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Pain Patterns
Page Page
Abdominal Muscles 942, 944, 945 Multifidi 917
Abdominis Obliqui Obliqui Capitis Superior
and Transversus 942 and Inferior 473
Abductor Digiti Minimi 787 Occipitalis 428
Adductor Pollicis 775 Occipitofrontalis 428
Anconeus 670 Opponens Pollicis 775
Anterior Neck Muscles 398 Orbicularis Oculi 417
BicepsBrachii 649 Palmaris Longus 744
Brachialis 661 Pectoralis Major 820,822
Brachioradialis 693 Pectoralis Minor 845
Buccinator 418 Platysma 417
Coracobrachialis 639 Posterior Cervicals 447
Deltoid 624 Pronator Teres 757
Diaphragm 863, 864 Pyramidalis 945
Digastric 398 Rectus Abdominis 944
Extensor Carpi Radialis and Recti Capitis Posteriores
Extensor Carpi Ulnaris 692 Major and Minor 473
Extensor Digitorum 715 Rotatores 917
Extensor Indicis 715 Rhomboid Major and Minor 614
Facial Muscles 417, 418 Scaleni 506
Finger Extensors 715 Semispinalis Capitis and
Flexores Carpi Radialis and Cervicis 447
Ulnaris 756 Serratus Anterior 888
Flexores Digitorum Superficialis Serratus Posterior Inferior 909
and Profundus 756 Serratus Posterior Superior 901
Flexor Pollicis Longus 757 Splenius Capitis and Splenius
Frontalis 428 Cervicis 433
Hand and Finger Flexors 756,757 Sternalis 858
Hand Extensors 692 Sternocleidomastoid 310
Iliocostalis Thoracis and Subclavius 823
Lumborum 915 Suboccipital Muscles 473
Infraspinatus 553 Subscapularis 598
Intercostal Muscles 863 Supinator 729
Interossei of the Hand 787 Supraspinatus 539
Lateral Pterygoid 380 Temporalis 351
Latissimus Dorsi 573 Teres Major 588
Levator Scapulae 493 Teres Minor 565
Longissimus Capitis 446 Thoracolumbar Paraspinals 915,917
Longissimus Thoracis 904 Trapezius 279, 280, 281
Masseter 331 Triceps Brachii 668, 669
Medial Pterygoid 366 Zygomaticus Major 417

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HEAD AND NECK
PAIN-AND-MUSCLE GUIDE
CHAPTER 5

UPPER BACK,
SHOULDER AND ARM
PAIN-AND-MUSCLE GUIDE
CHAPTER 18

FOREARM AND HAND


PAIN-AND-MUSCLE GUIDE
CHAPTER 33

TORSO
PAIN-AND-MUSCLE GUIDE
CHAPTER 14

Pictorial index. The muscles that are likely to refer pain to an illustrated region
of the body are listed in the Pain-and-muscle Guide to the corresponding Part of
the Manual. A Guide is found at the beginning of each Part, which is marked by
red thumb tabs.

Copyrighted Material
Travell & Simons'

Myofascial Pain
and Dysfunction:
The Trigger Point Manual
VOLUME 1. Upper Half of Body
Second Edition

Copyrighted Material
Travell & Simons'

Myofascial Pain
and Dysfunction:
The Trigger Point Manual
VOLUME 1. Upper Half of Body

Second Edition

DAVID G. SIMONS, M.D., FAAPM&R, M.S., DSC (HON.)


Clinical Professor, Rehabilitation Medicine
Emory University School of Medicine
Atlanta, Georgia

Clinical Professor
Department of Physical Medicine and Rehabilitation
University of California, Irvine

Formerly Clinical Chief


Electromyography and Electrodiagnosis Section
Rehabilitation Medicine Service
Veterans Affairs Medical Center
Long Beach, California

JANET G. TRAVELL, M.D. t

LOIS S. SIMONS, M.S., P.T.


Consultant, Myofascial Pain and Dysfunction

Illustrations by Barbara D. Cummings


with contributions by Diane Abeloff and Jason Lee

Williams &: Wilkins


A U'AVKKLY ( O M P A N Y

BALTIMORE PHILADELPHIA LONDON PARIS BANGKOK


BUKNOS AIKI-.S HOW. KOW, < MUNICH SVHNHV I'OKYO WROCLAW

t
Dr. Janet Travell's genius and medical insight identified in the first edition the clinical picture of individual myofascial
pain syndromes and many perpetuating factors. In addition, we were most fortunate to have had the benefit of her advice
in preparing some of this edition. She emphasized the importance of including a new chapter that covers the respiratory
muscles and supplied unique pearls of clinical wisdom that sprinkle this revision.

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Editor: Eric Johnson
Managing Editor: Linda Napora
Project Editor: Jeffrey S. Myers
Marketing Manager: Chris Cushner

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The publisher is not responsible (as a matter of product liability, negligence or otherwise) for any injury re-
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Printed in the United States of America


First Edition, 1 9 8 3

Library of Congress Cataloging-in-Publication Data

Simons, David G.
Travell & Simons' myofascial pain and dysfunction : the trigger point manual / David G. Simons, Janet
G. Travell. Lois S. Simons ; illustrations by Barbara D. Cummings, with contributions by Diane Abeloff and
Jason Lee. 2nd ed.
p. cm.
Rev. ed. of: Myofascial pain and dysfunction / Janet G. Travell, David G. Simons. c l 9 8 3 - c l 9 9 2 .
Includes bibliographical references and index.
Contents: v. 1. Upper half of body.
ISBN 0-683-08363-5 (v. 1)
1. Myofascial pain syndromesHandbooks, manuals, etc.
I. Travell, Janet G, 1 9 0 1 - . II. Simons, Lois S. III. Travell, Janet G., 1 9 0 1 - Myofascial pain and dys-
function. IV. Title.
[DNLM: 1. Myofascial Pain Syndromes. WE 5 0 0 S 6 1 1 t 1998]
RC925.5.T7 1998
616.7'4dc21
DNLM/DLC
for Library of Congress 98-36642
CIP

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1 2 3 4 5 6 7 8 9 10

Copyrighted Material
This Volume is dedicated to
Janet G. Travell, M.D.
1901 - 1997
To whom we all owe a great debt of gratitude
for her inspirational pioneering of this field
and for heading us in the right direction.

Copyrighted Material
Foreword

In my 1992 Foreword to the now-fa- mits me to predict a magnificent success.


mous mate, Volume 2, of the Trigger Point This is a gargantuan publishing effort that
Manual Volume 1,1 boldly opined that Vol- would have done Rabelais credit. But this
ume 2 was "... even better than the other Gargantua is not fantasy; it is hard-headed
[Vol.1] because it reflects an enormous new facts and a wise explication of many cur-
recharging of energy that further experi- rent ideas and new findings.
ence, interaction, and thought have stimu- The new edition clarifies for me the
lated.... This new volume," I went on to overlap of confusing similar conditions
say, "has the distinction of going beyond that must be distinguished. It illuminates
those areas [emphasized in the first edition improved testing methods and clearly puts
of Volume 1] to discuss rationale, new others into their place, often outside. The
principles arising from a ground-swell of authors are forthright and precise in the di-
experience, and the unique place of myo- agnostic criteria for an active trigger point
fascial pain syndrome in the spectrum of for general clinical use as a "... circum-
musculoskeletal disorders." scribed spot tenderness in a nodule of a
"Myofascial trigger points and their sig- palpable taut band and patient recognition
nificance in painful conditions are no of the pain evoked by pressure on the ten-
longer the rather controversial subject they der spot as being familiar."
were before Volume 1 appeared, nor are the The thorough discussion of the nature of
treatment methods taught by Drs. Travell trigger points and their electrodiagnostic
and Simons. These are firmly established characteristics is very valuable and timely,
and are increasingly being validated by as is the coverage of the histogenesis of
once skeptical clinical investigators ...[Vol- trigger points. Updating and expansion
ume 2] goes beyond and opens up new throughout the volume now make the two
ground in sensitizing clinicians to the im- volumes together one of the most impres-
portant interfaces between myofascial pain sive medical publishing efforts of modern
syndromes and articular (somatic) dys- times. Truly it becomes a tour de force. I
functions on the one hand and fibromyal- am proud to be its "godfather."
gia on the other hand. I applaud the wise
manner in which these issues are ad-
dressed, assessed, and integrated."
How can this scribbler do any better John V. Basmajian, O.C., O. Ont, MD,
than that eulogy to summarize his opinion FRCPC, FRCPS (Glasg]
of the macho younger mate of Volume 1 FACA, FAADMR, FSBM, FABMR,
when the latter now produces an offspring FAFRM-RACP (Australia), Hon Dip (St L C)
that outshines both its parents? My scan- Professor Emeritus, McMaster University
ning of the manuscript before its birth per- Hamilton, Ontario, Canada

vii

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At present, the only way to make a definite diagnosis Each muscle has individual characteristics which the
of a trigger point is by physical examination. This fig- examiner needs to learn. When active trigger points in
ure emphasizes the fact that the ESSENTIAL first step any muscle fail to respond to treatment, with few ex-
is to learn how to recognize by palpation the nodule ceptions one or more perpetuating factors need to be
and taut band that are characteristic of a trigger point. identified and resolved.

Copyrighted Material
Preface

The passing of Janet Travell, M.D., on 1 matic." In none of these patients did the
August 1997 at the age of 95 marked the doctors find objective evidence of disease
end of the era when she gave life to the to account for the patient's pain, but the
concept of myofascial trigger points (TrPs) skeletal muscles had not been examined.
and nurtured it through childhood. Others When Dr. Travell examined these patients,
must now lead the concept through adoles- all three groups had isolated tender spots
cence to maturity. in muscles which, when compressed, re-
As a memorial and tribute to Dr Travell's produced the patient's pain in the shoul-
unique contribution, the following selec- der, arm or chest. The common ailment
tion is quoted from the preface of the first was an unrecognized myofascial trigger
edition of this volume: "Dr. Travell de- point syndrome.
scribes in detail her introduction to myo- "Fortunately, these observations were
fascial trigger points in her autobiography, made in an environment rich in experi-
Office Hours: Day and Night. Although she mental expertise. She regularly taught
was brought up on the unitary concept of pharmacology to medical students whom,
disease that all of the patient's symptoms to answer their questions, she inspired to
should be explained by one diagnosis, she perform the appropriate experiments for
soon learned that life is not like that. The themselves in the laboratory. The inquisi-
man who has both heart disease and pul- tive students and faculty at the Cornell
monary tuberculosis may suddenly die of University Medical College helped Dr.
cancer of the lung. Patient complaints that Travell formulate her investigation of the
originate in the musculoskeletal system nature of trigger points and how they func-
usually have multiple causes responsible tion.
for the total picture. "She herself was inspired by the inter-
"Early in her medical career, Dr. Travell change of ideas and the criticism of leaders
served simultaneously on pulmonary, car- in basic and clinical research at the New
diology, and general medical services. On York Hospital, Cornell Medical College
all the services, the major complaint she Center. Foremost among these were Drs.
encountered among the patients was pain. Harry Gold, McKeen Cattell, Vincent du Vi-
The patient might be dying of a serious ill- gneaud, Ephraim Shorr, Harold G. Wolff,
ness, but when asked, "How are you?" Eugene F. Dubois, and the renowned neu-
would answer, "Well, ok, except I have this rologist, Frank Fremont-Smith, Director of
terrible pain in my shoulder. I can't sleep. the Josiah Macy Foundation. During the
I can't lie on that side." When asked the many years of their association, she was es-
cause of the pain, the resident on the pul- pecially indebted to her cardiologist col-
monary service would say that it was reflex laborator, Seymour H. Rinzler.
from the lung. On the cardiology service, "The successful care rendered Senator
in another hospital, patients had the same Kennedy five years prior to his election as
complaint of shoulder pain, but the resi- President led Dr. Travell to the position of
dent explained the pain as reflex from the White House Physician under Presidents
heart, of course. In the general medical John F. Kennedy and Lyndon B. Johnson.
clinic, a secretary who spent all day typing Except for that one short detour, she never
and pulling heavy file drawers would de- strayed from her primary focus on the di-
scribe precisely the same pain complaint; agnosis and management of myofascial
but its origin was said to be "psychoso- pain syndromes due to trigger points."
ix

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x Preface

TRANSITIONS Previously no distinction was drawn be-


tween trigger points located in the middle
This second edition of volume 1 of The portion of the muscle belly (central TrPs)
Trigger Point Manual is transitional in a and those located in a region of muscle at-
number of ways. Most important, it marks tachment (attachment TrPs). The tender-
the transition of the trigger point concept ness of each depends on different patho-
from the status of a syndrome of unknown physiological processes with significant
etiology to that of an experimentally estab- therapeutic implications that have yet to be
lished neuromuscular disease entity. Elec- adequately explored.
trophysiological and histopathological evi- In the first edition, an attempt was made
dence presented in Chapter 2 now makes it to document what we knew about myofas-
clear that dysfunctional motor endplates of cial TrPs, almost all of which was based on
skeletal muscle fibers are at the heart of the clinical observations. There is now the be-
pathophysiology that characterizes myo- ginning of a peer-reviewed body of litera-
fascial trigger points (TrPs). Many impor- ture with blinded, controlled studies that
tant details remain to be resolved. are scientifically credible. Many more are
This second edition is transitional also urgently needed. Such studies of the effec-
because it addresses the close interaction tiveness of TrP treatment by skilled clini-
between myofascial TrPs and articular (so- cians should contribute greatly to a more
matic) dysfunctions. This edition calls at- widespread recognition of the importance
tention to that relationship in practically of myofascial TrPs as a major source of
every chapter and presents it some detail musculoskeletal pain. To facilitate this
in Chapter 16, Posterior Cervical Muscles. transition, the present edition now calls at-
At present, these are often treated as unre- tention to specific clinical conditions wor-
lated problems that should be integrated in thy of investigation (see "Research Oppor-
clinical practice for the patient's sake. An tunities" in the Index).
osteopathic physician who is well ac-
quainted with myofascial TrPs has CHANGES IN THIS EDITION
achieved this integration in her practice This edition incorporates a number of
and has contributed to most of the chap- changes applicable to most chapters. All
ters. This edition can only call attention treatment sections (Section 12) have been
to specific examples of the closeness of extensively rewritten and now include a
the muscle-joint relationship. It barely number of trigger point release techniques
scratches the surface of what is needed. in addition to spray and stretch. Section 12
This edition marks the beginning of a in many of the chapters has been enhanced
transition from a volume by two authors to by the extensive experience and insight of
a volume with significant contributions by Mary Maloney, P.T., and her daughter Jill
others. The subject matter is rapidly out- Maloney Newman, P.T. Successful inactiva-
growing the comprehension of only two in- tion of active TrPs depends on restoring full
dividuals. range of pain-free motion. The most effec-
This edition presents the major progress tive technique(s) for achieving that goal de-
in our understanding of the pathophysio- pends on an appreciation of the trigger
logical basis for many of the clinical phe- point source of the pain, which muscle is
nomena associated with myofascial TrPs. involved, the patient's response, the clini-
We now know, based on histopathology, cian's training and skill, etc. This change in
that a palpable nodule and an associated emphasis is reflected in the new title of sec-
taut band are essential features of a myo- tion 12, Trigger Point Release. A rewritten
fascial TrP (and also of myogelosis). The Section 11 of every muscle chapter now is
importance of the nodularity was not em- called Differential Diagnosis and incorpo-
phasized in the first edition of volume 1. rates the material under its previous title,
Emphasis is now shifting from pain as the Associated Trigger Points, as a subheading.
cardinal feature of a myofascial TrP to in- Recent surface electromyographic stud-
creased muscle tension and its conse- ies confirm and emphasize the importance
quences. of the motor dysfunctions associated with

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Preface xi

TrPs. This fundamental and essentially un- Chapter 45 is an entirely new and ex-
explored effect of TrPs may be as important tensive chapter specifically on the di-
as, or even more important clinically than aphragm and the many functions of the in-
the referred pain that they cause. tercostal muscles. The chapter includes
Differences in several individual chap- respiratory mechanics and the contribu-
ters are noteworthy. Chapter 2 has been tion of other muscles to respiration.
completely rewritten and presents a new
understanding of the nature of myofascial OVERVIEW OF THIS EDITION
TrPs. It also considers the role of TrPs in Myofascial trigger points are a fre-
the family of syndromes related to occupa- quently overlooked and misunderstood
tional overload of muscles. source of the distressingly ubiquitous mus-
The considerable changes in the diag- culoskeletal aches and pains of mankind.
nostic and treatment sections of Chapter 3 This manual assembles in one place the in-
reflect the new understanding of the na- formation necessary for the student and the
ture of myofascial trigger points. Evidence practitioner to recognize and treat one ma-
of muscular dysfunctions as well as the jor source of musculoskeletal pain com-
identification of referred pain patterns are plaints, myofascial TrPs. Many other
emphasized, and effective physical treat- sources of muscle pain and their neuro-
ments include many more that are now physiological basis are presented in an-
available. other book, Muscle Pain, by Mense and Si-
A considerable part of the section on mons, that will be published by Williams &
systemic perpetuating factors in Chapter 4 Wilkins.
was rewritten and updated by Robert This first volume of The Trigger Point
Gerwin, M.D., based on clinical experience Manual presents introductory general in-
and research projects of his own. formation on all TrPs and also detailed de-
Most of the introduction to masticatory scriptions of single-muscle syndromes for
muscles in Chapter 5 was written by a the upper half of the body.
dentist, Dr. Bernadette Jaeger, and includes This book is specifically addressed to
a comprehensive section on the contribu- health care professionals who are con-
tion of TrPs to many different kinds of cerned for patients with musculoskeletal
headache. The masticatory muscle chap- pain problems and who have been well
ters themselves, Chapters 8-12, have bene- trained in (or are prepared to learn): mus-
fitted greatly from her expertise as well as cle anatomy, physiology, kinesiology, nec-
that of Mary Maloney, P.T., who is well ac- essary palpation skills, and how to recog-
quainted with the management of myofas- nize (and resolve) perpetuating factors. It is
cial TrPs in masticatory muscles. NOT intended as a procedural "cook
Chapters 16 (Posterior Cervical Muscles) book." It presents a basis for understanding
and 17 (Suboccipital Muscles) emphasize the cause of the patient's pain and ways of
the close relation between articular dys- eliminating the source of the pain, not just
functions and TrPs in those muscles. alleviating it.
Chapter 20 (Scalene Muscles) presents Usually, acute single-muscle syndromes
(in Section 11) new insights into the con- are easily managed. Often, however, the
troversial and frustrating subject of tho- patient presents with pain that represents a
racic outlet syndrome. composite pattern referred from several
Chapter 21 (Supraspinatus muscle) re- muscles; the practitioner must become a
views (in Section 11) rotator cuff disease sleuth and recognize the component parts.
and considers its relation to the motor and Much of the detective work lies in tracking
sensory disturbances caused by TrPs. down not only what specific stress or
In Chapter 36 (Supinator Muscle), Sec- stresses initiated the patient's trigger
tion 10 explores the contribution of TrPs to points, but also what additional factors
entrapment of the deep radial nerve, and may be perpetuating them. Chapter 4 of
Section 11 examines the close relation be- this manual reviews many of these factors.
tween TrPs and tennis elbow or lateral epi- The identification of perpetuating factors
condylitis. can require a thorough knowledge of body

Copyrighted Material
xii Preface

mechanics, kinesiology, and skillful medical illustrates what part of the body is included
detectiveworkinareasthatareoftenneglected under each of the four main parts of this
ordismissedasunimportant. volumethatfollowtheintroduction.Eachpart
This manual describes individually the is identified by a red thumb tab and begins
component parts of the myofascial jigsaw withapainandmuscleguide.Thisguideillus
puzzle.Thereadermustpiecethemtogetherto tratestheareaswithinthatregionandliststhe
fit the clinical picture of each patient, muscles that are most likely to refer pain to
remembering that no two persons are exactly each area. For convenience, the
alike. painandmuscle guide also lists the chapter
The handy listing of muscle pain patterns, numberofthechapterthatdealswithamuscle.
alphabetically arranged, is located inside the Everymusclechapterisuniformlyarranged
frontcover. with fourteen headings and begins with
The primary clue as to which muscle has a HIGHLIGHTS,asummaryofkeypointsinthat
TrPistherestrictionofpassiveandactiverange chapter. The sections of introductory Chapter
of motion due to pain. In addition, thepattern 3, Apropos of All Muscles, have the same
ofpainreferredfromanactiveTrPisavaluable fourteen numbered headings. Thus, each
guideastotheTrPsourceofthepain. section of Chapter 3 serves as a general
Sincethepainreferredfrommostmyofascial introduction to the corresponding section for
TrPs often appears at some distance from the every muscle. It presents information
triggerpoint,thepractitionercanbenefitfroma applicabletoallmuscles.InformationinChapter
guide that identifies which muscles most 3 that is critical to the management of a patients
commonlyreferpaintoaparticularareaofthe myofascial pain syndrome may not be repeated in
body. The pictorial index on the front fly leaf theindividualmusclechapter.

Copyrighted Material
Acknowledgments

We are especially indebted to four indi- served at active loci contributed signifi-
viduals who made considerable contribu- cantly to steering us in the right direction,
tions to this revision and who are listed on and his critical review of Chapter 2 was
the Contributor page and are identified in most helpful.
chapters to which they made a substantial Dr. Hong's numerous controlled clinical
contribution. They are Robert Gerwin, M.D., studies have helped greatly to give re-
Bernadette Jaeger, D.D.S., Mary Maloney, search substance to the clinical impres-
P.T., and Roberta Shapiro, D.O. In addition, sions of TrP characteristics.
Michael Kuchera, D.O., and I. Jon Russell, We are especially grateful to Jason Lee
M.D., PhD. meticulously reviewed and for carrying the major responsibility of typ-
made helpful contributions to Chapter 16. ing most of the revisions, for obtaining and
The research collaboration with Profes- organizing references, and for doing some
sor Chang-Zern Hong, M.D., in performing editing. Jason was a veritable genius with
both human studies and animal studies re- the care and feeding of the computers and
sulted in the electrodiagnostic characteri- exhibited a priceless talent for finding es-
zation of TrPs that was essential to the sential items that we had misplaced from
identification of their pathophysiology. time to time. Our thanks also go to Barbara
The support of Phyllis Page, M.D., Chief, Zastrow, who provided the secretarial ser-
Physical Medicine and Rehabilitation Ser- vices at the beginning of the revision, and
vice, Veterans Affairs Medical Center, to Frances Denmark, who competently and
Long Beach, California and of Raghavaiah cheerfully provided the assistance that en-
Kanekamedala, Director of the Electromyo- abled us to complete the work.
graphy Laboratory of the same service, was The observations made and questions
essential to the accomplishment of the raised by Jochen Sachse, M.D., while trans-
electrodiagnostic studies of TrPs in human lating the first edition into German identi-
subjects. The enthusiastic support of Pro- fied many necessary corrections. His ef-
fessor Robert Blanks, PhD, Departments of forts and expertise are much appreciated.
Anatomy and Neurobiology, University of The visit to the office of Michel Bouve,
California, Irvine, for the use of his labora- M.D., D.C. in Belgium redirected our atten-
tory facilities and the support by Professor tion to the critical functional importance of
Jen Yu, Chairman of the Department of the restricted range of motion caused by
Physical Medicine and Rehabilitation, TrPs even when the patient presents with
University of California, Irvine, made pos- little or no pain complaint. We now better
sible our investigation of the electrodiag- appreciate both theoretically and clinically
nostic characteristics of trigger spots in how increased muscle tension can be the
rabbits. fundamental, primary effect of TrPs and
In general, the long discussions with that pain can be a less constant, secondary
Professor Siegfried Mense over many phenomenon.
years concerning the nature of myofascial We express our deep respect and grati-
TrPs, and in particular their referred pain tude to Barbara D. Cummings for complet-
neurophysiology, helped greatly in the de- ing most of the drawings for this revision,
velopment of our understanding of the and to Diane Abeloff for contributing
pathophysiology of TrPs. Specifically, the the rest of the drawings. The computer-
discussions with Professor Mense concern- generated figures are a tribute to the com-
ing the nature of the potentials being ob- puter skills of Jason Lee. It was a pleasure
xiii

Copyrighted Material
xiv Acknowledgments

toworkwithourProjectEditor,JeffreyMyers, persistence and understanding helped to


who kindly made the additional changes sustain and encourage us, buoyed up by her
necessary in page proof and provided much delightful sense of humor which made us
additional information needed to ensure a laugh through the tears at times when we
qualityproduct. desperatelyneededlaughter.
Last, but by no means least in importance,
words cannot adequately express our deep
gratitude to our Managing Editor, Linda DavidG.Simons,M.D.Lois
Napora, for her close support and StathamSimons,M.S.,P.T.3176
encouragement throughout the enormous MonticelloStreetCovington,GA30014
undertaking of this revision. Her patient

Copyrighted Material
Contributors

Robert D. Gerwin, M.D.


Pain and Rehabilitation Medicine
Bethesda, Maryland

Bernadette Jaeger, D.D.S.


Associate Professor
UCLA Section of Diagnostic Sciences and Orofacial Pain
Los Angeles, California

Michael L. Kuchera, D.O., FAAO


Professor and Chairperson
Department of Osteopathic Manipulative Medicine
Kirksville College of Osteopathic Medicine
Kirksville, Missouri

Mary L. Maloney, R.P.T.


Naugatuck Physical Therapy and Maloney Rehabilitation Services
West Haven, Connecticut

I. Jon Russell, M.D., Ph.D.


Associate Professor of Medicine
Department of Medicine
Division of Clinical Immunology
Section of Rheumatology
The University of Texas Health Science Center
San Antonio, Texas

Roberta F. Shapiro, D.O., FAAPM&R


Assistant Clinical Professor
Department of Pediatrics
Department of Physical Medicine & Rehabilitation
Albert Einstein College of Medicine
New York, New York

xv

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Contents

Foreword by John V. Basmajian, O.C., O. ONT.,M.D vii


Preface ix
Acknowledgments xiii
Contributors xv

PART 1 INTRODUCTION
CHAPTER 1 Glossary 1
CHAPTER 2 General Overview 11
CHAPTER 3 Apropos of All Muscles 94
CHAPTER 4 Perpetuating Factors 178

PART 2 HEAD AND NECK PAIN


CHAPTER 5 Overview of Head and Neck Region 237
CHAPTER 6 Trapezius Muscle 278
CHAPTER 7 Sternocleidomastoid Muscle 308
CHAPTER 8 Masseter Muscle 329
CHAPTER 9 Temporalis Muscle 349
CHAPTER 10 Medial Pterygoid Muscle 365
CHAPTER 11 Lateral Pterygoid Muscle 379
CHAPTER 12 Digastric Muscle and Other Anterior Neck Muscles 397
CHAPTER 13 Cutaneous I: Facial Muscles (Orbicularis Oculi,
Zygomaticus Major, Platysma, and Buccinator) 416
CHAPTER 14 Cutaneous II: Occipitofrontalis 427
CHAPTER 15 Splenius Capitis and Splenius Cervicis Muscles . .432
CHAPTER 16 Posterior Cervical Muscles: Semispinalis Capitis,
Longissimus Capitis, Semispinalis Cervicis, Multifidi,
and Rotatores 445
CHAPTER 17 Suboccipital Muscles: Recti Capitis Posteriores
Major and Minor, Obliqui Inferior and Superior 472

PART 3 UPPER BACK, SHOULDER, AND ARM PAIN


CHAPTER 18 Overview of Upper Back, Shoulder, and Arm Region 485
CHAPTER 19 Levator Scapulae Muscle 491
CHAPTER 20 Scalene Muscles 504
CHAPTER 21 Supraspinatus Muscle 538
CHAPTER 22 Infraspinatus Muscle 552
CHAPTER 23 Teres Minor Muscle 564
CHAPTER 24 Latissimus Dorsi Muscle 572
CHAPTER 25 Teres Major Muscle 587
CHAPTER 26 Subscapularis Muscle 596
CHAPTER 27 Rhomboid Major and Minor Muscles 613
CHAPTER 28 Deltoid Muscle 623
xvii

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xviii Contents

CHAPTER 29 Coracobrachialis Muscle 638


CHAPTER 30 Biceps Brachii Muscle 648
CHAPTER 31 Brachialis Muscle 660
CHAPTER 32 Triceps Brachii Muscle (and the Anconeus) 667

PART 4 FOREARM AND HAND PAIN


CHAPTER 33 Overview of Forearm and Hand Region 685
CHAPTER 34 Hand Extensor and Brachioradialis Muscles 690
CHAPTER 35 Finger Extensor Muscles: Extensor Digitorum and Extensor Indicis 713
CHAPTER 36 Supinator Muscle 728
CHAPTER 37 Palmaris Longus Muscle 743
CHAPTER 38 Hand and Finger Flexors in the Forearm: Flexores Carpi
Radialis and Ulnaris, Flexores Digitorum Superficialis and
Profundus, Flexor Pollicis Longus (and the Pronator Teres) 753
CHAPTER 39 Adductor and Opponens Pollicis Muscles (Trigger Thumb) 774
CHAPTER 40 Interosseous Muscles of the Hand, Lumbricals, and
Abductor Digiti Minimi 786

PART 5 TORSO PAIN


CHAPTER 41 Overview of Torso Region 801
CHAPTER 42 Pectoralis Major Muscle (and the Subclavius) 819
CHAPTER 43 Pectoralis Minor Muscle 844
CHAPTER 44 Sternalis Muscle 857
CHAPTER 45 Intercostal Muscles and the Diaphragm 862
CHAPTER 46 Serratus Anterior Muscle 887
CHAPTER 47 Serratus Posterior Superior and Inferior Muscles 900
CHAPTER 48 Thoracolumbar Paraspinal Muscles 913
CHAPTER 49 Abdominal Muscles 940

Index to Volume 1 971


Index to Volume 2 1017

Copyrighted Material
PART 1
INTRODUCTION

CHAPTER 1
Glossary
The glossary comes first to ensure that the The glossary is in the front of the book to
reader knows what a term means as it is encourage frequent reference to it, when-
used in this manual and to help the reader ever needed. Comments concerning a defi-
become acquainted with unfamiliar terms. nition are added in italics.

Abduction: Movement away from the mid- muscle, refers a patient-recognized pain on
line. For fingers, it is movement away from direct compression, mediates a local twitch
the midline of the middle digit. For the response of muscle fibers when adequately
thumb, it is movement perpendicular to, stimulated, and, when compressed within
and away from, the plane of the palm. For the patient's pain tolerance, produces re-
the hand, at the wrist, it is radial deviation ferred motor phenomena and often auto-
of the hand, which is away from the mid- nomic phenomena, generally in its pain ref-
line of the body in the anatomical position. erence zone, and causes tenderness in the
For the arm, at the shoulder joint, abduc- pain reference zone. To be distinguished
tion moves the elbow in the frontal plane from a latent myofascial trigger point.
away from the midline of the body. For the
scapula, it is a gliding movement across Acute: Of recent onset (hours or days).
the posterior thorax away from the verte-
bral column. Adduction: Movement toward the midline.
For fingers, it is movement toward the mid-
Active Locus (of a Trigger Point): A minute line of the middle digit. For the thumb, it is
region in a muscle that exhibits sponta- movement perpendicular to, and toward,
neous electrical activity (often character- the plane of the palm. For the hand, it is ul-
ized as endplate noise) and that may or nar deviation at the wrist. For the arm, at
may not also exhibit spike activity charac- the shoulder joint, it is movement of the el-
teristic of single fiber action potentials. bow toward the midline of the body, move-
ment in the frontal plane from the abducted
Active Range of Motion: The extent of position of the arm. For the scapula, it is a
movement (usually expressed in degrees) gliding movement across the posterior tho-
of an anatomical segment at a joint when rax toward the vertebral column.
the movement is produced only by volun-
tary effort of the subject to move that part Agonists: Muscles, or portions of muscles,
of the body being tested. so attached anatomically that when they
contract they develop forces that comple-
Active Myofascial Trigger Point: A myofas- ment or reinforce each other.
cial trigger point that causes a clinical pain
complaint. It is always tender, prevents full Allodynia: Pain due to a stimulus that does
lengthening of the muscle, weakens the not ordinarily provoke pain (decreased
1

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2 Part 1 / Introduction

pain threshold; the response is a different Caudad: Away from the head, toward the
kind of sensation than that normally tail; usually synonymous with inferior; op-
evoked by the stimulus). posite of cephalad.

Analgesia: Absence of pain in response to Central Myofascial Trigger Point: A myo-


stimulation which would normally be fascial trigger point that is closely associ-
painful. ated with dysfunctional endplates and is
located near the center of muscle fibers.
Anatomical Position: The erect position of
the body with the face forward, each arm at Cephalad: Toward the head; usually syn-
the side of the body, forearms supinated so onymous with superior; opposite of caudad.
that the palms of the hands are facing for-
ward, fingers in extension, feet together Chronic: Long-standing (weeks, months or
with the toes directed forward. The terms years), but NOT necessarily irreversible.
posterior, anterior, lateral, medial, supe- Symptoms may be mild or severe.
rior, inferior, etc. are applied with the body-
in this position. Composite Pain Pattern: Total referred
pain pattern of two or more closely adja-
Antagonists: Muscles, or portions of mus- cent muscles. No distinction is made
cles, so attached anatomically that when among the referred pain patterns of the in-
they contract they develop forces that op- dividual muscles.
pose each other.
Contract-Relax: As used in this volume, it is
a gentle voluntary muscle contraction fol-
Anterior: Toward the front of the body
lowed by relaxation with encouragement of
(ventral); opposite of posterior (dorsal).
elongation of the muscle. To be distin-
guished from Hold-Relax, which is isometric.
Arm: In this volume, the arm includes only
the segment of the upper limb between the
Contraction (of muscle): Activation of the
shoulder and elbow, and does not include
contractile elements of muscle fibers by
the entire upper limb.
propagated action potentials. To be distin-
guished from Contracture.
Associated Myofascial Trigger Point: A
trigger point in one muscle that occurs Contracture (of muscle): Sustained intrin-
concurrently with a trigger point in an- sic activation of the contractile elements of
other muscle. One of these associated muscle fibers. With contracture, muscle
trigger points may have induced the shortening occurs in the absence of motor
other, or both may stem from the same unit action potentials. This physiological
mechanical or neurologic origin. definition, as used in this manual, must be
differentiated from the clinical definition,
Atlantoaxial Joint: Junction of the atlas which is shortening due to fibrosis. Con-
(CJ and the axis (C ).
2 tracture also must be distinguished from
contraction and spasm.
Attachment Trigger Point: A trigger point
at the musculotendinous junction and/or Coordinated (normal) Respiration: Expan-
at the osseous attachment of the muscle sion of the chest with simultaneous con-
that identifies the enthesopathy caused by traction of the diaphragm which increases
unrelieved tension characteristic of the intraabdominal pressure and protrudes
taut band that is produced by a central the abdomen during inhalation. To be dis-
trigger point. tinguished from paradoxical (abnormal)
respiration.
Bruxism: Clenching of the teeth, resulting
in rubbing, gritting, or grinding together of Coronal Plane: A frontal (vertical) plane
the teeth, usually during sleep. 6
that divides the body into anterior and pos-

Copyrighted Material
Chapter 1 / Glossary 3

terior portions and lies at right angles to a Flat Palpation: Examination by finger pres-
sagittal plane.
10
sure that proceeds across the muscle fibers
at a right angle to their length, while com-
Deep: Farther from the surface; opposite of pressing them against a firm underlying
superficial. structure, such as bone. Flat palpation is
used to detect taut bands and trigger
Distal: Farther from the trunk or point of points. To be distinguished from pincer
origin; opposite of proximal. palpation and snapping palpation.

Dysesthesia: An unpleasant abnormal sen- Flexion: In general, bending of hinge


sation, whether spontaneous or evoked. joints. In the upper limb, it is movement in
the anterior direction in a sagittal plane. In
Enthesitis: "Traumatic disease occurring at the case of the thumb, it is movement in
the insertion of muscles where recurring the ulnar direction in the plane of the
concentration of muscle stress provokes in- palm.
flammation with a strong tendency toward
fibrosis and calcification." The enthesopa-
7
Function (of a muscle): In this edition of
thy referred to in this book may, in time, volume 1, the actions (movements) of a
develop into an enthesitis. muscle are included under its function. No
sharp distinction is made between function
Enthesopathy: A disease process at muscu- and action.
lotendinous junctions and/or where ten-
dons and ligaments attach into bones or Functional Unit: A group of agonist and
joint capsules. It is characterized by local antagonist muscles that function together
tenderness and may, in time, develop into as a unit because they share common
enthesitis. spinal-reflex responses. The agonist mus-
cles may act in series or in parallel. Previ-
Erector Spinae Muscles: This group of ously identified as a Myotatic Unit.
muscles consists of the spinalis, the
longissimus, and the iliocostalis muscles, 1
Hold-Relax: As used in this volume, a gen-
which are the longest, most longitudinal, tle voluntary isometric muscle contraction
and most superficial of the paraspinal followed by relaxation. To be distinguished
musculature. from Contract-Relax, in which movement
takes place.
Essential Pain Zone (Area): The region of
referred pain (indicated by solid red areas Horizontal Abduction: Movement of the
in pain pattern figures) that is present in elevated arm about a longitudinal axis in
nearly every patient when the trigger point the transverse plane, away from the mid-
is active. To be distinguished from a line of the body.
spillover referred pain zone.
Horizontal Adduction: Movement of the
Extension: In general, straightening of elevated arm in the transverse plane to-
hinge joints. In the upper limb, it is move- ward the midline of the body.
ment in the posterior direction in a sagittal
plane. In the case of the thumb, it is move- Hyperesthesia: Increased sensitivity to
ment in the radial direction in the plane of stimulation, excluding the special senses.
the palm.
Hyperpathia: A painful syndrome charac-
Fibrositis: An outmoded term with multiple terized by abnormally painful reaction to a
meanings. Many authors in the past used it stimulus, especially a repetitive stimulus
to identify what were myofascial trigger (both threshold and response are increased).
points. Other authors have used the term
very differently (see Chapter 2). We avoid Hyperalgesia: An increased pain response
using the term because of its ambiguity. to a stimulus that is normally painful

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4 Part 1 / Introduction

(stimulus and response are in the same Lateral: Farther from the midsagittal plane
mode). of the body or from the midline of a struc-
ture; opposite of medial.
Hypoalgesia: Diminished pain in response
to a normally painful stimulus. Lateral Rotation (External Rotation, Ro-
tation Outward): Rotation of the anterior
Incisal Path: The path of a point in the surface of the limb away from the mid-
groove between the lower central incisor line of the body. For the scapula, it is up-
teeth in relation to the sagittal plane as the ward rotation about an anteroposterior
jaws are opened and closed. axis, with the inferior angle moving later-
ally and the glenoid cavity moving cra-
Inferior: Toward the soles of the feet; syn- nially.
onymous with caudal in the trunk; oppo-
site of superior. Local Twitch Response: A transient con-
traction of a group of tense muscle fibers
Involved Muscle: A muscle that has devel- (taut band) that traverse a trigger point.
oped one or more active or latent trigger The contraction of the fibers is in response
points. to stimulation (usually by snapping palpa-
tion or needling) of the same trigger point,
Ischemic Compression: Now revised and or sometimes of a nearby trigger point.
identified as Trigger Point Pressure Re- Sometimes the local twitch response has
lease. been erroneously called a jump sign.

Joint Play: Small movements within a Low Back Pain: Pain in lumbar, sacral,
synovial joint that are independent of, and/or gluteal areas; a descriptive term
and cannot be induced by, voluntary mus- that does not identify a diagnosis or cause.
cle contraction. Essential for normal,
pain-free, nonrestricted movement of the Lumbago: Pain in the mid and lower back;
articulation.
2
a descriptive term that does not identify a
diagnosis or cause.
Jump Sign: A general pain response of the
patient, who winces, may cry out, and may Medial: Closer to the midsagittal plane of
withdraw in response to pressure applied the body or to the midline of a structure;
on a trigger point. This term has been used opposite of lateral.
erroneously to describe the local twitch re-
sponse of muscle fibers to trigger-point Medial Rotation (Internal Rotation, Rota-
stimulation. tion Inward): Rotation of the anterior sur-
face of the limb toward the midline of the
Key Myofascial Trigger Point: A trigger body. For the scapula, it is downward rota-
point responsible for activating one or tion about an anteroposterior axis, with the
more satellite trigger points. Clinically, a inferior angle moving medially and the gle-
key trigger point is identified when inacti- noid cavity moving caudally.
vation of that trigger point also inactivates
the satellite trigger point. Motor Endplate: Soleplate ending where a
terminal branch of the axon of a motor neu-
Latent Myofascial Trigger Point: A myo- ron makes synaptic contact with a striated
fascial trigger point that is clinically quies- muscle fiber (cell).
cent with respect to spontaneous pain; it
is painful only when palpated. A latent Muscular Rheumatism [Muskel Rheuma-
trigger point may have all the other clini- tismus): Muscular pain and tenderness at-
cal characteristics of an active trigger tributed to "rheumatic" causes (especially
point and always has a taut band that in- exposure to cold). Sometimes used to iden-
creases muscle tension and restricts range tify myofascial trigger points. To be distin-
of motion. guished from articular rheumatism.

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Chapter 1 / Glossary 5

Myalgia: Pain in a muscle or muscles. The 8


Myofascitis (Myositis Fibrosa): Induration
term is used in two ways to signify: (1) dif- of a muscle through an interstitial growth
fusely aching muscles due to systemic dis- of fibrous tissue. Sometimes used erro-
9

ease, such as a virus infection, and (2) the neously in the past as synonymous with
spot tenderness of a muscle or muscles as myofascial trigger points.
in myofascial trigger points. The reader
must distinguish which use an author has Myogelosis: Circumscribed firmness and
in mind. tenderness to palpation in a muscle or
muscles associated with the patient's
Myofascial Pain Dysfunction Syndrome: A pain complaint. The name is derived
controversial, largely outmoded term that from the concept that the regions of cir-
has been considered to mean a syndrome cumscribed firmness were due to local-
largely of muscular origin, a complex psy- ized gelling of muscle proteins. Focal ten-
chophysiological phenomenon, or a syn- derness and palpable taut muscle fibers
drome primarily due to disturbed occlusal and nodules are also characteristic of
mechanics. myofascial trigger points. Most patients
diagnosed as having myogelosis also
Myofascial Pain Syndrome (Myofascial would be diagnosed as having myofascial
Syndrome): 1. (as used in this book) The trigger points.
sensory, motor, and autonomic symptoms
caused by myofascial trigger points. The
Myotatic Unit: See Functional Unit.
specific muscle or muscle group that
causes the symptoms should be identified.
Occipitoatlantal joint: Junction of the oc-
2. (as sometimes confusingly used by oth-
ers) A regional pain syndrome of any soft ciput (C ) and the atlas ( C J , sometimes re-
0
3

tissue origin. To avoid confusion, we rec-


13 ferred to as the atlanto-occipital (joint). 5

ommend that when anyone uses the term


myofascial pain syndrome, that person Occlusal Disharmony: Occlusal contacts
should specify which meaning applies that interfere with centric occlusion of the
file general or specific definition. teeth or with functional mandibular excur-
sions from centric occlusion. ' 4 12

Myofascial Trigger Point (clinical defini-


tion of a central trigger point): A hyperirri- Palpable (Taut) Band: See Taut Band.
table spot in skeletal muscle that is associ-
ated with a hypersensitive palpable nodule Paradoxical (abnormal) Respiration: Si-
in a taut band. The spot is painful on com- multaneous expansion of the chest and
pression and can give rise to characteristic contraction of abdominal muscles that
referred pain, referred tenderness, motor pulls the abdomen inward during inhala-
dysfunction, and autonomic phenomena. tion. To be distinguished from coordinated
Types of myofascial trigger points include: (normal) respiration.
active, associated, attachment, central,
key, latent, primary, and satellite. (Note es- Passive Range of Motion: The extent of
pecially the distinction between central movement (usually tested in a given plane)
and attachment myofascial trigger points). of an anatomical segment at a joint when
Any myofascial trigger point is to be distin- movement is produced by an outside force
guished from a cutaneous, ligamentous, without voluntary assistance or resistance
periosteal, or any other nonmuscular trig- by the subject. The subject must relax the
ger point. muscles crossing the joint.

Myofascial Trigger Point (etiological defin- Pincer Palpation: Examination of a part by


ition of a central trigger point): A cluster of holding it in a pincer grasp between the
electrically active loci each of which is thumb and fingers. Groups of muscle fibers
associated with a contraction knot and a are rolled between the tips of the digits to
dysfunctional motor endplate in skeletal detect taut bands of fibers, to identify trig-
muscle. ger point nodules and tender spots in the

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6 Part 1 / Introduction

muscle, and to elicit local twitch re- point, which usually occur at a distance
sponses. To be distinguished from flat pal- from the trigger point.
pation and snapping palpation.
Release (of muscle tightness): Any proce-
Posterior: Toward the back of the body dure that reduces the resting muscle ten-
(dorsal); opposite of anterior. sion (or muscle stiffness).

Pressure Release: See Trigger Point Pres- Sagittal Plane: A vertical anteroposterior
sure Release. plane that divides the body into right and
left portions. The midsagittal plane divides
Primary Myofascial Trigger Point: A cen- the body into right and left halves.
tral myofascial trigger point that was ap-
parently activated directly by acute or Satellite Myofascial Trigger Point: A cen-
chronic overload, or repetitive overuse of tral myofascial trigger point that was in-
the muscle in which it occurs and was not duced neurogenically or mechanically by
activated as a result of trigger-point activity the activity of a key trigger point. Distin-
in another muscle. guishing the mechanism responsible for
the key-satellite relationship can rarely be
Prone: Lying face downward; opposite of resolved by examination alone. The rela-
supine. tionship usually is confirmed by simulta-
neous inactivation of the satellite when the
Proximal: Closer to the trunk or point of key trigger point is inactivated. A satellite
origin; opposite of distal. trigger point may develop in the zone of
reference of the key trigger point, in an
Reactive Cramp: Synonymous with short- overloaded synergist that is substituting for
ening activation. the muscle harboring the key trigger point
(key muscle), in an antagonist countering
Reference Zone: see Zone of Reference. the increased tension of the key muscle, or
in a muscle linked apparently only neuro-
Referred Autonomic Phenomena: Vaso- genically to the key trigger point. Previ-
constriction (blanching), coldness, sweat- ously, only a trigger point that developed in
ing, pilomotor response, ptosis, and/or hy- the referred pain zone of another trigger
persecretion that occur in a region separate point was identified as a satellite trigger
from the trigger point causing these phe- point.
nomena. The phenomena usually appear
in the same general area to which that trig- Scoliosis: Lateral curvature of the spine.
ger point refers pain.
Screening Palpation: Digital examination of
Referred (Trigger-Point) Pain: Pain that a muscle to determine the absence, or pres-
arises in a trigger point, but is felt at a dis- ence, of palpable bands and tender trigger
tance, often entirely remote from its points using flat and/or pincer palpation.
source. The pattern of referred pain is re-
producibly related to its site of origin. The Secondary Trigger Point: Term previously
distribution of referred trigger-point pain used, but rarely in this edition. Trigger
rarely coincides entirely with the distribu- points previously identified as secondary
tion of a peripheral nerve or dermatomal trigger points are now classified as satellite
segment. trigger points. A secondary trigger point
was previously identified as one that de-
Referred (Trigger-Point) Phenomena: Sen- veloped in a synergist or an antagonist of
sory and motor phenomena such as pain, the muscle harboring the key trigger point.
tenderness, increased motor unit activity
(spasm), vasoconstriction, vasodilatation, Shortening Activation: Activation of latent
and hypersecretion caused by a trigger myofascial trigger points by unaccustomed

Copyrighted Material
Chapter 1 / Glossary 7

shortening of a muscle during stretch ther- plied force." 3. A force that tends to pro-
11

apy of its antagonist. An activated trigger duce distortion.


point increases tension of its muscle and
can cause severe referred pain. Square Brackets [ ]: In this volume square
brackets identify comments or interpreta-
Shoulder Joint: Glenohumeral joint. tions by the authors.

Stripping Massage (Deep-stroking Mas-


Snapping Palpation: A fingertip is placed sage): As described in Chapter 3 Section 12.
against the tense band of muscle at right
angles to the direction of the band and sud- Suboccipital Decompression: A tension-re-
denly presses down while the examiner lease procedure for the upper cervical re-
draws the finger back so as to roll the un- gion. It is performed with the patient in the
derlying fibers under the finger. (The mo- supine position and the examiner's finger-
tion is similar to that used to pluck a gui- tips placed in the suboccipital recess bilat-
tar string, except that the finger does not erally; initially, pressure is applied anteri-
slide over the skin but moves the skin with orly (toward the ceiling) so as to induce
it.) To most effectively elicit a local twitch regional extension at the OA, C and Clf 2

response, the band is palpated and junctions. Then traction is applied in a


snapped at the trigger point, with the mus- cephalad direction.
cle positioned to eliminate slack. To be dis-
tinguished from flat palpation and pincer Superficial: Closer to the surface; opposite
palpation. of deep.

Superior: Toward the vertex of the head;


Spasm: Increased tension with or without usually synonymous with cephalad; oppo-
shortening of a muscle due to nonvolun- site of inferior.
tary motor nerve activity. Spasm is identi-
fied by motor unit potentials that cannot be Supination: A movement of the forearm
terminated by voluntary relaxation. To be that positions the palm anteriorly when the
distinguished from contracture. body is in the anatomical position.

Supine: Lying face upward; opposite of


Spillover Pain Zone (Area): The region
prone.
where some, but not all, patients experi-
ence referred pain beyond the essential Synergistic Muscles: Muscles that rein-
pain zone, due to greater hyperirritability force or complement each other when they
of a trigger point. The spillover zone is contract.
indicated by red stippling in the pain-
pattern figures. To be distinguished from Taut Band: The group of tense muscle
an essential referred pain zone that is fibers extending from a trigger point to the
solid red. muscle attachments. The tension of the
fibers is caused by contraction knots that
Strain: Tissue and psychological reaction are located in the region of the trigger point.
to prolonged stress. Reflex contraction of the fibers in this band
produces the local twitch response.
Stretch: Any procedure that elongates the Thoracic Outlet: The triangular aperture
muscle fibers. With trigger points, the goal bounded anteriorly by the scalenus ante-
of the procedure is to release the increased rior muscle, posteriorly by the scalenus
muscle tension by elongating the shortened medius muscle, and interiorly by the first
sarcomeres of contraction knots. rib. Some other authors include all of the
superior opening of the thoracic cage.
Stress: 1. A physical or psychological over-
load that produces a tissue or psychologi- Transverse Plane: A horizontal plane that
cal reaction. 2. "The resisting force set up divides the body into upper and lower
in a body as a result of an externally ap- portions.

Copyrighted Material
8 Part 1 / Introduction

TriggerArea:Sometimesusedinthisvolumeas Zone of Reference: The specific region of the


synonymouswithanattachmenttriggerpoint. bodyata distancefromatriggerpoint,where
phenomena (sensory, motor, and/or
Trigger Point (Trigger Zone, Trigger Spot, autonomic) caused by the trigger point are
TriggerArea):SeeMyofascialTriggerPoint. observed.

TriggerPoint PressureRelease:Applicationof
slowly increasing, nonpainful pressure over a REFERENCES
trigger point until a barrier of tissue resistance 1. Clemente CD. Grays Anatomy, 30th ed. Philadelphia:
isencountered.Contactisthenmaintaineduntil Lea&Febiger,1985:466469,472(Fig.621).
the tissue barrier releases, and pressure is 2. GreenmanPE.PrinciplesofManualMedicine.Baltimore:
increasedtoreachanewbarriertoeliminatethe Williams&Wilkins,1996:99.
3. Ibid.(p.175).
triggerpointtensionandtenderness.Inthisedi 4. MahanPE.Personalcommunication,1981.
tion, Trigger Point Pressure Release replaces the 5. MaigneR.DiagnosisandTreatmentofPainofVertebral
term Ischemic Compression that was used in the Origin: A Manual Medicine Approach. Baltimore:
first edition. Other versions (some of which are Williams&Wilkins,1996:5455.
painful) are identified elsewhere as Acupressure, 6. McDonoughJTJr.StedmansConciseMedicalDic
tionary,2nded.Baltimore:Williams&Wilkins,
Myotherapy,Shiatzu,andasThumbTherapy. 1994:141.
7. Ibid,(p.339).
Trigger Point Release: Release of muscle 8. Ibid.(p.659).
tension by inactivating the trigger points that 9. Ibid.(p.664).
10. Ibid.(p.793).
are causing the taut bands which are
11. Ibid.(p.966).
responsible for the increased tension. 12. ShaberEP.Personalcommunication,1981.
ManymethodsofreleasearedescribedinSection12 13. SimonsDG.Myofascialpainsyndrome:onetermbut
ofChapter3. twoconcepts:anewunderstanding[editorial].
JMusculoskePain1995;3(1):713.

Copyrighted Material
Acronyms

AA: atlantoaxial (joint). GOT: glutamic oxaloacetic transaminase

ACh: acetylcholine GPT: glutamic pyruvate transaminase

ATP: adenosine triphosphate h: Hour

ATPase: adenosine triphosphatase HTC II: holo-transcobalamin II

ATrP: attachment trigger point Hz: Hertz (frequency)

C: centigrade (degrees) INH: isonicotinic acid hydrazide (isoni-


azid)
C : second cervical spinal nerve
2

IP: Interphalangeal (joint)


Ca : ionized calcium
2+

Kilo: kilogram
CBC: complete blood count
kg: Kilogram, a unit of weight equal to
Cbl: cobalamin (vitamin B ) 12
1,000 grams; approximately 2.2 pounds.

CK: creatine kinase LLLI: lower limb-length inequality


cm: centimeter
LTR: local twitch response
CTrP: central trigger point
m: Meter, a defined measure of distance;
approximately 39 inches.
DNA: deoxyribonucleic acid
MCP: metacarpophalangeal (joint)
EMG: electromyographic
MCV: mean corpuscular volume
ESR: erythrocyte sedimentation rate

ETK: erythrocyte transketolase Me-Cbl: methylcobalamin

F: Fahrenheit (degrees) Meq: milliequivalent

FIGLU: formiminoglutamate Me-THF: methyltetrahydrofolate

FMS: fibromyalgia syndrome mg: milligram (1/1,000 of one gram)

FT : free triiodothyronine
3
Mg: magnesium

FT : free levothyroxine
4 (Mg): magnesium concentrations

g: gram mg/dl: milligrams per decaliter

GABA: gamma aminobutyric acid MIU/L: milli international units per liter

Copyrighted Material
10 Part 1 / Introduction

mm: Millimeter, 1/1,000 of a meter; ap TM:temporomandibular


proximately1/25inch.
TMD:temporomandibulardisorders
Mm: millimolar (0.001 moles of solute per liter
ofsolution)
TMJ:temporomandibularjoint
MP:metacarpophalangeal(joint)
TOS:thoracicoutletsyndrome
MPD:myofascialpaindysfunction(syndrome)

MPS:myofascialpainsyndrome TPP:thiaminepyrophosphate

msec/div: milliseconds per division (of sweep


TRH:thyrotropinreleasinghormone
speed)
ng/ml: nanogram per milliliter (109 or TrP:triggerpoint
1/1,000,000,000ofonegram)
TrPs:triggerpoints
OA:occipitoatlantal(joint)

oz: ounce TSH:thyroidstimulatinghormone

pg/ml: picograms per milliliter (1012 or (jisec:microsecond,or0.001sec


1/1,000,000,000,000ofonegram)

PSIS:posteriorsuperioriliacspine (xV: microvolt, a measure of electrical ]


tential:106volt,or0.0000001volt
RBC:redbloodcell

RDA:recommended(required)dailyallowance
RDG:RobertD.GerwinRDI:recommended
dietaryintakeSEA:spontaneouselectrical
activitySI:Sacroiliac(joint)
SR: sarcoplasmic reticulum (see Figs. 2.5 and
2.13) sTSH: sensitive thyrotropin (test) T3:
3,5,3triiodothyronineT4:levothyroxine

T:fourththoracicvertebraorspinalnei

TBG:thyroxinebindingglobulin

THF:tetrahydrofolate

Copyrighted Material
CHAPTER 2
General Overview

HIGHLIGHTS: BACKGROUND (Section A) sum- an active TrP for general clinical use are circum-
marizes the prevalence and importance of myo- scribed spot tenderness in a nodule of a palpable
fascial trigger points (TrPs) and then reviews their taut band and patient recognition of the pain
place in the medical literature of this century. evoked by pressure on the tender spot as being
Many overlapping and some confusingly similar familiar. The DIFFERENTIAL DIAGNOSIS and
conditions currently identify muscle pain syn- CONFUSIONS section lists many conditions
dromes. Clear distinctions are important. The mimicked by TrPs. It emphasizes the importance
most distinctive CLINICAL CHARACTERISTICS of understanding and examining for the distin-
OF TRIGGER POINTS (Section B) are a history of guishing characteristics of fibromyalgia and artic-
pain related to muscular activity and characteris- ular dysfunctions as compared to myofascial
tic physical findings. Examination of the muscle TrPs. MUSCLE STRUCTURE AND FUNCTION
reveals circumscribed spot tenderness in a nod- (Section C) examines the motor unit, motor end-
ule that is part of a palpably tense band of mus- plate zone, and neuromuscular junction in some
cle fibers, patient recognition of the pain evoked detail. It updates an understanding of muscle
by pressure on the tender spot as being familiar, pain. NATURE OF TRIGGER POINTS (Section D)
pain referred in the pattern characteristic of TrPs first reviews the newly discovered Electrodiag-
in that muscle, a local twitch response (LTR), nostic Characteristics of Trigger Points which in-
painful limitation of stretch range of motion, and clude the demonstration of spontaneous electri-
some weakness of that muscle. Promising TEST- cal activity and spikes at active loci that are
ING methods that demonstrate the presence of closely associated with dysfunctional motor end-
TrPs include a specific needle electromyographic plates. Then it presents the newly identified His-
(EMG) technique, ultrasound, surface EMG, al- togenesis of Trigger Points that recognizes con-
gometry, and thermography. Referred motor dys- traction knots as the key feature which apparently
functions during activity can be tested using sur- are closely related to active loci. This leads to an
face EMG techniques. Appropriate TREATMENT Integrated Hypothesis of Trigger Points that pos-
of patients for TrPs may involve many forms of tulates a local energy crisis which results from the
stretch, several techniques to augment muscle dysfunctional endplates at active loci. Other Hy-
release, injection of TrPs, management of perpet- potheses are considered unlikely. The extensive
uating factors, and a home self-treatment pro- research on the Local Twitch Response is sum-
gram. Recommended DIAGNOSTIC CRITERIA of marized.

A. BACKGROUND 12 C. MUSCLE STRUCTURE AND FUNCTION 45


Prevalence 12 Muscle Structure and Contractile Mechanism . . . .45
Importance 13 The Motor Unit 47
Historical Review 14 The Motor Endplate Zone 49
Related Diagnostic Terms 18 Neuromuscular Junction 53
B. CLINICAL CHARACTERISTICS OF TrPS 19 Muscle Pain 54
Symptoms 19 D. NATURE OF TRIGGER POINTS 57
Physical Findings 21 Electrodiagnostic Characteristics of Trigger Points 57
Testing 22 Histopathological Characteristics of Trigger Points 67
Treatment 30 Integrated Trigger Point Hypothesis 69
Diagnostic Criteria 31 Other Hypotheses 78
Differential Diagnosis and Confusions 35 Local Twitch Response 82

11

Copyrighted Material
12 Part 1 / Introduction

A. BACKGROUND In an internal medicine group prac-


tice, 54 of 172 patients presented with a
257

Prevalence pain complaint. Sixteen [30%] of the pain


Myofascial trigger points (TrPs) are ex- patients met the criteria for myofascial
tremely common and become a painful TrPs. Four of these sixteen patients had
part of nearly everyone's life at one time or pain duration of less than 1 month, three
another. Latent TrPs, which often cause had pain for 1 to 6 months, and nine had
motor dysfunction (stiffness and restricted pain duration of more than 6 months.
range of motion) without pain, are far more A neurologist examining 96 patients
common than the active TrPs, which in ad- from a community pain medical center 90

dition cause pain. found that 9 3 % had at least part of their


Among 200 unselected, asymptomatic pain caused by myofascial TrPs and in
young adults, Sola, et a/. found focal ten-
261 7 4 % , myofascial TrPs were considered the
derness representing latent TrPs in the primary cause of the pain.
shoulder-girdle muscles of 5 4 % of the fe- Among 283 consecutive admissions to a
male, and 4 5 % of the male subjects. Referred comprehensive pain center, a primary or-
pain was demonstrated in 2 5 % of these sub- ganic diagnosis of myofascial syndrome was
jects with latent TrPs. A recent study of 269 assigned in 8 5 % of cases. A neurosurgeon
80

unselected female student nurses with or and a physiatrist made this diagnosis inde-
without pain symptoms showed a similar
228
pendently, based upon physical examina-
high prevalence of TrPs in masticatory mus- tion "as described by Simons and Travell." 255

cles. A TrP was identified by palpating a taut Of 164 patients referred to a dental
band for spot tenderness of sufficient sensi- clinic for chronic head and neck pain of at
tivity to cause a pain reaction. No effort was least 6 months duration, 5 5 % were found
made to distinguish active and latent TrPs, to have a primary diagnosis of myofascial
but a considerable number of TrPs were pain syndrome caused by active TrPs. 83

likely active because 2 8 % of subjects were Five lumbogluteal muscles of 97 patients


aware of pain in the temple area. In mastica- complaining of pain in the locomotor system
tory muscles, TrPs were found in 5 4 % of were examined in an orthopedic clinic. 84

right lateral pterygoid muscles, in 4 5 % of Forty-nine percent of the patients presented


right deep masseter, in 4 3 % of right anterior with latent TrPs and 2 1 % presented with ac-
temporalis, and in 4 0 % of intraoral exami- tive TrPs in the piriformis muscle.
nations of the right medial pterygoid mus- The wide range in prevalence of myo-
cle. Among the neck muscles, TrPs were fascial pain caused by TrPs that is reported
identified in 3 5 % of the right splenius capi- in different studies is likely due in part to
tis muscles and in 3 3 % of right upper trape- differences in the patient populations ex-
zius muscles. The insertion of the right up- amined and in the degree of chronicity.
per trapezius was also tender in 4 2 % of Probably even more important are differ-
those muscles with TrPs. Enthesopathy of ences in the criteria used to make the diag-
this muscle was common. 228
nosis of myofascial TrPs and, most impor-
Frohlich and Frohlich examined 100
84 tant, differences in the training and skill
asymptomatic control subjects for latent level of the examiners. Few of these stud-
TrPs in lumbogluteal muscles. They found ies gave a detailed description of the diag-
latent TrPs in the following muscles: qua- nostic examinations employed. A sum-
dratus lumborum (45% of patients), glu- mary of prevalence excluded papers that
242

teus medius (41%), iliopsoas (24%), glu- used the general definition 241
of a myo-
teus minimus (11%), and piriformis (5%). fascial pain syndrome. Active myofascial
Reports of the prevalence of myofascial TrPs are clearly very common and are a
TrPs in specific patient populations are major source of musculoskeletal pain and
available and, together, indicate a high dysfunction, but poor agreement on appro-
prevalence of this condition among indi- priate diagnostic criteria has been a serious
viduals with a regional pain complaint. handicap. A study has critically tested in-
The reports that follow are summarized in terrater reliability for 5 manual examina-
Table 2.1. tions in 5 different muscles among four
94

Copyrighted Material
Chapter 2 / General Overview 13

Table 2.1. Prevalence of Trigger Point Pain in Selected Patient Populations


Number % with
Region Practice Studied Myofascial Pain Source

General Medical 172(54) 30% Skootsky, etal., 1 9 8 9 257

General Pain Med. Center 96 93% Gerwin, 1995 90

General Comprehensive Pain 283 85% Fishbain, etal., 1986 80

Center
Craniofacial Head & Neck Pain Clinic 164 55% Fricton, etal., 1985 83

Lumbogluteal Orthopedic Clinic 97 21% Frohlich and Frohlich, 1995 84

experienced and trained examiners. The managers, dentists,


221
family
83, 102, 140, 271

study demonstrated good to excellent practitioners, gynecologists, neurol-


184204 213

agreement for all muscles and for all exam- ogists, nurses, orthopedic surgeons,
87 25 6,10,

inations except for one examination, 46


pediatricians, physical therapists,
1168 199,

which was not highly reliable for all mus- 200


physiatrists, rheumatolo-
31,139,219,220,223

cles tested. gists, and veterinarians.


82,89,215 143

In a population of hospitalized and ambu- Yet the muscles in general and TrPs in
latory Physical Medicine and Rehabilitation particular receive little attention as a major
Service patients with the fibrositis syndrome source of pain and dysfunction in modern
(mostly TrPs), the greatest number were be- medical school teaching and in medical
tween 31 and 50 years of age. These data
155
textbooks. This manual describes a ne-
agree with our clinical impression that indi- glected, major cause of pain and dysfunc-
viduals in their mature years of maximum tion in the largest organ of the body. The
activity are most likely to suffer from the contractile muscle tissues are a primary
pain syndromes of active myofascial TrPs. target of the wear and tear of daily activi-
With the reduced activity of more advanced ties, but it is the bones, joints, bursae and
age, the stiffness and restricted range of mo- nerves on which physicians usually con-
tion of latent TrPs tend to become more centrate their attention.
prominent than the pain of active TrPs. Severity. The severity of symptoms
caused by myofascial TrPs ranges from the
Importance
agonizing incapacitating pain caused by
Voluntary (skeletal) muscle is the largest very active TrPs to the painless restriction
single organ of the human body and ac- of movement and distortion of posture due
counts for nearly 5 0 % of body w e i g h t . 939173
to latent TrPs that are so commonly over-
The number of muscles counted in the body looked. The potential severity of pain from
depends on the degree of subdivision that is acute activation of a TrP is illustrated by
considered one muscle and on the number of one housewife who, while bending over
variable muscles that are included. Not cooking, activated a quadratus lumborum
counting heads, bellies, and other divisions TrP that felled her to the kitchen floor and
of muscles, the Nomina Anatomica reported caused pain so severe that she was unable
by the International Anatomical Nomencla- to reach up and turn the stove off to prevent
ture Committee under the Berne Conven- a pot from burning through its bottom. The
tion, lists 200 paired muscles, or a total of
136
patients with myofascial TrP pain in a gen-
400 muscles. Any one of these muscles can eral medicine practice reported visual ana-
develop myofascial TrPs that refer pain and log scale ratings of pain as high as or higher
motor dysfunction, often to another location. than pain due to other causes . 257

The clinical importance of myofascial Patients who have had other kinds of se-
TrPs to practitioners has been described in vere pain, such as that due to a heart at-
the literature for acupuncturists, 111, 187,
tack, broken bones, or renal colic, say that
anesthesiologists, -
208 23,
chronic pain
260
the myofascial pain from TrPs can be just

Copyrighted Material
14 Part 1 / Introduction

as severe. Despite their painfulness, myo- just beginning to sort out this complex
fascial TrPs are not directly life threaten- puzzle. One way of clarifying what TrPs
ing, but their painfulness can, and often are clinically is to define more clearly what
does, devastate the quality of life. they are not and how other diagnoses are
Cost. Unrecognized myofascial head- related. Major progress has been made this
ache, shoulder pain and low back pain that past decade by clearly distinguishing a
have become chronic are major causes of in- central cause of muscle pain and tender-
dustrial lost time and compensation applica- ness, fibromyalgia, from the primarily mus-
tions. Bonica pointed out that disabling
21 cular dysfunction, TrPs. The relation be-
chronic pain costs the American people bil- tween articular dysfunction that responds
lions of dollars annually. Low back pain to manual therapy and TrPs remains to be
alone costs the people of California $200 as clearly delineated. The updated re-
million annually. Analgesics to relieve view shows that repeatedly, an author or
238

chronic pain are costly and can be a signifi- the adherents to a school of thought will
cant cause of nephropathy. A considerable
97 concentrate on part of the total clinical pic-
portion of the chronic pain due to myofascial ture of myofascial TrPs, introduce a new
TrPs could have been prevented by prompt name, and overlook the rest of the picture.
diagnosis with appropriate treatment. Froriep is a pre-twentieth century au-
85

How many more people not included in thor who identified Muskel Schwiele as ex-
these studies do carry on, yet bear the misery tremely tender, palpable hardenings in mus-
of nagging TrP pain that would respond if it cles that, when treated, afforded the patient
were diagnosed and treated for what it is? much pain relief. By the turn of the century
When the myofascial nature of pain is un- Adler, in America, used the English term
2

recognized, such as the pain caused by TrPs muscular rheumatism and included the
in the pectoral muscles that mimics cardiac concept of pain radiating from the tender
pain, the symptoms are likely to be diag- spot. In England, Gowers, Stockman,101 264

nosed as neurotic, psychogenic, or behav- and Llewellyn and Jones introduced the
172

ioral. This adds frustration and self-doubt to term fibrositis for the same symptom com-
the patient's misery and blocks appropriate plex. In Germany, Schmidt used the Ger- 229

diagnosis and treatment. Active myofascial man counterpart to muscular rheumatism,


TrPs are largely responsible for that enig- Muskelrheumatismus. Other authors used
matic scourge of mankind, musculoskeletal the term Weichteilrheumatismus literally
pain. The total cost is incalculable, but enor- "soft-parts rheumatism" which is com-
mous, and most of it is unnecessary. monly translated into English as nonarticu-
lar rheumatism. The cause of the diagnosis
Historical Review remained controversial in every case.
The history of growth in our under- In 1919, Schade reported that the
226

standing of musculoskeletal pain is the hardness of previously tender ropiness in


history of the identification of specific muscles persisted during deep anesthesia
sources and causes of pain, including neu- and after death until rigor mortis obscured
ropathic sources, articular dysfunction, the difference. This finding discredited a
muscular origins, and modulation of cen- nerve-activated, muscular contraction
tral nervous system processing of pain. mechanism as the cause of the palpable
The history of muscle pain was reviewed bands, but is consistent with an endoge-
for much of this c e n t u r y ' and recently
216 235
nous contracture of sarcomeres being re-
has been updated. 238
sponsible. Schade later postulated a lo-
227

This review identifies, and Table 2.2


235 calized increase in the viscosity of muscle
lists, a number of historically noteworthy colloid and proposed the term "Myo-
publications that provide a background to gelosen," literally translated as "muscle
our present understanding of myofascial gellings" and identified in English as myo-
pain caused by TrPs. Progress has been gelosis. In the same year, two orthopaedic
slow and spotty. Pain and/or tenderness of surgeons in Munich, F. Lange and G.
the muscles may have distinctly different Eversbusch described tender points as-
163

causes that can produce confusingly simi- sociated with regions of palpable hardness
lar symptoms. The medical community is in muscles, that they termed "Muskel-

Copyrighted Material
Chapter 2 / General Overview 15

Table 2.2. Historical Muscle Pain Papers


Authorship, Year,
Term Used Muscular Findings & Reference

Muskelschwiele [Mus- Tender tight cord or band Froriep, 1843 85

cle callus]
Muscular rheumatism Tender, elongated infiltrations, radiating pain Adler, 1900 2

Fibrositis Tender fibrous beaded chains Gowers, 1 9 0 4 101

Chronic rheumatism Nodules: histologically, inflamed connective Stockman, 1 9 2 0 264

tissue
Fibrositis, Myofibrositis Tender nodules with radiating pain Llewellyn and Jones,
1915 172

Muskelrheumatismus, Tender, contracted muscle bundles Schmidt, 1 9 1 6 229

Myalgie [muscular
rheumatism, myalgia]
Myogelose [muscle Tender muscle indurations (persisted after Schade, 1.919 226

gelling] death)
Muskelharten [muscu- Tender indurations with or without muscular F. Lange, 1 9 2 5 162

lar indurations] contraction


Muskelharten, Myo- The first "trigger point manual;" referred pain M. Lange, 1 9 3 1 164

gelosen [muscular in- not mentioned


durations or gelling]
Muskelharten [muscu- Introduction of ethyl chloride spray Kraus, 1 9 3 7 156

lar indurations]
Referred pain Experimental demonstration of pain referred Kellgren, 1 9 3 8 149

from muscle
Muscular rheumatism Spot tenderness in indurated region, pain reac- Gutstein, 1 9 3 8 112

tion, and referred pain


Idiopathic myalgia Spot tenderness, referred pain, decreased Travell, era/., 1 9 4 2 276

ROM (her first description of TrPs)


Fibrositis Tender nodule, referred pain Kelly, 1 9 4 1
151

Myofascial TrPs Tender spot, referred pain, 32 pain patterns Travell, R, 1 9 5 2 278

Myofascial TrPs Early recognition of importance of TrPs in pa- Bonica, 1953 20

tients with pain


Trigger Areas Electromyographic activity of trigger areas first Weeks and Travell,
reported 1957 288

Fibrositissyndrom [fi- Reported non-specific dystrophic pathology in Miehlke, era/., I 9 6 0 1 9 3

brositis syndrome] more severe cases


Fibrositis syndrome Generalized chronic pain with multiple tender Smythe and Moldofsky
points (redefinition) 1977 258

Fibromyalgia Renamed the 1977 redefinition of fibrositis Yunus, era/., 1 9 8 1 300

Myofascial TrP Publication of Volume 1 of the Trigger Point Travell and Simons,
Manual 1983 279

Pressure pain Introduction of an algometer for measuring Fischer, 1986 72

threshold trigger point tenderness


Fibromyalgia Official diagnostic criteria for fibromyalgia Wolfe, era/., 1 9 9 0 294

Myofascial TrPs Publication of Volume 2 of the Trigger point Travell and Simons,
Manual 1992 280

Myofascial TrPs Electromyographic activity characteristic of Hubbard and Berkoff,


TrPs reported 1993 133

Localized twitch re- Value of the rabbit as an experimental model Hong and Torigoe,
sponse for the local twitch responses characteristic of 1994 128

myofascial TrPs

Copyrighted Material
16 Part 1 / Introduction

Table 2.2. Historical Muscle Pain Papers (Continued)


Authorship, Year,
Term Used Muscular Findings & Reference

Active Loci Use of the rabbit as an experimental model to Simons, etal., 1995 249

study the elecrical activity of TrPs


Myofascial TrPs New research data for selection of diagnostic Simons, 1996 242

criteria; experimental basis for the new dys-


functional endplate hypothesis
Myofascial TrPs Interrater reliability; identified TrP diagnostic Gerwin, etal., 1997 94

criteria
Myofascial TrPs Identification of likely pathogenesis Simons, 1997 244

harten," literally translated into English as treme tenderness in that band, reproduc-
"muscle hardenings" or "indurations." In tion of the patient's distant pain complaint
1925, F. Lange described the local twitch
162
by digital pressure on that spot, and relief
response. His student, M. Lange, " later 1 4
of the pain by massage or injection of the
equated these muscle hardenings to tender spot. Each author reported pain syn-
Schade's myogeloses. M. Lange used fin- dromes of specific muscles throughout the
gers, knuckles, or a blunt wood probe to body in large numbers of patients. All
apply forceful, ecchymosis-producing three had identified myofascial TrPs. How-
massage (Gelotripsie). His comprehensive ever, each used different diagnostic terms,
clinical book also presented the history
164
were apparently unaware of one another,
and experimental basis of the concept of and the commonality of their observations
myogeloses (prior to the discovery of the passed unnoticed for decades.
actin-myosin contractile mechanism). This One of the three, Michael Gutstein, was
work essentially ignored the referred pain born in Poland and first published as Gut-
aspect of TrPs. stein from Berlin, then Gutstein-Good and
Before coming to the United States from finally as Good from Great Britain. In the
Germany, Hans Kraus, who was an early 12 or more papers that he published in
pioneer in this field, first reported the ther- Britain between 1 9 3 8 112
and 1957, he 99

apeutic use of ethyl chloride spray, for re- used many diagnostic terms to describe the
lief of Muskelharten in 1 9 3 7 , and for the
156
same condition: myalgia, idiopathic myal-
relief of fibrositis in 195 2 , and for the re-
157
gia, rheumatic myalgia, and nonarticular
lief of TrPs in 1 9 5 9 . He continued to pro-
158
rheumatism. He illustrated the referred
mote the importance of exercise and TrPs pain patterns of many patients as case re-
until his recent death. ports. He repeatedly held that the process
In 1938, Kellgren, working under the
149 responsible for the "myalgic spots" was a
influence of Sir Thomas Lewis, published a local constriction of blood vessels due to
major milestone paper. He established un- overactivity of the sympathetic fibers sup-
equivocally for most major postural mus- plying the vessels.
cles of the body that each muscle and Michael Kelly lived and published in
many fascial structures had a characteristic Australia. Throughout his series of nearly a
referred pain pattern when injected with a dozen papers, all on fibrositis between
small amount of painful salt solution. 1941 and 1 9 6 3 , he was impressed by
151 152

Shortly after this, three clinicians on three both the palpable hardness of the "nodule"
continents simultaneously and indepen- associated with the tender point in the
dently published a series of papers in Eng- muscle and by the distant referral of pain
lish emphasizing four cardinal features: a from the afflicted muscle. Kelly published
palpable nodular or band-like hardness in numerous case reports with referred pain
the muscle, a highly localized spot of ex- patterns. He gradually evolved the concept

Copyrighted Material
Chapter 2 / General Overview 17

that fibrositis was a functional, neurologi- different meaning to the many meanings
cal disturbance that originated at the myal- that had become associated with fibrosi-
gic lesion. He envisioned little or no local tis. The 1977 authors identified a con-
216 258

pathology, but a central nervous system re- dition of generalized pain marked by multi-
flex disturbance that caused the referred ple tender points when tested by palpation.
pain. Four years later, Yunus, et al. proposed 300

Janet Travell lived and published in the the term fibromyalgia as a more appropriate
United States. Her more than 40 papers on name for the 1977 redefinition of fibrositis.
myofascial TrPs have appeared between Since the diagnoses of either myofascial
1 9 4 2 and 1990, and the first volume of
276 275 TrPs or fibromyalgia now accounted for
The Trigger Point Manual was published in nearly all of the patients previously diag-
1983 followed by the second volume in nosed as having fibrositis, this became an
1992. She and Rinzler in 1952 reported the outmoded diagnosis. At that time, it was not
pain patterns of TrPs in 32 skeletal muscles, clear how closely the pathophysiology of fi-
as "The myofascial genesis of pain," 278 bromyalgia and TrPs related to each other;
which quickly became the classic source of the etiology of both was highly speculative.
this information. It was her opinion that any By 1990, rheumatologists under the
fibroblastic proliferation was secondary to a leadership of F. Wolfe officially estab-
294

local muscular dysfunction and that any lished diagnostic criteria for fibromyalgia.
pathologic changes occurred only after the The criteria were simple and the examina-
condition continued for a long time. She be- tion easily and quickly performed, which
lieved that the self-sustaining characteristic helped focus the attention of the medical
of TrPs depends on a feedback mechanism community on this syndrome. Since then,
between the TrP and the central nervous sys- remarkable progress has been made toward
tem. Of those three pioneers, only Travell's identifying its cause. It is now firmly estab-
influence withstood the test of time. lished that a central nervous system dys-
To date, only two biopsy studies are function is primarily responsible for the in-
known of sites selected specifically as creased pain sensitivity of fibromyalgia. 224

myofascial TrPs. One study reported


253
In the mid 1980s, A. F i s c h e r pro- 71,74

biopsies of TrPs in the leg muscles of dogs duced a pressure algometer that provided a
and the other reported findings in hu-
214
method for measuring the sensitivity of
man biopsies of myogelosis located at TrP myofascial TrPs and of fibromyalgia tender
sites. Biopsy studies of the tender nodule points.
of myogelosis or of fibrositis must have in- An important milestone of progress was
cluded many myofascial TrPs. The study reached by Hubbard and Berkoff in 1993
by Miehlke, et al. of the Fibrositissyn-
W3
when they convincingly reported needle
drom (fibrositis) was the most extensive EMG activity characteristic of myofascial
and thorough. They reported minimal find- TrPs. Weeks and Travell
133
had illus-
288

ings in mild cases and increasingly marked trated the phenomenon 36 years earlier.
nonspecific dystrophic findings in progres- The following year Hong and Torigoe 128

sively more symptomatic cases. If the demonstrated that the rabbit was a suitable
pathophysiology of TrPs is primarily a dys- experimental model for studying the LTR
function in the immediate region of indi- that is characteristic of human TrPs. In
vidual motor endplates, there is no reason 1995, Simons, et a i . confirmed in rabbit
248

to expect routine histological studies to re- experiments the electrical activity reported
veal the cause. However, a recent histolog- by Hubbard and Berkoff. These rabbit
ical study of the palpable nodules associ- studies, and a concomitant human
ated with myogelosis at TrP sites found study, strongly implicated a dysfunc-
249

substantiating evidence of contracture of tional endplate region as the prime site of


some individual muscle fibers. 214
TrP pathophysiology. 242

Throughout most of this century, the Another important step of progress was
term fibrositis described a condition that the report by Gerwin, et al. * of an inter-
9

was compatible with myofascial TrPs, al- rater reliability study that demonstrated
though ambiguously s o . In 1977, Smythe
216
reliable identification of myofascial TrP
and Moldofsky added another and very
258
criteria in 5 muscles. The integrated hy-

Copyrighted Material
18 Part 1 / Introduction

pothesis found in section D of this chapter ule. The diagnosis was completely redefined
moves our understanding of TrPs another in 1977, and the condition described by
258

major step forward. 244


the 1977 definition was officially estab-
lished in 1990 as fibromyalgia. According
294

Related Diagnostic Terms to the current definition of fibromyalgia, it is


The cause of muscle pain syndromes and a totally different condition that is unrelated
of musculoskeletal pain in general, has per- to the original concept of fibrositis. Fibrosi-
plexed the medical community for more tis is currently an outmoded diagnosis.
than a century. The subject has been Muskelharten. By 1921 the term
plagued by a multitude of terms that em- Muskelharten was well recognized in
3

phasized different aspects of basically the German literature and still appears in Ger-
same condition and that were reported in
235
man occasionally, but rarely in English. It
different languages. A brief review of some literally means "muscle indurations" and
of the more important diagnostic terms cur- refers to the palpable firmness of the tender
rently encountered will help to put the nodule responsible for the patient's pain.
available literature into perspective. Another German term, Myogelosen (liter- 4

Anatomically Oriented Terms. Through ally "muscle gellings") refers to the same
the years, many authors "discovered" a phenomena and the two terms have fre-
"new" muscle pain syndrome related to a quently been used interchangeably. The
specific part of the body and gave it a name term Muskelharten is often used to charac-
corresponding to that region. Characteristi- terize the physical findings and the term
cally, unrecognized myofascial TrPs con- Myogelosen to identify the diagnosis.
tributed significantly to the pain syndrome Myofascial Pain Syndrome. This term
identified. Common examples are tension has acquired both a general and a specific
headache, 140, 272,
occipital neuralgia,
287 103
meaning. The two meanings need to be dis-
the scapulocostal s y n d r o m e , and
192,203,204
tinguished. The general meaning in-
241

tennis elbow [see Chapter 36). cludes a regional muscle pain syndrome of
Fibromyalgia. Fibromyalgia is funda- any soft tissue origin that is associated with
mentally a different condition than TrPs, muscle t e n d e r n e s s and is commonly
160,298

but often presents with symptoms that are used in this sense by dentists. The other
14

confusingly similar to those caused by meaning is specifically a myofascial pain


chronic myofascial TrPs. Fibromyalgia is syndrome caused by TrPs. This is a focal hy-
characterized by a central augmentation of perirritability in muscle that can strongly
nociception which causes generalized modulate central nervous system functions
deep tissue tenderness that includes mus- and is the subject of this book.
cles. It has a different etiology than myo- Myofascitis. The term myofascitis is now
fascial TrPs but many of the tender points rarely (and should not be) used as synony-
diagnostic of fibromyalgia are also com- mous with myofascial TrPs. Myofascitis is
mon sites for TrPs and many patients have properly used to identify inflamed muscles.
both conditions. In the German literature, Myogeloses. The term myogeloses is the
fibromyalgia is usually equated with Gen- English form of a German term, Myogelosen,
eralizierte Tendomyopathie (generalized which is still commonly used and is gener-
tendomyopathy). Fibromyalgia is consid- ally considered synonymous with Muskel-
ered in more detail later in this chapter. harten [see above). The name myogeloses
Fibrositis. The term fibrositis appeared was based on an outmoded hypothesis to ac-
in the English literature in 1 9 0 4 and was
101 count for muscle contraction that was pro-
soon adopted into German as the Fibrositis- posed before the actin-myosin contractile
syndrom. For most of the century, fibrositis mechanism was discovered. A recent
was characterized by a tender palpable "fi- study indicates that myogeloses and TrPs
214

brositic" nodule by most of the authors us- identify the same condition approached
ing the term fibrositis. Many of these pa- from somewhat different diagnostic points
tients had TrPs. In time, fibrositis became an of view using different terminology.
increasingly controversial diagnosis be- Nonarticular Rheumatism. /Monarticu-
cause of multiple definitions and no satis- lar rheumatism is a commonly used, but
factory histopathological basis for the nod- not very clearly defined, general term for

Copyrighted Material
Chapter 2 / General Overview 19

soft tissue pain syndromes that are not as- complicated, more painful, and it becomes
sociated with a specific joint dysfunction or increasingly time-consuming, frustrating,
disease. The term is generally considered and expensive to treat.
as synonymous with soft tissue rheuma-
tism, which is the English translation for Symptoms
the German term Weichteilrheumatismus. Active TrPs produce a clinical complaint
This term was commonly used to describe (usually pain) that the patient recognizes
a range of conditions that also include myo- when the TrP is digitally compressed. La-
fascial pain caused by TrPs. Currently, the tent TrPs can produce the other effects char-
term nonarticular rheumatism is used to 218
acteristic of a TrP including increased mus-
identify muscle pain syndromes that are cle tension and muscle shortening (but do
not fibromyalgia and are not attributed to not produce spontaneous pain). Both active
myofascial TrPs. The literature reviews of and latent TrPs can cause significant motor
nonarticular rheumatism by Romano in- 218
dysfunction. It appears that the same fac-
clude conditions such as adhesive capsuli- tors which are responsible for the develop-
tis, periarticular arthritis, bursitis, epi- ment of an active TrP, to a lesser degree, can
condylitis, insertion tendinosis, and tennis cause a latent TrP. An active key TrP in one
elbow, which are frequently myofascial muscle can induce an active satellite TrP in
TrPs masquerading as another diagnosis. another muscle. Inactivation of the key TrP
Osteochondrosis. This term is used by often also inactivates its satellite TrP with-
Russian vertebroneurologists as an inclu- out treatment of the satellite TrP itself.
sive term to cover the interaction of neural Onset. The activation of a TrP is usually
and muscular conditions, such as fi- associated with some degree of mechanical
bromyalgia, myofascial TrPs, and spinal abuse of the muscle in the form of muscle
nerve compromise. overload, which may be acute, sustained,
Soft Tissue Rheumatism. This term is and/or repetitive. In addition, leaving the
usually used synonymously with nonartic- muscle in shortened position can convert a
ular rheumatism, described above. latent TrP to an active TrP and this process is
Tendomyopathy. Tendomyopathy is greatly aggravated if the muscle is con-
the English version of the German term tracted while in the shortened position. In
that is divided into general and local cate- paraspinal (and very likely other) muscles, a
gories. General tendomyopathy is consid- degree of nerve compression that causes
ered synonymous with fibromyalgia. The 65 identifiable neuropathic electromyographic
localized form often includes myofascial changes is associated with an increase in the
TrPs but is not as clearly defined. numbers of active TrPs. These TrPs may be
37

activated by disturbed microtubule commu-


B. CLINICAL CHARACTERISTICS OF nication between the neuron and the end-
TRIGGER POINTS plate since the motor endplate is the periph-
The clinical characteristics of TrPs un- eral core TrP pathophysiology.
der the headings of symptoms, physical The patient is aware of the pain caused
findings, and treatment are introduced and by an active TrP but may or may not be
presented only in overview in this section. aware of the dysfunction it causes. Latent
The rationale for each physical finding is TrPs characteristically cause some in-
noted in that subsection. Testing tech- creased muscle tension and limitation of
niques that are useful for experimental stretch range of motion, which often es-
purposes and some that have potential rou- capes the patient's attention or is simply
tine clinical application are dealt with in accepted. The patient becomes aware of
more detail here rather than in the muscle pain originating from a latent TrP only
chapters because they have yet to be estab- when pressure is applied to it. Sponta-
lished as a part of routine clinical practice. neous referred pain appears with increased
Diagnosis and treatment of acute single- irritability of the TrP, and it then is identi-
muscle myofascial pain syndromes can be fied as active. 125

simple and easy. When an acute myofascial The patient usually presents with com-
TrP syndrome is neglected and allowed to plaints due to the most recently activated
become chronic, it becomes unnecessarily TrP. When this TrP has been successfully

Copyrighted Material
20 Part 1 / Introduction

Supraspinal

Trigger
Direct G Indirect
A
E stimuli
stimuli
point
-Acute o v e r l o a d -Other trigger
- O v e r w o r k fatigue B points
F -Heart, gallbladder
-Radiculopathy
-Gross trauma a n d other
C visceral disease
-Joint dysfunction
D -Emotional
Pain Spinal distress
reference z o n e cord

Figure 2.1. Schematic of central nervous system in- gion of the reference zone that facilitates release of
teractions with a trigger point (X). Triple arrow A run- the trigger point. Arrow E signifies the activating effect
ning from the trigger point to the spinal cord repre- of indirect stimuli on the trigger point; dashed arrow F
sents sensory, autonomic and motor effects. Arrow B denotes effects of trigger points on visceral function.
from the spinal cord to the trigger point includes auto- Thick arrows G identify trigger point interactions at the
nomic modulation of the intensity of trigger point acti- supraspinal level. (Figure adapted from Travell JG.
vation. Arrow C to the pain reference zone represents Myofascial trigger points: clinical view. In: Bonica JJ,
the appearance of referred pain and tenderness at Albe-Fessard D, eds. Advances in Pain Research and
distant sites that may be several neurological seg- Therapy, Vol. 1. New York: Raven Press, 919-926,
ments removed from the trigger point. Arrow D indi- 1976.)
cates the influence of the vapocoolant spray in the re-

eliminated, the pain pattern may shift to nal colic. A perpetuating factor (see Chapter
that of an earlier, key TrP which also must 4) increases the likelihood of overload stress
be inactivated. If the key TrP is inactivated converting a latent TrP to an active TrP.
first, the patient may recover without fur- With adequate rest, and in the absence
ther treatment. of perpetuating factors, an active TrP may
The intensity and extent of the referred revert spontaneously to a latent state. Pain
pain pattern depends on the degree of irri- symptoms disappear, but occasional reacti-
tability of the TrP, not on the size of the vation of the TrP by exceeding that mus-
muscle. Myofascial TrPs in small, obscure, cle's stress tolerance can account for a his-
or variable muscles can be as troublesome tory of recurrent episodes of the same pain
to the patient as TrPs in large familiar over a period of years.
muscles. Pain Complaint. Patients with active
As illustrated in Figure 2.1, trigger myofascial TrPs usually complain of
points are activated directly by acute over- poorly localized, regional, aching pain in
load, overwork fatigue, direct impact subcutaneous tissues, including muscles
trauma, and by radiculopathy. and joints. They rarely complain of sharp,
Trigger points can be activated indirectly clearly-localized cutaneous-type pain. The
by other existing TrPs, visceral disease, myofascial pain is often referred to a dis-
arthritic joints, joint dysfunctions, and by tance from the TrP in a pattern that is char-
emotional distress. Satellite TrPs are prone to acteristic for each muscle. Sometimes the
develop in muscles that lie within the pain patient is aware of numbness or paresthe-
reference zone of key myofascial TrPs, or sia rather than pain.
within the zone of pain referred from a dis- Infants have been observed with point
eased viscus, such as the pain of myocardial tenderness of the rectus abdominis muscle
infarction, peptic ulcer, cholelithiasis, or re- and colic, both of which were relieved by

Copyrighted Material
Chapter 2 / General Overview 21

sweeping a stream of vapocoolant over the and loss of forearm muscle coordination
muscle, which helps to inactivate myofas- makes grasp unreliable. Objects sometimes
cial TrPs. slip unexpectedly from the patient's grasp.
When children with musculoskeletal The weakness results from reflex motor in-
pain complaints were examined for myo- hibition and characteristically occurs with-
fascial TrPs, the TrPs were found to be a out atrophy of the affected muscle. The pa-
common source of their pain. It is our im-
12 tient is prone to substitute intuitively
pression that the likelihood of developing without realizing that, for instance, he or
pain-producing active TrPs increases with she is carrying the grocery bag in the non-
age into the most active, middle years. As dominant but now-stronger arm.
activity becomes less strenuous in later The motor effects of TrPs on the muscle
years, individuals are more likely to be in which the TrPs are located are consid-
aware of the stiffness and restricted motion ered in detail below under Surface EMG.
resulting from latent TrPs. Sleep Disturbances. Disturbance of
Sola found that laborers who exercise
259
sleep can be a problem for patients with a
their muscles heavily every day, are less painful TrP syndrome. Moldofsky has
196

likely to develop active TrPs than are shown in a series of studies that many sen-
sedentary workers who are prone to inter- sory disturbances, including pain, can seri-
mittent orgies of vigorous physical activity. ously disturb sleep. This sleep disturbance
Our clinical experience has been similar. can, in turn, increase pain sensitivity the
Active TrPs are found commonly in pos- next day. Active myofascial TrPs become
tural muscles of the neck, shoulder and more painful when the muscle is held in
pelvic girdles, and in the masticatory mus- the shortened position for long periods of
cles. In addition, the upper trapezius, sca- time and also if body weight is compress-
lene, sternocleidomastoid, levator scapu- ing the TrP. Thus, for patients with active
lae and quadratus lumborum muscles are TrPs, sleep positioning can be critical to
very commonly involved. avoid unnecessarily disturbing their sleep.
Dysfunctions. In addition to the clini-
cal symptoms produced by the sensory dis- Physical Findings
turbances of referred pain, dysesthesias, A muscle harboring a TrP is prevented
and hypesthesias, patients also can experi- by pain from reaching its full stretch range
ence clinically important disturbances of of motion, and is also restricted in its
autonomic and motor functions. strength and/or endurance. Clinically, the
Disturbances of autonomic functions TrP is identified as a localized spot of ten-
caused by TrPs include abnormal sweating, derness in a nodule in a palpable taut band
persistent lacrimation, persistent coryza, of muscle fibers. Restricted stretch range of
excessive salivation, and pilomotor activi- motion and palpable increase in muscle
ties. Related proprioceptive disturbances tenseness (decreased compliance) are more
caused by TrPs include imbalance, dizzi- severe in more active TrPs. Active TrPs are
ness, tinnitus, and distorted weight per- identified when patients recognize the
ception of lifted objects. pain that is induced by applying pressure
Disturbances of motor functions caused to a TrP as "their" pain. The taut band
94

by TrPs include spasm of other muscles, fibers usually respond with an LTR when
weakness of the involved muscle function, the taut band is accessible and when the
loss of coordination by the involved mus- TrP is stimulated by properly applied snap-
cle, and decreased work tolerance of the ping palpation. The taut band fibers re-
involved muscle. The weakness and loss of spond consistently with a twitch response
work tolerance are often interpreted as an when the TrP is penetrated by a needle.
indication for increased exercise, but if this Taut Band. By gently rubbing across
is attempted without inactivating the re- the direction of the muscle fibers of a su-
sponsible TrPs, the exercise is likely to en- perficial muscle, the examiner can feel a
courage and further ingrain substitution by nodule at the TrP and a rope-like indura-
other muscles with further weakening and tion that extends from this nodule to the at-
deconditioning of the involved muscle. tachment of the taut muscle fibers at each
The combination of weakness in the hands end of the muscle. The taut band can be

Copyrighted Material
22 Part 1 / Introduction

snapped or rolled under the finger in ac- whether elicited by snapping palpation or
cessible muscles. With effective inactiva- by needle penetration. 246

tion of the TrP, this palpable sign becomes Limited Range of Motion. Muscles
less tense and often (but not always) disap- with active myofascial TrPs have a re-
pears, sometimes immediately. stricted passive (stretch) range of motion
Tender Nodule. Palpation along the because of pain, as demonstrated by Mac-
taut band reveals a nodule exhibiting a donald. An attempt to passively stretch
177

highly localized, exquisitely tender spot the muscle beyond this limit produces in-
that is characteristic of a TrP. When the ten- creasingly severe pain because the in-
der spot was tested for tenderness, dis- volved muscle fibers are already under
placement of the algometer by 2 cm pro- substantially increased tension at rest
duced a statistically significant decrement length. The limitation of stretch due to
in pain threshold algometer readings. 212
pain is not quite as great with active move-
Clinically, displacement of the application ment as with passive lengthening of the
of pressure by 1-2 mm at a TrP can result in muscle, at least partly due to reciprocal in-
a markedly reduced pain response. hibition. When the TrP is inactivated and
This strong localization of tenderness in the taut band is released, range of motion
the vicinity of a TrP corresponds to the local- returns to normal. The degree of limitation
ized sensitivity of the experimental muscle produced by TrPs is much more marked in
for eliciting LTRs as demonstrated in rabbit some muscles (e.g., subscapularis) than
experiments. A 5 mm displacement to ei-
128 others (e.g., latissimus dorsi).
ther side of the trigger spot (at right angles to Painful Contraction. When a muscle
the taut band) resulted in almost total loss of with an active TrP is strongly contracted
response. However, the response faded out against fixed resistance, the patient feels
more slowly when stimulated over a range of pain. This effect is most marked when an
177

several centimeters from the trigger spot attempt is made to contract the muscle in a
along the taut band. See Local Twitch Re- shortened position.
sponse in section D at the end of this chapter. Weakness. Although weakness is gen-
Recognition. Application of digital erally characteristic of a muscle with active
pressure on either an active or latent TrP myofascial TrPs, the magnitude is variable
can elicit a referred pain pattern character- from muscle to muscle and from subject to
istic of that muscle. However, if the patient subject. Electromyographic studies indi-
"recognizes" the elicited sensation as a fa- cate that, in muscles with active TrPs, the
miliar experience, this establishes the TrP muscle starts out fatigued, it fatigues more
as being active and is one of the most im- rapidly, and it becomes exhausted sooner
portant diagnostic criteria available when than normal m u s c l e s . - These changes
116 118

the palpable findings are also p r e s e n t . 94,242


are presented in more detail under surface
Similar recognition is frequently observed electromyography in Section B of this
when a needle penetrates the TrP and en- chapter. The weakness may reflect reflex
counters an active l o c u s . -
123 249
inhibition of the muscle by the TrPs.
Referred Sensory Signs. In addition to
referring pain to the reference zone, TrPs Testing
may refer other sensory changes such as No laboratory test or imaging technique
tenderness and dysesthesias. This referred has been generally established as diagnos-
tenderness has been measured in experi- tic of TrPs. However, three measurable
ments by Vecchiet, et a/. 283
phenomena help to substantiate objec-
Local Twitch Response. Snapping pal- tively the presence of characteristic TrP
pation of the TrP frequently evokes a tran- phenomena and all are valuable as re-
sient twitch response of the taut band search tools. Two of them, surface EMG
fibers. This is fully described in Section 9 and ultrasound, also have much potential
of Chapter 3. Its pathophysiological nature for clinical application in the diagnosis
is considered in Section D of this chapter. and treatment of TrPs.
Twitch responses can be elicited both from Needle Electromyography. In 1957,
active and latent TrPs. In one study, no dif- Weeks and Travell anticipated the 1993
288

ference was noted in twitch responses Hubbard and Berkoff report of finding
133

Copyrighted Material
Chapter 2 / General Overview 23

Figure 2.2. High-resolution ultrasound image


of a local twitch response in the taut band
fibers of a trigger point. The twitch was
elicited by needle penetration of the trigger
point in a taut band of a right infraspinatus
muscle. The band across the middle of the
figure that was seen by ultrasound imaging to
contract is identified by white arrows. The
transient contraction coincided with the pa-
tient's verbal report that he felt his typical pain
and experienced the referred pain to his
shoulder and arm. (Reprinted with permission
from Gerwin RD, Duranleau D. Ultrasound
identification of the myofascial trigger point
[Letter]. Muscle Nerve 20:767-768, 1997.)

EMG activity identified as specific to myo- addition, the TrP can produce referred
fascial TrPs. Subsequent rabbit and human spasm and referred inhibition in other
studies have confirmed the presence
248,250,252
muscles. With the recent appearance of on-
of spontaneous low-voltage motor endplate line computer analysis of EMG amplitude
"noise" activity as well as high voltage spike and mean power spectral frequency, a few
activity that is highly characteristic of myo- pioneer investigators have reported the ef-
fascial TrPs but not pathognomonic. The fects of TrPs on muscle a c t i v i t y . The 56,116

source of the associated high-voltage spikes reports indicate that TrPs can influence
can be ambiguous. When the endplate noise motor function of the muscle in which
activity is observed, it is a strongly confirma- they occur, and that their influence can be
tory finding and an invaluable research tool. transmitted through the central nervous
A detailed consideration of this phenome- system to other muscles. To date, there has
non appears in section D of this chapter. not been a sufficient number of well-
Ultrasound Imaging. Visualization of controlled studies to establish the clinical
an LTR using ultrasound was first noted by reliability and application of these obser-
Michael Margolis, M.D. This observation
181 vations, but the few reports of these TrP ef-
was followed up by Gerwin and Duran- fects are very promising.
leau.91, 92
The published finding is illus- On one hand, the strong clinical effects
trated in Figure 2.2. This imaging proce- of TrPs on sensation, as evidenced by TrP
dure not only provides a second way, in tenderness and referred pain, have been
addition to EMG recording, of substantiat- well-documented in this volume. It is well
ing and studying the LTR, but also has a known that strong cutaneous stimuli (e.g.,
strong potential for providing a much electric shocks) can cause reflex motor ef-
needed available imaging technique that fects (e.g., flexion reflex). If skin can
114

could be widely used to objectively sub- modulate motor activity and TrPs can mod-
stantiate the clinical diagnosis of TrPs. This ulate sensory activity, it should be no sur-
test, however, would require the examiner prise that TrPs can also strongly affect mo-
to use the skill-demanding snapping palpa- tor activity. In fact, the motor effects of
tion technique, or to insert a needle into the TrPs may be the most important influence
TrP, in order to elicit the twitch response. they exert, because the motor dysfunction
Surface Electromyography. Trigger they produce may result in overload of
points cause distortion or disruption of other muscles and spread the TrP problem
normal muscle function. Functionally, the from muscle to muscle. Accumulating evi-
muscle with the TrP evidences a three-fold dence now indicates that the muscles tar-
problem: it exhibits increased responsive- geted for referred spasm from TrPs also
ness, delayed relaxation, and increased fa- usually have TrPs themselves. These motor
tigability, which, together, increase over- phenomena of TrPs deserve serious compe-
load and reduce work tolerance. In tent research investigation.

Copyrighted Material
24 Part 1 / Introduction

An increased responsiveness of some af- tween the decline in median power fre-
fected muscles is indicated by abnormally quency and the decline in strength of max-
high amplitude of EMG activity when the imum voluntary contraction, tested inter-
muscle is voluntarily contracted and loaded. mittently. The increasing fatigue of the
Clinical evidence suggests that some mus- muscle was demonstrable as increasing
cles tend to be shortened and abnormally ex- weakness.
citable, while others appear to be weak and There is general acceptance of median
inhibited. The upper trapezius is iden-
142,170
power frequency as a valid criterion of mus-
tified as an excitable muscle and EMG stud- cle fatigue. Headley reported delayed re-
118

ies showed that, although the muscle covery following fatiguing exercise in 55
showed no abnormal motor unit activity at patients with muscle-related cumulative
rest, when it harbored TrPs it tended to "over- trauma disorder (CTD). Myofascial TrPs
react" when voluntarily contracted. During
56
were very common in the involved muscles
flexion/extension movements of the head, in this group. Median power spectral analy-
the upper trapezius and/or sternocleidomas- sis of sEMG activity of bilateral lower
toid muscles with TrPs presented surface trapezius muscles was monitored pre- and
EMG amplitudes over 2 0 % greater than post-exercise and after a 7 minute rest.
asymptomatic muscles in 8 0 % of cases. 56
There was a statistically significant differ-
Headley demonstrated a similar, marked
117
ence between pre- and postexercise mean
augmentation of EMG activity in upper power spectral values. The postexercise
trapezius muscles harboring TrPs as com- values of affected muscles showed minimal
pared to the uninvolved muscle on the con- recovery in seven minutes whereas normal
tralateral side when the patient attempted to muscles recover 70-90% within 1 minute.
shrug both shoulders equally. Delayed relaxation is commonly seen in
Preliminary studies indicate that TrPs muscle-overload work situations. 118
This
can refer inhibition or excitation to func- failure to relax is a common surface EMG
tionally related muscles, especially if the finding during repetitive exercises of mus-
target muscles also have TrPs. In several in- cles with myofascial TrPs. Headley em- 118

stances referred motor effects were ob- phasized the importance of the brief surface
served electromyographically from latent EMG gaps observed in normal records of
TrPs, indicating that these motor effects repetitive movements. Loss of these gaps can
may be produced by a TrP independent of contribute significantly to muscle fatigue. G.
its pain-producing characteristics. This ap- Ivanichev 138
demonstrated delayed relax-
parently specific motor effect of TrPs is an ation (loss of clean gaps with loss of muscle
unexplored but fertile field for TrP research. coordination) in a study of hand extensor
The presence of a TrP may characteristi- muscles with TrPs or flexor muscles with
cally induce excitation in some muscles TrPs when subjects were doing rapid alter-
and inhibition in others. If so, the presence nating movements of extension and flexion
of TrPs may help to explain why some mus- at the wrist. The presence of a sustained low-
cles frequently develop the clinical picture level EMG activity when the muscle could
of being inhibited, and others become ex- and should be relaxed is sometimes referred
cessively responsive to clinical activation. to as a static load. Delayed or missing relax-
Hagberg and Kvarnstrom 115
demon- ation accelerates fatigue of the muscle.
strated accelerated fatiguability electro- Figure 2.3 illustrates schematically the
myographically and in terms of work toler- EMG changes observed in muscles with
ance of the trapezius muscle that had TrPs. The involved muscle shows a fatigue
myofascial TrPs as compared to a con- pattern at the beginning of a repetitive
tralateral muscle that was pain-free. The task and then accelerated fatiguability
EMG amplitude increased and median with delayed recovery. These features
118

power frequency decreased significantly in apparently are hallmarks of the motor dys-
the involved muscle as compared to the function of muscles containing myofascial
uninvolved muscle. Both of these changes TrPs.
are characteristic of initial fatigue. Man- In addition, the TrP can also induce mo-
nion and Dolan showed, during fatiguing
179
tor activity (referred spasm) in other mus-
exercise, a nearly linear relationship be- cles. Headley illustrated an example of
116

Copyrighted Material
Chapter 2 / General Overview 25

At Start Moderate Prolonged 7 Min


Rest Activity Activity Activity Rest

Figure 2.3. Comparison of surface electromyographic points start out as if the muscle is already fatigued
response to fatiguing exercise of normal muscle (black and show that the muscle reaches exhaustion more
lines) and muscle with active myofascial trigger points quickly (and is slower to recover) than normal muscle.
(red lines). The averaged amplitude (open circles) and These changes are accompanied by accelerated fa-
mean power frequency (solid circles) of the elec- tigue and weakness of the muscle with trigger points.
tromyographic record from the muscle with trigger

this phenomenon where pressure on a TrP onds that pressure was being applied. This
in a right soleus muscle induced a strong response failed to occur following inactiva-
spasm response in the right lumbar tion of the triceps TrP. The upper trapezius
paraspinal muscles. Figure 2.4 illustrates a muscle in this case also had TrPs, and its
similar response with pressure applied to a response fits with the impression that mus-
TrP in the long head of the triceps brachii cles with TrPs are more readily activated
muscle inducing a strong motor unit re- (and therefore are more likely to become
sponse (spasm) in the ipsilateral upper target muscles for referred spasm) than
trapezius muscle only during the 20 sec- muscles free of TrPs. This may be another

Copyrighted Material
26 Part 1 / Introduction

Seconds

Figure 2.4. Motor activation of the upper trapezius marked increase in surface electromyographic activity
muscle in response to painful pressure applied to a (referred spasm) corresponds to the period of me-
trigger point in the long head of the ipsilateral triceps chanical stimulation of the trigger point. (Redrawn
brachii muscle. The bar marks the period of painful with permission from the data of Barbara J. Headley,
pressure applied to the triceps trigger point. The PT.)

indication of sensitization of TrP-involved These examples are analogous to the ac-


a motor neurons. Research studies are tivated segment concept described in an
needed to elucidate this issue. osteopathic study by Korr, et al. In their 15i

Certain muscles tend to be targets of re- study, the spasm was demonstrated by the
ferred spasm so TrPs in a number of distant paraspinal muscles acting as target muscles
muscles can accentuate EMG activity and at the level of a vertebra showing pressure
irritability of a target muscle. The upper sensitivity that was considered indicative
trapezius, masseter, posterior cervicals, of an articular dysfunction. A previous re-
and lumbar paraspinal muscles appear to port noted that the spasm response was
be common target muscles. These are also most marked when pressure was applied to
muscles that are prone to develop tight- a pressure-sensitive vertebra. 50

ness, according to Janda. 142


Spasm may be referred by TrPs indepen-
Carlson, et al. demonstrated the TrP-
32
dent of pain referral. Headley noted that
116

target muscle relationship for referred some distant TrPs which referred spasm to
spasm between the upper trapezius and the the paraspinal muscles were not prone to
ipsilateral masseter muscle. Following TrP refer pain and were rated as only mildly
injection of the trapezius muscle, there was painful on application of pressure. She re-
a significant reduction in pain intensity ported that inactivation of these spasm-
ratings and EMG activity in the masseter inducing TrPs resulted in marked reduc-
muscle. Every one of the patients in the tion of low back pain. Although these
study had localized TrP tenderness in the "latent" TrPs were not themselves referring
masseter TrP, location, reinforcing the sus- pain, they apparently were inducing al-
picion that target muscles characteristi- gogenic activity in the back muscles.
cally develop TrPs, but not necessarily ac- The capacity of TrPs to refer inhibition
tive TrPs. can cause major disruption of normal mus-

Copyrighted Material
Chapter 2 / General Overview 27

cle function. Headley 117


illustrated two set of local pain (pressure pain threshold),
clear examples of movement-specific inhi- the onset of referred pain (referred pain
bition where the muscle worked well dur- threshold), and intolerable pressure (pain
ing a test movement but did not contract at tolerance). Most commonly, the pressure
all during a movement for which it would required to reach pain threshold is mea-
normally serve as prime or assistive mover. sured directly from a spring scale cali-
A frequently-seen example of referred inhi- brated in kilograms, Newtons, or pounds.
bition is an anterior deltoid muscle that is Since the pressure is applied through a cir-
strongly inhibited during shoulder flexion cular foot plate, its diameter is a factor and
but is recruited essentially normally dur- the actual measurement being made is
ing shoulder abduction. In these cases, the stress (Kg/cm ) applied to skin. Since one
2

normal functional pattern returned with of the most common algometers has a foot
inactivation of the problematic TrP in the plate area of 1 cm , the meter reading in Kg
2

infraspinatus muscle (Headley, personal is numerically the same as Kg/cm , so no2

communication, 1996). numerical conversion is needed.


Another reported example of referred in- A convenient hand-held spring algome-
hibition was an active TrP in the quadra-
117
ter that is commercially available was de-
tus lumborum that inhibited gluteal mus- scribed in 1986, and standard values were
72

cles. Normal function of the gluteal muscles published in 1987. Since then, the spring
73

was restored when the quadratus lumborum algometer has been widely used in research.
TrP was inactivated. The immediate restora- This device is useful for making a measure-
tion of normal strength and normal median ment of pain pressure threshold at a TrP site
power spectral frequency during repetitive so the initial tenderness can be compared to
activity strongly suggests that the recruited measurements following a therapeutic or
muscle was not lacking strength before the experimental intervention. It is relatively
test, but was probably neurologically inhib- objective, since the subject need not see the
ited by the quadratus lumborum TrP. With meter display, but the reading does depend
sufficient repetitions in a work situation, on the subject's report of a subjective sensa-
these abnormal patterns appear to become tion. It is very useful for research studies
well "learned" when the muscle no longer and helpful in many clinical situations, but
returns immediately to a normal pattern the user must be aware of three kinds of lim-
with inactivation of the TrP. Now it becomes itations when applying it to TrPs.
necessary to retrain the muscle to a normal First, the measurement, per se, indicates
pattern after inactivation of the responsible absolutely nothing about the source or
TrPs. Surface EMG biofeedback from the in- cause of the tenderness being measured.
hibited muscle(s) can facilitate retraining. The tenderness may be due to myofascial
All of these motor phenomena and their TrPs, to tender points of fibromyalgia, to
complexity suggest that the motor dysfunc- bursitis, to severe spasm, etc. Therefore, by
tions caused by TrPs are as complicated itself, tenderness cannot serve as a diag-
and important as the sensory story empha- nostic criterion. The cause of the tender-
sized in the first edition of the Trigger Point ness must be determined by other diagnos-
Manual. These motor dysfunctions alone tic observations.
could constitute a book. However, an enor- Second, the absolute value obtained at
mous amount of competent, thoughtful any one site can be strongly influenced by
surface EMG research will be needed be- variations in the thickness and compliance
fore that book can be written. of subcutaneous tissues from subject to
Algometry. Sensitivity to pain in pa- subject and by inherent differences in the
tients with TrPs has been measured as the sensitivity of different muscles. 73

pain threshold to electrical stimulation ' 283


Third, the relatively high degree of skill
284
or to applied pressure. Pressure algome- required to use this instrument effectively,
try has been most commonly reported. and the exquisite specificity of the location
Pressure algometry involves induction of a of the TrP being measured are generally un-
specific pain level in response to a mea- derrated. The precise location of maximum
sured force applied perpendicularly to the tenderness of that TrP must first be estab-
skin. Three endpoints are reported: the on- lished by palpation and with the subject's

Copyrighted Material
28 Part 1 / Introduction

cooperation. Since the tenderness of the al. that referred pain frequently can be
232

nodule in a taut band is being measured, elicited from normal muscle with the ap-
the foot plate must be centered over the plication of sufficient pressure in subjects
point of maximum tenderness in the nod- with no pain complaint. The presence of
ule, and pressure must be aimed precisely local tenderness at these apparently nor-
in the direction of maximum tenderness. mal-muscle sites is more likely in subjects
The foot plate must remain in this position who are suffering from TrP pain and is to
throughout the measurement. If the foot be expected in patients with fibromyalgia.
plate slips off the nodule and compresses Hong, et al. found that referred pain
125

the tissue adjacent to the nodule (which it could be elicited from every active TrP
is very prone to do), an entirely different site, but from only 4 7 % of the latent TrP
and erroneously high reading is obtained. sites. Stated another way, it took less pres-
For these reasons, errors in measuring TrP sure to elicit referred pain from an active
tenderness are nearly always underestima- TrP than from a latent TrP. As would be ex-
tions, not overestimations. By placing a pected, all three kinds of thresholds were
finger on each side of the nodule or taut significantly lower (P < 0.01) at active
band and positioning the foot plate be- TrPs than at latent TrPs. The more irritable
tween the fingers, the fingers can serve as a the TrP, the lower its pain threshold. How-
guide to maintain the footplate position ever, there was considerable overlap be-
over the point of maximum tenderness. tween values obtained from active and la-
These difficulties can be at least partly tent TrPs, so threshold measurements
ameliorated by averaging the lowest two of alone were not sufficient to distinguish ac-
three readings if they are in reasonable tive from latent TrPs. This study demon-
agreement. strates that pressure algometry can be a
What constitutes appropriate interpreta- powerful research tool and useful clinical
tion of results from algometry of TrPs was re- tool.
cently greatly clarified by Hong, et al. The
125
An incomplete, single-subject, illus-
authors examined three sites associated with trated report indicates that pressure pain
77

latent and with active TrPs in the middle fin- thresholds measured at intervals along the
ger extensor of the extensor digitorum com- taut band are lowest at the TrP and that both
munis muscle by algometry. The three sites TrP and taut band thresholds increase con-
were on the TrP, on the taut band 2 cm distal siderably following needling and injection
to the TrP, and a control (normal muscle) site of the TrP. Systematic controlled studies of
1 cm further distal to the taut-band site and pressure thresholds throughout the length
1 cm lateral to the taut band site. At each site, of the taut band including the attachment
three kinds of thresholds were measured: are needed. The essentials for such a re-
onset of (local) pain, onset of referred pain, search study have been identified. 243

and intolerable pain. The results are pre- Another form of pressure algometer is
sented graphically in Figure 2 of their paper. an electronic pressure-sensitive film that
The authors 125
showed convincingly can be placed on the finger tip. Such a de-
that eliciting referred pain in the expected vice was described as a palpometer. All of
16

pattern for that muscle is not a specific the versions tried so far had a problem
finding of TrPs. Instead, its presence is pri- with adequate sensitivity and linearity of
marily dependent on the amount of pres- instrumental response at small pressure
sure applied to the site. In all 25 examina- values, where resolution and accuracy are
tions, referred pain was elicited from both most important. Since some degree of sen-
the active TrP site and its taut band site (2 sation as to what is being palpated is trans-
cm removed from the TrP). At the control mitted through the film to the finger tip, a
site of patients with active TrPs, referred properly engineered device may have a sig-
pain was elicited in half of the examina- nificant advantage over the spring scale
tions before reaching pain tolerance. In the system. The palpometer approach has the
subjects with latent TrPs, characteristic re- advantage that it is electronic and that the
ferred pain was elicited from control sites results can be recorded readily and the
in one-quarter of the examinations. These data entered directly into a computer for
findings agree with those of Scudds, et analysis and storage.

Copyrighted Material
Chapter 2 / General Overview 29

Thermography. Thermograms can be ever, research studies are needed to inves-


recorded by infrared radiometry or with tigate whether this reflex hypothermia is
films of liquid crystal. Recording infrared distinguishable from that which may occur
radiation (electronic thermography) with when painful pressure is applied to a ten-
computer analysis provides a powerful tool der articular dysfunction, area of bursitis,
for the accurate rapid visualization of skin or an area of enthesopathy.
temperature changes over large areas of the
body. This technique can demonstrate cu- A thermographic hot spot was used by
taneous reflex phenomena characteristic of Kruse and Christiansen as an initial
161

myofascial TrPs. The less expensive con- identifier of the likely location of a TrP.
tact sheets of liquid crystal have limita- Then, the presence of the TrP was con-
tions that make reliable interpretation of firmed by physical examination. This pro-
the findings considerably more difficult. cedure eliminated from consideration
Each of these thermographic techniques TrPs that might not be thermographically
measures the skin surface temperature to a active.
depth of only a few millimeters. The temper- Fischer and Chang 79
examined the
ature changes correspond to changes in the gluteal region of 14 consecutive low back
circulation within, but not beneath, the skin. pain patients for thermographic hot spots.
The endogenous cause of these temperature Hot spots were examined for spot tender-
changes is usually sympathetic nervous sys- ness in 13 muscles and 1 ligament. Re-
tem activity. Thermographic changes in skin duced pressure threshold readings were
temperature, therefore, are comparable in significantly correlated [P< 0.01) with hot
meaning to changes in skin resistance or spots compared to contralateral control
changes in sweat production. However, elec- sites. Hot spots were likely to be tender
tronic infrared thermography is superior to sites, but the report left open the question
these other two measures in convenience of whether these sites were tender because
and in spatial as well as temporal resolution. of TrPs, fibromyalgia tender points, or
In summary, the following research other causes.
studies indicate that just finding a hot spot Swerdlow and Dieter examined 165
265

on the thermogram is NOT sufficient to patients who suffered whiplash injury


identify a TrP beneath it. A similar temper- and found 139 of them had TrPs in the up-
ature change can be expected from radicu- per, middle, or lower trapezius muscles.
lopathy, an articular dysfunction, enthe- Using Fischer's thermographic criteria, 74

sopathy, or due to a local subcutaneous they found 4 0 % false-positives and 20%


inflammation. The thermographic hot spot false-negatives among these patients,
of a TrP is described as a discoid region 5 which is unacceptable as a diagnostic cri-
to 10 cm in diameter, displaced slightly terion.
from directly over the TrP. Five studies
71
Scudds, et a/.
231a
examined the backs of
reported a region of hyperthermia over the 49 fibromyalgia patients and 19 myofas-
TrP (a total of 170 T r P s ) ; ' ' ' -
52 53 74
none
1% 161
cial pain patients using infrared thermog-
reported a finding of hypothermia. No such raphy under resting conditions in con-
agreement exists with regard to skin tem- junction with a dolorimeter study of
perature changes in the region of referred referred pain. They found that the average
pain. However, available data suggest an skin temperature of the myofascial pain
interesting possibility. Undisturbed TrPs patients was 0.65%C warmer than the fi-
referring spontaneous autonomic cuta- bromyalgia patients. Apparently this
neous effects may tend to induce hyper- study identified TrPs only by spot tender-
thermia in a limited area of the skin over- ness and referral of pain, which another
lying the TrP, whereas mechanical study showed can also occur in normal
stimulation of the TrP that causes addi- subjects. All TrPs caused referred pain,
232

tional pain induces a "reflex" hypothermia and half of the most tender spots in fi-
that is dependent on the stimulus. This re- bromyalgia patients also referred pain.
flex hypothermia phenomenon may be a This result may mean that half of the fi-
far more discriminating criterion of a TrP bromyalgia patients also had TrPs, which
than the hyperthermia over the TrP. How- is consistent with the finding of another

Copyrighted Material
30 Part 1 / Introduction

investigator who looked for that possibil- palpation. Pressure threshold of the TrP
ity, or it may mean that some tender
90
and corresponding control sites was deter-
points that are not TrPs may also refer mined by algometry. Pressure was then ap-
pain. These studies do suggest that pa- plied to the TrP until the subject felt
tients selected primarily for myofascial referred pain, and it was maintained for 1
TrPs are more likely to exhibit hyperther- minute while thermograms were recorded
mia than patients with fibromyalgia. Ap- every 15 seconds.
parently, the active loci responsible for Initially, the region of the TrP site always
TrPs not only can cause referred pain, but showed increased temperature compared
they also can refer local cutaneous hyper- to its control site. The referred-pain zone,
thermia. A thermographic research study initially, often showed a lesser increase. 161

is needed of TrPs identified by adequate With compression of the TrP, the areas of
diagnostic criteria (see Section B of this thermal response (in the direction of re-
chapter), and of tender points that are not ferred pain) showed a statistically signifi-
TrPs in fibromyalgia patients. cant reduction in temperature, whereas
Diakow conducted a study to see if
53 corresponding control sites showed a non-
active TrPs exhibited a region of hyper- significant increase in temperature. The re-
thermia extending toward the pain refer- gion of thermal response was remarkably
ence zone beyond the usual hot spot as more extensive than the region of referred
compared to latent TrPs, which were as- pain. The pressure threshold values at TrP
sumed not to do so. In addition, he ana- sites were significantly (P < 0.001) lower
lyzed a subgroup who showed evidence (reflecting more tenderness) than at control
of articular dysfunction that would be sites.
likely to cause hyperthermia in the same
region to which a TrP might refer hyper- The literature to date fails to address a
thermia. By eliminating this subgroup of number of critical questions concerning
25 patients (leaving 104), the discrimina- thermographic changes associated with
tion of active versus latent TrPs on the ba- TrPs. Since many acupuncture practitioners
sis of Cohen's Kappa statistic improved use a skin-resistance point finder to locate
from 0.44 to 0.55 (bad to poor) and speci- the appropriate place to insert the needle for
ficity improved from 0.70 to 0.82 (fair to inactivating a TrP (or for treating a pain-type
good). These results suggest that articular acupuncture point), it would be of consider-
dysfunction can be an additional source able interest to explore in a blinded research
of hot spots, which fits with Korr's stud- study, the region of a hot spot for a point of
ies of facilitated segments. 154
low resistance and determine to what extent
Two studies indicated that when re- a point of low resistance is located within
ferred pain is produced by compressing the hot spot and how consistently a low-re-
the TrP, the reference zone becomes hy- sistance point has a TrP (active or latent)
pothermic. Travell examined one patient nearby, beneath it. The presence of a TrP
who showed this very clearly. 279 should be determined by adequate diagnos-
Kruse and Christiansen 161
did a well- tic criteria applied by examiners tested for
controlled study of temperature change in good interrater reliability. Since several re-
the reference zone of TrPs in response to search studies show that the dysfunction
pressure stimulation of middle trapezius characteristic of TrPs is modulated by sym-
TrPs. The criteria used for diagnosis of TrPs pathetic nervous system activity, "- - re-
33 167 186

were not specifically stated but given only search studies of the effects of TrPs on sym-
by a general reference to the first edition of pathetic control of skin perfusion should
Volume 1 of this Manual. Infrared thermo- improve our understanding of the func-
grams were obtained bilaterally from 5 pre- tional relationships between myofascial
scribed upper extremity locations of 11 TrPs and the autonomic nervous system.
student volunteers with symptomatic TrPs
in the middle trapezius muscle and from Treatment
11 asymptomatic controls. Initially ther- Effective treatment of a myofascial pain
mograms were used to locate thermally ac- syndrome caused by TrPs usually involves
tive TrPs which were confirmed as TrPs by more than simply applying a procedure to

Copyrighted Material
Chapter 2 / General Overview 31

the TrPs. It is often necessary to consider behaviors which tend to reinforce dys-
and deal with the cause that activated the function and suffering. Many patients
TrPs, to identify and correct any perpetuat- have suffered grievously and needlessly
ing factors (which often are different than because a series of clinicians unac-
what activated the TrPs), and to help the quainted with myofascial TrPs erro-
patient to restore and maintain normal neously applied the psychogenic label
muscle function. to them covertly if not overtly.
This volume includes a number of re- 3. Myofascial pain syndromes are self-lim-
lease and injection techniques, many of iting and will cure themselves. An acute
which were not considered in the previous uncomplicated TrP activated by an un-
edition. These techniques are considered in usual activity or muscle overload can re-
detail in Chapter 3, Section 12 of this vol- vert spontaneously to a latent TrP
ume. These treatment approaches include within a week or two, IF the muscle is
the use of simple muscle stretch, augmented not overstressed (used within tolerance,
muscle stretch, postisometric relaxation, which may be limited) and IF there are
reciprocal inhibition, slow exhalation, eye no perpetuating factors. Otherwise, if
movement, TrP pressure release, massage, the acute syndrome is not properly man-
range of motion, heat, ultrasound, high-volt- aged, it evolves needlessly into a
age galvanic stimulation, drug treatment, chronic myofascial pain syndrome.
biofeedback, and new injection techniques. 4. Relief of pain by treatment of skeletal
There are a number of common miscon- muscles for myofascial TrPs rules out se-
ceptions about the treatment of TrPs. rious visceral disease. Because of the re-
ferred pain nature of visceral pain, appli-
1. Simply treating the TrP should be suffi- cation of vapocoolant spray or infiltration
cient. Occasionally this may be true IF of a local anesthetic into the somatic ref-
the stress that activated the TrP is not re- erence zone can temporarily relieve the
current and IF there are no perpetuating pain of myocardial infarction, angina,
factors present. Otherwise, the TrP is and acute abdominal disease with no ef-
likely to be reactivated again by the same fect on the visceral pathology. 290

stress. Ignoring perpetuating factors in-


Diagnostic Criteria
vites recurrence. After the TrPs have per-
sisted for some time, failure to retrain The lack of general agreement as to appro-
the muscle to normal function or failure priate diagnostic criteria for examining trig-
to reestablish its full-stretch range of mo- ger points has been an increasingly serious
tion results in a degree of persistent mo- impediment to more widespread recognition
tor dysfunction. of myofascial trigger points and to compati-
2. The pain cannot be as severe as the pa- ble studies of the effectiveness of treatment.
tient says and must be largely psy- Interrater Reliability. Of four recent
chogenic. The patients are trying to studies on interrater reliability of TrP ex-
communicate their suffering. Believe aminations, the first three reported unsatis-
them. It feels severe to them. Patients in factory to marginal interrater reliability.
a general medical practice rated their The fourth study showed why such results
pain as severe as, or more severe than were obtained. It demonstrated convinc-
pain from other causes such as pharyn- ingly the need for all examiners to be both
gitis, cystitis, angina, and herpes experienced and trained in order to per-
zoster.257
In addition, an appreciable form reproducible examinations. This sec-
amount of the pain reported by many tion will summarize these studies and the
patients with fibromyalgia comes from lessons learned.
their TrPs. The pain of fibromyalgia Four well-designed studies have re-
rates fully as severe as the pain of cently evaluated the reliability of various
rheumatoid arthritis. It is severe enough myofascial TrP examinations. Results are
to cause central nervous system changes summarized in Table 2.3. In 1992 Wolfe,
characteristic of chronic pain. Because et a l . reported a study, part of which in-
293

of their chronic TrP and fibromyalgia volved the evaluation of 8 muscles in 8


pain, these patients often develop pain patients by 4 physicians experienced in

Copyrighted Material
32 Part 1 / Introduction

Table 2.3. Interrater Reliability of Examinations for Trigger Point Characteristics, Kappa
Values

Wolfe, et al., Nice, et al., Njoo, et al., Gen/i/in, et al.,


Examination 1992 293
1992 ,9S
1994*' 1995 93
Mean

Spot Tenderness 0.61 0.66 0.84 0.70


Jump Sign 0.70 0.70
Pain Recognition 0.30 0.58 0.88 0.59
Palpable Band 0.29 0.49 0.85 0.54
Referred Pain 0.40 0.38 0.41 0.69 0.47
Twitch Response 0.16 0.09 0.44 0.23
Mean 0.35 0.38 0.49 0.74

examining patients for TrPs. The muscles Njoo and Van der Does reported the
201

examined included the levator scapulae, examination of 2 muscles (quadratus lum-


supraspinatus, anterior scalene, upper borum and gluteus medius) in 61 patients
trapezius, infraspinatus, pectoralis major, with low back pain by 2 examiners picked
sternocleidomastoid, and the iliocostalis/ from a pool of 1 physician in general prac-
longissimus muscles in the T -L region.
10 1 tice and 4 medical students. Each medical
Each of the four examiners had many student was well-trained by the physician
years of independent experience, but had over a 3 month period but was inexperi-
no chance prior to this study to agree on a enced. The average kappa values for the 6
technique for examining the upper body examinations were essentially equal for
TrPs (they were untrained, experienced the quadratus lumborum and gluteus
examiners). The physicians examined medius muscles, indicating that for them,
each muscle for 5 findings characteristic those muscles were about equally difficult
of TrPs (Table 2.3). Since subsequent stud- to examine. Four of the five examiners
ies reported interrater reliability results in were well-trained but inexperienced.
terms of the kappa statistic, two co-au- Their interrater reliability was better than
thors of this study [Simons and Skootsky] that in previous studies, but not good.
analyzed the original data for the kappa Gerwin, et al. reported a double study
94

statistic, which corrects for chance agree- in which 4 experienced physicians exam-
ment. The examiners achieved poor inter- ined 5 muscles bilaterally in each of 10 sub-
rater reliability. jects with myofascial TrPs. The first study
Nice, et a l . reported on the examina-
198 was conducted with the assumption that
tion of three sites in the thoracolumbar the four experienced examiners employed
paraspinal muscles of 50 patients with essentially the same examination tech-
low back pain by 12 experienced full-time nique. They achieved the same poor inter-
physical therapists who routinely treated rater reliability of other experienced un-
patients with low back pain. "A practice trained examiners.
session was held to allow the therapists to However, in a second study by the same
practice this method on each other until four physicians, but following a three-
all physical therapists reported that they hour training session, agreement among
felt capable of using the method on pa- doctors was assessed statistically and
tients."198
This was inadequate training found to be reliable before proceeding
because there was no evaluation of uni- with the study. The study showed that ex-
formity of technique. Again, these were amination of the extensor digitorum com-
experienced but inadequately trained ex- munis and latissimus dorsi muscles was
aminers and they also achieved poor in- most reliable. Examination of the stern-
terrater reliability. ocleidomastoid and upper trapezius mus-

Copyrighted Material
Chapter 2 / General Overview 33

cles was less reliable, and examination of should employ both experienced and trained
the infraspinatus muscle was least reli- examiners who have been tested for inter-
able, which suggests that, of the five mus- rater reliability BEFORE the study is con-
cles tested, it is the most difficult to ducted. The necessary skill can be learned.
examine reliably. Fricton, in a diagnostic study of masticatory
myofascial pain, likewise found that experi-
The results of the four studies are sum- enced raters were more reliable than inexpe-
marized in Table 2.3, from which a number rienced raters and also concluded that find-
of inferences can be drawn. The table ings by palpation are technique-sensitive. 82

shows, across the bottom row, the mean Looking at Table 2.3 from another point
kappa value of all examinations for each of view, one can examine the mean kappa
study. The examiners in these studies fell values of all four studies in terms of each
into 3 categories: experienced and un- examination technique tested [see right
trained, trained and inexperienced, trained hand column of Table 2.3). In Table 2.4A,
and experienced. Two studies, Wolfe, et the difficulty of the examinations was
al. and Nice, et al.
233
tested experienced
198
ranked according to the mean kappa values
but untrained examiners and obtained un- derived from these four studies.
satisfactory mean kappa values of 0.35 and Diagnostic Value of Examinations. A
0.38, respectively. On the other hand, Njoo second question must be considered, "What
and Van der Does tested well-trained but
201
is the diagnostic value of the examination
inexperienced examiners, who reached a technique in terms of its specificity for iden-
barely satisfactory mean kappa value of tifying trigger points?" An estimate of the
0.49. Gerwin, et al. tested well-trained
33
relative diagnostic value of each measure
and experienced examiners who achieved without regard to other findings is presented
a good mean kappa value of 0.74. In the in the last column of Table 2.4A. These esti-
subsequent publication of this study as a mates are based on considerations presented
paper, the fact that the Kappa statistic is
94
below. However, they need confirmation or
inappropriate when all examiners report modification by experimental studies that
the same finding in a subject was consid- examine the sensitivity and specificity of
ered. Avoiding that mistake showed that each examination, and combinations of ex-
the reliability was actually good to excel- aminations as controlled research studies.
lent, considerably better than that reported
An examination for spot tenderness or the
in the initial abstract, but the abstract
93
jump sign is essentially the same test. The
data were used in Table 2.3 so that the
vigorousness of the jump sign is an indicator
Kappa statistics results of the four studies
of the amount of pressure applied and the
could be compared directly.
degree of spot tenderness. Either of these
Clearly, a clinical or experimental re- tenderness findings alone has limited diag-
search study of human myofascial trigger nostic value because of ambiguity as to the
points, to obtain the most meaningful results, cause of tenderness. The tenderness might

Table 2.4A. Comparative Reliability of Diagnostic Examinations for Trigger Points,


Estimate of the Relative Difficulty Performing the Examinations, and
Estimated Relative Diagnostic Value of each Examination by Itself,
Regardless of Other Findings

Presence of No. of Studies Mean Kappa Difficulty Diagnostic Value Alone

Spot Tenderness 3 0.70 + +*


Pain Recognition 3 0.59 ++ +++
Palpable Band 3 0.54 +++ + +*
Referred Pain 4 0.47 +++ +
Twitch Response 3 0.23 ++++ ++++
*The combined presence of these two will likely have a high diagnostic value for sufficiently skilled examiners.

Copyrighted Material
34 Part 1 / Introduction

be due to myofascial TrPs, fibromyalgia, en- tender points of fibromyalgia that are not also
thesopathy, bursitis, tendinitis, etc. The re- TrPs. However, tender points of fibromyalgia
sponse observed is strongly dependent on per se should not have the other palpable
the amount of pressure applied. For reli-
125
trigger point characteristics.
able results, the pressure must be quantita- Scudds, et al. did a related study
232

tively standardized in some way. If a quanti- when they located tender muscular spots
tative estimate of spot tenderness is desired, that referred sensation in 5 4 % of healthy
properly administered pressure algometry 72
subjects, nearly half of whom described the
73
is superior to testing for the jump sign. sensation as pain. The authors did not ex-
Pain recognition is a relatively reliable amine the sensitive locations for other evi-
test, as long as patients understand that the dence of latent TrPs. The study by Sola, et
examiner is asking them IF they recognize al. found a similar percentage of latent
261

the pain as a familiar one that they have ex- TrPs in an unselected population, suggest-
perienced recently. They are NOT to iden- ing that many of the pain-referring spots
tify a referred pain that is new and not fa- found by Scudds, et al. were latent TrPs.
miliar to them. If the patient recognizes the Hong, et al. showed that the threshold to
125

pain generated by pressure on a TrP, then produce a referred pain pattern was
that tender spot can be considered a source reached with less pressure on an active TrP
(trigger) that is contributing to at least part than on a latent one. The additional pres-
of the patient's pain problem. sure required to progress from the pain
The finding of a palpable taut band, by threshold to the referred pain threshold
itself, may be ambiguous because it can was less at all three sites in muscles with
sometimes be observed in pain-free subjects active TrPs than in muscles with latent
without other clinical evidence of TrP phe- TrPs. However, there was no sharp line of
nomena. '201
The presence of a palpable
293 distinction between active and latent TrPs
nodule in the taut band has not been tested with regard to the pressure needed to elicit
as a possible criterion of myofascial TrPs unrecognized referred pain.
but some clinicians observe the phenome- Although eliciting referred pain that
non routinely and the nodule is to be ex- is not recognized by the patient but con-
pected based on the pathogenesis of TrPs. forms to the expected pain pattern for that
Normal palpable structures such as intra- muscle does not identify a latent TrP un-
muscular septa should not be tender. The ambiguously, it can be very helpful diag-
value of examining for a taut band alone is nostically. The spontaneous referred pain
further limited by the inaccessibility of pattern reported by the patient is a very
many muscles to satisfactory manual palpa- helpful indicator of where to start looking
tion. However, although never tested exper- for TrPs.
imentally, the presence of spot tenderness Twitch responses are strongly associated
combined with a palpable band and nodule with the presence of TrPs and this finding is
should prove highly reliable, if the exam- probably the most specific single clinical test
iner is skillful at detecting these structures. of a TrP. However, the extent to which
123

Addition of a palpable nodule at the tender twitch responses can be elicited from other
spot as a criterion may enhance diagnostic parts of the muscle, particularly in an area of
sensitivity. Historically, this has been a cri- enthesopathy, has not been critically evalu-
terion for diagnosing fibrositis, Myogelosen, ated. Enthesopathy by definition is found
Muskelharten, and muscular rheumatism. only in the region of attachment at the ends
Recognized referred pain that reproduces of the muscle fibers, whereas TrPs are closely
the patient's pain complaint identifies an ac- associated with endplates, which are located
tive TrP and adds greatly to the specificity of near the middle of muscle fibers. The clinical
the diagnosis. An unrecognized referred pain diagnostic usefulness of the twitch response
that corresponds to the known referral zones is limited to those muscles in which it can be
of the TrP being examined is nonspecific. 125 reliably identified visually, by palpation, or
No study is known that has examined under by ultrasound imaging. The local twitch re-
controlled conditions specifically how com- sponse is the most difficult of the diagnostic
monly this referred pain can be elicited from signs to elicit reliably manually, and rela-

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Chapter 2 / General Overview 35

tively few examiners have developed the were performed. A consensus document
needed skill. On the other hand, it does seem that establishes official diagnostic criteria
to be highly specific and is readily elicited by is an urgent need.
needle penetration of the trigger point.
The addition of ultrasound imaging may Differential Diagnosis and Confusions
greatly increase the importance of testing Three possible sources of musculoskele-
for an LTR. The LTR requires a high level of tal pain are common and are commonly
skill for reliable results, but, with ultra- overlooked: myofascial TrPs, fibromyalgia,
sound imaging, it also has the potential for and articular dysfunction that requires
providing a specific, objective, recordable, manual mobilization. These three condi-
clinically available imaging test for myo- tions often interact with one another, re-
fascial TrPs. The ultrasound test can pro- quire different diagnostic examination
vide an objective measure of the relative techniques, and need significantly differ-
skill of examiners. ent treatment approaches.
Pain-restricted range of motion is a fun- One current source of confusion is use
damental characteristic of TrPs that has not of the term myofascial pain syndrome for
been subjected to testing for interrater reli- two different concepts. Sometimes, myo-
241

ability among examiners. fascial pain syndrome is used in a general


Recommendation. Clearly, there is no sense that applies to a regional muscle
one diagnostic examination that alone is a pain syndrome of any soft tissue origin. 108,

satisfactory criterion for routine clinical i6o, 1 9 4 . 2 0 7 , 2 9 8 , 2 9 9 Historically, the term myo-

identification of a trigger point. Based on fascial pain syndrome has been used in the
experimental information now available, 94
restricted sense of that syndrome which is
the combination of spot tenderness in a caused by TrPs within a muscle belly (not
palpable band and subject recognition of scar, ligamentous, or periosteal T r P s ) . '
88,255

the pain are minimum acceptable criteria. 260,278,279 m c e g the general usage includes
The criteria currently recommended for di- many conditions that cause muscle pain
agnosing a myofascial TrP are listed in without reference to and in absence of
Table 2.4B. Most important: at present, TrPs, the use of that terminology is am-
every author reporting a study of myofas- biguous and very confusing to those who
cial TrPs should identify in the methods think in terms of TrPs, which is only one of
section specifically which TrP examina- the conditions included in the general-us-
tions were used as diagnostic criteria and age term. For authors, one unambiguous
should describe in detail exactly how they approach is to specify myofascial pain syn-

Tabie 2.4B. Recommended Criteria for Identifying a Latent Trigger Point or an Active
Trigger Point

Essential Criteria
1. Taut band palpable (if muscle accessible).
2. Exquisite spot tenderness of a nodule in a taut band.
3. Patient's recognition of current pain complaint by pressure on the tender nodule (identifies an
active trigger point).
4. Painful limit to full stretch range of motion.
Confirmatory Observations
1. Visual or tactile identification of local twitch response.
2. Imaging of a local twitch response induced by needle penetration of tender nodule.
3. Pain or altered sensation (in the distribution expected from a trigger point in that muscle) on
compression of tender nodule.
4. Electromyographic demonstration of spontaneous electrical activity characteristic of active loci
in the tender nodule of a taut band.

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36 Part 1 / Introduction

drome due to TrPs or use the term regional fascial TrP pain is so common and because
muscle pain syndrome to identify the more patients are most likely to experience the
general usage. The unmodified, unspeci- pain at sites other than the TrP location,
fied use of the term myofascial pain is dis- the clinician is prone to miss the diagnosis
couraged. unless he or she considers the possibility
This section begins with a listing of of, and specifically searches for, the distant
common diagnoses that often are made TrP culprit(s).
mistakenly without considering the possi- Fibromyalgia Syndrome. Two of the
bility of TrPs. Patients are frequently re- three most common muscle pain syn-
ferred to myofascial TrP experts with one dromes, fibromyalgia and myofascial pain
of these diagnoses (and often a patient has due to TrPs, are now recognized as quite
been given several of them), but when the separate c l i n i c a l ' and etiological enti-
90 126

patient's pain problem was actually caused ties. 224


Since both conditions are likely
242

by unrecognized or inadequately treated to cause severe muscle pain and frequently


myofascial TrPs. co-exist but need a different treatment ap-
Next, this section discusses other condi- proach, it is of great importance for the pa-
tions that are closely related to myofascial tient's sake that any clinician dealing with
TrPs. Commonly both conditions are pre- a patient who has muscle pain be able to
sent. This confusing situation makes it par- clearly distinguish these two conditions.
ticularly important to draw a sharp For one who is interested in understanding
diagnostic distinction when the two condi- what fibromyalgia is, what it means to the
tions require different treatment ap- patient, and how best to manage it, the
proaches. The related conditions considered reader is referred to an authoritative, com-
include: fibromyalgia, articular dysfunc- prehensive, readable book for patients
tions, temporomandibular dysfunctions, oc- written by a nurse and a physician. For 81

cupational myalgia, nonmyofascial TrPs, one interested in a manual that similarly


and the posttraumatic hyperirritability syn- identifies the clinical nature of both fi-
drome. Also, the relation between acupunc- bromyalgia and chronic myofascial pain
ture and myofascial TrPs is considered. caused by TrPs, the reader is referred to the
Myofascial Trigger Points Mistakenly Di- Survival Manual by Starlanyl and
agnosed as Other Conditions. Those clini- Copeland. Dr. Starlanyl is a physician
263

cians who have become skilled at diagnosing who herself has both conditions and has
and effectively managing myofascial TrPs learned how she can deal with them. A
frequently see patients who were referred to third useful patient manual is focused on
them by other practitioners as a last resort. myofascial TrPs. It is written by a physical
These patients commonly arrive with a long therapist who learned about TrPs through
list of diagnostic procedures and diagnoses, personal experience. " 118

none of which satisfactorily explained the At the beginning of this decade, the
cause of, or relieved, the patient's pain. Table American College of Rheumatology estab-
2.5 lists examples of these diagnoses. Beside lished official criteria for the classification
each diagnosis are listed likely TrP sources of of fibromyalgia (Table 2.6). Anyone writ-
294

that pain. This frustrating situation is under- ing a paper that identifies subjects as hav-
standable because very few medical schools ing fibromyalgia should adhere closely to
or physical therapy schools teach myofascial these criteria. Likewise, in examining pa-
TrPs as a regular part of the curriculum, so tients for the possibility of fibromyalgia,
most physicians and therapists now in prac- these are the only criteria that determine
tice have received at most a hit-or-miss officially whether or not that is the appro-
exposure to myofascial TrPs. For most clini- priate diagnosis. This is a clinical opera-
cians, their understanding of, and compe- tional definition that makes no pretense at
tence achieved in, diagnosing myofascial identifying an etiology. In fact, Simms, et
TrPs must have been achieved through sup- al. * studied tenderness in 75 anatomical
23

plemental learning following graduation. sites comparing fibromyalgia patients and


This list reminds us that every skeletal normal control subjects. Simms, et al. con-
muscle of the body can develop TrPs, and cluded that of the previously proposed 18
many of them commonly do. Since myo- tender points, only 2 were included in

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Chapter 2 / General Overview 37

Table 2.5. Common Referral Diagnoses Received When Overlooked TrPs were Actually
the Cause of Patients Symptoms
Some Likely Trigger Point Trigger Point Manual
Initial Diagnosis Sources Chap. # (Volume 1)

Angina Pectoris (atypical) Pectoralis major 42


Appendicitis Lower rectus abdominis 49
Atypical Angina Pectoralis major 42
Atypical Facial Neuralgia 274
Masseter 8
Temporalis 9
Sternal division of sternocleidomastoid 7
Upper trapezius 6
Atypical Migraine Sternocleidomastoid 7
Temporalis 9
Posterior cervical 16
Back Pain, Middle Upper rectus abdominis 49
Thoracic paraspinals 48
Back Pain, L o w 255
Lower rectus abdominis 49
Thoracolumbar paraspinals 48
see Volume 2 muscles
(Bicipital) Tendinitis Long head of biceps brachii 30
Chronic Abdominal Wall P a i n 106
Abdominal muscles 49
Dysmenorrhea Lower rectus abdominis 49
Earache (enigmatic) Deep masseter 8
Epicondylitis Wrist extensors 34
Supinator 36
Triceps brachii 32
Frozen Shoulder Subscapularis 26
Myofascial Pain Dysfunction Masticatory muscles 8-11
Occipital Headache 103
Posterior cervicals 16
Postherpetic Neuralgia Serratus anterior 46
Intercostals 45
Radiculopathy, C 6 Pectoralis minor 43
Scalenes 20
Scapulocostal Syndrome Scalenes 20
Middle trapezius 6
Levator scapulae 19
Subacromial Bursitis Middle deltoid 28
Temporomandibular Joint Disorder Masseter 8
Lateral pterygoid 11
Tennis Elbow Finger extensors 35
Supinator 36
Tension Headache 140
Sternocleidomastoid 7
Masticatory muscles 8-11
Posterior cervicals 16
Suboccipital muscles 17
Upper trapezius 6
Thoracic Outlet Syndrome 127
Scalenes 20
Subscapularis 26
Pectoralis minor and major 43,42
Latissimus dorsi 24
Teres major 25
Tietze's Syndrome Pectoralis major enthesopathy 42
Internal intercostals 45

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38 Part 1 / Introduction

Table 2.6. The American College of Rheumatology 1990 Criteria for the Classification
of Fibromyalgia*

1. History of widespread pain.


Definition. Pain is considered widespread when all of the following are present: pain in the
left side of the body, pain in the right side of the body, pain above the waist, and pain below
the waist. In addition, axial skeletal pain (cervical spine or anterior chest or thoracic spine or
low back) must be present. In this definition, shoulder and buttock pain are considered as pain
for each involved side. "Low back" pain is considered lower segment pain.
2. Pain in 11 of 18 tender point sites on digital palpation.
Definition. Pain on digital palpation must be present in at least 11 of the following 18 tender
point sites:
Occiput: bilateral, at the suboccipital muscle insertions.
Low cervical: bilateral, at the anterior aspects of the intertransverse spaces at C5-C7.
Trapezius: bilateral, at the midpoint of the upper border.
Supraspinatus: bilateral, at origins, above the scapular 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.
Digital palpation should be performed with an approximate force of 4 kg.
For a tender point to be considered "positive" the subject must state that the palpation was
painful. "Tender" is not to be considered "painful."
Note: For classification purposes, patients are said to have fibromyalgia if both criteria are
satisfied. Widespread pain must have been present for at least 3 months. The pres-
ence of a second clinical disorder does not exclude the diagnosis of fibromyalgia.

Reprinted by permission from Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 crite-
ria for the classification of fibromyalgia: Report of the Multicenter Criteria Committee. Arthritis Rheum 1990; 33:160-170.

what they found to be the 19 most dis- bromyalgia was at first thought to originate
criminating points. The tender sites se- in skeletal muscles, a careful histological
lected as diagnostic criteria are quite arbi- and ultrastructural study has shown no ab-
trary, but adequately representative of the normality of skeletal muscles that was suf-
patient's total-body, physiologically en- ficiently common for that to be considered
hanced sensitivity to pain. the cause of fibromyalgia. ' 18 224

Fibromyalgia can be thought of as a set On the other hand, the etiology of myo-
of core features and two types of ancillary fascial TrPs is clearly a focal muscular dys-
features. The core features are generalized function which can exert a strong influence
pain and tenderness over 11 of 18 pre- on all major parts of the nervous system,
scribed anatomical sites. Characteristic an- and can lead to spinal level neuroplastic
cillary features occur in over three-quarters changes that help to convert an acute pain
of individuals: fatigue, nonrestorative problem into a chronic one.
sleep, and morning stiffness. Less common There is strong research support for a
findings, in perhaps 2 5 % of cases, include: systemic, metabolic/neurochemical patho-
irritable bowel syndrome, Raynaud's phe- genesis of fibromyalgia. Fibromyalgia is
nomenon, headache, subjective swelling, considered an upward modulation of pain
nondermatomal paresthesia, psychological sensitivity throughout the body. Extensive
stress, and marked functional disability. research in recent years has led to the
Patients with fibromyalgia experience at "serotonin deficiency hypothesis" that 224

least as much pain as those with other involves measurable disturbance in noci-
painful disease states. Even though fi-
183
ception, including serotonin regulation of

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Chapter 2 / General Overview 39

the hypothalamic pituitary axis and the pi- cial pain due to TrPs from fibromyalgia. The
tuitary adrenal axis, and substance P. There following comments relate to this table.
is a close relationship between substance P Trigger points occur with nearly equal
and calcitonin gene-related peptide that prevalence in male and female subjects, 261

also appears to be involved. Experimen- 224


whereas usually between 4 to 9 times as
tal evidence also indicates that N-methyl- many females as males are observed to
D-aspartate receptors of the central nervous have fibromyalgia, 182
depending on the
system are involved in the pain mecha- population studied.
nisms of fibromyalgia. A specific and of-
262
Since fibromyalgia is by definition char-
ten hard-to-detect thyroid dysfunction may acterized by widespread, generalized pain
be a commonly overlooked, but treatable, and tenderness, this provides a basic dis-
factor in fibromyalgia. Muscle nocicep-
176
tinction from a myofascial TrP, which causes
tive input may contribute to the pathogen- a specific localized pain and tenderness pat-
esis or severity of fibromyalgia. 18
tern originating from a lesion in a muscle.
Many studies show that a considerable When examined, muscles harboring
number of fibromyalgia patients also have TrPs feel tense because of the contraction
myofascial TrPs. In three studies, the per- knots and taut bands, whereas muscles of a
centages of fibromyalgia patients who also patient with fibromyalgia feel softer and
have TrPs were reported as 1 0 0 % to 6 8 % . ' 7 0
more doughy, unless the fibromyalgia pa-
go, 104 A study of 22 fibromyalgia patients 119
tient also has TrPs in the muscle being ex-
found that 4 0 % needed TrP injections, and amined. The muscles of fibromyalgia pa-
8 9 % of those injected reported relief. One tients show increased compliance.
early author considered the presence of Restricted range of motion is character-
myofascial TrPs an essential feature of pri- istic of TrPs, whereas hypermobility is rel-
mary fibromyalgia. layson45
considered
144
atively common in children 86
and in
injection of TrPs an important part of treat- adults who have fibromyalgia.
292

ing fibromyalgia syndrome. Others ' 217 230


Patients with myofascial pain are exam-
emphasized the clinical importance of ined for myofascial TrPs as described in
clearly distinguishing fibromyalgia and this volume, whereas fibromyalgia patients
myofascial TrPs. are examined for tender points. Myofascial
Distinguishing myofascial TrPs and fi- TrPs and fibromyalgia tender points are
bromyalgia is relatively simple when the equally tender at the cutaneous, subcuta-
myofascial TrPs are acute, but can be much neous, and intramuscular levels. However,
more difficult when the myofascial TrPs the two conditions are sharply distin-
have evolved into a chronic pain syndrome guished by the fact that locations other
through neglect or inappropriate treatment. than tender point sites in fibromyalgia pa-
Fibromyalgia, by definition, is a chronic tients are as tender at all three depths of
pain syndrome. Table 2.7 lists a number of tissue as are their tender point sites, 284

clinical features that distinguish myofas- whereas non-TrP sites in myofascial pain

Table 2.7. Clinical Features Distinguishing Myofascial Pain due to Trigger Points (TrPs)
from Fibromyalgia

Myofascial Pain (TrPs) Fibromyalgia

1 female : 1 male 4-9 females : 1 male


Local or Regional pain Widespread, general pain
Focal tenderness Widespread tenderness
Muscle feels tense (taut bands) Muscle feels soft and doughy
Restricted range of motion Hypermobile
Examine for trigger points Examine for tender points
Immediate response to injection of TrPs Delayed and poorer response to injection of TrPs
2 0 % also have fibromyalgia 90
7 2 % also have active TrPs 90

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40 Part 1 / Introduction

patients have been shown to measure the function), Korr and associates demonstrated
same high pain thresholds as correspond- decreased pain thresholds, increased sym-
ing sites in normal subjects. Fibromyal-
284
pathetic activity (decreased skin resistance),
gia patients are abnormally tender almost and facilitation of motor pathways. With
154

everywhere. Myofascial pain patients are other coworkers, Korr demonstrated a


50

abnormally tender only at sharply circum- muscular component to the facilitated seg-
scribed TrP sites and specific sites of re- ment. They reported a marked increase in
ferred tenderness. paraspinal muscle activity associated with
Recently, tender points have been desig- dysfunctional articular segments. However,
nated as fibrositic tender points. This is
183 they apparently were unaware of myofas-
an unfortunate misnomer since there is no cial TrPs and how they related to the muscle
palpable or pathological evidence that tenderness that the authors associated
muscular fibrosis is involved in fibromyal- closely with the articular dysfunction.
gia. It is equally inappropriate as a name for There is a remarkable analogy between
TrPs with rare exceptions. this concept of a facilitated segment that
TrPs injected in myofascial pain patients can strongly influence the three compo-
who also have fibromyalgia showed a de- nents of the nervous systemmotor, sen-
layed and poorer response than TrPs in- sory, and autonomicand the nervous sys-
jected in patients who have myofascial pain tem effects that can be caused by
syndrome without fibromyalgia. 125
myofascial TrPs. The important relation-
Articular Dysfunctions. Articular dys- ship between the muscles and articular
functions that require manual mobilization dysfunction is well recognized by many
make up one of the three major categories clinicians, but has been badly neglected as
of musculoskeletal pain syndromes that a subject for serious research investigation.
are often overlooked. The pain in these Karel L e w i t published observations
168,169

syndromes is commonly caused by TrPs. and studies from his extensive experience
Traditional medical physicians pioneered as a neurologist practicing manual medi-
an understanding of TrPs while osteo- cine and described the close relationship
pathic physicians, chiropractors, and prac- between articular dysfunction and myofas-
titioners of orthopedic medicine have de- cial TrPs. He emphasizes the importance of
veloped and promoted manual medicine addressing therapeutically the muscle-
techniques. Until recently, the two have, dysfunction component and the articular-
for the most part, followed separate paths. dysfunction component of musculoskele-
The osteopathic pioneer F. Mitchell for tal pain syndromes when both are
many years taught, and eventually pub- present. 170
The increased tension of TrP
lished, his insight into the close relation- taut bands and their facilitation of motor
ship between articular dysfunctions and activity can maintain displacement stress
the muscular system. However, his writ-
195
on the joint while abnormal sensory input
ings show no evidence that he was aware from the dysfunctional joint can reflexly
of the important role of myofascial TrPs. activate the TrP dysfunction. The two con-
Currently, at least one college of osteopa- ditions can aggravate each other.
thy emphasizes the importance of the close Since publication of the Trigger Point
relation between TrPs and articular dys- Manual in 1983, the chiropractic profession
function. Rarely do medical schools teach has become increasingly interested in myo-
mobilization of joints. Physical therapy cur- fascial TrPs as such. One of their members
ricula are more likely to include the diagno- has presented the only published report of 175

sis and treatment of articular dysfunctions which we are aware that looked specifically
than that of myofascial pain due to TrPs. at the relationship between articular dys-
An outstanding osteopathic pioneer in function and TrPs. In this preliminary test,
the establishment of physiological dysfunc- he examined the relative amount of EMG ac-
tions associated with articular dysfunction, tivity that appeared in paraspinal muscles
Irvin Korr, explored and promoted the con- of normal, slightly involved, and severely
cept of the facilitated segment. In the seg- involved segments in response to pressure
mental vicinity of an "osteopathic lesion" on a distant TrP. He found that induction of
(vertebra with evidence of articular dys- additional pain by pressure on a distant ac-

Copyrighted Material
Chapter 2 / General Overview 41

tive TrP markedly augmented the EMG ac- tently overlooking a major treatable cause of
tivity in muscles of severely subluxed seg- muscle pain, confusion and frustration are
ments as compared to normal segments. bound to follow. One study queried doc-
55

This finding indicates that articular dys- tors as to their understanding of the term
function can effectively increase the respon- "repetitive strain injury" and found that, be-
siveness of motor neurons of adjacent mus- cause diagnostic criteria are so variable
cles to nociceptive input from distant TrPs. among papers, the term is effectively mean-
Occupational Myalgias. The subject of ingless. Half of the doctors who responded
occupational myalgias has attracted increas- were of the opinion that there was no gen-
ing interest in recent years. A MEDLINE uine organic condition corresponding to
search from 1990 through 1995 recovered their assessment of what that term means.
56 abstracted articles on the subject. The 11 The other half thought it was a genuine dis-
different terms used by the authors fell into ease entity but showed little agreement as to
3 groups: cumulative trauma, repetitive what they thought was wrong. One likely
strain, and overuse. Twenty of the papers possibility is that a TrP origin of the pain is
dealt with cumulative trauma, of which 18 being overlooked by most practitioners con-
used the term "cumulative trauma disor- cerned with this condition.
der." In the repetitive strain group, only 12 Fortunately, most authors approached
of the 28 papers used the term "repetitive resolution of occupational myalgias by re-
strain injury." Others used "repetitive mo- ducing the overload and/or overuse when-
tion injuries" and "repetitive motion stud- ever possible. This way, the mechanical
ies." Seven of the 8 in the overuse group perpetuating factors that could have been
were labeled "overuse syndrome." This is aggravating TrPs were ameliorated or elim-
another example of many authors using dif- inated, allowing the muscle to partially, or
ferent terms to identify essentially the same occasionally completely, recover normal
muscle pain syndrome. All authors had one function.
root concern-patients developed muscu- However, if the source of pain and dys-
loskeletal pain symptoms as a result of work function of occupational myalgias were
activity. Many authors expressed frustration specifically related to TrPs in the muscle
at the lack of a satisfactory explanation for being overused, local TrP management of
the cause of the pain itself. that muscle would expedite return to nor-
A cardinal feature of myofascial TrPs is mal function. The employees or patients
that they are activated either by an acute could be trained to recognize activities that
overload or repeated overuse. The one com- abused the involved muscles and to tailor
mon denominator of all 56 articles is the as- routine activities and stretching exercises
sociation of musculoskeletal pain with over- to maintain normal function of those mus-
load and/or overuse of the muscle. Placing a cles, which would greatly reduce the like-
muscle in an awkward position that requires lihood of reactivation. R o s e n empha-
219,220

sustained contraction of specific muscles in sizes the importance of the awareness of


order to maintain that posture is one of the TrPs in the management of painful muscles
most common examples of overuse. that are used beyond their "critical load,"
Headley emphasized how commonly the
118 especially among performing artists.
symptoms of patients with cumulative Trigger Points and Acupuncture. The
trauma disorder are caused by myofascial distinction between TrPs and acupuncture
TrPs. She demonstrated electromyographi- points for the relief of pain is blurred for a
cally abnormal function of muscles caused number of good reasons. First, the mecha-
by the TrPs in these patients. This study sup- nisms responsible for the pain relief associ-
ports the clinical experience of the authors ated with the two concepts have until very
and practicing c l i n i c i a n s .
178282
recently been enigmatic or controversial.
Remarkably, NOT ONE of these 56 occu- Second, as reported by Melzack, et al., wv

pational myalgia abstracts indicated that the there is a high degree of correspondence
author(s) had considered the possibility that ( 7 1 % based on their analysis) between
myofascial TrPs may be contributing to the published locations of TrPs and classical
workers' or patients' problems. This is a se- acupuncture points for the relief of pain.
rious oversight for all concerned. By consis- Third, a number of studies report similar

Copyrighted Material
42 Part 1 / Introduction

results when needling TrPs using acupunc- point. However, essentially the same sen-
ture needles as when using hypodermic sory phenomenon is frequently observed
needles with injected s o l u t i o n .
110,123,141
when injecting a TrP and the local twitch
The evidence that TrP phenomena origi- response is observed. In a study of the
123

nate in the vicinity of dysfunctional end- analgesia obtained by electroacupuncture,


plates is presented later in this chapter. the authors concluded that the effect may
210

Classical acupuncture points are identified be the result of intense stimulation of TrPs.
as prescribed points along meridians de- Another version of "acupuncture" used
fined by ancient Chinese documents. As for the treatment of TrPs involved insertion
Melzack, et al. showed, the ancient Chi-
187
of the needle to only a depth of approxi-
nese clinicians were astute enough to rec- mately 4 mm into the skin and subcuta-
ognize the importance of many common neous tissue overlying the TrP. 7, 8
Com-
TrP locations and to include them in their pared to needle penetration of the TrP, this
charts of acupuncture points for pain. insertion technique must involve an en-
Currently, there are a number of practi- tirely different mechanism that depends on
tioners of acupuncture who use a modified nervous system modulation of TrP activ-
definition of acupuncture points which ity. This technique requires a controlled
247

would selectively identify TrP locations. Bel- clinical study to confirm its efficacy for
grade 13
states that "tender points are TrPs and, if effective, needs further re-
acupuncture points and can often be chosen search to identify its mechanism.
for therapy." If one defines an acupuncture Ward examined 12 acupuncture sites
286

point for treatment of pain as a tender spot, that were also common TrP sites in either a
one is using a cardinal definition of TrPs as a trapezius or infraspinatus muscle for the
criterion for an acupuncture point, which electrical activity characteristic of an ac-
would increase the likelihood of treating a tive locus in a TrP (see Section D, Nature of
TrP and calling it an acupuncture point. Sup- Trigger Points). Characteristic endplate
porting this concept, Loh, et al. compared
174
spike activity was observed in every case.
acupuncture therapy with medical treatment In conclusion, frequently the acupunc-
for migraine and muscle tension headaches. ture point selected for the treatment of pain
They found that benefit from acupuncture is actually a TrP. Sometimes, it is not a TrP.
was more likely to occur when the subject Because of the fundamental differences in
was treated at local tender muscular points. mechanism, approach to management, and
However, some classical acupuncture points prognostic implications, it is important
for pain cannot be myofascial TrPs, such as that clinicians identify TrPs as such so they
those in the ear. Central myofascial TrPs oc- can institute an appropriate home program
cur in the midfiber region of a muscle belly. and correct perpetuating factors, if present.
It is now well-established that pain relief Nonmyofascial Trigger Points. Trigger
experienced from classical acupuncture points that refer pain also may be observed
points is associated with an endorphin re- in what appears to be normal skin, in scar
sponse in the central nervous system. 13
tissue, fascia, ligaments, and the perios-
However, the reduction of pain by inactivat- teum. The reason for sensitization of noci-
ing a TrP is produced by eliminating the no- ceptors at these sites needs to be clarified,
ciceptive focus in a muscle that is responsi- but must be different from the central TrP
ble for the pain. The fact that nociceptive mechanism that is closely associated with
input from the TrP can cause some central motor endplates.
modulation of endorphins tends to con-
69
Sinclair reported skin TrPs in 8 of 30
256

fuse the issue but does not change the pri- healthy young adults. He found sharply
mary muscular site of the TrP mechanism. circumscribed TrP areas while exploring
One student of acupuncture, Pomer- the body by pinching the skin between the
anz, 208
emphasized the importance of the finger and thumb. He studied 18 skin TrPs
Deqi phenomenon for identifying an intensively in 4 of these subjects and per-
acupuncture point. The Deqi phenomenon formed a skin biopsy. Generally, a sharp,
is described as a sensation of fullness, dis- stinging, moderately severe pain was re-
tension, and pins and needles when the in- ferred either locally or remotely to the skin
serted needle encounters the acupuncture from a cutaneous TrP. The area of referred

Copyrighted Material
Chapter 2 / General Overview 43

pain also showed modulation of sensation which referred pain to the ankle and foot.
(referred tenderness or referred dysesthe- Myofascial TrPs resulting from acute sprains
sia) by stimulation of the TrP. Some of the knee, ankle, wrist and metacarpopha-
reference zones were within the same seg- langeal joint of the thumb have been re-
mental distribution, but others had no seg- ported to cause referred pain, which was at
mental relation to their skin TrPs. first elicited and then permanently relieved
Trommer and Gellman reported seven
281 by injection of each TrP with physiologic
patients in whom skin TrPs referred pain or saline. Leriche identified ligamentous
268 2 7 7 166

numbness to other skin areas that were of- TrPs following fracture or sprain; the TrPs re-
ten nearby, sometimes remote. The skin sponded completely to 5 or 6 injections of a
TrPs were found by pricking the skin with a local anesthetic. Gorrell reviewed the
100

needle, exploring for a sensitive spot that re- anatomy of the ankle ligaments and de-
produced the patient's symptoms. In every scribed a technique for the identification and
case, the symptoms were relieved by re- injection of ligamentous TrPs at this joint.
peated intracutaneous injections, but only Kraus briefly reviewed the literature
159

if they were made precisely at the skin TrP. on ligamentous TrPs and noted that they
These studies do not suggest a con- are easily localized for injection, which of-
stancy in the referred pain patterns of cuta- ten gives immediate pain relief and a
neous TrPs like that observed for myofas- postinjection soreness lasting up to 10
cial TrPs. Also, there was no indication in days. Hackett illustrated patterns of pain
113

these reports, nor in our observations, that referred from the iliolumbar, sacroiliac,
the reference zones of skin TrPs bear any sacrospinal, and sacrotuberous ligaments;
relation to the reference zones of TrPs in he recommended injection of a sclerosing
underlying muscles. agent, which was not widely accepted be-
In our experience, scar TrPs (in skin or cause his technique caused too many com-
mucous membranes) refer burning, prick- plications. Dittrich found TrPs in the
54

ling, or lightning-like jabs of pain. De- aponeurosis of the latissimus dorsi muscle
falque reported using alcohol injection to
49 where it joins the lumbodorsal fascia; the
treat TrPs in postoperative scars of 69 pa- TrPs referred pain to the shoulder region.
tients, and 9 1 % of the patients experienced Two authors, de Valera and Raftery re- 51

permanent cure or marked improvement. ported trigger areas in three pelvic liga-
Such scar TrPs can often be inactivated by ments, the sacroiliac, sacrospinous and
precise intracutaneous injection with 0.5% sacrotuberous, which, when strained, be-
procaine solution. In refractory cases, the come tender to palpation, refer pain, and
addition of a soluble steroid to the local respond to injection with a local anesthetic.
anesthetic solution used for injection of the Tenderness at a musculotendinous junc-
scar TrP can be effective. Bourne injected
22
tion may be enthesopathy secondary to
the scar TrPs with triamcinolone acetonide taut-band tension of a TrP in the muscle
and lidocaine hydrochloride. Travell simi- belly or may be a local tendinous TrP.
larly used dexamethasone sodium phos- Weiser described point tenderness at the
289

phate with 0.5% procaine, injecting a few insertion of the semimembranosus muscle
tenths of a milliliter at any one location. in 98 patients who complained of sponta-
Nonmyofascial TrPs may also be found neous pain at the medial aspect of the knee.
in fascia, ligaments, and joint capsules. The pain was reproduced by local pressure
Kellgren demonstrated experimentally
149 or tension at that insertion site. Symptoms
that fascial epimysium of the gluteus were relieved by injecting 2% lidocaine hy-
medius muscle referred pain several cen- drochloride with triamcinolone into the
timeters distally when injected with 0.1 ml tender spot. Unless the clinician also exam-
of 6% saline solution, and that a tender ines the muscle for taut bands and TrPs, it is
spot in the tendon of the tibialis anterior, not clear what is the cause of the tenderness
similarly injected, referred pain to the me- and therefore how to prevent its recurrence.
dial aspect of the ankle and instep. Kellgren established an experimental
150

Travell reported that an acute sprain of


269
basis for periosteal TrPs by demonstrating
the ankle was accompanied by the develop- that the periosteum also can refer pain in
ment of four TrPs in the joint capsule, each of response to injection of hypertonic saline,

Copyrighted Material
44 Part 1 / Introduction

just as the muscles do. Among 160 experi- from such stimulation is slow. Even with
ments designed to determine the nature of mild exacerbations, it may take the pa-
referred pain originating from deep tissues, tients many minutes or hours to return to
Inman and Saunders reported that nox-
134
the baseline pain level. Severe exacerba-
ious stimulation of the periosteum by tion of pain may require days, weeks, or
scratching it with a needle, by injecting it longer to return to baseline. These patients
with 6% salt solution, or by applying a may have multiple TrPs which are not the
measured pressure elicited severe referred primary cause of their condition, but
pain that sometimes radiated for consider- which do contribute to their misery and re-
able distances. Tenderness was referred to quire special consideration in treatment
the muscles and bony prominences within because of the adverse consequences of
the pain reference zone, as also happens strong sensory stimulation, especially
with myofascial TrPs. Repeated stimula- pain.
tion of the same periosteal or ligamentous Patients with posttraumatic hyperirri-
attachments consistently referred pain in tability syndrome almost always give a his-
the same direction, but the extent of radia- tory of having coped well in life prior to the
tion varied with the intensity of the stimu- injury, having paid no more attention to
lus. Unfortunately, the authors did not re- pain than did their friends and family. They
port the distribution of these specific were no more sensitive to ordinary stimuli
periosteal referred pain patterns. Auto- than other persons. From the moment of
nomic reactions to the stimulation, such as the initial trauma, however, pain suddenly
sweating, blanching, and nausea were fre- became the focus of life. They must pay
quently observed in the subjects. close attention to the avoidance of strong
Clinically, the periosteum can be a potent sensory stimuli; they must limit activity be-
source of referred pain. Relief of this re-
107 cause even mild to moderate muscular
ferred pain may be obtained by injecting pe- stress or fatigue intensifies the pain. Efforts
riosteal TrPs, analogous to the relief obtained to increase exercise tolerance may be self-
by injecting myofascial or cutaneous TrPs. 165 defeating. Such patients, who suffer
Posttraumatic Hyperirritability Syn- greatly, are poorly understood and, through
drome. The term "posttraumatic hyperir- no fault of their own, are difficult to help. It
ritability syndrome" was i n t r o d u c e d135,237 may be worth considering an unconven-
to identify a limited number of patients tional but knowledgeable approach, such
with myofascial pain who exhibit marked as that of Goldstein, for these patients.
98

hyperirritability of the sensory nervous In patients with posttraumatic hyperirri-


system and of existing TrPs. A similar syn- tability, the sensory nervous system behaves
drome was described earlier by Margoles much as the motor system does when the
as the stress neuromyelopathic pain syn- spinal cord has lost supraspinal inhibition.
drome. These patients may be sometimes
180
With increased motor responsiveness, a
identified as suffering from severe sudden- strong sensory input of almost any kind can
onset fibromyalgia that is associated with activate nonspecific motor activity (spasm)
physical trauma and myofascial TrPs. This for an extended period of time. Similarly in
syndrome follows a major trauma, such as patients with hyperirritability syndrome, a
an automobile accident, a fall, or a severe strong sensory input can increase the ex-
blow to the body that is apparently suffi- citability of the nociceptive system for long
cient to injure the sensory modulation periods. In addition, these patients may show
mechanisms of the spinal cord or brain lability of the autonomic nervous system
stem. The patient has constant pain, which with skin temperature changes and swelling
may be exacerbated by the vibration of a that resolve with inactivation of regional
moving vehicle, by the slamming of a door, TrPs. Since routine medical examination of
by a loud noise (a firecracker at close hyperirritability syndrome patients fails to
range), by jarring (bumping into something show any organic cause for their symptoms,
or being jostled), by mild thumps (a pat on they are often disposed of by assigning them
the back), by severe pain (a TrP injection), a psychological or behavioral diagnosis.
by prolonged physical activity, and by Any additional fall or motor vehicle acci-
emotional stress (such as anger). Recovery dent that would ordinarily be considered

Copyrighted Material
Chapter 2 / General Overview 45

minor can severely exacerbate the hyperirri- and myosin filaments. Ionized calcium trig-
tability syndrome for years. Unfortunately, gers the interaction between the filaments,
with successive traumas, the individual may and adenosine triphosphate (ATP) provides
become increasingly vulnerable to subse- the energy. The ATP releases a myosin head
quent trauma. A common finding is a series from the actin after one power "stroke" and
of relatively minor motor vehicle accidents immediately "recocks" it for another cycle.
or falls over a period of several years that cu- The ATP is converted to adenosine diphos-
mulatively became severely incapacitating. phate (ADP) in the process. The presence of
Similar phenomena were subsequently calcium immediately triggers another cycle.
described as the cumulative trauma disor- Many such power "strokes" are needed to
der and the jolt syndrome.
30 01 produce the random rowing motion that is
required of many myosin heads of many fil-
C. MUSCLE STRUCTURE AND aments to accomplish one smooth twitch
FUNCTION contraction.
To understand the nature of myofascial In the presence of both free calcium and
TrPs, it is necessary to understand several ATP, the actin and myosin continue to in-
197

aspects of basic muscle structure and func- teract, expending energy and exerting force
tion that are not usually emphasized. In to shorten the sarcomere. This interaction of
addition to the material presented here, actin and myosin, that produces tension and
this subject is also treated in detail in consumes energy, cannot happen if the sar-
Chapter 8 of a companion text. 191
comeres are lengthened (the muscle
stretched) until no overlap remains between
Muscle Structure and Contractile the actin and the myosin heads. This has
Mechanism started to happen in the lower panel of Fig-
A striated (skeletal) muscle is an assem- ure 2.5, where the actin filaments are beyond
bly of fascicles, each of which is a bundle the reach of half of the myosin heads (cross
of roughly 100 muscle fibers (Fig. 2.5, fiber bridges). The contractile force that any one
in upper panel). Each muscle fiber (a mus- sarcomere can exert on activation depends
cle cell) encloses approximately 1000-2000 strongly on its length. The force drops off
myofibrils in most skeletal muscles. A rapidly as the sarcomere approaches maxi-
myofibril consists of a chain of sarcomeres mum or minimum length (fully stretched or
connected serially, end-to-end. The basic fully shortened). Therefore, each sarcomere
contractile unit of skeletal muscle is the of a muscle can generate maximum force
sarcomere. Sarcomeres are connected to only in the midrange of its length but it can
each other by their Z lines (or bands) like expend energy in the fully shortened posi-
links in a chain. Each sarcomere contains tion trying to shorten further.
an array of filaments that consist of actin The calcium is normally sequestered in
and myosin molecules which interact to the tubular network of the sarcoplasmic
produce the contractile force. The middle reticulum (Fig. 2.5, upper panel, and Fig.
panel of Figure 2.5 shows a resting-length 2.6) that surrounds each myofibril. Calcium
sarcomere with complete overlap of actin is released from the sarcoplasmic reticulum
and myosin filaments (maximum contrac- that surrounds each myofibril when a prop-
tile force). During maximum shortening agated action potential reaches it from the
the myosin molecules impinge against the surface of the cell through " T " tubules (Fig.
" Z " band blocking further contraction (not 2.6). Normally, after it has been released, the
shown). The lower panel shows a nearly free calcium is quickly pumped back into
fully stretched sarcomere with incomplete the sarcoplasmic reticulum. The absence of
overlap of actin and myosin molecules (re- free calcium terminates the contractile ac-
duced contractile force). tivity of the sarcomeres. In the absence of
The myosin heads of a myosin filament ATP, the myosin heads remain firmly at-
are a form of the enzyme adenosine triphos- tached (failure to "recock") and the muscle
phatase that contacts and interacts with the becomes stiff as in rigor mortis.
actin to produce a contractile force. These A well illustrated, more detailed de-
contacts are seen through the electron mi- scription of the entire contractile mecha-
croscope as cross bridges between the actin nism is available. 3

Copyrighted Material
Muscle

Fascicle Fiber Fibril

Sarcoplasmic
reticulum

Muscle shortened

Ca ATP

Actin Myosin Cross


bridges

M u s c l e stretched
Sarcomere
Ca Z line

A band
I band I band

Figure 2.5. Structure and contractile mechanism of brings the Z lines together and shortens the sarcom-
normal skeletal muscle. The muscle is a bundle of fas- ere, which is the source of the contractile force that
cicles (light red), each of which consists of striated shortens the muscle. The portions of the actin fila-
muscle cells or fibers (fiber). One fiber contains on the ments in two sarcomeres that are adjacent to a Z line
order of 1000 myofibrils (fibril). The myofibril is sur- and are free of myosin filaments form an / band. The
rounded by a network of saclike structure, the sar- presence of myosin filaments determines the extent of
coplasmic reticulum (sarcoplasmic reticulum). Insets: the A band. The presence of only an A band in the ab-
adenosine triphosphate (ATP) and free calcium (Ca ) ++
sence of an I band indicates maximum shortening
activate the cross bridges of the myosin (shaded rods) (complete overlap of filaments).
to tug on the actin filaments (open rods). This pull

Copyrighted Material
Chapter 2 / General Overview 47

Molecular T Tubule
Feet (Action Potential)

Calcium Storage

Myosin Actin

Terminal
Cisternae Sarcoplasmic Triad
T Tubule Reticulum

Z Line Z Line
M Line
I Band I Band
H Band

A Band

Figure 2.6. One sarcomere shown schematically in where the actin molecular filaments (thin lines) attach
longitudinal section that also shows a triad and sar- to the Z-line and the I band includes as much of the
coplasmic reticulum in cross section (see Fig. 2.5 for actin filaments as are free of myosin cross bridges.
orientation). The human sarcoplasmic reticulum is a The M line is produced by the overlapping interweav-
tubular network that surrounds the myofibrils in a ing tails of the myosin molecules, which head away
muscle fiber of skeletal muscle. It is the reservoir for from the M line in both directions.
calcium, which is normally released by action poten- One triad (two terminal cisternae and one T tubule
tials that are propagated along the surface of the mus- seen in red box) is shown in more detail in the upper
cle cell (sarcolemma) and along the T-tubules (open schematic. The depolarization (that is caused by the
circles), which are invaginations of the sarcolemmal action potential propagated along the T-tubule) is
membrane. The lower schematic portrays one sar- transferred through molecular feet to induce calcium
comere (the functional unit of skeletal muscle) that ex- release (red arrows) from the sarcoplasmic reticulum.
tends from one Z-line to the next Z-line. The Z-line is Calcium (red dots) interacts with the contractile ele-
where sarcomeres join to form a chain of interlaced ments to induce contractile activity, which continues
links. The A band is the region occupied by myosin until the calcium is pumped back into the sarcoplas-
molecules (brush-like structures) and their projecting mic reticulum or until the ATP energy supply becomes
myosin heads. The I band includes a central Z-line depleted.

The Motor Unit and the multiple motor endplates where


Motor units are the final common path- each nerve branch terminates on one mus-
way through which the central nervous cle fiber (cell). The motor unit includes all
system controls voluntary muscular activ- of those muscle fibers innervated by one
ity. Figure 2.7 schematically illustrates a motoneuron. In summary, a motor unit in-
motor unit, which consists of the cell body cludes one a-motoneuron and all of the
of an a-motoneuron in the anterior horn of muscle fibers that it supplies. Any one
the spinal cord, its axon, (which passes muscle fiber normally receives its nerve
through the spinal nerve and then through supply from only one motor endplate and
the motor nerve and enters the muscle therefore only one motoneuron. The mo-
where it branches to many muscle fibers), toneuron determines the fiber type of all of

Copyrighted Material
48 Part 1 / Introduction

Spinal cord

Anterior horn

Spinal nerve Cell body of motor neuron


Axon

M u s c l e nerve

Motor a x o n

Figure 2.7. Schematic of a motor unit. The motor unit (solid black circle). Approximately 10 motor units in-
includes the cell body of a motor neuron, its axon, all terdigitate at any one location so that one axon sends
its arborizations, and the muscle fibers that it supplies a branch to approximately every tenth muscle fiber.
(usually about 500). In human skeletal muscle, each fi-
nal arborization terminates at one motor endplate

the muscle fibers that it supplies. In pos- nerve fiber (axon) through each of its ar-
tural and limb muscles, one motor unit borizations to the specialized nerve termi-
supplies between 300 and 1500 muscle nal that helps to form the neuromuscular
fibers. The smaller the number of fibers junction (motor endplate) on each muscle
that are controlled by individual motoneu- fiber. On arrival at the nerve terminal, the
rons of a muscle (smaller motor units), the electrical action potential is relayed chem-
finer is the motor control in that muscle. ically across the synaptic cleft of the neu-
When the cell body of a motor neuron in romuscular junction to the postjunctional
the anterior horn initiates an action poten- membrane of the muscle fiber. There the
tial, the potential propagates along the message again becomes an action potential

Copyrighted Material
Chapter 2 / General Overview 49

that propagates in both directions to the Location of Motor Endplates


ends of the muscle fiber, causing the fiber to Understanding the location of motor
contract. The nearly synchronous firing of endplates is very important for the clinical
all the muscle fibers innervated by one neu- diagnosis and management of myofascial
ron produces a motor unit action potential. TrPs. If, as appears to be the case, the
One motor unit of a human limb muscle pathophysiology of TrPs is intimately asso-
usually spans a territory 5-10 mm in diam- ciated with endplates, one would expect to
eter. The diameter of one motor unit in
29
find TrPs only where there are motor end-
the biceps brachii muscle can vary from plates. Endplates in nearly all skeletal
2-15 mm. This allows space for the inter- muscles are located near the middle of
mingling of the fibers of approximately 15- each fiber, midway between its attach-
30 motor units. Both EMG and glycogen- ments. This principle in human muscles
depletion studies show that the density of was illustrated schematically (Fig. 2.8) by
muscle fibers supplied by one neuron is Coers and Woolf, who were outstanding
44

greater in the center of the motor unit terri- pioneers in the study of motor endplates.
tory than toward its periphery. Two re- 29
Aquilonius, et al. presented a detailed
5

cent studies of the diameter of masseter analysis of the location of endplates in the
motor units reported mean values of 8.8 human adult biceps brachii, tibialis ante-
3 . 4 m m and 3.7 2 . 3 m m , the latter
185 267
rior and sartorius muscles. Christensen il- 36

ranging between 0.4 mm and 13.1 mm. De- lustrated the midfiber distribution of end-
tailed three-dimensional analysis of the plates in stillborn infants in the opponens
distribution of fibers in five motor units of pollicis, brachioradialis, semitendinosus
cat tibialis anterior muscles showed some (two transverse bands of endplates), biceps
marked variations in diameter throughout brachii, gracilis (two distinct transverse
the length of a motor unit. Thus, the size
222
bands), sartorius (scattered endplates), tri-
of a taut band, if it were produced by only ceps brachii, gastrocnemius, tibialis ante-
one motor unit, could vary greatly and rior, opponens digiti quinti, rectus femoris,
could have more or less sharply defined extensor digitorum brevis, cricothyroid,
borders depending on the uniformity of and deltoid muscles.
muscle fiber density within that motor
unit. A similar variability could result from As the above illustrations show, the
the involvement of selected muscle fibers principle applies regardless of the fiber
of several interdigitating motor units. arrangement of the muscle. For that reason,
knowledge of the arrangement of fibers in a
muscle is essential to understanding the
The Motor Endplate Zone
arrangement of the endplates within that
The motor endplate is the structure that muscle and, therefore, where one can ex-
links a terminal nerve fiber of the motoneu- pect to find TrPs. Fiber arrangements of
ron to a muscle fiber. It contains the muscles include: parallel, parallel with
synapse where the electrical signal of the tendinous insertions, fusiform, fusiform
nerve fiber is converted to a chemical mes- with two bellies, unipennate, bipennate,
senger (acetylcholine [ACh]) which in turn multipennate, and spiral (Fig. 2.9).
initiates another electrical signal in the cell Among skeletal muscles, there are at
membrane (sarcolemma) of the muscle least four kinds of exceptions to the general
fiber. guideline that there is one endplate zone lo-
The endplate zone is the region where cated in the midbelly region of the muscle.
motor endplates innervate the fibers of the
muscle. This region is now known as the 1. Several human muscles, including the
motor point. The motor point is identi-
153
rectus abdominis, the semispinalis capi-
fied clinically as the area where a visible or tis, and the semitendinosus have in-
palpable muscle twitch can be elicited in scriptions dividing the muscle into ser-
response to minimal surface electrical ial segments each of which has its own
stimulation. Originally the motor point endplate zone, as illustrated in murine
was erroneously thought to represent the muscles in Figure 2.10A, B, C, and E. In
hilar region where the motor nerve enters comparison, Figure 2.10D and F show
the muscle. 4
the usual endplate arrangement.

Copyrighted Material
50 Part 1 / Introduction

A B

C
Figure 2.8. Location of endplates in human skeletal circumpennate (feather-like) arrangement of muscle
muscles of different structure. The red lines represent fibers in the flexor carpi radialis, and palmaris longus.
muscle fibers; the black dots represent motor end- C, sinuous arrangement of endplates in middle deltoid
plates of those fibers and the black lines represent muscle fibers that have a complex pennate configura-
aponeurotic attachments. Endplates are consistently tion. (Adapted with permission from Coers C. Contri-
found in the midregion of each muscle fiber. A, linear bution a I'etude de la jonction neuromusculaire. II.
endplates in muscle with short fibers that are arranged Topographie zonale de I'innervation motrice terminale
between parallel aponeuroses, as seen in the gastroc- dans les muscles stries. Arch Biol Paris 64.-495-505,
nemius muscle. B, loop arrangement of endplates in 1953.) 42

Copyrighted Material
Chapter 2 / General Overview 51

Figure 2.9. Parallel and fusiform fiber arrangements length for all of its fibers. See Figure 2.8 to see how
provide greater length change at the expense of force, the location of motor endplates would relate to these
Pennate arrangements provide more force at the ex- various fiber arrangements. (Adapted with permission
pense of length change. Note that the attachments of from Clemente CD. Gray's Anatomy of the Human
muscle fibers in each muscle provide nearly equal Body. 30th ed. Philadelphia: Lea & Febiger, 1985:429.)

Copyrighted Material
52 Part 1 / Introduction

A B C D

E F
Figure 2.10. Photomicrographs and schematic draw- cilis posterior muscle. C is the computer-generated
ings showing the location of endplates in mouse skele- version of B for comparison. This muscle shows two
tal muscles based on the study by Schwarzacher us- bands of endplates. D, photomicrograph of the di-
ing the cholinesterase stain technique of Koelle aphragm showing the endplate zone running mid-
modified by Coers to emphasize motor endplates. In 231
way between the ends of the muscle fibers.
the computer-generated schematics (C, E, F), red E, schematic of endplate arrangement in the semi-
lines represent muscle fibers; black dots represent tendinosus muscle and F, in the gluteus maximus mus-
motor endplates of those fibers and black lines repre- cle. (Photomicrographs reproduced with permission
sent muscle fiber attachments either directly to bone or from Schwarzacher VH. Zurlage der motorischen end-
to an aponeurosis. A is a photomicrograph and B is the platten in den skeletmuskeln. Acta Anat 30:758-774,
published schematic drawing made from it of the gra- 1957. Schematics were derived from the same source.)

Copyrighted Material
Chapter 2 / General Overview 53

2. The human sartorius muscle has end- important for understanding the pain and
plates scattered throughout the muscle. autonomic phenomena associated with TrPs.
The endplates supply parallel bundles
of short fibers that interdigitate through- Neuromuscular Junction
out the length of the muscle with no Different species have different topo-
well defined endplate zone. The hu-
44
graphical arrangements of the nerve termi-
man gracilis is described by one author 36
nal at an endplate. The frog has extended
as having two transverse endplate zones linear synaptic gutters. Rats and mice have
like the semitendinosus, but as having a variation in which the gutters are curled
multiple interdigitating fibers with a and convoluted as illustrated in Figure
scattered endplate distribution like the 2.11. Figure 2.12 shows the usual human
sartorius by others. This interdigitat-
44
arrangement. Cholinesterase stain of an
ing configuration is unusual in human endplate (Fig. 2.12A) clearly shows multi-
skeletal muscles and the endplate ple more or less separate groups of synap-
arrangement in these two muscles may tic clefts. With sufficient separation, this
be highly variable among individuals. arrangement might effectively function as
3. A review of compartmentalization multiple small synapses, which could ac-
within a muscle emphasized that each
62 count for multiple sets of spikes originat-
compartment is isolated by a fascial ing from one active locus in one muscle
plane. A separate branch of the motor fiber (see Section D). Figure 2.12B is a
nerve innervates the endplate zone of schematic of this human endplate arrange-
each compartment. Each compartment is ment seen in cross section.
also functionally distinct. Examples The neuromuscular junction is a synapse
given are the proximal and distal parti- which, like many in the central nervous sys-
tions of the extensor carpi radialis longus tem, depends on ACh as the neurotransmit-
and the distal partitions of the flexor ter. The basic structure and function of a
carpi radialis muscle. The masseter mus- neuromuscular junction is presented sche-
cle also shows evidence of motor unit matically in Figure 2.13. The nerve terminal
compartmentalization. Relatively few
185
produces packets of ACh. This process con-
human muscles have been studied for sumes energy that is largely supplied by mi-
this feature. It may be quite common. tochondria located in the nerve terminal.
4. The gastrocnemius muscle is an example The nerve terminal responds to the ar-
of the arrangement of muscle fibers that rival of an action potential from the a-mo-
increases strength by reducing range of toneuron by the opening of voltage-gated
motion. The fibers are strongly angulated calcium channels. These channels allow
so that one individual fiber is only a small ionized calcium to move from the synaptic
percent of the total muscle length. Conse- cleft into the nerve terminal. The channels
quently the endplate zone runs centrally are located on both sides of the specialized
down most of the length of each compart- portion of the nerve membrane that nor-
ment of the muscle. An example of this mally releases packets of ACh in response
arrangement is shown in Figure 2.8A. to ionized calcium.
The simultaneous release of many pack-
Figure 2.11 schematically portrays two ets of ACh quickly overwhelms the barrier
motor endplates and the small neurovascu- of cholinesterase in the synaptic cleft. Much
lar bundles that cross the muscle fibers as the of the ACh then crosses the synaptic cleft to
terminal axons supply motor endplates. 60
reach the crests of the folds of the postjunc-
The linear arrangement of endplates that fol- tional membrane of the muscle fiber where
lows the path of such a neurovascular bun- the ACh receptors are located (Fig. 2.13).
dle is oriented across the direction of the However, the cholinesterase soon decom-
muscle fibers. The neurovascular bundle
544
poses any remaining ACh, limiting its time
includes nociceptor sensory nerves and au- of action. The synapse can now respond
tonomic nerves that are closely associated promptly to another action potential.
with these blood vessels. The close proxim- The normal random release of individ-
ity of these structures to motor endplates is ual packets of ACh from a nerve terminal

Copyrighted Material
54 Part 1 / Introduction

BLOOD
VESSEL

NOCICEPTOR MOTOR
AXON AXON

Figure 2.11. Sketch overview of two mammalian mo- the endplate on the right, the action potentials of that
tor endplates and the neurovascular bundle associ- fiber have a positive-first deflection. This is one way of
ated with them. The nerve terminals of a motor axon localizing motor endplates electromyographically. The
are twisted into a compact neuromuscular junction action potential configurations at the bottom of the
that is imbedded into the slight elevation of the end- figure correspond to the waveforms that would be
plate region on the muscle fiber. The motor nerve recorded at various locations along the foreground
fibers are accompanied by sensory nerve fibers and muscle fiber. (Adapted with permission from Figure 5
blood vessels. Autonomic nerves are found in close of Salpeter MM. Vertebrate neuromuscular junctions:
association with these small blood vessels in muscle General morphology, molecular organization, and
tissue. Action potentials recorded at the endplate re- functional consequences. In: Salpeter MM, ed. The
gion of a muscle fiber show an initially negative de- Vertebrate Neuromuscular Junction. New York: Alan
flection. Beyond a very short distance to either side of R. Liss, Inc., 1987:1-54.) 225

produces well separated individual minia- membrane (sarcolemma) throughout the


ture endplate potentials. These individual muscle fiber.
miniature endplate potentials are not prop-
agated and die out quickly. On the other Muscle Pain
hand, the mass release of ACh from nu- The current understanding of the neuro-
merous vesicles in response to an action physiology of muscle pain is a subject that
potential arriving at the nerve terminal de- requires a separate book for adequate cov-
polarizes the postjunctional membrane erage. The subject was summarized in
191

enough for it to reach its threshold for ex- 1993, 188


and u p d a t e d .
1 8 9 1908240

citation. This event initiates an action po- In brief outline, several endogenous sub-
tential that is propagated by the surface stances are known to sensitize muscle no-

Copyrighted Material
Chapter 2 / General Overview 55

Figure 2.12. Structure of a motor endplate. Photomi- B, Schematic of cross section through the motor end-
crograph of the subneural apparatus and a schematic plate region. This unmyelinated terminal nerve ends in
cross section of the terminal arrangement in human six terminal expansions (black globules). Each termi-
muscle. A, Photomicrograph of human endplate re- nal expansion has its own synaptic gutter and system
gion, stained by a modified Koelle's method to reveal of postsynaptic folds. The dotted lines represent the
cholinesterase, shows the multiple groups of discrete Schwann cell extension that attaches to the sar-
synaptic clefts of the subneural apparatus. This termi- colemmal membrane of the muscle cell and isolates
nal motor nerve ending of one endplate shows 11 dis- the content of the synaptic cleft from the extracellular
tinct round or oval couplets. This structural form is milieu. The vertical parallel lines represent the stria-
distinctly different than the tortuous and plexiform ter- tions (Z lines) of the muscle fiber. (Reproduced with
minals in rats and mice. (Reproduced with permission permission from Coers C Contribution a I'etude de la
from Coers C. Structural organization of the motor jonction neuromusculaire. Donnees nouvelles concer-
nerve endings in mammalian muscle spindles and nant la structure de I'arborisation terminale et de I'ap-
other striated muscle fibers. In: Bouman HD, Woolf pareil sousneural chez I'homme. Arch Biol Paris
AL, eds. The Innervation of Muscle. Baltimore: 64:133-147, 1953.) 41

Williams & Wilkins, 1960:40-49.) 43

Calcium

Figure 2.13. Schematic cross section of part of a neu- up arrows). This calcium causes the release of many
romuscular junction, which transmits a nerve action packets of acetylcholine (ACh) into the synaptic cleft
potential across the synapse via a chemical messen- (larger down arrows). Receptors specific for ACh de-
ger so it becomes a muscle action potential. In re- polarize the postsynaptic membrane of the muscle
sponse to an action potential propagated down the fiber sufficiently to open sodium channels deep in the
motor nerve, the synaptic membrane of the nerve ter- folds of the postjunctional membrane. Sufficient de-
minal opens voltage-gated calcium channels, allowing polarization of these sodium channels initiates a prop-
an influx of calcium from the synaptic cleft (small red agated action potential in the muscle fiber.

Copyrighted Material
56 Part 1 / Introduction

ciceptors. They include bradykinin, E-type low back and referred leg pain are neither
prostaglandins, and 5-hydroxytryptamine, well localized nor attributable to a specific
which, in combination, can potentiate sen- tissue without additional information.
sitization effects. The release of prosta- The overwhelming majority of dorsal
glandins from nearby sympathetic fibers by horn cells that have visceral input also
noradrenalin may influence the TrP mech- have a somatic input that is nociceptive. 33

anism at the endplate. There is evidence As one becomes more aware of the ubiqui-
that prostaglandin-induced sensitization of tousness of referred pain, both neurophys-
nociceptors is mediated by cyclic adeno- iologically and clinically, it becomes ap-
sine monophosphate (cyclic AMP). Other parent that a patient's pain is likely to be
factors known to enhance sensitization lo- referred from a site other than the location
cally are increases in hydrogen ion con- of the original pain complaint. It is un-
centration (Ph decreased to 6.1), and sub- likely that branching of primary afferent
stance P. Peripheral sensitization of
188
fibers is responsible for referred pain ex-
nociceptors would be responsible for local cept in rare instances. 190

tenderness to pressure and most likely also An awareness of neuroplastic changes 296

for referred pain. Which of these, or other in the central nervous system is a relatively
substances, are responsible for sensitizing new and fundamental development with
nociceptors in the region of active loci of profound clinical implications. An acute
TrPs is not known at this time, but this is- nociceptive input can induce prolonged
sue offers a fertile field for research inves- changes in the processing of nociceptive
tigation that may involve drugs. signals in the central nervous system that
Several phenomena occurring at the involves both functional and structural
spinal cord level can be related to referred changes. Neurophysiological evidence of
pain. Experiments monitoring the response the "wind-up" of neuronal activity has re-
of a dorsal horn cell to deep-tissue (includ- cently been summarized by Yaksh and
ing muscle) stimulation can establish the Abram. More prolonged nociceptive in-
295

location and extent of the receptive field(s) put can induce more long-lasting changes
of that neuron. Injection of a pain-inducing that may not be reversible with time alone.
substance into the muscular receptive field Yu and colleagues have shown neuro-
296

of a nociceptor neuron can result in the ap- plastic sensitization of sensory nerves that
pearance of additional receptive fields in increased responsiveness to stimulation in
that l i m b . This phenomenon is attributed
121
cutaneous and in deep receptive fields of
to the "awakening" of "sleeping" nocicep- muscle by injecting a temporarily noxious
tive pathways in the spinal cord. The sensi- (painful) substance (mustard oil) into the
tivity of the original nociceptive-only dor- tongue muscle of anesthetized rats. Nox-
sal horn cells can increase enough to ious stimulation of one muscle influenced
become responsive to more gentle, nonno- the responsiveness of another muscle to
ciceptive stimuli. Similar phenomena can stimulation.
be observed when the noxious substance is Much of the suffering from chronic pain
injected into another muscle in the same is preventable if the acute pain is controlled
limb but outside of the original receptive promptly and effectively. Clinical exam-
field.
121190
ples of the importance of this principle are
Inputs from several tissues to one sen- increasing rapidly. Specifically with regard
sory lumbar spinal neuron are common. In to myofascial TrPs, Hong and Simons 127

a study of cats, most of the 188 units stud-


95 demonstrated that the length of treatment
ied (77%) were hyperconvergent and re- required for patients who had developed a
sponded to nociceptive input from two or pectoralis myofascial TrP syndrome as the
more deep tissues: facet joints, periosteum, result of whiplash injury was directly re-
ligaments, intervertebral disc, spinal dura, lated to the length of time between the ac-
low back/hip/proximal leg muscles and cident and the beginning of TrP therapy.
tendons. Most of these units (93%) also had With longer initial delay, more treatments
a cutaneous nociceptive site. This finding
95 were required and the likelihood of com-
corresponds to the clinical experience that plete symptom relief decreased.

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Chapter 2 / General Overview 57

The use of local analgesia at the time of the TrP or palpable nodule. Adding to the
surgery to prevent nociceptive signals from problem, differences in terminology often
reaching the spinal cord is helpful, but is
295
made it difficult to know whether or not
more effective if combined with meticu- different investigators were examining pa-
lous post- surgical pain control. The con- tients with basically the same medical con-
cept of preventive analgesia has been ap- dition but identifying it by different names
plied successfully by blocking pain from that emphasized similar but somewhat dif-
the TrP with preinjection blocks prior to a ferent diagnostic aspects.
TrP i n j e c t i o n .
7678
Katz, et al. * showed that
1 8
Our current understanding of TrPs results
preventing acute surgical pain, in turn, from the convergence of two independent
prevented progression to chronic pain and lines of investigation, one electrodiagnostic
that there was a direct relation between the and the other histopathological. Fitting to-
severity of acute postoperative pain and gether the lessons from each leads to an Inte-
the severity of subsequent chronic postop- grated Hypothesis that appears to explain the
erative pain. nature of TrPs. It is now becoming clear that
Recent investigations show that differ- the region we are accustomed to calling a TrP
ent areas of the brain become activated in or a tender nodule is a cluster of numerous
response to an experimentally induced microscopic loci of intense abnormality that
acute pain as compared to chronic neuro- are scattered throughout the nodule. The TrP
pathic pain. Neuropathic pain shows by
130 is like a nest of hornets that contains multi-
positron emission tomography a striking ple minute sources of intense trouble. The
preferential activation of the right anterior critical TrP abnormality now appears to be a
cingulate cortex (Brodman area 24), regard- neuromuscular dysfunction at the motor
less of the side of the painful mononeu- endplate of an extrafusal skeletal muscle
ropathy. Activation of this region of the fiber, in which case myofascial pain caused
brain is associated with emotional distress by TrPs would be a neuromuscular disease.
(suffering). Acute pain activates both mo- This section reviews the research data that
tor and sensory portions of the cortex pro- provides the basis for this concept.
ducing a cognitive and motor behavioral
experience rather than an emotional expe- Electrodiagnostic Characteristics of
rience. These findings emphasize the im- Trigger Points
portance of the affective-motivational di- The basis for the electrodiagnostic ap-
mension in chronic ongoing neuropathic proach to the study of TrPs was anticipated
pain that is not involved in acute pain. by Weeks and Travell in 1 9 5 7 when they
288

Chronic pain causes suffering that is reported and illustrated that TrPs in the
processed differently in the brain than is resting trapezius muscle exhibited a series
the experience of acute pain. These neuro- of high frequency spike-shaped discharges
physiological facts emphasize the impor- while at the same time adjacent sites in this
tance to the patient and to the health care muscle were electrically silent. Unfortu-
delivery system of preventing chronic pain nately, this observation was not effectively
and properly interpreting patients' de- pursued. In 1993, Hubbard and Berkoff 133

scriptions and behavior. Newly-activated reported similar electrical activity as being


myofascial TrPs that are poorly identified characteristic of myofascial TrPs. Their pa-
and poorly managed can become a major per, like the previous 1957 report, called
unnecessary cause of expensive, misery- attention only to high-amplitude (>100 u.V)
producing chronic pain. spike potentials as being characteristic of
TrPs. Hubbard and Berkoff hypothesized
D. NATURE OF TRIGGER POINTS that the source of the electrical activity was
Trigger points have been difficult to un- abnormal muscle spindles and rejected the
derstand because there has been no possibility that the potentials might be
method of studying them electrophysiolog- coming from extrafusal motor endplates.
ically, and those investigating pathology When Simons, Hong, and Simons started
were looking for characteristic histological to investigate the electrical activity in TrPs
changes distributed uniformly throughout described by Hubbard and Berkoff, they 133

Copyrighted Material
58 Part 1 / Introduction

Figure 2.14. Typical recording of the spontaneous but a ten-times higher sweep speed of 10 msec per
electrical activity (SEA) and spikes recorded from an division that was used in subsequent studies by oth-
active locus of a trigger point at two different sweep ers ' who also have observed the low amplitude
248 250

speeds. A, recording at the same slow sweep speed noise component as well as the polarity of initial de-
of 100 msec/div used by Hubbard and Berkoff to re-133
flection of the spikes from active loci. This additional
port this electrical activity. Only spikes of unknown ini- information is of critical importance for understanding
tial polarity are identifiable. B, a similar amplification the source and nature of these potentials.

employed a five-fold higher amplification active locus was adopted to identify such a
and ten- fold increase in sweep speed for site of electrical activity. These three au-
their recordings. It was immediately appar- thors used the same kind of needle and the
ent that there were two significant compo- same slow insertion technique reported by
nents to the electrical activity. In addition Hubbard and Berkoff.
to the intermittent and variable high-ampli- In time, it became increasingly apparent
tude spike potentials, there was a consis- to the three investigators with the help of S.
tently present, lower amplitude (maximum Mense, that the potentials found at the active
of about 60 u.V) noise-like component. loci of TrPs corresponded completely to the
Figure 2.14A shows the electrical activ- potentials that are recognized by elec-
ity that Simons, Hong, and S i m o n s 248 tromyographers as normal motor endplate
recorded at the same slow speed that Hub- potentials. However, they did not conform to
bard and Berkoff reported. Only spikes are the miniature endplate potentials described
distinguishable in this record and the po- by physiologists. Electromyographers iden-
larity of their onset is not identifiable. Fig- tify the low-amplitude component (like SEA
ure 2.14B presents similar electrical activ- of TrPs) as endplate noise and the high-am-
ity recorded at the same amplification but plitude spike component as endplate
with a ten-fold increase in sweep speed. In spikes. The similarity can be seen by com-
153

this record, the noise-like low-amplitude paring Figures 2.14B and 2.15B. The end-
potentials are clearly apparent and distin- plate potentials in Figure 2.15 are presented
guishable from the spike activity, and the as normal endplate activity in a current elec-
negative polarity of the initial deflection of trodiagnostic textbook. This interpretation
153

each spike potential is clearly evident. is based on the study reported by Wieder-
To deal with the potential terminology holt. At this point, it became necessary for
291

confusion inherent in this situation, the the three investigators to resolve what ap-
three investigators adopted the noncom- peared to be the incompatible "facts" that the
mittal term spontaneous electrical activity SEA and spikes characteristic of active loci
(SEA) to identify this noise-like compo- in symptom-producing TrPs were generally
nent. 248
Since spikes only, SEA only, or considered to be normal endplate activity.
both components might appear from one of Spontaneous Electrical Activity. To re-
these minute needle sites, the neutral term liably identify SEA of TrPs electromyo-

Copyrighted Material
Chapter 2 / General Overview 59

cal potentials identified as normal endplate activity of endplate activity showing both the continuous end-
the tibialis anterior muscle and published in a current plate noise and occasional spikes. (Reprinted with
textbook of electrodiagnosis. Recordings are at the permission from Kimura J. Electrodiagnosis in Dis-
153

higher sweep speed of 10 ms per division. A, endplate eases of Nerve and Muscle, Vol. 2. Philadelphia: F.A.
spikes recorded at low amplification; the relatively Davis, 1989.)
low-amplitude noise-like component is barely appar-

graphically, it is necessary to use a relatively One should not expect to record normal
high amplification (20 U. V/division) and fast miniature endplate potentials with such a
sweep speed (10 msec/division). If the nee- large needle. However, the SEA of an active
dle examination is conducted using the locus is a different matter. Individual
thrust technique normally employed by miniature endplate potentials have been
electromyographers, the examiner is likely very difficult to detect extracellularly using
to pass an active locus without recognizing a microelectrode because of the minute
67

it or to elicit a local twitch response instead source and because their potentials are
of finding SEA. A very gentle insertion tech- propagated such a short distance along the
nique is required that includes back and outer surface of the postjunctional mem-
forth rotation of the needle between the brane, and because the potentials reappear
thumb and finger as it is slowly advanced. so infrequently at any one location.
On these higher-amplification records, the On the other hand, if excessive ACh re-
peak amplitudes of spikes are often off scale lease induces greatly increased and contin-
but their presence is unmistakable and the uous electrical activity that produces a
polarity of their initial deflection from the contraction knot (see p. 69, Fig. 2.24), the
baseline is observable in detail. resultant higher-voltage endplate poten-
The SEA presented here was recorded tials would be more readily detectable
with the commonly used, disposable, with the relatively large needle electrode,
teflon-coated, monopolar EMG needle. The and much of the endplate region would
exposed tip of this needle is relatively likely be active continuously (not active
large compared to the diameter of a mus- intermittently at a few isolated minute lo-
cle fiber or of the endplate region of a mus- cations). The double-size, contraction knot
cle fiber. Figure 2.16 shows the relative region would increase the target size that
size of the needle and muscle fibers. The could now be 100 u,m or more in diame-
exposed tip of a needle was approximately ter. 2 1 4 , 2 5 3
0.45 mm (450 u,m) long. The mean diame- Evidence indicates that the SEA may be
ter of normal muscle fibers varies with present spontaneously regardless of the
fiber type ranging from 41 to 59 u,m. 57
presence of the EMG needle. Since the nee-
Therefore, either side of the exposed tip dle is carefully advanced slowly and
would contact approximately 9 muscle smoothly, it usually evokes very few, small
fibers of 50 |xm diameter. insertion potentials. As the needle slowly

Copyrighted Material
60 Part 1 / Introduction

100p

Figure 2.16. Schematic that shows the relative size of ameter. The exposed needle tip (without the teflon
the exposed tip of a standard teflon-coated elec- coating) can extend about 450 u.m and therefore
tromyographic needle as compared to normal muscle could be in contact with approximately 18 muscle
fibers. Muscle fibers are generally about 50 u,m in di- fibers, counting both sides of the needle.

advances through the TrP region in this showed that a biphasic motor unit poten-
electrically quiet background, the examiner tial with an initial negative deflection fol-
occasionally hears a distant rumble of noise lowed by a rapid rate of rise indicates that
that swells to full SEA dimensions as the the recording needle is close to (within 1
needle continues to advance. This "acquisi- mm of] the origin of the action potential (a
tion" of SEA at an active locus in a TrP is il- motor endplate). The trace in the lower box
lustrated in Figure 2.17A and presents a of Figure 2.17B shows the regular firing
record of the needle approaching the im- pattern of one voluntarily recruited motor
mediate vicinity of the SEA. The transition unit. The upper trace in the upper box of
represents a fraction of a millimeter of nee- Figure 2.17B presents in detail the action
dle displacement. Sometimes the SEA can potential that is shown between the +
be increased or decreased by simply apply- marks in the lower trace. It has the intitial
ing gentle side pressure to the hub of the negative deflection followed by rapid rise
EMG needle. The distance of the needle to peak negative voltage and the biphasic
from the discrete source of the electrical ac- waveform characteristic of a motor unit ac-
tivity can be that critical. tion potential recorded at its origin, the
Early in the study of the electrical activ- motor endplate. 27
This potential was
ity found at active l o c i , the investiga-
248,250 recorded at the site of a trigger point active
tors needed to test whether or not active locus. The lower trace of the upper box in
loci were located at motor endplates. Fig- Figure 2.17B was recorded from an adja-
ure 2.17B shows a recording of a voluntary cent control site about 1 cm away. Its wave-
motor unit action potential and illustrates form (a triphasic potential without a sharp
one strong indication that SEA originated spike) shows that the recording needle was
at a motor endplate. Buchthal, et al. 27 not located at the origin of that electrical

Copyrighted Material
Chapter 2 / General Overview 61

Figure 2.17. Two examples of electrical activity contraction of the muscle. The upper trace in the up-
recorded at active loci in trigger points. A, The slow per box of B displays in detail (at 2.5 times the ampli-
sweep-speed, 1 second recording in the lower box tude and 10 times the sweep speed) the sixth action
obtained as the needle approached an active locus potential in the lower box. The abrupt initially negative
shows the quiet baseline becoming increasingly ac- diphasic spike of this upper trace indicates that the
tive due to endplate noise (spontaneous electrical ac- recorded potential originated within a few microme-
tivity) at the same time that the investigators heard a ters of the search needle, which means it had to be
corresponding development of a noise-like (seashell) that close to the motor endplate. The lower trace of
sound. The last 0.1 sec of that record from the search the upper box of B was recorded from an adjacent
needle is displayed at increased amplification and ten control site in the endplate zone but out of the trigger
times the sweep speed in the upper trace of the up- point and shows a triphasic, rounded, initially negative
per box in A. It shows typical spontaneous electrical deflection of longer duration from different muscle
activity of approximately 20 u.V amplitude. The lower fibers of the same motor unit. This potential did not
trace of the upper box displays the quiet baseline pre- originate at a motor endplate. That both potentials
sent throughout this record that was simultaneously came from the same motor unit was confirmed by a
recorded from a control needle at a site near to, but constant time relationship in all nine repetitions of
outside of, the trigger point. them throughout the 1 second record. This experi-
B, The 1 second recording in the lower box of B ment illustrates how one can establish independently
displays repetitive discharges of 1 motor unit recorded the presence of an endplate in the absence or pres-
from an endplate location found by the appearance of ence of spontaneous electrical activity. The finding
spontaneous electrical activity of a trigger point active supports the concept that the spontaneous electrical
locus. The motor unit activity is in response to the activity observed in a trigger point active locus arises
subject performing (on request) a minimal voluntary in the immediate vicinity of, or from, a motor endplate.

activity. However, it is a simultaneous search experiment. A confirmatory result


recording from another fiber (or fibers) of would indicate that the motor neurons
the same motor unit. The potential in the with dysfunctional endplates are more ex-
upper trace was recorded from the site of citable than others.
an active locus originating within a mil- The issue of whether the endplate po-
limeter or less from a motor endplate. This tentials now recognized by electromyogra-
kind of single-fiber potential, voluntarily phers as endplate noise arise from normal
recruited and originating at an active locus, or abnormal endplates is critical and ques-
was a consistent finding. Frequently, when tions conventional belief. Figure 2.18 illus-
the subjects initiated a gentle voluntary trates the difference between normal min-
contraction, they first recruited only the iature endplate potentials (Fig. 2.18A and
same motor unit that included the muscle C) and abnormal endplate noise (Fig. 2.18B
fiber that was exhibiting SEA. This indica- and D) which corresponds to the SEA of
tion of selective recruitment needs to be active loci in TrPs.
studied quantitatively in a controlled re- Since publication of the paper by

Copyrighted Material
62 Part 1 / Introduction

Figure 2.18. Physiological studies of the endplate po- C, normal, infrequent, individual, monophasic minia-
tentials characteristic of normal endplates (A and C) ture endplate potentials. D, response to exposure of
and of dysfunctional endplates (B and D) under rest- the endplate region to incompatible blood serum. This
ing conditions. A and B, are early intracellular record- continuous noise-like (abnormal) discharge appears
ings published in 1956. A, two normal (isolated,
171
the same as the so-called normal endplate noise
monophasic, low amplitude) miniature endplate po- component of motor endplate potentials as usually
tentials. B, a continuous series of overlapping, super- described by electromyographers and the same as
imposed, noise-like, higher-amplitude abnormal po- the spontaneous electrical activity observed in trigger
tentials produced by almost any mechanical points. This noise-like electrical discharge was caused
disturbance of the endplate region. (A and B repro- by a nearly 1000-fold increase in the rate of acetyl-
duced with permission from Liley AW. An investigation choline release from the resting nerve terminal. (C and
of spontaneous activity at the neuromuscular junction D reproduced with permission from Ito Y, Miledi R,
of the rat. / Physiol 332:650-666, 1956) Vincent A. Transmitter release induced by a "factor" in
C and D are slower-speed physiological research rabbit serum. Proc R Soc Lond B 387:235-241, 1974.)
recordings made in 1974 with greater amplification. 137

Wiederholt in 1 9 7 0 , electromyographers
291
arises from a functionally disturbed end-
have accepted his apparently mistaken plate. In 1956, Liley observed that even a
171

conclusion that potentials similar to what relatively minor mechanical disturbance


we now identify as SEA represent normal applied to the endplate region could greatly
miniature endplate potentials. Electromyo- increase the frequency of the postjunctional
graphers commonly identify the low-am- membrane potentials, from a normal maxi-
plitude potentials as "seashell" noise. 153
mum of 118/sec to as high as 1,000/sec (an
Wiederholt was correct in concluding that increase of one order of magnitude). Minor
the low-amplitude potentials arose from mechanical stimuli (minor traumas) that
endplates, and illustrated one recording of produced this effect included pulling gently
a few discrete monophasic potentials hav- on the motor nerve, vibration of the end-
ing the configuration of normal miniature plate region, and visible dimpling of the sur-
endplate potentials as described by physi- face of the muscle fiber by touching it with
ologists. However, the continuous noise- an electrode. These mechanical stimuli con-
like endplate potentials that he also illus- verted the discharge pattern from normal to
trated and that we observe from active loci abnormal, and once converted, the pattern
have an entirely different configuration remained abnormal (Fig. 2.18B). 171

and have an abnormal origin. Two decades later, studies by Miledi


Three studies by physiologists, two of and coworkers identified excessive release
which appeared following Wiederholt's of acetylcholine packets as the cause of the
study, indicate that the SEA (endplate noise) increased electrical activity. These studies

Copyrighted Material
Chapter 2 / General Overview 63

were published several years after Wieder- SEA, they would have had no reason to men-
holt's seminal paper. In 1971 Heuser and
291
tion it, because the authors might have con-
Miledi 120
demonstrated that exposure of sidered it to be normal endplate potentials
the endplate region to lanthanum ions pro- that are to be expected in the endplate zone
duced a 10,000-fold (four orders of magni- and not worthy of mention. Previous investi-
tude) increase in the release of ACh result- gators had been similarly misled.
ing in so many miniature endplate Based on his clinical experience and
potentials that it produced a noise-like pat- early studies of SEA, Hong proposed that
122

tern where individual potentials were no the clinically identified TrP consists of mul-
longer discernable. In a subsequent tiple discrete sensitive spots. It now appears
study, exposure of the endplate region to
137
that those sensitive spots are abnormal end-
a foreign serum produced a similar result plates evidencing SEA and are scattered
that is illustrated in Figure 2.18D. If a sim- among uninvolved normal endplates. This
ilarly disturbed nerve terminal extends the configuration based purely on electrophysi-
length of a TrP contraction knot [see page ological evidence, is illustrated schemati-
69), then the entire postjunctional mem- cally as a cross section of the muscle fibers
brane covered by the nerve terminal could of a TrP in Figure 2.19 (also see Fig. 2.21).
be expected to evidence the endplate noise Subsequent r e p o r t s concluded
19,37,248 250

(SEA). The discharge of ACh into the that the electrical activity which is charac-
synaptic cleft is illustrated schematically teristically found in TrPs is the same as the
in Figure 2.13. motor endplate potentials recognized as
Recently, Ertekin, et al. reported a
m normal by electromyographers. The
153,291

marked increase in the number of minia- dysfunction seen in TrPs is NOT normal.
ture endplate potentials during an attack of Spikes. It is now recognized by elec-
hypokalemic periodic paralysis. This indi- tromyographers that spikes which originate
cates that low serum potassium can also in the endplate region are action potentials
lead to abnormally increased (but much of the skeletal muscle fiber supplied by that
less severe and also reversible) release of endplate. To confirm this concept and to
153

ACh under resting conditions. eliminate the possibility that SEA originates
This "acetylcholine noise," as Miledi and in intrafusal fibers of a dysfunctional mus-
associates called it in their papers, looks re- cle spindle, the taut band was monitored as
markably like the potentials produced by far as 2.6 cm from the endplate for the same
Liley, the endplate noise of electromyog-
171 action potentials that originated at the end-
raphers, and the SEA found in TrPs. Their plate as spikes. The same potentials were
findings suggest that the SEA which identi- observed at both locations. These distant
251

fies active loci in TrPs is produced by grossly potentials must have been propagated by
increased release of ACh due to a serious extrafusal rather than intrafusal fibers since
disturbance of normal endplate function that distance was more than twice the total
and that the endplate noise identified by length of an intrafusal muscle fiber. 132

electromyographers is the signature of a dys- Contrary to the experience with SEA


functional endplate. Endplate dysfunction during needle exploration of TrPs, spikes
can be caused by a number of conditions. were not recognized or anticipated at a dis-
Investigators in one recent study con- tance, but appeared suddenly, often simul-
cluded that there were no abnormal EMG taneously with SEA. Since spikes are often
findings in TrPs. The examiners apparently
59
10 times the voltage of SEA, when they oc-
used the standard clinical EMG insertion cur with SEA and the SEA was apparent
technique, which is less likely than a slow from a distance, the spikes should have
gentle needle movement to reveal the SEA of been equally apparent when the needle
TrPs. The relatively low gain of 50 uV/divi- was more than three times (square root of
sion that was reported by the authors might 10) as far from the source of the voltage. Re-
have revealed the SEA of active loci, but the peatedly, very light side pressure on the
investigators would have needed to be look- hub of the EMG needle terminated the
ing for such a low-amplitude phenomenon. spike potentials, while release of the pres-
They made no mention of seeing endplate sure or added pressure in the other direc-
noise and spikes. Even if they had identified tion restored them. These observations left

Copyrighted Material
64 Part 1 / Introduction

Figure 2.19. Schematic drawing of a cross sectional showing spontaneous electrical activity (forms with
view through a trigger point {dotted circle). This red crescents). The locations and frequency of normal
schematic gives an indication of the relative frequency endplates (black crescents bordering muscle fibers)
and distribution of active loci. It identifies muscle were identified by initially negative motor unit poten-
fibers that did not have endplates included in this sec- tials produced by a minimal voluntary contraction. See
tion (clear forms), fibers with normal endplates (forms text for more explanation. Drawing based on pub-
with black crescents), and fibers with active loci lished d a t a . ' '
242 248 249

the impression that the presence or absence tion of which mechanism is operating is an
of spikes in only moderately active (irrita- important issue that needs to be resolved
ble) TrPs depends significantly on the me- by research experiments.
chanical disturbance (stimulus) introduced Available data indicate that spikes occur
by the needle at active loci of the TrP. 251
when a sufficient number of ACh packets
When numerous spikes were present, it are released to depolarize the postjunctional
was not uncommon to see three or four dif- membrane to the threshold for excitation of
ferent trains of spikes each of which had its the Na channel receptors located in the
+

own waveform characteristics and repeti- depths of the synaptic folds (Fig. 2.13).
tion rate. This observation suggested three Opening of these channels then initiates a
or four different sites of origin within one propagated action potential in that muscle
endplate or, less likely, individual sites of fiber. The mechanical pressure exerted by
origin from a cluster of involved endplates. the needle or related mechanical distur-
If multiple trains of spikes originate from bances apparently facilitates ACh release
one muscle fiber, the multiple pockets of sufficiently to produce spikes in moderately
synaptic folds illustrated in Figures 2.12A dysfunctional endplates. Severely dysfunc-
and B may account for this phenomenon, tional endplates of very active TrPs produce
provided that a train of spike potentials spikes spontaneously without stimulation.
originated independently from the individ- This clinical impression needs to be clari-
ual synaptic pockets. If the multiple trains fied by carefully designed experiments.
of spikes originate in a cluster of endplates, One must be aware of the danger of as-
each source would be propagated in a dif- suming that spikes alone observed in a TrP
ferent but nearby muscle fiber. Determina- originate at an active locus when no SEA is

Copyrighted Material
Chapter 2 / General Overview 65

Figure 2.20. Schematic showing the three lo-


cations that were explored for active loci. One
was a trigger point site selected as a clinically
identified trigger point in a taut band. Another
was an endplate zone site that was in the in-
dependently and electrically identified end-
plate zone, but was outside of any clinically
identifiable trigger points. The third was a taut
band site that was beyond the endplate zone
and also not at a trigger point. All of the trigger
points were found to be located in the endplate
zone. The distribution of endplates (thin ovals)
determines the extent of the endplate zone.
The taut band was identified by palpation.

identified. We define an active locus only as out spikes as the criterion of an active lo-
a TrP site where SEA occurs, or where SEA cus, 11 muscles (a total of 264 needle ad-
occurs with spikes. It can be difficult to dis- vances) were examined (Table 2.8). The
tinguish spikes originating at a dysfunctional study showed active loci to be four times
endplate from a series of motor unit action more common in TrPs than in the endplate
potentials originating at the same endplate. zone outside of a TrP (35:9). No active 252

Distribution of Active Loci in a Muscle. loci were observed in the taut band outside
A recent study examined the location of
249 of the endplate zone. Clearly, the SEA
active loci in different parts of a muscle (noise) type of endplate electrical activity is
with a TrP. The trigger point was always significantly related to myofascial TrPs.
found to be located within the endplate This same SEA was significantly related to
zone, the boundaries of which had been trigger spots of rabbits (similar to human
determined independently. This study ex- TrPs) as compared to adjacent nontaut band
amined three test sites (Fig. 2.20) for active sites. However, it is also clear that the iso-
248

loci: in the TrP, in the endplate zone out- lated observation of SEA alone does not as-
side of a TrP, and in the taut band associ- sure one that the needle is located in a clin-
ated with that TrP but outside the TrP and ically identifiable TrP. It may represent a
outside of the endplate zone. A fourth lo- site of mechanical stress on the synaptic
cation (control) was monitored in the same connection, or an immune system reaction.
muscle, but outside each of the three test It might also be too small a group of active
sites. Each of the three sites was explored loci to be clinically detectable.
systematically (Fig. 2.21) by inserting the The question arose, "If the SEA and
needle sequentially into three divergent spike potentials that we are observing arise
tracks, stopping eight times in each track. from dysfunctional endplates, then why
A recording was made whenever observing don't we also see the normal configuration
SEA alone, spikes alone, SEA with spikes, of individual miniature endplate poten-
a local twitch response, and also whenever tials observed by physiologists and occa-
the needle had advanced approximately sionally by electromyographers?" 28, 63, 291

1.5 mm and no activity had been located. Those normal miniature endplate poten-
After each advance very gentle side pres- tials that have been observed were re-
sure was applied to the hub of the teflon corded using coaxial needle electrodes,
monopolar EMG needle to see if activity which characteristically have a smaller ex-
appeared or changed. Needle advancement posed surface (0.03 m m ) compared to the
2 28

was very slow with gentle rotation of the tip of a monopolar needle (0.08 mm ). The 2

needle back and forth to facilitate its coaxial configuration also makes the nee-
smooth entry through the muscle tissue. dle more directional in sensitivity. Both of
Using the presence of SEA with or with- these factors could be important consider-

Copyrighted Material
66 Part 1 / Introduction

Figure 2.21. Schematic of search pattern at one ex- spontaneous electrical activity. The electromyo-
perimental site. The large dotted oval represents the graphic needle was very slowly advanced eight times
region of the clinically identified trigger point. The thin in each of three diverging tracks (labeled 1, 2, and 3).
filled ovals represent active loci. The thin open ovals Each needle advance was approximately 1.5 mm.
represent normal endplate locations that show no

Table 2.8. Prevalence of Spontaneous Electrical Activity (SEA) with or without Spikes at
3 Sites, Based on 264 Needle Advances at Each Site

Trigger point Site Endplate Zone Taut Band

SEA Only 21 7*
SEA with Spikes 14 0**
SEA Present
(with or without spikes) 35 9ns 0ns

P values compared to TrP site: * = 0.024; ** < 0.005; *** < 0.001; ns > 0.05

ing the minute area of extracellular end- SEA at the TrP. One can confirm the pres-
plate membrane from which a normal end- ence of a functional motor endplate by the
plate potential can be recorded. The first 67
presence of diphasic motor unit action po-
two reports - illustrated both the end-
28 63
tentials that have a sharp initial negative
plate noise pattern and the lower-ampli- spike. In accordance with the volume con-
tude individual miniature endplate pat- duction theory and as observed by
58

tern, which is what would be expected if Buchthal, et al., this waveform occurs
27

some recordings came from dysfunctional only when the potentials originate in the
endplates and others from normal end- region of the needle tip. Figure 2.11 illus-
plates. Figure 2.16 illustrates the relative trates how the waveform changes when it is
size of a monopolar teflon-coated EMG recorded at its endplate point of origin and
needle and the diameter of a muscle fiber, after it has propagated a short distance in
which is also the approximate size of the either direction along the muscle fiber. Fig-
endplate that surrounds it. ure 2.17B illustrates the differences in
In studies of active loci, - - it be-
249 2 5 2 5 2 waveform when action potentials of the
came important to confirm the presence of same motor unit are recorded simultane-
normal endplates in addition to the appar- ously at the origin of propagation at the
ently abnormal ones that were generating endplate of one muscle fiber (Fig 2.17B)

Copyrighted Material
Chapter 2 / General Overview 67

Figure 2.22. Distribution of active loci (that showed located at an endplate. Three positions (open circles)
spontaneous electrical activity and endplate response showed quiet baseline without evidence of an end-
to voluntary contraction) and of endplate locations plate. One record (horizontal bar) was not counted
without active loci in a trigger point. Endplates were because it was ambiguous as to the presence of an
recognized by the origin-waveform produced by gen- endplate. These findings indicate that the "abnormal"
tle voluntary contraction. A total of 18 positions were endplate potentials of trigger point active loci are
tested along two needle tracks. Nine positions (solid found scattered among "normal" endplates that do
circles) were identified as endplates without sponta- not evidence spontaneous electrical activity and that
neous electrical activity. All 3 positions (asterisks) the SEA abnormality is located at an endplate.
where an electrically active locus was found were also

and from other fibers of the same motor unit If spikes originate at an active locus and
at a site away from their endplates. are propagated action potentials in just that
Using the technique described above to one muscle fiber, and if the taut band rep-
locate SEA, we examined several TrPs for resents taut muscle fibers passing through
the presence of SEA and for normal (SEA- the TrP, then it should be possible to record
free) motor endplate locations by sampling a train of spikes simultaneously from the
8 locations in each of two tracks in a TrP. active locus and from the taut band some
The subject was asked to make a minimal distance from the TrP. This was observed in
voluntary contraction at each location. several human subjects and in several rab-
Figure 2.22 graphically presents the re- bits. In one human subject the distance
251

sults. Of the 16 locations tested in the TrP between the TrP and the recording needle
(which was in the endplate zone), three in the taut band was 2.6 cm, twice the total
locations were active loci (SEA appeared length of an intrafusal muscle fiber.
and also negative voluntary spikes), nine
were at an endplate (negative voluntary Histopathological Characteristics of
spikes without SEA), and four were at nei- Trigger Points
ther an endplate nor an active locus (no ev- Contraction knots, a characteristic histo-
idence of electrical activity beyond back- pathologic finding in TrPs and in tender pal-
ground). This is consistent with the pable nodules, have been repeatedly noted
concept that a group of dysfunctional mo- but their significance not appreciated. In
tor endplates are at the heart of the TrP 1951, Glogowski and Wallraff reported 96

mechanism and that the dysfunctional finding numerous "knotenformig gequol-


endplates are a minority located among lene Muskelfasern " (knot-like swollen mus-
normal endplates. cle fibers) in biopsies of Muskelharten

Copyrighted Material
68 Part 1 / Introduction

(Myogelosen) (muscle indurations or myo- sists of stretched sarcomeres to compen-


gelosis) in human subjects. sate for the contractured ones in the knot
In 1960, Miehlke, et al. reported
193
segment. In addition, a pair of contraction
"bauchige Anschwellungen" (bulging knots separated by empty sarcolemma are
swellings) of muscle fibers in longitudinal illustrated in the upper right of the inset
sections, and also much variable width (part B) of Figure 2.25. This f e a t u r e 96,253

and staining intensity in cross sections of may represent one of the first irreversible
muscle fibers, in biopsies taken from re- complications that result from the contin-
gions of Muskelharten (muscle indurations ued presence of the contraction knot.
or nodules) in patients with Fibrositissyn- The muscle fibers containing contrac-
drom (fibrositis). tion knots are clearly under increased ten-
In 1976, Simons and Stolov used TrP cri-
253
sion both at the contraction knot and be-
teria to examine canine muscles for a tender yond. The total muscle schematic in Figure
spot in a palpable taut band comparable to 2.25A illustrates that this sustained ten-
that observed in human patients. With ani- sion could produce local mechanical over-
mals under anesthesia, the same location in load of the connective tissue attachment
the muscle was identified by palpation and structures in the vicinity where the taut
widely biopsied. Some isolated, large, round band fibers attach. This sustained tissue
muscle fibers and some groups of these distress could be expected to induce the re-
darkly staining, enlarged, round muscle lease of sensitizing agents that would sen-
fibers appeared in cross sections (Fig. 2.23). sitize local nociceptors, producing local
In longitudinal sections, the corresponding tenderness and the characteristics of an at-
feature was a number of contraction knots. tachment TrP
An individual knot appeared as a segment of In 1996, Reitinger, et al. biopsied in
21i

muscle fiber with extremely contracted sar- fresh cadavers the still-palpable nodules of
comeres. This contractured segment showed myogelosis that were located in the gluteus
a corresponding increase in diameter of the medius muscle where trigger point 1 and
muscle fiber, as illustrated in Figure 2.24. trigger point 2 are found as described by
The structural features of contraction Travell and Simons. Cross sections
280

knots, one of which is illustrated in Figure showed the previously described, large,
2.24, are portrayed schematically in the rounded, darkly staining muscle fibers and
lower half of Figure 2.25. This figure pre- a statistically significant increase in the av-
sents a likely explanation for the palpable erage diameter of muscle fibers in the myo-
nodules and the taut bands associated with gelosis biopsies compared to nonmyo-
TrPs. The inset below in Figure 2.25B gelotic control biopsies from the same
shows three single contraction knots scat- muscle. Electron microscopic cross sec-
tered among normal muscle fibers. Figures tions showed an excess of the A-Band and
2.24 and 2.25B illustrate that beyond the lack of the I-Band configuration. Exclusive
thickened segment of contractured muscle presence of A-Band in the absence of
fiber at the contraction knot, the muscle I-Band occurs only in fully contracted sar-
fiber becomes markedly thinned and con- comeres. It is highly likely that this fully-
15

Figure 2.23. Giant round muscle fiber in the center


of the figure is surrounded by open space that may
have resulted from a local severe energy crisis. This
space may contain substances that could sensitize
adjacent nociceptive nerve fibers. In addition to the
normal-size irregularly shaped muscle fibers sur-
rounding the giant fiber, there are four abnormally
small fibers, two above to the right, and two below
to the left, that may be the segments of muscle
fibers which are narrowed because of a contraction
knot elsewhere in that fiber.

Copyrighted Material
Chapter 2 / General Overview 69

Figure 2.24. Longitudinal section of an example of the bottom of the figure. The fiber diameter is markedly in-
contraction knots seen in biopsies of canine muscles, creased in the region of the knot and abnormally de-
in this case the gracilis. An exquisitely tender spot in creased on either side of it. The irregularity of the sar-
a taut band of the muscle was selected as the biopsy colemma along the upper border of the fiber (in the
site. These are two essential trigger point criteria. The center of the contraction knot) may represent an end-
striations (corresponding to sarcomere length) indi- plate. The distortion of the sarcomere alignment in ad-
cate severe contracture of the approximately 100 sar- jacent muscle fibers represents sheer stresses in
comeres in the knot section of the muscle fiber. The those fibers that may, in time, play a part in the prop-
sarcomeres on both sides of the knot show compen- agation of this dysfunction to neighboring muscle
satory elongation compared to the normally spaced fibers.
sarcomeres in the muscle fibers running across the

contracted electron microscopic pattern knot in Figure 2.24 fits the appearance one
seen in cross sections and the large round would expect if the motor endplate for that
fibers correspond to the (fully contrac- muscle fiber was centered over and extended
tured) contraction knots seen in longitudi- the length of the contraction knot. A defini-
nal sections under light microscopy. tive experiment to confirm this impression is
Two features of Figure 2.24 suggest that described under Confirmation of the Inte-
the SEA does originate at a contraction knot grated Trigger Point Hypothesis that follows.
and that the contraction knot may be caused
by a dysfunctional endplate. First, this figure Integrated Trigger Point Hypothesis
illustrates a longitudinal section of a con- This section includes several diagnos-
traction knot, which, in this case, is a seg- tic categories that have German names,
ment of muscle fiber that includes about 100 which are explained in the historical re-
maximally contractured sarcomeres. Nor- view part of section A of this chapter. It is
mally sarcomeres range in length from about presented from the point of view that
0.6 u,m when fully shortened to about 1.3 |xm TrPs are fundamentally the same disease
when fully extended, which is a full 1:2 process as other diagnoses based on ten-
length ratio. Based on a minimum sarco-
15
der nodules which are responsible for the
mere length of 0.6 u,m, the 100 sarcomeres of patient's pain, diagnoses that may em-
the contraction knot would extend 60 urn. phasize some aspects, and that have dif-
This is within the 20 to 80 u>m range in the ferent names which are often in other lan-
length of normal motor endplates, depend- guages.
ing on the muscle. Second, although one
225
The integrated hypothesis combines in-
cannot be sure of this in the absence of formation from electrophysiological and
cholinesterase stain, the irregularity of the histopathological sources. The energy cri-
upper border in the middle of the contraction sis part of the hypothesis began to take

Copyrighted Material
70 Part 1 / Introduction

Figure 2.25. Schematic of a trigger point complex of periencing maximal contracture of its sarcomeres. The
a muscle in longitudinal section. The schematic iden- sarcomeres within one of these enlarged segments
tifies three regions that can exhibit abnormal tender- (contraction knot) of a muscle fiber are markedly
ness {red). It also illustrates contraction knots that shorter and wider than the sarcomeres of the neigh-
most likely: make a trigger point feel nodular, cause boring normal muscle fibers which are free of con-
the taut band, and mark the site of an active locus. traction knots. In fibers with these contraction knots
A, the central trigger point {CTrP) which is found in (note the lower three individual knots), the sarcomeres
the endplate zone, contains numerous electrically ac- in the part of the muscle fiber that extends beyond
tive loci, and contains numerous contraction knots. both ends of the contraction knot are elongated and
The local tenderness of the CTrP is identified by a red narrow compared to normal sarcomeres. At the top of
oval. A taut band of muscle fibers extends from the this enlarged view is a pair of contraction knots sepa-
trigger point to the attachment at each end of the in- rated by an interval of empty sarcolemma between
volved fibers. The sustained tension that the taut band them that is devoid of contractile elements. This con-
exerts on the attachment tissues can induce a local- figuration suggests that the sustained maximal ten-
ized enthesopathy that is identified as an attachment sion of the contractile elements in an individual con-
trigger point {ATrP). The local tenderness of the en- traction knot could have caused mechanical failure of
thesopathy at the ATrP is identified by a red circle the contractile elements in the middle of the knot. If
with a black border. that happened, the two halves would retract, leaving
B, this enlarged view of part of the central trigger an interval of empty sarcolemma between them. In
point shows the distribution of five contraction knots patients, the CTrP would feel nodular as compared to
and is based on Figures 2.23 and 2.24. The vertical the adjacent muscle tissue, because it contains nu-
lines in each muscle fiber identify the relative spacing merous "swollen" contraction knots that take up addi-
of its striations. The space between two striations cor- tional space and are much more firm and tense than
responds to the length of one sarcomere. Each con- uninvolved muscle fibers.
traction knot identifies a segment of muscle fiber ex-

Copyrighted Material
Chapter 2 / General Overview 71

Figure 2.26. Schematic of the energy crisis hypothe- lease of acetylcholine can result in excessive release
sis which postulates a vicious cycle (red arrows) of of calcium from the SR (black arrow). This calcium
events that appears to contribute significantly to myo- produces maximal contracture of a segment of mus-
fascial trigger points. The function of the sarcoplasmic cle which creates a maximal energy demand and
reticulum (SR) is to store and release ionized calcium chokes off local circulation. The ischemia interrupts
that induces activity of the contractile elements, which energy supply which causes failure of the calcium
causes sarcomere shortening. An initiating event such pump of the sarcoplasmic reticulum, completing the
as trauma or a marked increase in the endplate re- cycle.

form about 20 years ago and has been ity is abnormal depolarization of the
evolving ever since. The energy crisis con- postjunctional membrane that could con-
cept is compatible with recent electrodiag- tinue indefinitely based on continuing ex-
nostic findings, both of which fit the newly cessive ACh release from a dysfunctional
recognized histopathological picture. nerve terminal. In this way, maximum con-
Energy Crisis Component. This con- tracture of the muscle fibers in the vicinity
cept developed from efforts to identify a of the motor endplate could persist indefi-
pathophysiological process that could nitely without motor unit action potentials.
account for: (1) the absence of motor unit The sustained contractile activity of the
action potentials in the palpable taut band sarcomeres would markedly increase meta-
of the TrP when the muscle was at rest, (2) bolic demands and would squeeze shut the
the fact that TrPs are often activated by rich network of capillaries that supply the
muscle overload, (3) the sensitization of nutritional and oxygen needs of that region.
nociceptors in the TrP, and (4) the effec- Circulation in a muscle fails during a sus-
tiveness of almost any therapeutic tech- tained contraction that is more than 3 0 % to
nique that restores the muscle's full stretch 5 0 % of maximum effort. This combination
length. The energy crisis concept was in- of increased metabolic demand and im-
troduced in 1 9 8 1 and was recently up-
254
paired metabolic supply could produce a se-
dated. '190 239
vere but local energy crisis. This functional
Figure 2.26 shows the basic concept of component of the energy crisis should be re-
the energy crisis hypothesis. It postulated versible in a short period of time.
an increase of the calcium concentration The C a pump that returns the calcium
+ +

outside of the sarcoplasmic reticulum pos- into the sarcoplasmic reticulum is depen-
sibly due to mechanical rupture of either dent on an adequate supply of adenosine
the sarcoplasmic reticulum or of the
239
triphosphate (ATP) and appears to be more
muscle cell membrane (sarcolemma). A 17
sensitive to low ATP levels than the con-
sufficient increase in calcium would maxi- tractile mechanism. Thus an impaired
mally activate actin and myosin contractile uptake of calcium into the sarcoplasmic
activity. However, if the damage were re- reticulum would expose the contractile el-
pairable, the abnormality would be tempo- ements to a further increase in calcium
rary. It is now apparent that a more likely concentration and contractile activity. This
mechanism for sustained contractile activ- completes a vicious cycle. In addition, the

Copyrighted Material
72 Part 1 / Introduction

severe local hypoxia and tissue energy cri- dure and very desirable to repeat this ex-
sis would be expected to stimulate produc- periment using modern instrumentation
tion of vasoreactive substances that could and current diagnostic criteria of a TrP.
sensitize local nociceptors. 2. One elegantly instrumented and vali-
Thus, the hypothesis accounts for: (1) the dated study reported in German exam-
26

lack of motor unit action potentials because ined affected muscle for focal hypoxia
of the endogenous contracture of the con- and reported remarkably positive re-
tractile elements rather than a nerve-initi- sults. The study reported the findings in
ated contraction of the muscle fibers; (2) the tender, tense indurations (Muskelharten)
frequency with which muscle overload ac- in the back muscles of three patients di-
tivates TrPs and may reflect the marked me- agnosed as having Myogelosen (myogelo-
chanical vulnerability of the synaptic cleft sis). Figure 2.27 presents the graphic re-
region of an endplate; (3) the release of sub- sults of the three patients examined in
stances that could sensitize nociceptors in this way. The first 5 to 8 mm of sensor ad-
the region of the dysfunctional endplate of vancement shows the normal random
the TrP as a result of tissue distress caused variation of tissue oxygen tension with
by the energy crisis; and (4) the effective- successive 0.7 mm steps of advancement
ness of essentially any technique that elon- as the oxygen sensor approached the ten-
gates the TrP portion of the muscle to its full der induration [TrP]. As the probe ap-
stretch length even briefly, which could proached the palpable border of the ten-
break the cycle that includes energy-con- der induration, the tissue oxygen tension
suming contractile activity. increased as if there were a compen-
This fourth point can be explained by satory hyperemia surrounding the region
the fact that the continued activity of the of hypoxia. After reaching a peak, the tis-
actin-myosin interaction depends on phys- sue oxygen tension fell abruptly to
ical contact between the actin and myosin nearly (but not quite) zero, indicating
molecules, which occurs fully when the profound hypoxia in the central region of
sarcomere is approximately midlength or the induration. It is noteworthy that the
less. The molecules lose overlap contact at volume of the region of increased oxygen
full length. This principle is illustrated in tension which surrounded the central re-
the lower part of Figure 2.5. With cessation gion of oxygen deficit was at least as large
of contractile activity because of actin- as the volume of hypoxic tissue.
myosin separation, both the energy con- 3. The contraction knots and electronmicro-
sumption and compression of capillaries scopic findings described above confirm
would be relieved. This opportunity to re- the presence of contractured sarcomeres.
store energy reserves could help to block
two critical steps in the energy-crisis cycle. In addition, the tendinous attachment of
Based on this hypothesis, the TrP region many of the fibers with these shortened seg-
should have three demonstrable character- ments would be likely to develop enthesitis
istics: (1) be higher in temperature than because of the abnormally increased, sus-
surrounding muscle tissue because of in- tained tension exerted by the double source
creased energy expenditure with impaired of tension in each involved muscle fiber.
circulation to remove heat, (2) be a region Although no experimental investigation
of significant hypoxia because of ischemia, of the development of enthesitis, where
and (3) have shortened sarcomeres. taut bands attach at the ends of the muscle,
has been reported to date, its frequent clin-
1. The only two published reports that ical occurrence is illustrated repeatedly
specifically measured intramuscular TrP throughout this volume and confirmed by
temperature were an early report by Trav- clinicians who look for it.
ell in 1 9 5 4 and another described very
270
Integrated Trigger Point Hypothesis.
briefly in Russian in 1976 by Popelian- When combined, the electrophysiological
skii, et al. Both recorded a focal in-
209
and histological lines of evidence indi-
crease in temperature in the region of the cate that a TrP is essentially a region of
TrP. It would be a relatively simple proce- many dysfunctional endplates, and that

Copyrighted Material
Chapter 2 / General Overview 73

Sensor Advancement (mm) Sensor Advancement (mm) Sensor Advancement (mm)

Palpable border of the induration Normal mean p 0 2

Figure 2.27. Tissue oxygen saturation values vere oxygen deficiency recorded as the probe ap-
recorded by an oxygen probe that progressed in 0.7 proached the center of the induration. Note the com-
mm steps through normal muscle and then into a ten- parable region of increased oxygen saturation sur-
der, tense induration-Muskelharten (another name for rounding the central region of hypoxia. (Data
a TrP)-in three patients with Myogelosis. Arrow marks reproduced with permission from Bruckle W, Suckfull
the palpable border of the induration. The dashed line M, Fleckenstein W, et al. Gewebe-p02-Messung in
indicates the mean oxygen saturation of adjacent nor- der verspannten Ruckenmuskulatur [m. erector
mal muscle. The area marked in red identifies the se- spinae]. Zeitschrift fur Rheumatologie 49:208-216,

each dysfunctional endplate is associated These potentials are so numerous that they
with a section of muscle fiber that is max- superimpose to produce endplate noise or
imally contracted (a contraction knot). SEA, and a sustained partial depolariza-
The spontaneous electrical activity and tion of the postjunctional membrane. The
spikes that characterize active loci within excessive demand for production of ACh
TrPs are currently recognized by elec- packets in the motor nerve terminal would
tromyographers as 'normal" endplate po- increase its energy demand (evidenced by
tentials. However, physiological experi- abnormal mitochondria in the nerve termi-
ments have shown that these potentials are nal). The increased activity of the postjunc-
not normal, but are the result of a grossly tional membrane and sustained depolar-
abnormal increase in ACh release by the ization would impose an additional local
nerve terminal. It appears very likely that a energy demand. Increased numbers of sub-
contraction knot is located at an endplate sarcolemmal mitochondria and abnormal
and that it is caused by this endplate dys- mitochondria have been noted repeatedly
function. The following hypothesis pro- in past studies. This mechanism may be re-
poses a likely relationship between the dys- sponsible for the presence of many ragged
functional endplate and the contraction red fibers in muscles with characteristics
knot. The hypothesis provides a model that that are compatible with the presence of
can be used to design critical experiments myofascial TrPs.
with which to verify, refine, or refute the The calcium channels that trigger re-
hypothesis. lease of calcium from the sarcoplasmic
Figure 2.28 presents the integrated TrP reticulum are voltage gated, normally by
hypothesis schematically. The hypothesis depolarization of the T tubule at the triad
is based on continuous excessive ACh re- where the T tubule communicates with the
lease from a dysfunctional motor nerve ter- sarcoplasmic reticulum. The T tubule is
minal into its synaptic cleft. Impaired part of the same sarcolemmal membrane
cholinesterase function would potentiate that forms the postjunctional membrane.
the effect. The excessive ACh activates The sustained depolarization of this mem-
ACh receptors in the postjunctional mem- brane is one mechanism that might account
brane to produce greatly increased num- for a tonic increase in the release of cal-
bers of miniature endplate potentials. cium from the sarcoplasmic reticulum to

Copyrighted Material
74 Part 1 / Introduction

Dysfunctional Endplate Region

Autonomic
nerve
Nociceptive
fibers
nerve
fibers Motor
Sensitizing nerve terminal
substances Excess
acetylcholine
release

Energy crisis

Increased Depolarization
energy
Decreased demand SR Muscle
energy
C a l c i u m release fiber
supply
S a r c o m e r e contracture

C o m p r e s s i o n of vessels

Figure 2.28. Integrated hypothesis. The primary dys- would increase energy demand. The sustained mus-
function hypothesized here is an abnormal increase cle fiber shortening compresses local blood vessels,
(by several orders of magnitude) in the production thereby reducing the nutrient and oxygen supplies
and release of acetylcholine packets from the motor that normally meet the energy demands of this region.
nerve terminal under resting conditions. The greatly The increased energy demand in the face of an im-
increased number of miniature endplate potentials paired energy supply would produce a local energy
produces endplate noise and sustained depolariza- crisis, which leads to release of sensitizing sub-
tion of the postjunctional membrane of the muscle stances that could interact with autonomic and sen-
fiber. This sustained depolarization could cause a sory (some nociceptive) nerves traversing that region.
continuous release and uptake of calcium ions Subsequent release of neuroactive substances could
from local sarcoplasmic reticulum (SR) and pro- in turn contribute to excessive acetylcholine release
duce sustained shortening (contracture) of sar- from the nerve terminal, completing what then be-
comeres. Each of these four highlighted changes comes a self sustaining vicious cycle.

produce the local sarcomere contracture of traction knot would greatly increase the lo-
the contraction knots. The increased vol- cal energy and oxygen demand.
ume occupied by the contraction knots The concept of sustained contracture of
would also explain why clinicians describe sarcomeres in the muscle fiber supplied by
palpating a nodule at the TrP along with the affected endplate is compatible with
the narrower taut band. This contracture the previously proposed energy crisis hy-
process appears to occur in the immediate pothesis reviewed in detail above. The
vicinity of an endplate. A sustained release severe energy crisis in the vicinity of the
of calcium from the sarcoplasmic reticu- endplate can be expected to release neuro-
lum would increase the energy demand of active substances that sensitize and modify
the calcium pumps in the sarcoplasmic the function of any sensory and autonomic
membrane that return the calcium into the nerves in that region. As noted in Section
sarcoplasmic reticulum. The sustained C above, small blood vessels, sensory
contracture of the sarcomeres in the con- nerves, and autonomic nerves normally are

Copyrighted Material
Chapter 2 / General Overview 75

part of the same neurovascular bundle or erally lasted for 4 months. Apparently very
complex that includes the motor nerve. few subjects realized complete relief. The
Sensitization of local nociceptors could phentolamine study is more convincing
account for the exquisite tenderness of the than the phenoxybenzamine study and is
TrP, the referred pain originating at the TrP, strongly supported by a subsequent rabbit
and the origin of a local twitch response. study. In that study, intravenous injec-
33a

Several lines of experimental evidence sug- tion of phentolamine caused as much as a


gest that autonomic (especially sympa- 6 8 % decrease in SEA in 80 seconds. Ap-
thetic) nervous system activity can strongly parently, roughly two-thirds of the ACh re-
modulate the abnormal release of acetyl- lease was dependent on local sympathetic
choline from the nerve terminal. nervous system effects.
The clinical effectiveness of Botulinum A In addition, in conjunction with a hu-
toxin injection for the treatment of myofas- man study of active loci in TrPs, the in- 249

cial TrPs helps to substantiate dysfunc-


1 34,297
vestigators confirmed a previous observa-
tional endplates as an essential part of the tion that in many subjects spike activity
131

pathophysiology of TrPs. This toxin specifi- associated with SEA in the upper trapezius
cally acts only on the neuromuscular junc- muscle was clearly increased by normal
tion, effectively denervating that muscle cell. resting inhalation and was inhibited by ex-
Studies by Gevirtz and associates sup- halation. Exaggerated respiratory efforts in-
port indications that the autonomic ner- creased the response. T h e y also noted an
249

vous system can modulate spike activity increase in the amplitude of SEA during
(and therefore the rate of release of ACh inhalation.
packets) at a motor endplate. Trigger point
The possibility that the presence of ex-
EMG activity was increased by psychologi-
cess calcium in the vicinity of the con-
cal stressors both in normal subjects and 186

tractile elements is due to an excess of


in patients with tension-type headache. 167

calcium release compared to calcium up-


These two reports did not specify whether
take into the sarcoplasmic reticulum is
the TrP EMG activity being measured was
supported by a case report. Two pa-
233

SEA or spikes or some combination of both.


tients prone to trigger points in the right
More recently, Hubbard published ad-
132
gluteus medius muscle experienced a
ditional experimental data indicating that flare and became refractory to the usually
the amount of electrical activity is strongly successful injection after taking a calcium
influenced by the autonomic nervous sys- channel blocker, alodipine besylate, for
tem. All intramuscular injections em- hypertension. Treatment became effective
ployed EMG guidance to place the injected again in the absence of alodipine. This
solution close to the source of the TrP EMG calcium-channel blocker inhibits the re-
potentials. Four patients were injected uptake of calcium into the sarcoplasmic
with phentolamine intramuscularly and in reticulum of vascular smooth muscle and
two patients phentolamine was injected in- cardiac muscle. If this is also true of skele-
travenously. In all six studies, the TrP EMG tal muscle, the resultant increase in cal-
activity subsided for the duration of the cium to stimulate contracture of sarco-
phentolamine effect. Phentolamine is a meres in the TrP region would aggravate
competitive a-adrenergic blocker. 132
In a the vicious cycle of Figure 2.28.
series of uncontrolled studies, a total of
108 patients received EMG-guided TrP in- Clinical Correlations. If multiple active
jections of phenoxybenzamine, which is a loci are part of the same pathophysiological
long-lasting adrenergic, noncompetitive a- process as multiple contraction knots, and
receptor blocking agent that can produce a if this relationship applies equally to TrPs
chemical sympathectomy with no effect on and to tender nodules, it would represent a
the parasympathetic system. It has an in- major step forward in our understanding of
travenous half-life of 24 hours. Between enigmatic myogenic pain. Based on the in-
one-half and two-thirds of the patients ex- tegrated hypothesis just described, many of
perienced at least 2 5 % pain relief within 1 the clinical features of this clinical condi-
month following treatment and relief gen- tion can now be explained.

Copyrighted Material
76 Part 1 / Introduction

Two aspects of Figure 2.24 suggests that, fibers in the taut band extend beyond the
in fact, the SEA does originate at a contrac- nodule unchanged. The contraction knots
tion knot and that the contraction knot may represent additional volume (Fig. 2.25).
be caused by a dysfunctional endplate. As- The spot tenderness of both TrPs and
suming this pathophysiological interpreta- nodules would be the result of sensitized
tion is correct, it explains a number of clin- nociceptors. The nociceptors are most likely
ical features that apply to both TrPs and sensitized by substances released as a result
myogelosis, although in both cases, some of the local energy crisis and tissue distress
features commonly have been overlooked. which is associated with these histopatho-
The taut band of a TrP would be caused logical changes and endplate dysfunction.
by the increased tension of involved mus- The enthesopathy (tenderness at the mus-
cle fibers both because of the tension pro- cle attachment where the taut band termi-
duced by the maximally shortened sarco- nates) is explained by the inability of the
meres in the contraction knot and also muscle attachment structures to withstand
because of the increased (elastic) tension the unrelieved sustained tension produced
produced by all the remaining elongated by the taut band. In response, these tissues
(and therefore thin) sarcomeres. Ordinarily develop degenerative changes that are likely
a muscle fiber runs from its musculotendi- to produce substances which could sensitize
nous attachment at one end of a muscle to local nociceptors. Fassbender and Wegner 66

its musculotendinous attachment at the presented histological evidence in fibrositis


other end; in fusiform muscles, that is (nonarticular rheumatism) patients for the
nearly the full length of the muscle. kind of degenerative changes to be expected
Figure 2.24 shows clearly the abnormally in regions of TrP-induced enthesopathy.
shortened and abnormally lengthened sar- The myoglobin response to massage of fi-
comeres of the muscle fiber that contains brositic nodules can be explained on the ba-
the contraction knot (in the center of the fig- sis of the observed histopathological
ure). These abnormal lengths contrast to the changes in nodules. Repeated deep mas-
normal resting length of sarcomeres in the sage of the fibrositic nodules (TrPs) pro-
uninvolved muscle fibers running across duced transient episodes of myoglobinuria
the lower part of the figure. With the in- that were not produced by similar massage
volvement of a sufficient number of muscle of normal m u s c l e . The intensity of myo-
47,48

fibers within several fascicles, the increased globin response, the degree of tenderness,
tension of the involved muscle fibers and firmness of the nodule progressively
should be palpable as a taut band running faded out with repeated treatments (Fig.
the length of the muscle. This full-length 2.29). The distended sarcoplasm of these
description applies if the muscle fibers run contraction knots could well be more vul-
nearly parallel to the long axis of the mus- nerable to rupture by mechanical trauma
cle, and the muscle has no inscriptions. and external pressure than normal fibers. If
The palpable nodule of TrP-related diag- massage applied by the therapist resulted
noses, such as fibrositis and myogelosis, in cell rupture, the cell would spill myoglo-
can be explained by the presence of multi- bin and most likely destroy the involved
ple contraction knots (Fig. 2.25). Since a sar- neuromuscular junction as a functional
comere must maintain a nearly constant structure, thus effectively terminating the
volume, it becomes broader as it shortens. contracture and associated energy crisis. As
The sarcomeres in a contraction knot appear more and more contraction knots within
at least twice the diameter of the distant sar- the nodule were eliminated, the patient
comeres beyond the contraction knot in the would experience increasing relief of
same fiber. The nodule feels larger than sur- symptoms.
rounding tissue because of the greater vol- The development of histopathological
ume occupied by the contraction knots and complications that could contribute to
it feels firmer because of the highly con- chronicity and make treatment more diffi-
densed state of the contractile elements in cult is suggested by two observations. First,
each knot. The region of contraction knots Figure 2.24 clearly illustrates marked dis-
feels larger than the rest of the taut band be- tortion of the striations (sarcomere arrange-
cause the normal fibers and stretched-thin ment) in adjacent muscle fibers for some

Copyrighted Material
Chapter 2 / General Overview 77

Figure 2.29. Median values resulting from repeated tension index was proportional to the extent of mus-
deep massage of the same fibrositic nodules (TrPs) in cle tension before a treatment. This index (small black
13 patients. Plasma myoglobin levels increased 10- closed circles) declined progressively to the tenth
fold following the first treatment. By the tenth treat- treatment reaching one-fourth of the value that it had
ment, the response had declined to the same low level at the time of the first treatment. Graph based on data
observed in normal muscle. The "fibrositic" palpable in Table I of Danneskiold-Samsoe, et al., 1983. 47

distance beyond the contraction knot. This by Simons and Stolov in their Figure 9
253

would produce unnatural shear forces be- and by Reitinger, et al. in their Abb. 3c.
214

tween fibers that could seriously (and Second, the occasional finding of a seg-
chronically) stress the sarcolemma of the ment of empty sarcolemmal tube between
adjacent muscle fibers. If the membrane two contraction knots (Fig. 2.25) may
were stressed to the point that it became represent an additional irreversible com-
pervious to the relatively high concentra- plication of a contraction knot. Miehlke, et
tion of calcium in the extracellular space, al.
193
described "Entleerung einzelner
it could induce massive contracture that Sarkolemmschlauche" (emptying of indi-
would compound the shear forces. Ben- vidual sarcolemmal tubes). Reitinger, et
nett described this mechanism clearly
17
al. described "Muskelfasern mit optisch
21i

and how it could lead to severe local con- leerem, zystichen Innenraum (Myofibril-
tracture of the muscle contractile elements. lenverlust?)" [muscle fibers with an opti-
This mechanism might account for the cally empty, cystic interior (loss of myofib-
"keulenformige gequollene Muskelfasern" rills?)]. Simons and Stolov, in their
253

(club shaped swollen muscle fibers) de- Figure 13, illustrated and described the
scribed by Glogowski and Wallraff, which 96
complete emptying of the sarcolemmal
look like elongated versions of a contrac- tube between two contraction knots (Fig.
tion knot. If this happens, it might occur 2.25). This configuration appears as if the
anywhere along a muscle fiber where it has sustained maximal tension of the contrac-
been affected by an adjacent contraction tile elements in a contraction knot caused
knot. This could explain the tendency for mechanical failure of the contractile ele-
clumping of giant fibers mixed with un- ments in the middle of the knot. This al-
usually small fibers (segments of stretched lowed the two halves to retract, leaving an
sarcomeres) that is seen in cross sections. interval of empty sarcolemma between
This tendency for clumping was illustrated them. Electronmicroscopic illustrations by

Copyrighted Material
78 Part 1 / Introduction

Fassbender ' show disintegration of the


64 66
encouraged by commercial interests. 148

actin filaments where they attach to the Z- The term tension headache is a good ex-
line suggesting that this is the location in ample of this myth in action. The term
the chronically contractured sarcomeres originated with the assumption that mus-
where the mechanical failure may begin. cle spasm (involuntary contraction) was
These additional histopathological com- responsible for the headache and that re-
plications could contribute to chronicity laxing the pericranial muscles would re-
and may relate to the transition from latent lieve it. In 1991, an editorial in the journal
to active TrPs. PAIN reviewed this issue and empha-
202

Confirmation. A relatively simple sized that it was unambiguously clear that


study could validate the integrated hypoth- increased EMG activity did not account
esis. The investigators would need to iden- for the muscle tenderness and pain of ten-
tify myofascial TrPs with tender nodules sion-type headache. The author had no
that are responsible for the patient's pain satisfactory alternative solution. A subse-
complaint; locate the SEA of an active locus quent study reinforced this conclusion. 145

in the TrP electrodiagnostically; mark 242

that location electrolytically with iron from A current variation of this pain-spasm-
the EMG n e e d l e ; ' biopsy the site; fix
147 291
pain concept, the stress-hyperactivity-pain
the biopsy by liquid nitrogen; and prepare theory, seems equally invalid for the
38

longitudinal sections that are stained for same reasons.


iron, for acetylcholinesterase, and a
147,291 291
Muscle Spindle Hypothesis. In their
base stain such as one of the trichromes. 214
initial communication, Hubbard and
If the iron-stained regions include contrac- Berkoff, and again Hubbard in his more
133

tion knots with motor endplates attached to recent report, concluded that the source
132

them, it would greatly advance understand- of EMG activity in TrPs was a dysfunc-
ing of, and the acceptance of the diagnoses tional muscle spindle. T h e y gave three
133

of TrPs and TrP-related conditions that are reasons for dismissing the possibility that
characterized by tender nodules and/or taut these potentials might arise from motor
bands. Descriptions of this critical experi- endplates: (1) the activity is not localized
ment, and the rationale for it have been enough to be generated in the endplate,
published. 244 245
(2) the activity does not have the expected
location, and (3) the activity does not have
Other Hypotheses
the expected waveform morphology.
Pain-Spasm-Pain Cycle. The old con- Existing literature and our experimental
cept of a pain-spasm-pain cycle does not findings contradict these three assertions.
stand up to experimental verification ei-
ther from a physiological point of view 191
1. The degree of localization that is de-
or from a clinical point of view.
105
scribed under the headings Active Loci
Physiological studies show that muscle and Spikes above corresponds closely to
pain tends to inhibit, not facilitate, reflex that previously described in the classi-
contractile activity of the same muscle. 191
cal paper on the source of motor end-
Walsh explained clearly how this mis-
285
plate potentials. 291

conception has been strongly reinforced 2. Recent s t u d i e s '


248
explicitly exam-
249,252

by a misunderstanding of normal human ined the distribution within the muscle


motor reflexes based on spinalized cat ex- of the electrically active loci and found
periments and how the misconception that they are chiefly in a TrP, to some ex-
has persisted throughout the 20th cen- tent also in the endplate zone, but were
tury. not found outside of the endplate zone.
In 1989, Ernest Johnson, editor of the
146 Muscle spindles are scattered through-
American Journal of Physical Medicine out a muscle as shown in Figure 2.30 35

summarized overwhelming evidence that and in Figure 2 . 3 1 . Muscle spindles


211

the common perception of muscle pain clearly are not concentrated just in the
being closely related to muscle spasm is a endplate zone where TrPs are found. The
myth and that the myth has been strongly studies associated with Figures 2.17 and

Copyrighted Material
Chapter 2 / General Overview 79

Figure 2.30. Distribution of muscle spindles {small


black ovals) in the semitendinosus (ST) and soleus
muscles of the cat. The semitendinosus muscle is di-
vided into two segments that are separately innervated.
However, the muscle spindles are uniformly distributed
throughout the length of both segments and not con-
centrated in the endplate zone as are motor endplates.
(Reproduced with permission from Chin NK, Cope M,
Pang M. Number and distribution of spindle capsules in
seven hindlimb muscles of the cat. In: Barker D, ed.
Symposium on Muscle Receptors. Hong Kong: Univer-
sity Press, 1962:241-248.)

Figure 2.31. An example of the distribution of muscle spindles


in the sternocleidomastoid muscle of a 14 weeks old human fe-
tus. The spindles are distributed rather uniformly throughout the
muscle and not clustered in the midbelly region of the muscle as
are the motor endplates. (Reproduced with permission from
Radziemski A, Kedzia A, Jakubowicz M. Number and localiza-
tion of the muscle spindles in the human fetal sternocleidomas-
toid muscle. Folia Morphol 50(1/2)65-70, 1991.)

Copyrighted Material
80 Part 1 / Introduction

2.22 demonstrate that active loci occur at guished from true miniature endplate
motor endplates. potentials, which are considerably more
3. The reader can judge with regard to the difficult to locate and record.
waveform morphology by comparing 2. The presence of action potentials origi-
the spikes with SEA in our recordings nating at an endplate that was also the
from an active locus (Fig. 2.14B) with site of a TrP active locus was illustrated
the endplate potentials illustrated in a in Figures 2.17B and 2.22. These are
current electromyography text (Fig. motor endplates of extrafused fibers.
2.15). The amplitude and sweep speed The type of needle used would be me-
with which a recording is made can pro- chanically (Fig. 2.16) unable to pene-
duce great differences in waveform ap- trate the capsule of a muscle spindle to
pearance, which can be very misleading reach an intrafusal motor endplate.
(Fig. 2.14A). At similar sweep speeds Muscle spindles usually lie in loose
the SEA and endplate potentials have connective tissue.
the same waveform morphology. 3. The demonstration that the spikes from
Other authors agree that these spikes a TrP active locus can propagate at least
and spontaneous electrical activity found 2.6 cm along the taut band precludes
251

in TrPs arise from motor endplates. 19, 37 a muscle-spindle intrafusal-fiber origin.


Brown and Varkey also attributed the
24 This distance is twice the total length of
spontaneous electrical activity to poten- a human muscle spindle and four times
tials of the endplate zone and attributed the half-fiber distance measured in this
spikes to postsynaptic muscle-fiber action experiment.
potentials that were presynaptically acti- 4. In addition, the clinical effectiveness of
vated by mechanical irritation, with which Botulinum A toxin injection for the
we agree. treatment of myofascial TrPs sup-
1,34,297

There are four additional reasons why ports the endplate hypothesis.
one must very seriously question the valid-
ity of the hypothesis that the heart of the If muscle-spindles were the location of
TrP dysfunction lies in dysfunctional mus- TrPs, it would not help to explain the close
cle spindles rather than in dysfunctional relation between TrPs and taut bands, since
motor endplates. propagated action potentials originating
from motor neurons are not responsible for
1. If the conclusion that these potentials the tension of the band. It is true that a
arise from dysfunctional muscle spin- muscle-spindle is an attractive source for
dles is correct, then Wiederholt's com- the afferent limb of the local twitch re-
prehensive EMG, histological and phar- sponse. However, it is not necessary to pos-
macological study 291
reached an tulate a dysfunctional muscle spindle. Fur-
erroneous conclusion and electromyog- ther research studies are needed to resolve
raphers ever since have been misled. It whether muscle spindles ever contribute
may be difficult to convince the elec- to the local twitch response in any way.
tromyographic community that what Two issues need clarification. The re-
they have identified as endplate poten- cent report by Hubbard of finding one
132

tials are really muscle-spindle poten- muscle spindle in one biopsy needs to be
tials. If the potentials described by Hub- put in perspective. The first histological
bard are other than endplate potentials, study using iron deposition as an accurate
then where in his studies are the end- marker in 1955 reported that in all 28
147

plate potentials identified by elec- sites of electrical activity in rat muscles


tromyographers? Because most of the "no other structures of muscle, including
studies by physiologists describing ab- muscle spindles, had any consistent
normal endplate potentials correspond- relationship to the area containing the
ing to SEA did not appear in print until iron deposits." They 147
did not use a
after his paper, Wiederholt did not real- cholinesterase stain and so were unable to
ize that the potentials commonly identi- identify motor endplates. Wiederholt 291

fied as endplate noise must be distin- used both iron stain and cholinesterase

Copyrighted Material
Chapter 2 / General Overview 81

stain when he strongly associated the has presented extensive EMG evidence that
source of the electrical activity with end- neuropathic changes are significantly re-
plates. He made no mention of muscle lated to the presence of TrPs in the
spindles, although it would be no surprise paraspinal musculature. There is much
if a muscle spindle appeared in a few of clinical evidence that compression of motor
his sections since they are widely distrib- nerves can activate and perpetuate the pri-
uted in the muscle, including the end- mary TrP dysfunction at the motor endplate.
plate region. The methylene blue injec- Fibrotic Scar Tissue Hypothesis. The
tion used by Hubbard to localize the site concept that the palpable firmness of the tis-
for evaluation is well known for its ten- sues at the TrP represents fibrotic (scar) tis-
dency to diffuse along the fascial planes sue is based on the assumption that dam-
where muscle spindles are located. As the aged muscle tissue has healed by scar
author noted, this one biopsy, which con- formation. This concept derives from his-
75

tradicts previous studies, is not conclu- tological findings in a few most severely in-
sive. volved subjects in studies of Muskelharten,
The report that in two subjects EMG-
132 Myogelosen, Fibrositis, and Weichteil-
guided intramuscular TrP injections of cu- rheumatismus reported in the German liter-
rare had no effect on either the amplitude or ature throughout this century. Patients with
frequency of the TrP-EMG activity would myofascial TrPs would have been included
seem to be convincing evidence that the under the diagnostic criteria used for these
EMG activity did not come from motor end- studies but so would almost any other mus-
plate activity. However, in several pilot cular affliction with tender indurations.
tests using intravenous injection of curare Only two studies have reported biopsies
in the rabbit (Hong, Simons, Simons, un- of TrPs, one on dogs and one on human
253

published data) the investigators learned subjects. Both studies presented strong
214

that unless one establishes, by some inde- evidence for the presence of contraction
pendent means such as motor nerve stimu- knots and neither found fibrosis. In addi-
lation, that the motor endplates are effec- tion, the recently discovered endplate dys-
tively blocked by the curare, one cannot function described in this chapter and taut
draw any conclusions with confidence con- bands caused by sarcomere contraction
cerning its effect on the electrical activity of fully account for the clinical findings of pa-
active loci. This confirmation was lacking tients with myofascial TrPs without invok-
in the Hubbard study. To be seriously con- ing fibrosis as part of the process. The rapid
sidered, this experiment needs to be re- resolution of the palpable taut band with
peated with proper controls. specific TrP treatment argues against the fi-
One other study suggested that spikes
205 brosis explanation. A review by Simons 235

arise from intrafusal muscle fibers. Those of all biopsies of tender nodules reported for
authors discussed why spikes are not ec- much of this century found that the authors
topic discharges of motor axons but did not consistently reported little or no scar tissue
consider the possibility that spikes are the and, when present, it was observed only in
result of mechanically induced release of a relatively few clinically severe cases.
abnormal amounts of acetylcholine at the It is possible that if the endplate dys-
neuromuscular junction of an extrafusal function is allowed to persist for an ex-
fiber. However, all of their data were con- tended period of time, it may eventually
sistent with this latter mechanism of spike lead to chronic fibrotic changes. How
generation. Muscle spindles may, at times, quickly and under what circumstances this
contribute to TrP phenomena, but it seems might occur must be resolved with appro-
extremely unlikely that muscle spindles priate research studies. The increasing re-
are the primary site of the TrP mechanism. fractoriness to local TrP therapy with
longer periods before effective treatment is
Neuropathic Hypothesis. In 1980, started can just as well be attributed to
127

Gunn proposed that the cause of TrP hy-


109 plastic changes of the central nervous sys-
persensitivity is neuropathy of the nerve tem when subjected to prolonged nocicep-
serving the affected muscle. Recently, Chu 37 tive input as to fibrotic changes in the mus-

Copyrighted Material
82 Part 1 / Introduction

cle. This central mechanism is now well tances away from it. Responses were unob-
documented experimentally. tainable 5 mm to either side of the trigger
spot, were greatly attenuated when applied
Local Twitch Response in the taut band 1 cm from the trigger spot to-
The local twitch response (LTR) is a brisk ward the recording needle, and were vesti-
transient contraction of the palpable taut gial in the taut band 3 cm from the trigger
band of muscle fibers elicited by mechanical spot. The vigor of the twitch response was
stimulation of the TrP in that taut band. Me- very sensitive to small displacements of
chanical stimulation may be produced by only a few millimeters when the stimulus
needle penetration of the TrP, by mechan-
246 was applied to muscle fibers adjacent to the
ical impact applied directly to the muscle 128 trigger spot, and was similarly attenuated by
(or applied through the skin over the TrP), or displacement a few centimeters along the
by snapping palpation of the TrP. 246 same fibers that pass through the trigger
Clinically, the response is most valuable spot. These findings correspond to the loca-
as a confirmatory sign. When injecting a tion of tenderness at TrPs in human patients.
TrP, an LTR signals that the needle has Responsiveness to snapping palpation is
reached a part of the TrP that will be thera- greater at the nodule or TrP as compared to a
peutically effective. It is often not practi-
123 distance from it along the taut band. The
cal to include the LTR as a primary diag- findings also correspond to the meticulous
nostic criterion of a TrP because an LTR accuracy with which one must stimulate the
can be prohibitively painful to the patient sensitive locations in the taut band and not
when it is elicited, it is often inaccessible adjacent tissue in order to evoke the LTR.
to manual palpation because of overlying Figure 2.32B examines the effect of tap-
fat and/or muscle, and the LTR requires a ping the trigger spot and recording the
particularly high degree of manual skill for twitch response with a needle in the taut
reliable detection. However, when it does
94
band and with the needle placed 5 mm to
occur in the course of examination of a ten- either side of the taut band. The latter posi-
der nodule or taut band, the LTR is strong tions showed vestigial twitch responses.
evidence for the presence of a TrP. The rab- The action potentials of the twitch response
bit localized twitch response has proven to were propagated in just those fibers passing
be a valuable research tool for investigating through the trigger spot and did not involve
the nature of twitch r e s p o n s e s . 128,129
adjacent muscle fibers. The twitch response
Topographic Extent of the Local Twitch was highly localized to the trigger spot and
Response. To date, most experimental in- to the taut band passing through it.
vestigations of the local twitch response Origin and Propagation of the Local
(LTR) examined the localized twitch re- Twitch Response. No studies to deter-
sponse which is the rabbit counterpart of mine the specific structure(s) responsible
the LTR. The pioneering study by Hong for the origin of the LTR are known to date.
and Torigoe in 1 9 9 4 identified a trigger
128
Clinically, the strong relation between the
spot (comparable to the human TrP) in the appearance of LTRs during successful
rabbit biceps femoris muscle by locating a needling of a TrP and the severe pain fre-
123

taut band using pincer palpation and test- quently experienced by the subject when a
ing along its length for a maximum twitch twitch response occurs suggests that it can
response to snapping palpation. This loca- originate from stimulation of sensitized no-
tion was designated the trigger spot. Me- ciceptors in the region of the TrP.
chanical stimulation was standardized by The a-motoneurons with endplates suf-
using a solenoid-driven rod to impact the fering from excessive ACh release appear to
surface of the muscle at selected locations. be preferentially responsive to the strong
The response was recorded electromyo- sensory spinal input from these sensitized
graphically with a monopolar teflon-coated nociceptors. This possibility is reinforced
EMG needle placed in the taut band sev- by the observation that snapping palpation
eral centimeters distal to the trigger spot. of one TrP resulted in simultaneous LTRs in
Figure 2.32A from this study compares the taut band of that TrP and in a taut band
the vigor of the twitch response to taps on of another nearby muscle. It is possible that
the trigger spot and to taps applied short dis- adequate mechanical stimulation of any

Copyrighted Material
A

B
Figure 2.32. Electromyographic recordings demon- spot, almost none to either side, and progressively
strating the spatial specificity of the rabbit localized less as the point of stimulation moved farther from the
twitch response with regard to the region of the trigger trigger spot.
spot that was stimulated mechanically to elicit the re- B, The arrow indicates the point of mechanical
sponse and with regard to the region of the taut band stimulation by a tap delivered with a solenoid-driven
from which the response could be recorded. The solid thin rod. The three electromyographic tracings were
black line represents the taut band (marked respon- obtained in, and 5 mm to either side of, the taut band.
sive band) that was selected for testing by manual The recordings near but not in the taut band show
palpation. only distant waveforms.
A, specificity of the point of stimulation in the region These observations substantiate the clinical im-
of the trigger spot in the taut band. Electromyographic pression that the local twitch response is specific to
recordings of twitch responses were obtained from a mechanical stimulation of the trigger spot (point) re-
needle inserted in the taut band distant from the trig- gion and is ordinarily propagated only by the taut
ger spot. Stimuli were delivered directly on the trigger band fibers passing through the trigger spot. (Repro-
spot, to either side of it, and along the taut band to- duced with permission from Hong CZ, Torigoe Y. Elec-
ward the recording needle, as indicated by labels on trophysiological characteristics of localized twitch re-
the recordings and location of the label lines. The sponses in responsive taut bands of rabbit skeletal
most vigorous response was observed at the trigger muscle. / Musculoske Pain 2(2)^ 7-43, 1994.)

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84 Part 1 / Introduction

Figure 2.33. Evidence that the local twitch response is ized twitch responses in milliseconds. As soon as the
a spinal reflex not dependent on higher centers. spinal cord was severed, the localized twitch re-
A, schematic of procedure for a localized twitch re- sponse disappeared due to spinal shock. As the ani-
sponse experiment. First, the spinal cord of the fully
129
mal recovered from spinal shock, the localized twitch
anesthetized rabbit was completely severed. Later, response slowly returned. However, after the motor
the motor nerve was severed. B, results of the local- nerve was severed, localized twitch responses be-
ized twitch response experiment. Abscissa: time came unobtainable and remained that way. Based on
elapsed in minutes; Ordinate: mean duration of local- published data. 129

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Chapter 2 / General Overview 85

nidus of sensitization in the muscle, includ- no twitch response was obtainable. As the
ing bursitis or enthesopathy in the region spinal cord recovered from spinal shock
where the muscle attaches, may be able to caused by the spinal surgery, the duration of
initiate an LTR. Although LTRs were signif- twitch responses recovered to their presur-
icantly more likely to occur at a TrP site than gical level. Following sectioning of the sci-
out of a TrP, the fact that responses did oc-
248
atic nerve, the duration of twitch responses
cur as the result of needling two other sites again fell to zero and remained there until
supports the possibility of less specific sites the end of the experiment an hour later.
of origin for this response than just active These results indicate that the rabbit local-
loci at motor endplates. ized twitch response is propagated essen-
Hong and coworkers reported several tially as a spinal reflex that is not dependent
studies that examined propagation of the on supraspinal influences.
rabbit localized twitch response. The initial A human study followed changes in
124

rabbit study reported that vigorous twitch


128
the local twitch response during the recov-
responses to mechanical stimulation with a ery phase after a brachial plexus injury that
solenoid device were terminated by anes- resulted in complete loss of nerve conduc-
thetizing the muscle nerve supplying the tion. The EMG activity of twitch responses
muscle or by severing it with scissors. A recovered in parallel with the recovery of
subsequent study of five rabbits examined
129
nerve conduction. This result is consistent
the effect on the twitch response by first with the other evidence that the twitch re-
transecting the spinal cord at the T , T , or T
4 5 6 sponse is largely if not completely a spinal
level and later cutting the sciatic nerve, as il- reflex. The reflex pathway is illustrated
lustrated in Figure 2.33A. Figure 2.33B pre- schematically in Figure 2.34.
sents the duration of localized twitch re- In a study of the motor innervation of
266

sponses recorded before and repeatedly the cat gastrocnemius muscle, the authors
after each procedure. Immediately follow- described and illustrated what portion of
ing spinal cord transection rostral to seg- the muscle contracted in response to electri-
ments supplying the biceps femoris muscle, cal stimulation of one fascicle of the motor

Figure 2.34. Schematic of the most likely reflex path- flex. The apparent increase in responsiveness of a-
way followed by a local twitch response originating in motoneurons whose endplates exhibit the sponta-
a myofascial trigger point. The open black circle with neous electrical activity of active loci would account
red rays identifies the active locus and its associated for a preferential response of an involved motor unit
sensitized nociceptor fibers of a myofascial trigger (or units) (dark red lines) which are present in the taut
point. The dotted red line represents the nociceptor band. The muscle fibers of uninvolved motor units are
pathway to the dorsal horn neuron (solid red circle) light red lines. The local twitch is the motor response
which connects through internuncial neurons to ven- resulting from the activation of the involved motor
tral horn cells. The open black circle in the ventral unit(s) of the taut band. The arrows show the direction
horn locates a motor neuron. The curved black line of action potentials in the nerve and in the muscle
represents one motor unit of the return limb of the re- fibers.

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86 Part 1 / Introduction

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Copyrighted Material
CHAPTER 3

Apropos of All Muscles

HIGHLIGHTS: Considerations that apply gener- muscle groups have a reduced stretch range of
ally to all the muscles are consolidated in this motion (ROM). Pain is commonly caused in a
chapter. Detailed knowledge of the REFERRED muscle with TrPs by contracting it in the shorted
PAIN (AND TENDERNESS) pattern is usually a position. TRIGGER POINT EXAMINATION of a
valuable help in identifying which muscle(s) are muscle requires a knowledge of the location and
responsible for myofascial trigger point (TrP) pain. direction of its fibers in relation to those of neigh-
The precise location of all of the patient's per- boring muscles. Objective confirmation of a TrP
ceived pain is drawn on a body form to aid in di- requires special examination techniques for lo-
agnosis and for future reference. An area of re- cating its taut band, nodule, and spot tenderness
ferred tenderness corresponds approximately to by palpation. The diagnosis of an active trigger
the distribution of the referred pain described by point is established by patient recognition of the
the patient. Understanding the muscle's pain elicited by pressure on the TrP and may be
ANATOMY helps one to integrate knowledge of confirmed by eliciting a local twitch response
its chief action(s), functional relations to other (LTR) from it. Nerve ENTRAPMENT may occur
muscles, how to find it for examination, how to because of pressure by the palpable bands of
stretch (lengthen) it, and the location of its TrPs taut muscle fibers that are associated with myo-
for injection. The FUNCTION of a muscle reveals fascial TrPs, when the nerve passes through the
what movements and stress situations are likely muscle between taut bands, or when it is com-
to activate and perpetuate TrPs in it. The FUNC- pressed between such a band and bone. The
TIONAL UNIT identifies other muscles that are cause of the neurological symptoms and signs of
functionally closely related and, therefore, also neurapraxia that result is easily misinterpreted if
likely to develop TrPs because of referred motor this mechanism of entrapment is not recognized.
effects and interacting mechanical stresses. DIFFERENTIAL DIAGNOSIS must consider
SYMPTOMS of myofascial pain and dysfunction symptoms which appear to come from trigger
that appear suddenly often begin after a clearly points but are caused by another diagnosis and
remembered movement or event at a specific also other diagnoses which the patient has re-
time and place. In other cases, excessively pro- ceived because of symptoms that are caused by
longed or repetitive efforts insidiously activate trigger points. TRIGGER POINT RELEASE can
TrPs in the abused muscles. The stressful move- be accomplished using spray and stretch or us-
ment or conditions responsible for ACTIVATION ing voluntary contraction and release techniques
AND PERPETUATION OF TRIGGER POINTS in that include postisometric relaxation, reciprocal
a particular muscle must be identified and elimi- inhibition, contract-relax, and muscle energy
nated or modified to prevent the same stresses technique. Direct manual techniques include trig-
from reactivating and perpetuating the TrPs fol- ger point pressure release, deep stroking mas-
lowing treatment. PATIENT EXAMINATION dis- sage, and strumming. Indirect methods also can
tinguishes between the primary effects of in- be used, and all of these methods can be sup-
creased muscle tension and muscle shortening plemented with accessory techniques and
caused by the primary TrP pathophysiology and modalities.
the secondary tension, reflex, and nerve sensiti-
zation effects. Examination begins with observa- TRIGGER POINT INJECTIONS require first,
tion of the patient's posture, movements, and accurate localization of the TrP by palpation and
body structure and symmetry, and it includes then, confirmation of precise placement of the
screening movements that quickly identify which needle based on needle-elicited pain and a local
94 twitch response. Enough finger pressure is ap-

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Chapter 3 / Apropos of All Muscles 95

plied to insure hemostasis. After injection, the pa- home and the elimination of perpetuating factors
tient should perform three full cycles of slow ac- (Chapter 4). Particularly among patients with
tive range of motion to reestablish normal func- chronic myofascial pain, these considerations
tion of the muscle. CORRECTIVE ACTIONS usually determine the duration of relief experi-
include both a stretch exercise program for use at enced after treatment of the involved muscles.

1. REFERRED PAIN (AND TENDERNESS) 95 Palpable Tender Nodule and Taut Band 117
Patient's Pain History 95 Referred Pain 119
Drawing the Pain Pattern 97 Local Twitch Response 121
Interpretation of Initial Pain Patterns 100 Central and Attachment Trigger Points 122
Interpretation of Pain Patterns on Return Visits .101 Key and Satellite Trigger Points 122
2. ANATOMY 102 10. ENTRAPMENT 123
Terminology 102 11. DIFFERENTIAL DIAGNOSIS 125
Fiber Arrangement 102 12. TRIGGER POINT RELEASE 126
Supplemental References 103 Spray and Stretch 127
3. INNERVATION 104 Voluntary Contraction and Release Methods . . .138
4. FUNCTION 104 Trigger Point Pressure Release 140
5. FUNCTIONAL UNIT 104 Deep Stroking (and Other) Massage 141
6. SYMPTOMS 104 Indirect Techniques 143
History 105 Myofascial Release 143
Limited Range of Motion 109 Accessory Techniques 143
Weakness 109 Modalities 146
Other Non-pain Symptoms 109 Pain Relief 147
Depression 110 Caveats 149
Sleep Disturbances 110 13. TRIGGER POINT INJECTION 150
Prognosis 110 Why Inject? 151
7. ACTIVATION AND PERPETUATION OF TRIGGER What to Inject? 151
POINTS 110 How to Inject? 155
Sudden Onset 111 How Many Injections? 163
Gradual Onset 111 Ligamentous Sprains 165
8. PATIENT EXAMINATION 112 Postinjection Procedures 165
Patient Mobility and Posture 112 Reasons for Failure of Injection of Trigger Points 166
Neuromuscular Functions 112 14. CORRECTIVE ACTIONS 166
Referred Tenderness 114 Patient Compliance 166
Cutaneous and Subcutaneous Signs 115 Appropriate Activities 167
Compression Test 116 Activity Goals 169
Joint Play 116 Application of Heat 170
9. TRIGGER POINT EXAMINATION 116 Posture and Positioning 170
Diagnostic Criteria 117 Exercises 171

1. REFERRED PAIN (AND TENDERNESS) Patient's Pain History


The patient's pattern of referred pain Surprisingly, the patient is rarely aware
and tenderness is often the key to identify- of a trigger point (TrP) in the muscle that
ing the muscle(s) responsible for a myofas- causes the myofascial pain; pain evoked by
cial pain syndrome. This section explains lying on an infraspinatus TrP at night is
how to draw a representation of the pa- perceived in the shoulder, not at the guilty
tient's pain, and how to interpret the loca- TrP in the muscle overlying the scapula.
tion of the pain. Identification of the areas However, when the patient stretches or
of referred tenderness is covered under loads the involved muscle, he or she is
Section 8. likely to feel discomfort in the regions of

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96 Part 1 / Introduction

taut band attachments. The myofascial TrP peripheral (away from the center of the
pain patterns presented throughout this body), mostly central (predominantly in
manual were described by patients as situ- the direction of the center of the body), and
ated deep (subcutaneous and muscular) local (only in the immediate vicinity and
and aching in character, unless stated oth- surrounding the TrP). Examples illustrat-
erwise in our description. ing these three kinds of pain patterns ap-
Regardless of the mode of onset, pear in Figure 3.1. Some TrPs produce pain
whether abrupt or gradual, pain referred patterns that are combinations of these
from myofascial TrPs is characterized as three. Many patterns include the TrP and
steady, deep, and aching, rarely as burning. sometimes it is the most painful location.
It is to be distinguished from the prickling Other patterns do not include the TrP it-
pain and numbness associated with pares- self, which can be very misleading to the
thesias and dysesthesias of peripheral clinician and to the patient.
nerve entrapment or of nerve root irrita- In general, referral at least partly in the
tion. However, two skin muscles, the peripheral direction is most common (85%
platysma and palmaris longus, refer a nee- of patterns). Half of all patterns (48%) refer
dle-like prickling sensation superficially. only in the direction of the periphery. In
Throbbing pain is more likely to be due to addition, 2 0 % of all patterns include both
vascular disease or dysfunction. Occasion- peripheral and central referral, and 17% of
ally, a myofascial TrP initiates sharp, lan- peripheral patterns include a strong local
cinating, or lightning-like stabs of pain. pattern. Just 1 0 % of the patterns have only
The patterns of pain referred from TrPs a local pattern and just 5% refer only in a
in a muscle are reproducible and pre- central direction.
dictable. Knowledge of these patterns is These data suggest that once it is estab-
used to locate the muscles most likely to be lished where the patient hurts, one is
causing the spontaneous pain, much as one much more likely to find the TrP located
suspects which viscus is diseased by its toward the center of the body from the re-
specific pattern of referred pain. The diag- ferred pain than to find the TrP located pe-
nostic value of the patient's pain patterns ripheral to the pain complaint. These data
depends strongly on the accuracy and de- also warn that only a total of 27% of pat-
tail with which the exact location and ex- terns include a substantial local compo-
tent of the pain are mapped. nent of TrP-generated pain. If a clinician
Generally, the specificity of the pain pat- depends on finding the TrP at the spot
terns in this manual was established first where a patient points when he or she
by determining which muscle contained shows where the pain is, the clinician is
the TrP through observing the location of likely to be wrong nearly three quarters of
movement produced by a local twitch re- the time. The Trigger Point Wall Charts and
sponse (LTR), or (when the muscle was not Trigger Point Flip Charts published by
accessible for eliciting an LTR) by noting Williams & Wilkins are a great aid in this
other anatomical landmarks when inject- regard.
ing the TrP. Next, when injecting the TrP, When the TrPs are more active, the ex-
the clinician asked the patient to note care- tent of referred pain is greater, the pain is
fully the location of any associated pain more intense, pain is more likely to persist
when the needle produced an LTR in that at rest, the TrPs are more tender, the taut
TrP. The location of this pain was consid- bands are more tense, and LTRs are more
ered the referred pain pattern of a TrP in vigorous. 71

that muscle of that patient. In this volume, the solid red area in
It would be helpful if there were a gen- each drawing of referred pain and tender-
eral rule that predicted the direction of the ness depicts the essential pain zone, which
referred pain pattern of a TrP based on the is present in nearly every patient when the
location of the muscle. This possibility was identified TrP is active. Spillover pain
investigated. The direction of referral of
144
zones, which may or may not be present,
the 147 pain patterns of volumes 1 and 2 of appear as red stippling. A black (or white)
the Trigger Point Manual was classified as X published on pain pattern drawings

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Chapter 3 / Apropos of All Muscles 97

Mostly central c Local

B
Peripheral
A
Figure 3.1. Examples of the three directions in which from biceps brachii trigger points with some pain in
trigger points (Xs) may refer p a i n . A, peripheral the region of the distal tendinous attachment of the
projection of pain from suboccipital and infraspinatus muscle. C, local pain from a trigger point in the serra-
trigger points. B, mostly central projection of pain tus posterior inferior muscle.

identifies a common location of the TrP, or "My shoulder hurts," some will indicate
TrPs, in that muscle; this provides only a pain in front of or behind the shoulder; one
general guide. The TrPs may be located reaches back to the scapula; another grabs
anywhere in the endplate zone(s) of the the entire shoulder indicating pain deep in
muscle. The location of the endplate the joint; and yet another rubs the upper
zone(s) depends on the arrangement of arm. Therefore, the clinician needs to ask
fibers in that muscle (see Chapter 2, Sec- the patient to delineate the pain on his or
tion D). her body using one finger; then the practi-
tioner can draw its pattern on the blank
Drawing the Pain Pattern form. The patient should then examine the
In addition to observing the patient's drawing for accuracy and completeness.
posture and examining for limitation in This procedure enhances the precision of
range of motion (see Section 8 in this chap- the record, and improves communication.
ter), a precise pictorial representation of The locations of all the patient's separate
the patient's pain is a valuable aid for lo- pain patterns and the date of the first ap-
cating TrPs causing myofascial pain. Verbal pearance of each are noted for future refer-
descriptions are often imprecise and mis- ence. Other authors also strongly endorse
leading so a blank body form can be used the use of pain d r a w i n g s . - Precise
12 113,117

routinely to record the patient's descrip- delineation of the patient's pain areas is re-
tion of the pain. Figures 3.2, 3.3, and 3.4 quired to match them with the known pain
are forms useful for this purpose. The same patterns of individual muscles and to
form also can be used to record the loca- record progress.
tion and tenderness measure of the TrPs It is common practice to give the patient
when they have been located. The form be- a blank body form and ask him or her to in-
comes a valuable medical record. dicate with symbols where the pain is felt.
Communication concerning pain sensa- This is useful for identifying patients who
tions is difficult, at best. When patients say, have the widespread pain of fibromyalgia

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98 Part 1 / Introduction

Figure 3.2. Body form: full figure, front and left side.

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Chapter 3 / Apropos of All Muscles 99

Figure 3.3. Body form: full figure, right side and back.

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100 Part 1 / Introduction

Figure 3.4. Body form: head, front and sides.

and not just the regional pain of myofascial tients complain of referred pain in the fin-
TrPs. These generalized drawings are of lit- gernails. With this start, the patient begins
tle help for distinguishing which muscle(s) to realize that discriminating answers are
harbor active TrPs. The specific detailed possible. The patients begin to understand
pain pattern is often the key to a prompt that this examiner takes the details of their
accurate diagnosis. pain complaints seriously and will not dis-
To record the distribution of the pa- count their description of the pain as oth-
tient's pain, one can follow the conventions ers may have done. After the patient's pain
in this volume. The area that hurts most se- patterns have been recorded, it is often
verely, and/or most frequently, is drawn in very helpful for the patient (and the clini-
solid red. Regions that are sometimes cian) to see the pattern of that patient's
painful, or are less painful, are stippled; the pain on a flip chart or wall chart of TrP
lighter the stippling, the less painful the Pain Patterns. Patients are relieved to real-
area. Red is reserved for aching pain; an- ize that they have not been imagining the
other color such as green, or check marks, pain, as they ofttimes have been led to be-
can be used for numbness and tingling. lieve, and that many other patients have
After examining the patient, an X is experienced the same pain. This opportu-
used to record the location of each TrP. Af- nity to demonstrate the muscles that con-
ter treatment, black diagonal lines can be tain the TrPs which are causing their pain
used to record the areas that were sprayed is especially helpful when the pain pattern
and stretched. A circled X can be used to is a composite of several TrPs. Details are
locate a TrP injection site. Marginal notes important, such as which side of the limb
tell the date of onset and the associated hurts, and whether the pain skips across a
event (if any), unusual depth of pain (if su- joint or concentrates in the joint. It does in-
perficial or deep in the bones and joints), justice to the patient and to the diagnosis
and any unusual quality other than aching. to depend on generalizations.
The dates of onset permit reconstruction of When a TrP is identified and its location
the evolution of a series of pain patterns. has been marked by an X on the Pain-Pat-
When mapping back pain, it is important tern form, the TrP tenderness may be docu-
to record the orientation of the pain as in- mented by a dated pressure algometry
dicated by the patient's finger movement, reading recorded beside the X.
up and down, or across the back.
Sometimes a patient will state, "I hurt Interpretation of Initial Pain Patterns
all over." When asked if the nose hurts, the Is the drawing a simple, one-muscle,
answer is almost always, "No." Nor do pa- myofascial TrP pain pattern? Is it a com-

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Chapter 3 / Apropos of All Muscles 101

posite of several such patterns that are su-


perimposed, or does it have a distribution
that is foreign to TrP pain patterns and,
therefore, most likely of non-myofascial
origin? To answer these questions one
needs to be familiar with the individual
myofascial referred pain patterns, to know
that myofascial pain caused by TrPs is
rarely symmetrical, and to know that it
rarely assumes a glove-and-stocking or
hemialgia distribution. The extent of a
175

muscle's referred pain pattern tends to en-


large as the irritability (activity) of the TrP
increases.
A referred pain pattern may be compos-
ite in two ways. A total pattern may com-
prise overlapping patterns from different
muscles, so that the extent of the pattern
exceeds that of one muscle. Figure 3.5 il-
80

lustrates how this can look when the pa-


tient complains of headache.
On the other hand, if TrPs in several
muscles all refer pain to the same area (e.g.,
the shoulder), the area may be a little
larger, but also will be more painful and
hyperesthetic than if the symptoms came
from only one muscle. Inactivation of only FIGURE 3.5. Common "tension type headache" pain
pattern caused by overlapping referral patterns of
one of the contributing TrPs may produce
pain (red) from trigger points in the temporalis (white
little amelioration of the patient's pain; Xs), suboccipital (uppermost black X), sternocleido-
whereas, inactivation of all of them can mastoid (middle black X), and upper trapezius (fowesf
achieve complete relief. black X) muscles. (Adapted with permission from
No two patients' problems are exactly Jaeger B: Differential diagnosis and management of
alike. A few patients exhibit marked varia- craniofacial pain. Chapter 11. In: Endodontics. Ed. 4.
tions in the expected referred pain pattern, Edited by Ingle Jl, Bakland LK. Williams & Wilkins,
sometimes due to a genetic variation in Baltimore, 1994:550-607.) 80

central nervous system transmission, com-


parable to an anomalous muscle. Rarely are mally tender, the treatment was successful.
such variations in pattern symptoms of However, if the patient returns claiming
hysteria. "no improvement," an accurate record of
The history should indicate whether the the previous pain pattern becomes critical.
pain pattern has been stable, or whether it The earlier record is compared with a new
has evolved over months or years. If the drawing representing the patient's pain
pattern is stable, the pain is likely to re- and algometer readings of TrP tenderness.
solve promptly with specific myofascial If the patient has the same degree of ten-
TrP therapy. The progressive involvement derness in the same TrPs and the same pain
of many muscles is a strong indication that pattern as before treatment, one must ask
perpetuating factors (Chapter 4) must be how long pain relief lasted following treat-
eliminated for lasting pain relief. ment. If pain relief was complete for some
hours or days, one can assure the patient
Interpretation of Pain Patterns on that a muscular cause of the pain is pre-
Return Visits sent, and that it can be relieved, at least
When the patient returns pain free with temporarily. However, repeated treatment
complete restoration of full range of motion without first resolving the perpetuating fac-
and the prior TrP sites are no longer abnor- tors that make the TrPs so hyperirritable is

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102 Part 1 / Introduction

likely to be fruitless. A major effort should where attachment TrPs may occur. Chapter
then focus on identifying and eliminating 2 reviews the reasons for these phenom-
the perpetuating factors. ena. Some individual muscle chapters re-
On the other hand, if careful comparison flect this new understanding more fully
of a current "no improvement" pain pat- than others.
tern with the patterns of the patient's pre-
vious visit shows a distinct improvement, Terminology
and if some of the muscles previously
treated no longer contain tender TrPs, this The names of the muscles come from
represents satisfactory progress. Compari- Nomina Anatomica. English usage fol-
7

son of the new drawing with the initial lows the American edition of Gray's
chart of the prior pain patterns may iden- Anatomy of the Human Body. 33
In this
tify a pain distribution in the location of a manual, the words "origin" and "inser-
previous pain. In this case, one set of TrPs tion" are avoided except in instances
has been inactivated, but the absence of where the relation is unambiguous, as with
that pain has unmasked the referred pain finger attachments. Not uncommonly, the
pattern of the next most active TrPs. Often, functions of the nominal origin and inser-
the patient is not aware of a slight shift in tion become reversed, particularly during
pain location until reminded by comparing movement when muscles are likely to be
the old and new pictorial records. Without strained and TrPs activated; use of the term
the accurately recorded pain patterns for "attachment" helps one to keep an open
comparison, the clinician and the patient mind and to think of muscle functions in
might overlook the progress being made. realistic terms, permitting interpretation of
Occasionally, the pattern may be new to the specific stress situation described by
that patient; a TrP has been newly activated the patient. To stretch a muscle therapeuti-
and must be managed as any acute myofas- cally, it usually matters not which end is
cial TrP syndrome. fixed and which end is moved.
Unless stated otherwise, descriptions of
2. ANATOMY muscle attachments refer to the person in
the upright position, standing straight, face
By knowing all of a muscle's attach-
forward, and the arms and forearms at the
ments, one can deduce the major actions of
side with the forearm supinated (anatomi-
the muscle, where to find it for palpation,
cal position, Fig. 3.2). Therefore, above is
and the direction of its fibers. The anatomi-
equivalent to cephalad, superior, or proxi-
cal drawings of each muscle in this volume
mal, and below is equivalent to caudad, in-
present the muscle alone with its bony at-
ferior, or distal.
tachments. The bones to which the muscle
attaches are stippled more darkly than
other bones. When necessary, additional Fiber Arrangement
drawings of regional anatomy show the A description of the fiber arrangement
muscle's relation to nearby muscles and in muscles is commonly overlooked in
structures. Anatomy textbooks were anatomy texts, lost in the hiatus between
scoured for the needed views of muscles. gross and microscopic anatomy. It is rarely
When questions remained, dissections described adequately, except in a few older
were studied in the anatomy laboratory. Al- texts, such as Bardeen and Eisler. All the
6 43

though an anatomical variation may occur fibers of any one muscle are of nearly equal
in only a small percent of the population, it length, but usually with staggered attach-
is 1 0 0 % to the patient who has the variation ments at the ends; muscle fibers usually at-
and to the clinician caring for the patient. tach to aponeuroses or to bone in a paral-
It has now become clear that knowledge lelogram arrangement. In long muscles
of the location of the endplate zone(s) in a with short fibers, such as the gastrocne-
muscle is of fundamental importance to mius, the aponeuroses overlap each other,
understanding where central TrPs can be or an aponeurosis at one end of the fibers
found. Knowing the location of myotendi- overlaps a bony attachment at the other
nous junctions and tendo-osseous attach- end. Individual muscle fibers may be
22,27

ments is important for understanding placed so diagonally, as in the soleus, that

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Chapter 3 / Apropos of All Muscles 103

Table 3.1 A Few of the Strongest Muscles Arranged in Their Order of Calculated
Cross-sectional Area, Derived from Weber. 184

Cross-sectional Mean Fiber Total Muscle


Muscle Area Length Weight

cm 2
cm gm
External intercostal 79 1.5 126
Multifidus 68 2.9 210
Internal intercostal 47 1.5 77
Longissimus thoracis 32 7.2 223
Deltoid 32 9.0 305
Triceps brachii, short head 26 5.8 161
Subscapularis 25 6.2 164
Infraspinatus and teres minor 17 7.4 132
Biceps brachii, long head 16 9.7 168
Triceps brachii, long head 16 7.7 131
Internal abdominal oblique 14 7.0 107
Serratus anterior 13 13.7 186
Cucularis (trapezius) 13 10.9 146
Brachialis 13 8.4 117
Pectoralis major, sternal 12 14.7 187
External abdominal oblique 10 10.9 115
Flexor digitorum profundus 10 6.7 68

the fiber length is barely one-half the the selection of muscles for transfer of ten-
length of the whole muscle. don attachment. 22

In 1851, Weber studied the structure


184
The relative length of individual fibers
of muscle and its relation to function by to total muscle length has important func-
measuring the weight and mean fiber tional consequences. Muscles like the
105

length of each muscle in the body. Table quadriceps, scalenes, and gastrocnemius
3.1 extracts data for a number of the larger with relatively short fibers (low fiber
muscles. The cross-sectional area of each length/muscle length ratios) are designed
muscle was calculated by the formula S = for force production. Muscles like the bi-
P/pL where S = the cross-sectional area, in ceps, hamstrings, and tibialis anterior
cm ; P = the weight of the whole muscle,
2
have high fiber length/muscle length ra-
in grams; p = the specific gravity of mus- tios and are designed to produce high ve-
cle, 1.0583 gm/cm ; and L = the mean
3
locity movement. Muscles designed to
length of the fibers in that muscle, in cen- produce force have endplate zones that
timeters. This kind of measurement may tend to run the length of the muscle,
vary greatly from person to person depend- whereas muscles designed for rapid move-
ing on body build, occupation, the degree ment have endplates zones that run rela-
and kind of physical activity, etc. Subse- tively transverse to the muscle (depending
quent studies 22
have reported results
181
on muscle structure), but always near the
comparable to those of Weber. midpoint of the muscle fibers (see Chapter
Assuming similar fiber diameters among 2 section C).
muscles, the cross-sectional area is nearly
proportional to the relative strength of each Supplemental References
muscle, since this area also is proportional As a service to those who teach muscle
to the number of myofibrils contracting in anatomy and to those interested in differ-
parallel. This concept has been applied to ent anatomical views or in a more detailed

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104 Part 1 / Introduction

understanding of a muscle, additional il- ported by patients that, when overloaded


lustrations are listed at the end of Section or repeated, produced TrPs in that muscle.
2 of each muscle chapter, under Supple-
mental References. 5. FUNCTIONAL UNIT
The functional unit to which a muscle
3. INNERVATION belongs includes the muscle(s) that rein-
The spinal and peripheral nerves that force and counter its actions as well as the
usually supply each muscle are identified joint(s) which the muscle crosses. The inter-
in this section. In many muscles, there is dependence of these structures functionally
considerable individual variation; rarely is reflected in the organization and neural
do anatomists agree completely on the seg- connections of the sensorimotor cortex.
mental innervation of a muscle. The functional unit is emphasized be-
cause the presence of an active TrP in one
4. FUNCTION muscle of the unit increases the likelihood
Since the actions of a muscle that pro- that other muscles of the unit also will de-
vide the functions for which it is used are velop TrPs. Dysfunction (weakness and
so closely intertwined, these two issues are shortening) of the affected muscle tends to
considered together under one heading in overload other muscles of that functional
this edition. unit. When inactivating TrPs in a muscle,
Understanding the actions of muscles is one must be concerned about TrPs that
valuable diagnostically and therapeuti- may develop secondarily in muscles that
cally. Diagnostically, an accurate descrip- are interdependent.
tion of the precise movement made by the The physiological definition of a myo-
patient at the time that the TrP was acti- tatic unit (the term used in the previous
vated, together with a knowledge of which edition) includes the synergists, which
muscles are used to produce and to control help the prime mover (agonist), and the an-
that movement, helps to determine which tagonists, 135
because these muscles are
muscles were likely to have been strained linked by interacting reflex pathways. 106,188

at the time. The strained muscles are then The term functional unit is used in this
examined for restricted range of motion edition and includes the muscles noted
and tender nodules to see if they harbor ac- above and also muscles that do not neces-
tive TrPs. sarily share common reflexes, but which
Therapeutically, a knowledge of the have close functional relationships. An ex-
movements and activities that depend upon ample of one relationship is muscles that
the muscles being treated is needed in order extend the line of pull of the affected mus-
to explain proper body mechanics to the pa- cle during total body movements (e.g., the
tient. The patient must understand precisely external abdominal oblique extends the
what movements and activities should be line of pull of the serratus anterior muscle).
modified or avoided to prevent further mus- Another example is found in stabilizing
cular overload and perpetuation of the TrPs. muscles, such as the upper trapezius and
In this manual, actions of muscles are levator scapulae muscles when they help
described as the movement of a segment at control the scapula during forceful lifting
a joint; for example, the brachioradialis movements of the upper limb on that side.
muscle flexes the forearm at the elbow.
Terms describing directions of movement 6. SYMPTOMS
are defined in Chapter 1. With a thorough knowledge of individ-
Four sources of information were used ual myofascial pain syndromes and of TrP
to summarize the actions of a muscle: (1) referred pain patterns, one can often, with
the actions listed in anatomy texts based a careful history, not only identify the di-
on the attachments of the muscle; (2) the agnosis of myofascial pain but also deter-
movements produced by stimulating the mine which muscles are most likely caus-
muscle electrically; (3) electromyographic ing the pain. The chapters that follow note
studies that reported which movements or specific features of individual muscle syn-
efforts generated motor action potentials in dromes. This section describes the features
that muscle; and (4) the movements re- of the patient's history that help to identify

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Chapter 3 / Apropos of All Muscles 105

myofascial pain syndromes and to distin- is helpful. However, the fact that the pa-
guish them from other painful conditions. tient has an electrostatic air cleaner may
The myofascial TrPs may be activated not be sufficient. One patient reported us-
acutely by an obvious cause of muscular ing it every night, but further inquiry re-
strain or may become symptomatic insidi- vealed that she also opened her bedroom
ously due to less obvious chronic muscular windows every night. She liked fresh air
overload. In either case, symptoms may con- and did not realize that her air cleaner had
tinue for months or years if the myofascial no chance of eliminating the pollens that
TrP source of the pain is not recognized and were coming in from outdoors.
treated. This situation often, but not always, The list of medications should include
leads to the syndrome of chronic pain, all medications currently being taken, in-
which is likely to become a way of life and
156
cluding vitamin and mineral supplements.
may require attention to learned pain be- The patient is asked to bring a bottle of
havior, as well as the TrP origin of pain.
47
every medication so that the actual dosage
This manual concentrates on the latter. can be established. This includes prescrip-
tion and over-the-counter drugs, as well as
History nutritional supplements. A list of the med-
Travell emphasized the importance of ications taken in the past that caused side
taking a thorough and thoughtful history in effects or d i d not relieve the pain is also
patients with chronic musculoskeletal important.
pain. The following material on the patient The patient is asked to send, in advance,
history is abstracted from a chapter written a copy of all medical records in his or her
by Travell in 1 9 9 0 .
172
possession and to request any others to be
Preliminary Review of Records. The sent by any recent consulting physicians,
completeness of the history is increased by especially orthopedic and neurological
a preliminary review of the patient's story consultations. These records are carefully
and records. Before the first visit, the patient reviewed before the patient's initial visit.
is requested to submit a chronology of life Interview with Patient. While taking the
events, a chronology of medical events, and history, patient comfort should be ensured
a complete list of current and recent med- by demonstrating the principles of good
ications including nutritional supplements. body mechanics to them. A footrest can be
The chronology of life events should give provided when the patient's legs are too
dates and places of residence, education, short for the feet to rest firmly on the floor;
marriages, children living (age and where additional armrest height can be supplied
they live), sports activities, travel, and em- when the elbows do not reach the armrests of
ployment (what kind, where, for whom). the chair; a butt-lift (ischial-lift) can be
The chronology of medical events placed under the small hemipelvis when the
should include illnesses, infections, acci- patient's body is tilted because of this asym-
dents (fractures, falls, etc.), surgical proce- metry; a small pillow positioned in the lum-
dures, dental procedures, pregnancies and bar hollow helps maintain effortlessly a nor-
miscarriages, allergies (tests and hyposen- mal lumbar curve of the spine and helps the
sitizations), and vaccinations. The patient patient to sit erect rather than with the head
may overlook a significant accident if no and shoulders hunched forward. Patients are
fracture occurred, but further interrogation often amazed to discover the degree of im-
will elicit the full history. mediate relief that can be obtained by reliev-
The patient is generally aware of in- ing muscular strain due to these mechanical
halant allergies, but special care must be perpetuating factors. This relief helps the pa-
taken to check for food allergies and what tient appreciate the strong impact that these
foods cause symptoms. Myofascial TrPs are factors can have on his or her pain.
aggravated by high histamine levels and A towel or scarf can be provided to pro-
active allergies. Marking the skin to test for tect the patient's shoulders when a chilling
dermatographia is a simple way of identi- draft causes direct cooling of the muscles.
fying high histamine levels. If the hands and feet are cold, a dry heating
For inhalant allergies, reducing expo- pad placed on the abdomen warms the
sure by the use of electrostatic air cleaners core of the body and sends more blood into

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106 Part 1 / Introduction

the limbs (reflex heat). Contrary to the pa- tient may be asked, "Are these all the areas
tient's previous experience, with the where you have pain?"
needed postural and environmental correc- "Yes."
tions he or she may now be able to sit for "Do your feet hurt?"
one-half or three-quarters of an hour "Why, yes! All my life."
through the intensive medical history, as "Why didn't you mention them?"
comfortable at the end as at the start. "Doesn't everyone's feet hurt?"
To effectively understand the history, it Another patient may fail to mention
is important to empathize but not to iden- headaches, and then reply to a specific
tify with the patient. Empathy is estab- question, "They're normal. I've had them
lished by putting oneself in patients' shoes, as long as I can remember."
objectively seeing their life problems from Another helpful question is, "What do
their point of view, understanding their you do to get relief?" One woman, when
jobs, their personal relationships, and their asked how she relieved her backache (in-
emotional stresses. Identification with the terscapular), confided that she lay on a
patient often results in emotional involve- warm iron and rubbed the pain away.
ment that is destructive to the doctor-pa- "Oh, dear, I never told anyone else that
tient relationship and can be damaging to before. You will think I'm crazy."
the doctor's own mental health. "No, that is exactly what I would expect
Pain Distribution. If the pain is con- you to do to help relieve the pain from
stant and in multiple locations, the patient those muscles in your upper back."
is likely either to say, "I hurt all over," or to It is important to convince the patient
focus on the most intense pain, not men- that whatever the pain history, it is believ-
tioning other pains until the most severe able to you.
pain is relieved. Some patients are afraid of being labeled
Learning to discriminate where it really hypochondriacs or psychological cripples
does hurt is essential. One patient said she if they reveal all the places where they
had pain in her "TMJ." She had received hurt. Some have been convinced by other
temporomandibular joint arthrograms and practitioners that they really are crazy to
multiple tests and treatments by many den- think that they have so much pain.
tists and physicians for her "TMJ pain." Also, patients should be assured that
When asked to point to where the pain was you do not think they are "doctor shop-
located, she put her finger on the mastoid ping" because they have seen so many
process behind the ear. She never had any physicians for their long-standing severe
pain in the TMJ region. This lack of pain problem. Rather, they are to be com-
anatomical knowledge causes similar prob- mended for their determination to get well
lems for the shoulder, buttock, low back, and regain their normal function.
and other parts of the body. Review of Body Systems. A brief review
When the patient complains of "pain all of the major body systems helps to ensure
over," the doctor must ask, "Do you have that a significant medical problem is not
pain in the nose? The earlobe? The knee?" overlooked. In reviewing the gastrointesti-
When the patient says " n o " to one or more nal tract, the history should be explored for
of these questions, the patient realizes that diarrhea, constipation, nausea, heartburn,
the pain is not felt all over and that the abdominal pain, hemorrhoids, blood in the
clinician needs to know the precise distri- stools, and the like. When a patient is low in
bution of pain. By mapping the specific folate, diarrhea is likely to occur intermit-
pain patterns one can begin to identify the tently with explosive, watery stools. Consti-
likely locations of the trigger points re- pation often is associated with low thyroid
sponsible for the pain complaints. function and/or vitamin B inadequacy. Ex-
t

An accurate picture of all the areas of cessive flatus may be dietary or due to loss
pain is very important. After completing of normal intestinal bacterial flora.
the pain distribution on a body form that Simple questionnaires are easily mis-
has each pain shaded in red (the same leading. When one patient was asked if she
body form used for the pain diary between had diarrhea, she answered, "Oh, no." As
visits can be used for this purpose), the pa- she was leaving the office, she asked for a

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Chapter 3 / Apropos of All Muscles 107

prescription for paregoric. When queried, gry." She changed her question: "Are there
she replied, "Oh, I'm going to the theater any foods that you avoid?"
tonight and, if I didn't take the paregoric, "Oh, yes. I'm a complete vegetarian."
during the performance I probably would In his previous medical questionnaire,
have to rush out to the bathroom." She did his doctor had marked his diet as normal.
not have diarrhea; she took paregoric regu- His myofascial pain had started insidi-
larly as a preventive. ously soon after he stopped eating meat,
Sleep. If patients report that they fowl, fish, and dairy products. He took no
"sleep poorly," further questioning is in or- vitamin or other nutritional supplements.
der. Is it because they cannot fall asleep or He had a marked vitamin B deficiency.
12

because sleep is interrupted repeatedly dur- The history should also determine
ing the night? Do they wake up early and are whether meals are prepared ahead of time
unable to go back to sleep? Most important, and placed on heated trays under fluores-
what disturbs their sleep? In what position cent lighting, as in a doctors'/nurses' dining
do they sleep? (There may be a mechanical room, a home for the elderly, fast food stop,
cause of pain that interferes with sleep.) Do school cafeteria, or even at a first-class ho-
they have "restless legs" (folic acid defi- tel buffet. This exposure of food to heat and
ciency)? Do they have a chronic urinary fluorescent light causes rapid degradation
tract infection and nocturia or an enlarged and loss of vitamin C and some B vitamins.
prostate so that they have to get up at night The quality of the diet is determined not
to empty the bladder? only by what the patient eats but by how
One patient, when asked if he had to get this food is prepared. Are the potatoes fried
up at night to urinate, replied: "Oh, no." or peeled and boiled? If boiled, are they cut
"Was there ever a time when you did into pieces to cook faster, which permits
have to urinate at night?" the water-soluble vitamins and minerals to
"Yes. Now, all the time, several times leach out? If the raw spinach leaves are
every night." soaked in water to wash them well, this
"But I thought you said you didn't have leaches out folic acid. Thus raw/green sal-
to get up at night." ads, fruits, milk, vegetables, and the like do
"That's right, I don't. I use a bedside not always provide an adequate, balanced
urinal." diet. Some individuals have an unusually
Many times, the cause of sleep distur- high requirement for specific vitamins.
bance is specifically identifiable and cor- Work Situation. A careful history of
rectable. A baby may cry at night because it precisely what the patient ordinarily does at
doesn't have enough blankets and is cold. work (or at home) is fundamentally impor-
Body warmth is also important for myofas- tant. Many times, if the patient experiences
cial pain patients. When the muscles be- intermittent pain, it is helpful for the patient
come cool at night, they contract to generate to keep a written record of any onset of pain
heat, and this tension can activate latent trig- throughout the day and to relate it to activi-
ger points. An electric blanket is most help- ties at the time. The many sources of strain
ful, even during the summer in an air-condi- include an awkward positioning of a key-
tioned, cool room. Often, only the spouse is board, documents, computer monitors, or of
aware of the painless jerking of "restless reading and writing material, visitors seated
legs" at night. A supplement of folic acid, at one side that require the patient to turn
several milligrams daily, frequently resolves the head and neck to face the individual
this source of sleep disturbance. with whom he or she is talking, holding a
Diet. Questions regarding what foods telephone receiver between chin and shoul-
the patient avoids may be as informative as der, or abuse of the muscles in housework.
those regarding what foods they eat. Pa- An important source of overlooked mus-
tients may assure you that they eat a well- cle strain is a long-standing loss of range of
balanced, normal diet. When Dr. Travell motion in one arm, that requires the oppo-
questioned one man about his diet, he site afflicted extremity to be overworked.
replied, "I have a wonderful appetite!" She One patient, a dentist, had myofascial pain
repeated the question as to what he ate, in the non-dominant arm and a painless
and he smiled and said, "I'm always hun- middle finger of the dominant right hand

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108 Part 1 / Introduction

that he could not flex beyond 90 degrees. be delayed as long as 12 to 20 hours. Such
When asked why, the patient said, "I broke a time delay makes it easy to overlook the
the finger when I was a youngster, 50 years cause of recurrence of the TrP pain. Usu-
ago, and the joint has been locked ever ally, further activation of an existing latent
since." TrP produces pain almost immediately. If
While talking to the patient, gentle exam- the patient is subject to recurrence of se-
ination of the finger revealed that, indeed, it vere episodic pain every few days, one
did bend. The middle finger's long extensor should consider the possibility of episodic
muscle harbored latent TrPs that restricted hypoglycemia. In this case, onset of pain
stretch but caused no pain. His muscles had should relate to eating and/or exercise and
learned to guard that part of the body. One the patient can be tested for overreaction to
brief application of the vapocoolant spray- a glucose tolerance test. The energy crisis
passive stretch procedure promptly restored at the TrP worsens when there is serious
the full range of finger flexion. The dysfunc- loss of its energy supply.
tion of the dominant right hand had caused Pain patterns mapped on successive vis-
compensatory overload and myofascial pain its tell the story of progressive improvement
syndromes of the nondominant extremity. with some pain areas disappearing and oth-
Timing of Pain. Myofascial TrPs may ers diminishing in size. A new area of pain
cause constant pain, intermittent pain, or may mean that a less active TrP has been
no pain complaint. These differences in
172
"unmasked" by eliminating a more severe
presentation affect diagnostic symptoms. pain from a TrP in the same functional unit.
Patients in constant pain caused by TrPs are
usually unaware of activities that aggravate About the same time Travell published
the pain. They already have such intense the above clinical description, other au-
172

pain that they do not perceive an increase, thors showed experimentally that patients
and so cannot distinguish what makes it with only latent TrPs can experience local
worse. Similarly, they may be aware of ten- TrP tenderness and TrP referred tender-
derness at the TrP, but may not distinguish n e s s with restricted range of motion that
177

a change in their referred pain when pres- is limited by discomfort. However, patients
sure is applied to the TrP, partly because the avoid that degree of movement so they do
TrP is so hypersensitive that only a little not present with a pain complaint. Not
pressure reaches local pain tolerance. only is the function of that muscle com-
Most patients with active TrPs experience promised, but the latent TrP also can refer
intermittent pain that is characteristically motor dysfunction to other muscles with-
aggravated by specific movements and may out referring pain. The absence of pain can
be alleviated at least temporarily by a certain make it difficult to suspect and identify the
position. These patients may have some rel- latent TrPs responsible for the referred mo-
atively pain-free days, especially if their pain tor dysfunction. This situation is common
is associated with muscle stress induced at among masticatory muscles.
work. They can usually identify what activi- Myofascial pain may start abruptly or
ties makes them worse, and what position or gradually. With abrupt onset, the patient
situation provides relief. The patient must remembers clearly the first date of the pain
learn not to be spartan and to avoid the "good and can usually describe in precise detail
sport" syndrome, and must learn how to pro- the exact event or movement, such as
tect the abused muscle(s) from unnecessary reaching back for something. Pain of grad-
overload. This group of patients is ideal for ual onset is usually due to chronic over-
patient education. They can learn to "listen" load of muscles; myofascial pain may also
to their muscles and respond appropriately. appear during or after a period of viral in-
Latent TrPs give no primary pain clues, fection, visceral disease, or psychogenic
and must be identified by postural stress and may develop in association with
changes, muscle dysfunction, and physical radiculopathy of its nerve supply. 31,32

examination. Regardless of the mode of onset,


Patients and clinicians need to under- whether abrupt or gradual, pain referred
stand that the onset of pain following acti- from myofascial TrPs is characterized as
vation of a TrP due to muscle overload can steady, deep, and aching, rarely as burning.

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Chapter 3 / Apropos of All Muscles 109

It is to be distinguished from the prickling 2. By slow, steady passive stretching of the


pain and numbness associated with pares- involved muscles, particularly when the
thesias and dysesthesias of peripheral patient is seated under a warm shower
nerve entrapment or of nerve root irrita- or in a warm bath.
tion. However, two skin muscles, the pla- 3. When moist heat is applied over the TrP.
tysma and palmaris longus, refer a needle- The pain is decreased much less when
like prickling sensation superficially. the heat is applied over the reference
Throbbing pain is more likely to be due to zone.
vascular disease or dysfunction. Occasion- 4. By short periods of light activity with
ally, a myofascial TrP initiates sharp, lanci- movement (not by isometric contraction).
nating, or lightning-like stabs of pain. 5. By specific myofascial therapy (Sections
When TrPs in several muscles refer pain 12 and 13 of this chapter).
to one target area, such as the shoulder, or The development of a new pain during
to a naturally sensitive area like the nipple, treatment must be diagnosed on its own
the zone of referred tenderness may be- merits and may not be myofascial in origin.
come intolerant of the lightest touch and
exquisitely sensitive to pressure. Limited Range of Motion
An essential part of the history is to de- This is rarely the chief complaint, but it
termine in detail which activities and pos- is a fundamental characteristic of TrPs that
tures aggravate the pain and which ones re- is readily identified by the pain that devel-
lieve it. ops as the muscle approaches full stretch
Myofascial TrP pain is characteristically range of motion. Limitation of motion and
aggravated: increased stiffness are worse in the morn-
ing and recur after periods of overactivity
1. By strenuous use of the muscle, espe- or immobility during the day. This painful
cially in the shortened position. Defin- stiffness is apparently due to the abnormal
ing precisely the movement that in- tension of the palpable bands and to ten-
creases the pain provides a major clue to sion-induced sensitivity of the taut-band
the muscle that harbors the responsible fiber attachments.
TrPs.
2. By passively stretching the muscle. Weakness
However, active stretch by voluntary Frequently, patients are aware of weak-
contraction of the antagonist may only ness of certain movements, as when pour-
rarely cause pain because the patient ing milk from a carton, turning a doorknob,
subconsciously learns to limit this or carrying groceries in one arm. This
movement. The patient is aware of re- yields clues as to which muscles are in-
stricted range of motion and "weak- volved. The muscle learns to limit the
ness," but may not think of the affected force of its contraction below the pain
muscle as painful. threshold of the central and attachment
3. By pressure on the TrP. TrPs.
4. By placing the involved muscle in a Weakness may be a reflection of inhibi-
shortened position for a prolonged pe- tion referred from a TrP in another muscle
riod. Pain and stiffness are often at their (for example, inhibition of the anterior del-
worst when the patient gets out of bed in toid by a TrP in the infraspinatus muscle). 64

the morning, or when getting up from a


chair after sitting immobile for a while. Other Non-pain Symptoms
5. By sustained or repeated contraction of Patients may report excessive lacrima-
the involved muscle. tion, nasal secretion, pilomotor activity
6. By cold, damp weather, viral infections, and occasionally changes in their sweat
and periods of marked nervous tension. patterns, but TrP activity is rarely seriously
7. By exposure to a cold draft, especially considered as the source of these symp-
when the muscle is fatigued. toms. An involved limb may feel cold as
compared with the opposite one due to
Myofascial TrP pain is decreased:
reflex vasoconstriction. The examiner
should be alert for symptoms of postural
1. By a short period of rest.

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110 Part 1 / Introduction

dizziness, spatial disorientation, and dis- TrPs and makes them less responsive to
turbed weight perception. All of these phe- treatment.
nomena can be caused by myofascial TrPs;
some are specific to particular muscles, Sleep Disturbances
others are not.
A careful history identifies the serious-
ness and nature of sleep disturbance. De-
Depression
pressed patients tend to fall asleep readily,
A major, well-recognized contributor to but awaken in the night and have trouble
depression is chronic pain. On the other sleeping again. They arise in the morning
hand, depression may lower the pain feeling more tired than when they went to
threshold, intensify pain, and impair the bed, suggesting fibromyalgia. Some pa-
response to specific myofascial therapy. tients are awakened by their myofascial
Patients who have suffered myofascial pain, others by noises. Each is managed in
pain for months or years are likely also to terms of the cause.
have developed secondary depression and
sleep disturbances, and to have restricted
Prognosis
their activity and exercise. The ensuing re-
striction of body movement and the in- Acute myofascial pain due to TrPs
creased psychic tension aggravate their caused by a clearly identifiable strain of
TrPs, causing a vicious cycle. All contribu- one muscle is, as a rule, able to be fully re-
tory factors should be identified and cor- lieved and normal function restored. The
rective actions taken. longer the period between the acute onset
Depression must be recognized. If un- of pain and the beginning of treatment,
treated, or undertreated, it blocks recovery the greater the number of treatments that
from myofascial syndromes. It is diagnosed will be required over a longer period of
by a variety of clues. Physiologic clues are time. 73

insomnia, anorexia and weight loss, impo- Patients who have had a stable pattern
tence or decreased libido, or blurred vi- of referred TrP pain for months or longer,
sion. Mental-outlook symptoms include a without extension to other muscles, are
sad mood, thoughts of suicide or death, likely to respond better to treatment than
and strong feelings of guilt. Other clinical patients with progressively more severe
changes are inability to concentrate, poor symptoms. When the pain has spread and
memory, indecisiveness, mumbled speech, is gaining momentum with successively
and a negative reaction to suggestion. So- more muscles becoming involved, multi-
cially, the patient exhibits a desire to be ple perpetuating factors must be elimi-
alone, disinterest in favorite activities, a nated before specific myofascial therapy
drop in job performance, and neglect of can provide sustained relief.
personal appearance and hygiene.
Folic acid or pyridoxine deficiency and 7. ACTIVATION AND PERPETUATION OF
low thyroid function are potent contributors TRIGGER POINTS
to depression, and may, in addition, increase Acute events that precipitate a sudden
neuromuscular irritability and TrP pain. An onset of symptoms and the chronic stresses
analysis of the problem should include, that are likely to produce a gradual onset of
"What are the unique characteristics of this TrP symptoms are both considered here.
patient who has the pain?," not just, "What One time traumatic occurrences can acti-
TrP involvement does this patient have?" vate TrPs but are not responsible for per-
With developing depression, patients petuating them. Other factors, such as
describe increasingly restricted move- those considered in Chapter 4, are respon-
ments and activity as their way to avoid sible for maintaining their activity. Situa-
pain. After a few weeks, most patients have tions that cause repeated or chronic mus-
discontinued their previous exercise pro- cular overload can activate TrPs and then
gram, and the unstretched muscles become perpetuate them. In this latter case, the
increasingly deconditioned and irritable. muscular stress is both an activating and a
This potentiates their tendency to develop perpetuating factor. Obviously, from a clin-

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Chapter 3 / Apropos of All Muscles 111

ical management point of view, these two This activation of a latent TrP can be
kinds of onset can result in quite different avoided by adding procaine to make a
sets of problems that require different ther- 0.5% solution. The procaine also reduces
apeutic considerations and approaches. postinjection soreness compared to dry
Therefore, sudden onset and gradual onset needling . 67

are considered separately in this section. Latent TrPs may be activated incidental
to spray-and-stretch therapy. While one
Sudden Onset group of muscles is being passively
When asked, "Do you remember the day stretched, their antagonists are shortening
your pain started?," most patients will re- much more than usual. Fortunately, if la-
spond either with a clear affirmative or a tent TrPs in the antagonists are painfully
fuzzy negative. If affirmative, the details of activated in this way, they can be inacti-
posture and movement occurring at the vated quickly by then spraying and stretch-
time of onset permit estimation of the de- ing them.
gree of stress that was imposed on various During injection of an especially active
muscles. Sometimes, the pain was felt at TrP, the intense referred pain may activate
the moment of stress; at other times, the latent TrPs in muscles in the reference
patient remembers feeling "something hap- zone. For instance, injection of scalene
pen" or hearing "a snap" at the moment of muscles has activated TrPs in the
stress, but the pain developed gradually brachialis muscle, which entrapped the ra-
several hours later, reaching a maximum in dial nerve and caused paresthesia and tin-
12-24 hours. Either is considered an acute gling of the thumb. Similarly, severe pain
single-event onset. The delayed onset can referred to a somatic area due to an acute
be a response to another soft tissue injury visceral lesion, such as myocardial infarc-
(as described under Low-Back Pain in tion or appendicitis, is likely to activate
Chapter 41) that causes reflex spasm and TrPs in the painful region of the chest wall
can induce secondary TrPs. or abdomen. 165

The mechanical stresses that tend to ac- Latent TrPs in a fatigued muscle, espe-
tivate myofascial TrPs acutely include cially in the calf or neck and shoulders,
stresses such as a wrenching movement, may be activated by direct cooling of the
automobile accidents, falls, fractures (in- overlying skin, as by a cold draft from air
cluding chip fractures), joint sprains, dislo- conditioning or an open car window.
cations, or a direct blow to the muscle. 165

Acute onset also may be associated with an Gradual Onset


episode of excessive or unusual exercise, Locating the cause of active TrPs that de-
such as packing and handling boxes when veloped gradually due to chronic overload
moving. 165
Most of the time, myofascial can be difficult, but it is important because
TrPs due to such one-time gross trauma are the chronic strain, if continued, perpetu-
easily inactivated as soon as any associated ates and may intensify the TrPs. Typical
soft-tissue injury has healed; however, the causes of sustained postural overload are
TrPs may persist for years if untreated. poor work habits, such as a slouched pos-
Intramuscular injection of medicinal ture or a keyboard operator lifting the
substances given inadvertently at the site shoulders to reach an elevated keyboard. If
of a latent TrP may activate i t .
163,166
The pa- the source of strain is not obvious, the pa-
tient feels a local pain before the solution tient must help to identify it. The patient
is injected when the needle tip reaches a should be instructed in the kind of move-
TrP. If the injection is delayed for a few sec- ments that would overload the involved
onds, this pain can be distinguished from a muscle, and then watch for daily activities
second intense referred pain caused by ac- that use that motion. The patient should
tivation of the TrP when a locally irritant also note any movement or activity that in-
medication is injected. It is wise to palpate creases the referred pain, and then avoid it,
for a non-tender area to insert the needle or learn how to perform the activity (if es-
and to relocate the needle before injection, sential) without overloading the muscles.
if its insertion encounters TrP tenderness. Minutes spent tracking down precisely

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112 Part 1 / Introduction

what activated the TrPs can prevent recur- Only identical twins have identical genetic
rences and save hours of frustrating treat- origins, and no two people have the same
ment time and treatment failure. exposure to environmental influences dur-
Synergistic muscles that axe overloaded ing development. Even identical twins
by substituting for an involved muscle, or have different fingerprints. When it comes
are in sustained contraction to protectively to musculoskeletal pain, there is no one-
splint an involved muscle are themselves shot, cure-all silver bullet.
likely to develop secondary TrPs.
A muscle that is immobilized in the Patient Mobility and Posture
shortened position for prolonged periods The patient's spontaneous posture and
tends to develop active TrPs. This was 165
movements should be observed while he or
demonstrated by the increased likelihood she walks, sits, or removes articles of cloth-
that patients with acute coronary thrombo- ing [see Chapter 4 1 , Section C for com-
sis would develop a painful or frozen ments regarding posture and movement).
shoulder syndrome due to myofascial TrPs People with painfully active TrPs tend to
when they were kept flat on their backs in move slowly and protectively. They avoid,
bed without regular, gentle, active motion or explore gingerly, movements that might
of the upper extremities. 169
painfully stretch or load muscles with TrPs,
Nerve compression, such as in the radicu- and they may be compensating for muscles
lopathy caused by a ruptured intervertebral that are weak because the muscles are re-
disc, favors the development of TrPs in the flexly inhibited by TrPs in the same or other
muscles supplied by the compressed nerve muscles. Some key observations: Does the
root (postdisc syndrome). Less severe
165,190 patient use arms and hands bilaterally in
radiculopathy also can activate TrPs. 31,32 their full range of motion? Does the body,
The "nervous tension" associated with rather than only the head, turn when the
emotional stress or psychological tension patient looks around? In the sitting posi-
can induce T r P s . The associated in-
80,96,165 tion, is the spine crooked and one shoulder
creased TrP activity most likely is medi-
97,116 lower than the other? Is the face symmetri-
ated by autonomic nervous system activity. cal? Does the patient perform spontaneous
Muscle pain syndromes are commonly stretching movements for relief; if so, what
seen in patients with any of a number of vi- muscles are being stretched?
ral diseases, including acute upper respira-
tory tract infections. 38 Neuromuscular Functions
This heading includes examination for
8. PATIENT EXAMINATION restricted stretch range of motion, weak-
This section considers the examination ness, distorted weight perception, and
of the patient for dysfunctions and phe- weak deep-tendon reflexes. Restriction of
nomena that characteristically are pro- stretch is the primary effect of the increased
duced by TrPs. It assumes that the clinician muscle tension and shortening caused by
has taken or reviewed the patient's com- the TrP mechanism. The restriction is aug-
plete medical history, and that the patient mented by pain arising secondarily from
has received a general medical examina- sensitized nociceptors in central TrPs and
tion that paid special attention to neuro- at attachment TrPs. On the other hand,
logical function in order to distinguish weakness is caused secondarily by reflex
symptoms of neurological origin from motor inhibition induced by TrPs in the
those of myofascial TrP origin. The exami- same muscle or in other muscles.
nation of the muscle itself for evidence of Some people have inherently poor mus-
TrPs is covered in Section 9, Trigger Point cular coordination; they move jerkily and
Examination. This patient examination quickly. Some individuals are tense and
section distinguishes between primary TrP maintain a residual and unnecessary co-
effects that are the direct result of the TrP contraction of antagonist muscles. These
pathophysiology and secondary effects are among the most difficult patients to
that are induced by the TrP activity. It is treat because they keep misusing and abus-
important to understand these basic princi- ing their muscles. On the other hand, the
ples because no two patients are alike. muscles of highly coordinated athletes

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Chapter 3 / Apropos of All Muscles 113

quickly learn to inhibit specific move- stricted to a greater degree by subscapu-


ments to avoid pain and thus develop laris TrPs than by TrPs in other shoulder
weakness. With treatment, these athletic muscles. The Hand-to-shoulder- blade Test
patients are likely to reestablish their nor- range of motion is restricted the most by
mal function quickly. infraspinatus and anterior deltoid TrPs.
Restriction of Movement. A muscle con- Supination and pronation of the forearm
taining active TrPs is functionally shortened are also tested because restricted range of
and somewhat weakened. Attempts to pas- these motions can overload the shoulder
sively extend the muscle to its fully muscles as they attempt to compensate.
stretched length cause pain at less than nor- The stiffness and the relatively painless,
mal range. This painful restriction of the pas- but progressive, restriction of movement
sive stretch range of motion can be quickly that characterize decrepitude of advancing
detected by screening tests. Range of motion age are often due largely to latent TrPs. These
in the shortened position shows little or no latent TrPs do not spontaneously refer pain.
restriction, but additional contraction effort They cause muscle shortening and can re-
in this position is likely to be painful. The strict stretch range of motion without the pa-
characteristic painfulness to passive stretch tient being aware of the limitation because
in one direction and to active contraction in the muscles have learned to restrict move-
the other was reported specifically for 10 ment to within the painless range. These la-
muscles by Macdonald. Any movement,
109
tent TrPs respond as well to specific myofas-
especially a quick maneuver, that markedly cial therapy and a regular stretching program
increases tension in the muscle, either as do active TrPs, relieving this decrepitude.
stretching or contracting it, can cause pain. Although the range of motion of a mus-
In order to identify active or latent TrPs cle with TrPs does not test passively as be-
that may limit range of motion and thus in- ing restricted at the shortened end of the
fluence dysfunction, as Boeve suggested,
18
range, such a muscle is intolerant of being
the examiner should: (1) identify limited left relaxed in the shortened position for a
range of motion by performing specific period of time, and quickly develops a
range of motion testing for a particular seg- cramp-like pain on voluntary contraction
ment; (2) take up slack to the point of ten- in the shortened position. This pain can be
sion before changing the position; (3) ask explained theoretically as the result of in-
the patient where he or she feels the tension tensification of the shortening process at
or where it hurts; (4) search (palpate) there the contraction knots responsible for the
for a taut band and TrP. Boeve identified
18
TrP phenomena. Placing the muscle in a
the TrPs that were located in this way as shortened position reduces the tension of
relevant TrPs. Such TrPs can produce dys- the taut band, which could allow addi-
function whether or not they produce pain. tional contraction of sarcomeres in the
As a screening test for normal range of region of the contraction knot, thereby
head and neck muscles, the seated patient increasing the energy demand and intensi-
should be able to place the chin firmly on fying its local energy crisis. This would in-
the chest, to look straight up at the ceiling, crease sensitization of local nociceptors
to turn the head at least 9 0 % so that the (refer to Chapter 2, Section D). However,
chin points to the acromion, and to place gentle voluntary contraction with the mus-
the ear close to the shoulder without cle in the lengthened position should help
shrugging. For screening shoulder-girdle to normalize sarcomere lengths throughout
muscles with the Mouth-Wrap-around Test muscle fibers with contraction knots and
(Fig. 18.2), the hand should cover at least contribute to recovery.
half of the mouth with the arm behind the The Scalene-cramp Test [see Fig. 20.4)
head. When performing the Hand-to-shoul- gives an example of cramping caused by
der-blade Test (Fig.22.3), the fingertips on contracting a muscle with TrPs in the short-
the non-dominant side normally reach to ened position. In addition to causing this
the spine of the contralateral scapula. cramping, TrPs in a scalene muscle can
Reach with the dominant hand is usually 1 cause weakness and restricted range of mo-
or 2 cm less than with the non-dominant tion in the extensor digitorum communis
hand. The Mouth Wrap-around Test is re- as evidenced by the Finger-flexion Test {see

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114 Part 1 / Introduction

Fig. 20.6). The weakness may be explained trol. It requires inactivation of the respon-
by reflex motor inhibition referred from the sible TrPs and often requires reeducation
scalene TrPs to the extensor digitorum of the patient's motor control to "unlearn"
communis. The restricted range of motion the dysfunctional, poorly coordinated ac-
is caused by satellite TrPs induced in the tivity pattern caused by the TrP.
extensor digitorum communis by the key Distorted Weight Perception. Testing
scalene TrPs. These motor referred phe- for the disturbance of weight appreciation
nomena are comparable to the pain re- caused by sternocleidomastoid TrPs is de-
ferred from scalene TrPs to the same region. scribed in Chapter 7, Section 8. Loss of fine
Weakness. It is important to think be- coordination among the muscles of masti-
yond the obvious weak function of a mus- cation due to active TrPs in those muscles
cle or muscle group and not to assume that is described in Chapter 5.
all it needs is strengthening exercises. The Weak Deep-tendon Reflexes. Myofas-
clinician must determine why if is weak cial TrPs in a muscle can reduce the brisk-
and the type of weakness. Myofascial TrPs ness of the deep-tendon reflex response
contributing to or causing the weakness elicited by tapping the tendon of that mus-
may be in the same muscle and/or in func- cle. A weak or even absent ankle jerk due to
tionally related muscles. active TrPs in the soleus muscle demon-
Weakness resulting from TrPs may be de- strates this when, within minutes following
tected by testing for static or dynamic mus- inactivation of the TrPs, the previously weak
cle strength and the two methods can result ankle jerk equals that of the normal side.
in completely different answers. Static test-
ing, as performed in conventional testing of Referred Tenderness
muscle strength, attempts to produce a vol- Referred pain and referred tenderness
untary contraction of just the muscle being are closely related neurophysiologically.
tested. This action depends strongly on di- Most of the animal studies that are inter-
rect cortical control of muscle contraction. preted as relevant to the neurophysiologi-
Dynamic testing monitors muscle activity cal mechanisms responsible for referred
while the subject is performing functionally pain are actually studies of referred tender-
meaningful tasks that have been learned and ness. -
120
One study in human subjects of
145

that require muscle coordination. This activ- active TrPs (pressure induced local and re-
ity is largely under cerebellar control and is ferred pain) and of latent TrPs (pressure
much more susceptible to reflex inhibition. produced local pain only) was reported by
The monitoring of dynamic weakness may Vecchiet, et al. They examined the ten-
177

be done by palpation, but may be done quan- derness to electrical stimulation in the TrP
titatively and more accurately with record- region, in the pain reference zone, and in
ings using surface electromyography (EMG). contralateral control regions. Measures
Sudden premature cessation of effort by were taken of skin, subcutaneous, and in-
the patient during static testing may be due tramuscular sensitivity to electrical stimu-
to painful loading of distant stabilizing lation at each site. Pain thresholds were
muscles, to painful loading of the muscle significantly reduced intramuscularly at
being tested, or to a sudden inhibition of both sites (TrP region and pain reference
effort just short of painful loading that has zone) for both kinds of TrPs (active and la-
been "learned" by the muscle being tested. tent), but thresholds were more markedly
Determined effort by the subject can over- reduced by active TrPs and most markedly
ride at least some of this learned pain inhi- reduced at the TrP compared to the pain
bition, and the amount and location of the reference zone. The same pattern applied
pain associated with this kind of aug- to subcutaneous thresholds except that
mented strength testing can help to locate they were lowered only in the more active
the inhibiting TrPs. Inactivation of these TrPs. Pain thresholds were consistently
inhibiting TrPs may completely restore lower in patients with more active TrPs.
normal strength. Pain sensitivity in the reference zone re-
lates strongly to the irritability of the TrP.
On the other hand, the reflexly induced
weakness identified during dynamic test- A subsequent study reported similar
178

ing is not under such direct cortical con- findings where pain thresholds to electri-

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Chapter 3 / Apropos of All Muscles 115

cal stimulation were significantly de- mottled, dimpled appearance of the skin in
creased at TrP sites in skin, subcutaneous panniculosis indicates a loss of normal elas-
and muscular tissues, as compared to an ticity of the subcutaneous tissue, apparently
uninvolved control site in another muscle. due to turgor and congestion. This "peau 114

Trigger point referred tenderness must de orange," or orange peel effect, and the
be distinguished from enthesopathy. Trig- persistent indentations of the "matchstick
ger point referred tenderness is distributed test," but without evidence of pitting
diffusely throughout the involved area and edema, have been beautifully illustrated for
is not well localized. Enthesopathy pre- the skin of the back under the term troph-
sents a circumscribed tenderness specifi- edema. However, Dorland defines troph-
62 3

cally in the regions of muscle attachment. edema as "a disease marked by permanent
When enthesopathy is caused by central edema of the feet or legs, which is not what
TrPs, the tenderness is localized where the the authors described.
62

taut bands (of the TrPs) attach. Boos observed that panniculosis is asso-
21

ciated occasionally with the symptoms of


Cutaneous and Subcutaneous Signs "Muskelrheumatismus" (muscular rheu-
Dermographia. Dermographia has been matism), "Muskelhartspann" (muscular firm
strongly identified with the fibrositis syn- tension), and "Myogelosen" (myogeloses or
drome (the use of the term fibrositis was muscle gellings), because topographically
closely related to myofascial TrPs). We 91 the panniculosis is distributed simi-
find that dermographia in the skin overlying larly in all of those conditions. McKeag 114

muscles with active myofascial TrPs occurs considered panniculosis a form of fibrosi-
most often over muscles of the back of the tis. All four of these diagnostic terms fre-
neck, shoulders and torso, and less fre- quently were used to identify findings
quently over limb muscles. Regular use of characteristic of myofascial TrPs. Boos 21

an antihistamine may be indicated. No ex- noted that freely mobile cutaneous tissue
perimental investigation is known that has excludes panniculosis. We find panniculo-
systematically explored the relation be- sis in a distribution and with a frequency
tween myofascial TrPs and this phenome- similar to that of dermographia (above), but
non. One is needed. not necessarily in the same patients.
Panniculosis. Despite the early use of Panniculosis should be distinguished
the term p a n n i c u l i t i s
5,114
and the subse- from adiposa dolorosa and from fat herni-
21

quent interchangeable use of panniculosis ations. 35, 1 1 4

and panniculitis to characterize diffuse It is not known why some patients with
subcutaneous induration, panniculitis is
21
myofascial TrPs show dermographia and/
now described in a current rheumatology or panniculosis, and others do not. These
text as a nodular condition of the skin
126
conditions may be different forms of mild
that is associated with erythema nodosum autoimmunity. In panniculosis, the subcu-
and with the termination of steroid ther- taneous tissue exhibits increased viscosity
apy. This description of panniculitis does that responds to the application of barrier
not fit the condition we identify here as release pressure in a manner suggestive of
panniculosis. In panniculosis, one finds a thixotropy. This increased viscosity
146, 1 8 3

broad, flat thickening of the subcutaneous may be related to sympathetic nervous sys-
tissue with an increased consistency that tem activity and seems to have some chan-
feels coarsely granular. It is not associated
21
nel of interaction with the TrP mechanism
with inflammation. Panniculosis is usually in underlying TrPs. Skin rolling applied as
identified by hypersensitivity of the skin a series of treatments can normalize the
and the resistance of the subcutaneous tis- panniculosis and can also relieve underly-
sue to "skin rolling." ing TrP activity or make the TrPs more re-
Skin rolling is accomplished by picking sponsive to treatment. A well-designed
up a fold of skin and subcutaneous tissue study is needed that critically evaluates the
between the fingers and the thumb, and relation between TrP activity and the pres-
moving the hand across the surface by ence of overlying panniculosis. The study
rolling the fold forward, as clearly described could employ separate treatment of the
and illustrated by Maigne. The peculiar,
111 TrPs and of the panniculosis, observing

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116 Part 1 / Introduction

what effect the treatment of one has on the treating the patients promptly for restricted
other. joint play, especially if inactivating the
TrPs does not fully restore normal range of
Compression Test motion or if the TrPs recur promptly.
When a patient presents with myofascial In 1964, Mennell described how to ex-
118

pain felt only during movement (not at rest), amine for loss of joint play throughout the
manually compressing the muscle responsi- body and how to restore it. Since that time,
ble for that movement (while the movement joint play has become recognized and appre-
is being performed) sometimes prevents the ciated by the osteopathic profession, and
59,79

referred pain. For example, when sternoclei- by many physical therapists, but is often ne-
domastoid TrPs cause pain on swallowing, glected by others. The movement of joint
firmly squeezing a roll of the skin overlying play can not be induced by voluntary mus-
that sternocleidomastoid can block the pain cular effort or by passive movement of a joint
and render swallowing temporarily pain- through its functional range. It is normally a
free. Section 8 of Chapter 34 describes the painless accessory movement that is essen-
compression test for TrPs in the hand exten- tial to normal pain-free joint function and
sors that cause pain during handgrip. Painful must be performed passively by an examiner.
abduction of the arm caused by a TrP in the It is usually a movement of only a few mil-
upper trapezius is relieved by firm pressure limeters that occurs roughly perpendicular
on that muscle with the palm of the hand in to a major plane of voluntary movement at
the midscapular line during abduction. 89
that joint. Lost joint play often can be re-
This Compression Test can be used to stored quickly by a simple, gentle manipula-
demonstrate to the patient the myofascial tion performed by one who is skilled in the
TrP origin of the pain without imposing ad- appropriate technique for that joint.
ditional pain. When patients have already
heard numerous explanations for their 9. TRIGGER POINT EXAMINATION
pain from many doctors, they are naturally Limitations of stretch range of motion
incredulous of yet another and unfamiliar and records of referred pain patterns help
explanation for their pain. First augment- to identify which muscles to examine for
ing the patient's pain by pressure on the active TrPs; palpation and observation of
TrP, and then relieving it by the Compres- TrP phenomena confirm which muscles
sion Test, helps to convince the patient are responsible for the myofascial pain.
that the pain has a definite muscular This section deals with how to examine
source which responds to treatment. The a muscle for TrPs. The anatomy drawing(s)
neurological mechanism that makes the in each chapter can assist the examiner in
compression test effective may relate to the locating a specific muscle. To confirm its
mechanism responsible for the effective- location, with one hand the examiner re-
ness of vapocoolant spray. These mecha- sists a voluntary movement by the patient
nisms deserve experimental investigation. that contracts the muscle, and with the
other hand palpates for muscle contraction.
Joint Play While the muscles are being examined
Loss of joint play is a common cause of for TrPs, the patient should be comfortable
pain-producing joint dysfunction that and warm. The muscle must be relaxed;
commonly interacts strongly with myofas- otherwise, the distinction between tense
cial TrPs. This joint dysfunction is consid- bands and adjacent slack muscle fibers is
ered an important component of osteo- diminished or lost.
pathic somatic dysfunction by Jacobs and Before the examiner attempts to palpate
Falls, who state that, "The restoration of
79
a muscle for TrPs, the examining digits
joint play appears to be the basis for the must have the fingernails trimmed very
success of synovial joint mobilization us- short. This is especially critical during pin-
ing direct or indirect action treatment tech- cer palpation and when attempting to elicit
niques in osteopathic manipulation." Joint digital LTRs. An appreciable length of fin-
play examination and treatment are fre- gernail not only causes the patient unnec-
quently simple and full recovery can often essary (sometimes severe) pain, but the
be greatly expedited by examining and skin pain caused by long fingernails is

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Chapter 3 / Apropos of All Muscles 117

readily misinterpreted as TrP tenderness. sometimes almost perfect for the detec-
One common reason for unreliable results tion of spot tenderness, a taut band, pres-
when attempting to elicit LTRs is failure to ence of referred pain, and reproduction
use the finger tip because the fingernail of of the subject's symptomatic pain. How-
the palpating finger is inadequately ever, agreement on the presence or ab-
trimmed. The skin pain from the fingernail sence of an LTR was not as satisfactory
prevents application of sufficient pressure for its use as a clinical diagnostic crite-
to elicit the LTR, and the fingernail me- rion of a TrP. The reliability for the iden-
chanically interferes with use of the tip of tification of LTRs was poorest in the in-
the finger to apply the pressure. Adequate fraspinatus. The LTR is a difficult and
trimming of fingernails is a fundamental relatively unreliable diagnostic test when
requirement that is commonly ignored. the response is elicited manually. How-
For those who have difficulty in recog- ever, it is valuable as a strongly confir-
nizing TrPs by palpation, a dermometer, or matory diagnostic finding when elicited
similar device to measure skin conduc- manually and is especially valuable when
tance or skin resistance, is sometimes used elicited during the needling of TrPs.
to explore the skin surface for points of It now appears that the most reliable di-
high conductance (low skin resistance), agnostic criterion of TrPs on examination
which apparently often overlie active TrPs. of the muscle is the presence of exquisite
This device may be helpful, but has not tenderness at a nodule in a palpable taut
been shown to be highly reliable. Use of band. If, in addition, the patient recognizes
the dermometer for identifying TrPs needs pain that is elicited by digital pressure on
experimental evaluation of its reliability (or needle penetration of) the TrP as his or
and, if reliable, investigation of the neuro- her clinical pain complaint, the TrP is clin-
physiological basis for its effectiveness. ically active, not just latent. Associated
Palpating TrPs can severely exacerbate phenomena, such as a characteristic pat-
the patient's referred pain activity for a day tern of referred pain or an LTR, are strongly
or two. For this reason, it is critically im- supportive evidence. Other features, not
portant to examine a muscle for TrPs only critically evaluated but strongly character-
if the examiner then applies specific myo- istic of TrPs, are limited stretch range of
fascial therapy such as spray and stretch motion and increased tension of the muscle
followed by moist hot packs to muscles observed during the patient examination.
with TrPs. When the examiner neglects
this caveat, patients with myofascial TrP Palpable Tender Nodule and Taut Band
pain come to dread a physical examination Several other authors have recognized
that includes palpating muscles for TrPs. how critical the details of the palpation
The clinical rule is: palpate for TrPs in only technique are for locating taut b a n d s . '
131 158

those muscles that can be treated during The optimal elongation of a muscle for pal-
the same visit. This consideration also pating taut bands (which is usually the first
should be incorporated into research pro- step in palpating the TrP) is at a position
tocols whenever practical. that is slightly longer than the position of
ease. In this case, the uninvolved muscle
Diagnostic Criteria fibers are still slack, but the taut band fibers
The reliability with which the physi- are placed under additional tension by
cal features of TrPs could be determined lengthening the muscle to the point of a
was evaluated by four experienced physi- perceptible increase in resistance to move-
cians who, following a three hour train- ment. This places the taut band fibers un-
ing session immediately before the study, der increased tension without tensing the
examined five pairs of muscles for five uninvolved fibers (Fig. 3.6A) and produces
physical characteristics of TrPs in each of the maximum palpable distinction be-
ten subjects. 52
The muscles examined tween the normal tonus of the uninvolved
were the infraspinatus, latissimus dorsi, fibers and the increased tension of the taut
upper trapezius, extensor digitorum, and band fibers. This is also the optimal ten-
sternocleidomastoid. Agreement among sion for eliciting LTRs and for making LTRs
examiners was at least substantial and most visible. The stretch may be on the

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118 Part 1 / Introduction

Taut (palpable) bands in muscle

Taut
bands

Relaxed
muscle
fibers
A
Local twitch response

Local
twitch
of band

B
Figure 3.6. Longitudinal schematic drawing of taut sure. The trigger point is the most tender spot in the
bands, myofascial trigger points (dark red spots), and band. B, rolling the band quickly under the fingertip
a local twitch response seen in longitudinal view of the (snapping palpation) at the trigger point often pro-
muscle (light red). A, palpation of a taut band (straight duces a local twitch response that usually is most
lines) among normally slack, relaxed muscle fibers clearly seen as skin movement between the trigger
(wavy lines). The density of red stippling corresponds point and the attachment of the muscle fibers.
to the degree of tenderness of the taut band to pres-

verge of causing pain, but should evoke, at along the taut band to locate the nodule
most, only mild local discomfort. Optimal that corresponds to a circumscribed
tension is usually about two-thirds of the slightly enlarged region of decreased com-
muscle's normal stretch range of motion, pliance. This nodular region is also the lo-
but may be only one-third or less with very cation of maximum tenderness (the TrP).
active TrPs. The reduction in range of mo- Three kinds of palpation can be used:
tion varies greatly among muscles. flat palpation, pincer palpation, and deep
A taut band feels like a palpable cord of (probing) palpation. Flat palpation is used
tense muscle fibers among the normally for relatively superficial muscles which
pliable fibers. Such palpable tense muscle have only one surface accessible for palpa-
fibers were described as "matted together" tion (e.g., the extensor digitorum commu-
by Wilson. The examiner should palpate
189
nis). Pincer palpation is used when oppo-

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Chapter 3 / Apropos of All Muscles 119

site sides of the muscle are accessible and When intervening tissue makes the mus-
the belly of the muscle can be grasped be- cle inaccessible to flat or pincer palpation,
tween the digits (e.g., the sternocleidomas- the examiner must use deep palpation.
toid, lateral border of the latissimus dorsi, This means placing the fingertip over an
biceps brachii, and part of the pectoralis area of skin that overlies the motor-point
major). Deep or probing palpation must be region or attachment of the muscle sus-
used for deep muscles with considerable pected of harboring TrPs. Localized tender-
tissue between them and the skin (e.g., the ness that is elicited only when the finger
quadratus lumborum, gluteus minimus, pressure is directed in one specific direc-
and piriformis muscles). tion is compatible with the diagnosis of ei-
In this manual, flat palpation refers to ther a central or attachment TrP if pressure
the use of a fingertip that employs the mo- elicits pain recognized by the patient as his
bility of the subcutaneous tissue to slide the or her pain complaint. Additional evi-
patient's skin across the muscle fibers. This dence, such as restricted stretch range of
movement permits detection of changes in motion and characteristic referred pattern
the underlying structures (Fig. 3.7). First, are helpful in making a provisional diag-
the skin is pushed to one side of the area to nosis when the usual palpable findings are
be palpated (Fig. 3.7A) and the finger slides inaccessible. Favorable response to spe-
across the fibers to be examined (Fig. 3.7B), cific myofascial TrP therapy helps to con-
allowing the skin to bunch on the other side firm the diagnosis.
(Fig. 3.7C). Any ropy structure (taut band) Sufficient pressure on an active TrP al-
within the muscle is felt as it rolls under most always elicits at least withdrawal,
the finger. A taut band feels like a cord that wincing, or vocalization by the patient. In
can range from 1 mm to 4 mm or more in di- the past, if the withdrawal were sufficiently
ameter depending on the severity of the vigorous the response was identified as a
TrP. The sensation of applying snapping "jump sign." This jerk response was noted
palpation across the taut band can be com- by Good in 1949 with regard to TrP charac-
55

pared to what plucking a violin or guitar teristics that he called myalgic pain, and by
string imbedded in the muscle might feel Kraft et ai. in 1968 with regard to TrP char-
91

like. In a muscle that has many TrPs, five or acteristics that they called fibrositis. Kraft
six such bands, or cords, may lie in such later dubbed this response the "jump sign."
close proximity to one another that they This response served as a rough indication
seem to merge. If the examiner tips the pal- of the tenderness of the TrP that depended
pating finger up on end to palpate with the strongly on how much pressure was ap-
end of the terminal phalanx, individual plied. Now the tenderness can be measured
bands may be distinguishable. This tech- quantitatively using an algometer. The ex-
nique requires a very short fingernail. treme sensitivity to applied pressure that
For examination of the abdomen, flat elicits the jump sign is not by itself consid-
palpation using "fingertip" pressure lo- ered to be a sufficient diagnostic criterion of
cates spot tenderness in the abdominal a TrP, but it is characteristic of an active TrP.
wall, while "flathand" pressure using the
flat part of the finger or hand is more likely Referred Pain
to elicit tenderness of underlying vis- The referred patterns that are character-
cera. Static pressure with the finger flat
158
istic of myofascial TrPs as presented in this
can be expected to detect little more than Manual are not unique to just the TrP itself.
underlying tenderness in any muscle. Patterns that are similar or nearly identical
The technique of pincer palpation is may be elicited from other structures in-
performed by grasping the belly of the mus- cluding zygapophyseal joints, muscle tis-
19

cle between thumb and fingers (Fig. 3.8A) sue that is two centimeters removed from
and pressing the fibers between them with the TrP but still in the taut band, and at-
71

a back-and-forth rolling motion to locate tachments of the muscle that exhibit en-
taut bands (Fig. 3.8B). When a taut band is thesopathy.
identified, it is explored along its length to Compression of either an active or latent
locate the nodule and spot of maximum central TrP can reproduce the typical pat-
tenderness, which identifies a TrP. tern of referred pain of a given muscle, and

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120 Part 1 / Introduction

Figure 3.7. Cross-sectional schematic drawing show-


ing flat palpation of a taut band {black ring) and its trig-
ger point (red spot). Flat palpation is used for muscles Figure 3.8. Cross-sectional schematic drawing show-
(light red) that are accessible only from one side of the ing pincer palpation of a taut band (black ring) at a
muscle, such as the infraspinatus. A, skin pushed to trigger point (red spot). Pincer palpation is used for
one side to begin palpation. B, fingertip slides across muscles (light red) that can be picked up between the
muscle fibers to feel the cord-like texture of the taut digits, such as the sternocleidomastoid, pectoralis
band rolling beneath it. C, skin pushed to other side at major and latissimus dorsi. A, muscle fibers sur-
completion of movement. The same movement per- rounded by the thumb and fingers in a pincer grip. B,
formed vigorously is snapping palpation. hardness of the taut band felt clearly as it is rolled be-
tween the digits. The change in the angle of the distal
phalanges produces a rocking motion that improves
discrimination of fine detail. C, the palpable edge of
the taut band is sharply defined, as it escapes from
between the fingertips, often with a local twitch re-
sponse.

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Chapter 3 / Apropos of All Muscles 121

sometimes other sites of tenderness in The LTR is readily elicited and per-
muscle (such as enthesopathy) can also re- ceived in the muscles that permit pincer
spond to pressure with similar referred palpation. Other superficially placed mus-
pain patterns. Hypertonic saline injected cles, such as the deltoid, gluteus max-
into the muscle consistently produces imus, vastus medialis, and the finger and
these patterns. Eliciting a characteristic wrist extensors, are likely to exhibit
pain pattern at a muscle site is compatible strong LTRs in response to snapping pal-
with it being a TrP, but the finding by itself pation with a fingertip. An LTR is not
is not diagnostic of a TrP. likely to be elicited by palpation of deep
These characteristic referred pain pat- muscles, like the subscapularis or multi-
terns are most valuable as a preliminary fidi, but it can be elicited by needle con-
guide as to which muscle(s) may harbor tact with the TrP.
TrPs that are responsible for the patient's Most muscles exhibit a vigorous LTR
pain, and are useful for helping patients only if they harbor active TrPs, but the
understand the source of their pain. middle finger extensor, in most adults,
Gerwin et al. in their interrater relia-
52
contains a latent TrP that responds with a
bility study noted that the one criterion readily visible LTR. In one study, the LTR
which distinguished an active TrP from a was most reliably observed in this muscle
latent TrP was the patient's recognition of as compared to four others apparently
52

his or her pain complaint when the active because the response here is so accessi-
TrP was compressed. ble, so common, and so easily elicited. An
LTR in this muscle extends the middle
Local Twitch Response finger, which makes it obvious. For this
In 1955, Travell and Weeks and
165, 1 6 6 test the relaxed arm rests on a table or
Travell 185
reported a localized twitch of armrest of a chair, and the wrist hangs
part of the muscle when the TrP was rolled over the edge. The tender spot is located
under the fingers. The twitch could be vig- in a palpable band of the middle finger
orous enough to cause a perceptible jerk of extensor about 2 cm distal to the lateral
the body part. Travell previously had ob- epicondyle [see Fig. 35.1 A). With the fore-
served this twitch response when a needle arm and hand to be tested fully relaxed,
was inserted into a trigger area. The EMG 163 the TrP is rolled under the fingertip with
characteristics of LTRs were reported in rapid, strongly applied, snapping palpa-
1976 by Simons, but the LTR was then
143 tion [see Fig. 35.4), and the extensor re-
misnamed the "jump sign," which refers to sponse of the middle finger is ob-
a different phenomenon, as noted above. served. '143 149

The LTR is a transient contraction of es- The LTR elicited by snapping palpation
sentially those muscle fibers in the tense or needle penetration has been studied
band that are associated with a TrP (Fig. electromyographically. 149
The LTR lasted
3.6B). It may be seen as a twitch or dim- from 12-76 msec in response to needle
pling of the skin near the terminal attach- stimulation. Clinical evidence and ani-
69

ment of the fibers, or palpated through the mal research s t u d i e s


74,75
indicate that the
skin with the examining hand. The re- LTR depends upon a spinal-level reflex
sponse is elicited by a sudden change of mechanism.
pressure on the TrP, usually produced by In summary, Gerwin, et al. showed 52

transverse snapping palpation of the TrP that in many muscles it requires so much
across the direction of the muscle fibers training and skill to elicit LTRs reliably by
(taut band), or by needle penetration into palpation, that for most clinicians an LTR
the TrP. ' The optimal muscle length for
143 149
is generally not a satisfactory criterion for
eliciting an LTR by snapping palpation is making the diagnosis of myofascial pain
the same as that for examining the muscle caused by TrPs. When an LTR is elicited
for taut bands as described above. The manually in the presence of other palpable
closer to the TrP that the taut band is stim- indicators of a TRP, it is a strongly confir-
ulated by snapping, the more vigorous is matory finding. However, Hong demon- 67

the LTR. strated that an LTR is a valuable indicator

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122 Part 1 / Introduction

of having found the mark whenever ples. Incorporation of an understanding of


needling TrPs. these two kinds of TrPs and the therapeutic
ramifications should provide a major op-
Central and Attachment Trigger Points portunity for advancement in the clinical
Elucidation of the pathophysiology re- practice of myofascial pain in the coming
sponsible for central and attachment TrP years.
phenomena, as illustrated in Figure 2.25
(and its associated text), makes it necessary Key and Satellite Trigger Points
to distinguish central TrPs located in the
A Key Myofascial TrP is one that is re-
endplate zone of a muscle and attachment
sponsible for the activity of one or more
TrPs that occur in a region of attachment of
satellite trigger points. Clinically, a key TrP
the muscle. Fischer recognized the im-
46

becomes apparent when inactivating it also


portance of this distinction from a thera-
inactivates its satellite TrPs without direct
peutic point of view. The difference in
treatment of the satellite TrPs themselves.
pathophysiological mechanisms involved
This relationship was noted occasionally
is also important.
in the first edition of this volume. Many ad-
The primary central TrP abnormality is ditional pairs of key and satellite TrPs are
associated with individual dysfunctional presented in Table 3.3, which is based
endplates in the endplate zone (or motor largely on observations reported by Hong. 68

point). This dysfunction produces a local Figure 3.10 illustrates key TrPs in the up-
energy crisis that results in sensitization of per trapezius and sternocleidomastoid
local nociceptors. This dysfunction can muscles with corresponding satellite TrPs
produce contraction knots which then pro- in the digastric, masseter, and temporalis
duce a nodule and a taut band of tense muscles.
muscle fibers.
Key and satellite TrPs are related TrPs.
The attachment TrPs result from the sus- Sometimes the "hierarchy" appears clear,
tained increased tension of these muscle but which TrP came first (or which is
fibers at the attachment point. This sus- most important) is not always evident.
tained tension can produce enthesopathy What is clear is that TrPs in certain mus-
with swelling and tenderness where the cles are related to TrPs in certain other
muscle fibers attach to an aponeurosis, ten- muscles; successfully treating one of these
don, or bone. Some muscles have sufficient related TrPs may also inactivate the other.
separation between the muscle fiber-to-ten- The role as to which muscle harbors the
don attachment and tendon-to-bone at- key TrP may sometimes reverse. Knowl- 102

tachment that one end of the muscle may edge of these relationships is used to ex-
have two distinctly different attachment amine for Key TrPs that might be over-
TrPs. looked when the patient complains
Figure 3.9 illustrates the location of a chiefly of symptoms produced by the
central TrP and of two corresponding at- satellite TrP.
tachment TrPs in the temporalis muscle.
Sensitization of local nociceptors causes Whiteside 187
described an interesting
the pain in both kinds of TrPs, but the example of a three-step satellite TrP phe-
processes by which the sensitization devel- nomenon. A final-year physiotherapy stu-
ops are different in each. Table 3.2 lists the dent complained of a toothache that de-
clinical findings characteristic of central veloped in her right upper jaw along with
TrPs as compared to attachment TrPs and an ache in her right upper trapezius mus-
includes the cause of each finding. cle when she studied for long periods of
In the first edition of this volume, no time. She had received extensive dental
distinction was drawn between central and treatment including a root canal without
attachment TrPs. Although the time avail- relief. In response to firm pressure on a
able to incorporate this new understanding TrP in the right lower trapezius she said,
into all individual muscle chapters was "I am getting the dull ache in the upper
limited, a major effort was made to identify trapezius that I get when I study." In re-
the difference for the most obvious exam- sponse to pressure on an upper trapezius

Copyrighted Material
Chapter 3 / Apropos of All Muscles 123

Figure 3.9. Example of a central trigger point X and and the lower one occurs where the tendon attaches
two attachment trigger points (black circles) both of to bone. In this situation, an additional attachment TrP
which correspond to regions of tension caused by the (not identified) could occur where the fibers of the taut
central trigger point. The uppermost attachment trig- band from the TrP attach superiorly directly to the
ger point occurs at the musculotendinous junction, skull.

TrP she said, "I am now getting pain in the


lenting pressure exerted on the nerve can
right temporal region, but I've not had
produce neurapraxia (loss of nerve con-
pain in that area before." In response to
duction) but only in the region of compres-
pressure on a right temporal TrP she re-
sion. Table 3.4 lists nerves that can be en-
sponded, "Now I'm getting pain in the
trapped by a muscle in this manner.
tooth that bothers me when I study."
Occasionally, there is EMG evidence of
some neurotmesis (axonal loss) in addition
10. ENTRAPMENT to neurapraxia.
When a nerve passes between taut The patient with one of these entrap-
bands in a muscle, or when a nerve lies be- ments is likely to present with two kinds
tween taut TrP bands and bone, the unre- of symptoms: aching pain referred from

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124 Part 1 / Introduction

Table 3.2 Comparisons Between Central Trigger Points (TrPs) and Attachment
Trigger Points

Finding Most Likely Cause

Central TrPs In motor endplate zone Dysfunctional endplates


Nodule Contraction knots
Local and referred pain Nociceptors sensitized by local energy crisis
Taut band beyond nodule Contraction Knot Tension

Attachment TrPs In attachment zone Taut band tension


Palpable induration Inflammatory reaction
Local and referred pain Nociceptors sensitized by persistent taut band
tension
Taut band at attachment TrP Contraction knots in central TrP

Table 3.3 Listing of Muscles Observed to Exhibit Corresponding Key Trigger Points and
Satellite Trigger Points*

Key Trigger Point Satellite Trigger Points

Sternocleidomastoid Temporalis*
Masseter*
Lateral Pterygoid*
Digastric
Orbicularis Oculi*
Frontalis*
Upper Trapezius Temporalis*
Masseter
Splenius
Semispinalis Capitis
Levator Scapulae*
Rhomboid Minor*
Occipitalis*
Lower Trapezius Upper Trapezius
Scaleni Serratus Posterior Superior*
Pectoralis Major* and Minor*
Deltoid
Extensor Digitorum Communis*
Extensor Carpi Radialis and Ulnaris
Long Head, Triceps Brachii*
Infraspinatus Anterior Deltoid*
Biceps Brachii
Latissimus Dorsi Long Head, Triceps Brachii*
Flexor Carpi Ulnaris

" F r o m Hong CZ. Considerations and recommendations regarding myofascial trigger point injection. J Mus-
culoskel Pain 2 ( l ) : 2 9 - 5 9 , 1 9 9 4 .

TrPs in the involved muscle, and the pain of myofascial origin usually find
nerve compression effects of numbness their symptoms aggravated by chilling
and tingling, hypoesthesia, and some- the muscle, and relieved by heat on the
times hyperesthesia. Patients with nerve TrPs.
entrapment prefer cold packs on the neu- The signs and symptoms of partial neu-
rogenically painful region; patients with rapraxia may sometimes be relieved within

Copyrighted Material
Chapter 3 / Apropos of All Muscles 125

Temporalis TrP

Masseter TrP
Digastric TrP

Sternocleidomastoid TrP
Upper trapezius TrP

Figure 3.10. Examples of key trigger points (TrPs), muscles. It shows a key sternocleidomastoid trigger
shown as red Xs, and corresponding satellite trigger point initiating satellite trigger points in the temporalis
points (black Xs) in other muscles. A key TrP in one and posterior digastric muscles. (Credit is given to
muscle can induce satellite TrPs in other muscles (ar- M.J. Tolic, M.D., for suggesting the concept of this fig-
rows). This figure illustrates key upper trapezius TrPs ure.)
initiating satellite TrPs in the temporalis and masseter

minutes after inactivation of the responsi- tional unit that are also likely to develop
ble myofascial TrPs, which immediately TrPs.
relaxes the taut bands. Effects of more se- In the first edition, when differential di-
vere compression may require days or agnosis was considered as it is here, it was
weeks for recovery. usually included as a subheading under
Section 7, Activation of Trigger Points, or
11. DIFFERENTIAL DIAGNOSIS distributed throughout the chapter. This
Section 11 was previously named Asso- section now identifies other diagnoses that
ciated Trigger Points and has been re- are commonly applied to patients when
named Differential Diagnosis. The associ- the pain is caused by TrPs. Table 2.5 lists
ated trigger point information is now examples of 24 of these conditions. This
covered in a subheading, Related Trigger section also considers the problem of mis-
Points. The material under this subheading diagnosing one of those other conditions as
identifies the other muscles of the func- TrPs and not treating it appropriately.

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126 Part 1 / Introduction

Table 3.4 Nerve Entrapments by Myofascial Taut Bands in Muscles That Are Included
in This Volume

Entrapped Nerve Muscle Chapter

Accessory Sternocleidomastoid 7
Brachial Plexus, lower trunk Pectoralis Minor 43
Brachial Plexus Anterior and Middle Scalenes 20
Digital Interossei, hand 40
Greater Occipital Semispinalis Capitis 16
Intercostal Intercostal 45
Musculocutaneous Coracobrachialis 29
Radial Triceps Brachii 32
Radial, sensory Brachialis 31
Radial, superficial sensory Extensor Carpi Radialis Brevis 34
Radial, deep Supinator 36
Serratus Anterior, motor nerve Middle Scalene 20
Spinal, posterior primary rami Thoracolumbar Paraspinal 48
Supraorbital Frontalis 14
Ulnar Flexor Digitorum, deep, superficial 38
Ulnar Flexor Carpi Ulnaris 38
Ulnar, deep (motor) branch Opponens Digiti Minimi 40

12. TRIGGER POINT RELEASE rarely applicable to the muscle itself. Ex-
amined in terms of muscle tension caused
by TrPs, many of these procedures are ap-
With Contributions by
propriate for treating TrPs, although the au-
Mary L. Maloney, P.T. thors rarely recognize the possibility (like-
lihood) that TrPs are a significant part of
The title of this section has changed the picture.
from "Stretch and Spray" to "Trigger Point This section is organized in terms of the
Release." The change reflects the shift in kinds of procedures used to relieve the TrP
emphasis from only one manual therapeu- tension causing the pain and considers
tic technique to an appreciation of the why each approach is likely to contribute
wide variety of effective techniques avail- to relief. It considers passive muscle
able and an indication of the clinical use- stretch techniques, techniques that involve
fulness of each. This section presents a ra- voluntary contraction, manipulation of the
tionale for each technique that is based on TrP, and modalities. In addition, this sec-
the new understanding of the nature of tion identifies helpful accessory tech-
T r P s . ' It calls attention to how various
147 148
niques, notes methods used simply to re-
treatment techniques that are commonly lieve the pain rather than eliminate its
used today relate to myofascial TrPs. cause, and lists a number of caveats.
There are many techniques published Intensive examination for perpetuating
and practiced to relieve the tissue tensions factors is called for when the patient has
associated with musculoskeletal pain. chronic myofascial pain, or if the severity
Each professional group dealing with this of involvement is progressive.
problem has its own terminology and fa- When deciding which of the many avail-
vorite methods. Rarely do these practition- able treatment methods to use, it is impor-
ers identify what is causing the pain or tant to consider whether the TrPs being
present a convincing explanation of why treated are central TrPs in the endplate zone
their procedure relieves it. Some practi- of the muscle or are attachmentTrPs located
tioners do explain why they think the tis- where the muscle attaches to its aponeuro-
sues are tense, but these explanations are sis, tendon, or a bone. Stretching (lengthen-

Copyrighted Material
Chapter 3 / Apropos of All Muscles 127

ing) the muscle inactivates central TrPs, but middle finger knuckle. As the spray was
may tend to aggravate the overloaded mus- momentarily applied over the joint, the girl
cle attachments. The attachment TrPs are was startled and jerked her hand away.
more likely to respond to manual therapy Then, mystified, the girl said "That feels
that is directed to the regions where central better; put some right here." A second brief
TrPs are located and therapy that concen- pass of vapocoolant over the other side of
trates on relieving the strain on the attach- the joint completely relieved her pain and
ments caused by the TrP-induced shorten- restored the full range of motion. Refrig-
169

ing of the taut band fibers. eration anesthesia with frosting of the skin
Generally, central TrPs become less irrita- was not an essential mechanism.
ble in response to warmth. However, some- Rinzler and Travell, 138
and then Trav-
times patients find relief by application of ell, succeeded in relieving pain due to
162, 1 6 9

cold. Attachment TrPs may be more respon- acute coronary thrombosis by applying the
sive to cold than to heat, especially when spray to the skin over the area of pain re-
they are very irritable. Since the attachment ferred from the heart. This effectiveness of
TrPs are the result of the tension from the taut vapocoolant spray in relieving the pain of
bands of the central TrPs, inactivation of the myocardial ischemia was demonstrated ex-
central TrP is essential; on the other hand, re- perimentally. The spray did nothing to re-
137

ducing the sensitivity of the attachment TrPs lieve the ischemia; it relieved only the pain.
may greatly facilitate inactivation of their It inhibited the perception of referred vis-
central TrPs. The optimal therapeutic inter- ceral pain.
vention for central TrPs compared to that for In our experience, spray and stretch is the
attachment TrPs is an issue that needs com- single most effective noninvasive method to
petent experimental investigation. inactivate acute TrPs. However, many other
Recovery of full function may involve noninvasive techniques require no supplies
more than just TrP inactivation and relief of and are better suited to use by the patient at
pain, especially in patients who have home. When the simpler approaches fail to
chronic pain. If the muscle has learned dys- give satisfactory results, many times the ad-
function that restricts both its strength and dition of spray and stretch (often in combi-
coordination during functional activities, it nation with other techniques) brings success.
must be retrained to normal function. This A single-muscle syndrome of recent onset
requires adequate monitoring of the rate of frequently responds with full return of pain-
muscle fatigue and loss of strength during free function when two or three sweeps of
exercise and functional activity. Surface spray are applied while the muscle is being
EMG can be a valuable quantitative tool for extended gently to its full stretch length. In
160

measuring fatigue and in addition can pro- addition, when many muscles in one region
vide biofeedback for retraining. of the body, such as the shoulder, are in-
volved and the TrPs are interacting strongly
Spray and Stretch with one another, spray and stretch is a prac-
In 1952, Hans Kraus described how
123 tical means of releasing an entire functional
he discovered that spraying ethyl chloride group of muscles together to make more
on the skin relieves musculoskeletal rapid progress toward pain relief. The spray-
pain. Kraus was looking for a substitute for and-stretch technique does not require the
alcohol-soaked towels exposed to live precise localization of the TrP that is needed
steam that were then used in Germany by for injection; it requires only identification of
wrestlers as a treatment for painful where the taut bands are located in the mus-
sprains. 123
Kraus recommended ethyl
93 cle to ensure that those fibers are released.
chloride spray for initial treatment, and The essential therapeutic component is
then depended heavily on active range of the stretch. "Stretch is the action, spray is
motion and exercise for eventual recovery. distraction." However, the expression "spray
Dr. Travell became aware of his freezing and stretch" is preferred to "stretch and
spray technique through his 1941 paper on spray" because it is important that the spray
"surface anesthesia." Her first use of it
92
be applied before or concurrently with, but
was on a young girl who had sprained her not after, the muscle is stretched. Stretch

Copyrighted Material
128 Part 1 / Introduction

without some additional technique to release The effectiveness of the spray for help-
muscle tension and suppress pain is likely to ing the stretch to release central TrPs
aggravate TrPs, especially attachment TrPs. (when attachment TrPs are also present)
Myofascial TrPs in the muscles of young may depend on the vapocoolant spray's
children and babies are especially respon- suppression of pain from the attachment
sive to spray-and-stretch therapy. In this
10
TrPs, which would otherwise be intolerant
age group, many of the other techniques of any additional tension. This effect of
which require more patient participation the spray would be comparable to its po-
are not applicable. Most children have tent analgesic effect on burns, sprains, car-
been well trained to be needle-shy. diac ischemia, and referred visceral pain.
Spray and stretch is especially useful See Chapter 2, Part B for more on this
immediately after TrP injection during the mechanism.
period that the local anesthesia remains. Vapocoolants. To be effective for re-
This combination procedure helps to inac- leasing TrP tension in order to stretch the
tivate any residual TrP activity and to at- muscle, the vapocoolant must be dispensed
tain full stretch range of motion. as a fine stream, not as the dispersed spray
Much of the shoulder pain in patients which is used for spraying paint or hair.
with hemiplegia arises in TrPs caused by the Two sprays are currently commercially
overload of spasticity and strain on the re- available: Fluori-Methane and ethyl chlo-
maining functional musculature. During the ride. Both are sterile as dispensed and can
first few weeks following a stroke, much be sprayed on a sterile field without conta-
temporary relief can be obtained by spray minating it. However, neither is consid-
1

and stretch of both agonists and antagonists ered to be an antiseptic nor will they kill
in the shoulder region, applied twice daily. germs.
Liberson described wheeling a drum of
104
Both volatile liquids exert pressure in a
vapocoolant equipped with a hose and spray closed container at room temperature. The
nozzle through the Physical Medicine and pressure forces a stream of the room-temper-
Rehabilitation Ward twice daily to spray and ature liquid out of the inverted bottle upon
stretch the patients with hemiplegia in order opening of the control valve. The warmer is
to reduce their pain and increase their func- the container, the higher is the pressure.
tion more rapidly during the early weeks of Upon leaving the nozzle, the stream of liq-
recovery. After 4 - 8 weeks, as the degree of uid immediately begins to evaporate, which
paralysis and spasticity stabilizes, the relief cools the stream as it passes through the air
of TrP pain becomes more lasting. Such re- to the skin. For a distance of approximately
lief of pain encourages the patient to strive half a meter (about 18 inches) the stream
for function, and influences the results of re- continues to get colder until it impacts the
habilitation by improving the patient's ef- skin, where it continues to evaporate and
forts to use marginally functional muscles. 35
further cool the skin. At short distances from
Immediately following major trauma the skin, the stream has less time to cool and
such as fracture, dislocation, or whiplash in- so impacts the skin at a temperature nearer
jury, cold packs should be applied to the to room temperature. When held far enough
muscles to reduce tissue swelling. Spray and from the skin and directed at one spot, the
stretch, with heat, should be deferred until stream of either spray can produce subfreez-
3 - 5 days later as the local reaction to trauma ing temperatures; this is to be avoided.
subsides. However, the anti-inflammatory Because ethyl chloride is a potentially
effect of the vapocoolant spray alone, when serious health hazard and is colder than
applied at once, is remarkably helpful for re- desirable for TrP applications, Travell as-
169

lieving the pain of sprains and burns. sisted in the development of a safe alterna-
Patients who have myofascial pain and tive, Fluori-Methane, which is a mixture
hyperuricemia may not respond well to of two fluorocarbons: 8 5 % trichloromono-
spray and stretch because pain recurs fluoromethane and 15% dichlorodi-
quickly. The response is better to injection fluoromethane. Fluori-Methane is non-
of TrPs. This may be explained by the de- flammable, chemically stable, non-toxic,
position of uric acid crystals in an acid en- non-explosive and does not irritate the
vironment at the TrP. skin.

Copyrighted Material
Chapter 3 / Apropos of All Muscles 129

Unfortunately these fluorocarbons cause PATIENT PREPARATION. Adequate body


serious degradation of the upper atmos- warmth is critical for a favorable muscular
phere ozone layer and are no longer manu- response to treatment. If, on arrival, the pa-
factured or approved for commercial pur- tient feels chilly or the hands and the feet
poses. A temporary medical exception has are cold, a dry heating pad can be applied
been granted for Fluori-Methane while a to the abdomen to raise the core tempera-
suitable substitute is being developed. A ture and cause reflex vasodilatation in the
promising substitute is undergoing testing limbs. This is important in cold climates,
and when approved will be marketed as chilly rooms, and whenever a patient feels
"Gebauer Spray and Stretch" by the same cool. A blanket should cover the portion of
company that sells Fluori-Methane. The the patient not exposed for treatment.
new product will be dispensed from a can A simple and often effective alternative
with a different valve mechanism rather to the application of heat is neutral warmth
than from the familiar glass bottle. Most of that is obtained by covering the patients
the illustrations in this edition show the with a wool scarf, sweater, or small blanket
operator using the new product. to keep them warm by conserving their
Ethyl chloride is too cold for optimum own body heat. However, the muscle relax-
release of TrP tension as usually applied. It ation gained by the warmth can be lost due
is a rapidly acting general anesthetic that to chilling when the source of warmth is
has a dangerously low margin of safety, is suddenly removed.
flammable and is explosive when 4 - 1 5 % of Hypoglycemia aggravates TrPs. Before
the vapor is mixed with air. It has been 123
application of a specific myofascial ther-
responsible for accidental anesthetic apy like spray and stretch, the patient
deaths of patients and a physician. If 169
should be asked if he or she has eaten re-
ethyl chloride spray is used, rigorous pre- cently to avoid potential hypoglycemia.
cautions must be observed. Fire hazards For patients with a suspicious history, a
must be eliminated, and neither the patient banana, glass of milk, cheese, flavored
nor the clinician should inhale the heavy "drinking" gelatin in orange juice, or a cup
vapor. Ethyl chloride should never be
160,170
of instant soup may prevent a painfully ad-
given to a patient for home use. verse reaction to therapy soon afterward.
Urticaria owing to cold allergy has not The portions of the skin to be sprayed
been observed in response to spraying with should be bare. Spray penetrates the hair
Fluori- Methane for myofascial therapy, and unless it is heavily greased or thickly mat-
was observed only once with ethyl chlo- ted, but wigs and toupees must be removed.
ride. There is no evidence that inhalation
170
Patients should be given an initial refer-
of Fluori-Methane in doses and concentra- ence with which to judge improvement in
tions to which patients are exposed during their range of motion following treatment,
treatment for TrPs is toxic. It has an odor so that they can be aware of progress fol-
that is unpleasant to some patients, and un- lowing treatment. To the patient, a move-
necessary exposure should be avoided. ment feels as if it "goes as far as it can go"
Most of the articles by Travell describ- both at a restricted range and at the full
ing the use of spray refer to ethyl chloride range of motion. During initial testing, the
because they were written before Fluori- patients learn the extent of their movement
Methane became available. She cautioned by answering specific questions. "How
readers to substitute Fluori-Methane for wide does your mouth open; two or three
ethyl chloride when they refer to those knuckles?" "How far can you see around
articles. behind you?" "Can your fingertips reach
Spray Technique. Detailed descrip- around the back of your head and cover
tions of the vapocoolant spray technique your mouth?" or "Can you reach your back
have been p u b l i s h e d . ' ' ' ' '
51 119 160 164
Re-170 193 pants pocket?" A mirror helps patients to
production of the referred pain by pressure see and remember what they were able to
on a TrP helps the patient to more fully un- do. The measurement should be retested
derstand why treatment is directed primar- following treatment so that the patient can
ily to the tender region in the muscle and not fully appreciate the difference. Since we
primarily to the region of pain complaint. are as concerned with function as with

Copyrighted Material
130 Part 1 / Introduction

pain, it is important that patients fully ap- Repeat using


preciate the improvement in their function.
The involved muscle cannot be effec-
parallel sweeps
tively stretched if it is not fully relaxed, and Spray over
full relaxation needs a comfortable, warm, pain pattern
well-supported patient. All the limbs must
be positioned comfortably when the patient
is in the recumbent position. In the seated
Spray skin
position, the patient's pelvis and shoulder-
girdle axis must be leveled by adding an is- over muscle Stretch
chial lift to compensate for any discrepancy muscle
in the size of the two halves of the pelvis. passively
The patient is given a lumbar pad to correct
a stooped posture (see Chapter 4 1 , Section
C). If the operator is extending the patient's
head, the patient is asked to lean the head
back against the operator, who supports it
so that the neck muscles can fully relax.
If the patient is tensely holding the
Anchor arm
breath, the practitioner can make a remark end of muscle
like, "Don't forget to breathe," to remind
the patient to release the tension. As
demonstrated by Basmajian, relaxation is
9

not a passive process, but an active one


that requires learning how to consciously
turn off motor unit activity.
For many patients, the trick is to divert
attention from themselves and to concen- Patient seated relaxed
trate on the support. They must feel the
armrests of the chair supporting their fore- Figure 3.11. Sequence of steps to use when stretch-
arms, or think about the support of the ing and spraying any muscle for myofascial trigger
mattress on which they are lying. For those points, as applied to this partial stretch of the upper
who find this difficult, deep breathing with trapezius muscle. 7, patient supported in a comfort-
the diaphragm is encouraged; then spray able relaxed position. 2, one end of the muscle (light
and stretch is applied to the muscle as the red) anchored. 3, skin sprayed with repeated parallel
patient slowly exhales. For most patients, sweeps of the vapocoolant over the length of the
normal coordinated diaphragmatic (ab- muscle in the direction of pain pattern (dark red dots).
All of the muscle belly and its attachments are in-
dominal) breathing is much more relaxing
cluded. 4, after the first sweep of spray, pressure is
than paradoxical chest breathing.
applied to take up the slack in the muscle and is con-
To effectively stretch a muscle, one end of tinued as additional sweeps of spray are applied. 5,
it must be anchored so that the operator can sweeps of the spray are extended to cover the re-
exert tension on it toward the other end. Fre- ferred pain pattern of that muscle. 6, steps 3, 4 and 5
quently, the patient's body weight or gravity may be repeated 2 or 3 times until the skin becomes
can be used as the anchor. Sometimes, the cold to the touch or when the range of motion reaches
patient can fix one end of the muscle by sit- maximum. Application of heat and then several cycles
of full active range of motion follow. See Figure 3.12
ting on the hand when a scalene or upper
for details of the spray technique.
trapezius muscle is being stretched.
SPRAY PROCEDURE. Figure 3 . 1 1 summa-
rizes the sequence of steps in the spray-and- the muscle as it develops. Initial sweeps of
stretch technique, as applied to the trapez- the jet stream of spray are applied over the
ius muscle. First, the patient must be trapezius muscle and continued over the
positioned comfortably and well supported complete pain pattern to begin releasing
to permit voluntary relaxation. One end of muscle tension before taking up the slack to
the muscle should be anchored so that lengthen the muscle toward its stretch posi-
movement of the head will take up slack in tion. The spray (or ice) is applied in parallel

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Chapter 3 / Apropos of All Muscles 131

sweeps only in the direction of the referred covering first the full length of the muscle
pain. This spray procedure can be repeated and then covering the complete pain refer-
until full muscle length is achieved, or no ence zone. It is important to include cover-
further progress occurs. However, any given age of the attachments at both ends of the
area of skin should be covered only two or muscle as well as the muscle belly.
three times before rewarming. After the The bottle is held about 30 cm (12 in)
skin has rewarmed, several cycles oifull ac- from the skin (Fig. 3.12). Slow, even sweeps
tive range of motion complete one spray- that progress over the skin at about 10 cm (4
and-stretch treatment of that muscle. in)/sec are spaced to provide a slight over-
The valve that seals the nozzle of the Flu- lap of the tracks of wet spray. Two or three
ori-Methane bottle permits only an on-off superimposed sweeps are usually maxi-
application with no intermediate control. mum; the skin must then be rewarmed. Six
Partial opening of the valve results in drip- sweeps over the same skin area, without re-
ping of vapocoolant from the nozzle and de- warming, are too many because that many
flection of the stream. The Fluori-Methane sweeps can cool the underlying muscle
bottle must be held inverted so that the liq- (Fig. 3.13). It is best to spray a slightly
uid will flow from the nozzle. When it is larger area than just the referred pain pat-
held upright, only vapor emerges. The re- tern. No therapeutic harm is done with
placement product that is being developed some additional coverage and it may help
will come in cans that are held upright and to release TrP tension in adjacent muscles.
operated much like a hair spray or paint If the spray is too cold for the patient,
can, and its valve probably will not provide moving the line of spray more quickly across
proportional control either. the skin will help. If the spray is still too
The closer the bottle is held to the skin, cold, the bottle or can should be held closer
the warmer is the stream of vapocoolant on to the skin than the usual 12 inches. If a
impact. One can demonstrate this easily on colder spray than usual is desired, the spray
oneself by how cold the stream feels when distance can be increased to 18 inches.
the bottle is held at various distances from The patient should tell the operator if it
the skin. Notice the sharp pain produced at feels as if the spray should be directed over
the site of frosting when one spot is a line of muscle fibers that are being
sprayed too long (about 6 seconds) and missed. Many times the patient can clearly
causes freezing of the skin. This should be feel the line of muscle tension that needs to
avoided. An instant of frosting is painful
186
be released and can describe or point to
but innocuous. Prolonged frosting can just where the spray needs to be directed to
cause a blister and ulceration. relieve the tension. Vapocooling such an
When the spray is initially applied over overlooked region usually further releases
very irritable TrPs, the skin may be unbear- muscle tension and provides increased
ably hypersensitive to the cold. This initial range of motion. It is remarkable how pre-
distress can be mitigated by using a bottle cisely the skin (that the patient wants to be
saved for its fine-bore nozzle, by holding a sprayed) overlies the abnormally tense
bottle (can) close to the skin, and by waft- muscle fibers. It also is remarkable how the
ing the jet stream across the skin rapidly. muscle tension sometimes melts away as
Many patients who are receiving spray the stream of spray reaches the most dis-
therapy for the first time are severely star- tant portion of the referred pain pattern.
tled by the cold spray if they are not warned When vapocoolant is applied to the
what to expect. The effect of the spray face, the eye on that side should be cov-
should be demonstrated to them first on the ered. If Fluori-Methane spray accidentally
operator's hand, and then on the patient's hits the conjunctiva or the eardrum it is
hand before starting treatment. The jet startling and painful, but not damaging. Pa-
stream of vapocoolant is most effective tients with asthma and other respiratory
when directed at an acute angle to the skin conditions may not tolerate vapocoolant
(approximately 3 0 % ) , not perpendicularly, spray near the face unless the practitioner
and when applied in parallel sweeps along covers the patient's nose with a small cloth
the direction of the muscle fibers. The spray or a hand. Ice stroking (see below) may re-
sweeps are applied in one direction only, place the spray for these patients.

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132 Part 1 / Introduction

Figure 3.12. Schematic drawing showing how the jet direction of the muscle fibers, and progress toward
stream of vapocoolant is applied. Unidirectional the referred pain zone (red stippling). The spray con-
sweeps cover, first, parallel lines of skin over those tainer is held at an acute angle usually 30 cm (12 in)
muscle fibers that are stretched the tightest, then over from the skin, as the spray sweeps over the skin at a
the rest of the muscle and its pain pattern. Sequential rate of about 10 cm (4 in)/sec. Held closer, spray is
sweeps of spray (thick black arrows) should follow the warmer. Farther away, it is colder.

Vapocoolant spray also can be applied STROKING WITH ICE. The sensory and re-
advantageously as a pre-spray preliminary flex effects of a jet stream of vapocoolant
to other manual techniques such as manual spray (such as Fluori-Methane) can be ob-
release, myofascial release, a muscle en- tained also to a considerable degree by
ergy technique, or whenever both hands of stroking with ice. Water frozen in a plastic
the practitioner are required for a manual or paper cup is a convenient form for ap-
release technique. plying the ice. A stirring stick inserted in
Self-spray by the patient with Fluori- the cup before freezing the water provides
Methane can be useful during the transition a convenient handle to hold the ice, or a
period, while the perpetuating factors are well-insulated plastic foam cup can be
still being identified and resolved, and by pa- used. The ice is exposed by tearing back
tients who seem unavoidably prone to reac- part of the cup, and an edge of the ice is ap-
tivation of TrPs and therefore need to be able plied to the skin in unidirectional parallel
to quickly inactivate TrPs for themselves. Pa- strokes, following the spray patterns pre-
tients generally learn quickly to self-spray sented in each muscle chapter. The
their masticatory and calf muscles. However, stroking movements progress slowly, at the
it requires unusually skillful selective relax- same rate as the spray ( 1 0 cm (4 in)/sec).
ation to effectively spray and stretch by one- This application of the sharp edge of ice
self the shoulder-girdle, arm and neck mus- simulates the jet stream of vapocoolant
cles. Fortunately, there are effective alternate spray. The practitioner should hold a small
techniques for self treatment if patient self- cloth ready to blot the skin as needed to
spray is not practical or convenient. prevent melting ice from wetting the skin.

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Chapter 3 / Apropos of All Muscles 133

Sweeps Sweeps
Pectoral M.
(2.2 cm)
Subcutaneous
(0.8 cm)
Skin
surface

Room temp. 24.0C


Rectal temp. 37.5C

Minutes

Spray

Figure 3.13. Skin surface, subcutaneous and muscle sweeps traversed the same path directly over the sen-
temperature effects produced by the correct (A) and sors. When a given skin area was covered only once
incorrect (B) use of vapocoolant spray. Temperatures (A), the fall in muscle temperature was negligible,
were recorded by a tier of three thermal sensors in 0.2C; when the skin and tier of sensors were covered
needles from: (1) pectoral muscle (upper line) at a by six superimposed sweeps (B), the muscle temper-
depth of 2.2 cm, (2) subcutaneous tissue (middle ature dropped more, 1.5C, starting during the appli-
curve) at a depth of 0.8 cm, and (3) skin surface (bot- cation and continuing to drop as the cold penetrated
tom curve). The jet of vapocoolant was applied in one to deeper tissues. This shows the importance of spac-
direction in six even sweeps at 10 cm/sec for a total ing sweeps of spray, of not superimposing them, and
of 2 min (shading). A, (bottom left) sweeps covered of not covering the same area of skin too many times
adjacent parallel skin areas, and only one sweep tra- too quickly.
versed the tier of sensors. B, (bottom right) all six

The skin must remain dry, because RATIONALE FOR VAPOCOOLING AND ICING.
dampness reduces the rate of the change in Properly applied, the vapocoolant or ice
skin temperature produced by the ice- stroking causes a sudden drop in skin tem-
stroking. Wetness also prolongs and dif- perature and has a physical impact that
fuses the cooling effect, which delays re- produces additional tactile stimulation.
warming of the skin. The ice block can be The continuous motion of the stream of
covered with thin plastic as long as the spray causes a continuing barrage of alarm-
stroking edge of the ice is thin and cold. ing impulses to the spinal cord. This input
The clinician should avoid cooling the un- has an inhibitory effect on locally gener-
derlying muscle when stroking with ice, ated pain as demonstrated by its effective
just as when applying vapocoolant spray. analgesic effect in sprained ankles, burns,

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134 Part 1 / Introduction

and ischemic contraction of forearm mus- lease of central TrPs. The value of spray
cles and as indicated schematically in Fig- and stretch may lie in the fact that both
ure 3.14. This neural mechanism helps the kinds of TrPs need to be relieved and that
patient maintain relaxation of the muscle this technique addresses both. Apparently,
when otherwise the degree of stretch being the effectiveness of stretch is improved if
achieved might cause enough discomfort the irritated nociceptors of the attachment
to initiate involuntary protective contrac- TrPs have been desensitized. These consid-
tion of the muscle to prevent further erations need additional experimental in-
lengthening. As described in Chapter 2 vestigation that takes into consideration
Part C, the autonomic nervous system can the difference between central and attach-
significantly influence the intensity of ac- ment TrPs and the relative sensitivity of
tivity of the TrP mechanism at the motor each in a particular patient.
endplate. The spray effect on the skin ap- OTHER USES FOR VAPOCOOLANTS. Ethyl
parently also can inhibit this autonomic chloride spray was initially used for joint
activation at the spinal cord level as illus- sprains; Fluori-Methane is equally effec-
123

trated in Figure 3.14. tive. The sooner the vapocoolant is applied


There are substitute stimuli that also after the sprain, the more fully it relieves
can produce these effects of spray. They in- pain and swelling, thereby permitting imme-
clude the application of sweeps of ice, and diate limited use to restore normal function
the serial prickling produced by running a quickly. Vigorous stretching must be avoided
neurologist's pin wheel along lines that fol- in the presence of torn tissues, but the joint's
low the spray pattern. range of motion should be progressively
reestablished as quickly as recovery permits.
The close reflex relationship between
skin sensation and function of the underly- The vapocoolant spray is remarkably ef-
ing muscle was demonstrated by studies of fective for chilling the skin to numb it for
human withdrawal reflexes to noxious skin painless TrP injections, and for relieving
186

stimuli on both the trunk and lower ex- the pain and preventing the blistering of
tremity. Electromyographic recordings of a thermal burns. It reduces secondary hyper-
gentle, sustained voluntary contraction of algesia, erythema, and swelling as demon-
multiple muscles throughout the region strated in experimental studies. Burns
163 1 7 3

measured increases and decreases in the of second-degree severity that were sprayed
EMG activity induced by shock stimuli to repeatedly (as necessary to keep them pain-
the skin. Activity of muscles beneath the free) did not blister, compared with un-
site of skin stimulation was facilitated, and treated control burns that did blister. The
that of other muscles was generally inhib- spray is applied to the painful area as soon
ited.
63
Early and late responses were iden-
95 as possible after the burn (preferably within
tified. Early responses were likely to cause 5 or 10 seconds) until it stops hurting. It is
movement that terminated weight bearing helpful to keep a bottle in the kitchen by
of that limb, and to remain constant, re- the stove. The spray is reapplied immedi-
gardless of changes in the location of the ately as soon as pain recurs. The number of
stimulus. Late responses were modifiable, repetitions required depends on the sever-
and after several trials, they were adapted ity of the burn. On minor first-degree burns,
to move the limb away from the stimulus. 63 one application may be sufficient to imme-
Skin reflexes of the back and abdomen in- diately and completely eliminate pain.
duced movement away from the stimulus. 95
Vapocoolant spray applied to the
painful regions in acute myocardial in-
The direction of spraying, across the farction can be remarkably effective in re-
muscle and then over the pain pattern, was lieving the pain without changing the
initially determined by subjective testing course of the cardiac pathology. A few
137 1 6 2

on patients by Dr. Travell. She observed the applications can sometimes fully replace
direction of spraying that the patients pre- morphine or comparable analgesics.
ferred and that gave the maximum relief of Vapocoolant spray relieved or delayed
tension and pain. The spray may be espe- pain during experimental ischemic con-
cially effective in quieting attachment TrPs traction of forearm muscles. The same
174

and the stretch may be specific for the re- mechanism may apply to relief of attach-

Copyrighted Material
Chapter 3 / Apropos of All Muscles 135

Cold and impact alarm


Cold spray
Pain Pain

Inhibition
Trigger point

Autonomic effect

Stretched Muscle contraction


Skin muscle

Figure 3.14. Schematic representation of likely neural mechanism. Thus the pain prevents further elongation
pathways that could account for the effectiveness of of the muscle. The sudden cold and the tactile stimu-
vapocoolant applied to skin overlying an active central lus of the stream of vapocoolant spray inhibit the pain
myofascial trigger point (dark red). The trigger point and the reflex motor and autonomic responses in the
limits range of motion of the muscle, and an attempt central nervous system (black bar). This pain-sup-
to lengthen the muscle beyond its limited range of pressing effect now permits more effective relaxation
comfort causes pain. This pain of stretching can in- and gentle lengthening of the muscle. In addition,
duce involuntary muscle contraction to return the spray over muscle attachment trigger points appears
muscle to a comfortable length and can increase sym- to reduce their sensory irritability.
pathetic activity that stimulates the trigger point

ment TrP tenderness. The spray also re- Stretch (Lengthening) Technique. Al-
lieves the pain of bee stings, and is re-
123
most any method that gently stretches
ported as helpful in controlling the pain of (lengthens) a muscle with TrPs and increases
postherpetic neuralgia. 157
its pain-free range of motion is beneficial. In
Some veterinarians and animal trainers a controlled experiment, application of the
81

use vapocoolant spray to relieve myofas- spray-and- stretch technique reduced the in-
cial TrPs, including spot tenderness, in the tensity of referred pain and reduced the sen-
muscles of horses and dogs. ' Because
123 83 84 sitivity of the TrPs being treated. However, a
some animals can react so vigorously to rapid, forceful stretch by itself causes pain,
the cold spray, some veterinarians simply protective contraction, and reflex spasm of
reassure the animal in order to use manual the muscle, all of which hurt the patient and
TrP pressure release and stretch tech- obstruct further elongation of the muscle.
niques to inactivate the TrPs. Drs. Travell Some method of suppressing these reactions
and Simons have found spray and stretch must be added in order to release TrP ten-
of TrPs in dogs and cats very effective if in- sion. Rapid stretch and a "bouncing" stretch
tolerable coldness of the spray is con- are to be avoided; they tend to irritate TrPs,
trolled by application technique, and if the not release them. It is often possible, with a
animal is properly reassured. A veterinar- newly activated or a moderately irritable
ian, Dr. Frank is completing a doctoral
48 TrP, to inactivate it immediately by simply
thesis that demonstrates the effectiveness passively, slowly stretching the muscle
of TrP pressure release techniques for in- without spray. However, the release without
activating myofascial TrPs and restoring spray can be expedited and made less un-
full function in seriously afflicted dogs. comfortable when stretch is combined with

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136 Part 1 / Introduction

simple augmentation maneuvers such as co- the application of vapocoolant spray. This
ordinated exhalation, postisometric relax- second edition of Volume 1 emphasizes a
ation, contract-relax, and reciprocal inhibi- much more gentle stretch and uses the term
tion. It could be very instructive to try this "take up the slack" to identify just enough
approach immediately on yourself the next force to lengthen the muscle to the next bar-
time you activate a TrP, wherever you are. rier (to the onset of resistance to further
Two approaches to stretching the mus- elongation).
cle are available: elongating the muscle by Initially, the operator should gently
moving the joint(s) it crosses or elongating lengthen the muscle until it reaches the bar-
it by direct manual traction applied to the rier (a rapidly increasing resistance to fur-
muscle. Passive movement of the joint(s) ther movement) and then hold that degree
crossed by the muscle was emphasized in of tension. This degree of muscle stretch
the first edition of this volume and can be should not be painful to patients, but they
used for patient self-treatment. This second will feel a degree of muscle tension. As un-
edition also embraces the direct traction hurried, rhythmic, intermittent sweeps of
approach and includes numerous valuable vapocoolant are applied, the gentle pressure
methods for augmenting stretch in addition is maintained to keep the muscle stretched
to spray that include postisometric relax- to the barrier. Maintaining complete relax-
ation, reciprocal inhibition, slow exhala- ation of the muscle being stretched may re-
tion, directed eye movement, and contract- quire concentrated effort on the part of the
relax. These various techniques can be patient, careful monitoring by the operator,
used in many different combinations and and verbal reinforcement as necessary. As
integrated with augmentation techniques. the muscle "gives up" and releases its ten-
The remarkable effectiveness of almost sion, the operator smoothly takes up the
any technique that elongates the muscle and slack to reestablish a new stretch position
restores it to full stretch length can be ex- that again engages the barrier.
plained by the integrated hypothesis (see The effectiveness of this spray-and-
Chapter 2 Part D). The contracture of the sar- release technique is often increased by al-
comeres in the contraction knots of a TrP ternating the application of spray with
must be released in some way. Lengthening postisometric relaxation that is augmented
the contractured sarcomeres of the contrac- by coordinated cycles of respiration. Fol-
tion knots by gentle sustained stretch with lowing each period of contraction and re-
augmentation techniques apparently in- laxation, the muscle is repositioned to en-
duces gradual reduction in the overlap be- gage the new restrictive barrier.
tween actin and myosin molecules and re- Jerking the muscle or sudden loading by
duces the energy being consumed. When the the patient must be avoided during and af-
sarcomeres reach full stretch length, there is ter stretch. Reaching the full normal length
minimal overlap and greatly reduced energy of the muscle is essential for complete in-
consumption. This breaks an essential link activation of its TrPs and relief of their re-
in the energy crisis vicious cycle. The sus- ferred pain and achieving the final few de-
tained increased tension on contractured grees of stretch may be critical.
sarcomeres may cause tearing of the actin at- A skill that for some operators is difficult
tachments to the Z lines as observed ultrami- to learn is "tuning in" to the tenseness of
croscopically by Fassbender. This tearing,
44
the patient's muscles and accurately identi-
when complete, could produce the segments fying the barrier, which occurs at a very
of empty sarcolemma observed by light mi- specific position. Some muscles, especially
croscopy among muscle fibers in muscle large strong ones, may need a little "coax-
biopsies selected at TrP sites in dogs and at
152
ing" at the barrier to get them to release, but
TrP sites in patients with myogelosis. 136
excessive force hurts the patient, results in
STRETCH OF SPRAY AND STRETCH. The key post-treatment soreness, and increases the
to treating TrPs is to lengthen the muscle irritability of attachment TrPs. The opera-
fibers that are shortened by the TrP mecha- tor must ask patients to speak up immedi-
nism. Following publication of the first edi- ately if the procedure becomes painful and
tion of this volume, a rather forceful pas- warn them not to be stoical. The concept of
sive stretch was sometimes associated with "no pain-no gain" does NOT apply here.

Copyrighted Material
Chapter 3 / Apropos of All Muscles 137

After completing full stretch, the return must be done at a slow rate of no more than
to resting length must be smooth and grad- one impact per second and at least one im-
ual, and the patient must not overload a pact every 5 seconds; the slower rates within
muscle by suddenly lifting the weight of this range are likely to be more effective.
that part of the body with it. This procedure may enhance or substitute
If the muscle seems "stuck" short of full for intermittent cold with stretch. Dr. Travell
range of motion, instead of repeating ex- considered it particularly applicable to the
actly the same spray-and-stretch proce- quadratus lumbomm (self-applied), bra-
dure, a number of modifications and alter- chioradialis, long extensors of the fingers,
nate techniques may be tried by (1) and to the peroneus longus and brevis mus-
sweeping the spray over functionally par- cles. It should not be applied to anterior or
allel or neighboring muscles that also may posterior compartment leg muscles because
be shortened by latent TrPs and could be of a possible compartment syndrome if it
"hanging up" the muscle being stretched; caused intramuscular bleeding or swelling.
(2) by asking the patient to help gently to Poststretch Procedures. The most im-
stretch the muscle by contracting its antag- portant poststretch (or postinjection) proce-
onists thereby reaping the additional re- dure is to have the patient actively perform
wards of reciprocal inhibition (however, if three FULL cycles of the range of motion
the patient tries too hard and cocontracts that fully lengthens and fully shortens every
the involved muscle, it can defeat this pur- muscle that was treated. This movement
pose); (3) by trying several cycles of post- helps to normalize muscle function at the
isometric relaxation with directed eye sarcomere level and to reestablish normal
movements and coordinated exhalation, coordination with other muscles of its func-
emphasizing coordinated "abdominal" (di- tional unit. It encourages the patient to use
aphragmatic) breathing; (4) by applying that muscle throughout its full normal range
TrP pressure release; (5) or by having the in ordinary daily activities. At this time, the
patient perform several cycles of the full practitioner should teach the patient how to
active range of motion for that muscle and perform the same movement(s) at home.
then resume spray and stretch. A program of home stretch exercises is
DIRECT STRETCH RELEASE. Muscle stretch important, particularly when postural trunk
by direct application of manual effort is and lower limb muscles are involved. The
identified in this volume as Stretch Re- patient benefits by soaking in a warm bath at
lease. Two hands are used to stretch the home as soon as possible after the spray-and-
muscle by placing the hands near the at- stretch treatment. The patient should avoid
tachments of the muscle and gently sepa- strenuous activity and therefore should NOT
rating them until a tissue barrier is en- go traveling, go sightseeing, or go shopping
countered. This tension elongates the immediately after treatment, but should al-
muscle and the associated connective tis- low the muscles to rest and recover normal
sues. This stretch release is preceded by function. The patient should be instructed
pre-spraying with vapocoolant or stroking in advance to plan appropriately limited ac-
with ice to help release the muscle tension. tivity following treatment. Strenuous swim-
Authors who write about Myofascial Re- ming should be avoided, but it is desirable
lease describe a similar technique but rarely for the patient to perform, in a warm pool,
associate its effectiveness with the inactiva- unstrained stretching and range-of-motion
tion of TrPs, and they do not apply intermit- activities that cause no pain. Thus, "lazy"
tent cold. They use more generalized termi- stretching with the body supported by the
nology and emphasize release of the fascial water is excellent. Specific stretching exer-
tissues rather than release of muscle tight- cises for the patient to do at home are essen-
ness. Release of both tissues is important. tial. They maintain and help to extend the
PERCUSSION AND STRETCH. This tech- range of motion achieved by treatment.
nique begins by passively lengthening the Although no controlled experiments
muscle just to the onset of resistance. The on the effect of heat following TrP ther-
clinician or patient uses a hard rubber mal- apy are known to have been reported, it
let or reflex hammer to hit the TrP at pre- was Dr. Travell's conviction that dry heat
cisely the same place about 10 times. This applied to myofascial TrPs was not as ef-

Copyrighted Material
138 Part 1 / Introduction

fective as moist heat and that post-treat- gentle intermittent muscular contractions
ment muscle soreness is markedly re- may be very effective at normalizing sar-
duced by applying a hot pack for a few comere lengths of involved muscle fibers.
minutes immediately after spray and The action potentials resulting from the
stretch (or injection). Certainly, use of voluntary effort cause contraction of the
heat rewarms the skin for reapplication elongated sarcomeres on both sides of the
of spray or icing of the same area, if contraction knot. This added tension tends
needed. Used at the end of treatment, ap- to pull open the contractured sarcomeres
plied heat leaves the patient feeling in the contraction knot. As soon as this
warm and reassured, which promotes fur- process begins to separate the actin and
ther reduction of muscle tension by en- myosin molecules in the contractured sar-
couraging mental relaxation. The art of comeres, those sarcomeres consume less
medicine can, at times, be as important energy because fewer myosin heads inter-
as the science. act with actin. This tends to relieve the
In this manual, when moist heat is men- energy crisis which could lead to the re-
tioned, it is assumed to be an Hydrocolla- duction of the amount of excessive acetyl-
tor Steam Pack or comparable hot pack. A choline being released. If this analysis is
convenient alternative for home use is a correct, it should be beneficial during each
waterproof electric heating pad covered relaxation period to keep taking up slack as
with dampened flannel. A piece of plastic it develops in the muscle. Chapter 2, Sec-
that covers the exposed side of the pad can tion D explains this etiological mechanism
be tucked in around its edges to protect in detail.
sheets, clothing and hair from getting wet. Postisometric Relaxation (PIR). The
Patients who are instructed to use electric postisometric relaxation (PIR) technique in-
heating pads at home must be warned to use troduced by Karel Lewit" is a modified con-
the low setting; if they fall asleep with the tract-relax method that for most muscles in-
switch on high, they may burn themselves corporates augmentation by coordinated
seriously. A hand-pumped spray bottle of respiration and eye movements. This tech-
water is a convenient device with which to nique has been specifically identified by Le-
dampen the cover of the waterproof heating wit as useful in the treatment of myofas-
101

pad. A thin wet towel wrapped around an cial TrPs with detailed instructions for their
old-fashioned hot water bag has been used treatment in many individual muscles.
effectively in place of a hot pad or pack. The basic concept of PIR is to contract
the tense muscle isometrically against resis-
Voluntary Contraction and tance and then to encourage it to lengthen
Release Methods during a period of complete voluntary re-
These methods all employ some degree laxation. Whenever possible, gravity is
of voluntary (active) contraction followed used to "encourage" release of the muscle
by relaxation. A reduction in muscle stiff- tension and take up the slack. For PIR to be
ness (tension) following the contraction effective, the patient must be relaxed and
provides an increase in range of motion the body well supported. The muscle is pas-
during the period of relaxation. This ap- sively and gently lengthened to the point of
proach is the basis for some of the sim- taking up the slack (reaching the barrier or
plest, most available, most popular, and the point of initial resistance). If this initial
most effective techniques for inactivating positioning causes pain, either the extent of
myofascial TrPs. Included among them are the movement has been excessive or the pa-
contract-relax, postisometric relaxation, a tient has actively resisted the movement.
combination of postisometric relaxation Postisometric relaxation begins by hav-
and reciprocal inhibition, hold-relax, and ing the patient perform an isometric con-
muscle energy techniques. traction of the tense muscle at its maximum
The new understanding of the nature of pain-free length, while the clinician stabi-
TrPs provides a rationale as to why this ap- lizes that part of the body to prevent mus-
proach is so effective. Since the primary cle shortening. Contraction should be
TrP etiology appears to be a contraction slight ( 1 0 - 2 5 % of maximum voluntary
knot at a dysfunctional motor endplate, contraction ). After holding this contrac-
101

Copyrighted Material
Chapter 3 / Apropos of All Muscles 139

tion for 3 - 1 0 sec, the patient is instructed ation and release of muscle tension when
to "let go" and to relax the body com- stretching a muscle to inactivate its TrPs.
pletely. During this relaxation phase, the To invoke reciprocal inhibition, the mus-
clinician gently takes up any slack that de- cles that oppose the muscle being stretched
velops in the muscle, noting the increase in are voluntarily contracted to actively assist
range of motion. Care is taken to maintain the stretching movement. Thus, the muscle
the stretched length of the muscle and not to be stretched is reciprocally inhibited.
let it return to a more neutral position dur- This method can be used alone to aug-
ing subsequent cycles of isometric contrac- ment a simple stretch, or it can be com-
tion and relaxation. 101
bined with other techniques such as spray
Combining PIR with reflex augmentation and stretch. Apparently, this neuromuscu-
of relaxation 100,101
greatly enhances its ef- lar mechanism for releasing TrP tension in-
fectiveness. Augmentations include the use volves more than inhibition of alpha mo-
of coordinated respiration and eye move- torneuron activity. The tension-release
ments as described below. Reciprocal inhi- mechanisms also may be dependent on au-
bition can also be incorporated to enhance tonomic effects that are related to the inhi-
release of tight muscles. The effectiveness bition of spontaneous electrical activity
of the contract-relax technique used in (SEA) and spike activity of TrPs during ex-
postisometric relaxation was demonstrated halation, and their augmentation by in-
experimentally as preisometric contrac- halation and mental stress.
tion. These are two different names for es-
110
Contract-relax. The principle of con-
sentially the same technique. In this con- tract-relax appears in many forms with
trolled study, the authors demonstrated
110
many names throughout the musculoskele-
that hamstring muscle stretch which was tal treatment literature. The "muscle energy
limited by pain increased significantly (p < technique" is highly regarded by osteo-
0.01) following a 6 second voluntary con- pathic physicians and is described under a
traction of the muscle. The authors were separate heading below. The term contract-
perplexed by the fact that measured EMC relax, as originally taught by Knott and
was essentially unchanged before and after Voss was recommended for treatment of
90 1 8 0

stretch under all conditions, because they marked limitation of the range of passive
had accepted the common assumption that motion with no active motion available in
increased resistance to stretch arose from the muscle opposing the tight muscle. As
motor unit activity. Their results substanti- they described it, contract-relax employed
ate our understanding that much increased maximum contraction in a pattern move-
stiffness of painful muscles is due to the ment followed by relaxation of the tight
viscoelastic properties of the muscle which muscle to permit active shortening of the
can be strongly influenced by the tension of opposing weak muscle. Release of tightness
the taut bands that are induced by TrPs. 151a
in that muscle permitted improvement in
A good way to become skilled in the use the range of motion. Through the years, the
of PIR is to practice it on oneself to relieve exact meaning of the term has become some-
muscle stiffness associated with prolonged what diffuse. There are now numerous vari-
immobilization of muscles. This stiffness ations (and applications) of the basic princi-
becomes increasingly apparent with ad- ple that muscle tension is reduced im-
vancing age, when it becomes critically im- mediately following voluntary contraction.
portant to maintain full range of motion of In this volume, contract-relax used for
muscles, especially of postural muscles, in treating TrPs is a gentle, voluntary, mini-
order to maintain normal mobility mally resisted contraction of the tight mus-
throughout the body. cle. The contraction is followed by relax-
Reciprocal Inhibition. Reciprocal inhi- ation to permit passive elongation of the
bition is not only an involuntary spinal- muscle to a new stretch length. Contract-
level reflex but is effective when a contrac- relax is the basic procedure in the PIR
tion is initiated at the cortical level. When method of Lewit. 101

one muscle is activated, its antagonist is re- Hold-relax. Hold-relax is a variant of


flexly inhibited. The use of reciprocal inhi- the contract-relax technique that is not
bition is valuable for augmenting relax- commonly used for treating TrPs, but may

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140 Part 1 / Introduction

be employed when there is no joint move- quate treatment of somatic dysfunction re-
ment desired during or after the procedure. lieves the TrPs. The concept of TrPs and
It consists of isometric contraction of the many examples in specific muscles are
tight muscle followed by relaxation, but well described by Kuchera and Kuchera 94

not by elongation of the tight muscle. in a separate chapter that emphasizes their
When used in the treatment of muscles importance.
with TrPs, hold-relax is commonly com- There is much to be gained if practition-
bined with manual techniques applied di- ers identify the active TrPs and any associ-
rectly to the muscle, such as deep stroking ated joint dysfunction so that each can be
massage and TrP pressure release. treated specifically with an appropriate
Muscle Energy Technique. Muscle en- technique. Often, the appropriate tech-
ergy techniques are closely related to tech- nique simultaneously (and serendipi-
niques used for release of TrPs and there- tously) corrects both conditions.
fore are of considerable interest. They are
osteopathic procedures that by definition 57 Trigger Point Pressure Release
"are used to mobilize joints in which The new term trigger point pressure re-
movement is restricted, stretch tight mus- lease replaces the previous term and con-
cles and fascia, improve local circulation, cept of ischemic compression. TrP pressure
and balance neuromuscular relationships release is known to be effective at central
to alter muscle tone." TrPs where there is a rationale for its use.
Kuchera and Kuchera clearly identify
94 However, its value when applied to attach-
three muscle energy techniques. The first is ment TrPs needs to be evaluated experi-
isometric contraction, which is the one mentally. Clinical evidence and the nature
most commonly used, generally for im- of TrPs indicate that, when applying digital
proving restricted motion at an articula- pressure to a TrP to inactivate it, there is no
tion. This technique corresponds to the need to exert sufficient pressure to produce
contract-relax method described in this ischemia . Since the core of the TrP already
manual for restoring restricted motion at an is suffering severe hypoxia surrounded by
articulation (caused by muscle tightness increased tissue oxygen tension, there is no
due to TrPs). The second technique, iso- reason to expect that additional ischemia
tonic contraction, is commonly identified as such would be helpful. Treatment needs
as a concentric (shortening) contraction, to release the contractured sarcomeres of
that in this case is resisted by the clinician. the contraction knots in the TrP.
The third muscle energy technique, isolytic The technique that was previously de-
contraction, is the same as what is com- scribed as ischemic compression is essen-
monly identified as an eccentric (lengthen- tially what Prudden called myotherapy, 133

ing) contraction, but again is resisted by the and was adopted by a group of practition-
clinician. These techniques involve volun- ers of this technique who identified them-
tary muscle contractions by the patient selves as myotherapists.
against a specific counterforce provided by Instead of ischemic compression, we
a clinician, whereby the patient, not the recommend the application of TrP pressure
clinician, provides the corrective force. release. This technique is less vigorous
Since two of the four stated objectives than ischemic compression and employs
of muscle energy recognize the importance the barrier release concept. The pressure
101

of correcting muscular abnormalities in or- release approach seems to be equally or


der to effectively mobilize restricted more effective clinically and is NOT likely
joints, many of the procedures effectively to produce appreciable additional is-
stretch the trouble-making tight muscles chemia. This approach is tailored to the
with their associated fasciae. In many needs of the individual's muscles, is more
cases, the resisted patient contractions ef- "patient friendly", and therefore is more
fectively produce the contract-relax ma- likely to be used by the patient. The patient
neuver. Since many of these maneuvers learns what optimal pressure feels like for
would therefore be effective for the treat- subsequent self-treatment. The barrier re-
ment of TrPs, it is not surprising when lease approach, however, does require a
Greenman observes that frequently ade-
59
higher order of manual skill.

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Chapter 3 / Apropos of All Muscles 141

To apply TrP pressure release, the clini- Shiatzu. Shiatzu and acupressure
77 28

cian lengthens the muscle to the point of are terms used to describe a technique
increasing resistance within the comfort comparable to the old concept of is-
zone and then applies gentle, gradually in- chemic compression but are not concep-
creasing pressure on the TrP until the fin- tually related to TrPs. However, the de-
ger encounters a definite increase in tissue scriptions of the treatment strongly
resistance (engages the barrier). At that suggest that TrPs are often the painful
point the patient may feel a degree of dis- condition that is being treated with shi-
comfort but should not experience pain. atzu. These treatments are promoted for
This pressure is maintained (but not in- other conditions in addition to the relief
creased) until the clinician senses relief of of pain. Shiatzu and acupressure are
tension under the palpating finger. The pal- philosophically quite different from the
pating finger increases pressure enough to concept of myofascial TrPs, but in prac-
take up the tissue slack and to encounter tice many of the treatments appear quite
(engage) a new barrier (the finger "follows" similar.
the releasing tissue). The clinician again
maintains only light pressure until more of Deep Stroking (and Other) Massage
the muscle tension releases ("lets go") un- The technique of deep-stroking massage
der the finger. During this period the clini- (which is also called stripping massage)
cian may change the direction of pressure was historically the first widely accepted
to achieve better results. This process of technique for treating fibrositis (many de-
TrP pressure release can be repeated for scriptions of which fit myofascial TrPs ) 142

each band of taut muscle fibers in that and was widely practiced at the beginning
muscle. The virtue of this technique is that of the 20th century. This method is proba-
it is painless and imposes no additional bly the most effective way to inactivate cen-
strain on any attachment TrPs, and thereby tral TrPs when using a direct manual ap-
avoids aggravating them. This digital tech- proach, and it can be used to treat TrPs
nique is particularly well suited to muscles without producing excessive joint move-
like the infraspinatus and serratus muscles ment. The rationale is clear.
that are relatively thin and overlie bone.
Deep-stroking massage is effective in the
The effectiveness of this approach can hands of clinicians who are skilled in its
often be enhanced by including supple- use. Massage should be applied with close
mental techniques. These additional tech- attention paid to restrictive barriers and
niques should not cause pain either. In ad- their release. The patient must be positioned
dition to simply taking up the slack in the comfortably so that the muscle to be treated
muscle before beginning the procedure, the is completely relaxed and lengthened with-
entire muscle can be maintained at a slack- out pain to the point that there is no residual
free length throughout the process. Release slack in the muscle as a whole. The skin
of the TrP may be further enhanced by oc- should be lubricated if the subcutaneous tis-
casionally performing a contract-relax ma- sues are tense and immobile. The thumbs or
neuver alternated with reciprocal inhibi- a finger of both hands are placed so they trap
tion. The goal is to release the contraction a taut band between them just beyond the
knots in the TrP and release the tension band's TrP. As the digits encounter the
they cause in the muscle fibers comprising nodularity of the TrP that is caused by its
the taut band. contraction knots [see Fig. 2.25), pressure is
This barrier release approach may fail to exerted to engage the restrictive barrier. The
afford relief because (1) the TrP is too irri- digits progress no faster than tissue release
table to tolerate any additional mechanical occurs as the nodularity "gives" to some ex-
stimulation; (2) the operator misjudged the tent. The purpose of the pressure directed
pressure required to reach the barrier; (3) along the length of the taut band is to elon-
the operator pressed too hard, causing pain gate the maximally shortened (contrac-
and autonomic responses with involuntary tured) sarcomeres of the contraction knots
tensing by the patient; and (4) the patient to release their tension. The stroking mas-
has perpetuating factors that make the TrPs sage should be continued along the length of
hyperirritable and resistant to treatment. the remaining taut band beyond the TrP to

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142 Part 1 / Introduction

the attachment of the band, helping to re- strumming finger runs across the taut bands
store the stretched sarcomeres to normal at the level of the TrPs over the nodules
length by continuing to exert traction on the from one side of the muscle to the other.
shortened contraction knots. This also helps The operator's finger pulls perpendicularly
to relieve the taut band tension and any en- across the muscle fibers rather than along
thesopathy in the attachment region. the length of the fibers. This method ap-
The next massage stroke should go in plies specifically to central TrPs, which are
the reverse direction starting on the same near the middle of the muscle belly.
taut band but on the other side of the Strumming consists of pulling the finger
nodule to further release the contractured across the middle of the muscle fibers
sarcomeres. This stroke now helps to re- slowly until the nodule at the TrP is en-
lease the abnormal tension on the other countered. Light contact is maintained at
half of the taut band and at the other mus- that point until the operator senses tissue
cle attachment. release under the finger. The finger contin-
Excessive pressure or speed of movement ues pulling across the nodule in steps as
is likely to rupture contraction knots, de- tension releases. Relaxed deep coordinated
stroying the corresponding motor endplates abdominal (diaphragmatic) breathing by
as functional structures and increasing the the patient facilitates general relaxation
painfulness of the procedure. If the proce- during the exhalation phase.
dure were to rupture the sarcolemmal mem- This technique is particularly applica-
brane at the contraction knots, the muscle ble to a few muscles like the masseter and
fiber would spill myoglobin. In addition to medial pterygoid, which permit direct pal-
the effect of stretch, this rupture process pation of the muscle through only a thin
may be one reason for the effectiveness of layer of mucosa rather than through thick
vigorous application of deep massage, as cutaneous and subcutaneous tissues.
suggested by the following experiments. Friction Massage. The purpose of fric-
Danneskiold-Samsoe and c o - w o r k e r s
4041
tion massage is to mobilize the superficial
found that application of deep massage to tissues over the underlying structures in
the "tender nodules" of "fibrositis" or of order to improve their mobility. This cor-
11

"myofascial pain" (which were consistent responds to the technique of skin rolling to
with the clinical characteristics of TrPs) re- relieve the subcutaneous tightness of pan-
lieved the signs and symptoms of most pa- niculosis (Section 8, above) and is also an
tients after 10 massage sessions. Those ex- accessory technique. It is not considered to
periencing pain relief had a transient be a specific TrP therapy.
elevation of serum myoglobin levels fol- Ice Massage. Ice massage can be ap-
lowing the initial therapy sessions, but not plied in two different ways with different
after the final sessions when symptoms had objectives. One method is the intermittent
been relieved and the tenderness and ten- use of ice in lieu of the vapocoolant spray as
sion of the nodule being massaged had sub- a variation of spray and stretch, as described
sided. The results of this research effort are earlier in this chapter. The other method is
illustrated in Figure 2.29. Control massage the local application of cold for pain relief,
of normal muscle did not appreciably in- which is considered later in this section.
crease serum myoglobin. This finding sug- Periosteal Therapy. Periostbehandlung
gests that the muscle fibers of TrPs and their (periosteal therapy) is essentially an unre-
contraction knots are more susceptible to lated rhythmic massage technique that is
mechanical trauma than uninvolved fibers applied to bony prominences of the body 179

and that local tissue manipulation can in- and should not to be confused with myo-
activate the symptom-producing TrPs. fascial TrP therapy. Waves of pressure are
This technique is not the deep friction applied for 2-4 min; each half-wave of in-
massage of Cyriax, which he applied
37 creasing or decreasing pressure lasts 4-10
across the long axis of the muscle fibers. sec. The finger, thumb, or knuckle pressure
The Cyriax technique is more closely re- is applied to the periosteum near painful
lated to strumming that is described below. areas. We agree with the authors that the
179

Strumming. Strumming is similar to mechanism of pain relief in this case is dis-


deep-stroking massage except that the tinctly different from that of Druckpunkte

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Chapter 3 / Apropos of All Muscles 143

(pressure points), which usually have been appeared to be purely bony locations where
described in terms that are compatible with a muscular attachment would be unlikely.
myofascial TrPs. Lewit considers Jones points as tender
101

spots in soft tissue. These tender spots are


Indirect Techniques often found at muscle attachments where
The osteopathic technique for releasing enthesopathy could occur and cause the
tender points described by Jones in 1 9 8 1 85
tenderness.
in terms of strain and counterstrain (the If these tender points of Jones are often at
term still used by osteopathic physicians )53
the same location as myofascial attachment
has now evolved into a 1997 book on posi- TrPs, it should be simple to verify. First, one
tional release therapy by a chiropractor could note if a central TrP is present in a taut
and a physical therapist that is predi-
39
band of muscle fibers that attach where the
cated on the osteopathic paradigm of so- Jones tender point has been located. If so, it
matic dysfunction. This indirect technique would be of interest to measure the irritabil-
uses body positioning for releasing tender ity of both the central and attachment TrP
points which are conceived of as foci of sites before and after treatment. The central
constriction in the myofascial tissues. The TrP could be treated by trigger-point therapy
tender points they describe appear to have (e.g., by injection or local pressure release
little relation to fibromyalgia tender techniques), or the Jones point could be
points, but may fit into the concept of myo- treated by positional release therapy, orboth
fascial attachment TrPs. The authors 39
treatments could be applied to a third group
make no clear distinction between fi- of subjects. Each therapeutic approach may
bromyalgia tender points and myofascial have advantages that are complementary.
TrPs.
Kuchera and Kuchera characterize
94 Myofascial Release
Jones's strain-and-counterstrain technique Myofascial release is a system of therapy
clinically as follows: About 146 tender that combines principles and practice from
points can be identified. The muscle pain, soft tissue technique, muscle energy tech-
weakness, and subjective hurt is on one as- nique, and inherent force craniosacral tech-
pect of the body and the Jones tender point nique. It includes a highly subjective
59

is characteristically on the other aspect of transfer of energy from the therapist to the
that part of the body, usually in a muscle patient. It is strongly promoted by John
141

antagonist. At the position of comfort, the Barnes and practiced by numerous physi-
8

point becomes flaccid on repeated testing cal therapists. It is another example of a


and the position is one of mild strain. The clinical practice that is sometimes effective
position of comfort generally is held for up for myofascial TrPs, but the patient is not
to 90 seconds, until release is detected by examined for them, so the extent to which
gentle intermittent test palpations, then the the patient is benefitting from relief of TrPs
body parts are returned SLOWLY to their goes unrecognized. Unfortunately, any ad-
neutral position. Poor posture may cause ditional benefit of specifically addressing
recurrence of these "myofascial points" the patients' remaining TrPs is forfeited.
that are presumed to be caused by some
form of functional strain.94
Accessory Techniques
In the original book on strain and coun- A number of techniques can assist and
terstrain by Jones, 85
he illustrated and supplement the specific TrP therapies de-
named the location of 65 tender points. Most scribed above. Controlled respiration and
of the names identified bony landmarks that directed eye movement are two techniques
did not identify what muscle(s) attached at of great value and are applicable to many
that location. Of the 65 points, 9 were iden- of the TrP release techniques. The others
tified at the attachment region of a named have more limited application.
muscle. Forty-four points were located ei- Phased Respiration. As one slowly
ther at the region of a muscular attachment exhales, muscles throughout the body
where one might find an attachment TrP, or, generally tend to relax. With inhalation,
occasionally, at the belly of a muscle where muscular activity is facilitated. One
101

a central TrP might be located. Twelve points noteworthy exception is the relaxing effect

Copyrighted Material
144 Part 1 / introduction

that a deep inhalation (yawn) has on the direction. This applies to lifting the head
jaw-closing mandibular elevator muscles. and torso as well as to stooping and trunk
Since exhalation encourages relaxation of rotation. Direction of gaze does not facilitate
most muscles, it can be very helpful to co- movement toward side b e n d i n g . How-
100101

ordinate an exhalation phase of respiration ever, looking up does facilitate straighten-


with the release phase of most muscle- ing up from the side-bent position. These
stretching techniques as described. To be eye movements should not be exaggerated,
effective, respiration must be sufficiently because a maximum-effort movement may
slow and deep. 101
Effectiveness also im- have an inhibitory effect. 100,101

proves if the patient uses coordinated This phenomenon is directly applicable


diaphragmatic (abdominal) breathing. Ab- for enhancing stretch-type release tech-
dominal breathing is particularly impor- niques used to release TrP tightness in mus-
tant when attempting to relax neck mus- cles. By looking in the direction of move-
cles. Paradoxical breathing should be ment needed to release specific muscle
avoided; it is inefficient and may send tightness, the release process is augmented.
mixed messages to the autonomic nervous The mechanism for this effect may be
system as to whether the individual is in- similar to the mechanism for the influence
haling or exhaling. that respiration has on the electrical activ-
When phased respiration is used in con- ity in active loci of TrPs, which was noted
junction with a technique such as contract- above. However, the direction of gaze was
relax that involves muscle contraction and not specifically tested in those experiments.
relaxation phases, the muscle contraction It should be tested since eye motion and
phase should be synchronized with inhala- respiration are related. Lewit et al. clearly
103

tion and the relaxation phase with exhala- demonstrated a significant synkinetic effect
tion. Patients who have difficulty adopting between the rate of alternating the direction
a slow, deep respiratory pattern may be of upward-downward gaze and the respira-
helped by pausing, breathing naturally sev- tory rate. The rate of respiration followed
eral times, and relaxing between each cycle the rate of eye motion over a 2:1 range.
of contraction-relaxation. Skin Rolling. The manual technique of
For the torso, inhalation facilitates mov- skin rolling as described in Chapter 2 of this
ing toward the neutral erect position and volume with regard to panniculosis has
exhalation facilitates relaxation as one been found to be useful clinically both for
leans away from an erect posture. Leaning diagnosis and treatment of this condition.
forward is naturally associated with exha- Therapeutically, skin rolling seems to work
lation and relaxation. best over the shoulders and upper back and
The following experimental evidence least well over the buttocks. The nature of
108

suggests a significant relation between res- panniculosis and the reason that relieving
piration and TrP activity. While conducting the panniculosis apparently helps to re-
a study of active loci in human TrPs, the
151 lieve TrP activity remain speculative. They
authors confirmed a previous observation deserve to be investigated further.
of another investigator. In many subjects,
76
Biofeedback. Biofeedback alone is not
spike activity associated with SEA of the specific myofascial TrP therapy, but it can
TrPs in the upper trapezius muscle was be helpful in two ways. First, it can be used
turned on by normal resting inhalation and to help the patient avoid unnecessary in-
was turned off by exhalation. The authors creased resting muscle activity which con-
also noted a corresponding waxing and tributes to TrP irritability and activation.
waning in the amplitude of SEA. The effect Many patients express their anxiety and
was augmented by exaggerated respiration. frustration through general muscular ten-
Neither set of potentials represented nearby sion, which abuses their muscles. Biofeed-
motor unit potentials or distant ones. back training applied to the problem mus-
Directed Eye Movement, Clinical obser- cles can help these patients to become
vations have shown that the direction of aware of unnecessarily sustained activation
gaze facilitates the movement of the head of their muscles. It can be an effective tool
and trunk in the direction of the patient's for teaching them how to recognize and
gaze and inhibits movement in the opposite control the excess tension. Meditation prac-

Copyrighted Material
Chapter 3 / Apropos of All Muscles 145

ticed for this same purpose can enhance the differences in the response of some patients
patient's ability to reestablish muscular re- to the application of heat versus cold to the
laxation and emotional tranquility. TrP region deserves critical investigation.
Another, potentially much more impor- Iontophoresis and Phonophoresis. Ion-
tant, application of biofeedback is the use tophoresis is the process of using an elec-
of surface EMG for identifying muscular tric potential of low voltage direct current
incoordination, referred inhibition, and re- to move a solute of ions across a mem-
ferred spasm caused by TrP activity. Used brane. In the case of TrP therapy, the move-
as feedback, surface EMG can be an impor- ment is through the epidermis and dermis
tant tool in retraining the affected muscles into underlying tissues. The degree of pen-
to normal muscle balance and function fol- etration depends partly on the barrier
lowing inactivation of the responsible TrPs properties of the tissues to the penetrating
( See Chapter, 2 Part B, Surface EMG). substances. The maximum depth of pene-
Heat and Cold. Heat applied to the sur- tration is probably about 1 cm and the
face of the skin penetrates poorly. It causes direct current has a caustic and sclerotic
reflex dilatation of skin blood vessels, in- effect that must be considered. Ion-
140

creasing circulation that quickly removes tophoresis has been used to deliver ionic
the heat and distributes it throughout the drugs, including hydrocortisone, lido-
rest of the body. Thus, the only effect it caine, and salicylate. The use of recombi-
would be likely to have with regard to un- nant DNA technology promises the pro-
derlying TrPs would be a general increase duction of protein and peptide drugs
in circulation in that part of the body. It amenable to this therapy. 153

would also tend to make the patient feel The effectiveness and any advantages of
cozy and warm, helping in relaxation. this modality for medicating attachment
On the other hand, application of surface TrPs would need to be established by ade-
cold tends to penetrate progressively more quately controlled experiments. Usually,
deeply into the underlying tissues the injecting the medication directly into the
longer it is applied. As the cold penetrates, desired location is more direct, reliable,
it causes vasoconstriction which reduces provides better control of the dose, and ex-
the heat that would have been supplied by poses only the tissue to be treated to the
the local circulation. The cold numbs the medication. However, injection does in-
tissues, which is why application of cold volve instrumental invasiveness.
can be effective for relief of neurogenic pain. Phonophoresis employs therapeutic ul-
Immediately following major trauma trasound to drive the substance through
such as fracture, dislocation, or whiplash the dermis. This medium is commonly
injurycold packs should be applied to used to treat musculoskeletal conditions
the traumatized muscles to reduce pain using hydrocortisone, lidocaine, or as-
and tissue swelling without regard to TrPs. pirin. A controlled study demonstrated
140 26

When this acute phase has passed in a few effective penetration of dexamethasone
days, TrP therapy should be considered. and hydrocortisone acetate by ultrasound
In the past, clinicians have found that for into the subcutaneous tissue, but not into
relief of TrP distress many patients pre- submuscular tissue. The details of tech-
ferred the application of heat rather than nique can be critical to success. 87

cold. However, some patients preferred Although no scientific papers are known
cold applications to TrPs for relief of their to have been published on the usefulness
myofascial pain. This seemed contradictory of either of these techniques for the treat-
and enigmatic. It may be that central TrPs ment of TrPs, some clinicians have found
are more responsive to warmth and that at- them useful for the administration of
tachment TrPs are more responsive to cold. steroids into an active TrP area. Since the
No controlled study is known that has injection of steroid into central TrPs rarely
explored the effectiveness of heat versus appears to prove more beneficial clinically
cold when applied to TrPs as therapy. than nonsteroid needle techniques, it is un-
There is a possibility that cold applied to likely that attempts to medicate the central
attachment TrPs would reduce the sensory TrP region using these modalities would be
hyperirritability of the enthesopathy. The beneficial. However, steroid application to

Copyrighted Material
146 Part 1 / Introduction

attachment TrPs may be a different story, utes, the intensity is gradually increased
and the beneficial effects observed by clin- with frequent queries as to patient sensa-
icians may have been the result of steroid tions, until the intensity has been in-
treatment of attachment TrPs. The hazards creased to, but not beyond the original pain
of steroids also must be fully considered. threshold level. Usually, the patient no
Since painfully active attachment TrPs longer feels pain at this level of stimulation
limit the usefulness of stretch techniques, a and the TrP is less tender and irritable. 128

noninvasive method for markedly reduc- The Medco-sonolator combines ultra-


ing their irritability could be quite useful. sound with electrical stimulation of suffi-
The advantages and disadvantages of cient intensity so that the increased current
phoretic penetration of steroids as com- flow through the point of low skin resis-
pared to injection need to be investigated tance (that frequently, but unreliably occurs
with regard to this modality. over the TrP) generates a prickly sensation.
Microamperage. Although the use of This technique may be helpful in finding a
microamperage therapy for myofascial TrPs possible location of a TrP for those who
has been enthusiastically promoted by man- have not yet mastered the necessary palpa-
ufacturers, we know of no well controlled tion skills. This combination therapy has
experimental studies that demonstrate effi- been reported to be helpful clinically. 20,129

cacy, nor is there a convincing rationale at The mechanism by which ultrasound


this time for its use in the treatment of TrPs. could effectively inactivate TrPs is un-
The whole field of cutaneous procedures to known. The ultrasound undoubtedly
treat underlying TrPs needs critical investi- causes tissue heating, which could aggra-
gation to resolve whether there is an vate the local energy crisis by increasing
unidentified mechanism operating, or other metabolic rate at the TrP and thereby stress
factors are responsible for whatever favor- key TrP tissues to the point of no return. The
able clinical results are observed. 150
heat may have more specific effects to in-
hibit the release of acetylcholine and reduce
Modalities endplate dysfunction. The mechanical exci-
Therapeutic Ultrasound. Clinically, tation of tissues at the molecular level by ul-
many therapists find the application of ul- trasound may play a role in these processes.
trasound an effective means of inactivating Well-designed, well-controlled experi-
TrPs. Unfortunately, no controlled study mental studies on the effect of ultrasound
specific to its effectiveness on TrPs is on competently diagnosed active TrPs are
known. Ultrasound transmits vibrational needed to fill this challenging void in our
energy at the molecular level, approxi- knowledge.
mately 5 0 % of which reaches a depth of 5 High Voltage Galvanic Stimulation.
cm. These vibrations not only generate heat The waveforms characteristic of this kind
within the tissue, but can have additional, of electrical stimulation are relatively high-
but less clearly understood, chemical ef- frequency brief spikes of at least 150 volts
fects due to intense molecular excitation with very rapid rise times and no duration
that may play a role in TrP applications. of peak-voltage. This form of stimulation is
The clinical use of therapeutic ultrasound selectively more effective on large diame-
is well summarized by Santiesteban. 140
ter motor nerves than on smaller diameter
One clinically successful technique sensory nerves, which makes it better tol-
starts with a setting of 0.5 watt/cm and 2 erated than square-wave potentials as a
uses a slow dwell technique with a circular way of stimulating muscle nerves electri-
motion that completes one circle in 1 or 2 cally. A description of the parameters of
140

s e c . The circle is tight enough to provide


193 various types of electrical stimulation is
a small overlap over the TrP in the center of presented by Kahn. 86

the circle. In another technique that em- The use of high voltage (and high fre-
ploys essentially the same movement of quency) galvanic stimulation is common
the applicator, the power is first increased practice among some therapists as a pri-
to the threshold pain level (approximately mary modality for the treatment of TrPs. It
1.5 watt/cm ] and then reduced to one-half
2
sometimes is used as preliminary treat-
of that intensity. Over the next 2 to 3 min- ment and more commonly is applied fol-

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Chapter 3 / Apropos of All Muscles 147

lowing stretch and/or injections. Clinical


134
to achieve increased mobility and a degree
experience suggests that one effective tech- of muscle stretching that otherwise might
nique is to increase the intensity of cyclic not occur.
(not continuous) electrical stimulation to Stimulation is sometimes applied along
the point of gentle muscular contractions. the spine, or over acupuncture points, or
Rachlin recommends electrical stimu-
134
over reference zones where the pain is felt,
lation routinely following TrP injection or over the TrPs where the pain originates.
and needling. He describes using an inter- Generally, electrode placement is an em-
mittent current (sinusoidal, surged, or piric matter that depends on what posi-
ramped) for 15 minutes. If spasm were pre- tioning provides the patient with the most
sent, he recommends preceding the inter- relief. Stimulation over the central TrPs
mittent current with 10 minutes of tetaniz- may give different results than stimulation
ing current to fatigue the muscle in order to over the corresponding attachment TrPs.
achieve more complete relaxation follow- This could be explored systematically.
ing stimulation. If the patient rejects the Drug Therapy. In the management of
use of electrical stimulation (because of patients with myofascial pain syndromes,
discomfort), he suggests moist heat as a one can consider the role of drugs with re-
substitute. spect to pain relief, muscle relaxants,
Muscle spasms can be released by appli- sleep, and trouble-making drugs.
cation of high frequency galvanic stimula- PAIN RELIEF. No nonnarcotic medica-
tion, if the muscle is continuously stim-
140
tion is known that is specific for the pain
ulated to exhaustion. 112
generated by central myofascial TrPs. The
The application of intermittent or cyclic new understanding of the pathophysiology
stimulation sufficient to cause gentle mus- of TrPs opens the door to identifying drugs
cle contraction and then relaxation may be that specifically inactivate the TrP mecha-
considered an involuntary (effortless) form nism. The specific effectiveness of drugs
of contract-relax, which, when done volun- on attachment TrPs is unexplored. Since
tarily by the patient, is very effective. The the enthesopathy causing the pain and ten-
electrical stimulation allows the patient to derness at that location is a reaction to the
feel contraction of the appropriate muscle, stress of the taut band on attachment struc-
and this assists the patient to learn an ap- tures, it is likely that some anti-inflamma-
propriate voluntary contraction for a home tory drugs, including steroids, may provide
exercise. effective relief if administered locally on
site in effective dosage.
Pain Relief Available nonsteroidal anti-inflamma-
Transcutaneous Electrical Nerve Stimu- tory drugs given orally afford little relief
lation. Transcutaneous electrical nerve from pain originating in central TrPs. How-
stimulation is well established as one means ever, they can be very helpful for alleviat-
of obtaining temporary, sometimes pro- ing the postinjection soreness that is likely
longed, pain relief. Although it is not a treat- to peak a day or two after injection, espe-
ment modality for myofascial TrPs, it is an cially when dry needling without a local
accessory technique. The electrical stimulus anesthetic has been used. This alleviation
consists of relatively low-voltage square reflects the fact that the tissue injury of
waves of variable polarity, duration and fre- needling induces an inflammatory reaction
quency. This stimulus is not suitable for that is fundamentally different from the
muscle stimulation because it tends to stim- pathophysiology of the TrP itself.
ulate small sensory nerves more readily than When a nonsteroidal anti-inflammatory
the larger motor nerves, and therefore is rel- drug was injected in high concentrations at
atively more painful than high voltage gal- the TrP, its prostaglandin-suppressing ac-
vanic stimulation. Santiesteban reviewed 140
tion seemed to help relieve pain originating
the treatment parameters and clinical appli- from TrPs. Prostaglandins are likely one of
49

cations of this kind of electrical stimulation. the more important agents involved in the
The nonspecific relief of pain afforded sensitization of nociceptors in a TrP. This
by this modality can, in addition to im- drug would not be expected to have any ef-
proving the quality of life, help the patient fect on the primary endplate dysfunction.

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148 Part 1 / Introduction

Successful management of a chronic laxants, but it is important also to accurately


myofascial pain syndrome relieves the pa- identify and treat the source of the spasm.
tient's pain so that analgesic medication is SLEEP. Most patients with persistent
no longer needed. However, at the start of myofascial TrP pain have difficulty sleep-
specific treatment, before the patient ob- ing and show abnormal sleep patterns
tains sustained relief, medication may be when monitored in a sleep laboratory. In 4

necessary. To help wean the patient off of many patients, it is the referred pain gener-
drugs, a time-contingent schedule, rather ated by active TrPs that disturbs sleep. In
than the usual pain-contingent schedule, patients with pain and in normal subjects,
should be established. A pain cocktail can disturbed sleep tends to aggravate pain the
be very helpful. 47
next day. This subject has been well re-
125

Chapter 5, Section D in this manual out- viewed by Moldofsky. 124

lines a general treatment approach for In treating patients with myofascial pain
chronic headaches, facial, neck, or shoul- that disrupts sleep, top priority needs to be
der pain that have a significant myofascial given to inactivating the TrPs that are
TrP component. It can readily be adapted chiefly responsible for insomnia. The pa-
to the other muscles. tient should be shown what sleeping posi-
Successful management of muscu- tion will minimize myofascial pain and be
loskeletal pain depends on an accurate di- encouraged to take medication as neces-
agnosis. Is the pain muscular, articular, sary to obtain restful sleep.
and/or neurologic in origin? In current Three antihistamines, which are non-
medical practice most medical practition- habit-forming, are recommended for better
ers are poorly trained in the diagnosis and sleep. Dimenhydrinate (Dramamine) and
manual treatment of the common muscular diphenhydramine hydrochloride (Bene-
and articular sources of pain. Common ini- dryl) have a common antihistamine that
tial reactions of practitioners to these enig- has a soporific effect on most people. The
matic musculoskeletal complaints are to 50-mg tablet of dimenhydrinate is available
(1) procrastinate, hoping it will go away without prescription and packs a stronger
spontaneously, (2) prescribe a drug, (3) wallop than a 25-mg capsule of diphenhy-
consider surgery, or (4) rationalize it as psy- dramine, which is also available in a 50-mg
chogenic or behavioral, which can be con- capsule. The 25-mg dose can usually be re-
sidered a form of denial. The patients de- peated during the night, if necessary, with-
serve better. out excessive morning hang-over. Gener-
MUSCLE RELAXANTS. The rationale for ally, sleep medication should be taken
the use of muscle relaxants has been based one-half hour before retiring.
largely on the erroneous concept that mus- Promethazine (Phenergan) has a longer
cle pain causes spasm of the same muscle, duration of action than dimenhydrinate,
which in turn causes more muscle pain. and may be helpful to individuals who fall
Since this pain-spasm-pain concept has asleep easily, but have trouble remaining
failed the test of experimental investiga- asleep. This antihistamine also has a po-
tion [see Chapter 2, Part C), we see no ra-
121
tent calming effect that is valuable for pa-
tionale for muscle relaxants in the treat- tients who are anxious. Usually, one 12.5
ment of myofascial pain caused by TrPs. mg tablet at bedtime suffices.
Often the increased muscle tension that A natural sleep-inducing hormone, mela-
is identified as "spasm" related to muscu- tonin, is now available without prescription
loskeletal pain is actually caused by taut in a bewildering array of amounts available
bands of TrPs. Muscle relaxants have no ef- per tablet (from a few hundred micrograms
fect on muscle fibers that are in contracture to more than a milligram) with no guidance
because of dysfunctional endplates. On the as to how to use it. It is specifically useful to
other hand, true spasm (identified as EMG reestablish a normal sleep-waking cycle. A
motor unit activity) can be reflexly induced dose of 200-500 /xg taken one-half hour be-
by TrPs or by other sources such as joint fore bedtime will expedite going to sleep
dysfunctions or ruptured surface fibers of an and help to prevent early awakening. Best
intervertebral disc [see Chapter 4 1 , Part B). of all, there is no need for a hang-over effect
This spasm can be responsive to muscle re- the next morning because its influence is ef-

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Chapter 3 / Apropos of All Muscles 149

fectively negated by continued exposure to sure release, deep stripping massage, hold-
bright light. We recommend use of no more relax with mild (not vigorous) contraction,
than the minimum dose required to obtain indirect techniques, TrP injection, high volt-
the desired effect, and recommend that age galvanic stimulation, and ultrasound.
melatonin be taken only intermittently, be- The muscles of these patients may require
cause the long-term effect of regular large strengthening with stabilizing exercises.
doses (1 mg or more) has not been reported. Hypermobility syndrome is covered in
TROUBLE-MAKING DRUGS. Small to mod- more detail in Volume 2, Chapter 2, Sec-
erate amounts of caffeine may help to min- tion 7 of this manual.
imize TrPs by increasing vasodilatation in Shortening Activation (Reactive Cramp-
the skeletal musculature. However, exces- ing). When a tight muscle (e.g., right mid-
sive intake of coffee and/or cola drinks that dle scalene) is suddenly released, shorten-
contain caffeine (more than two or three ing activation (a reactive cramp) may
cups, bottles, or cans daily) is likely to ag- develop in an antagonist muscle (e.g., the
gravate TrP activity. A cup of coffee may left levator scapulae). As the tight muscle
contain 50-150 mg of caffeine. As a rule, (right middle scalene) is lengthened well be-
drip coffee contains more than percolated, yond its accustomed limit in the process of
which contains more caffeine than instant inactivating its TrPs, the antagonist (left lev-
coffee. Most of the canned soft drinks
34
ator scapulae) is simultaneously shortened
contain 30-50 mg of caffeine. However, caf- to less than its accustomed minimum
feine-free soft drinks are now widely avail- length. If the antagonist harbors latent (or
able. Many combination analgesic drugs mildly active) TrPs, they suddenly and
contain caffeine that may add significantly strongly may be activated by being placed
to the total caffeine load without the pa- (and held briefly) in this unaccustomed
tient's realizing it unless someone analyzes shortened position. The patient can then ex-
in detail the patient's caffeine intake. perience severe cramplike referred pain
Regular excessive alcohol consumption from the TrPs in this muscle that is an an-
may indirectly perpetuate TrPs through tagonist to the previously tight muscle. This
chemically reduced serum and tissue fo- reaction may be immediate, or it can de-
late levels and because of poor eating velop half an hour or so following treatment.
habits. Ingestion of alcohol reduces the ab- The delayed reaction may be caused by the
sorption of folic acid, while increasing the patient making use of the new stretch range
body's need for it. of the treated muscle, thus placing the un-
The habit of tobacco smoking markedly treated antagonist muscle in the shortened
increases the need for vitamin C, which is position after leaving the treatment session.
poorly stored in the body. The marked cap- Shortening activation can be avoided by
illary fragility associated with low ascorbic systematically treating both the agonist
acid levels greatly increases the tendency and antagonist groups of muscles partially,
for tissue bleeding at injection sites. Injec- one after the other. The reaction occurs
tion of TrPs in smokers should be post- more often in flexors, like the biceps
poned until adequate tissue levels of vita- brachii, finger flexor, and hamstring mus-
min C are assured (see Vitamins, in Chapter cles, than in the corresponding extensors.
4). Clinical experience indicates that to- Lengthening treatment of the sternocleido-
bacco smoking aggravates TrPs directly. mastoid or quadratus lumborum muscle on
one side is likely to activate latent TrPs in
Caveats its contralateral mate. Treatment of the
Hypermobility. Treatment with a subscapularis may activate TrPs in the
stretching technique that fully lengthens a supraspinatus and infraspinatus muscles.
muscle is contraindicated across joints that Occasionally, stretch of the abdominal
are truly hypermobile. When there are TrPs musculature initiates paraspinal cramping.
in muscles that cross hypermobile joints, Reasons for Failure. When the patient
these TrPs should be inactivated using tech- fails to show lasting improvement following
niques applied directly to the central TrPs spray and stretch (assuming that myofascial
without stretching the muscle as a whole. pain due to TrPs is the correct diagnosis,
These alternative therapies include TrP pres- and assuming that the muscle causing the

Copyrighted Material
150 Part 1 / Introduction

dysfunction is the one that was treated) the warmed immediately with a hot pack or
following should be considered: pad. Recurrence is more likely if the pa-
PERPETUATING FACTORS. When active tient fails to actively move the treated part
myofascial TrPs do not subside after cor- through its fully shortened and lengthened
rectly applied spray and stretch, one or more range of motion several times to reestablish
perpetuating factors are usually responsible. normal function.
INADEQUATE COVERAGE. If the spray is ap- CHRONICITY. Pain recurs when aggravat-
plied only to the reference zone where the ing or perpetuating factors are present and
patient complains of pain, it usually misses reactivate the TrPs. However, chronicity
the skin overlying the TrP that is causing the alone need not prevent an immediate but
pain. When TrPs in several widely separated temporary response to specific myofascial
muscles refer pain to the same area, stretch- therapy.
ing and spraying some, but not all, of these
muscles will provide only partial relief. 13. TRIGGER POINT INJECTION
PATIENT TENSION. For effective passive There are three different approaches to
stretch, the patient must fully relax the the needle-inactivation of the active loci in a
muscles being treated. Frequently tension central TrP. Generally, we recommend injec-
in postural muscles spills over, and the pa- tion of a local anesthetic without cortico-
tient must assume a relaxed body position steroid and no adrenalin. Dry needling can
and feel relaxed all over to fully relax the be effective but results in more postinjection
muscles being treated. soreness. Only under special circumstances
POOR SPRAY TECHNIQUE. The vapo- would one inject Botulinum toxin A. Effec-
coolant is less effective if the stream of tive treatment using either the injection of a
spray is passed too quickly over the skin, local anesthetic or dry needling depends on
or if the spray container is held too close to mechanical disruption and inactivation of
the skin. On the other hand, the same skin the active loci in that TrP. Inactivation of
area should not be sprayed so often, or so TrPs by injecting Botulinum toxin A de-
slowly, that the underlying muscle be- pends on its specific pharmacological de-
comes chilled. The line of spray must be structive effect on motor endplates.
directed over the line of muscle fibers that It is essential to clearly define just what is
are under maximum tension so that the meant by one injection. The number of in-
topographically related skin reflex effects jections should be counted in terms of the
of vapocooling can release them. number of TrP sites injected, not the num-
INCOMPLETE SPRAY AND STRETCH. Addi- ber of times some solution has been de-
tional cycles of spray and stretch, with re- posited within one TrP site. One TrP site has
warming after each cycle, need to be re- a highly variable number of active loci that
peated as long as the range of motion must be inactivated and all of the loci in one
increases significantly with each cycle, or TrP can be needled or injected with one skin
until full range is reached. penetration. Using a nonmyotoxic local
INADEQUATE STRETCH TECHNIQUE. The anesthetic (which is the kind of anesthetic
TrPs will persist if too much or jerky force is recommended) or dry needling, many nee-
used to passively stretch the muscle. Firm dle movements within the TrP are normally
stretch before spraying can cause painful required. When a local anesthetic is used,
spasm and seriously impair relaxation. one should inject only a small amount (< 1
INCOMPLETE STRETCH. Residual tautness ml) at any one location within the TrP. The
remains when the muscle is stretched to clinician must obtain twitch responses from
less than its FULL range of motion. Adja- all of the remaining active loci in that TrP in
cent muscles often need releasing before order to ensure effective treatment.
this full range can be reached. If stretch is Some clinicians depend on the injection
limited by structural impediments, such as of large amounts of seriously myotoxic
an old fracture, osteoarthritis or idiopathic drugs like Botulinum toxin A or concen-
scoliosis,164
local manual release tech- trated long acting local anesthetics in the
niques will be required. general vicinity of a point of tenderness,
POOR POSTTREATMENT. Muscle soreness hoping to inject a TrP. When myotoxic
is likely to be greater if the skin is not re- drugs are considered unavoidable for injec-

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Chapter 3 / Apropos of All Muscles 151

tion of TrPs, it is much better to inject Injection is indicated when a few TrPs
small amounts precisely where the con- remain that are unresponsive to manual
traction knots of the TrP are located. Selec- methods, when skilled manual TrP therapy
tive injection of small amounts of these is not available, when there are only a few
substances wherever the needle elicits an relatively acute TrPs and the treatment
LTR in a TrP is much less damaging to the time is severely limited, and when the pa-
muscle as a whole, and is just as effective, tient has hyperuricemia and symptoms of
as a large amount. EMG monitoring for the gout. Injections can be helpful when the
spontaneous electrical activity of an active muscle cannot be stretched for mechanical
locus is an even more specific indicator of reasons, or when stretch should be limited
a site for injection. because of hypermobility.
When reporting TrP injections, for each Patients with both fibromyalgia and
injection the clinician should specify the myofascial TrPs are much more sensitive to
muscle injected, and whether it was a painful therapeutic techniques (which, for
central TrP or an attachment TrP that was them, are likely to be counterproductive)
injected. than are patients with TrPs but without fi-
bromyalgia. Patients with both conditions
Why Inject? respond to TrP injections, but they do not
The decision whether to treat TrPs by respond as well as patients with only myo-
manual methods (described in the preced- fascial TrPs. 72

ing Section 12) or by injection depends It is a serious mistake to judge the effi-
strongly on the training and skill of the cacy of TrP treatment by manual methods
practitioner. Ideally, both approaches or by injection if the practitioner was not
should be equally available to the patient both well trained AND experienced in the
and used when indicated. Manual methods techniques used for the muscles reportedly
are noninvasive, available for the patient to treated. Knowledgeable, skillful practition-
learn to use for self-treatment, and can be ers of TrP therapy can be difficult to locate.
used to release multiple TrPs at the same So often, when patients give a history of be-
time in one muscle or a group of TrPs in sev- ing treated for TrPs without benefit, careful
eral muscles that serve the same function. questioning makes it clear that treatment
However, manual methods are more likely was given without adequate examination
to require several treatments and the bene- for TrPs or was not performed in a manner
fit of treatment may not be as fully apparent that one would expect to be effective.
for a day or two, as compared to injection. It
requires considerable time and effort to ac- What to Inject?
quire the skill needed to use manual tech- Dry needling is as effective as injection of
niques or to inject TrPs effectively. an anesthetic for relief of TrP symptoms, IF
Manual methods are specifically indi- the needle elicits LTRs, which occur when
67

cated when the TrP is acute, when the goal the needle encounters active loci of the TrP.
is to train the patient in effective methods Conversely, if no LTR occurs, dry needling
of self-management of the pain and dys- and injection of nontoxic anesthetics are
function, when the patient is severely nee- equally ineffective. Postinjection soreness
67

dle-shy, or when the central TrPs in the is more likely to occur, is more severe, and is
middle of the muscle belly are not accessi- of longer duration following dry needling. 67

ble to injection (iliacus and psoas muscles) Various injection techniques have in-
for most clinicians. cluded the use of procaine, lidocaine,
One well-performed injection can fully longer acting local anesthetics, isotonic
inactivate a TrP immediately, which is re- saline, epinephrin, a corticosteroid, Botu-
assuring to the clinician and the patient. linum A toxin, and several forms of dry
Identification and injection of key TrPs can needling, each of which will be considered.
produce impressive results. Success de- Dry Needling versus Injection. In com-
pends strongly on the accuracy of the clin- parative studies dry needling was
67, 82

ician's aim. This accuracy depends strongly found to be as effective as injecting an


on the precision with which the TrP was lo- anesthetic solution such as procaine or li-
calized and on the skill of the clinician. docaine in terms of immediate inactivation

Copyrighted Material
152 Part 1 / Introduction

of the TrP. In the Hong study of the re-


67
Procaine is the ester of p-aminobenzoic
sponse of trapezius muscle TrPs to 0.5% li- acid and ethanol with a tertiary dieth-
docaine or to dry needling, both groups ex- ylamino group attached at the other end of
perienced essentially the same amount of the alcohol. It is hydrolyzed rapidly in the
improvement immediately and 2 weeks blood serum by procaine esterase to p-
later. However, within 2 - 8 hours, 4 2 % of aminobenzoic acid and diethylamino
the lidocaine-injected patients and 1 0 0 % ethanol. The diethylamino ethanol is an
56

of the dry-needled patients developed lo- antiarrhythmic agent, but more weakly so
cal soreness. The soreness of the patients than procaine, and is fortunately an effec-
treated by dry needling had significantly tive anti-convulsant, because convulsions
greater intensity and duration than the are one of the toxic effects of the whole
soreness of lidocaine-injected patients. procaine molecule. The other product of
56

These results indicate that the critical hydrolysis, p-aminobenzoic acid, is some-
therapeutic factor in both cases is mechan- times considered a member of the vitamin
ical disruption by the needle. This is con- B complex because it is needed for the syn-
sistent with the understanding that disrup- thesis of folic acid by those bacteria that
tion of the TrP contraction knots can produce the vitamin. The potassium56

terminates the basis for a local energy cri- salt of p-aminobenzoic acid is sold under
sis and its sensitization of nearby nerves. the name Potaba as an antifibrotic agent.
Procaine Injection. Dr. Travell recom- Most local anesthetics, including pro-
mended a procaine concentration of 0.5% in caine, block nerve conduction by competi-
physiological saline because greater concen- tively replacing calcium at its membrane
trations showed no additional increase in binding site. Depolarization of the nerve
36

anesthetic effect. No serious harm is done


167
membrane is essential for the propagation of
by using a 1% solution. However, the higher an action potential and depends on the flow
concentration has no known advantage. An of sodium ions through sodium channels
accidental nerve block will last longer and from the inside to the outside of the mem-
the higher concentration has a correspond- brane. Normally, the displacement of cal-
ingly greater toxicity to the muscle and sys- cium from its binding site facilitates the flow
temically. The maximum amount of pro- of sodium ions across the membrane through
caine that should be injected at one time is 1 the channels. Blockage of this calcium bind-
g ire That would permit the injection of 100 ing site impedes the flow of sodium ions,
ml of 1 % procaine. Since only a few tenths of which prevents depolarization and the prop-
a milliliter of local anesthetic are deposited agation of an action potential. ' 29 56

at a time within a TrP, it rarely is necessary to Local anesthetics based on this mecha-
inject a total of more than 20 ml at one visit. nism selectively affect small, usually un-
With 0.5% procaine, accidental injection myelinated, fibers as compared to large
of 2 ml into an artery or vein creates no prob- myelinated nerve fibers and thus block
lem, if adequate hemostasis is applied to the pain perception more than voluntary mo-
vessel. Injection with the same strength solu- tor control. Unlike most local anesthetics,
56

tion near a nerve causes only mild sensory procaine is not rapidly absorbed from mu-
loss for a maximum of about 20 minutes, cous membranes. 29

which is well tolerated if the patient was pre- A bacteriostatic agent commonly added
viously warned that this might happen. to procaine is sodium bisulfite, which can
These statements are not true if the injected be irritating and contribute to postinjection
solution contains epinephrine, which is soreness. This effect can be reduced by di-
never recommended for the injection of TrPs. luting 2% procaine solution to 0.5% with
Procaine is the least myotoxic among isotonic saline solution, which is not so ir-
the local anesthetics that are commonly in- ritating to the muscles as sodium bisulfite
jected. Pain sensation following nerve and has local anesthetic properties of its
block reappeared in 19 minutes after 1% own. The 0.5% strength of procaine is
56 1 9 3

procaine, and in 40 minutes after 1% lido- not commercially available.


caine. Procaine and chloroprocaine have
36
Lidocaine Injection. A 1% solution of
the lowest systemic toxicity of the com- lidocaine is commonly used successfully
monly used local anesthetics. 29
instead of procaine to inject TrPs. The ef-

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Chapter 3 / Apropos of All Muscles 153

fectiveness of these two anesthetic agents the pain of enthesopathy with injection of
for reducing postinjection soreness has not corticosteroids supports this possibility.
been compared experimentally. The definitive treatment for attachment
Lidocaine is not merely a longer-acting TrPs is inactivation of the central TrPs re-
form of procaine. These two agents have dif- sponsible for them. However, prompt reduc-
ferent intermediate chains and different aro- tion in the tenderness and irritability of the
matic residues. Unlike other amide local
56
region of enthesopathy at the attachment TrP
anesthetics, lidocaine is an aminoacyl is therapeutically beneficial to the patient's
amide. Lidocaine is more effective in a neu- comfort and most likely helps to reduce the
tral solution; procaine is more potent in an irritability of the corresponding central TrP.
alkaline solution. Procaine is hy-
36, 139
Although we know of no controlled
drolyzed in the blood stream; lidocaine is re- study that critically evaluated the effec-
moved from tissues through solubility in fat tiveness of steroid therapy specifically for
and is metabolized primarily in the liver. 29
attachment TrPs, the report by Day et al. i2

Isotonic Saline Injection. Sola and on the treatment of tennis elbow is strongly
Kuitert treated a series of 100 patients with
154
suggestive that steroid therapy is quite ef-
myofascial TrPs by injecting isotonic saline fective in this situation. This study is sum-
(which also contained a bacteriostatic agent) marized and its relation to attachment TrPs
with multiple needle penetrations in a fan- is presented in Chapter 36, Section 13.
wise pattern. These patients experienced The use of long-acting (deposit) steroids
therapeutic results equal to those previously is not recommended for the injection of
reported with the injection of a local anes- TrPs. Such a preparation may, by itself, be
thetic. Frost et a/. did a controlled, double-
50
destructive to muscle fibers. It can in-
132

blind comparison between isotonic saline crease the danger of muscle and connective
and a long-acting anesthetic, mepivacaine. tissue tears. Long-acting steroids are gener-
They injected tender areas of the muscle that ally irritating to nerves and can produce
showed localized changes in the consistency complications. Use of deposit steroids en-
58

of the muscle, and from which the patient's hances the danger of a systemic Cushing-
pain could be evoked (TrPs). Using these TrP oid reaction with repeated injections.
criteria for the precise localization of the in- Repeated use of corticosteroid injections
jection, they found that the saline afforded followed by ultrasound has been reported
equal, or more pain relief than injection of to produce depression and atrophy of skin
the same volume of 0.5% mepivacaine, and subcutaneous tissue that resulted in
which is myotoxic. Most bacteriostatic saline the need for surgical repair. 88

for injection contains at least 0.9% benzyl al- Myotoxicity. Procaine and lidocaine
cohol as the bacteriostatic agent, which has are the least myotoxic of the local anes-
local anesthetic properties of its o w n .
56193
thetics that are commonly injected intra-
Corticosteroid Injection. Corticosteroids muscularly, and lidocaine is clearly more
are potent anti-inflammatory agents and myotoxic than procaine. Myotoxicity, par-
therefore appropriate for the treatment of ticularly of the longer-acting anesthetics, is
conditions characterized by an inflamma- strongly related to the concentration in-
tory reaction. The pathophysiology of a cen- jected. It is unlikely that solutions stronger
tral TrP in the muscle endplate zone involves than 0.5% are any more effective when in-
sensitization of nociceptors secondary to a jecting TrPs. Solutions stronger than 1%
local energy crisis. The clinical experience become increasingly and significantly
to date indicates that nonsteroidal anti-in- myotoxic. Longer acting anesthetics tend
flammatory drugs are not effective in reduc- to be more myotoxic than shorter acting
ing the nerve sensitization in central TrPs. ones. Epinephrine severely increases myo-
Addition of injected steroids here apparently toxicity without conferring any apprecia-
offers no advantage. On the other hand, the ble clinical advantage when injecting TrPs.
nerve sensit