17-items rated on a 4-point Likert scale from 1 = strongly disagree to 4 =
strongly agree. Since the original work, the scale has been adapted into a shorter 11-item
question scale (TSK-11) that has similar psychometric properties.34 The TSK has come
under scrutiny lately, as it may not be a good screening tool to predict pain and functional
outcomes following rehabilitation.35 We include it in our list since it has a long history of use
in research and in the clinic, and still has value.

• Keele STarT Back Screening Tool (SBST): The previous tools measure specific
psychological variables (fear and catastrophization), whereas the SBST measures broader
variables, or yellow flags, as potential predictors of an at-risk patient to move into chronicity
to help stratify care and improve outcomes. The SBST is a tool with 9 items. Patients
answer “agree” or “disagree” on eight questions and one question is answered with a
5-point Likert scale. Based on the number of points scored from the responses, patients
are classified into low, medium, or high risk. This classification system and then stratifying
patients into different care pathways has shown some promise in improving management
of patients and reducing overall costs.36 The SBST is similar to the Orebro Musculoskeletal
Pain Screening Questionnaire (OMPSQ), which we will discuss next, and seems to predict
functional outcomes better than the OMPSQ.37

• Orebro Musculoskeletal Pain Screening Questionnaire (OMPSQ): The OMPSQ is another

tool that serves as a broader yellow flag assessment. It aims at classifying patients into
various risk groups related to future disability. The original OMSPQ has 25 items38 and
there has also been a short version39 developed with only 10 items that show similar
predictive abilities. Patient responses are scored on a 1-100 scale with scores greater than
50 indicating higher risk for future work disability. As stated, the OMPSQ is similar to the
SBST and is potentially better at predicting pain and work outcomes.37

• Optimal Screening for Prediction of Referral and Outcome – Yellow Flags (OSPRO-
YF) The last tool that we will explore is the OSPRO-YF.40 This is a concise yellow flag
assessment tool that estimates patient scores on many of the full-length psychological
questionnaires for low mood, anxiety, fear, catastrophization, pain acceptance and others.
It comes in three forms: 17-item, 10-items, and 7-items with minimum accuracy scores
of 85%, 81%, and 75% respectively. The Academy of Orthopedic Physical Therapy has
developed a scoring portal for clinicians to evaluate patient responses. (orthopt.org/yf/) This
tool is still early in its development but shows promise as a way of synthesizing multiple
questionnaires into one quick and easy tool to use in the clinic.

216 PRINCIPLE 10 | THE IMPORTANCE OF ASSESSING FOR YELLOW FLAGS

The bottom line is that clinicians need another way to screen for yellow flags in addition to
history taking. Tools like the OMSPQ and SBST help classify a patient’s risk of disability,
potentially providing direction for the level of care that may be needed to reduce chronicity.
Both have good psychometric properties, so pick one and start using it with your patients.
Other items like FABQ, PCS, and TSK can identify psychological yellow flag variables that
are known risk factors for disability. The OSPRO-YF is a promising tool to synthesize various
patient questionnaires like the FABQ, PCS, and TSK into one short questionnaire. Again, pick
one and start using it to get a more complete understanding of each patient you treat.

10.10: Social
The patient questionnaires covered up to this point are
used to assess psychosocial factors, but the reality is,
most of the variables they assess are psychological. The
social element of the biopsychosocial model of care is
probably the least understood, because of its complexity
and the lack of studies around it.41 Social determinants
of health are some of the biggest predictors and
challenges facing our current healthcare system; those
with chronic pain are not an exception to this issue.42,43
Income inequality and the differing lifestyles of patients
have a strong influence on their overall health. As healthcare providers, each of us needs
to take an active role with individual patients, and in our communities, if we want to make
a positive impact on social and economic issues, including: socioeconomic status, early life
development, social exclusion and support, addiction, healthy food, transportation availability,
job security, and others. Conducting a thorough history and taking time to more fully
understand a patient’s condition from the biological, biomechanical, psychological and social
perspectives is vital to enhance the level of care provided. This enhanced care is provided
through empathetic listening and by assisting these individuals with resources and making
referrals to other healthcare professionals.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 217

Conclusion
The psychosocial variables, or yellow flags, a patient is affected by cannot be ignored no
matter how big a role biomedical problems play in their current condition. We treat people—
and people are biological, psychological, and social creatures; so we have to assess all aspects
of that person. This does not mean we will treat all of those areas, but we need to listen and
understand so we can adjust our treatment plans and prognosis, along with making referrals,
if needed. Listening well begins with thorough history taking. As we hear the patient’s story
we can explore each of the yellow flag
variables in more depth and use patient
report screening tools.

We’d be shortsighted to finish this

principle this way, in lieu of what we
discussed in Principle 8 and the call
to action by the late Louis Gifford.44
In Gifford’s iconic writings he often
included “pink flags” to represent the
good things patients present. Using a
stoplight as our analogy: Red means
stop; Yellow means caution; Green
means go, we opted to call these green
flags. Manual therapists, by virtue of
their clinical interaction (everything we
potentially do—Principle 1) may also “paint” yellow flags green via our interactions. Education,
even biomedical, regarding a painful low back, done in a safe clinical environment by a clinician
that really cares and exhibits exceptional skill, especially orthopedically, may in fact positively
influence a yellow “fear” flag by painting it green. It is thus argued that woven into the manual
skills, TA and clinical encounter manual therapist should not only be able to recognize yellow
flags but may in fact influence them in a positive way.

218 PRINCIPLE 10 | THE IMPORTANCE OF ASSESSING FOR YELLOW FLAGS

Principle 10 References
1. 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.
2. Lek M, Karczewski KJ, Minikel EV, et al. Analysis
of protein-coding genetic variation in 60,706
humans. Nature. 2016;536(7616):285.
3. Noë A. Out of our heads: Why you are not your
brain, and other lessons from the biology of
consciousness. Macmillan; 2009.
4. Main CJ, George SZ. Psychologically informed
practice for management of low back pain:
future directions in practice and research.
Physical therapy. 2011;91(5):820-824.
5. Vlaeyen JW, Linton SJ. Fear Avoidance and its
consequences in chronic musculoskeletal pain:
a state of the art. Pain. 2000;85(3):317-332.
6. Ulirsch JC, Weaver MA, Bortsov AV, et al. No
man is an island: Living in a disadvantaged
neighborhood influences chronic pain
development after motor vehicle collision. Pain.
2014;155(10):2116-2123.
7. Sterling M, Jull G, Kenardy J. Physical and
psychological factors maintain long-term
predictive capacity post-whiplash injury. Pain.
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8. Linton SJ. Occupational psychological factors
increase the risk for back pain: a systematic
review. Journal of occupational rehabilitation.
2001;11(1):53-66.
9. Waddell G. 1987 Volvo award in clinical
sciences. A new clinical model for the treatment
of low-back pain. Spine. 1987;12(7):632-644.
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back pain. Baillière’s clinical rheumatology.
1992;6(3):523-557.
11. Kendall N, Linton S, Main C. Guide to Assessing
Psycho-social Yellow Flags in Acute Low Back
Pain: Risk Factors for Long-Term Diability and
Work Loss. Wellington, New Zealand: Accident
Compensation corporation in the New Zealand
Guidelines Group;1997.
12. Kendall N, Linton S, Main C. Psychosocial Yellow
Flags for Acute Low Back Pain: ‘Yellow Flags’ as
an analogue to ‘Red Flags’. European Journal of
Pain. 1998;2(1):87-89.
13. Kendall N, Watson P. Identifying psychosocial
yellow flags and modifying management. Topical
issues in pain. 2000;2:131-139.
14. Watson P. Psychosocial predictors of outcome
from low back pain. Topical Issues of Pain.
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15. Watson P, Kendall N. Assessing psychosocial
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111-131.
16. Linton SJ, Halldén K. Can We Screen
for Problematic Back Pain? A Screening
Questionnaire for Predicting Outcome in Acute
and Subacute Back Pain. The Clinical journal of
pain. 1998;14(3):209-215.
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17. Moore JE. Chronic low back pain and
psychosocial issues. Phys Med Rehabil Clin N
Am. 2010;21(4):801-815.
18. Hasenbring MI, Verbunt JA. Fear-avoidance
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models of behavior and their consequences for
clinical practice. The Clinical journal of pain.
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19. Konish L. This is the real reason most Americans
file for bankruptcy. 2019; https://www.cnbc.
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americans-file-for-bankruptcy.html. Accessed
9/20/19.
20. Mercuri M, Gafni A. Medical practice variations:
what the literature tells us (or does not) about
what are warranted and unwarranted variations.
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Conquered America. Journal of the History of
Medicine and Allied Sciences. 2008;63(2):
139-177.
22. Crombez G, Vlaeyen JW, Heuts PH, Lysens R.
Pain-related fear is more disabling than pain
itself: evidence on the role of pain-related
fear in chronic back pain disability. Pain.
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23. Kroska EB. A meta-analysis of fear-avoidance
and pain intensity: The paradox of chronic pain.
Scandinavian Journal of Pain. 2016;13:43-58.
24. Hassett AL, Clauw DJ. Does psychological stress
cause chronic pain? The Psychiatric clinics of
North America. 2011;34(3):579-594.
25. Edwards RR, Dworkin RH, Sullivan MD, Turk DC,
Wasan AD. The role of psychosocial processes
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pain. The Journal of Pain. 2016;17(9):T70-T92.
26. Mee J, Sumsion T, Craik C. Mental health clients
confirm the value of occupation in building
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27. Bigos SJ, Battie MC, Spengler DM, et al. A
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 PRINCIPLE 11

Additional Treatments Complement

Manual Therapy

11.1: PNE+ ................................................................ 223

11.2: Pain Neuroscience Education ...... 226

11.3: Nutrition and Sleep Hygiene.......... 227

11.4: Breathing ....................................................... 228

11.5: Graded Motor Imagery ....................... 228

11.6: Safe, Healing Environment with

Compassion and Empathy .............. 228

11.7: Manual Therapy, Neural

Mobilization and Soft Tissue/
Trigger Point Therapy .......................... 229

11.8: Modalities ...................................................... 229

11.9: Relaxation, Meditation,

Mindfulness and Yoga ........................ 230

11.10: Exercise—Aerobic, Stabilization

and Resistance Training,
Isometrics and More ............................ 231

11.11: Aquatic Therapy....................................... 232

11.12: So What? ........................................................ 233

Conclusion...................................................................... 233

Principle 11 References ...................................... 234

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 221

One for All and All for One
Chronic pain is complex; therefore, its treatment must be complex, right? Given the myriad
of neurophysiological and psychosocial issues associated with the development and
maintenance of a chronic pain state, we must realize that the solution is unlikely to be a
singular approach or singular profession. The more complex pain becomes, the more
multimodal and multidisciplinary treatment will need to be. For the manual therapist, this
once again (see Introduction) underscores the Swiss army knife mentality which includes
adding other approaches to a clinical repertoire of manual therapy. The good news is that
there are numerous evidence-based treatments available for the manual therapist that can
help people in pain. In this section we will delve into the various potential “pain” treatments,
from a manual perspective.

Before we delve into the various additions to manual therapy, we want to explore two questions
and their respective answers:

Question 1: Can you be a manual therapist without knowing anatomy?

• This seems like a very benign question and the

answer is simple: no. Sure, an administrative
assistant can touch someone, but we’re talking
about skillful delivery of a manual treatment to
address pain and disability. Again, the answer
is, no. Knowledge of anatomy, pathoanatomy
and biomechanics is needed to carefully
position a patient with cervicogenic headaches
into a prone position with adequate cervical
rotation to expose the upper cervical spine
joints for treatment. Prior to this technique, a
series of screening tests (with adequate and
much needed knowledge) is performed to
enhance safety and determine the appropriate
technique. Anatomy thus has its place. Manual therapists, by virtue of their craft, are
experts in this area—well done and don’t give it up or neglect it.

222 PRINCIPLE 11 | ADDITIONAL TREATMENTS COMPLEMENT MANUAL THERAPY

Question 2: Can you help someone in pain, especially chronic pain, without
knowing anatomy?

• The answer? An overwhelming…YES! Many non-manual therapy trained clinicians help

tens of thousands of people with pain daily, without the use of anatomical knowledge. The
reality is that we can enhance a person’s life (without the use of touch) by teaching them
skills like mindfulness, how to set goals, breathing exercises, sleep hygiene, nutritional
counseling, etc. Anatomy has a time and a place, likely more important in nociceptive
based clinical presentations (be it acute, sub-acute or chronic), but perhaps not in the
more sensitized patient population. Again, this points to the shift—as pain mechanisms
shift and various biological and physiological processes unfold, the importance of
anatomical findings becomes less relevant. What does this mean? Simply that there are so
many other non-manual ways to help people presenting with pain in our clinics and, once
again, the open-minded modern manual therapist stands to benefit from broadening their
horizons, while the close-minded traditional manual therapists are doing themselves and
their patients a major disservice.

The discussion that follows is exactly that: How can manual therapists embrace other non-
manual treatments to help patients?

11.1: PNE+
There is a lack of convincing evidence for the
usefulness of education in musculoskeletal
conditions as a standalone intervention.1-4
This also applies to PNE, which has been
increasingly used by manual therapists
as a means to teach people about pain.5-
7
Various systematic reviews show that
education, by itself, is not as powerful
as when it is combined with physical
treatments, especially movement-based
treatments including exercise and manual
therapy.5-7 This has led to the evolution of
the PNE+ concept for chronic pain—PNE plus the addition of “other” (especially movement-
based) treatments. The critical part: PNE evidence is now beginning to point to the idea that
it facilitates or enhances movement, which is what provides the shift in pain and function.8,9
A good analogy is to think of PNE as a primer, versus a primary treatment. For example,
in a recent RCT, PNE plus exercise was compared to exercise only and the graphs clearly
show PNE resulting in no meaningful shift by itself, but when added to exercise, it enhances
the efficacy of the movement approach.8,9 PNE thus, in essence, prepares (i.e., decreased
fear-avoidance, decreased pain catastrophization and fostering healthy beliefs regarding pain)
people to move more, which is likely the critical element in their recovery.10

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 223

Changes in pain disability
Interaction effect: P<.001
60
education exercise follow-up
50

40

30
NS
20
P=.04 P=.01 P=.01 Control Group
10
PNE+ Group
0
Baseline Post Education 3 months 6 months 12 months

Figure 11.1: Changes in pain disability over time between PNE+ and a biomedical control group

Changes in pain vigilance & awareness

Interaction effect: P<.001
50
education exercise follow-up
40
NS P=.001 P=.005 P=.01 Control Group
30

PNE+ Group
20

10

0
Baseline Post Education 3 months 6 months 12 months

Figure 11.2: Changes in pain vigilance and awareness over time between PNE+ and a biomedical control group

From a manual therapy perspective, PNE+ studies have been conducted with the addition
of spinal mobilization and manipulation,11 and soft tissue massage,11 as well as muscle and
neural tissue mobilization.11,12 Additionally (within current manual therapy approaches),
PNE+ has also been combined with trunk and neck stabilization approaches,11-14 as well as
dry needling.15

224 PRINCIPLE 11 | ADDITIONAL TREATMENTS COMPLEMENT MANUAL THERAPY

PNE+ is also important when considering the opioid epidemic as it relates to chronic pain.
The current opioid epidemic prompts healthcare providers, including manual therapists, to
ask, “What do we do?” Various PNE+ treatments, including manual therapy,16-18 have been
studied extensively for their ability to turn on
the non-pharmacological, naturally occurring

PNE+
endogenous systems, thus decreasing the need
for pharmaceutical delivery of opioids. The body of
evidence in favor of the PNE+ approach versus the
current use of opioids is impressive. Additionally,
it can provide significant benefit with little to no
side effects. Below is a listing of various PNE+
treatments that have been shown to help enhance
naturally occurring endogenous mechanisms,
which can as part of the PNE+ program be used
to replace the need for pharmaceutical delivery
of opioids:

• PNE19-21 • Aerobic exercise49-52

• Nutrition22-25 • Humor53-55

• Breathing26-28 • Aquatic therapy56,57

• Biofeedback29-31 • Social interaction58-60

• Graded motor imagery32-34 • Coping skills61-63

• Safe, healing environment with • Sleep hygiene64-66

compassion and empathy35-37
• Soft tissue/trigger point therapy67-69
• Manual therapy16-18
• Stabilization and resistance training70-73
• Neural mobilization 38-40

• Journaling74-76
• Modalities41-43
• Stretches, movement and body
• Yoga44-46 awareness77,78

• Relaxation and meditation27,47,48 • Posture and position of power

and confidence79,80

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 225

By no means is this list complete, but it provides overwhelming
evidence that various, currently available, non-pharmacological
treatments can help with pain. Many of these can be (i) used
by a manual therapist or (ii) be seen from a manual therapy
perspective. If we use the PNE+ list as a starting point, we have
a multimodal treatment plan that includes manual therapy. The
new-age, biopsychosocial manual therapist (makes for a big name tag) may look at this list
and see manual treatments as part of this approach including manual therapy,16-18 neural
mobilization,38-40 soft tissue and trigger point therapy,67-69 thus once again underscoring the
overall premise of the book that pain science and manual therapy are not mutually exclusive.
The PNE+ model clearly shows how manual therapists need to expand their horizons and
explore other additional potential treatments alongside manual therapy including sleep
hygiene, yoga, nutrition, etc. Also note how overarching themes, already covered, play a role
in modulating pain including safe, healing and welcoming environments.35-37 PNE+ has been
explained extensively in the PNE textbook by Louw, et al., and readers wanting more in-depth
information of each of the PNE+ treatments are referred to that text.81 What follows is a short
review of some of the PNE+ treatments along with some clinical thoughts and pearls in the
context of this book’s main theme: Blending pain science and manual therapy.

11.2: Pain Neuroscience Education

If PNE didn’t exist, neither would the controversy around whether pain science should be
“hands-on” or “hands-off,” and this book would not be needed. PNE as a cognitive (educational)
intervention puts into question the need for hands-on treatment. At this point of the book, we
believe we have clearly demonstrated PNE and hands-on treatments can and should coexist.
In fact, just view Principle 11.1, showcasing the efficacy of PNE combined with movement
(exercise). Principle 1 showed how PNE, by positively influencing pain catastrophization and
fear-avoidance, in essence dampens the sensitivity of the nervous system, thus allowing a
“window” for graded touch, i.e., manual therapy. This notion is underscored with the current
idea that PNE by itself, is not that powerful when used as a treatment to alter pain and
disability, but prepares (along with
motivational interviewing) a patient
for the all-important movement part,
be it active (exercise) or passive
(manual therapy) or a combination
of both. This blend, however,
requires manual therapists to clean
their “manual language” to avoid
biomechanical and biomedical
descriptions of manual therapy, but
rather describe manual therapy as
a means of facilitating movement
versus “fixing” something.

226 PRINCIPLE 11 | ADDITIONAL TREATMENTS COMPLEMENT MANUAL THERAPY

11.3: Nutrition and Sleep Hygiene
Nutrition and sleep hygiene are best viewed as “add-ons” for the manual therapist. This can
be accomplished by referral to a specialist, i.e., licensed dietician, or with knowledge and
skills acquired by the manual therapist. While working with a patient, the therapist may want
to spend some time discussing nutrition and providing information and advice or reviewing
a sleep hygiene program. This would definitely be the case for the manual therapist who
has special knowledge or training in the various add-on approaches. For example, studies
have shown magnesium plays a role in neuropathic pain82 and a manual therapist treating a
patient with carpal tunnel syndrome may choose to cover all the necessary PNE, along with
manual treatments, stretches and a home exercise program, in addition to discussing optimal
magnesium intake in the patient’s diet.

Many people in pain have poor sleeping habits. How do we “correct”

sleep? We return to good sleep habits with a sleep hygiene program. A
patient is taught the various aspects of healthy sleep habits (and why
they’re important) and then systematically, over a period of time, works
to adopt them. This leads to a healthy sleep pattern or, if not, may
indicate the need for further medical testing to determine if there are
other issues (e.g., sleep apnea). When a manual therapist is treating
headaches, sleep hygiene is an important factor since the brain does
the majority of its “housekeeping” at night (chemically-speaking),83,84 and if treatment is “only”
focused on manual treatment, a key factor is ignored, especially in tension-type headaches
and migraines.84 What do MIT (Massachusetts Institute of Technology) rats dream of at night?
Running on an exercise wheel.85 Motor patterns (movement patterns) are solidified during
sleep, which is why sleep and athletic performance is correlated.86,87 A manual therapist spends
countless hours during patient visits focusing on motor control exercises with (and without)
manual therapy to optimize movement. Yet, they may spend little to no time addressing sleep
hygiene, which plays a major role in solidifying these patterns.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 227

11.4: Breathing
How many times have you seen a patient hold their breath while exercising and had to remind
them to….breathe! How often have you worked “with” breathing when performing a thoracic
spinal manipulation: “Breathe in; breathe out and….thrust.”88 Breathing is an important
element of manual treatments. By itself, we know breathing is incredibly important when it
comes to pain as it helps with stress reduction, sympathetic and parasympathetic function,
etc. As an add-on, manual therapists may wish to teach patients simple breathing strategies
to ease pain and facilitate relaxation.

11.5: Graded Motor Imagery

GMI is described in detail in Principle 7. Once again,
one of the key tenants for the blend of manual therapy
and pain science are the potential “neuroplastic”
changes that can be positively influenced via tactile stimulation and/or discrimination, i.e.,
manual therapy. From imagined movements (motor imagery) to sensory discrimination and
localization, various options may help the modern manual therapist to change manual therapy
from a passive to a more active assisted (from a brain perspective at least) treatment.

11.6: Safe, Healing Environment with Compassion

and Empathy
A precaution to manual treatment, even contraindication in some cases, is patient safety. This
is not just biomedically speaking, i.e., vertebrobasilar insufficiency, but also psychosocial,
i.e., abuse. Clinical environments must be safe from the moment a patient enters the clinic,
starting with the paperwork that includes personal information that the patient is sharing. This
continues with the interview, to the physical examination and treatment. As described in earlier
sections, oxytocin is a powerful chemical released during touch and strengthens bonds. In
fact, it could be argued manual therapists may empower closer bonding with patients than
non-manually trained clinicians. This beautiful blend of talking to a patient, touching a patient
skillfully and creating a safe, healing environment powerfully influences pain.

228 PRINCIPLE 11 | ADDITIONAL TREATMENTS COMPLEMENT MANUAL THERAPY

11.7: Manual Therapy, Neural Mobilization and
Soft Tissue/Trigger Point Therapy
Need we say more? Review Principle 1 and the various
mechanisms behind manual treatment in modulating
a pain experience. These treatments can be used in
isolation (single high-velocity cervical thrust to easy pain
and asymmetry in movement), or in combination (neck
mobilization with added neural mobilization or soft
tissue/trigger point therapy).

11.8: Modalities
Gate Control is more than 50 years old and new concepts of the pain neuromatrix, the interplay
between the neural and immune systems, and neuroplasticity, etc., push us to new frontiers
in pain, but the theory still has validity. Altering nociception can (and usually does) alter a pain
experience, so yes, modalities that primarily alter nociception (bottom-up approach) can also be
considered. For example, in the sports medicine world a current controversy is “itis,” referring
to the notion that tendinitis may not truly be an inflammatory issue and thus not truly an “itis,”
questioning the use of cryotherapy (ice). Neurophysiologically speaking, however, it is well
established that C-fiber activity into the dorsal horn can be modulated by applying ice to an
injured area.89 It can be argued that modulation of the C-fibers (barrage into the CNS) may play
a significant role in the development and maintenance of a pain experience.90,91 How does this
apply to the manual therapist? Clinically it may actually be quite advantageous to use “cooling”
alongside with manual therapy to ease pain. In this scenario, manual treatment of an area is
interspersed with 30-90 seconds of ice application. For example: a cervicogenic headache
whereby mobilization to the upper cervical spine is interspersed with ice massage to the upper
cervical spine/occipital region to decrease afferent barrages into the CNS. On the other end of
the spectrum, hot moist heat has been shown to be effective in treating pain, sometimes even
more so than some common over-the-counter pain medicines.92 In psychology it is now well
understood that patients remember two events during a clinical encounter with a patient—a
“peak” event (i.e., pushing a knee to get optimal range of motion) and the last thing they do, which
may include a “relaxing” modality after some manual
treatment, for example some electrical stimulation with or
without heat or cold on an affected area. Yes, we get it,
on the whole therapeutic modalities have limited efficacy
(as do most treatments by themselves). Consider the fact
that a modern manual therapist may clinically reason the
cost/benefit and risk/benefit of these interventions in
comparison to other treatments. They will then consider
the patient’s beliefs, the context of the situation, and a
proper explanation of the effects and efficacy of the
modality and find there may be benefit to using them
when treating the patient’s pain. Therefore, a skilled blend
of manual treatment and modalities may be more powerful
than each of them as a stand-alone treatment.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 229

11.9: Relaxation, Meditation, Mindfulness and Yoga
There are plenty of books (and even whole sections) in bookstores and libraries dedicated
to each of these topics. Because stress and pain go hand-in-hand, it’s extremely important
that today’s manual therapist have the knowledge, skillset and resources to teach patients
about relaxation, meditation, mindfulness and yoga and/or refer them to other specialists,
when necessary. A manual therapist may choose to add these techniques to his/her clinical
repertoire, combined with manual therapy, or refer the patient to a colleague or another
specialist for further assistance.

Relaxation styles, approaches to therapy, and schools of thought are varied. However, there
is growing evidence that using multiple relaxation techniques can produce positive changes
in many individuals, including those with chronic conditions.93-98 Therapists might explore
various strategies with their patients, being sure to make it as uncomplicated as possible.99,100

Meditation is a practice where an individual operates, trains the mind, or induces a mode of
consciousness to allow the mind to engage in peaceful thoughts.93,101 Meditation is often used
to clear the mind, reduce stress, promote relaxation or train the mind.48,101-103 In addition to
relaxation exercises, mindfulness, yoga, tai chi, etc., there is growing interest in meditation.
With numerous different philosophies and approaches, there are not only individual book
titles, but complete aisles of books dedicated to each of these topics.

Mindfulness is often clumped together with relaxation and meditation. This psychological
process of bringing one’s attention to the internal and external experiences occurring in the
present moment can be developed through the practice of meditation and other training.27,47,94,104
The term “mindfulness” is a translation of the Pali term “sati,” which is a significant element
of some Buddhist traditions. There is an increasing interest in, and evidence for, the use of
mindfulness for people with chronic pain.94,104

230 PRINCIPLE 11 | ADDITIONAL TREATMENTS COMPLEMENT MANUAL THERAPY

11.10: Exercise—Aerobic, Stabilization and Resistance
Training, Isometrics and More…
It could be argued that the most common multimodal add-on
to manual therapy is some form of exercise. Principle 1 showed
how manual techniques result in immediate motor control and
muscle recruitment patterns in people with pain. In almost all
current best-evidence guidelines for musculoskeletal pain,
exercise is at the top, as it should be. Movement is the biggest
pain killer on earth, and when it’s performed by the patient
(locus of control): Double win! Aerobic exercise powerfully
engages the endogenous mechanisms. For example, a
6-mile run produces 6 milligrams of morphine in the brain!105
Where does that leave people who cannot move that much?
Recent studies have shown that isometric exercises produce
not only a local (where the contraction is being done), but
remote and centrally acting endogenous effect.52,106 Yes, you
heard correct: A person with knee pain may actually experience less knee pain (during a
treatment) while doing isometric contractions of a hand grip dynamometer with their hand—
how neat! What about doing isometrics during manual treatments? As for spinal stabilization,
current evidence is lacking, but what about patient perceptions? How many patients come
in believing the cause of their back pain is their “core” and if you were to teach them some
“core” exercises they believe they would get better? Combining some of the evidence for the
efficacy of exercising trunk stabilizers with patient (and clinician) beliefs may be advantageous.
(Once again, we are compelled to highlight that such “stabilization” exercises must be framed
correctly and not drive fear or increase thoughts of vulnerability). In various chronic pain
states, resistance exercises have been shown to help reduce pain and improve disability.107,108
There’s more: Stretches, along with body awareness, have been shown to enhance the
endogenous opioids,77,78 which again, is part of most day-to-day treatments performed by
manual therapists. How many manual therapists add stretches and body awareness/postural
“correction” strategies at the end of a session as part of the session and/or home exercise
program? Again, the aim is not to provide a full dissertation of exercise and pain (it’s been
done) but8 remind readers of the importance of this common treatment performed by manual
therapists with or without manual therapy.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 231

11.11: Aquatic Therapy
No, we do not think manual therapists should buy wetsuits, snorkels and flippers to do manual
therapy—unless they want to! There is evidence that aquatic therapy can be useful for patients
with chronic pain such as fibromyalgia.109,110 In recent PNE studies, PNE has been successfully
combined with aquatic therapy.111 Just like most of the other movement-based approaches,
aquatic therapy has shown an ability to turn on the various endogenous mechanisms.56,57
The warmth of the water and the buoyancy helps patients move more than they might be
able to on land. This freedom to move allows for increased blood flow and oxygen and, from
a larger neuroscience perspective, allows healthy stimulation and mapping of body parts
in the somatosensory and motor homunculi. Specific to the treatment followed during the
aquatic therapy session, therapists are encouraged to follow the exercise principles already
discussed, including focusing on cardiovascular exercise, conditioning (resistance) exercise
versus strength, and general stabilization. As with the land-based exercises, therapists should
be careful about the way they explain the approach, e.g., not doing “strengthening” exercises
in the pool, which implies weakness. What about manual therapy? Yes, clinicians may choose
to jump in the water and help mobilize stiff joints, thus taking advantage of the buoyancy and
warmth, or (as with many of the PNE+ treatments), be added to a manual therapy regimen.

232 PRINCIPLE 11 | ADDITIONAL TREATMENTS COMPLEMENT MANUAL THERAPY

11.12: So What?
What does all of this mean? In order to truly be a manual therapist who follows the
biopsychosocial model, a broader perspective (and treatment plan) is needed, especially
for chronic pain, which is offered above. Yes, a manual therapist may choose to “only” do
manual therapy, but this is not the norm—it’s usually blended with other treatments, many of
which positively influence pain, disability, fear-avoidance, pain catastrophization, etc., thus in
essence…blending pain science and manual therapy.

Conclusion
The struggles clinicians face when treating persistent pain are well documented (see
Introduction). In many cases clinicians will report “they don’t know what to do” with people
struggling with persistent pain. Principle 11 showcases a series of non-manual treatments that
may be used to help people in pain, especially persistent pain. If we add the various “manual”
treatments into this, including mobilization, manipulation, soft tissue treatments, graded motor
imagery and neurodynamics, we are left with increasing options to help people in pain. This
principle showcases how the modern manual therapist must look beyond the technique in
front of them (manual therapy) as the sole treatment of choice, especially when it comes to
persistent pain. The critical element would be to determine who needs manual therapy and if
they do, when, how strong and how much? This we further explore in Principle 12.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 233

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107. Brosseau L, Wells GA, Tugwell P, et al. Ottawa
Panel Evidence-Based Clinical Practice
Guidelines for Aerobic Fitness Exercises in the
Management of Fibromyalgia: Part 1. Physical
therapy. 2008/07/01/ 2008;88(7):857-871.
108. Valkeinen H, Hakkinen A, Alen M, Hannonen
P, Kukkonen-Harjula K, Hakkinen K. Physical
Fitness in Postmenopausal Women with
Fibromyalgia. Int J Sports Med. Oct 24 2007.
109. Evcik D, Yigit I, Pusak H, Kavuncu V.
Effectiveness of aquatic therapy in the treatment
of fibromyalgia syndrome: a randomized
controlled open study. Rheumatol Int. Jul
2008;28(9):885-890.
110. Louw A, Puentedura EL, Mintken P. Use of an
abbreviated neuroscience education approach
in the treatment of chronic low back pain:
a case report. Physiother Theory Pract. Jan
2012;28(1):50-62.
111. Pires D, Cruz EB, Caeiro C. Aquatic exercise and
pain neurophysiology education versus aquatic
exercise alone for patients with chronic low back
pain: a randomized controlled trial. Clin Rehabil.
Jun 2015;29(6):538-547.
 PRINCIPLE 12

Putting More Thought

into Treatment Choices

12.1: Evidence Based Practice .................. 240

12.2: Subgrouping Patients .......................... 243

12.3: “Chronic” Pain .......................................... 247

12.4: Psychosocial Risk Factors ............... 249

12.5: Chronic Nociceptive-

Dominant Pain .......................................... 251

12.6: Neuroplasticity .......................................... 252

12.7: Who Does Not Need

Manual Therapy? ..................................... 253

12.8: The Big Picture…and

Manual Therapy ....................................... 258

Conclusion...................................................................... 258

Principle 12 References ...................................... 259

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 239

Right Treatment, Right Time,
Right Patient
Our overall goal in showing you how pain science and manual therapy approaches can and
should coexist culminates with Principle 12: Who needs manual therapy? Who needs pain
science? Who needs a blend of the two? How much of each do they need?

12.1: Evidence Based Practice

In recent years, there has been a lot of interest and discussion surrounding
the notion of subgrouping patients, especially those with LBP.1 As rates
of disability associated with LBP increased over the last decade, so too,
has the number of potential treatments.2,3 Quick searches on PubMed,
“Dr. Google” and “Professor Wikipedia” result in a plethora of potential
treatments for LBP:

• Acupuncture • Feldenkrais • Nerve blocks

• Alexander technique • Facet blocks and • Ointments
denervation
• Anthroposophic medicine • Pilates
• Fusion
• Back school • Relaxation techniques
• Healing
• Balneotherapy • Spa treatment
• Herbal medicine
• Bed Rest • Stabilization
• Holistic therapy
• Behavioral therapy • Stretching
• Homeopathy
• Body awareness therapy • Surgery
• Hydrotherapy
• Biofeedback • Taping
• Injections
• Cardiovascular fitness • Therapeutic conversation
training • Ionic modulation
• Thermotherapy
• Cervical Collar • Iontophoresis
• Traction
• Connective tissue • Laser therapy
• TENS – high & low
massage
• Magnet therapy frequency
• Craniosacral therapy
• Manipulation • Trigger point dry needling
• Cupping
• Massage • Trigger point injection
• Diet
• Medication • Ultrasound
• Disc injections
• Meditation • Vibration
• Electrotherapy
• Mobilization • Yoga
• Epidural anesthesia
• Moxibustion • Zone therapy
• Exercise
• Multimodal rehabilitation

240 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

 Guru RCT
Expert Systematic
Clinician Review
Pioneers Scientist

So, which one’s work? Surely, disciples of each approach would say theirs is best, to the
exclusion of other approaches. By the way, how do we (did we) know treatments work?
Until the advent of Evidence Based Medicine (EBM), results were mainly based on personal
observations (which included significant bias). In addition, as more and more money was
increasingly being spent on healthcare, various stakeholders (government, industries,
employers, third-party payers, etc.) demanded more from treatments, including “proof” that
they worked. This shift occurred in medicine (including manual therapy) in the mid 1990s.4,5
In manual therapy, to that point, treatments and treatment choices were made primarily based
on the education the clinician had received; their own personal experience; teachings by their
“guru,” etc. Now, with the advent of EBM, and the need to prove the effectiveness of particular
treatments before choosing to use them, the pendulum has shifted towards EBM, including
adopting the EBM pyramid of hierarchy of evidence. Now, defending treatment choices
resembled “poker-style” betting with clinicians facing off: “I see your systematic review, but
raise you a meta-analysis,” inferring their choice was superior.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 241

Another problematic issue caused by the introduction of EBM was that clinicians began to
perceive the value of an intervention based only on published research. Suddenly, treatments
which had been successfully used for decades were deemed ineffective and “did not work”
if no published evidence existed. Although this may seem ridiculous, it illustrates how our
society often makes extreme shifts in one direction or the other, including in our beliefs about
which patient treatments should be used. Surely, treatments “worked,” but the advent of EBM
identified that more research investigating efficacy was needed, attracting both critics and
proponents to either side of the EBM discussion. On the clinical side, it is now well established
and understood that EBM includes at minimum three key elements: latest scientific evidence,
patient expectations and clinical experience.6 On the flipside, EBM did usher in a new era of
unprecedented research that fueled the development and growth of different professions while
showing the efficacy of various non-pharmacological, evidence-based treatments, including
manual therapy. So, what is the evidence for treating LBP or neck pain, which constitute
nearly two-thirds of all outpatient PT visits?
Table 12.1: Various current evidence-based recommendations for treating low back and
neck pain

LBP* Neck Pain*

• Motor control exercise7 • Acupuncture18

• Therapeutic aquatic exercise8 • Manual therapy19-22

• Massage, especially when combined with exercises • Exercise19,22,23

and education.9
• Traction24,25
• Exercise programs starting four to six weeks post-surgery 10

• Posture23
• Acute or sub-acute LBP, intensive patient education 11

• Nothing helps;
• Moderate evidence that lumbar supports help12 More research is
needed24,26-31
• Traction as a single treatment for LBP is probably not
effective13

• A subgroup of patients likely to benefit from mechanical

traction may exist14

• It appears that patients with low back pain likely to

respond to manipulation can be accurately identified
before treatment15

• Manipulative treatment with stabilizing exercises16

• Lumbar mobilization17

*These listings constantly change and are updated based on research and what is shown here highlights
efficacy (based on high-RCTs, systematic reviews and/or meta-analyses) for treatment and is not an updated-
authoritative listing of evidence.

242 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

An unfortunate side effect of EBM was the devaluing of patient experiences and treatment
choices being boiled down to averages of averages, thus losing out on the individual needs
of each patient based on their clinical presentation. In the early 2000s, an exciting line of
research, born out of EBM, emerged which soon had proponents on either side of the fence:
Clinical Prediction Rules (CPRs) and subgrouping of patients.

12.2: Subgrouping Patients

It all started with a simple, logical idea: If 100 patients with LBP visited a clinic and all of
them received the same treatment, e.g., a lumbar spine manipulation technique, surely some
would benefit, while others would not. Similarly, some may get better with a treatment focused
on spinal stabilization exercises or lumbar traction. What if we could predict ahead of time
who would benefit from spinal manipulation, stabilization, traction or any other treatment?
This thought process was in direct contrast to EBM which tended to group large numbers
of patients together and assumed patient samples of LBP were entirely homogenous. The
evolution of the CPRs and subgrouping is best described by Childs and Flynn: “Using broad
inclusion criteria results in a heterogeneous sample that may include many patients for whom
no benefit is expected, thus masking the intervention’s true value.”32

Stabilization Directional
Preference

Manipulation Traction

Red Flags Yellow Flags

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 243

As tools to assist in the decision-making process, improve diagnostic accuracy and predict
outcomes, CPRs are not unique to PT. In fact, CPRs are used extensively in the medical
community for accuracy in diagnosing ankle fractures33 and cervical radiculopathy,34 to help
predict the likelihood of death from coronary heart disease,35 and to determine when to order
cervical radiographs.36 From the discussion of subgrouping and the idea that some patients
needed certain treatments and others not, including the emergence of screening for red
flags (no treatment; refer out), and the presence of psychosocial yellow flags, a new model of
subgrouping for LBP emerged over the next few years.1 In a CPR study, a group of patients
all receive the same treatment which, based on selected criteria, is either deemed a success
or a failure after the application of the treatment. Statistical analysis is then used to determine
which characteristics the success group has in common and, basically, if a certain number of
these are present, what the predicted success would be. In manual therapy, the first (and likely
most influential CPR), was developed by Flynn and colleagues in 2002.15 In this study, testing
the delivery of a lumbopelvic manipulation to patients presenting with LBP, they showed that
five predictors were associated with success: Duration of LBP 16 days or less; no symptoms
distal the knee; a fear-avoidance beliefs questionnaire (FABQ) subscale for work of 18 or less;
at least one hip internal rotation more than 35 degrees in prone and hypomobility at one or
more of the lumbar levels.15 Soon after the development of the lumbopelvic manipulation CPR,
Childs and colleagues validated the rule, thus strengthening the argument for subgrouping.37
In the cervical spine, authors also alluded to the notion of subgrouping. For example, Jull
and her research team in Queensland firmly believed that neck pain should be classified
as either idiopathic or whiplash-associated, since the mechanisms, clinical presentation and
accompanying psychosocial variables are very different.38 Additionally, if we subdivide neck
pain into additional categories such as radicular and non-radicular; presence of headaches
vs. no headaches; and if headaches are present, is it cervicogenic, a tension-type or migraine,
it is easy to see that neck pain also constitutes a huge subgrouping.39 Again, in line with
this reasoning, a CPR for neck pain was developed by Cleland and colleagues in 2007.40 In
this CPR study, it was shown that patients with neck pain responded favorably to a series of
thoracic manipulations if they had the following predictors: Duration of symptoms 30 days or
less; symptoms not distal to the shoulder; looking up does not aggravate symptoms; FABQ
physical activity subscale below 11; decreased upper thoracic (T3-T5) kyphosis and cervical
extension ROM less than 30 degrees. Even though the subsequent validation study did not
succeed in confirming the rule for thoracic manipulation for neck pain, the body of work
furthered the notion of subgrouping.

In the meantime, Puentedura and colleagues developed a CPR for neck manipulation affecting
neck pain,41 indicating positive outcomes predicted by: Duration of symptoms 38 days or
less; positive expectation that neck manipulation will help; difference in cervical rotation
ROM to either side at least 10 degrees and pain with a spring (posterior-anterior) testing
of the middle cervical spine. No specific CPR has been developed for thoracic pain. So,
what does all of this mean? Remember, our goal is to be able to better answer the question,
“Who needs what type of manual therapy intervention, when considered from a pain science
perspective?” Based on the CPR research related to manual therapy, we can start developing
some broad generalizations:

244 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

 Lumbar Spine Manipulation
for LBP
• Pain < 16 days
An argument can be made
that manual therapy is
Thoracic Spine Manipulation definitely indicated in
for Neck Pain acute and sub-acute
• Pain < 30 days spinal pain

Cervical Spine Manipulation

for Neck Pain
• Pain < 30 days

An argument can be made

Lumbar Spine Manipulation certain psychosocial
for LBP factors may indicate
• Low FABQ-WS a positive outcome for
manual therapy:
- Low fear-avoidance
- Positive expectation
Thoracic Spine Manipulation
for Neck Pain
• Low FABQ-WS
An argument can be made
certain psychosocial
factors may indicate a
Cervical Spine Manipulation negative outcome for
for Neck Pain manual therapy:
- High fear-avoidance
• Positive expectation - Negative expectation

Additionally, reviewing the various manual therapy CPRs and the growing body of evidence
pertaining to psychosocial risk factors such as fear avoidance and pain catastrophization,
additional decisions pertaining to psychosocial risk factors can be made as well:

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 245

This includes the current interest in tools such as the Keele STarT Back Screening Tool (Keele
SBST). The Keele SBST is a 9-item questionnaire that contains questions that are established
predictors for disabling LBP. Each item is answered with ‘‘agree’’ or ‘‘disagree,’’ except the
bothersome item which uses a Likert scale of ‘‘not at all’’ to ‘‘extremely.’’ The overall score is
used to separate patients into low and medium risk subgroups. The distress subscale is used
to separate medium risk subgroup into medium and high risk. It is used to identify potential
‘‘at-risk’’ patients for potential long-term chronic problems.42 These patients need careful
assessment and intervention with suitable cognitive and behavioral strategies.43

Using this information, we can develop a process of identifying patients who might respond
favorably to manual therapy (green = go; red = stop; and yellow = caution).

Interview / Clinical Reasoning

Identify time Identify psychosocial

phase of pain risk factors

Acute Chronic Low Medium High

Risk Risk Risk

Figure 12.1: Potential algorithm for hands-on manual therapy choices based on duration of pain and
psychosocial risk factors

246 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

12.3: “Chronic” Pain
The next question is whether or not we should apply manual treatments to patients with chronic
pain. Traditionalists would argue “yes” (we’ve been doing it for years), while pain science-influenced
clinicians would say “no” due to the following issues: patients becoming dependent on manual
therapy (locus of control); high probability of sudden and unpredicted increase of symptoms (flare);
chronic pain being “far more complex than just issues in the tissues”; lack of evidence and more.
The term chronic pain, however, gives us little information about the underlying pain mechanisms
and only describes pain in terms of its duration. In Principle 3, we discuss various pain mechanisms
and it’s now commonly taught that pain mechanisms can be divided into nociceptive dominant,
peripheral neurogenic dominant or CS (nociplastic) dominant.44-49 In Principle 3, we showed that if
patients meet certain clusters of signs and symptoms, they are more likely to fit into one of these three
categories, which should drive the treatment decision, including the choice of manual therapy, versus
the ubiquitous term “chronic pain.” In nociceptive dominant pain mechanisms, it is easy to make the
case for manual therapy, since the patterns are very tissue-specific and fit clinical patterns associated
with manual therapy.49 In peripheral neurogenic pain mechanisms, manual therapy is often used.
First, in neurodynamic interventions, the physical handling of a sensitized nervous system, actively
and passively, is part of the history of manual therapy (see Introduction) and is slowly but surely gaining
evidence for its use, especially in neurogenic pain states.50 Second, in neurodynamic approaches a
lot of emphasis is placed on creating adequate space for the neuromeningeal structures, essentially
creating healthy “containers” for movement.51,52 Manual techniques such as cervical spine lateral glides
are shown to be beneficial for neck pain, radiculopathy and upper extremity pain.53-55 Neurogenic
pain states, however, include potential significant pain experiences, e.g., acute radiculopathy which is
often non-responsive to pharmacological interventions, which implies caution with aggressive manual
treatments. The final category of CS (nociplastic) is often associated with very little, or no “hands-on,”
given the pain mechanisms, presence of allodynia, potential “flare,” locus of control, etc.56 If we agree
that in CS hands-on treatment (directed at a specific mechanical issue) should not be the first choice,
or potentially not a choice at all, until the question of “who needs manual therapy” model can be more
clearly studied for patients with central sensitized pain states.

Interview / Clinical Reasoning

Identify Identify time Identify psychosocial

mechanism phase of pain risk factors

Nociceptive Neuropathic Central Acute Chronic Low

sensitization Medium High
Risk Risk Risk

Figure 12.2: Expansion of the proposed algorithm of manual therapy selection by adding pain mechanisms

This model provides guidance for therapists deciding whether or not to include manual
therapy treatment:
• Green: manual therapy, including high velocity, is a go
• Yellow: manual therapy can be done, but with caution
• Red: concern and potential “no” for manual therapy

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 247

At this point, we recognize the fact that many readers may disagree with this, especially since
they may have some very strong beliefs about manual therapy. By no means are we suggesting
this categorization is definitive or final. What we are suggesting is that a more comprehensive
reasoning process needs to occur when determining whether or not a patient needs manual
therapy. In addition to traditional indications for manual therapy, the clinician must consider
hypothesized pain mechanisms as well as other interacting biopsychosocial factors in treatment
planning. The good news? We’re not done yet, and it gets more complicated (and interesting).
For example, what if we can “shift” an allodynic pain state, which is often associated with
CS (nociplastic), to become less sensitive and, in essence, allow for a manual approach?56
In Principle 1 (mechanisms of manual therapy), we highlighted a paper discussing this very
notion, pertaining to PNE. There is a growing body of evidence, including studies utilizing
PPT measurements, neurodynamic tests and fMRI, which have indicated the ability of PNE
to positively influence a hypervigilant nervous system.57-62 If this is the case, it highlights two
key issues. One: Pain science and manual therapy can and should coexist. Two: Designating
CS as “red” (i.e., not to proceed with manual therapy) may not be entirely accurate. In some
patients with a CS dominant pain state (red), we can shift them to less sensitive, thus some are
more…“yellow” (i.e., proceed with caution). Perhaps it is time to update our emerging model,
showing that some patients with CS may in fact become candidates for a manual approach?
Within this model it can be argued that graded mobilization (i.e., Maitland) may in fact be
a case of graded exposure, which would be appropriate.56 Within this model it can then be
argued that graded mobilization, i.e., Maitland,63 may in fact be a case of graded exposure to
manual treatment, which may be appropriate.

Interview / Clinical Reasoning

Identify Identify time Identify psychosocial

mechanism phase of pain risk factors

Nociceptive Neuropathic Central Acute Chronic Low

sensitization Medium High
Risk Risk Risk

Figure 12.3: Adaptation of the proposed algorithm after strategies aimed at dampening the sensitivity of the
nervous system

248 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

12.4: Psychosocial Risk Factors
Since we’ve decided to revisit the model that determines who needs manual therapy, we might
as well explore the potential to shift other categories as well. In the psychosocial category,
screening tools such as the FABQ, TSK, PCS and the Keele SBST are increasingly used to
screen for patients at high risk for developing chronicity:

• FABQ: Presence of avoidance behavior is associated with increased risk of prolonged

disability and work loss. It is proposed that FABQ-PA >14 and FABQ-W scores >34 and
are associated with a higher likelihood of not returning to work.64,65

• PCS: The PCS utilizes a 13-item, 5-point Likert scale with higher scores indicating elevated
levels of catastrophizing. Previous studies utilizing the PCS have shown a median score of
18; that of healthy individuals and in patients with pain the PCS is generally higher, with a
score over 30 reported as a high level of pain catastrophization.66

• TSK: The TSK measures a person’s pain-related fear of movement and (re)injury with
total scores ranging from 17 to 68, and higher scores indicate more fear of movement
and/or re-injury.67

• Keele SBST: The overall score is used to separate into low and medium risk subgroups.
The distress subscale is used to separate medium risk subgroup into medium and high risk.
It is used to identify potential ‘‘at-risk’’ patients for potential long-term chronic problems.42

So what? It is recommended that for patients that score above the cut-off scores for the
aforementioned psychosocial scales, treatments should be geared towards cognitive and
behavioral treatments, including CBT, PNE, multidisciplinary care, etc.43,68-70 One of the
intents of this treatment approach would be to positively influence fear-avoidance, distress,
kinesiophobia and pain catastrophization. In PNE, for example, all of these psychosocial risk
factors have been shown to be positively influenced, thus reducing their risk for chronicity.57
This would imply psychosocial “red” could be moved to “yellow” or even “green.” Could a
patient with high levels of risk, after a few sessions on PNE, possibly with additional treatments
such as mindfulness, relaxation or gentle exercise, experience decreased levels of risk and
once again “become” a manual therapy candidate? Some may argue we’re pushing too hard
and trying to make everything fit this model because we’re sold on the concept. First, what we
are mentioning here is not uncommon in clinical practice and
many clinicians already screen for, and often address issues
such as high levels of fear. And over time, as fear decreases,
increased physical loads of exercise and movement,
including passive (manual) movement can be achieved.57,68,70
Second, and critically important is the notion of, what do we
do with these high-risk patients? It is suggested they receive
multidisciplinary care, which we agree with, but it is also a risky
proposition as it steers patients towards the medical model
which is riddled with pathways towards medicalization.71

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 249

For example, it is now well established that from a medical perspective a large part of the
opioid epidemic starts in the emergency department with early exposure to narcotics.72 It has
been shown that patients who access rehabilitation (PT, chiropractic, etc.) first, have between
a 70-90% reduced exposure to opioids (WebPT™ conference 2018), which should drive the
notion that today’s manual therapists should be able to (i) screen for and (ii) address various
psychosocial issues, and only if non-responsive, consider referral to a multidisciplinary team.
Please note, we acknowledge that issues such as depression and patients potentially harming
themselves is different and should be screened for and managed in the proper manner.73 What
we’re talking about is levels of fear-avoidance and pain catastrophization, which presents itself
in very high numbers in most musculoskeletal conditions. Time to update our flowchart again.

Interview / Clinical Reasoning

Identify Identify time Identify psychosocial

mechanism phase of pain risk factors

Nociceptive Neuropathic Central Acute Chronic Low

sensitization Medium High
Risk Risk Risk

Figure 12.4: Adaptation of the proposed algorithm since psychosocial variables can also be positively
influenced

250 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

12.5: Chronic Nociceptive-Dominant Pain
Since we’re updating our chart, we might as well address another area of concern: chronic pain.
As stated before, chronic pain implies duration of pain and does not provide much information
about the underlying processes. This is why we push the pain mechanism work by Gifford and
Smart and colleagues. A common misconception is that chronic pain implies CS (nociplastic),
which is likely where most of the concern comes from in terms of “hands-on” or “hands-off.”
We need to realize that (shockingly) we also get chronic, nociceptive-based pain states, which
we think most “pain” therapists forget, which in turn may be good candidates for manual
therapy. For example, in a high-level RCT for CLBP, Cecchi and colleagues tested three different
treatment interventions: Back school (15h of education); PT (15h combining mobilization
and exercise); and spinal manipulation (4-6 sessions per week for 4-6 weeks as needed).74

Interview / Clinical Reasoning

Identify Identify time Identify psychosocial

mechanism phase of pain risk factors

Nociceptive Neuropathic Central Acute Chronic Low

sensitization Medium High
Risk Risk Risk

Central

Nociceptive

Figure 12.5: Further expansion of the algorithm to differentiate between nociceptive and central chronic pain

Patients were followed for one year and all groups improved, however the manipulation group
had better functional improvement at the one-year follow up compared to the other groups.
How did they define “CLBP?” – “non-specific LBP reported ‘often’ to ‘always’ at least for the
past six months.” In another high-level RCT specific for spinal stenosis and LBP, Whitman and
colleagues applied manual therapy to patients with a mean duration of five years, with 62% of
the manual therapy (versus 41% of the exercise group) yielding positive results one year later.75
No, this is not a definitive listing of manual therapy efficacy for CLBP, but rather showing
that not all chronic pain is associated with increased sensitivity. This further implies (again),
the modern manual therapist has to become aware of CS and screen appropriately. If not
centrally sensitized, patients with chronic, nociceptive-dominant pain states are candidates
for manual therapy.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 251

12.6: Neuroplasticity
Unfortunately (or fortunately), we can keep going. For example, in Principle 7 we delve into the
various aspects of neuroplasticity and along with Principle 1, try and make the case for hands-
on treatments to be seen as a form of sensory integration and/or discrimination.76 Where does
this fit in? We know that these neuroplastic changes are typically associated with chronic pain,
but also now shown to occur fast, including acute pain and threat of pain. This once again
implies that we should, from a neuroplastic perspective, consider acute and chronic pain as
potential “hands-on” candidates as a means to reorganize cortical maps.

Interview / Clinical Reasoning

Identify Identify time Identify psychosocial

mechanism phase of pain risk factors

Nociceptive Neuropathic Central Acute Chronic Low

sensitization Medium High
Risk Risk Risk

Plasticity Central

Nociceptive

Figure 12.6: Final rendering of the algorithm to include neuroplasticity into the various potential clinical
presentations and their relative potential indication for the use of manual therapy

252 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

This process could go on and on, but let’s come to some conclusions:

• There must be a more deliberate and evidence-based approach to selecting treatments

• Screening and using validated tools, with cut-off scores are non-negotiable, and should
screen for pain mechanisms and risk factors

• Categories are not fixed and can be shifted forward and back with or without treatment

• The choice of manual therapy is dynamic and should be based on the fluidity within
these categories

• Patients in the “red” categories may become candidates for manual therapy

• Patients in the “green” or “yellow” categories may become averse to manual therapy

• Careful reassessment is constantly needed, including psychosocial and pain

mechanism models

12.7: Who Does Not Need Manual Therapy?

At this point, manual therapists are likely
salivating as we show (very biased), how often
“no-manual therapy” patients may, in fact,
become candidates for manual therapy. On
the flipside, pain science experts are already
writing nasty letters (if that’s still a thing),
reviews and blogs about this book which will
irreparably harm people in pain and put the
pain movement back 30 years! Our goal is to
merely make the case that these two worlds are
not mutually exclusive. Yes, for a patient with
fibromyalgia, widespread sensitivity, who has recently undergone a painful divorce, and is
now facing high levels of fatigue and sleep deprivation, a central posterior-anterior mobilization
at C5 will likely do very little to help. In fact, it may make the patient worse by virtue of a
heightened sensitivity of the nervous system and potential fueling of a biomechanical belief
of why they hurt. This once again underscores the need for manual therapists to develop a
working knowledge of pain science. Now is a good time to ask the question: Who does NOT
need manual therapy?

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 253

• Safety issues/red flags: Manual therapists excel at screening
for red flags and including a review of systems, often more
so than their “pain” counterparts, since it’s an integral part
of diagnostic and clinical reasoning.77-79 Precautions and
contraindications to manual therapy, as well as treatment in
general may obviously preclude the use of manual therapy.

• CS and allodynia: As stated before, neither CS nor allodynia are necessarily red flag
items, since both can be influenced to become less of an issue in the patient’s clinical
presentation.56,57 Manual therapy, however, should not be the first choice in these patient
populations by virtue of their sensitivity and underlying biological, physiological and
psychological issues. Furthermore, if CS and/or allodynia is non-responsive to treatments
such as PNE, GMI or CBT, it should not be a treatment choice. Again, we need manual
therapy proponents to realize the complexity of pain and strongly urge them to “think
bigger” in these complex pain states, i.e., sleep hygiene, nutrition, goal setting, relaxation,
exercise and more, or as we often say at seminars: Manual therapy should NOT be in your
top five choices, maybe not even top 10….in lieu of what we just mentioned.80

• High psychosocial risk patients: Per the various screening tools (e.g., Keele SBST),
patients in this category likely need multidisciplinary and multimodal interventions with
a heavy cognitive approach.43 This is well established and documented. Again, if the
various risk factors can be positively influenced by therapeutic interventions, lowering
them accordingly, manual therapy may become a treatment choice.56,68 On the flipside,
patients who are deemed to have a high risk for chronicity and have been non-responsive
to cognitive interventions should not become candidates for manual therapy interventions.
Instead, they may need further psychological screening and/or management.

• Addicted to manual therapy: The use of manual therapy should also be carefully
reconsidered in patients who become “addicted” to manual therapy, especially spinal
manipulation. It is believed that during high-velocity manipulations and/or “cracking
one’s knuckles” powerful centrally mediated endorphins are released in the brain (i.e.,
the PAG), which provides the euphoric sensation associated with the manipulation as
well as immediate hypoalgesia.81,82 Apart from developing a dependency on passive
treatment (locus of control), patients may seek repeated manipulation as a means to
stimulate endorphin release, which over time may habituate responses to manipulation
thus lessening the effect of such treatments.

254 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

• Locus of control: It is well described: The more complex the pain; the more comprehensive
the treatment.83,84 Furthermore, it is often stated, the more chronic pain is, the more active
the treatment must be.83 We support those statements and, once again, urge clinicians
not to run towards manual therapy as the first choice in complex pain scenarios. A big
criticism against the use of manual therapy for chronic pain is that it makes patients
depend on an external source for help. In this case, the clinician becomes the key factor
in the treatment, thus shifting the locus of control externally (away from the patient). It is
thus proposed that teaching people skills to enhance self-efficacy such as coping skills,
relaxation, stretches, etc., is more advantageous as they develop the skills needed to help
themselves (internal locus of control). Once again, we support these statements. Clinically,
patients with a strong external locus of control may be identified with statements such
as “just fix me,” treatment choices focusing on passive treatment such as hot packs or
therapeutic ultrasound (or manual therapy) or a resistance (and excuses) for not engaging
in active strategies such as exercise. A model that is gaining a lot of interest in the pain
world, borrowed from behavioral medicine, is the transtheoretical model of health behavior
change model.86 This model, which describes various stages in facilitating behavior change
is now being explored for treatments such as PNE, but can also powerfully be used by
manual therapists. The “best” place for patients to be when entering a clinic would be in
the preparation stage, since they are ready for action. Typically, these patients have already
decided to make a change, are committed to change and receptive to treatment choices.
The most difficult patients are those in the pre-contemplation phase. These patients have
no intent to change; they do not see a reason to change and are not interested in your
help.86 Clinically, we often recognize them as patients who tell you they don’t want to
be there or add “I’m only here because my doctor sent me; my work sent me, etc.”
These patients will likely prefer passive treatments and show little to no interest in active
treatments such as exercise. Manual therapists should caution themselves not to foster a
passive-only approach to patients in this phase.

1
E
PRECONT MPLATION

No recognition
of need for
CO

or interest
CE

NTE
NAN

5 in change 2
MPLA
MAINTE

Ongoing
practice of new,
TION

Thinking about
healthier behavior changing

Adopting Planning for

new habits change
P

RE
ION PA
RAT
ACT ION
4 3

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 255

• Biomedical reinforcement: This may be the hardest to follow through with, since it requires
being honest with yourself. If manual therapy and your approach and description of manual
therapy fosters a biomedical model, which is known to increase fear, pain catastrophization
and ultimately pain: STOP! Manual therapy—deeply rooted in orthopedics, likely more
than any other realm of rehabilitation/therapy needs a serious clean-up of its language
(Principle 5). It is now well established that the health of a person’s tissues and their pain
experience are poorly correlated.84 Some people have various tissue issues (injury, aging,
etc.), yet experience little to no pain, while in others their tissues appear healthy (scans,
tests, etc.), yet they experience significant pain.87 What patients believe in terms of the
health of their tissues powerfully influences their pain. By having a manual therapist overly
focusing and explaining various tissues issues, along with using provocative terminology,
may induce catastrophization, which in turn fuels fear avoidance, followed by disability
and increased pain and thus a vicious cycle ensues.88

• Safety with touch: Unfortunately, manual therapists must recognize that many people
suffering from pain have experienced really bad things in life, including abuse. This may
be psychological abuse, physical abuse or even sexual abuse.89-91 Johan Vlaeyen, the
pioneer behind the fear-avoidance model has been quoted as saying patients may not
necessarily have fear, but rather have a lack of safety (Pain in Motion Conference 2015—
Brussels, Belgium). For patients who have experienced physical or sexual abuse touch
can be very threatening, especially from a clinician they barely know or even someone of
the opposite sex. It can be argued (luckily) that many of the current screening tools familiar
to manual therapists (PCS, FABQ, CSI, etc.) may pick up clinical manifestations associated
with past abuse, but they are not specific to these issues. Manual therapists should ensure
the clinical environment is safe, including the use of hands-on treatments.

256 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

• Nocebo: Manual therapy exerts a powerful placebo effect.41,92,93 Patients who believe it will
work respond better than those who do not.41 Conversely, the nocebo effect can explain why
patients who believe a treatment won’t work will respond poorly to the chosen treatment
intervention, including manual therapy. How do we know if someone does not want/
believe in manual therapy? Typically, information gathered during the interview can provide
powerful clues, including statements about previous treatments and their outcomes, such
as manual therapy. For example, a patient may state that “the last therapist” did a certain
manual therapy technique or regimen and “they were in pain for days” may be enough
to warrant careful consideration of manual therapy. Comments like these, or the patient’s
response to an explanation of examination findings or planned interventions, may also be
helpful when determining if manual therapy is a good choice or not.

This list can go on and on, and once again, should not be seen as
the authoritative list of “no-hands-on,” but, rather open the reader’s
eyes to the fact that hands-on and hands-off treatment choices are
fluid and dependent on numerous factors. So what? What does all
of this mean? As you near the end of this book, we may have to go
back to the Introduction. In the heyday of manual therapy, all patients
received manual therapy, and if we asked if people with chronic pain
should receive manual therapy, we’d be greeted with an overwhelming “yes!” Fast forward
to the last 10-15 years with the advent of the pain revolution, brain scans, pain neuromatrix,
neuroimmune responses, psychosocial variables and neuroplasticity and the answer would
be a resounding “NO!”

Manual Therapy for Chronic Pain Manual Therapy for Chronic Pain Manual Therapy for Chronic Pain

Yes No Yes No Yes No

In Quebec City in 2012 at IFOMPT, David Butler, one of the foremost pain experts and a
pioneer in pain science, cautioned the manual therapy world not to leave behind the “bio” of
the biopsychosocial approach. This book is dedicated to Butler’s call—we cannot forget the
“bio.” In fact, we have a mandate to touch; patients want to be touched; patients respond well
to touch, and it works on so many levels, even from a pain science perspective. Maybe the
pendulum should be shifted ever so slightly back. No, we also don’t believe it’s a 50-50 shift,
but definitely a shift backward towards the middle.

INTEGRATING MANUAL THERAPY AND PAIN NEUROSCIENCE 257

12.8: The Big Picture…and Manual Therapy
Pain is indeed complex, and we cannot have you walk away from this book and think that for
chronic pain, manual therapy is a primary and first choice. The more complex the pain; the
more complex and intertwined the treatment. In complex chronic pain states, one approach
or one profession does not have the answer, nor will they ever, including manual therapy (and
for that sake PNE, GMI, neurodynamics, etc.). Manual therapy, including mobilization and/
or manipulation, neurodynamics, massage, trigger point therapy, etc., all form part of this
treatment plan, but it’s only a part. Recent pain research has shown that PNE approaches
are gaining efficacy, but PNE as an intervention by itself is very limited. In fact, education by
itself is very limited in changing behavior. Researchers showed that when PNE is combined
with movement, including manual therapy, it is far superior to PNE alone, culminating in the
concept of PNE+, with the plus referring to adjunct treatments supporting PNE.

Conclusion
A good place to start the conclusion is to view the 22 points of the PNE+ program (Principle
11) and see heartwarming (for the manual therapist) words like manual therapy, biofeedback,
neural mobilization, GMI, soft tissue/trigger point therapy, stabilization and resistance training,
stretches, etc. Can we be any clearer as we scream from the rooftops: “Pain science and
manual therapy can and should co-exist!” The most powerful tool we can teach you is when to
use the word “AND” in determining whether to implement manual therapy treatment. Instead
of asking, “Should pain science be hands-on OR hands-off?” we need to realize the answer is
a resounding: “Pain science is both hands-on AND hands-off!”

258 PRINCIPLE 12 | PUTTING MORE THOUGHT INTO TREATMENT CHOICES

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Integrating Manual Therapy and Pain Neuroscience
The modern clinician faces more challenges than ever before, including a worldwide pain epidemic
and skepticism among critics about the efficacy of hands-on treatments. This first-of-its-kind text,
for beginning and experienced clinicians, demonstrates that pain science and manual therapy are
not mutually exclusive—they work better together. Clinicians who understand this and adopt
techniques that combine the two are better prepared to help patients, especially the millions
suffering from chronic pain.

Broken down into 12 principles, the book delves into concepts like clinical reasoning, nociception,
neuroplasticity, therapeutic alliance, psychosocial factors and additional treatments to complement
hands-on therapy—showing how the implementation of these concepts can contribute to
successful outcomes.

This text is informed by more than 100 years of combined experience between four world-renowned
therapists and pain science experts. Filled with examples, recent research, and pearls of wisdom,
the book was written to help clinicians overcome the challenges they face and influence treatment
outcomes by treating the body AND the brain.

Adriaan Louw Emilio Puentedura Stephen Schmidt Kory Zimney

PT, PhD PT, DPT, PhD, OCS, PT, MPhysio, OCS, PT, DPT
GDMT, FAAOMPT FAAOMPT

An educator, scientist and
physical therapist, Adriaan has
been practicing and teaching
pain science and manual
therapy for more than 25
years. He is the co-founder and
co-owner of the International
Spine and Pain Institute and
holds adjunct faculty positions
at St. Ambrose University and
the University of Nevada, Las
Vegas. Adriaan is the Director of
Post-professional education for
Evidence in Motion.
Emilio, who is also known as
“Louie,” has been involved in
orthopedic manual therapy and
neurodynamics for more than
39 years, working in outpatient
settings with a focus on spinal
conditions, and presenting
seminars on the various
approaches to manipulative
therapy. Following a long tenure
at the University of Nevada,
Las Vegas, he is now Clinical
Professor of Baylor University’s
DPT program.
Steve is a physical therapist
with more than 25 years of
experience treating patients
with persistent pain,
neurological disorders and
musculoskeletal problems. He
is a faculty member for the
Kaiser Vallejo PNF program,
a senior faculty member
for the International Spine
and Pain Institute and has
taught numerous national and
international seminars on pain
neuroscience education.
Kory has been a physical
therapist for more than 25
years, working primarily in
orthopedics. In 2013, he
became a full-time faculty
member at the University
of South Dakota where he
teaches courses related to
rehab neuroscience, spine, and
evidence-based practice. He is
also a senior faculty member
with the International Spine
and Pain Institute.

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