Myofascial Manipulation

Myofascial Manipulation
Myofascial Manipulation
Theory and Clinical Application
THIRD EDITION
Robert I. Cantu
Alan J. Grodin
Robert W. Stanborough
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The author has made every effort to ensure the accuracy of the information herein. However,
appropriate information sources should be consulted, especially for new or unfamiliar
procedures. It is the responsibility of every practitioner to evaluate the appropriateness of a
particular opinion in the context of actual clinical situations and with due considerations to new
developments. The author, editors, and publisher cannot be held responsible for any typographical
or other errors found in this book.
Photo used in design on opener pages reprinted from Histology (p. 212) by A. W. Ham and D. H.
Cormack with permission of J.B. Lippincott Co.,© 1979.
Library of Congress Cataloging-in-Publication Data
Cantu, Robert I.
Myofascial manipulation : theory and clinical application/ Robert I. Cantu, Alan J. Grodin,
Robert W. Stanborough. - 3rd ed.
p. cm.
Includes bibliographical references and index.
ISBN 978-1-4164-0498-9 (Print) ISBN 978-1-4164-0600-6 (e-book PDF)
1. Myofascial pain syndromes-Physical therapy. 2. Manipulation (Therapeutics)
I. Grodin, Alan J. II. Stanborough, Robert W. III. Title.
RC925.5.C26 2012
616.794-dc22
Art Director: Jason Crosier

Designer: Jan Mullis
This book is designed in Minion Pro and Univers.
Printed in the United States of America

1 2 3 4 5 6 7 8 9 10 20 19 18 17 16 15 14 13 12 11
To the Good Shepherd ... who restores my soul.
R.I.C.
To my wife, Carol,
and my children,
Jason, Evan, Seth, and Lisa,
for their support and tolerance
of my personal and professional life.
A.J.G.
To my wife, Becky,
for her never-ending patience and support,
and to my children,
Abby and Jake,
whose inquisitive nature is ever-inspiring.
R.W.S.
Contents
Con tributor s . ................................................................ xi

Fore,vord .................................................................. .x 111
. ..
Pfre ace .................................................................... xv11
Ackno ,vledgm ents .. ........................................................ .xx i
PART I
Historical Development and Current Theories
of Myofascial Manipulation ................................ 1
CHAPTER 1
Hi stori cal Basis for My ofasc ial Ma nipul ation ......................... 3
Robert I. Cantu and Robert W. Stanborough
Anc ient Times . ........................................................ .4
Mode rn Tim es: The Trend Toward Mobility and Diagnos is of Pathology ...... 10
Futur e Cons iderations .................................................. 13
CHAPTER 2
M od ern The ori es and System s of My ofasc ial Ma nipul ation . . . . . . . . . . . 17
Robert I. Cantu, Alan J.Grodin, and Robert W. Stanborough
Autonomic Approaches ................................................. 17
Mechan ical Approaches ................................................. 21
Movemen t Approaches ................................................. 25
Conc lusion . .......................................................... .28
PART II
Scientific Basis for Myofascial Manipulation .................. 31
CHAPTER 3
Hi stolo gy and Biom ech ani cs of My ofasc ia .......................... 33
Robert I. Cantu and Robert W. Stanborough
VII
v111 Contents
Histology and Biomechanics of Connective Tissue ......................... 33

Histolog y and Biomechanics of Muscle ................................... 54
Histology and Biomechanics of Junctional Zones ........................... 58
Conclusion . .......................................................... .63
CHAPTER 4
Histopathology of Myofascia and Physiology
of Myofascial Manipulation .................................. 69
Robert I. Cantu, Alan J. Grodin, and Robert W Stanborough
Histopathology of Myofascia ............................................ 69
Physiology of Myofascial Manipulation ................................... 80
Conclusion . .......................................................... .86
CHAPTER 5
Neuromechanical Aspects of Myofascial Pathology
and Manipulation .......................................... 91
Clayton D. Gable
Basic Afferent Neurology of Connective Tissue ............................ 92
Receptor Influence on Movement ....................................... 105
Muscle Tone.......................................................... 111
Application to Specific Therapeutic Techniques ........................... 117
Conclusion . ......................................................... . 121
CHAPTER 6
Muscle Pain Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
Jan Dommerholt and Robert W Stanborough
Soft Tissue Lesion and Mechanical D ysfunction ........................... 126
Myofascial Pain Syndrome ............................................. 128
Fibromyalgia ........................................................ . 149
PART Ill
Evaluation and Treatment of the Myofascial System .......... 181
CHAPTER 7
Basic Evaluation of the Myofascial System. . . . . . . . . . . . . . . . . . . . . . . . . 183
Robert I. Cantu, Alan J. Grodin, and Robert W Stanborough
Histor y ............................................................. . 184
Postural and Structural Evaluation ...................................... 185
Contents IX
Active Movement Analysis ............................................. 193

Compressive Testing of the Spine ........................................ 195
Palpatory Examination ................................................ 195
CHAPTER 8
Atlas of Therapeutic Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199
Robert I. Cantu, Alan J.Grodin, and Robert W Stanborough
Techniques for the Lumbar Spine ...................................... 205
Techniques for the Lumbopelvic/Lower Quarter Area ..................... 248
Techniques for the Thoracic/Upper Thoracic Spine and Upper Extremity ..... 279
Techniques for the Cervical Spine ...................................... 305
Index .. .................................................................... .317

About the Authors .......................................................... 327
Contributors
Jan Dommerholt, PT, DPT, MPS, FAAPM

Director of Rehabilitation Services
Bethesda Physiocare
Bethesda,Maryland
Vice President
International Myofascial Pain Academy
Schaflhausen, Switzerland
Clayton D. Gable, PT, PhD

Assistant Professor
Department of Physical Therapy
The University of Texas Health Science Center at San Antonio
San Antonio, Texas
XI
Foreword
If you have picked up this book, chances are high that you are not a greenhorn in
the field of rehabilitation and manual therapy . Most likely you belong to the most
experienced and knowledgeable bodywork practitioners in your community , or
are on your way there . Or-less likely-you chose this book as an attempt to boost
your image in the eyes of your peers . The book you have selected is one of the
absolute masterpieces in the field. The previous edition sits on the bookshelves of
virtually all the leading massage and bodywork schools worldwide and decorates
the desks of hundreds of ambitious authors and teachers within this field.
Most massage and other manual therapies direct their techniques toward en-
hanced functioning of muscular tissues; improved vascular , lymphatic flow; or
better skeletal positioning . Myofascial therapies , on the other hand , target more
specifically the muscular connective tissues (myofasciae). These tissues include
broad sheets of dense connective tissues such as the fascia lata of the lateral thigh
or the plantar fascia of the sole of the foot. They also include a complex network
of thin connective tissue bags and sheets on the insides of muscles as well as sur-
rounding the muscles . Most muscle electromyography experts agree that muscle
activity at rest is electrically silent. The passive tissue stiffness of muscles at rest
therefore appears to depend to a large degree on the local properties of this fas-
cial network . One of the advantages of myofascial therapies , as described in this
book, is that they include a detailed repertoire of working techniques for address-
ing fascial contractures and adhesions , which often underlie musculoskeletal pain
problems .
For several decades , fascia has been neglected as the "Cinderella" of orthope-
dic medicine . Medical doctors were introduced to this tissue by learning to "clean
it off" in their dissection courses to reveal the distinct organs enveloped within .
These colorless tissues were regarded mainly as packing material , which some-
times assists the muscles as passive force transmitters . However, during the last
few years, new measurement tools have shown that fascial tissues serve many
important functions in the body and contain some surprising tissue properties .
The First International Fascia Research Congress , held at Harvard Medical School
in Boston in 2007, signaled an important turning point and was celebrated with
worldwide acknowledgment. There is now global recognition that this underesti-
mated contextual tissue plays a much more important role in health and pathology
than was estimated during previous decades .
XIII
xiv Foreword
Among the many surprising fascial properties that are now being discovered
and investigated are two that I would like to mention briefly: the proprioceptive
importance of fascia and the discovery of active fascial tonicity . Although in the
past it was often assumed that mechanoreceptors in joint capsules and associated
ligaments were the main input devices for proprioception , more recent investiga-
tions have revealed that these ')oint receptors" are mostly stimulated only at the
end ranges of available movements and provide very little input during regular
everyday movements . In contrast , fascial membranes are often positioned much
farther away from the movement axes and are therefore in much better positions
to register smaller movements around these joints . These sheets are densely popu-
lated by sensory nerve endings , which are excellent input devices for propriocep-
tion . It has therefore been postulated that myofascial manipulations may largely
work by stimulating those fascial receptors , with resulting physiological as well as
neuromuscular responses from the central nervous system . If you want to study the
specific fascial mechanoreceptors in detail-for example , to direct your manual
techniques more specifically toward their different subtypes-this book provides
detailed information . Chapter 6, "Muscle Pain Syndromes ," in this new edition
contains the best description of fascial innervation that I have seen .
The other property I wish to mention is fascial tonicity . Recent evidence sug-
gests that fascia contains its own active motricity; it can contract and relax au-
tonomously , independent of the skeletal musculature . Laboratory work with rat as
well as human fascia by our group (Fascia Research Project , University of Ulm,
Germany) and by the group working with Ian Naylor (Bradford University, United
Kingdom) has shown that fascia contains contractile connective tissue cells, called
myofibroblasts . The cells enable fascia to actively contract , both in the form of
smooth muscle-like temporary contractions and in chronic tissue contractures
that include tissue remodeling (as in frozen shoulder or Dupuytren contracture) .
How to best influence the active tonus regulation of fascia therapeutically-via
mechanostimulation as well as other means-is currently an exciting subject of
interdisciplinary research .
In contrast to most fields of academic exploration , the field of myofascial ther-
apies continues to be dominated by the existence of so-called schools . Each school
is organized around a charismatic founder and emphasizes a specific manual mo-
dality and a particular explanatory concept. Although such distinction served well
in providing followers with an almost tribal social affiliation , it has also attenuated
a healthy culture of questioning , cross-pollination , and mental collaboration . This
book is one of the rare exceptions in the field. Rather than focusing on only one
school and providing a semireligious body of congruent belief concepts (and ig-
noring contrasting concepts that are taught elsewhere) , it describes with academic
precision the different schools and concepts that have been able to describe their
work in an anatomical language . It clearly distinguishes proven facts from current
assumptions and provides accurate references behind the different sources of in-
formation . Nevertheless , rather than being an academic textbook only, it is written
Foreword xv
in a practical and reader-friendly manner and does include several excellent practi-
cal descriptions of clinical working approaches .
Be warned , dear reader-and I am writing that of course with a twinkle in
my eye-that if you are looking for a cozy home to help you feel superior and
safe with one newly learned method of fascial manipulation and one related belief
concept , this book will not help you sleep more comfortably . However , if you have
picked up this book as an experienced practitioner who is interested in expand-
ing your understanding of fascial manipulation , and if you seek to be exposed to
an internationally recognized , state-of-the-art review of different techniques and
concepts , then you have found the true masterpiece within this field .
Dr. Robert Schleip

Director,Fascia Research Project
Division of Neur op hysiology, Ulm Un iversity, Germ any
Preface
Preface to the Third Edition

We continue to be amazed and humbled at the ongoing demand for Myofascial
Manipulation since release of the second edition in 2001. Although the format of
the first, second, and third editions has remained consistent, the principles and
concepts within have been reworked and modified to stay consistent with the re-
search to date. As with many areas of science, the field of rehabilitation and man-
ual therapy continues to grow and, therefore, requires that professionals meet the
responsibility of staying current and relevant in the clinic. New terms have made
their way into the field of soft tissue manipulation. Architectural terms such as
tensegrity,for example, are now being used in the literature.
The techniques provided in the second edition have proved to be "bread and
butter" not only for its readers but also for its authors. Despite the addition of new
techniques, this third edition is by no means intended to be exhaustive in content
or techniques. These techniques merely represent the ongoing growth of research,
knowledge, and clinical experience we wish to share with our readers. Our hope
is that this edition will continue to provide therapists with the background for the
skills they practice, an understanding of current concepts to enrich and justify
their practice, and sufficient treatment principles and techniques to provide the
best manual care possible. Quality and efficiency of care have become ever more
urgent and necessary in this era of shrinking reimbursements and with the aging,
yet active, population.
We have added techniques to the third edition based on the requests made
during our years of teaching. Those added have proven to be just as essential in
our clinics as those provided previously. A DVD accompanies the text to provide
additional instruction.
Once again, Chapters 5 and 6 have been completely rewritten owing to tre-
mendous insight gained from the continually growing body of research. The First
International Fascia Research Congress, held in Boston, in October of 2007, was
considered a smashing success. Much of the research presented has been incorpo-
rated in this edition. The Second International Fascia Research Congress, held in
Amsterdam, in October of 2009, was equally successful in moving our knowledge
of myofascia forward, and some of the information presented there has also been
incorporated in this book.
XVII
xv111 Preface
The three main divisions of the book have remained. Part I provides the his-
torical background of manual therapy and current theories, Part II provides the
scientific basis for myofascial manipulation, and Part III provides a system for
evaluation and treatment of the myofascial system.
Readers familiar with the previous editions will feel right at home with this
edition. We hope new readers will find this edition useful and refer to it often in
clinical practice . Enjoy!
ROBERT I. CANTU
A LAN J. GRODIN
ROBERT W. STANBOROUGH
Preface to the First Edition

In his classic book, Joint Pain, John Mennell wrote that "no textbook in the field
of orthopedics can be entirely original." On first reflection, this statement seems
a bit contradictory, in light of the fact that Mennell was quite an innovator and
one of the early advocates of using arthrokinematic rules for joint mobilization.
On further reflection, however, his ideas and philosophies, while quite innova-
tive, were based on a combination of knowledge and clinical experience he at-
tained throughout his years as a medical student and as a physician. The knowl-
edge and experience he gained over the years were molded and integrated in a
way that became uniquely his own. His system became his "handwriting," or his
style.
Handwriting is a good analogy for personal style. A person's handwriting is
a totally unique self-expression. The uniqueness comes from the actual process
of learning how to write, from years of practicing that handwriting, and from
the particular function the handwriting serves in the person's life. A physician
who has taken voluminous notes throughout school primarily for his or her own
benefit will have very different handwriting from the architect who has to submit
drawings with very legible writing. The letters formed in the handwriting, as well
as the spelling, are not unique, but the way the letters are represented by the indi-
vidual are.
So it is with this book on myofascial manipulation. For us, it is a combination
of acquired knowledge and clinical experience that, over the years of treating pa-
tients, has evolved into a particular philosophy or system that is unique. For any-
one to say that they were the first in history to "invent" certain techniques would
be presumptuous. What we attempt to do in this book is to take the most current
body of research in myofascia and integrate this cognitive knowledge with psycho-
motor skill to produce a concrete system of evaluation and treatment acceptable to
a profession that is striving for higher professional recognition.
This textbook is divided into three parts that reflect its major purposes. The
first part outlines the evolution of myofascial manipulation, incorporating both
its history and the latest schools of thought. The second part and purpose of this
Preface XIX
text book out lines the scientific basis of myofascial manipulation. Management
of certain clinical problems is also discussed. Part III focuses on evaluation and
treatment techniques that have repeatedly proved effective in the clinical setting
and includes an atlas of therapeutic techniques.
For the sake of clarity throughout the text, manual therapy is divided into
joint manipulation and soft tissue manipulation. As understanding of connective
tissue has increased, the distinction between joint and soft tissue manipulation has
become somewhat clouded. Joint manipulation has been defined as "the skilled
passive movement of a joint." The tissues being mobilized, however, are all histo-
logically classified as connective tissues, and in this respect, any type of manual
therapy can be considered soft tissue manipulation. The distinction made in this
text is in the arthrokinematics, or lack of arthrokinematics, in the application of
the techniques. Soft tissue manipulation is generally less concerned with arthro-
kinematic rules than is joint manipulation; a majority of the techniques are not
concerned with individual joints but with myofascial relationships and the interre-
lations of the joints to the soft tissues. For the purposes of this text, we have defined
myofascial manipulation as: The forceful passive movement of the musculofascial
elements through its restrictive direction(s), beginning with its most superficial
layers and progressing into depth while taking into account its relationship to the
joints concerned.
Myofascial Manipulation is not meant to be a panacea or an exhaustive criti-
cal review of the literature, but a representation of what we feel strongly about
clinically. These are techniques that we use every day, integrating them with joint
mobilization, alternate somatic therapies, and exercise. Our hope is that this in-
formation will be integrated into the readers' arsenal of techniques and into their
philosophy of treatment, so that each clinician's style, or "handwriting," will be-
come more distinct as well as more effective.
ROBERT I. CANTU
ALAN J. GROD I N
Preface to the Second Edition

When we published the first edition of Myofascial Manipulation in 1992, we were
not fully aware of the interest and pent-up demand for this material. Since 1992, the
book has continued to sell copies, and this has been a humbling experience for us.
We believe there are several reasons for the continued interest in this material.
First, an underlying philosophy and strategy for the book was to provide good
"bread and butter" techniques that were effective on patients, were relatively easy
to learn, and were practical to use in the current arena of managed care. For the
second edition, we have added a number of other "bread and butter" techniques,
being careful not to add any "fluff" to merely make the book bigger. What are still
represented in this edition are the myofascial techniques that the authors have
used successfully over the years on a daily basis on literally thousands of patients.
xx Preface
Second, the first edition relied heavily on basic science principles. We went to
the literature, for example, to explain the mechanisms of injury and repair, and to
delineate pain of mechanical versus nonmechanical origin. We carefully extrapo-
lated and integrated these principles into the principles of management and treat-
ment of soft tissue dysfunction. For the second edition, we wanted to strengthen
that scientific foundation. To that end, we enlisted the help of gifted professionals
and content experts, to add material, and to retool and revise existing material
in the previous edition. The chapter on neuromechanical aspects of myofascial
pathology and manipulation, for example, adds a dimension of understanding
we did not offer before. Also, the chapter on muscle pain syndromes (i.e., pain of
mostly nonmechanical origin) was completely rewritten due to the explosion of
research in that area. The chapter on the histopathology of connective tissue has
also been completely updated due to advances in research over the last 8 years.
As we mentioned in the first edition, Myofascial Manipulation is not designed
to be a panacea for manual therapy, but a great utility tool to be used in conjunc-
tion with joint mobilization and exercise. In our courses, we often refer to that
triad (soft tissue mobilization, joint mobilization, and exercise) as the "pinball
triad of manual therapy." This is because the three aspects of treatment are virtu-
ally inseparable and totally integrated in the clinic. The savvy clinician knows how
to effectively "bounce off" all three aspects of treatment to arrive at the desired,
optimal result.
We respectfully submit the second edition of Myofascial Manipulation for
your consideration as a tool to help expand the horizons of our profession. Man-
aged care, Medicare cutbacks, market saturation of therapists, and turf erosion
have put us in a position where it is no longer an option for us to be the very best.
Our professional lives and the health and longevity of our profession in general
depend on it. We hope that this tool will be useful in helping us all forge ahead to
expand our individual and collective horizons.
ROBERT I. CANTU
ALAN J. GRODIN
Acknowledgments
The authors thank the following persons for their assistance in the preparation of
this edition: To Rebecca J. Stanborough, BA, MFA, for her help in proofreading
and copyediting the manuscript; Glen Coad for his photographic and cinematog-
raphy excellence; and Melissa Nunnally, DPT, and Marisa Ball, DPT, MTC, for
being the "patients" in Chapters 7 and 8.
Once again we wish to acknowledge all the professors who adopted the second
edition for their courses and curriculums as well as all the readers who have pro-
vided feedback. Thank you.
From the Second Edition

The authors thank the following persons for their assistance in the preparation of
this volume: To Trevor Roman for shooting the photos in Chapter 8, and to Debbie
Cobb and Brad Foresythe for being the "therapist and patient" in Chapter 8.
The authors also acknowledge all the professors who adopted the first edition
for their courses and curriculums-the long-term success of this book is due to
your support and votes of confidence. Thank you.
From the First Edition

The authors thank the following people for their invaluable assistance in the pro-
duction of this book: Karen Barefield, PT, for her drawings in Chapters 6 and 7;
Paula Gould for her photography in Chapters 6 and 7; Carolyn Law, MPT, for her
help in editing the manuscript, from both a content and a grammatical stand-
point; and Lisa Richardson, for being the "patient" in Chapters 6 and 7.
XXI
PART I
Historical Development
and Current Theories
of Myofascial Manipulation
Historical Basis
for Myofascial Manipulation
Rob ert I. Ca ntu and Rob ert W. Sta nbo rough
Myofascial manipulation is as old as history itself- humans have been perform-

ing myofascial manipulation as long as humans have been touching. Throughout
history, many different systems and supporting theories for the treatment of mus-
culoskeletal pain and dysfunction have come and gone. Today, the originality of
any current system of manual medicine is generally found in the underlying phi-
losophy, not in the techniques themselves. The underlying theory and philosophy
of any manual therapy system will dictate the sequencing of technique and will
attempt to explain both the results and the proposed mechanisms of action. The
techniques may be old, but the packaging is new. Underlying theories may alter the
way the treatment is performed and may vary or modify the technique. The advent
of the scientific age has yielded a tremendous wealth of research, which in turn has
changed the theory and philosophy of modern manual medicine.
The existing schools of thought in manual medicine have been shaped not
only by current science but also by what was learned by researchers in the past.
We treat based on what we know or think we know. The purpose of this chapter is
to chart briefly the evolution of manual therapy, with an emphasis on myofascial
manipulation. A greater appreciation for the current philosophy and techniques
can be gleaned from studying historical trends.
The evolution and persistence of manual medicine throughout the years have
been remarkable, especially considering that the medical communities once dis-
approved of such treatment, and the scientific basis of the field has been heavily
researched only within about the last 60 years. This research has fostered a redefi-
nition of manual medicine and has verified how much can be accomplished with
manual therapy.
The history of manual medicine can be divided into four basic periods. The
first period, which begins in ancient history and ends roughly at the close of the
nineteenth century, emphasized position. Joint pain, including spinal pain, was
a result of a "luxation or subluxation" of one or more of the joints. The emphasis
was placed on restoring the position of the spinal vertebrae to relieve pain. In the
3
4 HISTORICAL DEVELOPMENT AND CURRENT THEORIES
second period, starting with the early twentieth century, the philosophy and theory
of manual medicine began to emphasize mobility. Restoring mobility to a joint that
"was locked" became the focus of manual medicine . The science of arthrokinema-
tics developed, and terms such as accessory movements appeared. This spurred the
curiosity of researchers in the middle and late twentieth century, who pushed the
study of manual medicine into a third phase -u nderstanding how manual therapy
affects the biomechanics of connective tissue. They viewed the increased mobility of
the joints as a result of mechanical changes in connective tissues. Largely because
of the chronicity and recurrence of many types of back pain, the focus of the pres-
ent period of research in manual medicine is on neural mechanisms of back pain
and movement reeducation (see Chapter 5, "Neuromechanical Aspects of Myofas-
cial Pathology and Manipulation"). The science of motor learning and control will
have much to offer in this area. The immediate future of manual therapy lies in the
combination of passive manual therapy techniques and movement reeducation or
motor learning techniques for prophylaxis. The philosophy and history of each
movement is discussed in the following sections.
Ancient Times
Early recordings of manual medicine date back to the time of Hippocrates around
the year 400 BC. Two relevant works, "On the Joints" and "On Setting the Joints by
Leverage," describe various combinations of manipulations, massage, and traction
performed on a patient prone on a wooden table. 1 Much of Hippocrates' work in
early manual medicine can probably be attributed to the popularity of wrestling in
his day. Entries in early manuscripts include descriptions of both joint manipula-
tion and massage in treatment of a dislocated shoulder.
And it is necessary to rub the shoulder gently and smoothly. The physician must
be experienced in many things, but assuredly also in rubbing; for things that have
the same name have not the same effects. For rubbing can bind a joint which is
too loose and loosen a joint that is too hard. However, a shoulder in the condition
described should be rubbed with soft hands and, above all things, gently; but the
joint should be moved about, not violently but so far as it can be done without
producing pain. 2<p4>
In the treatment of back pain, Hippocrates describes treatment of humpback,

which is alternately translated "kyphosis." Hippocrates is probably referring to a
kyphosis of the lumbar spine. He describes two treatments for this condition, con-
sisting of mechanical traction and extension exercises. 3
If possible, the patient is first given a steam bath ... then he is placed on his stom -
ach on a wooden board [for traction] .... The physician places the flat of one of his
hands on the kyphosed portion of the patient's back, and his other hand on the
top of the first. ... He presses vertically, or in the direction of the head, or in the
direction of the buttocks [Figure 1.1].The physician ... takes into consideration
whether the reduction should naturally be made straight downward, or towards
Historical Basis for Myofasc ial Manipulation 5
Figure 1.1 The Hippocratic method of traction and manual pressure as described by Galen. Source:
Reprinted with permission from E. H. Schoitz, Manipulation Treatment of the Spinal Column From the
Medical-Historical Standpoint, Part I, Journal of the Norwegian Medical Association (1958;78:359- 372).
Copyright© 1958, Norske Laegeforening.
Figure 1.2 Method for "repositioning of an outward dislocation" of the spinal column. Source:Reprinted
with permission from E. H. Schoitz, Manipulation Treatment of the Spinal Column From the Medical-
Historical Standpoint, Part I, Journal of the Norwegian Medical Association (1958;78:359- 372). Copyright
© 1958, Norske Laegeforening.
the head, or towards the hip. This method of repositioning is harmless; indeed,
it will do no harm even if one sits on the hump while extension is applied ... nay
there is nothing against putting one's foot on the hump and making gentle suc-
cession by bringing one's weight upon it [Figure l.2]. 1<P4)
The description of lumbar extension for treatment of lumbar "kyphosis" is

early testimony to some of the popular extension techniques for treatment of
discogenic lesions in which a loss of lordosis is common. The idea of "reposition-

ing" is definitely an early theme in the ancient documented literature on manual
medicine.
Claudius Galenus, or Galen, a Greek physician who lived in the years AD 129-
199, contributed much written material on early manual medicine, including
18 commentaries on Hippocrates. 1 His primary contribution was documentation
of early neurological investigations. He recognized seven of the cranial nerves, dif-
ferentiated between sensory and motor nerves, and was the first to treat paresthe-
sias and extremity pain by treating the spine. Galen described one such incident
in which a patient developed paresthesias and loss of sensation in the third to fifth
digits of the hand after falling from a wagon. Galen described the problem as be-
ing localized in the first spinal nerve 1 and healed the patient by treating the neck.
Much of the emphasis in Galen's work again focused on the "repositioning" of an
outward dislocation of the spinal column.
Although the advent of the Middle Ages brought a decline in medical advance-
ment, an Arabic physician named Avicenna wrote a large work around the year
AD 1000 summarizing the medical knowledge of the day. In the work, references
are made to manual medicine, with descriptions and illustrations similar to the
Hippocratic method . The Hippocratic method had survived, virtually unchanged
in technique, well into the Middle Ages. It can be argued that many of the tech-
niques (especially traction and extension principles) are still being used today.
Renaissance
The most well-known contributor to manual medicine in the Renaissance period
was the French surgeon Ambroise Pare, who lived in the l SOOs.1•4 Pare was also
instrumental in the development of some of the early orthopedic surgical tech-
niques. The positional theory was still strong, as evidenced in the following quote:
The exogenous causes of dislocation include falls, hard blows, and prolonged
work in a greatly bent position, e.g. among vineyard workers .... If the vertebrae
are dislocated and far apart, a good method is to lay the patient on a board, face
down, fasten him to it with bands beneath his armpits, around his trunk and
thighs, then pull from top and bottom as hard as possible, but without violence.
If such tension cannot be tolerated, no treatment can be applied. Then you may
place your hands on the out -curving part and press the projecting vertebrae. 4
Again, during this period evidence exists for traction and manipulation into ex-
tension, with the fundamental theory being repositioning of the vertebra as in the
Hippocratic method .
Bone Setters
From the mid- 1600s well into the nineteenth century, the "bone setters" of En-
gland flourished. Bone setters, considered "quacks" by traditional medical practi-
tioners, had no formal training; their art was generally passed on from parents to
children, generation after generation. Bone setters were known locally, had other
primary occupations, and usually treated

"con amore" (a term used to imply "without
pay").
Bone setters derived their name from
their basic philosophy that small bones can
move out of place and that healing takes
place when the bones are restored to their
original positions. One of the most well-
known bone setters was Sarah Mapp, a
vagrant peasant woman, who was sought
out by commoners and nobility alike (Fig-
ure 1.3). The fact that members of the no-
bility sought out bone setters infuriated the
Figure 1.3 The bone setter Sarah Mapp (Crazy
Sally). Source:Reprinted with permission from traditional medical community. For many
E. H. Schoitz, Manipulation Treatment of the Spinal years, the medical community hotly de-
Column From the Medical-Historical Standpoint, bated the subject of bone setting, with some
Part I, Journal of the Norwegian Medical Associa-
physicians being shunned for speaking in
tion (1958;78:359- 372). Copyright© 1958, Norske
Laegeforening. their favor.
This controversy is exemplified by
Wharton Hood, a medical doctor in the
community, who learned the practice of bone setting from one of his patients,
whom he had treated for a systemic illness. Realizing the effectiveness of such
treatment in his own practice, Hood wrote boldly in the journals of the day in
favor of bone setting:
I obtained information, which surgeons do not learn, and which, if related to
anatomical knowledge, is of the greatest possible value from the prophylactic
and therapeutic viewpoints ... It is entirely evident that quackery, among other
things, is an expression of the extent to which the authorized physicians have
failed to fulfill their patient's quite reasonable desires or demands. If the physi-
cian does not know how to fulfill or pursue these needs, it is his duty to study
them, and in no respect can he fulfill his duty merely by criticizing quacks for
his failures. 1<P5>
Another physician of the day who defended manual medicine was English sur-
geon Sir James Paget (1814-1 899), a respected medical school professor. In a lecture
to his students and later in an editorial to one of the medical journals, he wrote,
Few of you will enter into practice today without having a so-called bone setter
as a competitor. There is little point in presenting a lecture on the injuries which
these persons cause; it is more important to consider the fact that their treatment
can do some good .... Learn then to imitate what is good and avoid what is bad in
the practice of bone setters. Fas est ab hoste doceri! (It is advisable to learn from
one's opponent.) l(p6)
Still another surgeon of the day wrote, "The success of certain bone setters is
due -i n addition to their skill -t o the lack of practice and ignorance with which
the practicing physician is equipped as concerns injuries to and diseases of the

joints." 1
One of the best-known bone setters, Herbert Barker, who practiced from the
late 1800s until 1927,vainly attempted to obtain credibility and good standing in
the medical community by inviting physicians to observe his work and offering
to perform demonstrations. His work was effective enough to attract members of
the British royal family, actors, and politicians. Despite his successful treatments
and his willingness to submit his work to the medical community's scrutiny, he
was still shunned by the physicians of the day. Finally, frustrated by the arrogant
attitudes of his contemporary physicians, Barker wrote,
Strong as the love of service to suffering is among many doctors as a whole; there
exists some things much stronger and less worthy in prejudice and jealousy,
which have from the beginning of time darkened the pages of surgical history,
and smirched its record of noble endeavors. 5
Eventually, the medical community could no longer argue with the success of
bone setters, and in 1925 an editorial in Lancet stated,
The medical history of the future will have to record that our profession has
greatly neglected this important subject ... the fact must be faced that the bone
setters have been curing multitudes of cases by movement ... and that by our
faulty methods, we are largely responsible for their very existence. 6
Osteopathic Medicine and Chiropractic

While controversy was raging over England's bone setters, a similar controversy
existed in America during the 1800s and early 1900s. America's first bone setters
were practicing by the mid- 1800s in Rhode Island and Connecticut and were criti-
cized by skeptics, just as in England. 4
In the mid-1860s, Andrew Taylor Still, who had attended but never finished
medical school, was helping his father cure native Indians and "simple folks" in the
Midwest, when he lost three of his children to spinal meningitis. Disgusted with
the traditional practice of medicine, he founded the practice of osteopathic medi-
cine in 1874, probably influenced by the bone setters of his time. Taylor maintained
that it was God who "asked him to fling in the breeze the banner of osteopathy." 7
Being a very religious man, Still dedicated his first textbook to God : "Respectfully
dedicated to the Grand Architect and Builder of the Universe." 7 His basic theory
was that the human organism had the innate strength to combat disease and, as a
vital machine of structure and function, would remain healthy as long as the body
remained structurally normal. If the structure was abnormal, the function would
be adversely affected. Still maintained that the causes of all diseases were
dislocated bones, abnormal, dislocated ligaments or contracted muscles, par -

ticularly in the spine, exercising a mechanical pressure on the blood vessels and
nerves, a pressure that in part produces ischemia and necrosis, and in part an
obstruction of the "vital juices" through the nerves .7
Thus, the rule of the artery and the rule of structure governing function be-
came the cornerstones of osteopathic thought. Unfortunately, the treatment
scheme included "cures" for all sorts of systemic diseases. Fortunately, osteopathic
medicine continued to evolve into a more scientific and realistic philosophy. In
1956, the Register of Osteopaths in England compiled the osteopathic Blue Book,
which stated in part that "osteopathy is a system of therapeutics which lays chief
emphasis upon the diagnosis and treatment of structural and mechanical derange-
ments of the body." 8 By imposing these limitations, osteopathic physicians and
osteopathic practice have become more accepted even though the theories are still
debated. Three areas in osteopathic medicine that are currently applicable to myo-
fascial manipulation are muscle energy techniques, positional release techniques,
and strain/counterstrain techniques. 9 - 11
In 1895, 21 years after Still had founded osteopathic medicine, David Daniel
Palmer founded chiropractic. Some of the cure-all claims of osteopathic practice
were being relinquished and were subsequently adopted by chiropractors. Palmer
learned his technique through rediscovery of the ancient Hippocratic methods
and from osteopathic medicine. He did, however, claim to be the founder of a new
.
science.
But I maintain to have been the first who repositioned dislocated vertebrae by us-
ing the spinous process and the transverse process as levers ... and starting from
these fundamental facts to have founded a science that is destined to revolution -
ize the theory and practice of the healing art. 7
Dr. Charles Still, son of the founder of osteopathic medicine, maintained

that Palmer had acquired his skills from a certain student at the Kirksville Os-
teopathic School and wrote, "Chiropractic is the malignant tumor on the body of
osteopathy." 7
The original premise of chiropractic can be summed up as the "law of the
nerve":
1. A vertebra can become subluxated.

2. A subluxation is apt to affect the structures that pass th rough the interverte -
bral foramen (nerves, blood vessels, and lymphatic vessels).
3. As a result the reof, a disruption of the function can occur at the correspond-
ing segment in the spinal cord with its spinal and autonomic nerves, so that
the conduction of nerve impulses becomes impaired.
4. As a result the reof, the innervations of certain parts of the organism change
abnormally, so that they become functionally or organically sick, or they be-
come disposed to disease.
5. An adjustment (reposition)of a subluxated vertebra causes the structures
passing th rough the intervertebral foramen to be released, whereby the nor-
mal innervation of the organs is restored, so that they become functionally
and organically rehabilitated ?
From ancient times to the end of the nineteenth century, manual medicine
had been practiced with an apparent high degree of success. The emphasis during
this era was on repositioning a subluxation for the reduction of pain and restora-
tion of health . With traditional medicine coming closer to embracing the value of
manual medicine, the advent of the scientific age spurred new clinical investiga-
tions and research on the subject. Today, the subluxation philosophy has been par-
tially replaced with the mobility philosophy in explaining the theories of manual
medicine.
Modern Times: The Trend Toward Mobility

and Diagnosis of Pathology
In the early 1920s, physician participation in manual medicine became more com-
mon, especially in Great Britain, where the practice had been hotly debated for
many years. One of the first physicians to publish extensively and authoritatively
on the subject was Edgar Cyriax, father of the late James Cyriax. Dr. James Cyriax
is best remembered as one of the first to recognize discogenic pathology as a cause
of back pain. 9•12
In the late 1920s, the utilization of basic science, especially arthrokinemat-
ics, became a significant factor in the study and philosophy of manual medicine,
which influenced both scientists and medical personnel to explore further the the-
ory of manual medicine. R. K. Ghormley was one of the first scientists to describe
the facet joints as a possible cause of low-back pain. 13 He contended that arthritic
changes in the facet joints narrowed the intervertebral foramen, causing sciatic
pain. Unfortunately, the condition he described was largely untreatable, and the
hypothesis was later obscured by the idea of discogenic pathology as a cause of
low-back pain and sciatica. 14
Basic science and arthrokinematics continued to influence and redefine man-
ual medicine, however, and in the late 1940s and early 1950s, James Mennell pub-
lished several volumes, including Physical Treatment by Movement, Manipulation
and Massage 15 and The Science and Art of Joint Manipulation. 16 Mennell was a
strong advocate of intimate joint mechanics and the use of appropriate mobili-
zation based on those same mechanics. He is believed to have been the first to
coin the term accessory motion to describe involuntary motions that are neces-
sary in a joint for proper movement. He was also a strong proponent of the facet
hypothesis in the evaluation and treatment of back pain, and he recognized lack
of mobility of the facet joints as being a causative factor in back pain. Mennell's
early recognition of periarticular soft tissue dysfunction as a causative factor in
back pain is significant in the development of the theoretical basis of soft tissue
manipulation.
Also in the late 1940s and early 1950s, James Cyriax published the first edition
of his now classic Textbook of Orthopaedic Medicine. 17 The greatness of this publi-
cation lies in the differential diagnosis of musculoskeletal disorders and dysfunc-
tions of the extremities. The work remains unsurpassed to this day. Cyriax's work
is of special significance in the area of myofascial manipulation in the recognition,
categorization, and differential diagnosis of the body's various soft tissues. The
fact that pain could be caused by dysfunction of various or selective soft tissues,
including, but not limited to, periarticular connective tissue, is a foundation of
soft tissue manipulation today. Cyriax was also the first to introduce the concept
of "end feel" in the diagnosis of soft tissue lesions. Cyriax summarizes his own
philosophy as follows:
In particular, I have tried to steer manipulation away from the lay notion of a
panacea - the chief factor delaying its acceptance today. My only important dis -
covery, on which the whole of this work rests, is the method of systematic exami-
nation of the moving parts by selective tension. By this means, precise diagnoses
can be achieved in disorders of the radio-translucent moving tissues. 17(pxi)
The recognition of radiotranslucent moving tissues as the cause of pain is a

cornerstone in the validation of treatment of soft tissue pathology, even though
Cyriax deviated somewhat from his philosophy when evaluating and treating the
spine. Oddly, his views on low-back pain remained strongly and narrowly in the
realm of discogenic lesions, which is perplexing in light of the extremely system-
atic evaluation of the soft tissues advocated in extremity dysfunction.
Historically, the shift toward mobility and soft tissues in the etiology of back
pain is quite evident by the mid - twentieth century. The trend continued with
James Mennell's son, John, who was another advocate of the mobility philosophy.
John Mennell operationally defined the different terms, which by this time had be-
come confusing. In his book Joint Pain, Mennell argued that the principal cause of
pain arose from the synovial joints of the back, and not the disc. 18 He argued that
there was no reason why the synovial joints of the spine should respond to trauma
and/or therapeutic measures any differently from any other synovial joint of the
body. Mennell outlined the etiological factors that give rise to joint pain:
1. Intrinsic joint trauma
2. Immobilization that includes therapeutic immobilization, disuse, and aging
3. The healing of a more serious pathological condition in the musculoskeletal
system
Mennell also advocated the following concepts in operationally defining man-

ual therapy terminology:
1. There is a normal anatomical range of mechanical play movements in syno -
vial joints. It is prerequisite to efficient pain -free movement. This is joint
play.
2. Loss of joint play results in a mechanical pathological condition manifested
by impaired (or lost) function and pain. This is joint dysfunction.
3. Mechanical restoration of joint play by a second party is the logical treatment
of joint dysfunction. This is joint manipulation. 19
Thus, by moving joints in selective ways, the connective tissues surrounding the
joint are appropriately stretched and normal movement is restored . The extensibil-
ity of the surrounding tissues is what ultimately allows for normal arthrokinemat-
ics in the joint.
Another person responsible for bringing arthrokinematics into the evaluation

and treatment of joint pain was Norwegian physiotherapist Freddy Kaltenborn.
Influenced by James Cyriax, Kaltenborn's classic text on extremity mobilization
was the first that consistently and comprehensively used arthrokinematic prin-
°
ciples to restore function to joints. 2 Kaltenborn was the first to advocate heav-
ily the convex/concave rule for joint mobilization. He defined mobilization as "a
component of manual therapy referring to any procedure that increases mobility of
the soft tissues (soft tissue mobilization) and/or the joints (joint mobilization)." 20
The implication made by Mennell, James Cyriax, and others is that restor-
ing the mobility of the joint restores normal function and thereby reduces pain.
A strong proponent of this idea was Stanley Paris, who wrote that the treatment
of spinal pain involved treatment of the dysfunction and not of the pain itself.
Paris wrote, "Dysfunction is the cause of pain. Pain follows dysfunction - pain
cannot precede dysfunction. Pain does not warn of anything, it states 'something
is wrong."' 3,21- 23 According to Paris and others, normalizing mobility and func-
tion in the spine will effectively reduce or eliminate the pain. Paris further opera-
tionally defined the various accessory motions of joints in the following manner:
(1) component motions are those motions occurring in a joint during active mo-
tion that are necessary for the motion to take place normally, and (2) joint play
motions are those motions that are not under voluntary control and that occur
only in response to outside forces. 21
Paris developed a comprehensive evaluative system that included, in part, the
evaluation of passive segmental mobility of the individual joints of the spine. He
also classified manipulation into three distinct categories:
1. Distract ion: when two articular surfaces are separated from one another. Distrac -
tions are used to unweigh t the joint surfaces, to relieve pressure on an intra -articular
structure, to stretch a joint capsule, or to assist in the reduction of a dislocation.
2. Nonthrust art iculation: when the joint is either oscillated within the limits of
an accessory motion or taken to the end of its accessory range and then oscillated or
stretched. Articulations are used mechanically to elongate the connective tissues, includ -
ing adhesions, and neurophysiologically to fire cutaneous, muscular, and joint receptor
mechanisms.
3. Thrust man ipulation: when a sudden high -velocity, short -amplitude motion is de -
livered at the pathological limit of an accessory motion. The purpose is to alter positional
relationships, snap an adhesion, or produce neurophysiological effects.21
Another proponent of the mobility theory is G. D. Maitland of Australia. His

treatment system includes "graded oscillations" of grades I-I V.24 The oscillations
are thought to work by increasing mobility as well as modulating pain through
neurophysiological effects.
The mobility theory became so dominant in manual therapy that in the 1970s
the chiropractic profession redefined its philosophy to include movement abnor-
malities, while retaining its subluxation theory. Several studies, as early as the
1980s, used fluoroscopy to show changes in mobility of spinal facet joints after a
thrust manipulation. 25 These studies are impressive and validate the effectiveness
of manual therapy for increasing mobility.
The next logical step in the evolution of manual medicine was the emphasis on
the histology and biomechanics of connective tissue. Because restoration of mo-
tion is manual therapy's primary goal, and because all the periarticular tissues af-
fected during manual therapy are connective tissues (soft tissues), understanding
the biomechanics of connective tissues became paramount. Substantial research
was performed by Akeson, Amiel, Woo, and others to determine the biomechani-
cal characteristics of normal and immobilized connective tissues. This research
provided the building blocks for much of what is known today. The findings of
this research are discussed in detail in Chapter 3, "Histology and Biomechanics of
Myofascia," and Chapter 4, "Histopathology of Myofascia and Physiology of Myo-
fascial Manipulation." Advances in the understanding of connective tissue have
helped explain the effectiveness of manual therapy, especially that of myofascial
manipulation.
Such advances increasingly support the need for an integrated treatment ap-
proach. Research to date is beginning to shed light on some of the biomechanical
mysteries of soft tissue as well as some of its functions, not previously known or
merely suspected . Not only does connective tissue help hold the body together, but
it is a living, responsive, ever-changing tissue. One area that is gaining notoriety
is that of "tensegrity." As described by Buckminster Fuller, tensegrityis an archi-
tectural concept referring to structures under continuous tension. It is a concept
observed even at the cellular level in the cytoskeleton. 26 This concept is further de-
veloped in Chapter 4, "Histopathology of Myofascia and Physiology of Myofascial
Manipulation," and Chapter 5, "Neuromechanical Aspects of Myofascial Pathol-
ogy and Manipulation." Additionally, preliminary findings suggest that the ability
of connective tissue to contract may be similar to that of smooth muscle (discussed
in Chapter 4).27- 29
Future Considerations
Manual therapy continues to evolve. The number of journals dedicated to this
profession and to soft tissue work alone has increased tremendously. Although
manual therapy can be an effective tool for treating and managing spinal prob-
lems, the incidences of chronic low-back pain continue to soar. One state alone
showed a significant increase within a 14-year period (3.9% in 1992 to 10.2% in
2006), which may exemplify similar increases nationally. 30 Integrative therapies
and theories of movement science, in conjunction with manual techniques, can
help overcome patient fear avoidance and may lead to education, wellness, and
prevention.
The idea of exercise for prevention of low-back pain is widely sanctioned, and
conventional exercise can be considered movement science in rudimentary form.
Manual techniques can correct the dysfunction, and movement therapies may
help prevent future recurrence. Together, they create a much needed and more
complete form of treatment.
Myofascial manipulation not only produces mechanical and autonomic re-
sults but also fosters the continued growth of modulated central nervous system
mechanisms. The idea that myofascial manipulation can be a form of "sensory-
motor education," helping to establish more efficient movement patterns, is
strongly emerging to complement motor learning theories. 31 Such topics are gain-
ing momentum. The topic under current investigation is whether connective tissue
is an unrecognized, whole body communication system. It may be the "missing
link needed to improve cross-system integration in both biomechanical science
and medicine." 32<P3l
References
1. Schoitz E. Manipulation treatment of the spinal column from the medical-historical standpoint.
TidsskrNor Laegeforen.1958;78:359- 372.
2. De Domenico G. Beard'sMassage:Principlesand Practiceof Soft TissueManipulation. St. Louis,
MO: Saunders Elsevier; 2007.
3. Loubert P, Paris SY. Foundationsof ClinicalOrthopaedics.Saint Augustine, FL: Institute Press;
2008.
4. Lomax E. Manipulative therapy: a historical perspective from ancient times to the modern era.
In: Goldstein M, ed. The ResearchStatus of SpinalManipulative Therapy.Bethesda, MD: Na -
tional Institute of Neurological and Communicative Disorders and Stroke; 1975.
5. Hood W On the so-called bone setting, its nature and results. Lancet. 1867:336- 338, 441-443,
499- 501.
6. Paget J. Clinical lecture on cases that bone-setters cure. BMJ. 1867.
7. Schoitz E. Manipulative treatment of the spine from a medical-historical point of view. II: Oste-
opathy and chiropractic. TidsskrNor Laegeforen.1958;78:429- 438.
8. Schoitz E. Manipulative treatment of the column from the medical-historical point of view.
III: The last 100 years. J NorwegMed Assoc. 1958;78:946- 950.
9. Deig D. PositionalReleaseTechniques.Course notes. Krannert Graduate School of Physical
Therapy, University of Indianapolis, IN; 1991.
10. Jones L. Spontaneous release by positioning. The Doctor of Osteopathy. 1964;4:109- 116.
11. Jones L. Strain and Counterstrain. Colorado Springs, CO: American Academy of Osteopathy;
1981.
12. Cyriax E. CollectedPapers on Mechano-1herapeutics.London, UK: Bale and Danielson; 1924.
13. Ghormley R. Low back pain with special reference to the articular facets. JAMA.
1933;101:1773- 1777.
14. Mixter W, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal.
New Engl Surg Soc. 1934;2:210- 215.
15. Mennell J. Physical Treatment by Movement, Manipulation and Massage. Boston: Little,
Brown & Co; 1945.
16. Mennell JB. The Scienceand Art of Joint Manipulation. London, UK: Churchill; 1949.
17. Cyriax J. Textbook of OrthopaedicMedicine. Vols 1, 2. London, UK: Bailliere Tindall; 1982.
18. Mennell JM. Joint Pain. Boston: Little, Brown; 1964.
19. Mennell JM. History of the development of medical manipulative concepts: medical termi-
nology. In: Goldstein M, ed. The ResearchStatus of Spinal Manipulative Therapy.Monograph
No. 15. Bethesda, MD: National Institute of Neurological and Communicative Disorders and
Stroke; 1975:19-24.
20. Kaltenborn F. Manual Mobilization of the Joints: 1he Extremities. 6th ed. Minneapolis, MN:
Orthopaedic Physical Therapy Products; 2002.
21. Paris S. The Spine:Etiology and Treatment of Dysfunction IncludingJoint Manipulation. Saint
Augustine, FL: Institute of Graduate Physical Therapy; 1979.
22. Paris S. Mobilization of the spine. Phys 1her. 1979;59:988- 995.
23. Paris S. Spinal manipulative therapy. Clin Orthop. 1983;179:5561.
24. Maitland GD. PeripheralManipulation. Woburn, MA: Butterworth-Heinemann; 1981.
25. Atlanta Craniomandibular Society/Life Chiropractic College Joint Seminar. August 1987;
Atlanta, GA.
26. Chen C, Ingber, DE. Tensegrity and mechanoregulation: from skeleton to cytoskeleton. In:
Findley T, Schleip R, ed. Fascia Research:Basic Scienceand Implicationsfor Conventional and
Complementary Health Care. Boston: Elsevier; 2007:20 - 32.
27. Schleip R, Klingler W, Lehmann-Horn F. Active fascia l contractility: fascia may be able to
contract in a smooth muscle-like manner and thereby influence musculoskeletal dynamics.
Med Hypotheses. 2006;65:273 - 277.
28. Schleip R, Klingler W, Lehmann-Horn F. Fascia is able to contract in a smooth muscle-like
manner and thereby influence musculoskeletal mechanics. In: Liepsch D, ed. Proceedingsof
the 5th World Congressof Biomechanics.Munich, Germany: Medimond: International Pro-
ceedings; 2006:51- 54.
29. Schleip R, Klingler W, Lehmann-Horn F. Active contraction of the thoracolumbar fascia: in-
dications of a new factor in low back pain research with implications for manual therapy. In:
Vleeming A, Mooney V, Hodgers P, eds. Paper presented at: 5th Interdisciplinary World Con-
gress on Low Back & Pelvic Pain, 2004, Melbourne. www.fasciaresearch .de/MelbourneReport
.pdf. Accessed December 3, 2010.
30. Freburger J, Jackman AM, Castel LD. The rising prevalence of chronic low back pain. Arch
Intern Med. 2009;169:251- 258.
31. Juhan D. Job'sBody:A Handbookfor Bodywork. Barrytown, NY: Station Hill Press; 1987.
32. Langevin H. Connective tissue: a body-wide signaling network? Med Hypotheses.
2006;66:1074 - 1077.
Modern Theories and Systems
of Myofascial Manipulation
Robert I. Ca ntu, A lan J. Grodin, and Robert W. Sta nbo rough
This chapter provides an overview of some of the alternate somatic therapies con-
sidered myofascial in nature. Its purpose is neither to give the reader a comprehen-
sive background of each individual system nor to include every system currently
being practiced - such undertakings would be books in themselves. The systems
reviewed represent those that have most influenced the authors over the years and
that have contributed to the development of personal treatment philosophies. The
manual therapist interested in myofascial manipulation should also have a basic
working knowledge of the fundamental philosophies behind various systems and
theories both to become a more educated consumer in the continuing education
market and to understand the orientation of the respective practitioners.
Modern theories and systems are arranged in three categories: autonomic, or
reflexive, approaches; mechanical approaches; and movement approaches. Auto-
nomic approaches are those that exert therapeutic effect on the autonomic ner-
vous system, mechanical approaches are those that actually attempt mechanical
changes in the myofascia by direct application of force, and movement approaches
are those that attempt to change aberrant movement patterns and establish more
optimal ones. Ideally, the manual therapist should have a basic working knowledge
of theories or systems in all three areas, along with some application techniques
from each approach.
Autonomic Approaches
The autonomic, or reflexive, approaches attempt to exert their effect through the
skin and superficial connective tissues. 1•2 MacKenzie defined the autonomic, or
reflexive, component as "that vital process which is concerned in the reception of
a stimulus by one organ or tissue and its conduction to another organ, which on
receiving a stimulus produces the effect." 3<P47l Soft tissue mobilization performed
for autonomic effect stimulates sensory receptors in the skin and superficial fas-
cia. These stimuli pass through afferent pathways to the spinal cord and may be
17
channeled through autonomic pathways, producing effects in areas corresponding

to the dermatomal zones being mobilized. 4
The idea of affecting various body areas by stimulating the skin and superficial
connective tissue has been used in areas apart from soft tissue mobilization. For
example, part of the theory of transcutaneous electrical nerve stimulation (TENS)
is that direct stimulation of large myelinated nerve fibers overrides noxious stimuli
traveling to higher centers of the central nervous system. Therefore, TENS has ap-
plication not only for pain control but also for control of postsurgical nausea or
menstrual cramping.
Affecting the autonomic system is an important stepping-stone to more ag-
gressive, mechanical work, especially in acute patients. In subacute patients, auto-
nomic techniques are most often used at the beginning and at the end of treatment
to provide entry and exit from mechanical technique. The effects of autonomic
technique should not be overemphasized, however. Some practitioners have used
this autonomic phenomenon to justify treatment of disorders unrelated to the
neuromusculoskeletal system. Although the autonomic effect cannot be denied,
judgment should be exercised by the clinician in evaluating the extent of auto-
nomic treatment.
Connective Tissue Massage (Bindegewebsmassage)

Connective tissue massage (CTM) was developed in the 1920s by German phys-
iotherapist Elizabeth Dicke 1 and later expanded by Maria Ebner. 2 The system was
conceptualized and put into practice in rudimentary form in the late 1920s when
Dicke was suffering from a prolonged illness caused by an "impairment of the
circulation" in her right leg, later diagnosed as endarteritis obliterans. The leg was
cold and discolored, with significant but diffuse numbness and loss of distal pulses.
The attending physicians prescribed a prolonged period of bed rest. Had bed rest
failed to diminish the symptoms, amputation would have been considered as a last
resort . Dicke was in bed for a 5-month period, during which time she understand-
ably developed significant low-back pain. As she began to palpate her own back,
she found exquisite tenderness, hypersensitivity, and palpatory changes in the area
of the iliac crest and sacrum. She stated that she felt "a thickened infiltrated area
of tissue, and opposite it, an increased tension of the epidermis and dermis." 1 As
many people do to painful and sensitive areas, she gently massaged the superficial,
tender areas, which produced relief. Over time, the low-back pain diminished and,
more important, notable changes occurred in the lower extremity. As her symp-
toms resolved, she initially felt itching, fallowed by warm flushes and increased
sensation. She then began exploring the extremity itself and found other hyper-
sensitive areas, especially along the border of the greater trochanter and the ilio-
tibial tract. She very gently and superficially stroked these areas, and improvement
continued. Within 3 months her symptoms had subsided, and shortly thereafter
she was able to resume her full duties as a physiotherapist.
Out of her experiences, Dicke gradually constructed a systematic treatment
method . From this pursuit, she also extrapolated a treatment of organic pain,
Mode rn Theories and Systems of Myofascia l Manipulation 19
which is beyond the realm of this book The effects outlined by Dicke that are per-
tinent to modern manual therapy are as follows:
1. CTM can directly influence connective tissue that is locally altered by illness
(i.e., scars, local blood supply, and other disturbances).
2. CTM can set general circulation in order. Subcutaneous connect ive tissue is
extremely vascularized and can absorb varied quantities of blood as a result
of constriction or dilation.
3. CTM can release nerve impulses along quite specific paths by means of re -
flexes that are locked into the central nervous system. It can create reactions
in distant organs. Dicke refers to certain aspects of this phenomenon as the
"cutivisceral reflex." 1 Dicke uses the example of the application of a mother's
warm hand to alleviate a child's stomachache. Obviously, the intestine would
not be affected from the surface of the skin, and the reaction must be due
to an autonomic response affecting the intestines via the skin. The skin and
subcutaneous tissues, which are highly innervated and vascularized, are the
primary tissues for the reception of outside tactile stimuli.
The CTM system is very systematic and protocol oriented if performed as

Dicke taught. Each stroke, for example, is performed three times, with the right
side always first. Most strokes are performed with the middle finger of the hand,
with the other hand always in light contact with the patient. Lubrication is never
used, and the low back and sacral areas are always treated first. Treatment is never
administered without first treating the basic section of the low back, sacrum, and
coccyx, with a "build-up" to the affected area. What must be remembered about
CTM and about all other "systems" is that they are merely systems. Astute clini-
cians can and should modify these systems while assisting patients in the course
of their recovery.
CTM exerts its effect using the skin and subcutaneous connective tissue. This
makes CTM primarily a superficial form of myofascial manipulation (in terms of
depth of penetration), one that provides much needed techniques on the "lighter"
end of the manual technique spectrum. Manual therapists often move too quickly
into moderate or deep-level technique, instead of gradually entering the myofas-
cial system.
CTM offers other therapeutic advantages when integrated properly into
the overall treatment scheme. In a patient who is autonomically hypersensi-
tive, CTM provides the type of technique that can quiet the system. Such an
acute patient can be described as having a reflex sympathetic dystrophy (RSD)-
type back. Often seen in the hands and feet, RSD is a hyperactivity of the sym-
pathetic nervous system that creates chronic intense pain and hypersensitivity,
cold clammy feeling, cold sweat in the area, nausea with attempted palpation,
and eventually trophic changes including shiny skin and bone and hair loss. A
patient with an RSD-type back may display some of these symptoms, although
without most of the accompanying signs. The patient may exhibit hypersensi-
tivity to palpation, a cold clammy feel to the back with attempted palpation or
treatment, and a nausea response. The superficiality of CTM makes it a prime
choice of technique, because it primarily affects the autonomic nervous system.

The CTM technique also allows the patient to grow accustomed to the clini-
cian's hands in a very nonthreatening manner, further promoting relaxation and
rapport .
In cases where deeper myofascial restrictions exist, the CTM technique pro-
vides a good entry into the deeper tissues. If the clinician penetrates the layers of
myofascia too rapidly, reflex guarding of the deep myofascia may result, rendering
treatment more difficult. Moving from superficial to deep treatment facilitates the
accessing and treating of the deeper myofascial elements. The clinician thus allows
the body to open itself to treatment, which becomes less forceful with less potential
for tissue microtrauma and exacerbation of pain. Deep technique does not need to
be aggressive, if the deep tissue is accessed appropriately.
Hoffa Massage
Albert Hoffa's text, published in 1900 and later revised by Max Bohm in 1913, rep-
resents more classical massage techniques, such as eflleurage, petrissage, tapote-
ment, and vibration. 4- 6 Although most therapists learn these as standard massage
techniques in entry-level programs, they are recognized and discussed because of
their importance in the overall treatment scheme . Some clinicians may disregard
this type of massage, regarding it as too basic to include in the realm of advanced
manual therapy; however, leaving behind traditional myofascial manipulation
techniques can handicap even the most advanced manual therapists. A technique
is not necessarily more effective just because it is more complex.
Some may consider these techniques to be more mechanical in nature, but
the strokes can be lighter and designed to be relaxing, which categorizes them
as reflexive, or autonomic. Many myofascial manipulation systems are neither
exclusively reflexive nor exclusively mechanical but may lean toward one more
than the other. Hoffa massage certainly inclines toward the reflexive. Hoffa states
that forces used should be gentle and "light-handed" so the patient feels very little
pain. 5 Hoffa advocates that massage should never last more than 15 minutes, even
for the whole body.
As with CTM, Hoffa massage emphasizes using autonomic, or reflexive, tech-
nique as an entryway for other, more mechanical techniques. With Hoffa mas-
sage or CTM, the patient is prepared - and more specifically, the myofascia is pre-
pared - for techniques designed to promote histological changes in the myofascial
tissues. The changes can be made without forceful maneuvers that can create mi-
crotrauma or exacerbate painful conditions. Some of Hoffa's basic massage strokes
are described as follows:
Effleurage techniques slide or glide over the skin with a smooth, continuous mo -
tion. Pressure may be light to moderate, as when applying oil or warming an area,
or may be deep, as when facilitating venous return in heavily muscled areas ....
When effleurage is performed with moderate pressure, slowly and smoo thly on
the back, it may stimula te the parasympathetic nervous system and evoke the
relaxation response. 4<P73>
Petrissagetechniques lift, wring or squeeze soft tissue in a kneading motion or

press or roll the tissues under or between the hands ... may be performed with
one or two hands ... to 'milk' a muscle of accumulated metabolites, increase
circulation, and assist venous return. Petrissage may also help separate muscle
fibers and evoke muscular relaxation.4<p36)
Tapotement consists of a series of brisk percussive movements following each
other in rapid, alternating fashion .... The movement ... is light, rapid, and
rhythmic. The hands should "bounce off" the surface as they make contact, light-
ening the impact.4<P95)
Hoffa was one of the first clinicians to describe massage in an actual textbook.
The fundamental strokes of traditional massage are still performed widely today,
although many variations have been introduced . Hoffa's massage techniques are
considered basic by modern standards, but advanced manual therapists continue
to use his techniques in their treatment schemes.
Mechanical Approaches
Mechanical approaches differ from autonomic approaches in that they seek to
make mechanical, or histological, changes in the myofascial structures. Superfi-
cial tissue rolling to mobilize adhesions, elongation of a superficial fascial plane,
and stretching of a hamstring are examples of mechanical techniques. The pur-
pose of each is to improve the mechanical mobility of the tissue treated . As pre-
viously stated, mechanical techniques should generally be performed following
some form of an autonomic technique. Even if the patient is not suffering acute
pain, a few minutes of an autonomic technique may facilitate the application of
a mechanical technique. The application of a mechanical technique is not neces-
sarily aggressive. For the most part, tissue mobility should not be forced; instead,
the clinician should make changes gradually, properly going through the "layers"
until the deeper tissues are accessed. That is not to say that aggressive, more force-
ful mechanical technique is an inferior form of treatment; at times, such forceful
technique is necessary to free up long-standing restrictions. Gentler technique,
however, should always be attempted first.
Remember that the systems described in the following subsections are just
that: systems - they can be very protocol oriented and very ordered. An eclectic
approach is useful, because each patient is different and will respond to each tech-
nique differently. Principles may be borrowed from any system, however, and may
be effective if used at the proper time and in the proper sequence.
Rolfing ® (Structural Integration) *

Structural integration, a system created by Ida Rolf, PhD, is used to correct inef-
ficient posture or to integrate structure. Rolf believed that myofascial components
determined the adequacy of the joint and that by "integrating" the myofascia to
normal or more toward normal, the patient would have more "normal" movement.
*Rolfing• is a registered service mark of the Rolf Institute of Structural Integration.

-
"7
--..
--- -
;
--
-
- - --- _.., -·
-- - ;
© 1958 Id• P. Rolf l

Figure 2.1 The concept of balancing posture in a gravitational field, with the body consisting of various
blocks. Source:Reprinted from Rolfing:Re-establishingthe Natural Alignment and Structural Integration of
the Human Bodyfor Vitality and Well-Being(p. 33) by I. Rolf with permission of the Rolf Institute of Struc-
tural Integration,© 1998.
According to Rolf, changes in the body, which she called "functional disorganiza-
tion," are a direct result of exposure to the continuous force of gravity.7 Although
her work included emphasis on the client's entire being, the tissue of focus during
treatment is fascia, as it constantly reorganizes and responds to stresses. She often
likened the relationship of fascia and muscle to that of the fibrous pulp and juice
of a citrus fruit. She equated the fibrous pulp to the fascial connective tissue as the
organ of structure or posture .7,8 Rolfs treat-
Table 2.1 The Rolfing "Recipe" ment technique involves manual soft tissue
Sessions 1-3: sleeve sessions manipulation with the goal of balancing
1. Respiration the body with the forces of the gravitational
2. Balancing under the body (legs and feet) field (Figure 2.1). This is achieved using a
3. Lateral line-front to back (sagittal plane
standardized, nonsymptomatic approach to
balance)
soft tissue manipulation, administered in-
Sessions 4-7: core sessions dependent of specific pathologies.
4. Base of the body/mid line (balance left to The treatment involves what is called
right) "the recipe" of 10 one-hour sessions, each
5. Rectus abdominus/psoas for pelvic balance
6. Sacrum-weight transfer from head to feet
emphasizing a particular aspect of posture
7. Balance of head/neck to the rest of the (Table 2.1). Treatment begins at the periph-
body ery, the outside, and works in. Two or three
advanced sessions may be added, as well as
Sessions 8-10: integration sessions
subsequent occasional "tune-up" sessions.
8. Individual upper and lower half relationship
9. Individual upper and lower half relationship
Rolf's work established a number of
10. Balance of the whole system insights, including the fact that the fascial
Source:Rolf I. Rolfingand PhysicalReality.Rochester, network is continuous throughout the body.
VT: Healing Arts Press; 1977. It is said to become denser and shorter as it
Modern Theories and Systems of Myofascia l Manipulation 23
l
heals. Such "thickenings," if left untreated,
can transmit strain in many directions,
leading to distal restrictions, much like a
snag in a sweater can create strain and fiber
distortion throughout (Figure 2.2).7 Based
on this philosophy and others, her treatment
principle states that "if tissue is restrained,
and balanced movement demanded at a
nearby joint, tissue and joint will relocate in
a more appropriate equilibrium.'' 7
Another premise underlying Rolfing is
that a person's psychological components
are manifested in structure and that chang-
ing the structure can change the psycholog-
ical component. Rolfing strives to integrate
the structural with the psychological:
The technique of Structural Integra -
tion deals primarily with the physical
man; in practice, considerations of the
physical are inseparable from consid-
erations of the psychological. ... Emo-
tional response is behavior, is function.
All behavior is expressed through the
musculoskeletal system .... A man's
emotional state may be seen as the
Figure 2.2 The fascial sweater concept showing
that a fascial restriction in one area will strain ar- projection of his structural imbal -
eas away from the restriction and cause abnormal ances. The easiest, quickest and most
movement patterns. Reprinted from Rolfing:Re- economical method of changing the
establishing the Natural Alignment and Structural coarse matter of the physical body
Integration of the Human Bodyfor Vitality and Well- is by direct intervention in the body.
Being (p. 39) by I. Rolf with permission of the Rolf
Change in the coarser medium alters
Institute of Structural Integration,© 1998.
the less palpable emotional person and
his projections. 9
Picture the slouched posture of a person under considerable stress or fatigue.

Whether due to physical manifestation of the psychological state or simply poor
postural habits, to the structural integrationist or Rolfer, balance and harmony of
movement are the goal to be achieved.
Trager ®*
Tragering is a mechanical soft tissue and neurophysiological reeducation approach
developed by Milton Trager, MD. The approach has no rigid procedures or proto-
cols like some other systems. It uses the nervous system to make changes, rather
than making mechanical changes in the connective tissues themselves. The Trager
*Trager• is a registered service mark of the Trager Institute.
practitioner "uses the hands to communicate a quality of feeling to the nervous sys-
tem, and this feeling then elicits tissue response within the client." 10 Trager began
developing his system in his late teens, while training as a boxer. He subsequently
left boxing to protect his hands and to pursue the development of his system. Eight
years later, Trager undertook formal medical training, earning his medical doctor-
ate at the University Autonoma de Guadalajara in Mexico. He opened his private
practice in 1959 in Waikiki and, in the early 1970s, began teaching his system on
an individual basis in California. The Trager Institute was formed, and there are
currently thousands of Trager practitioners throughout the world.
Tragering is directed toward the unconscious mind of the patient : "For every
physical non-yielding condition there is a psychic counterpart in the unconscious
mind, and exactly to the degree of the physical manifestation." 11 The system uses
gentle passive motions that emphasize mobilization techniques, concentrating on
traction and rotation, and a system of active movements termed Mentastics. The
intensity of the movements is in the moderate range, with integration of cervical
and lumbar traction. The oscillations and rocking techniques serve as relaxation
techniques that encourage the patient to relinquish control gradually. Finally, the
active movement part of the treatment serves as a neuromuscular reeducation
technique similar in principle to that of the Feldenkrais method (discussed later in
this chapter). The idea is to alter the patient's neurophysiological set and give the
patient the tools to maintain the changes. 12 The therapist is not attempting to make
mechanical changes in the soft tissues but is trying to alter the neuromuscular set
to establish more normal movement patterns.
Myofascial Release
The term myofascial releasewas first used in reference to specific soft tissue tech-
niques in 1981.Robert Ward, DO, Anthony Chila, DO, FAAO, and John Peckman,
DO, are credited with coining this term when they taught courses titled "Myo-
fascial Release" at Michigan State University. 13 Two distinct styles of myofascial
release techniques exist: direct and indirect. Most of the techniques provided in
this text are from the direct approach.
The intent of the direct technique is to improve the mobility of soft tissue
through application of a slow, controlled mechanical stress directly into a restric-
tion. This is usually done using fingers, thumbs, forearms, or elbows. Pressure is
gradually increased or repeated until the mobility of the tissue is felt to improve.
The tissue may be manipulated while the patient is either passive or actively mov-
ing, depending on the patient's tolerance.
Indirect techniques are applied similarly, with a drastic difference in the
amount of force used. The force used in indirect techniques, compared with that
in direct techniques, is lower in intensity but much longer in duration, which gives
the tissues an opportunity to "melt," or release. These techniques are considered
gentler and are often used when patients are tender or extremely guarded. For
that reason, patient feedback is essential and considered a key component of the
treatment.
Regardless of the style, director indirect, using heavy-handed or light force, the
goal of myofascial release is to increase mobility of the tissue in order to improve
the underlying mechanics of the tissue and ultimately restore proper function.
Movement Approaches
The movement approaches differ from the others in that the patient actively partic-
ipates in therapy. Both autonomic and mechanical approaches rely on the clinician
to impart the changes and movement. In the movement approaches, the clinician
guides the patient through a series of movements to change aberrant patterns and
retrain into more efficient movements and postures.
Proprioceptive Neuromuscular Facilitation

Proprioceptive neuromuscular facilitation (PNF) is a treatment approach devel-
oped in the 1940s by Herman Kabat, MD, PhD, and expanded upon by his physical
therapist assistants Margaret Knott and Dorothy Voss, for the purpose of treating
patients with poliomyelitis. As a movement approach, the basic principles of PNF
are to (1) always keep the treatment approach positive, reinforcing what the patient
can do on both physical and psychological levels; (2) help patients achieve their
highest level of function; and (3) direct the entire human being in each treatment
and not a specific problem or body segment. 14
PNF uses diagonal movements based on synergistic patterns. Two antagonis-
tic patterns make up a "diagonal" and exist for each extremity, the neck, and the
trunk. Each pattern is used to address dysfunction caused by muscle weakness,
poor coordination, and joint restriction. Although a variety of techniques are used,
some of the most commonly taught (some of which are used in this text) are rhyth-
mic initiation, rhythmic stabilization, contract - relax, and hold - relax. General
goals (functional activities) and specific goals (treatment activities) are established
to promote functional movement through facilitation, inhibition, strengthening,
and relaxation of muscle groups. Muscle overload is used when strengthening or
stabilizing, as forces are applied from proximal to distal. 14
Alexander Technique
F. Matthias Alexander was a Shakespearian orator at the turn of the twentieth
century. He developed a consistent problem in projecting his voice. He studied
the relationship of head and neck posture to voice projection and, from that study,
developed a system of movement that can teach the entire body to become more
efficient, regardless of the activity. The technique objectives are improvements in
both posture and body mechanics. Many vocalists, musicians, and other perform-
ing artists use the Alexander technique to improve efficiency.
Because Alexander's recurrent laryngitis persisted despite prolonged peri-
ods of rest, he set up a system of mirrors through which he could observe him-
self speaking in his professional oratorical voice. He observed a tendency to pull
his head back, depress his larynx, and inhale through his mouth. After repeated
practice sessions, he was able to hold his head and neck in a more efficient posture,
and with time, his voice projection improved and his laryngitis subsided. As time
passed, Alexander noticed that the "dysfunctional" head tilting was not an iso-
lated movement but was coordinated with other dysfunctional patterns through-
out his body, such as lifting the chest, arching the back, and tensing the legs and
feet. 15 Alexander theorized that in each human being, there existed an integrating
mechanism that produced more optimal coordination and functioning. Alexan-
der wrote,
I discovered that a certain use of the head in relation to the neck, and of the head
and neck in relation to the torso and other parts of the organism ... constituted a
primary control of the mechanisms as a whole . .. and that when I interfered with
the employment of the primary control of my manner, this was always associated
with a lowering of the standard of my general functioning. 16
Position and motion of the head and neck are, therefore, the cornerstones of
the Alexander technique. The student of the Alexander technique learns to acti-
vate this primary locus of control in the head and neck and to keep it functioning
during activities of daily living. The instructor's approach is usually to give palpa-
tory as well as verbal feedback as the student learns new positions and movement
patterns. As the student masters new patterns, less palpatory and verbal feedback
is given, until the student can independently achieve proper control patterns. Al-
exander was very experiential and deliberate in his approach, reasoning that, like
music teachers who suggest that their students practice slowly, patterns are best
learned slowly and with positive reinforcement.
The technique involves three stages: (1) awareness of the habit, (2) inhibition of
the habit, and (3) conscious control of the habit. These three stages constitute what
Alexander termed "conscious learning," in that the participant deliberately and
actively tries to change old habits while incorporating new ones.
Awareness of the habit carries great importance in the Alexander technique.
For Alexander, public speaking triggered the dysfunctional patterns. He found
he had difficulty even recognizing the patterns that were so detrimental to his
voice projection. He hypothesized that the brain no longer identified the aberrant
patterns of movement as dysfunctional but rather considered them to be normal.
Simply looking in the mirror to correct an aberrant postural or movement dys-
function was insufficient to change the pattern. Developing an awareness of the
pattern was the first step.
Once Alexander recognized the dysfunctional pattern, inhibition of the move-
ment was necessary, but again, being aware of the pattern was not enough to change
it, because the habit was too well established. He began to speak while consciously
trying to "turn off" the dysfunctional pattern. He then used conscious control to
"inhibit" the dysfunctional pattern and integrate the new one.
Some of these principles are integrated into the sequencing of overall treat-
ment. If a patient exhibits poor posture resulting from myofascial restrictions and
Mode rn Theories and Systems of Myofa scial Manipulation 27
movement imbalances, the clinician can use mechanical approaches to free up the
restriction, allowing the patient to assume optimal posture without undue effort.
If new posture is emphasized too early in the treatment sequence, the patient of-
ten may not have the body awareness or the ability to assume it. The new posture,
then, can increase the patient's original pain and establish a negative reinforce-
ment loop. If the clinician addresses mechanical restrictions and emphasizes body
awareness, the patient becomes aware of the problem, is able to inhibit the old
pattern, and can consciously work toward establishing the new pattern, with more
efficient effort.
Alexander's concepts have been used and expanded by others for working with
head and neck posture in relation to mandibular position. As is widely known,
head and neck posture and movement affect mandibular position and function;
the Alexander technique aptly applies to the evaluation and treatment of temporo-
mandibular joint (TMJ) disorders. Whether used for treatment of TMJ, neck, or
other spinal dysfunctions, the Alexander technique merges logically with the au-
tonomic and mechanical approaches in helping myofascial dysfunctional patients
achieve desired changes.
Feldenkrais Method
The Feldenkrais approach seeks to retrain the body away from aberrant movement
patterns into more efficient ones. Moshe Feldenkrais, DSc, was a versatile Israeli
engineer, physicist, and athlete. He participated in soccer and judo, but a persis-
tent knee injury resulting from soccer play led him to explore human movement
from an engineering perspective. His movement approach is based on the idea that
movement abnormalities occur in response to past trauma, rendering one more
susceptible to reinjury. His approach is designed to help the body reprogram the
brain to integrate the whole mind - body entity.
The Feldenkrais method has two basic approaches, separated only for conve-
nience. The first is an experiential approach, termed "Awareness Through Move-
ment," 17 in which the patient receives a series of verbal commands designed to
weaken old movement patterns and to establish new ones. The second is a hands-
on approach termed "Functional Integration." 18 Feldenkrais disliked separating
the two, especially if
the distinction is made that one is for "sick" or "brain damaged" people, and the
other is for "normal, healthy" people. Which of us, after all, is not brain damaged
in the sense that we allow many areas of our brains to atrophy through misuse or
nonuse? We can have terrible posture and movement patterns and habits which
are distorting and damaging to our bodies and brains and still be classified as
"normal." Who are we, then to call other people brain damaged simply because
their particular deficiency produces visible effects that we label" disease" ?19
The idea that all persons exhibit some abnormal movement either from previ-
ous trauma or old habit patterns is a cornerstone of the Feldenkrais method. As
with the Alexander technique, gentle sequences of movement allow for slow, delib-
erate changing of abnormal, inefficient movement patterns into normal, efficient
movements.
Conclusion
Examples of the three types of approaches (autonomic, mechanical, and move-
ment) described in this chapter merge well with the philosophy and scheme of
treatment presented in this book As later chapters illustrate, the sequencing of
treatment that we recommend includes beginning superficially with a manual ap-
proach and working gradually into deeper tissues. Once the clinician has accessed
and affected deeper tissues, limitations within the joints can be examined and/
or treated. The clinician can then work to elongate the structures that have be-
come facilitated. When optimal length and mobility are established, the focus is
on neuromuscular reeducation, using a variety of strengthening or motor control
techniques to prevent recurrence. Eventually postural integration should be im-
plemented. The progression from a light manual approach (autonomic) to a deep
manual approach (mechanical) and then to an emphasis on movement and pos-
ture (movement approach) is the key to complete treatment.
References
1. Dicke E, Schliaek H, Wolff A. A Manual of ReflexiveTherapyof the ConnectiveTissue.Scarsdale,
NY: Sidney S Simon Publishers; 1978.
2. Ebner M. ConnectiveTissueManipulation. Malabar, FL: Robert E. Kreiger Publishing Co; 1985.
3. MacKenzie J. Angina Pectoris.London: Henry Frowde and Hodder and Stroughton; 1923.
4. Tappan F, Benjamin P. Tappan'sHandbookof HealingMassageTechniques:Classic,Holistic,and
EmergingMethods. 3rd ed. Stamford, CT: Appleton and Lange; 1998.
5. Hoffa A. Technickder Massage.14th ed. Stuttgart, Germany: Ferdinand Enke; 1900.
6. Bohm M. Massage:Its Principlesand Technique.Philadelphia, PA: WB Saunders; 1913.
7. Rolf I. Rolfing:Re-establishingthe Natural Alignment and StructuralIntegrationof the Human
Bodyfor Vitality and Well-Being.Rochester, VT: Healing Arts Press; 1989.
8. Rolf I. Rolfingand PhysicalReality.Rochester, VT: Healing Arts Press; 1990.
9. Rolf I. Rolfing:The Integrationof Human Structures.Rochester, VT: Healing Arts Press; 1977.
10. Juhan D. The Trager approach - psychophysical integration and mentastics. The TragerJour-
nal. 1987;Fall:1.
11. Trager M. Trager psychophysical integration and mentastics. The TragerJournal. 1982;Fall:5.
12. Witt P. Trager psychophysical integration: an additional tool in the treatment of chronic spi-
nal pain and dysfunction. Whirlpool. Summer 1986.
13. Manheim C. The Myofascial ReleaseManual. 4th ed. Thorofare, NJ:SLACK;2008.
14. Adler S, Beckers D, Buck M. PNF in Practice:An Illustrated Guide. 3rd ed. Heidleberg, Ger-
many: Springer Medizin Verlag; 2008.
15. Rosenthal E. The Alexander technique: what it is and how it works. Med Prob/Perform Art.
1987;June:53- 57.
Modern Theor ies and Systems of Myofascia l Manipulation 29
16. Alexander F. The UniversalConstant in Living. New York: Dutton; 1941:10.

17. Feldenkrais M. Awareness ThroughMovement. New York: Harper & Row; 1972.
18. Rywerant Y. The FeldenkraisMethod: Teachingby Handling. San Francisco: Harper & Row;
1983.
19. Rosenfeld A. Teaching the body how to program the brain in Moshe 's "miracle." Smithsonian.
January 1981.
PART II
Scientific Basis
for Myofascial Manipulation
Histology and Biomechanics
of Myofascia
Rob ert I. Ca ntu and Rob ert W. Sta nbo rough
The foundations of orthopedic physical therapy are based on the understanding of

human anatomy and biomechanics. Soft tissue, which often guides, directs, and /
or limits movement, is at the very core of biomechanics. Manual physical thera-
pists, as musculoskeletal specialists, need to have in-depth knowledge of the mi-
croscopic and macroscopic structures of the connective tissue (particularly fascia),
muscle, and junctional zones. They also need to understand the mechanics of soft
tissue and its relation to osseus structures, because manual therapy treatments are
aimed at correcting adaptations within connective tissue with the goal of restoring
movement and function. Such knowledge will aid physical therapists in compre-
hending and assessing tissue changes due to trauma or immobilization and will
enable therapists to properly remobilize the myofascial tissues.
Histology and Biomechanics of Connective Tissue

Connective tissue makes up 16% of a person's total body weight and stores 23% of
the body's total water content. 1 Connective tissue forms the base of the skin and
numerous other structures, including fascia, muscle sheaths, nerve sheaths, ten-
dons, ligaments, joint capsules, periosteum, aponeuroses, and blood vessel walls. It
also forms the bed and framework of the internal organs, 1•2 as well as the building
blocks of bone, adipose, and cartilage . Based on its inherent mechanical proper-
ties, connective tissue has a functional capacity but also plays an important role
in the body's defense against invading microorganisms and as a contributor in
tissue repair and reconstruction after injury. 3•4 The importance of these roles to
the manual therapist will be discussed in Chapter 4, "Histopathology of Myofascia
and Physiology of Myofascial Manipulation."
Most of the structures affected by soft tissue or joint manipulation are con-
nective tissues. For example, when a facet joint is manipulated, the joint capsule
itself, which is connective tissue, is affected, as are the surrounding periarticular
The auth ors gratefully ackn owledge the contributions of Deborah Cobb to earlier versions of this chapter.
33
34 SCIENTIFIC BASIS FOR MYOFASCIAL MAN IPULATION
connective tissues, ligaments, and fascia. The joint itself is simply a space between
two articulating surfaces that allows for movement and that is guided, and some-
times limited, by the connective tissue surrounding the joint.
This chapter begins with a review of the scientific literature related to normal
histology and the biomechanics of connective tissue. Although much of the bench-
mark research dates from earlier in history, it is still accurate and consistent with
more recent research. This information lays the groundwork for an understanding
of how trauma, immobilization, and remobilization affect the connective tissues.
Histology
The four basic types of tissue found in the human body are muscle, nerve, epi-
thelium, and connective tissue. 2 Connective tissue is subclassified into connective
tissue proper, cartilage, and bone. Connective tissue proper is further subclassified
by orientation and density of fiber types. 5 The three basic connective tissue types
are dense regular, dense irregular, and loose irregular (Figure 3.1).5 These tissue
Collagen Nerve ~- Adipose cells ~ Elastin Macrophage Pericyte Capillary
Ground Fibroblast
Eosinophil Substance · Neulrophil..,..._,- Masi cell Lymphocyte Plasma Cell
Figure 3.1 A diagrammatic reconstruction of loose connective tissue showing the characteristic cell
types, fibers, and intercellular spaces. Source: Reprinted from Gray's Anatomy, ed. 35 (p. 32) by R. Warwick
and P. L. Williams with permission of Elsevier, © 1973.
Histology and Biomechanics of Myofascia 35
Table 3.1 Histological Makeup of Connective Tissue

I. Cells
A. Fibroblasts: synthesize collagen. elastin. reticulin. and ground substance.
B. Fibrocytes: mature version of fibroblast, found in stable mature connective tissue.
C. Myofibroblasts: contract via actin and myosin to pull tissues together.
D. Macrophages and histiocytes: "big eaters" found in traumatic, inflammatory, or
infectious conditions; clean and debride area of waste and foreign products.
E. Mast cells: secrete histamine (vasodilator) and heparin (anticoagulant).
F. Plasma cells: produce antibodies; present only in infectious conditions.
II. Extracellular Matrix
A. Fibers
1. Collagen: very tensile
a. Type I: connective tissue proper (loose and dense)
b. Type 11:hyaline cartilage
c. Type Ill: fetal dermis. lining of arteries
d. Type IV: basement membranes
2. Elastin: more elastic, found in lining of arteries. Also ligamentum flavum and
ligamentum nuchae.
3. Reticulin: delicate meshwork for support of internal organs and glands.
B. Ground substance: viscous gel with high water concentration. Provides medium
in which collagen and cells lie.
1. Purpose
a. Diffusion of nutrients and waste products
b. Mechanical barrier against bacteria
c. Maintains critical interfiber distance, preventing microadhesions
d. Provides lubrication between collagen fibers
e. More abundant in early life; decreases with age
2. Components
a. Glycosaminoglycans:
lubricating effect, maintenance of
critical interfiber distance, etc.
b. Proteoglycans: primarily bind water
types are described in detail later in this chapter (see "Biomechanics of Connective
Tissue").
The Cells of Connective Tissue

Connective tissue comprises cells and extracellular matrix (fibers and ground sub-
stance; Table 3.1). These cells can be divided into a fixed cell population of fibro-
blasts; adipocytes; persistent mesenchymal stem cells; and mobile wandering cells
consisting of macrophages, lymphocytes, plasma cells, eosinophilic leukocytes,
and mast cells.6 Fibroblasts are found in all connective tissues, whereas the other
cells are found primarily in pathological states.
Fibroblasts. Fibroblasts, considered the true connective tissue cells, are the most
prevalent in connective tissue. These cells are the primary secretory cells in con-
nective tissue and are responsible for the synthesis of all components of connec-
tive tissue, including collagen, elastin, and ground substance. They adhere to and
lay down the fibers. In highly cellular tissues, fibroblasts may mix with collagen
fibers to become reticular cells. 3•4 In mature stable connective tissue, fibroblasts
are converted into fibrocytes, which are mature, nonsecretory versions of the fi-
broblast. Fibroblasts and fibroblastic activity are influenced by various factors, in-
cluding mechanotransduction, steroid hormone, and dietary content. Fibroblasts
are nonphagocytic.
Myofibroblasts. Myofibroblasts are cells that have the ability to contract. Dur-
ing wound healing, myofibroblasts use their actin and myosin to draw the dam-
aged tissues together. Although their contractile abilities are often beneficial,
they can also result in pathological responses within connective tissue, such as in
Dupuytren disease.
Myofibroblasts are found in both fascia and intramuscular connective tissue.
They exist in particularly high densities within the perimysium and are thought
to play a role in passive muscle stiffness or resting tension. Myofibroblast-induced
stiffness is "U-shaped" in that it responds similarly to mechanostimulation of ei-
ther high stresses or the absence of stress .7The thickening effects are seen as early
as 2 days after a muscle is immobilized in a shortened position 8 (see Chapter 4,
"Histopathology of Myofascia and Physiology of Myofascial Manipulation").
Macrophages. Other types of cells, not exclusive to connective tissue, are found
primarily in traumatized or infectious states. Macrophages (a term meaning "big
eater") are responsible for phagocytosing waste products, damaged tissue, and for-
eign matter. In traumatized states, macrophages primarily phagocytose damaged
cells and damaged macromolecular connective tissue fibers, debriding the area
in preparation for repair. In infectious or inflammatory states, macrophages are
capable of phagocytosing bacteria or other invading microorganisms. 3•4 Macro-
phages may be the signal for vascular regeneration to begin.
Mast cells. Mast cells were given their name because they appeared "stuffed with
granules" (mast is German for "well fed"). They are mobile and are important de-
fensive cells, which are formed primarily in loose connective tissue. Mast cells are
responsible for constantly secreting small amounts of the anticoagulant heparin
into the bloodstream. The significance of this is still not known. 6 The disruption
of mast cells also results in the release of histamine. Within the mast cell granules,
histamine is bound to heparin. Histamine causes vasodilation in neighboring
noninjured vessels, resulting in increased permeability. The release of histamine is
linked to inflammatory reactions, allergies, and hypersensitivities. 1- 6
Mast cells can be hypersensitized by certain antigens introduced into the body,
facilitating cell production of histamine, 2 which may explain why individuals with
numerous allergies and diffuse myofascial pain can have an increased histamine
response to soft tissue manipulation. Plasma cells are somewhat related to mast
cells in that they are present primarily during infectious states. They are part of the
immune system and are responsible for synthesizing antibodies.
Other connective tissue cells. With the exception of the fibroblast and fibrocyte,
all other cells found in connective tissue are also related to the reticuloendothelial
Histo logy and Biomechan ics of Myofasc ia 37
Figure 3.2 Photomicrograph of loose connective tissue. The connective tissue fibers lie in a bed of ground
substance. c = collagen; e = elastin; f = fibroblast. Source:Reprinted from Histology (p. 212) by A. W. Ham
and D. H. Cormack with permission ofJ. B. Lippincott Co.,© 1979.
system. This widely scattered system consists of phagocytic and immunologi-

cal cells and associated organs and tissues related to first-line defense of the
body against invading microorganisms and foreign particles. 3 Aside from con-
nective tissue, the cells of the reticuloendothelial system are found in the blood
and in the reticular tissue of the spleen, liver, and meninges. The body's connec-
tive tissue framework is an integral part of the reticuloendothelial system be-
cause of the mechanical barrier that connective tissue provides against invading
. .
m1croorgan1sms.
The Extracellular Matrix

The only component of connective tissue other than cells is the extracellular ma-
trix (Table 3.1; Figure 3.2). The matrix is composed primarily of collagen, elas-
tin, and reticulin fibers, as well as ground substance. Collagen fibers are the most
tensile resistant of the three fiber types, as well as the most common. Elastin and
reticulin fibers also resist tensile forces but are more elastic. The inert properties
of the extracellular matrix account for the functional characteristics of the differ-
ent types of connective tissue. Connective tissue fibers, with their tensile strength
and elasticity, are the basis for the mechanical support. Ground substance, with
its water-binding capacity, is the basis for lubrication and diffusion of nutrients in
connective tissues. 6
Collagen is divided into four major types: Type I is found primarily in ordi-
nary loose and dense connective tissue; Type II is found primarily in hyaline car-
tilage; Type III is found lining the fetal dermis; and Type IV is found in basement
membranes. Manual therapy techniques are most likely to affect Type I collagen.
The characteristics of each type are described later.
Elastin fibers are less tensile than collagen and have more elastic characteris-
tics. The lining of arteries contains a high percentage of elastin. The ligamentum
nuchae of the spine also contains a high percentage of elastin. 9•10 Reticulin is the
least tensile of the connective tissue fibers; it is found primarily in the delicate
meshwork supporting the body's internal organs and glands.
Another important component of connective tissue is ground substance. This
is the viscous, hydrophilic, gel-like medium in which the cells and fibers are em-
bedded. Ground substance has several primary functions. It contains a high pro-
portion of water, and this accounts for the first of its primary functions-diffusion
of nutrients and waste products. A second function of the ground substance is
to provide a mechanical barrier against invading bacteria and microorganisms.
Connective tissue cells, being part of the reticuloendothelial system, provide the
first line of defense against invading organisms. A third function of ground sub-
stance is to maintain the so-called critical interfiber distance. Collagen fibers that
approximate one another can potentially adhere together if a certain distance is
not maintained between them. The ground substance, which provides some of the
tissue volume, can effectively maintain the distance between fibers, preventing
microadhesions and maintaining extensibility. Ground substance content in con-
nective tissue seems to decrease with age, possibly contributing to a decrease in
flexibility with aging.
The primary components of ground substance are glycosaminoglycans (GAGs)
and water. GAGs are also referred to as "acid mucopolysaccharides" in the older
literature. GAGs are either sulfated or nonsulfated. The nonsulfated GAGs, such as
hyaluronic acid, are hydrophilic and bind to water, which makes up approximately
70% of the total connective tissue content. 3- 5
Hyaluronic acid, which has long been used to help restore joint function in
the veterinary world, has received Food and Drug Administration approval for
use in the injection of human joints. Chondroitin, which is another component
of ground substance, is sold in alternative medicine settings, purportedly to help
joint function. The idea of using nonhormonal components of connective tissue to
help restore the tissue is a budding idea that may have a significant impact on the
long-term treatment of injured or arthritic joints.
Biosynthesis of Collagen
Collagen synthesis begins in the fibroblast by the absorption of amino acids into
the cell. In the rough endoplasmic reticulum of the cell, the amino acids are syn-
thesized into polypeptide chains. From the polypeptide chains, protocollagen (or
procollagen), a precursor of collagen, is synthesized. Strands of protocollagen are
linked in a triple helix in the cell to form strands of tropocollagen. Tropocollagen,
Histology and Biomechanics of Myofa scia 39
Synt es s o'
round m~ opolysaccha• .es
ubsta 1 olg apparatu,
an• .i~d t c to r te n
l Aminoacids including
praline and lysine
8 Aggregationof collagen
fibrils t o form Assembly of
collagen fibres
2
polypept ide chain
and bundles of fibres
7 Aggregation of
tropocollagen to
form collagen fibrils
3 Hydroxylation of
prol1ne and lysine
in polypeptide chain
•
"
-.r -
J
2.80"•
6 Passageof tropocollagen
to extracellular space 4 Assembly of three
hydroxylat ed
polypeptidechains
5 Addition of
into one
carbohydrate moiety
tropocollagen molecule
Figure 3.3 A schemati c dra wing representing the biosynthesis of collagen by fibroblasts. Source: Reprinted
from Gray's An atomy, ed. 35 (p. 38) by R. War wick and P. L. Williams with permissi on of Elsevier, © 1973.
which is the molecular unit of collagen, is then passed through the cell membrane
into the interstitial spaces. In the extracellular space, tropocollagen strands are
linked in series and in parallel in a quarter-stagger arrangement to form collagen
fibrils (Figure 3.3). Initially, the tropocollagen molecules are hydrostatically at-
tracted to each other and form hydrostatic bonds. Eventually, the collagen matures
and the weak hydrostatic bonds are converted to stronger covalent bonds. 11
To review briefly, hydrostatic bonds are those in which polarized molecules, or
molecules of different polarities, are attracted and weakly bonded to one another.
Covalent bonds are those in which the two bonding atoms bind with a shared elec-
tron. The energy required to break a covalent bond is much greater than the energy
required to break a hydrostatic bond . This accounts for the increasing strength of
collagenous tissue during maturation. Collagen fibrils eventually band together
to form collagen fibers. The configuration of mature collagen can be likened to
the structure of common rope . Small strands intertwine to form threads, threads
intertwine to form larger strands, and so forth (Figure 3.4).
TROPO-
MICROFIBRIL SUBFIBRIL FlBRIL FIBER
COLLAGEN
(x ray) (x ray) (x ray) (EM, SEM)
(x ray)
(EM) (EM) (EM, SEM) (OM)
•.h ..
35nm
staining periodicity
fibroblasts
1.5nm 3.5nm 10-20nm 50-500nm 50-300µm
SIZE SCALE
Figure 3.4 Architectural hierarchy of dense regular connective tissue, from the tropocollagen molecule
to the collagen fiber. Source:Adapted with permission from J.Kastelic, A. Galeski, and E. Baer, The Multi-
composite Structure of Tendon, Connective Tissue Research (1978;6:11-23). Copyright© 1978, Gordon and
Breach Science Publishers.
Biomechanics of Connect ive Tissue

General Characteristics and Definition of Terms
All injuries, whether to bone or connective tissues, are caused by forces acting on
these tissues. To prevent and treat these injuries, the manual therapist must first
have a working knowledge of the basic guiding biomechanical principles that apply
to soft tissues. When a force is applied to connective tissues, producing a mechani-
cal stress, the tissues tend to resist any change in size or shape. However, some de-
formation or change in length may occur as a result of the stress. This deformation
is called strain. Strain is determined by comparing change in length with the nor-
mal length. Strain is expressed in deformation per unit length, or percent change.
Tissue strain can be caused by stresses such as a push, pull, twist, tension, com-
pression, or shear. The last three are more common in connective tissue injury. 12
Tension is a pulling force along the length of the tissue. An example of this
is in a whiplash injury. The cervical spine is flexed and extended with force. The
posterior and anterior ligaments are tightened or stretched and subjected to ten-
sion stress. 12,13
Compression occurs when stress is applied along the length of a tissue, causing
the tissue to decrease in length and increase in perimeter. In an upright position,
compression forces are distributed through the intervertebral discs. As the two
surfaces of the vertebrae move closer together, the vertical tension of fibrous an-
nulus is reduced and tissue bulges out under compression. 12,13
Shearing occurs when one part of a tissue slides over another. This occurs
when forces meet each other in opposite directions. An example of this is when LS
slides forward over Sl, leading to a higher incidence of disc herniation. 12,13
Histology and Biomechan ics of Myofasc ia 41
Plastic Region
Point of Failure
s Point of Yield
T
R
E
s
s Elastic Region
STRAIN
Figure 3.5 Stress- strain curve.
Stress-strain curve. As previously mentioned, when stress is applied to a tissue,

it results in deformation or strain. The strain, or change in length, can be tempo-
rary or permanent. A graphic representation of this relationship is demonstrated
as a stress - strain curve (Figure 3.5). Initial change in length requires little force.
As more stress is applied to the tissue, the change in length diminishes. In other
words, greater amounts of force are required to effect small amounts of change.
The early part of the curve, sometimes called the toe region,represents the elastic
component of connective tissue. This part of the curve usually represents tem-
porary length changes in the tissue. When the tissue stretches beyond the elastic
range, it reaches a point at which the deformation becomes permanent. This point
is called the point of yield. If stress continues, the tissue moves into the plastic
region.The tissue is now permanently deformed but does not rupture. As the im-
posed stress increases further, the curve reaches its limit at the point offailure.12
Viscoelasticmodel of connective tissue. The viscoelastic concept can be explained

further using a simple engineering model. Connective tissue is often referred to
as being viscoelasticin nature. It contains both a viscous (permanent) deforma-
tion characteristic and an elastic (temporary) deformation characteristic. The two
characteristics combine to give connective tissue its unique qualities. 14- 18 This
model incorporates a spring (elastic) and a hydraulic cylinder (plastic) linked in
series to help depict this deformation quality (Figure 3.6).
The elasticcomponent of connective tissue represents the temporary change in
length that occurs when it is subjected to a stretch (spring portion of model). The
42 SCIENTIFIC BASIS FOR MYOFASCIAL M AN IPULATION
Collagen Tendons
fibers Ligamen ts
(A) + Connective Joint capsules
Grou nd tissue Aponeuroses
substance Fascia
matrix etc .
Viscous proper ties --------i►► Plastic stretch
(B)
Tensile
Hydraulic cylinder model forc.e
Elastic prope rties -------1►► Elastic stretch
(C)
Tensile
Spring model force
I
I
1twlW1► I•
( D) I Tensile
I force
I
I
Elastic I Viscous
elements I elements
I
Figure 3.6 (A) The primary and secondary organization of connective tissue in the bod y. (B) Schematic
representation of a viscous element in material capable of permanent (plastic) deformation. (C) Schematic
representation of an elastic element in material capable of reco verable (elastic) deformation. (D) A simpli -
fied model of collagenous tissue. Connective tissue is a viscoelastic material: When stretched, it behaves as if
it has both viscous and elastic elements connected in series. Source:Reprinted with permission from Sapega
AA, Quedenfeld TC, Moyer RA, Butler RA. "Biophysical Factors in Range -of-Motion Exercise. " The Physi-
cian and Sports Medicine, Vol. 9, No. 12, p. 58, © 1981, McGraw -Hill Companies.
ELASTICMODEL elastic component has a poststretch recoil in

i'Rl: J..OIIO
which all length or extensibility gained dur-
~ ing the stretch or manipulation is lost over a
short period of time as the tissue returns to
its original shape (Figure 3.7). In the elastic
Figure 3. 7 Schematic representation of the vis- model, the spring recoils when tension or
coelastic model of elongation - elastic component force is removed. The elastic component is
in which no permanent elongation occurs after
application of tensile force. Source:Reprinted from
not well understood but is believed to be the
Myofascial Manipulation: Theory and ClinicalMan- slack taken out of the connective tissue fi-
agement (p. 4) by A. J.Grodin and R. Cantu with hers. For example, irregular connective tis-
permission of Forum Medicum Inc., © 1989.
sue has a loose basket-weave configuration
of collagen fibers. When a stretch is placed
on the tissue, the slack is taken out as the fibers align themselves in the general di-
rection of the stretch (Figure 3.8). When the stretch is removed, the fibers assume
their previous orientation and the change in length is lost.
The viscous (or plastic) component represents the permanent deformation
characteristic of connective tissue. After a stretch or manipulation, part of the
length or extensibility gained remains even after a period of time (hydraulic cylin-
der portion of model). There is no postma-
nipulation recoil in the viscous component
(Figure 3.9). In the model, the hydraulic cyl-
inder has been opened or manipulated and
does not close. Some permanent changes
result from breaking intermolecular and in-
A tramolecular bonds between collagen mol-
ecules, fibers, and cross-links, among other
things (see "Connective Tissue Plasticity,"
later in chapter).
Figure 3.10 is a simple demonstration
of the viscoelastic model, showing the vis-
cous and elastic portions of the model com-
bined and arranged in series. After a force
is applied to the connective tissue through
B
stretch or manipulation, a net change in
length is achieved. Some of the change is
Figure 3.8 Diagram showing the weave pattern of quickly lost, while some remains.
collagen, with A and B representing elastic stretch The combination of viscous and elastic
and recoil of collagen fibers, respectively. Source:Re- properties allows for connective tissue to re-
printed from R. Donatelli and H. Owens-Burkhart, 13
Effects of Immobilization on the Extensibility of
spond by creep and relaxation. Creep oc-
Periarticular Connective Tissue, Journal of Ortho- curs when a load is applied to a tissue over a
paedic and Sports Physical Therapy,Vol. 3, pp. 67- 72, prolonged period of time, as in progressive
with permission of the Orthopaedic and Sports Sec-
stretching. This allows a gradual elongation
tions of the American Physical Therapy Association.
of the tissue. The degree of deformation is
PLASTIC(VISOUS)MODEL determined more by the duration of force

Jq.LOOI> -•LI!;~ 'R:>St u».b
applied to the tissue than by the amount of
force. A lesser load over a greater period of
time will produce a larger amount of creep
and less tissue stiffness than a greater load
applied at a faster rate. 19•20 An elevation in
temperature will also cause corresponding
Figure 3.9 Schematic representation of the vis-
coelastic model of elongation - plastic component increases in creep. Hence, when stretching
in which deformation remains after the application tight connective tissue, warmed tissue held
of tensile force. Source:Reprinted from Myofascial for a sustained period will be more pliable
Manipulation: Theory and ClinicalManagement than cold tissue stretched quickly. 12,13
(p. 5) by A. J.Grodin and R. Cantu with permission
of Forum Medicum Inc.,© 1989. If force is applied intermittently, as in
repeated progressive stretching, a progres-
sive elongation may be achieved. In Fig-
ure 3.llA , strain, or percent elongation, is plotted against time for the purposes
of illustrating this phenomenon. Initiall y, there is a rapid elongation, representing
the "taking up of the slack," which is a contribution of the elastic portion of con-
nective tissue. As time passes, less elongation is achieved, representing the contri-
bution of the viscous portion of connective tissue. When the stress is eventually
released, the elastic portion recoils as some of the gained length is lost, while the
changes in the viscous portion remain. This phenomenon is consistent with the
elastic characteristics of connective tissue. Not all the change in length is lost be-
cause the tissue was stretched into the viscous, or plastic, range.
If the stress is reapplied to the tissue, the stress-stain curve looks identical but
starts from a new length position achieved after the first stretch (Figure 3.llB ).
Again, the elongation is initially very rapid, but it gradually slows as the tissue
makes the transition from elasticity to plas-
VISCOELASTIC MODEL
~IO'O ticity. When the stress is again released,
some loss of length results, but a portion
of changed length is also retained. With
each progressive stretch, the tissue has
some gain in total length that is considered
permanent.
This phenomenon appears often in the
clinical setting. For example, when a re-
stricted joint capsule is stretched, a certain
Figure 3.10 Schematic representation of the vis-
increase in range of motion may be achieved
coelastic model of elongation - some elongation is
lost and some is retained after the application of during a particular treatment session. The
tensile force. Source:Reprinted from Myofascial Ma- patient may return a day or two later with
nipulation: Theory and ClinicalManagement (p. 5) a range of motion greater than the original
by A. J.Grodin and R. Cantu with permission of
range but less than that achieved at the end
Forum Medicum Inc.,© 1989.
of the previous treatment. In other words,
Strain Strain Stress Released

(E long ati on)
____, ✓
Stress Released (E long ati on)
I
'\
Stress Reapplied
A .; , Ti me 1-------- -- B - Time--- - - --------,
Figure 3. 11 (A) Elongation of connective tissue (strain) plotted against time. (B) Repeated elongations
of connective tissue (strain) plotted against time. Source:Reprinted from Myofascial Manipulation: Theory
and ClinicalManagement (pp. 5- 6) by A. J.Grodin and R. Cantu with permission of Forum Medicum Inc.,
© 1989.
some range is lost due to the elastic component, but some is retained due to the
plastic component.
Although the plastic component represents a permanent elongation, connec-
tive tissue is still capable of losing the elongation. The half-life of collagen is 300 -
500 days in mature nontraumatized conditions. 21 Over time, new collagen is laid
down to replace older collagen. New collagen is laid down according to stresses (or
lack of stresses) applied to the tissue. If the tissue is not stressed for long periods of
time, it will adaptively shorten as collagen is laid down in the context of the length
of the tissues and lack of applied stress. Wolff's law, which states that "bone adapts
to the stresses applied," 10 is also true of connective tissue. All connective tissue
seeks metabolic homeostasis commensurate with the stresses being applied to it.
Wolff's law, however, when applied to connective tissue, has a functional as well
as a dysfunctional aspect. Abnormal stresses chronically applied to connective tis-
sues may result in dysfunction in the tissues and the adjacent structures supported
by that tissue (fascia, facet joints, etc.). A clinical example of this phenomenon
is the connective tissue band that develops in the patient with spondylolisthesis.
Because the spine in this condition cannot withstand the anterior shear forces ap-
plied daily, the body responds by laying down connective tissue, in time forming a
connective tissue band. Normal stresses, or carefully controlled stresses (i.e., those
stresses imparted externally by the clinician in the form of manipulation or by the
patient in the form of exercises), may positively change the metabolic and physi-
cal homeostasis of the tissue. Collagen production is thus less haphazard, more
organized, and laid down in a quantity and direction more suited to optimal tissue
function. This concept is more fully developed in Chapter 4, "Histopathology of
Myofascia and Physiology of Myofascial Manipulation."
Specific Characteristics
Various types of connective tissue have spe-
cific characteristics. Such characteristics
support the function of each type.
Dense regular connective tissue. Ligaments

and tendons are categorized as dense regular
connective tissue. Dense, parallel arrange-
ment of collagen fibers characterizes dense
regular connective tissue (Figure 3.12). The
high proportion of collagen to ground sub-
Figure 3.12 Drawing of dense regular connective stance and the parallel arrangement of the
tissue, showing the parallel arrangement of colla-
gen fibers. Source:Reprinted from Gray'sAnatomy,
fibers account for the high tensile strength
ed. 35 (p. 40) by P. Williams and R. Warwick with and limited extensibility of these tissues.
permission of Elsevier, © 1973. Because of the histological makeup of these
tissues, they are the least responsive to
manual work. Because of the compactness and density of collagen fibers and the
relatively small proportions of ground substance, the tissue is not highly meta-
bolic, and not very vascular, accounting for the increased healing time required
after trauma.
The primary function of tendon is to attach muscle fibers to bone and to
transmit forces expended by muscle to the bone with limited elongation, allowing
for tension or joint movement. 22 •23 The collagen fibers in tendons are in a par-
allel arrangement, providing the highest unidirectional tensile strength possible.
The stress-strain relationship of tendons is similar to that of other connective tis-
sues, with some minor differences. When
- - a tendon is stressed, the toe region (elastic

component) of the stress-strain curve is
generally smaller because of the parallel ar-
rangement of collagen fibers; this indicates
less realignment of fibers than is found in
other connective tissues during tension.
The toe region is generally followed by a
moderately linear region with a slightly
greater slope, which is indicative of the ten-
don's greater stiffness. With further tensile
deformation, small dips or hitches appear
Figure 3.13 Drawing ofligamentous tissue, show-
ing overall parallel arrangement of fibers, but some-
in the curve, and these dips and hitches may
what less parallel than tendon. Source:Reprinted represent early tissue microfailure. Finally,
from Gray'sAnatomy, ed. 35 (p. 40) by P. Williams with further loading, the tissue fails com -
and R. Warwick with permission of Elsevier,
pletely, and the stress-strain curve drops to
© 1973.
zero. 22,24
Table 3.2 Classification of Connective Tissue
Tissue type Specific structures Characteristics of the tissue

Dense regular Ligaments, tendons Dense, parallel arrangement of
collagen fibers; proportionally
less ground substance
Dense irregular Aponeurosis, periosteum, joint Dense, multidirectional
capsules, dermis of skin, areas arrangement of collagen
of high mechanical stress fibers; able to resist
multidirectional stress
Loose irregular Superficial fascial sheaths, muscle Sparse, multidirectional
and nerve sheaths, support sheaths arrangement of collagen
of internal organs fibers; greater amounts of
elastin present
The primary function of ligament is to check excessive motion in joints and

to guide joint motion. 22 •23 Ligaments have a less consistent parallel arrangement
of collagen fibers than does tendon 25 (Figure 3.13). Under light microscopy, the
orientation of the collagen in ligament shows an undulating configuration known
as "crimp." 26 This crimp phenomenon is thought to be responsible for the mildly
elastic characteristics of ligament. The ligament functions biomechanically as a
spring, until all of the crimp is straightened out and, subsequently, becomes more
tensile when the collagen fibers are actually stressed. The ultimate biomechanical
result is that ligaments have somewhat less tensile strength per unit area than ten-
don, but they have slightly more yield (Table 3.2).
Dense irregular connective tissue . Dense

irregular connective tissue includes, but is
not limited to, joint capsules, aponeuroses,
periosteum, and fascial sheaths under high
degrees of mechanical stress. The major dif-
ference between dense irregular and dense
regular connective tissue is the orientation
of collagen fibers. In dense irregular con-
nective tissue, the collagen fibers are aligned
multidirectionally to withstand multidirec-
tional stresses (Figure 3.14). The lumbodor-
sal fascia, for example, has many different
attachments and is pulled in different direc-
Figure 3. 14 Drawing of dense irregular con-
tions during the spine's normal function.
nective tissue, showing the multidirectional fiber
orientation as well as the high density of collagen fi-
bers. Source: Reprinted from Gray's Anatomy, ed. 35 Loose irregular connective tissue . Loose ir-
(p. 40), by P. Williams and R. Warwick with permis- regular connective tissue includes, but is
sion of Elsevier,© 1973.
not limited to, the superficial and some
48 SCIENTIFIC BASIS FOR MYO FASCIA L MAN IPULATION
deep fascia, as well as muscle and nerve sheaths. The supportive framework of the
lymph system and the internal organs is also classified as loose irregular connec-
tive tissue . Loose irregular connective tissue is generally characterized by a sparse,
multidirectional framework of collagen and elastin. Loose irregular connective
tissue contains a greater amount of ground substance per unit area than other
types of connective tissues. Because of sparse concentrations of collagen in this
type of tissue, loose irregular connective tissue is the most elastic and typically has
the greatest potential for change when manipulated by external forces.
Contractility of connective tissue. Connective tissue has long been viewed as in-
active or inert tissue. Its role was primarily thought to be tissue containment, pro-
viding structure and stability to neighboring tissues and joints. Although all its
functions are not yet completely understood, research suggests that fascia also has
an active role through myofibroblast contraction. 27•28
Such contractions are unique, in that they can produce a shortened collagen
matrix, which results in long-term changes without an ongoing contraction. 29
Contraction of collagen matrix or connective tissue may contribute, particularly
in the low back, to vertebral stability or harm by becoming stiff and preventing
freedom of movement. Shortened tissue locks the collagen in an interstitial and
incremental manner as collagen fibrils slip past one another and then relink, much
like a ratchet turns and resets while tightening a bolt. 29
Myofibroblasts are derived from fibroblasts, the most common cell found in
connective tissue. They are responsible for the synthesis of collagen, elastin, reticu-
lin, and ground substance. Fibroblasts are usually protected or "stress-shielded"
within the extracellular matrix. When an injury occurs, or when tissues are ex-
posed to excessive ongoing stress, their protection can be jeopardized. As a result,
they differentiate into myofibroblasts through a two-step process. 29 Two principal
factors are required for this transformation to take place: (1) transforming growth
factor /31 (TGF-/31) and (2) mechanical stress, the latter being the primary fac-
tor. 30 TGF-/31 is produced by platelets, macrophages, parenchymal cells, or injured
epithelial cells. Fibroblasts first differentiate into proto-myofibroblasts by forming
cytoplasmic actin-containing stress fibers. If continually exposed to both TGF-/31
and mechanical stress, the proto-myofibroblasts further differentiate into a myo-
fibroblast, gaining the distinct ability to contract. 31 This process has long been
known and is most often seen during tissue repair.
The contractility of the myofibroblast is due to an inherent contractile appa-
ratus consisting of actin microfilaments and nonmuscle myosin. 29 Myofibroblasts
are identified in tissue by their expression of a-smooth muscle actin (a-SMA),
which is a common and reliable molecular marker. 32•33
Myofibroblasts are known to be present and active in granulation tissue as
part of a mechanotransduction system, whereby forces are transmitted from the
myofibroblasts themselves to the surrounding extracellular matrix. 31 This system
is so extensive that it has been suggested that fibroblasts, myofibroblasts, and their
elaborate connections may form a complex cellular network capable of integrative

communication throughout the whole body. 34 ,35
Myofibroblasts are also known to be present in normal human fascia, specifi-
cally the fascia lata, plantar fascia, and lumbar fascia. 28 The density of myofibro-
blasts has been found to be significantly higher in human lumbar fascia than in
rodent and porcine lumbar fascia. 27•28 The differences in myofibroblast density may
be due to variations in the amount of stress the lumbar fascia experiences between
bipeds and quadrupeds. Such reasoning would be consistent with additional find-
ings suggesting that density level is directly related to activity level. Of the 39 hu-
man tissue samples tested (ages 17-91; 25 male, 7 female), density was highest in
the younger subjects, under 32 years of age (128/mm 2 + 51/mm 2 ); less dense in the
middle-age subjects, ages 54-56 (13/mm 2 + 8/mm 2 ); and least dense in subjects
older than age 70 (12/mm 2 + 3/mm 2 ). 27
Myofibroblasts have been known to produce sufficient force for wound clo-
sure. What was unknown until recently was whether contracting myofibroblasts
could alter the collagen matrix such that connective tissue might tighten and/or
shorten enough to impede movement or function. In an attempt to measure such
forces, myofibroblasts have been stimulated using a variety of means, such as elec-
trical stimulation and chemical and mechanical stressors. 28 Schleip et al. were able
to produce a relaxation response using nitric oxide as well as electrical stimula-
tion at 20 Hz (7 V, 2 ms). They were unsuccessful in producing myofibroblast con-
tractions using caffeine, acetylcholine, potassium-enriched solution, epinephrine,
or adenosine, but they did produce significant contractile responses using hista-
mine, oxytocin (a hormone responsible for uterine contraction during labor), and
mepyramine (also known as pyrilamine), an antihistamine that targets histamine
H 1 receptors. 28
Yahia et al. were also able to elicit contractions by repeatedly stretching sam-
ples of thoracolumbar fascia samples. 36 Samples of thoracolumbar fascia were
taken through a series of stretches not exceeding 6% deformation. After the first
series of stretches, researchers permitted the tissues to rest for 30 minutes, and
then they performed another set of stretches. After a subsequent resting period of
60 minutes, researchers took the fascia samples through a third series of stretches.
The force needed to deform the tissue to 6% with each series of stretches progres-
sively increased, suggesting a contractile response of the tissue. Similar responses
were seen with tissues when a fixed strain was applied instead of repeated strain,
and the opposite response was noted when samples were tested using a fixed load.
In the last group, tissues relaxed over time, slowly decreasing the load on the tis-
sue. Such tissue responses are now thought to be due to a myofibroblastic response.
Using the force difference between stretches as measured by Yahia et al. 36
(1.5 N, 0.153 kgf or 0.337 lbf), Schleip et al. calculated forces that could reach as
high as 38 N (3.875 kgf or 8.543 lbf) in a horizontal cross-section of thoracolumbar
fascia measuring 71 mm X 0. 53 mm at the L3 vertebral level A force of this mag-
nitude could certainly make a change in a tissue's mobility for better or worse. 37•38
50 SCIENTIFIC BASIS FOR M YOFASCIAL MAN IPULATION
Connective tissue plasticity. If connective tissue, or at least fascia, has the ability
to contract or develop a contracture, does it have the capacity to return to a re-
laxed state? If so, how? If not, does it remain shortened similar to muscle, thereby
restricting motion, impeding function, or causing pain and pathology?
A number of pathological conditions can result in such limitations, including
Dupuytren disease 39 and, some have suggested, frozen shoulder. 40 •41 Patients with
chronic low-back pain also experience nonpathological changes. 42 Langevin et al.
found, on average, a 25% greater perimuscular connective tissue thickness in the
lumbar region (L2/L3) in subjects with chronic low-back pain than in a group
without low-back pain.
Rolf explained connective tissue changes based on the gel-sol principle and
piezoelectric effect. Rolf explained that tissue, as a colloidal substance, can func-
tion in two different forms: a gel and a sol.43 The gel state is thick and dense. Heat
or a mechanical stimulus can be used to make the gel more fluid or soluble (sol).
Juhan uses the term thixotropy to describe the viscous transition from gel to sol.44
Ketchup is a familiar thixotropic substance; it is often found in a more gelatinous
state, especially if left unused for a period of time, but it can quickly be made a sol
by shaking the bottle. Within connective tissue, the piezoelectric principle results
in increased mobility of tissue as pressure that is applied to tissues disrupts the
balance of charges, stimulating fibroblasts to produce collagen. 45 Although these
explanations clarify the long-term changes produced by soft tissue manipula-
tion, they do not adequately account for the short-term changes experienced dur-
ing a single treatment session. Schleip et al. suggest that such early changes are
produced via a neurophysiological response. Ruffini organs and interstitial mus-
cle receptors, better termed interstitial myofascial receptors,are the key to such
changes. 38
Both Ruffini organs and interstitial receptors (Types III and IV) are found
within connective tissue. They respond to slow, deep, steady pressure delivered in
a tangential direction. Manual stimulation produces changes in tone, vasodilation,
and local fluid dynamics (plasma extravasation) via the autonomic nervous system.
This process has been described as an "intrafascial circulation loop" (Figure 3.15).
Short-term and long-term soft tissue changes produced by myofascial manip-
ulation seem to include several combined processes. Among these are an intrafas-
cial circulation loop, regulation of the hypothalamus and central nervous system
(not discussed here), and the contractility of connective tissues (Figure 3.16).
Fascia as a force transmitter. The term myofascial manipulation suggests ma-

nipulating tissue consisting of both muscle (myo) and fascia. Manipulation of
both is necessary because forces transition through both tissues, and each has its
own properties and responses. Muscle has the ability to generate dynamic move-
ment via a contraction. The actin and myosin interact to make the muscle shorter
(concentric) or longer (eccentric), depending on the type of contraction, produc-
ing forces that create or control movement. This ability of muscle has been shown
Palpable tissue ------♦ Tissue manipulations Stimulation of

response mechanoreceptors
Local fluid
dynamics Interstitial & Ruffini
Autonomic
nervous system
Figure 3.15 The "intrafascial circulation loop" (based on Mitchell & Schmid, 1977). Fascia is densely in-
nervated by interstitial tissue receptors. The autonomic nervous system uses their input (plus that of some
Ruffini endings) to regulate local fluid dynamics in terms of an altered blood pressure in local arterioles and
capillaries plus in plasma extravasation and local tissue viscosity. The change might then be felt by the hand
of a sensitive practitioner. Source:Reprinted from Journal of Bodywork and Movement Therapies,Vol. 7
No. 2, Schleip, R., Fascial Plasticity - A New Neurobiological Explanation: Part 2, p. 105. Copyright© 2003,
with permission from Elsevier.
Palpable tissue _______

response
I. Manipulation of tissue 1
.
------+ Stimulation of
mechanoreceptors
Interstitial & Ruffini
lntrafascial Autonomic
smooth muscle cells nervous system
Figure 3. 16 The "Fascial Contraction Loop" (based on Yahia and on Staubesand). Embedded between
the collagen fibers of fascia are smooth muscle cells, which are regulated by the autonomic nervous system.
Their activation can cause an active intrafascial tissue contraction. Source:Reprinted from Journal of Body-
work and Movement Therapies,Vol. 7 No. 2, Schleip, R., Fascial Plasticity - A New Neurobiological Explana-
tion: Part 2, p. 109. Copyright© 2003, with permission from Elsevier.
repeatedly using fully dissected muscles, where forces at the proximal and distal
ends have been found to be equal. 46 - 49 Although fascia is believed to assist in hin-
dering movement, until recently, it has not been clear whether fascia plays any role
in force transmission. The assistance of fascia in force transmission is now known
to be significant. If fascia did not assist with movement, the forces required to pro-
duce body movements would be so enormous that much of the musculoskeletal
system's efficiency would be lost.
As muscles generate force or the body responds to outside forces, the fascia and
connective tissue act as an energy broker. Fascia absorbs chemical or mechanical
energy, temporarily stores it in the form of potential energy, and redistributes it
kinetically. The role of fascia as a force transmitter can be seen throughout simple
ambulation. Ambulation is initiated by a concentric contraction, but it quickly
becomes a function using primarily a combination of eccentric contractions and
connective tissue transmission for the purpose of efficiency. As the foot hits the
ground and the center of gravity moves over the foot, energy is absorbed, stored,
and reused through connective tissue. The actual force production by the muscle
is thereby reduced significantly.
When tissues become restricted and more rigid, their ability to absorb energy
lessens. Muscles therefore have to work harder to produce mechanical energy as
potential energy is lost. This can be likened to the potential energy lost while try-
ing to run on soft sand: Muscles are required to generate more energy to create
motion. Each step requires an extra concentric effort to pick up the legs and keep
them moving forward, because the kinetic energy is lost in the give of the sand.
This energy model is called the "legs carry trunk model."
When connective tissue is mobile, the system is much more efficient. Graco-
vetsky describes this more efficient model as the "spine engine" model 50 •51 Based
on his model, as the foot hits the ground, eccentric contractions are produced to
control forward movement and prevent falling. The viscoelastic qualities of con-
nective tissue allow it to absorb ground reaction forces through the lower extrem-
ity connective tissue, even reaching the spine to produce rotation. A contraction
of the gluteus maximus, along with the swing of the opposite arm, preloads the
thoracolumbar fascia, preparing it to further absorb ground reaction forces as
potential energy. 52 As the forces transmit through the connective tissue, they are
eventually released as kinetic energy as the thoracolumbar fascia springs back, re-
versing the rotation of the spine and initiating opposite hip flexion and arm swing,
creating a pendulum effect. 52
Fascia, as a continuous tissue, has been shown to be a force transmitter in a
number of animal studies. Force is transmitted through fascia via intramuscular,
intermuscular, or extramuscular force transmission. In intramuscular force trans-
mission, force is transmitted within the muscle from the endomysial - perimysial
fascial network onto adjacent fibers. 53 - 55 In intermuscular force transmission,
force is transmitted through the connective tissue between the neighboring mus-
cles.56·57 In extramuscular force transmission, force is transmitted through vari-
ous connective tissues, such as compartmental fascia or general fascia/connective
tissue surrounding blood vessels or nerves. 48 •55 •58 - 61 The influence of these fascia
connections is such that passive changes in length and active forces measured at
the proximal and distal portions of the muscle are not equal. 62- 64 Additionally,
although performed on animals, several studies have shown that fascial connec-
tions are significant enough to affect both synergistic and antagonistic related
muscles. 48,59,65,66
Similar results have been shown in human studies. Smeulders et al. showed
how critical the intermuscular connections are by measuring the active and pas-
sive length-force characteristics of the flexor carpi ulnaris (FCU). 67 While per-
forming an FCU transposition in children with cerebral palsy, Smeulders et al.
were able to measure the length-force of the FCU at specific points of dissection as
the muscle separated from its surrounding fascial connections. Kreulen et al. used
this method of measurement to determine the biomechanical effects of dissect-
ing the FCU. 68They measured the length of the FCU before and after dissection.
While keeping the wrist in neutral (0° flexion), they measured the length of FCU
while intact (221 + 36.2 mm), after tenotomy from the pisiform (216 + 37.7 mm),
and following the dissection of the muscle belly (204 + 36.9 mm) from its sur-
rounding fascia connections. The dissected muscle shortened significantly further
(196 + 36.3 mm) following an electronically stimulated tetanic contraction.
Passive excursion measurements were also taken before and after dissection. 68
Measurements were taken to compare the passive movement of maximal wrist
flexion and maximal extension. With the muscle and tendon intact, the difference
noted was 18.0 + 4.0 mm. After tenotomy, the excursion measured 16.0 + 3.8 mm
(89% of the original excursion despite the tendon being cut). Finally, after com-
plete dissection, the maximal passive wrist flexion/extension excursion measured
2.0 + 1.9 mm (11%of the original excursion).
De Bruin et al. also measured the flexion torque of the FCU during a simi-
lar dissection. 69While performing an FCU transposition in eight patients, they
measured the isometric torque under the same conditions examined above: before
tenotomy, after tenotomy of the distal tendon, and after dissection of the muscle
belly from its fascia connections. The wrist flexion torque decreased, on average,
to 80% following tenotomy and decreased further to 59% following complete dis-
section. A decrease between an intact tendon and tenotomy would certainly be ex-
pected, but the 21% difference between tenotomy and dissection further suggests
that myofascial connections are significant force transmitters.
Kawakami and colleagues have examined the influence of fascia connections
by using ultrasound to measure fascicle lengths during contractions. Longitudinal
ultrasonic images were taken of the tricep surae muscles (medial gastrocnemius,
lateral gastrocnemius, and soleus) in 12 different positions (15° dorsiflexion, 0°,
15°, and 30° plantarflexion, each with the knee in 0°, 45°, and 90° knee flexion). 70
Fascicle lengths were measured between the superficial and deep aponeuroses. The
fascicle lengths were longest when the ankle joint was positioned in 15° dorsi-
flexion with 0° knee flexion and shortest when positioned in 30° plantarflexion
with 90° knee flexion. These measurements were used as a platform to investigate
the role of muscle versus connective tissue in function. Fukunaga et al. exam-
ined the force transmission roles of muscle and connective tissue during ambula-
tion. 71 The researchers measured the lengths of muscle fascicles during toe-off,
swing, heel strike, and double/single support phases of the walks of six healthy
male volunteers (age 25 + 3 years, height 169 + 3 cm, body mass 69 + 8 kg). The
authors compared the results to corresponding measurements taken within the

musculoskeletal complex and tendon. The findings showed significant recoiling
abilities of the Achilles tendon during a major portion of the loading phase and
near-isometric behavior of the gastrocnemius as the fascicles maintained a near-
constant length. Kawakami et al. gathered similar measurements while examining
muscle versus connective tissue during the stretch - shortening cycle of a contrac-
tion. 72 Their findings showed near-isometric contractions of the gastrocnemius
during the eccentric phase, producing greater muscle power and elastic recoil of
the tendinous tissues, both of which support economic locomotion theories such
as Gracovetsky's presented above.
The results of these studies indicate that the force-transmitting qualities of
connective tissue, including intramuscular, intermuscular, and extramuscular
pathways, enable a large part of human motion. The system is most efficient when
connective tissues are mobile, making the flow of such forces more fluid. When the
myofascial tissues are immobilized, hindered, or nontransmitting, the forces may
be damaging to the tissue.
Histology and Biomechanics of Muscle

As stated previously, myofascial tissues account for the majority of soft tissue af-
fected by orthopedic manual therapy. A large portion of myofascial tissue is mus-
cle tissue. The manual physical therapist needs a basic understanding of muscle
tissue to have an appropriate empirical understanding of myofascial manipula-
tion. Knowledge of trauma, immobilization, and remobilization of muscle tissue
must be built on scientifically based principles, as outlined herein. Discussion of
the histology and physiology of muscle tissue occupies whole chapters in many
textbooks; the purpose of this section is to provide a basic overview of muscle
histology and how it relates to connective tissue . Much of the knowledge of mam-
malian skeletal muscle comes from studies of frog skeletal muscle, because frogs'
muscles are anatomically and histologically similar to those of mammals.
Histology
Muscle is histologically categorized into three types: skeletal, smooth, and cardiac.
This section focuses primarily on skeletal muscle. Skeletal, or striated, muscle is so
named because of its banded appearance under light microscopy. The striations
reflect the functional contractile unit of the muscle, called the sarcomere.Muscle
is also functionally characterized by fiber type, based on speed of contraction or
relaxation, biochemistry and metabolism, and circulation.
Mechanism of Growth in Skelet al Muscle

The total number of actual muscle fibers in a muscle is reached sometime before
birth. Longitudinal growth in a muscle is accomplished in early years by an in-
crease in the length of the individual sarcomeres and by addition of sarcomeres.
Increases in diameter are accomplished by the addition of myofilaments in parallel
arrangement. Likewise, the muscle shortens by losing sarcomeres and decreases

in diameter by losing myofilaments. With prolonged disuse, the muscle fibers
degenerate and the tissue is replaced with less metabolically active connective tis-
sue. Human skeletal muscle, however, does have some limited regeneration po-
tential. Satellite cells, which are believed to be a persisting version of the prenatal
myotubes found inside basement membranes, can become activated to produce a
limited number of new muscle fibers. The number of new fibers that can be pro-
duced, however, cannot compensate for the amount lost during major muscle
trauma or degeneration.
Cellular and Histological Organization of Skeletal Muscle

The contractile proteins of striated muscle are actin and myosin. The actin and
myosin interact in a ratchet-type manner to shorten the muscle (Figure 3.17). Actin
and myosin filaments are contained in the sarcomere. The transverse alignment of
sarcomeres in adjacent myofilaments gives this tissue the striated appearance. The
striations result from a series of bands (Z-, A-, and I-bands ), which reflect compo-
nents of the sarcomere. The distance between two Z-bands reflects the length of
Myosin Actin + myosin Actin

•
**
***:*.
*->!<;**: •
•
•
•
•
•
•
•
• • • •
•
• •
***:* • • • •
• • • • •
** • •
I
I "4;
I
I
•• I
/
I / Ill
111
'
/ 111
-... 111
>--, .... 111

111
, 111
',I I II
,
M
• • '
z
111
•..•
'-..--J
H Sarcomere
A I
Figure 3.17 Diagram showing the organization of skeletal muscle and the mechanism of shortening.
Source:Reprinted from Gray'sAnatomy, ed. 35 (p. 479) by P. Williams and R. Warwick with permission of
Elsevier, © 1973.
Muscle the sarcomere and will vary depending on

the contractile state of the muscle. The A-
band, which represents myosin molecules,
does not change in length during contrac-
tion, whereas the I-band, which represents
'
.•' •'
' '' ' areas where actin does not overlap myosin,
I
, ':
'
changes depending on the contractile state
Fasciculus ,'
Groupof --
;, I
II
of the muscle.
musclefibers I
I
Sarcomeres are arranged in series to
,
I
form cylindrical organelles called myo-

I
,
I
I
I filaments. Myofilaments are arranged in
;,
bundles and are contained in the myofibril,
which is the muscle's cellular unit. Each
myofibril is surrounded by loose connective
tissue called the endomysium. Myofibrils
j
'
I
I
are multinucleated cells that also contain
I
' . mitochondria, lysosomes, ribosomes, and

...
\
\ . glycogen. Myofibrils are grouped together
' ' ...
into bundles called fasciculi (Figure 3.18).
Perimysium, also loose connective tissue,
Myofibril
separates and envelops each fasciculus in a
type of sheath. Finally, fasciculi are grouped
together to form individual muscles, which
are wrapped in a loose connective tissue
Myofilaments sheath called the epimysium.
Biomechanics of Muscle
The connective tissues of skeletal muscle
have important roles in the optimal func-
Myosin
tion of muscle. These connective tissues
provide a certain amount of coherence in
the muscle while allowing an appropriate
.
Actin
•. • •. • .• ....
•,..
Figure 3. 18 Diagram showing architectural hi-

•• •
•
•
degree of mechanical freedom. The con-
nective tissue layers also serve to carry the
erarchy of muscle tissue. Source: Reprinted from blood supply to the tissue and ramify to
Gray's Anatomy, ed. 35 (p. 481) by P. Williams and form a rich capillary network in the muscle
R. Warwick with permission of Elsevier,© 1973. fiber.26 Additionally, they allow the penetra-
tion of nerves along with this blood supply
to provide for diffusion of nutrients and
ions as necessary for muscular metabolism and excitation. 3 The endomysium is
particularly significant in these roles, because it most closely approximates the in-
dividual muscle fibers. Perimysium is thought to provide both a cushioning effect,
through force transmission, and a stiffening effect, particularly in tonic muscles,
because tonic muscles contain significantly more perimysium than do phasic

muscles. 8 •73
Muscle Fiber Types

Human muscle is a mixture of Type I and Type II fibers. The percentage of each
fiber type varies from individual to individual, and the composition of an indi-
vidual's muscle fiber is directly related to muscle function. 26 Muscles are gener-
ally categorized according to the predominant fiber type present throughout the
muscle.
The following fiber type classification is currently the most widely used .74
Fibers are classified as Type I, Ila , lib , or Ilm (Table 3.3). Type I fibers are slow
twitch fibers, named for their slow contraction times. They are also the lowest in
glycogen stores but have the richest concentration of mitochondria and myoglo-
bin. Because of these characteristics, Type I fibers are the slowest to fatigue. The
postural muscles of the body have a predominance of Type I fibers. Type Ila fibers
(also called fast twitch/oxidative or fast red fibers) are intermediate fibers that have
a faster contraction time than Type I fibers while remaining moderately fatigue
resistant. A high concentration of myoglobin and mitochondria is still present in
these fibers. Type lib muscle fibers (also called fast twitch/glycolytic or fast white
fibers) have faster contraction times and rely more on glycolytic pathways for en-
ergy metabolism. Type lib fibers have a lower concentration of myoglobin and
mitochondria and are not fatigue resistant. Finally, a superfast fiber, Type Ilm , has
been identified in mammalian muscle tissue, including human muscle tissue. This
type of fiber is found primarily in the jaw muscles and contains a unique myosin
that distinguishes it from the other fibers. 75 Muscles that have a greater percent-
age of Type II fibers, that cross two joints, and that work eccentrically are much
Table 3.3 Classification of Muscle Fiber Types
Functional Functional
Fiber type classification Metabolic characteristics characteristics
Type I Slow twitch High concentrations of myo- Slow contraction
globin, increased numbers of times, fatigue
mitochondria, low content of gly- resistant
cogen, oxidative metabolism
Type Ila Fast twitch/ Moderately high concentrations Faster contraction
oxidative of myoglobin, increased numbers times than Type I.
(fast red) of mitochondria, glycolytic/ less fatigue
oxidative (mixed) metabolism resistant
Type llb Fast twitch/ High glycogen content, gly- Fast contraction
glycolytic colytic metabolism, decreased times, fatigues
(fast white) numbers of mitochondria easily
Type llm Superfast Contains unique myosin configu- Very fast contraction
ration, high glycogen content, times
lycolytic metabolism
more susceptible to strain injuries. The most common site of those injuries is at the
musculoskeletal junction. 26
Histology and Biomechanics of Junctional Zones

The junctional zones in the myofascial tissues include the myotendinous junction
and the ligament, tendon, and joint capsule insertions to bone . Early studies indi-
cate that although injury can occur in any portion of the myofascial tissues, injury
to the junctional zones is quite common. 76 Numerous stress - strain studies indicate
that most tissue failures occur at or near the myotendinous junction. 77 - 82 Myofas-
cial restrictions are commonly found near the junctional zones because of the fre-
quency of injury to these areas, and the clinician should be aware of these areas in
myofascial evaluation. A basic understanding of the histology and biomechanics
of junctional zones is, therefore, preliminary to a study of their histopathology and
to an empirical understanding of myofascial evaluation and treatment.
Histology of Myotendinous Junction

The attachment of the muscle is generally through tendon. The muscle belly at-
taches to tendon at the musculotendinous junction on each side of the belly. These
musculotendinous junctions are highly specialized areas.
Several histological differences occur in the transitional area between muscle
fibers and tendon that give it unique functional characteristics. First, the cell mem-
brane forms a continuous interface between intercellular components of muscle fi-
bers and extracellular components of connective tissue. The cell membrane at this
junction becomes highly folded or convoluted, allowing the contractile intercellu-
lar components to interdigitate with the extracellular components. 83- 90 The folding
of the cell membrane increases the surface area, thereby reducing the stress per
unit area on the membrane. The folds hold the membrane at a low angle in rela-
tion to the forces coming from the muscle fibers, placing the membrane primarily
under shear forces. If the folds did not exist, the junctional membrane would ex-
perience vector forces at right angles to the membrane surfaces. This would create
a tensile load at the junction. Studies indicate, however, that cell membranes are
highly resistant to shear forces that would increase their surface area. 91 The design
of the folds allows for much higher force transmission before tissue rupture.
Finally, the membranous folds increase the potential adhesive area in the
musculotendinous junction, 92 •93 thereby decreasing the load per unit area be-
ing transmitted from the muscle. Interestingly, muscles with predominantly fast
twitch muscle fibers have an increased folding of the junctional membranes. This
phenomenon is probably related to the fact that higher forces are developed in
fast twitch muscles than in slow twitch muscles, and greater cumulative tensile
strength is required to sustain and transmit such forces.
Another significant histological characteristic of the myotendinous junction is
decreased sarcomere length and extensibility. 94•95 This characteristic results in the
myotendinous junction first being loaded by terminal sarcomeres and subsequently
being fully loaded by the rest of the sarcomeres in the muscle belly. More signifi-
cantly, the decreased extensibility of the terminal sarcomeres also makes the tissue
in this area more vulnerable to tearing, as evidenced by the frequency of injury in
the experimental models. 94•95 The clinical implications are discussed further in
Chapter 4.
Biomechanics of the Myotendinous Junction

As previously mentioned, the intercellular contractile units must ultimately be
coupled with the collagen fibers of the tendon for transfer of forces to take place.
This is accomplished architecturally in the following manner. Thin myofilaments,
believed to be derivatives of actin, attach from the terminal Z disks of the myofi-
brils to a thickened cell area of the inner cell membrane called the subsarcolemma.
The contractile proteins of the muscle sarcomeres, therefore, have an attachment
to the cell membrane. The outer portion of the cell membrane is similarly attached
to a basement membrane that runs parallel to the cell membrane. The basement
membrane contains Type IV collagen and high-molecular-weight glycoproteins.
The basement membrane is then attached to collagen fibers of the tendon. 84 -s7,s9,90
All of the components of the myotendinous junction are coupled in a parallel
arrangement, rather than in series. As previously mentioned, the cell membrane
can accommodate shear forces more optimally than tensile forces, and the archi-
tecture of the myotendinous junction reflects this efficiency.
Connective Tissue Insertion to Bone

The insertions of tendons, ligaments, and joint capsules to bone vary somewhat
in their histological architecture. As with the myotendinous junction, the archi-
tecture is designed to dissipate tensile forces and minimize stress concentrations.
Despite their architectural design, these junctions are common sites of injury and
remain areas of weakness during loading. As with the other areas examined in
this chapter, a basic review of the histology and biomechanics of these junctions is
necessary to understand their response to trauma and pathology.
Within an area of 1 mm, the connective tissue is transformed into hard tissue
(Figures 3.19A and B). Two types of insertions are identified in the literature: direct
and indirect. Direct insertions have four distinct histological zones that represent
the transition of the tissues from soft connective tissues to bone. 96
Zone 1 consists of the actual tendon or ligament. The histology of this zone
does not differ much from the histology of ordinary tendon, ligament, or capsule.
Collagen fibers are found here embedded in the matrix or ground substance, as
are fibroblasts. Zone 2 consists of fibrocartilage. The cells in this region resem-
ble chondroblasts or chondrocytes. Zone 3 consists of mineralized fibrocartilage,
where mineral deposits are found around collagen fibrils. Finally, Zone 4 consists
of bone, where the collagen fibrils merge with the fibrils of the bone matrix.
Indirect insertions do not have specifically defined zones, as do the direct
insertions. The connective tissue fibers tend to blend more with the periosteum,
which in turn attaches to bone. These transitional fibers are sometimes referred to
'•
.~~
I
• ..
'-
A
-
•
• - -
•
•
• • • •
. ' "' . •
•
•
r ,.
, •
• ..
•
• -
-
.. •
B
Figure 3.19 (A) Direct insertions. The four distinct zones seen in the supraspinatus insertion. The four
zones are tendon (T), uncalcified fibrocartilage (FC), calcified fibrocartilage (C-FC), and bone (B). Blood
vessels (BY) are absent from the fibrocartilage zones. The tidemark (TM) between the calcified and un-
calcified zones of articular cartilage (AC) is continuous with that at the insertion of the tendon. Source:
Reprinted with permission from M. Benjamin, E. J.Evans, et al., The Histology of Tendon Attachments to
Bone in Man, Journal of Anatomy, No. 149, pp. 89- 100, © 1986, Cambridge University Press. (B) Femoral
insertion of rabbit medial collateral ligament. The deep fibers of the ligament (L) pass into bone through the
fibrocartilage (F). The arrow indicates the line of calcification. Source:Reprinted with permission from S.-Y.
Woo, M. A. Gomez, et al., The Biomechanical and Morphological Changes in the Medial Collateral Liga-
ment of the Rabbit After Immobilization and Remobilization, Journal of Bone & Joint Surgery,Figure 6-A,
Vol. 69A, p. 1207, © 1987,Journalof Bone & Joint Surgery.
as Sharpey's fibers. 96 These fibers are described as originating in the periosteum

and perforating the underlying bone, anchoring the periosteum to underlying
bone. 23 No fibrocartilage is seen in indirect insertions. 23•97
A common feature of the two insertional types is the presence of superficial
and deep fibers. The superficial fibers generally attach to periosteum, which in
turn attaches to bone. The deep fibers insert into bone or by way of fibrocartilage.
The main difference is that the direct insertion has a fibrocartilaginous transi-
tional zone, whereas the indirect insertions do not. Another commonality is that
the junctional zones of ligament, tendon, and capsule are relatively avascular com-
pared with the tissue on either side of the zone. 98,99
The attachment sites of ligament, tendon, and joint capsule to bone also vary
in their biomechanics because of differences in the forces imparted by these tis-
sues. Obviously, the tendon-bone junction will have greater forces because of the
forces generated by muscle, whereas the ligament and joint capsule-bone junc-
tion will have lesser forces. Studies conducted by Noyes et al. have demonstrated
the resilience of the tendon-bone junction. 100 These researchers analyzed several
samples of patellar tendon to determine stress-strain characteristics of the ten-
don proper, the entire bone-tendon-bone unit, and the actual attachment site.
The attachment sites undergo more significant strain (elongation) before receiving
significant stresses, indicating that strains in this region are greater than in any
other region. This allows for more force dissipation at this region but also makes
this region more vulnerable.
Biotensegrity of the Musculoskeletal System

Muscle contraction produces movement of the human body. As muscles generate
force, connective tissue helps transmit the force and guide the movement through
its connections to bone. The balance of force
moving back and forth between structures
is best described through the architectural
principle of tensegrity. Tensegrity is used
to describe architectural structures that are
kept mechanically stable by distributing
and balancing stresses. The stability is not
dependent on the strength of the individual
members of the structure but rather on a
combined effort of resisted compression
and tension (see Figure 3.20).
There are two types of tensegrity
structures. 101 The first are those developed
by Buckminster Fuller, whereby rigid,
Figure 3.20 A combination of rubber bands and compression-resistant frames in the shapes
solid dowels shows the prestressed balance of the
of triangles, pentagons, or hexagons are
tensegrit y structure.
fixed so as to produce continual tension
across all members. Geodomes are examples of such structures. The second type,
developed by Kenneth Snelson, involves compression-resistant structures and
tensile-resistant structures that are organized in a way that prestresses them. The
compression-resistant structures stretch or tense the structures of tensile resis-
tance, and the tensile-resistant structures compress the compression-resistant
structures. Each balances out the other, producing continuous tension and local
compression. The benefit of the latter is that it provides both strength and move-
ment and can be applied to nature and to the entire human body. For example, as
a sculptor, Fuller created numerous self-standing structures that appear to float or
to defy gravity. Some mimic the shape of a swan's neck.
Geodesic forms or spherical shapes composed of interconnecting triangles are
found throughout nature. Structures such as carbon atoms, viruses, enzymes, or-
ganelles, cells, and small organisms are stabilized by having interconnecting sides,
as a way of minimizing energy and mass while maximizing structural integrity.
Cells rely on the principle of tensegrity to maintain a delicate balance between
mobility and strength. The cytoskeleton of each cell can provide both mobility and
strength, because it is composed of an internal framework. The cytoskeleton has
three different types of molecular protein polymers: the microfilament, intermedi-
ate filament, and microtubules. 102 Altering the mechanical forces across the cyto-
skeleton can cause biochemical reactions and can alter the genetic programs of a
cell.103, 104 Cells spread flat are more likely to divide, cells that have no force on them
or that are prevented from spreading activate apoptosis, and cells with mid-range
forces (not too extended or retracted) neither divide nor die. Instead, they differen-
tiate into specific tissues. 105 In essence, force directs the function of the cell. If cells
are stretched, as they are by the myofibroblasts during wound healing, the signal is
clearly to divide and produce more cells. If cells are plentiful, as in the end stages of
remodeling, forces are reduced. The reduction causes the cells to become rounded
and die. Somewhere in between is homeostasis, with mid-range forces, and cells
can differentiate for the purpose of normal tissue function.
Cells make up tissues that provide specific functions or make up organs. Tis-
sues such as the skin perform either specific or a variety of functions during which
they experience force changes. Linear stiffness keeps the tissues intact and can
prevent tissue damage. When skin is pulled, resistance will be felt at some point. It
is thought that more tensegrity "members" line up in the direction of the applied
stress, which determines the stiffness of the tissue. 106•107 Up to a certain point, tis-
sues are able to temporarily deform, but they will eventually change their nature
as a response to sustained forces. Such changes result from prolonged postures due
to sitting, standing, or other static positions. Likewise, linear stiffness or linear
resistance is most likely the force responsible for absorption, storage, and reuse of
the loading forces produced during ambulation as an effort to conserve energy and
provide efficiency of movement.
The principle of tensegrity is clear to see on a macroscopic scale of the hu-
man body. The compression-resistant bones pull up against gravity and yet remain
stabilized by the continual tension produced by resistant muscles, tendons, liga-

ments, and fascia. The balance of the constant tension and localized compression
has been experienced by anyone who has floated in water or by astronauts who
have floated in space. With gravity removed and the body at complete rest, the
arms, legs, and trunk all flex slightly and do not straighten out.
The rigidity of tensegrity is what enables a person to stand or sit upright. The
constant tension of tensegrity gives the body its shock absorption qualities and
prevents everyday forces, such as falling, stepping off the curb, or jumping a last
step, from breaking bones and dislocating joints. Tensegrity allows for fluid move-
ment while holding everything together, as is necessary when reaching out to pick
up a drink, book, or child. The arm reaches out, while the muscles in the legs and
trunk contract to create proximal stability. The muscles in the shoulder complex
lift the weight of the arm, producing compression in the joints, which help to sta-
bilize the appendage. Disruption in the push - pull relationship can lead to tissue
changes, as seen in a forward head posture. The forward position pulls on the pos-
terior tensile-resistant structures, potentially leading to increased passive tension,
thickening in an effort to become stronger, and joint compression. The increased
compression of the bone, according to Wolff's law, results in the production of
more bone, such as osteophytes. Maintaining good posture and healthy tissues can
minimize injury by preserving the balance between the push of the osseus struc-
tures that resist compression and the pulling force of the soft tissue structures that
hold the skeleton together.
Conclusion
The information covered in this chapter serves as an overview of the scientific re-
search available regarding soft tissue. A thorough understanding of basic anatomy
and biomechanics is necessary for the manual physical therapist to be successful
in treatment of the myofascial tissues. Additionally, an understanding of the fluid
qualities of connective tissue, as well as its ability to act as a force transmitter via
the principles of tensegrity, assists the therapist to set realistic goals for manual
treatment. Knowledge of these concepts also is helpful with patient education, be-
cause they can easily be described in lay terms.
As the evidence regarding soft tissue and myofascial manipulation expands,
the pieces of the puzzle start to fit. More and more data demonstrate how immobi-
lization can limit motion, as well as how manipulation can reverse the limitations.
Practitioners compete daily for patients, and insurance company reimbursements
are steadily decreasing; in such an environment, it is essential for manual physical
therapists to educate patients as well as to maintain professional credibility within
the medical community. It is imperative to blend and balance the art and science
of the profession, especially as the science expands and particularly in the areas of
myofascial manipulation.
References
1. Dicke E, Schliack H, Wolff A. A Manual of Reflexive Therapyof the ConnectiveTissue.Scars-
dale, NY: Sidney S. Simon Publishers; 1978.
2. Ham AW,Cormack DH. Histology.Philadelphia: JB Lippincott; 1979.
3. Warwick R, Williams PL. Gray'sAnatomy. 35th ed. Philadelphia: WB Saunders; 1973.
4. Standring S. Gray'sAnatomy. 40th ed. London: Churchill Livingstone Elsevier; 2008.
5. Copenhaver WM, Bunge RP,Bunge MB. Bailey'sTextbookof Histology.Baltimore: Williams &
Wilkins; 1971.
6. Geneser F. Textbookof Histology.Philadelphia: Lea & Febiger; 1986.
7. Neidlinger-Wilke C, Wilke H, Claes L. Cyclic stretching of human osteoblasts affects pro-
liferation and metabolism: a new experimental method and its application.! OrthopRes.
l 994;12:70- 78.
8. Williams P, Goldspink G. Connective tissue changes in immobilized muscle. J Anat.
1984,Mar:343-350.
9. Fielding JW,Burstein AH, Frankel VH. The nuchal ligament. Spine. 1976;1:3-14.
10. Nachemson AL, Evans JH. Some mechanical properties of the third human lumbar interlami-
nar ligament (ligamentum flavum). J Biomech. 1968;1:211- 220.
11. Cummings G, Crutchfield CA, Barnes MR. Soft Tissue Changesin Contractures.Atlanta, GA:
StokevillePublishing; 1985.
12. Norris C. SportsInjuries:Diagnosisand Management. Oxford: Butterworth Heinmann;
1993.
13. Bernhardt D. Sports PhysicalTherapy.New York:Churchill Livingstone; 1986.
14. Sapega AA, Quedenfeld TC, Moyer RA, Butler RA. Biophysicalfactors in range-of-motion
exercise. Phys Sportsmed.1981;9:57- 65.
15. Warren CG, Lehmann JF,Koblanski JN. Heat and stretch procedures: an evaluation using rat
tail tendon. Arch PhysMed Rehabil.1976;57:122-126.
16. Woo S-Y,Ritter D. The biomechanical and biochemical properties of swine tendons: long-term
effects of exercise on the digital extensors. Connect TissueRes. 1980;7:177-183.
17. Fung YC. Elasticity of soft tissues in simple elongation. Am J Physiol.1967;213:1532-1544.
18. Hooley CJ, McCrum NG, Cohen RE. The viscoelastic deformation of tendon. J Biomech.
1980;13:521-528.
19. De Deyne P, Meyer R, Paley D, Herzenberg J. The adaptation of perimuscular connective tissue
during distraction osteogenesis. Clin Orthop RelatRes. October 2000:259- 269.
20. Iatridis J, Yandow J, Langevin H. Subcutaneous tissue mechanical behavior is linear and visco-
elastic under uniaxial tension. Connect TissueRes. 2003;44:208- 217.
21. Neuberger A, Slack HG. The metabolism of collagen from liver, bone, skin and tendon in the
normal rat. BiochemJ.1953;53:47- 52.
22. Frankel VH, Nordin M. BasicBiomechanicsof the SkeletalSystem. Philadelphia: Lea & Febiger;
1980.
23. Woo SL,Gomez MA, Sites TJ, Newton PO, Orlando CA, Akeson WH. The biomechanical and
morphological changes in the medial collateral ligament of the rabbit after immobilization and
remobilization.! BoneJoint SurgAm. 1987;69:1200-1211.
24. Viidik A. Tensile strength properties of Achilles tendon systems in trained and untrained rab-
bits. Acta Orthop Scand. 1969;40:261-272.
25. Kennedy JC, Hawkins RJ,Willis RB, Danylchuck KD. Tension studies of human knee liga-
ments: yield point, ultimate failure, and disruption of the cruciate and tibial collateral liga-
ments. ! BoneJoint SurgAm. l 976;58:350- 355.
Histology and Biomechan ics of Myofascia 65
26. Barlow Y,Willoughby J. Pathophysiology of soft tissue repair. Br Med Bull. l 992;48:698- 711.
27. Schleip R, Klingler W, Lehmann-Horn F. Active contraction of the thoracolumbar fascia: indi-
cations of a new factor in low back pain research with implications for manual therapy. In:
5th InterdisciplinaryWorld Congresson Low Back & PelvicPain. Melbourne: World Federation
of Occupational Therapists; 2004.
28. Schleip R, Klingler W, Lehmann-Horn F. Fascia is able to contract in a smooth muscle-like
manner and thereby influence musculoskeletal mechanics. In: Liepsch D, ed. 5th World Con-
gressof Biomechanics.Munich, Germany: Medimond International Proceedings; 2006:51- 54.
29. Tomasek J, Gabbiani G, Hinz B, Chaponnier C, Brown R. Myofibroblasts and mechano-
regulation of connective tissue remodelling. Nat Rev Mol CellBiol. 2002;3:349- 363.
30. Wipff P, Hinz B. Myofibroblasts work best under stress. J Bodyw Mov 1her.2009;13:121- 127.
31. Gabbiani G. The myofibroblast in wound healing and fibrocontractive diseases.! Pathol.
2003;200:500- 503.
32. Serini G, Gabbiani G. Mechanisms of myofibroblast activity and phenotypic modulation. Exp
CellRes. 1999;1:273- 283.
33. Powell DW, MifflinRC, Valentich JD, Crowe SE, Saada JI, West AB. Myofibroblasts.I: Para-
crine cells important in health and disease. Am J Physiol.1999;277(1Pt l):Cl-C9.
34. Langevin H, Cornbrooks C, Taatjes T. Fibroblasts form a body-wide cellular network. Histo-
chem CellBiol. 2004;122:7-1 5.
35. Langevin H. A body-wide signaling network? Med Hypotheses.2006;66:1074-1 077.
36. YahiaL, Rhalmi S, Newman N, Isler M. Sensory innervation of human thoracolumbar fascia:
an immunohistochemical study. Acta OrthopScand. 1992;63:195-197.
37. Schleip R. Fascial plasticity- a new neurobiological explanation: Part I. J Bodyw Mov 1her.
2003;7:ll -1 9.
38. Schleip R. Fascial plasticity- a new neurobiological explanation: Part 11.J Bodyw Mov 1her.
2003;7:104- 116.
39. Rayan G. Dupuytren disease: anatomy, pathology, presentation, and treatment.! BoneJoint
SurgAm. 2007;89:189-1 98.
40. Bunker T, Anthony P. The pathology of frozen shoulder: a Dupuytren-like disease. J BoneJoint
Surg Br. 1995;77:677- 683.
41. Mengiardi B, Pfirmann C, Gerber C, Hadler J, Zanetti M. Frozen shoulder: MR arthrographic
findings. Radiology.2004;233:486- 492.
42. Langevin H, Sevens-Tuttle D, Fox J, et al. Ultrasound evidence of altered lumbar connective
tissue structure in human subjects with chronic low back pain. BMC MusculoskeletDisord.
2009;10:151.
43. Rolf I. Rolfing:Re-establishingthe Natural Alignment and StructuralIntegrationof the Human
Bodyfor Vitality and Well-Being.Rochester: Healing Arts Press; 1989.
44. Juhan D. Job'sBody:A Handbookfor Bodywork 3rd ed. Barrytown, NY: Station Hill Press;
1998.
45. Oshman J. EnergyMedicine. Edinburgh: Churchill Livingstone; 2000.
46. De Ruiter C, De Haan A, Sargeant A. Repeated force production and metabolites in two me-
dial gastrocnernius muscle compartments of the rat. J Appl Physiol.1995;79:1855-1861.
47. Meijer HJ, Rijkelijkhuizen JM, Huijing PA. Myofascial force transmission between antagonistic
rat lower limb muscles: effects of single muscle or muscle group lengthening.! Electromyogr
IGnesiol. 2007;17:698- 707.
48. Rijkelijkhuizen J, Baan G, de Haan A, de Ruiter C, Huijing P. Extramuscular myofascial force
transmission for in situ rat medial gastrocnernius and plantaris muscles in progressive stages
of dissection.! Exp Biol. 2005;208:129- 140.
49. De Ruiter C, De Haan A, Sargeant A. Physiological characteristics of two extreme muscle

compartments in gastrocnemius medialis of the anaesthetized rat. Acta PhysiolScand.
1995;153:313-324.
50. Gracovetsky S. Gracovetsky on walking. StructuralIntegration.2003;3 l :4- 8.
51. Gracovetsky S. Is the lumbodorsal fascia necessary? J Bodyw Mov 1her.2008;12:194-1 97.
52. Zorn A, Schmitt F, Hodeck K, Schleip R, Klingler W. The elastic function of the lumbar fascia
in human gait. In: European Workshopon Movement Science.Amsterdam 2007.
53. Purslow P, Trotter J. The morphology and mechanical properties of endomysium in series-
fibred muscles: variations with muscle length. ! Muscle Res CellMotil. 1994;15:299- 308.
54. Huijing P, Baan G, Rebel G. Non-myotendinous force transmission in rat extensor digitorum
longus muscle. J Exp Biol. 1998;201:683- 691.
55. Huijing P. Muscular force transmission: a unified, dual or multiple system? A review and some
explorative experimental results. Arch PhysiolBiochem.1999;170:292-311.
56. Maas H, Baan G, Huijing P. lntermuscular interaction via myofascial force transmission: ef-
fects of tibialis anterior and extensor hallucis longus length on force transmission from rat
extensor digitorum longus muscle. J Biomech.2001;34:927- 940.
57. Maas H, Meijer H, Huijing P. lntermuscular interaction between synergists in rat originates
from both intermuscular and extramuscular myofascial force transmission. CellsTissuesOr-
gans. 2005;181:38- 50.
58. Huijing P, Baan G. Extramuscular myofascial force transmission within the rat ante-
rior tibial compartment: proximo-distal differences in muscle force. Acta PhysiolScand.
2001;173:297- 311.
59. Yucesoy C, Koopman B, Baan G, Grootenboer H, Huijing P. Effects of inter- and extramuscu-
lar myofascial force transmission on adjacent synergistic muscles: assessment by experiments
and finite-element modeling. J Biomech.2003;36:1797- 1811.
60. Huijing P. Epimuscular myofascial force transmission between antagonistic and synergis-
tic muscles can explain movement limitations in spastic paresis. J ElectromyogrKinesiol.
2007;17:708- 724.
61. Huijing P, Baan G. Myofascial force transmission via extramuscular pathways occurs between
antagonistic muscles. CellsTissuesOrgans.2008;188:400-414.
62. Huijing P, Baan G. Myofascial force transmission causes interaction between adjacent
muscles and connective tissue: effects of blunt dissection and compartmental fasciotomy on
length force characteristics of rat extensor digitorum longus muscle. Arch PhysiolBiochem.
2001;109:97-1 09.
63. Huijing P, Baan G. Myofascial force transmission: muscle relative position and length deter-
mine agonist and synergist muscle force. J Appl Physiol.2003;94:1092-11 07.
64. Huijing P, Jaspers R. Adaptation of muscle size and myofascial force transmission: a review of
some new experimental results. Scand J Med Sci Sports.2005;15:349- 380.
65. Meijer H, Rijkelijkhuizen J, Huijing P. Effects of firing frequency on length-dependent myofas-
cial force transmission between antagonistic and synergistic muscle groups. Eur J Appl Physiol.
2008;104:501- 513.
66. Yucesoy C, Baan G, Huijing P. Epimuscular myofascial force transmission occurs in the rat
between the deep flexor muscles and their antagonistic muscles. J ElectromyogrKinesiol.
2010;20:118-1 26.
67. Smeulders MJ, Kreulen M, Hage JJ, Huijing PA, van der Horst CM. Intraoperative measure-
ment of force-length relationship of human forearm muscle. Clin Orthop Relat Res.January
2004:237- 241.
68. Kreulen M, Smeulders MJ, Hage JJ, Huijing PA. Biomechanical effects of dissecting flexor carpi
ulnaris. J Bone Joint Surg Br. 2003;85:856- 859.
Histology and Biomechan ics of Myofascia 67
69. de Bruin M, Smeulders M, Kreulen M. lntermuscular myofascial connections of FCU could

contribute to wrist flexion torque in the spastic arm of cerebral palsy patients. In: Huijing P, ed.
2nd InternationalFasciaResearchCongress2009. Amsterdam; 2009.
70. Kawakami Y,Ichinose Y,Fukunaga T. Architectural and functional features of human triceps
surae muscles during contraction.! Appl Physiol.l 998;85:398- 404.
71. Fukunaga T, Kubo K, Kawakami Y,Fukashiro S, Kanehisa H, Maganaris C. In vivo behaviour
of human muscle tendon during walking. ProcBiol Soc.2001;268:229- 233.
72. Kawakami Y,Muraoka T, Ito S, Kanehisa H, Fukunaga T. In vivo muscle fibre behavior during
counter-movement exercise in humans reveals a significant role for tendon elasticity.! Physiol.
2002;540:635- 646.
73. Borg T, Caulfield J. Morphology of connective tissue in skeletal muscle. TissueCell.
1980;12:197-207.
74. Gauthier GF. Skeletal muscle fiber types. In: Engel AG, Banker BQ, Franzini-Armstrong C,
eds. Myology.New York:McGraw-Hill; 1986:255-284.
75. Rowlerson A, Pope B, Murray J, et al. A novel myosin present in cat jaw-closing muscles.
J Muscle Res CellMotil. 1981;1:255-438.
76. McMaster PR Tendon and muscle ruptures: clinical and experimental studies on the causes
and location of subcutaneous ruptures.! BoneJoint Surg. 1933:705-722.
77. Garrett WE Jr. Muscle strain injuries. Am J SportsMed. 1996;24(6Suppl):52- 58.
78. Almekinders LC, Garrett WE Jr. Histopathology of muscle tears in stretching injuries. Trans
OrthopRes Soc. 1984;9:306.
79. Garrett WE Jr, Almekinders LC. Biomechanics of muscle tears in stretching injuries. Trans
OrthopRes Soc. 1984;9:384.
80. Garrett WE Jr., Nikolaou PK, Ribbeck BM, Glisson RR, Seaber AV.The effect of muscle archi-
tecture on the biomechanical failure properties of skeletal muscle under passive extension.
Am J SportsMed. 1988;16:7-12.
81. Nikolaou PK, Macdonald BL, Glisson RR, Seaber AV,Garrett WE Jr. Biomechanical and histo-
logical evaluation of muscle after controlled strain injury. Am J SportsMed. 1987;15:9-14.
82. Garrett WE Jr., Rich FR, Nikolaou PK, Vogler JB 3rd. Computed tomography of hamstring
muscle strains. Med Sci Sports Exerc.1989;21:506-514.
83. Gelher D, Moore DH. Observations of the myotendon junction in mammalian skeletal muscle.
Z ZellforschMikrosk Anat. 1960;2:325- 336.
84. Mackay B, Harrop TJ, Muir AR. The fine structure of the muscle tendon junction in the rat.
Acta Anat (Basel).1969;73:588- 602.
85. Tidball JG, Daniel TL. Myotendinous junctions of tonic muscle cells:structure and loading.
CellTissueRes. 1986;245:315-322.
86. Eisenberg BR, Milton RL. Muscle fiber termination at the tendon in the frog's sartorius: a ste-
reological study. Am J Anat. 1984;171:273- 284.
87. Tidball JG. The geometry of actin filament-membrane associations can modify adhesive
strength of the myotendinous junction. CellMotil. 1983;3:439- 447.
88. Trotter JA, Hsi K, Samora A, Wofsy C. A morphometric analysis of the muscle-tendon junc-
tion. Anat Rec. 1985;213:26- 32.
89. Mair WG, Tome FM. The ultrastructure of the adult and developing human myotendinous
junction. Acta Neuropathol.1972;21:239- 252.
90. Trotter JA, Eberhard S, Samora A. Structural connections of the muscle-tendon junction. Cell
Motil. l 983;3:431-438.
91. Evans EA, Hochmuth RM. Mechanochemical properties of membranes. Current Topicsin
Membranesand Transport.1978;10:l-64.
92. Bikerman JJ. Stresses in proper adhints. In: The Scienceof AdhesiveJoints.2nd ed New York:
Academic Press; 1968:192-263.
93. Lubkin JL. The theory of adhesive scarf joints. Journalof AppliedMechanics.1957;24:255- 260.
94. Gordon AM, Huxley AF, Julian FJ. Tension development in highly stretched vertebrate muscle
fibres. J Physiol.1966;184:143-169.
95. Huxley AF, Peachey LD. The maximal length for contraction in vertebrate striated muscle.
J Physiol(Lond). 1961;156:150-165.
96. Cooper RR, Misol S. Tendon and ligament insertion: a light and electron microscopic study.
J BoneJoint Surg. l 970;52:Al - A21.
97. Benjamin M, Evans EJ, Copp L. The histology of tendon attachments to bone in man. J Anat.
1986;149:89-100.
98. Scapinelli R. Studies on the vasculature of the human knee joint. Acta Anat (Basel).
l 968;70:305- 331.
99. Arnoczky SP, Rubin RM, Marshall JL. Microvasculature of the cruciate ligaments and its re-
sponse to injury: an experimental study in dogs. J Bone Joint SurgAm. 1979;61:1221-1229.
100. Noyes FR, DeLucas JL, Torvik PJ. Biomechanics of anterior cruciate ligament failure: an
analysis of strain-rate sensitivity and mechanisms of failure in primates.! Bone Joint Surg
Am. 1974;56:236-253.
101. Ingber DE. The architecture of life. Sci Am. 1998;278:48-57.
102. Ingber DE. Tensegrity and mechanotransduction. J Bodyw Mov 1her. 2008;12:198 - 200.
103. Matthews BD, Overby DR, Mannix R, Ingber DE. Cellular adaptation to mechanical stress:
role of integrins, Rho, cytoske letal tension and mechanosensitive ion channels.! CellSci.
2006;119:508 - 518.
104. Ingber DE. Tensegrity -based mechanosensing from macro to micro. Prog BiophysMol Biol.
2008;97:163-1 79.
105. Ingber DE. Mechanical control of tissue morphogenesis during embryological development.
Int J Dev Biol. 2006;50:255 - 266.
106. Wang N, Ingber D. Mechanotransduction across the cell surface and through the cytoskel-
eton. Science. 1993;21:1124-1127.
107. Wang N, Naruse K, Stamenovic D, et al. Mechanical behavior in living cells consistent with
the tensegrity model. ProcNatl Acad Sci US A. 2001;98:7765 - 7770.
Histopathology of Myofascia
and Physiology of Myofascial
Manipulation
Robert I. Ca ntu, A lan J. Grodin, and Robert W. Sta nbo rough
Histopathology of Myofascia
Understanding any treatment technique requires knowledge of the basic process of
soft tissue healing. In the previous chapter, the normal histology and biomechan-
ics of myofascial tissues are presented. With that groundwork laid, this chapter ad-
dresses the histopathology and pathomechanics of those same tissues. A review of
classic and recent literature is provided to help readers understand posttraumatic
scar formation and the effects of immobilization and remobilization on myofascial
tissues. With an awareness of the changes that occur in the myofascial tissues un-
der dysfunctional conditions, a manual therapist can set realistic treatment goals
and choose the most appropriate treatment techniques to accomplish them. The
intuitive aspects of myofascial manipulation must always be balanced by a solid
understanding of tissues and their response to dysfunction.
Pathophysiology of Soft Tissue Repair

By its most basic definition, a wound is a disruption of unity. Because vertebrates
lack the ability to regenerate exact duplicates of injured parts, response to injury
comes in the form of repair through granulated scar tissue. The scar formation
process is not cyclic but rather is a linear process with a sequence of recurring
stages. The literature varies as to whether a wound undergoes three or four distinct
phases. 1- 4 We divide the scar process into four distinct phases: (1) the inflamma-
tory phase, (2) the granulation phase, (3) the fibroblastic phase, and (4) the matu-
ration phase. 5•6 Different tissues heal at different rates, and within a single wound,
areas in various phases of healing may be seen. 1 The changes may also be affected
The authors gratefully acknowledge the contributions of Deborah Cobb to earlier versions of this chapter.
69
acute inflammation
fibrous repair
remodelling and contraction
months
1 2 3 4 5 6 7 8
• ice, compression , elevation, gentle movements
• protect weak joint, ensure joint is stable, remove hematoma
• allow new collagen to feel normal tensions
• prevent undesirable shortening, e.g., muscles, joint capsules
Figure 4.1 Encouraging favorable healing conditions. Source:Reprinted with permission from P. Evans,
The Healing Process at Cellular Level: A Review. Physiotherapy,Vol. 66, No. 8, pp. 256- 259, © 1980, Phys-
iotherapy Canada, and G. Hunter, Specific Soft Tissue Mobilization in the Treatment of Soft Tissue Lesions,
Physiotherapy,Vol. 80, No. 1, pp. 15- 21, © 1994, Physiotherap y Canada.
by an individual's age and fitness level.7Clinicians should understand when each

phase is likely to begin and end.
Inflammation, a normal prerequisite to healing, is the first phase seen after a
trauma. This phase begins immediately and may last 24 - 48 hours. Injury causes
chemical and mechanical changes that alter blood flow. This alteration, in turn,
leads to the cardinal signs of inflammation: heat, redness, swelling, and pain. The
inflammatory response to injury is the same regardless of the injuring agent or the
location of the injury. 8 Whole blood poured directly into a wound will coagulate
and temporarily seal off the injured vessels and lymphatic channels. This trau-
matic exudate acts to temporarily seal the wound. Histamine is released by the
injured tissues, resulting in vasodilation and the appearance of a reddened, hot,
and swollen region. 1 Prostaglandins, formed from cell membrane phospholipids
when cell damage occurs, produce pain. 2 Phagocytosis then occurs to prevent in-
fection in the wound and prepare the wound for healing. Phagocytosis is initiated
by short-lived polymorphonuclear leukocytes, which first attach to bacteria and
then dissolve and digest them. Shortly after, macrophages appear to continue the
phagocytic process and to begin influencing scar production. 9 The role of macro-
phages in recruiting fibroblasts has a significant effect on the final amount of scar-
ring produced. 1 During the inflammatory phase of the healing process, movement
in the wound area would be disadvantageous, as it could lead to further tissue
and/or clot disruption. Modalities aimed at decreasing inflammation and proper
positioning, in addition to appropriate anti-inflammatory medications, are of the
most value at this point (Figure 4.1).
The granulation phase begins when the macrophages and histiocytes debride
the area. The granulation stage is so named because of the appearance of capil-
lary buds, which, under a microscope, look like granules. Healing cannot proceed
further unless this increased connective tissue vascularity can meet the metabolic
demands of the healing tissues. Immobilization is essential during this phase to
Histopatho logy of Myofascia and Physiology of Myofasc ial Manipulation 71
lntramolecular Cross-links
Collagen filament
Cross-link Amino acid chains

A
Intermolecular Cross-links
Cross-link - ~
Collagen filament [
Figure 4 .2 Collagen bonding increases tensile strength: (A) Weak intramolecular cross-links form be-
tween amino acid chains within one collagen filament. (B) Stronger intermolecular cross-links form from
one collagen filament to another. Source:Reprinted from Hardy, A., Biology of Scar Tissue, Physical Ther-
apy, Dec. 1989, Vol. 69, No. 12, with permission of the American Physical Therapy Association.
permit vascular regrowth and to prevent further microhemorrhages and tissue

breakdown. 1,10 Heat application at this point may cause increased bleeding in the
fragile healing tissues. 11
Rebuilding of tissue begins in the fibroblastic phase. Fibroblasts proliferate,
and collagen synthesis is accelerated. As the fibroblasts proliferate, new collagen is
laid down in a disorganized manner in the area of the wound. The strength of the
wound is determined not by the amount of collagen laid down but by the bonding
of the collagen filaments or cross-links (Figure 4.2).3 The cross-linking allows for
early controlled movement without disruption of the wound. Controlled move-
ment will cause the fibrils to align lengthwise along the line of stress of the heal-
ing structure. 12 Because vascularity remains high during this phase, the immature
scar still has a characteristic pink coloring. Wound closure usually occurs at this
stage, and the time frame varies depending on the vascularity and metabolic rate
of the tissue. In tissues with high metabolic activity (muscles, skin, etc.), wound
closure occurs in 5- 8 days. In tissues with lower metabolic activity (ligament and
tendon), wound closure occurs in 3- 5 weeks. 6 During this phase, gentle handling
of the wound is essential, and gentle manual therapy techniques may be appro-
priate. Soft tissue manipulation designed to break up scar tissue will inflame the
wound, leading to further collagen deposits. 5•6
The final stage of scar formation is the maturation or remodeling phase. This
stage may last from 3 weeks to 12 months. 4 During this phase, collagen must
change in order to reach maximum function. A reduction in wound size, a re-
alignment of collagen fibers, and an increase in the strength of the scar are all
characteristics of this phase. Arem and Madden confirmed that a physical change
in scar length could be achieved through the application of low-load, long-dura-
tion stress during this phase. 12 Throughout this phase, the scar tissue is responsive
to manual therapy, but the progress will be somewhat slowed. Without controlled
stress or manipulation during this phase, however, tensile strength of the scar will
not improve, and optimal function will be diminished.
Cycle of Fibrosis and Decreasing Mobility in Connective Tissue

The fibrotic process is histologically distinct from the scar formation process. The
fibrotic process in connective tissue is a homogeneous process involving an entire
tissue area or the entire tissue "fabric" and does not have clear-cut stages as does
the scar tissue formation process. The fibrotic process is cyclical, whereas scar for-
mation is a linear process having a distinct end. The fibrotic process in connective
tissue can continue as long as the irritant is present.
The fibrotic process is generally initiated by the production of an irritant, pos-
sibly traumatic exudates from nearby, acutely inflamed, traumatized tissue or a
low-grade irritation or inflammation of the tissue. The low-grade irritation may be
caused by arthrokinematic dysfunction, poor posture, overuse, habit patterns, or
structural and movement imbalances. A rotator cuff irritation, for example, may
be caused by a poor tennis serve, poor sleeping postures, occupational overuse
syndromes, or other causes. The mechanical irritant produces a low-grade inflam-
mation, which then starts the process. With an inflammatory response, macro-
phages are activated to clean and debride the area. Inflammatory exudates, along
with damaged collagen and other waste products, are carried away. The increased
metabolic activity in the area stimulates the body to increase the area's vascularity.
With increased vascularity and debridement of damaged collagen (from micro-
trauma), fibroblasts are activated to replace lost collagen. Because the inflamma-
tory process is generally painful, the joint is not moved in proper fashion. The
collagen forms haphazardly, because adequate stress is not being placed on the tis-
sue, and cross-linking with preexisting collagen fibers begins. Myofibroblasts then
appear, as they do during the scar formation process. The myofibroblasts, which
contain significant amounts of actin and myosin in the cytoplasm, anchor to ad-
jacent collagen fibers and contract, shrinking the tissue. The tissue shrinkage re-
sults in further dysfunctional movement, which, in turn, creates more mechanical
Chronic irritant
~
Abnormal movement Macrophages activated
(biomechanics)
Shrinkage of connective Increased vascularity

tissue
Increased myofibroblastic Increased

activity fibroblastic activity
Increased production of connect ive tissue

(fibrosis)
Figure 4.3 Cycle of fibrosis and decreasing mobility.
stresses and more chronic irritant (Figure 4.3). As long as an irritant is present, the
cycle continues.
Since the introduction of technologically advanced imaging, changes in soft
tissue have been documented. Palpable taut bands identified in patients diagnosed
with myofascial pain syndrome have been confirmed visually using magnetic res-
onance elastography. 13- 15 Soft tissue changes have also been visually recorded in
patients with low-back pain (LBP). Langevin et al. examined 107 human subjects
(60 with LBP and 47 without LBP).16 Using diagnostic ultrasound, they compared
the perimuscular connective tissue thickness bilaterally, 2 cm lateral to the mid-
point of the L2- L3 interspinous ligament. Subjects with LBP had, on average,
25% greater thickness than those without LBP, after adjusting for body mass index.
Researchers found no differences related to sex, age, or activity level.
Response of Myofascial Tissue to Immobilization

Connective tissue has characteristic histological and biomechanical responses
to immobilization. Much of the research currently available focuses on animal
studies. These studies examine connective tissue from various parts of the body
for histological and biomechanical effects of immobilization. Human studies, al-
though limited, are starting to emerge. Although animal studies provide a certain
amount of insight, therapists should exercise caution when generalizing results
from animal studies to a human rehabilitation population. Furthermore, many of
the studies discussed in this chapter deal with the response of "normal," or non-
traumatized, connective tissue to immobilization and do not necessarily address
the response of traumatized and/or scar tissue. In the general orthopedic setting,
connective tissue that has been immobilized has also been traumatized. Trauma
has an effect on the histology and biomechanics of the healing of connective tis-
sue. It is also important to consider the process of scar formation and the effects of
immobilization on the developing scar tissue. We address these clinical consider-
ations in detail because the response of normal connective tissues to immobiliza-
tion provides a basis for understanding traumatized conditions.
Nontraumatized Connective Tissue

When a nontraumatized joint is subjected to immobilization, stress-deprived con-
nective cells exhibit changes within 4-10 days. 17·18Intrinsic changes to periarticu-
lar connective tissues begin to limit mobility. Many of the early animal studies on
immobilized connective tissue were performed by Akeson, Woo, and their associ-
ates.19-24In studies utilizing primarily knee joints, laboratory animals were immo-
bilized by internal fixation for periods from 2 to 9 weeks. A pin was placed from
the proximal third of the femur to the distal third of the tibia, presumably to avoid
traumatizing the knee joint. The animals were then euthanized at various lengths
of immobilization, and the periarticular tissues were analyzed microscopically,
histochemically, and biomechanically. From a microscopic standpoint, the authors
found fibrofatty infiltrate, especially in the capsular folds and recesses. The longer
the immobilization, the greater the amount of infiltrate found. A more protracted
period of immobility also resulted in a change in the infiltrate's appearance, which
became more fibrotic. The fibrous infiltrate created macroscopic adhesions in the
recesses and capsular folds.
Histological and histochemical analyses showed several significant changes,
the primary one being a significant loss in ground substance with no significant
collagen loss. The primary components of lost ground substance were the glycos-
aminoglycans and water. The authors reported a 30% -40 % loss in both sulfated
and nonsulfated groups. Because the primary purpose of the nonsulfated group
(hyaluronic acid) is to bind water, the water loss is easily explained.
As noted in Chapter 3, "Histology and Biomechanics of Myofascia," one of
the primary purposes of the ground substance is to lubricate the area between
adjacent collagen fibers. Collagen fiber lubrication is associated with the mainte-
nance of the so-called critical interfiber distance, which is the distance that must
be maintained between collagen fibers to allow them to glide smoothly and to
prevent microadhesions between fibers. When the critical interfiber distance is not
maintained, the collagen fibers approximate and eventually become cross-linked
by newly synthesized collagen. Also, because collagen fibers are laid down accord-
ing to the stresses (or lack of stresses) applied, collagen in immobile connective tis-
sue is arranged haphazardly. 25The newly synthesized collagen then binds adjacent
collagen fibers, decreasing the extensibility of the tissue (Figure 4.4).
Several factors explain why significant amounts of ground substance are
lost, yet collagen is not. First, the half-life of nontraumatized collagen is 300 -
500 days, whereas the half-life of ground substance is 1.7-7 days. 26-28Also, with
immobilization times of less than 12 weeks,

collagen synthesis occurs at the same rate as
collagen degradation. After 12 weeks, how-
ever, the rate of collagen degradation ex-
ceeds the rate of synthesis, and net amounts
of collagen are lost. 29
Biomechanical analyses indicate that
moving an immobilized joint requires
10 times more torque than is needed to move
a normal joint. After several repetitions, the
Figure 4.4 Drawing showing the laying down of amount of torque required to move the im-
newly synthesized collagen, forming cross-links mobilized joint was reduced to 3 times that
onto existing collagen fibers. These cross-links are
for a normal joint. The biomechanical im-
believed to be responsible for decreased extensibility
in immobilized connective tissue. Source:Reprinted plication is that fibrofatty macroadhesions
from R. Donatelli and H. Owens-Burkhart, Effects and microscopic adhesions in the form of
of Immobilization on the Extensibility of Periar- increased collagen cross-linking contribute
ticular Connective Tissue, Journal of Orthopaedic
to the decreased extensibility of the connec-
and Sports PhysicalTherapy,Vol. 3, pp. 67- 72, with 19 24
permission of the Orthopaedic and Sports Sections tive tissue. -
of the American Physical Therapy Association. Schollmeier et al. immobilized the fore-
limbs of 10 beagles for 12 weeks. At the end
of that time, the passive range of motion
of the glenohumeral joints was markedly decreased and intra-articular pressure
was raised during movements. The capsule showed hyperplasia of the synovial
lining and vascular proliferation of the capsular wall. Functional and structural
changes began to reverse after remobilization and returned to normal limits after
12 weeks. 30
In a study of rat ankles immobilized for 2- 6 weeks, Reynolds et al found
slightly different results. This study found that dense connective tissues remodel
in such a way that mobility is unaffected after 2 weeks of immobilization but is
markedly limited after 6 weeks of immobilization. 31 The authors attribute these
changes to dense connective tissue undergoing remodeling between the 2- and
6-week periods. Earlier studies implied that cyclic manipulation of the immobi-
lized joints caused rupture of the remodeled tissues, which limited early mobility.
In Figure 4.5, following each yield point, the angle of the slope of the curve is un-
changed. This finding supports the idea that the remodeled tissue, which initially
limited motion, had not ruptured; rather, discrete adhesions between folds of tis-
sues were responsible for the limitation.
Langenskiold et al. performed a study on immobilized, healthy rabbits. 32 The
authors found that casting for 5- 6 weeks significantly decreased knee flexion.
The resumption of normal activity, however, restored 90% of joint mobility after
3 weeks. When immobilization was increased to 7 or 8 weeks, only 28% of knee
flexion returned after 10 weeks of reconditioning. It took as long as 12 months for
some of the animals to regain full mobility. The study suggests that the longer the
75 t
:j:
~
(/)
Q)
Q)
~
Cl
Q)
-0
~
C
0
50
\
)(
Q)
25 11 *
;;:::
11
(/)
~
0
*
0 *
..0
0 20 40
Loading Time (seconds)
Figure 4.5 Diagrammatic representation of the qualitative difference in pattern of dorsiflexion between
limbs casted for 6 weeks (:j:)and all other limbs (t). In all ankles casted for 6 weeks, the curve exhibited
intermediate plateaus (11),followed by small but sudden slipping further into dorsiflexion (*), suggesting
rupture of an adhesion with each slip. Source:Reprinted from C. A. Reynolds, G. S. Cummings, and P. D.
Andrew, et al., The Effect ofNontraumatic Immobilization on Ankle Dorsiflexion, Journal of Orthopaedic
and Sports Therapy,Vol. 23, No. 1, p. 31, with permission of the Orthopaedic and Sports Sections of the
American Physical Therapy Association.
period of immobilization, the more difficult it becomes to regain normal tissue

structure and mobility.
In a study by Evans et al., experimentally immobilized rat knees were remobi-
lized by high-velocity manipulation, by range of motion, or both. 25 The investiga-
tors found that with manipulation, the macroadhesions ruptured, and partial joint
mobility was restored. If joint motion was allowed subsequent to the manipula-
tion, functional range was regained. Range of joint motion, along with freedom of
movement, produced the same effect, although more gradually; after 35 days the
joints were histologically indistinguishable. Rat knee joints immobilized for more
than 30 days, however, did not regain full functional range. Again, the results sug-
gest that movement restores the normal histological makeup of connective tissue,
but the longer the period of immobilization, the lower the potential for achieving
optimal results.
In summary, immobilization of connective tissue generally results in loss of
ground substance with no net collagen loss (with immobilization periods of less
than 12 weeks). The loss of ground substance also allows for significant water loss.
Histologically, this results in decreased tissue extensibility due to the inability of
the collagen fibers to maintain the critical interfiber distance and the subsequent
formation of microscopic collagen cross-links. At the macroscopic level, immobi-
lization causes the formation of fibrofatty macroadhesions that become progres-
sively more fibrotic with increased immobilization times. The studies also indicate
that all periarticular connective tissues responded in the same basic fashion. Liga-
ment- and capsule-surrounding fascia all had the same basic response to immo-
bilization. Remobilization of the tissues reverses the effects, if the immobilization
Histopathology of Myofa scia and Physiology of Myofa scial Manipulation 77
period has not been unduly long. More research is needed on duration of mobility
and changes occurring within the connective tissues. Clinicians need to consider
the early changes occurring in the immobilized connective tissues and adjust their
treatment plans accordingly. Before 4-6 weeks, the stress-deprived, weakened cells
may require gentle mid-range movement and protection from excessive forces;
however, after 6 weeks, treatment protocols should incorporate sufficient stress
to induce connective remodeling, which can accommodate lengthened positions
until full joint mobility is achieved. 28
Traumatized Connective Tissue

Questions have arisen regarding how traumatized connective tissue's response to
immobility varies from the response of nontraumatized tissue. The previously dis-
cussed studies focused on the response of nontraumatized connective tissue to
immobilization. Some consider internal fixation of a limb to be a trauma-inducing
form of immobilization, even though the fixation is located some distance from
the tissue studied. In a study performed by Flowers and Pheasant, nontraumatized
human digits were casted for a period of several weeks and then examined. 33 The
range of motion lost during the immobilization period was regained within one
treatment session of approximately 20 minutes. The implication of this study and
of the previous immobilization studies is that when connective tissues of syno-
vial joints are immobilized in the presence of inflammatory exudates, joint con-
tractures occur. Studies show that these contractures result from remodeling and
shortening of connective tissues. When a limb is immobilized without inflamma-
tory exudates being present, no contracture occurs, even after weeks. 5•6 Appar-
ently, a catalyst-traumatic exudate-is needed to begin the process of contrac-
ture. Also, methods of fixation may affect tissue changes.
The rigid fixation in the previously discussed studies allowed for virtually no
movement, whereas the cast fixation in Flowers and Pheasant's study 33 may have
allowed enough movement to prevent tissue changes. This phenomenon can be
seen in a clinical setting. For example, when a distal radial fracture is casted, an
extra callus often forms because of the less than optimal union. From a rehabili-
tation standpoint, the functional range of motion of the wrist, hand, and radio-
ulnar joints is usually restored. If the fracture is fixated with an external fixator,
the union is typically much cleaner, with less callus formation. Functional range
of motion is typically not fully restored, however, especially in the wrist and radio-
ulnar joints.
The clinical implications are threefold . First, patients entering physical ther-
apy for rehabilitation following injury or surgery and subsequent immobilization
will have connective tissue changes as just described . Second, a combination of
two processes is occurring: scar formation and fibrosis. Scar formation occurs in
areas that sustained direct insult and are in need of regeneration and repair. Fi-
brotic changes occur in tissues surrounding the scar area that were not directly
traumatized but were affected chemically by the traumatic exudates. Third, trau-
matic exudates infiltrate these surrounding, nontraumatized areas and, acting as
chemical catalysts, create changes in the connective tissues.
Scar tissue versus.fibrosis. Scar formation and fibrosis are two different histologi-
cal processes, although some similarities exist. Scar formation is a localized re-
sponse, with activity limited to a traumatized area, whereas fibrosis is a homoge-
neous change in the "fabric" of the connective tissue. Limitation in mobility caused
by scar tissue results from the lack of extensibility of the scar tissue and from the
adhesions formed with adjoining healthy connective tissue. Fibrotic changes cause
the entire tissue to become less extensible, which then limits movement. Also, as
previously mentioned, fixation methods may exacerbate the effects. Semirigid im-
mobilization (immobilizer or cast) may allow sufficient movement to decrease the
effects of immobilization.
For example, a shoulder may be frozen because of a macroscopic scar adhesion
in the folds of the inferior capsule, in which case a manipulation under anesthesia
would tear the scar adhesion and restore mobility. A frozen shoulder may also be
caused by a capsulitis, where the entire capsule shrinks (an analogy here is the
size 5 capsule and a size 8 glenohumeral joint-the sock is simply too tight). The
distinction is that motion is limited by homogeneous changes in the capsule rather
than a single scar adhesion. A manipulation under anesthesia may not be as suc-
cessful in the latter case, because an entire tissue is responsible for the immobility.
The benefit of increased mobility is outweighed by the potential damage to the
capsule fabric and the restimulation of the fibrotic cycle.
Muscle Tissue
The response of muscle tissue to immobilization is less simplistic and more multi-
factorial than the response of connective tissue to immobilization. Being a contrac-
tile tissue, a muscle can be passively or actively immobilized, and the muscle may
be immobilized in a shortened or lengthened position. The muscle may be inner-
vated or denervated and predominantly slow twitch or predominantly fast twitch.
Because muscle is highly metabolic, it can undergo various metabolic changes,
depending on its activity level. The purpose of this section is to outline briefly the
histological response of muscle tissue to immobilization and to review the factors
influencing immobilized muscle most applicable to myofascial manipulation.
One of the classic works on muscle response to immobilization was performed
by Tabary et al. 34 In this study, cat soleus muscles were immobilized at various
lengths and for various durations. The animals were immobilized by plaster
cast. Some of the animals were euthanized, and the muscles were biomechani-
cally and histologically analyzed. The passive length-tension was increased in
muscles immobilized in the shortened position, probably because of the connec-
tive tissue changes within and surrounding the muscle. Muscles immobilized in
the lengthened position had no significant changes in the passive length-tension
characteristics. From a histological standpoint, the muscles immobilized in the

shortened position had a 40% loss of sarcomeres, with an overall decrease in fi-
ber length. The muscles immobilized in the lengthened position exhibited a 19%
increase in sarcomeres and an overall increase in fiber length. After 4 weeks of
remobilization, the number of sarcomeres in the muscles returned to normal. This
study illustrates the principle that to keep sarcomeres at optimal lengths, muscle
tissue will adapt to change in length by increasing or decreasing sarcomeres.
In a follow-up study by Tabary and Tardieu, muscle changes caused by pro-
longed active shortening were studied .35 Sciatic nerves of guinea pigs were stimu-
lated for 12 hours to produce muscle contractions while held in a shortened or
lengthened position. The muscles stimulated in the shortened range had a 25% loss
of sarcomeres after only 12 hours of contraction. Within 48-72 hours, sarcomeres
were completely recovered in the muscles. The implication of these studies is that
passively shortened muscles lose sarcomeres at a much slower pace than actively
shortened muscles.
Kauhanen et al. immobilized the vastis intermedius muscle of 13 rabbits in
a shortened position for 2-28 days. 36 After 3 days of immobilization, the muscle
displayed a 15% decline in muscle fiber diameter. By 2 weeks, fatty changes were
prominent and muscle fiber diameter had decreased to 56%. By 4 weeks, severe
fibrotic damage of myofibrils was observed and fiber diameter had decreased to
47% of control values.
Leiva et al. also immobilized the vastis intermedius of rabbits into the ex-
tended position. 37 As the duration of the immobilization increased, progressive
disorganization of myofibrils occurred, with breaking up of Z-bands and an in-
crease in the number and size of plasmic lipid vacuoles. This study suggests, as
does the prior study, that adverse mechanisms are in effect at the onset of disuse
atrophy.
Kannus et al. found that, after 3 weeks of immobilization, a significant de-
crease occurred in the mean percentage of intramuscular connective tissue. 38 They
also found an increase in the relative number of muscle fibers with pathological
alterations.
Kawakami and colleagues did a series of studies in humans. They examined
the strength and cross-section of the thigh of healthy male subjects after 20 days
of bed rest. 39•40 They confirmed that strength is related to muscle cross-section. 41
Both were decreased, but no changes were noted in the pennation angles of the
atrophied muscle, suggesting that muscle architecture does not change with atro-
phy of up to 10% and that loss of strength is most likely due to decreased ability to
activate the motor units.
The clinical implication of these findings relates to the types of immobiliza-
tion that occur in the practice setting. Immobilization may occur artificially (ex-
ternal or internal fixation) or as a physiological mechanism (muscle guarding).
In the clinical setting, immobility may be due to trauma, past or present. A good
example is the whiplash injury, in which immobilization is caused intrinsically by
the cervical and upper thoracic paravertebral muscles, the scapulothoracic mus-
cles, and the shoulder girdle muscles. In many cases, the surrounding muscula-
ture remains tonically active long after the facet or ligamentous strain has healed.
The body learns a new recruitment pattern for the surrounding muscles, and this
hypertonic pattern remains long after healing. The muscles are then actively "im-
mobilized," causing some of the histological changes mentioned previously. Often,
the most difficult part of the therapeutic process is dealing with this hypertonicity,
which is secondary to the original injury.
Physiology of Myofascial Manipulation

Massage has been used for centuries in various cultures around the world . Massage
may be described as systematic, therapeutic, and functional stroking and knead-
ing of the soft tissues of the body. The terms myofascial manipulation, soft tissue
manipulation, and soft tissue mobilization are used interchangeably with massage.
Many studies of the effects of massage published before the 1950s involved ani-
mal subjects, but more recent research has been performed on humans. The ef-
fects of massage, as shown by these studies, include circulatory changes, blood
flow changes, capillary dilation, cutaneous temperature change, and metabolic
changes, with noted changes in scar healing and collagen distribution.
Effects of Massage on Blood Flow and Temperature

The effects of massage on blood flow in the extremities of 17 adult men and women
were analyzed by Wakim et al. 42 Groups were subdivided into those with no medi-
cal problems, those with rheumatoid arthritis, those with flaccid paralysis, and
those with spasmatic paralysis. The subjects received two types of massage: (1) a
moderate depth stroking and kneading massage described as a modified Hoffa-
type massage, and (2) a deeper vigorous, stimulating, kneading, and percussion
massage (as practiced in some European schools of physical therapy). Therapists
treated upper and lower extremities, and the massage lasted 15 minutes.
Wakim et al. concluded that a consistent and significant increase in total blood
flow and cutaneous temperature occurred after deep stroking and kneading mas-
sage of the extremities in healthy subjects, patients with rheumatoid arthritis,
and subjects with spasmatic paralysis. A much milder effect was noted with the
more superficial Hoffa-type massage and primarily in the group with paralysis.
The greatest increase in circulation after deep stroking and kneading massage to
the extremities occurred in subjects with flaccid paralysis. Significant increases in
blood flow and temperature were still apparent in all groups receiving deep mas-
sage when these signs were remeasured at 30 minutes. Blood flow increases dimin-
ished markedly after 30 minutes. Deep stroking, or kneading, or vigorous stimu-
lating massage of the extremities did not result in consistent, significant changes
in blood flow of the contralateral unmassaged extremity. The primary significance
of Wakim et al.'s study is that temperature change in the extremities, resulting
from increased blood flow to the part, may well depend on the manner in which
the massage is administered. The authors found that the moderate-depth Hoffa
massage affected only the blood flow of subjects with flaccid paralysis, whereas the
deep stimulating massage had the effect of increasing the blood flow of all subjects
studied. 42
Effects of deep kneading massage on venous blood flow were also examined
by Wolfson using animal models (dogs).43 A "deep, kneading type of massage"
was applied to the limbs above and below the knee (after anesthetizing). Wolfson
measured blood flow by cannulation of the femoral vein during anesthesia. The
blood draining outward was measured and reinjected into the opposite limb at
the same rate the blood was being removed . The massage initially caused a fairly
rapid increase in blood flow followed by a decrease in blood flow to a rate less than
normal. This decrease in blood flow continued throughout the administration of
the massage. Following cessation of the massage, blood flow slowly returned to
normal. Thus, Wolfson concluded that massage causes an increase in the rate of
blood flow by mechanically emptying the blood vessels and allowing them to refill
with fresh blood .
The findings in these studies are similar. Deep kneading massage, as per-
formed on human as well as animal models, increases the blood flow to the area
being treated. Caution should be exercised, however, when generalizing the results
of animal studies to the human population.
The reaction of normal blood vessels to mechanical stimuli was microscopi-
cally examined by Carrier. 44 Gross visual observation of skin reaction was made
following mechanical stimulation of the skin by a blunt instrument. With light
stroking, the area in the path of the stroke blanched after a latent period of 15-
20 seconds. The blanching lasted for several minutes. A harder stimulus resulted in
a hyperemic line in the immediate path of the stimulus. With microscopic inves-
tigation, light pressure resulted in instantaneous opening of all capillaries in the
microscopic field. A heavier pressure opened the underlying capillary for a longer,
unspecified, duration.
Carrier's observations 44 may correspond with the results of the studies by
Wakim et al and Wolfson. 42 •43 If the moderate-depth Hoffa-type massage (non-
stimulating) is similar to the light stroke produced by a blunt instrument in Car-
rier's study, an immediate superficial capillary reaction is an effect of massage. The
light stroke or Hoffa massage creates capillary dilation but for too short a duration
to affect blood volume, blood flow, or temperature in the underlying stroked area.
When vigorous stimulating massage is administered, the result is a longer lasting
dilation of the underlying capillaries, which creates a change in both blood flow
and skin temperature. Both the vigorous stimulating massage and lighter Hoffa-
type massage are used in myofascial manipulation.
In other research, Pemberton described the work of Clark and Swenson, who
studied the capillary circulation in the ear of a rabbit following massage .45 A per-
manent window was surgically created in the rabbit's ear, allowing observation
of the capillaries. Following massage, the researchers noted an increase in rate

of blood flow, as well as actual changes in the vessel walls. The vessel wall change
was evidenced by the "sticking" and emigration of leukocytes. Clark and Swenson
concluded that massage is accompanied or followed by an increased interchange
of substances between the bloodstream and the tissue cells. The vessel wall change
heightens the tissue metabolism.
Although Clark and Swenson did not define massagein their study, the find-
ings of increased blood flow and vessel wall change support the notion that mas-
sage, or soft tissue manipulation, affects the vascularization of the region underly-
ing the massage . Clark and Swenson's conclusion coincides with the findings of
Carrier, 44 who observed an immediate capillary reaction underlying the stimulus
of light and heavy pressure. Martin et al. studied cutaneous temperature of an ex-
tremity following modified Hoffa massage in healthy adults and those with rheu-
matoid arthritis. 46 Length of massage varied from 5 to 10 minutes.
Cutaneous temperature of the digits was measured with thermocouples. The
results indicated that after massage of an extremity, superficial cutaneous tem-
perature increased in the extremity for a period of 15- 90 minutes. In a related
investigation, the peripheral cutaneous temperature was examined after back mas-
sage. With three subjects, massage caused no change in the cutaneous temperature
of the extremities.
Despite design and variable differences, the studies presented all concur on
one point: massage causes capillaries to dilate in the region underlying the mas-
sage. If capillary dilation occurs, increased blood volume and flow occur, resulting
in an increased temperature in the area of the massage.
Effect of Massage on Metabolism

Massage can also affect the metabolic processes, including the vital signs and
bodily waste products. A review of the literature on massage's effects on human
metabolism was performed by Cuthbertson. 47 Cuthbertson concluded that there
was increased output of urine after massage, especially following abdominal mas-
sage. The excretion of acid was not consistently altered, and there was no change in
nitrogen content, inorganic phosphorus, or sodium chloride. The increased urine
output occurred within 3 hours of the massage; the total net output of urine in a
24-hour period was unchanged. Among healthy patients in the survey, there was
no increase in basal consumption of oxygen, in pulse rate, or in blood pressure.
The above metabolic effects apply to a systemic process. Localized increase in basal
consumption may occur, although localized effects have been inconclusive.
Because massage does not influence the basal metabolism, a likely explanation
for the increased urine output is the effect of massage on the circulation of the
part concerned. Increased blood volumes and blood flow through the area being
massaged may cause the area to dispose of excess fluids during and after massage,
thereby increasing urine output.
Ironson et al. examined the benefits of massage on individuals with the hu-
man immunodeficiency virus (H IV). Twenty-nine homosexual men (20 with H IV,
9 without H IV) received daily massage for 1 month. After the 1 month of massage,
a significant increase in the number of natural killer cells was noted in the H IV-
positive men. Thus, massage appears to enhance the immune system's cytotoxic
capacity. Further research in this area is required .48
The findings of increased blood flow, increased temperature, and increased
metabolism in the area being massaged have strong clinical implications. They
support the notion that massage is definitely indicated in areas where increased
tissue circulation and nutrition are desired.
Physiological Reflexive (Autonomic) Effects of Massage

The literature on the reflexive, or autonomic, effects of massage consists of studies
showing the results of connective tissue massage distal to the area being treated. In
support of connective tissue massage, Ebner reported that viscera, blood vessels,
and supporting tissue and muscle cannot function as separate entities. 49 Connec-
tive tissue massage stimulates the circulation to an area of the body that, in turn,
reflexively opens up increased circulatory pathways to other regions of the body.
The cause for the initial increase in circulation is secondary to the mechanical
tension created by the connective tissue massage strokes, which thereby stimulates
the tissue.
Ebner studied the skin temperature of three patients after connective tissue
massage. 49 Ebner found an increase in skin temperature (1°C to 2°C) of the foot
following 20 minutes of connective tissue massage, which was performed on the
sacral and lumbar segments of the back. Volker and Rostovksy (as reported by
Ebner) also carried out experiments using connective tissue massage and found
a maximum increase in temperature distal to the area being massaged approxi-
mately 30 minutes after the massage ended.
The mechanical friction of the massage stroke stimulates the structures within
the connective tissue, primarily the mast cell. As the mast cell is stimulated, it pro-
duces histamine, which is a vasodilator. The vasodilation increases blood flow to
the area treated and to other areas receiving histamine through the bloodstream.
The increased permeability of the capillaries and small venules allows for quicker
and more complete diffusion of waste products from the tissues to the blood . The
blood components, when filtered by the kidney and excreted as urine, show in-
creased nitrogen content, inorganic phosphorus, and sodium chloride, as reported
by Cuthbertson. 47 The increased circulation caused by connective tissue massage
(stimulating massage) through the reflexive nature of histamine release follows
the findings of Carrier, Martin, et al., and Wakim et al. when stimulating massage
is performed .42 •44•46 Chapter 2, "Modern Theories and Systems of Myofascial Ma-
nipulation," fully elaborates on the autonomic effects of myofascial manipulation.
Effects of Massage on Fibroblastic Activity/Collagen Synthesis

During the Healing Process
Research has shown that controlled motion of soft tissues influences the heal-
ing process. 5o- 53 As discussed in prior sections, the soft tissues of the body are
Injury
i----------,✓
-
.c
O>
C
~
t;
Q)
<I)
C
~
________________ _
....._
Time
Figure 4.6 General trend of increase in tensile strength of injured soft tissue during healing process.
Source:Reprinted with permission from P. Evans, The Healing Process at the Cellular Level, Physiotherapy,
Vol. 66, No. 8, pp. 256- 259, © 1980, Physiotherapy Canada, and G. Hunter, Specific Soft Tissue Mobilisation
in the Treatment of Soft Tissue Lesions, Physiotherapy,Vol. 80, No. 1, Jan 1994, pp. 15- 21. © 1994, Physio-
therapy Canada.
subjected to both internally and externally generated forces. Without stress ap-
plied through the tissues, the tensile strength will decrease. 53 Stearns observed
the effect of movement on the fibroblastic activity in healing connective tissues
and concluded that fibrils form almost immediately. 54 External factors were re-
sponsible for assuming an orderly arrangement of these fibrils. Cyriax and Russell
asserted that gentle passive movements of the soft tissues will prevent abnormal
adherence of the fibrils without affecting their proper healing. 55
The manual therapist should use his or her knowledge of the stages of heal-
ing to determine when specific massage techniques should be used (Figure 4.6).
Chapter 3, "Histology and Biomechanics of Myofascia," discussed the soft tissue's
inability to withstand stress immediately after injury. It is, therefore, important to
protect the injured tissues from stress during the early inflammatory stage. The
fibrin bond holding the wound together can easily be disrupted, ultimately leading
to an increase in the amount of scar tissue formed. 56 Because collagen does not ap-
pear in the wound for 4 - 6 days after injury, the value of friction and deep massage
before this time is questionable. 57
As the tissues move into the regeneration phase, fibroblasts begin to lay down
collagen, and the tensile strength increases. Gentle transverse friction is often used
at this point. The repetitive force is applied perpendicular to the fibers of the tissue
as an imitation of the muscle's normal mobility. It is used with progressive force
to help broaden but not stretch or tear the healing fibers in an effort to enable
pain-free movement as the tissues heal. 58 The increased movement will encourage
realignment, lengthening, and strengthening of fibers.
ASTYM, or augmented soft tissue manipulation, has proven to be effective

during the regeneration stage. ASTYM is a system that uses specially designed in-
struments to assist the therapist in manipulating soft tissue, followed by stretching
or exercise. One without the other does not produce optimal results. A therapist
uses specially designed instruments with lubricant to gently "catch" the fibrotic
tissue, producing a mechanical stimulus. This, in turn, triggers the neurophysi-
ological response of tissue healing via collagen synthesis. Prescribed stretches or
exercises are immediately incorporated to produce controlled stresses through the
tissues. A model using rat Achilles tendon injuries revealed that ASTYM leads to
an increase in fibroblast recruitment and activation, as well as an increase in fibro-
nectin production. 59Increasing fibroblast activity increased the healing process in
this animal model. 60 Carefully applying tension during this phase will help col-
lagen fibers to align properly. 61,62
As the remodeling phase begins, the rate of collagen synthesis equals that of
collagen lysis. Evans found that collagen fibers tend to contract and decrease scar
tissue mobility at this point. 56Collagen cross -linking adds strength to the wound
but can also lead to a decrease in mobility. During this phase, the wound should
undergo continual tension to promote good fiber orientation and scar tissue ex-
tensibility. The use of deep massage techniques may be appropriate at this time to
decrease adhesions and break down scar. 55One study on friction massage done
for 10 minutes a day over 3 months on pediatric burn patients with hypertrophic
scarring failed to show any increase in pliability or height of the scar. 63Further
studies using longer or more frequent treatment sessions should be done before
concluding that massage is ineffective in the treatment of hypertrophic scarring.
Effect of Massage on Collagen Distribution

Manual therapists have long supported the theory that the mechanical proper-
ties of connective tissue change as a result of massage or manual therapy. The
theory is primarily based on palpation skills and the changes perceived to take
place as a direct result of a treatment (see "Connective Tissue Plasticity" in
Chapter 3, "Histology and Biomechanics of Myofascia"). The thickness of a tis-
sue may vary depending on area of the body, 64 sex,65 age, 66 hormonal status, 67
disease, 68 medication, 69 mechanical forces, 70 sun exposure, 70 or hand domi-
nance. 64Changes to the mechanics of tissue as a result of massage, at least in the
superficial tissues, have been attributed to changes in the structure of collagen
distribution. 71
Pohl measured the superficial tissues of 30 subjects before and after treatment.
She identified palpable thickenings in the superficial tissues, locating tissues that
felt hard, firm, cold, stiff, and even painful. 71 Once the thickenings had been iden-
tified, she measured the collagen distribution in these areas using high-resolution,
high-frequency (22 MHz) ultrasound. Scans showed peaks at the points of high-
est collagen density, usually seen at the epidermis and as the tissue transitions
from dermis to subcutis. Following the pretreatment measurement, Pohl treated
the thickened tissues using skin rolling, a common technique where the superficial
tissues are rolled, pressed, and squeezed between the fingers and thumb.
After noticing changes, including increased warmth, greater mobility, and
palpably thinner tissues, she remeasured the collagen distribution. Although no
baseline data are available, the same data were measured and treatment performed
on 10 nonafflicted areas. A comparison of the data from the subjects' afflicted tis-
sues and nonafflicted tissues provides some insight as to the changes clinically
perceived. No pre- and posttreatment differences were found in the nonafflicted
tissues; however, a significant change was noted in the afflicted tissues. The differ-
ence of the mean height of the highest peak in the dermis pretreatment (M = 3.72,
SD = 0.68) and posttreatment (M = 2. 59, SD = 0.55) was highly significant (t test
for matched pairs, t29 = -8.03, P < 0.000 1).71 These measurements suggest less
collagen density and a more homogeneous tissue as a result of superficial soft tis-
sue manipulation.
Conclusion
The literature supports the use of myofascial techniques to influence the healing
of soft tissues. The choice of technique by the physical therapist should be based
in part on the stage of healing of the injured tissue. Gentle techniques may be
beneficial early on to ensure an orderly arrangement of fibrils and to prevent adhe-
sions. In the later stages of healing, deeper techniques may be more appropriate to
decrease adhesions, improve scar extensibility, and increase overall mobility of the
soft tissues. A good manual therapist not only must understand the histopathology
of myofascia and the stages of healing but also must remember to use this knowl-
edge when choosing treatment techniques. Choosing the appropriate technique at
the appropriate time is essential to successful treatment.
References
1. Hardy MA. The biology of scar formation. Phys 1her. 1989;69:1014- 1024.
2. Norris DA. Sports Injuries:Diagnosisand Treatmentfor PhysicalTherapists.Oxford: Butter-
worth-Heinmann; 1993.
3. van der Meulen JC. Present state of knowledge on processes of healing in collagen structures.
Int J SportsMed. 1982;4- 8.
4. Kellett J. Acute soft tissue injuries - a review of the literature. Med Sci SportsExerc.
1986;18:489- 500.
5. Cummings GS. Soft Tissue Contractures: Clinical Management Course Notes. Georgia State
University; March 1989.
6. Cummings GS, Crutchfield CA, Barnes MR. OrthopaedicPhysicalTherapySeries:Soft Tissue
Changesin Contractures.Atlanta, GA: Stokesville Publishing; 1983.
7. Lachman S. Soft TissueInjuries in SportsMedicine. Oxford, UK: Blackwell Publishing; 1988.
8. Hettinga DL. Inflammatory response to synovial joint stiffness. In: Orthopaedicand Sports
PhysicalTherapy.2nd ed. St. Louis: CV Mosby; 1990.
9. Leibovich SJ, Ross R. The role of the macrophage in wound repair: a study with hydrocortisone
and antimacrophage serum. Am JPathol. 1975;78:71- 100.
10. Lotze MT, Duncan MA, Gerber LH, Woltering EA, Rosenberg SA. Early versus delayed
shoulder motion following axillary dissection: a randomized prospective study. Ann Surg.
1981;193:288-295.
11. Paletta FX, Shehadi SI, Mudd JG, Cooper T. Hypothermia and tourniquet ischemia. Plast
Reconstr Surg Transplant Bull. 1962;29:531-538.
12. Arem AJ, Madden JW. Effects of stress on healing wounds: I. Intermittent noncyclical tension.
J Surg Res. 1976;20:93-102.
13. Chen Q, Bensamoun S, Basford J, Thompson J, An K. Identification and quantification
of myofascial taut bands with magnetic resonance elastography. Arch Phys Med Rehabil.
2007;88:1658 -1 661.
14. Bensamoun S, Ringleb S, Littrell L, et al. Thigh muscle stiffness assessed with magnetic reso-
nance elastography in hypothyroid patients before and after medical treatment.! Magn Reson
Imaging. 2007;26:708 - 713.
15. Chen Q, Basford J, An K. Ability of magnetic resonance elastography to assess taut bands.
Clin Biomech (Bristol,Avon). 2008;23:623 - 629.
16. Langevin H, Stevens-Tuttle D, Fox J, et al. Ultrasound evidence of altered lumbar connective
tissue structure in human subjects with chronic low back pain. BMC Musculoskelet Disord.
2009;10:l - 9.
17. Videman T, Eronen I, Friman C, Langenskiold A. Glycosaminoglycan metabolism of
the medial meniscus, the medial collateral ligament and the hip joint capsule in experi-
mental osteoarthritis caused by immobilization of the rabbit knee. Acta Orthop Scand.
1979;50:465-470.
18. Videman T, Michels son JE, Rauhamaki R, Langenskiold A. Changes in 35S-sulphate uptake
in different tissues in the knee and hip regions of rabbits during immobilization, remobiliza-
tion and the development of osteoarthritis. Acta Orthop Scand. 1976;47:290- 298.
19. Woo SL, Matthews JV, Akes on WH, Amiel D, Convery FR. Connective tissue response to im-
mobility: correlative study ofbiomechanical and biochemical measurements of normal and
immobilized rabbit knees. Arthritis Rheum. 1975;18:257-264.
20. Akeson WH, Woo SL, Amiel D, Coutts RD, Daniel D. The connective tissue response to im-
mobility: biochemical changes in periarticular connective tissue of the immobilized rabbit
knee. Clin Orthop Relat Res. 1973;356- 362.
21. Akeson WH, Amiel D, LaViolette D, Secrist D. The connective tissue response to immobility:
an accelerated ageing response? Exp Gerontol. 1968;3:289-301.
22. Akeson R. Human lung organ-specific antigens on normal lung, lung tumors, and a lung
tumor cell line. J Natl CancerInst. 1977;58:863- 869.
23. Akeson WH, Amiel D, Woo SL. Immobility effects on synovial joints the pathomechanics of
joint contracture. Biorheology.1980;17:95-110.
24. Akeson WH, Amiel D, LaViolette D. The connective-tissue response to immobilit y: a study of
the chondroitin-4 and 6-sulfate and dermatan sulfate changes in periarticular connective tis-
sue of control and immobilized knees of dogs. Clin Orthop Relat Res. 1967;51:183-197.
25. Evans EB, Eggers GWN, Bulter JK, Blumel J. Experimental immobilization and mobilization
of rat knee joints. J Bone Joint Surg. 1960;42A:737-758.
26. Neuberger A, Slack HG. The metabolism of collagen from liver, bone, skin and tendon in the
normal rat. Biochem J.1953;53:47-52.
27. Schiller S, Mathews MB, Cifonelli JA, Dorfman A. The metabolism of mucopolysaccharides
in animals: III. Further studies on skin utilizing C14-glucose, C14-acetate, and S35-sodium
sulfate. J Biol Chem. 1956;218:139-145.
28. Schiller S, Mathews MB, Goldfaber L, Ludowieg J, Dorfman A. The metabolism of mu-
copolysaccharides in animals: II. Studies in skin utilizing labeled acetate. J Biol Chem.
1955;212:531-535.
29. Amiel D, Akeson WH, Harwood FL, Frank CB. Stress deprivation effect on metabolic turn-
over of the medial collateral ligament collagen: a comparison between nine- and 12-week
immobilization. C/in Orthop Relat Res. 1983:265-270.
30. Schollmeier G, Sarkar K, Fukuhara K, UhthoffHK. Structural and functional changes in the
canine shoulder after cessation of immobilization. Clin Orthop Relat Res. 1996:310-315.
31. Reynolds CA, Cummings GS, Andrew PD, Tillman LJ. The effect of non-traumatic immobili-
zation on ankle dorsiflexion. J Orthop Sports Phys 1her. 1996;23:27- 33.
32. Langenskiold A, Michelsson JE, Videman T. Osteoarthritis of the knee in the rabbit produced
by immobilization: attempts to achieve a reproducible model for studies on pathogenesis and
therapy. Acta Orthop Scand. 1979;50:l-14.
33. Flowers KR, Pheasant SD. The use of torque angle curves in the assessment of digital stiffness.
J Hand 1her. 1988:69-74.
34. Tabary JC, Tabary C, Tardieu C, Tardieu G, Goldspink G. Physiological and structural
changes in the cat's soleus muscle due to immobilization at different lengths by plaster casts.
J Physiol. 1972:231-244.
35. Tabary JC, Tardieu G. Experimental rapid sarcomere loss with concomitant hypoextensibility.
Muscle Nerve. 1981:198-203.
36. Kauhanen S, Leiva I, Petilla M, Michelsson JE. Recovery of skeletal muscle after immobiliza-
tion of rabbit hindlimb: a light microscopic study. APMIS. 1996;104:797-804.
37. Leiva I, Kauhanen S, Michaelsson JE. Abnormal mitochondria and sarcoplasmic changes in
rabbit skeletal muscle induced by immobilization. APMIS. 1998;106:1113-1123.
38. Kannus P, Jozsa L, Jarvinen TL, et al. Free mobilization and low- to high-intensity exercise in
immobilization-induced muscle atrophy.! Appl Physiol. 1998;84:1418- 1424.
39. Kawakami Y, Muraoka Y, Kubo K, Suzuki Y, Fukunaga T. Changes in muscle size and archi-
tecture following 20 days of bed rest. J Gravit Physiol. 2000;7:53 - 59.
40. Kawakami Y, Akima H, Kubo K, et al. Changes in muscle size, architecture, and neural ac-
tivation after 20 days ofbed rest with and without resistance exercise. Eur J Appl Physiol.
2001;84:7-1 2.
41. Funkunaga T, Miyatani M, Tachi M, Kouzaki M, Kawakami Y, Kanehisa H. Muscle volume
is a major determinant of joint torque in humans. Acta PhysiolScand. 2001;172:249- 255.
42. Wakim KG, Terrier JC, Elkins EC. The effects of percutaneous stimulation on the circulation
in normal and in paralyzed extremities. Fed Proc. 1948;7:128.
43. Wolfson H. Studies on effect of physical therapeutic procedures on function and structures.
JAMA. 1931;96:2020.
44. Carrier EB. Studies on physiology of capillaries: reaction of human capillaries to drugs and
other stimuli. Am J Physiol. 1922;61:528-547.
45. Pemberton R. Physiology of massage. In: AMA Handbook of PhysicalMedicine and Rehabili-
tation. Philadelphia: Blakinston Co; 1950:133.
46. Martin GM, Roth GM, Elkins EC, Krusen FH. Cutaneous temperature of the extremities of
normal subjects and patients with rheumatoid arthritis. Arch PhysMed Rehabil. 1946;27:665.
47. Cuthbertson DP. Effect of massage on metabolism: a survey. GlasgowMed J.1933;2:200-213.
48. lronson G, Field T, Scafidi F, et al. Massage therapy is associated with enhancement of the im-
mune system's cytotoxic capacity. Int J Neurosci. 1996;84:205-217.
49. Ebner M. Connective Tissue Manipulation. Malabar, FL: Robert E. Kreiger Publishing; 1985.
50. Takai S, Woo SL, Horibe S, Tung DK, Gelberman RH. The effects of frequency and duration of
controlled passive mobilization on tendon healing.! Orthop Res. 1991;9:705- 713.
51. Frank C, Akeson WH, Woo SL, Amiel D, Coutts RD. Physiology and therapeutic value of pas-
sive joint motion. C/in Orthop Relat Res. 1984:113-125.
52. Gomez MA, Woo SL, Amiel D, Harwood F, Kitabayashi L, Matyas JR. The effects of increased
tension on healing medical collateral ligaments. Am JSports Med. 1991;19:347-354.
53. Forrester JC, Zederfeldt BH, Hayes TL, Hunt TK. Wolff's law in relation to healing skin.
J Trauma. 1970;10:770-779.
54. Stearns ML. Studies on the development of connective tissue in transparent chambers in the
rabbit ear. Am JAnat. 1940;67:55-97.
55. Cyriax J, Russell G. Textbook of OrthopedicMedicine. London: Tindall and Cass all Ltd; 1990.
56. Evans P. The healing process at the cellular level. Physiotherapy.1980;66:256-259.
57. Hunter G. Specific soft tissue mobilization in the treatment of soft tissue lesions. Physiother-
apy. 1994;80:15-21.
58. Chamberlain GJ. Cyriax 's friction massage: a review. J Orthop Sports Phys 1her. 1982;4:16-22.
59. Davidson C, Ganion L, Gehlsen G, Verhoestra B, Roepke J, Sevier T. Rat tendon morpho-
logic and functional changes resulting from soft tissue mobilization. Med Sci Sports Exerc.
1997;29:313-319.
60. Melham T, Sevier T, Malnofski M, Wilson J, Helfst R. Chronic ankle pain and fibrosis success-
fully treated with a new non-invasive augmented soft tissue mobilization technique (ASTM):
a case report. Med Sci Sports Exerc. 1998;30:801-804.
61. Tipton CM, Matthes RD, Maynard JA, Carey RA. The influence of physical activity on liga-
ments and tendons. Med Sci Sports. 1975;7:165-175.
62. Postacchini F, De Martino C. Regeneration of rabbit calcaneal tendon maturation of collagen
and elastic fibers following partial tenotomy. Connect Tissue Res. 1980;8:41-47.
63. Patino 0, Novick C, Merlo A, et al. Massage in hypertrophic scar. JBurn Care Rehabii.
1999;20:268-271.
64. Smalls L, Wickett R, Visscher M. Effect of dermal thickness, tissue composition, and body site
on skin biomechanical properties. Skin Res Technol.2006;12:43 - 49.
65. Roberts M, Andrews G, Caird F. Skinfold thickness on the dorsum of the hand in elderly. Age
Ageing. 1975;4:8-15.
66. Hall D, Blacket A, Zajac A, Switala S, Airey C. Changes in skinfold thickness with increasing
age. Age Ageing. 1981;10:19-23.
67. Quatresooz P, Pierard-Franchimont C, Gaspard U, Pierard G. Skin climacteric aging and hor-
mone replacement therapy.! Cosmet Dermatol. 2006;5:3 - 8.
68. Pitt P, O'Dowd T, Brincat M, Moniz C, Studd J, Berry H. Reduction of skin collagen with in-
creased skin thickness in postmenopausal women with rheumatoid arthritis. Rheumatology.
l 986;25:263 - 265.
69. Cossmann M, Welzel J. Evaluation of the atrophogenic potential of different glucocorticoids
using optical coherence tomography, 20-MHz ultrasound and profilometry: a double-blind,
placebo-controlled trial. Br J Dermatol. 2006;155:700 - 706.
70. Kligman A, Takase Y. Cutaneous Aging. Tokyo: University of Tokyo Press; 1988.
71. Pohl H. Changes in the structure of collagen distribution in the skin caused by a manual tech-
nique.! Bodyw Mov 1her. 2010;14:27- 34.
N euromechanical Aspects
of Myofascial Pathology
and Manipulation
Clayton D . Gable
The mere motion of muscular and/or fascial tissues through stretching feels good
to humans and many other vertebrate animals. The tendency to stretch upon
awakening in the morning, or upon completing a long journey by airplane or car,
is nearly universal . Even pets seem to love a good, long stretch. Walsh cited E. K.
Borthwick, Emeritus Professor of Classics at Edinburgh University, for the follow-
ing account:
The verb "stretch" (reiyv, teino) is the common form and is used by Homer of
stretching of a bow, reins, etc.- "to stretch oneself in running." Aeschylus uses it
of straining the voice. Galen uses it of stretching tendons, etc.
The noun, rovoa (tonos), is apparently attested in Xenophanes (sixth century

BC philosophic poet) of exertion or striving after virtue or courage. It is used by
Aeschylus of stretching flax; in Herodotus and Aristophanes of bed and chair
cords; in Plato and Aeschines, of pitch of voice, or accent; in Aristoxenus and
subsequent musical writers of pitch-key; in the medical writer Soranus (second
century AD) of power of contracting muscles. 1(p6)
As one can surmise from the passage above, muscle contraction has, for almost
2,000 years, been associated with stretching.
Given that stretching is such an integral part of normal human and verte-
brate behavior and has given rise to the study of the influence of various sensory
mechanisms on movement, it is necessary to review some neurology associated
with myofascial tissues. To that end, in this chapter, I review the basic neurology
of myofascial tissues, emphasizing the afferent or stimulus perception side of the
equation. In addition, I review some of the more contemporary findings regard-
ing (1) the influence of somatosensory receptors on movement control, (2) muscle
tone, and (3) the interaction of biomechanical properties of myofascial tissues and
the nervous system.
91
Following the review of the basic science regarding neurology and movement
control is a discussion of how science relates to the clinical application.
Basic Afferent Neurology of Connective Tissue

A detailed presentation of the current neuroscience related to receptor anatomy
and physiology is beyond the scope of this text. What follows is a summary of
classical and recent understandings of peripheral receptors in the skin and vari-
ous connective tissues of myofascia. These receptors fall into four major catego-
ries: mechanoreceptors, nociceptors, thermoreceptors, and chemoreceptors. All of
these receptors influence or are influenced by movement, temperature, physiology,
and/or pathology. Also, all receptors influence movement and movement con-
trol, and they all influence, directly or indirectly, cardiovascular and respiratory
physiology.
Mechanoreceptors
Mechanoreceptors are exactly what the name implies; they are peripheral sensory
receptors of mechanical events. They transduce mechanical energy into nerve im-
pulses, which are then transmitted to the central nervous system via their afferent
neuron axons. They are located throughout the musculoskeletal system, the vascu-
lar tree, and the skin. They include specialized neuronal structures and free nerve
endings (Table 5.1).
Each of the various mechanoreceptors listed in Table 5.1 has its own anatomy,
firing characteristics, threshold, conduction velocity, and - most important for a
clinician- functional and physiological effects. Therefore, the following subsec-
tions review some of the pertinent characteristics and functional implications of
the various receptors. It is important to note that even those receptors listed in
Table 5.1 as being primarily located in the skin contribute to proprioception and
kinesthesia. Gardner and colleagues state the following:
Three types of mechanoreceptors in muscle and joints signal the stationary posi -
tion of the limb and the speed and direction of limb movement: (1) specialized
stretch receptors in muscle termed muscle spindle receptors; (2) Golgi tendon
organs, receptors in the tendon that sense contractile force or effort exerted by a
group of muscle fibers; and (3) receptors located in joint capsules that sense flex-
ion or extension of the joint. 2<p443>
It is with this statement in mind that the following review is offered .
Meissner's Corp uscles

Meissner's corpuscles are specialized structures located in glabrous (hairless)
skin of mammals (e.g., palms, soles of feet, lips). They adapt rapidly in response
Neuromechanical Aspects of Myofascial Pathology and Manipulation 93
Table 5.1 Mechanoreceptors
Fiber size
Receptor type and group Location and information transduced
Meissner's corpuscle A/3 Skin: touch
Pacinian corpuscle A/3 Skin: flutter
Fibrous connective tissue: compressive stimuli
Ruffini's corpuscle A/3 Skin: steady indentation
Fibrous connective tissue: tension on structures such
as ligaments
Merkel's receptor A/3 Skin: steady indentation
Hair-guard. hair-tylotrich A/3 Skin: steady indentation
Hair-down A/3 Flutter
Primary muscle spindle Aa Dynamic change of length
la
Secondary muscle spindle A/3 Muscle length. mostly static
II
Golgi tendon organ Aa Tension on a tendon
II
Joint capsule receptors A/3 Extremes of joint position (i.e .. maximum tension on
(Type 11) II joint capsule)
Muscle afferents (Ill) Ao Mechanical. chemical. and thermal stimuli in muscle
111
Muscle afferents (IV) C Mechanical. chemical. and thermal stimuli in muscle
IV
Free nerve endings A-C Mechanical chemical. thermal. and pain
to mechanical stimuli, such as skin indentation (Figure 5.1). The rapidly adapting
characteristic is common to several skin mechanoreceptors. It indicates that a rap-
idly adapting receptor will respond to a stimulus event with an action potential,
and then the receptor will go silent for a period of up to several seconds failing
receipt of another mechanical event.
In the case of a Meissner's corpuscle, a single indentation of 70- 1,000 µm
into the skin would result in a single action potential with a subsequent silent
period of up to several seconds. Although this behavior would appear to be some-
what dysfunctional, rapidly adapting receptors have another characteristic. They
are responsive to repetitive stimuli (at various frequencies) with repeated action
potentials.
Meissner's corpuscles, specifically, respond to repetitive stimuli, such as si-
nusoidal indentations of the skin, at frequency ranges of 2 or 3 Hz up to around
300 Hz. Compared with Pacinian corpuscles, this range is a relatively slow fre-
quency range. As previously mentioned, this range of stimulus indentation is from
70- 1,000 µm, with the greatest sensitivity between 10 and 100 Hz of stimulus (Fig-
ure 5.2). With a rapidly adapting system, the perception of relatively low-frequency
THICK(HAIILESS)Sl<JN SKIN
THIN(HAIRY)
0perq (poro) Shiftofhair

of-duct
Hair-
Figure 5.1 The organization of skin, comparing the structures found in thick, hairless skin with thin,
hairy skin. The epidermis has been partially peeled back to show the interdigitating dermal and epider-
mal papillae. Source: Reprinted from Gray's Anatomy, ed. 40 (p. 146) by S. Stranding with permission of
Churchill Livingstone Elsevier,© 2008.
and low-amplitude indentations of the skin is possible. In particular, the density of

Meissner's corpuscles is higher in glabrous skin of such structures as the hands. 2
This is most beneficial for the therapist in palpation and during treatment. The
property of rapid adaptation gives the Meissner's corpuscles excellent temporal
resolution in perception of rapid and subtle change. It does nothing, however, to
explain their superior spatial sensitivity.
Meissner's corpuscles have two other characteristics for which their superior
spatial resolution may be accountable. First, Meissner's corpuscles are mechani-
cally coupled with the surrounding subcutaneous tissues by thin strands of con-
nective tissue. These strands promote the transmission of adequate stimulating
force to several surrounding corpuscles for a given pinpoint stimulus area. The
second characteristic is related partially to this mechanical coupling but mostly to
the fact that the receptivefield for Meissner's corpuscles is very small (2- 4 mm in
diameter).
Meissner's corpuscle
1000 I
-
I
-E ,I
I
C
_,.,
(/) -
:::1.
,,,
-0 0C 100
c ·-
...,
;'
...,
......
0
::, ~
E
~-g
C
Q) -
10
Pacinian corpuscle
10 (50) 100 (300) 1000

Frequency (Hz)
Figure 5.2 Sensitivity to skin indentation. Source:Reprinted with permission from J.H. Kandel et al.,
eds., Principlesof Neural Science,3rd ed., pp. 533- 547, © 1991, McGraw-Hill Companies.
A receptivefield can be thought of as an isolated area of skin that receives

stimulation and the area that perceives a stimulus. In an area of skin with small
receptive fields, stimulus of a small point results in perception of stimulus that is
restricted to just that small point. Conversely, an area with large receptive fields
will result in perception of stimulus to a large area, even with only a small point
stimulated.
The impact of Meissner's corpuscles on practitioners of manual therapeutic
technique would be difficult to overstate. With their excellent spatial resolution
and ability to perceive relatively small differences in texture, tissue density, and so
forth, Meissner's corpuscles are invaluable to the manual practitioner.
Pacinian Corp uscles

Pacinian corpuscles are located in the subcutaneous tissue of both hairy and gla-
brous skin. Although the skin is the largest organ with the greatest density of Pa-
cinian corpuscles, it certainly is not the only location where they are found. As
early as 1882, Hagen-Torn found Pacinian corpuscles in the joint capsules of vari-
ous animals. 3 Gardner investigated joint capsules further and with better tech-
nology. He failed to find Pacinian corpuscles in the articular capsule but did find
them in the fibrous periosteum near articular or ligamentous attachments. 4 Zimny
et al. reported finding Pacinian corpuscles in the anterior and posterior horns of
knee menisci, accompanied by Ruffini endings, free nerve endings, and Golgi ten-
don organs. 5
A great deal is known about the anatomy and function of Pacinian corpuscles.
They consist of a specialized nerve ending surrounded by connective tissue lami-
nae. This connective tissue lamina make the corpuscle a rapidly adapting receptor,
responsive to stimuli at frequencies from 15 to 1000 Hz. This rapidly adapting

quality allows the corpuscles to be sensitive to rapid change in stimulus intensity.
As with other mechanoreceptors, the Pacinian corpuscle is sensitive to mechanical
energy. In fact, it is extraordinarily sensitive (down to a level of less than 1-µm skin
indentation, which will result in an action potential from the Pacinian corpuscle).
Even though Pacinian corpuscles are very sensitive to mechanical energy, their
very large receptive fields make them exceedingly poor for localization. Recall that
the receptive field of a Meissner's corpuscle is from 2 to 4 mm in diameter with
excellent localization. In contrast, the receptive fields of Pacinian corpuscles are so
large that in experimental stimulation of Pacinian corpuscles, humans were able
to localize only to one finger or to the medial half of the palm.
Ruffini Corpuscles
Ruffini corpuscles are found in the subcutaneous tissue beneath both hairy and
glabrous skin. 2 They are also found in the superficial layers of fibrous joint cap-
sules and other connective tissue surrounding joints. 6 Their intertwining with the
connective tissue is functional, because they are stimulated by the displacement of
the collagen fibers surrounding them. They are slowly adapting receptors and have
very large receptive fields. One major advantage of their slowly adapting charac-
teristic is of functional significance: because they do not "turn off" following a
stimulus but continue to fire with a consistently applied stimulus, they contribute
to steady-state position sense and tactile sensation.
Merkel's Receptors
Merkel's receptors are probably the most peripheral of all the sensory receptors.
They are located in the epidermis of glabrous (hairless) skin. They have unusual re-
ceptors, in that the receptors appear to synapse with epithelial cells. This synapse,
or connection, of epithelial cells directly with the Merkel's receptors results in an
action potential for the neuron serving the receptor with any mechanical stimulus
to its related epithelial cell(s). Like Ruffini endings, Merkel's receptors are slowly
adapting, but unlike them, Merkel's receptors have very small receptive fields.
Theref ore, these endings can respond to very small stimuli and localize well with
their 2- to 4-mm-sized fields along with their capacity to continue to send "tonic"
signals to the central nervous system without a change in stimulus intensity. 2
Hair Receptors
Hair receptors are divided functionally into two categories based principally on
the type of stimulus to which they respond . Tylotrich (stiff) hair receptors are
responsive to steady skin indentation, and down hair receptors are sensitive to
flutter. Basically, hair receptors are specialized nerve endings incorporated in the
connective tissue at the base of a follicle and are very sensitive to mechanical defor-
mation of the hair. Their implications for clinical practice of the manual therapist
Neuromechanical Aspects of Myofasc ial Pathology and Manipulation 97
Staticbag,
fiber
Dynamicbag,
fiber Longchain
fiber
Shortchain
fibers
Dynamicy-efferent
Staticy-efferent{ ____ +-t-~-it"'l"---:li"""!lr"'I-Hr"

II
II
Afferentfibers
la
Staticy-efferent
Staticp-etferent
Dynamic
p-etferent
Collateralsto
extrafusalmuscle
Figure 5.3 Nuclear bag and nuclear chain fibers in a neuromuscular spindle. Dynamic /3-and y-efferents
innervate dynamic bag 1 intrafusal fibers, whereas static /3-and y-efferents innervate static bag 2 and
nuclear chain intrafusal fibers. Source: Adapted from Gray's Anatomy, ed. 40 (p. 61) by S. Stranding with
permission of Churchill Livingstone Elsevier,© 2008.
are most likely restricted to an awareness of their presence and the knowledge that
they, like most any receptor, can be sensitized under conditions of paraesthesia. 7
Muscle Spindles
Muscle spindles are located in striated (skeletal) muscle and transduce changes
in length of the muscle. They fall into three categories and are named for their
shape and function (Figure 5.3). The dynamic nuclear bag fibers transduce infor-
mation about rapid changes in length and the rate of change of length. They are
most heavily concentrated in phasic muscles. The static nuclear bag spindles (so
named because of the central bunching of the muscle fiber nuclei) transduce more
tonic information about spindle length. Nuclear chain fibers (muscle fiber nuclei
are evenly distributed throughout the muscle fiber) transduce information about
slower changes in length and are more concentrated in tonic muscles. The physi-
ology of muscle spindles, as well as their influence on muscle tone, is worthy of
discussion here.
Muscle spindles are specialized encapsulated structures that are arranged in
parallel with skeletal muscle fibers (Figure 5.3). They consist of (1) a group of spe-
cial muscle fibers (intrafusal fibers), which are located in the spindle; (2) sensory
axons that terminate as a spiral ending around the intrafusal fibers; and (3) motor
axons (gamma efferent fibers), which adjust the sensitivity of muscle spindles. For
clarification of the differential physiology of muscle spindles, it is helpful to dis-
cuss the two sensory endings (i.e., afferent fibers) that transduce length informa-
tion from the spindles.
Primary endings. Primary endings consist of branches of a Group Ia afferent

axon. Primary endings terminate on all three types of intrafusal fibers in the mus-
cle spindle. The spiral endings wrap around the central or equatorial region of the
muscle spindles. The structure of the membrane of both primary and secondary
endings contains stretch-sensitive channels that, when activated, depolarize the
axolemma of the primary and/or secondary endings, sending an impulse up the
afferents to the spinal cord. Primary endings exhibit a property known as velocity
sensitivity,where they increase their firing rate with a sudden and rapid change in
length. This velocity sensitivity is manifested both with rapid shortening and with
lengthening. In the case of rapid shortening, the primary endings lapse in their fir-
ing and then continue firing at a lower frequency when the shortening halts. With
lengthening, the primary endings will demonstrate increased firing rates that are
dependent on the rate of the lengthening (stretching). Consequently, primary end-
ings respond vigorously with increased firing rates when stimulated briefly, such
as with a tap or vibration. In addition to their sensitivity to velocity of stretch, they
are also very sensitive to changes in length, demonstrating increased firing rates
with stretches of as little as 0.1 mm.
Secondary endings. Group II afferents branch into secondary endings, which in-
nervate the static nuclear bag fibers and the nuclear chain fibers in a spiral fashion,
like the primary endings. The secondary endings function similarly to the slowly
adapting receptors already discussed. That is to say, secondary endings exhibit a
fairly steady firing rate in either the presence or the absence of movement. These
slowly adapting receptors are, therefore, ideal for signaling the length of muscle
without the need for movement to increase their sensitivity.
Gain adjustment of muscle spindles. As can be surmised from the previous dis-
cussion and Figure 5.4, when the extrafusal muscle fibers of a muscle contract in
response to a stimulus from an alpha motor neuron, the intrafusal fibers would be
left slack. Therefore, there would be a silent period in the firing of both the primary
and secondary endings. To eliminate this silent period, the gamma motor neuron
Sustained stretch
of muscle
la discharge I I 11I I I 11I I I
----J t
Tension /
Pull
B Weight
Stimulate alpha
motor neuron
111 IIII IIIII I
t
C Contraction
Stimula te alpha
la responses ls "filled In"
motor neuron
'
+ t
11111111111111111111
Stimulate gamma
motor neuron
t
Contraction
Figure 5.4 During active muscle contractions the ability of the spindles to sense length changes is main-
tained by activation of gamma motor neurons. (Adapted from Hunt and Kuffler, 1951.) (A) Sustained ten-
sion elicits steady firing of the Ia afferent. (B) A characteristic pause occurs in ongoing discharge when the
muscle is caused to contract by stimulation of its alpha motor neuron alone. The Ia fiber stops firing because
the spindle is unloaded by the contraction. (C) If during a comparable contraction a gamma motor neuron
to the spindle is also stimulated, the spindle is not unloaded during the contraction and the pause in Ia dis-
charge is "filled in." Source:Adapted with permission from C. C. Hunt and S. W. Kuffier, Stretch Receptor
Discharges During Muscle Contraction,Journal of Physiology,Vol. 113, pp. 298-315, © 1951, The Physiologi-
cal Society.
system activates the intrafusal fibers and maintains the sensitivity of the spindles.
When the gamma motor neuron system activates the intrafusal fibers simultane-
ously with the alpha motor neuron system, the extrafusal fibers are also activated,
and the sensitivity of the primary and secondary endings is maintained. 8
Golgi Tendon Organs

Golgi tendon organs (GTOs) transduce information about tension. They are lo-
cated at the musculotendinous junctional zones. The GTOs transduce mechanical
information through specialized nodes on free nerve endings. GTOs are free nerve
endings with specialized nodes on their

- Musclefibers
branches that respond to the mechanical
deformation from collagen fibers placed on
stretch. These free nerve endings comprise
lb afferent
branches of lb afferent neurons that become
unmyelinated after entry into the GTO. The
structure of the collagen strands inside a
GTO is a braided arrangement. To appreci-
ate the manner in which longitudinal ten-
sion affects these strands, one can think
about the way a so-called Chinese finger
trap works. When tension is applied to the
muscle, it approximates the braided strands
Axon of the GTO and compresses the branches of
. '
I ' 1- -1-Collagen the lb afferent neurons (Figure 5.5). GTOs
''
_ fiber
' ,....__._,........__,......_
_, are extremely sensitive to changes in ten-
sion on the connective tissue in which they
250µm
are located. This sensitivity has been docu-
Figure 5.5 Golgi tendon organs. Source:J.E.
Swett and T. W. Schoultz, Mechanical Transduction
mented at levels as low as the force gener-
in the Golgi Tendon Organ: A Hypothesis. Archives ated by a twitch contraction of a single mo-
de Italiennes de Biologie,113:374-382, © 1975, tor unit in the triceps surae of a cat (i.e., very
Archives de ltaliennes de Biologie. few grams of force).9
Another important feature of the GTO
is in its combination with muscle spindles.
The primary endings from dynamic nuclear bag fibers experience a pause in their
firing during contraction of a muscle. In contrast, the GTOs are highly active,
with contraction of a muscle secondary to the tension exerted on them by the
muscle.
Implications of Muscle Spindles and Golgi Tendon Organs

Although the impact of the alpha and gamma motor neuron system is broadly
understood by most practitioners of manual therapeutics, the impact of pathology
in connective tissue may require some discussion. Intrafusal fibers are arranged
in parallel to the extrafusal muscle fibers. Muscle spindles measure approximately
4-5 mm in length and 1 mm in diameter. With their parallel arrangement, they
are connected to either end of the muscle's attachment by long collagen-containing
fibers. GTOs are arranged in series with the extrafusal muscle fibers and are ap-
proximately 1 mm in length and 300 - 500 µm in diameter. For that reason, a
change in the mechanics of a muscle secondary to injury can change the firing
patterns of either or both of these proprioceptors.
The following scenario serves as a demonstration: An athlete sustains a con-
tusion to the distal third of the medial head of the gastrocnemius muscle. This
occurred 5 days prior to the appointment, and the edema has resolved fairly well.
Neuromechanical As pects of Myofa scial Pathology and Manipulation 101
During gait, the gastrocnemius is active from mid-stance (as a decelerator) until
toe-off (as an accelerator). Assuming a relatively normal foot posture and equal
forces, rate of change of length, and length changes being generated by the medial
and lateral head of the gastrocnemius, the afferent stimuli coming from the medial
and lateral head of the gastrocnemius would, under nonpathological conditions,
be approximately equal. With the current condition-that is, with a contusion in
the process of healing and bearing some scar tissue-the afferent information is
different between the two heads of the gastrocnemius. In the medial head, the
afferent information is altered because of the scarring of the collagenous connec-
tions of the intrafusal fibers. This results in a mechanical "mislink" from collag-
enous cross-bridges and scarring and results in a perceived change in length that
reflects the actual change in length. In addition to the mismatch between the two
heads of the gastrocnemius relative to the length of the muscles, there is a problem
with tension information from the GTOs.
The serial arrangement of the GTOs makes them sensitive to tension gener-
ated along the mechanical chain of the muscle. Therefore, changes in the visco-
elastic properties of the muscle to which it is attached can produce a differential
in tension (particularly at the initiation of contraction). This differential tension
produces another mismatch between the tendinous origin of the medial and lat-
eral heads and even creates the possibility of differences within the fascicles of the
medial head attaching to the Achilles tendon. With the decreased elasticity of the
muscle from the collagenous cross-bridges and scarring, there is a relatively higher
tension perceived by the medial head compared with the lateral head . In addition
to all of the collagenous cross-bridges, which have affected the elasticity of the
muscle, there is also the problem of changes in viscosity of the muscle (intrafusal
and extrafusal fibers) and all the surrounding connective tissue (see Chapter 3,
"Histology and Biomechanics of Myofascia," for a review of viscoelasticity). These
changes in viscosity and elasticity contribute to an afferent information mismatch,
when compared with the conditions under which most tasks are learned.
Joint Capsule Receptors

Joint receptors include an impressive array of receptor types. Among them, the
Ruffini endings are classified as Type I receptors by Wyke. 10 They tend to be more
heavily concentrated in the proximal extremity joint capsules and are slowly
adapting. Their proximal concentration makes them ideally suited to provide pos-
tural information about static positions given the fact that proximal stability is
necessary to allow distal movement.
Pacinian corpuscles are Type II receptors and are located in the deeper layers
of the joint capsule and the fat pad. They also tend to be concentrated near the
bony attachments of the joint capsule. Of interest is the fact that Pacinian cor-
puscles are virtually silent in inactive joints and are activated with the onset and
cessation of movement. Of course, this behavior is consistent with their rapidly
adapting characteristic, as seen in their skin counterparts.
Golgi-Mazzoni endings (anatomically similar to GTOs) are classified by Wyke

as Type III and are located among the collagen fibers of the extrinsic and intrin-
sic ligaments of larger joints (e.g., knee collateral and cruciate ligaments). 10 Along
with their similarity to GTOs comes a similar functional characteristic. They are
most active in their firing patterns at extremes of position inflexion/extension or
other motions that stress the ligaments.
Wyke's Type IV joint receptors are primarily free nerve endings. 10 They are
located in the fibrous joint capsule, fat pads, ligaments, and walls of blood ves-
sels. They tend to be unmyelinated and are high-threshold, nonadapting pain
receptors.
The great variety of joint receptors creates quite a symphony of propriocep-
tive information within the central nervous system. Their primary function is the
transduction of joint position; however, the relative amount of information that
is provided by joint receptors is small, compared with that provided by muscle
spindles and other mechanoreceptors.
A majority of joint receptors are activated at the extremes of range (i.e., situ-
ations with greater tension on the capsules or ligaments). Greater firing rates are
also likely in the event of scarring of the capsule. In other words, the joint receptors
would perceive the joint to be at an extreme of range of motion before that extreme
is actually achieved. Such a situation could easily arise in the case of any surgery
with a capsulotomy or capsulorrhaphy. The same situation would also occur in the
case of an inflammatory condition resulting in scarring of the joint capsule, as in
adhesive capsulitis of the shoulder, or a change in the viscoelastic properties of the
capsule or ligaments. 6,10
A change in the relative tension on a joint capsule, as in adhesive capsulitis,
would result in a differential level of inhibition and/or excitation between sides of
the body. There is probably a difference between sides of the body based on move-
ment pattern history, as in the case of handedness. If that relative difference were
changed as a result of injury, however, the background levels of muscle tone would
alter the movement patterns. Such a change has been described by Juli and Janda
and is commonly observed by clinicians observing scapulohumeral rhythm. 11
With this difference in relative levels of facilitation or inhibition, the motor com-
mands sent to the shoulder to perform a well-learned task (e.g., tennis serve or
baseball pitch) would be insufficient to accomplish the task or could be disturbed
by spinal-level reflex mechanisms. In either case, the movement patterns become
dysfunctional. The resulting movement patterns may either introduce inaccuracy
into the performance or lead to faulty movements and overuse injuries.
Small-Diameter Muscle Afferents (III and IV)

Another group of afferent fibers that is often overlooked includes the Group III
and IV muscle afferents (not to be confused with Wyke's terminology for joint
receptors). Group III and IV muscle afferents are thinly myelinated and unmy-
elinated, respectively. Group III afferents are located in the interstitial spaces of
Neuromechanical As pec ts of Myofa scial Pathology and Manipulation 103
skeletal muscle, either close to or within the adventitia of arterioles and venules. 12
Von During and Andres specifically found Group IV endings in the adventitia of
small veins and even in the lymphatic vessels. 13
The research on the reflexive effects of Group III and IV muscle afferents has
concentrated primarily on their effects on ventilation and circulation. In that
realm, they have been found to have some very powerful effects on both systems.
On the sensory input side of the reflex equation, the III and IV afferents respond
to mechanical, chemical, and thermal stimuli. On the output side of the equation,
the responses appear to be related not only to systemic changes in respiration and
cardiac output but also to local changes in muscle blood flow. The for mer has been
well documented in the cardiorespiratory literature and the latter in literature re-
viewed in Chapter 4, "Histopathology of Myofascia and Physiology of Myofascial
Manipulation." 14
Considering the therapeutic techniques presented in this book and their in-
dications, it is worthwhile to discuss mechanisms of stimulation of the Group III
and IV receptors in a general sense, as they relate to myofascial technique. First,
Group III and IV receptors respond to both mechanical stimulation and muscu-
lar contraction. The mechanical stimulation most often used in research is that
of non-noxious probing. 15 The basic conclusions have shown that more force is
required to stimulate the receptive fields of Group III and IV afferents than is re-
quired for muscle spindles and GTOs. Group III and IV receptors are even differ-
entially sensitive to mechanical stimulation. 14 The second and third mechanisms
are related to chemoreception and a sensitizing effect of chemicals to mechanical
stimulation. These are considered in the following paragraphs.
Non-noxious probing will stimulate a majority of Group III receptors,
with noxious probing generating explosive bursts of impulses from many more
Group III receptors. In contrast, almost all Group IV receptors require a noxious
level of probing, and then only a few bursts of impulses will occur. The level of
probing (non-noxious and noxious) referred to in these studies exceeds the level of
stimulus required by muscle spindles and GTOs by several orders of magnitude,
making the forces very similar to those applied in even some of the gentlest tech-
niques presented in this book.
Approximately half of the Group III receptors respond immediately with a vig-
orous increase in afferent discharge during muscular contraction. The remaining
half tend to respond as the exercise session progresses (i.e., after > 30 seconds of
isometric contraction or rhythmical contraction). This finding indicates that about
half of the receptors may be more chemically sensitive rather than mechanically
sensitive. Unlike the Group III receptors, Group IV receptors tend to rarely dis-
charge with muscle contraction in the early stages. As the contraction progresses
and is maintained, however, the frequency of their discharge increases. This find-
ing would also support a primarily chemoreceptive role for the Group IV receptors.
Other studies regarding the chemoreceptive properties of these two recep-
tors have been perf armed with a wide variety of drugs, including papaverine,
isoproterenol 16 (both vasodilators), bradykinins, 17 arachidonic acid 18 and lactic

acid, 19 indomethacin, and aspirin. 20 The most important findings for the man-
ual therapist relate to changes in the mechanical sensitivity of the receptors in
response to some of these chemicals. Specifically, there are increases in sensitivity
to mechanical stimuli with the metabolic and inflammation by-products. On the
positive side, increased concentrations ofbradykinin and cyclooxygenase metabo-
lites (both strongly associated with inflammation and injury) are likely to increase
the sensitivity of Group III and IV afferents to contraction and mechanical prob-
ing. Contrary to these findings, indomethacin and aspirin, both of which decrease
a muscle's ability to produce prostaglandins and thromboxanes, decreased the
sensitivity of the receptors to contraction.
Given that the sensitivity of Group III and IV muscle receptors is positively
affected by naturally occurring inflammation by-products and negatively affected
by anti-inflammatory drugs, the clinician needs to consider these effects during
treatment. In the case of an inflammatory process (either acute or chronic), there
would be a tendency for a greater increased blood flow in a muscle that was in-
flamed but also undergoing manipulation, possibly resulting in intramuscular
edema. If the patient had taken anti-inflammatory agents, however, the sensitivity
to mechanical stimulation would be decreased, and therefore the negative effects
of increasing edema would be mitigated. Basically, such a line of reasoning would
serve as a precaution for use of myofascial manipulation on an inflamed muscle.
To summarize, the mechanoreceptors of the mammalian body are numer-
ous and diverse in their anatomy and function. Some are exceedingly sensitive to
mechanical stimuli (e.g., Merkel's receptors and Pacinian, Ruffini, and Meissner's
corpuscles), whereas others require more vigorous stimulation (e.g., Group III and
IV muscle afferents). Despite their diversity, these mechanoreceptors have two
things in common. First, they are all physically attached to connective tissues and
thereby perceive mechanical events. Second, they all provide afferent information
to the central nervous system, which then exhibits reflexive effects in the periph-
ery. Some of those reflexive effects are directly motoric in nature, and others are
more autonomic in nature. Some of these reflexive effects are reviewed in various
levels of detail later in this chapter, but no discussion of peripheral receptors is
complete without some attention to nociception and chemoreception.
Nociceptors
Nerve fibers that are selectively responsive to stimuli that may potentially dam-
age tissue or to stimuli from actual tissue damage are called nociceptors. They fall
into three major categories - mechanical, thermal, and polymodal - depending
on the form of stimulus required. These three categories can be further classified
according to their afferent nerve fibers. The thermal and mechanical stimuli are
transmitted via Aofibers and the polymodal stimuli via the C fibers. Aofibers
are thinly myelinated fibers that conduct impulses at 5- 30 m/second. C fibers are
unmyelinated fibers that carry impulses at 0.5- 2 m/second.
Table 5.2 Chemical or Agent Effect on Nociceptors

Chemical or agent Source Effect on nociceptors
Potassium Damaged cells Activation
Serotonin Platelets Activation
Bradykinin Plasma kininogen Activation
Histamine Mast cells Activation
Prostaglandins Arachidonic acid-damaged Sensitization
cells (inflammation product)
Leukotrienes Arachidonic acid-damaged Sensitization
cells
Substance P Primary afferent Sensitization
Source: H.L. Fields, Pain, p. 32, © 1987.Reproduced with permission of the McGraw -Hill Companies.
In addition to their conduction velocity characteristics and their respective

modes of stimuli, another important characteristic of pain should be considered.
This characteristic is related heavily to chemoreception. Chemoreception is typi-
cally considered a sensory modality reserved for the tongue and nose, but in the
case of pain, it becomes of extreme importance. Nociceptors demonstrate two re-
sponses to a large number of chemicals and naturally occurring agents. The chem-
icals either activate them or sensitize them. Activation is manifested by an action
potential of the nerve, whereas sensitization is a lowering of the stimulus threshold
required to produce an action potential. Some of the agents are listed in Table 5.2.21
Receptor Influence on Movement

Having considered the role of the afferent, further explanation regarding the re-
flexive and higher order of sensory influences on movement and autonomic func-
tion must be given to complete the neurophysiology of myofascial manipulation.
Because many manual therapy students are already familiar with these topics, the
explanations in this section are concise. For further information, refer to Kandel
and colleagues' classic book Principles of Neural Science.22
Basics of M ot or Contr ol
The spinal cord, brainstem, and cerebral cortex achieve motor control through
hierarchical and sometimes parallel processes. Each has its own independent level
of control, and each interacts with the others to accomplish full motor control.
Figure 5.6 displays a relatively simple diagram of the motor system. 23 The fol-
lowing sections emphasize the "sensory consequences of movement upon move-
ment" component of the model in Figure 5.6. Furthermore, some discussion is
included about the influence of myofascial pathology on the sensory consequences
of movement.
Cerebral cortex
Motor areas
""" ' ...
Tha lamus
., Basal ,-.
)
'
ganglia
. Brain
', Cerebellum
" stem
Muscle
. Spinal cord ., contraction

and
movement
'
Sensory
receptors
Sensory consequenc es of movement
Figure 5.6 Motor system levels of control. Source:Reprinted with permission from E. R. Kandel et al.,
eds., Principlesof Neural Science,3rd ed., pp. 533- 547, © 1991, McGraw-Hill Companies.
Muscle Stretch Reflex

Probably the best understood and most studied of the influences of peripheral re-
ceptors on movement is that of the muscle stretch reflex (MSR), previously known
as the deep tendon reflex. The MSR is a monosynaptic reflex with input from the
primary and secondary endings in the muscle spindle, with the major portion of
the stimulus coming from the primary endings. During the MSR, the stimulus
to the primary endings, in the form of a sudden lengthening of the muscle, is
conducted by the Group Ia afferent. The Ia afferent synapses directly on an alpha
motor neuron for the same muscle and excites it to the level of an action potential.
This results in transmission of a motor impulse to the stimulated muscle and con-
traction of the muscle. All of this occurs in very short order, requiring only about
40-60 milliseconds. 8
As described previously, the influence of pathology in the connective tissue
can be considerable on the MSR. An alteration in the parallel link of the muscle
spindle to its tendinous connection can occur with faulty links to other connec-
tive tissue outside of the target muscle. Connections via scarring or newly formed
cross-bridges of collagen to the skin, intermuscular septa, other tendons, or even
bone can occur in connective tissue patho logy. Such connections could alter the
MSR to either a heightened or a lowered level of activity, depending on the stimu-
lus applied to them. In the case of pathomechanical cross-bridge formation, such
an increase in the sensitivity of the MSR would alter the spinal-level mechanisms
of muscle tone regulation. Juli and Janda hypothesized that these changes would
result in an increase of dynamic muscle tone in the agonist muscle .11 With changes
in dynamic muscle tone and subsequent changes in movement patterns, the me-
chanical stresses would be different on the system, resulting in connective tissue
remodeling in response to Wolff's law.
Consider, for example, a patient, 3 weeks status after distal third femoral frac-
ture with an intramedullary rod, supine, with the lower leg hanging over the end
of a treatment mat and the knee in flexion. With the scarring that occurs, there
will be adhesions between the vastus lateralis, rectus femoris, and vastus interme-
dius. Each of these muscles has a resting tone. If the adhesions have formed in such
a way that they differentially affect the rate of change of length in the muscles as
they slide together and against each other, however, sensory mismatch will occur.
Accompanying this sensory mismatch will be a differential MSR response among
the three muscles that was not present before the scarring occurred. This example
of the impact of connective tissue pathology on the MSR is only one of many pos-
sible scenarios. Likewise, this example illustrates the impact of such a pathome-
chanical situation on the MSR. Multiple other interactions are possible, a few of
which are presented in the following section.
Golgi Tendon Organs

Golgi tendon organs (GTOs), when stimulated by a change in tension, have an
inhibitory effect on the agonist muscle and a facilitatory effect on the antagonist
muscle. The mechanism of this event is much more complex than that of the MSR.
In the case of the MSR, there is a monosynaptic connection of the muscle spindle
afferent fibers that synapse with the alpha motor neuron for output. The afferent
input from the GTO synapses on the Group l b inhibitory interneurons. These in-
terneurons receive input from multiple sources before synapsing themselves with
the motor axons of either the agonist or the antagonist muscles. Originally thought
to be a protective mechanism to prevent tendon rupture, this same mechanism of-
fers great utility for the manual therapist in relaxation of agonist muscle guarding
and/or facilitating antagonist retraining during therapeutic exercises. The recep-
tors for the GTO are specialized nodes on an axon that respond to mechanical
deformation with an action potential. Therefore, the mechanical event necessary
to fire the GTO does not have to be stretch; it could be direct pressure on the mus-
culotendinous junction. The outcome regarding muscle tone is the same whether
stimulated by tension or other mechanical input.
Some of the Group l b inhibitory neurons receive converging input from Ia
afferents from muscle spindles, low-threshold cutaneous afferents (e.g., Merkel's
receptors and Pacinian corpuscles), and joint receptors, and excitatory as well as
inhibitory input from several descending pathways. All of these combined inhib-
itory and excitatory inputs have major implications for fine motor control. The
GTOs and the other inputs to the Group l b inhibitory interneurons provide for
fine control of exploratory behaviors where the amount of force being generated is
critical. Therefore, the implication for these receptors' importance when learning
to perform manual therapy is obvious. 24
In addition to the implications for fine control and control in exploratory
behaviors, there are ramifications for patients and their motor control. The most
conspicuous example of problems with the GTO is tendinitis. In the case of Achil-
les tendinitis, an inflammation of the musculotendinous junction would result
in interfascicular edema inside the tendon. This edema changes the viscoelastic
properties of the musculotendinous junction, resulting in a change in the tension
on the braided collagen fibers that surround GTOs. Besides the change in the me-
chanics of the GTO, the chemical makeup of the GTO also undergoes ambient
change. With greater concentrations of bradykinin and cyclooxygenase metabo-
lites (by-products of inflammation), it is possible that the sensitivity of the GTO is
increased in the same way that the sensitivity of Group III and IV muscle afferents
is altered by these agents. If the GTO sensitivity were increased by inflammation
by-products, then the increased GTO firing rates would further inhibit the agonist
and facilitate the antagonist and, thereby, interfere with normal motor control and
movement patterns.
Joint Receptors
As previously described, joint receptors come in a variety of shapes, sizes, func-
tional characteristics, and locations in the joints. Discussion is restricted here to
the Golgi-Mazzoni and the ligamentous free nerve endings because they are the
most superficial of the joint receptors and are the most easily stimulated in the
practice of myofascial manipulation. The Golgi-Mazzoni receptors are similar to
GTOs and exhibit very similar effects on motor control at a reflex level. In like
manner, the free nerve endings transmit information to the spinal cord and syn-
apse on Group lb inhibitory interneurons. Both of these joint receptors are rapidly
adapting receptors and are also known to be essentially silent in immobile joints.
They are stimulated most at the extreme ranges of motion. Therefore, from a func-
tional viewpoint, the surface of a joint capsule in which the receptors are located
dictates which muscles are the agonists and which are the antagonists. In the case
of the posterior capsule of the knee, rapid knee extension would result in an in-
hibitory effect on the quadriceps at the end of range, whereas rapid knee flexion
would stimulate the joint receptors in the anterior capsule and cause inhibition of
the hamstrings at the extreme of knee flexion.
An example of the inhibitory properties of an abnormal stimulus to joint re-
ceptors was provided by Kennedy and colleagues. In their classic paper of 1982,
they demonstrated that an effusion (60 cc) of the knee would result in a 30%- 50%
decrement in the electrical activity of the quadriceps, as measured by the Hoffman
reflex, with the greatest inhibition occurring in the vastus medialis. Although they
did not distinguish the particular types of receptors, they were able to show that
the receptors in proximity to the joint cavity itself were very important. Under
the conditions of effusion, the quadriceps were inhibited; however, when a local
anesthetic was added to the effusion, the inhibition all but disappeared. 25 Clini-
cally, these findings add even further motivation for the therapist to control joint
effusion and, failing that, to make conservative recommendations for strenuous
activity of the lower extremity. If such a small joint effusion can inhibit the quad-
riceps, then failure to control the effusion could lead to serious injury from inhibi-
tion of the surrounding musculature. One can only assume that similar findings
would be seen in other diarthrodial joints with similar muscular inhibition. Such
findings clearly demonstrate that a mechanical stress on the rapidly adapting re-
ceptors, such as the Pacinian corpuscles, is (most likely) inhibitory to quadricep
motor units. Indeed, these findings offer compelling evidence that in the presence
of edema or bleeding following thrust manipulation procedures, there would be a
reflex inhibition of musculature surrounding that joint or related to that joint neu-
rologically. The findings of Kennedy et al. are consistent with findings reported in
prior and subsequent literature, confirming that joint receptors are more sensitive
to extremes of range. The mechanical stress placed on the joint capsule served to
stimulate the joint receptors in the same manner as extremes of range of motion
would.
Skin Receptors and Position Sense

The influence of skin receptors and other mechanoreceptors located in deeper tis-
sues on motor activation levels has been documented for almost 100 years. Simple
reflexes such as the flexion withdrawal reflex are spinal -level systems evoked by
stimulation of nociceptors. Other stimuli of a noxious nature, such as a slightly
caustic agent, placed on the leg of a spinalized frog will produce the even more
sophisticated movement of attempting to wipe away the stimulating agent. 26
Hagbarth demonstrated in 1952 that a pinch stimulus to the skin of the dorsal
aspect of the hind limb of a cat (i.e., opposite surface of the muscle) inhibits the
output of motor neurons to the tibialis anterior, whereas the same stimulus pre-
sented to the skin on the ventral aspect (i.e., over the tibialis anterior) facilitates
motor neuron activity. 27 These and similar findings form the foundation for many
of the facilitatory and inhibitory handling techniques employed by physical and
occupational therapists today. Many of these facilitatory and inhibitory techniques
were originated by clinicians working with clients with neurological problems.
One common technique is that of maintained pressure over the anterior thigh,
which is inhibitory to the quadriceps after an initial burst of electromyographic
(EMG) activity.
The findings of changes in motor output as a result of manual contact and
other stimulus input are well known. Another aspect of the effect of sensory in-
put from the skin on motor output that is less well known is the contribution of
skin mechanoreceptors to position sense. Psychophysical studies (i.e., behavioral

measures of perception) such as those performed by Burgess et al. and Matthews
failed to demonstrate a significant deterioration of kinesthetic sense in response to
anesthetizing the skin. 28 ,29
The psychophysical findings initially seem to indicate that skin mechano-
receptors have little if any influence on position sense. The work just cited, how-
ever, operates from a negative assumption. Burgess et al. assumed that because
elimination of skin receptors failed to negatively impact the performance of the
task, mechanoreceptors in the skin had no impact on position sense. 27 Collins
et al., however, investigated the threshold of perception of a muscle twitch at the
wrist and found it to be attenuated by as much as 60% with voluntary movement
of the same arm. An experimental manipulation of stretching the skin on the dor-
sum of the hand produced a 79% reduction in twitch detection threshold and a
58% reduction in position sense accuracy when compared with controls. 30
Cohen et al. performed single-cell recordings from the sensory strip of the
cortex in monkeys to investigate the relative effect of passive and active move-
ment and skin stretch on cortical cell activity. They recorded from cortical cells
while passively moving the monkeys' arms into flexion and abduction. They also
recorded from the same cells while stretching the skin of the medial upper arm.
They demonstrated that 84% of the cell recordings that responded to passive
movement also responded to skin stretch. Inversely, 84% of the cells that did not
respond to passive movement also did not respond to skin stretch. 31
The findings from the studies by Collins et al. and Cohen et al. present fairly
convincing evidence that skin mechanoreceptors serve as a source of position
sense information. 30•31 In addition, whether they contribute to the position sense
information is not dependent on external forces being applied directly to the skin.
On a functional note, the data from the experiment by Collins et al. indicated
that, as one would expect, there was a directional bias for skin receptor firing or
lack of firing. 30 This bias produced a tendency for more phasic firing of the recep-
tors as the monkey reached with the left hand toward a target in the upper right
quadrant, in contrast to a tonic firing of receptors as the monkey reached with the
left hand toward a target in the upper left quadrant. Considering the mechanics of
the situation and the extensibility of skin, these findings are not surprising.
The implication for cutaneous mechanoreceptor information functioning as
position sense information is obvious. In the case of the slowly adapting receptors
in the skin, a constant abnormal mechanical stimulus from an adhesion would
result in an alteration in the cumulative position sense information, even in the
absence of motion or extremes of motion. On the other hand, an adhesion would
apply forces that would easily stimulate rapidly adapting receptors when the sub-
ject engaged in either rapid or extremes of movement. These same receptors, as
discussed previously, have either facilitating or inhibitory effects on muscles that
are agonists or antagonists for movements normally associated with input from
that area of skin.
Nociception
The influence of pain on movement and control, brought on by peripheral stimula-
tion, is probably the most obvious sign of change in movement control. The initial
response to acute pain from mechanical or thermal stimuli is transmitted to the
nervous system via AS fibers, which are myelinated, rapidly conducting fibers. The
withdrawal reflex seen in even spinalized animals is very fast. The response to pain
of a more polymodal nature, such as that mediated by inflammation by-products
and other neuroactive agents, is typically more complicated.
Polymodal pain is carried on C fibers, which are slowly conducting fibers.
Polymodal pain, most likely because of its continuing nature, also has the char-
acteristic of inducing some type of behavioral response. This response may be at a
spinal level or virtually any other level of the nervous system. The responses can
vary from obvious muscle guarding in the surrounding musculature to inhibition
of a muscle. The aim of both muscle guarding and muscle inhibition is to decrease
the movement that leads to pain.
One misconception that has been propagated from one author to the next is
the "pain - spasm - pain" cycle. Unfortunately, as Walsh 1 and Simons and Mense 32
eloquently point out, this hypothesis is based on a misunderstanding of the in-
volved motor reflexes. The original hypothesis stated that pain increased y -motor
neuron activity, which would stimulate or increase the sensitivity of the muscle
spindle and result in an increased a-motor neuron activity and muscle contrac-
tion. The major problem with this theory is the fact that muscle pain does not re-
sult in increased EMG activity. Furthermore, the timing and intensity of the EMG
activity does not correlate with the reported levels of pain.
These findings related to nociception present a contradiction to the practitio-
ner of manual therapy and any acute observer of posture and movement. It is rela-
tively easy to identify muscle asymmetries in bulk as well as in muscular activity
during movement. If muscular pain and the apparent increases in muscle tone are
not caused by spasm, then what produces the increase in muscle tone? This ques-
tion is actually twofold : First, what does pain have to do with increased muscle
tone? Second, what is muscle tone/spasm? The following sections explain some of
the thinking regarding these topics.
Muscle Tone
Muscle tone has long been associated with muscular contraction; however, it is
actually more complex than just a contraction. Certainly, a typical muscle con-
traction or level of muscle tone, explained according to the sliding filament theory,
cannot occur without an electrical action potential. In the case of muscle spasm
or "normal" resting muscle tone, an action potential is not typically discernible
via electromyography; therefore, it must entail more than just an electrogenic ac-
tivation of the actomyosin complex. Simons and Mense have offered an excellent
Muscle tone
(general tone)
Viscoelastic tone Contractile activity

(specific tone)
Elastic stiffness Viscoelastic Contractu re Electrogenic Electrogen ic

stiffness (no EMG spasm contraction
activity) (pathologic) (norma l)
Figure 5. 7 Muscle tone. Source:Adapted from Understanding and Measurement of Muscle Tone as Re-
lated to Clinical Muscle Pain, Pain, No. 75 (pp. 1- 17) by D. G. Simons and S. Mense with permission of
W. B. Saunders Company,© 1998. This figure has been reproduced with permission of the International As-
sociation for the Study of Pain© (!ASP©). The figure may not be reproduced for any other purpose without
permission.
review of muscle tone and its relation to clinical muscle pain. 32 In it, they divide
muscle tone into two types: electrogenic tone and viscoelastic tone (Figure 5.7).
Electrogenic Muscle Tone

Electrogenic tone can be categorized into three levels. The first level is resting
muscle tone. This muscle tone has historically been explained as a postural low-
level tonic discharge of motor neurons. As explained by Walsh, 1 a misconception
begun by Waller was based on a generally inapplicable experiment reported by
Brondegeest in 1860. Waller, and later the Sherrington school, explained resting
muscle tone with the muscle stretch reflex. Such an explanation would, by defini-
tion, require an action potential to be generated in a-motor neurons. Activation of
a-motor neurons would activate motor units, which would be perceptible by elec-
tromyography. All efforts to document resting muscle tone via electromyography
have failed. 33- 35 This is not to deny that some form of contracture is occurring in
the muscle. Physiologists tend to define contracture as an endogenous shortening
of the muscular contractile apparatus in the absence of EMG activity initiated by
anterior horn cells.36 According to this definition, cross-bridges form, but not as a
result of an action potential from the myoneural junction.
The second level of electrogenic muscle tone is what Simons and Mense refer
to as electrogenic spasm. This particular type of contraction is involuntary and
directly associated with measurement EMG activity from that muscle. 32 Voluntary
muscular contraction is the third and last level of muscle tone and requires no
explanation.
Before progressing to a more in-depth explanation of findings regarding vis-
coelastic tone, it is useful to discuss in a little more depth ideas related to clinical
muscle spasm. As previously stated, a pain-spasm-pain cycle is an insupportable

hypothesis in the sense of an electrogenic spasm. As any manual therapist who has
worked on a human or other mammal will attest, however, pain and changes in
compressibility of muscular tissue are easily discernible by palpation. In this re-
gard, the findings related to trigger points and tension-type headache are particu-
larly revealing. In tension-type headache, it is easy to palpate taut bands of muscle.
These bands, while often associated with trigger points, do not demonstrate ob-
servable EMG activity. The trigger points themselves, however, have been shown to
demonstrate localized electrical activity in the confined area of the trigger point. 37
It appears that these taut bands of muscle are the result of the same contracture
mechanisms described by physiologists.
Other forms of muscle contraction of particular interest to clinicians fall into
two categories. In the first form, known as involuntary guarding, unnecessary
muscular contraction limits movement. The second form could best be described
as inefficient use. Most clinicians are aware that because of guarding, pain avoid-
ance, and other causes, patients will move in manners that are inefficient. These
inefficient movement patterns can have serious consequences. Consider, for ex-
ample, a marathon runner who gets a blister over the head of the fifth metatarsal
at mile 3 of the race. Such a minor injury has been known to have consequences
of a femoral head stress fracture by the end of the marathon. The same such inef-
ficient use can occur with painful muscles and/or trigger points. Lack of appropri-
ate relaxation between contractions of the upper trapezius has been demonstrated
by Elert et al., and lvanichev demonstrated that muscles with trigger points failed
to relax appropriately during alternating movements as they became fatigued. 38 •39
An understanding of these various levels of muscle tone that are associated
with electrical activity in the muscle is certainly important for the clinician. Also,
an insight into the influences of various receptors on a-motor neuron and y -motor
neuron activity is useful for understanding control. Because this volume relates
more specifically to the manipulation of myofascial tissues, the following section
on viscoelasticity has important implications for practitioners seeking to under-
stand the rapid results that can be expected with myofascial manipulation.
Viscoelastic Muscle Tone

The viscoelastic muscle tone, or specific tone, is made up of an elastic component
and a viscoelastic component (Figure 5.7). The purely elastic component, by defini-
tion, requires a steady force to produce a deformation of the substance, which in
this case is myofascial connective tissue. Collagen and other structural proteins of
myofascial tissue are not the only components of connective tissue. These tissues
also contain various other proteins in addition to their obvious structural systems.
These other substances are primarily in fluid form and have various degrees of vis-
cosity, or "fluid stiffness." The primary component of the noncontractile fluid com-
ponent is water, which is retained by the nonsulfated glycosaminoglycans (GAGs)
and makes up about 70% of the extracellular matrix. The second component is the
sulfated version of GAGs, which account for the tissue cohesiveness. Another fluid
component of myofascial tissue is actin. Although actin certainly makes up a large
complement of muscle itself, it is also abundantly present in noncontractile fluid
and serves cell motility and intracellular structure functions. This protein is actu-
ally fluid in its purified form and, much like syrup, will form strings when picked
up on a glass rod or other stirring device.
The GAGs, actin, and myosin all contribute to the viscoelasticity of myofascial
tissue. Unlike elasticity, the stiffness of viscoelasticity is velocity dependent. Also,
it is worthy of note that unlike the velocity dependence of spasticity, the relation-
ship between viscoelasticity and velocity of movement is purely mechanical. The
mechanical viscoelasticity characteristic and the structural elasticity of the struc-
tural proteins combine to make up the specific tone of a muscle that is unrelated
to contractile activity.
Viscoelasticity of muscle, or viscoelastic tone, affects movement and postural
control The sensory mechanisms that produce the sensation(s) from the musculo-
skeletal system that prompt mammals to stretch after remaining still are relatively
undefined . Concerning posture, there are mechanical properties of muscle (largely
unexplored until recently) that tend to support a resting stiffness of muscles in
posturally supported humans that is unrelated to EMG activity, with the exception
of occasional corrective bursts of activity. The properties of myofascial tissues that
prompt the stretching behavior and account for maintenance of static balance,
however, have been the subject of an abundance of study, resulting in a focus on
the property of thixotropy.
Thixotropy
Defined
Thixotropy, from the Greek words thixis (touch) and tropos (turning or change-
able), is a term that is new to many people across the spectrum of clinicians who
use manual therapeutics. It is not, however, new to physiologists involved in the
study of muscle and tissue mechanics. Thixotropy describes a state of stiffness of
a fluid that is dependent on the history of movement. A number of common sub-
stances exhibit thixotropy. Tomato catsup is probably the most common. After
sitting in the bottle, catsup becomes very stiff and difficult to get out of the bottle.
With just a little stirring, however, the stiffness decreases substantially. 40
Thixotropy is a physical property of muscle and other tissues and not a re-
sponse to some neurophysiological event. The mere act of moving a substance with
thixotropic properties will result in a reduction of stiffness. The reverse is also true:
if a thixotropic substance remains still for a given period of time (which varies
depending on the substance), the substance will become stiffer.
To measure thixotropy, physiologists have used torque motors with very small
torques of approximately 0.1 newton meters (Nm). Under conditions of a sinusoi-
dal motion of the wrist, the amplitude of a motion of the wrist is about 0.02 radians
(1.14°). With a movement of the wrist in an amplitude of approximately 0.075 ra-

dians for only three cycles, the amplitude of the passive wrist movement with the
same 0.1 Nm of torque increases to about 0.06 radians (3.42 °). These amplitudes
are very small so as to avoid stirring the muscle; however, it is important to note
that a brief interruption of as little as 2.5 seconds returned stiffness to its original
levels. Also of note is the fact that this stiffness, which is restorable in as little as
2.5 seconds, is possible at most any length with the exception of a position of ex-
treme stretch. Clearly, the amount of stirring and the amount of interruption of
motion can be very small. 41
Possible Mechanisms of Thixotropy in Muscle

Several investigators have hypothesized that the thixotropic properties of muscle
originate at the cross-bridge mechanisms in muscle. Campbell and Lakie propose
that the thixotropic behavior of relaxed skeletal muscle may be explained by a ten-
dency for some of the cross-bridges to connect even in the absence of an action po-
tential.42 Campbell and Lakie summarize their explanation of thixotropy, which
they attribute to a model of undetached cross-bridge mechanisms, in this way:
"The molecular motors of muscle may be idling rather than switched off when
the muscle is relaxed." 42<P957l As described by Hill, the early stage of the tension
response to movement appears to be dependent on the duration of the rest pe-
riod (no movement) and the filamentary release tension, which occurs later in the
movement and is linked to the stretch velocity. 43
Another hypothesis that can explain the thixotropy of muscle, put forward
by Mutungi and Ranatunga 44 and other investigators, attributes the viscoelastic
properties of relaxed skeletal muscle to titin filaments. Titin filaments are excep-
tionally large structural proteins in muscle, which link the thick myosin filaments
to the Z-lines of muscle. Titin filaments tend to adopt a random-coil configuration
when relaxed. They uncoil with stretching. Consequently, titin does not offer a
very viable explanation for thixotropy of muscle, but with its increase in tension
at extremes of range, it may contribute to the resistance felt in muscle when it is
stretched to near its limits of range of motion. 44 •45
Clinical Implications ofThixotropy

Considering the ranges of motion used in measurement of thixotropy, it is ques-
tionable whether thixotropy has any practical application to clinical practice.
Thixotropy is thought to explain the phenomenon of palpable "muscle spasms"
that are found on examination of patients with myofascial trigger points. As pre-
viously cited, highly localized electrical activity has been found in myofascial
trigger points. These same trigger points have been identified by Simons 46 as cor-
responding anatomically with the intramuscular portion of motor nerve termi-
nals. It is possible that the localized electrical activity is adequate to sensitize no-
ciceptors in the area of a myofascial trigger point. The nociceptive agents released
may also destabilize the T-tubules enough to result in a higher calcium concen-
tration within myofibrils. This would result in a larger number of cross-bridges
being formed between the myosin heads and troponin, which would increase the
stiffness (i.e., thixotropy). Such an increase in cross-bridges would decrease the
pliability of muscle in the immediately surrounding muscle tissue. This phenom-
enon would explain why deep massage is beneficial for increasing the pliability of
the muscle around trigger points. According to the pain-spasm-pain cycle, deep
massage of a myofascial trigger point should increase the pain, thereby increas-
ing the spasm, which causes even more pain. This does not always occur in prac-
tice; in fact, many practitioners can testify that deep massage can "decrease the
spasm."
Neurophysiological Implications of Thixotropy

The mechanical properties of thixotropy reviewed in the previous sections apply to
the largest complement of muscle, the extrafusal fibers. Extrafusal fibers are only
part of the picture, however. According to Proske et al., thixotropy, as a mechani-
cal property, has a profound influence on muscle spindles and their afferent neu-
rons.40These influences are too numerous to review here, but the resting discharge
of primary spindle afferents and their sensitivity to muscle stretch are dependent
on the previous history of movements and/or contraction. In several studies, re-
searchers have demonstrated that when a conditioning movement or contraction
is performed, such as an isometric contraction in the shortened position, the af-
ferent discharge from muscle spindles is increased .8 The reverse is observed in an
isometric contraction in the lengthened position. This phenomenon is not a facili-
tation of the spinal cord mechanisms but rather a sensitization or desensitization,
as the case may be, of the muscle spindle.
Another potential influence of thixotropy can be postulated based on the
biochemical, biophysical, and neurophysiological properties of joint capsules and
other connective tissues. First, the biochemistry and biophysics of the sulfated
GAGs have shown them to be responsible for the cohesiveness of connective tis-
sue. Second, with this increased cohesiveness comes an increased initial resistance
to active or passive stretch. Consequently, one would expect an initial afferent
discharge from joint receptors after a joint has remained still for a few minutes.
Indeed, Walsh and Wright demonstrated that thixotropy occurs at the human
hip, with the amplitude of the resonant frequency of a sinusoidally abducting/
adducting hip almost doubling in response to a stirring motion of large ampli-
tude. 47Whether this thixotropic resistance to initial movement actually produces
an increased afferent discharge very early in the time course of the movement re-
mains to be tested. Nevertheless, if the fluid mechanics of a joint capsule, mus-
culotendinous junction, or direct muscular attachment to bone were changed by
inflammation by-products, then the afferent output from those receptors could
certainly be either increased or decreased . Such an event may explain some of the
faulty movement patterns or holding patterns described by Juli and Janda. 11
I have reviewed the basic receptor anatomy and physiology for most of the
somatosensory system, with the exception of the vestibular system. I have also
reviewed some of the interactions of the somatosensory system with the motor
output system, with particular emphasis on that portion related to the myofas-
cial system. I now turn to the direct application of this physiology and biophysics
background .
Application to Specific Therapeutic Techniques

In the following sections, I outline applications of the science heretofore presented.
Each application takes the following form: (1) a very brief discussion of the par-
ticular technique to which application is made; (2) a discussion of the pathology/
pathomechanics addressed by the particular technique; (3) a proposed theoretical
mechanism, whereby these techniques may influence the somatosensory system;
and (4) proposed mechanisms for motor control alterations that are engendered by
the technique under consideration.
Anterolateral Fascial Elongation

The anterolateral fascial elongation technique (shown in Chapter 8, Figures 8.126
and 8.127) is an important technique because its logical and neuromechanical
characteristics can apply to virtually all of the superficial techniques described
in this book. The anterior lateral fascial elongation technique, as described later
in Chapter 8, primarily stretches the superficial fascial sheath in a diagonal pat-
tern across the anterior surface of the body. In doing so, the technique treats a
number of restrictions at various levels. At the interface between the skin and the
superficial fascia, there may be restrictions secondary to blunt trauma and scar-
ring. In the superficial fascia itself, and in its interface with the pectoralis major
and the external oblique abdominals, the sheath is continuous from the proximal
humerus, clavicle, and anterior shoulder down to the contralateral crest of the
ilium, thoracolumbar fascia, anterior superior iliac spine, inguinal ligament, and
the pubis.
Restrictions of the superficial fascia of the anterior trunk have mechanical
implications for posture and for virtually all movements of the trunk and upper
and lower extremities. Certainly, there are mechanical restrictions of mobility, but
given that patients develop such faulty postural habits, the pathomechanical im-
plications for the body as a whole are most likely seated in position sense. Restric-
tions in the superficial fascia would result in a continuous and abnormal stimulus
of the slowly adapting mechanoreceptors in the skin and all the succeeding layers
of the superficial fascia . Because the mechanical restriction in the skin and super-
ficial fascia is very similar to that found in the experiment perf armed by Cohen et
al.,31 some direct postulates are in order.
Cohen et al. found increased activity of somatosensory cortical cells repre-
senting skin receptive fields in the axilla and the skin of the medial proximal
arm associated with parallel skin stretching, passive movement, and active move-
ment. 31 They demonstrated the same highly correlated activity in a variety of tasks,
including reaction time tasks, holding tasks, and active movement of the arm. The
shortened range of skin produced very little activity in tactile receptors of the
axilla and upper arm. This is in contrast to movements into shoulder flexion or
shoulder flexion with abduction, which increased the activity. 46 Furthermore, the
greater the stretch in either amplitude or movement, the greater the firing rate of
phasic (rapidly adapting) receptors (e.g., Pacinian corpuscles).
These findings are completely logical and intuitive when considered in con-
junction with the human postural phenomena observed by clinicians. Consider a
patient 3 - 4 weeks following a cholecystectomy via a left upper quadrant incision
rather than a laparoscopic procedure. A phasic stimulus of skin receptors during
erect sitting or right shoulder flexion would be perceived as a "greater than rest-
ing or normal position" burst of activity. In that case, the patient would return to
a position that was more in line with resting position. If a mechanical restriction
resulted in an abnormal phasic stimulus or tonic stimulus, then the interpretation
by the system would be that the patient was in a stretched position when, in fact,
the position might be neutral. Consequently, the patient would tend to move into
a position that decreases the firing activity of the phasic and/or tonic receptors.
This position is then perceived, via the skin receptive fields, as normal, and further
shortening of the superficial fascia occurs. This faulty receptor activity and the
position sense activity it provides soon become the basis for postural perception.
Historically, the theoretical basis for such behavior has been pain avoidance.
Certainly, pain avoidance behavior is a reasonable and patent argument in the
early stages, but after several weeks of healing, the pain disappears. What remains
is the new position sense reference from skin and superficial fascia receptors.
Another hypothesis concerning the continued behavior of avoiding elonga-
tion is that of alteration in motor programs (motor memories) to fit the new and
dysfunctional behavior. Considering the amount of practice required to change
a very well-learned motor program, this is not likely. Consider, for example, at-
tempting to change one's signature. It is possible, but on a practical level, it is not
probable owing to the huge volume (millions of repetitions) of practice required.
It is likely this new position sense stimulus acts to inhibit the very muscles that
would elongate the skin's rapidly and slowly adapting receptors. Similar inhibition
is also seen in the Golgi tendon organ and Golgi-Mazzoni type joint receptors.
Such a postulate is based on the findings of numerous investigators of the
inhibitory influences of GTOs and joint receptors on motor output. It is also in
agreement with Janda's model of altered muscle function and motor performance
resulting from "inadequate proprioceptive stimuli," which is probably more cor-
rectly stated as inappropriate or mismatched proprioceptive stimuli. 31 One excep-
tion is noted, which is that the logic described cannot validly be applied to the Bin-
degewebsmassage type of stroke or the skin rolling. This is because their goals and
physiology are not directly connected to the evidence supplied by Cohen et al. 31
Iliac Crest Release Technique

The iliac crest release technique is useful to consider, because it is a moderately
deep technique (shown in Chapter 8, Figures 8.24 and 8.25). It is executed by ap-
plying an anterior-directed force through the fingers, moving from the border of
the iliac crest anteriorly and superiorly on to the thoracolumbar fascia and then to
the insertion of the deep erector spinae and quadratus lumborum. This technique
addresses restriction of the thoracolumbar fascia and the muscular and ligamen-
tous attachments. Bogduk and Macintosh discussed the anatomy of the thoraco-
lumbar fascia with its two layers connecting to the crest of the ilium. 48 This anat-
omy makes its mechanics somewhat complicated and allows the thoracolumbar
fascia to contribute to stabilization of the spine in virtually all movements, with
the possible exception of side bending to the same side. 11
There is some disagreement concerning the density of mechanoreceptors
in the thoracolumbar fascia. An assumption that the connective tissue in this
structure is no different from that found in the shoulder, knee, and ankle would
lead one to conclude that the receptors consist of free nerve endings, Pacinian
corpuscles, Ruffini endings, Golgi-Mazzoni endings, and others associated with
ligamentous structure. Bednar et al., however, failed to find a significant density
of mechanoreceptors in the thoracolumbar fascia of patients with chronic back
pain. 49 They concluded that there were differences in the density of receptors be-
tween healthy subjects and persons with back pain. One major caveat concerning
their study is that it was performed with standard histological staining and no
specifics were noted concerning the area of the thoracolumbar fascia from which
samples were taken during surgery. Yahia et al. found Ruffini endings and Vata-
Pacini corpuscles (a specialized form of Pacinian corpuscles). These samples were
also taken from surgical patients. Also, Yahia et al.'s samples were prepared with
immunohistochemical staining techniques that targeted neural filament protein. so
With the documented presence of Ruffini endings and Pacinian-like corpus-
cles in the thoracolumbar fascia, it is likely that a restriction of the thoracolumbar
fascia would produce an abnormal afferent stimulus. This abnormal stimulus from
normal motions or positions would result in an abnormally excited or inhibited
level of activity for the motor units of the abdominal , paraspinal , and quadratus
lumborum musculature. Therefore, decreasing restrictions with the iliac crest re-
lease technique would help to correct this abnormal afferent outflow. Such a cor-
rection would allow the relative levels of excitation and inhibitions to return to
levels dictated by the normal motor programs as opposed to inappropriate pro-
prioceptive signals.
Diaphragmatic Techniques
Techniques for correcting restrictions in the diaphragm and inferior border of the
rib cage are important in helping patients who are having difficulty with postural
reeducation. The techniques progress from a gentle stretching of the superficial to
middle layer restrictions just inferior to the anterior rib cage, to those that involve
grasping the inferior portion of the rib cage, in a seated position, and stretching
it superiorly and anteriorly while asking the patient to sit up straighter and inhale
deeply (shown in Chapter 8, Figures 8.54 through 8.57).
Diaphragmatic techniques address restrictions that are very deep in the tho-
racic and abdominal cavities. Although directly addressing restrictions in the tho-
racic cavity is not possible, it is possible to affect restrictions in the mediastinum
by stretching the diaphragm and deep fascia of the abdomen and diaphragm. Such
restrictions can lead to or be the result of multiple postural problems, such as for-
ward head, protracted shoulders, and a general slumped posture in sitting.
The pathomechanics of slumped posture and forward head are fairly well un-
derstood. With an increasingly forward-head posture comes a tendency for the ribs
and sternum to move inferiorly and posteriorly. This leads to a shortening of the
connective tissue in the abdomen and the thorax. With decreasing length comes
a tendency for increased afferent activity from the tension receptors (e.g., GTOs,
Ruffini endings, Pacinian corpuscles). An increase in tension on these receptors,
especially on the GTOs, of the central tendon of the diaphragm has been shown to
elicit a complex inhibitory effect on the external intercostals and the diaphragm. so
All of this inhibitory activity results in a reduction in lung volume. Over time, as
lung capacity is diminished by these inhibitory processes, the connective tissue
would remodel to its new length, resulting in a new "set" for the normal tension on
the tendon. The manipulation techniques described herein allow for a lengthening
of the diaphragm along its anterior borders, with a resultant, postulated reduction
in the inhibitory activity of the GTOs.
Erector Spinae Muscle Play

Erector spinae muscle play is a relatively simple technique to perform and, de-
pending on the vigor with which it is done, can have exclusively neurophysiologi-
cal effects or, when performed more aggressively, can have mechanical effects. The
technique basically consists of bending the muscle as if bending a garden hose
(shown in Chapter 8, Figures 8.15 and 8.16). The technique can also be modified as
in the quadriceps and hamstring technique to include bending and some muscle
rolling and lifting actions. No matter what particular technique is used, the result
is a multidirectional mechanical stress with the least emphasis on longitudinal
stretching.
The major benefit of the technique appears to be in improving the mobility of
muscle on muscle and of individual muscle fascicles on other muscle fascicles. If a
restriction occurs between two fascicles or two muscles, then the resulting altered
mechanics produces a sensory mismatch and inappropriate proprioception from
the muscle. Such a case has been described in the earlier section "Implications of
Muscle Spindles and Golgi Tendon Organs."
Although the influences of intermuscular and/or interfascicular adhesions on
afferent and efferent neural activity are fairly common knowledge among thera-
pists, there are other pathological problems related to such adhesions, as well as
benefits related to a transverse muscle play technique.
The pathology of such adhesions and, more important, the changes in in-
tramuscular pressure caused by them relate to influences of thixotropy and the
Group III and IV afferents. Adhesions of such a nature can lead to a local irrita-
tion of the muscle and a destabilization of the cell membrane adequate to cause
a release of calcium into the myofibrils. This release of calcium will result in the
formation of cross-bridges without benefit of an action potential and increased
thixotropic resistance to stretch. Increases in intramuscular pressure have been di-
rectly associated with increased afferent action potentials of the Group III and IV
afferents coming from the arterioles, venules, and connective tissue in proximity
to these structures. Such afferent activity results in cardiovascular and pulmonary
changes on a systemic level and an autonomic response of increased blood flow at
a local level.
The treatment techniques themselves also have direct effects on the thixot-
ropy of the system and the Group III and IV afferents. The muscle play motion of
the muscle would provide a mechanical stimulus to aid in decreasing the thixo-
tropic resistance to motion. Next, the technique would have direct effects on the
Group III afferents, with resultant changes in local blood flow, in addition to sys-
temic cardiovascular and pulmonary effects. The changes in thixotropy engen-
dered by the techniques most likely also extend to changing the outflow from the
muscle spindles themselves, with all the cascade of effects from them.
Conclusion
Much of the material presented in the early sections of this chapter may appear
to be weighted heavily toward basic science. It is highly probable, however, that
a significant part of benefit derived from the techniques is neurophysiological in
origin because of the rapidity of the effects and the relatively longer period of time
required for remodeling. A number of these techniques can be viewed as methods
to prepare the patient to be able to move in a manner that will lead to more func-
tional remodeling of collagen.
Practitioners should certainly apply the science and neurophysiology where
valid, but they should also exercise caution when extending their explanation too
far afield from the intent of the science. Furthermore, the practitioner should re-
member that many manual techniques appear to have no rational explanation but
consistently appear to benefit patients. Consequently, the practitioner should use
the science for explanation, when possible, while continuing to use the art of man-
ual therapy to heal and investigating the explanations for the effects seen.
References
1. Walsh EG. Muscles,Massesand Motion: 1he Physiologyof Normality,Hypotonicity,Spasticityand
Rigidity.New York:Cambridge University Press; 1992.
2. Gardner EP,Martin JH, JessellTM. In: ER Kandel, JH Schwartz, TM Jessell,eds. Principlesof
Neural Science.4th ed. New York:McGraw-Hill; 2000:430- 449.
3. Hagen-Torn 0. Entwicklung and Bauder Synoviamembranen. Archivfar MikroskopischeAnat-
omie. 1882;21:591- 663.
4. Gardner E. Nerve terminals associated with the knee joint of the mouse. Anat Rec.
1942;83:401- 419.
5. Zimny ML, Schutte M, Dabezies E. Mechanoreceptors in the human anterior cruciate ligament.
Anat Rec. l 986;214:204 - 209.
6. Zimny ML. Mechanoreceptors in articular tissues. Am JAnat. 1988;182:16-32.
7. Basbaum AI, Jessell TM. The perception of pain. In: ER Kandel, JH Schwartz, TM Jessell, eds.
Principlesof Neural Science.4th ed. New York: McGraw-Hill; 2000:472- 491.
8. Pearson K, Gordon J. Spinal reflexes. In: ER Kandel, JH Schwartz, TM Jessell, eds. Principlesof
Neural Science.4th ed. New York: McGraw-Hill; 2000:713- 736.
9. Houk J, Henneman E. Responses of Golgi tendon organs to active contractions of the soleus
muscle of the cat. JNeurophysiol.1967;30:466-481.
10. Wyke B. The neurology of joints. Ann R Coll Surg Engl. 1967;41:25-50.
11. Jull GA, Janda V. Muscles and motor control in low back pain: assessment and management.
In: LT Twomey, JR Taylor, eds. Physical Therapyof the Low Back. New York: Churchill Living-
stone; 1987.
12. Stacey MJ. Free nerve endings in skeletal muscle of the cat. JAnat. 1969;105:231-254.
13. Von During M, Andres KH. Topography and ultrastructure of group III and IV nerve termi-
nals of cat gastrocnemius-soleus muscle. In: W Zenker, WL Neuhuber, eds. The Primary Affer-
ent Neuron: A Survey of Recent Morpho-Functional Aspects. New York: Plenum; 1990:35-41.
14. Kaufman MP. Afferents from limb skeletal muscle. In: JA Dempsey, AI Pack, eds. Regulation
of Breathing.2nd ed. New York: Marcel Dekker; 1995:583- 617.
15. Kumazawa TN, Mizumura K. Thin-fibre receptors responding to mechanical, chemical and
thermal stimulation in the skeletal muscle of the dog. JPhysiol. 1977;273:179-194.
16. Haouzi P, Hill JM, Lewis BK, Kaufman MP. Responses of group III and IV muscle afferents
to distension of the peripheral vascular bed. JAppl Physiol. 1999;87:545-553.
17. Mense S. Nervous outflow from skeletal muscle following chemical noxious stimulation.
J Physiol.1977;267:75-88.
18. Rotto DM, Schultz HD, Longhurst JC, Kaufman MP. Sensitization of group III muscle
afferents to static contraction by products of arachidonic acid metabolism.! Appl Physiol.
1990;68:861- 867.
19. Sinoway LI, Hill JM, Pickar JG, Kaufman MP. Effects of contraction and lactic acid on dis-
charge of group III muscle afferents in cats. JNeurophysiol. 1993;69:1053-1059.
20. Rotto DM, Hill JM, Schultz HD, Kaufman MP. Cyclo-oxygenase blockade attenu-
ates the responses of group IV muscle afferents to static contraction. Am JPhysiol.
1990;259:H745-H750.
21. Fields HL. Pain. New York: McGraw-Hill; 1987.
22. Kandel ER, Schwartz JH, Jessell TM. Principlesof Neural Science.4th ed. New York: McGraw-
Hill; 2000.
23. Ghez C. The control of movement. In: ER Kandel, JH Schwartz, TM Jess ell, eds. Principlesof
Neural Science.3rd ed. New York: Appleton & Lange; 1991:533-547.
24. Houk J, Crago PE, Rymer WZ. Functional properties of the Golgi tendon organs. In: Spinal
and SupraspinalMechanisms of Voluntary Motor Control and Locomotions, vol 8, Progressin
ClinicalNeurophysiology.Basel: Karger; 1980:33-43.
25. Kennedy JC, Alexander IJ, Hayes KC. Nerve supply of the human knee and its functional
importance. Am JSports Med. 1982;10:329-335.
26. Berkinblit MB, Feldman AG, Fukson 01. Adaptability of innate motor patterns and motor
control mechanisms. Behav Brain Sci. 1986;9:585-638.
27. Hagbarth KE. Excitatory and inhibitory skin areas for flexor and extensor motoneurons. Acta
PhysiolScand Suppl. 1952;26:l-58.
Neuromechan ical Aspects of Myofasc ial Patho logy and Manipulation 123
28. Burgess PR, Wei JY,Clark FJ, Simon J. Signaling of kinesthetic information by peripheral sen-
sory receptors. Annu Rev Neurosci. 1982;5:171-187.
29. Matthews PB. Proprioceptors and their contribution to somatosensory mapping: complex
messages require complex processing. Can JPhysiolPharmacol. 1988;66:430-438.
30. Collins DF, Cameron T, Gillard DM, Prochazka A. Muscular sense is attenuated when hu-
mans move. J Physiol. 1998;508:635-643.
31. Cohen DAD, Prud ' homme MJL, Kalaska JF. Tact ile activity in primate cortex during active
arm movements: correlation with receptive field properties.! Neurophysiol. 1994;71:161-172.
32. Simons DG, Mense S. Understanding and measurement of muscle tone as related to clinical
muscle pain. Pain. 1998;75:l-17.
33. Clemmesen S. Some studies on muscle tone. Proc R Soc Med. 1951;44:637-646.
J PhysMed. 1953;32:85-92.
34. Ralston HJ, Libet B. The question oftonus in skeletal muscle. Am
35. Basmajian JV. New views on muscular tone and relaxation. Can Med Assoc J.1957;77:203-205.
36. DiMauro S, Tsujino S. Non-lysosomal glycogenoses. In: AG Engel, C Franzini-Armstrong,
eds. Myology. 2nd ed, vol 2. McGraw-Hill; 1994:1554-1576.
37. Simons DG, Hong CZ, Simons LS. Prevalence of spontaneous electrical activity at trigger
spots and control sites in rabbit muscle. JMusculoskelet Pain. 1995;3:35-48.
38. Elert J, Dahlqvist SR, Almay B, Eisemann M. Muscle endurance, muscle tension and personal-
ity traits in patients with muscle or joint pain: a pilot study. JRheumatol. 1993;20:1550-1556.
39. Ivanichev GA. Painful Muscle Hypertonus (in Russian). Kazan: Kazan University Press; 1990.
40. Proske U, Morgan DL, Gregory JE. Thixotropy in skeletal muscle and in muscle spindles: a
review. ProgNeurobiol. 1993;41:705- 721.
41. Walsh EG. Muscles,Masses and Motion: 1he Physiologyof Normality, Hypotonicity, Spasticity
and Rigidity. New York: Cambridge University Press; 1992.
42. Campbell KS, Lakie M. A cross-bridge mechanism can explain the thixotropic short-range
elastic component of relaxed frog skeletal muscle. JPhysiol. 1998;510:941- 962.
43. Hill DK. Tension due to interaction between the sliding filaments in resting striated muscle:
the effect of stimulation.! Physiol. 1968;199:637-684.
44. Mutungi G, Ranatunga KW. The viscous, viscoelastic and elastic characteristics of resting fast
and slow mammalian (rat) muscle fibres. JPhysiol. 1996;496:827-836.
45. Linke WA, Bartoo ML, lvemeyer M, Bolla ck GH. Limits of titin extension in single cardiac
myofibrils. JMuse Res CellMotil. 1996;17:425-438.
46. Simons DG. Clinical and etiological update on myofascial pain due to trigger points. JMuscu-
loskelet Pain. 1996;4:93-121.
47. Walsh EG, Wright GW. Postural thixotropy at the human hip. Q JExp Physiol.
1988;73:369- 37 7.
48. Bogduk N, Macintosh JE. The applied anatomy of the thoracolumbar fascia. Spine.
1984;9:164-170.
49. Bednar DA, Orr FW, Simon GT. Observations on the pathomorphology of the thoracolumbar
fascia in chronic mechanical back pain: a microscopic study. Spine. 1995;20:1161-1164.
50. Yahia L, Rhalmi S, Newman N, Isler M. Sensory innervation of human thoracolumbar fascia:
an immunohistochemical study. Acta Orthop Scand. 1992;63:195-197.
Muscle Pain Syndromes
Jan Dommerholt and Robert W. Stanborough
Muscle pain is a common feature of both acute and chronic pain problems and
affects people of all ages, although chronic muscle pain is less common in younger
populations. 1- 3 Patients with muscle pain are frequently referred to physical thera-
pists for evaluation and treatment ; therefore, physical therapists need to under-
stand the nature of pain and of muscle pain in particular. Clinicians need to be
familiar with the mechanisms of referred pain, peripheral and central sensitiza-
tion, and the best evidence-informed treatment options. 4 •5 Depending on the diag-
nosis, myofascial manipulation may or may not be a part of the patient's rehabilita-
tion program.
Muscle pain is experienced as an aching, diffuse, and difficult-to-localize pain,
which often features referred pain into deep somatic tissues. 3 It can be either tran-
sient, as in delayed onset of muscle soreness, 6 or more persistent .7 Parameters for
the treatment of persistent pain are not included in the American Physical Therapy
Association's "Guide to Physical Therapy Practice," 8 and relatively few physical
therapists have expressed special interest in chronic pain ,9 perhaps because of
lack of understanding. Unfortunately, one study suggested that 96% of orthopedic
physical therapists preferred not to treat patients with chronic pain problems. 10
Although physical therapists are well trained in addressing dysfunction, which
is often a source of pain, they are poorly represented in pain management societ-
ies, and few schools of physical therapy have adopted specific pain curricula for
physical therapists, as suggested by the International Association for the Study of
Pain. 9•11
Muscle pain is distinctly different from cutaneous pain and activates specific
cortical structures, including the anterior cingulate gyrus. 12- 14 Muscles feature
specialized muscle nociceptors, which are free nerve endings connected to the
central nervous system by thin myelinated (Group III) or unmyelinated (Group
IV) afferent fibers. 15 - 17 These nociceptors are particularly effective in inducing
neuroplastic changes in the spinal dorsal horn. 18 Under nonpathological circum-
stances, there is a dynamic balance between activation of dorsal horn neurons and
the descending inhibitory pain-modulating pathways, which are very effective in
inhibiting muscle pain. 19,20
125
Persistent muscle pain has been described as fibrositis , myofasciitis , muscu-

lar rheumatism , rheumatoid myositis , muscle hardening, myogelosis, myofascial
pain, and myalgia, among others .7 Sometimes patients with complaints of persis-
tent muscle pain are thought to be suffering from a presumed somatoform disor-
der, but there is little evidence to support this notion. 21 A thorough medical and
physical evaluation is needed to identify any possible underlying myofascial cause
of chronic pain, rather than considering the pain problem to be psychogenic in
nature .22 •23
Muscle pain syndromes can be classified into distinct categories, including
soft tissue mechanical dysfunction, myofascial pain, and fibromyalgia, although
fibromyalgia is moving more and more toward being considered a neurological
disorder. Soft tissue mechanical dysfunction is an acute and local pathology, such
as a partial tear in a muscle . Although there are overlapping characteristics, pain
originating from soft tissue mechanical dysfunction can be specifically identified
during the course of a thorough musculoskeletal examination. Often, the patient's
history reveals the etiology of soft tissue mechanical dysfunction. For example, tis-
sues may fail from a fall, twist, or repetitive motion and then develop into a muscle
tear or strain, a ligament sprain, a tendon tear, or tendonitis. Myofascial pain is
often viewed as a regional pain problem; however, it can be regional or widespread .
In one study, up to 45% of patients with chronic myofascial pain had generalized
pain in three or four quadrants. 24 By definition, fibromyalgia is always widespread
and chronic. 25 Based on current evidence, fibromyalgia is no longer considered a
"muscle pain" syndrome. 26 The purpose of this chapter is to explore the etiology,
symptomatology, pathophysiology, and medical/therapeutic management of these
common pain problems and to discuss the role of the physical therapist and physi-
cian in the evaluation and treatment of patients with these conditions.
Soft Tissue Lesion and Mechanical Dysfunction

Definition and Characteristics
Pain continues to be one of the primary reasons patients seek help from medical
professionals. Fibromyalgia, with its lack of specific diagnostic findings and dif-
fuse pain patterns, represents one end of a spectrum of pain severity and complex-
ity, and soft tissue mechanical dysfunction represents the other end . Mechanical
dysfunction is simply where tissue has failed, because of either its inability to resist
a one-time force or its inability to withstand a repetitive stress over time . In either
case, the etiology is mechanical in nature, which provides patients with the abil-
ity to reproduce their pain or make it better or worse. With soft tissue mechanical
dysfunction, there is usually an overuse or direct trauma to the tissue produc-
ing an inflammatory response. A partial or full tear, as in a hamstring tear or
"pull"; a gastrocnemius tear; lateral epicondylitis; and de Quervain's disease are
forms of soft tissue mechanical dysfunction. Facet hypo mobility or hypermobility,
muscular or movement imbalances, discogenic pathologies, and sacroiliac joint
Mus cle Pain Syndromes 127
dysfunction also represent mechanica l dysfunction characterized by soft tissue le-

sions. These dysfunctions can be medically diagnosed and evaluated for specific
pathologies. Treatment may be provided based on the findings of the examination,
the stage of the condition, and the reactivity of the tissues and the patient.
In order to accurately diagnose and treat soft tissue mechanical dysfunction, a
thorough and systematic examination should be performed. Initially, gross move-
ments should be used to isolate stresses as muscles contract and are stretched, at
which time the therapist takes note of what makes the patient's symptoms better
or worse. The soft tissues surrounding the articulations (i.e., capsules and liga-
ments) should also be stressed using accessory mobility testing. To localize the
dysfunction to the specific lesion, tissues may be further isolated using special tests
or palpation for tenderness. The purpose is to identify and define areas of somatic
dysfunction and to localize a lesion site.
Somatic dysfunction can be defined as impaired or altered function of related
components of the somatic system (body framework), skeletal, arthrodial, and
myofascial structures. The criteria for dysfunction include the following:
•!• Structural or functional asymmetry of related parts of the musculoskeletal
system, ascertained by observation and palpation
•!• Abnormality of texture in the musculoskeletal system soft tissues (skin,
fascia, muscle, ligament, or joint capsule), ascertained by observation and
palpation
•!• Range -of-motion abnormality of a joint, several joints, or regions of the
musculoskeletal system (either restricted or hypermobile qualitat ive changes
in range of motion, such as cogwheel movement, hesitations, and compensa -
tions), ascertained by observations and palpation, utilizing both active and
passive testing
Management of Soft Tissue Mechanical Dysfunction

A patient's clinical history will usually offer substantial clues about causes of the
dysfunction, such as trauma, overuse, or lifestyle, among others. The evaluation
will reveal specific findings that will allow for systematic development of a treat-
ment plan specific to the particular pathology or dysfunction. Of the three catego-
ries described, soft tissue mechanical dysfunction usually requires shorter term
treatment and has the best prognosis for recovery.
Treatment of soft tissue mechanical dysfunction is usually guided by the stages
of healing - inflammation, granulation, proliferation, and maturation - described
in Chapter 4, "Histopathology of Myofascia and Physiology of Myofascial Ma-
nipulation." Support should be provided during inflammation and granulation,
to allow the tissue to heal. Controlled movements may be implemented during
the proliferation phase to aid in collagen alignment. Finally, in the maturation, or
remodeling, stage, controlled stresses should be continued and increased to facili-
tate healing along the lines of stress. During the linear process of tissue healing, a
careful balance must be struck between providing "controlled stresses," to ensure
healing according to the tissues' demands, and preventing further damage, result-
ing in delayed healing or excessive scar tissue. If healing is prolonged, what began
as a soft tissue mechanical dysfunction may develop into secondary myofascial
pain. Trigger points may develop and become the main source of pain, necessitat-
ing appropriate treatment.
Myofascial Pain Syndrome

Definition
Myofascial pain has been defined differently by various authors or disciplines.
Some describe myofascial pain as a regional pain problem of any soft tissue ori-
gin. 27In dentistry, myofascialpain dysfunction syndrome has become the preferred
term, described as muscle pain with or without limitations in mouth opening as
a feature of temporomandibular dysfunction. 28The validity and accuracy of the
temporomandibular dysfunction criteria have recently been questioned, how-
ever.29Gunn described myofascial pain as a chronic pain condition that occurs in
the musculoskeletal system without obvious injury or inflammation. 30According
to Gunn, myofascial pain is always the result of peripheral neuropathy, which he
defined as "a condition that causes disordered function in the peripheral nerve." 31
The most commonly used definition, by Simons et al., describes myofascial pain as
"a muscle pain disorder characterized by the presence of a myofascial trigger point
within a taut band, local tenderness, referral of pain to a distant site, restricted
range of motion, and autonomic phenomena." 32<P 3l
Dr. Janet Travell, White House physician to former Presidents Kennedy and
Johnson, is considered the initiator of the myofascial pain literature, although other
writers described trigger point phenomena as far back as the 16th century, 33and
the first textbook on trigger points was published in 1931 by Lange in Germany. 34
One of Travell's main contributions was a detailed mapping of common muscle-
referred pain patterns. 35·36Simons, Travell, and Simons describe myofascial trig-
ger points in almost all skeletal muscles of the body. 32·37In the older European
literature, the term myogelosiswas commonly used to describe myofascial trig-
ger points. 38In this chapter, the Simons, Travell, and Simons criteria are applied.
There is limited scientific research of the reliability and validity of the criteria, but
in clinical practice, they appear to be acceptable. 39- 41The lack of validated criteria
has not stopped researchers and clinicians from studying trigger point phenomena
and their clinical management. 42- 46
The American College of Rheumatology has established criteria for the di-
agnosis of fibromyalgia, 47 and often, patients who present with widespread myo-
fascial pain are diagnosed with that disorder. Myofascial trigger points are not
often considered as a potential source of their pain 47; however, in the presence
of widespread trigger points, the diagnosis of myofascial pain would be the pre-
ferred diagnosis. 25•49Myofascial pain can exist in isolation without involvement of
other structures and can also be associated with other musculoskeletal disorders.
Muscle Pain Syndromes 129
Myofascial pain has been described as the most common diagnosis responsible for
chronic pain and disability, but it is also considered the most commonly missed
diagnosis. 22 •48 This may be due in part to the fact that physical therapy literature
rarely includes reference to trigger points. Several studies have shown that patients
with osteoarthritis, tension-type headaches, and migraines have more clinically
relevant trigger points than do healthy controls. 50 - 53 Although trigger points are
often associated with cervicogenic and tension-type headaches, not all headaches
feature trigger points. Nummular headache, for example, is a primary headache
disorder, characterized by mild to moderate and pressure-like pain circumscribed
to a single round or elliptical area of the head surface, but without active trigger
points in the neck and shoulder muscles. 54 - 56
The role of trigger points is adequately described in other studies and case
reports, including those of facet joint dysfunction, disc herniations, neck pain,
and postlaminectomy syndromes. 57- 60 Trigger points can also occur in associa-
tion with other medical conditions, ranging from nerve entrapments and myocar-
dial infarction to endometriosis, prostatitis, and interstitial cystitis. 61- 67 Although
trigger points are often missed and underdiagnosed, their presence does not ex-
clude other pertinent problems. Caution is therefore warranted, because clinicians
should not focus exclusively on trigger points. Although trigger points are recog-
nized as a source of pain, they are merely a symptom of an underlying dysfunc-
tion. Because trigger points are part of nearly every musculoskeletal pain problem,
it is debatable whether myofascial pain should be considered an actual syndrome. 5
Many recent studies seem to support the concept that a myofascial trigger point
is a manifestation of peripheral and central sensitization, 4 •68 •69 or it may indicate
an actual disease process of muscle rather than a poorly defined syndrome. 70 In
this context, there is no diagnostic or clinical benefit to the patient in making the
distinction between primary and secondary myofascial pain syndrome . The ex-
amination and treatment should be the same.
Diagnosis
The main criterion for the diagnosis of myofascial pain is the presence of an active
myofascial trigger point, an exquisitely sensitive region in a taut band of skeletal
muscle .71 Simons et al. define a trigger point as "a hyperirritable spot in skeletal
muscle that is associated with a hypersensitive palpable nodule in a taut band ." 32 (P 3l
Trigger points have been reported in all age groups except infants. 2 •72- 76 An active
trigger point produces symptoms, including local or referred pain or other pares-
thesia. A latent trigger point does not induce pain without being stimulated .32
Most patients complain of diffuse pain and are not aware that specific myo-
fascial trigger points may cause or contribute to their pain. The diagnosis of
myofascial pain is made by systematic palpation of taut bands and myofascial
trigger points, following a review of the patient's history, and by a thorough
musculoskeletal examination, including an assessment of posture and functional
movement patterns. 32 The patient's pain pattern and range-of-motion restrictions
Table 6.1 Criteria for Identifying a Myofascial usually point the clinician to the involved
Trigger Point muscles. The minimum acceptable criteria
Diagnostic criteria for trigger point diagnosis are the presence
1. Full stretch, limited by pain of a hyperirritable spot within a palpable
2. Taut band palpable taut band of a skeletal muscle, combined
3. Tender spot or nodule within a taut band
with the patient's recognition of the re-
4. Reproducible pain of patient's complaint
ferred pain elicited by the trigger point (Ta-
Confirmatory observations ble 6.1). These criteria, when applied by an
1. Local twitch response experienced therapist, have obtained good
2. Referred pain in the expected distribution of interexaminer reliability. 71 The presence of
that muscle
3. Endplate noise or spontaneous electrical
a local twitch response, referred pain, or
activity (SEA) demonstrated by an reproduction of the person's symptomatic
electromyographic study pain increases the certainty and specificity
Source: Alfven G. The pressure pain threshold (PPT) of the diagnosis of myofascial pain. A local
of certain muscles in children suffering from recurrent twitch response is a brief, involuntary con-
abdominal pain of non -organic origin: an algometric
study. Acta Paediatr. 1993;82:481- 483. traction of the taut band that can be seen,
Source: Simons D. Understanding effective treat- palpated, felt with the needle during trig-
ments of myofascial trigger points. J Bodyw Mov Ther. ger point injections or dry needling, and
2002;6:81- 88.
recorded electromyographically. It is me-
diated primarily through the spinal cord
without supraspinal influence_n -so The patient's body type and the specific muscle
involved will determine the ease of soliciting a local twitch response. The degree of
stimulation required to reproduce a patient's usual pain can also help determine
whether a trigger point should be considered active or latent. Active trigger points
have a lower pain threshold than that of latent trigger points.
The interrater reliability of the myofascial trigger point examination has been
studied by several authors. 71•81- 88 The reliable identification of trigger points re-
quires anatomical knowledge, adequate manual ability, training, and clinical prac-
tice. Older studies showing lack of interrater reliability were marked by a variety of
methodological problems, including a lack of identification of taut bands, inexpe-
rience of examiners in assessing muscle trigger points, incorrect positioning of the
patient or the examiner, incorrect palpation techniques, variation in the amount
of manual force exerted on the palpated point, and the duration of force applied.
One problem common to all interrater reliability studies is that the trigger point
criteria established by Simons et al. 32 have not been validated. 39- 41 Nevertheless,
Gerwin et al. established excellent interrater reliability for the five major features
of the trigger point: palpable taut band, tenderness, local twitch response, referred
pain, and reproduced pain. 71 They observed that individual features of the trig-
ger point are differentially represented in different muscles. For example, the lo-
cal twitch response was easier to obtain and, therefore, more commonly found in
the extensor digitorum communis than in the infraspinatus muscle. 71 Sciotti et
al. confirmed that clinicians can reliably identify latent trigger points in the tra-
pezius muscle, 87 whereas Bron et al. showed that experienced physical therapists
can reach excellent reliability with palpation of trigger points in various shoulder
muscles. 81
In spite of these studies, recent systematic reviews of the reliability of the trig-
ger point diagnosis concluded that high-quality studies are still needed to confirm
the currently used clinical diagnostic criteria in different populations. 39- 4t,43The
taut band, trigger point, and local twitch response are objective criteria, identi-
fied solely by palpation, and do not require a verbal response from the patient.
Various authors have suggested methods to objectively quantify the amount of
pressure required to elicit a painful response from a trigger point using algometry
or palpometry; however, in clinical practice it remains difficult to determine the
distinguishing features of active and latent myofascial trigger points, because both
are painful with compression. 89·90 Pressure algometry is influenced by nociceptors
in the skin and subcutaneous tissues. 91 Chen et al. confirmed the presence of taut
bands with magnetic resonance elastography, 92·93whereas Sikdar et al. used ultra-
sound imaging and vibration sonoelastography to visualize taut bands and trig-
ger points. 94•95Previous efforts to visualize trigger points with sonography were
not successful. 96·97Gerwin and Duranleau showed local twitch responses with ul-
trasound .97Other authors have suggested that extracorporeal shockwave therapy
might help clinicians confirm the presence of trigger points, but few studies have
demonstrated its validity and utility .98- 101
Although Janda maintained that systematic palpation can differentiate be-
tween myofascial taut bands and general muscle spasms, 102electromyography is
now the gold standard to differentiate taut bands from contracted muscle fibers. 103
A taut band is an endogenous localized contracture within the muscle without
activation of the motor endplate. 104 Spasms can be defined as electromyographic
activity as the result of increased neuromuscular tone of the entire muscle and are
the result of nerve-initiated contractions. From a physiological perspective, the
term contracture is more appropriate than contraction when describing chronic
involuntary shortening of a muscle without electromyographic activity. In clinical
practice, the use of electromyography as a diagnostic tool is limited primarily to
research studies. 105- 107Surface electromyography can be used in the management
of trigger points especially to assess and treat abnormal tension and dysfunctional
movement patterns. 102·108·109
The diagnostic process must include the usual differential diagnostic consid-
erations and must rule out other pathological processes. For example, in the ex-
amination of a patient with knee pain, the clinician should consider radiculopathy,
ligamentous, meniscal, and capsular injuries; patellofemoral joint dysfunction;
bursitis; tendinitis; and arthritis. The clinician must also appreciate referred pain
patterns and the biomechanical implications of taut muscle bands and myofascial
trigger points in the quadriceps, hamstrings, gluteus maximus and iliotibial band,
adductors, and calf muscles. 110 After establishing an initial diagnosis of myofascial
pain, the clinician must determine whether any mechanical, systemic, or psycho-
logical perpetuating factors are contributing to the formation or persistence of
myofascial trigger points. Major mechanical factors to be considered in the diag-

nosis and management of myofascial pain syndrome include spinal mechanical
dysfunction, anatomic variations, and poor posture . Myofascial trigger points and
taut bands may also contribute to further mechanical dysfunction.
Mechanical dysfunction is one of the main problems associated with myofas-
cial pain. Physical therapists use soft tissue and joint manipulation techniques to
correct mechanical dysfunction. Patients with soft tissue mechanical dysfunction
may also present with pertinent myofascial trigger points. For example, consider-
ing that knee joint motion is accompanied by simultaneous coactivation of the
quadriceps and hamstring muscles, any mechanical discrepancy in either muscle
group will affect the resultant joint motion and could influence joint stability.
Certain medical conditions, most notably those that affect the muscle energy
system or otherwise interfere with muscle metabolism, can interfere with recovery
from myofascial pain. 111These conditions include hypothyroidism and deficien-
cies of ferritin, folic acid, vitamin B12, and vitamin D. Less common systemic fac-
tors include gout, hypercalcemia, and infections such as recurrent Candida albi-
cans and parasitic diseases. 25Although the link between myofascial dysfunction
and these conditions has been observed empirically, scientific support is still lack-
ing .111Psychological perpetuating factors may include depression, anxiety, stress-
ful life circumstances, anger, and hopelessness. Patients with myofascial pain were
reported to have significantly more severe depression and greater difficulty with
social relationships than patients having certain other pain syndromes, such as
arthritis. 112- 115
Some authors have questioned the validity of myofascial pain or its under-
lying mechanisms. 116- 119 Quintner and Cohen suggested that all myofascial pain
phenomena are the result of secondary hyperalgesia of peripheral neural origin. 119
Ample scientific evidence from human and animal studies substantiates the ex-
istence and clinical importance of myofascial trigger points and myofascial pain.
Clinical Characteristics
In clinical settings, patients with myofascial pain usually complain of diffuse pain
confined to one or more regions of the body, as opposed to complaints of wide-
spread pain, which often accompany fibromyalgia. In some instances, patients de-
scribe sharp pain over myofascial trigger points that they can easily identify . In
other cases, the pain complaint is related to referred pain from myofascial trigger
points, and patients have difficulty locating the source of pain. Taut bands and
myofascial trigger points can be identified upon palpation. Because some patients
perceive that clinicians do not take pain complaints seriously, they may be sur-
prised when a clinician elicits a familiar pain complaint by compressing myofas-
cial trigger points. Validating a pain complaint in this manner can be an impor-
tant step in establishing a therapeutic relationship.
Myofascial pain may follow a sequence of events associated with postural
imbalances, leading to joint hypermobility or hypomobility and abnormal bio-
mechanical functioning. A prime example is the forward-head posture, a common

precursor to myofascial pain. 120 - 123 Patients with chronic myofascial pain may re-
port other symptoms associated with pain, such as sleep disturbances, fatigue, and
increased irritability. Clinical symptoms can be divided into motor and mechani-
cal dysfunction, sensory dysfunction, and autonomic dysfunction.
Motor and Mechanical Dysfunction

Both active and latent myofascial trigger points may cause dysfunction, includ-
ing restrictions in range of motion and muscle weakness. 124 In patients with acute
myofascial pain, restrictions in range of motion are due primarily to pain and
shortening of muscle fibers. In chronic cases, altered movement patterns, kinesio-
phobia, and soft tissue and joint dysfunction can further contribute to restrictions
in range of motion. 125 Muscle weakness without atrophy is often seen with myofas-
cial pain and may be due to pain, restrictions in range of motion, kinesiophobia,
inhibition of gamma motoneuron activity, or reflex inhibition of anterior horn cell
function as a result of painful sensory input. Because myofascial trigger points
may be directly related to articular dysfunction, muscles and related joints should
be considered as single functional units and examined during the initial evalua-
tion. Spinal manipulation can reduce the pressure threshold of trigger points in
the trapezius muscle. 60
Many persons with myofascial pain present with anatomical variations that
may contribute to myofascial trigger point formation. It is not unusual that a par-
ticular anatomical variation does not cause any dysfunction prior to an event that
results in the onset of myofascial pain, yet it becomes a significant factor during
the recovery. For example, a patient with a significant leg length discrepancy may
never have experienced low back pain; however, following a motor vehicle acci-
dent, the discrepancy may become a critical perpetuating factor for myofascial
trigger points in the quadratus lumborum muscle, among others. 126
According to Simons and colleagues, the most common anatomical variations
are leg length discrepancy, small hemipelvis, short upper arm syndrome, and long
second metatarsal syndrome. 32 •37 Leg length discrepancies may be due to congeni-
tal, developmental , traumatic, or pathological changes in one of the osseous links
of the lower extremity kinetic chain. In such cases, a distinction must be made be-
tween a structural and a functional leg length discrepancy. Structural discrepan-
cies are due to true anatomical differences in length of the femur or tibia, whereas
functional discrepancies can be caused by hip adductor contractures, hip capsule
tightness, unilateral innominate rotations, or poor arch support . Leg length dis-
crepancies and pelvic asymmetries may produce muscle imbalances and postural
adjustments, resulting in the development of myofascial trigger points. 127 Short
upper arms result in pronated shoulders, pectoral muscle shortening, and abnor-
mal loading of neck and trunk muscles, as the individual attempts to find a com-
fortable position when seated. Another cause of biomechanical stress on muscle
that leads to persistent myofascial trigger points is a long second metatarsal bone.
In this situation , the normal , stable tripod support of the foot created by the first
and second metatarsal bones and the heel may not occur. Instead, in some indi-
viduals with such a foot configuration, weight is carried on a knife-edge from the
second metatarsal head to the heel, overloading the peroneus longus. Clinicians
may consider the use of orthotics to correct myofascial dysfunction of the peroneal
muscles. 128 Diagnostic callus formation occurs in these individuals in the areas of
abnormal loading - that is, under the second metatarsal head and on the medial
aspect of the foot at the great toe and first metatarsal head .
Abnormal postures can result in muscle imbalances, the formation of myo-
fascial trigger points in adaptively shortened or lengthened muscles, joint hypo-
mobility and hypermobility, and nerve compression. Forward-head posture is the
most common postural deviation in patients with chronic pain, including patients
with myofascial pain. 120 •122 •123 •129•130 The biomechanical and myofascial aspects of
the forward-head posture are fully discussed in Chapter 7, "Basic Evaluation of
the Myofascial System." The following are typical symptoms in this particular
.
scenario:
•!• Intermi ttent cervical, thoracic, or lumbar pain
•!• Unilateral or bilateral headaches, including migraine and tension-type
headaches
•!• Facial pain
•!• Myofascial trigger points in multiple muscle sites
•!• Upper extremity referred pain or paresthesia in the absence of neurological
findings
•!• Difficulty sitting for a long period of time, especially in deep, soft chairs or
bucket seats that accentuate forward-head posture
•!• Pain or ache on prolonged standing
•!• Decreased pain with rest or gentle movements
Fricton, a dentist who has specialized in myofascial pain, analyzed the most
common postural problems of patients with myofascial pain in the head and neck
regions. In addition to forward-head posture, patients presented with poor tongue
position, scoliosis, abnormal lumbar lordosis, and occlusal problems. 123
Several studies have shown that occupational groups with constrained work
postures and repetitive arm movements are at increased risk for developing myo-
fascial pain. 131•132 Work tasks with high repetition frequency and static muscle
loading may actually decrease the pain pressure threshold and result in allodynia
and hyperalgesia. 133 Constrained work postures may result in decreased circu-
lation and the release of nociceptive substances directly into muscle tissue. 134• 135
Awkward postures are common in the workplace and include excessive wrist flex-
ion and extension, ulnar and radial abduction, forearm supination and pronation,
extended reaches beyond the shoulder-reach envelope, and pinch grips that are
either too wide or too narrow. 136 •137 Particular occupational groups at increased
risk include musicians, data entry operators and typists, industrial workers, and
assembly line workers. 138- 144 Andersen et al. reported the onset of myofascial pain
in various occupational groups with monotonous repetitive work 131 In a study of

patients with cumulative trauma disorders, 94.5% were diagnosed with myofascial
pain. 132 Treaster et al. observed that experienced typists developed myofascial trig-
ger points after only 30 minutes of continuous typing. 141 Piano students exhibited
significantly decreased pressure thresholds over latent trigger points in the wrist
extensor muscles after only 20 minutes of piano playing. 145 Several studies have
confirmed that trigger points are a common feature of lateral epicondylalgia. 1'1{), 147
Skubick et al. demonstrated that asymmetrical loading of the sternocleidomastoid
muscles and cervical paraspinal muscles can result in carpal tunnel syndrome. 148
A more recent study showed that 30% of patients suspected of having carpal tun-
nel syndrome presented with trigger points in the infraspinatus muscle. 67
Sensory Dysfunction
Active myofascial trigger points not only feature local pain but also refer pain to
a distant site. Vecchiet and colleagues described a significant lowering of the pain
threshold over active trigger points, not only in the muscular tissue but also in
the overlying cutaneous and subcutaneous tissues, when measured by electrical
stimulation. With latent trigger points, the sensory changes did not involve the
cutaneous and subcutaneous tissues. In patients diagnosed with fibromyalgia, hy-
peralgesia was present in all three tissues, not only over fibromyalgia tender points
but also in other nonpainful regions. 149 - 151
Several studies support the observation that active and latent trigger points
show features of peripheral sensitization as well as neuroplastic changes within
the spinal dorsal horn. 4 •152 •153 Ge et al. demonstrated that nociceptive stimulation
of latent myofascial trigger points with glutamate injections increased the occur-
rence of local muscle cramps. Nearly 93% of subjects developed muscle cramps fol-
lowing glutamate injection into latent trigger points but not into the non-trigger
point regions. Injections with isotonic saline did not produce any muscle cramps
in latent trigger points or in normal muscle tissue. The authors suggested that la-
tent trigger points may feature a focal increase in sensitivity. 154 The presence of al-
lodynia or non-nociceptive hypersensitivity at latent trigger points was confirmed
by Li et al. 155 Eleven healthy volunteers were injected with hypertonic saline, glu-
tamate, or isotonic saline into a latent trigger point. Painful injections in trigger
points induced a higher pain score than did painful injections in normal muscle
tissue. Latent trigger points with a higher pain score produced more referred pain
than did latent trigger points with a lower pain score. 155 In another study, stimu-
lation of active trigger points in the upper trapezius or levator scapulae muscles
produced contralateral local twitch responses in the same muscle in 61.5% of the
subjects, whereas stimulation of latent trigger points did not produce any contra-
lateral local twitch responses. 156 These studies of latent and active trigger points
seem to suggest that the sensitivity of latent and active trigger points may represent
a gradual spectrum. More active trigger points seem to present with more features
of peripheral and central sensitization.
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Figure 6.2 Referred pain patterns from myofascial trigger points in the infraspinatus muscle mimic
a C6 radiculopath y. Source:Reprinted with permission from Mediclip, Manual Medicine 2, version l.Oa.,
Williams & Wilkins.
Referred pain can be particularly challenging to clinicians, because the loca-

tion of pain reported by patients frequently does not match the actual cause of the
pain complaint. Headley maintained that muscle inhibition due to trigger points
is particularly common in areas of referred pain. 157 Referred pain patterns are not
necessarily restricted to single segmental pathways or to peripheral nerve distri-
butions. Although typical referred pain patterns have been established, there is
considerable variation across patients 32,37,iss (Figures 6.1 and 6.2).
Usually, the pain in reference zones is described as "deep tissue pain" of a
dull and aching nature. The term referredpain is not entirely accurate. Patients do
not always experience pain but may feel other referred paresthesia , such as burn-
ing or tingling sensations. 32·37·159- 164 Referred paresthesia may also mimic or be
responsible for other pain problems, such as tinnitus, tension-type headaches, and
migraines. 70·153·161·165Mechanically stimulating an active trigger point may repro-
duce a patient's symptoms, either immediately or after a delay of up to 15 seconds.
Mechanical stimulation can consist of manual pressure, needling of the trigger
point, movement of the involved body region, and postural strains, such as for-
ward-head posture or pressure on the gluteal muscles in sitting . Pain following
pressure stimulation is probably due to the simultaneous activation of cutaneous
and muscle nociceptors. 166 Even physiological muscle tone at rest may stimulate
an active trigger point, indicative of hypersensitivity of the nervous system. Nor-
mally, skeletal muscle nociceptors require intense stimulation and do not respond
to moderate local pressure, contractions, or muscle stretches. 167·168It is important
to note that referred pain is not specific to myofascial trigger points; however, it is
more common and much easier to elicit over trigger points. 169Normal muscle tis-
sue and other body tissues, such as skin, fascia, zygapophyseal joints, and internal
organs, may also refer pain to distant regions, making referred pain elicited by
stimulation of a tender location a nonspecific finding. 170- 176
It is important that clinicians be familiar with the referred pain patterns of
trigger points. During the history taking, clinicians will be directed to the involved
muscles based on the location of the subjective pain complaint. For example, when
patients complain of pain or paresthesia down the arm, the clinician should not
only consider possible nerve root involvement but also immediately consider trig-
ger points in the scalene muscles; the shoulder muscles, including the rotator
cuff muscles and the pectoralis minor muscle 177- 181; and the arm muscles. 146•182,183
Knowledge of referred pain patterns is also relevant for the development of a treat-
ment plan. Treatment of trigger points in the infraspinatus muscle can inactivate
trigger points in the anterior deltoid and wrist extensors. 184 Trigger points in the
masseter muscle can be treated by deactivating trigger points in the trapezius mus-
cle.185General facial pain can be due to trigger points in the sternocleidomastoid,
masseter, temporalis, or trapezius muscles, 185- 191whereas pain down the leg could
originate in the gluteal muscles. 178
Autonomi c Dysf unction

Autonomic phenomena associated with trigger points may include vascular
changes; secretory, pilomotor, and trophic changes; ptosis; changes in skin tem-
perature; and hypersecretion. 171·192 Autonomic changes are not specific for myo-
fascial pain, because most pain syndromes have an autonomic component. Tro-
phic changes may lead to the development of so-called satellite trigger points in
the area of referred pain. 32·184The autonomic aspects of trigger points have not
been subjected to many scientific studies. Shultz et al. observed a higher elec-
trical resistance of the skin overlying trigger points than of tissue not overlying
trigger points, which may indicate an autonomic component to the trigger point
Muscle Pain Syn dromes 139
phenomena. 193 Zhang et al. noted an attenuated skin blood flow response after
painful stimulation of latent trigger points compared with normal muscle tissue ,
indicating increased sympathetic vasoconstriction at the location of latent trigger
points. 194 Increasing sympathetic flow via breath-holding also raised the electrical
activity of trigger points. 195 Sympathetic hyperactivity at trigger points was con-
firmed by Ge et al.192 In their study of patients with unilateral shoulder pain , they
observed that an increased sympathetic outflow to muscles decreased the pressure
pain threshold following mechanical stimulation of trigger points. An increase
of intrathoracic pressure increased local and referred pain intensities. 192 Psycho-
logical arousal or stress significantly increased the electrical activity of myofascial
trigger points , whereas autogenic relaxation and the administration of the sympa-
thetic blocking agent phentolamine reduced the activit y, which seems to indicate
that trigger points are indeed associated with the autonomic nervous system. 196 - 199
Pathogenesis
Research has advanced the study of myofascial trigger points considerably. Hu-
man and animal studies have confirmed that trigger points have a specific electri-
cal discharge , as Weeks and Travell established in 1957.105 - 107, 199 - 210 The electrical
activity is a local phenomenon , which is not mediated through the spine or supra-
spinal influences. 203 Simons and colleagues reported action potentials of 10-50
µV and intermittent biphasic spikes of 100-600 µV, and they established that the
electrical activity of trigger points is in fact endplate noise resulting from an exces-
sive release of acetylcholine at the motor endplate. 101,209 ,210 In 1956, Liley described
the spontaneous electrical activity that occurs at the motor endplate ,211 which was
confirmed in 1970 by Wiederholt. 212 Endplate noise is an indication of the irrita-
bility of trigger points 107 but is also an expression of sympathetic dysfunction. 195
Several researchers have explored the effect of therapeutic interventions on end-
plate noise . For example , laser treatments to trigger points in the biceps femoris of
rabbits reduced the endplate noise significantly in one study. 105
A motor endplate is the synapse between the terminal ends of motor neurons
and skeletal muscle. The terminal branches of a single motor neuron end in multi-
ple presynaptic boutons. 213 For an understanding of the role of the motor endplate
in the pathogenesis of trigger points , a brief review of normal muscle physiology
is required .214
Normal Muscle Contraction

Following an a-motor neuron nerve impulse and subsequent depolarization of the
nerve cell membrane , voltage-gated Ca 2+ channels are opened , which causes an
influx of Ca 2+ and a quantal release of acetylcholine , adenosine triphosphate , and
other molecules into the synaptic cleft. Acetylcholine release is also modulated by
the concentration of acetylcholinesterase , which under normal circumstances hy-
drolyzes acetylcholine into acetate and choline. When two acetylcholine molecules
bind to a nicotinic acetylcholine receptor across the synaptic cleft in the muscle ,
the receptor opens a ligand-gated cation channel, which in turn facilitates a so-
dium (Na+) influx and a potassium (K+)efflux across the muscle cell membrane.
Each single quantum of acetylcholine depolarizes the postsynaptic cell and triggers
a miniature endplate potential. A sufficient number of miniature endplate poten-
tials will produce a depolarization and an action potential, which travels along the
T-tubules, triggers the dihydropyridine and ryanodine receptors in the sarcoplas-
mic reticulum, and causes a release of Ca 2+ from the sarcoplasmic reticulum.
Ca 2+triggers a shift in position of tropomyosin in the muscle sarcomere, which
exposes the myosin-actin binding sites, leading to the formation of cross-bridges
and muscle contractions. The release of cross-bridges is dependent on adenosine
triphosphate. Other proteins, including titin, nebulin, troponin, tropomodu-
lin, and desmin, also play significant roles. Titin is the largest known vertebrate
protein and connects myosin filaments to the Z-line with cross-links to other
sarcomeres. Titin is also linked to actin via its so-called PEVK segment, which
is thought to limit the degree of muscle contraction, because myosin filaments
are caught against this "viscous bumper." The myosin filaments, therefore, are
somewhat comparable to a drag net. 215- 219One interesting feature of titin is that
during sarcomere contractions, titin filaments are folded into a sticky gel on the
Z-line, which unfolds into a springlike structure during muscle elongation. 215·216•219
Nebulin inhibits cross-bridge formation until actin is activated by Ca 2+. Nebulin
is linked to desmin and myopalladin and contributes to cytoskeletal stability and
integrity. 220-224
Trigger Point Contractures

In 1981, Simons and Travell developed the "energy crisis hypothesis" to explain the
pathogenesis of trigger points. 32The ongoing contractures compromise the local
circulation and reduce the oxygen supply, triggering several vicious cycles. The
oxygen saturation in a trigger point is far below normal levels, 225which leads to
hypoxia, a decrease in pH, and hypoperfusion. 226-228In addition, the production
of adenosine triphosphate will be impaired, because its production is oxygen de-
pendent. The lack of adenosine triphosphate not only maintains the actin-myosin
cross-bridges and the contractures but also leads to an increase of acetylcholine, a
failure of the calcium pump, increased levels of Ca 2+, and a Ca 2+-induced Ca 2+ re-
lease.104•229The increase in Ca 2+ is another feedback mechanism, which reinforces
the muscle contractures. Termination of a muscle contraction is normally accom-
plished by pumping Ca 2+ back into the sarcoplasmic reticulum against a large con-
centration gradient. With an impaired calcium pump, the intracellular calcium
concentration stays elevated, and the actin and myosin filaments become continu-
ously activated. 229Shenoi and Nagler confirmed that an impaired reuptake of cal-
cium into the sarcoplasmic reticulum can cause myofascial trigger points. They
reported that calcium channel blockers caused myofascial trigger points, presum-
ably based on their ability to prevent calcium reuptake. 230Increased Ca 2+ may also
damage the mitochondria, leading to ragged red fibers, which have been observed
in trigger points. 231•232 In biopsy studies of myofascial trigger points, Gariphianova

described pathological changes, including a decrease in the quantity of mitochon-
dria, possibly indicating metabolic distress. 233
Hypoxia contributes to several other vicious cycles. It leads to an acidic milieu,
muscle damage, and an excessive local release of multiple nociceptive substances,
including calcitonin gene - related peptide, bradykinin, and substance P.234 Hy-
poxia may also trigger an immediate increased acetylcholine release at the motor
endplate. 235 Calcitonin gene- related peptide enhances the release of acetylcho-
line from the motor endplate, decreases the effectiveness of acetylcholinesterase,
and sensitizes the nicotinic receptors. An acidic pH enhances the release of cal-
citonin gene- related peptide and down-regulates acetylcholinesterase and causes
hyperalgesia .236 - 238
When Simons and Travell developed the energy crisis hypothesis, the impaired
calcium pump was an essential component. 32 More recently, the energy crisis hy-
pothesis was further developed into the "integrated trigger point hypothesis,"
which incorporates more recent research including insights from the pain sci-
ences. 32 Several authors have since expanded the integrated trigger point hypoth-
esis. 236 •239•240 A key aspect of the current thinking about the pathogenesis of trigger
points is the presence of excessive acetylcholine at the motor endplate, which has
been confirmed by human and animal studies. 105 - to7, 199 - 210 The surplus of acetyl-
choline results in a constant activation of the muscle contractile system. Excessive
acetylcholine can be due to an insufficiency of acetylcholinesterase, an acidic pH,
hypoxia, a lack of adenosine phosphate, and certain genetic mutations. 235 •236 •24 0
Drugs and particular chemicals, such as calcitonin gene - related peptide, diisopro-
pyl fluorophosphate, or organophosphate pesticides, and an increased sensitivity
of the nicotinic acetylcholine receptors across the synaptic cleft can also lead to ex-
cessive levels of acetylcholine. 235 •236 •24 0 Increasing evidence suggests that injections
with botulinum toxin are effective in deactivating myofascial trigger points. This
evidence, in turn, supports the idea that at least part of the problem may be due
to excessive levels of acetylcholine and a dysfunctional motor endplate. 205 ,24 1- 245
Botulinum toxin is a neurotoxin that blocks the release of acetylcholine from pre-
synaptic cholinergic nerve endings. 246 In addition, botulinum toxin has an anti-
nociceptive effect, blocking the release of calcitonin gene - related peptide from the
nerve terminal. 241,247,248 In a rodent study, the administration of botulinum toxin
resulted in a complete functional repair of dysfunctional endplates. 249
Dommerholt and Shah suggested that at the sarcomere level, myosin filaments
may actually break through the actin - titin barrier because of the excessive ace-
tylcholine levels.250 It is then also conceivable that the myosin filaments may be-
come mired in the sticky substance of titin, which may explain why stretching taut
bands with active trigger points is usually ineffective .251 When actin and myosin
filaments are maximally contractured at the trigger point, the I-band of the sar-
comere would no longer be present. Several histological studies have confirmed
this absence. 252 •253 Fassbender observed degenerative changes of the I-bands, in
addition to capillary damage, a focal accumulation of glycogen, and a disintegra-

tion of the myofibrillar network. 254 Gerwin and colleagues suggested that the most
likely mechanisms leading to trigger point formation are eccentric contractions
in unconditioned muscle, unaccustomed eccentric contractions, (sub)maximal
concentric contractions, low-level contractions, uneven intramuscular pressure
distributions, and direct trauma. 5 •255 Eccentric loading has also been linked to the
development of trigger points. 256 The recruitment of muscle fiber during low-level
contractions follows stereotypical patterns in most subjects, with smaller motor
units recruited before and derecruited after larger motor units. 257- 259 Such low-
level contractions result in muscle fiber degeneration, an increase in the release
of Ca 2+ and cytokines, and energy depletion, which are known patterns for the
development of trigger points. 260 - 264 This model, which Hagg called the Cinderella
hypothesis, is indeed applicable to the formation of trigger points. 141•257
Peripheral and Central Sensitization

Information from the pain sciences contributes to understanding of the nature
of myofascial trigger points. Muscles have specific nociceptors for a wide range of
substances, including prostaglandins, protons, serotonin, bradykinin, adenosine
triphosphate, and glutamate, among others. These receptors are dynamic in nature
and can be activated mechanically and chemically. 265 Following noxious stimula-
tion, the receptors release several neuropeptides, including substance P and calci-
tonin gene-related peptide, which stimulate vasodilatation and increase the local
microvasculature. 266 •267 Vasodilatation leads to activation of mechanoreceptors
and increased sensitivity of the receptor. 15•268 In addition, the neuropeptides trig-
ger the release of several other substances, including histamine, bradykinin, sero-
tonin, and prostaglandins. 269 Many harmful cycles exist, whereby nociceptive sub-
stances keep stimulating receptors, leading to more release of other nociceptors.
Bradykinin, serotonin, and prostaglandins are the most important substances re-
sponsible for muscle pain. When present in combination, these substances produce
more pain than when present individually. 270 Interestingl y, the receptor sensitivity
varies depending on the presence and concentration of nociceptive substances. 271
An ongoing barrage of nociceptive afferent from trigger points into the dorsal
horn can alter the responsiveness of the dorsal horn and lead to increased local
pain or referred pain to other spinal cord segments. Persistent nociceptive activity
is a prerequisite for dorsal horn changes. 272 Trigger points are not the only source
of afferent nociceptive input. Afferent barrage from joints, skin, and viscera can
also result in central sensitization by the unmasking of "sleeping" receptors and
low-threshold mechanosensitive neurons. 159•273 - 275 The afferent input from these
newly effective receptors may result in spatial summation in the dorsal horn and
the appearance of new receptive fields. This means input from previously ineffec-
tive regions can now stimulate the neurons. 152•276 These changes in the dorsal horn
explain the allodynia of a myofascial trigger point. Changes in the dorsal horn and
peripheral sensitization can cause hyperalgesia.
Gunn maintains that myofascial pain is not dependent on nociceptive input. 30

According to Gunn, the symptoms of myofascial pain are explained entirely by
functional deficiencies of the peripheral nervous system. Gunn's hypothesis con-
tradicts the many scientific studies that have confirmed the nociceptive nature of
active and latent myofascial trigger points. 151,152,154,155,180, 194,275
The modified convergence projection theory proposed by Mense is based
on the pathophysiological unmasking process of interneurons within the dorsal
horn. 152•162 After identifying an original receptive field of the biceps femoris muscle
of a rat, Mense injected a painful dose of bradykinin in the tibialis anterior mus-
cle. Bradykinin levels have been shown to increase during pain, ischemia, static
muscle contractions, and inflammation. The effects of bradykinin injections on
the dorsal horn show similarities with the effects of myofascial trigger points. 152•162
The activity of the neuron corresponding with the receptive field was measured by
an electrode placed in the spinal cord. After 5 minutes, the original receptive field
had expanded; after 15 minutes, the original receptive field no longer responded
only to painful stimuli but also to moderate mechanical stimuli. Because the in-
terneurons are located over various segments, pain may be experienced in regions
outside the segmental innervation of the myofascial trigger point, which distin-
guishes Mense's hypothesis from the conventional convergence theory. 2n Tem-
poral summation is also clinically relevant in widespread pain condition. 166 This
mechanism may result in the formation of satellite trigger points in the area of the
enlarged receptive field. 5•184 The temporal delay observed in the onset of referred
pain is probably the result of the time needed to unmask interneurons with sub-
stance P and glutamate. It is likely that a similar process exists for craniomandibu-
lar muscles, even though they do not receive input from the spinal cord. 17.278- 280
New or enlarged receptive fields were identified after injection of mustard oil in
the masseter muscle. 278 The modified convergence projection theory offers a con-
ceivable model for the referred pain phenomena seen in myofascial pain and has
been confirmed in many recent studies of patients with tension-type headaches
and migraines. 4 •56 •69•153•160,161,191,192,281•282 Pain in the elbow, commonly referred to
as epicondylitis, or tennis elbow, may in fact be due to trigger points in shoulder
or arm muscles. 146•184 Patients with osteoarthritis of the hip and knee had signifi-
cantly more trigger points in the muscles crossing these joints than did healthy
controls. 50•57 Patients with pelvic floor pain have more trigger points in the ab-
dominal muscles, gluteal muscles, and hip adductors. 283 - 286
One of the most important studies conducted in the past decade originates
from the National Institutes of Health, in which Shah and colleagues analyzed
the local biochemical milieu of trigger points using a sophisticated microdialy-
sis system capable of collecting small volumes of approximately 0.5 µ L and sub-
nanogram sizes smaller than 75 kDa. 228 The researchers found significantly higher
concentrations of many chemicals in the immediate vicinity of active trigger
points when compared to latent trigger points and normal muscle tissue; these
chemicals included substance P, calcitonin gene-related peptide, bradykinin,
serotonin, norepinephrine, tumor necrosis factor-a, and interleukin-la. The lo-

cal environment of active trigger points was also significantly more acidic. 228 A
lower pH can modify the threshold sensitivity of nociceptors for prolonged peri-
ods of time without any evidence of tissue damage. 237•287 A low pH also inhibits
acetylcholinesterase, which would increase the levels of acetylcholine and support
the development of taut bands and trigger points. 236 A second study by Shah and
colleagues confirmed and expanded the results of their first study. In addition,
the researchers found increased levels of interleukin-6 and interleukin-8 in the
trapezius muscle, but slightly increased levels of all the analytes in the gastrocne-
mius muscle. 227•288 The importance of many of these substances and their effect on
neuroplastic changes in the dorsal horn have already been discussed. Cytokines
play a significant role in pain mechanisms, muscle hyperalgesia, and muscle injury
repair. 289 - 296 Again, there are many feedback loops in between these chemicals.
It is beyond the scope of this chapter to provide a more detailed analysis of the
relevancy of all the analytes. The interested reader is referred to the pain science
literature on the same topic. 250
Several studies have established that muscle pain, including pain from trigger
points, activates particular cortical structures. 14 Electrical stimulation and com-
pression of trigger points in the trapezius muscle resulted in enhanced brain activ-
ity in somatosensory and limbic regions, including the anterior cingulate cortex,
while suppressed activity was noted in the hippocampus. 13•297 The anterior cingu-
late cortex is also involved with the emotional, affective component of pain, which
may indicate possible links between muscle pain and stress-related changes. 14
Autonomic Aspects
The etiology of the autonomic aspects of trigger points has not been fully explored.
Based on studies of the impact of psychological arousal on the electrical activity
of trigger points, Hubbard suggested that myofascial trigger points may be due to
dysfunctional muscle spindles, 197 an opinion shared by Partanen and colleagues
as recently as 2009.298 •299 They maintained that the endplate spikes are action po-
tentials of intrafusal muscle fibers and that the "active spots" are in fact muscle
spindles. Simons et al. refuted this, however, by demonstrating that the spike po-
tentials are propagated by extrafusal muscle fibers and not by intrafusal fibers. 27
Liley showed, as early as 1956, that the spontaneous electrical activity is a conse-
quence of the release of acetylcholine at motor endplates. 211
Direct connections between the sympathetic nervous system and muscle fi-
bers have been established and may be critical for future studies. 300 - 302 In 1981,
Barker and Saito demonstrated that some extrafusal muscle fibers are autonomi-
cally innervated. 303 Ljung et al. demonstrated that the extensor carpi radialis bre-
vis muscle is supplied with heterogeneously distributed sympathetic and sensory
innervations in relation to small blood vessels. 304 Viscero-autonomic afferent input
may also trigger point formation via viscero-somatic reflexes.240 The research by
Shah and colleagues found increased levels of norepinephrine and serotonin in the
immediate milieu of active trigger points, which may be associated with increased
autonomic activity in the motor endplate of trigger points. 227•228 Intramuscular
injections of the a-adrenergic antagonist phentolamine decreased endplate noise
from trigger spots in rabbits, whereas the acetylcholine antagonist curare had no
impact. 199 Injections of serotonin antagonists also reduced pain levels significantly
when compared to injections of anesthetics. 305 •306 Gerwin et al. suggested that
a- and /3-adrenergic receptors at the motor endplate may provide a possible mech-
anism for autonomic interactions, 255 which in rodents increased the release of ace-
tylcholine after stimulation. 307
Management of Myofascial Pain

The goals for treatment of myofascial pain are restoration of normal tissue mobil-
ity by deactivating myofascial trigger points and facilitating a return to function.
As with any treatment plan addressing pain problems, the treatment plan can be
divided into a pain-control phase and a training, or conditioning, phase. 5 Dur-
ing the pain-control phase, the emphasis is on reducing the nociceptive aspects
of trigger points through deactivating clinically relevant active and latent myo-
fascial trigger points. Physical therapists may employ manual trigger point
therapy, physical therapy dry needling, or trigger point injections where legally
allowed. They may also employ other manual therapy interventions, breathing ex-
ercises, relaxation therapy, electrotherapeutic modalities, early posture training,
and physical conditioning. During the conditioning phase, the emphasis shifts to
further improving physical functioning, core stability, cardiovascular endurance,
and aerobic conditioning. Trigger point therapy is always part of a broader treat-
ment approach. 5 A recent paper defined clinical prediction rules to assist in identi-
fying patients with chronic tension-type headaches who are likely to benefit from
trigger point therapy. 308
Manual therapy is one of the basic treatment options for myofascial pain. 309
Therapists may perform manual techniques using manual palpation and pressure
application or by inserting a solid filament needle into a trigger point to evoke a
local twitch response, known as physical therapy dry needling. Physical therapists
use dry needling in Australia, Belgium, Canada, Chile, Denmark, Ireland , the
Netherlands, New Zealand, Norway, South Africa, Spain, and the United King-
dom, among other countries. As of August 2009, physical therapy dry needling
was noted to be formally within the scope of physical therapy practice in 12 U.S.
states: Alabama, Colorado, Georgia, Kentucky, Maryland, New Hampshire, New
Mexico, Ohio, Oregon, South Carolina, Texas, and Virginia. Maryland also allows
physical therapists to administer trigger point injections. 309 Physical therapy dry
needling is a form of mechanical stimulation. The mechanical effects of physical
therapy dry needling and injection therapies for trigger points were established
in 1944.310 Physical therapy societies and associations around the world, includ-
ing Australia, Canada, Ireland , the Netherlands, and New Zealand, among oth-
ers, have acknowledged that physical therapy dry needling is within the scope of
physical therapy practice. In spring 2009, the Executive Committee of the Ameri-
can Academy of Orthopaedic Manual Physical Therapy endorsed the practice of
physical therapy dry needling. Despite the widespread acceptance and the body of
research documenting its efficacy, the American Physical Therapy Association has
not yet endorsed dry needling by physical therapists but does not find the practice
inconsistent with its "Guide to Physical Therapy Practice." 8
The underlying mechanisms of physical therapy dry needling are still not en-
tirely understood. Physical therapy dry needling can change the chemical environ-
ment of trigger points and may restore normal functioning of acetylcholinesterase
and the acetylcholine receptors as part of muscle regenerative processes. 227•228 •311•312
Superficial physical therapy dry needling, which involves placing a needle into the
tissues overlying a trigger point at a depth of no more than 5-10 mm, may involve
stimulation of Aofibers when the needle is manipulated, release oxytocin, acti-
vate mechanoreceptors coupled with C-fiber afferents, or stimulate the anterior
cingulate cortex. 13•297•313 - 317 It is likely that physical therapy dry needling directed
at myofascial trigger points involves central pain mechanisms, but to date there is
no direct evidence. Hui et al. reported specific changes in the limbic system and
subcortical gray structures following acupuncture needling. 318
Several other studies have implicated the limbic system. 319 - 322 Takeshige and
colleagues confirmed that treatment of acupuncture and nonacupuncture points
involved the descending inhibitory system. 323 •324 Research of the mechanisms of
physical therapy dry needling techniques is still in the beginning stages.
No form of myofascial trigger point treatment should be offered as a stand-
alone intervention. Clinicians should avoid learning and using physical therapy
dry needling, or any other type of treatment, as a quick trick. Physical therapy
dry needling, as well as manual myofascial trigger point release, is better imple-
mented as one part of a comprehensive management plan. Although some patients
may express initial reluctance regarding physical therapy dry needling, many will
be encouraged to learn that the techniques can inhibit nociceptive input, often
within a few treatment sessions. Any intervention that causes extreme anxiety for
a patient, however, may not be the preferred initial choice of treatment. 153•325 - 333
Several studies support using soft tissue manipulation techniques either instead
of or in conjunction with physical therapy dry needling. 44 •334 - 341 The practitioner
must evaluate and, when indicated, treat both soft tissue and joint dysfunctions. 60
The intratissue and intertissue mobility of the functional unit must be evaluated
and treated as well.
In states that prevent the use of physical therapy dry needling, other interven-
tions may be used. Effective soft tissue techniques include myofascial manipula-
tion, massage therapy techniques, sustained pressure over the myofascial trigger
point, trigger point release with a microstimulation applicator, stretch and spray
techniques combined with postisometric relaxation, or muscle energy/hold - relax
techniques. 44, 334- 340
A trigger point release involves sustained pressure applied to the myofascial
trigger point using a flat palpation or pincer grip while the patient performs gentle
muscle contraction. This technique is commonly used, and its effectiveness is

based on the endplate (integrated) hypothesis, which states that sarcomeres within
the trigger point are hypercontracted and are transmitting increased resting ten-
sion through the neighboring sarcomeres. 309The gentle pressure as applied to the
myofascial trigger point is held while the patient is asked to repeatedly and gently
contract and relax the muscle until the tension is released and the pain and nod-
ule are reduced, indicating a resetting of the sarcomere length (several sections in
Chapter 8, "Atlas of Therapeutic Techniques," describe trigger point release tech-
niques). 309Trigger point releases should always be followed up with a gentle 30- to
60-second stretch to the involved muscle. It may also be followed up with general
myofascial manipulation to both the muscle released and its surrounding muscu-
lature as part of a comprehensive rehabilitation plan.
Physical therapy dry needling is not without risk and requires training and
a thorough knowledge of anatomy, indications, and contraindications. 309It has
been practiced at least since 1979, and few adverse effects have been reported, other
than minor complications such as posttreatment soreness and minor hematomas.
The main risk of physical therapy dry needling is pneumothorax, which has rarely
been reported. However, considering the number of physical therapists using
physical therapy dry needling and the number of acupuncturists and physicians
using similar techniques in their practices worldwide, the risk of pneumothorax
is very small .
The scientific support of physical therapy dry needling is growing. 309Shah
and colleagues established that causing a local twitch response with a solid fila-
ment needle can reduce the concentrations of several nociceptive substances in
the immediate environment of active trigger points. 227 ·228·288 A Cochrane review
supported the use of physical therapy dry needling in the treatment of patients
with chronic low back pain. 342Physical therapy dry needling applied to myofascial
trigger points reduced the sensitivity of more distal trigger points. 184Interestingly,
treatment of myofascial trigger points in the extensor carpi radialis longus muscle
or of acupuncture points in the arm also reduced the sensitivity of trigger points in
the trapezius muscle. 343•344Physical therapy dry needling can easily be combined
with electrotherapy, but little scientific guidance exists for the optimal treatment
parameters. 309,345,346
In addition to treating trigger points in peripheral muscles, Gunn advocated
evaluating and treating the paraspinal muscles at the levels of segmental innerva-
tion. 30A recent study confirmed that the combination of treating multifidi mus-
cles and peripheral muscles was slightly more effective than treating only trigger
points in peripheral muscles. 330To address hypoxia at the trigger point site, it is
important to improve the local circulation, which will contribute to decrease any
abnormal nociceptive input, and to restore optimal movement patterns.
Physical therapists (only in Maryland) and physicians may elect to use trigger
point injections. The mechanisms and outcome of physical therapy dry needling
and trigger point injections are equally effective. 42•45•78·309·331·346•347Injectables in-
clude procaine hydrochloride and lidocaine . Because procaine is no longer widely
available , a 0.25% lidocaine solution is recommended and was found to be more

effective than stronger solutions. 348 •349 There is no scientific support for using in-
jections with vitamin B12 , steroid, or nonsteroidal anti-inflammatories. Steroid in-
jections may induce myopathy. There is theoretical support for trigger point injec-
tions with bee venom, but no clinical outcome studies have been reported. 350 Bee
venom may activate brainstem catecholaminergic neurons and a2 adrenergic and
serotonergic pathways of the descending inhibitory system. 351- 353 Injections with
serotonin antagonists and botulinum toxin have shown positive results in several
studies. 242 •244 •245 •305 ,306 ,355 •356 However, injectable serotonin antagonists are not uni-
versally available . Some studies suggest that physical therapy dry needling would
cause more posttreatment soreness, but when injections are compared with physi-
cal therapy dry needling using a solid filament needle, there were no significant
differences. 78,331,347
There is limited support for the use of modalities in the treatment of myofas-
cial trigger points. Comparing laser, ultrasound, transcutaneous electrical nerve
stimulation, and other forms of electrotherapy, laser proved to be the most effec-
tive modality. 44 •105 •338 •356 - 366 Extracorporeal shockwave therapy reduced pain levels
and improved isokinetic force production in one randomized controlled study. 100
Correcting structural and functional discrepancies may require specific mus-
cle stretches, neurodynamic manipulations, joint manipulations, orthotics, or
postural reeducation. Patients with chronic myofascial pain usually present with
poor postures and muscle imbalances, with both adaptively shortened and length-
ened muscles. Strengthening shortened muscles will not correct muscular imbal-
ances and abnormal posture, and doing so may cause further aggravation of active
myofascial trigger points, as well as increase pain and dysfunction . Overstretching
must be avoided because it may stimulate myofascial trigger points. Before isotonic
training and conditioning programs can be initiated, abnormal postures must be
corrected . During the pain control phase of the program, patients can correct their
postures and muscle imbalances by gently stretching shortened muscles, improv-
ing neural mobility, and restoring basic function. Correction and prevention of
abnormal postures require a comprehensive program that includes exercises to re-
store normal dynamic vertebral stabilization and mobility, motor control, muscle
balances, strength, endurance, and breathing patterns. Many patients are aero-
bically deconditioned, which, combined with poor posture, may cause adaptive
shortening of the auxiliary respiratory muscles, such as the scalenes; restricted
chest expansions; and paradoxical breathing. Paradoxical breathing should be
corrected with functional abdominal breathing. 367
Certain work tasks or activities of daily living may predispose a patient to
chronic musculoskeletal overload, increasing the risk of myofascial dysfunction.
Considering activity-related aspects of myofascial pain will enhance treatment
outcomes. Modifying the workplace or the patient's work habits can be critical . If
a patient continues to be exposed to certain workplace or other stress factors with-
out modification of the conditions, the potential cause of myofascial dysfunction
may not be addressed adequately .
Throughout the treatment process, much attention should be paid to edu-

cating the patient regarding the etiology of pain, perpetuating factors, and self-
management. In working with patients with chronic myofascial pain, the clinician
must assess and address psychosocial issues. Patients must learn to modify their
behaviors and avoid overloading the muscles without resorting to total inactivity.
Fibromyalgia
Definition
Fibromyalgia, initially labeled fibrositis, was believed to be a connective tissue dis-
order and type of muscular rheumatism. 368 The term fibromyalgia was later in-
troduced when it became increasingly apparent that no inflammation ("itis") was
°
associated with the connective tissue, only pain ("algia").369 •37 Fibromyalgia syn-
drome (FMS) is often diagnosed by using inclusion criteria set forth by the Ameri-
can College of Rheumatology (ACR).48 Although the word fibromyalgia is sugges-
tive of a musculoskeletal syndrome limited to fibrous and muscular tissues, it is
now defined as a medical condition, characterized and defined by the hallmark
of chronic widespread nonarticular musculoskeletal pain. 371 It is a diffuse central
nervous system disorder with pain and dysfunctional sensory processing. 26 It af-
fects nearly 2% of the U.S. population, occurs in women 10 times more frequently
than in men (3.4% female vs. 0. 5% male), and is usually diagnosed between ages 20
and 50 but has been observed in both younger and older individuals. 372 Annual
treatment costs in 1996 averaged $2,275.00 per patient. 373
Diagnosis
FMS is an idiopathic, chronic condition characterized by widespread, diffuse pain,
including above and/or below the waist and on the right and/or left sides of the
body, as well as multiple tender points. 48 •374- 376 In 1990, the ACR defined fibromy-
algia using two classification criteria. These criteria have since become readily ac-
cepted as diagnostic, even though their validity and reliability for clinical practice
have not been established. 25 •48 The first is a history of chronic, widespread, diffuse
pain lasting longer than 3 months, and the second is pain elicited in at least 11 of
18 identifiable but arbitrarily selected tender points using a palpatory force of 4 kg
per unit area. 48 The tender points sites include the following nine paired locations
(Figure 6.3):
Occiput:Bilateral, at the suboccipital muscle insertions
Low cervical:Bilateral, at the anterior aspects of the intertransverse spaces at
C5- C7: under 5 cm
Trapezius: Bilateral, at the midpoint of the upper border
Supraspinatus: Bilateral, at origins, above the scapula spine near the medial
border
Second rib: Bilateral, at the second costochondral junctions, just lateral to the
junctions on upper surfaces
Lateral epicondyle:Bilateral, 2 cm distal to the epicondyles

Gluteal:Bilateral, in upper outer quadrants of buttocks in anterior fold of
muscle
Greater trochanter:Bilateral, posterior to the trochanteric prominence
Knee:Bilateral, at the medial fat pad proximal to the joint line
A third complaint often noted but not part of the classification criteria is sleep
disturbance, with patients reporting fatigue even after waking. 3n - 379
A proper diagnosis is most important when examining patients with symp-
toms commonly attributed to FMS. Physicians who still rely solely on a simplistic
Insertion of
the subocci pital
Under the muscle
lower sternomastoid
muscle
~
.....
•
-
l'
\
,,_ ·'
Origin of the Mid upper
Near the supraspinatus trapezius muscle
second costochondral muscle
junction
2 cm distal
to the lateral
epicondyle l
I
,
I
Upper outer
quadrant of
At the prominence
the buttock
of the greater I At the \
trochanter medial
lat pad
of the
knee
1'
Figure 6.3 Fibrom yalgia tender points. Source:Reprinted with permission. D. L. Goldenberg. Diagnos-
tic and Therapeutic Challenges ofFibrom yalgia, Hospital Practices1989, Vol. 24, No. 9A, p. 39. © 1989
McGra w-Hill Companies. Illustration by Laura Dupre y.
tender point count will not be able to distinguish FMS from other chronic wide-
spread pain syndromes with similar symptoms, such as hypothyroidism, disturbed
sleep, growth hormone deficiency, metabolic insufficiencies, myofascial pain, my-
algias secondary to medication use, irritable bowel syndrome, nonulcer dyspepsia,
esophageal dysmotility, parasitic infestations, myoadenylate deaminase deficiency,
chronic prostatitis, vulvodynia, rheumatic and infectious diseases, psychological
diagnoses, hypermobility syndrome, and whiplash syndrome, among others. 25 •380
Tenderness assessed by the tender point count does not distinguish FMS from
other pain syndromes but may be an indication of allodynia, hyperalgesia, or pe-
ripheral and central sensitization. 381- 383 When a diagnosis of FMS is seen as an end
point rather than an opportunity to explore what may be causing the widespread
pain and associated symptoms, the established medical differential diagnostic
process is not applied. Although the FMS criteria state that the diagnosis is one of
inclusion, which should be made irrespective of other diagnoses, common sense
dictates that a physician would need to exclude other possible diagnoses to make a
diagnosis of FMS. In other words, FMS is actually a diagnosis of exclusion. 25 The
widespread nature of FMS is not sufficient to make the diagnosis. Using a tender
point count to establish the widespread nature of a particular pain problem may
lead to many false positives. 384 - 386 Localized musculoskeletal pain is relatively rare
and usually coexists with pain in other body regions.
Patients diagnosed with FMS commonly present with considerable comor-
bidities, including headaches, 48•387 anxiety and depression, 374 •388 - 391 irritable bowel
syndrome, 377•392 •393 and a number of other ailments, making the differential diag-
nosis extremely difficult when using the established classification criteria alone.
This is especially true when considering the extent to which symptoms overlap
with those of chronic fatigue syndrome and other chronic pain conditions. Both
FMS and chronic fatigue syndrome share symptoms of muscle pain, sleep distur-
bance, fatigue, cognitive dysfunction, abdominal pain, muscle weakness, reduced
activity, and migratory arthralgias. 378•394 Both are chronic pain disorders believed
to have an underlying central nervous system abnormality, although some chemi-
cal differences have been shown. Immunological dysregulations, such as the ab-
normal 2'-5' oligoadenylate (2-SA) synthetase/RNase L pathway, have been de-
tected in patients with chronic fatigue syndrome, but never in those diagnosed
with FMS.394•395 Patients with chronic fatigue syndrome also show significantly
lower blood perfusion in the brainstem compared with controls. 394 Of most inter-
est is the difference in levels of substance P. Those diagnosed with FMS or FMS and
chronic fatigue syndrome combined have elevated levels of substance P, whereas
those diagnosed with chronic fatigue syndrome alone do not. 394, 396
Although not yet definitive, new diagnostic methods involving the nervous
system seem promising. In the meantime, the sole use of the 1990 ACR classifi-
cation criteria has been challenged and no longer appears to be an acceptable or
reliable diagnostic method. 25•375 The criteria have several significant limitations,
which may explain why fewer health care providers currently use them in clinical
practice compared to a decade ago. 375 As a response to its limitations and because
so many patients failed to satisfy the 1990 classification criteria, the ACR has pro-
vided a provisional, updated case definition and diagnostic criteria that do not
require a tender point examination. 397
Wolfe et al. examined 829 patients previously diagnosed with FMS as part
of a two-phase multicenter study. 397 During the first phase, data were collected
from both patients and physicians for the purpose of developing questionnaires.
Patients were asked to complete a regional pain scale (renamed the Widespread
Pain Index [WPI]), a categorical scale for symptoms, a visual analog scale, and the
Health Assessment Questionnaire II functional disability scale, as well as to iden -
tifyprelisted symptoms experienced within the last 3 months. In the second phase,
participating physicians were asked to examine patients using the ACR tender
point count and to complete categorical scales for pain, fatigue, sleep disturbance,
cognitive symptoms, waking unrefreshed, and overall (global) severity using the
same categorical scoring as the patients. Physicians were also asked to indicate
whether patients complained of muscle pain, irritable bowel syndrome, fatigue,
cognitive problems, muscle weakness, headache, abdominal pain or cramps, par-
esthesias, dizziness, sleep problems, depression, constipation, diarrhea, interstitial
cystitis, anxiety, and muscle tenderness. Using a similar list of symptoms, physi-
cians were asked to categorize patients as having "few or no somatic symptoms,"
"a moderate number of symptoms," or a "great deal of symptoms." Using the data
collected, Wolfe et al. created a symptom severity scale to be used in conjunction
with the WPI during the examination process. 397
According to the updated criteria, listed in Table 6.2, a patient may be di-
agnosed with FMS if the following three conditions are met: (1) WPI score > 7
and symptom severity scale score > 5 or WPI score = 3 -6 and symptom sever-
ity scale score > 9; (2) symptoms have been present at a similar level for at least
3 months; and (3) the patient does not have a disorder that would otherwise ex-
plain the pain.
The provisional diagnostic criteria presented are not meant to replace the 1990
ACR classification criteria but were designed to supplement them. By addressing
the limitations of the tender point examination, the provisional criteria improve
the 1990 classification sensitivity. The provisional criteria also, for the first time,
enable recording of current and past symptom severity as these change through
the course of the patient's life.
Pathogenesis
During the past decade, the research regarding pain syndromes has expanded
considerably. The purpose of this book, however, is to provide sufficient back-
ground, research, and management for those soft tissue dysfunctions that best re-
spond to myofascial manipulation. Although FMS is no longer considered a soft
tissue or mechanical dysfunction, 25 •398 such patients are continually being referred
to physical therapists. As musculoskeletal specialists, physical therapists need to
Table 6.2 Fibromyalgia Diagnostic Criteria

Criteria
A patient satisfies diagnostic criteria for fibromyalgia if the following 3 conditions are met:
(1) Widespread pain index (WPI) > 7 and symptoms severity (SS) scale score > 5 or WPI 3-6
and SS scale score > 9
(2) Symptoms have been present at a similar level for at least 3 months.
(3) The patient does not have a disorder that would otherwise explain the pain.
Ascertainment
(1) WPI: note the number of areas in which the patient has had pain over the last week. In how
many areas has the patient had pain? Score will be between O and 19.
Shoulder girdle, left Hip (buttock, trochanter). left Jaw. left Upper back
Shoulder girdle, right Hip (buttock, trochanter). right Jaw. right Lower back
Upper arm. left Upper leg, left Chest Neck
Upper arm. right Upper leg, right Abdomen
Lower arm. left Lower leg, left
Lower arm. right Lower leg, right
(2) SS scale score:
Fatigue
Waking unrefreshed
Cognitive symptoms
For each of the 3 symptoms above, indicate the level of severity over the past week using the
following scale:
0 = no problem
1 = slight or mild problems. generally mild or intermittent
2 = moderate, considerable problems. often present and/or at a moderate level
3 = severe: pervasive, continuous, life-disturbing problems
Considering somatic symptoms in general. indicate whether the patient has:•
0 = no symptoms
1 = few symptoms
2 = a moderate number of symptoms
3 = a great deal of symptoms
The SS scale score is the sum of the severity of the 3 symptoms (fatigue, waking unrefreshed,
cognitive symptoms) plus the extent (severity) of somatic symptoms in general. The final score
is between O and 12.
*Somatic symptoms that might be considered: muscle pain, irritable bowel syndrome, fatigue/tiredness, thinking
or remembering problem, muscle weakness, headaches, pain/cramps in the abdomen, numbness/tingling, diz-
ziness, insomnia, depression, constipation, pain in the upper abdomen, nausea, nervousness , chest pain, blurred
vision, fever, diarrhea, dry mouth, itching, wheezing, Raynaud 's phenomenon, hives/welts, ringing in ears , vomit -
ing, heartburn, oral ulcers, loss of/change in taste, seizures, dry eyes, shortness of breath, loss of appetite, rash,
sun sensitivity, hearing difficulties, easy bruising, hair loss, frequent urination, painful urination, and bladder
spasms.
Note . Reprinted from Wolfe F, Clauw DJ, Fitzcharles MA, et al. "The American College of Rheumatology Prelimi -
nary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity." Arthritis Care and Research.
2010;62:607,with permission of John Wiley & Sons, Inc.
understand the current thinking about FMS to be able to provide the best evi-
dence-informed treatment.
The most widely accepted pathogenic models regarding FMS point to abnor-
malities in central nervous system sensory processing. The term central sensitiza-
tion is appearing more often in the literature to describe FMS. FMS is commonly
labeled a "central pain" or "neuropathic pain" syndrome. 399 - 403 Dysregulation of

the pain pathways and neurotransmitter irregularities enable pain amplification,
making individuals hypersensitive to both painful and nonpainful stimuli, such
as touch, temperature, light, sound, and smell. 369•372 ,404 - 4 osPatients diagnosed with
FMS are not a homogeneous group, and it is unlikely that all nonpain symptoms,
such as disturbed sleep, fatigue, cold intolerance, dry eyes, and dizziness, can fully
be explained by the sensitization model. 409 Yunus maintains that FMS is part of
a spectrum of overlapping central sensitivity syndromes. 410 There is no evidence
suggesting that the reported chronic widespread pain experienced by patients with
FMS is a result of tissue pathology, structural abnormalities, or peripheral sensiti-
zation, which are usually related to inflammation. 411 When compared with healthy
individuals, patients diagnosed with FMS rated painful responses to stimuli as
greater in magnitude, longer lasting, and more frequently painful, supporting the
position of neuropathic dysregulation. 412 •413 Many factors may be responsible for,
or at least contribute to, central sensitization. A growing body of evidence suggests
that biochemical abnormalities are the primary factors, due to the lack of descend-
ing analgesic activity. 26 •375•414- 416
Evidence shows that levels of norepinephrine and serum serotonin are reduced
in patients with FMS,406 •417 which is thought to be a contributing factor of central
sensitization. Serum serotonin is responsible for presynaptically inhibiting the re-
lease of neurotransmitters involved in the pain processes. Inhibited neurotrans-
mitters include substance P but may also include others, such as the excitatory
amino acid glutamate, which has been found in concentrations more than dou-
ble in patients with FMS compared with controls. 418 Substance P and glutamate
modulate postsynaptic responses by aiding in the transmission of pain signals via
the primary afferent neurons. Levels of substance P and glutamate have also been
found to be elevated in the cerebrospinal fluid of patients with FMS and to corre-
spond with patients' levels of reported pain intensity. 419 - 421 Elevated levels of sub-
stance P lower the synaptic excitability threshold within the spinal cord, resulting
in sensitizing neurons away from the local stimulus. Such sensitization can span
long distances in the spinal cord, expanding receptive fields to both nociceptive
and non-nociceptive afferent impulses. 412 •422 •423 These changes can cause hyperal-
gesia and allodynia through multiple spinal segments and may be responsible for
the widespread, diffuse pain reported by so many patients with FMS.274, 408 ,412 •424
Recently, researchers have used functional imaging techniques, such as mag-
netic resonance imaging, single photon emission computed tomography, and posi-
tron emission tomography. One study found hypoperfusion in the anterior and
posterior cingulate, the amygdala, the medial frontal and parahippocampal gyrus,
and the cerebellum and found hyperperfusion of the radioligand within the so-
matosensory cortex, all of which disturb sensory processing. 425 •426 Other studies
have demonstrated attenuated dopaminergic activity and a reduced availability of
µ-opioid receptors in patients with FMS.427- 429
Management of Fibromyalgia
Individuals with FMS typically do not respond to treatments otherwise effective
in treating damaged or inflamed tissues (i.e., ice, nonsteroidal anti-inflammatory
drugs, steroid injections, or surgical procedures). The management plan typi-
cally includes pharmacological and nonpharmacological interventions. Pharma-
cological therapies may include medications such as antidepressants, analgesics,
muscle relaxants, anticonvulsants, and others. 407 Nonpharmacological therapies
may include aerobic and strengthening exercise, massage, chiropractic manipu-
lation, cognitive-behavioral therapy, sleep hygiene, and a number of alternative
therapies.
Pharmacological Management
The U.S. Food and Drug Administration has approved pregabalin, duloxetine,
and milnacipran for treating FMS, although these drugs do not necessarily dem-
onstrate acceptable efficacy for the majority of patients. 430Nevertheless, several
studies offer support for the administration of these medications for patients with
FMS to reduce overall pain levels, the number of tender points, stiffness, and fa-
tigue.374•43
1-438Nonsteroidal anti-inflammatory medications are often used but
have limited effectiveness. 439Tricyclic antidepressants, such as amitriptyline, have
been studied extensively because of their ability to block the reuptake of serotonin
or norepinephrine. They are effective in reducing pain and fatigue and improving
sleep but have resulted in problems with tolerability. 440-442Cyclobenzaprine, when
used at bedtime, has been shown to improve sleep and to reduce pain. 443-447 Selec-
tive serotonin reuptake inhibitors, such as fluoxetine, paroxetine, and citalopram,
have not been as effective as would be expected but do provide relief for some
patients. 431
•448-450Tramadol, a central-acting nonopioid analgesic with limited
opioid activity, has been shown to reduce pain as much as 20% when compared
with a placebo, especially when combined with acetaminophen. 451 •452Opioids are
commonly used in the management of patients with FMS, in spite of limited re-
search. 380The number of medications and their effects far exceed the limitations
and purpose of this text. It should be noted that no single medication has been
labeled as "the" drug of choice for patients with FMS, and no cure currently exists.
However, physical therapists and other clinicians should at least be familiar with
the names, indications, effects, and common side effects of some of the more com-
monly prescribed medications used in treating persons with FMS.
Nonpharmacological Management
Nonpharmacological therapies include exercise, massage, cognitive-behavioral
therapy, and a number of alternative therapies. Acupuncture, 453-456massage, 457and
osteopathic or chiropractic manipulation 458•459provide some short-term reduction
in pain, but the quality of the methodology of such studies is not strong. Exercise
is the most relevant intervention for the physical therapist. As with any referral,
a thorough musculoskeletal examination should be performed to determine not

only the best course of treatment but also whether any treatable musculoskeletal
impairments are present. If so, an impairment must be treated within the frame-
work and limitations of FMS. For this reason, therapists should understand the
limitations and precautions of exercise when treating FMS, as well as how it can be
used to help manage this condition and improve the patient's quality of life.
In studies of patients with FMS, exercise has been examined for its effect on
the intensity of pain, the number of tender points, depression, fatigue, anxiety,
general well-being, and functional improvement. The majority of evidence con-
tinues to support the use of low-intensity aerobic exercise as the best physical
intervention for FMS management. 460 - 462 Some evidence suggests that the use
of aerobic exercise, with or without biofeedback, results in a significant improve-
ment in depression for patients with FMS compared with untreated controls. 463- 466
Those with FMS showed reduced anxiety and depression when aerobic exercise
was combined with education about their condition. 467- 470 Reduced pain has also
been documented, including a reduction in the number of tender points, as a result
of exercise. 464•466 •471- 474 There is also much evidence supporting the use of exercise
in that it can significantly improve the feelings of well-being and increase levels of
physical function, regardless of reported levels of pain. 464, 466 ,471- 473,475,476
The types of exercise used and the duration vary from study to study. Types
include resisted strengthening, stretching, land-based aerobic exercises, pool ex-
ercises, and a combination of any of the foregoing. Burckhardt et al. compared an
untreated control group with an FMS group that performed an hour of aerobics,
consisting of walking, swimming, or cycling (one time per week for 6 weeks), fol-
lowed by a 6-week home exercise program, totaling 12 weeks of exercise. 4n The
FMS group reported decreased pain and an improvement in the sense of global
well-being. 477 In 1999, Gowans et al. compared an untreated control group with
an FMS group that performed pool exercises during a 6-week period . The exer-
cise regimen consisted of a IO-minute warm-up, followed by walking, jogging,
side-stepping, and arm exercises at 75% maximum heart rate and a IO-minute
cooldown. 478 The results showed significantly reduced levels of fatigue and self-
efficacy with a 6-minute walk test. 478 In 200 1, Gowans et al. compared an un-
treated control group with an FMS exercise group for 23 weeks. The exercise group
performed both pool- and land-based exercises. The exercise routine began with a
5-minute warm-up, followed by 20 minutes of aerobic exercise at 60%- 75% maxi-
mum heart rate. 47 1 The exercises progressed from gentle arm and leg pool exercises
during week 1 to running in the pool by week 6. In week 7 the regimen was in-
creased to include pool- and land-based exercises (slow, continuous walking over
land two times per week and one time per week in the pool), fallowed by intermit-
tent jogging two times a week in the gym and one time a week in the pool. The
results were similar, resulting in an improvement of patients' global well-being and
physical function. 471
Although most research agrees that low-intensity aerobic exercise is beneficial

in managing FMS, no specific protocol has been developed, leaving physical thera-
pists to decide what is best for their patients. In an attempt to determine the best
type of aerobic exercise, Brosseau et al. graded 16 studies related to aerobic exercise
and FMS.4{> 0 Ten studies showed statistical significance and clinical importance,
defined as an improvement of more than 15% relative to a control, based on panel
expertise and empirical results, but only five demonstrated any clinical benefit.
Of these five, two favored pool-based aerobics, 479•480one favored a progression/
combination of pool- and land-based aerobic exercises, 471and two favored land-
6 481
based aerobic exercise.4{> • Based on this evidence, the American Pain Society
strongly encourages aerobic exercise at moderate intensity, two to three times a
week, and also recommends the avoidance of exercise-induced pain and noncom-
pliance.4{>1,482•483At best, with any patient, a therapist should increase the intensity
of an exercise program slowly, taking into consideration adverse affects such as ex-
acerbation of pain. A well-progressed exercise program can provide benefit only as
long as it is followed. Buckelew et al. found benefits even after 2 years of the initial
implementation,4{>4 but Wigers et al. found no benefit in a 4.5-year follow-up study,
due to the fact that participants had abandoned their exercise routines.4{>6
Refere nces
1. McBeth J, Jones K Epidemiology of chronic musculoskeletal pain. Best PractRes Clin Rheuma-
tol. 2007;21:403-425.
2. Vecchiet L. Muscle pain and aging. JournalMusculoskeletalPain. 2002;10:5- 22.
3. Lindell L, Bergman S, Petersson IF, Jacobsson LT, Herrstrom P. Prevalence of fibromyalgia and
chronic widespread pain. Scand J Prim Health Care.2000;18:149- 153.
4. Fernandez-de-las-Penas C, Cuadrado ML, Arendt-Nielsen L, Simons DG, Pareja JA. Myofas-
cial trigger points and sensitization: an updated pain model for tension-type headache. Cepha-
lalgia.2007;27:383- 393.
5. Dommerholt J, Bron C, Franssen JLM. Myofascial trigger points: an evidence-informed review.
Journalof Manual and Manipulative Therapy.2006;14:203- 221.
6. Byrne C, Twis C, Eston R. Neuromuscular function after exercise-induced muscle damage:
theoretical and applied implications. SportsMed. 2004;34:49- 69.
7. Simons DG. Muscle pain syndromes: part 1. Am J PhysMed. 1975;54:289- 311.
8. American Physical Therapy Association. Guide to physical therapy practice, second edition.
Phys Ther.2001;81:9- 746.
9. Dommerholt J. Physical therapy in an interdisciplinary pain management center. Pain Practi-
tioner.2005;14:32- 36.
10. Wolff MS, Michel TH, Krebs DE, Watts NT. Chronic pain: assessment of orthopedic physical
therapists' knowledge and attitudes. Phys Ther.1991;71:207- 214.
11. Scudds R, Solomon P. Pain and its management: a new pain curriculum for occupational
therapists and physical therapists. PhysiotherCan. 1995;47:77- 78.
12. Arendt-Nielsen L, Sluka KA, Nie HL. Experimental muscle pain impairs descending inhibi-
tion. Pain. 2008;140:465-471.
13. Niddam DM, Chan RC, Lee SH, Yeh TC, Hsieh JC. Central representation ofhyperalgesia
from myofascial trigger point. Neuroimage.2008;39:1299- 1306.
14. Svensson P, Minoshima S, Beydoun A, Morrow TJ, Casey KL. Cerebral processing of acute
skin and muscle pain in humans. J Neurophysiol.1997;78:450- 460.
15. Mense S. Algesic agents exciting muscle nodceptors. Exp Brain Res. 2009;196:89- 100.
16. Taguchi T, John V, Hoheisel U, Mense S. Neuroanatomical pathway of nociception originating
in a low back muscle (multifidus) in the rat. Neurosci Lett. 2007;427:22 - 27.
17. Sessle BJ. Acute and chronic craniofacial pain: brainstem mechanisms of nociceptive transmis-
sion and neuroplasticity, and their clinical correlates. Crit Rev OralBiol Med. 2000;1 l :57- 91.
18. Wall PD, Woolf CJ. Muscle but not cutaneous C-afferent input produces prolonged increases
in the excitability of the flexion reflex in the rat. J Physiol.1984;356:443 - 458.
19. Fields HL, Basbaum Al. Central nervous system mechanisms of pain modulation. In: Melzack
R, Wall PD, eds. Textbookof Pain. Edinburgh, UK: Churchill Livingstone; 1999:309- 329.
20. Millan MJ. The induction of pain: an integrative review. ProgNeurobiol.1999;57:1-164.
21. Kirmayer LJ, Looper KJ.Abnormal illness behaviour: physiological, psychological and social
dimensions of coping with distress. Curr Opin Psychiatry.2006;19:54- 60.
22. Hendler NH, Kozikowski JG. Overlooked physical diagnoses in chronic pain patients involved
in litigation. Psychosomatics.1993;34:494-501.
23. Hendler NH, Zinreich J, Kozikowski JG. Three-dimensional CT validation of physical com-
plaints in "psychogenic pain" patients. Psychosomatics.l 993;34:90- 96.
24. Gerwin R. A study of 96 subjects examined both for fibromyalgia and myofascial pain
(abstract). Journalof MusculoskeletalPain. 1995;3(suppl 1):121.
25. Dommerholt J, Issa T. Differential diagnosis: myofascial pain. In: Chaitow L, ed. Fibromyal-
gia Syndrome:A Practitioner'sGuide to Treatment.Edinburgh, UK: Churchill Livingstone;
2009:179- 213.
26. Clauw DJ. Fibromyalgia: update on mechanisms and management.! Clin Rheumatol.
2007;13:102-1 09.
27. Simons DG. Myofascial pain syndrome: one term but two concepts: a new understanding
(editorial). Journalof MusculoskeletalPain. l 995;3:7-1 3.
28. Dworkin SF, Sherman J, Mancl L, Ohrbach R LeResche L, Truelove E. Reliability, validity, and
clinical utility of the research diagnostic criteria for Temporomandibular Disorders Axis II
Scales: depression, non-specific physical symptoms, and graded chronic pain. J OrofacPain.
2002;16:207- 220.
29. Steenks MH, de Wijer A. Validity of the research diagnostic criteria for temporomandibu-
lar disorders Axis I in clinical and research settings.! OrofacPain. 2009;23:9-1 6; discussion
17-27.
30. Gunn CC. The Gunn Approach to the Treatmentof ChronicPain. 2nd ed. New York: Churchill
Livingstone; 1997.
31. Gunn CC. Radiculopathic pain: diagnosis, treatment of segmental irritation or sensitization.
Journalof MusculoskeletalPain. 1997;5:119- 134.
32. Simons DG, Travell JG, Simons LS. Travelland Simons'MyofascialPain and Dysfunction:1he
TriggerPointManual. 2nd ed, vol 1. Baltimore: Lippincott Williams & Wilkins; 1999.
33. Baldry PE. Acupuncture, TriggerPointsand MusculoskeletalPain. Edinburgh, UK Churchill
Livingstone; 2005.
34. Lange M. DieMuskelhiirten (Myogelosen).Munich: JF Lehmann's Verlag; 1931.
35. Travell JG, Rinzler S, Herman M. Pain and disability of the shoulder and arm: treatment by
intramuscular infiltration with procaine hydrochloride. JAMA.1942; 120:417-422.
36. Travell JG, Rinzler SH. The myofascial genesis of pain. PostgradMed. 1952;1 l :452- 434.
37. Travell JG, Simons DG. MyofascialPain and Dysfunction:1he TriggerPointManual, vol 2.
Baltimore: Williams & Wilkins; 1992.
38. Simons DG. Triggerpunkte und Myogelose. ManuelleMedizin. 1997;35:290-294.

39. Lucas N, Macaskill P, lrwig L, Moran R, Bogduk N. Reliability of physical examination
for diagnosis of myofascial trigger points: a systematic review of the literature. Clin J Pain.
2009;25:80- 89.
40. Tough EA, White AR, Richards S, Campbell J. Variability of criteria used to diagnose myo-
fascial trigger point pain syndrome - evidence from a review of the literature. C/inJ Pain.
2007;23:278- 286.
41. Myburgh C, Larsen AH, Hartvigsen J. A systematic, critical review of manual palpation for
identifying myofascial trigger points: evidence and clinical significance. Arch Phys Med Reha-
bil. 2008;89:1169-11 76.
42. Cummings TM, White AR. Needling therapies in the management of myofascial trigger point
pain: a systematic review. Arch PhysMed Rehabil.2001;82:986- 992.
43. McEvoy J, Huijbregts PA Reliability of myofascial trigger point palpation: a systematic review.
In: Dommerholt J, Huijbregts PA, eds. MyofascialTriggerPoints:Pathophysiologyand Evidence-
Informed Diagnosisand Management. Boston: Jones & Bartlett; 2011 :65- 88.
44. Rickards LD. The effectiveness of non-invasive treatments for active myofascial trigger point
pain: a systematic review of the literature. Int J OsteopathicMed. 2006;9:120-1 36.
45. Tough EA, White AR, Cummings TM, Richards SH, Campbell JL. Acupuncture and dry
needling in the management of myofascial trigger point pain: a systematic review and meta-
analysis of randomised controlled trials. Eur J Pain. 2009;13:3-1 0.
46. Vernon H, Schneider M. Chiropractic management of myofascial trigger points and myo-
fascial pain syndrome: a systematic review of the literature. ! Manipulative Physiol1her.
2009;32:14- 24.
47. Wolfe F, Smythe HA, Yanus MB, et al The American College ofRheumatology 1990 criteria
for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis
Rheum. 1990;33:160-172.
48. Fricton JR. Myofascial pain syndrome: characteristics and epidemiology. Adv Pain Res 1her.
1990;17:107-128.
49. $ahinN, Karata~ 0, Ozkaya M, Cakmak A, Berker E. Demographics features, clinical find-
ings and functional status in a group of subjects with cervical myofascial pain syndrome. Agri.
2008;20:14- 19.
50. Bajaj P, Graven-Nielsen T, Arendt-Nielsen L. Osteoarthritis and its association with muscle
hyperalgesia: an experimental controlled study. Pain. 2001;93:107-1 14.
51. Calandre EP, Hidalgo J, Garcia-Leiva JM, Rico-Villademoros F. Trigger point evaluation in
migraine patients: an indication of peripheral sensitization linked to migraine predisposition?
Eur J Neurol. 2006;13:244- 249.
52. Giamberardino MA, Tafuri E, Savini A, et al Contribution of myofascial trigger points to
migraine symptoms.! Pain. 2007;8:869- 878.
53. Marcus DA, ScharffL, Mercer S, Turk DC. Musculoskeletal abnormalities in chronic headache:
a controlled comparison of headache diagnostic groups. Headache.1999;39:21-27.
54. Fernandez-de-las-Penas C, Cuadrado ML, Barriga FJ, Pareja JA. Pericranial tenderness is not
related to nummular headache. Cephalalgia.2007;27:182-1 86.
55. Fernandez-de-las-Penas C, Cuadrado ML, Barriga FJ, Pareja JA Local decrease of pressure
pain threshold in nummular headache. Headache.2006;46: 1195-1198.
56. Fernandez-de-las-Penas C, Cuadrado ML, Barriga FJ, Pareja JA. Active muscle trigger
points as sign of sensitization in chronic primary headaches. Journalof MusculoskeletalPain.
2009;17:155-1 61.
57. Bajaj P, Bajaj P, Graven-Nielsen T, Arendt-Nielsen L. Trigger points in patients with lower limb
osteoarthritis. Journalof MusculoskeletalPain. 2001;9:l 7- 33.
58. Fernandez-de-las-Penas C, Alonso-Balnco C, Alguacil-Diego IM, Miangolarra JC. Myofascial

trigger points and postero-anterior joint hypomobility in the mid-cervical spine in subjects
presenting with mechanical neck pain; a pilot study. J Man Manip 1her.2006;14:88- 94.
59. Fernandez-de-las-Penas C, Fernandez Carnero J, Miangolarra-Page JC. Musculoskeletal dis-
orders in mechanical neck pain: myofascial trigger points versus cervical joint dysfunction.
Journalof MusculoskeletalPain. 2005;13:27- 35.
60. Ruiz-Saez M, Fernandez-de-las-Penas C, Blanco CR, Martinez-Segura R, Garcia-Leon R.
Changes in pressure pain sensitivity in latent myofascial trigger points in the upper trapezius
muscle after a cervical spine manipulation in pain-free subjects.! Manipulative Physiol1her.
2007;30:578- 583.
61. Doggweiler-Wiygul R. Urologic myofascial pain syndromes. Curr Pain HeadacheRep.
2004;8:445- 451.
62. Jarrell J, Robert M. Myofascial dysfunction and pelvic pain. CanadianJournalof CME. Febru-
ary 2003:107-11 6.
63. Zermann DH, lshigooka M, Doggweiler R, Schmidt RA. Chronic prostatitis: a myofascial pain
syndrome? Infect Urol.1999;12:84-92.
64. Delaney JP, Leong KS, Watkins A, Brodie D. The short-term effects of myofascial trigger point
massage therapy on cardiac autonomic tone in healthy subjects.! Adv Nurs. 2002;37:364- 371.
65. Simons DG. Cardiology and myofascial trigger points: Janet G. Travell's contribution. Tex
Heart Inst J.2003;30:3- 7.
66. FitzGerald MP, Anderson RU, Potts J, et al. Randomized multicenter feasibility trial of myo-
fascial physical therapy for the treatment of urological chronic pelvic pain syndromes.! Urol.
2009;182:570- 580.
67. Qerama E, Kasch H, Fuglsang-Frederiksen A. Occurrence of myofascial pain in patients with
possible carpal tunnel syndrome: a single-blinded study. Eur J Pain. 2009;13:588- 591.
68. Fernandez-de-las-Penas C, Galan-del-Rfo R, Fernandez-Carnero J, Pesquera J, Arendt-Nielsen
L, Svensson P. Bilateral widespread mechanical pain sensitivity in women with myofascial tem-
poromandibular disorder: evidence of impairment in central nodceptive processing.! Pain.
2009;10:1170-1178.
69. Fernandez-de-las-Penas C, Schoenen J. Chronic tension-type headache: what is new? Curr
Opin Neurol. 2009;22:254- 261.
70. Dommerholt J, Huijbregts PA. MyofascialTriggerPoints:Pathophysiologyand Evidence-
Informed Diagnosisand Management. Boston: Jones & Bartlett; 2011.
71. Gerwin RD, Shannon S, Hong CZ, Hubbard D, Gevirtz R. lnterrater reliability in myofascial
trigger point examination. Pain. 1997;69:65- 73.
72. Alfven G. The pressure pain threshold (PPT) of certain muscles in children suffering
from recurrent abdominal pain of non-organic origin: an algometric study. Acta Paediatr.
l 993;82:481- 483.
73. Cimbiz A, Beydemir F, Manisaligil U. Evaluation of trigger points in young subjects. Journal
of MusculoskeletalPain. 2006;14:27- 35.
74. Kao MJ, Han TI, Kuan TS, Hsieh YL, Su BH, Hong CZ. Myofascial trigger points in early life.
Arch PhysMed Rehabil.2007;88:251- 254.
75. Zapata AL, Moraes AJ, Leone C, Doria-Filho U, Silva CA. Pain and musculoskeletal pain syn-
dromes in adolescents.! AdolescHealth. 2006;38:769- 771.
76. von Stillpnagel C, Reilich P, Straube A, et al. Myofascial trigger points in children with tension-
type headache: a new diagnostic and therapeutic option. J ChildNeurol. 2009;24:406- 409.
77. Hong C-Z, Torigoe Y. Electrophysiological characteristics of localized twitch responses in re-
sponsive taut bands of rabbit skeletal muscle. Journalof MusculoskeletalPain. 1994;2:17-43.
78. Hong CZ. Lidocaine injection versus dry needling to myofascial trigger point: the importance
of the local twitch response. Am J Phys Med Rehabil.l 994;73:256 - 263.
79. Hong CZ. Persistence of local twitch response with loss of conduction to and from the spinal
cord Arch PhysMed Rehabil.1994;75:12-16.
80. Hong CZ, Torigoe Y, Yu J. The localized twitch responses in responsive bands of rabbit skel-
etal muscle are related to the reflexes at spinal cord level Journalof MusculoskeletalPain.
1995;3:15- 33.
81. Bron C, Franssen J, Wensing M, Oostendorp RA. lnterrater reliability of palpation of myofas-
cial trigger points in three shoulder muscles. J Man Manip 1her.2007;15:203 - 215.
82. Donnelly JM, Palubinskas L. Prevalence and inter-rater reliability of trigger points. Journal of
MusculoskeletalPain. 2007;15(suppL 13):16 (abstract).
83. Hsieh CY, Hong CZ, Adams AH, et al. Interexaminer reliability of the palpation of trigger
points in the trunk and lower limb muscles. Arch Phys Med Rehabil.2000;81:258 - 264.
84. Lew PC, Lewis J, Story I. Inter-therapist reliability in locating latent myofascial trigger points
using palpation. Man 1her. 1997;2:87 - 90.
85. Nice DA, Riddle DL, Lamb RL, Mayhew TP, Rucker K. lntertester reliability of judgments
of the presence of trigger points in patients with low back pain. Arch Phys Med Rehabil.
l 992;73:893 - 898.
86. Njoo KH, Van der Does E. The occurrence and inter-rater reliability of myofascial trigger
points in the quadratus lumborum and gluteus medius: a prospective study in non-specific low
back pain patients and controls in general practice. Pain. 1994;58:317 - 323.
87. Sciotti VM, Mettak VL, DiMarco L, et al. Clinical precision of myofascial trigger point location
in the trapezius muscle. Pain. 2001;93:259 - 266.
88. Wolfe F, Simons DG, Fricton J, et al. The fibromyalgia and myofascial pain syndromes: a pre-
liminary study of tender points and trigger points in persons with fibromyalgia, myofascial
pain syndrome and no disease. J Rheumatol. l 992;19:944 - 951.
89. Bendtsen L, Jensen R, Jensen NK, Olesen J. Muscle palpation with controlled finger pressure:
new equipment for the study of tender myofascial tissues. Pain. 1994;59:235-239.
90. Fischer AA. Pressure threshold measurement for diagnosis of myofascial pain and evaluation
of treatment results. ClinJ Pain. 1986;2:207-214.
91. Fenger-Gr0n LS, Graven-Nielsen T, Arendt-Nielsen L, Svensson P, Steengaard-Pedersen K,
Jensen TS. Muscular sensibility assessed by electrical stimulation and mechanical pressure.
Journalof MusculoskeletalPain. l 998;6:33- 44.
92. Chen Q, Basford J, An KN. Ability of magnetic resonance elastography to assess taut bands.
Clin Biomech (Bristo~Avon). 2008;23:623 - 629.
93. Chen Q, Bensamoun S, Basford JR, Thompson JM, An KN. Identification and quantifica-
tion of myofascial taut bands with magnetic resonance elastography. Arch Phys Med Rehabil.
2007;88:1658 -1 661.
94. Sikdar S, Shah JP, Gebreab T, et al. Novel applications of ultrasound technology to visualize
and characterize myofascial trigger points and surrounding soft tissue. Arch Phys Med Rehabil.
2009;90:1829 - 1838.
95. Sikdar S, Shah JP, Gilliams E, Gebreab T, Gerber LH. Assessment of myofascial trigger points
(MTrPs): a new application of ultrasound imaging and vibration sonoelastography. Conj Proc
IEEEEngMed Biol Soc.2008;2008:5585 - 5588.
96. Lewis J, Tehan P. A blinded pilot study investigating the use of diagnostic ultrasound for de-
tecting active myofascial trigger points. Pain. 1999;79:39-44.
97. Gerwin RD, Duranleau D. Ultrasound identification of the myofascial trigger point. Muscle
Nerve. 1997;20:767-768.
98. Bauermeister W The diagnosis and treatment of myofascial trigger points using shockwaves.
In: Myopain '04:Abstractsfrom the 6th WorldCongressof MyofascialPain and Fibromyalgia.
Munich: Haworth; 2004:13.
99. Bauermeister W Diagnose und Therapie des Myofaszialen Triggerpunkt Syndroms <lurch Lo-
kalisierung und Stimulation sensibilisierter Nozizeptoren mit fokussierten elektrohydraulische
Stosswellen. Medizinisch-OrthopadischeTechnik 2005;5:65- 74.
100. Muller-Ehrenberg H, Licht G. Diagnosis and therapy of myofascial pain syndrome with fo-
cused shock waves (ESWT). Medizinisch-Orthopadische Technik. 2005;5:l - 6.
101. Muller-Ehrenberg H, Thorwesten L. Improvement of sports-related shoulder pain after treat-
ment of trigger points using focused extracorporeal shock wave therapy regarding static and
dynamic force development, pain relief and sensomotoric performance. Journal of Musculo-
skeletal Pain. 2007;15(suppl. 13):33.
102. Janda V. Muscle spasm: a proposed procedure for differential diagnosis. Journal of Manual
Medicine. 1991;6:136-139.
103. Franssen JLM. Handboek OppervlakteElektromyografie.1995, Utrecht, The Netherlands:
De Tijdstroom.
104. Mense S. Pathophysiologic basis of muscle pain syndromes. In: Fischer AA, ed. Myofascial
Pain: Update in Diagnosisand Treatment. Philadelphia, PA: WB Saunders; 1997:23-53.
105. Chen KH, Hong CZ, Kuo FC, Hsu HC, Hsieh YL. Electrophysiologic effects of a thera-
peutic laser on myofascial trigger spots of rabbit skeletal muscles. Am J Phys Med Rehabii.
2008;87:1006 - 1014.
106. Kuan TS, Hsieh YL, Chen SM, Chen JT,Yen WC, Hong CZ. The myofascial trigger point re-
gion: correlation between the degree of irritability and the prevalence of end plate noise. Am J
PhysMed Rehabil. 2007;86:183 -1 89.
107. Simons DG. Review of enigmatic MTrPs as a common cause of enigmatic musculoskeletal
pain and dysfunction.! ElectromyogrKinesiol. 2004;14:95 -1 07.
108. Headly BJ. Evaluation and treatment of myofascial pain syndrome utilizing biofeedback. In:
Cram JR, ed. ClinicalElectromyographyfor Surface Recordings.Nevada City, CA: Clinical
Resources; 1990:235-254.
109. Headly BJ. Chronic pain management. In: O'Sullivan SB, Schmitz TS, eds. PhysicalRehabili-
tation: Assessment and Treatment. Philadelphia, PA: FA Davis; 1994:577-600.
110. Dommerholt J, Grobli C. Knee pain. In: Whyte-Ferguson L, Gerwin RD, eds. Clinical
Mastery of Myofascial Pain Syndrome. Baltimore: Lippincott, Williams & Wilkins; 2005:
359- 389.
111. Dommerholt J, Gerwin RD. Nutritional and metabolic perpetuating factors in myofascial
pain. In: Dommerholt J, Huijbregts PA, eds. Myofascial TriggerPoints: Pathophysiologyand
Evidence-InformedDiagnosisand Management. Boston: Jones & Bartlett; 2011:51- 64.
112. Altindag 0, Gur A, Altindag A. The relationship between clinical parameters and depression
level in patients with myofascial pain syndrome. Pain Med. 2008;9:161- 165.
113. Cassisi JE, Sypert GW, Lagana L, Friedman EM, Robinson ME. Pain, disability, and psycho-
logical functioning in chronic low back pain subgroups: myofascial versus herniated disc
syndrome. Neurosurgery. 1993;33:379-385.
114. Faucett JA. Depression in painful chronic disorders: the role of pain and conflict about pain.
J Pain Symptom Manage. 1994;9:520-526.
115. Zautra AJ, Marbach JJ, Raphael KG, Dohrenwend BP, Lennon MC, Kenny DA. The exami-
nation of myofascial face pain and its relationship to psychological distress among women.
Health Psychology.1995;14:223- 231.
116. Bohr T. Problems with myofascial pain syndrome and fibromyalgia syndrome. Neurology.
1996;46:593-597.
117. Bohr TW. Fibromyalgia syndrome and myofascial pain syndrome. Do they exist? Neurol
Clin. 1995;13:365-384.
118. Hey LR, Helewa A. Myofascial pain syndrome: a critical review of the literature. Physiother
Can. 1994;46:28-36.
119. Quintner JL, Cohen ML. Referred pain of peripheral nerve origin: an alternative to the
"myofascial pain" construct. Clin J Pain. 1994;10:243-251.
120. Fernandez-de-las-Penas C, Alonso-Blanco C, Caudrado ML, Gerwin RD, Pareja JA. Trig-
ger points in the suboccipital muscles and forward head posture in tension-type headache.
Headache. 2006;46:454 - 460.
121. Fernandez-de-las-Penas C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA. Myofas-
cial trigger points and their relationship to headache clinical parameters in chronic tension-
type headache. Headache. 2006;46:1264 -1 272.
122. Fernandez-de-las-Penas C, Cuadrado ML, Pareja JA. Myofascial trigger points, neck
mobility, and forward head posture in episodic tension-type headache. Headache.
20 07;47 :662- 672.
123. Fricton JR, Kroening R, Haley D, Siegert R. Myofascial pain syndrome of the head and
neck: a review of clinical characteristics of 164 patients. Oral Surg OralMed Oral Pathol.
1985;60:615-623.
124. Grobli C. Klinik und Pathophysiologie von myofaszialen Triggerpunkten. Physiotherapie.
1997;32:17-26.
125. Cummings GS, Tillman LJ. Remodeling of dense connective tissue in normal adult tissues.
In: Currier DP, Nelson RM, eds. Dynamics of Human BiologicTissues. Philadelphia, PA: FA
Davis; 1992:45- 73.
126. Dommerholt J. Whiplash injury, muscle pain and motor dysfunction. In: Mense S, Gerwin
RD, eds. Muscle Pain:Diagnosisand Treatment. Heidelberg, Germany: Springer-Verlag;
2010:247- 288.
127. Janda V. Muscle strength in relation to muscle length, pain, and muscle imbalance. In:
Harms-Ringdahl K, ed. Muscle Strength. Edinburgh, UK: Churchill Livingstone; 1993:83-91.
128. Saggini R, Giamberardino MA, Gatteschi L, Vecchiet L. Myofascial pain syndrome of the
peroneus longus: biomechanical approach. Clin J Pain. 1996;12:30-37.
129. Fernandez-de-las-Penas C, Alonso-Blanco C, Cuadrado ML, Pareja JA. Neck mobility and
forward head posture are not related to headache parameters in chronic tension-type head-
ache. Cephalalgia.2007;27:158 -1 64.
130. Fernandez-de-las-Penas C, Simons D, Cuadrado ML, Pareja J. The role of myofascial trigger
points in musculoskeletal pain syndromes of the head and neck. Curr Pain Headache Rep.
2007;11:365 - 372.
131. Andersen JH, Krergaard A, Rasmussen K. Myofascial pain in different occupational groups
with monotonous repetitive work. Journal of Musculoskeletal Pain. 1995;3(suppl 1):57.
132. Lin TY, Teixeria MJ, Fischer AA, et al. Work-related musculoskeletal disorders. In: Fischer
AA, ed. Myofascial Pain: Update in Diagnosisand Treatment. Philadephia, PA: WB Saun-
ders; 1997:113-118.
133. Farrell J, Littlejohn G. Association between task performance and tender point pain thresh-
old to pressure in normal subjects. Journal of Musculoskeletal Pain. 1997;5:19- 47.
134. Gerdle B, Hilgenfeldt U, Larsson B, Kristiansen J, S0gaard K, Rosendal L. Bradykinin and
kallidin levels in the trapezius muscle in patients with work-related trapezius myalgia, in
patients with whiplash associated pain, and in healthy controls: a rnicrodialysis study of
women. Pain. 2008;139:578 - 587.
135. Larsson B, BjiirkJ, Kadi F, Lindman R, Gerdie B. Blood supply and oxidative metabolism in
muscle biopsies of female cleaners with and without myalgia. Clin J Pain. 2004;20:440 - 446.
136. Feuerstein M, Hickey PF. Ergonomic approaches in the clinical assessment of occupational
musculoskeletal disorders. In: Turk DC, Melzack R, eds. Handbook of Pain Assessment. New
York: Guilford Press; 1992:71- 99.
137. Kuorinka I, Forcier L. Work Related Musculoskeletal Disorders (WMSDs):A ReferenceBook
for Prevention. Bristol, UK: Taylor & Francis; 1995.
138. Dommerholt J. Performing arts medicine - instrumentalist musicians part I: general consid-
erations.! Bodyw Mov 1her. 2009;13:311- 319.
139. Dommerholt J. Performing arts medicine - instrumentalist musicians part III: case reports.
J Bodyw Mov 1her. 2010;14:127- 138.
140. Rosen NB. Myofascial pain: the great mimicker and potentiator of other diseases in the per-
forming artist. Md Med J.1993;42:261-266.
141. Treaster D, Marras WS, Burr D, Sheedy JE, Hart D. Myofascial trigger point develop-
ment from visual and postural stressors during computer work. J ElectromyogrKinesiol.
2006;16:115-1 24.
142. Straker L, Burgess-Limerick R, Pollock C, Maslen B. The influence of desk and display de-
sign on posture and muscle activity variability whilst performing information technology
tasks. Appl Ergon. 2009;40:852 - 859.
143. Straker L, Skoss R, Burnett A, Burgess-Limerick R. Effect of visual display height on mod-
elled upper and lower cervical gravitational moment, muscle capacity and relative strain.
Ergonomics.2009;52:204 - 221.
144. Alund M, Larsson SE, Lewin T. Work-related chronic neck impairment: neck motion analy-
sis in female traverse crane operators. Scand J RehabilMed. 1992;24:133-1 39.
145. Chen SM, Chen JT, Kuan TS, Hong J, Hong CZ. Decrease in pressure pain thresholds of
latent myofascial trigger points in the middle finger extensors immediately after continuous
piano practice. Journal of Musculoskeletal Pain. 2000;8:83 - 92.
146. Fernandez-Carnero J, Fernandez-de-Las-Penas C, de la Llave-Rinc6n AI, Ge HY, Arendt-
Nielsen L. Prevalence of and referred pain from myofascial trigger points in the forearm
muscles in patients with lateral epicondylalgia. Clin J Pain. 2007;23:353- 360.
147. Fernandez-Carnero J, Fernandez-de-Las-Penas C, de la Llave-Rinc6n AI, Ge HY, Arendt-
Nielsen L. Bilateral myofascial trigger points in the forearm muscles in patients with
chronic unilateral lateral epicondylalgia: a blinded, controlled study. Clin J Pain. 2008;24:
802- 807.
148. SkubickDL, Clasby R, Donaldson CCS, et al. Carpal tunnel syndrome as an expression of
muscular dysfunction in the neck. J Occup Rehabil. 1993;3:31-43.
149. Vecchiet L, Giamberardino MA, de Bigontina P. Comparative sensory evaluation of parietal
tissues in painful and nonpainful areas in fibromyalgia and myofascial pain syndrome. In:
Gebhart GF, Hammond DL, Jensen TS, eds. Proceedingsof the 7th World Congresson Pain
(Progressin Pain Researchand Management). Seattle, WA: IASP Press; 1994:177-1 85.
150. Vecchiet L, Giamberardino MA, Dragani L. Latent myofascial trigger points: changes in
muscular and subcutaneous pain thresholds at trigger point and target level. Journal of
Manual Medicine. 1990;5:151-154.
151. Vecchiet L, Pizzigallo E, Iezzi S, Affaitati G, Vecchiet J, Giamberardino MA. Differentiation
of sensitivity in different tissues and its clinical significance. Journal of Musculoskeletal Pain.
1998;6:33-45.
152. Mense S. Nociception from skeletal muscle in relation to clinical muscle pain. Pain.
1993;54:241-289.
153. Giamberardino MA, Tafuri E, Savini A, et al. Contribution of myofascial trigger points to
migraine symptoms.! Pain. 2007;8:869 - 878.
154. Ge HY, Zhang Y, Boudreau S, Yue SW, Arendt-Nielsen L. Induction of muscle cramps by no-
ciceptive stimulation of latent myofascial trigger points. Exp Brain Res. 2008;187:623- 629.
155. Li LT, Ge HY, Yue SW, Arendt-Nielsen L. Nociceptive and non-nociceptive hypersensitivity
at latent myofascial trigger points. C/in J Pain. 2009;25:132 -1 37.
156. Audette JF, Wang F, Smith H. Bilateral activation of motor unit potentials with unilateral
needle stimulation of active myofascial trigger points. Am J PhysMed Rehabil. 2004;83:368 -
374, quiz 375- 377, 389.
157. Headley BJ. Evaluation and treatment of myofascial pain syndrome utilizing biofeedback.
In: Cram JR, ed. ClinicalElectromyographyfor Surface Recordings.Nevada City, CA: Clinical
Resources; 1990:235-254.
158. Dejung B, Griibli C, Colla F, Weissmann R. Triggerpunkttherapie.Bern, Switzerland: Hans
Huber; 2003.
159. Arendt-Nielsen L, Svensson P. Referred muscle pain: basic and clinical findings. Clin J Pain.
2001;17:11-1 9.
160. Fernandez-de-las-Penas C, Ge HY, Arendt-Nielsen L, Cuadrado ML, Pareja JA. Referred
pain from trapezius muscle trigger points shares similar characteristics with chronic tension
type headache. Eur J Pain. 2007;11:475- 482.
161. Fernandez-de-las-Penas C, Ge HY, Arendt-Nielsen L, Cuadrado ML, Pareja JA. The local
and referred pain from myofascial trigger points in the temporalis muscle contributes to
pain profile in chronic tension-type headache. C/in J Pain. 2007;23:786 - 792.
162. Mense S. Referral of muscle pain: new aspects. American Pain Society Journal. 1994;3:l - 9.
163. Vecchiet L, Dragani L, de Bigontina P, Obletter G. Experimental referred pain and hyperal-
gesia from muscles in humans. In: Vecchiet L, Lindblom U, Albe-Fessard D, Fessard DA,
Giamberardino MA, eds. New Trends in Referred Pain and Hyperalgesia.Amsterdam: El-
sevier Science; 1993:239- 249.
164. Vecchiet L, Giamberardino MA. Referred pain: clinical significance, pathophysiology and
treatment. In: Fischer AA, ed. Myofascial Pain: Update in Diagnosisand Treatment. Philadel-
phia, PA: WB Saunders; 1997:119-136.
165. Rocha CA, Sanchez TG . Myofascial trigger points: another way of modulating tinnitus. Prog
Brain Res. 2007;166:209 - 214.
166. Nie H, Graven-Nielsen T, Arendt-Nielsen L. Spatial and temporal summation of pain evoked
by mechanical pressure stimulation. Eur J Pain. 2009;13:592 - 599.
167. Mense S, Meyer H. Different types of slowly conducting afferent units in cat skeletal muscle
and tendon.J Physiol.June 1985:403-417.
168. Mense S, Stahnke M. Responses in muscle afferent fibres of slow conduction velocit y to con-
tractions and ischaemia in the cat. J Physiol. September 1983;383-397.
169. Hong CZ, Chen YN, Twehous D, Hong DH. Pressure threshold for referred pain by compres-
sion on the trigger point and adjacent areas. Journal of Musculoskeletal Pain. 1996;4:61-79.
170. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns, I: a study in nor-
mal volunteers. Spine. 1990;15:453-457.
171. Hong CZ, Simons DG. Pathophysiologic and electrophysiologic mechanisms of myofascial
trigger points. Arch Phys Med Rehabil. 1998;79:863-872.
172. Gibson W, Arendt-Nielsen L, Graven-Nielsen T. Referred pain and hyperalgesia in human
tendon and muscle belly tissue. Pain. 2006;120:113 -123.
173. Gibson W, Arendt-Nielsen L, Graven-Nielsen T. Delayed onset muscle soreness at tendon -
bone junction and muscle tissue is associated with facilitated referred pain. Exp Brain Res.
2006;174:351- 360.
174. Giamberardino MA, Affaitati G, Iezzi S, Vecchiet L. Referred muscle pain and hyperalgesia
from viscera . Journal of Musculoskeletal Pain. 1999;7:61-69.
175. Gibson SJ, Littlejohn GO, Gorman MM, Helme RD, Granges G. Altered heat pain thresholds
and cerebral event-related potentials following painful CO 2 laser stimulation in subjects
with fibromyalgia syndrome. Pain. 1994;58:185-193.
176. Mizumura K. Peripheral mechanism of muscle pain: an update. Curr Anaesth Crit Care.
2009;20:183 - 187.
177. Crotti FM, Carai A, Carai M, Sgaramella E, Sias W. Post-traumatic thoracic outlet syndrome
(TOS). Acta Neurochir Suppl. 2005;92:13 - 15.
178. Facco E, Ceccherelli F. Myofascial pain mimicking radicular syndromes. Acta Neurochir
Suppl. 2005;92:147- 150.
179. Weed ND. When shoulder pain isn't bursitis: the myofascial pain syndrome. PostgradMed.
1983;74:97-98, 101-102, 104.
180. Ge HY, Fernandez-de-Las-Penas C, Madeleine P, Arendt-Nielsen L. Topographical mapping
and mechanical pain sensitivity of myofascial trigger points in the infraspinatus muscle. Eur
J Pain. 2008;12:859 - 865.
181. Escobar PL, Ballesteros J. Teres minor: source of symptoms resembling ulnar neuropathy or
CS radiculopathy. Am J Phys Med Rehabii. 1988;67:120-122.
182. Hwang M, Kang YK, Kim DH. Referred pain pattern of the pronator quadratus muscle.
Pain. 2005;116:238- 242.
183. Hwang M, Kang YK, Shin JY,Kim DH. Referred pain pattern of the abductor pollicis longus
muscle. Am J PhysMed Rehabil. 2005;84:593 - 597.
184. Hsieh YL, Kao MJ, Kuan TS, Chen SM, Chen JT,Hong CZ. Dry needling to a key myo-
fascial trigger point may reduce the irritability of satellite MTrPs. Am J Phys Med Rehabil.
2007;86:397- 403.
185. Carlson CR, Okeson JP, Palace DA, Nitz AJ, Lindroth JE. Reduction of pain and EMG activ-
ity in the masseter region by trapezius trigger point injection. Pain. 1993;55:397-400.
186. Wright EF. Referred craniofacial pain patterns in patients with temporomandibular disor-
der.! Am Dent Assoc. 2000;131:1307-1 315.
187. Turp JC, Kowalski CJ, O'Leary N, Stohler CS. Pain maps from facial pain patients indicate
a broad pain geography.! Dent Res. 1998;77:1465-1472.
188. Svensson P, Graven-Nielsen T. Craniofacial muscle pain: review of mechanisms and clinical
manifestations.! Orofac Pain. 2001;15:117- 145.
189. Reeh ES, elDeeb ME. Referred pain of muscular origin resembling endodontic involvement:
case report. Oral Surg OralMed Oral Pathol. 1991;71:223-227.
190. Mascia P, Brown BR, Friedman S. Toothache of nonodontogenic origin: a case report.
J Endod. 2003;29:608 - 610.
191. Ge HY, Madeleine P, Wang K, Arendt-Nielsen L. Hypoalgesia to pressure pain in referred
pain areas triggered by spatial summation of experimental muscle pain from unilateral or
bilateral trapezius muscles. Eur J Pain. 2003;7:531- 537.
192. Ge HY, Fernandez-de-las-Penas C, Arendt-Nielsen L. Sympathetic facilitation ofhyperal-
gesia evoked from myofascial tender and trigger points in patients with unilateral shoulder
pain. Clin Neurophysiol. 2006;117:1545- 1550.
193. Shultz SP, Driban JB, Swanik CB. The evaluation of electrodermal properties in the identifi-
cation of myofascial trigger points. Arch Phys Med Rehabil. 2007;88:780 - 784.
194. Zhang Y, Ge HY, Yue SW, Kimura Y, Arendt-Nielsen L. Attenuated skin blood flow re-
sponse to nociceptive stimulation of latent myofascial trigger points. Arch Phys Med Rehabil.
2009;90:325 - 332.
195. Chung JW, Ohrbach R, McCall WD Jr. Effect of increased sympathetic activity on electrical
activity from myofascial painful areas. Am J Phys Med Rehabii. 2004;83:842 - 850.
196. Banks SL, Jacobs DW, Gevirtz R, Hubbard DR. Effects of autogenic relaxation training on
electromyographic activity in active myofascial trigger points. Journal of Musculoskeletal
Pain. 1998;6:23- 32.
197. Hubbard DR. Chronic and recurrent muscle pain: pathophysiology and treatment, and re-
view of pharmacologic studies. Journal of Musculoskeletal Pain. 1996;4:123-1 43.
198. McNulty WH, Gevirtz RN, Hubbard DR, Berkoff GM. Needle electromyographic evaluation
of trigger point response to a psychological stressor. Psychophysiology.1994;31:313-316.
199. Chen JT, Chen SM, Kuan TS, Chung KC, Hong CZ. Phentolamine effect on the spontaneous
electrical activity of active loci in a myofascial trigger spot of rabbit skeletal muscle. Arch
PhysMed Rehabil. 1998;79:790-794.
200. Chen JT, Chung KC, Hou CR, Kuan TS, Chen SM, Hong CZ. Inhibitory effect of dry nee-
dling on the spontaneous electrical activity recorded from myofascial trigger spots of rabbit
skeletal muscle. Am J Phys Med Rehabil. 2001;80:729 - 735.
201. Chen JT, Chen SM, Kuan, TS, Chung KC, Hong CZ. Phentolamine effect on the spontane-
ous electrical activity of active loci in a myofascial trigger spot of rabbit skeletal muscle. Arch
PhysMed Rehabil. 1998;79:790-794.
202. Couppe C, Midttun A, Hilden J, et al. Spontaneous needle electromyographic activity in
myofascial trigger points in the infraspinatus muscle: a blinded assessment. Journal of Mus-
culoskeletalPain. 2001;9:7-1 7.
203. Hong CZ, Yu J. Spontaneous electrical activity of rabbit trigger spot after transect ion of spi-
nal cord and peripheral nerve. Journal of Musculoskeletal Pain. 1998;6:45-58.
204. Hubbard DR, Berkoff GM. Myofascial trigger points show spontaneous needle EMG activity.
Spine. 1993;18:1803-1807.
205. Kuan TS, Chen JT,Chen SM, Chien CH, Hong CZ. Effect ofbotulinum toxin on end-
plate noise in myofascial trigger spots of rabbit skeletal muscle. Am J Phys Med Rehabil.
2002;81:512- 520; quiz 521- 523.
206. Macgregor J, Graf von Schweinitz D. Needle electromyographic activity of myofascial trigger
points and control sites in equine cleidobrachialis muscle: an observational study. Acupunct
Med. 2006;24:61 - 70.
207. Mense S, Simons DG, Hoheisel U, Quenzer B. Lesions of rat skeletal muscle after local block
of acetylcholinesterase and neuromuscular stimulation.! Appl Physiol. 2003;94:2494 - 2501.
208. Weeks VD, Travell J. How to give painless injections. In: AMA Scientific Exhibits 1957.New
York: Grune & Stratton; 1957:318-322.
209. Simons D. Clinical and etiological update of myofascial pain from trigger points. Journal of
Musculoskeletal Pain. 1996;4:93-121.
210. Simons DG. Do endplate noise and spikes arise from normal motor endplates? Am J Phys
Med Rehabil. 2001;80:134 - 140.
211. Liley AW. An in vestigation of spontaneous activity at the neuromuscular junction. ! Physiol.
1956;132:650-666.
212. Wiederholt WC. "End -plate noise" in electromyography. Neurology. 1970;20:214-224.
213. Arrowsmith JE. The neuromuscular junction. Surgery (Oxford).2007;25:105 -111.
214. Dommerholt J, McEvoy J. Myofascial trigger point release approach. In: Wise CH, ed. Ortho-
paedic Manual Physical Therapy:FromArt to Evidence. Philadelphia, PA: FA Davis. In press.
215. Gregorio CC, Granzier H, Sorimachi H, Labeit S. Muscle assembly: a titanic achievement?
Curr Opin CellBiol. 1999;11:18-25.
216. Lindstedt SL, Reich TE, Keim P, LaStayo PC. Do muscles function as adaptable locomotor
springs? J Exp Biol. 2002;205(Pt 15):2211- 2216.
217. Nagy A, Cacciafesta P, Grama L, Kengyel A, Malnasi-Csizmadia A, Kellermayer MS. Differ-
ential actin binding along the PEVK domain of skeletal muscle titin. J CellSci. 2004;117
(Pt 24):5781- 5789.
218. Niederlander N, Reynaud F, Astier C, Chaussepied P. Regulation of the actin-myosin inter-
action by titin. Eur J Biochem. 2004;271:4572 - 4581.
219. Wang K, McCarter R, Wright J, Beverly J, Ramirez-Mitchell R. of the sarcomere matrix in
skeletal muscles: the titin - myosin composite filament is a dual-stage molecular spring. Bio-
phys J.1993;64:1161-11 77.
220. Bang ML, Mudry RE, McE!hinny AS, et al. Myopalladin, a novel 145-kilodalton sarco-
meric protein with multiple roles in Z-disc and I-band protein assemblies.! Cell Biol.
2001;153:413- 427.
221. Clark KA, McElhinny AS, Beckerle MC, Gregorio CC. Striated muscle cytoarchitecture:
an intricate web of form and function. Annu Rev CellDev Biol. 2002;18:637- 706.
222. Jin JP, Wang K. Nebulin as a giant actin-binding template protein in skeletal muscle
sarcomere: interaction of actin and cloned human nebulin fragments. FEBSLett.
1991;281(1-2):93-96.
223. McElhinny AS, Kazmierski ST, Labeit S, Gregorio CC. Nebulin: the nebulous, multifunc-
tional giant of striated muscle. Trends CardiovascMed. 2003;13:195- 201.
224. McElhinny AS, Schwach C, Valichnac M, Mount-Patrick S, Gregorio CC. Nebulin
regulates the assembly and lengths of the thin filaments in striated muscle. J Cell Biol.
2005;170:947- 957.
225. Briickle W, Suckfiill M, Fleckenstein W, Weiss C, Muller W. Tissue p02 measurement in
taut back musculature (m. erector spinae) [in German]. Z Rheumatol. 1990;49:208-216.
226. Maekawa K, Clark GT, Kuboki T. Intramuscular hypoperfusion, adrenergic receptors, and
chronic muscle pain. J Pain. 2002;3:251- 260.
227. Shah JP, Danoff JV, Desai MJ, et al. Biochemicals associated with pain and inflammation
are elevated in sites near to and remote from active myofascial trigger points. Arch PhysMed
Rehabil. 2008;89:16 - 23.
228. Shah JP, Phillips TM, Danoff JV,Gerber LH. An in-vivo rnicroanalytical technique
for measuring the local biochemical milieu of human skeletal muscle. J Appl Physiol.
2005;99 :1977-1 984.
229. Martonosi AN. Regulation of calcium by the sarcoplasrnic reticulum. In: Engel AG, and
Franzini-Armstrong G, eds. Myology. New York McGraw-Hill; 1994:553-584.
230. Shenoi R, Nagler W. Trigger points related to calcium channel blockers (letter). Muscle
Nerve. 1996;19:256.
231. Henriksson KG, Bengtsson A, Lindman R, Thornell LE. Morphological changes in muscle in
fibromyalgia and chronic shoulder myalgia. In: H. Vrer0y, Merskey H, eds. Progressin Fibro-
myalgia and Myofascial Pain. Amsterdam: Elsevier; 1993:61-73.
232. Heffner RR, Barron SA. The early effects of ischemia upon skeletal muscle mitochondria.
J Neurol Sci. 1978;38:295-315.
233. Gariphianova MB. The ultrastructure of myogenic trigger points in patients with contrac-
ture of mimetic muscles (abstract). Journal of Musculoskeletal Pain. 1995;3(suppl 1):23.
234. Graven-Nielsen T, Arendt-Nielsen L. Induction and assessment of muscle pain, referred
pain, and muscular hyperalgesia. Curr Pain Headache Rep. 2003;7:443 - 451.
235. Bukharaeva EA, Salakhutdinov RI, Vyskocil F, Nikolsky EE. Spontaneous quantal and
non-quantal release of acetylcholine at mouse endplate during onset of hypoxia. PhysiolRes.
2005;54:251 - 255.
236. Gerwin RD, Dommerholt J, Shah JP. An expansion of Simons' integrated hypothesis of trig-
ger point formation. Curr Pain Headache Rep. 2004;8:468 - 475.
237. Sluka KA, Kalra A, Moore SA. Unilateral intramuscular injections of acidic saline produce
a bilateral, long-lasting hyperalgesia. Muscle Nerve. 2001;24:37- 46.
238. Sluka KA, Price MP, Breese NM, Stucky CL, Wemmie JA, Welsh MJ. Chronic hyperalge-
sia induced by repeated acid injections in muscle is abolished by the loss of ASIC3, but not
ASIC!. Pain. 2003;106:229 - 239.
239. McPartland JM. Travell trigger points: molecular and osteopathic perspectives.! Am Osteo-
path Assoc. 2004;104:244 - 249.
240. McPartland JM, Simons DG. Myofascial trigger points: translating molecular theory into
manual therapy.! Man Manip 1her. 2006;14:232 - 239.
241. Aoki KR. Review of a proposed mechanism for the antinociceptive action ofbotulinum
toxin type A. Neurotoxicology.2005;26:785- 793.
242. Gobel H, Heinze A, Reichel G, Hefter H, Benecke R, Dysport Myofascial Pain Study Group.
Efficacy and safety of a single botulinum type A toxin complex treatment (Dysport) for the
relief of upper back myofascial pain syndrome: results from a randomized double-blind
placebo-controlled multicentre study. Pain. 2006;125:82- 88.
243. Kern U, Martin C, Scheicher S, Muller H. Long-term treatment of phantom- and stump
pain with botulinum toxin type A over 12 months: a first clinical observation [in German].
Nervenarzt. 2004;75:336- 340.
244. Mense S. Neurobiological basis for the use ofbotulinum toxin in pain therapy.! Neurol.
2004;251 (suppl 1):11-17.
245. Reilich P, FheodoroffK, Kern U, et al. Consensus statement: botulinum toxin in myofascial
pain. JNeurol. 2004;251 (suppl 1):136-138.
246. Hackett R, Kam PC. Botulinum toxin: pharmacology and clinical developments: a literature
review. Med Chem. 2007;3:333- 345.
247. Bach-Rojecky L, Lackovic Z. Antinociceptive effect ofbotulinum toxin type A in rat model
of carrageenan and capsaicin induced pain. CroatMed J.2005;46:201- 208.
248. Luvisetto S, Marinelli S, Cobianchi S, Pavone F. Anti-allodynic efficacy ofbotulinum neuro-
toxin A in a model of neuropathic pain. Neuroscience.2007;145:l - 4.
249. de Paiva A, Meunier FA, Molg6 J, Aoki KR, Dolly JO. Functional repair of motor endplates
after botulin um neurotoxin type A poisoning: biphasic switch of synaptic activity between
nerve sprouts and their parent terminals. ProcNatl A cad Sci US A. 1999;96:3200- 3205.
250. Dommerholt J, Shah J. Myofascial pain syndrome. In: Ballantyne JC, Rathmell JP, Fishman
SM, eds. Bonica'sPain Management. Baltimore: Lippincott Williams & Williams; 2010.
In press.
251. Wang K, Yu L. Emerging concepts of muscle contraction and clinical implications for myo-
fascial pain syndrome (abstract). In: Focuson Pain 2000. Mesa, AZ: Janet G. Trave ll, MD
Seminar Series; 2000.
252. Reitinger A, Radner H, Tilscher H, Hanna M, Windisch A, Feigl W. Morphologische Unter-
suchung an Triggerpunkten . Manuelle Medizin. 1996;34:256-262.
253. Windisch A, Reitinger A, Traxler H, et al. Morphology and histochemistry of myogelosis.
Clin Anat. 1999;12:266-271.
254. Fassbender HG. Morphology and pathogenesis of soft-tissue rheumatism [in German].
Z Rheumaforsch. 1973;32:355-374.
255. Gerwin RD, Dommerholt J, Shah J. An expansion of Simons ' integrated hypothesis of trigger
point formation. Curr Pain Headache Rep. 2004;8:468 - 475.
256. ltoh K, Okada K, Kawakita K. A proposed experimental model of myofascial trigger points
in human muscle after slow eccentric exercise. Acupunct Med. 2004;22:2 -1 2; discussion
12- 13.
257. Hagg GM. The Cinderella hypothesis. In: Johansson H Wirdhorst U, Djupsjobacka M,
Passatore M, eds. Chronic Work-RelatedMyalgia. Gavle, Sweden: Gavle University Press;
2003:127-1 32.
258. Forsman M, Taoda K, Thorn S, Zhang Q.Motor-unit recruitment during long-term isomet-
ric and wrist motion contractions: a study concerning muscular pain development in com-
puter operators. Int JInd Ergon. 2002;30:237- 250.
259. Zennaro D, Laubli T, Krebs D, Krueger H, Klipstein A. Trapezius muscle motor unit activity
in symptomatic participants during finger tapping using properly and improperly adjusted
desks. Hum Factors.2004;46:252 - 266.
260. Febbraio MA, Pedersen BK. Contraction-induced myokine production and release: is skel-
etal muscle an endocrine organ? Exerc Sport Sci Rev. 2005;33:114-119.
261. Gissel H. Ca 2+ accumulation and cell damage in skeletal muscle during low frequency stimu-
lation. Eur JAppl Physiol.2000;83:175 - 180.
262. Gissel H, Clausen T. Excitation-induced Ca(2+) influx in rat soleus and EDL muscle:
mechanisms and effects on cellular integrity. Am JPhysiolRegul Integr Comp Physiol.
2000;279:R917 - R924.
263. Lexell J, Jarvis J, Downham D, Salmons S. Stimulation-induced damage in rabbit fast-twitch
skeletal muscles: a quantitative morphological study of the influence of pattern and fre-
quency. Cell Tissue Res. 1993;273:357-362.
264. Pedersen BK, Febbraio M. Muscle-derived interleukin-6: a possible link between skeletal
muscle, adipose tissue, liver, and brain. Brain Behav Immun. 2005;19:371- 376.
265. Mense S. The pathogenesis of muscle pain. Curr Pain Headache Rep. 2003;7:419- 425.
266. Ambalavanar R, Dessem D, Moutanni A, et al. Muscle inflammation induces a rapid in-
crease in calcitonin gene-related peptide (CGRP) mRNA that temporally relates to CGRP
immunoreactivity and nociceptive behavior. Neuroscience.2006;143:875 - 884.
267. Snijdelaar DG, Dirksen R, Slappendel R, Crul BJ. Substance P. Eur JPain. 2000;4:121- 135.
268. Mense S, Simons DG. Muscle Pain: UnderstandingIts Nature, Diagnosis,and Treatment.
Philadephia, PA: Lippincott, Williams & Wilkins. 2001:385.
269. Massa ad CA, Safieh-Garabedian B, Poole S, Atweh SF, Jabbur SJ, Saade NE. Involvement of
substance P, CGRP and histamine in the hyperalgesia and cytokine upregulation induced by
intraplantar injection of capsaicin in rats. JNeuroimmunol. 2004;153:171-1 82.
270. Jensen K, Tuxen C, Pedersen-Bjergaard U, Jansen I, Edvinsson L, Olesen J. Pain and tender-
ness in human temporal muscle induced bybradykinin and 5-hydroxytryptamine. Peptides.
1990;11:1127-1132.
271. Marceau F, Sabourin T, Houle S, et al. Kinin receptors: functional aspects. Int Immunophar-
macol. 2002;2:1729 -1 739.
272. Curatolo M, Arendt-Nielsen L, Petersen-Felix S. Evidence, mechanisms, and clinical im-
plications of central hypersensitivity in chronic pain after whiplash injur y. Clin JPain.
20 04;20:469 - 476.
273. Marchettini P, Simons DA, Caputi G, Ochoa JL. Pain from excitation of identified muscle
nociceptors in humans. Brain Res. 1996;740:109-116.
274. Graven-Nielsen T, Arendt-Nielsen L. Peripheral and central sensitization in musculoskeletal
pain disorders: an experimental approach. Curr Rheumatol Rep. 2002;4:313- 321.
275. Bendtsen L, Jensen R, Olesen J. Qualitatively altered nociception in chronic myofascial pain.
Pain. 1996;65:259-264.
276. Hoheisel U, Mense S, Simons DG, Yu XM. Appearance of new receptive fields in rat dorsal
horn neurons following noxious stimulation of skeletal muscle: a model for referral of mus-
cle pain? Neurosci Lett. 1993;153:9-1 2.
277. Ruch TC. Pathophysiology of pain. In: Ruch TC, Patton HD, eds. Physiologyand Biophysics:
1he Brain and Neural Function. Philadelphia, PA: WB Saunders; 1979:272-324.
278. Hu JW, Sessle BJ, Raboisson P, Dallel R, Woda A. Stimulation of craniofacial muscle af-
ferents induces prolonged facilitatory effects in trigeminal nociceptive brainstem neurons.
Pain. 1992;48:53-60.
279. Svensson P, Bak J, Troe st T. Spread and referral of experimental pain in different jaw mus-
cles.! OrofacPain. 2003;17:214- 223.
280. Svensson P, List T, Hector G. Analysis of stimulus-evoked pain in patients with myofascial
temporomandibular pain disorders. Pain. 2001;92:399 - 409.
281. Fernandez-de-las-Penas C, Ge HY, Cuadrado ML, Madeleine P, Pareja JA, Arendt-Nielsen L.
Bilateral pressure pain sensitivity mapping of the temporalis muscle in chronic tension-type
headache. Headache. 2008;48:1067 -1 075.
282. Fernandez-de-las-Penas CF, Cuadrado ML, Gerwin RD, Pareja JA. Referred pain from the
trochlear region in tension-type headache: a myofascial trigger point from the superior
oblique muscle. Headache. 2005;45:731- 737.
283. Anderson RU. Management of chronic prostatitis - chronic pelvic pain syndrome. Urol Clin
North Am. 2002;29:235 - 239.
284. Anderson RU. Traditional therapy for chronic pelvic pain does not work: what do we do
now? Nat Clin Pract Urol.2006;3:145 - 156.
285. Anderson RU, Wise D, Sawyer T, Chan C. Integration of myofascial trigger point re-
lease and paradoxical relaxation training treatment of chronic pelvic pain in men. J Urol.
2005;174:155-1 60.
286. Anderson RU, Wise, D, Sawyer T, Chan CA. Sexual dysfunction in men with chronic prosta-
titis/chronic pelvic pain syndrome: improvement after trigger point release and paradoxical
relaxation training.! Urol.2006;176:1534- 1538.
287. Issberner U, Reeh PW, Steen KH. Pain due to tissue acidosis: a mechanism for inflammator y
and ischemic myalgia? Neurosci Lett. 1996;208:191-194.
288. Shah JP, Gilliams EA. Uncovering the biochemical milieu of myofascial trigger points using
in vivo rnicrodialysis: an application of muscle pain concepts to myofascial pain syndrome.
JBodyw Mov 1her. 2008;12:371- 384.
289. Hoheisel U, Unger T, Mense S. Excitatory and modulatory effects of inflammator y cyto -
kines and neurotrophins on mechanosensitive group IV muscle afferents in the rat. Pain.
2005;114:168- 176.
290. Loram LC, Fuller A, Cartmell T, Mitchell B, Mitchell D. Behavioural, histological and
cytokine responses during hyperalgesia induced by carrageenan injection in the rat tail.
PhysiolBehav. 2007;92:873- 880.
291. Loram LC, Fuller A, Fick LG, Cartmell T, Poole S, Mitchell D. Cytokine profiles during
carrageenan-induced inflammatory hyperalgesia in rat muscle and hind paw. J Pain.
2007;8:127- 136.
292. Loram LC, Themistocleous AC, Fick LG, Kamerman PR. The time course of inflammatory
cytokine secretion in a rat model of postoperative pain does not coincide with the onset of
mechanical hyperalgesia. Can JPhysiolPharmacol. 2007;85:613- 620.
293. Luo G, Hershko DD, Robb BW, Wray CJ, Hasselgren PO. IL-lbeta stimulates IL-6 produc-
tion in cultured skeletal muscle cells through activation of MAP kinase signaling pathway
and NF-kappa B. Am J PhysiolRegul Integr Comp Physiol. 2003;284:Rl249 - Rl254.
294. Samad TA, Moore KA, Sapirstein A, et al. lnterleukin-lbeta-mediated induction of Cox-2 in
the CNS contributes to inflammatory pain hypersensitivity. Nature. 2001;410:471- 475.
295. Schafers M, Sorkin LS, Sommer C. Intramuscular injection of tumor necrosis factor-alpha
induces muscle hyperalgesia in rats. Pain. 2003;104:579 - 588.
296. Tidba ll JG. Inflammatory processes in muscle injury and repair. Am J PhysiolRegul Integr
Comp Physiol. 2005;288:R345 - R353.
297. Niddam DM, Chan RC, Lee SH, Yeh TC, Hsieh JC. Central modulation of pain evoked from
myofascial trigger point. Clin JPain. 2007;23:440 - 448.
298. Partanen J. End plate spikes in the human electromyogram: revision of the fusimotor theory.
JPhysiolParis. 1999;93:155- 166.
299. Partanen JV, Ojala TA, Arokoski JP. Myofascial syndrome and pain: a neurophysiological
approach. Pathophysiology.2010;17:19- 28.
300. Grassi C, Passatore M. Action of the sympathetic system on skeletal muscle. Ital J Neurol Sci.
1988;9:23-28.
301. Grassi C, Passatore M. Spontaneous sympathetic command to skeletal muscles: functional
implications. Funct Neurol. 1990;5:227-232.
302. Grassi C, Passatore M. Anti-fatigue action exerted by the sympathetic nervous system in the
rabbit digastric muscle. Funct Neurol. 1991;6:255- 258.
303. Barker D, Saito M. Autonomic innervation of receptors and muscle fibres in cat skeletal
muscle. Proc R Soc Lond B Biol Sci. 1981;212:317-332.
304. Ljung BO, Forsgren S, Friden J. Sympathetic and sensory innervations are heterogeneously
distributed in relation to the blood vessels at the extensor carpi radialis brevis muscle origin
of man. Cells Tissues Organs. 1999;165:45- 54.
305. Ettlin T. Trigger point injection treatment with the 5-HT3 receptor antagonist tropisetron in
patients with late whiplash-associated disorder: first results of a multiple case study. Scand J
Rheumatol Suppl. 2004;119:49 - 50.
306. Muller W, Stratz T. Local treatment oftendinopathies and myofascial pain syndromes with
the 5-HT3 receptor antagonist tropisetron. Scand J Rheumatol Suppl. 2004;119:44 - 48.
307. Bowman WC, Marshall IG, Gibb AJ, Har borne AJ. Feedback control of transmitter release
at the neuromuscular junction. Trends Pharmacol Sci. 1988;9:16-20.
308. Fernandez-de-las-Penas C, Cleland JA, Cuadrado ML, Pareja JA. Predictor variables for
identifying patients with chronic tension-type headache who are likely to achieve short-term
success with muscle trigger point therapy. Cephalalgia.2008;28:264 - 275.
309. Simons D. Understanding effective treatments of myofascial trigger points. J Bodyw Mov
1her. 2002;6:81- 88.
310. Steinbrocker 0. Therapeutic injections in painful musculoskeletal disorders. JAMA.
1944;125:397-401.
311. Gaspersic R, Koritnik B, Erzen I, Sketelj J. Muscle activity-resistant acetylcholine receptor
accumulation is induced in places of former motor end plates in ectopically innervated re-
generating rat muscles. Int J Dev Neurosci. 2001;19:339- 346.
312. Sadeh M, Stern LZ, Czyzewski K. Changes in end-plate cholinesterase and axons during
muscle degeneration and regeneration.! Anat. 1985;140:165-176.
313. Lund I, Lundeberg T. Are minimal, superficial or sham acupuncture procedures acceptable
as inert placebo controls? Acupunct Med. 2006;24:13 -1 5.
314. Lundeberg T, Uvniis-Moberg K, Agren G, Bruzelius G. Anti-nociceptive effects of oxytocin
in rats and mice. Neurosci Lett. 1994;170:153-157.
315. Mohr C, Binkofski F, Erdmann C, Biichel C, Helmchen C. The anterior cingulate cortex
contains distinct areas dissociating external from self-administered painful stimulation:
a parametric fMRI study. Pain. 2005;114:347- 357.
316. Olausson H, Lamarre Y, Backlund H, et al. Unmyelinated tactile afferents signal touch and
project to insular cortex. Nat Neurosci. 2002;5:900 - 904.
317. Uvniis-Moberg K, Bruzelius G, Alster P, Lundeberg T. The antinociceptive effect of non-
noxious sensory stimulation is mediated partly through oxytocinergic mechanisms. Acta
PhysiolScand. 1993;149:199-204.
318. Hui KK, Liu J, Makris N, et al. Acupuncture modulates the limbic system and subcortical
gray structures of the human brain: evidence from fMRI studies in normal subjects. Hum
Brain Mapp. 2000;9:13- 25.
319. Biella G, Sotgiu ML, Pellegata G, Paulesu E, Castiglioni I, Fazio F. Acupuncture produces
central activations in pain regions. Neuroimage. 2001;14:60- 66.
320. Hsieh JC, Tu CH, Chen FP, et al. Activation of the hypothalamus characterizes the acupunc-
ture stimulation at the analgesic point in human: a positron emission tomography study.
Neurosci Lett. 2001;307:105-1 08.
321. Wu MT, Hsieh JC, Xiong J, et al. Central nervous pathway for acupuncture stimulation: lo-
calization of processing with functional MR imaging of the brain: preliminary experience.
Radiology.1999;212:133-1 41.
322. Wu MT, Sheen JM, Chuang KH, et al. Neuronal specificity of acupuncture response: a fMRI
study with electroacupuncture. Neuroimage. 2002;16:1028 -1 037.
323. Takeshige C, Kobori M, Hishida F, Luo CP, Usami S. Analgesia inhibitor y system in-
volvement in nonacupuncture point-stimulation-produced analgesia. Brain Res Bull.
1992;28:379-391.
324. Takeshige C, Sato T, Mera T, Hisamitsu T, Fang J. Descending pain inhibitory system in-
volved in acupuncture analgesia. Brain Res Bull. 1992;29:617-634.
325. Ceccherelli F, Rigoni MT, Gagliardi G, Ruzzante L. Comparison between superficial and
deep acupuncture in the treatment of lumbar myofascial pain: a double-blind randomized
controlled study. Clin J Pain. 2002;18:149 -1 53.
326. Cummings M. Myofascial pain from pectoralis major following trans-axillary surgery.
Acupunct Med. 2003;21:105 -1 07.
327. Dilorenzo L, Traballesi D, Morelli A, et al. Hemiparetic shoulder pain syndrome treated
with deep dry needling during early rehabilitation: a prospective, open-label, randomized
investigation. Journal of Musculoskeletal Pain. 2004;12:25 - 34.
328. Lewit K. The needle effect in the relief of myofascial pain. Pain. 1979;6:83-90.
329. Lucas KR, Polus BI, Rich PS. Latent myofascial trigger points: their effect on muscle activa-
tion and movement efficiency.! Bodyw Mov 1her. 2004;8:160 -1 66.
330. Ga H, Choi JH, Park CH, Yoon HJ. Dry needling of trigger points with and without para spi-
nal needling in myofascial pain syndromes in elderly patients. ! A/tern Complement Med.
2007;13:617- 624.
331. Ga H, Koh HJ, Choi JH, Kim CH. Intramuscular and nerve root stimulation vs . lidocaine
injection to trigger points in myofascial pain syndrome.! Rehabil Med. 2007;39:374 - 378.
332. McMillan AS, Nolan A, Kelly PJ. The efficacy of dry needling and procaine in the treatment
of myofascial pain in the jaw muscles. J OrofacPain. 1997;11:307-314.
333. Moseley GL. A pain neuromatrix approach to patients with chronic pain. Man 1her.
2003;8:130 - 140.
334. Fernandez-de-las-Penas C, Campo MS, Carnero JF, Miangolarra-Page JC. Manual therapies
in myofascial trigger point treatment: a systematic review. J Bodyw Mov 1her. 2005;9:27 - 34.
335. Fernandez-de-las-Penas C, Alonso-Blanco C, Fernandez-Carnero J, Miangolarra-Page JC.
The immediate effect of ischemic compression technique and transverse friction massage
on tenderness of active and latent myofascial trigger points: a pilot study. J Bodyw Mov 1her.
2006;10:3 - 9.
336. Gemmell H, Miller P, Nordstrom H. Immediate effect of ischaemic compression and trigger
point pressure release on neck pain and upper trapezius trigger points: a randomized con-
trolled trial. Clin Chiropractic.2008;11:30 - 36.
337. Hanten WP, Olson SL, Butts NL, Nowicki AL. Effectiveness of a home program of ischemic
pressure followed by sustained stretch for treatment of myofascial trigger points. Phys 1her.
2000;80:997 -1 003.
338. Hong CZ, Chen YC, Pon CH, Yu J. Immediate effects of various physical medicine modali-
ties on pain threshold of the active myofascial trigger points. Journal of Musculoskeletal
Pain. 1993;1:37-53.
339. Mennell J. Spray-stretch for the relief of pain from muscle spasm and myofascial trigger
points. J Am Podiatry Assoc. 1976;66(11):873-876.
340. Blikstad A, Gemmell H. Immediate effect of activator trigger point therapy and myo-
fascial band therapy on non-specific neck pain in patients with upper trapezius trigger
points compared to sham ultrasound: a randomized controlled trial. Clinical Chiropractic.
2008;11:23 - 29.
341. Hou CR, Tsai LC, Cheng KF, Chung KC, Hong CZ. Immediate effects of various physical
therapeutic modalities on cervical myofascial pain and trigger-point sensitivity. Arch Phys
Med Rehabil. 2002;83:1406 - 1414.
342. Furlan AD, van Tulder M, Cherkin D, et al. Acupuncture and dry-needling for low back
pain: an updated systematic review within the framework of the Cochrane Collaboration.
Spine. 2005;30:944 - 963.
343. Tsai CT, Hsieh LF, Kuan TS, Kao MJ, Chou LW, Hong CZ. Remote effects of dry needling on
the irritability of the myofascial trigger point in the upper trapezius muscle. Am JPhys Med
Rehabil. 2010;89:133-1 40.
344. Chou LW, Hsieh YL, Kao MJ, Hong CZ. Remote influences of acupuncture on the pain in-
tensity and the amplitude changes of end plate noise in the myofascial trigger point of the
upper trapezius muscle. Arch PhysMed Rehabil. 2009;90:905 - 912.
345. Lee SH, Chen CC, Lee CS, Lin TC, Chan RC. Effects of needle electrical intramuscular stim-
ulation on shoulder and cervical myofascial pain syndrome and microcirculation. J Chin
Med Assoc. 2008;71:200 - 206.
346. Mayoral del Moral 0. Fisioterapia invasiva del sfndrome de dolor miofascial. Fisioterapia.
2005;27:69 - 75.
347. Kamanli A, Kaya A, Ardicoglu 0, Ozgocmen S, Zengin FO, Bayik Y. Comparison oflido-
caine injection, botulinum toxin injection, and dry needling to trigger points in myofascial
pain syndrome. Rheumatol Int. 2005;25:604 - 611.
348. lwama H, Akama Y. The superiority of water-diluted 0.25% to near 1% lidocaine for trigger-
point injections in myofascial pain syndrome: a prospective, randomized, double-blinded
trial. Anesth Analg. 2000;91:408 - 409.
349. lwama H, Ohmori S, Kaneko T, Watanabe K. Water-diluted local anesthetic for trigger-point
injection in chronic myofascial pain syndrome: evaluation of types of local anesthetic and
concentrations in water. RegAnesth Pain Med. 2001;26:333- 336.
350. Dommerholt J, Gerwin RD. Neurophysiological effects of trigger point needling therapies.
In: Fernandez de las Penas C, Arendt-Nielsen L, Gerwin RD, eds. Tension Type and Cervi-
cogenicHeadache:Pathophysiology,Diagnosisand Management. Boston: Jones & Bartlett;
2010:247- 259.
351. Kim HW, Kwon YB, Han HJ, Yang IS, Beitz AJ, Lee JH. Antinociceptive mechanisms associ-
ated with diluted bee venom acupuncture (apipuncture) in the rat formalin test: involvement
of descending adrenergic and serotonergic pathways. Pharmacol Res. 2005;51:183- 188.
352. Kwon YB, Kim JH, Yoon JH, et al. The analgesic efficacy of bee venom acupuncture
for knee osteoarthritis: a comparative study with needle acupuncture. Am J Chin Med.
2001;29:187-1 99.
353. Kwon YB, Lee JD, Lee HJ, et al. Bee venom injection into an acupuncture point reduces ar-
thritis associated edema and nociceptive responses. Pain. 2001;90:271- 280.
354. Ashkenazi A, Silberstein S. Botulinum toxin type A for the treatment of headache: why we
say yes . Arch Neurol. 2008;65:146 - 149.
355. Silberstein N. More than a cosmetic fix. Combined with physical therapy, botulinum toxin
type A can help provide relief for chronic muscle pain. Rehab Manag. 2007;20:44, 46.
356. Al tan L, Bingol U, Aykay M, Yurtkuran M. Investigation of the effect of GaAs laser therapy
on cervical myofascial pain syndrome. Rheumatol Int. 2005;25:23 - 27.
357. Ceccherelli F, Altafini L, Lo Castro G, Avila A, Ambrosio F, Giron GP. Diode laser in cervi-
cal myofascial pain: a double-blind study versus placebo. Clin J Pain. 1989;5:301- 304.
358. Garn AN, Warming S, Larsen LH, et al. Treatment of myofascial trigger-points with
ultrasound combined with massage and exercise: a randomised controlled trial. Pain.
1998;77:73-79.
359. Hakgiider A, Birtane M, Giircan S, Kokino S, Turan FN. Efficacy of low level laser therapy in
myofascial pain syndrome: an algometric and thermographic evaluation. Lasers Surg Med.
2003;33:339 - 343.
360. Ilbuldu E, Cakmak A, Disci R, Aydin R. Comparison of laser, dry needling, and placebo
laser treatments in myofascial pain syndrome. Photomed Laser Surg. 2004;22:306 - 311.
361. Lee JC, DT Lin, Hong CZ. The effectiveness of simultaneous thermotherapy with ultrasound
and electrotherapy with combined AC and DC current on the immediate pain relief of myo-
fascial trigger points. Journal of Musculoskeletal Pain. 1997;5:81-90.
362. Majlesi J, Unalan H. High-power pain threshold ultrasound technique in the treatment of
active myofascial trigger points: a randomized, double-blind, case-control study. Arch Phys
Med Rehabil. 2004;85:833 - 836.
363. Snyder-Mackler L, Barry AJ, Perkins AI, Soucek MD. Effects of helium-neon laser irradia-
tion on skin resistance and pain in patients with trigger points in the neck or back Phys
1her. 1989;69:336-341.
364. Snyder-Mackler L, Bork C, Bourbon B, Trumbore D. Effect of helium-neon laser on muscu-
loskeletal trigger points. Phys 1her. 1986;66:1087-1090.
365. Srbely JZ, Dickey JP. Randomized controlled study of the antinociceptive effect of ultra-
sound on trigger point sensitivity: novel applications in myofascial therapy? Clin Rehabil.
2007;21:411- 417.
366. Srbely JZ, Dickey JP, Lowerison M, Edwards AM, Nolet PS, Wong LL. Stimulation of myo-
fascial trigger points with ultrasound induces segmental antinociceptive effects: a random-
ized controlled study. Pain. 2008;139:260 - 266.
367. Chaitow L. Breathing pattern disorders, motor control, and low back pain. J OsteopMed.
2004;7:33- 40.
368. Inanici F, Yunus MB. History offibromyalgia: past to present. Curr Pain Headache Rep.
2004;8:369 - 378.
369. Smythe HA, Moldofsky H. Two contributions to understanding of the "fibrositis" syndrome.
Bull Rheum Dis. 1977;28:928-931.
370. Yunus MB. Fibromyalgia syndrome: a need for uniform classification.! Rheumatol.
1983;10:841-844.
371. Chakrabarty S, Zoorob R. Fibromyalgia. Am Fam Physician.2007;76:247- 254.
372. Wolfe F, Ross K, Anderson J, Russell IJ, Hebert L. The prevalence and characteristics of
fibromyalgia in the general population. Arthritis Rheum. 1995;38:19-28.
373. Wolfe F, Anderson J, Harkness D, et al. A prospective, longitudinal, multicenter study of ser-
vice utilization and costs in fibromyalgia. Arthritis Rheum. 1997;40:1560-1570.
374. Arnold LM, Lu Y, Crofford LJ, et al. A double-blind, multicenter trial comparing duloxetine
with placebo in the treatment of fibromyalgia patients with or without major depressive dis-
order. Arthritis Rheum. 2004;50:2974 - 2984.
375. Clauw DJ. Fibromyalgia: a label for chronic, widespread pain. Medscape Rheumatology.
2008. http://www.medscape.org/viewarticle/575198. Accessed December 12, 2010.
376. Clauw DJ, Crofford LJ. Chronic widespread pain and fibromyalgia: what we know, and what
we need to know. Best Pract Res Clin Rheumatol. 2003;17:685 - 701.
377. Aaron LA, Buchwald D. A review of the evidence for overlap among unexplained clinical
conditions. Ann Intern Med. 2001;134:868 - 881.
378. Aaron LA, Burke MM, Buchwald D. Overlapping conditions among patients with chronic
fatigue syndrome, fibromyalgia, and temporomandibular disorder. Arch Intern Med.
2000;160:221 - 227.
379. Harding SM. Sleep in fibromyalgia patients: subjective and objective findings. Am J Med Sci.
1998;315:367-376.
380. Williams DA, Clauw DJ. Understanding fibromyalgia: lessons from the broader pain re-
search community.! Pain. 2009;10:777 - 791.
381. Croft P, Burt J, Schollum J, Thomas E, Macfarlane G, Silman A. More pain, more ten-
der points: is fibromyalgia just one end of a continuous spectrum? Ann Rheum Dis.
1996;55:482-485.
382. Graven-Nielsen T, Sorensen J, Henriksson KG, Bengtsson M, Arendt-Nielsen L. Central
hyperexcitability in fibromyalgia. Journal of Musculoskeletal Pain. 1999;7:261-271.
383. Henriksson KG. Is fibromyalgia a central pain state? Journal of Musculoskeletal Pain.
2002;10:45 - 57.
384. Kamaleri Y, Natvig B, Ihlebaek CM, Benth JS, Bruusgaard D. Number of pain sites is associ-
ated with demographic, lifestyle, and health-related factors in the general population. Eur J
Pain. 2008;12:742 - 748.
385. Kamaleri Y, Natvig B, lhlebaek CM, Bruusgaard D. Localized or widespread musculoskeletal
pain: does it matter? Pain. 2008;138:41- 46.
386. Kamaleri Y, Natvig B, lhlebaek CM, Bruusgaard D. Does the number of musculoskeletal
pain sites predict work disability? A 14-year prospective study. Eur J Pain. 2009;13:426 - 430.
387. Marcus DA, Bernstein C, Rudy TE. Fibromyalgia and headache: an epidemiologi-
cal study supporting migraine as part of the fibromyalgia syndrome. Clin Rheumatol.
2005;24:595 - 601.
388. Martinez-Lavin M. Overlap of fibromyalgia with other medical conditions. Curr Pain Head-
ache Rep. 2001;5:347- 350.
389. Perez-Stable EJ, Miranda J, Munoz RF, Ying YW. Depression in medical outpatients: under-
recognition and misdiagnosis. Arch Intern Med. 1990;150:1083-1088.
390. Ackenheil M. Genetics and pathophysiology of affective disorders: relationship to fibromyal-
gia. Z Rheumatol. 1998;57(Suppl 2):5- 7.
391. Burckhardt CS, O'Reilly CA, Wiens AN, Clark SR, Campbell SM, Bennett RM. Assessing
depression in fibromyalgia patients. Arthritis Care Res. 1994;7:35- 39.
392. Bennett R. Fibromyalgia: present to future. Curr Rheumatol Rep. 2005;7:371- 376.
393. Sperber AD, Atzmon Y, Neumann L, et al. Fibromyalgia in the irritable bowel syndrome:
studies of prevalence and clinical implications. Am J Gastroenterol.1999 ;94:3541- 3546.
394. Meeus M, Nijs J. Central sensitization: a biopsychosocial explanation for chronic wide-
spread pain in patients with fibromyalgia and chronic fatigue syndrome. Clin Rheumatol.
2007;26:465 - 473.
395. Nijs J, De Meirleir K. Impairments of the 2-5A synthetase/RNase L pathway in chronic fa-
tigue syndrome. In Vivo. 2005;19:1013-1 021.
396. Evengard B, Nilsson CG, Lindh G, et al. Chronic fatigue syndrome differs from fibromyal-
gia: no evidence for elevated substance P levels in cerebrospinal fluid of patients with chronic
fatigue syndrome. Pain. 1998;78:153-155.
397. Wolfe F, Clauw DJ, Fitzcharles MA, et al. The American College of Rheumatology prelimi-
nary diagnostic criteria for fibromyalgia and measurement of symptom severity. Arthritis
Care Res. 2010;62:600 - 610.
398. Dommerholt J. Fibromyalgia: time to consider a new taxonomy? Journal of Musculoskeletal
Pain. 2000;8:41 - 47.
399. Rowbotham MC. Is fibromyalgia a neuropathic pain syndrome? J Rheumatol Suppl.
2005;75:38- 40.
400. Staud R. New evidence for central sensitization in patients with fibromyalgia. Curr Rheuma-
tol Rep. 2004;6:259.
401. Staud R. Biology and therapy offibromyalgia: pain in fibromyalgia syndrome. Arthritis Res
1her. 2006;8:208.
402. Staud R, Doming M. Evidence for abnormal pain processing in fibromyalgia syndrome. Pain
Med. 2001;2:208 - 215.
403. Woof C. Pain: moving from symptom control toward mechanism-specific pharmacologic
management. Ann Intern Med. 2004;140:441 - 451.
404. Bennett RM. Emerging concepts in the neurobiology of chronic pain: evidence of abnormal
sensory processing in fibromyalgia. Mayo Clin Proc. 1999;74:385-398.
405. Crofford LJ, Clauw DJ. Fibromyalgia: where are we a decade after the American College of
Rheumatology classification criteria were developed? Arthritis Rheum. 2002;46:1136 -11 38.
406. Julien N, Goffaux P, Arsenault P, Marchand S. Widespread pain in fibromyalgia is related to
a deficit of endogenous pain inhibition. Pain. 2005;114:295- 302.
407. Mease P. Fibromyalgia syndrome: review of clinical presentation, pathogenesis, outcome
measures, and treatment.! Rheumatol Suppl. 2005;75:6 - 21.
408. Staud R, Smitherman ML. Peripheral and central sensitization in fibromyalgia: pathogenetic
role. Curr Pain Headache Rep. 2002;6:259 - 266.
409. Jones KD, Deodhar P, Lorentzen A, Bennett RM, Deodhar AA. Growth hormone perturba-
tions in fibromyalgia: a review. Semin Arthritis Rheum. 2007;36:357- 379.
410. Yunus MB. Central sensitivity syndromes: a new paradigm and group nosology for fibro-
myalgia and overlapping conditions, and the related issue of disease versus illness. Semin
Arthritis Rheum. 2008;37:339 - 352.
411. Simms RW, Roy SH, Hrovat M, et al. Lack of association between fibromyalgia syndrome
and abnormalities in muscle energy metabolism. Arthritis Rheum. 1994;37:794-800.
412. Staud R, Vierck CJ, Cannon RL, Mauderli AP, Price DD. Abnormal sensitization and tem-
poral summation of second pain (wind-up) in patients with fibromyalgia syndrome. Pain.
2001;91:165-1 75.
413. Staud R, Vierck CJ, Robinson ME, Price DD. Spatial summation of heat pain within and
across dermatomes in fibromyalgia patients and pain-free subjects. Pain. 2004;111:342- 350.
414. Clauw DJ. Pharmacotherapy for patients with fibromyalgia. J Clin Psychiatry.2008;69
(suppl 2):25- 29.
415. Crofford LJ, Demitrack MA. Evidence that abnormalities of central neurohormonal systems
are key to understanding fibromyalgia and chronic fatigue syndrome. Rheum Dis Clin North
Am. 1996;22:267- 284.
416. Mense S. Descending antinociception and fibromyalgia. Z Rheumatol. 1998;57(suppl
2):23- 26.
417. Russell I, Vaeroy H, Javors M, Nyberg F. Cerebrospinal fluid biogenic amine metabo-
lites in fibromyalgia/fibrositis syndrome and rheumatoid arthritis. Arthritis Rheum.
1992;35:550-556.
418. Sarchielli P, Di Filippo M, Nardi K, Calabresi P. Sensitization, glutamate, and the link be-
tween migraine and fibromyalgia. Curr Pain Headache Rep. 2007;11:343 - 351.
419. Pillemer SR, Bradley LA, Crofford LJ, Moldofsky H, Chrousos GP. The neuroscience and en-
docrinology offibromyalgia. Arthritis Rheum. 1997;40(11):1928-1939.
420. Russell IJ. Advances in fibromyalgia: possible role for central neurochemicals. Am JMed Sci.
1998;315:377- 384.
421. Russell IJ, Orr MD, Littman B, et al. Elevated cerebrospinal fluid levels of substance P in pa-
tients with the fibromyalgia syndrome. Arthritis Rheum. 1994;37(11):1593- 1601.
422. Liu H, Brown JL, Jasmin L, et al. Synaptic relationship between substance P and the sub-
stance Preceptor: light and electron microscopic characterization of the mismatch between
neuropeptides and their receptors. ProcNatl Acad Sci US A. 1994;91:1009-1013.
423. Staud R. Evidence of involvement of central neural mechanisms in generating fibromyalgia
pain. Curr Rheumatol Rep. 2002;4:299 - 305.
424. Sorensen J, Graven-Nielsen T, Henriksson KG, Bengtsson M, Arendt-Nielsen L. Hyperexcit-

ability in fibromyalgia. J Rheumatol. 1998;25:152- 155.
425. Guedj E, Cammilleri S, Niboyet J, et al. Clinical correlate of brain SPECT perfusion abnor-
malities in fibromyalgia. JNucl Med. 2008;49:1798 - 1803.
426. Guedj E, Taieb D, Cammilleri S, et al. 99mTc-ECD brain perfusion SPECT in hyperalgesic
fibromyalgia. Eur JNucl Med Mol Imaging. 2007;34:130 -1 34.
427. Harris RE, Clauw DJ, Scott DJ, McLean SA, Gracely RH, Zubieta JK. Decreased central
mu-opioid receptor availability in fibromyalgia. JNeurosci. 2007;27:10000 -1 0006.
428. Wood PB, Patterson JC 2nd, Sunderland JJ, Tainter KH, Glabus MF, Lilien DL. Reduced pre-
synaptic dopamine activity in fibromyalgia syndrome demonstrated with positron emission
tomography: a pilot study. J Pain. 2007;8:51- 58.
429. Wood PB, Schweinhardt P, Jaeger E, et al. Fibromyalgia patients show an abnormal dop-
amine response to pain. Eur JNeurosci. 2007;25:3576 - 3582.
430. Lawson K. Pharmacological treatments of fibromyalgia: do complex conditions need com-
plex therapies? Drug Discov Today. 2008;13:333 - 340.
431. Arnold LM, Hess EV, Hudson JI, Welge JA, Berno SE, Keck PE Jr. A randomized, placebo-
controlled, double-blind, flexible-dose study offluoxetine in the treatment of women with
fibromyalgia. Am JMed. 2002;112:191- 197.
432. Arnold LM, Russell IJ, Diri EW, et al. A 14-week, randomized, double-blinded, pla-
cebo-controlled monotherapy trial of pregabalin in patients with fibromyalgia. JPain.
2008;9:792 - 805.
433. Crofford LJ, Appleton BE. The treatment of fibromyalgia: a review of clinical trials. Curr
Rheumatol Rep. 2000;2:101-1 03.
434. Crofford LJ, Rowbotham MC, Mease PJ, et al; Pregabalin 1008-105 Study Group. Pregabalin
for the treatment of fibromyalgia syndrome: results of a randomized, double-blind, placebo-
controlled trial. Arthritis Rheum. 2005;52:1264 -1 273.
435. Mease PJ, Russell IJ, Arnold LM, et al. A randomized, double-blind, placebo-controlled,
phase III trial of pregabalin in the treatment of patients with fibromyalgia. JRheumatol.
2008;35:502 - 514.
436. Pae CU, Marks DC, Han C, Patkar AA, Masand PS. Duloxetine: an emerging evidence for
fibromyalgia. Biomed Pharmacother.2009;63:69 - 71.
437. Russell IJ, Mease PJ, Smith TR, et al. Efficacy and safety of duloxetine for treatment of fibro-
myalgia in patients with or without major depressive disorder: results from a 6-month, ran-
domized, double-blind, placebo-controlled, fixed-dose trial. Pain. 2008;136:432 - 444.
438. Vitton 0, Gendreau M, Gendreau J, Kranzler J, Rao SG. A double-blind placebo-controlled
trial of milnacipran in the treatment of fibromyalgia. Hum Psychopharmacol.2004;19(suppl
l):S27- S35.
439. Russell IJ, Fletcher EM, Michalek JE, McBroom PC, Hester GG. Treatment of primary
fibrositis/fibromyalgia syndrome with ibuprofen and alprazolam: a double-blind, placebo-
controlled study. Arthritis Rheum. 1991;34:552- 560.
440. Bennett RM. A double-blind, randomized, controlled study of amitriptyline, nortriptyline
and placebo in patients with fibromyalgia: an analysis of outcome measures. Curr Rheumatol
Rep. 2002;4:286 - 292.
441. O'Malley PG, Balden E, Tomkins G, Santoro J, Kroenke K, Jackson JL. Treatment of fibro-
myalgia with antidepressants: a meta-analysis.! Gen Intern Med. 2000;15:659 - 666.
442. Carette S, Bell MJ, Reynolds WJ, et al. Comparison of amitriptyline, cyclobenzaprine, and
placebo in the treatment of fibromyalgia: a randomized, double-blind clinical trial. Arthritis
Rheum. 1994;37:32- 40.
443. Bennett RM, Gatter RA, Campbell SM, Andrews RP, Clark SR, Scarola JA. A comparison
of cyclobenzaprine and placebo in the management of fibrositis: a double-blind controlled
study. Arthritis Rheum. 1988;31:1535-1542.
444. Quimby LG, Gratwick GM, Whitney CD, Block SR. A randomized trial of cyclobenzaprine
for the treatment of fibromyalgia. JRheumatol Suppl. 1989;19:140-143.
445. Santandrea S, Montrone F, Sarzi-Puttini P, Boccassini L, Caruso I. A double-blind crossover
study of two cyclobenzaprine regimens in primary fibromyalgia syndrome.! Int Med Res.
1993;21:74- 80.
446. Tofferi JK, Jackson JL, O'Malley PG. Treatment of fibromyalgia with cyclobenzaprine: a
meta-analysis. Arthritis Rheum. 2004;51:9 -1 3.
447. Jaeschke R, Adachi J, Guyatt G, Keller J, Wong B. Clinical usefulness of amitriptyline
in fibromyalgia: the results of23 N-of-1 randomized controlled trials. JRheumatol.
1991;18:447-451.
448. Maes M, Verkerk R, Delmeire L, Van Gastel A, van Huns el F, Scharpe S. Serotonergic mark-
ers and lowered plasma branched-chain-amino acid concentrations in fibromyalgia. Psychia-
try Res. 2000;97:11- 20.
449. Anderberg UM, Marteinsdottir I, von Knorring L. Citalopram in patients with fibromyalgia:
a randomized, double-blind, placebo-controlled study. Eur J Pain. 2000;4:27 - 35.
450. Capaci K, Hepguler S. Comparison of the effects of amitriptyline and paroxetine in the
treatment of fibromyalgia syndrome. Pain Clinic. 2002;14:223 - 228.
451. Biasi G, Manca S, Manganelli S, Marcolongo R. Tramadol in the fibromyalgia syndrome:
a controlled clinical trial versus placebo. Int J Clin Pharmacol Res. 1998;18:13- 19.
452. Bennett R, Kamin M, Karim R, Rosenthal N. Tramadol and acetaminophen combination
tablets in the treatment of fibromyalgia pain: a double-blind, randomized, placebo-con-
trolled study. Am JMed. 2003;114:537- 545.
453. Assefi NP, Sherman KJ, Jacobsen C, Goldberg J, Smith WR, Buchwald D. A randomized
clinical trial of acupuncture compared with sham acupuncture in fibromyalgia. Ann Intern
Med. 2005;143:10 -1 9.
454. Berman BM, Ezzo J, Hadhazy V, Swyers JP. Is acupuncture effective in the treatment of
fibromyalgia? J Fam Pract. 1999;48:213-218.
455. Deluze C, Bosia L, Zirbs A, Chantraine A, Vischer TL. Electroacupuncture in fibromyalgia:
results of a controlled trial. BMJ. 1992;305:1249 - 1252.
456. Harris RE, Tian X, Williams DA, et al. Treatment of fibromyalgia with formula acupuncture:
investigation of needle placement, needle stimulation, and treatment frequency.! A/tern
Complement Med. 2005;11:663 - 671.
457. Brattberg G. Connective tissue massage in the treatment offibromyalgia. Eur JPain.
1999;3:235-244.
458. Blunt KL, Rajwani MH, Guerriero RC. The effectiveness of chiropractic management of
fibromyalgia patients: a pilot study. JManipulative Physiol 1her. 1997;20:389-399.
459. Gamber RG, Shores JH, Russo DP, Jimenez C, Rubin BR. Osteopathic manipulative treat-
ment in conjunction with medication relieves pain associated with fibromyalgia syndrome:
results of a randomized clinical pilot. JAm Osteopath Assoc. 2002;102:321- 325.
460. Brosseau L, Wells GA, Tugwell P, et al; Ottawa Panel Members. Ottawa Panel evidence-
based clinical practice guidelines for aerobic fitness exercises in the management of fibromy-
algia: part 1. Phys 1her. 2008;88:857 - 871.
461. Busch AJ, Schachter CL, Overend TJ, Peloso PM, Barber KA. Exercise for fibromyalgia: a
systematic review. J Rheumatol. 2008;35:1130 -1 144.
462. Jones KD, Adams D, Winters-Stone K, Burckhardt CS. A comprehensive review of 46 exer-
cise treatment studies in fibromyalgia (1988- 2005). Health Qua/ Life Outcomes. 2006;4:67.
463. Altan L, Bingol U, Aykay M, Koy Z, Yurtkuran M. Investigation of the effects of pool-based
exercise on fibromyalgia syndrome. Rheumatol Int. 2004;24:272 - 277.
464. Buckelew SP, Conway R, Parker J, et al. Biofeedback/relaxation training and exercise inter-
ventions for fibromyalgia: a prospective trial. Arthritis Care Res. 1998;11:196-209.
465. Hakkinen A, Hakkinen K, Hannonen P, Alen M. Strength training induced adaptations

in neuromuscular function of premenopausal women with fibromyalgia: comparison with
healthy women. Ann Rheum Dis. 2001;60:21- 26.
466. Wigers SH, Stiles TC, Vogel PA. Effects of aerobic exercise versus stress management treat-
ment in fibromyalgia: a 4.5 year prospective study. Scand JRheumatol. 1996;25:77- 86.
467. Cedraschi C, Desmeules J, Rapiti E, et al. Fibromyalgia: a randomised, controlled trial of
a treatment programme based on self management. Ann Rheum Dis. 2004;63:290 - 296.
468. Mannerkorpi K, Ahlmen M, Ekdahl C. Six- and 24-month follow-up of pool exercise therapy
and education for patients with fibromyalgia. Scand JRheumatol. 2002;31:306 - 310.
469. Mannerkorpi K, Nyberg B, Ahlmen M, Ekdahl C. Pool exercise combined with an education
program for patients with fibromyalgia syndrome: a prospective, randomized study. JRheu-
matol. 2000;27:2473 - 2481.
470. Zijlstra TR, van de Laar MA, Bernelot Moens HJ, Taal E, Zakraoui L, Rasker JJ. Spa treat-
ment for primary fibromyalgia syndrome: a combination of thalassotherapy, exercise
and patient education improves symptoms and quality of life. Rheumatology (Oxford).
2005;44:539 - 546.
471. Gowans SE, deHueck A, Voss S, Silaj A, Abbey SE, Reynolds WJ. Effect of a randomized,
controlled trial of exercise on mood and physical function in individuals with fibromyalgia.
Arthritis Rheum. 2001;45:519- 529.
472. King SJ, Wessel J, Bhambhani Y, Sholter D, Maksymowych W. The effects of exercise
and education, individuall y or combined, in women with fibromyalgia. J Rheumatol.
2002;29:2620 - 2627.
473. Schachter CL, Busch AJ, Peloso PM, Sheppard MS. Effects of short versus long bouts of aero-
bic exercise in sedentary women with fibromyalgia: a randomized controlled trial. Phys 1her.
2003;83:340 - 358.
474. Sprott H. What can rehabilitation interventions achieve in patients with primary fibromyal-
gia? Curr Opin Rheumatol. 2003;15:145- 150.
475. Jentoft E, Kvalvik AG, Mengshoel AM. Effects of pool-based and land-based aerobic ex-
ercise on women with fibromyalgia/chronic widespread muscle pain. Arthritis Rheum.
2001;45:42- 47.
476. Williams DA, Cary MA, Groner KH, et al. Improving physical functional status in
patients with fibromyalgia: a brief cognitive behavioral intervention.! Rheumatol.
2002;29:1280 - 1286.
477. Burckhardt CS, Mannerkorpi K, Hedenberg L, Bjelle A. A randomized, controlled clini-
cal trial of education and physical training for women with fibromyalgia. JRheumatol.
1994;21:714-720.
478. Gowans SE, deHueck A, Voss S, Richardson M. A randomized, controlled trial of exercise
and education for individuals with fibromyalgia. Arthritis Care Res. 1999;12:120-128.
479. Gusi N, Tomas-Carus P, Hakkinen A, Hakkinen K, Ortega-Alonso A. Exercise in waist-high
warm water decreases pain and improves health-related quality of life and strength in the
lower extremities in women with fibromyalgia. Arthritis Rheum. 2006;55:66 - 73.
480. Meiworm L, Jakob E, Walker UA, Peter HH, Keul J. Patients with fibromyalgia benefit from
aerobic endurance exercise. Clin Rheumatol. 2000;19:253 - 257.
481. McCain GA, Bell DA, Mai FM, Halliday PD. A controlled study of the effects of a supervised
cardiovascular fitness training program on the manifestations of primary fibromyalgia. Ar-
thritis Rheum. 1988;31:1135-1141.
482. Burckhardt CS, Goldenberg DL, Crofford LJ, et al. Guidelinesfor the Management of Fibro-
myalgia Syndrome Pain in Adults and Children. Glenview, IL: American Pain Society; 2005.
483. Busch AJ, Barber KA, Overend TJ, Peloso PM, Schachter CL. Exercise for treating fibromyal-
gia syndrome. CochraneDatabase Syst Rev. 2007:CD003786.
PART Ill
Evaluation and Treatment

of the Myof ascial System
Basic Evaluation of the
Myofascial System
Robert I. Cantu, Alan J.Grodin, and Robert W. Stanborough
The principal focus of this chapter is the evaluation of the myofascial system. Myo-
fascial assessment, however, represents only one aspect of the total biomechanical
evaluation of the spine, and the results of any myofascial evaluation should always
be correlated with other findings to assess accurately the functional (or dysfunc-
tional) status of the spine and extremities. For that reason, this chapter will neces-
sarily ref er to other aspects of the biomechanical evaluation.
Dysfunction is defined by Dorland's Illustrated Medical Dictionary, 31st Edition,
as a "disturbance, impairment, or abnormality of the functioning of an organ." 1
More specifically, somatic dysfunction can be defined as "impaired or altered func-
tion of related components of the somatic system. Somatic dysfunction is a state of
altered mechanics, palpable changes of integrity, increased or decreased mobility
and autonomic changes." 2 A therapist diagnoses dysfunction in the same man-
ner as a physician diagnoses pathology: through correlation of findings. When a
physician is looking for pathology in relation to low-back pain, the diagnosis is not
made based on radiology or physical examination alone. In the case of discogenic
pathology, for example, the physician uses the history, physical examination, ra-
diological findings, and electromyograms (EMGs) to determine if true discogenic
radiculopathy exists. If the patient has a magnetic resonance image (MRI) with
a positive finding for discogenic lesion, in the absence of any other finding, the
herniation may not be the cause of the pain and dysfunction. The physician who
diagnoses discogenic pathology on the basis of MRI alone would be premature in
making the diagnosis. If, however, the patient is experiencing low-back pain; has
referred pain in the lower extremity; and has diminished reflexes, selective muscle
weakness, and positive EMG and MRI results, the findings together definitively
correlate for discogenic pathology.
The physical therapist diagnoses significant dysfunction in the same way.
All findings from the history, visual, palpatory, and movement examinations are
correlated to determine dysfunction. Postural asymmetry caused by a leg-length
discrepancy, without the existence of other indicators, may not be dysfunctional.
183
184 EVAL UATION A ND TREATMENT OF THE MYOFASCIAL SYSTEM
Active movement abnormalities alone are not necessarily dysfunctional. Segmen-

tal hypermobility and hypo mobility, in and of themselves, are not necessarily dys-
functional. Connective tissue changes, in the absence of other findings, are not
dysfunctional. If several findings from the evaluation are abnormal, however, a
strong statement can be made for dysfunction. For example, a patient may have
symptoms including localized unilateral low-back pain, a postural fulcrum at
14- 5, an exaggerated lumbar curve reversal on forward bending (with a fulcrum
of motion at 14- 5), tenderness to palpation at the 14- 5 interspace, increased erec-
tor spinae muscle tone in the lumbar spine, hypermobility of the 14- 5 segment,
and thickened connective tissue in the area. In this unusually clear-cut theoretical
scenario, a dysfunction of 14- 5 exists, with 14- 5 hypermobility, movement im-
balance as a result of the hypermobility, increased thickness of connective tissue in
the area resulting from the body's attempt to stabilize the imbalance, and protec-
tive muscle guarding with altered muscular recruitment patterns. Although none
of these abnormalities alone constitutes dysfunction, the combination of abnor-
malities does. Treatment can be initiated by addressing the combination of factors
that contribute to the overall dysfunction.
The aspects of myofascial evaluation considered in this chapter are the history,
postural and structural evaluation, movement analysis, and palpatory examina-
tion. The findings of such should also be correlated with passive motion analysis.
Emphasis is on the myofascial aspects of the evaluation.
History
Cyriax stated that the patient's history is of great importance, especially in spinal
conditions. 3 Most clinicians have a standardized routine questionnaire and his-
torical format, but several key questions should always be asked when looking for
myofascial-type pain syndromes.
1. What is the quality of the pain? Myofascial pain is usually dull and aching, as well
as poorly localized. If the patient is reporting specific, sharp pain, which is easily repro -
duced, specific pathology may exist rather than a myofascial -type syndrome.
2. How is the patient sleeping at night? One of the critical factors in myofascial pain
is the disturbed sleep pattern. Typically, the patient will report difficulty going to sleep
and frequent awakenings during the night. Patients usually report feeling unrefreshed and
fatigued in the morning.
3. What pattern does the pain follow during the day? A typical daytime pattern for
myofascial pain is increased stiffness and pain in the early morning, with a slight drop -off
in symptoms at mid -morning, and with the pain remaining somewhat constant through -
out the day. Increased activity usually aggravates the condition, but the symptoms remain
regional and diffuse.
4. Can a position of comfort or relief be identified? Patients should be able to identify
a position of relief, even if only temporary, where pain may be decreased by minimizing
stresses through the contractile tissues. In the case of active trigger points, the position of
relief is often an alternating pattern of contracting and resting the muscle in a midrange
position.
Basic Evaluation of the Myofasc ial System 185
Postural and Structural Evaluation

The first part of any objective evaluation for somatic dysfunction consists of ob-
serving posture. Posture can be defined as balance and muscular coordination
and adaptation with minimal expenditure of energy. It is the position the body
assumes in preparation for the next movement, yet it is not necessarily a static
position. 4 Posture is dynamic, requiring constant changes in muscular forces and
creation of connective tissue tensions. Looking at the skeletal aspects of posture
without considering the dynamic aspects results in a shallow, incomplete picture
of the postural influences of dysfunction. It is the muscles that provide movement,
and both muscle and connective tissue maintain position. Body posture may give
preliminary clues to the location of a movement disturbance or to an area where
stress may occur because of overuse or trauma. Posture observation directs the
clinician's focus to a particular area or areas of the system that may be significantly
dysfunctional.
Observation of Posture
The patient should be viewed from anterior, posterior, and lateral angles to en-
sure accurate assessment (Figures 7.1 through 7.3). In integrating the myofascial
-..-
-=-
Figure 7 .1 Postural examination: anterior view. Figure 7 .2 Postural examination: posterior view.
186 EVALUATION AND TREATMENT OF THE MYOFASCIAL SYSTEM
system into postural evaluation, the clini-

cian should look for muscle asymmetry,
connective tissue asymmetry, and increased
muscular activity that may correlate with
abnormal structural deviations. Because
muscles may span several joints, and be-
cause the fascial planes can be restricted
over large areas of the body, the entire body
should be viewed from the feet up to the
• subcranial area .
Muscle asymmetry may be a result of
prolonged shortening or lengthening of a
muscle group, due, for example, to a leg-
length discrepancy or a pelvic obliquity.
Connective tissue asymmetry may be due
to abnormal stresses applied to an area, cre-
ating a localized proliferation of connective
tissue, as in a spondylolisthesis. Increased
muscular activity is usually a precursor to
muscle asymmetry and is usually found in
more acute cases.
Figure 7.3 Postural examination: lateral view. Although observing body asymmetry
is important, the clinician must remember
that the human body is, by nature's design,
asymmetrical. Hand, leg, and eye dominance may contribute to myofascial and
structural asymmetry. The critical factor in determining whether the asymmetry
is significant is its correlation to other relevant evaluative findings.
Postural observations give the clinician some insights into the overall equilib-
rium of the spine. When looking at joint equilibrium in the spine, consider that a
joint can be stable and in an optimal functional position only if there is equilib-
rium between the forces acting on it. A good example of myofascial disequilibrium
in the spine is the dysfunction caused by the forward-head posture. (See the sec-
tion entitled "Postural Effects of the Forward-Head Posture" for more details.)
In the forward-head posture, the midcervical facet joints are in the "up and
forward position," or forward bent. There is generally a loss of lordosis in this area,
with a tendency toward hypermobility (Figure 7.4). In the upper cervical and sub-
cranial area, the facet joints are in the "down and back position," or backward
bent, to compensate for the forward bending in the lower cervical spine and to
keep the eyes in horizontal. This creates compression of the facet joints, which
can lead to hypomobility and a shortening of the posterior myofascial structures.
Because the greater occipital nerve pierces the subcranial myofascia, compression
of this nerve can create occipital and frontal headaches. The anterior cervical spine
compensates by lengthening, changing the length-tension relationships, and con-
tributing to a weakness in the area.
In the forward-head posture, the man-

dible tends to open, so the masseters and
temporalis are engaged to keep the mouth
closed. This leads to new, but abnormal,
hyperactive muscle patterns, where the
muscles become facilitated and can create
dysfunctions such as nocturnal bruxism,
which can lead to degenerative changes in
the temporomandibular joint.
In the upper thoracic area, the facets
are again in a forward bent position, with
the posterior myofascial structures on a
stretch. In the anterior chest wall, the myo-
fascial structures are held in a shortened
position. The shoulder girdle complex is
held in a protracted position, with the gle-
nohumeral joint tending to go toward inter-
nal rotation. Because the anterior thorax is
held in a shortened position, diaphragmatic
breathing is compromised and the acces-
sory muscles of respiration are facilitated,
Figure 7 .4 Forward-head posture. leading to a potentially elevated first rib, a
compromise of the costoclavicular space,
and an increasing susceptibility to thoracic
outlet-type symptomatology. The lumbar spine can be either hyperlordotic or hy-
polordotic. If hypolordotic, a stretching of posterior structures occurs, resulting in
hypermobility and possible strain on the posterior aspect of the disc.
Postural Effects of the Forward-Head Posture

•!• Backward bending (extension) of the occiput/atlas
•!• Shortening of suboccipital muscles, resulting in potential impingement of
the greater or lesser occipital nerves
•!• Forward bending of the midcervical facet joints
•!• Cervical imbalance with a tendency toward degenerative joint disease from
CS through C7
•!• Imbalance between the sternocleidomastoid, the levator scapula, and the
trapezius
•!• Imbalance between the anterior cervical musculature (including the supra -
hyoid and infrahyoid muscles) and posterior cervical extensors
•!• Hyperactivity of masseters and temporalis to counter mandible's tendency to
open
•!• Shoulder girdle protraction with internal rotation (latissimus, subscapularis,
pectoralis, and teres major involvement)
•!• Muscular imbalance leading to abnormal muscle firing (some muscles be -
come facilitated with trigger points)
•!• Maintenance of joints and soft tissues in shortened range, leading to restric -
tion of joint capsules and loss of proprioception
•!• Elevation of the first rib by increased scalene activity
•!• Anterior and posterior restriction of the first rib articulations
•!• Tendency toward thoracic outlet symptomatology
•!• Increased thoracic kyphosis with decreased lumbar lordosis
•!• Increased activity of the accessory respiratory muscles due to poor diaphrag -
matic breathing and poor expansion of the lower rib cage
Myofascial Aspec ts of the Forward- Head Posture

The myofascial aspects of the forward-head posture correlate well with the me-
chanical aspects. Janda refers to the effects of myofascial imbalances on postural
imbalances. 2 •5 The principles he propounded include the relationship of "tonic"
(sometimes called "postural") and "phasic" muscles and their correlation to ago-
nist/antagonist muscle groups. In histological terms, tonic and phasic muscles are
differentiated by oxidative capacity and ability to generate large or small amounts
of force for short or long periods of time. The terms tonic and phasic, in the context
of Janda's work and for the purposes of this discussion, relate more to how the
muscle responds to dysfunction. In the myofascial context, a tonic muscle is one
that responds to dysfunction or abnormal stress by increasing in tone, or becom-
ing tight, whereas aphasic muscle is one that responds to dysfunction by becom-
ing inhibited or weak. 6 In the agonist/antagonist scheme, usually one muscle or set
of muscles responds to dysfunction by tightening, while the other responds with
inhibition or weakness. An obvious example of this is the quadriceps and ham-
strings. The quadriceps rarely become short and tight, whereas the hamstrings
tend to tighten and shorten regularly. If the knee is injured, the quadriceps are
usually inhibited, become weak, and atrophy, whereas the hamstrings rarely show
these results. These agonist/antagonist relationships play a vital role in postural
problems of the spine. Janda mapped out alternating patterns of faulty agonists/
antagonists spanning regions of the body, designating specific postural syndromes:
upper crossed, lower crossed, and layered syndromes. 7- 9
The upper crossed syndrome is observed in the posture's lateral view. It is
characterized by changes in the posterior short/tight tonic groups (upper trape-
zius and levator scapulae), phasic scapular stabilizers (low and mid-trapezius), and
anterior postural musculature (sternocleidomastoid, pectoralis major/minor), as
well as inhibited/weak phasic scapular stabilizers (lower/mid trapezius) and deep
cervical flexors. Connecting the like muscle groups with a line, anterior/posterior
tonic and anterior/posterior phasic, results in an X shape or cross, hence the term
upper crossed syndrome (Figure 7.5). The forward-head posture described is by far
the most common presentation in the clinic; however, a small percentage of pa-
tients present with an axially extended posture .
The lower crossed syndrome is mapped out in much the same way. It is char-
acterized by changes in the posterior - tonic posterior thoracolumbar erectors and
Phasic Tonic
long us colli upper trapezius
deep neck flexors levator scapulae
Tonic Phasic
pectoralis group low/mid trapezius
rhomboids
Phasic
abdominals
erector spinae
quadratus lumborum
Tonic
iliopsoas Phasic
gluteal group
Figure 7 .5 Upper and lower crossed syndromes.
phasic gluteus medius and maximus - and the anterior - postural hip flexors (ilio-
psoas, rectus femoris) and phasic abdominals. The patient presents with a forward
pelvic tilt, increased lumbar lordosis, and slightly flexed hips (Figure 7.5). Altered
patterns of hip extension are often seen in ambulation, with compensatory exten-
sion of the lumbar spine.7•10
The layered syndrome is observed in the posterior view. From top to bottom,
an alternating pattern adaptation can be seen in the tonic and phasic muscles, in-
cluding the tonic upper trapezius/levator scapulae, phasic mid- and low trapezius,
tonic thoracolumbar erectors, phasic gluteus medius/maximus, and tonic ham-
strings (Figures 7.6 and 7.7).
Janda suggested that treatment should first focus on restoring proper length
to the tonic muscles before strengthening the phasic. 11 He based this on Sher-
rington's law of reciprocal inhibition. Although not confirming Sherrington's law,
researchers have shown that the deep cervical musculature becomes inhibited in
the presence of neck pain, 12•13 while superficial flexors of the cervical spine (i.e., the
postural
: uppertrapezlus
levatorscapulae
Phasjc: infraspinatus
mid/lowtrapezius
mombolds
Postural: erector
splnae
Phaslc: glutealgroup
Postural: hamstrings
Figure 7 .6 Layered syndrome: posterior view.
sternocleidomastoid and anterior scalene) become overactive with delayed relax-

ation following head and upper-limb movements or prolonged isometric contrac-
tions.13-15 These tissue responses are believed to be the body's attempt to redistrib-
ute loads between agonist and antagonists within the spine. 16Likewise , the upper
trapezius has been shown to respond to repetitive upper limb movements with
hyperactivity. 14
Changes in behavior, as described above, are also fallowed by changes in
structure and function in prolonged or habitual conditions, resulting in decreased
muscle endurance, 17- 20strength, 19-21and efficiency.18
Cervical Spine
In the forward-head posture, the cervical lordosis is decreased, as is the straight-
line distance between the occiput and the cervicothoracic junction. This rela-
tionship places the cervical erector spinae in a shortened position, which over a
Basic Evaluation of the Myofascial System 191
Table 7.1 Cervical/Upper Thoracic Agonist/

Antagonist Relationships
Tonic (postural) Phasic
Cervical erector Anterior cervical
sp1nae musculature
Upper trapezius/ Latissimus dorsi
levator scapulae
Pectoralis major Low/mid-trapezius
( upper part) (upper part)
Pectoralis minor Rhomboids
period of time permanently shortens the

muscle. This is especially true in the upper
cervical spine. The anterior musculature,
on the other hand, is in an elongated posi-
tion, which eventually creates a permanent
lengthening. Because the muscle groups
respond to dysfunction by shortening and
weakening, the forward-head posture is
further enhanced (Table 7.1).
Thoracic Spine
In the forward-head posture, there is an
increased kyphosis of the thoracic spine.
The straight-line distance between the
manubrium and the umbilicus, as well
as the straight-line distance between gle-
nohumeral joints, is decreased. This places
Figure 7.7 Layered syndrome: lateral view. the pectoralis major and minor, along with
the upper trapezius, in a shortened position.
In the myofascial system, the pectoralis ma-
jor and minor muscles respond to dysfunction by tightening, as does the upper
trapezius. The middle and lower trapezius and rhomboid muscles weaken in re-
sponse to dysfunction, which further facilitates the thoracic dysfunction. Once
again, antagonistic muscle groups respond in opposite ways to facilitate the same
dysfunction. As noted, the anterior of the diaphragm, which, in turn, facilitates
the upper thoracic accessory breathing muscles, further compounds the problem.
Table 7.2 summarizes these changes.
Lumbar Spine
In the lumbar spine, two situations commonly exist. The first, excessive lumbar
lordosis, can be correlated to dysfunctional muscle groups (lower crossed syn-
drome). The increased lumbar lordosis includes a tightening of the lumbar erector
Table 7.2 Muscle Agonist/Antagonist Groups of the Cervicothoracic Area

With Resulting Dysfunctions
Response to
Muscle group Action dysfunction Results of dysfunction
Upper trapezius • Shoulder elevation Tightens • Scapula elevation/
levator scapulae • Assists shoulder adduction
adduction • Cervical joint compression
• Cervical backward • Restricted axial extension
bending and side • Limited cervical side
ending bending and rotation
Pectoralis major • Shoulder flexion Tightens • Restricted shoulder flexion
( upper part) • Humeral horizontal • Restricted horizontal
adduction adduction
Pectoralis minor • Scapular protraction Tightens • Scapular abduction with
• Accessory breathing inferior angle outward
rotation
• Winging of scapulae
inferior border
• Increased thoracic
kyphosis
Rhomboids middle/ • Scapular adduction Weakens • Scapular abduction with
lower trapezius • Fixes scapulae inferior inferior angle outward
angle to thoracic wall rotation
• Winging of scapulae
inferior border
• Increased thoracic
kyphosis
Cervical erector • Cervical backward Tightens • Loss of forward bending
sp1nae bending (extension) • Loss of axial extension
• Holds cervical spine in
forward-head posture
Anterior cervical • Cervical forward Weakens • Weakness in forward
musculature bending (flexion) bending
• Loss of axial extension
• Inability to pull out of
forward-head posture
spinae, psoas muscle groups, iliacus, and tensor fasciae latae. The antagonistic
groups, which include the abdominals and the gluteus maximus, weaken, further
facilitating the dysfunction. Corresponding
Table 7.3 Lumbar /Lumbopelvic Agonist/ joint dysfunction includes hypomobility of
Antagonist Relationships
the lumbar segments, with tightening of the
Tonic (postural) Phasic posterior structures (Tables 7.3 and 7.4).
lliopsoas/tensor fasciae Gluteus maximus The other scenario, in which there
latae
is a loss of lumbar lordosis, pits the ham-
Hamstrings Quadriceps
strings and posterior hip structures against
Hip adductors Gluteus medius
the erector spinae as antagonistic groups
Gastrocnemius-soleus Dorsiflexors
(layered syndrome). This situation is more
Erector spinae Abdominals
common in men with early to moderate
Basic Evaluation of the Myofascial System 193
Table 7.4 Muscle Agonist/Antagonist Groups of the LumbopelvicArea and Resulting Dysfunction
Response to
Muscle group Action dysfunction Results of dysfunction
lliopsoas • Hip flexi on Tightens • Restricted hip extension
• Assists in external • Tight anterior hip capsule
rotation & adduction • Increased lumbar lordosis
• Backward bending of • Decreased posterior
the lumbar spine rotation of ilium
• Restricted hip extension,
external rotation &
adduction
Tensor fasciae • Anterior rotation of ilium Tightens • Decreased posterior
latae • Hip flexion, internal rotation of ilium
rotation, abduction • Restricted hip extension,
• Backward bending of external rotation &
lumbar spine adduction
• Assists knee flexion • Contributes to increased
lumbar lordosis
Gluteus maximus • Hip extension Weakens • Loss of hip extension
• Posterior rotation of • Decreased posterior
ilium rotation of ilium
Hip adductors • Hip adduction Tightens • Restricted hip abduction
• Assists hip flexion • Restricted posterior
• Anterior rotation of ilium rotation of ilium
Gluteus medius • Hip abduction Weakens • Limited hip abduction
• Hip internal rotation • Loss of lateral hip
(anterior fibers) stabilization
• Hip external rotation
(posterior fibers)
Erector spinae • Extension of spine Tightens • Increased lumbar lordosis
Abdominals • Flexion of spine Weakens • Anterior pelvis tilt
• Increased lumbar lordosis
degenerative joint disease of the lumbar spine. The tightness in the hamstrings
and posterior capsule of the hips pulls the spine into forward flexion, holding the
erector spinae in a lengthened position, leading to progressive weakness. The cor-
responding dysfunction is usually joint hypermobility with eventual instability of
the lumbar spine.
When evaluating posture, the clinician should consider these myofascial re-
lationships and how they correlate to structure. These findings may then be cor-
related to the remainder of the evaluation.
Active Movement Analysis

Evaluation of active movements gives the clinician more valuable information
regarding possible pathology of the spine or extremities that may be correlated
with postural findings. In evaluating active range of motion from a myofascial
standpoint, the clinician should first look regionally, then segmentally. Regional
observation will usually reveal myofascial abnormalities, whereas segmental ob-

servation reveals more specific joint abnormalities. Entire spine motion should
be observed, with the patient being instructed to move segmentally starting in
the cervical area and proceeding through the thoracic and lumbar spine. Spinal
movements should be observed in total at least once, regardless of the suspected
area of pathology. The area of pathology should then be examined specifically.
The purpose of performing both regional and segmental observations is to dif-
ferentiate symptomatic from nonsymptomatic dysfunction. Dysfunction that is
symptomatic in one area of the body can be caused by a primary dysfunction in
another area that is not symptomatic but requires treatment to resolve the patient's
overall symptoms and dysfunction. This is especially true when examining the
myofascial system because the fascial planes are more regional, as are the resulting
dysfunctions.
Restriction of movement in the posterior musculature and fascia of the lower
extremity, with corresponding hypermobility of the lumbar spine, exemplifies re-
gional, asymptomatic dysfunction that causes symptomatic dysfunction elsewhere.
If a patient complains of low-back pain and exhibits an exaggerated lumbar curve
reversal with active movements, the pelvic component of forward bending may
be limited as a result of tight hips, short hamstrings, and/or shortened posterior
fascial planes. Over time, the posterior structures of the lumbar spine can become
elongated and weak as the lumbar spine becomes hypermobile or even unstable. In
such a case, the primary dysfunctions to address include the hips, hamstrings, and
posterior fascial structures, in order to balance the stresses distributed through the
hip and low back in overall forward bending. Such a patient will usually present
with a flattened lumbar lordosis. The loss of lordosis often correlates with regional
movement patterns as a result of the primary and secondary dysfunctions. Look-
ing only segmentally in the lumbar spine can prevent the clinician from finding
primary causes of dysfunction.
As in a standard structural examination, all the cardinal plane movements,
including side bending, forward bending, and rotation, should be observed. Quad-
rant movements should also be observed, because daily movements and resulting
dysfunctions occur in multiple planes. This is particularly important when deal-
ing with the multidirectional qualities of the myofascial system. The multiplanar
motions that are useful to observe are (1) forward bending with side bending, and
rotation to the same side; and (2) backward bending with side bending, and rota-
tion to the same side. The first combined set of motions follows a very functional
movement pattern that usually helps assess, among other things, the flexibility of
the myofascial planes on the contralateral side of the movement. The second com-
bined movement is generally used to assess compressive joint lesions of the spine
on the same side the movement is occurring. When the same extension quadrant
is observed from the anterior view, the anterior fascial planes can be evaluated
for restrictions. Because the diaphragm and anterior fascial planes may become
restricted in the forward-head posture, observing the backward-bending quadrant
movement from an anterior angle is important.
Compressive Testing of the Spine

Compressive testing of the spine is usually considered a special test of the spine,
but it should be routinely performed. A convenient time to perform this test is after
active movement testing. The concept behind compressive testing is to assess the
amount of "spring" that the spine has when a direct compression is imparted. Gen-
erally, patients with accentuated curvatures will have an increased springiness,
indicating increased lever arms for the effects of gravity and increased stresses on
myofascial structures. The spines of patients with decreased curvatures (axially
extended cervical spine along with decreased lordosis in the lumbar spine) will
not have enough "spring," leading to decreased shock attenuation during normal
everyday activities. Ballistic or impact exercise such as jogging or aerobic exercise
may further accentuate the dysfunction. Postural reeducation after normalization
of myofascial tone can help correct this dysfunction.
Palpatory Examination
Once posture and active movements are assessed, the clinician may begin to esti-
mate where the significant dysfunctions exist. The palpatory examination reveals
yet more information that may be correlated to previous findings and offers a clear
picture of possible goals and treatment approaches.
The palpatory examination includes, but is not necessarily limited to, the fol-
lowing: (1) palpation of the myofascial structures in the form of layer palpation,
(2) palpation of joint structures, and (3) assessment of passive segmental mobility.
Palpation of myofascial structures is primarily emphasized here, including layer
palpation and passive mobility of muscles and fascial mobility.
Layer Palpation
Layer palpation is a systematic method of assessing the mobility and condition of
the myofascial structures, starting from the most superficial structures and pro-
gressing into the deepest palpable structures. Layer palpation is extremely impor-
tant, especially because a common error in both assessment and treatment is to
press through the superficial tissues and delve into the deeper structures without
consideration of possible superficial tissue adaptations. The tissues that can be pal-
pated include the skin, subcutaneous fascia, blood vessels, muscle sheaths, muscle
bellies, musculotendinous junctions, tendons, deep fascia, ligaments, bone, and
joint spaces.
The clinician should be able to palpate in depth the location of the structures
during the palpatory examination. Developing layer palpation requires training of
both tactile and visual senses. The development of tactile skills includes the ability
to detect tissue texture abnormalities and tissue resistance, taking into consider-
ation how tissues at one level of depth differ from the surrounding tissues at the
same depth or on the contralateral side. Table 7.5 lists contrasting terms that are
helpful in describing results from layer palpation.
Table 7.5 Descriptive Terms for Layer Palpatory Examination
superficial-deep acute-chronic
compressible-rigid painful-non pai nfu I
moist-dry circumscribed-diffuse
soft-hard rough-smooth
hypermobile-hypomobile thick-thin
Table 7.6 Palpatory Examination
Examination type Elements of evaluation Structures to palpate

Superficial • Light touch • Skin
• Tissue temperature and moisture • Superficial connective tissue
• Mobility of superficial fascia
• Skin rolling
Deep • Compression: palpation through • Muscle sheaths
layers of tissue perpendicular to • Muscle bellies
the tissue • Tendons
• Shear: movement of tissues • Myotendinous junction
between layers perpendicular to • Joint capsule
tissue • Periosteal layer
For practical purposes, the layer palpation format may be categorized into su-
perficial and deep palpation (Table 7.6). The superficial palpatory examination in-
cludes assessment of tissue temperature and moisture, as well as use of light touch
to determine the extensibility and integrity of the superficial connective tissues.
Tissue rolling is an important part of layer palpation, because it gives the clinician
information about the extensibility of the subcutaneous connective tissue (Fig-
ure 7.8). In tissue rolling, the skin and superficial connective tissue are lifted up,
away from the deeper tissues. Both the extensibility of the tissues and its integrity
can be palpated .
The deep palpatory examination includes compression, a perpendicular pal-
pation through layers of tissue, and shear. Shear is movement of the tissues be-
tween layers, also moving perpendicular to the tissue. The palpable structures are
muscle sheaths, muscle bellies, tendons, myotendinous junctions, tenoperiosteal
junctions, joint capsules, and the deep periosteal layers of tissue . Tissue texture
abnormalities and restrictions are noted in the deeper tissues. Transverse muscle
play is an effective assessment tool for determining the mobility of a muscle or
muscle group within the enveloping fascial sheath. In muscle play, the muscle is
"bent" in order to assess the transverse flexibility of the muscle . This concept is
discussed in greater depth in Chapter 8, "Atlas of Therapeutic Techniques."
Once the evaluation is completed, the findings are correlated to define the spe-
cific dysfunction, and treatment is initiated accordingly. Reevaluation should take
place before, during, and after a treatment for the purpose of treatment modifica-
tions, to provide optimal outcomes and to accommodate for changes made .
Figure 7 .8 Skin rolling.
References
l. Dorland'sIllustratedMedical Dictionary,31st ed. Philadelphia: Saunders Elsevier; 2007.
2. Grodin A, Cantu R. Myofascial Manipulation (course notes). St. Augustine, FL: University of
St. Augustine for Health Sciences; 2003.
3. Cyriax J. Textbookof OrthopaedicMedicine:Vol. 1. Diagnosisof Soft TissueLesions.8th ed. Lon-
don, UK: Bailiere Tindall; 1982.
4. Steindler A. Kinesiology.Springfield, IL: Charles C Thomas; 1977.
5. Janda V. Muscles, central nervous motor regulation and back programs. In: Korr IM, ed. The
NeurobiologicMechanismsin Manipulative Therapy.New York: Plenum Press; 1978:27-42.
6. Janda V. Muscle weakness and inhibition (pseudoparesis) in back pain syndromes. In: Grieve G,
ed. Modern Manual Therapyof the VertebralColumn. New York: Churchill Livingstone; 1986:
197-201.
7. Janda V. Muscles as a pathogenic factor in back pain. In: ProceedingsIFOMPT 4th Conference.
Christchurch, New Zealand; 1980.
8. Janda V.Musclesand Motor Controlin Low Back Pain:Assessmentand Management. New York:
Churchill Livingstone; 1987.
9. Janda V.Musclesand CervicogenicPain Syndromes.New York: Churchill Livingstone; 1988.
10. Janda V, Bullock-Saxton J. Postureand Muscle Form Assessment [DVD]. United States: Ortho-
pedic Physical Therapy Products; 1996.
11. Janda V. Pain in the locomotor system. In: Proceedingsfrom the Second Annual Interdisciplin-
ary Symposium: Rehabilitation in Chronic Low Back Disorders.Los Angeles; 1988.
12. Falla D, Juli G, Hodges PW. Feedforward activity of the cervical flexor muscles during volun-
tary arm movements is delayed in chronic neck pain. Exp Brain Res. 2004;157:43 - 48.
13. Falla D, Jull GA, Hodges PW. Patients with neck pain demonstrate reduced electromyo-
graphic activity of the deep cervical flexor muscles during performance of the craniocervical
flexion. Spine. 2004;29:2108 - 2114.
14. Falla D, Bilenkij G, Jull G. Patients with chronic neck pain demonstrate altered patterns
of muscle activation during performance of a functional upper limb task. Spine. 2004;29:
1436-1 440.
15. Fernandez-de-las-Penas C, Falla D, Arendt-Nielsen L, Farina D. Cervical muscle co-activation
in isometric contractions is enhanced in chronic tension-type headache patients. Cephalalgia.
2008;28:744 - 751.
16. Falla D, Farina D, Dahl MK, Graven-Nielsen T. Muscle pain induces task-dependent changes
in cervical agonist/antagonist activity.! Appl Physiol. 2007;102:601- 609.
17. Falla D, Farina D. Muscle fiber conduction velocity of the upper trapezius muscle during
dynamic contraction of the upper limb in patients with chronic neck pain. Pain. 2005;
116:138-145.
18. Falla D, Jull G, Edwards S, Koh K, Rainoldi A. Neuromuscular efficiency of the sternocleido-
mastoid and anterior scalene muscles in patients with chronic neck pain. Disabil Rehabil.
2004;26:712 - 717.
19. O'Leary S, Jull G, Kim M, Vicenzino B. Cranio-cervical flexor muscle impairment at maxi-
mal, moderate, and low loads is a feature of neck pain. Man 1her. 2007;12:34 - 39.
20. Watson D, Trott PH. Cervical headache: an investigation of natural head posture and upper
cervical flexor muscle performance. Cephalalgia. 1993;13:272-284.
21. Jordan A, Mehlsen J, Ostergaard K. A comparison of physical characteristics between patients
seeking treatment for neck pain and age-matched healthy people. JManipulative Physiol 1her.
1997;20:468-475.
Atlas of Therapeutic Techniques
Robert I. Cantu, Alan J. Grodin, and Robert W. Stanborough
The atlas of therapeutic techniques included in this chapter is by no means a com-

prehensive list of all myofascial interventions. It merely represents a compilation
of techniques that have consistently proven to be effective for many patients in the
clinic. The purpose of the book, and specifically of this chapter, is to give the clini-
cian a solid and basic understanding of myofascial techniques. Every practicing
clinician can and should modify these techniques to meet the individual needs of
each patient and clinician. The techniques then become personalized and, there-
fore, unique to that particular practitioner. New techniques are born in this way,
and many evolve into specific systems of treatment. Myofascial manipulation has
been performed for centuries and has evolved into its present-day state through
constant adaptation. Undoubtedly, myofascial manipulation will continue to
evolve into more effective applications as the body of knowledge increases.
Before discussing individual techniques, certain terms are defined and treat-
ment concepts and procedures discussed, for the sake of clarity and consistency
throughout the chapter.
Joint versus soft tissue manipulation: Some difficulty may arise in drawing
the line between what is soft tissue manipulation and what is joint manipulation.
If a joint is operationally defined as "a space built for motion," then any tissue
surrounding the "joint" may be considered soft tissue. Ligament, capsule, perios-
teum, and fascia are all histologically classified as connective tissue. When dealing
with the joint, the following concept may be applied: Anything that is not bone is
connective tissue. Technically speaking, then, joint manipulation is a form of soft
tissue manipulation because the extensibility of the connective tissue surrounding
the joint is being changed.
For the purpose of clarity in this text, however, the operational definition of
a joint should be expanded. A joint may be defined as a space built for motion in
which movement is governed by (a) arthrokinematic rules and (b) connective tis-
sue extensibility. The term arthrokinematics is the distinguishing factor in separat-
ing soft tissue manipulation from joint manipulation. Joint restrictions occur and
are treated in characteristic arthrokinematic fashion. Manipulation techniques
must be applied following arthrokinematic rules in order to restore extensibility.
199
Myofascial restrictions, on the other hand, are not as predictable because they can
occur outside the realm of specific joint arthrokinematics. Restrictions of the su-
perficial fascia, a loose irregular connective tissue, for example, may occur in many
planes and in many different and unpredictable directions. The treatment is based
on localizing the restriction and moving into the direction of restriction, regard-
less of whether the direction follows the arthrokinematics of the nearby joint.
Herein lies one of the problems with myofascial manipulation: Treatment has
a tendency to become subjective and abstract. The danger of losing credibility is
higher than in joint manipulation, because treatment is based on "what the thera-
pist is feeling." There is no doubt that "good hands" and an "intuitive mind" are of
great value in manual therapy, specifically in myofascial manipulation. A balance
should exist, however, between scientific scrutiny and clinical intuition. Treatment
that relies heavily on one while deemphasizing the other will not be balanced and,
therefore, will not be as effective. This text represents myofascial manipulation
in a biomechanical and kinesiological sense, respecting and integrating nearby
joint arthrokinematics as much as possible. In this way, myofascial manipulation
is represented in the most concrete empirical form possible, without negating the
intuitive aspects of the treatment technique.
Sequencing of treatment: The sequence in which technique is applied will
generally make the difference between success and failure. There are two impor-
tant questions: Where in the entire treatment scheme does myofascial manipula-
tion fit? And how does the clinician sequence individual myofascial technique for
optimal results? Each patient is different, and each clinician will determine the
sequence of treatment on an individual basis; however, the guidelines discussed
below may be helpful in deciding treatment sequencing for individual patients. A
general scheme of treatment follows.
1.Myofascial manipulation of involved and regional areas associated with local in-
volvement. With joint manipulation, treatment often focuses on individual joints being
moved in specific directions. Myofascial manipulation, however, initially focuses on
larger areas or regions of treatment. Individual joint restrictions often have significant
myofascial components. Passive segmental mobility of individual joints may change with
regional treatment of myofascia because the tissue may cross one or more joints. Releas-
ing myofascial tissues prior to joint manipulation also allows joint manipulation to be
performed with less force application. If the myofascial component of the restriction is
first released, the mechanical restriction of the joint can more easily and more specifically
be assessed and treated. The general progression of myofascial manipulation considers the
following factors:
a. Direct beforeindirect technique. For the most part, all the techniques described
in this text are direct in nature. In other words, the techniques locate the restriction and
move into the direction of the restriction. The concept is that the shortest distance be-
tween any two points is a straight line, and the shortest distance through a restriction is
directly through the restriction. If the changes cannot be made with direct technique be-
cause of pain, autonomic responses, or severity of the restriction, then indirect technique
maybe used.
At las of Therapeutic Techniques 201
b. Superficialto deep. Common sense dictates that application of myofascial tech -

nique begins superficially and progresses in depth as changes are made, or in search of
deeper myofascial restrictions. Treatment that progresses from superficial to deep also
allows the patient to gradually grow accustomed to the clinician's hands, facilitating re -
laxation and allowing for unforced penetration to deeper levels. Deeper technique is not
synonymous with more aggressive technique. If the deeper connective tissues are properly
accessed, they may be treated effectively without potential microtrauma and exacerbation
of symptoms. Instead of breaking down the doors, the clinician allows the body to open
the doors for easy and less damaging access into a deeper area.
2. Joint manipulation after treatment of myofascia. As the myofascia releases, joint
manipulation becomes easier, and individual joint restrictions are more easily isolated. At
times, however, if the myofascial restriction is unyielding, joint manipulation may become
necessary to free up the myofascia. Type III joint mechanoreceptors, which are stimulated
by joint manipulation, inhibit surrounding muscular activity. Joint and myofascial ma -
nipulation are "played off" one another, in that joint manipulation inhibits myofascia, and
myofascial manipulation facilitates joint manipulation.
3. Joint and myofascial elongation.Once extensibility has been improved in the myo -
fascia and the joints, elongation and stretching may be approached with greater efficiency.
Elongation (distinct from stretching) refers primarily to the spine. Force is applied to
decompress the spine as if to "open the accordion." Elsewhere in the body, myofascial
elongation is applied via stretch or tissue traction. For example, myofascial manipulation
should always be performed on a hamstring prior to stretch to allow for greater tissue
extensibility.
4. Neuromuscular reeducation. Stretching and strengthening exercises and move -
ment approaches (i.e., Feldenkrais, 1 Alexander2) are appropriate at this time. The alter -
nate somatic movement therapies correspond with the concepts of myofascial and joint
manipulation, but their effectiveness is limited if the tissue is not first prepared. The new
extensibility of the tissue - obtained from the myofascial and joint manipulation, stretch -
ing, and elongation - facilitates the promotion of new movement patterns. Patients are
encouraged at this time to stretch, strengthen, and move in new, more efficient patterns.
5. Posturalinstruction. Once the restrictions are removed and the patient freely moves
in new, more efficient patterns, the potential exists for postural reeducation. If postural in -
struction, which is necessary for most patients, is given at the beginning of the treatment
sequence, the patient cannot effectively assume the expected postures, further enforcing
aberrant movement. The patient tires from moving against his or her own restrictions, and
a negative feedback loop is established. The patient reports, for example, that "it is easier to
slump than to try to sit erect:' and the poor postural pattern is actually reinforced. With
new freedom of movement, good posture is easier and is positively reinforced.
Positioning of patient and therapist: The therapist needs to keep in mind two
important concepts related to positioning. First, to achieve maximal therapeutic
effect, both patient and therapist should be situated in the most efficient positions
possible . This concept may seem elementary, yet it is often forgotten in the day-
to-day treatment of patients. Any inefficiency in the therapist's application of the
treatment is transferred to the patient. The patient senses this inefficiency in the
manual technique and is unable to relax fully.
The second aspect of positioning, included in the discussion of specific tech-

niques below, is the generous use of pillows, especially between the patient and the
therapist. When positioning patients, especially in the side-lying position, a pillow
should always be placed between the therapist and the patient. The pillow provides
a mechanical barrier between patient and therapist, which helps prevent needless
body contact. "Filling the gap" between therapist and patient provides stability to
the patient while in a side-lying position and aids in the biomechanical delivery of
the technique.
Because physical longevity is required during manual therapy, and because
the patient may outsize the therapist, the therapist's use of body weight, ground,
and lever arms is important.
1. Useof body weight. The therapist can optimize use of body weight by using adjust-
able-height tables or by standing on a stool or step. The ability to lean over the patient acts
as a significant force multiplier, whether the patient is prone, side-lying, or supine.
2. Useof the ground to facilitate weight shifting. When the therapist is using a push-
pull type of technique, weight shifting allows the therapist to access the lower kinetic
chain. This is often achieved as the therapist uses a diagonal stance. Rather than being
"all arm," the therapist uses the lower kinetic chain as a force multiplier. The hands also
become more relaxed in the application of the technique. The technique becomes more
forceful even though the hands become softer.
3. Use of lever arms as a force multiplier. The longer the lever arm, the greater and
more focused the force becomes. This concept is especially important in joint manipu-
lation but is also applicable to soft tissue manipulation. A precautionary note is in or-
der at this point: The longer the lever arm is, the greater the force multiplication and the
greater the risk of injury. Some manual therapists advocate the use of shorter lever arms
for greater safety, and their point is well taken. The manual therapist should be careful
when lengthening the lever arm, recognizing the force multiplication that is occurring.
Care and protection of hands: The hands are the primary treatment modality
for the manual therapist and do not come with a replacement guarantee. Because
of the significant and repetitive stresses that the hands withstand, great care should
be taken to use them properly, in the most effective and efficient way possible. If a
manual therapist works on 15 patients a day, 5 days per week, the therapist is lay-
ing hands on more than 3,700 bodies per year. Those numbers accumulate over the
course of a career. The hands are very durable body parts; however, the principles
of Wolff's law (good stress/bad stress) apply to patient and therapist, bone and
soft tissue alike . Practicing correct application of technique and following proper
hand-care procedures are essential for ensuring longevity of the manual thera-
pist's career. The following are some suggestions for hand care.
1. Whenever possible, use techniques that do not hyperflex or hyperextend any joints.
Suggested techniques include the chisel grip (Figure 8.1), octopus grip (Figure 8.2), and
half-chisel grip (Figure 8.3). End -range maneuvers will only accelerate joint hypermobil-
ity problems, leading to early arthritic changes. The thumbs, when used together, should
support each other and should be aligned with the metacarpals, which in turn should be
aligned with the radius. When used individually, the thumb and proximal interphalangeal
At las of Therapeutic Techn iques 203
Figure 8.1 Chisel grip.
Figure 8.2 Octopus grip.
(PIP) joint of the index finger can be used together to form a very stable contact surface
(Figures 8.2 and 8.4).
2. Adapt for size difference between therapist and patient . If the patient is large, and
the desired depth of penetration is not practical, the therapist should not use the fingers or
Figure 8.3 Half -chisel grip.
Figure 8.4 Power grip.
thumb. The fists and elbows are excellent alternat ives. The the rapist can palpate with the
fingers but should treat with the elbows or fists.
3. Wash hands in cold water after each patient treatment . If the the rapist experiences
any inflammat ion in the hands du ring a pat ient treatment, the cold water may act as a
cryotherapy/anti -inflammatory treatment. Using warm water 15- 20 times per day may
have a cumulative inflammatory effect, whereas use of cold water may slow down the
process.
4. Protect the hands during off-hours. When gardening or performing any type of
work that may be hard on the hands, the therapist should wear gloves. Manual therapists
actually incur more microtrauma to their hands during off-hours, when the hands should
be getting much -needed rest.
5. Use of lubricant. A small amount of lubricant should be used, especially in tech -
niques involving longer stroking. The amount of lubricant should be just enough to de-
crease noxious skin friction, but not enough to cause slipping of the hand on the body.
A certain amount of traction on the skin is necessary for appropriate delivery of the
technique.
Techniques for the Lumbar Spine

Bindegewebsmassage-Type Stroke (see DVD)
Purpose : This technique is a reflexive or autonomic technique; it is used when
the patient shows signs of being autonomically facilitated or extremely hypersen-
sitive3 (Figures 8.5 to 8.8). Many patients exhibit acute symptoms that mimic a
reflex sympathetic dystrophy. The skin, for example, is hypersensitive with a cold
clammy feel or touch, and the patient is easily nauseated. For a patient with such
symptoms, starting with a deep touch is usually painful and counterproductive.
The technique suggested here offers an entryway into deeper technique by quieting
the autonomic system.
Figure 8.5 Bindegewebsmassage: stroke initiation.

Figure 8.6 Bindegewebsmassage: stroke completion.
Figure 8.7 Bindegewebsmassage: stroke initiation.
Patient position: Prone , with lumbar spine in neutral position.

Therapist position: Standing over patient, perpendicular to patient.
Hands: Contact is made with the pads or tips of the last three fingers. The
pisiform is the axis of motion for the technique.
Figure 8.8 Bindegewebsmassage: stroke completion.
Execution: The therapist places the stabilizing hand on the patient to gen-
tly stabilize the subcutaneous connective tissue. The manipulating hand is placed
gently on the patient, with the pisiform being the axis of motion for the tech-
nique. Starting with the elbow of the manipulating hand close to the body, the
therapist moves it from the body, bringing the fingers away from the stabilizing
hand in a sweeping motion. Then the therapist lifts the manipulating hand and
repeats the stroke. The technique is repeated at a deliberate pace, moving about
an area of the spine as indicated by restrictions. The technique is superficial, ap-
plied only to the superficial, subcutaneous connective tissue. The technique is
generally comfortable and, at worst, should be only mildly uncomfortable. The
goal of this technique is to quiet the autonomic system, not to create mechanical
changes.
Long Axis Distraction of Superficial Connective Tissue

Purpose: The purpose of this technique is to elongate the superficial connec-
tive tissues, usually in the cephalic-caudal direction (Figures 8.9 to 8.11). Because
the subcutaneous connective tissue is multidirectional in fiber orientation, diago-
nal restrictions may occur and should be treated . This technique can also be per-
formed on a deeper level to provide an elongation of the spine itself.
Patient position: Although prone position with the lumbar spine in neutral is
demonstrated here, the technique can be performed in any position depending on
the location of the restriction. In the supine position, for example, the technique
can be used to treat restrictions in the anterior chest or abdomen.
Figure 8.9 Long axis distraction of superficial connective tissue: stroke initiation.
Figure 8.10 Long axis distraction of superficial connective tissue: stroke completion.
Therapist position: Standing over patient, perpendicular to direction of

restriction.
Hands: Hands are placed in a crossed position on the patient, directly in line
with the restriction.
At las of Therapeut ic Techn iques 209
Figure 8.11 Long axis distraction of superficial connective tissue: stroke from above.
Execution: The therapist applies gentle posterior-anterior pressure until the

subcutaneous fascial level is reached. A gentle distraction is then applied in the
direction of the restriction, usually cephalocaudal, as the hands are pushed apart.
The technique can be performed in the midline, off-center, diagonally, or in any
direction of restriction. When being performed in the midline with a deeper pres-
sure, a distraction and elongation of the spine will result. Care must be exercised
with the deeper version of the technique in patients with degenerative joint disease
or discogenic lesions.
Medial-Lateral Fascial Elongation

Purpose: The purpose of this technique is to elongate the superficial fascia in
a medial-lateral direction (Figures 8.12 and 8.13). As with the previous technique,
the long axis distraction of superficial connective tissue, the application may be
superficial as well as deep. The most superficial application of the technique is
autonomic, whereas any deeper application is primarily mechanical A minimal
amount of lubricant is applied to the patient's back to prevent skin irritation.
Patient position: Prone, with lumbar spine in neutral position.
Therapist position: Standing perpendicular to patient, with more cephalic
hand braced on treatment table for support and efficiency in application of tech-
nique. The other elbow is placed in the area of the lumbosacral junction, with the
forearm and hand resting lightly on the patient.
Execution: The therapist applies enough gentle posterior-anterior pressure
with the elbow and forearm until the level of superficial subcutaneous fascia is
Figure 8.12 Medial -lat eral fascial elongation: stroke initiation.
Figure 8.13 Medial - lateral fascial elongation: stroke completion.
reached. A lateral elongation force is then applied, as the elbow and fore arm slide
laterally and around the body. Most of the pressure is at the elbow and the proxi-
mal one-third of the ulna. The rest of the forearm and hand are merely resting on
the patient, in a relaxed position, as the technique is executed. Deeper pressure
may be gradually applied to the muscular and periosteal levels as the subcutaneous
fascia releases and as patient tolerance dictates.
Tissue Rolling (see DVD)

Purpose: The purpose of this technique is mechanical assessment and altera-
tion of restrictions in the superficial fascia (Figures 8.14 and 8.15).
Therapist position: Standing diagonally over patient.
Execution of assessment: The skin and subcutaneous fascia are gently lifted in
a posterior direction at different levels and areas of the spine. Generally, the tissue
is assessed just off the midline of the spine and in a caudal-to-cephalic direction.
Typically, the fascia directly over the spine has much less mobility because it an-
chors to superficial bony structures such as the spinous process. This decrease in
mobility should not be considered dysfunctional.
As with other superficial techniques, the assessment may be in medial-lateral
or diagonal directions because of the multidirectionality of the superficial connec-
tive tissue. Some patients will be quite restricted in all planes; this may be a gen-
eral function of body type or may represent generalized restrictions. The clinician
must not only base the clinical judgment on the superficial fascial assessment but
must also correlate the findings with other components of the evaluation.
Therapeutic application: The therapist gently lifts the skin and superficial
subcutaneous connective tissue in a posterior direction with both hands. Using
each hand alternately, the clinician rolls the skin, never releasing the hold on the
Figure 8.14 Tissue rolling.

Figure 8.15 Tissue rolling, close up.
skin and subcutaneous tissue. Generally, the skin is rolled from caudal to cephalic,
but other directions such as medial to lateral or diagonals can be pursued . One
can imagine balancing a drop of water on the lifted portion of the skin as the roll
is applied. When a restriction is encountered, the rolling can be stopped, and a
gentle posterior stretch or oscillation can be applied . (Although the figures show
skin rolling in the region of the back, the technique may be applied anywhere in
the body where restrictions are found in the superficial subcutaneous connective
tissue.)
Long Axis Laminar Release (see DVD)

Purpose: The first purpose of this technique is to elongate and decompress
the spine. The second purpose is to identify localized lesions in the medial border
of the erector spinae. As the therapist identifies these lesions, the motion may be
stopped and a sustained pressure may be applied.
Patient position: Prone, with lumbar spine in neutral position. Preferably, the
neck also should be in a neutral position and not rotated. The patient's head should
be as close as possible to the head of the table to allow the therapist to complete the
technique through the iliac area.
Therapist position: Standing at head of table in diagonal stance, one foot in
front of other.
Hands: The hands are placed gently over the patient with the fingers and
thumbs facing in a caudal direction using the octopus grip (Figure 8.2). The
thumbs, while supporting each other and in line with the radius, are placed in the
groove between the erector spinae and the

spine. The thumb alignment allows for the
most efficient application of technique and
the least amount of biomechanical compro-
mise for the therapist's hands. The technique
should be performed with both thumbs on
one side of the spine at a time, one thumb
just behind the other, for the greatest force
production. A bilateral technique can also
be performed, but the depth of penetration
is somewhat compromised, as is the stabil-
ity of the therapist's hands.
Execution: Starting in the upper tho-
racic area and with moderate pressure in
the groove between the erector spinae and
the spine, the therapist moves the thumbs
caudally into the lumbar and lumbosacral
areas while the entire hand maintains con-
tact with the superficial tissue (Figure 8.16).
As the hands reach the lumbosacral junc-
tion, the palms separate to engage the iliac
Figure 8.16 Long axis laminar release: stroke crests, and a gentle traction force is applied
initiation. (Figure 8.17). After several strokes, lesions
Figure 8.17 Long axis laminar release: stroke completion with distraction.
along the groove may be identified. These lesions are manifestations of local in-
creases in muscle tone, reflexive muscle guarding, or connective tissue thicken-
ings. The lesions may be results of acute inflammation or may be remnants of older
trauma, holding patterns, or chronic fibrotic changes. The movement of the hands
may be stopped at any time to apply localized, sustained pressure over the lesions.
Muscle Play of Erector Spinae (see DVD)

Purpose: In this technique, the therapist manipulates the fascial sheath or
casing surrounding the erector spinae. Muscle play is defined as the ability of the
muscle to expand and move within its compartment independent of joint move-
ment or voluntary muscle contraction. Many fascial restrictions occur in planes
perpendicular to or diagonal to the direction of the muscle fibers. Muscle sheaths
are classified as loose connective tissue that has multidirectional fiber orientation.
By manipulating the connective tissue sheath surrounding or encasing the muscle
or groups of muscle, muscular contraction can occur more efficiently, circulation
to the muscle is improved, and movement in the localized and general areas is
improved.
Therapist position: Standing perpendicular to patient.
Hands: Hand position for this technique is extremely important. The move-
ment can be likened to the bending of a garden hose (Figure 8.18). If one imagines
a garden hose being an encasement in which improvement of mobility is desired,
,,
\
\.
----10
0
Figure 8.18 Muscle play of erector spinae: force distribution. Force applied through the thumbs "bends"
the muscle.
bending the hose is one way to accomplish this goal. For the technique, the tips of
the thumbs are placed on the lateral border of the erector spinae, while the thumbs
remain positioned so they are in line with the radius of the forearms. This ensures
that forces are distributed throughout the arm and are not localized in the inter-
phalangeal, metacarpophalangeal, or carpometacarpal joints. (Having the thumbs
in any other position will quickly produce fatigue.) The pads of the index fingers
are placed lightly over the medial border of the erector spinae. The palms of the
hands are resting lightly over the lateral aspect of the patient's body (Figures 8.19
and 8.20).
Execution: This technique is performed in an oscillatory manner using a
medial-lateral force, initially applied through palms of the hands, producing an
oscillatory movement through patient's body at each spinal segment. This rhythm
will vary from patient to patient and will also depend on the patient's general state
of relaxation. Moving too quickly or slowly will result in either a log-rolling type
of motion or a motion that is out of resonance. Once a satisfactory rhythm and
excursion are attained, the thumbs, which are contacting the lateral border of the
erector spinae, begin to create the bending force in synchrony with the rhythm
of the rest of the body. The primary force is now at the thumbs, with the palms
retaining a degree of force to maintain the oscillation. The "power" portion of
the stroke is from lateral to medial with the thumbs; the index fingers are merely
monitoring the position of the hand on the erector spinae. To ensure that a bend-
ing movement is being executed (as opposed to only a medial-lateral movement),
Figure 8.19 Mus cle play of erector spinae.

Figure 8.20 Muscle play of erector spinae: hand placement.
the elbows must move from a position away from the body to a position toward the
body during the power portion of the stroke. In other words, the elbows are held
away from the body at the initiation of the stroke (shoulder abduction) and are
moved toward the body during the stroke (shoulder adduction).
If a restriction is identified in a medial-to-lateral direction, the hand position
is changed or reversed. The therapist must, therefore, move to the other side of the
table to perform the technique so the thumbs are contacting the medial border
of the erector spinae. The "power" portion of the stroke is still delivered through
the thumbs, but now in a medial-to-lateral direction. Different levels of the erec-
tor spinae may be treated simply by moving the hands in a cephalic or caudal
direction, being sure that the thumbs contact the lateral borders of the erector
.
sp1nae.
"Ironing" of Erector Spinae Muscle Group

Purpose: The purpose of this technique is to produce tonal inhibition of the
erector spinae muscle group while applying gentle unilateral traction to the lum-
bar spine (Figure 8.21). Because longitudinal manipulation is usually less noxious
and more sedative than cross-fiber manipulation, this is an excellent technique for
applying moderately deep pressure when the patient is in considerable discomfort
.
or pain.
Therapist position: Standing, directly facing patient at approximate level of
lumbosacral area.
Figure 8.21 "Ironing" of erector spinae muscle group.
Hands: The top hand is placed over the iliac crest to "anchor" the pelvis. The
bottom hand is crossed over the top hand and placed over the erector spinae mus-
cle mass as close to the lumbosacral junction as possible. The table should be low
to allow for the use of the therapist's body weight.
Execution: A small amount of lubrication is used. The palm of the bottom
hand pushes into the erector spinae muscle group and slides slowly and firmly in
a cephalic direction. This technique is deep, but the therapist uses the entire heel
of the hand to create a strong but diffuse technique. During the technique, the top
hand remains anchored onto the iliac crest, allowing for a moderate distraction of
the lumbar area.
Bony Clearing of the Iliac Crest

Purpose: This technique is designed to first evaluate the fascial attachments
at the iliac crest and then soften the fascia, especially at the insertion of the deep
erector spinae and quadratus lumborum (Figures 8.22 and 8.23). This technique
also serves to prepare the iliac crest surface area for the next series of techniques
(iliac crest release).
Execution: In the first part of the technique, the fingers of both hands are
placed directly over the superior border of the iliac crest. For better mechanical
advantage, the fingers of one hand are placed over the fingers of the hand mak-
ing contact with the patient. The technique starts on the superior border of the
iliac crest, as close to the midline as possible. The fingers scour along the superior
Figure 8.22 Bony clearing of the iliac crest: bilateral hand support.
Figure 8.23 Bony clearing of the iliac crest: power grip.
border of the iliac crest laterally and at moderate depth. A small amount of lubri-
cant should be used to avoid skin irritation.
In the second part of the technique, the "power grip" shown in Figure 8.4 is
used to gain further depth. Again starting as medially as possible, the therapist
scours along the superior border of the iliac crest, using the reinforced thumb and
PIP joints as the contact on the patient. This technique should be used for thera-
pists with hypermobility in the metacarpophalangeal or other joints of the digits.
Iliac Crest Release

Purpose: The iliac crest release and lateral sacral release techniques are used
to manipulate the fascial planes in the area of the iliac crest, the top one-third of
the ilium, and the lateral border of the sacrum. The area of the iliac crests contains
connective tissue thickenings from various muscular and fascial attachments and
is vulnerable to myofascial restrictions. Movement restrictions in forward bend-
ing, side bending, and backward bending can originate here. The posterior por-
tions of the fascial planes create the forward-bending restrictions, whereas the
anterior portions create backward-bending restrictions.
Patient position: Prone. Should the connective tissue need to be placed in a
slackened position for deeper penetration, the hip may be extended manually by
the therapist or statically with pillows (Figure 8.24).
Therapist position: Standing diagonally over patient, approximately perpen-
dicular to iliac crest.
Hands: The optimal hand position for this technique is to have the middle
fingers approximating one another for support, forming a chisel grip (Figure 8.1).
This position allows for a four-finger contact on the iliac crest or lateral border
of the sacrum. The index fingers are "dummy" fingers, one being below and one
Figure 8.24 Iliac crest release: hip extension.

being above the middle fingers. The fifth digits are also "dummy" in that they do
not participate in actually manipulating tissue.
Execution: The therapist places the fingers over the border of the iliac crest
and applies a posterior-anterior force through the fingers (Figures 8.25 and 8.26).
Figure 8.25 Iliac crest release: prone.
Figure 8.26 Iliac crest release: contact.

A very slight extension of the fingers occurs during the power portion of the stroke
as the fingers deliver a repetitive stroke in an oscillatory manner. By correctly ap-
plying the force, the fingers will slide off the border of the ilium into the connec-
tive tissue. When the fingers are withdrawn posteriorly in preparation for the next
stroke, they move back on the border of the ilium. Contact with the patient is
never broken during the repetitive application of the technique, except to move to
other areas of the iliac crest. The crest may and should be manipulated from the
most lateral palpable aspect to the most medial palpable aspect, because the entire
border of the iliac crest is susceptible and vulnerable to myofascial restrictions.
The depth of penetration of the stroke is moderate and depends on patient toler-
ance. Although this may be a tender area for some, many patients will be restricted
in this area without experiencing any tenderness. The clinician should treat this
area based on objective findings in the evaluation and not merely on subjective
complaints.
A variation of this technique is to apply the same force, but contact 1 or
2 inches inferior to the border of the ilium and into the connective tissue. Force is
applied into the connective tissue of the ilium, manipulating the entire expanse of
the ilium, or at least palpating for restrictions. The fingers should manipulate the
deeper connective tissues and should not slide off the ilium.
Lateral Sacral Release

This technique is very similar to the iliac crest release but targets a different tis-
sue: the fascia of the lateral border of the sacrum. The piriformis attaches close
by, and patients with low back, hip, sacroiliac, and leg pain can benefit from this
technique, especially those with diffuse hip and leg pain proximal to the knee. The
lateral sacral release is an excellent technique to use in conjunction with the bilat-
eral sacral release technique, which is discusssed next.
Therapist position: Standing perpendicular to patient.
Hands: The optimal hand position for this technique is to have the middle
fingers approximating one another for support, forming a chisel grip (Figure 8.1).
Execution: The fingers start just off the sacrum and push onto the lateral sur-
face of the sacrum in a rhythmical fashion (Figures 8.27 and 8.28). A very slight
extension of the fingers occurs during the power portion of the stroke as the fin-
gers deliver a repetitive stroke, lateral to medial, in an oscillatory manner. Contact
with the patient is never broken during the repetitive application of the technique.
The sacrum moves under the fingers following the push stroke and back into posi-
tion due to the rocking motion of the patient's body.
Because the sacroiliac joint occupies the cephalic half of the sacrum, the iliac
crest release and sacral release may be done together, with hands moving from the
ilium to the sacrum. In such cases, the therapist" detours" from the iliac crest onto
the lateral aspect of the posterior superior iliac spine and moves caudally toward
the inferior-lateral angles of the sacrum. Used in combination, the techniques
cover the bony surfaces starting just lateral to the anterior superior iliac spine and
progressing medially and caudally to the sa-

crococcygeal junction.
r·
Bilateral Sacral Release
Purpose: The purpose of this technique
is to manipulate the connective tissue as
it attaches to the sacral borders. This may
become necessary before attempting to
manipulate the sacrum out of various po-
sitional faults or movement dysfunctions.
Freeing up the myofascial restrictions often
facilitates manipulation of the sacrum. This
area may also be restricted in conjunction
with iliac crest restrictions due to the fascia
lata's insertion at the anterior superior iliac
spine, lateral border of the iliac crest, lateral
borders of the sacrum, coccyx, and sacro-
tuberous ligament. To fully manipulate the
insertion of the fascia lata, the therapist
should manipulate the lateral border of the
Figure 8.27 Lateral sacral release. sacrum.
Patient position: Prone, with lumbar
spine in neutral position.
Therapist position: Standing perpen-
dicular to patient.
Hands: The hands are brought together
so that the thumbs and index fingers of
each hand are making contact with one
another.
Execution: Anatomically, only the dis-
tal half of a sacral border is palpable. The
proximal half of the sacrum articulates with
d , the ilium and is not palpable. To ensure that
l , contact is being made on the sacrum, the

therapist should approach the sacrum with
the bottom hand below the level of the sa-
• crum (distal to the sacrum), until contact is

made bilaterally with the patient's buttock.
The bottom hand then palpates in a cephalic
direction until the inferior lateral angles of
the sacrum are palpated (Figures 8.29 and
8.30). The top hand then contacts the bot-
tom hand in the manner described above.
Figure 8.28 Lateral sacral release: bony contact.
A repetitive caudal-to-cephalic motion is
performed following the lateral border of

the sacrum. The direction of the technique
should be V-shaped, consistent with the
shape of the sacrum. If the fingers are only
moving cephalically and not spreading,
contact with the lateral borders of the sa-
crum is not being maintained.
The technique may also be executed
unilaterally using the same hand position
as the iliac crest release described previ-
ously (Figure 8.1). The lateral border of the
sacrum is located the same way as described
above. Once the lateral border is located,
contact is made with the fingertips. The fin-
gers are then moved in a caudal-to-cephalic
motion, maintaining contact on the lateral
border of the sacrum.
Medial-Lateral Pull-Away
Purpose: The first purpose of this tech-
Figure 8.29 Bilateral sacral release. nique is autonomic or reflexive in nature.
As with other autonomic techniques, it de-
sensitizes the patient who is extremely acute
and gains entryway to deeper technique. As
the patient's condition allows or dictates,
deeper pressure is applied until the level of
the erector spinae is reached, changing the
emphasis of the technique from autonomic
to mechanical The erector spinae can be
gently manipulated from a medial to lateral
direction.
Patient position: Side-lying, with hips
and knees semiflexed. A pillow should be
placed between patient and therapist both
for biomechanical advantage and for mod-
esty. The patient is moved close to the edge
of the table until snug against the pillow.
Therapist position: Standing over pa-
tient, snug against pillow.
Hands: The hands are placed gently
over the patient. The therapist makes con-
tact with the whole hand, while the finger-
tips rest over the medial border of the lum-
Figure 8.30 Bilateral sacral release: contact.
bar erector spinae.
Figure 8.31 Medial-lateral pull-away.
Execution: The stroke begins very gently at approximately the level of the
subcutaneous fascia and works from medial to lateral (Figure 8.31). Initially, the
pressure is evenly distributed throughout the hand. As the patient tolerates, more
pressure is exerted through the fingertips until a moderate to deep pressure is be-
ing consistently exerted.
Ouadratus Lateral Erector Spinae Release (see DVD)

Purpose: The purpose of this technique is to prepare the quadratus lumborum
and the lateral fascial structures of the lumbar spine for elongation and stretch
techniques. The technique involves sustained pressure and has the primary goal
of reducing active tonic contractions of the quadratus lumborum. After the tone
in the quadratus is diminished, the elongation and stretch techniques applied are
more effective and efficient.
Patient position: Side-lying, with the hips and knees in approximately 70° of
flexion.
Therapist position: Standing perpendicular to patient, with pillow between
patient and therapist. If an adjustable-height table is available, the table level should
be lowered to approximately hip level, making patient waist level.
Hands: The therapist uses the mid-forearm of the inferior arm in this tech-
nique. The forearm is placed in the soft tissue of the mid-lumbar area, between the
12th rib and the iliac crest. If the forearm is angled posteriorly, the lateral border
of the erector spinae will be contacted . If the forearm is angled anteriorly, the qua-
dratus lumborum will be contacted . As an alternate position, the web space and
Figure 8.32 Quadratus - lateral erector spinae release: forearm contact.
metacarpophalangeal joint of the top hand can be placed on the quadratus lumbo-
rum as the bottom hand positions to hike the hip.
Executi on : The top hand is placed gently on the patient for support and to
minimize patient movement. The middle aspect of the forearm (ulnar surface) is
wedged into the groove between the 12th rib and the iliac crest (Figure 8.32). Light
to moderate pressure is placed down onto the muscle groups and sustained for a
period of time until a release of muscular tone is achieved or until it is obvious that
no change will be made. The forearm may be moved anterior and posterior (back
and forth), as the therapist flexes and extends the shoulder, making a very deliber-
ate "sawing" type of motion.
As an alternate technique, the therapist can use the bottom hand to contact
the greater trochanter and push it cephalically to "hike" the hip and create side-
bending in the lumbar spine (Figure 8.33). This is done to put the quadratus lum-
borum in a slackened position. Simultaneously, the first metacarpophalangeal of
the top hand makes contact with the quadratus, pushing firmly in a medial direc-
tion to access its deeper fibers for the purpose of tone reduction.
Side-Bending Elongation Ouadratus Stretch

Purpose: This technique should be used generally to elongate the posterolat-
eral and anterolateral fasciae of the lumbar and thoracic spines and, specifically,
to stretch the quadratus lumborum. In chronic unilateral pain conditions, the
painful side often retracts, contracts, and generally shortens. The manifestation
of such a condition can be assessed posturally or with active movements. Both the
Figure 8.33 Quadratus-lateral erector spinae release: hand contact.
connective tissues and contractile tissues may become dysfunctional and exhibit
changes consistent with immobilization.
More specifically, this technique may be used to prepare for correction of lat-
eral shift conditions of more than 3 weeks' duration. As discussed in Chapter 3,
"Histology and Biomechanics of Myofascia," muscle decreases in length by losing
sarcomeres-the process takes approximately 3 weeks. Tissue held in a shortened
range for longer than 3 weeks has undergone contractural changes, which must be
addressed before shift correction can be attempted.
Finally, this technique may be used to decompress compressive lesions such
as nerve impingement syndromes. Aside from backward bending, side bending is
the least stressful movement on the disc, followed by, in increasing order of stress,
forward bending and rotation. In rehabilitation of discogenic lesions, the side-
bending elongation maneuver may decompress a nerve root by taking the disc
into the second-least-stressful maneuver.
Patient position: Side-lying.
Therapist position: Standing perpendicular to patient with pillow between
therapist and patient. The top forearm contacts the lateral thorax/rib cage, while
the bottom forearm is placed between the ilium and the greater trochanter.
Hands: The fingers contact the medial border of the erector spinae .
Execution: To localize forces in the lumbar area, the hips and knees are bent to
90° and the patient's feet are lowered off the table. Care must be taken while lower-
ing the feet off the table not to provoke any symptoms. Once the feet are off the
Figure 8.34 Side-bending elongation quadratus stretch.
table, pressure is exerted in a cephalic direction with the top forearm and in a cau-
dal direction with the bottom forearm. At the same time, the fingers move from
medial to lateral on the erector spinae, strumming the tissues as they elongate. The
forearms are localizing most of the stretch on the quadratus. The hands are pri-
marily aiding this movement by gently releasing the erector spinae (Figure 8.34).
In this position, a gentle hold - relax technique may be performed by asking
the patient to gently push the ilium into the therapist's bottom forearm. The pa-
tient should not be allowed to remain with the legs off the table for more than
30 - 45 seconds, because the lever arms of the lower extremity are applying consid-
erable forces into the lumbar spine.
To diffuse the forces and provide a more general elongation of the lumbar and
thoracic spines, the therapist asks the patient to fully flex the shoulder and hold
the top of the treatment table. The legs are then lowered off the table, as previously
described . The forces may be applied through the arm - hand contacts described
above, or a traction - elongation force may be applied through the palms of the
hands, as shown in Figure 8.35. The therapist can apply an elongation of the lateral
connective tissue of the lumbar and thoracic spines and even into the connective
tissues of the shoulder girdle complex.
In some cases, where the quadratus lumborum has been hypertonic but not
necessarily shortened, it may be necessary to create more length in the quadratus
than possible with the previously described quadratus lumborum technique. To
create more length, the therapist rotates the patient's trunk to the Tl 2/Ll segment.
Figure 8.35 Side-bending elongation quadratus stretch: crossed arms.
Figure 8.36 Side-bending elongation quadratus stretch, with rotation.
During this rotation, rib 12 is rotated away from the pelvis, allowing for lengthen-
ing of the more cephalic aspect of the quadratus lumborum. Once rotated, the legs
are placed off the table and a side-bending force is placed on the pelvis as previously
described (Figure 8.36). The top arm continues to side-bend at approximately 30°
off center. The therapist should not continue to rotate. The change in angle of the
side-bending provides a more aggressive stretch of the quadratus lumborum. Note
of caution: Discogenic lesions are a strong precaution here, because the rotation
could compromise a discogenic lesion.
L3 Deep Soft Tissue Manipulation

Purpose: The purpose of this technique is to alter the connective tissue in the
mid-lumbar area, and specifically around the L3 area. Because L3 is generally the
apex of the lumbar curve, and the site of hypomobility, myofascial preparation of
the area is necessary prior to joint manipulation. The transverse process of L3, be-
ing the longest in the lumbar spine, can easily be palpated.
Patient position: Side-lying, with hips and knees in a semiflexed position and
a pillow placed between therapist and patient.
Therapist position: Standing over patient, with patient snug against pillow.
Hands: The middle fingertips are used for this technique.
Execution: Starting laterally, the transverse process of L3 is palpated. Once on
the transverse process, the fingers are moved superiorly, posteriorly, inferiorly, and
anteriorly to contact the connective tissue surrounding the L3 transverse process.
Firm and progressive pressure can be applied using an oscillatory motion depend-
ing on patient tolerance (Figures 8.37 and 8.38).
Passive segmental mobility may be tested in any plane just before and just
after the technique is applied. Because soft tissue and joint manipulation are of-
ten used together, and because joint restrictions may often be due to soft tissue
Figure 8.37 L3 deep soft tissue manipulation.

0.,
Figure 8.38 L3 deep soft tissue manipulation: contact.
restrictions, passive segmental mobility may be altered with this or any other myo-
fascial technique.
Forward-Bending Laminar Release

Purpose: The purpose of this technique is to elongate the posterior myofascial
tissues of the lumbar spine. This may be necessary in hyperlordotic postures or
in preparation for joint manipulations. As discussed earlier, soft tissue and joint
manipulation have a unique relationship in that either the soft tissues or the joint
may be contributing to a hypomobility. Passive segmental mobility of a joint may
change dramatically after releasing soft tissue. On the other hand, joint manipula-
tion may have a profound effect on the surrounding myofascial tissues by way of
stimulating joint receptors. This technique is often performed before, during, and
after joint manipulation to complement specific joint maneuvers.
Patient position: Side-lying in a semifetal position.
Therapist position: Standing perpendicular over patient. The therapist stabi-
lizes the patient's top knee by placing it in the area of the therapist's anterior hip
for control and ease of execution.
Hands: The top "stabilizing" hand is placed over the thoracolumbar junction,
and the forearm is placed parallel with the spine. The bottom "manipulating" hand
is placed initially in the area of the upper lumbar spine in contact with the erec-
tor spinae, with the fingers slightly flexed. The forearms should be parallel to each
other (Figure 8.39).
Execution: To execute the technique, the fingers of the manipulating hand
are moved caudally down the length of the erector spinae while the patient's hip is
Figure 8.39 Forward-bending laminar release: stroke initiation.
Figure 8.40 Forward-bending laminar release: stroke completion.
simultaneously flexed. The leg movement is executed through the therapist's hip
and pelvis. The therapist pulls the patient's knee toward the chest, causing hip flex-
ion, a posterior pelvic tilt, and consequently forward bending in the lumbar spine,
thereby decreasing the lumbar lordosis (Figure 8.40). This allows for elongation of
the posterior tissues coming from hip flexion as well as from the caudal stroking
of the therapist's bottom hand.
If a specific joint restriction is found, this technique may be somewhat lo-
calized to prepare the surrounding soft tissues prior to a joint manipulation. The
hip is first flexed to forward-bend the lumbar spine to the level of the restriction.
During this time the fingers are palpating between the spinous processes for the
forward-bending restriction. Once movement is felt at the appropriate level, the
hip is extended slightly to slacken the tissue at that level. The top stabilizing hand
is brought down to a position just cephalic to the restricted level. The bottom hand
is brought up to a level almost contacting the top hand. The therapist then strokes
over the erector spinae in a caudal direction the length of two to three segments
while the hip is flexed through a short arc of movement. This allows for tissue to
be elongated both by the hip flexion and by the caudal pull of the bottom hand.
Passive intervertebral mobility should be assessed prior to an appropriate number
of repetitions of this technique .
Longitudinal Posterior Hip Release

Purpose: This technique is an extension of the previous technique, the for-
ward-bending laminar release, but is sometimes used separately for lesions in the
area of the posterior hip. Piriformal lesions and parasacral lesions, as well as exten-
sibility problems in the posterior hip, are effectively treated with this technique.
Patient position: Side-lying in the semifetal position, with top knee stabilized
in anterior hip of therapist.
Therapist position: Standing perpendicular to patient, stabilizing patient's
top knee with anterior hip. This allows the therapist to have an effective mechani-
cal advantage while giving the patient a sense of security.
Hands: The therapist's top hand is placed so that the palm gently contacts the
anterior superior iliac spine. The bottom hand is positioned over the buttock, with
the fingertips just distal to the sacroiliac joint.
Execution: The top hand gently stabilizes the ilium while the patient's hip is
gently flexed . The therapist accomplishes this by leaning in a cephalic direction
with his or her pelvis. Simultaneously, the bottom hand strokes from just distal to
the posterior superior iliac spine to the ischial tuberosity and laterally in a paratro-
chanteric direction (Figure 8.41). Most of the pressure is applied through the fin-
gertips, but the palm remains in contact throughout.
Forward-Bending Laminar Release-Quadruped

Purpose: The purpose of this technique is to elongate the posterior soft tissues
of the lumbar or thoracic spines. This technique may serve as an alternative to the
forward-bending laminar release in side-lying position. If the patient is too large
for the therapist to manage in side-lying, the quadruped position may be used.
Specificity is sacrificed somewhat in order to gain some mechanical advantage.
One advantage to this technique is that the patient actively participates rather than
.
rema1n1ng passive.
Figure 8.41 Longitudinal posterior hip release.
Patient position: Quadruped position, with pillow placed on patient's poste-

rior leg.
Therapist position: Standing at patient's side at a 45° angle. The therapist may
need to be on a stool, or, if an adjustable-height table is used, the table should be
lowered.
Hands: For optimal stability and efficiency, the therapist holds a thumb against
the PIP joint of the index finger as shown in Figure 8.42. Contact is made using
both the PIP joint and the tip of the thumb. The inferior hand is placed on the
lumbosacral region closest to the therapist, while the superior hand contacts the
patient's shoulder, which will be used to guide the patient into flexion.
Execution: The therapist instructs the patient to bend forward first at the cer-
vical spine and gradually recruit motion into the thoracic spine. As movement is
recruited into the thoracic spine, the therapist asks the patient to start rocking
back on his or her heels as the therapist guides the speed of the movement. This
motion begins to recruit movement from lower lumbar to upper lumbar areas. As
the patient recruits this movement, the therapist longitudinally strokes the erector
spinae unilaterally with the bottom hand, starting from the sacrum and moving
toward the thoracolumbar junction (Figure 8.42). The top hand is used as a guid-
ing hand to dictate the quantity and pace of the patient's movement.
A cephalic-to-caudal stroke may also be applied to manipulate the tissues in
the lumbar region at end range of their movement. To perform the technique, the
therapist simply switches hand contacts so the bottom hand rests on the ilium
to help guide the movement and the top hand manipulates the erector spinae
Figure 8.42 Forward-bending laminar release: quadruped, caudal to cephalic.
Figure 8.43 Forward-bending laminar release: quadruped, cephalic to caudal.
unilaterally starting at the mid-thoracic spine and progressing down to the sa-
crum (Figure 8.43).
If specific restrictions are located along the erector spinae, the patient may be
placed in a crouched static position while the therapist manipulates the restricted
tissues in either a caudal-to-cephalic direction or a cephalic-to-caudal direction

(Figure 8.44).
This technique may also be used in the upper thoracic region, again with the
patient assuming a crouched position. The therapist stands at the head of the table
and manipulates one side of the upper thoracic tissues at a time (Figure 8.45).
Figure 8.44 Forward-bending laminar release: quadruped, stationary.
Figure 8.45 Forward-bending laminar release: quadruped, upper quadrant.

Forward-Bending Laminar Release-Sitting (see DVD)

Purpose: The purpose of this technique is to elongate the posterior myofascial
structures of the lumbar, thoracic, and, to a certain extent, cervical spines. As with
the previously described quadruped technique, the patient actively participates in
the technique; the technique also allows for working with patients larger than the
therapist or with patients who cannot assume a quadruped position because of a
knee or shoulder impairment. Specificity is somewhat sacrificed, but significant
mechanical advantage is gained in performing the technique in a sitting position.
Patient position: Sitting.
Therapist position: Standing directly behind patient.
Hands: The power grip is used, as illustrated in Figure 8.46. The positioning
of the thumb next to the PIP joint of the index finger is very stable and prevents
compromise of the joints of the hand.
Execution: The patient is first asked to forward-bend segmentally, starting
from the cervical spine, recruiting into the thoracic spine, and finally into the
lumbar spine. Once the patient understands the concept of segmental movement,
both sides of the spine are treated simultaneously as the thumb- PIP joint complex
of each hand is placed over the erector spinae at the cervicothoracic junction in a
downward position. For optimal mechanical advantage, the elbows should be di-
rected upward, while the thumb-PIP joint
complex should be directed downward. The
patient is asked to forward-bend segmen-
tally, and the therapist strokes the erector
spinae longitudinally at the level the move-
ment is being recruited (Figure 8.47). If a lo-
calized restriction is found, the patient may
be asked to stop the movement at the point
of the restriction while the therapist applies
a sustained pressure.
The same technique may be applied
unilaterally and with a rotatory component
by asking the patient to forward-bend di-
agonally. The patient is asked to follow the
lateral border of the leg with the arms. This
maneuver allows for a functional combina-
tion of forward bending, side bending, and
rotation. The therapist stands to one side of
the patient in a diagonal stance. The thera-
pist's hand closest to the patient is placed
on the patient's shoulder, providing guid-
ance and dictating the pace and quantity
Figure 8.46 Forward-bending laminar release:
of movement. The manipulating hand con-
sitting, stroke initiation.
tacts the erector spinae of the upper thoracic
.;
j
•
•
l
1 •
'..'
. •I
•
'
.• '• •
.. • •
'
•
'
•
• .. I
/I i'
\ I·, 1
I
/,'
- . ,I J fJ,il k t\:
Figure 8.47 Forward-bending laminar release: Figure 8.48 Lamina release: sitting, bending, and
sitting, bending initiation. rotation.
spine and moves in the caudal direction along the convexity created as the patient
moves segmentally into the diagonal plane. Again, the therapist manipulates the
erector spinae at the level of movement recruitment (Figure 8.48). If a movement
restriction and/or myofascial restriction is encountered, the patient may be asked
to stop, and the therapist may apply a sustained pressure.
This technique may also be applied to the cervical spine either bilaterally (Fig-
ure 8.49) or unilaterally as the therapist uses one hand to guide the patient's head
and neck, generally into a diagonal direction, and uses the other hand to stroke
down the cervical paravertebral muscles (Figure 8.50).
Contraindi cations: This technique should not be used with patients who have
discogenic backs or necks, because a loaded spine is being taken into forward
bending.
Lumbar Myofascial Roll

Purpose: This technique is an excellent preparatory technique for a mid-lum-
bar roll joint manipulation. Many times, a mid-lumbar joint manipulation is dif-
ficult to execute because of myofascial restrictions or active muscle guarding. The
patient may be apprehensive of rotating the spine to the degree that is required in
Figure 8.49 Forward-bending laminar release: Figure 8.50 Lamina release: seated upper
sitting, bilateral upper quadrant bending. quadrant.
the mid -lumbar joint manipulation. Decreasing myofascial restrictions not only
allows the patient to relax into rotation but also facilitates locking a specific joint
of the lumbar spine.
Patient position: Side-lying with pillow placed between therapist and
patient.
Therapist position: Standing facing patient at level of lumbar spine. The top
hand is placed over the patient's subclavicular-pectoral area, while the bottom
hand is placed over the mid-lumbar area. The patient's knee is placed in the ante-
rior portion of the therapist's hip.
Hands: The fingers of the bottom hand are placed on the medial aspect of the
erector spinae.
Execution: The lumbar spine is bent forward to a mid-range by flexing the
patient's hip and recruiting motion into the lumbar spine. The lumbar spine is
then rotated by pulling the patient's bottom arm until movement is recruited into
the lumbar spine. In the therapist position described above, the lumbar spine is
rotated from both contact points. The erector spinae muscles are simultaneously
stroked diagonally with the fingers, as the rotatory force is applied through the top
arm (Figure 8.51). The lumbar spine may be rotated close to end range but should
Atlas of Therapeutic Techniques 239
Figure 8.51 Lumbar m yofascial roll.
not be taken to the limit of motion. As relaxation and elongation are achieved, the
spine may be taken to end range to perform the joint manipulation.
Lateral Shear Correction

Purpose: This technique is performed to normalize the lateral shear forces
in the lumbar spine, which may be abnormal and/or asymmetrical owing to past
trauma. An excellent use of this technique is for resolving a discogenic lesion when
the patient has ceased experiencing a lateral shift for a period of time. When the
patient is tested for lateral shear (passively shifted), he or she will usually adopt
the position of the previous shift quite easily and will be markedly restricted when
sheared in the opposite direction. Normalizing this myofascial imbalance is the
primary purpose of the technique.
This technique should not be confused with the lateral shift correction tech-
nique, which is typically performed on a laterally shifted patient. The lateral shear
technique has application for neuromuscular retraining at end-stage discogenic
rehabilitation but should not be used early in the discogenic rehabilitation process,
especially when a lateral shift is still present. The technique of choice in the pres-
ence of a lateral shift is the lateral shift correction technique.
Test Procedure
To determine if a lateral shear imbalance exists, the therapist stands behind the pa-
tient and passively moves the patient into a lateral shift position (Figure 8. 52). This
.... .
i I
••
~l-!\t • •
' is accomplished by placing one hand on the
L
\
I
\·\
•
ilium and the other hand on the acromion-
;
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•
shoulder girdle area. The therapist places
:l\·..: i
I force through the tissues by simultaneously
stabilizing the ilium in a lateral direction
. I' r'. .,
I : ), (i.e., in the transverse plane) while apply-
'{
ing downward pressure on the acromion-
shoulder girdle in a 45° diagonal direction.
The vector on the acromion-shoulder girdle
is a combination of lateral force (in the hori-
zontal plane) and compressive force. If the
patient's trunk moves easily to the right and
is restricted in movement to the left, the pa-
tient is restricted in left lateral shear.
The next step is determining whether
the restriction is merely postural or whether
a true myofascial restriction exists. To
make this determination, the therapist has
the patient lie prone in a neutral position,
and the therapist again tests lateral shear,
this time primarily from the pelvis. If the
Figure 8.52 Lateral shear examination. patient's pelvis moves easily to the left and
is restricted in movement to the right, the
patient is said to be restricted in left lateral
shear. Remember, movement of spine is always referred to in terms of the superior
vertebrae move on the inferior. The direction of the shear is always based on the
direction the vertebral movements in the same way. In standing, if the trunk is
restricted in movement to the left, a left lateral shear restriction exists. In the prone
position, a left lateral shear is re-created with ilial movement to the right, which
results in trunk motion to the left. If ilial movement to the right is restricted, the
restriction is still said to be in left lateral shift .
If a movement restriction exists when the patient stands but normalizes when
the patient is prone, the condition is not as significant and is usually more easily
treated. If a movement restriction exists when the patient is standing and remains
when the patient is prone, the condition has become more entrenched and can po-
tentially be more detrimental if left unchecked. Either way, treatment is necessary
to correct the dysfunction.
Lateral Shear Correction Technique

Therapist position: Standing perpendicular to and over patient at level of pa-
tient's pelvis.
Hands: The therapist may use the palm of the hand or a fist to make contact on
the ilium, between the ilium and the greater trochanter of the hip (Figure 8.53).
Figure 8.53 Lateral shear correction.
Executi on : The restriction is engaged by gently shearing the pelvis laterally.

Once resistance is met, the patient is asked to hold his or her position and then to
relax (hold - relax stretch). As the patient relaxes, the pelvis is sheared further later-
ally until the restriction is once again engaged, and the process is repeated . After
several repetitions, the lateral shear is reevaluated, with the patient in both prone
and standing positions.
Two things are accomplished in this technique. The first is a neuromuscular
"repassing" to eliminate muscular holding patterns created by old trauma. The sec-
ond is releasing restrictions in the noncontractile elements that became restricted
as a result of prolonged dysfunction in the contractile elements.
Diaphragm Release
Purpose: Diaphragm release techniques are designed to free up restrictions
in the anterior fascia just caudal to the rib cage and to manipulate the diaphragm.
In a forward-head, protracted-shoulder, slumped position, the anterior elements
collapse, thereby reducing diaphragmatic excursion, which can lead to increased
activity in the secondary accessory breathing muscles. Also, for the patient to per-
form postural reeducation techniques successfully and elongate the thoracic area,
the contracted area of the anterior chest and abdomen must be supple and mobile.
Any of these techniques can be used successfully to eliminate pain referred to the
shoulder via the diaphragm. Three techniques are shown, ranging from the least
aggressive to the most aggressive; the general progression should follow the pa-
tient's tolerance level.
242 EVAL UATION AND TREATMENT OF THE MYOFASCIAL SYSTEM
Position 1: Supine
Patient position: Supine, with knees and hips slightly flexed, supported by
bolster or pillow.
Therapist position: Standing or sitting at side of patient. The seated position is
biomechanically more advantageous for the therapist.
Hands: The therapist's top hand is placed over the bottom portion of the rib
cage. The bottom hand is placed at the anterior-medial border of the rib cage, just
lateral to the xiphoid process and in the connective tissue just inferior to the rib
cage (Figure 8.54).
Execution: The top hand gently pushes the connective tissue in a medial and
caudal direction in order to slacken the tissue just inferior to the rib cage. This
allows the fingers of the bottom hand to wrap underneath the rib cage (to patient
tolerance). The stroke is applied, following the border of the rib cage medial to
lateral (Figure 8.55). Care should be taken not to push into the floating ribs while
moving laterally with the stroke. In this position, only a superficial or moderate
level of penetration can be achieved .
Position 2: Side-Lying
Patient position: Side-lying, with hips and knees flexed to 90°.
Therapist position: Standing behind patient, pillow between therapist and pa-
tient for stability and barrier.
Hands: The hand position is similar to that described for Position 1. The top
hand is placed on the lower portion of the rib cage, while the bottom hand is placed
at the caudal border of the rib cage, just lateral to the xiphoid process .
Figure 8.54 Diaphragm release: supine, stroke initiation.

Figure 8.55 Diaphragm release: supine, stroke completion.
Figure 8.56 Diaphragm release: side-lying.
Executi on : With the patient more flexed in side-lying, more slack is placed in
the superficial connective tissue. The first technique actually manipulates both the
connective tissue and the diaphragm. The second technique bypasses the super-
ficial connective tissue to engage the deeper connective tissue under the rib cage.
The therapist uses the top hand once again to move the connective tissue medially
and caudally, allowing the bottom hand to slide under the rib cage (Figure 8.56).
The stroke is again applied in a medial-to-

lateral direction, with care not to hit the
floating ribs.
Position 3: Sitting
Patient position: The beginning posi-
tion for this technique is the slumped sitting
posture. This puts the tissues in the greatest
amount of slack and allows the therapist
greater access to the tissues underneath the
rib cage. As the technique progresses, how-
ever, the therapist may ask the patient to as-
sume a more erect posture so the therapist
can manipulate the rib cage.
Therapist position: Standing behind
patient with pillow between therapist and
patient. The patient leans into the therapist
in a slumped position.
Hands: Whereas the previous tech-
niques are unilateral, this technique is bi-
lateral. Both hands slide underneath the
Figure 8.57 Diaphragm release: sitting. rib cage medially, just lateral to the xiphoid
process.
Execution: The manipulation is again
executed in a medial-to-lateral direction, with the patient in the slumped position.
At an appropriate time, the hands firmly grip the rib cage, and the patient is asked
to inhale deeply and attempt a more erect posture. The rib cage is manipulated
anteriorly (Figure 8.57).
Psoas Release
Purpose: Manipulation of the psoas muscle is clearly indicated when actual
shortening exists, which may create mobility problems into hip extension as well
as the lumbar spine, especially with forward-bent posture. In an axially extended
posture (flat-back posture), however, the psoas may be hypertonic in an effort to
increase lordosis or to guard a lesion, where axial flexion of the lumbar spine is
the primary dysfunction producing symptoms. In either case, a restriction may be
present or pain may be referred to the low back.
Patient position: Supine position, with hips and knees flexed approximately
30°-45 ° and supported on pillows or therapist's leg to put muscle in slackened
position (Figure 8.58). If the muscle does not exhibit enough slack, the hips may
be flexed to 90°, over the therapist's leg (Figure 8.59). This technique should be
performed on an adjustable-height table for optimal biomechanical advantage.
Therapist position: Standing at patient's side . If necessary, therapist places
one leg on the table; the patient's legs are then placed over the therapist's leg. The
Figure 8.58 Psoas release: legs supported 30°- 45°.
Figure 8.59 Psoas release: leg supported 90°.
therapist may use his or her position to change the amount of hip flexion during
application of the technique.
Hands: The therapist uses fingertips to contact the psoas. The psoas is ap-
proached from a 45° angle as the hands are placed lateral to the rectus abdominus,
slightly inferior to the umbilicus.
Figure 8.60 Psoas release: side-l ying.
Execution: Because the psoas is located along the lumbar vertebrae and corre-
sponding discs, a significant depth must be achieved through the abdomen. Care
must be taken to progress slowly into the appropriate depth, asking the patient
about the relative comfort of the technique. Ease of depth may be achieved by
sinking with every exhalation of the patient. As more depth is achieved through
the abdomen, "landing" on a more rigid structure indicates arrival onto the psoas.
The psoas will be more rigid than the soft tissue of the abdomen. The patient will
also report a different sensation, usually more noxious when the psoas is palpated,
especially if the psoas is dysfunctional. Proper location may be confirmed by ask-
ing the patient to slightly flex the hip, which will cause the muscle to fire into the
therapist's fingers.
Because longitudinal stroking of a muscle is generally less noxious than trans-
verse stroking, the psoas should be gently manipulated using a longitudinal stroke
at first. Only after longitudinal stroking has been applied should a transverse
stroke be attempted . Once the technique is terminated, the hands should be gradu-
ally removed from the abdomen. In some cases, the psoas may be more accessible
with the patient in a side-lying position. The therapist may use the thumbs to ac-
cess and release the psoas (Figure 8.60).
lliacus Release
Purpose: The iliacus muscle can be treated for limited extension of the hip
or as an extension of a psoas release. Even though the iliacus does not have an
At las of Therapeutic Tec hniques 247
Figure 8.61 Iliacus: 30° flexion.
insertion into the spine, a shortening dys-

function of the iliacus can anteriorly rotate
the pelvis, creating a backward-bending
dysfunction of the spine.
Patient position: Supine, with hips
flexed to approximately 30° and supported
by pillows or bolster (Figure 8.61). As with
the psoas, if not enough slack is placed on
the tissue, the hip may be flexed by the ther-
apist, up to approximately 110°.
tient. If necessary, therapist grasps patient's
lower extremity to impart hip flexion (Fig-
ure 8.62).
Hands : The therapist places the palm
of the hand over the anterior superior iliac
spine and wraps the fingers over the ilium,
contacting the anterior surface of the ilium.
The fingers contact with the iliacus at the
most accessible portion of the insertion
(Figure 8.63).
Execution: The technique begins with
Figure 8.62 Iliac us release: 110° flexion.
a proximal-to-distal stroking of the muscle
Figure 8.63 Iliacus release: contact.
(longitudinal stroking). As patient tolerance or muscle response dictates, the

stroke is shifted into a cross-stroking of the iliacus (lateral to medial).
Techniques for the Lumbopelvic/Lower Quarter Area

Greater Trochanter Rocking (see DVD)
Purpose: This technique is designed for gentle inhibition of the lateral rotators
of the hip and for the hamstrings. This is an excellent preparatory technique for
more extensive work in the piriformis, posterior hip, and hamstrings. Application
of this technique will generally yield an increase in straight-leg raise and in hip
internal rotation.
Patient pos ition: Supine.
Therapist pos ition: Standing or sitting at patient's side. The seated position is
biomechanically more advantageous for the therapist.
Hands: The fingers of the top hand will contact the posterior surface of the
greater trochanter, while the bottom hand gently grasps the leg in the area of the
distal femur, just proximal to the knee joint (Figures 8.64 and 8.65).
Execution: A gentle internal rotation motion is initiated with the bottom hand,
while an anterior pressure is simultaneously applied with the top hand through the
greater trochanter, further facilitating internal rotation of the hip (Figure 8.66).
The motion is repeated in an oscillatory fashion at a deliberate speed. The tech-
nique is generally performed in the mid-range of internal rotation and is gradually
moved toward end range. The manipulat-

ing hand may progress medially to further
inhibit the external rotators. Internal rota-
tion and straight-leg raising should be reas-
sessed after this technique.
Transverse Muscle Play

of Quadriceps (see DVD)
Purpose: The concept of muscle play
is applied to the quadriceps muscle where
the surrounding fasciae are manipulated to
provide more room for the quadriceps to
contract and expand. The "bending of the
water hose" analogy applies, but the tech-
nique has a different "look" compared with
the muscle play of the erector spinae (Fig-
ure 8.19) because of the size of the quadri-
ceps, compared with that of the erector spi-
nae, and the location around the femur.
Patient position: Supine.
Therapist position: Standing at pa-
tient's side at level of mid-femur in diagonal
Figure 8.64 Trochanter rocking.
stance.
Figure 8.65 Trochanter rocking: superior hand placement, bony contact.

p :,
Figure 8.66 Trochanter rocking: superior hand placement, close up.
Hands: The bottom hand grasps the quadriceps and femur distally, just proxi-
mal to the knee. The top hand grasps the quadriceps anywhere on the muscle belly
where a restriction is identified . The top hand palm is placed laterally over the
vastus lateralis.
Execution: Firmly grasping the distal aspect of the quadriceps with the bot-
tom hand, the top hand lifts and rolls the quadriceps over the femur and exerts
a shearing force through the quadriceps in a lateral-to-medial direction (Fig-
ure 8.67). The force is applied through the palm of the hand without sliding. The
technique is designed to move the muscle, not to slide over the muscle, which is
more of a massage technique. The technique is generally performed in a lateral-
to-medial direction because more restrictions seem to occur in the vastus late-
ralis, but it may also be applied in a medial-to-lateral direction by moving to the
patient's other side and shearing the quadriceps in a medial-to-lateral direction
(Figure 8.68). The technique may also be performed in diagonal planes if a restric-
tion occurs in that plane.
Alternately, both hands may be placed over the quadriceps to engage more
surface area but with the sacrifice of stabilization (Figure 8.69), or force can be ap-
plied through the tips of the thumbs to address a specific restriction, similar to the
erector spinae muscle play (Figure 8.70).
Some patients may not tolerate transverse muscle play of the quadriceps in
either a lateral-to-medial or a medial-to-lateral direction, even with light pressure.
In such cases, an anterior-to-posterior force is often tolerated (Figure 8.71), allow-
ing the therapist then to progress to the previous directions.
Figure 8.67 Transverse muscle play of quadriceps: lateral to medial.
Figure 8.68 Transverse muscle play of quadriceps: medial to lateral.
The main difference between soft tissue manipulation and joint manipulation
is that in joint manipulation, arthrokinematic rules must be followed. In soft tissue
manipulation, restrictions may occur in any plane and at any depth, and manipu-
lation of the restriction does not depend on arthrokinematics.
Figure 8 .69 Transverse muscle play of quadriceps: Figure 8 .70 Transverse musc le play of quadriceps:
bilatera l grip . using thumbs .
Figure 8 .71 Transverse muscle play of quadriceps: anterior to posterior .

lliotibial Band Paratrochanteric Manipulation (see DVD)

Purpose: The iliotibial band (ITB) is an area commonly involved in lower ki-
netic chain problems, knee dysfunction, and hip and low-back dysfunction. Many
diffuse "referred pain" syndromes in the lower extremity can be traced to iliotibial
dysfunctions. Treatment of this area becomes important to a variety of problems,
even if the patient has no conscious awareness of pain in the area. Many times the
patient will be exquisitely tender over the area of the ITB and surrounding tissues
when other dysfunctions are symptomatic nearby.
This technique actually addresses four distinct areas: (1) the connective tissue
"groove" between the ITB and the lateral hamstrings, (2) the groove between the
ITB and the lateral quadriceps, (3) the superficial tissues overlying the ITB, and
(4) the ITB itself Because loose irregular connective tissue is the most easily manip-
ulated, the surrounding connective tissue will more readily respond than the ITB.
This technique also addresses the paratrochanteric area. The connective tissue
surrounding the greater trochanter is also often dysfunctional; this includes tissue
that is superior, inferior, anterior, and posterior to the greater trochanter.
Patient position: Supine with hip and knee flexed, but with foot on treat-
ment table. In a more aggressive form of the technique, the patient is asked to flex
and adduct the hip and to hold the position to place the posterior hip in a more
stretched position (not shown). The therapist's position, hand placement, and ex-
ecution of the technique are the same in either position.
Therapist position: Standing at patient's side.
Hands: The power grip described previously (Figure 8.4) is used in this tech-
nique. The thumb and the PIP joint of the index finger contact one another and
become the point of contact with the patient. The elbow should point up toward
the ceiling for the best mechanical advantage while applying the technique.
Execution:
(1) Posterior border of the 1TB (i.e., lateral hamstrings and ITB): The ther-
apist's top hand (pictured left) stabilizes the patient's leg at the knee joint. The
thumb and PIP joint of the bottom hand (pictured right) contact the groove be-
tween the ITB and the hamstrings distally. With the elbow pointing upward, a
longitudinal force is applied to manipulate tissues following the border of the ITB
and the hamstring proximally. When the area of the greater trochanter is reached,
the therapist changes direction of the stroke and continues to encircle the greater
trochanter, ensuring manipulation of the paratrochanteric tissues (Figure 8.72).
(2) Anterior border of the 1TB (i.e., lateral quadriceps and ITB): The thera-
pist's bottom hand (pictured right) stabilizes the patient's leg at the knee joint. The
thumb and PIP joint of the top hand (pictured left) contact the groove between the
ITB and the quadriceps distally. With the elbow pointing upward, a longitudinal
force is applied to manipulate tissues following the border of the ITB and quad-
riceps, again until the greater trochanter is reached . The stroke continues over
the anterior border of the greater trochanter, encircling the greater trochanter and
ending posteriorly (Figure 8.73).
Figure 8. 72 lliotibial band paratrochanteric Figure 8. 73 lliotibial band paratrochanteric ma-

manipulation: posterior border. nipulation: anterior border.
(3) Direct technique over the 1TB: The

therapist uses his or her bottom hand (pic-
tured left) to stabilize the patient's leg at the
knee and his or her other hand as a loose fist
to manipulate the superficial tissues directly
overlying the 1TB (Figure 8.74). A longitu-
dinal stroke is applied in the distal-to-prox-
imal direction. The elbow/forearm may also
be used to distribute the forces over a large
contact surface. Care must be taken not to
exert more medial-to-lateral force than the
tissue can tolerate. The elbow/forearm con-
tacts the 1TB, and the stroke proceeds from
distal to proximal directly over the 1TB and
greater trochanter (Figure 8.75).
Both hands may also be used to stroke
directly over the 1TB (Figure 8.76). The
above techniques may be repeated with the
patient holding the leg in hip flexion and
adduction, to stretch the posterior elements
Figure 8. 7 4 lliotibial band paratrochanteric
of the hip and for greater access to the 1TB
manipulation: direct technique.
proximally.
Figure 8. 75 lliotibial band paratrochanteric Figure 8. 76 lliotibial band paratrochanteric

manipulation: forearm contact. manipulation: bilateral hand contact.
Hold-Relax Stretch of Hip

Purpose: The purpose of this technique is to stretch the posterior hip cap-
sule and surrounding periarticular soft tissues. A typical patient presentation is
a middle-aged man with a flattened lumbar lordosis, hypermobile lumbar facet
joints, tight hamstrings, and restricted posterior hip connective tissues. With little
pelvic contribution to forward bending, the lumbar spine becomes progressively
more hypermobile and symptomatic. Additional long-term effects are facet and/or
disc degeneration. The focus of treatment lies in establishing a balance of stresses
between the low back and the hip during forward bending. To accomplish greater
movement balance, the periarticular structures of the hip must be manipulated
before movement reeducation can begin.
The therapist can prepare the tissues for the more aggressive stretching of this
technique by first applying the iliotibial band paratrochanteric manipulation tech-
nique previously described.
Position 1: Hip Flexion!Adduction

Patient position: Supine, with hip flexed and adducted.
Therapist position: Standing over patient, facing patient. The patient's leg is
placed so it is in contact with the therapist's chest. The knee should approximate
256 EVAL UATION AND TREATMENT OF THE MYOFASCIAL SYSTEM
Figure 8.77 Hold-relax stretch of hip: table stabilization.
the therapist's axillary or pectoral area. (Female therapists should use a folded
towel as a mechanical barrier.)
Hands: The therapist either grasps the treatment table with one hand on either
side, thus "strapping" the patient to the table, or, for added stability, grasps the pa-
tient's leg with one hand and the opposite side of the table with the other hand.
Execution: With the patient in a firm grasp, the therapist asks the patient to
push the leg into the therapist's chest. The patient is then asked to release the con-
traction, and the therapist "takes up the slack," moving the hip into further flexion-
adduction (Figure 8.77). Occasionally, a patient will complain of anterior hip pain
while the technique is being executed. A possible explanation is that the anterior
capsule may be pinching with the extreme amount of flexion being applied to the
hip. If this occurs, the hip may be taken out of extreme flexion to emphasize the
technique's adduction component. The therapist stabilizes the pelvis at the ante-
rior superior iliac spine with the top hand. The leg is grasped with the bottom arm
and adducted with a slight external rotation component (Figure 8.78). The addi-
tion of external rotation and the increase in adduction will compensate for the loss
of flexion and regain the tissue tension lost with the loss of hip flexion.
Position 2: Hip Flexion, External Rotation, Adduction

An alternate method may be used when the patient continues to experience an-
terior hip pain with the above techniques. A combination of hip flexion, exter-
nal rotation, and adduction is applied to take the tissues to their end range be-
fore the hold-relax stretch. Applying hip external rotation prior to adduction
Figure 8.78 Hold-relax stretch of hip: anterior superior iliac spine stabilization.
Figure 8.79 Hold-relax stretch of hip: triplanar, contralateral side.
should make the anterior capsule taut, thereby making it less likely to be pinched
(Figure 8.79).
Patient position: Supine, with hip taken into 90° flexion, end-range external
rotation, and end-range adduction.
Therapist position: Standing against table on opposite side of hip to be

manipulated.
Hands: The lower leg is cradled in the therapist's bottom hand to control hip
flexion and rotation. The top hand clasps the patient's knee to control hip adduc-
tion and abduction.
Execution: As the forces accumulate, the patient should report feeling a tight-
ening of structures in the posterior hip or buttock. The patient is then asked to
resist further movement into flexion, external rotation, or adduction, depending
on the direction with the greatest restriction. The patient is then asked to relax as
the therapist "takes up the slack," and the process is repeated. Because the tissues
are taken into end range using a combination of three movements, very little force
is needed to manipulate. Care should be taken when applying resistance and '"tak-
ing up the slack."
Hamstring Manipulation (see DVD)

Purpose: The purpose of these techniques is to manipulate the hamstrings in
preparation for aggressive stretching. The hamstrings may be restricted in a longi-
tudinal direction, medial-lateral direction, or in a diagonal plane. Identifying and
treating lesions in the appropriate plane and position may release specific restric-
tions and may increase flexibility of the hamstrings prior to stretching.
Patient position: Supine, with hip and knee initially flexed to approximately
90°, and leg resting over therapist's shoulder.
Therapist position: Seated on treatment table facing patient.
Longitudinal Stroking
Hands: Contact with the patient is made with a loose fist (i.e., with the meta-
carpophalangeal joints of the hand) (Figure 8.80), bilateral power grips (Fig-
ure 8.81), or a forearm (Figure 8.82). Contact is initiated on the distal aspect of the
hamstrings.
Execution: With the patient's leg relaxed over the therapist's shoulder, the
therapist applies firm pressure into the distal aspect of the hamstrings with the fist
or elbow. The therapist strokes the hamstrings longitudinally, in a distal-to-prox-
imal direction, to the insertion at the ischial tuberosity. If a restriction lies in the
proximal hamstring near the ischial tuberosity, the hip may be flexed beyond 90°.
If the therapist identifies a specific restriction, the elbow may be used to apply
a sustained pressure on the restriction. The stroke should be stopped when the re-
stricted area is reached. The pressure should be sustained for an appropriate period
until changes in the restriction are palpable or until it is obvious that no change is
going to occur.
Splay Technique (see DVD)

Hands: The hands gently grasp the posterior-middle aspect of the lower ex-
tremity so the thumbs are in contact with the distal portion of the hamstrings
or hamstring tendons. The hands palpate between the muscle bellies as they
Figure 8.80 Hamstring manipulation: loose fist Figure 8.8 1 Hamstring manipulation: bilateral
contact. power grip contact.
move proximately, relocating to the mid-

dle one-third of the muscle bellies. The
thumbs should approximate one another
(Figure 8.83).
Executi on : Once the thumbs are in
contact with the middle one-third of the
muscle belly, deep pressure is applied by
placing the thumbs between the medial and
lateral hamstrings. The thumbs then apply
both medial and lateral forces to splay or
pull the hamstrings apart. The thumbs do
not slide over the hamstring muscle bellies.
Rather, the thumbs are grasping the muscle
bellies and pulling them apart. This tech-
nique can be thought of as a specific form
of muscle play for the middle hamstrings.
Proximal Hamstring Stretch

Figure 8.82 Hamstring manipulation: forearm
is to isolate a stretch of the proximal ham-
contact.
string. Hamstring injuries generally fall
---
Figure 8.83 Hamstring manipulation: splayed Figure 8.84 Proximal hamstring stret ch.
hands.
into two basic categories: mid-belly injuries and proximal injuries. Proximal inju-
ries can be more serious, more recurrent, and more difficult to treat than mid-belly
lesions. The proximal injury can sometimes act similar to an epicondylitis, where
the injury is in the tenoperiosteal junction. By isolating a stretch to the proximal
hamstring, the therapist can more effectively aid in the remodeling of the proxi-
mal tissues.
Patient position: Supine, with leg resting on therapist's shoulder.
Therapist position: Standing on one leg, with other leg on treatment table.
Hands: The therapist places his or her hands around the patient's knee. This
will help to provide a traction force and control the amount of knee flexion.
Execution: The therapist first performs a straight -leg raise until the patient
feels a mild hamstring stretch. The patient is then asked to localize the stretch. If
the stretch is felt in the distal or mid-belly of the hamstring, the therapist allows
the patient's knee to bend slightly. Keeping the slight bend constant, the therapist
continues to flex the hip until the patient again feels the stretch. At this point,
the patient should feel the stretch more proximally because the distal aspect has
been slackened and the proximal aspect has been further stretched . The therapist
repeats the process, allowing the patient's knee to flex slightly more, and then flex-
ing the hip further. The process is repeated until the stretch is felt closest to the
origin at the ischial tuberosity (Figure 8.84). To further localize the stretch, a slight
traction force can be placed on the leg while stretching. The traction serves to pull
slightly more on the origin of the muscle at the ischial tuberosity.
lschial Tuberosity Cross-Friction

Purpose: Many hamstring injuries and/or dysfunctions occur at the junctional
zone (i.e., the insertion of the hamstrings into the ischial tuberosity). Healing and
restoration of proper function may be facilitated with a deep cross-frictional type
of manipulation over this area.
Therapist position: Standing over patient in diagonal position.
Hands: The therapist may use the fingertips or the tips of the thumbs for this
technique. The most stable position of the hands for application of the technique
is the chisel grip (Figure 8.1). The fingers are placed over the insertion of the ham-
strings, just distal to the ischial tuberosity.
Execution: The fingers palpate deeply until firm pressure is placed on the
hamstring insertion and junctional zone. The fingers oscillate in a medial-to-
lateral direction, consistent with the concept of cross-friction. The fingers are then
moved proximally onto the ischial tuberosity (Figure 8.85). The periosteum of the
ischial tuberosity may also be damaged or dysfunctional. The same medial-to-
lateral movement is applied over the ischial tuberosity and into the sacrotuberous
ligament, as fibers of the hamstrings have been found attached to the ligament. 4
This technique should be applied aggressively to the point where it is seminoxious
to the patient.
Figure 8.85 lschial tuberosity cross-friction.

Gluteal Fascial Plane Manipulation

Purpose : Multiple fascial planes or connective tissue sheaths exist between
the gluteal musculature that, when restricted, may limit active hip extension. Be-
cause the greater trochanter moves anteriorly with hip extension, restrictions in
this fascial sheath may limit hip extension. The area is not usually painful and is
rarely tender, but it may create hip or lumbar dysfunctions if not extensible.
Patient position: Prone, with lumbar spine in neutral position (Figure 8.86).
To add tension to the tissue, the hip may be held or positioned in the extended
position (Figure 8.87).
Therapist position: Standing over patient in diagonal position. If the therapist
chooses to extend the hip manually (as opposed to positioning the hip with pil-
lows), he or she grasps the lower extremity with the bottom hand, leaving the top
hand free to execute the technique. If the therapist does not hold the lower extrem -
ity, both hands should be used in executing the technique.
Hands : The chisel grip (Figure 8.1) hand position is used. The index and ring
fingers approximated together provide the stability necessary to perform a tech-
nique at this depth. The pressure is exerted through the fingertips.
Execution: The direction of force is primarily in a posterior-to-anterior direc-
tion, with a slight horizontal component. As in the iliac crest release technique,
an oscillatory motion is performed repetitively in an anterior direction. To apply
tension to the fascial sheath, the therapist extends the hip or positions it on pillows.
As a follow-up technique, the hip may be stretched into extension.
Figure 8.86 Gluteal fascial plane manipulation.

Figure 8.87 Gluteal fascial plane manipulation: hip extension.
Cross-Friction of Piriformis Insertion

Purpose: This technique helps prepare the piriformis for direct contact on the
muscle belly if the piriformis muscle is reactive and cannot tolerate direct pres-
sure, or if direct pressure is not resulting in any palpable changes or changes in
symptoms.
Therapist position: Standing at patient's side at level of hip.
Hands: The bottom hand grasps the leg at the ankle and bends the knee to 90°.
The fingers of the top hand are placed on the posterior superior iliac spine, and the
thumb of the top hand is placed on the musculature of the buttock. The piriformis
insertion is located by gently rotating the leg internally and externally with the
bottom hand as the thumb moves through the soft tissue above the lateral aspect
of the greater trochanter. As the hip is gently rotated internally and externally, the
thumb moves distally and laterally until arriving at the first bony prominence.
The prominence should be the superior/posterior border of the greater trochanter
(Figure 8.88).
Execution: Once in position, the thumb should remain stationary. The tech-
nique is applied by mid-range and pain-free rotation of the hip. As the rotation oc-
curs, the thumb will come on and off the greater trochanter. A fairly deep pressure
can be applied, but only to patient tolerance . Care must be taken not to take the hip
into excessive internal rotation if the piriformis is very reactive.
Figure 8.88 Cross-friction of piriformis insertion.
Piriformis Release in Prone

Purpose: These techniques are used if the patient's dysfunction lies in a hy-
pertonic muscular state of the piriformis rather than in a connective tissue dys-
functional state. These techniques are designed primarily to decrease underlying
muscle tone and secondarily to affect connective tissue . The techniques are per-
formed in a graded fashion depending on the overall pain and reactivity of the
piriformis muscle.
The issue must be raised here as to whether or not the so-called piriformis
syndrome exists. Some say that the syndrome does not exist, but the average cli-
nician, in practice, cannot deny the involvement of the piriformis or manifesta-
tions of piriformis hypertonicity. The clinical reality is that piriformis syndrome
in a pure sense is rare, but piriformis involvement related to other dysfunctions is
seen quite often. When in a hypertonic state, the piriformis may produce a trigger
point, which has been shown to refer pain into the buttock and down the posterior
leg above the knee .
In all cases the piriformis muscle belly should be located by triangulating be-
tween the following three bony landmarks: (1) the posterior superior iliac spine,
(2) the greater trochanter, and (3) the ischial tuberosity.
Therapist position: Standing at patient's side, perpendicular to patient.
Hands: The hand position in the technique will vary depending on the reac-
tivity of the muscle and the tolerance of the patient. The general progression of
Figure 8.89 Piriformis release in prone: open hand.
the technique goes through three different hand positions: (1) palm of the hand,
(2) elbow, and (3) PIP joints of both hands.
Execution:
(1) Using the palm of the hand: The therapist applies gentle pressure to the
piriformis muscle using the bony landmarks above. With the knee bent to 90°, the
hip is gently rotated externally to put the piriformis on slack (Figure 8.89). Pres-
sure is gently increased through the manipulating hand until the level of the piri-
formis is reached. A sustained pressure is applied, provided the pressure does not
create an increase in tone. As the piriformis relaxes, more pressure can be applied
progressively. If the piriformis releases, even partially, the patient's tolerance will
increase, allowing the next variation of the technique.
(2) Using the elbow: With the lower extremity extended, the same sustained
pressure may be applied to the piriformis using the elbow (Figure 8.90). The el-
bow allows for the application of more localized pressure. As the piriformis re-
leases and as the pain decreases, progressive pressure can be applied for further
inhibition.
(3) Using bilateral PIP joints: Finally, again with the lower extremity ex-
tended, the PIP joints of both hands may be used to apply even more localized
pressure (Figure 8.91). If the patient is able to tolerate it, a gentle oscillatory motion
created with wrist flexion-extension can be performed to further inhibit and me-
chanically manipulate the piriformis.
Figure 8.90 Piriformis release in prone: elbow/forearm.
Figure 8.91 Piriformis release in prone: bilateral proximal interphalangeal joints.

Figure 8.92 Transverse muscle play of hamstrings: lateral to medial.
Transverse Muscle Play of Hamstrings (see DVD)

Purpose: As described in the earlier section "Transverse Muscle Play of Quad-
riceps," the concept of transverse muscle play can be used to manipulate the fascial
sheath surrounding the hamstrings to provide more space for the hamstrings to
contract and expand.
Therapist position: Standing at patient's side at level of mid-femur.
Hands: The bottom hand grasps the hamstrings and femur distally, just proxi-
mal to the knee joint for stabilization. The top hand grasps the hamstrings any-
where on the muscle belly where a restriction is identified. The palm of the hand
is initially placed over the lateral hamstring, just posterior to the 1TB. Both hands
may also be used to gain a greater contact surface.
Execution: Grasping the distal aspect of the hamstrings and femur, the bot-
tom hand stabilizes with a counterpressure as the top hand shears the hamstrings
in a lateral-to-medial direction (Figure 8.92). The major force is applied through
the palm of the hand. The hand does not slide over the skin. It simply bends the
muscle. The technique may also be performed in a medial-to-lateral direction if
the restriction is present (Figure 8.93). The therapist should approach the patient
from the other side of the table so a medial-to-lateral force may be applied with
the palm of the top hand. If a restriction is felt in a posterior-to-anterior direction,
the force may be applied accordingly using the palm of the hand (Figure 8.94).
----
Figure 8.93 Transverse muscle play of hamstrings: medial to lateral.
Remember, restrictions can occur in any direction or plane, and the technique
direction should be modified to treat the restriction adequately.
Transverse Muscle Play of Hamstrings and Adductor Magnus:

Posterior-to-Anterior Pressure
Purpose: As previously described in concept, this technique is designed to
manipulate the surrounding fascial sheaths of the adductor muscles. This is an
excellent preparatory technique for adductor stretching.
Therapist position: Standing at patient's side, holding leg with knee bent at
90°. Placing the medial hamstring on slack makes it easier to sink to the depth of
the hip adductors.
Hands: The palm of the top hand is used to apply the anterior pressure on the
adductor group so the thumb of the manipulating hand is always pointing caudal.
Execution: The palm of the hand makes contact with the adductor muscles
and partially with the medial hamstring. Pressure is applied toward the treatment
table to create the bending movement of the adductors (Figure 8.95).
Transverse Muscle Play of Gastrocnemius-Soleus

Purpose: The fascial sheath surrounding the gastrocnemius -soleus mus-
cle group is manipulated to increase extensibility and allow for more efficient
Figure 8.94 Transverse muscle play of ham- Figure 8.95 Transverse muscle play of hamstrings
strings: posterior-to-anterior pressure to lateral and adductor magnus: posterior-to-anterior pres-
tissues. sure to adductors.
contraction and expansion of the muscle group. Longitudinal stretching is also

facilitated after application of this technique.
Patient position: Prone, with lumbar spine in neutral position. Feet should be
off the table, or preferably a towel roll or pillow should be placed under the distal
anterior tibia to protect the ankles.
Therapist position: Standing perpendicular to patient at level of mid-tibia.
Hands: The bottom hand grasps the distal aspect of the gastrocnemius-
soleus muscle group just proximal to the Achilles tendon. The top hand grasps the
gastrocnemius-soleus muscle group at the level of the muscle where the restric-
tion is identified. Both hands may be used to attain a more optimal "bend" in the
muscle (Figure 8.96).
Execution: The bottom hand grasps the distal aspect of the gastrocnemius-
soleus muscle group firmly for stabilization, and the palm of the top hand shears
the muscle from lateral to medial (Figure 8.97). The hand does not slide over the
skin. Sliding over the skin modifies the technique into a pure massage technique,
which will prevent reaching the deeper, targeted tissues. As with the similar,
previously described techniques, the technique may be performed in a medial-
to-lateral or a posterior-to-anterior direction, depending on the direction of
Figure 8.96 Transverse muscle play of gastrocnemius-soleus: bilateral grip.
Figure 8.97 Transverse muscle play of gastrocnemius-soleus.
the restriction. The clinician should be sensitive to restrictions and follow them
with the technique, because no arthrokinematic rules apply. The success of the
treatment often depends on whether the direction of application was properly
identified.
Bony Clearing of the Tibia

Purpose: The purpose of this technique is to clear fascia from the anterior
and posterior compartments as they adhere to the tibia. Many lower kinetic chain
problems, especially in athletes participating in ballistic sports (running, basket-
ball, soccer, etc.), develop fascial adhesions related to so-called shin splints. The
bony clearing techniques are effective in manipulating the fascia as it adheres to
the tibia. This technique can be used for both anterior and posterior compartmen-
tal syndromes.
Therapist position: Standing or sitting at foot of table.
Hands: The thumb pushes off the border of the tibia, creating a "wedge" be-
tween the bone and the approximating soft tissue. The thumb is positioned either
anterior or posterior, depending on the compartment that is affected.
Execution: A small amount of lubrication is used. The thumb drives a wedge
between the bone (tibia crest) and the approximating soft tissues distally. The
thumb then moves proximally, continuing to stay in the wedge, and also continu-
ing to approximate the tibia (Figure 8.98). In compromised areas, either the wedge
will not be as deep or adhesions will make the wedge nonexistent. These adhe-
sions need to be manipulated. To manipulate tissues from the posterior side, the
patient's knee is bent, and the foot is placed on the table to provide slight slack in
the tissues (Figure 8.99).
If the therapist has weak thumbs or hypermobile carpometacarpal joints, a
"dummy thumb" grip may be used or the patient may be placed in prone position,
as described next.
I
l X
Figure 8.98 Bony clearing of the tibia: anterior tibia.

Bony Clearing of the Tibia Using

the Dummy Thumb
When using the dummy thumb, the thera-
pist must treat from the opposite side of the
table to protect his or her own back. An
anterior-posterior force may be applied to
wedge between the bone and the soft tis-
sues. The therapist may work the full length
of the tissues, moving from distal to proxi-
mal, repositioning after each manipulation
(Figure 8.100).
Bony Clearing of the Tibia in Prone

When the therapist performs bony clear-
ing of the tibia in prone, the patient must be
positioned with the spine in a neutral posi-
tion. The patient's knee is flexed to 90 ° and
stabilized against the therapist's body. The
lateral border of the index finger, while sup-
ported by the other three fingers, is used to
manipulate the tissues. A slicing motion is
made, wedging the lateral border of the in-
dex finger into the tissues between the tibia
Figure 8.99 Bony clearing of the tibia: posterior
and the neighboring soft tissue (Figures
tibia.
8.101 to 8.103).
'
Figure 8.100 Bony clearing of the tibia: dumm y thumb.
Figure 8.101 Bony clearing of the tibia: prone, Figure 8.102 Bony clearing of the tibia: prone,
half -chisel grip . thenar eminence .
'
,,
Figure 8.103 Bony clearing of the tibia: with movement .

This technique can be performed purely as a passive technique, as described

above, or may be applied with active plantar flexion and dorsiflexion. If the tech-
nique is applied with active movement, very little lubricant, if any, should be used.
Lateral Fascial Distraction of the Tibia

Purpose : The purpose of this technique is to stretch the posterior compart-
ment fascia that is adhered to the tibia medially. As with the bony clearing of the
tibia technique, described above, this technique is effective in the treatment of
lower leg compartment syndromes, shin splints, and so forth, that are caused by
excessive ballistic lower kinetic chain activity.
Patient position: Prone, with lumbar spine in neutral position, knee flexed to
90° and foot slightly plantar flexed.
Therapist position: Seated on side of table at patient's lower leg.
Hands: The lateral hand is placed distally and will be used as a cantilever. The
palm of the medial hand is placed on the mid-belly of the gastrocnemius-soleus
muscle group, as close to the tibia as possible without actually contacting it.
Execution: The therapist puts a medial-to-lateral pressure on the gastrocne-
mius-soleus muscle group, pulling it away from the tibia . The technique starts
in the mid-belly but can move proximally
or distally, depending on the location and
severity of the restriction (Figure 8.104).
The therapist carefully attempts to push
the muscle laterally into the plastic range,
keeping an eye on patient reaction. This
technique can be quite painful if the fas-
cia along the tibia-gastrocnemius border is
compromised.
-X Lateral Elongation
of Peroneal Tissue
Purpose: The purposes of this tech-
nique are to elongate the soft tissue struc-
tures of the lateral leg and to address re-
strictions that may have developed between
the tibialis anterior, extensor digitorum,
peroneus longus, and triceps surae. The fas-
cia of the lateral lower extremity is continu-
ous from the iliotibial band down across the
peroneal group to the foot.
Patient position: Side-lying, with lower
leg supported on pillow.
Figure 8.104 Lateral fascial distra ction of the
Therapist position: Standing or sitting
tibia.
at foot of table.
\
Figure 8.105 Lateral elongation of peroneal Figure 8.106 Lateral elongation of peroneal tis-
tissue. sue: with movement.
Hands: The therapist provides slight anterior-posterior stabilization by cup-

ping the lower leg between the leg and pillow. The manipulating hand, in the shape
of a loose fist, is placed on the distal aspect of the peroneal group muscle bellies.
Execution: Using a small amount of lubrication, the therapist applies suffi-
cient lateral-to-medial force to reach the level of the subcutaneous fascia. A caudal-
to-cephalic force is applied to distract the subcutaneous fascia (Figure 8.105). The
stroke should end just distal to the superior fibular head. The therapist repeats the
stroke, gently progressing in depth, being careful not to press into the periosteum
of the fibula.
The technique may be applied more specifically and between muscle bellies us-
ing a two-finger contact or with active movement from the patient (Figure 8.106).
Contact is made with the middle finger supported by the index finger. The stroke
is applied in the same depth and manner, caudal to cephalic, but can be applied
between muscle bellies and/or with active ankle inversion/eversion.
Cross-Friction of Gastrocnemius-Soleus Musculotendinous Junction

Purpose: Many patients involved in ballistic-type sports and activities develop
fascial thickening in the musculotendinous junction of the gastrocnemius-soleus
muscle group. This phenomenon may occur with or without muscular shortening.
The purpose of this technique is to manipulate the musculotendinous junction
and the fascia immediately surrounding it.
Patient position: Prone, with lumbar

spine in neutral position, the knee flexed to
90°, and the foot moderately plantar flexed.
Therapist position: Seated at side of
table at lower leg of patient. The patient's leg
is resting against the therapist.
Hands: The therapist's hands gently
grasp the patient's lower leg so that the fin-
gers come to rest directly over the muscu-
lotendinous junction of the gastrocnemius-
soleus muscle group.
Execution: The therapist applies firm
pressure over the musculotendinous junc-
tion using the fingers and applies a firm
cross-frictional movement across the junc-
tion, watching for the patient's response
(Figure 8.107). This area can be exquisitely
tender in active patients participating in
ballistic-type sports and activities. The ther-
apist holds the tissue in the shortened range,
which creates slack and allows for access to
Figure 8.107 Cross-friction of gastrocnemius-
deeper tissues. A stretch can immediately
soleus musculotendinous junction.
follow the application of this technique.
Lower Extremity/Posterior Quadrant Fascial Elongation (see DVD)

Purpose: The superficial fascia of the lower extremity is one continuous
cylinder anchoring to the sacrum and iliac crest. Changes in the lower extrem-
ity fascia often result in changes within the lumbar spine, and vice versa . The
purpose of this technique is to elongate the superficial fascial sheaths continu-
ously as they travel up the posterior-lateral lower extremity and into the lumbar
spine. Because the primary target is loose connective tissue, elongation is time
dependent.
Therapist position: Standing at foot of table.
Hands: The therapist uses both hands to grasp the patient's ankle and provide
a gentle distraction of the lower extremity.
Execution: As the lower extremity is distracted, the therapist slowly applies
forces, taking the lower extremity into flexion, internal rotation, and adduction
(Figure 8.108). As the tissues creep, movement should continue through the lower
extremity into the posterior knee, then into the hip, and eventually into the low
back and trunk. The movement is continued until the patient's leg is crossed and
the patient's lower trunk is fully rotated into side-lying, but this is not necessary
and depends on the flexibility of the tissues (Figure 8.109). The patient may feel
tension in the way of a good stretch in the lower extremity, in the posterior knee
Figure 8.108 Lower extremity/posterior quadrant fascial elongation.
Figure 8.109 Lower extremity/lower quadrant fascial elongation: completion.
or hip, and even into the low back. Once a maximal stretch is achieved, the patient
should be slowly retuned to the starting position. The technique may be repeated
two or three times. Treatment is based not on pain but rather on postural exami-
nation and functional limitations.
Plantar Fascia Manipulation

Purpose: Although the plantar aponeurosis is cushioned by a thick layer of
adipose tissue, restriction may result in dysfunction or foot pain. Patients diag-
nosed with plantar fasciitis often find relief through manipulation of the plantar
fascia. The purpose of this technique is to manipulate both the aponeurosis and
the superficial tissues overlying the aponeurosis. (This technique is shown with the
patient in prone position but may also be performed with the patient in a supine
position.)
Therapist position: Standing at foot of table.
Hands: Both hands are used to grasp the patient's ankle and provide a gentle
distraction of the lower extremity.
Execution: Beginning at the calcaneus, the therapist applies a longitudinal
stroke to the full length of the plantar surface of the foot, from proximal to distal
(Figure 8.110). The stroke is initially applied with the foot in plantar flexion, allow-
ing the tissues to have some slack, but the foot may be taken into dorsiflexion as
mobility improves or the subject's reactivity decreases. The pressure of the stroke
may also be increased with decreased subject reactivity but should always begin
gently and superficially.
Movement may be added to this technique, either passively or actively.
Passively, the therapist may further elongate the tissues by simultaneously strok-
ing in a proximal-to-distal direction while taking the foot into dorsiflexion. The
Figure 8.110 Plantar fascia manipulati on.

same can be done actively as the patient dorsiflexes in time with the proximal-to-
distal stroke.
Techniques for the Thoracic/Upper Thoracic Spine

and Upper Extremity
Lateral Elongation of Upper Thoracic Area
Purpose: The purpose of this technique is to elongate the soft tissue structures
of the upper thoracic area (posterior and anterior). The technique is especially ap-
plicable for patients with protracted shoulder girdle complexes and forward-head
postures. After application of the technique, the shoulder girdle and upper tho-
racic spine assume a more relaxed and retracted position. This technique should
be used before attempting postural reeducation techniques. Initially, the clinician
emphasizes both the anterior and posterior structures of the upper thoracic area.
As the technique progresses, more emphasis is placed on the anterior structures.
Three alternate hand placements are described, each of which progresses into
deeper tissues of the anterior chest.
Patient pos ition: Supine, with head flat on treatment table.
Therapist pos ition : Seated at head of table, at 45° angle to patient.
Anter ior- Poster ior Techniqu e

Hands: The therapist's hand closest to the patient is placed posteriorly,
so that the fingertips are just lateral to the spinous processes of the upper tho-
racic spine. The hand should be resting superior to the spine of the scapula. The
other hand is placed inferior to the clavicle, with the fingertips just lateral to the
sternum.
Executi on : The primary force of the technique comes from the fingertips, even
though contact is maintained through the palm of the hands. The stroke begins
medially and progresses laterally, as the therapist pulls the hands toward the gle-
nohumeral joint (Figures 8.111and 8.112). Once the stroke is completed, the hands
are quickly placed in the start position again, and the pull stroke is repeated. The
pressure is placed through each hand and is moderate in depth.
Deep Anter ior Techniqu e

Hands: To approximate deeper structures, both hands are placed anteriorly.
One hand is placed over the other, again over the tissues inferior to the clavicle.
The fingertips are just lateral to the sternum.
Executi on : As the stroke is applied through the whole hand, in a medial-
to-lateral direction, the force is focused through the fingertips (Figure 8.113).
Deeper pressure may be applied through the hands and fingertips as the tissues
soften.
Figure 8.111 Lateral elongation of upper thoracic area: stroke initiation.
Figure 8.112 Lateral elongation of upper thoracic area: stroke comp letion .
Rib Splaying: Ribs 1-3

Note: This hand placement provides the most aggressive form of lateral elon-
gation of the upper thoracic area. The depth of penetration is to the intercostal
spaces (Figure 8.114).
Figure 8.113 Lateral elongation of upper thoracic area: deep anterior technique.
Therapist position: Standing, facing

patient.
Hand s: Contact is made using the
power grip shown in Figure 8.4.
Execution: The stroke begins medially
in the intercostal space of ribs 1 and 2. The
intercostal space is followed laterally until
no longer palpable (a short distance). The
stroke is then performed in the intercostal
space of ribs 2 and 3. (In men, the stroke is
also repeated in the intercostal space of ribs
3 and 4.)
Unilateral Posterior/Anterior
Articulation of First Rib
Purpose: This technique is essentially a
joint manipulation technique, but it blends
well with the lateral elongation and rib
techniques, especially if rib dysfunction is
present. With increased myofascial tone in
the subclavicular area, the upper thoracic
Figure 8.114 Lateral elongation of upper thoracic area, and the scalene muscles, joint me-
area: rib splaying.
chanics in the first rib can easily become
dysfunctional. The purpose of this tech-

nique is not to change the position of the
first rib but rather to increase mobility.
Patient position: Supine, with head flat
on treatment table.
Therapist position: Seated at head of
table, at 45° angle to patient.
Hands : The bottom hand (which is usu-
ally the hand closest to the patient) palpates
the posterior aspect of the first rib near the
t costotransverse junction. This can be ac-
complished by first palpating the posterior
aspect of the upper trapezius. The clinician
then continues caudally and medially until
bone is palpated. This bone is the first rib.
If the finger is too lateral, the border of the
scapula will be palpated . If the finger is too
medial, the spinous process will be pal-
/ pated. The top hand palpates just lateral to
the first sternocostal articulation. The clini-
cian may first palpate the sternoclavicular
Figure 8.115 Unilateral posterior - anterior artic- junction with the index finger and slip the
ulation of first rib. middle finger onto the first rib, just caudal
and lateral to the sternoclavicular joint.
Execution: The clinician applies a moderate oscillatory movement, in both
anterior-to-posterior and posterior-to-anterior directions (Figure 8.115). Enough
pressure should be applied to create movement in the first rib. The rate of oscilla-
tion should be 2-3 oscillations per second .
First Rib Shoulder Depression Technique (see DVD)

Purpose: This technique is largely inhibitory in nature, although the first rib
can be gently articulated . The rhythm created by the rib and shoulder articulation
provides a form of biofeedback for the patient and can indicate to the clinician,
as well as to the patient, the degree of inherent relaxation or tension in the up-
per thoracic area. This subtle form of biofeedback helps release tone in the upper
thoracic area, prepares the tissue for deeper or more specific myofascial work, and
facilitates joint manipulation.
Patient position: Supine, with head flat on treatment table .
Therapist position: Seated at head of table at 45° angle to patient.
Hands: The hand closest to the patient palpates the posterior aspect of the
first rib, as described in the previous technique. Palpating the posterior aspect of
the upper trapezius, the clinician then continues caudally and medially until bone
is palpated . This bone is the first rib. If the finger is too lateral, the border of the
scapula will be palpated, and if the finger is

too medial, the spinous process will be pal-
pated . The other hand is placed on the su-
perior aspect of the shoulder joint complex.
Execution: Execution of this technique
involves two separate movements: (1) the
bottom hand manipulates the rib in an an-
terior direction, and (2) the other hand de-
presses the shoulder caudally (Figure 8.116).
The two motions occur simultaneously in
a slow, deliberate rhythm (approximately 2
oscillations per second). During execution,
the patient may become aware of increased
tone, tension, or holding patterns and may
spontaneously relax. The tissue is then pre-
pared for other techniques as necessary.
Bilateral Upper Thoracic Release

(see DVD)
Purpose: The purpose of this tech-
nique is to release the deep paravertebral
Figure 8.116 First rib shoulder depression musculature of the upper thoracic spine.
technique. The technique is accomplished in two dis-
tinct maneuvers. The first is moderate
depth, cephalic-caudal movement, and the second is a deep anterior-posterior
movement.
Patient position: Supine, with head flat on treatment table.
Therapist position: Seated at head of table directly behind patient.
Hands: The hands slide onto the paravertebral musculature of the upper tho-
racic spine (to approximately T4). The fingers make firm contact with the paraver-
tebral musculature.
Execution: The first maneuver is a gentle cephalic-caudal oscillation with
moderately deep pressure on the upper thoracic paravertebrals. The oscillations
should be performed at a rate of approximately 2 per second, producing a rocking
motion throughout the patient's entire body. The manipulating oscillations should
be one level at a time, progressively moving up the thoracic spine, and returning to
T4 to repeat the movement (Figures 8.117 and 8.118). In the second maneuver, the
direction of the movement changes from cephalic-caudal to anterior-posterior
articulations. Although this may be considered an anterior-posterior manipu-
lation of the upper thoracic spine, the firm pressure applied through the layers
of muscle is done so for the purpose of releasing underlying tone. The clinician
should exercise caution in guarding his or her hands, because this technique re-
quires maximum force through the fingers. Fatigue will occur quickly, and the
1 ....
-
Figure 8.117 Bilateral upper thoracic release.
Figure 8.118 Bilateral upper thoracic release: hand placement.
clinician should proceed to another technique. Efficiency and ease of application

of the technique are essential for effective technique delivery. Any strain or inef-
ficiency on the clinician's part will be transferred to the patient and reduce the
potential effect of the technique.
Pectoralis Major Muscle Play/

Pectoralis Minor Manipulation
(see DVD)
Purpose: In the forward-head posture,
the pectoralis major and minor may be-
come shortened and restricted. This short-
ening creates an inability to stand or sit
erect without significant effort from the pa-
tient. Before neuromuscular reeducation or
postural training can occur effectively, the
pectorals must have adequate extensibility.
Pectoralis Major
Patient position: Supine, with shoulder
flexed 90°-120 °.
tient at 45° angle. The therapist may place
a leg on the table to allow the patient's arm
to rest in a relaxed position (Figures 8.119
to 8.121).
Hands: The therapist's thumbs slide
underneath the pectoralis major, and the
Figure 8.119 Pectoralis major muscle play/pecto-
hands grasp the muscle firmly between the
ralis minor manipulation.
thumbs and fingers.
//
Figure 8.120 Pectoralis major and minor muscle play: close up.
Execution: The technique can be lik-

ened to the bending of a garden hose. The
pectoralis muscle is grasped firmly between
the thumbs and fingers and is gently lifted
and/or bent away from the thorax. The
movement can be a sustained movement or
an oscillatory movement, depending on the
patient's comfort level.
Pectoralis Minor
Hands: With one hand maintaining
the same position as described above, the
thumbs are moved posteriorly until in con-
tact with the pectoralis minor. The muscle
may be difficult to palpate, but if the ribs are
palpable, the muscle is being palpated.
Execution: The thumbs are pressed
onto the pectoralis minor, and a gentle
"cross-friction type" technique may be per-
formed. Care must be taken because the
Figure 8.121 Pectoralis major and minor mus cle pectoralis minor area is very tender even if
play: hand contact.
not dysfunctional.
Seated Pectoral Anterior Fascial Stretch

Purpose: The purpose of this technique is to stretch the anterior structures
(fascia, pectoralis major, pectoralis minor) to allow for more erect posture.
Patient position: Seated, with hands behind head, or with elbows straight.
Therapist position: Standing behind patient, with hip or knee stabilizing pa-
tient's thoracic spine and acting as fulcrum. A pillow should be placed between
patient and therapist.
Hands:
Bilateral stretch: The hands grasp the middle part of the upper arm.
Unilateral stretch: The inside hand of the therapist grasps the upper part of
the patient's arm. The outside hand is placed on the middle part of the anterolat-
eral rib cage.
Execution:
(1) Bilateral stretch: The pressure is applied in a lateral, posterior, and cephalic
direction for maximum elongation (Figure 8.122). The patient is asked to breathe
deeply to increase elongation anteriorly.
(2) Unilateral stretch: Using the inside arm and body, the therapist pulls the
patient's arm posteriorly and superiorly, stretching the anterior fascia. The thera-
pist places his or her outside hand on the rib cage to stabilize or to push caudally
to further engage the anterior superficial fascia (Figure 8.123).
Figure 8.122 Seated pectoral anterior fascial Figure 8.123 Seated pectoral anterior fascial
stretch: bilateral. stretch: unilateral.
Subscapularis
Purpose: The subscapularis is generally not an area reported by the patient to
be painful; however, the area may be significantly restricted and extremely ten-
der to palpation. Because the internal rotators are held in a shortened position
during the forward-head, protracted-shoulder posture, the subscapularis and the
surrounding myofascia become restricted, acting as barriers to efficient postural
reeducation.
Patient position: Supine, with shoulder flexed from 90° to 170°, depending on
the restriction and comfort level of patient.
Therapist position: Standing at head of table at 45° angle to patient. The thera-
pist holds the patient's arm close to the therapist's body to provide a slight traction
force.
Hands: The therapist may place hands on the patient in three different ways,
depending on how aggressively the therapist wishes to deliver the technique. The
therapist may use the palm of the hand, the thumb, or the fingertips, in order from
least aggressive to most aggressive.
Execution:
(1) Using the palm of the hand: The patient's arm, which is in some degree
of flexion, is gently distracted. The palm of the other hand is placed on the lateral
X
X
Figure 8.124 Subscapularis: half-chisel grip. Figure 8.125 Subscapularis: thenar eminence
contact.
border of the scapula, as close to the glenohumeral joint as possible. While placing
gentle distraction on the arm, the therapist uses the palm to stroke caudally and
toward the inferior angle of the scapula. If fascial restrictions exist, the stroke may
be lengthened to include the lateral fascial sheaths between the scapula and the
ilium (Figure 8.125).
(2) Using the thumb: In the same position, the therapist uses the thumb to
stroke caudally. Thumb placement is more specific; it should be located on the
anterior surface of the lateral border of the scapula. While distracting the arm, the
therapist moves the thumb caudally over the anterolateral border of the scapula
toward the inferior angle (Figure 8.124).
(3) Using the.fingertips: Specific restrictions, either in the lateral aspect of the
subscapularis or in the fascial sheath between the scapula and the thorax, may be
treated using the fingertips. The tips of the index, middle, and ring fingers palpate
the anterior surface of the lateral scapula and apply gentle pressure. Either sus-
tained pressure or a slow oscillatory movement can be used (Figure 8.125).
Anterolateral Fascial Elongation

Purpose: The anterior fascial planes are often restricted, especially in the
slumped posture or in various shoulder pathologies. The purpose of this technique
is to elongate the superficial fascial sheaths of the anterior thorax.
, Position 1: Supine
flexed 120°-170 °.
Therapist position: Standing behind
patient, grasping patient's arm and provid-
ing distraction of arm.
Hands: The therapist places the entire
surface of the hand just below the patient's
nipple line. Male therapists treating fem ale
patients should carefully drape the patient
and should stay well below breast tissue.
Execution: As the arm is tractioned
into flexion, a traction force is applied to the
superficial fascia, first in the direction of the
umbilicus (Figure 8.126). The therapist may
change the direction of the force and direct
it more diagonally toward the contralateral
anterior superior iliac spine or into a more
cardinal plane direction toward the ipsilat-
eral anterior superior iliac spine. The shoul-
der should be in as much flexion as possible
to allow for maximal stretch of the connec-
Figure 8.126 Anterolateral fascial elongation. tive tissues. The use of skin lubricants for
this technique is discouraged.
Position 2: Side-Lying With Rotational Component

Purpose: If the myofascia is restricted in a rotational direction, the technique
may be modified as follows.
Patient position: Side-lying, with spine in a rotated position.
Therapist position: Standing behind patient.
Hands: In the same position as described for Position 1.
Execution: The therapist distracts the shoulder and simultaneously provides a
rotational force on the spine . The other hand, which is positioned on the anterior
myofascia, is moved toward the umbilicus or the contralateral anterior superior
iliac spine (Figure 8.127). The myofascia of the anterior chest, axilla, and abdomen
will be effectively stretched in this position.
Scapular Framing (see DVD)

Purpose: Scapular framing is designed to manipulate myofascial restrictions
on all three borders of the scapula. This technique should routinely be performed
on scapulothoracic problems, problems of the upper thoracic and mid-thoracic
spine, cervical problems, and certain shoulder problems.
Patient position: Side-lying, with pillow between patient and therapist. Pa-
tient's arm should be resting comfortably on pillow.
Figure 8.127 Anterolatera l fascial elongation: rotation component .
Therapist position: Standing facing

patient, with pillow pressing against bod y.
There should be a "sn ug" fit between the pa-
tient , pillow, and therapist.
Medial Border
Hands: The top hand is lightl y placed
on the shoulder, and the bottom hand is
placed just off the medial border of the
scapula, between the scapula and the tho-
. .
rac1c sp1nous processes.
Execution: With the top hand , the ther-
apist slightly retracts the patient's shoulder
to slacken the tissue. Meanwhile , the fingers
of the bottom hand stroke from cephalic to
caudal along the length of the medial bor-
der of the scapula (Figure 8.128).
Upper Border
Hands: The fingertips of both hands are
placed over the upper trapezius muscle me-
Figure 8.128 Scapular framing: medial border.
dially at the cervicothoracic junction.
Figure 8.129 Scapular framing: upper border. Figure 8.130 Scapular framing: lateral border.
Execution: With firm pressure, the fingertips stroke the upper border of the
scapula and upper trapezius muscle from proximal to distal (i.e., from the cervi-
cothoracic junction to the glenohumeral joint). A gentle stretch is applied with the
palms of the hand as the scapula is stroked (Figure 8.129).
Lateral Border
Hands: The palm of the bottom hand is placed over the shoulder joint to sta-
bilize the area. The palm of the top hand is placed over the lateral border of the
scapula.
Execution: While the bottom hand is stabilizing the shoulder, the palm of
the top hand strokes the lateral border of the scapula caudally with firm pressure
(Figure 8.130). Specific finger pressure may be applied if trigger points or restric-
tions are found.
Alternate Technique for Upper Border

Patient position: Side-lying, with arm holding a pillow.
Execution: Standing at the head of the table in a diagonal stance, the therapist
exerts a caudal force through the patient's shoulder to produce a gentle stretch in
the upper trapezius (Figure 8.131).
Figure 8.131 Scapular framing: upper border alternate.
Alternate Technique for Lateral Border

Patient position: Side-lying. Patient is asked to grasp the top of the treatment
table with the upper hand. This flexes the shoulder and tightens the myofascia in
the lateral border of the scapula.
Execution: As the patient holds the treatment table, the therapist uses the palm
of his or her top hand to firmly stroke the lateral border of the scapula caudally
(Figure 8.132). The technique may continue toward the ilium if fascial restrictions
are encountered.
Myofascial Trigger Point Release (lnfraspinatus) Flat Palpation

Purpose: This technique is used to inhibit myofascial trigger points anywhere
within the infraspinatus muscle and can produce results such as increased mobil-
ity of the muscle and neighboring tissues, increased shoulder A/PROM (active/
passive range of motion), and decreased pain locally and within its referred pain
pattern down the arm. 5
Patient position: Side-lying, with upper extremity resting on a pillow that is
placed between patient and therapist.
Therapist position: Standing at patient's side.
Hands: Using a flat palpation, the therapist identifies the myofascial trigger
point by palpating perpendicular to the muscle fibers, which run diagonally from
the humerus to the medial border of the scapula. After identifying a taut band, the
therapist guides his or her fingers in parallel, along the taut band, to locate a thick,
firm nodule.
Figure 8. 132 Scapular framing: lateral border alternate.
Figure 8. 133 Myofascial trigger point release: flat palpation (infraspinatus).
Executi on : Once the nodule within the band or myofascial trigger point is
identified, the therapist applies gentle compression into the muscle belly to elicit
the patient's symptoms (Figure 8.133). The patient is asked to contract and relax
by performing the muscle's action (in this case, external rotation) followed by a
moment of complete relaxation. The therapist maintains the force until the symp-
toms subside and the tissue is felt to relax, being careful not to exacerbate the
patient's pain. Once the myofascial trigger point has been released, the therapist
should follow up with a local myofascial release technique and a passive stretch.
(This method of palpation and treatment can be used on a number of other muscles.)
Myofascial Trigger Point Release (Upper Trapezius) Pincer Palpation

Pur pose: This technique is used to inhibit myofascial trigger points anywhere
within the upper trapezius muscle, producing results such as increased mobility
of the muscle and its neighboring tissues, increased shoulder A/PROM, and de-
creased pain locally as well as within its referred pain pattern into the head/neck
or down the arm. 5
Pati ent pos iti on : Supine, with head flat on treatment table .
Therapist pos iti on : Sitting or standing at head of table at 45° angle to patient.
Hand s: The therapist clasps the upper trapezius muscle using a pincer grip
formed with the fingers and thumb. Palpation is performed perpendicular to the
muscle fibers, which run in a diagonal direction from the occiput and the cervical
spine to the acromion and the lateral one-third of the clavicle. As the tissues are
gently pushed and pulled back and forth, the therapist should identify a taut band.
The therapist then palpates along the taut band to find a thick, firm nodule.
Exec uti on : After identifying the nodule within the band or myofascial trigger
point, the therapist gently compresses it between the fingers and thumb to elicit
the patient's symptoms (Figure 8.134). The patient is then asked to gently contract
and relax the muscle by performing the muscle's action. In this case, the patient
should execute shoulder elevation or a small shoulder shrug and then completely
relax. The therapist maintains pressure until the symptoms subside and the tissues
are felt to relax. No increased pressure should be applied . Once the myofascial trig-
ger point has been released, the therapist should follow up with a local myofascial
release technique and a passive stretch. (This method of palpation and treatment
can also be used on a number of other muscles.)
Scapular Manipulation
Pur pose: Once the scapular soft tissues have been prepared by using tech-
niques such as scapular framing, the scapula may be manipulated off the thoracic
cage. This allows for more aggressive stretching of the scapulothoracic myofascia.
Two variations of this technique can be performed .
Pati ent pos iti on : Side-lying, with a pillow between patient and therapist, and
patient's arm resting comfortably on the pillow.
Therapist pos iti on : Standing at patient's side.
Hand s: Two variations of this technique may be performed : (1) The top hand
grasps the shoulder joint anteriorly, while the fingers of the bottom hand slide onto
the undersurface of the scapula. (2) In the alternate technique, the bottom hand
slides under the arm and around the scapula until the fingers can slide onto the
scapula's undersurface (Figure 8.135). The top hand also contacts the scapula so
Figure 8.134 Myofascial trigger point release: pincer palpation (upper trapezius).
Figure 8.135 Scapular manipulation: set-up.
the fingers can slide onto the undersurface of the scapula. The shoulder and chest
of the therapist contact the patient's shoulder anteriorly for stability.
Executi on : Once the fingers of the bottom hand have grasped the medial bor-
der of the scapula, the therapist lifts the scapula and shoulder girdle complex off
Figure 8.136 Scapular manipulation.
the thoracic cage, resulting in an aggressive stretch of the scapulothoracic myo-

fascia (Figure 8.136). This technique succeeds if the patient is smaller than or the
same size as the therapist.
With both hands grasping the medial border of the scapula, and the therapist's
shoulder stabilizing anteriorly, the scapula is lifted off the thoracic cage. This tech-
nique is successful with patients who are larger than the therapist.
Upper Extremity and Posterior Quadrant

Fascial Elongation (see DVD)
Purpose: The superficial fascia of the upper extremity, like that of the lower
extremity, is one continuous cylinder. It is continuous with the posterior trunk
fascia anchoring to the spinous processes, iliac crest, and sacrum. Changes in the
upper extremity fascia may continue to neck and shoulder soft tissue changes, and
vice versa. The purpose of this technique is to elongate the superficial and inter-
muscular fascial sheaths as they travel up the posterior-lateral upper extremity
and into the trunk. Because the primary target is loose connective tissue, elonga-
tion is time dependent.
Therapist position: Standing at head of patient.
Hands: Both hands are used to grasp the patient's right and left wrists, provid-
ing a gentle distraction of the upper extremity.
Execution: Only one upper extremity is treated at a time. As both upper ex-
tremities are tractioned, one is slowly taken into a flexion, internal rotation, and
Figure 8.137 Upper extremity and posterior quadrant fascial elongation: initiation.
Figure 8.138 Upper extremity and posterior quadrant fascial elongation: completion.
adduction (Figure 8.137). As the tissues creep, the therapist should continue to
move the upper extremity, causing the patient to feel a stretch through the upper
extremity, into the shoulder complex, and eventually into the trunk (Figure 8.138).
The movement may be continued until the patient is fully rotated, but this is not
necessary. It is dependent on the restrictions and flexibility of the patient. The

patient should report feeling tension in the way of a good stretch . Once a maxi-
mal stretch is achieved, the therapist should slowly return the patient to the start-
ing position. The technique may be repeated two or three times. Treatment is not
based on pain but rather on postural examination and functional limitations.
Thoracic Rotational Laminar Release (see DVD)

Purpose: Previous techniques emphasized the scapulothoracic and scapulo-
humeral relationships and musculature . This technique penetrates to the depth of
the paravertebral muscles, manipulating the muscles and, to a certain extent, the
joints into a rotational direction.
Patient position: Side-lying, with a pillow between patient and therapist, and
patient's arm resting comfortably on pillow.
Therapist position: Standing, facing patient with pillow between therapist
and patient.
Hands: The top hand is placed over the anterior aspect of the glenohumeral
joint. The fingers of the posterior hand are between the medial border of the scapu-
lar and spinous processes (Figure 8.139).
Execution: The primary distinction between this technique and scapular
framing of the medial border is in the depth of penetration and the rotational
component imparted to the thoracic spine. To execute the technique, the therapist
uses the fingers of the bottom hand to stroke cephalic to caudal with deep pressure,
------
Figure 8.139 Thoracic rotational laminar release: stroke initiation.

Figure 8.140 Thoracic rotational laminar release: stroke completion.
while using the top hand to retract the shoulder complex and rotate the thoracic
spine (Figure 8.140). The fingers act as a fulcrum of rotation for the thoracic spine
as they slide down the length of the thoracic spine. If the therapist feels segmental
restrictions as the technique is being performed, the stroke may be stopped and
the restricted segment may be oscillated into rotation.
Transverse Fascia I Stretch of the Biceps

Purpose: The purpose of this technique is to increase the medial-lateral mobil-
ity of the biceps in preparation for stretching or strengthening. Certain low-grade
peripheral entrapment neuropathies respond well to stretching of the biceps in a
medial-to-lateral direction. This seems to free up the nerves as they pass through
just posterior and medial to the biceps. Certain proximal humeral fractures cause
the binding down of the biceps, and this transverse fascial stretch will be beneficial
for this type of condition as well.
Therapist position: Standing outside patient's arm if treatment is applied in
lateral-to-medial direction, and inside patient's arm if technique is applied in me-
dial-to-lateral direction.
Hands: The heel of the therapist's hand is placed lateral to the muscle if the
technique is going from lateral to medial and is placed medial to the muscle if
the technique is going from medial to lateral.
Execution: The heel of the hand pushes

the biceps in a transverse direction (lateral
to medial, or medial to lateral) until all the
"slack" is taken out of the muscle. Once the
tissue is at the end of the elastic range, the
therapist pushes into the plastic range to get
the final stretch (Figure 8.141). The stretch is
held 3-5 seconds and then repeated.
Biceps Stretch
Purpose : The purpose of this technique
is to apply a focused stretch of the biceps
muscle .
slightly off table. If a less aggressive version
of the technique is desired, the patient may
be placed in the side-lying position to ac-
complish a lighter version of the stretch.
Therapist position: Seated level with
patient's neck or shoulder.
Figure 8.141 Trans verse fascial stretch of the Hands: The top hand is placed over the
biceps. patient's shoulder at the acromion and cora-
coid process for stabilization and to prevent
the shoulder from lifting from the table. The bottom hand is placed on the distal
arm, just proximal to the wrist.
Execution: The therapist gently extends the patient's shoulder. At the same
time, the elbow is fully extended and the radioulnar joints are fully pronated.
About the time the patient begins to feel a stretch, a slight traction force may be
placed through the arm (Figure 8.142). The therapist should ask the patient to tell
when a moderate stretch is felt. Because of the long lever arm, it is difficult to tell
when the biceps muscle/tendon is in a plastic stretch. After a 5- to IO-second hold,
the arm is released, and the stretch may be repeated.
Forearm "Ironing"
Purpose: As described earlier in the chapter for the lumbar erector spinae, the
"ironing" techniques are useful to decrease underlying tone and move fluid within
the tissues. If an area is particularly tender, longitudinal stroking is always less
painful than cross-stroking. This technique is effective for a wide array of elbow,
forearm, wrist, or hand dysfunctions. Although not shown, the technique can also
be applied to the flexor and the extensor surfaces of the forearm.
Patient position: Supine or seated.
Therapist position: Standing or sitting at patient's side .
Figure 8.142 Biceps stretch.
Hand position: The inside hand of the therapist gently grasps the patient's
wrist and flexes it. The outside hand is positioned on the distal aspect of the fore-
arm, just proximal to the wrist.
Execution: Using a small amount of lubrication, the palm of the therapist's
hand bears down on the soft tissues and begins to stroke in a distal-to-proximal
direction, stopping at the elbow (Figure 8.143). The pressure is firm, but the hand
and fingers remain relaxed, so the technique feels firm but not painful. The thera-
pist should use some body weight to avoid the technique coming primarily from
the arm.
Muscle Splay of the Forearm

Purpose: As with muscle splay of the hamstring, the idea is to stroke deeply
in the fascial planes separating muscles or muscle groups. When muscle groups
slide more freely on one another, their ability to be actively shortened or passively
lengthened is enhanced, creating greater efficiency of contraction and/or flexibil-
ity. Treatment of the flexor surface is described here, but the extensor surface may
be treated as well
Patient position: Supine or sitting, with forearm on treatment surface.
Therapist position: Standing or sitting lateral to patient, facing patient.
Hands : One hand flexes the patient's wrist, while the index and middle finger
find a "wedge" between muscle groups. Alternately, the thumb can be used, but the
therapist must be careful to avoid overuse injury of the thumb.
Figure 8.143 Forearm "ironing. "
...
Figure 8.144 Muscle splay of the forearm.
Execution: Starting distally, the therapist wedges between muscle groups with
the index and middle finger (or thumb), applying firm pressure. Using a small
amount of lubricant, the fingers slide proximally following the wedge created dis-
tally (Figure 8.144). Lack of a wedge or space between fibers may indicate fascial
adhesions. The therapist should identify and focus on these areas, working longi-
tudinally, from proximal to distal, until the fascia is freed up.
Transverse Muscle Bending of the Forearm

Purpose: Analogous in theory to previously described muscle bending tech-
niques, the purpose of this technique is to manipulate the forearm musculature in
a transverse direction. This allows the contractile tissues to move more freely in
their respective fascial compartments.
Therapist position: Standing or sitting at patient's side, using leg to stabilize
patient's forearm.
Hands: One hand stabilizes the forearm distally. The other hand gently grasps
the flexor (or extensor) surface of the forearm.
Execution: The palm of the hand pushes the muscle mass of the forearm
firmly in a transverse direction through the elastic range and into the plastic range
to encourage permanent deformation of the fascia (Figure 8.145). Multiple angles
can be applied. For example, the flexor mass may be pushed away from or toward
the ulna. The brachioradialis may be pushed anterior or posterior. The extensor
surface can also be moved in either transverse direction. The therapist must "think
with the hands" to determine where the re-
strictions are, and move in the direction of
the restriction.
) Palmar Stretch
is to stretch the palmar fascia and the pal-
X mar surface of the hand.
Patient position: Supine or sitting.
Therapist position: Standing or sitting ,
facing palm of patient 's hand.
Hands: The hand position is very im -
portant in this technique. Both of the
therapist's little fingers are placed between
the patient's index and middle fingers. The
therapist's fingers are then interdigitated
through the patient's fingers, with the mid-
dle and ring fingers of the therapist in the
web space of the patient's hand. The thera-
·- - •' pist's index fingers pull over the patient's

hand, and the thumbs are available for mas-
sage during the stretch.
Figure 8.145 Transverse muscle bending of the
Execution: The therapist's fingers that
forearm.
are interdigitated, along with the index
Figure 8.146 Palmar stretch. Figure 8.147 Retinacular stretch.
fingers, open the patient's hand to create a stretch. At the same time, the thumbs
can be used to massage the palmar surface of the hand when the stretch is occur-
ring (Figure 8.146). If the elbow is flexed and the wrist is in neutral, the palmar
fascia will be localized. If the elbow and wrist are extended, the stretch will also
include the wrist flexor muscles.
Retinacular Stretch
Purpose: Related to the previous technique, the retinacular stretch is designed
to open the carpal tunnel in a medial-to-lateral direction and to increase the ex-
tensibility of the retinaculum.
Patient position: Supine or sitting.
Therapist position: Standing or sitting, facing palmar surface of patient's
hand.
Hands: The therapist's thenar eminences are placed over the patient's distal
forearm and wrist. The therapist's fingers are on the dorsal surface of the patient's
hand to apply counterpressure.
Execution: The therapist applies firm pressure into the patient's wrist and dis-
tal forearm with the thenar eminences as the fingers apply counterpressure on the
dorsal surface of the hand. A firm stretch is applied from midline outward to the
ulna and radius. As the therapist's hands separate, firm pressure is maintained for
maximal stretch (Figure 8.147).
Techniques for the Cervical Spine

Elongation of Paravertebral Muscles
Purpose: This is a preparatory technique for other more aggressive myofascial
and joint manipulation techniques. As defined early in this chapter, elongation
differs from stretching in that elongation's purpose is not necessarily to lengthen
the muscle but rather to elongate the spine (the analogy of elongating an accor-
dion may be helpful). This technique, used with superficial penetration, also has a
strong autonomic inhibitive effect.
Patient pos ition: Supine, with head flat on table.
Therapist position: Sitting at head of treatment table.
Hands: The fingers are placed over the lower cervical - upper thoracic paraver-
tebral muscles.
Execution: The technique is executed by lightly stroking the length of the
cervical paravertebral muscles, from upper thoracic to subcranial muscles (Fig-
ure 8.148). The depth of penetration may gradually be increased with progressive
stroking.
Axial Flexion of the Cervical Spine (see DVD)

Purpose: This technique is one of the few described in this text that can be
used as either a direct or an indirect technique. The idea behind its use as an indi-
rect technique is to take the neck into the direction of restriction, thereby freeing
the restriction and allowing greater axial extension. A useful analogy is that of
Figure 8. 148 Elongation of paravertebral muscles.

a dresser drawer that is stuck and cannot be opened . By closing the drawer, one
makes the drawer become free to open. This technique can be divided into two
specific components: (1) a general axial extension of the cervical spine and (2) a
specific axial extension at the occiput-atlas (OA) joint.
Patient position: Supine, with head flat on treatment table .
Therapist position: Sitting at head of table .
Hands: The palms of the hands cradle the base of the occiput while the fingers
contact the lower cervical paravertebral musculature (Figure 8.149).
Execution: The head and neck are brought into a straight axial flexion (mov-
ing the head directly toward the ceiling). The fingers are simultaneously stroking
the lower cervical paravertebrals in a medial-to-lateral direction (Figure 8.150).
With each repetition, the fingers are moved up a level until they are in contact with
the subcranial musculature.
At this point, the technique may be applied more specifically in the area of
the OA joint. The therapist again flexes the head and neck axially, while apply-
ing firm pressure at the OA joints bilaterally with the fingertips. The fingers are
no longer stroking in a medial-to-lateral direction but are maintaining the pres-
sure on the OA joints. The neck may be axially extended into a diagonal plane
to check for unilateral restrictions. If a unilateral OA restriction exists, the neck
may be axially flexed in the same diagonal plane in an attempt to free up the
restriction.
This technique may be used as a direct technique with patients who exhibit
an axially extended posture. Although this posture is seen less often than the for-
ward-head posture, the technique may be used to move the neck directly into the
restriction.
Cervical Laminar Release

Position 1: Sitting
Purpose: This technique is used to elongate the cervical paravertebral muscu-
lature and to improve cervical forward bending.
Patient position: Sitting.
Therapist position: Standing behind patient.
Hands: In the bilateral technique, both hands are placed on the paravertebral
muscles with the thumbs and PIP joints of the index fingers contacting the patient.
In the unilateral technique, one hand is on the patient's head to monitor the diago-
nal movement of the patient's head and neck.
Execution: The therapist first asks the patient to forward-bend the cervical
spine segmentally. As the flexion occurs, the therapist's hands stroke caudally
through the mid-cervical, cervicothoracic, and upper thoracic areas. If unilateral
technique is preferred, the monitoring hand gently guides the patient into a diago-
nal pattern as the other hand gently strokes unilaterally through the cervical, cer-
vicothoracic, and upper thoracic areas (see Figures 8.49 and 8.50 in earlier section,
"Forward-Bending Laminar Release-Sitting").
Figure 8.149 Axial flexion of the cervical spine: stroke initiation.
Figure 8.150 Axial flexion of the cervical spine: stroke completion.
Position 2: Supine
Purpose: This technique is used to elongate the cervical myofascia.
Therapist position: Sitting at head of table.
Hands: One hand cradles the head at the occiput and brings the cervical spine
into a forward-bent position. The other hand makes contact with the cervical
Figure 8.151 Cervical laminar release.
paravertebral muscles, bilaterally, using the thumb on one side and the PIP joint of
the index finger on the other side.
Execution: One hand holds the neck statically in the forward-bent position
while the other hand strokes gently from approximately mid-cervical to cervico-
thoracic junction (Figure 8.151).
Diagonal Stretch of Cervical Cervicothoracic Myofascia

Purpose: This technique stretches the posterior myofascial structures as well
as the upper trapezius and levator scapula muscles.
Therapist position: Sitting at head of table .
Hands: One hand cradles and positions the head in a combination of forward
bending, side bending, and rotation. The rotation can be to either the same or
the opposite side as the forward bending, depending on the restriction. The other
hand is placed firmly on the patient's shoulder.
Execution: With the patient positioned, the therapist uses one hand to apply
gentle to moderate pressure caudally on the shoulder, while applying pressure with
the other hand to move the head into forward bending, side bending, and rotation
(Figure 8.152).
Manipulation of Subcranial and OA Myofascia

Purpose: This technique is useful in releasing subcranial myofascia and for
manipulating the OA joints. This technique allows patient participation and,
Figure 8.152 Diagonal stretch of cervical cervicothoracic myofascia.
therefore, may be considered a muscle energy technique. The idea behind the tech-
nique is stabilization of the occiput and movement of the atlas. The patient is axi-
ally flexing and extending the neck while the occiput is held rigid.
Therapist position: Standing or sitting. The patient's head will be cradled by
the therapist's arm and shoulder.
Hands: As the therapist cradles the patient's head with one arm and shoulder,
the therapist uses the hand on that side to firmly grasp the occiput. The other hand
is placed over the hand grasping the occiput as additional reinforcement.
Execution: With the therapist firmly holding the head, the patient is asked to
axially flex and extend the neck gently (Figure 8.153). The head is not allowed to
move, so the neck is actually moving on the head. The atlas is allowed to translate
anteriorly and posteriorly on a nonmoving occiput. After several repetitions, the
patient is allowed to rest his or her head on the table, and the amount of resting
axial flexion is reassessed.
Masseter Manipulation
Purpose: Prior to any intraoral soft tissue manipulation of the temporoman-
dibular joint (TMJ), the clinician should always attempt extraoral soft tissue ma-
nipulation aimed at restoring mobility of the joint. This technique inhibits the
masseters, allowing for a more comfortable and increasingly functional opening
of the mandible. The functional opening may be significantly increased without
having to perform intraoral maneuvers.
Patient position: Supine, with head flat

on treatment table.
Therapist position: Sitting at head of
table.
Hands: The tips of the index, middle,
and ring fingers are placed on the masseters
just below the TMJ line.
Execution: With moderate depth of
pressure, the therapist strokes along the
length of the masseters away from the TMJ
(Figure 8.154). After several strokes, the pa-
tient is asked to open the mouth in a subtle
and relaxed manner as the stroke is being
applied. As the masseters are stroked, the
relaxed mandible will open further, and a
gentle opening stretch may be applied at the
end of the technique .
Temporalis Manipulation
Purpose: As with the masseter, the
temporalis should be manipulated prior to
Figure 8.153 Manipulation of subcranial and any manipulation of the TMJ. This tech-
occiput-atlas myofascia.
nique inhibits the temporalis muscles and
Figure 8.154 Massester manipulation.

Figure 8.155 Temporalis manipulation.
therefore may allow for a more comfortable and increased opening of the man-
dible or decreased headache pain.
Hands: The finger pads of the index, middle, and ring fingers are placed on the
temporalis muscle bellies bilaterally.
Execution: Beginning with moderate pressure, the therapist makes small cir-
cular strokes with the hands, gradually increasing in size while manipulating with
a push-pull stroke (Figure 8.155). The push-pull stroke is created by flexing and
extending the fingers. The majority of the force is applied through the push (i.e.,
the finger extension). The therapist slowly and gently moves around the muscle
until the entire muscle is treated. After several strokes, the patient may be asked to
time opening of the mouth with the push stroke in an effort to further relax and
elongate the tissues.
Frontal Facial Decompression

Purpose: The purpose of this technique is twofold. First, the hand position can
be used to provide a gentle subcranial traction. Second, the technique can be used
to inhibit the frontalis muscle or to provide a fascial stretch to the frontal, nasal,
and facial fascias. This technique is useful in cases of parieto-occipital headaches
or sinus headaches.
Figure 8.156 Frontal facial decompression.

Hands: One hand gently cradles the occiput, while the other hand is placed
directly over the frontal area of the patient's face, with the therapist's thumb point-
ing in the direction of the therapist.
Execution: The therapist gives a slight traction with the bottom hand. With
the palmar surface of the top hand in full contact over the frontalis, the thera-
pist simultaneously applies a fascial traction and holds for 15- 30 seconds (Fig-
ure 8.156). The emphasis of this technique is on the frontal fascial stretch and fron-
tal decompression.
Retro-Orbital Decompression
Purpose: Related to the previous technique, the purpose of this technique is
to stretch the retro-orbital fascia and the fascia around the nasal suture. This tech-
nique is especially indicated for patients with retro-orbital headaches and sinus
headaches.
Hands: The bottom hand gently cradles the base of the occiput. The palm of
the top hand makes contact with the frontal area, while the fingers are positioned
as follows: The index and ring finger are placed over the left and right orbital bones,
Figure 8.157 Retro-orbital decompression.
just inside the eyebrow, well away from the eyes, and the middle finger is placed
just over the nasal suture.
Execution: A gentle traction is applied through the occiput with the bot-
tom hand. The palm of the top hand places a mild traction over the frontal fas-
cia, while the fingers apply a fascial traction over the retro-orbital and nasal fas-
ciae (Figure 8.157). The therapist must be careful to make absolutely no contact
with the eyes. The fascial stretch is applied firmly with the pads of the fingers for
10-20 seconds.
Sternocleidomastoid Muscle Play

Purpose: This technique decreases tone of the sternocleidomastoid (SCM)
muscles. Even if the muscle is relaxed in the supine position, the SCM may still be
exquisitely tender to palpation because of overuse in the erect posture .
Therapist position: Sitting at head of table, gently cradling patient's head in
very slight backward-bent position.
Hands: One hand is cradling the occiput, while the other hand is positioned
with the thumb placed on the cephalic portion of the SCM near the mastoid
process.
Execution: The therapist rotates the patient's neck and adds a slight amount
of backward bending of the cervical spine. The thumb of the other hand is placed
Figure 8.158 Sternocleidomastoid muscle play.
Figure 8.159 Sternocleidomastoid muscle play: alternative.
on the SCM near the insertion at the mastoid process (Figure 8.158). The SCM is
gently stroked from cephalic to caudal. The SCM may also be cross-stroked at any
point along the muscle belly where trigger points, tender areas, or areas of hyper-
tonicity are encountered (Figure 8.159).
References
1. Feldenkrais M. Advances ThroughMovement. New York:Harper & Row; 1972.
2. Rosenthal E. The Alexander technique: what it is and how it works. Med Prob/PerformArt.
1987;2:53- 57.
3. Dietze E, Schliack H, WolffA. A Manual of Reflexive Therapyof the ConnectiveTissues.Scarsdale,
NY: Sidney Simon; 1978.
4. Pool-Goudzwaard AL, Vleeming A, Stoeckart R, Snijders CJ, Mens JM. Insufficient lumbopelvic
stability: a clinical, anatomical and biomechanical approach to "a-specific" low back pain. Man
1her. 1998;3:12-20.
5. Simons DG, Travell JG, Simons LS, Cummings BD.MyofascialPain and Dysfunction:1he Trig-
ger PointManual: Vol. 1. UpperHalf of Body, 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 1998.
Index
Accessory movement Autonomic aspects of myofascial pain syndrome,

component motions, 12 138-139, 144-1 45
definition and origin of term, 10 Autonomic effects of massage, 83
historical development, 4 Avicenna, 6
joint play motions, 12 Axial flexion of cervical spine, 305 - 306, 307
types of, 12
ACR (American College ofRheumatology), 149 Back pain. See Low-back pain (LBP)
Active movement analysis, 193-194 Barker, Herbert, 8
Acupuncture Biceps
for fibromyalgia, 155 biceps stretch, 300
for myofascial pain management, 146 transverse fascia l stretch of, 299- 300
Acute pain, 111. See also Pain Biceps stretch, 300
Aeschylus, 91 Bilateral sacral release, 222 - 223
Afferent neurology of connective tissue Bilateral upper thoracic release, 283 - 284
free nerve endings, 93 Bindegewebsmassage, 18- 20
Golgi tendon organs (GTOs), 92, 93, 99-1 01, 118, Bindegewebsmassage-type stroke, 205 - 207
120 Bio mechanics
hair receptors, 93, 96- 97 of connective tissue, 4, 40- 54
joint capsule receptors, 92, 93, 101- 102, 108-109 of junctional zones, 59- 63
mechanoreceptors, 92-1 04 of muscles, 56- 58
Meissner 's corpuscles, 92- 95 Biotensegrity of musculoskeletal system, 61- 63
Merkel's receptors, 93, 96 Blood flow, massage 's effects on, 80- 82
muscle spindles, 92, 93, 97-1 01 Body posture. See Postural and structural
nociceptors, 104-105 evaluation
Pacinian corpuscles, 93, 95- 96, 101, 118, 119, Bohm, Max, 20
120 Bone setters (17th -1 9th centuries), 6- 8
Ruffini corpuscles, 50, 93, 96, 101, 119, 120 Bony clearing
small-diameter muscle afferents (III and IV), 93, of iliac crest, 217- 219
102-104, 121 of tibia, 271- 274
Alexander, F. Matthias, 25- 27 Borthwick, E. K., 91
Alexander technique, 25- 27, 201
American College ofRheumatology (ACR), 149 Cells of connective tissue, 35- 37
American Physical Therapy Association, 125 Central sensitization
Anterolateral fascia l elongation, 117-118, 288 - 289 fibromyalgia, 153-154
Antidepressants, 155 myofascial pain syndrome, 142-144
Aponeuroses, 47 Cervical cervicothoracic myofascia, diagonal stretch
Arthrokinematics, 4, 10, 11- 12, 199-200 of, 308
Assessment of myofascial system. See Evaluation of Cervical laminar release, 306 - 308
myofascial system Cervical spine
ASTYM (augmented soft tissue manipulation), 85 axial flexion of, 305- 306, 307
Augmented soft tissue manipulation (ASTYM), 85 cervical laminar release, 306 - 308
Autonomic approaches to myofascial manipulation, diagonal stretch of cervical cervicothoracic myo-
17- 21 fascia, 308
317
318 Index
Cervical spine (continued) functions of, 33- 34

elongation of paravertebral muscles, 305 general characteristics of, and definitions of
evaluation of, 190-191 terms, 40- 46
frontal facial decompression, 311- 312 histology of, 34- 40
manipulation of subcranial and OA myofascia, insertion of, to bone, 59- 61
308 - 309 loose irregular connective tissue, 47- 48
masseter manipulation, 309- 310 pathophysiology of soft tissue repair, 69- 72
retro-orbital decompression, 312- 313 percentage of body weight and storage of water
sternocleidomastoid (SCM) muscle play, 313- 314 content by, 33
temporalis manipulation, 310- 311 photomicrograph of, 37
therapeutic techniques, 305- 314 plasticity of, 50
Cervicothoracic area, muscle agonist/antagonist response of, to immobilization, 73- 80
groups of, 192 stress - strain curve, 41, 44- 45
Chila, Anthony, 24 types of, 34
Chiropractic, 9-1 0, 12, 155 types of injuries to, 40
Chisel grip, 202, 203 viscoelastic model of, 41- 45
Chondroitin, 38 Wolff's law, 45
Chronic fatigue syndrome, 151 Connective tissue massage (CTM), 18-20
Citalopram, 155 Contractility of connective tissue, 48- 49
Collagen Contraction of muscles, 50- 51, 131, 139-140
in basement membrane, 59 Contractures of trigger points, 131, 140-142
biosynthesis of, 38- 40 Convex/concave rule for joint mobilization, 12
critical interfiber distance, 74 Creep and relaxation, 43- 44
cross-links and, 71, 74, 75 Critical interfiber distance, 74
in dense irregular connective tissue, 47 Cross-friction of gastrocnemius - soleus musculo-
in dense regular connective tissue, 46 tendinous junction, 275- 276
diagram of, 34 Cross-friction of piriformis insertion, 263- 264
distribution of, 85- 86 Cross-links, 71, 74, 75
in extracellular matrix, 35, 37- 40 CTM (connective tissue massage), 18-20
half-life of, 45, 74 Cutaneous pain, 125
in loose irregular connective tissue, 48 Cyclobenzaprine, 155
lubrication of, 74 Cyriax, Edgar, 10
massage's effects on, 83- 86 Cyriax, James, 10-12, 184
response of, to immobilization, 74- 75
types of, 35, 38 Dense irregular connective tissue, 47
viscoe lastic model of connective tissue and, 43, 45 Dense regular connective tissue, 46- 47
weave pattern of, 43 Diagnosis. See also Evaluation of myofascial system
wound healing and, 71- 72, 83- 85 of dysfunction, 183-184
Compression, definition of, 40 of fibromyalgia (FMS), 149-152, 153
Compressive testing of spine, 195 in modern times, 10-13
Connective tissue of myofascial pain syndrome, 129- 132
afferent neurology of, 92-1 05 of soft tissue lesion and mechanical dysfunction,
biomechanics of, 40- 54 127
cells of, 35- 37 Diagonal stretch of cervical cervicothoracic myo-
classification of, 47 fascia, 308
collagen, 35, 37- 40 Diaphragm release, 241- 244
contractility of, 48- 49 Diaphragmatic techniques, 119-120
dense irregular connective tissue, 47 Dicke, Elizabeth, 18-19
dense regular connective tissue, 46- 47 Distraction, 12
diagram of, 34 Dry needling. See Physical therapy dry needling
extracellular matrix, 35, 37- 40 Duloxetine, 155
fascia as force transmitter, 50- 54 Dupuytren disease, 50
fibrosis cycle and decreasing mobility in, 72- 73, Dysfunction
77- 78 criteria for somatic dysfunction, 127
Index 319
definition of, 183 postural and structural evaluation, 185- 193

definition of somatic dysfunction, 183 questions for, 184
diagnosis of, 183- 184 skin rolling, 196, 197
motor and mechanical dysfunction in myofascial thoracic spine, 191, 192
pain syndrome, 133-135 Exercise
myofascial pain dysfunction syndrome, 128 for fibromyalgia, 155- 157
sensory dysfunction in myofascial pain syn- for low-back pain (LBP), 13
drome, 135-138 Extension exercises, 4- 6
soft tissue lesion and mechanical dysfunction, Extracellular matrix, 35, 37- 40
126-128
somatic dysfunction, 127, 183 Facet hypothesis, 10
Fascia as force transmitter, 50- 54
Ebner, Maria, 18 Fascial contraction loop, 50, 51
Effieurage massage techniques, 20 Fascial sheaths, 47
Elastin, 35, 37, 38 Fasciculi, 56
Electrogenic muscle tone, 112-113 FCU (flexor carpi ulnaris), 53
Electromyograms (EMGs), 183 Feldenkrais method, 24, 27- 28, 201
Elongation Fibroblastic phase of wound healing, 71- 72
anterolateral fascial elongation, 288- 289 Fibroblasts
lateral elongation of peroneal tissue, 274- 275 contractility of connective tissue, 48- 49
lateral elongation of upper thoracic area, 279- 281 description and functions of, 35- 36
lower extremity/posterior quadrant fascial elon- during healing process, 71- 73, 83- 85
gation, 276- 277 massage 's effects on, during healing process,
medial - lateral fascial elongation, 209- 211 83- 85
of paravertebral muscles, 305 Fibrocytes, 35
in sequencing of treatment, 201 Fibromyalgia (FMS)
side-bending elongation quadratus stretch, comorbidities with, 151
225- 229 definition of, 126, 149
upper extremity and posterior quadrant fascial diagnosis of, 149-1 52, 153
elongation, 296- 298 incidence of, 149
EMGs (electromyograms), 183 management of, 155-157
End feel, 11 nonpharmacological management of, 155- 157
Endomysium, 56 pathogenesis of, 152-154
Endplate (integrated) hypothesis, 147 pharmacological management of, 155
Energy crisis hypothesis, 140- 141 tender points, 150-151
Epimysium, 56 treatment costs for, 149
Erector spinae Fibrosis cycle, 72- 73, 77- 78
"ironing" of, 216- 217 Fibrositis, 149
long axis laminar release, 212- 214 First rib shoulder depression technique, 282- 283
muscle play of, 214- 216 Flexor carpi ulnaris (FCU), 53
quadratus lateral erector spinae release, 224- 225, Fluoroscopy, 12-1 3
226 Fluoxetine, 155
Erector spinae muscle play, 120-121 FMS. See Fibromyalgia (FMS)
Evaluation of myofascial system. See also Diagnosis Forearm
active movement analysis, 193-194 forearm "ironing," 300- 301
cervical spine, 190-191 muscle splay of, 301- 303
compressive testing of spine, 195 transverse muscle bending of, 303
forward-head posture, 186-190 Forearm "ironing," 300 - 301
history of, 184 Forward-bending laminar release, 230- 232
lateral shear examination, 239- 240 Forward-bending laminar release - quadruped,
layer palpation, 195-197 232- 235
lumbar spine, 191-193 Forward-bending laminar release - sitting, 236- 237
observation of posture, 185-193 Forward -head posture, 186-190
palpatory examination, 195-197 Free nerve endings, 93
320 Index
Frontal facial decompression, 311- 312 Histopathology

Frozen shoulder, 50 fibrosis cycle and decreasing mobility in connec-
Fuller, Buckminster, 13, 61- 62 tive tissue, 72- 73, 77- 78
Functional imaging techniques, 154 of myofascia, 69- 80
pathophysiology of soft tissue repair, 69- 72
GAGs (glycosaminoglycans), 35, 38, 113-114, 116 response of myofascial tissue to immobilization,
Gain adjustment of muscle spindles, 98- 99 73- 80
Galen, 6, 91 scar formation, 77- 78
Gastrocnemius - soleus, transverse muscle play of, Historical basis for evaluation of myofascial system,
268- 270 184
Gastrocnemius - soleus musculotendinous junction, Historical basis for myofascial manipulation
cross-friction of, 275- 276 ancient times, 3- 6
Gel- sol principle, 50 bone setters (17th-1 9th centuries), 6- 8
Ghormley, R. K., 10 chiropractic, 9-1 0, 12
Gluteal fascial plane manipulation, 262- 263 modern trend toward mobility and diagnosis of
Glycosaminoglycans (GAGs), 35, 38, 113-114, 116 pathology, 10-13
Golgi-Mazzoni receptors, 102, 108, 118 osteopathic medicine, 8- 9
Golgi tendon organs (GTOs), 92, 93, 99-1 01, 107- Renaissance, 6
108, 118, 120 Hoffa massage, 20- 21
Granulation phase of wound healing, 70- 71 Hold - relax stretch of hip, 255- 258
Greater trochanter rocking, 248- 249, 250 Hood, Wharton, 7
Ground substance, 35, 37, 38, 74 Humpback (kyphosis), 4- 6
GTOs (Golgi tendon organs), 92, 93, 99- 101, 107- Hyaluronic acid, 38
108, 118, 120
Iliac crest
Hair receptors, 93, 96- 97 bony clearing of, 217- 219
Half-chisel grip, 202, 204 release, 119, 219- 221
Hamstring Iliac crest release, 119, 219- 221
hamstring manipulation, 258- 259 lliotibial band (1TB) paratrochanteric manipula-
longitudinal stroking, 258 tion, 253- 255
proximal hamstring stretch, 259- 261 Imaging techniques, 154, 183
splay technique, 258- 259 Immobilization
transverse muscle play of hamstrings, 267- 268 fibrosis cycle and, 72- 80
transverse muscle play of hamstrings and adduc- muscle tissue and, 78- 80
tor magnus: posterior-to-anterior pressure, nontraumatized connective tissue and, 74- 77
268 response of myofascial tissue to, 73- 80
Hamstring manipulation, 258- 259 traumatized connective tissue and, 77- 78
Hands Inefficient use, 113
care and protection of, 202- 205 Inflammation, 70
chisel grip, 202,203 Injections. See Trigger point injections
half-chisel grip, 202,204 Interstitial myofascial receptors, 50
lubricant for, 205 Intrafascial circulation loop, 50, 51
octopus grip, 202, 203 Involuntary guarding, 113
power grip, 204 "Ironing"
washing of, 204 - 205 of erector spinae muscle group, 216- 217
Hippocrates, 4- 6, 9 forearm "ironing," 300- 301
Hips lschial tuberosity cross-friction, 261
hip flexion, external rotation, adduction, 256- 1TB.See lliotibial band (1TB) paratrochanteric
258 manipulation
hip flexion/adduction, 255- 256
hold - relax stretch of, 255- 258 Joint, definition of, 199
Histology Joint capsule receptors, 92, 93, 101- 102, 108- 109
of connective tissue, 34- 40 Joint capsules
of junctional zones, 58- 59 as dense irregular connective tissue, 47
of muscles, 54- 56 insertion of, to bone, 59- 61
Index 321
Joint manipulation versus soft tissue manipulation, forward-bending laminar release, 230- 232
199-200 forward-bending laminar release - quadruped,
Joint mobilization, convex/concave rule for, 12 232- 235
Joint pain, 11 forward-bending laminar release- sitting, 236- 237
Junctional zones iliac crest release, 219- 221
biomechanics of, 59- 63 iliacus release, 246 - 248
biotensegrity of musculoskeletal system, 61- 63 "ironing" of erector spinae muscle group, 216- 217
connective tissue insertion to bone, 59- 61 L3 deep soft tissue manipulation, 229- 230
histology of, 58- 59 lateral sacral release, 221- 222
musculotendinous junctions, 58- 59 lateral shear correction, 239- 241
long axis distraction of superficial connective tis-
Kabat, Herman, 25 sue, 207- 209
Kaltenborn, Freddy, 12 long axis laminar release, 212- 214
Knott, Margaret, 25 longitudinal posterior hip release, 232
Kyphosis (humpback), 4- 6 lumbar myofascial roll, 237- 239
medial - lateral fascial elongation, 209- 211
L3 deep soft tissue manipulation, 229- 230 medial - lateral pull-away, 223- 224
Lange, M., 128 muscle play of erector spinae, 214- 216
Lateral elongation psoas release, 244- 246
of peroneal tissue, 274- 275 quadratus lateral erector spinae release, 224- 225,
of upper thoracic area, 279- 281 226
Lateral fascial distraction of tibia, 274 side-bending elongation quadratus stretch,
Lateral sacral release, 221- 222 225- 229
Lateral shear correction, 239- 241 therapeutic techniques, 205- 248
Lateral shear examination, 239- 240 tissue rolling, 196, 197, 211- 212
Layer palpation, 195-197 Lumbar/lumbopelvic area, muscle agonist/
Layered syndrome, 189, 190, 191 antagonist groups of, 192
LBP. See Low-back pain (LBP) Lumbopelvic area, muscle agonist/antagonist
"Legs carry trunk" model, 52 groups of, 192
Ligaments Lumbopelvic/lower quarter area
as dense regular connective tissue, 46- 47 bony clearing of tibia, 271- 274
function of, 47 cross-friction of gastrocnemius - soleus musculo-
insertion of, to bone, 59- 61 tendinous junction, 275- 276
Long axis distraction of superficial connective tis- cross-friction of piriformis insertion, 263- 264
sue, 207- 209 gluteal fasc ial plane manipulation, 262- 263
Long axis laminar release, 212- 214 greater trochanter rocking, 248- 249, 250
Longitudinal posterior hip release, 232 hamstring manipulation, 258- 259
Loose irregular connective tissue, 47- 48 hold - relax stretch of hip, 255- 258
Low-back pain (LBP) iliotibial band (1TB) paratrochanteric manipula-
causes of, 10 tion, 253- 255
exercise for, 13 ischial tuberosity cross-friction, 261
fibrotic process and decreasing mobility in con- lateral elongation of peroneal tissue, 274- 275
nective tissue, 73 lateral fascia l distraction of tibia, 274
incidence of, 13 lower extremity/posterior quadrant fascial elon-
Lower crossed syndrome, 188- 189 gation, 276- 277
Lower extremity/posterior quadrant fascial elonga- piriformis release in prone, 264- 266
tion, 276- 277 plantar fascia manipulation, 278- 279
Lubricant for hands, 205 proximal hamstring stretch, 259- 261
Lumbar myofascial roll, 237- 239 therapeutic techniques, 248- 279
Lumbar spine transverse muscle play of gastrocnemius - soleus,
bilateral sacral release, 222- 223 268- 270
bindegewebsmassage-type stroke, 205- 207 transverse muscle play of hamstrings, 267- 268
bony clearing of iliac crest, 217- 219 transverse muscle play of hamstrings and adduc-
diaphragm release, 241- 244 tor magnus: posterior-to-anterior pressure, 268
evaluation of, 191-193 transverse muscle play of quadriceps, 249- 252
322 Index
Macrophages,35,36 fibromyalgia, 126, 149-157

Magnetic resonance imaging (MRI), 154, 183 myofascial pain syndrome, 126, 128-1 49
Maitland, G. D., 12 physical therapists and treatment of patients with
Manipulation, 12. See also Myofascial manipulation chronic pain, 125
Manual medicine. See Historical basis for myofas- soft tissue lesion and mechanical dysfunction,
cial manipulation; Myofascial manipulation; 126-128
Therapeutic techniques Muscle play
Mapp, Sarah, 7 of erector spinae, 214- 216
Massage. See Myofascial manipulation; Therapeutic pectoralis major muscle play/pectoralis minor
techniques; and specifictypes of massage, such manipulation, 285- 286
as Hoffa massage transverse muscle play of gastrocnemius - soleus,
Masseter manipulation, 309- 310 268- 270
Mast cells, 35, 36 transverse muscle play of hamstrings, 267- 268
Maturation or remodeling phase of wound healing, transverse muscle play of hamstrings and adduc-
72 tor magnus: posterior-to-anterior pressure, 268
Mechanical approaches to myofascial manipulation, transverse muscle play of quadriceps, 249- 252
21- 25 Muscle spasms, 111, 113, 115-116, 131
Mechanoreceptors,92 -1 04 Muscle spindles, 92, 93, 97-1 01
Medial - lateral fascial elongation, 209- 211 Muscle splay
Medial -l ateral pull-away, 223- 224 of forearm, 301- 303
Medications. See Pharmacological management of hamstring, 258- 259
Meissner's corpuscles, 92- 95 Muscle stretch reflex (MSR), 106-107
Mennell, James, 10 Muscle tone
Mennell, John, 11 electrogenic muscle tone, 112-113
Merkel's receptors, 93, 96 muscular contraction compared with, 111-11 2
Metabolism, massage 's effects on, 82- 83 thixotropy, 114-117
Middle Ages, 6 viscoelastic muscle tone, 113-114
Milnacipran, 155 Muscles
Mobility philosophy, 4, 10-13 biomechanics of, 56- 58
Mobilization, definition of, 12 cellular and histological organization of skeletal
Modified convergence projection theory, 143 muscle, 55- 56
Motor and mechanical dysfunction, myofascial pain classification of muscle fiber types, 57- 58
syndrome,133 -1 35 contraction of, 50- 51, 131, 139-140
Movement diagram of architectural hierarchy of muscle tis-
basics of motor control, 105-106 sue, 56
description of movement approaches to myofas- histology of, 54- 56
cial manipulation, 25- 28 mechanism of growth in skeletal muscle, 54- 55
Golgi tendon organs (GTOs), 107-108 normal muscle contraction, 139-140
historical development of movement reeduca- response of, to immobilization, 78- 80
tion, 4 sarcomeres of, 54- 56, 59, 140, 147
joint receptors, 108- 109 Musculotendinous junctions, 58- 59
muscle stretch reflex (MSR), 106-107 Myofascia
receptor influence on, 105- 117 connective tissue histology and biomechanics,
skin receptors and position sense, 109-110 33- 54
Movement reeducation, 4,201 histopathology of, 69- 80
MRI, 154, 183 junctional zones histology and biomechanics,
MSR (muscle stretch reflex), 106-1 07 58- 63
Muscle afferents (small-diameter), 93, 102-104, 121 muscle histology and biomechanics, 54- 58
Muscle agonist/antagonist groups response of, to immobilization, 73- 80
of cervicothoracic area, 192 Myofascial assessment. See Evaluation of myofascial
oflumbar/lumbopelvic area, 192 system
oflumbopelvic area, 192 Myofascial manipulation. See also Therapeutic tech-
Muscle pain syndromes niques; and specifictherapeutic techniques
cutaneous pain compared with, 125 autonomic approaches, 17-21
different terms for, 128 fascia as force transmitter, 50- 54
Index 323
future considerations, 13-1 4 Pacinian corpuscles, 93, 95- 96, 101, 118, 119, 120
historical basis for, 3-1 0 Paget, Sir James, 7
mechanical approaches, 21- 25 Pain. See also Low-back pain (LBP); Muscle pain
modern theories and systems of, 17-28 syndromes
modern trend toward mobility and diagnosis of acute pain, 111
pathology, 10-13 cutaneous pain, 125
movement approaches to, 25- 28 nociception and nociceptors, 104-105, 111
physiology of, 80- 86 pain - spasm - pain cycle, 111, 113, 115-1 16
Myofascial pain dysfunction syndrome, 128 polymodal pain, 111
Myofascial pain syndrome. See also Evaluation of referred pain, 136-138, 253
myofascial system Widespread Pain Index (WPI), 152
autonomic aspects, 144- 145 Pain - spasm - pain cycle, 111,113, 115-11 6
autonomic dysfunction, 138- 139 Palmar stretch, 303- 304
clinical characteristics of, 132-139 Palmer, David Daniel, 9
definition of, 126, 128-129 Palpatory examination, 195- 197
diagnosis of, 129-132 Paravertebral muscles, elongation of, 305
management of, 145-149 Pare, Ambroise, 6
motor and mechanical dysfunction, 133-135 Paris, Stanley, 12
normal muscle contraction, 139-140 Paroxetine, 155
pathogenesis of, 139-145 Pathophysiology of soft tissue repair, 69- 72
peripheral and central sensitization, 142-144 Peckman, John, 24
physical therapy for, 145- 147 Pectoralis major muscle play/pectoralis minor ma-
referred pain, 136- 138, 253 nipulation, 285- 286
sensory dysfunction, 135-138 Periosteum, 47
taut bands and, 73, 131, 132 Peripheral neuropathy, 128
trigger point contractures, 140- 142 Peripheral sensitization, 142-144
Myofascial release, 24- 25 Peroneal tissue, lateral elongation of, 274- 275
Myofascial trigger point release (infraspinatur) flat Petrissage massage techniques, 21
palpation, 292- 294 Pharmacological management, of fibromyalgia
Myofascial trigger point release (upper trapezius) (FMS), 155
pincer palpation, 294 Physical therapy
Myofascial trigger points. See Trigger points for chronic pain, 125
Myofibroblasts, 35, 36, 48- 49, 72- 73 diagnosis and, 183-184
Myofilaments, 54- 56, 59 dry needling, 145-1 46
Myogelosis, 128 for myofascial pain syndrome, 145- 147
Myotendinous junction trigger point injections, 147- 148
biomechanics of, 59- 63 trigger point release, 146-1 47
biotensegrity of musculoskeletal system, 61- 63 Physical therapy dry needling, 145- 146
connective tissue insertion to bone, 59- 61 Physiology of myofascial manipulation
histology of, 58- 59 blood flow and temperature, 80- 82
collagen distribution, 85- 86
Neural mechanisms, 4 fibroblastic activity/collagen synthesis during
Nociception and nociceptors, 104- 105, 111, 125. See healing process, 83- 85
also Muscle pain syndromes; Pain metabolism, 82- 83
Nonthrust articulation, 12 reflexive (autonomic) effects, 83
Nontraumatized connective tissue, response of, to Piezoelectric effect, 50
immobilization, 74- 77 Piriformis
Nuclear bag fibers, 97 cross-friction of piriformis insertion, 263- 264
Nuclear bag spindles, 97 piriformis release in prone, 264- 266
Nuclear chain fibers, 97- 98 Plantar fascia manipulation, 278- 279
Plasma cells, 35
OA myofascia, manipulation of, 308- 309 Plasticity, of connective tissue, 50
Octopus grip, 202,203 PNF (proprioceptive neuromuscular facilitation), 25
Opioids, 155 Polymodal pain, 111. See also Pain
Osteopathic medicine, 8- 9, 155 Position sense, 109-110
324 Index
Positional theory, 4- 10 RSD (reflex sympathetic dystrophy), 19-20

Positioning of patient and therapist, 201- 202 Ruffini corpuscles, 50, 93, 96, 101, 119, 120
Positron emission tomography, 154
Postural and structural evaluation Sacrum
cervical spine, 190-191 bilateral sacral release, 222- 223
forward-head posture, 186-1 90 lateral sacral release, 221- 222
lumbar spine, 191-193 Sarcomeres,54 - 56,59,140,147
observation of posture, 185- 193 Scapular framing, 289- 292
thoracic spine, 191, 192 Scapular manipulation, 294- 296
Postural instruction, 201 Scar formation, 77- 78
Power grip, 204 SCM. See Sternocleidomastoid (SCM) muscle play
Pregabalin, 155 Seated pectoral anterior fascia l stretch, 286 - 287
Primary endings of muscle spindles, 98 Secondary endings of muscle spindles, 98
Proprioceptive neuromuscular facilitation (PNF), Sensory dysfunction and myofascial pain syn-
25 drome, 135-138
Proteoglycans, 35 Sequencing of treatment, 200 - 201
Proximal hamstring stretch, 259- 261 Sharpey 's fibers, 59, 61
Psoas release, 244- 246 Shearing, definition of, 40
Sherrington 's law of reciprocal inhibition, 189
Quadratus lateral erector spinae release, 224- 225, Side-bending elongation quadratus stretch, 225- 229
226 Single photon emission computed tomography, 154
Quadriceps, transverse muscle play of, 249- 252 Skeletal muscles. See Muscles
Skin receptors, 109-110
Receptive field, 94- 95 Skin rolling, 196, 197
Receptor influence on movement Small-diameter muscle afferents (III and IV), 93,
basics of motor control, 105-106 102- 104, 121
Golgi tendon organs (GTOs), 107-108 Snelson, Kenneth, 62
joint receptors, 108- 109 Soft tissue lesion and mechanical dysfunction,
muscle stretch reflex (MSR), 106-107 126-128
nociception, 111 Soft tissue manipulation versus joint manipulation,
skin receptors and position sense, 109-110 199-200
Reciprocal inhibition, Sherrington 's law of, 189 Soft tissue repair, pathophysiology of, 69- 72
Referred pain, 136-138, 253 Somatic dysfunction, 127, 183
Reflex sympathetic dystrophy (RSD), 19- 20 Spasms, 111, 113, 115-116, 131
Reflexive approaches to myofascial manipulation, "Spine engine" model, 52
17- 21 Splay technique
Reflexive effects of massage, 83 forearm, 301- 303
Remodeling or maturation phase of wound healing, hamstring, 258- 259
72 Sternocleidomastoid (SCM) muscle play, 313- 314
Renaissance, 6 Still, Andrew Taylor, 8
Repositioning Still, Charles, 9
Galen's technique of, 6 Strain
Hippocratic method of, 4- 6 definition of, 40
osteopathy and repositioning of subluxation, 9-1 0 stress - strain curve, 41, 44- 45
Reticulin, 35, 37, 38 Stress - strain curve, 41, 44- 45
Reticuloendothelial system, 37 Structural Integration (Rolfing), 21- 23
Retinacular stretch, 304 Subcranial myofascia, manipulation of, 308- 309
Retro-orbital decompression, 312- 313 Subluxation theory, 9-1 0, 12
Ribs Subsarcolemma, 59
first rib shoulder depression technique, 282- 283 Subscapularis, 287- 288
unilateral posterior/anterior articulation of first
rib, 281- 282 Tapotement massage techniques, 21
Rolf, Ida, 21- 22, 50 Tautbands,73, 131,132
Rolfing (Structural Integration), 21- 23 Temperature, massage 's effects on, 80 - 82
Index 325
Temporalis manipulation, 310- 311 unilateral posterior/anterior articulation of first

Tendons rib, 281- 282
as dense regular connective tissue, 46 upper extremity and posterior quadrant fasc ial
function of, 46 elongation, 296- 298
insertion of, to bone, 59- 61 Thrust manipulation, 12
Tensegrity Tibia
of architectural structures, 13, 61- 62 bony clearing of, 271- 274
biotensegrity of musculoskeletal system, 61- 63 lateral fascia l distraction of, 274
Tension, definition of, 40 Tissue rolling, 196, 197, 211- 212
Therapeutic techniques Traction and manual pressure, 4- 5
care and protection of hands, 202- 205 Trager, Milton, 23- 24
cervical spine, 305- 314 Trager/Trager ing, 23- 24
joint versus soft tissue manipulation, 199-200 Tramadol, 155
lumbar spine, 205- 248 Transverse fascial stretch ofbiceps, 299- 300
lumbopel vic/ lower quarter area, 248- 279 Transverse muscle bending of forearm, 303
positioning of patient and therapist, 201- 202 Transverse muscle play of gastrocnemius - soleus,
sequencing of treatment, 200 - 201 268- 270
thoracic/upper thoracic spine and upper extrem- Transverse muscle play ofhamstrings, 267- 268
ity, 279- 304 Transverse muscle play of hamstrings and adductor
use of ground to facilitate weight shifting, 202 magnus: posterior-to-anterior pressure, 268
use of lever arms as force multiplier, 202 Transverse muscle play of quadriceps, 249- 252
use of therapist's body weight, 202 Traumatized connective tissue, response of, to im-
Thixotropy mobilization, 77- 78
clinical implications of, 115-116 Travell, Janet, 128
definition of, 50, 114-1 15 Treatment . See Therapeutic techniques
erector spinae muscle play and, 121 Tricyclic antidepressants, 155
mechanisms of, in muscle, 115 Trigger point injections, 147- 148
neurophysiological implications of, 116-117 Trigger point release, 146- 147
Thoracic rotational laminar release, 298- 299 Trigger points
Thoracic spine, evaluation of, 191, 192 autonomic aspects, 144-145
Thoracic/upper thoracic spine and upper extremity autonomic dysfunction, 138-139
anterolateral fascia l elongation, 288- 289 clinical characteristics of myofascial pain,
biceps stretch, 300 132-139
bilateral upper thoracic release, 283- 284 contractures of, 140-142
first rib shoulder depression technique, 282- 283 diagnosis of myofascial pain syndrome, 129-132
forearm "ironing," 300- 301 energy crisis hypothesis of, 140-141
lateral elongation of upper thoracic area, 279- 281 management of myofascial pain, 145- 149
muscle splay of forearm, 301- 303 motor and mechanical dysfunction, 133-1 35
myofascial trigger point release (infraspinatur) myofascial pain syndrome defined, 128-129
flat palpation, 292- 294 myofascial trigger point release (infraspinatur)
myofascial trigger point release (upper trapezius) flat palpation, 292- 294
pincer palpation, 294 myofascial trigger point release (upper trapezius)
palmar stretch, 303- 304 pincer palpation, 294
pectoralis major muscle play/pectoralis minor pathogenesis of, 139-149
manipulation, 285- 286 peripheral and central sensitization, 142- 144
retinacular stretch, 304 physical therapy dry needling, 145- 146
scapular framing, 289- 292 referred pain patterns of, 136-138
scapular manipulation, 294- 296 sensory dysfunction, 135-138
seated pectoral anterior fascia l stretch, 286- 287 trigger point injections, 147- 148
subscapularis, 287- 288 trigger point release, 146- 147
therapeutic techniques, 279- 304 Trochanterrocking,248 - 249,250
thoracic rotational laminar release, 298- 299
transverse fascial stretch of biceps, 299- 300 Unilateral posterior/anterior articulation of first rib,
transverse muscle bending of forearm, 303 281- 282
326 Index
Upper crossed syndrome, 188, 189 Widespread Pain Index (WPI), 152
Upper extremity and posterior quadrant fascial Wolff's law, 45
elongation, 296- 298 Wounds. See also Histopathology
U.S. Food and Drug Administration, 155 definition of, 69
favorable healing conditions, 70
Vata-Pacini corpuscles, 119 fibroblastic phase of, 71- 72
Viscoelastic model of connective tissue, 41- 45 granulation phase of, 70- 71
Viscoelastic muscle tone, 113-114 healing phases of, 69- 72
Voss, Dorothy, 25 inflammation of, 70
maturation or remodeling phase of, 72
Ward, Robert, 24 scar formation, 77- 78
Washing ofhands, 204- 205 WPI. See Widespread Pain Index (WPI)
About the Authors
Robert I. Cantu, MMSc, PT, MTC, is regional manager for Physiotherapy Associ-
ates in Atlanta, Georgia. He is also an instructor at the University of St. Augustine
for Health Sciences, where he has taught in the area of myofascial manipulation
for the last 21 years.
Alan J.Grodin, PT, MTC, is senior vice president for Sovereign Rehabilitation in
Atlanta, Georgia. He is also an instructor at the University of St. Augustine, where
he has taught in the area of myofascial manipulation for the last 27 years.
Robert W. Stanborough, PT, DPT, MHSc, MTC, CMTPT, FAAOMPT, is presi-

dent of First Coast Rehabilitation in St. Augustine, Florida. He is also a full-time
faculty member at the University of St. Augustine for Health Sciences, where he
has taught in the area of myofascial manipulation, as well as other subjects of phys-
ical therapy, for the last 8 years.
327

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8700 Shoal Creek Boulevard

Library of Congress Cataloging-in-Publication Data

Art Director: Jason Crosier

Printed in the United States of America

Con tributor s . ................................................................ xi

Histology and Biomechanics of Connective Tissue ......................... 33

Active Movement Analysis ............................................. 193

Index .. .................................................................... .317

Jan Dommerholt, PT, DPT, MPS, FAAPM

Clayton D. Gable, PT, PhD

Dr. Robert Schleip

Preface to the Third Edition

Preface to the First Edition

Preface to the Second Edition

From the Second Edition

From the First Edition

Myofascial manipulation is as old as history itself- humans have been perform-

In the treatment of back pain, Hippocrates describes treatment of humpback,

The description of lumbar extension for treatment of lumbar "kyphosis" is

discogenic lesions in which a loss of lordosis is common. The idea of "reposition-

primary occupations, and usually treated

the practicing physician is equipped as concerns injuries to and diseases of the

Osteopathic Medicine and Chiropractic

dislocated bones, abnormal, dislocated ligaments or contracted muscles, par -

Dr. Charles Still, son of the founder of osteopathic medicine, maintained

1. A vertebra can become subluxated.

Modern Times: The Trend Toward Mobility

The recognition of radiotranslucent moving tissues as the cause of pain is a

Mennell also advocated the following concepts in operationally defining man-

Another person responsible for bringing arthrokinematics into the evaluation

Another proponent of the mobility theory is G. D. Maitland of Australia. His

channeled through autonomic pathways, producing effects in areas corresponding

Connective Tissue Massage (Bindegewebsmassage)

The CTM system is very systematic and protocol oriented if performed as

choice of technique, because it primarily affects the autonomic nervous system.

Petrissagetechniques lift, wring or squeeze soft tissue in a kneading motion or

Rolfing ® (Structural Integration) *

*Rolfing• is a registered service mark of the Rolf Institute of Structural Integration.

© 1958 Id• P. Rolf l

Picture the slouched posture of a person under considerable stress or fatigue.

Proprioceptive Neuromuscular Facilitation

16. Alexander F. The UniversalConstant in Living. New York: Dutton; 1941:10.

The foundations of orthopedic physical therapy are based on the understanding of

Histology and Biomechanics of Connective Tissue

Collagen Nerve ~- Adipose cells ~ Elastin Macrophage Pericyte Capillary

Table 3.1 Histological Makeup of Connective Tissue

The Cells of Connective Tissue

system. This widely scattered system consists of phagocytic and immunologi-

The Extracellular Matrix

1.5nm 3.5nm 10-20nm 50-500nm 50-300µm

Biomechanics of Connect ive Tissue

Stress-strain curve. As previously mentioned, when stress is applied to a tissue,

Viscoelasticmodel of connective tissue. The viscoelastic concept can be explained

Viscous proper ties --------i►► Plastic stretch

Elastic prope rties -------1►► Elastic stretch

ELASTICMODEL elastic component has a poststretch recoil in

PLASTIC(VISOUS)MODEL determined more by the duration of force