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TT
DUTTON’S ORTHOPAEDIC
EXAMINATION, EVALUATION,
AND INTERVENTION
 NOTICE
Medicine is an ever-changing science. As new research and clinical experience broaden
our knowledge, changes in treatment and drug therapy are required. T e authors and the
publisher o this work have checked with sources believed to be reliable in their e orts
to provide in ormation that is complete and generally in accord with the standards
accepted at the time o publication. However, in view o the possibility o human error
or changes in medical sciences, neither the authors nor the publisher nor any other party
who has been involved in the preparation or publication o this work warrants that the
in ormation contained herein is in every respect accurate or complete, and they disclaim
all responsibility or any errors or omissions or or the results obtained rom use o the
in ormation contained in this work. Readers are encouraged to con rm the in ormation
contained herein with other sources. For example and in particular, readers are advised
to check the product in ormation sheet included in the package o each drug they plan to
administer to be certain that the in ormation contained in this work is accurate and that
changes have not been made in the recommended dose or in the contraindications or
administration. T is recommendation is o particular importance in connection with new
or in requently used drugs.
 DUTTON’S ORTHOPAEDIC
EXAMINATION, EVALUATION,
AND INTERVENTION
FOURTH EDITION

Mark Dutton, PT
Allegheny General Hospital
West Penn Allegheny Health System (WPAHS)
Adjunct Clinical Instructor, Duquesne University
School of Health Sciences
Pittsburgh, Pennsylvania

New York Chicago San Francisco Athens London Madrid Mexico City
Milan New Delhi Singapore Sydney oronto
Dutton’s Orthopaedic Examination, Evaluation, and Intervention, Fourth Edition

Copyright © 2017 by McGraw-Hill Education. All rights reserved. Printed in China. Except as
permitted under the United States Copyright Act o 1976, no part o this publication may be
reproduced or distributed in any orm or by any means, or stored in a data base or retrieval
system, without the prior written permission o the publisher.

Previous editions copyright © 2012, 2008, 2004 by he McGraw-Hill Companies, Inc.

1 2 3 4 5 6 7 8 9 DSS 21 20 19 18 17 16

ISBN 978-1-259-58310-0
MHID 1-259-58310-4

his book was set in Minion Pro by Aptara, Inc.

he editors were Michael Weitz and Brian Kearns.
he production supervisor was Catherine Saggese.
Project management was provided by Amit Kashyap, Aptara, Inc.
RR Donnelley was the printer and binder.

Library of Congress Cataloging-in-Publication Data

Names: Dutton, Mark, author.

itle: Dutton’s orthopaedic examination, evaluation, and intervention / Mark
Dutton.
Other titles: Orthopaedic examination, evaluation, and intervention
Description: Fourth edition. | New York : McGraw-Hill Education, [2016] |
Preceded by Dutton’s orthopaedic examination, evaluation, and intervention
/ Mark Dutton. 3rd ed. c2012. | Includes bibliographical re erences and
index.
Identi iers: LCCN 2016011470 | ISBN 9781259583100 (hardcover) | ISBN
1259583104 (hardcover)
Subjects: | MESH: Orthopedics–methods | Physical Examination–methods |
Musculoskeletal Diseases–diagnosis | Orthopedic Procedures–methods
Classi ication: LCC RD734 | NLM WE 168 | DDC 616.7/075–dc23 LC record available at
http://lccn.loc.gov/2016011470

McGraw-Hill Education books are available at special quantity discounts to use as premiums and
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 For my parents,
Ron and Brenda, who have always helped, guided, and inspired me
and to my two daughters, Leah and Lauren, who provide me with such joy.
 Your Legacy

Will you have earned the respect o your peers and the admiration o your critics?
Will you have acted humbly during success and grace ully in the ace o adversity?
Will you be remembered or how o ten you brought smiles to the hearts o others?
Will you have looked or the very best, and done your utmost to build worth, in others?
Will you have le t this world a better place by the li e you have lived?

Modif ed rom The Legacy You Leave ©2000 by Rick Beneteau

 Contents

Pre ace ix
SECTION IV
Acknowledgments xi
Introduction xiii THE EXTREMITIES
16 The Shoulder 577
17 Elbow 711
SECTION I 18 The Forearm, Wrist, and Hand 779
ANATOMY 19 Hip 869
1 The Musculoskeletal System 3 20 The Knee 966
2 Tissue Behavior, Injury, Healing, and Treatment 29 21 Lower Leg, Ankle, and Foot 1081
3 The Nervous System 64

SECTION V
SECTION II THE SPINE AND TMJ
EXAMINATION AND EVALUATION 22 Vertebral Column 1191
4 Patient/Client Management 163 23 The Craniovertebral Region 1209
5 Dif erential Diagnosis 218 24 Vertebral Artery 1246
6 Gait and Posture Analysis 287 25 The Cervical Spine 1256
7 Imaging Studies in Orthopaedics 344 26 The Temporomandibular Joint 1340
27 The Thoracic Spine 1382
28 Lumbar Spine 1425
SECTION III 29 The Sacroiliac Joint 1529

INTERVENTION
8 The Intervention 369 SECTION VI
9 Pharmacology or the Orthopaedic
Physical Therapist 398 SPECIAL CONSIDERATIONS
10 Manual Techniques 417 30 Special Populations 1569
11 Neurodynamic Mobility and Mobilizations 445
12 Improving Muscle Per ormance 463 Index 1613
13 Improving Mobility 521
14 Improving Neuromuscular Control 557
15 Improving Cardiovascular Endurance 566

vii

T e ourth edition o this book is an update o in ormation
and bibliography provided in the previous versions together
with a reorganization o various chapters.
T e United States currently spends more money on
healthcare per person than any other country in the world,
with current projections indicating that 20% o the gross
domestic product o the United States will be spent on
healthcare by the year 2019.1 As the population continues
to age, the treatment o musculoskeletal conditions, and
their subsequent expenses, will also increase. T is will
place an increasing burden on the clinician to provide value
or money—the achievement o a health outcome relative
to the costs incurred. Gone are the days when a clinician
can rely on an expensive shotgun approach to treatment.
Instead, emphasis is now placed on outcomes such as patient
satis action and accurate measures o clinical outcomes, or
Comments about this book may be sent to me at pt@mcgraw-hill.com.
Pre ace
it is the consistent measurement and reporting o clinical
outcomes that is the most power ul tool in moving toward a
value-based system.2
o that end, the aim o this book is to provide the reader
with a systematic and evidence-based approach to the
examination and intervention o the orthopaedic patient.
Such an approach must be eclectic because no single method
works all o the time. T us, this book attempts to incorporate
the most reliable concepts currently available.
I hope that this book will be seen as the best available
textbook, guide, review, and re erence or healthcare students
and clinicians involved in the care o the orthopaedic
population.
Mark Dutton, P
ix

From inception to completion, the various editions span almost
12 years. Such an endeavor cannot be completed without the
help o many. I would like to take this opportunity to thank the
ollowing:
T e aculty o the North American Institute o Manual
and Manipulative T erapy (NAIOM )—especially, Jim
Meadows, Erl Pettman, Cli Fowler, Diane Lee, and the
late Dave Lamb.
T e exceptional team at McGraw-Hill, or their superb
guidance throughout this object. T ank you especially
to Michael Weitz or his advice and support and to other
members o the initial lineup. Special thanks also to Brian
Kearns.
Acknowledgments
o the production crew o Aptara, especially the project
manager Amit Kashyap.
Bob Davis or his creative eye and the excellent photography.
Leah or agreeing to be the photographic model.
T e sta o Human Motion Rehabilitation, Allegheny
General Hospital including roy Baxendell, Susan Berger,
Diane Ferianc, Leslie Fisher, Keith Galloway, Dave Hahn,
Dean Hnaras, John Karp, Ronald Klingensmith, Randi
Marshak, Dan McCool, Renee Nacy, Dan Norkiewicz,
Darcy Skrip, Jodi Weiher, Melissa Willis, and Joe Witt.
o the countless clinicians throughout the world who
continually strive to improve their knowledge and clinical
skills.
xi

“T e very f rst step towards success in any occupation is
to become interested in it.”
—Sir William Osler (1849–1919)
Until the beginning o the last century, knowledge about the
mechanism o healing and the methods to decrease pain and
su ering were extremely limited. Although we may sco at
many o the interventions used in the distant past, many o
the interventions we use today, albeit less radical, have still to
demonstrate much more in the way o e ectiveness. T at may
soon change with the recent emphasis within many healthcare
pro essions on evidence-based clinical practice. T e process
o evidence-based practice is outlined in Table I-1. When
combining clinical expertise with the best available external
clinical evidence, clinicians can make in ormed decisions
regarding patient management, including the selection and
interpretation o the most appropriate evaluation procedures.
Also, intervention strategies based on the best available
TABLE I-1 The Process of Evidence -Based Practice
1. Identi y the patient problem. Derive a specif c question.
2. Search the literature.
3. Appraise the literature.
4. Integrate the appraisal o literature with your clinical expertise,
experience, patient values, and unique circumstances.
5. Implement the f ndings.
6. Assess outcome and reappraise.
Data rom Sackett DL, Strauss SE, Richardson WS, et al. Evidence Based
Medicine: How to Practice and Teach EBM. 2nd ed. Edinburgh, Scotland:
Churchill Livingstone; 2000.
Introduction
evidence will have a greater likelihood o success with the
least associated risk.3,4
T e goal o every clinician should be to enhance patient/
client satis action, increase ef ciency, and decrease unproven
treatment approaches.4 T e management o the patient/client
is a complex process involving an intricate blend o experience,
knowledge, and interpersonal skills. Obtaining an accurate
diagnosis requires a systematic and logical approach. Such
an approach should be eclectic because no single method
works all o the time. For any intervention to be success ul,
an accurate diagnosis must be ollowed by a care ully planned
and speci c rehabilitation program to both the a ected area
and its related structures. In this book, great emphasis is placed
on the appropriate use o manual techniques and therapeutic
exercise based on these considerations. Electrotherapeutic
and thermal/cryotherapeutic modalities should be viewed
as adjuncts to the rehabilitative process. T e accompanying
DVD to this book contains numerous video clips o manual
techniques and therapeutic exercises, which the reader is
encouraged to view. T e ollowing icon is used throughout
the text to indicate when such clips are available. [VIDEO]
REFERENCES
1. Sisko AM, ru er CJ, Keehan SP, et al. National health spending
projections: the estimated impact o re orm through 2019. Health Af .
2010; 29:1933–1941.
2. Porter ME. What is value in health care? New Engl J Med. 2010; 363:2477–
2481.
3. Sackett DL, Rosenberg WM, Gray JA, et al. Evidence based medicine:
what it is and what it isn’t. 1996. Clin Orthop Relat Res. 2007; 455:3–5.
4. Schroder JA. Manual therapy and neural mobilization: our approach and
personal observations. Orthop Pract. 2004; 16:23–27.
xiii
S EC TIO N I ANATOMY

C H AP TER 1 M s os
CHAPTER OBJECTIVES
At the completion of this cha pter,
the reader will be able to:
1. Describe the various types o biological tissue o the
musculoskeletal system.
2. Describe the tissue mechanics and structural di erences and
similarities between muscle, tendons, ascia, and ligaments.
3. Describe the di erent types o joints and their various
characteristics.
4. De ne the various terminologies used to describe the
joint position, movements, and relationships.
5. Give de nitions or commonly used biomechanical terms.
6. Describe the di erent planes o the body.
7. De ne the body’s center o mass and its location.
8. Describe the di erent axes o the body and the motions
that occur around them.
9. De ne the terms osteokinematic motion and
arthrokinematic motion.
10. Di erentiate between the di erent types o motion that
can occur at the joint sur aces.
11. Describe the basic biomechanics o joint motion in
terms o their concave–convex relationships.
12. De ne the terms close-packed and open-packed.
OVERVIEW
T e correct embryonic development o the musculoskeletal
system requires a coordinated morphogenesis o the un-
damental tissues o the body. T roughout the human body,
there are our major types o tissues:
Epithelial. Covers all internal and external body sur aces
and includes structures such as the skin and the inner
lining o the blood vessels.
T
ta
Syst m
Connective. Connective tissue (C ), which includes our
di erent classes: connective tissue proper, bone, cartilage,
and blood tissue. In the embryo, muscle tissue and its
ascia orm as a di erentiation o the paraxial mesoderm
that divides into somites on either side o the neural tube
and notochord. T e cartilage and bone o the vertebral
column and ribs develop rom the sclerotome which is the
anterior (ventral) part o the somite.1 T e dermomyotome,
which is the posterior (dorsal) part o the somite, gives
rise to the overlying dermis o the back and the skeletal
muscles o the body and limbs.1 Connective tissue
provides structural and metabolic support or other tissues
and organs o the body.
Muscle. Muscles are classi ed unctionally as either
voluntary or involuntary, and structurally as either
smooth, striated (skeletal), or cardiac. T ere are
approximately 430 skeletal muscles in the body, each o
which can be considered anatomically as a separate organ.
O these 430 muscles, about 75 pairs provide the majority
o body movements and postures.2
Nervous. Nervous tissue provides a two-way
communication system between the central nervous
system (brain and spinal cord) and muscles, sensory
organs, and various systems (see Chapter 3).
CONNECTIVE TISSUE
C proper has a loose, exible matrix, called ground substance.
T e most common cell within C proper is the broblast. Fi-
broblasts produce collagen, elastin, and reticular bers:
Collagen is a group o naturally occurring proteins. T e
collagens are a amily o extracellular matrix (ECM)
proteins that play a dominant role in maintaining
the structural integrity o various tissues and in
providing tensile strength to tissues. T e ECM is
ormed rom glycosaminoglycans (GAGs) subunits,
long polysaccharide chains containing amino sugars,
and are strongly hydrophilic to allow rapid di usion
o water-soluble molecules and easy migration o cells.
Proteoglycans, which are a major component o the ECM,
are macromolecules that consist o a protein backbone
3
 to which the GAGs are attached. T ere are two types
o GAGs: chondroitin sul ate and keratin sul ate.3,4 A
simple way to visualize the proteoglycan molecule is to
consider a test tube brush, with the stem representing the
protein core and the GAGs representing the bristles.5,6
Glycoproteins, another component o the ECM, consist o
bronectin and thrombospondin and unction as adhesive
structures or repair and regeneration.7
Elastic bers are composed o a protein called elastin. As
its name suggests, elastin provides elastic properties to the
tissues in which it is situated.8 Elastin bers can stretch,
A
but they normally return to their original shape when
N
the tension is released. T us, the elastic bers o elastin
A
T
determine the patterns o distention and recoil in most
O
organs, including the skin and lungs, blood vessels, and
M
Y
C . Bundles o collagen and elastin combine to orm a
matrix o C ascicles. T is matrix is organized within the
primary collagen bundles as well as between the bundles
that surround them.9
Reticular bers are composed o a type o collagen, which
is secreted by reticular cells. T ese bers crosslink to
orm a ne meshwork, called reticulin, which acts as a
supporting mesh in bone marrow, and the tissues and
organs o the lymphatic system, and the liver.
T e various characteristics o collagen di er depending
on whether it is loose or dense collagen. T e anatomic and
unctional characteristics o loose and dense collagen are
summarized in Table 1-1. Collagenous and elastic bers are
sparse and irregularly arranged in loose C but are tightly
packed in dense C .10
T e various types o C , as they relate to the musculoskeletal
system, are described as ollows:
Fascia
Fascia, or example, the thoracolumbar ascia and the plantar
ascia, is viewed as a loose C that provides support and protec-
tion to a joint, and acts as an interconnection between tendons,
aponeuroses, ligaments, capsules, nerves, and the intrinsic
components o muscle.11,12 Fascia may be categorized as brous
or non brous, with the brous components consisting mainly
o collagen and elastin bers, and the non brous portion con-
sisting o amorphous ground substance.13 T ree di erent types
o ascia have been identi ed, namely, super cial, deep, and vis-
ceral ascia. Various three-dimensional biomechanical models
o the human ascial system have been developed, which corre-
late dys unctional movement with various interrelated abnor-
mal amounts o tension throughout the network o ascia. In
TABLE 1-1 Loose and Dense Collagen
Joint Type Anatomic Location Fiber Orientation
Dense irregular connective Composes the external brous Parallel, tightly aligned bers Ligament: binds bones together and restrains
tissue layer o the joint capsule,
orms ligaments, bone,
aponeuroses, and tendons
Loose irregular connective Found in capsules, muscles, Random ber orientation
tissue nerves, ascia, and skin
4
particular, deep ascia has been implicated in being involved
with the deep venous return, in having a possible role in pro-
prioception, and responding to mechanical traction induced by
muscular activity in di erent regions.14 Histological studies o
deep ascia in the limbs show that it consists o elastic bers
and undulated collagen bers arranged in layers.15 Each colla-
gen layer is aligned in a di erent direction, and this permits a
certain degree o stretch as well as a capacity to recoil.16
Tendons
endons are dense, regularly arranged connective tissues,
composed o 70% water and 30% dry mass that attach mus-
cle to the bone at each end o the muscle. endons produce
joint motion by trans erring orce rom muscle to bone, and,
when stretched, store elastic energy that contributes to move-
ment. Also, tendons enable the muscle belly to be an optimal
distance rom the joint upon which it is acting. T e collagen
bers o tendons (70–80% o the collagen in tendons is type I,
with the remaining 20–30% o dry weight composed o pro-
teoglycans, GAGs, elastin, and other collagens—being type
III, V, and VII) are arranged in a quarter-stagger arrange-
ment, which gives it a characteristic banding pattern and pro-
vides high strength and stability.17 enoblasts, or immature
tendon cells, trans orm into tenocytes that synthesize colla-
gen and components o the ECM network.7 T e ECM sur-
rounds collagen and tenocytes and is composed o several
components or speci c unctions (e.g., glycoproteins, and
enascin-C, which may play a role in collagen ber orienta-
tion and alignment). endon structure is highly regular with
collagen- orming triple helices (tropocollagen), which pack
together to orm micro brils, which interdigitate to orm
brils, which coalesce to orm bers, which combine to orm
ascicles, which are bundled together to orm a tendon.18 T e
thickness o each tendon varies and is proportional to the size
o the muscle rom which it originates. Vascularity within the
tendon is relatively sparse and corresponds with the lower
metabolic/turnover rate o these tissues. Within the ascicles
o tendons, which are held together by loose C called endo-
tenon, the collagen components are oriented in a unidirec-
tional way. Endotenon contains blood vessels, lymphatics,
and nerves and permits longitudinal movements o individual
ascicles when tensile orces are applied to the structure. T e
C surrounding groups o ascicles, or the entire structure,
is called the epitenon. T e epitenon contains the vascular,
lymphatic, and nerve supplies to the tendon. A peritendinous
sheath (paratenon), which is composed o loose areolar con-
nective tissue in addition to sensory and autonomic nerve
bers, surrounds the entire tendon.19 T is sheath consists o
Mechanical Specialization
unwanted movement at the joints; resists
tension in several directions
Tendon: attaches muscle to bone
Provides structural support
two layers: an inner (visceral) layer and an outer (parietal)
layer with occasional connecting bridges (mesotenon). I
there is synovial uid between these two layers, the paratenon
is called tenosynovium; i not, it is termed tenovagium.9
endons are metabolically active and are provided with a
rich and vascular supply during development.20 endons receive
their vascular supply through the musculotendinous junction
(M J), the osteotendinous junction, and the vessels rom the
various surrounding tissues including the paratenon and meso-
tenon.18 endons in di erent areas o the body receive di erent
amounts o blood supply, and tendon vascularity can be com-
promised by the junctional zones and sites o riction, torsion, or
compression—a number o tendons are known to have reduced
tendon vascularity, including the supraspinatus, the biceps, the
Achilles, the patellar, and the posterior tibial tendon.18
T e mechanical properties o tendon come rom its highly
oriented structure. endons display viscoelastic mechanical
properties that con er time- and rate-dependent e ects on the
tissue. Speci cally, tendons are more elastic at lower strain rates
and sti er at higher rates o tensile loading (see Chapter 2).
endons de orm less than ligaments under an applied load and
are able to transmit the load rom muscle to bone.9 Material
and structural properties o the tendon increase rom birth
through maturity and then decrease rom maturity through
old age.18 Although tendons withstand strong tensile orces
well, they resist shear orces less well and provide little resis-
tance to a compression orce (see Chapter 2).
A tendon can be divided into three main sections:21
T e bone–tendon junction. At most tendon–bone
inter aces, the collagen bers insert directly into the
bone in a gradual transition o material composition. T e
physical junction o tendon and bone is re erred to as an
enthesis,22 and is an inter ace that is vulnerable to acute
and chronic injury.23 One role o the enthesis is to absorb
and distribute the stress concentration that occurs at the
junction over a broader area.
T e tendon midsubstance. Overuse tendon injuries can
occur in the midsubstance o the tendon, but not as
requently as at the enthesis.
M J. T e M J is the site where the muscle and tendon
meet. T e M J comprises numerous interdigitations
between muscle cells and tendon tissue, resembling
interlocked ngers. Despite its viscoelastic mechanical
characteristics, the M J is very vulnerable to tensile
ailure (see Chapter 2).24,25
Ligaments
Skeletal ligaments are brous bands o dense C that connect
bones across joints. Ligaments can be named or the bones
into which they insert (coracohumeral), their shape (deltoid
o the ankle), or their relationships to each other (cruciate).26
T e gross structure o a ligament varies according to location
(intra-articular or extra-articular, capsular), and unction.27
Ligaments, which appear as dense white bands or cords o
C , are composed primarily o water (approximately 66%),
and o collagen (largely type I collagen [85%], but with small
amounts o type III) making up most o the dry weight. T e
collagen in ligaments has a less unidirectional organization
than it does in tendons, but its structural ramework still pro-
vides sti ness (resistance to de ormation—see Chapter 2).28
Small amounts o elastin (1% o the dry weight) are present in
ligaments, with the exception o the ligamentum avum and
the nuchal ligament o the spine, which contain more. T e cel-
lular organization o ligaments makes them ideal or sustain-
ing tensile loads, with many containing unctional subunits
that are capable o tightening or loosening in di erent joint
positions.29 At the microscopic level, closely spaced collagen
bers ( ascicles) are aligned along the long axis o the liga-
ment and are arranged into a series o bundles that are delin-
eated by a cellular layer, the endoligament, and the entire liga-
T
h
ment is encased in a neurovascular biocellular layer re erred
e
to as the epiligament.26 Ligaments contribute to the stability
M
u
o joint unction by preventing excessive motion,30 acting as
S
guides or checkreins to direct motion, and providing proprio-
c
u
ceptive in ormation or joint unction through sensory nerve
l
O
endings (see Chapter 3) and the attachments o the ligament
S
to the joint capsule.31–33 Many ligaments share unctions. For
k
e
example, while the anterior cruciate ligament o the knee is
l
e
considered the primary restraint to anterior translation o the
T
A
tibia relative to the emur, the collateral ligaments and the pos-
l
terior capsule o the knee also help in this unction (see Chap-
S
Y
ter 20).26 T e vascular and nerve distribution to ligaments is
S
T
not homogeneous. For example, the middle o the ligament is
e
M
typically avascular, while the proximal and distal ends enjoy
a rich blood supply. Similarly, the insertional ends o the liga-
ments are more highly innervated than the midsubstance.
Cartilage
Cartilage tissue exists in three orms: hyaline, elastic, and
brocartilage.
Hyaline cartilage, also re erred to as articular cartilage,
covers the ends o long bones and permits almost
rictionless motion to occur between the articular sur aces
o a diarthrodial (synovial) joint.34 Articular cartilage
is a highly organized viscoelastic material composed o
cartilage cells called chondrocytes, water, and an ECM.
CLINICAL PEARL
Chondrocytes are specialized cells that are responsible or the
development o cartilage and the maintenance o the ECM.35
Chondrocytes produce aggrecan, link protein, and hyal-
uronan, all o which are extruded into the ECM, where they
aggregate spontaneously.4 The aggrecan orms a strong,
porous-permeable, ber-rein orced composite material with
collagen. The chondrocytes sense mechanical changes in
their surrounding matrix through intracytoplasmic laments
and short cilia on the sur ace o the cells.27
Articular cartilage, the most abundant cartilage within
the body, is devoid o any blood vessels, lymphatics, and
nerves.5,6 Most o the bones o the body orm rst as hya-
line cartilage, and later become bone in a process called
endochondral ossi cation. T e normal thickness o articu-
lar cartilage is determined by the contact pressures across
the joint—the higher the peak pressures, the thicker the 5
 cartilage.27 Articular cartilage unctions to distribute the
joint orces over a large contact area, thereby dissipating
the orces associated with the load. T is distribution o
orces allows the articular cartilage to remain healthy and
ully unctional throughout decades o li e. T e patellar has
the thickest articular cartilage in the body.
Articular cartilage may be grossly subdivided into our dis-
tinct zones with di ering cellular morphology, biomechani-
cal composition, collagen orientation, and structural proper-
ties, as ollows:
T e super cial zone. T e super cial zone, which lies
A
adjacent to the joint cavity, comprises approximately
N
10–20% o the articular cartilage thickness and
A
T
unctions to protect deeper layers rom shear stresses.
O
T e collagen bers within this zone are packed tightly
M
Y
and aligned parallel to the articular sur ace. T is zone
is in contact with the synovial uid and handles most o
the tensile properties o cartilage.
T e middle (transitional) zone. In the middle zone,
which provides an anatomic and unctional bridge
between the super cial and deep zones, the collagen
bril orientation is obliquely organized. T is zone
comprises 40–60% o the total cartilage volume.
Functionally, the middle zone is the rst line o
resistance to compressive orces.
T e deep or radial layer. T e deep layer comprises 30%
o the matrix volume. It is characterized by radially
aligned collagen bers that are perpendicular to the
sur ace o the joint, and which have a high proteoglycan
content. Functionally the deep zone is responsible or
providing the greatest resistance to compressive orces.
T e tidemark. T e tidemark distinguishes the deep
zone rom the calci ed cartilage, the area that prevents
the di usion o nutrients rom the bone tissue into the
cartilage.
Elastic (yellow) cartilage is a very specialized C ,
primarily ound in locations such as the outer ear, and
portions o the larynx.
Fibrocartilage, also re erred to as white cartilage,
unctions as a shock absorber in both weight-bearing
and nonweight-bearing joints. Its large iber content,
rein orced with numerous collagen ibers, makes
it ideal or bearing large stresses in all directions.
Fibrocartilage is an avascular, alymphatic, and
aneural tissue and derives its nutrition by a double-
di usion system.36 Examples o ibrocartilage include
the symphysis pubis, the intervertebral disk, and the
menisci o the knee.
Bone
Bone is a highly vascular orm o C , composed o collagen,
calcium phosphate, water, amorphous proteins, and cells. It
is the most rigid o the C s (Table 1-2). Despite its rigidity,
bone is a dynamic tissue that undergoes constant metabolism
and remodeling. T e collagen o bone is produced in the same
manner as that o ligament and tendon but by a di erent cell,
the osteoblast.10 At the gross anatomical level, each bone has a
distinct morphology comprising both cortical bone and can-
cellous bone. Cortical bone is ound in the outer shell. Can-
cellous bone is ound within the epiphyseal and metaphyseal
regions o long bones, as well as throughout the interior o
short bones.24 Skeletal development occurs in one o the two
ways:
Intramembranous ossi cation. Mesenchymal stem cells
within mesenchyme or the medullary cavity o a bone
initiate the process o intramembranous ossi cation. T is
type o ossi cation occurs in the cranium and acial bones
and, in part, the ribs, clavicle, and mandible.

TABLE 1-2 General Structure of Bone

Site Comment Conditions Result
Epiphysis Mainly develops under pressure Epiphyseal dysplasias Distorted joints
Apophysis orms under traction Joint sur ace trauma Degenerative changes
Forms bone ends Overuse injury Fragmented development
Supports articular sur ace Damaged blood supply Avascular necrosis

Physis Epiphyseal or growth plate Physeal dysplasia Short stature

Responsive to growth and sex hormones Trauma De ormed or angulated
Vulnerable prior to growth spurt Slipped epiphysis growth or growth arrest
Mechanically weak

Metaphysis Remodeling expanded bone end Osteomyelitis Sequestrum ormation

Cancellous bone heals rapidly Tumors Altered bone shape
Vulnerable to osteomyelitis Metaphyseal dysplasia Distorted growth
A ords ligament attachment

Diaphysis Forms sha t o bone Fractures Able to remodel angulation

Large sur ace or muscle origin Diaphyseal dysplasias Cannot remodel rotation
Signi cant compact cortical bone Healing slower than at metaphysis Involucrum with in ection
Strong in compression Dysplasia gives altered density and shape
Data rom Reid DC. Sports Injury Assessment and Rehabilitation. New York, NY: Churchill Livingstone; 1992.
6
 Endochondral ossi cation. T e rst site o ossi cation
occurs in the primary center o ossi cation, which is in
the middle o the diaphysis (sha ). About the time o
birth, a secondary ossi cation center appears in each
epiphysis (end) o long bones. Between the bone ormed
by the primary and secondary ossi cation centers,
cartilage persists as the epiphyseal (growth) plates
between the diaphysis and the epiphysis o a long bone.
T is type o ossi cation occurs in the appendicular and
axial bones.
T e periosteum is ormed when the perichondrium,
which surrounds the cartilage, becomes the periosteum.
Chondrocytes in the primary center o ossi cation begin
to grow (hypertrophy) and begin secreting alkaline phos-
phatase, an enzyme essential or mineral deposition. Cal-
ci cation o the matrix ollows, and apoptosis (a type o
cell death involving a programmed sequence o events
that eliminates certain cells) o the hypertrophic chon-
drocytes occurs. T is creates cavities within the bone. T e
exact mechanism o chondrocyte hypertrophy and apopto-
sis is currently unknown. T e hypertrophic chondrocytes
(be ore apoptosis) also secrete a substance called vascular
endothelial cell growth actor that induces the sprouting o
blood vessels rom the perichondrium. Blood vessels orm-
ing the periosteal bud invade the cavity le by the chondro-
cytes, and branch in opposite directions along the length
o the sha . T e blood vessels carry osteoprogenitor cells
and hemopoietic cells inside the cavity, the latter o which
later orm the bone marrow. Osteoblasts, di erentiated
rom the osteoprogenitor cells that enter the cavity via the
periosteal bud, use the calci ed matrix as a sca old and
begin to secrete osteoid, which orms the bone trabecula.
Osteoclasts, ormed rom macrophages, break down the
spongy bone to orm the medullary cavity (bone marrow).
T e unction o bone is to provide support, enhance lever-
age, protect vital structures, provide attachments or both
tendons and ligaments, and store minerals, particularly
calcium. From a clinical perspective, bones may serve as
use ul landmarks during the palpation phase o the exami-
nation. T e strength o bone is related directly to its density.
O importance to the clinician, is the di erence between
maturing bone and mature bone. T e epiphyseal plate or
growth plate o a maturing bone can be divided into our
distinct zones:37
Reserve zone: produces and stores matrix.
Proli erative zone: produces matrix and is the site or
longitudinal bone cell growth.
Hypertrophic zone: subdivided into the maturation
zone, degenerative zone, and the zone o provisional
calci ication. It is within the hypertrophic zone that
the matrix is prepared or calci ication and is here
that the matrix is ultimately calci ied. he hypertrophic
zone is the most susceptible o the zones to injury
because o the low volume o bone matrix and the
high amounts o developing immature cells in this
region.38
Bone metaphysis: the part o the bone that grows during
childhood.
Skeletal Muscle Tissue
T e microstructure and composition o skeletal muscle have
been studied extensively. T e class o tissue labeled skeletal
muscle consists o individual muscle cells or bers that work
together to produce the movement o bony levers. A single
muscle cell is called a muscle ber or myo ber. As muscle
cells di erentiate within the mesoderm, individual myo -
bers are wrapped in a C envelope called endomysium. Bun-
dles o myo bers, which orm a whole muscle ( asciculus),
are encased in the perimysium (Fig. 1-1). T e perimysium
is continuous with the deep ascia. T is relationship allows
T
the ascia to unite all o the bers o a single motor unit and,
h
e
there ore, adapt to variations in orm and volume o each
M
muscle according to muscular contraction and intramuscular
u
S
modi cations induced by joint movement.15 Groups o ascic-
c
uli are surrounded by a connective sheath called the epimy-
u
l
sium (Fig. 1-1). Under an electron microscope, it can be seen
O
S
that each o the myo bers consists o thousands o myo brils
k
e
(Fig. 1-1), which extend throughout its length. Myo brils are
l
composed o sarcomeres arranged in series.39
e
T
A
l
S
CLINICAL PEARL
Y
S
T
The sarcomere (Fig. 1 2) is the contractile machinery o
e
M
the muscle. The graded contractions o a whole muscle
occur because the number o bers participating in the
contraction varies. Increasing the orce o movement is
achieved by recruiting more cells into cooperative action.
All skeletal muscles exhibit our characteristics:40
1. Excitability, the ability to respond to stimulation rom the
nervous system.
2. Elasticity, the ability to change in length or stretch.
3. Extensibility, the ability to shorten and return to normal
length.
4. Contractility, the ability to shorten and contract in
response to some neural command. T e tension developed
in skeletal muscle can occur passively (stretch) or actively
(contraction). When an activated muscle develops tension,
the amount o tension present is constant throughout the
length o the muscle, in the tendons, and at the sites o the
musculotendinous attachments to the bone. T e tensile
orce produced by the muscle pulls on the attached bones
and creates torque at the joints crossed by the muscle. T e
magnitude o the tensile orce is dependent on a number
o actors.
One o the most important roles o C is to transmit
mechanically the orces generated by the skeletal muscle cells
to provide movement. Each o the myo brils contains many
bers called myo laments, which run parallel to the myo bril
axis. T e myo laments are made up o two di erent proteins:
actin (thin myo laments) and myosin (thick myo laments)
that give skeletal muscle bers their striated (striped) appear-
ance (Fig. 1-2).39
T e striations are produced by alternating dark (A) and
light (I) bands that appear to span the width o the muscle
ber. T e A bands are composed o myosin laments, whereas 7
 Epimys ium

Pe rimys ium

Fa s ciculus

Ca pilla ry
A
N
A
T
O
M
Y
Nucle us

Mitochondrion

Endomys ium
Myofibril
S a rcole mma

FIGURE 1-1 Microscopic structure o the muscle.

Myofibril
the I bands are composed o actin laments. T e actin la-
ments o the I band overlap into the A band, giving the edges
o the A band a darker appearance than the central region
(H band), which contains only myosin. At the center o each
e I band is a thin, dark Z line. A sarcomere (Fig. 1-2) repre-
er

ar
c om sents the distance between each Z line. Each muscle ber is
S
limited by a cell membrane called a sarcolemma (Fig. 1-1).
T e protein dystrophin plays an essential role in the mechani-
cal strength and stability o the sarcolemma.41 Dystrophin is
Myos in lacking in patients with Duchenne muscular dystrophy.
(thick fila me nt)

Actin
CLINICAL PEARL
(thin fila me nt) The sarcoplasm is the specialized cytoplasm o a muscle
cell that contains the usual subcellular elements along
with the Golgi apparatus, abundant myo brils, a modi ed
Tropomyos in endoplasmic reticulum known as the sarcoplasmic reticu-
Troponin complex lum (SR), myoglobin, and mitochondria. Transverse tubules
(T-tubules) invaginate the sarcolemma, allowing impulses
FIGURE 1-2 Troponin and tropomyosin action during a muscle
to penetrate the cell and activate the SR.
8 contraction.
 T e basic unction o muscle is to contract. T e word con-
traction, used to describe the generation o tension within
muscle bers, conjures up an image o shortening o muscle
bers during a resistance exercise. However, a contraction
can produce shortening or lengthening o the muscle, or no
change in the muscle length. T us, three types o contraction
are commonly recognized: isometric, concentric, and eccen-
tric (see Chapter 12).
Isometric contraction. Isometric exercises provide a
static contraction with a variable and accommodating
resistance without producing any appreciable change in
muscle length.42
Concentric contraction. A concentric contraction
produces a shortening o the muscle. T is occurs when
the tension generated by the agonist muscle is suf cient
to overcome an external resistance and to move the body
segment o one attachment toward the segment o its
other attachment.42
Eccentric contraction. An eccentric contraction occurs
when a muscle slowly lengthens as it gives in to an
external orce that is greater than the contractile orce it
is exerting.42 In reality, the muscle does not lengthen, it
merely returns rom its shortened position to its normal
resting length. Eccentric muscle contractions, which are
capable o generating greater orces than either isometric
or concentric contractions,43–45 are involved in activities
that require a deceleration to occur. Such activities include
slowing to a stop when running, lowering an object, or
sitting down. Because the load exceeds the bond between
the actin and myosin laments during an eccentric
contraction, some o the myosin laments probably are
torn rom the binding sites on the actin lament while
the remainder are completing the contraction cycle.46
T e resulting orce is substantially larger or a torn cross-
bridge than or one being created during a normal cycle o
muscle contraction. Consequently, the combined increase
in orce per cross-bridge and the number o active cross-
bridges results in a maximum lengthening muscle tension
that is greater than the tension that could be created
during a shortening muscle action.46,47
CLINICAL PEARL
Both concentric and eccentric muscle action comprise the
type o exercise called isotonic. An isotonic contraction is a
contraction in which the tension within the muscle remains
constant as the muscle shortens or lengthens.42 This state is
very di cult to produce and measure. Although the term
isotonic is used in many texts to describe concentric and
eccentric contractions alike, its use in this context is errone-
ous because in most exercise orms the muscle tension dur-
ing exercise varies based upon the weight used, joint veloc-
ity, muscle length, and type o muscle contraction.42
Four other contractions are worth mentioning:
Isokinetic contraction. An isokinetic contraction occurs
when a muscle is maximally contracting at the same speed
throughout the whole range o its related lever.42 Isokinetic
contractions require the use o special equipment that
produces an accommodating resistance. Both high-
speed/low-resistance and low-speed/high-resistance
regimens result in excellent strength gains.48–51 T e major
disadvantage o this type o exercise is its expense. Also,
there is the potential or impact loading and incorrect
joint axis alignment.52 Isokinetic exercises may also have
questionable unctional carryover.53
Econcentric contraction. T is type o contraction
combines both a controlled concentric and a simultaneous
eccentric contraction o the same muscle over two
T
separate joints.54 Examples o an econcentric contraction
h
include the standing hamstring curl, in which the
e
M
hamstrings work concentrically to ex the knee while the
u
hip tends to ex eccentrically, lengthening the hamstrings.
S
c
When rising rom a squat, the hamstrings work
u
concentrically as the hip extends and work eccentrically
l
O
as the knee extends. Conversely, the rectus emoris work
S
k
eccentrically as the hip extends and work concentrically as
e
l
the knee extends.
e
T
Isolytic contraction. An isolytic contraction is an
A
l
osteopathic term used to describe a type o eccentric
S
contraction that makes use o a greater orce than the
Y
S
patient can overcome. T e di erence between an eccentric
T
e
contraction and an isolytic contraction is that, in the ormer,
M
the contraction is voluntary whereas, in the latter, it is
involuntary. T e isolytic contraction can be used in certain
manual techniques to stretch brotic tissue (see Chapter 10).
Structures called cross-bridges serve to connect the actin
and myosin laments. Increased synthesis o actin and myo-
sin stimulates new myo brils that are added to the external
layers o the pre-existing myo brils.55 T e myosin laments
contain two exible, hinge-like regions, which allow the cross-
bridges to attach and detach rom the actin lament. Dur-
ing contraction, the cross-bridges attach and undergo power
strokes, which provide the contractile orce. During relax-
ation, the cross-bridges detach. T is attaching and detaching
is asynchronous, so that some are attaching while others are
detaching. T us, at each moment, some o the cross-bridges
are pulling, while others are releasing.
T e regulation o cross-bridge attachment and detachment
is a unction o two proteins ound in the actin laments:
tropomyosin and troponin (Fig. 1-2). ropomyosin attaches
directly to the actin lament, whereas troponin is attached
to the tropomyosin rather than directly to the actin lament.
CLINICAL PEARL
Tropomyosin and troponin unction as the switch or mus-
cle contraction and relaxation. In a relaxed state, the tropo-
myosin physically blocks the cross-bridges rom binding to
the actin. For contraction to take place, the tropomyosin
must be moved.
Each muscle ber is innervated by a somatic motor neu-
ron. One neuron and the muscle bers it innervates constitute
a motor unit or unctional unit o the muscle. Each motor
neuron branches as it enters the muscle to innervate a num-
ber o muscle bers. 9
 TABLE 1-3 Comparison of Muscle Fiber Types
Characteristics Type I
Size (diameter) Small
Resistance to atigue High
Capillary density High
Glycogen content Low
Twitch rate Slow
Energy system Aerobic
A
N
Maximum muscle shortening velocity Slow
A
T
O
Major storage uel Triglycerides
M
Y
CLINICAL PEARL
The area o contact between a nerve and muscle ber is
known as the motor end plate, or neuromuscular junction
(NMJ).
T e release o a chemical acetylcholine rom the axon ter-
minals at the NMJ causes electrical activation o the skel-
etal muscle bers. When an action potential propagates into
the transverse tubule system (narrow membranous tunnels
ormed rom and continuous with the sarcolemma), the volt-
age sensors on the transverse tubule membrane signal the
release o Ca2+ rom the terminal cisternae portion o the
SR (a series o interconnected sacs and tubes that surround
each myo bril).56 T e released Ca2+ then di uses into the sar-
comeres and binds to troponin, displacing the tropomyosin,
and allowing the actin to bind with the myosin cross-bridges
(Fig. 1-2). Whenever a somatic motor neuron is activated,
all o the muscle bers that it innervates are stimulated and
contract with all-or-none twitches. Although the muscle bers
produce all-or-none contractions, muscles are capable o a
wide variety o responses, ranging rom activities requiring a
high level o precision, to activities requiring high tension.
At the end o the contraction (the neural activity and action
potentials cease), the SR actively accumulates Ca2+ and muscle
relaxation occurs. T e return o Ca2+ to the SR involves active
transport, requiring the degradation o adenosine triphos-
phate (A P) to adenosine diphosphate (ADP)*.56 Because
SR unction is closely associated with both contraction and
relaxation, changes in its ability to release or sequester Ca2+
markedly a ect both the time course and magnitude o orce
output by the muscle ber.57
CLINICAL PEARL
The SR orms a network around the myo brils, storing and
providing the Ca2+ that is required or muscle contraction.
*T e most readily available energy or skeletal muscle cells is stored in the
orm o A P and phosphocreatine (PCr). T rough the activity o the enzyme
A Pase, A P promptly releases energy when required by the cell to per orm
10 any type o work, whether it is electrical, chemical, or mechanical.
Type II A Type II B
Intermediate Very large
Fairly high Low
High Low
Intermediate High
Fast Fast
Aerobic Anaerobic
Fast Fast
Creatine phosphate glycogen Creatine phosphate glycogen
On the basis o their contractile properties, two major types
o muscle ber have been recognized within skeletal muscle
based on their resistance to atigue: type I (tonic, slow-twitch
bers), and type II (phasic ast-twitch bers). ype II muscle
bers are urther divided into two additional classi cations
( ypes IIA and IIB) (Table 1-3). Scott et al.58 subdivide type II
bers into three classi cations, including a type IIIC.
ype I bers are richly endowed with mitochondria and
have a high capacity or oxygen uptake. T ey are, there ore,
suitable or activities o long duration or endurance (aerobic),
including the maintenance o posture. In contrast, ast-twitch
bers, which generate a great amount o tension within a short
period, are suited to quick, explosive actions (anaerobic),
including such activities as sprinting. T e type II ( ast-twitch)
bers are separated based on mitochondria content into those
that have a high complement o mitochondria (type IIA) and
those that are mitochondria-poor (type IIB). T is results in
type IIB bers having a tendency to atigue more quickly than
the type IIA bers ( able 1-3).
CLINICAL PEARL
In ast-twitch bers, the SR embraces every individual
myo bril. In slow-twitch bers, it may contain multiple
myo brils.59
T eory dictates that a muscle with a large percentage o
the total cross-sectional area occupied by slow-twitch type I
bers should be more atigue resistant than one in which the
ast-twitch type II bers predominate.
Di erent activities place di ering demands on a muscle
(Table 1-4).59 For example, dynamic movement activities involve
a predominance o ast-twitch ber recruitment, whereas pos-
tural activities and those activities requiring stabilization entail
more involvement o the slow-twitch bers. In humans, most
limb muscles contain a relatively equal distribution o each
muscle ber type, whereas the back and trunk demonstrate a
predominance o slow-twitch bers. Although it would seem
possible that physical training may cause bers to convert rom
slow twitch to ast twitch or the reverse, this has not been shown
to be the case.60 However, ber conversion rom type IIB to type
IIA, and vice versa, has been ound to occur with training.61
 TABLE 1-4 Functional Division of Muscle Groups Muscles serve a variety o roles depending on the required
movement:
Movement Group Stabilization Group
Prime mover (agonist). T is is a muscle that is directly
Primarily type IIa Primarily type I
responsible or producing a desired movement.
Prone to adaptive shortening Prone to develop weakness Antagonist. T is is a muscle that has an e ect directly
opposite to that o the agonist.
Prone to develop hypertonicity Prone to muscle inhibition
Synergist (supporter). his is a muscle that per orms
Dominate in atigue and new Fatigue easily a cooperative muscle unction relative to the
movement situations agonist. Synergists can unction as stabilizers or
Generally cross two joints Primarily cross one joint neutralizers.
Stabilizers ( xators). Muscles that contract statically to

T
h
Examples Examples
steady or support some part o the body against the pull

e
o the contracting muscles, against the pull o gravity,

M
Gastrocnemius/Soleus Fibularis (peronei)

u
or against the e ect o momentum and recoil in certain

S
Tibialis posterior Tibialis anterior vigorous movements.

c
u
Neutralizers. Muscles that act to prevent an undesired

l
Short hip adductors Vastus medialis and lateralis

O
action rom one o the movers.

S
Hamstrings Gluteus maximus, medius, and

k
e
minimus As previously mentioned, depending on the type o muscu-

l
e
lar contraction, the length o a muscle can remain the same

T
Rectus emoris Serratus anterior

A
(isometric), shorten (concentric), or “lengthen” (eccentric).

l
Tensor ascia lata Rhomboids T e velocity at which muscle contracts signi cantly a ects the

S
Y
tension that the muscle produces and subsequently a ects a

S
Erector spinae Lower portion o trapezius

T
muscle’s strength and power.66

e
M
Quadratus lumborum Short/deep cervical f exors Concentric contractions. As the speed o a concentric
contraction increases, the orce it is capable o
Pectoralis major Upper limb extensors
producing decreases.43,45 T e slower speed o contraction
Upper portion o trapezius Rectus abdominis is thought to produce greater orces than can be
produced by increasing the number o cross-bridges
Levator scapulae ormed. T is relationship is a continuum, with the
Sternocleidomastoid optimum velocity or the muscle somewhere between
the slowest and astest rates. At very slow speeds,
Scalenes the orce that a muscle can resist or overcome rises
Upper limb f exors
rapidly up to 50% greater than the maximum isometric
contraction.43,45
Data rom Jull GA, Janda V. Muscle and motor control in low back pain. In:
Twomey LT, Taylor JR, eds. Physical Therapy o the Low Back: Clinics in Physical Eccentric contractions. During a maximum-e ort eccentric
Therapy. New York, NY: Churchill Livingstone; 1987:258–278. contraction, as the velocity o active muscle lengthening
increases, orce production in the muscle initially
T e e ectiveness o muscle to produce movement depends increases to a point, but then quickly levels o .67–69 T e
on some actors. T ese include the location and orientation ollowing changes in orce production occur during an
o the muscle attachment relative to the joint, the limitations eccentric contraction:
or laxity present in the musculotendinous unit, the type o Rapid eccentric contractions generate more orce than
contraction, the point o application, and the actions o other do slower eccentric contractions.
muscles that cross the joint.2 During slow eccentric muscle actions, the work
produced approximates that o an isometric
CLINICAL PEARL contraction.43,45

Following the stimulation o muscle, a brie period elapses

be ore a muscle begins to develop tension. The length o this
period, the electromechanical delay (EMD), varies consider-
ably among muscles. Fast-twitch bers have shorter periods
o EMD when compared with slow-twitch bers.62 EMD is
a ected by muscle atigue, muscle length, muscle training,
passive muscle stretching, and the type o muscle activa-
tion.63 A tissue injury may increase the EMD and, there ore,
increases the susceptibility to uture injury i ull healing does
not occur.64 One o the purposes o neuromuscular re-educa-
tion (see Chapter 14) is to return the EMD to a normal level.65
CLINICAL PEARL
The number o cross-bridges that can be ormed is depen-
dent on the extent o the overlap between the actin and
myosin laments.70 Thus, the orce a muscle is capable o
exerting depends on its length. For each muscle cell, there
is an optimum length, or range o lengths, at which the
contractile orce is strongest. At the optimum length o
the muscle, there is a near-optimal overlap o actin and
11

myosin, allowing or the generation o maximum tension
at this length.
I the muscle is in a shortened position, the overlap o
actin and myosin reduces the number o sites available
or the cross-bridge ormation. Active insuf ciency o a
muscle occurs when the muscle is incapable o short-
ening to the extent required to produce a ull range o
motion (ROM) at all joints crossed simultaneously.2,54,71,72
For example, the nger f exors cannot produce a closed
st when the wrist is ully f exed, as they can when it is
in neutral position.
A
N
I the muscle is in a lengthened position compared with
A
its optimum length, the actin laments are pulled away
T
O
rom the myosin heads such that they cannot create as
M
many cross-bridges.46 Passive insuf ciency o the muscle
Y
occurs when the two-joint muscle cannot stretch to the
extent required or ull ROM in the opposite direction
at all joints crossed.2,54,71,72 For example, when an indi-
vidual attempts to make a closed st with the wrist ully
f exed, the active shortening o the nger and wrist f ex-
ors results in passive lengthening o the nger exten-
sors. In this example, the length o the nger extensors
is insu cient to allow ull ROM at both the wrist and the
ngers.73
T e orce and speed o a muscle contraction depend on
the requirements o the activity, which in turn, are dependent
on the ability o the central nervous system to control the
recruitment o motor units.2 T e motor units o slow-twitch
bers have lower thresholds and are easier to activate than
those o the ast-twitch motor units. Consequently, the slow-
twitch bers are recruited rst, even when the resulting limb
movement is rapid.74
As the orce requirement, speed requirement, or duration
o activity increases, motor units with higher thresholds are
recruited. ype IIa units are recruited be ore type IIb.75
CLINICAL PEARL
The term temporal summation re ers to the summation o
individual contractile units. The summation can increase
the muscular orce by increasing the muscle activation re-
quency.76
Although each muscle contains the contractile machin-
ery to produce the orces or movement, it is the tendon that
transmits these orces to the bones to achieve movement or
stability o the body in space.9 T e angle o insertion the ten-
don makes with a bone determines the line o pull, whereas
the tension generated by a muscle is a unction o its angle o
insertion. A muscle generates the greatest amount o torque
when its line o pull is oriented at a 90-degree angle to the
bone, and it is attached anatomically as ar rom the joint cen-
ter as possible.2
Just as there are optimal speeds o length change and opti-
mal muscle lengths, there are optimal insertion angles or each
o the muscles. T e angle o insertion o a muscle, and, there-
12 ore, its line o pull, can change during dynamic movements.46
T e angle o pennation is the angle created between the ber
direction and the line o pull. When the bers o a muscle
lie parallel to the long axis o the muscle, there is no angle
o pennation. T e number o bers within a xed volume o
a muscle increases with the angle o pennation.46 Although
pennation can enhance the maximum tension, the range o
shortening o the muscle is reduced. Muscle bers can con-
tract to about 60% o their resting length. Since the muscle
bers in pennate muscles are shorter than the no-pennate
equivalent, the amount o contraction is similarly reduced.
Muscles that need to have large changes in length without the
need or very high tension, such as the sartorius muscle, do
not have pennate muscle bers.46 In contrast, pennate muscle
bers are ound in those muscles in which the emphasis is on
a high capacity or tension generation rather than ROM (e.g.,
gluteus maximus).
CLINICAL PEARL
Skeletal muscle blood f ow increases 20- old during mus-
cle contractions.77 The muscle blood f ow increases in pro-
portion to the metabolic demands o the tissue, a relation-
ship ref ected by positive correlations between muscle
blood f ow and exercise. As body temperature elevates,
the speeds o nerve and muscle unctions increase, result-
ing in a higher value o maximum isometric tension and
a higher maximum velocity o shortening possible with
ewer motor units at any given load.78 Muscle unction is
most e cient at 38.5°C (101°F).79
During physical exercise, energy turnover in skeletal muscle
may increase by 400 times compared with muscle at rest and
muscle oxygen consumption may increase by more than 100
times.80 T e hydrolysis o A P to ADP and inorganic phos-
phate (Pi) provides the power or muscular activity. Despite
the large uctuations in energy demand just mentioned,
muscle A P remains practically constant and demonstrates
a remarkable precision o the system in adjusting the rate o
the A P-generating processes to the demand.81 T ere are three
energy systems that contribute to the resynthesis o A P via
ADP rephosphorylation. T ese energy systems are as ollows:
Phosphagen system. T e phosphagen, or A P-
PCr, system is an anaerobic process—it can proceed
without oxygen (O2). T e skeletal muscle cell stores
the phosphocreatine (PCr) and ADP, o which PCr
is the chemical uel source. At the onset o muscular
contraction, PCr represents the most immediate reserve
or the rephosphorylation o A P. T e phosphagen system
provides A P primarily or short-term, high-intensity
activities (i.e., sprinting), and is the major source o
energy during the rst 30 seconds o intense exercise, but
it is also active at the start o all exercises, regardless o
intensity.82 Once a muscle returns to rest, the supply o
A P-PCr is replenished. While the maximum power o
this system is great, one disadvantage o the phosphagen
system is that because o its signi cant contribution to
the energy yield at the onset o near-maximal exercise,
the concentration o PCr can be reduced to less than 40%
o resting levels within 10 seconds o the start o intense
 exercise, which translates into a small maximum capacity
o the system.83
Glycolytic system. T e glycolytic system is an anaerobic
process that involves the breakdown o carbohydrates—
either glycogen stored in the muscle or glucose delivered
through the blood—into pyruvate to produce A P in a
process called glycolysis. Pyruvate is then trans ormed
into lactic acid as a byproduct o the anaerobic glycolysis.
Because this system relies on a series o nine di erent
chemical reactions, it is slower to become ully active.
However, glycogenolysis has a greater capacity to provide
energy than does PCr, and there ore it supplements PCr
during maximal exercise and continues to rephosphorylate
ADP during maximal exercise a er PCr reserves have
become essentially depleted.82 T e process o glycolysis
can be in one o the two ways, termed ast glycolysis and
slow glycolysis, depending on the energy demands within
the cell. I energy must be supplied at a high rate, ast
glycolysis is used primarily. I the energy demand is not so
high, slow glycolysis is activated. T e main disadvantage o
the ast glycolysis system is that during very high-intensity
exercise, hydrogen ions dissociate rom the glycogenolytic
end product o lactic acid.81 T e accumulation o lactic
acid in the contracting muscle is recognized in sports and
resistance training circles. An increase in hydrogen ion
concentration is believed to inhibit glycolytic reactions
and directly inter ere with muscle excitation–contraction
and coupling, which can potentially impair contractile
orce during an exercise.82 T is inhibition occurs once
the muscle pH drops below a certain level, prompting
the appearance o phospho ructokinase (PFK), resulting
in local energy production ceasing until replenished by
oxygen stores.
CLINICAL PEARL
Lactic acid is the major energy source or providing the
muscle with ATP during exercise bouts that last 1–3 minutes
(e.g., running 400–800 m).
Oxidative system. As its name suggests, the oxidative
system requires O 2 and is consequently termed the
“aerobic” system. T e uel sources or this system are
glycogen, ats, and proteins. T is system is the primary
source o A P at rest and during low-intensity activities.
T e A P is resynthesized in the mitochondria o the
muscle cell such that the ability to metabolize oxygen
and other substrates is related to the number and
concentration o the mitochondria and cells. It is worth
noting that at no time during either rest or exercise does
any single energy system provide the complete supply
o energy. While being unable to produce A P at an
equivalent rate to that produced by PCr breakdown
and glycogenolysis, the oxidative system is capable o
sustaining low-intensity exercise or several hours.82
However, because o increased complexity, the time
between the onset o exercise and when this system is
operating at its ull potential is around 45 seconds.84
T e relative contribution o these energy systems to A P
resynthesis has been shown to depend upon the intensity
and duration o exercise, with the primary system used being
based on the duration o the event:85
0–10 seconds: A P–PCr. T ese bursts o activity develop
muscle strength and stronger tendons and ligaments, with
the A P being supplied by the phosphagen system.
10–30 seconds: A P–PCr plus anaerobic glycolysis.
30 seconds to 2 minutes: anaerobic glycolysis. T ese
longer bursts o activity, i repeated a er 4 minutes o
rest or mild exercise, enhance anaerobic power with the
T
h
A P being supplied by the phosphagen and anaerobic
e
glycolytic system.
M
u
2–3 minutes: anaerobic glycolysis plus oxidative system.
S
c
> 3 minutes and rest: oxidative system. T ese periods o
u
activity using less than maximum intensity may develop
l
O
aerobic power and endurance capabilities, and the
S
k
phosphogen, anaerobic glycotic, and anaerobic systems
e
l
supply the A P.
e
T
A
l
Respiratory Muscles
S
Y
S
Although the respiratory muscles share some mechanical simi-
T
e
larities with skeletal muscles, they are distinct rom skeletal
M
muscles in several aspects as ollows:86,87
Whereas skeletal muscles o the limbs overcome inertial
loads, the respiratory muscles overcome primarily elastic
and resistive loads.
T e respiratory muscles are under both voluntary and
involuntary control.
T e respiratory muscles are similar to the heart muscles,
in that they have to contract rhythmically and generate
the required orces or ventilation throughout the entire
li espan o the individual. T e respiratory muscles, however,
do not contain pacemaker cells and are under the control
o mechanical and chemical stimuli, requiring neural input
rom higher centers to initiate and coordinate contraction.
T e resting length o the respiratory muscles is a relationship
between the inward recoil orces o the lung and the outward
recoil orces o the chest wall. Changes in the balance o
recoil orces will result in changes in the resting length
o the respiratory muscles. T us, simple and everyday
li e occurrences such as changes in posture may alter the
operational length and the contractile strength o the
respiratory muscles.88 I uncompensated, these length changes
can lead to decreases in the output o the muscles, and hence,
a reduction in the ability to generate lung volume changes.88
T e skeletal muscles o the limbs, on the other hand, are not
constrained to operate at a particular resting length.
CLINICAL PEARL
The primary respiratory muscles o the body include the dia-
phragm; the internal, external, and transverse intercostals;
the levator costae; and the serratus posterior in erior and
superior.
13

JOINTS
Arthrology is the study o the classi cation, structure, and
unction o articulations (joints or arthroses). A joint rep-
resents the junction between two or more bones. Joints are
regions where bones are capped and surrounded by C s that
hold the bones together and determine the type and degree o
movement between them.89 An understanding o the anatomy
and biomechanics o the various joints is required to be able
to assess and treat a patient thoroughly. When classi ed ac-
cording to movement potential, joints may be classi ed into
A
two broad categories synarthrosis (nonsynovial) or diarthrosis
N
A
(synovial).
T
O
M
Synarthrosis
Y
T e type o tissue uniting the bone sur aces determines the
major types o synarthroses:89
Fibrous joints, which are joined by dense brous C .
T ree types exist:
Suture (e.g., suture o the skull).
Gomphosis (e.g., tooth and mandible or maxilla
articulation).
Syndesmosis (e.g., tibio bular or radioulnar joints).
T ese joints usually allow a small amount o motion.
Cartilaginous joints originally re erred to as
amphiarthrosis joints, are stable joints that allow or
minimal or little movement. T ese joints exist in humans
in one o two ways: synchondrosis (e.g., manubriosternal
joints) and symphysis (e.g., symphysis pubis). A
synchondrosis is a joint in which the material used to
connect the two components is hyaline cartilage.90 In a
symphysis joint, the two bony components are covered
with a thin lamina o hyaline cartilage and directly joined
by brocartilage in the orm o disks or pads.90
Diarthrosis
T is joint unites long bones and permits ree bone move-
ment and greater mobility. A broelastic joint capsule, which
characterizes these joints, is lled with a lubricating substance
called synovial uid. Consequently, these joints are o en
re erred to as synovial joints.
Examples include, but are not limited to, the hip, knee and
shoulder, and elbow joints. Synovial joints are urther classi-
ed based on complexity:
Simple (uniaxial): a single pair o articular sur aces one
male, or convex, sur ace and one emale, or concave, sur ace.
Examples include hinge joint and trochoid (pivot) joints.
Compound (biaxial): a single joint capsule that contains
more than a single pair o mating articulating sur aces.
T e two types o biaxial joint in the body include the
condyloid and saddle.
Complex (triaxial or multiaxial): contain an intra-articular
inclusion within the joint class such as a meniscus or disk
that increases the number o joint sur aces. T e two types
o joint in this category are plane joints and ball-and-
14 socket joints.
Synovial joints have ve distinguishing characteristics: a
joint cavity that is enclosed by the joint capsule, hyaline artic-
ular cartilage that covers the sur aces o the enclosed contigu-
ous bones, synovial uid that orms a lm over the joint sur-
aces, synovial membrane that lines the inner sur ace o the
capsule, and a joint capsule that is composed o two layers.90
All synovial joints o the body are provided with an array o
corpuscular (mechanoreceptors) and noncorpuscular (noci-
ceptors) receptor endings embedded in articular, muscular,
and cutaneous structures with varying characteristic behav-
iors and distributions depending on the articular tissue (see
Chapter 3). One intra-articular structure worth mentioning
is the articular disk or meniscus. A meniscus, which consists
o a dense ECM, is not covered by a synovial membrane and
occurs between articular sur aces where congruity is low. T e
cells o the meniscus are re erred to as brochondrocytes
because they appear to be a mixture o broblasts and chon-
drocytes.91 A meniscal disk may extend across a synovial joint,
dividing it structurally and unctionally into two synovial cav-
ities. Complete disks occur in the sternoclavicular and distal
radioulnar joints, while that in the temporomandibular joint
may be complete or incomplete.13 Peripherally disks are con-
nected to brous capsules, usually by vascularized connective
tissue, so that they become invaded by vessels and a erent and
motor nerves.13 Mechanoreceptors within the menisci unc-
tion as transducers, converting the physical stimulus o ten-
sion and compression into a speci c electrical nerve impulse
(see Chapter 3).92
Synovial joints can be broadly classi ed according to struc-
ture or analogy (Fig. 1-3) into the ollowing categories93:
Spheroid. As the name suggests, a spheroid joint is a reely
moving joint in which a sphere on the head o one bone
ts into a rounded cavity in the other bone. Spheroid
(ball-and-socket) joints allow motions in three planes
(Fig. 1-3) (see later). Examples o a spheroid joint sur ace
include the heads o the emur and humerus.
rochoid. T e trochoid, or pivot, joint is characterized
by a pivot-like process turning within a ring, or a ring on
a pivot, the ring being ormed partly o bone, partly o
ligament (Fig. 1-3). rochoid joints permit only rotation.
Examples o a trochoid joint include the humeroradial
joint and the atlantoaxial joint.
Condyloid (ovoid). T is joint is characterized by an ovoid
articular sur ace, or condyle (Fig. 1-3). One bone may
articulate with another by one sur ace or by two, but never
more than two. I two distinct sur aces are present, the
joint is called condylar, or bicondylar. T e elliptical cavity
o the joint is designed in such a manner as to permit the
motions o exion, extension, adduction, abduction, and
circumduction, but no axial rotation. T e wrist joint is an
example o this orm o articulation.
Ginglymoid. A ginglymoid joint is a hinge joint (Fig. 1-3). It
is characterized by a spool-like sur ace and a concave sur ace.
An example o a ginglymoid joint is the humeroulnar joint.
Ellipsoid. Ellipsoid joints are similar to spheroid joints
in that they allow the same type o movement albeit to
a lesser magnitude. T e ellipsoid joint allows movement
in two planes ( exion, extension; abduction, adduction)
 He a d of hume rus S ca pula

Ra dius Ulna

Pivo t jo int
Ball-and-s o c ke t

Hume rus Ulna

T
h
e
M
u
S
c
u
Ca rpa ls

l
O
Gliding jo int

S
k
e
Hing e jo int

l
e
T
A
l
Me ta ca rpa l Ca rpa l

S
Y
S
T
e
M
Me ta ca rpa l

Co ndylo id jo int

Saddle jo int

P ha la nx

FIGURE 1-3 Types o diarthrosis or synovial joints.

and is biaxial. Examples o this joint can Synovial Fluid

be ound at the radiocarpal articulation at the wrist
and the metacarpophalangeal articulation with the
phalanges.
Planar. As its name suggests, a planar joint is
characterized by at sur aces that slide over each
other. Movement at this joint does not occur about an
axis and is termed nonaxial. Examples o a planar joint
include the intermetatarsal joints and some intercarpal
joints.
Saddle (sellar). Saddle joints are characterized by a convex
sur ace in one cross-sectional plane and a concave sur ace
in the plane perpendicular to it (Fig. 1-3). Examples
o a saddle joint include the interphalangeal joints, the
carpometacarpal joint o the thumb, the humeroulnar
joint, and the calcaneocuboid joints.
In reality, no joint sur ace is planar or resembles a true geo-
metric orm; that is they resemble either the outer or inner
sur ace o a piece o eggshell.94
Articular cartilage is subject to a great variation o loading
conditions, so joint lubrication through the synovial uid
is necessary to minimize rictional resistance between the
weight-bearing sur aces. Fortunately, synovial joints are
blessed with a very superior lubricating system, which per-
mits a remarkably rictionless interaction at the joint sur-
aces. A cartilaginous lubricated inter ace has a coef cient
o riction* o 0.002.95 By way o comparison, ice on ice has
a higher coef cient o riction (0.03).95 T e composition o
synovial uid is nearly the same as blood plasma, but with a
decreased total protein content and a higher concentration
o hyaluronan.96
*Coef cient o riction is a ratio o the orce needed to make a body glide
across a sur ace compared with the weight or orce holding the two sur aces
in contact. 15
 CLINICAL PEARL
Hyaluronan is a critical constituent component o nor-
mal synovial f uid and an important contributor to joint
homeostasis.97 Hyaluronan imparts anti-inf ammatory and
anti-nociceptive properties to normal synovial f uid and
contributes to joint lubrication. It also is responsible or the
viscoelastic properties o synovial f uid,96 and contributes
to the lubrication o articular cartilage sur aces.
A
Indeed, synovial uid is essentially a dialysate o plasma to
N
which hyaluronan has been added.98 Hyaluronan is a GAG
A
T
that is continually synthesized and released into the synovial
O
M
uid by specialized synoviocytes.98,99 T e mechanical proper-
Y
ties o synovial uid permit it to act as both a cushion and a
lubricant to the joint. Diseases such as osteoarthritis, a ect the
thixotropic properties (thixotropy is the property o various
gels becoming uid when disturbed, as by shaking) o syno-
vial uid, resulting in reduced lubrication and subsequent
wear o the articular cartilage and joint sur aces.100,101 It is well
established that damaged articular cartilage in adults has a
very limited potential or healing (see Chapter 2) because it
possesses neither a blood supply nor lymphatic drainage.102
FIGURE 1-4 The anatomical position.
Bursae
Closely associated with some synovial joints are attened,
Proximal. Closer to the trunk.
saclike structures called bursae that are lined with a synovial
membrane and lled with synovial uid. T e bursa produces Distal. Away rom the trunk.
small amounts o uid, allowing or smooth and almost ric- Superf cial. oward the sur ace o the body.
tionless motion between contiguous muscles, tendons, bones, Deep. Away rom the sur ace o the body in the direction
ligaments, and skin.103–105 A tendon sheath is a modi ed o the inside o the body.
bursa. A bursa can be a source o pain i it becomes in amed
or in ected.

KINESIOLOGY
When describing movements, it is necessary to have a start-
ing position as the re erence position. T is starting position
is re erred to as the anatomic re erence position. T e anatomic
re erence position or the human body is described as the
erect standing position with the eet just slightly separated
and the arms hanging by the side, the elbows straight, and the
palms o the hand acing orward (Fig. 1-4).
Directional Terms
Directional terms are used to describe the relationship o body
parts or the location o an external object with respect to the
body.106 T e ollowing are commonly used directional terms:
Superior or cranial. Closer to the head.
In erior or caudal. Closer to the eet.
Anterior or ventral. oward the ront o the body.
Posterior or dorsal. oward the back o the body.
Medial. oward the midline o the body.
16 Lateral. Away rom the midline o the body.
MOVEMENTS OF
THE BODY SEGMENTS
In general, there are two types o motions: translation, which
occurs in either a straight or curved line, and rotation, which
involves a circular motion around a pivot point. Movements
o the body segments occur in three dimensions along imagi-
nary planes and around various axes o the body.
Planes of the Body
T ere are three traditional planes o the body corresponding
to the three dimensions o space: sagittal, rontal, and trans-
verse (Fig. 1-5).
Sagittal. T e sagittal plane, also known as the anterior–
posterior or median plane, divides the body vertically into
le and right halves o equal size.
Frontal. T e rontal plane, also known as the lateral or
coronal plane, divides the body equally into ront and back
halves.
Transverse. T e transverse plane, also known as the
horizontal plane, divides the body equally into top and
bottom halves.
 a ne
F ro n ta l p l
Ve rtica l a xis

AP
a xis

ML
a xis

T
h
e
M
u
S
c
Tra n s ve rs

u
e p la n e

l
O
S
k
e
l
e
T
A
l
S
Y
S
T
e
M
la n e
l p
Sa g itta
FIGURE 1-6 Axes o the body.

FIGURE 1-5 Planes o the body.

Because each o these planes bisects the body, it ol-
lows that each plane must pass through the center o grav-
ity (COG) or center o mass (COM).* Where a gravity eld
can be considered to be uni orm, the COG and COM are
the same (see later). I the movement described occurs in a
plane that passes through the center o gravity, that move-
ment is deemed to have occurred in a cardinal plane. An
arc o motion represents the total number o degrees traced
between the two extreme positions o movement in a spe-
ci c plane o motion.107 I a joint has more than one plane o
motion, each type o motion is re erred to as a unit o motion.
For example, the wrist has two units o motion: exion–
extension (anterior–posterior plane) and ulnar–radial devia-
tion (lateral plane).107
Few movements involved with unctional activities occur
in the cardinal planes. Instead, most movements occur in an
*T e COG, or COM, may be de ned as the point at which the three planes o
the body intersect each other. T e line o gravity is de ned as the vertical line
at which the two vertical planes intersect each other and is always vertically
downward toward the center o the earth.
in nite number o vertical and horizontal planes parallel to
the cardinal planes (see the discussion that ollows).
Axes of the Body
T ree re erence axes are used to describe human motion
(Fig. 1-6). T e axis around which the movement takes place is
always perpendicular to the plane in which it occurs.
Mediolateral. T e mediolateral (ML) or coronal, axis, is
perpendicular to the sagittal plane.
Vertical. T e vertical or longitudinal axis is
perpendicular to the rontal plane.
Anteroposterior (AP). T e AP axis is perpendicular to
the transverse plane.
Most movements occur in planes and around axes that are
somewhere in between the traditional planes and axes. T us,
nominal identi cation o every plane and axis o movement is
impractical. T e structure o the joint determines the possible
axes o motion that are available. T e axis o rotation remains
stationary only i the convex member o a joint is a per ect
sphere and articulates with a per ect reciprocally shaped 17
 Ce rvica l
Ce rvica l e xte ns ion
fle xion

Elbow
fle xion
S houlde r S houlde r
S houlde r e xte ns ion a bduction
fle xion Elbow
e xte ns ion
Hip
S houlde r
A
fle xion
a dduction
N
A
Finge r
T
S houlde r fle xion Finge r
O
Kne e circumduction e xte ns ion
M
fle xion
Y
Kne e
fle xion
Hip
Kne e e xte ns ion Hip
e xte ns ion a bduction
Hip
a dduction
Ankle Ankle
dors a l pla nta r
fle xion fle xion Hip
A B circumduction

Ce rvica l
la te ra l s ide
be nding

S houlde r
inte rna l
rota tion
Fore a rm
S houlde r prona tion
e xte rna l
rota tion Fore a rm
s upina tion

Wris t
Wris t a bduction
e xte ns ion Wris t Wris t
fle xion a dduction

Foot a nd a nkle
inve rs ion

Foot a nd a nkle Hip e xte rna l

e ve rs ion rota tion
Hip inte rna l
C rota tion FIGURE 1-7 Movements o the body.

concave member. T e planes and axes or the more common
planar movements (Fig. 1-7) are as ollows:
Flexion, extension, hyperextension, dorsi exion, and
plantar exion occur in the sagittal plane around an ML
axis. Exceptions to this include carpometacarpal exion
18 and extension o the thumb.
Abduction and adduction, side exion o the trunk,
elevation and depression o the shoulder girdle, radial and
ulnar deviation o the wrist, and eversion and inversion o
the oot occur in the rontal plane around an AP axis.
Rotation o the head, neck, and trunk; internal rotation
and external rotation o the arm or leg; horizontal
 adduction and abduction o the arm or thigh; and
pronation and supination o the orearm usually occur
in the transverse plane around the vertical axis. Rotary
motions involve the curved movement o a segment
around a xed axis, or center o rotation (COR). When a
curved movement occurs around an axis that is not xed,
but instead shi s in space as the object moves, the axis
around which the segment appears to move is re erred to
as the instantaneous axis o rotation or instantaneous COR
(see Moment Arm).
Arm circling and trunk circling are examples o
circumduction. Circumduction involves an orderly
sequence o circular movements that occur in the sagittal,
rontal, and intermediate oblique planes, so that the
segment as a whole incorporates a combination o exion,
extension, abduction, and adduction. Circumduction
movements can occur at biaxial and triaxial joints.
Examples o these joints include the tibio emoral,
radiohumeral, hip, glenohumeral, and the spinal joints.
Both the con guration o a joint and the line o pull o the
muscle acting at a joint determine the motion that occurs at
a joint:
A muscle whose line o pull is lateral to the joint is a
potential abductor.
A muscle whose line o pull is medial to the joint is a
potential adductor.
A muscle whose line o pull is anterior to a joint has
the potential to extend or ex the joint. At the knee,
an anterior line o pull may cause the knee to extend,
whereas, at the elbow joint, an anterior line o pull may
cause exion o the elbow.
A muscle whose line o pull is posterior to the joint has
the potential to extend or ex a joint (re er to preceding
example).
Center of Gravity
Every object or segment can be considered to have a single
COG, or COM—the point at which all the mass o the object
or segment appears to be concentrated. In a symmetrical
object, the COG is always located in the geometric center o
the object. However, in an asymmetrical object such as the
human body, the COG becomes the point at which the line
o gravity balances the object. T e line o gravity can best be
visualized as a string with the weight on the end (a plumb-
line), with a string attached to the COG o an object.108 I the
human body is considered as a rigid object, the COG o the
body lies approximately anterior to the second sacral verte-
bra (S2). Since the human body is not rigid, an individual’s
COG continues to change with movement with the amount
o change in the location depending on how disproportion-
ately the segments are rearranged.108 During static standing,
the body’s line o gravity is between the individual’s eet (base
o support). T e BOS includes the part o the body in con-
tact with the supporting sur ace and the intervening area.109
I an individual bends orward at the waist, the line o gravity
moves outside o the BOS. T e size o the BOS and its rela-
tion to the COG are important actors in the maintenance o
balance and, thus, the stability o an object. T e COG must
be maintained over the BOS i an equilibrium is to be main-
tained. I the BOS o an object is large, the line o gravity is
less likely to be displaced outside the BOS, which makes the
object more stable.108
Degrees of Freedom
T e number o independent modes o motion at a joint is
re erred to as the available degrees o reedom (DOF). A joint
can have up to 3 degrees o angular reedom, corresponding
to the three dimensions o space.110 I a joint can swing in one
T
h
direction or can only spin, it is said to have 1 DOF.111–114 T e
e
proximal interphalangeal joint is an example o a joint with
M
u
1 DOF. I a joint can spin and swing in one way only, or it
S
can swing in two completely distinct ways, but not spin, it
c
u
is said to have 2 DOF.111–114 T e tibio emoral joint, temporo-
l
O
mandibular joint, proximal and distal radioulnar joints, sub-
S
talar joint, and talocalcaneal joint are examples o joints with
k
e
2 DOF. I the bone can spin and also swing in two distinct
l
e
directions, then it is said to have 3 DOF.111–114 Ball-and-socket
T
A
joints, such as the shoulder and hip, have 3 DOF.
l
S
Y
S
CLINICAL PEARL
T
e
M
Joint motion that occurs only in one plane is designated
as 1 DOF; in two planes, 2 DOF; and in three planes, 3 DOF.
Because o the arrangement o the articulating sur aces—
the surrounding ligaments and joint capsules—most motions
around a joint do not occur in straight planes or along
straight lines. Instead, the bones at any joint move through
space in curved paths. T is can best be illustrated using Cod-
man’s paradox.
1. Stand with your arms by your side, palms acing inward,
thumbs extended. Notice that the thumb is pointing or-
ward.
2. Flex one arm to 90 degrees at the shoulder so that the
thumb is pointing up.
3. From this position, horizontally extend your arm so that
the thumb remains pointing up, but your arm is in a posi-
tion o 90 degrees o glenohumeral abduction.
4. From this position, without rotating your arm, return the
arm to your side and note that your thumb is now pointing
away rom your thigh.
Re erring to the start position, and using the thumb as
the re erence, the arm has undergone an external rotation
o 90 degrees. But where and when did the rotation take
place? Undoubtedly, it occurred during the three separate,
straight-plane motions or swings that etched a triangle in
space. What you have just witnessed is an example o a con-
junct rotation—a rotation that occurs as a result o joint sur-
ace shapes—and the e ect o inert tissues rather than con-
tractile tissues. Conjunct rotations can only occur in joints
that can rotate internally or externally. Although not always
apparent, most joints can so rotate. Consider the motions o
elbow exion and extension. While ully exing and extend-
ing your elbow a ew times, watch the pisi orm bone and 19
 orearm. I you watch care ully, you should notice that the
pisi orm and the orearm move in a direction o supination
during exion, and pronation during extension o the elbow.
T e pronation and supination motions are examples o con-
junct rotations.
Most habitual movements, or those movements that occur
most requently at a joint involve a conjunct rotation. How-
ever, the conjunct rotations are not always under volitional
control. In act, the conjunct rotation is only under volitional
control in joints with 3 DOF (e.g., glenohumeral and hip
joints). In joints with ewer than 3 DOF (hinge joints, such
as the tibio emoral and ulnohumeral joints), the conjunct
A
N
rotation occurs as part o the movement but is not under
A
voluntary control. T e implications or this become impor-
T
O
tant when attempting to restore motion at these joints: the
M
mobilizing techniques must take into consideration both the
Y
relative shapes o the articulating sur aces as well as the con-
junct rotation that is associated with a particular motion (see
Chapter 10).
JOINT KINEMATICS
Kinematics is the study o motion and describes how some-
thing is moving without stating the cause. Kinetics is the term
used to explain why an object moves the way it does due to
the orces acting on that object (see Chapter 2). In studying
joint kinematics, two major types o motion are involved: (1)
osteokinematic and (2) arthrokinematic.
Osteokinematic Motion
T e normal ROM o a joint is sometimes called the physi-
ologic or anatomic ROM. Physiologic movements o the
bones termed osteokinematics, are movements that can be
per ormed voluntarily, or example, exion o the shoul-
der. Osteokinematic motion occurs when any object orms
the radius o an imaginary circle about a xed point. T e
axis o rotation or osteokinematic motions is oriented
perpendicular to the plane in which the rotation occurs.106
T e distance traveled by the motion may be a small arc or
a complete circle and is measured as an angle, in degrees.
All human body segment motions involve osteokinema-
tic motions. Examples o osteokinematic motion include
abduction or adduction o the arm, exion o the hip or
knee, and side bending o the trunk. A number o ac-
tors determine the amount o available physiologic joint
motion, including
the integrity o the joint sur aces and the amount o joint
motion;
the mobility and pliability o the so tissues that surround
a joint;
the degree o so -tissue approximation that occurs;
the amount o scarring that is present115—interstitial
scarring or brosis can occur in and around the joint
capsules, within the muscles, and within the ligaments as
a result o previous trauma;
20
age—joint motion tends to decrease with increasing age;
gender—in general, emales have more joint motion than
males.
ROM is considered to be pathological when motion at a
joint either exceeds or ails to reach the normal physiologic
limits o motion (see Chapter 2).90
Moment Arm
o understand the concept o a moment arm, an understand-
ing o the anatomy and movement (kinematics) o the joint o
interest is necessary. Although muscles produce linear orces,
motions at joints are all rotary. For example, some joints can
be considered to rotate about a xed point. A good example
o such a joint is the elbow. At the elbow joint, where the
humerus and ulna articulate, the resulting rotation occurs pri-
marily about a xed point, re erred to as the COR. In the case
o the elbow joint, this COR is relatively constant through-
out the joint ROM. However, in other joints (e.g., the knee)
the COR moves through space as the knee joint exes and
extends because the articulating sur aces are not per ect cir-
cles. In the case o the knee, it is not appropriate to discuss a
single COR—rather we must speak o a COR corresponding
to a particular joint angle, or, using the terminology o joint
kinematics, we must speak o the instantaneous center o rota-
tion (ICR), that is, the COR at any “instant” in time or space.
T us, the moment arm is de ned as the perpendicular dis-
tance rom the line o orce application to the axis o rotation.
Arthrokinematic Motion
T e term arthrokinematics is used to describe the motions o
the bone sur aces within the joint. T ese movements cannot
be per ormed voluntarily and can only occur when resistance
to active motion is applied, or when the patient’s muscles are
completely relaxed. Both the physiologic (osteokinematic)
and joint play (arthrokinematic) motions occur simultane-
ously during movement and are directly proportional to each
other, with a small increment o arthrokinematic motion
resulting in a larger increment o osteokinematic motion.
Normal arthrokinematic motions must occur or a ull-range
o physiologic motion to occur. Mennell116,117 introduced the
concept that ull, painless, active ROM is not possible with-
out these motions and that a restriction o arthrokinematic
motion results in a decrease in osteokinematic motion. At
each synovial articulation, the articulating sur ace o each
bone moves in relation to the shape o the other articulating
sur ace. A normal joint has an available range o active, or
physiologic, motion, which is limited by a physiologic bar-
rier as tension develops within the surrounding tissues, such
as the joint capsule, ligaments, and C . Beyond the available
passive ROM, the anatomic barrier is ound. T is barrier
cannot be exceeded without disruption to the integrity o the
joint. Accessory or component motions, which are also not
under voluntary control occur during active motion. T ese
include examples such as rotation o the ulna during orearm
pronation and supination. At the physiologic barrier, there
is an additional amount o passive ROM. T is small motion,
 A B

Exte ns ion

S pin
Fe mur
s tatio nary

Roll

T
h
e
M
u
S lide

S
c
u
l
O
S
k
Roll a nd

e
l
s lide

e
T
A
Tibia

l
s tatio nary Exte ns ion
S pin

S
Y
S
T
e
M
FIGURE 1-8 Arthrokinematics o motion.

which is available at the joint sur aces, is re erred to as joint-

play motion. T e type and amount o motion occurring at the
joint sur aces is in uenced by the shape o their respective
joint sur aces. T ree undamental types o joint-play motions
exist based on the di erent types o joint sur aces (Fig. 1-8):118 A
Roll. A roll occurs when the points o contact on each

B
o
incongruent joint sur ace are constantly changing so

n
e
that new point on one sur ace meets a new point on the

m
o
opposite sur ace (see Fig. 1-8). T is type o movement

ti
o
n
is analogous to a tire on a car as the car rolls orward. In
J
o

a normal unctioning joint, pure rolling does not occur S ta tiona ry

in
t

alone but instead occurs in combination with joint sliding

g
lid

and spinning. T e term rock is o en used to describe

e

small rolling motions. Rolling is always in the same

direction as the swinging bone motion irrespective o
whether the sur ace is convex or concave (Fig. 1-8). I the
rolling occurs alone, it causes compression o the sur aces
on the side to which the bone is swinging and separation B
on the other side.
Slide. A slide is a pure translation i the two sur aces are
congruently at or curved. It occurs i only one point on
e
c

the moving sur ace makes contact with new points on the S ta tiona ry
a
rf
u

opposing sur ace (see Fig. 1-8). T is type o movement

tio
s

is analogous to a car tire skidding when the brakes are

t
in

ic

applied suddenly on a wet road. T is type o motion also

r
o

st
J

is re erred to as translatory motion. Although the roll o

e
R

a joint always occurs in the same direction as the swing

o a bone, the direction o the slide is determined by the
shape o the articulating sur ace (Fig. 1-9). T is rule is FIGURE 1-9 Gliding motions according to joint sur aces.
21
 o en re erred to as the concave–convex rule: I the joint
sur ace is convex relative to the other sur ace, the slide
occurs in the opposite direction to the osteokinematic
motion (see Fig. 1-9). I , on the other hand, the joint
sur ace is concave, the slide occurs in the same direction
as the osteokinematic motion (see Fig. 1-9). T e clinical
signi cance o the concave–convex rule is described in
Chapter 10.
Spin. A spin is de ned as any movement in which the
bone moves, but the mechanical axis remains stationary.
A spin involves a rotation o one sur ace on an opposing
A
sur ace around a vertical axis (see Fig. 1-8). T is type o
N
motion is analogous to the pirouette per ormed by a ballet
A
T
dancer. Spinning rarely occurs alone in joints but instead
O
occurs in combination with rolling and sliding. Spin
M
Y
motions in the body include internal and external rotation
o the glenohumeral joint when the humerus is abducted
to 90 degrees; and at the radial head during orearm
pronation and supination.
As osteokinematic and arthrokinematic motions are
directly proportional to each other, such that one cannot
occur completely without the other, it ollows that i a joint
is not unctioning correctly, one or both o these motions
may be at ault. When examining a patient with move-
ment impairment, it is critical that the clinician determine
whether the osteokinematic motion or the arthrokinematic
motion is restricted so that the intervention can be made
as speci c as possible. T is is particularly important when
trying to regain motion using traditional stretching meth-
ods which employ osteokinematic motions, as these meth-
ods magni y the orce at the joint and cause compression
o the joint sur aces in the direction o the rolling bone. In
contrast, using an arthrokinematic technique to increase the
joint play allows the orce to be applied close to the joint
sur ace and in the direction that replicates the sliding com-
ponent o the joint mechanics.
CLINICAL PEARL
Two other accessory motions are used by clinicians in vari-
ous manual techniques, compression and distraction:
Compression. This occurs when there is a decrease in
the joint space between bony partners and although it
occurs naturally throughout the body whenever a joint
is weight bearing, it can be applied manually to help
move synovial f uid and maintain cartilage health.
Distraction. This involves an increase in the joint space
between bony partners. The terms traction and dis-
traction are not synonymous, as the ormer involves a
orce applied to the long axis o a bone, which does
not always result in the joint space increasing between
the bony partners. For example, i traction is applied
to the sha t o the emur, it results in a glide occurring
at the hip joint sur ace, whereas i a distraction orce is
applied at right angles to the acetabulum, distraction at
the hip joint occurs.
22
In the extremities, osteokinematic motion is controlled
by the amount o exibility o the surrounding so tissues o
the joint, where exibility is de ned as the amount o inter-
nal resistance to motion. In contrast, the arthrokinematic
motion is controlled by the integrity o the joint sur aces
and the supporting tissues o the joint. T is characteristic
can be noted clinically in a chronic rupture o the anterior
cruciate ligament o the knee. Upon examination o that knee,
the arthrokinematic motion (joint slide or glide) is ound to
be increased, illustrated by a positive Lachman test, but the
ROM o the knee, its osteokinematic motion, is not a ected
(see Chapter 20).
In contrast, in the spine, the osteokinematic motion is con-
trolled by both the exibility o the surrounding so tissues
and by the integrity o the joint sur aces and the supporting
tissues o the joint. T is characteristic can be noted clinically
when examining the craniovertebral joint, where a restriction
in the arthrokinematic motion (joint slide or glide) can be
caused by either a joint restriction or an adaptively shortened
sub-occipital muscle (see Chapter 23).
T e examination o these motions and their clinical impli-
cations are described in Chapters 4 and 10.
Levers
A lever is a rigid object that is used to either multiply the
mechanical orce (e ort) or resistance orce (load) applied to
it around an axis. T e e ort orce attempts to cause movement
o the load. For simplicity sake, levers are usually described
using a straight bar that is the lever, and the ulcrum, which
is the point on which the bar is resting, and around which the
lever rotates. T at part o the lever between the ulcrum and
the load is re erred to as the load arm. T ree types o levers
are commonly cited:
First class: occurs when two orces are applied on either
side o the axis, and the ulcrum lies between the e ort
and the load (Fig. 1-10), like a seesaw. Examples in
the human body include the contraction o the triceps
at the elbow joint, or tipping o the head orward and
backward.
Second class: occurs when the load (resistance) is applied
between the ulcrum and the point where the e ort is
exerted (Fig. 1-10). T e magni ying e ects o the e ort
require less orce to move the resistance. Examples o
second-class levers in everyday li e include the nutcracker,
and the wheelbarrow—with the wheel acting as the
ulcrum. Examples o second-class levers in the human
body include weight-bearing plantar exion (rising up
on the toes) (Fig. 1-10). Another would be an isolated
contraction o the brachioradialis to ex the elbow, which
could only occur i the other elbow exors are paralyzed.
T ird class: occurs when the load is located at the end o
the lever (Fig. 1-10), and the e ort lies between the ulcrum
and the load, like a drawbridge or a crane. T e e ort is
exerted between the load and the ulcrum. T e e ort
expended is greater than the load, but the load is moved a
greater distance. Most movable joints in the human body
unction as third-class levers— exion at the elbow.
 Effort

Effort

T
h
Fulcrum

e
M
u
S
Loa d

c
Loa d Effort

u
Fulcrum

l
O
Fulcrum

S
Loa d

k
e
A Firs t-cla s s leve r B S e cond-cla s s leve r C Third-cla s s leve r

l
e
T
FIGURE 1-10 Classes o levers.

A
l
S
Y
S
T
When a machine puts out more orce than is put in, the wo types o kinematic chain systems are recognized:

machine is said to have a mechanical advantage (MA). T e
MA o the musculoskeletal lever is de ned as the ratio o
the internal moment arm to the external moment arm.
Depending on the location o the axis o rotation, the rst-
class lever can have an MA equal to, less than, or greater than
1.110 Second-class levers always have an MA greater than 1.
T ird-class levers always have an MA less than 1. T e major-
ity o muscles throughout the musculoskeletal system unc-
tion with an MA o much less than 1. T ere ore, the muscles
and underlying joints must “pay the price” by generating and
dispersing relative large orces, respectively, even or seem-
ingly low-load activities.110
KINEMATIC CHAINS
When a body moves, it does so by its kinematics, which in
the human body take place through arthrokinematic and os-
teokinematic movements. T e expression kinematic chain is
used in rehabilitation to describe the unction or activity o
an extremity or trunk in terms o a series o linked chains (see
Chapter 12). A kinematic chain re ers to a series o articu-
lated, segmented links, such as the connected pelvis, thigh,
leg, and oot o the lower extremity.110 According to kinematic
chain theory, each o the joint segments o the body involved
in a particular movement constitutes a link in the kinematic
chain. Because each motion o a joint is o en a unction o
other joint motions, the ef ciency o an activity can be depen-
dent on how well these chain-links work together.119
CLINICAL PEARL
The number o links within a particular kinematic chain var-
ies, depending on the activity. In general, longer kinematic
chains are involved with more strenuous activities.
e
M
closed kinematic chain (CKC) systems and the open kinematic
chain (OKC) systems (Table 1-5).120
Closed Kinematic Chain
A variety o de nitions or a CKC activity have been proposed:
1. Palmitier et al.121 de ne an activity as closed i both ends
o the kinetic chain are connected to an immovable rame-
work, thus preventing translation o either the proximal, or
distal joint center, and creating a situation whereby move-
ment at one joint produces a predictable movement at all
other joints.
2. Gray122 considers a closed-chain activity to involve xation
o the distal segment so that joint motion takes place in
multiple planes, and the limb is supporting the weight.
3. Dillman et al.123 describe the characteristics o closed-
chain activities to include relatively small joint move-
ments, low joint accelerations, greater joint compressive
orces, greater joint congruity, decreased shear, stimula-
tion o joint proprioception, and enhanced dynamic stabi-
lization through muscle coactivation.124
4. Kibler 124 de nes a closed-chain activity as a sequential
combination o joint motions that have the ollowing char-
acteristics:
a. T e distal segment o the kinetic chain meets
considerable resistance.
b. T e movement o the individual joints, and
translation o their instant centers o rotation occurs
in a predictable manner that is secondary to the
distribution o orces rom each end o the chain.
Examples o closed kinematic chain exercises (CKCEs)
involving the lower extremities include the squat and the leg
23
 TABLE 1-5 Differential Features of OKC and CKC Exercises
Exercise Mode Characteristics Advantages Disadvantages
Open kinematic 1. Single muscle group 1. Isolated recruitment 1. Limited unction
chain 2. Single axis and plane 2. Simple movement pattern 2. Limited eccentrics
3. Emphasizes concentric contraction 3. Minimal joint compression 3. Less proprioception and joint stability
4. Nonweight bearing with increased joint shear orces

Closed kinematic 1. Multiple muscle groups 1. Functional recruitment 1. Di cult to isolate

2. Multiple axes and planes 2.
3. Balance o concentric and 3.
eccentric contractions 4.
A
N
4. Weight-bearing exercise
A
T
Data rom Green eld BH, Tovin BJ. The application o open and closed kinematic chain exercises in rehabilitation o the lower extremity. J Back Musculoskel
O
Rehabil. 1992;2:38–51.
M
Y
press. T e activities o walking, running, jumping, climbing,
and rising rom the oor all incorporate closed kinetic chain
components. An example o a CKCE or the upper extremi-
ties is the push-up, or when using the arms to push down on
the armrests to rise out o a chair.
CLINICAL PEARL
In most activities o daily living, the activation sequence
o the links involves a closed chain whereby the activity is
initiated rom a rm base o support and trans erred to a
more mobile distal segment.
Open Kinematic Chain
It is accepted that the di erence between OKC and CKC
activities is determined by the movement o the end segment.
T e traditional de nition or an open-chain activity included
all activities that involved the end segment o an extremity
moving reely through space, resulting in isolated movement
o a joint.
Examples o an open-chain activity include li ing a drink-
ing glass and kicking a soccer ball. Open kinematic chain exer-
cises (OKCEs) involving the lower extremity include the seated
knee extension and prone knee exion. Upper extremity exam-
ples o OKCE include the biceps curl and the military press.
Many activities, such as swimming and cycling, tradition-
ally viewed as OKC activities, include a load on the end seg-
ment; yet the end segment is not “ xed” and restricted rom
movement. T is ambiguity o de nitions or CKC and OKC
activities has allowed some activities to be classi ed in oppos-
ing categories.123 T us, there has been a growing need or clari-
cation o OKC and CKC terminology, especially when related
to unctional activities.
T e works o Dillman et al.123 and then Lephart and
Henry125 have attempted to address the con usion. Dillman
et al.123 proposed three classi cations o activity to help clari y
the gray area between the CKC and the OKC activity. T ese
24
Functional movement patterns 2. More complex
Functional contractions 3. Loss o control o target joint
Increased proprioception and 4. Compressive orces on articular
joint stability sur aces
classi cations were based on the boundary condition, either
movable or xed, and the presence or absence o a load on the
end segment. An activity with a xed boundary and no load
does not exist, resulting in three classi cations:
1. Movable no load. T ese activities involve a movable end
with no load and closely resemble the extreme o an open-
chain activity. An example o this type o activity is hitting
a ball with a tennis racket.
2. Movable external load. T ese activities involve a movable
end with an external load and include a combination o
open- and closed-chain actions because they are charac-
terized by cocontractions o the muscles around the joints.
An example o this type o activity is the overhead shoul-
der (military) press.
3. Fixed external load. T ese activities involve a xed end
with an external load, and closely resemble the extreme o
a closed-chain activity. An example o this type o activity
is the push-up.
Lephart and Henry suggested that a urther de nition
could be made by analyzing the ollowing characteristics o
an activity:
T e direction o orce.
T e magnitude o the load.
Muscle action.
Joint motion.
Neuromuscular unction.
Under Lephart and Henry’s classi cation, activities could
be subdivided into our groups:
1. Activities that involve a xed boundary with an external
and axial load. An example o this type o activity is the use
o a slide board.
2. Activities that involve a movable boundary with an exter-
nal and axial load. An example o this type o activity is the
bench press.
3. Activities that involve a movable boundary with an exter-
nal and rotary load. An example o this type o activity is a
 resisted proprioceptive neuromuscular acilitation (PNF) TABLE 1-6 Close Packed Position of the Joints
motion pattern (see Chapter 10).
Joint Position
4. Activities that involve a movable boundary with no load.
Zygapophyseal (spine) Extension
An example o this type o activity is position training.
Although both the Dillman and Lephart and Henry mod- Temporomandibular Teeth clenched
els appear to be describing the same concept, the Lephart Glenohumeral Abduction and external rotation
and Henry model is distinct in that it incorporates diagonal
or rotary components to the movements. T ese diagonal and Acromioclavicular Arm abducted to 90 degrees
rotary movements eature in the vast majority o unctional Sternoclavicular Maximum shoulder elevation
activities.
Ulnohumeral Extension

T
h
Radiohumeral Elbow f exed 90 degrees; orearm

e
CLOSE-PACKED AND OPEN-

M
supinated 5 degrees

u
PACKED POSITIONS OF THE JOINT

S
Proximal radioulnar 5 degrees o supination

c
u
Distal radioulnar 5 degrees o supination

l
Joint movements usually are accompanied by a relative

O
S
compression (approximation) or distraction (separation) Radiocarpal (wrist) Extension with radial deviation

k
e
o the opposing joint sur aces. T ese relative compressions

l
Metacarpophalangeal Full f exion

e
or distractions a ect the level o congruity o the oppos-

T
ing sur aces. T e position o maximum congruity o the

A
Carpometacarpal Full opposition

l
opposing joint sur aces is termed the close-packed position

S
Y
o the joint. T e position o least congruity is termed the Interphalangeal Full extension

S
T
open-packed position. T us, movements toward the close-

e
Hip Full extension, internal rotation,
packed position o a joint involve an element o compres-

M
and abduction
sion, whereas movements out o this position involve an
element o distraction. Tibio emoral Full extension and external
rotation o tibia

Close Packed Position Talocrural (ankle) Maximum dorsif exion

T e close-packed position o a joint is the joint position that Subtalar Supination

results in:
Midtarsal Supination
T e maximal tautness o the major ligaments.
Tarsometatarsal Supination
Maximal sur ace congruity.
Minimal joint volume. Metatarsophalangeal Full extension
Maximal stability o the joint. Interphalangeal Full extension
Once the close-packed position is achieved, no urther
motion in that direction is possible. T is is the o en-cited rea-
son most ractures and dislocations occur when an external
orce is applied to a joint that is in its close-packed position. Maximal joint volume.
Also, many o the traumatic injuries o the upper extremities
result rom alling on a shoulder, elbow or wrist, which are Minimal stability o the joint.
in their close-packed position. T is type o injury, a all on T e open-packed position permits maximal distraction
an outstretched hand is o en re erred to as a FOOSH injury. o the joint sur aces. Because the open-packed position causes
T e close-packed positions or the various joints are depicted the brunt o any external orce to be borne by the joint cap-
in Table 1-6. sule or surrounding ligaments, most capsular or ligamentous
sprains occur when a joint is in its open-packed position. T e
open-packed positions or the various joints are depicted in
Open Packed Position
Table 1-7.
In essence, any position o the joint, other than the close-
packed position, could be considered as an open-packed posi-
tion. T e open-packed position, also re erred to as the loose-
packed position o a joint, is the joint position that results in:
CLINICAL PEARL
Slackening o the major ligaments o the joint.
Minimal sur ace congruity. The open-packed position is commonly used during joint
mobilization techniques (see Chapter 10).
Minimal joint sur ace contact.
25
 TABLE 1-7 Open Packed (Resting) Position of the Joints
Joint Position
Zygapophyseal (spine) Midway between f exion and extension

Temporomandibular Mouth slightly open ( reeway space)

Glenohumeral 55 degrees o abduction; 30 degrees o horizontal adduction

Acromioclavicular Arm resting by side

Sternoclavicular Arm resting by side

Ulnohumeral 70 degrees o f exion; 10 degrees o supination

A
N
Radiohumeral Full extension; ull supination
A
T
O
Proximal radioulnar 70 degrees o f exion; 35 degrees o supination
M
Y
Distal radioulnar 10 degrees o supination

Radiocarpal (wrist) Neutral with slight ulnar deviation

Carpometacarpal Midway between abduction–adduction and f exion–extension

Metacarpophalangeal Slight f exion

Interphalangeal Slight f exion

Hip 10–30 degrees o f exion; 10–30 degrees o abduction; and 0–5 degrees o external rotation

Tibio emoral 25 degrees o f exion

Talocrural (ankle) 10 degrees o plantar f exion; midway between maximum inversion and eversion

Subtalar Midway between extremes o range o movement

Midtarsal Midway between extremes o range o movement

Tarsometatarsal Midway between extremes o range o movement

Metatarsophalangeal Neutral

Interphalangeal Slight f exion

REFERENCES
1. Buckingham M, Bajard L, Chang , et al. T e ormation o skeletal
muscle: rom somite to limb. J Anat. 2003;202:59–68.
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C H AP TER 2 I
CHAPTER OBJECTIVES
At the completion of this cha pter,
the reader will be able to:
1. Describe the various types o stress that are applied to the
body.
2. Describe the various physiological processes by which the
body adapts to stress.
3. De ne the various common mechanisms o injury.
4. Describe the etiology and pathophysiology o
musculoskeletal injuries associated with various
types o body tissue.
5. Outline the pathophysiology o the healing process and
the various stages o healing o the various connective
tissues.
6. Describe the actors that can impede the healing process.
7. Outline the more common surgical procedures available
or musculoskeletal injuries.
8. Outline the principles behind postsurgical rehabilitation.
9. Describe the detrimental e ects o immobilization.
OVERVIEW
issues in the body are designed to unction while under-
going the stresses o everyday living. Body weight, riction,
and air or water resistance are all types o stresses that com-
monly act on the body. T e ability o the tissues to respond
to stress is due to the di ering viscoelastic properties o the
tissue, with each tissue responding to stress in an individual
manner based on design. Maintaining the health o the vari-
ous tissues is a delicate balance because insu cient, excessive,
or repetitive stresses can prove deleterious. Fortunately, most
tissues have an inherent ability to sel -heal—a process that is
an intricate phenomenon.
Ti Bh i ,
,H i ,
T t t
THE RESPONSE OF TISSUE TO STRESS
Kinetics is the term applied to de ne the orces acting on the
body. Posture and movement are both governed by the body’s
ability to control these orces. T e same orces that move and
stabilize the body also have the potential to de orm and injure
the body.1 A wide range o external and internal orces are
either generated or resisted by the human body during daily
activities. Examples o these external orces include ground
reaction orce, gravity, and applied orce through contact.
Examples o internal orces include structural tension, joint
compression, and joint shear orces (Fig. 2-1). Under the
right circumstances, the body can respond and adapt to these
stresses. T e terms stress and strain have speci c mechanical
meanings. Stress, or load, is de ned in units o orce per area,
and is used to describe the type o orce applied. Stress is inde-
pendent o the amount o material, but is directly related to
the magnitude o orce and inversely related to the unit area.2
Strain is de ned as the change in length o a material due to
an imposed load, divided by the original length.2 T e two
basic types o strain are a linear strain, which causes a change
in the length o a structure, and shear strain, which causes a
change in the angular relationships within a structure. It is the
concentration o proteoglycans in solution (see Chapter 1)
that is responsible or in uencing the mechanical properties
o the tissue, including compressive sti ness, sheer sti ness,
osmotic pressure, and the regulation o hydration.3
CLINICAL PEARL
Strain is the amount o elongation divided by the length
o the structure.
Stress is the orce in a structure divided by the cross-
sectional area.
T e inherent ability o a tissue to tolerate load can be observed
experimentally in graphic orm. When any stress is plotted on a
graph against the resulting strain or a given material, the shape
o the resulting load–de ormation curve depends on the kind
o material involved. T e load–de ormation curve, or stress–
strain curve, o a structure (Fig. 2-2) depicts the relationship
between the amount o orce applied to a structure and the
29

= and the waviness o the collagen pattern.
Origina l
s ha pe S he a r
A
N
A
= =
T
O
M
Y
Compre s s ion Te ns ion
FIGURE 2-1 Internal orces acting on the body.
structure’s response in terms o de ormation or acceleration.
T e horizontal axis (de ormation or strain) represents the
ratio o the tissue’s de ormed length to its original length. T e
vertical axis o the graph (load or stress) denotes the internal
resistance generated as a tissue resists its de ormation, divided
by its cross-sectional area. T e load–de ormation curve can be
divided into our regions, each region representing a biome-
chanical property o the tissue (Fig. 2-2):
oe region. Collagen bers have a wavy, or olded,
appearance at rest or on slack. When a orce that
lengthens the collagen bers is initially applied to
connective tissue, this slack range is a ected rst, and the
bers un old as the slack is taken up (see Crimp later).
T e toe region is an arti act caused by this take-up o
slack, alignment, and/or seating o the test specimen. T e
length o the toe region depends on the type o material
Elastic region. Within the elastic de ormation region, the
structure imitates a spring—the geometric de ormation
in the structure increases linearly with increasing load,
and a er the load is released the structure returns to
its original shape. T e slope o the elastic region o the
load–de ormation curve rom one point in the curve to
another, which corresponds to the physiological range o
a structure, is called the modulus o elasticity or Young’s
modulus, and represents the extrinsic sti ness or rigidity
o the structure—the sti er the tissue, the steeper the
slope. A key characteristic o passive tendon loading
is its sti ness—the orce in the tendon divided by the
amount o lengthening o the tendon.4 Young’s modulus
is a numerical description o the relationship between the
amount o stress a tissue undergoes and the de ormation
that results—stress divided by the strain. T e ratio o stress
to strain in an elastic material is a measure o its sti ness.
Young’s modulus is independent o specimen size and
is, there ore, a measure o the intrinsic sti ness o the
material. T e greater the Young’s modulus or a material,
the better it can withstand greater orces. Mathematically,
the value or sti ness is ound by dividing the load by the
de ormation at any point in the selected range. All normal
tissues within the musculoskeletal system exhibit some
degree o sti ness. Larger structures will have greater
rigidity than smaller structures o similar composition.
Sti ness is not necessarily a negative characteristic—
tendons transmit orce more e ectively and e ciently
when they are sti er.4
Plastic region. T e end o the elastic de ormation range,
and the beginning o the plastic de ormation range,
represents the point where an increasing level o stress on

REGIONS

LOAD (B)
(S TRES S ) Plas tic
Failure

Elas tic
(A)

To e

I II III IV DEFORMATION
S la ck Line a r P rima ry Comple te (S TRAIN)
ra nge phys iologica l fa ilure fa ilure
ra nge los s of
me cha nica l
prope rtie s

30 FIGURE 2-2 The stress–strain curve.

 the tissue results in progressive ailure and microscopic
tearing o the collagen bers. Further increases in
strain result in microscopic damage and permanent
de ormation. T e permanent change results rom the
breaking o bonds and their subsequent inability to
contribute to the recovery o the tissue. Unlike the elastic
region, removal o the load in this region will not result in
a return o the tissue to its original length.
Failure region. De ormations exceeding the ultimate
ailure point (Fig. 2-2) produce mechanical ailure o the
structure, which in the human body may be represented
Crimp
T e crimp o collagen is one o the major actors behind the
viscoelastic properties o connective tissue. Crimp, a collagen
tissue’s rst line o response to stress, is di erent or each type
o connective tissue, providing each with di erent viscoelas-
tic properties. Collagen bers are oriented obliquely when
relaxed. However, when a load is applied, the bers line up in
the direction o the applied orce as they uncrimp. Crimping
is seen primarily in ligaments, tendons, and joint capsules, and
occurs in the toe phase o the stress–strain curve (Fig. 2-2).

T
by the racturing o bone or the rupturing o a so

I
s
tissue.

s
CLINICAL PEARL

u
e
I a load is applied to the connective tissue and then

B
e
CLINICAL PEARL removed immediately, the material recoils to its original

H
a
size. I , however, the load is allowed to remain, the

v
Sti ness = orce/de ormation. The gradient in the linear material continues to stretch. A ter a period o a sustained

I
o
portion o the load-de ormation graph immediately a ter stretch, the stretching tends to reach a steady-state value.

r
,
the toe region o the load–displacement curve represents Realignment o the collagen bers in the direction o the

I
n
the sti ness value. The load–de ormation curve does not stress occurs, and water and proteoglycans are displaced

j
u
indicate the variable o time. rom the bers.

r
y
Elastic modulus = stress/strain. The larger the Young’s

,
H
modulus or a material, the greater stress needed or a

e
given strain.

a
Viscoelasticity

l
I
n
Viscoelasticity is the time-dependent mechanical prop-

g
,
Biological tissues are anisotropic, which means they can erty o a material to stretch or compress over time, and to

a
return to its original shape when a orce is removed. T e

n
demonstrate di ering mechanical behavior as a unction o

d
test direction. T e properties o extensibility and elasticity are mechanical qualities o a tissue can be separated into cat-

T
egories based on whether the tissue acts primarily as a solid,

r
common to many biologic tissues. Extensibility is the ability

e
uid, or a mixture o the two. Solids are described according

a
to be stretched, and elasticity is the ability to return to normal

T
length a er lengthening or shortening.5 to their elasticity, strength, hardness, and sti ness. Bone,

m
ligaments, tendons, and skeletal muscle are all examples o

e
n
elastic solids. Biological tissues that demonstrate attributes

CLINICAL PEARL
Unloading a tendon signi cantly in uences the mechanical
properties. For example, one study that looked at the
e ects o 4 weeks o unilateral lower limb suspension
ollowed by 6 weeks o rehabilitation ound that there was
a 17% decrease in the elastic modulus (lower sti ness)
a ter suspension, and the restoration o normal sti ness
a ter rehabilitation.6
Some protective mechanisms exist in connective tissue
to help respond to stress and strain, including crimp, visco-
elasticity, creep and stress relaxation, plastic de ormation,
and stress response.
CLINICAL PEARL
Protective tissue mechanisms include:
Crimp
Viscoelasticity
Creep and stress relaxation
Plastic de ormation
Stress response
T
o both solids and uids are viscoelastic. T e viscoelastic
properties o a structure determine its response to loading.
For example, a ligament demonstrates more viscous behav-
ior at lower loads whereas, at higher loads, elastic behaviors
dominate.7
Creep and Stress Relaxation
Creep and stress relaxation are two characteristics o visco-
elastic materials that are used to document their behavior
quantitatively.5
Creep is the gradual rearrangement o collagen bers, pro-
teoglycans, and water that occurs because o a constantly
applied orce a er the initial lengthening caused by crimp has
ceased. Creep is a time-dependent and transient biomechani-
cal phenomenon. Short duration stresses (<15 minutes) do
not have su cient time to produce this displacement; how-
ever, longer times can produce it. Once creep occurs, the tis-
sue has di culty returning to its initial length (see below).
Stress relaxation is a phenomenon in which stress or orce in
a de ormed structure decreases with time while the de orma-
tion is held constant.5 Unlike creep, stress relaxation responds
with a high initial stress that decreases over time until equi-
librium is reached and the stress equals zero, hence the label
“relaxation.” As a result, no change in length is produced. 31
 T us, stress to connective tissues can result in no change, a
semipermanent change, or a permanent change to the micro-
structure o the collagenous tissue. T e semipermanent or
permanent changes may result in either micro ailure.
Plastic De ormation
Plastic de ormation o connective tissue occurs when a tissue
remains de ormed and does not recover its prestress length.
Once all o the possible realignment has occurred, any urther
loading breaks the restraining bonds, resulting in micro ailure.
On average, collagen bers can sustain a 3% increase in elonga-
A
N
tion (strain) be ore microscopic damage occurs.8 Following a
A
brie stretch, providing the chemical bonds remain intact, the
T
O
collagen and proteoglycans gradually recover their original
M
alignment. T e recovery process occurs at a slower rate and
Y
o en to a lesser extent. T e loss o energy that occurs between
the lengthening orce and the recovery activity is re erred to
as hysteresis. T e more chemical bonds that are broken with
applied stress, the greater the hysteresis. I the stretch is o su -
cient orce and duration, and a su cient number o chemical
bonds are broken, the tissue is unable to return to its original
length until the bonds are re- ormed. Instead, it returns to a
new length and a new level o strain resistance. Increased tissue
excursion is now needed be ore tension develops in the struc-
ture. In essence, this has the e ect o decreasing the stabilizing
capabilities o the connective tissue.
Stress Response
Exercises may be used to change the physical properties o both
muscles/tendons and ligaments, as both have demonstrated
adaptability to external loads with an increase in strength:weight
ratios.9–11 T e improved strength results rom an increase in the
proteoglycan content and collagen cross-links.9–11
CLINICAL PEARL
Three biomechanical attributes o connective tissue can
have clinical signi cance:
Structural behavior
Material behavior
Viscoelastic behavior
TISSUE INJURY
So tissue injuries o all types are extremely common in the
general population. Studies have shown that there is a lin-
ear relationship between so tissue injuries and aging, with
ewer than 10% o individuals younger than 34 years being
a ected, in contrast to 32–49% o those older than 75 years
being a ected.12 Whether a stress proves to be bene cial or
detrimental to a tissue is very much dependent on the physi-
ologic capacity o the tissue to accept load. T is capacity is
dependent on some actors, among them:
T e health o the tissue. Healthy tissues can resist
32 changes in their shape. Any tissue weakened by disease
or trauma may not be able to resist adequately the
application o orce.
Age. Increasing age reduces the capacity o the tissues to
cope with stress loading.
Proteoglycan and collagen content o the tissue. Both
increasing age and exposure to trauma can result in
un avorable alterations in the proteoglycan and collagen
content o a tissue.
T e ability o the tissue to undergo adaptive change. All
musculoskeletal tissue can adapt to change. T is capacity
to change is determined primarily by the viscoelastic
property o the tissue.
T e speed at which the adaptive change occurs. T is
is dependent on the type and severity o the insult to
the tissue. Insults o low orce and longer duration may
provide the tissue an opportunity to adapt. In contrast,
insults o a higher orce and shorter duration are less
likely to provide the tissue time to adapt. T e distinction
between sudden and repetitive stress is important. An
acute stress (loading) occurs when a single orce is large
enough to cause injury on biological tissues; the causative
orce is termed macrotrauma. A repetitive stress (loading)
occurs when a single orce itsel is insu cient to cause
injury on biological tissues. However, when repeated or
chronic stress over a period causes an injury, the injury
is called a chronic injury, and the causative mechanism is
termed microtrauma. Etiologic actors or microtraumatic
injuries are o two basic types: intrinsic or extrinsic.
Intrinsic actors are physical characteristics that predispose
an individual to microtrauma injuries and include muscle
imbalances, leg length discrepancies, and anatomical
anomalies.13 Extrinsic actors, which are the most common
cause o microtrauma injuries, are related to the external
conditions under which the activity is per ormed. T ese
include training errors, type o terrain, environmental
temperature, and incorrect use o equipment.13
INJURY CLASSIFICATION
Injuries to the so tissues can be classi ed as primary or
secondary.
Primary, or macrotraumatic, injuries can be sel -in icted,
caused by another individual or entity, or caused by
the environment.14–17 T ese injuries include ractures,
subluxations, and dislocations, which are outside the scope
o practice or a physical therapist, and sprains, and strains,
which make up the majority o conditions seen in the
physical therapy clinic. For the purposes o the intervention,
primary injuries are classi ed into acute, subacute, or chronic.
Acute. T is type o injury is usually caused by
macrotrauma and indicates the early phase o injury
and healing, which typically lasts approximately 4–6
days unless the insult is perpetuated.
Subacute. T is phase occurs a er the acute phase and
typically lasts rom 10 to 17 days a er the acute phase
has ended but may last weeks in those tissues with
limited circulation, such as tendons.18
 Chronic. T is type o injury can have several de nitions.
On the one hand it may indicate the nal stage o healing
that occurs 26–34 days a er injury but can last 6 months
to 1 year depending on the tissue involved and the amount
o tissue damage. On occasion, a persistent in ammatory
state results in an accumulation o repetitive scar
adhesions, degenerative changes, and other harm ul e ects
re erred to as subclinical adaptations (see Chapter 8).
CLINICAL PEARL
Secondary or microtraumatic injuries are essentially the
in ammatory response that occurs with the primary
injury.19 Microtraumatic injuries include tendinopathy,
tenosynovitis, and bursitis.
TISSUE HEALING
Fortunately, the majority o tissue injuries heal without
complication in a predictable series o events (Fig. 2-3). T e
most important actor regulating the regional time line o

T
An acute-on-chronic injury involves a re-injury o the

I
healing is su cient blood ow.20 Many actors can deter-

s
tissue—an acute exacerbation o a chronic injury.

s
mine the outcome o the tissue injury, including those listed

u
e
B
e
H
a
He mo s tas is Inflammatio n Re pair Re mo de ling

v
I
o
r
As trocytic proce s s e s

,
e ncircle le s ion

I
n
Blood–bra in ba rrie r
No ECM de pos ition Incre a s e d glios is CNS: g lial s c ar

j
re e s ta blis he d

u
a nd limite d de ns ity

r
Re duce d infla mma tory a ngioge ne s is No le s ion tis s ue

y
ce ll re cruitme nt a nd

,
S eve ring of As trocyte s produce filling
de bride me nt; me dia te d

H
tis s ue s a nd by microglia , inhibitory mole cule s

e
preve nting a xona l Ne urons prote cte d
blood ve s s e ls

a
ma cropha ge s, a nd by glia l s ca r
re ge ne ra tion

l
a s trocyte s

I
Influx of

n
blood borne Axona l bre a kdown

g
ce lls a nd

,
a
prote ins Glio s is

n
Re le a s e of

d
s igna ling Mine ra liza tion (bone ) PNS: re g e ne ratio n
Os te obla s t, e pithe lia l,

T
mole cule s

r
by le ucocyte s CNS or S chwa nn ce ll Tis s ue re orga niza tion

e
prolife ra tion

a
Axons re inne rva te

T
Limite d ECM a nd ta rge t (P NS )
Injury

m
gra nula tion tis s ue

e
Full tis s ue s tre ngthe ning

n
S chwa nn ce ll condult (CT)/functiona l re cove ry
No n-CNS

T
a ids on a xon
(PHS, bone, s kin) re ge ne ra tion
P la te le t
a dhe s ion
a ctiva tion a nd
a ggre ga tion Mine ra liza tion Bo ne : no s c ar
Primary Full tis s ue
Fibrin forma tion
he aling s tre ngthe ning
S te mming of P ha gocyte s
a nd de bride me nt Re mova l exce s s
blood flow via tis s ue
he mos ta tic plug by le ucocyte s ;
me dia te d by
ma cropha ge s Se c o ndary
he aling
Re le a s e of
che moa ttra cta nts Bo ne
Se c o ndary
Axona l bre a kdown
he aling Cutane o us tis s ue :
c o llag e no us s c ar
Fibrobla s t
re cruitme nt
ECM de pos ition
Fibe r a lignme nt
Angioge ne s is a nd contra ction
S e conds to hours
Ce llula r a poptos is
Hours to days
Pa rtia l tis s ue
Days to we e ks s tre ngthe ning

We e ks to months

FIGURE 2-3 Stages o healing. 33

 TABLE 2-1 Factors Impacting Healing
Intrinsic (Local) Systemic Extrinsic
Extent o injury. Microtears involve only Age. The ability to heal injuries decreases Drugs. Nonsteroidal anti-in ammatory drugs and
minor damage, whereas macrotears with age corticosteroids decrease in ammation and
involve signi cantly greater destruction swelling, resulting in decreased pain

Edema. Swelling can cause increased Obesity. Oxygen pressure in the tissues is Absorbent dressings. The degree o
pressure that can impede nutrition to lower in obese patients. humidity greatly a ects the process o
the injured part, inhibit neuromuscular epithelialization—the epithelium regenerates
control, and retard the healing process twice as quickly in a moist environment

Hemorrhage. Bleeding produces the Malnutrition. Wound healing places a Temperature and oxygen tension. Hypothermia
A
same negative e ects on healing as higher than usual demand on a patient’s has a negative e ect on healing. Oxygen
N
A
does the accumulation o edema energy resources. In every stage o tension relates to the neovascularization o
T
wound healing, protein is needed. In the wound.
O
M
addition, adequate nutritional intake and
Y
body stores o all vitamins are essential.

Poor vascular supply. Wounds heal poorly Hormone levels. Hormones a ect the
and at a slower rate when the blood composition and structure o a variety o
supply is inadequate tissues.

Separation o tissue. A wound that has In ection. In ection can delay healing Physical modalities. These can be used to
smooth edges and good apposition promote an ef cient healing environment
will tend to heal by primary intention or an injury when used individually, or in
with minimal scarring. combination with other modalities or exercise

Muscle spasm. Spasm causes traction
on the already torn tissue, preventing
approximation.
General health. Comorbidity can play a
signi cant role in the overall healing
process. For example, diabetes can
impede tissue healing
Exercise. Exercise can help in the remodeling
process o all connective tissues. Wol ’s
law states that tissue remodeling and
the response to therapeutic exercise are
determined by the speci c adaptation o the
tissue to the imposed level o demand.

Atrophy. Consider a secondary

impairment to injury and subsequent
disuse

Degree o scarring. Scarring that occurs

normally, but hypertrophic scarring
produces keloids when the rate o
collagen production exceeds the rate
o collagen breakdown

in Table 2-1. Also, complications such as in ection, compro- phenomenon, in reality these events occur as an amalgama-
mised circulation, and neuropathy hurt the healing process tion o di erent reactions, both spatially and temporally.25
and can cause great physical and psychological stress to the T e various therapeutic approaches that can be used dur-
involved patient and his or her amily. ing each o these stages o healing are described in Chapter 8.

Stages o Tissue Healing Coagulation and Inf ammatory Stage

T e general stages o so tissue healing are described here,
whereas the healing o speci c structures is described later
under the relevant headings. A er microtrauma, macrotrauma,
or disease, the body attempts to heal itsel through a predict-
able series o overlapping events that include coagulation and
in ammation (acute), which begins shortly a er the initial
injury; a migratory and proli erative process (subacute), which
begins within days and includes the major processes o healing;
and a remodeling process (chronic), which may last or up to
a year depending on the tissue type, and is responsible or scar
tissue ormation and the development o new tissue.14,20–24
Whereas simpli cation o the complex events o healing
34 into separate categories may acilitate understanding o the
An injury to the so tissue triggers a process that represents
the body’s immediate reaction to trauma, which includes a
series o repair and de ensive events.20,26 Following an injury
to the tissues, the cellular and plasma components o blood
and lymph enter the wound. Capillary blood ow is disrupted,
causing hypoxia to the area. T is initial period o vasocon-
striction, which lasts 5–10 minutes, prompts a period o
vasodilation, and the extravasation o blood constituents.20
Extravasated blood contains platelets, which secrete sub-
stances that orm a clot to prevent bleeding and in ection,
clean dead tissue, and nourish white cells. T ese substances
include macrophages and broblasts.27 T e coagulation and
platelet release results in the excretion o platelet-derived
growth actor (PDGF),28 platelet actor 4,29 trans orming
growth actor-alpha ( GF-α),30 and trans orming growth
actor-beta ( GF-β).31 T e main unctions o a cell-rich tis-
sue exudate are to provide cells capable o producing the com-
ponents and biological mediators necessary or the directed
reconstruction o damaged tissue, while diluting microbial
toxins and removing contaminants present in the wound.25
In ammation is mediated by chemotactic substances,
including anaphylatoxins that attract neutrophils and mono-
cytes.
Neutrophils. Neutrophils are white blood cells (WBCs) o
the polymorphonuclear (PMN) leukocyte subgroup (the
others being eosinophils, and basophils) that are lled
with granules o toxic chemicals (phagocytes) that enable
them to bind to microorganisms, internalize them, and
kill them.
Monocytes. Monocytes are WBCs o the mononuclear
leukocyte subgroup (the other being lymphocytes).
T e monocytes migrate into tissues and develop into
macrophages, providing immunological de enses
against many in ectious organisms. Macrophages serve
to orchestrate a “long-term” response to injured cells
subsequent to the acute response.32
T e WBCs o the in ammatory stage serve to clean the
wound debris o oreign substances, increase vascular permea-
bility, and promote broblast activity.32 Other cell participants
include local immune accessory cells, such as endothelial
cells, mast cells, and tissue broblasts. T e PMN leukocytes,
through their characteristic “respiratory burst” activity, pro-
duce superoxide anion radical, which is well known to be
critical or de ense against bacteria and other pathogens.33
Superoxide is rapidly converted to a membrane permeable
orm, hydrogen peroxide (H 2O2), by superoxide dismutase
activity or even spontaneously.32 T e release o H 2O2 may
promote the ormation o other oxidants that are more stable
(have a longer hal -li e), including hypochlorous acid, chlora-
mines, and aldehydes.32 T e phagocytic cells that initiate the
innate immune response produce a set o proin ammatory
cytokines (e.g., NF-α, IL-1, and IL-6) in the orm o a cascade
that ampli es the local in ammatory response, in uences the
adaptive immune response, and serves to signal the central
nervous system (CNS) o an in ammatory response (Fig. 2-3).
T e extent and severity o this in ammatory response depend
on the size and the type o the injury, the tissue involved, and
the vascularity o that tissue.17,23,34–36
Local vasodilation is promoted by biologically active prod-
ucts o the complement and kinin cascades25:
T e complement cascade involves 20 or more proteins
that circulate throughout the blood in an inactive orm.25
A er tissue injury, activation o the complement cascade
produces a variety o proteins with activities essential to
healing.
T e kinin cascade handles the trans ormation o the
inactive enzyme kallikrein, which is present in both blood
and tissue, to its active orm, bradykinin. Bradykinin also
contributes to the production o tissue exudate through
the promotion o vasodilation and increased vessel-wall
permeability.37
Because o the variety o vascular and other physiological
responses occurring, this stage o healing is characterized by
swelling, redness, heat, and impairment or loss o unction. T e
edema is due to an increase in the permeability o the venules,
plasma proteins, and leukocytes, which leak into the site o
injury, resulting in edema.38,39 New stroma, o en called granu-
lation tissue, begins to invade the wound space approximately
4 days a er the injury.38,39 T e complete removal o the wound
debris marks the end o the in ammatory process.
Clinically, this stage is characterized by pain at rest or with
active motion, or when speci c stress is applied to the injured
structure. T e pain, i severe enough, can result in muscle
T
I
s
guarding and a loss o unction. T is is o en re erred to as
s
u
the protection phase based on the ocus o the intervention.
e
T e goals o the intervention during this phase are there ore
B
e
to minimize pain and edema, control in ammation, restore
H
ull, passive range o motion, prevent atrophy, maintain so
a
v
tissue joint integrity, and to enhance unction (see Chapter 8).
I
o
wo key types o in ammation are recognized: the nor-
r
,
mal acute in ammatory response and an abnormal, chronic,
I
n
or persistent in ammatory response. Common causes or a
j
u
persistent chronic in ammatory response include in ectious
r
y
agents, persistent viruses, hypertrophic scarring, poor blood
,
supply, edema, repetitive mechanical trauma, excessive ten-
H
e
sion at the wound site, and hypersensitivity reactions.40,41 T e
a
l
monocyte-predominant in ltration, angiogenesis, and brous
I
n
changes are the most characteristic morphologic eatures o
g
,
chronic in ammation. T is perpetuation o in ammation
a
involves the binding o neutrophilic myeloperoxidase to the
n
d
macrophage mannose receptor.42
T
r
e
a
Migratory and Proli erative Stage
T
m
T e second stage o so tissue healing, characterized by migra-
e
n
tion and proli eration, usually occurs rom the time o the
T
initial injury and overlaps the in ammation phase. Charac-
teristic changes include capillary growth and granulation tis-
sue ormation, broblast proli eration with collagen synthesis,
and increased macrophage and mast cell activities. T is stage
handles the development o wound tensile strength.
A er the wound base is ree o necrotic tissue, the body
begins to work to repair and close the wound (Fig. 2-3). T e
connective tissue in healing wounds is composed primarily o
collagen, types I and III43 cells, vessels, and a matrix that con-
tains glycoproteins and proteoglycans. Proli eration o colla-
gen results rom the actions o the broblasts that have been
attracted to the area and stimulated to multiply by growth ac-
tors, such as PDGF, GF-β, broblast growth actor (FGF),
epidermal growth actor, and insulin-like growth actor-1,
and tissue actors such as bronectin.25 T is proli eration
produces rst brinogen and then brin, which eventually
becomes organized into a honeycomb matrix and walls o
the injured site.44
T e wound matrix unctions as glue to hold the wound
edges together, giving it some mechanical protection while
also preventing the spread o in ection. However, the wound
matrix has a low tensile strength and is vulnerable to break-
down until the provisional extracellular matrix (ECM) is
replaced with a collagenous matrix. T e collagenous matrix
acilitates angiogenesis by providing time and protection to 35
Another random document with
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squamous, yellowish, sticky covering, under which the psoroptes lie
hidden and which affords them nourishment.
The crusts steadily grow thicker and lift the individual fibres of
wool, tearing them from their follicles, so that patches of skin
become bare. The patches thus formed increase in diameter, for the
acari leave the centre, where crust-formation is replaced by
abundant desquamation of the epidermis. The skin is thickened,
assumes the character of parchment, and in old-standing cases
becomes wrinkled.
The disease always commences along the back, withers, loins, and
the upper part of the quarters. Thence it spreads to the flanks and
sides of the chest. The psoroptes are almost exclusively confined to
recently affected points on the edges of the scabby patches. They are
visible to the naked eye, and appear as little whitish-brown points.
Scab is specially liable to attack a flock containing lambs and
yearling sheep, whose skin is thin, fine and supple, and therefore
more susceptible to their attacks. If a portion of a scabby flock be
shorn, the shorn animals will probably recover on account of the
psoroptes transferring themselves to the animals with long fleeces.
The diagnosis is easy. Psoroptic mange cannot be mistaken for
sarcoptic mange, on account of the different points affected.
Psoroptic mange only attacks regions covered by wool, and
sarcoptic mange those free of wool. A microscopical examination of
acari removed from the diseased animals will, however, immediately
remove all doubt.
Nor can the disease be confounded with phthiriasis, the
trichodectes being immediately distinguished from the psoroptes by
their greater size and the shape of their head. Moreover, they are
usually to be found on the front portions of the shoulders.
It is more likely to be mistaken for another disease, termed by
some writers seborrhœa and studied and described by Delafond
under the name of sebaceous folliculitis. This disease appears mostly
in autumn, and attacks animals much exposed to the weather and on
moist, cold soils. It begins with very violent pruritus, followed by
biting and loss of portions of the fleece. The skin is red, inflamed and
painful, and the wounds are covered with large quantities of
yellowish acid discharge of a sticky and offensive nature. The
treatment of this disease consists in placing the sheep in clean, dry,
well-ventilated sheds. Recovery is assisted by clipping and the
application of some emollient dressing to the diseased parts.
The ease with which the disease can be cured and the absence of
parasites enable one to readily distinguish it from psoroptic mange
(scab).
Prognosis. The disease is not specially grave, so long as only a
few animals are affected, for it is not difficult to cure by isolation,
good feeding, and proper external treatment; but if scab appears in a
flock, the freedom with which the animals intermingle is such that all
are rapidly attacked, and the irritation produced at once checks their
growth and causes loss in condition. Many ewes give birth to small,
feeble lambs, which are almost certain to die, and in any case the
wool is considerably diminished in value.
Delafond estimated that psoroptic mange formerly attacked one
thirty-fifth of all the sheep in France every year, causing damage to
the extent of five francs per head. At the present time, and since
proper sanitary laws have been instituted, it has become much less
common.
During the bad season of the year the mortality is greater, and may
reach as much as from 40 to 50 per cent. In cases where scab is
accompanied by some other disease, such as distomatosis, it may
even rise to 80 per cent.
The treatment is preventive and curative. Preventive treatment
consists in separating the healthy from the diseased animals and in
disinfecting the folds, sheds, etc.
Curative treatment. The first point in this treatment consists in
improving the diseased animal’s food both as to quality and quantity.
It is to be observed that the parasite has more difficulty in living on
robust and well-nourished animals. Moreover, observation shows
that transference from poor land to rich pastures is sometimes in
itself sufficient to bring about a spontaneous cure. Such, at least, is
the belief of the Spanish sheep farmers in Estramadura and of the
French shepherds.
The shepherd can do a great deal to arrest the course of the
disease. If he is careful, zealous, intelligent and observant he will
quickly note the first indications of the disease and, by isolating the
animals, check its spread.
The second point consists in shearing the diseased animals, and
this must be carried out at any season of the year. The money loss is
sometimes important, but must be met, for otherwise treatment is
impossible. In cases of localised scab, empyreumatic oil, oil of cade,
solutions of sulphuret of potassium, decoctions of black hellebore
(water 1 quart, fresh rhizome 4 ounces or dry rhizome 2 ounces),
decoction of tobacco and diluted tobacco juice (6 ounces in 1 quart of
water) have been recommended. Such local treatment, however, is
often useless, because incomplete.
When scab is generalised and it is impossible to define the parts
attacked, general treatment is indispensable and the diseased sheep
should be dipped.
As a preliminary, however, and in order to make sure that the
application will produce its effect, the animals after shearing should
be passed, twenty-four hours before the medicinal bath, through a
warm bath containing soap in order to soften and remove the scabs.
Applications of oil or some fatty substance will also soften the scabs,
which may afterwards be removed with a scraper without producing
bleeding. One pound of soft soap may be dissolved in fifty quarts of
water and each sheep plunged into this and scrubbed with a brush
for a few minutes. Washing alone removes a large number of the
parasites.
Whatever bath be used it should not be given until four or five
hours after the last feeding. The dips most popular in France are as
follows:—

Tessier’s Bath (1810).

For 100 sheep Arsenious acid 1½ parts or lbs.

Sulphate of iron 10 „
Water 100 „
 The above materials should be boiled for ten minutes, and, as a
consequence of the chemical fusion which occurs in the process, the
proportion of arsenious acid dissolved amounts to about 2 drachms
per quart instead of 3¾ drachms.
In this bath the arsenious acid acts as a parasiticide and the
sulphate of iron as an astringent, the latter checking the absorption
of toxic principles by the skin and sores, and preventing the sheep
from licking themselves.
Absorption by the skin is not so dangerous as has been believed.
Rossignol has shown that poisoning need not be feared in chemical
baths unless the proportion of dissolved arsenic is above 150 grains
per quart, especially if the period of immersion does not exceed five
minutes. Even pure solutions of arsenic, free from any astringent,
may be used, provided the quantity in the bath does not exceed 120
grains per quart.
The bath should, if possible, be kept warm—85° to 95° Fahr. (30°
to 35° C.).
Four men are generally employed for the operation. One drives in
the sheep, two others hold and brush them in the bath, and the
fourth holds the head of the animal above the liquid. Tessier
recommended gloves for the use of the operators, but experience has
shown that such a precaution is unnecessary. The udder, and
particularly the teats, of ewes with young may, if necessary, be
smeared with some fatty substance, such as vaseline or oil, in order
to guard against the astringent action of the liquid.
Each sheep is plunged in the bath for one or two minutes, or five
minutes at the most. All the diseased spots must be brushed, rubbed
and cleansed; but care must be taken not to make them bleed.
Tessier suggested leaving the animals for twenty-four hours in
some disinfected place, without straw or food, to prevent these
materials from being wetted by the liquid which runs from the fleece,
and which, if afterwards eaten, might have a poisonous effect. Here,
again, the danger has been exaggerated. Delafond has shown that
sheep may be given a fluid ounce of Tessier’s bath for eight days
running without producing the slightest unfavourable symptom.
Tessier’s bath is excellent from the therapeutic standpoint, but it
imparts a yellow tint to the fleece, which is thus rendered less
valuable. The mixture has therefore been modified in various ways.

Clément’s Bath (1846).

For 100 sheep Arsenious acid 1·5 parts or lbs.

Sulphate of zinc 5 „
Water 100 „

In this bath every quart contains about 2½ drachms of arsenious

acid. Its toxic power, therefore, is considerably greater than that of
Tessier’s bath.
Clément’s formula has one drawback. The sulphate of zinc may be
mistaken for a non-astringent alkaline sulphate (sulphate of soda),
and as a consequence poisoning may occur, as experience has shown.
Mathieu of Sèvres replaced the sulphate of iron by an equal
quantity of alum. In this case, each quart of the bath contains 2½
drachms of arsenious acid.
Clément’s and Mathieu’s formulæ have given just as good results
as Tessier’s.
A last formula is that of Professor Trasbot. The aloes is of very
little use, however, because it is almost insoluble.

For 100 sheep Arsenious acid 2 lbs.

Sulphate of zinc 10 „
Aloes 1 „
Water 25 gallons.

Condition of the animals after the bath.—On leaving the bath the
abraded parts are slightly cauterised. During the five or six following
days the skin is stiff, and covered with adherent crusts over the
points attacked by the parasites. The animals no longer scratch or
bite themselves.
Towards the eighth day the crusts fall, the skin appears supple and
of a pink colour, and the wounds cicatrise. In animals which have
suffered for a long time recovery is much slower, and may extend
over from thirty to fifty days. The wool again grows soft and bright,
while the sheep rapidly regain their spirits and condition. The
cicatrisation of the wounds is often accompanied by intense itching,
which must not be taken as a sign of the persistence of the disease. It
is well, however, to keep the animals under observation at this
period.
Under any circumstances, six weeks or two months should always
be allowed to elapse before giving a second bath. Should a few spots
appear to be attacked secondarily, they may be moistened with a
little of one of the bath liquids.
In Germany the creolin bath is generally employed:

For 100 sheep { Water 250 gallons or parts.

{ Creolin 6·5 „

Each sheep is bathed a second time after an interval of one week,

the animal being immersed for three minutes in the bath and
thoroughly scrubbed with a brush. The efficacy of this method,
however, is less certain.
In America, where the flocks are large and scabies is frequent,
sulphur baths are employed, the baths themselves being of great size.
The animals are forced to pass through them and remain there for
some minutes.
The size and value of American, Australian, and New Zealand
flocks demand that the modes of treatment practised and the
experience gained in these countries should receive something more
than passing notice. We therefore purpose giving a short résumé of
some parts of the very valuable monograph on sheep scab issued in
1897 by Dr. Salmon and Mr. Stiles, for the American Bureau of
Animal Industry.
In selecting a dip the question of expense will naturally arise; next,
the question as to whether or not scab actually exists in the flock to
be dipped. The facilities at hand, the set-back to the sheep, and the
length of the wool are also matters for consideration, as well as the
pastures into which the dipped sheep are to be placed.
Expense.—In estimating the expense one should consider not only
the actual outlay for the ingredients of the ooze, but the cost of fuel
and labour, the injury, if any, to the sheep, and the liability of not
curing the disease. It is much more economical to use an expensive
dip and cure scab, than it is to use a cheap dip and fail to cure it.
Does scab exist in the flock?—If scab does not actually exist and
the wool is long, the dipping in this case simply being a matter of
precaution, it is best not to select a dip containing lime.
The facilities at hand for preparing dip.—If fuel is very scarce, so
that it is impracticable to boil the mixture for at least two hours, the
lime-and-sulphur dips should not be selected.

Fig. 256.—A comparatively early case of common scab, showing a bare spot
and tagging of the wool.

The pastures.—In case it is necessary to place the dipped sheep on

the same pastures they occupied before being dipped, it is always
best to use a dip containing sulphur. If a proprietary dip is selected
under those circumstances, it is suggested that sulphur be added,
about 1 lb. of flowers of sulphur to every 6 gallons of dip. The object
in using sulphur is to place in the wool a material which will not
evaporate quickly, but will remain there for a longer period of time
than the scab parasites ordinarily remain alive away from their hosts.
By doing this the sheep are protected against reinfection.
Sulphur is one of the oldest known remedies for scab; its use is
best known in the tobacco-and-sulphur dip and in the lime-and-
sulphur dip. These home-made mixtures are the two dips which have
played the most important rôles in the eradication of scab from
certain English colonies, and their use is extensive in America.

The Tobacco-and-Sulphur Dip.

Fig. 257.—A slightly advanced case of common scab.

 The formula as given here, and as adopted by the New South
Wales sanitary authorities, appears to have first been proposed in
1854 by Mr. John Rutherford. “On the Hopkins Hill Station Mr.
Rutherford, with two dressings of these ingredients, then cured over
52,000 sheep which had been infected for eighteen months. Since
then millions of scabby sheep have been permanently cured in
Victoria in the same way, and in South Australia and New South
Wales hundreds of thousands of scabby sheep have also been
cleansed with tobacco and sulphur. Judging, therefore, from the
experience of the three colonies, there is no medicament or specific
yet known that can be compared with tobacco and sulphur as a
thorough and lasting cure for scab in sheep.” (Dr. Bruce, Chief
Inspector of Sheep for New South Wales.)
The proportions adopted by Rutherford, and afterwards made
official by the scab sanitary authorities, are—

Tobacco leaves 1 lb.

Flowers of sulphur 1 „
Water 5 gallons.

The advantage of this dip lies in the fact that two of the best scab
remedies, namely, tobacco (nicotine) and sulphur, are used together,
each of which kills the parasites, while the sulphur remains in the
wool and protects for some time against reinfection. As no caustic is
used to soften the scab, heat must be relied on to penetrate the
crusts.
Directions for preparing the dip.—Infusing the tobacco:—Place 1
lb. of gold-leaf or manufactured tobacco for every 6 gallons of dip
desired in a covered boiler of cold or lukewarm water, and allow to
stand for about twenty-four hours; on the evening before dipping
bring the water to near the boiling point (212° Fahr.) for an instant,
then remove the fire and allow the infusion to stand overnight.
Thoroughly mix the sulphur (1 lb. to every 6 gallons of dip desired)
with the hand in a bucket of water to the consistency of gruel.
When ready to dip, thoroughly strain the tobacco infusion from
the leaves by pressure, mix the liquid with the sulphur gruel, add
enough water to make the required amount of dip, and thoroughly
stir the entire mixture.

Lime-and-Sulphur Dips.

Under the term “lime-and-sulphur dips” is included a large

number, of different formulæ requiring lime and sulphur in different
proportions.
To give an idea of the variety of the lime-and-sulphur dips, the
following list is quoted, the ingredients being reduced in all cases to
avoirdupois pounds and United States gallons:
(1.) The original “Victorian lime-and-sulphur dip,” proposed by Dr.
Rowe, adopted as official in Australia:

Flowers of sulphur 20⅚ lbs.

Fresh slaked lime 10⁵⁄₁₂ „
Water 100 gallons.

(2.) South African (Cape Town) official lime-and-sulphur dip,

February 4th, 1897:

Flowers of sulphur 20⅚ lbs.

Unslaked lime 16⅔ „
Water 100 gallons.

(3.) Fort Collins lime-and-sulphur dip:

Flowers of sulphur 33 lbs.

Unslaked lime 11 „
Water 100 gallons.

(4.) A mixture which, used to some extent by the Bureau of Animal

Industry, contains the same proportions of lime and sulphur
(namely, 1 to 3) as the Fort Collins dip, but the quantities are
reduced to—
 Flowers of sulphur 24 lbs.
Unslaked lime 8 „
Water 100 gallons.

In case of fresh scab Formula No. 4 will act as efficaciously as the

dips with a greater amount of lime, but in cases of very hard scab a
stronger dip, as the Fort Collins dip, should be preferred; or, in
unusually severe cases, an ooze with more lime in proportion to the
amount of sulphur, such as the Victorian (No. 1) or the South African
(No. 2) dip might be used.

Prejudice against Lime-and-Sulphur Dips.

There is at present great prejudice (a certain amount of it justified,

no doubt) against the use of lime and sulphur, emanating chiefly
from the agents of patent or proprietary dips and from the wool
manufacturers.
In the first place, it is frequently asserted that lime and sulphur
does not cure scab. Experience in Australia and South Africa, as well
as in America, has shown beyond any doubt that a lime-and-sulphur
dip, when properly proportioned, properly prepared, and properly
used, is one of the best scab eradicators known.
It is claimed by some that it produces “blood poisoning.” But the
cases of death following the use of lime-and-sulphur dips have been
infinitesimally few when compared with the number of sheep dipped
in these solutions, and when compared with the deaths which have
been known to follow the use of certain proprietary dips. The details
of such accidents, so far as they have been reported, have not shown
that death was due to any property prepared and properly used lime-
and-sulphur dip. It is highly probable that the cases of so-called
“blood poisoning” of shear-cut sheep are generally due to an
infection with bacteria in stale dip containing putrefying material.
The greatest objection raised against the use of lime-and-sulphur
dip is that it injures the wool. This objection is raised by many wool
manufacturers and echoed with ever-increasing emphasis by the
manufacturers of prepared dips; while, after years of extensive
experience with properly prepared dip, its injury to the wool is
strongly and steadfastly denied by the Agricultural Department of
Cape Colony.
It is believed that a certain amount of justice is attached to this
objection to lime and sulphur as generally used; unless, therefore,
lime and sulphur can be used in a way which will not injure the wool
to an appreciable extent, we should advise against its use in certain
cases; in certain other cases the good accomplished far outweighs the
injury it does. Let us, therefore, examine into this damage and its
causes.

Fig. 258.—A more advanced case of common scab.

The usual time for dipping sheep is shortly after shearing, when
the wool is very short; whatever the damage at this time, then, it can
be only slight, and the small amount of lime left in the wool will
surely do but little harm.
In full fleece lime and sulphur will cause more injury. In Australia
the deterioration was computed by wool buyers at 17 per cent.,
although in Cape Colony the Department of Agriculture maintains
that if properly prepared, and if only the clear liquid is used, the
sediment being thrown away, the official lime-and-sulphur formula
will not injure the long wool. The United States Bureau of
Agriculture have found some samples of wool injured by dipping,
while on other samples no appreciable effect was noticeable.
If a lime-and-sulphur dip is used, care must be taken to give the
solution ample time to settle; then only the clear liquid should be
used, while the sediment should be discarded. In some of the above
tests on samples of wool it was found that the dip with sediment had
produced very serious effects, even when no appreciable effects were
noticed on samples dipped in the corresponding clear liquid.
Experience has amply demonstrated that a properly made and
properly used lime-and-sulphur dip is one of the cheapest and most
efficient scab eradicators known, but its use should be confined to
flocks in which scab is known to exist, and to shorn sheep, with the
exception of very severe cases of scab in unshorn sheep. It should
only be used when it can be properly boiled and settled. The use of
lime-and-sulphur dips in flocks not known to have scab, especially if
the sheep are full fleeced, cannot be recommended; in such cases
tobacco, or sulphur and tobacco, is safer and equally good.
All things considered, where it is a choice between sacrificing the
weight of sheep and to some extent the colour of the wool by using
tobacco and sulphur, and sacrificing the staple of the wool by using
lime and sulphur, the owner should not hesitate an instant in
selecting tobacco in preference to lime. The loss in weight by using
tobacco and sulphur is not much greater than the loss in using lime
and sulphur, while the loss in staple is of more importance than a
slight discoloration.
Preparation of the mixture.—Take 8 to 11 lbs. of unslaked lime,
place it in a mortar-box or a kettle or pail of some kind, and add
enough water to slake the lime and form a “lime paste” or “lime
putty.”[8]
8. Many persons prefer to slake the lime to a powder, which is to be sifted and
mixed with sifted sulphur. One pint of water will slake 3 lbs. of lime if the slaking is
performed slowly and carefully. As a rule, however, it is necessary to use more
water. This method takes more time and requires more work than the one given
above, and does not give any better results. If the boiled solution is allowed to
settle the ooze will be equally safe.
Sift into this lime paste three times as many pounds of flowers of
sulphur as of lime, and stir the mixture well.
Be sure to weigh both the lime and the sulphur. Do not trust to
measuring them in a bucket or to guessing at the weight.
Place the sulphur-lime paste in a kettle or boiler with about
twenty-five to thirty gallons of boiling water, and boil the mixture for
two hours at least, stirring the liquid and sediment. The boiling
should be continued until the sulphur disappears, or almost
disappears, from the surface; the solution is then of a chocolate or
liver colour. The longer the solution boils the more the sulphur is
dissolved and the less caustic the ooze becomes.
Pour the mixture and sediment into a tub or barrel placed near the
dipping vat and provided with a bung-hole about 4 inches from the
bottom, and allow ample time (two to three hours, or more if
necessary) to settle.
When fully settled draw off the clear liquid into the dipping vat,
and add enough water to make a hundred gallons. Under no
circumstances should the sediment be used for dipping purposes.
 Fig. 259.—A shorn sheep with large bare area due to scab.

To summarise the position of the United States Department of

Agriculture on the lime-and-sulphur dips:—When properly made
and properly used these dips are second to none and equalled by few
as scab eradicators. There is always some injury to the wool resulting
from the use of these dips, but when properly made and properly
used upon shorn sheep, it is believed that this injury is so slight that
it need not be considered; on long wool the injury is greater and
seems to vary with different wools, being greater on a fine than on a
coarse wool. This injury consists chiefly in a change in the
microscopic structure of the fibre, caused by the caustic action of the
ooze. When improperly made and improperly used the lime and
sulphur dips are both injurious and dangerous, and in these cases the
cheapness of the ingredients does not justify their use. In case scab
exists in a flock and the farmer wishes to eradicate it, he cannot
choose a dip which will bring about a more thorough cure than will
lime and sulphur (properly made and properly used), although it will
be perfectly possible for the farmer to find several other dips which
will, when properly used, be nearly or equally as effectual as any
lime-and-sulphur dip. There is no dip to which objections cannot be
raised.

Arsenical Dips.

There are both home-made arsenical dips and secret proprietary

arsenical dips. It is well to use special precautions with both, because
of the danger connected with them. One of the prominent
manufacturers of dips, a firm which places on the market both a
powder arsenical dip and a liquid non-poisonous dip, recently
summarised the evils of arsenical dips in the following remarkable
manner:
“The drawbacks to the use of arsenic may be summed up
somewhat as follows: (a) Its danger as a deadly poison. (b) Its drying
effect on the wool. (c) Its weakening of the fibre of the wool in one
particular part near the skin, where it comes in contact with the
tender wool roots at the time of dipping. (d) Its not feeding the wool
or stimulating the growth, or increasing the weight of the fleece, as
good oleaginous dips do. (e) The danger arising from the sheep
pasturing, after coming out of the bath, where the wash may possibly
have dripped from the fleece, or where showers of rain, after the
dipping, have washed the dip out of the fleece upon the pasture. (f)
Its occasionally throwing sheep off their feed for a few days after
dipping, and so prejudicing the condition of the sheep. (g) Its
frequent effect upon the skin of the sheep, causing excoriation,
blistering, and hardness, which stiffen and injure the animal,
sometimes resulting in death.”
Although this manufacturer has gone further in his attack upon
arsenic than the United States Bureau of Agriculture would have
been inclined to do, it must be remarked that when a manufacturer
of such a dip cannot speak more highly of the chief ingredient of his
compound than this one has done in the above quotations, his
remarks tend to discredit dips based upon that ingredient. Bruce, the
Chief Inspector of Live Stock for New South Wales, speaking of
arsenical dips, says: “Arsenic and arsenic and tobacco (with fresh
runs) cured 9,284 and failed with 9,271.”
It may be said, on the other hand, that arsenic really has excellent
scab-curing qualities; it enters into the composition of a number of
the secret dipping powders, and forms the chief ingredient in one of
the oldest secret dips used. This particular dip has been given second
place (with some qualifications) among the officially recognised dips
in South Africa.
Formulæ for arsenical dips.—Finlay Dun recommends the
following:—Take 3 lbs. each of arsenic, soda ash (impure sodium
carbonate) or pearl ash (impure potassium carbonate), soft soap, and
sulphur. A pint or two of naphtha may be added if desired. The
ingredients are best dissolved in 10 to 20 gallons of boiling water,
and cold water is added to make up 100 gallons. The head of the
sheep must, of course, be kept out of the bath.
A mixture highly endorsed by certain parties consists of the
following ingredients:

Commercially pure arsenite of soda 14 lbs.

Ground roll sulphur 34½ „
Water 432 gallons (U.S.)

The arsenite of soda is thoroughly mixed with the sulphur before

being added to the water.
Precautions in use of arsenical mixtures.—Any person using an
arsenical dip should bear in mind that he is dealing with a deadly
poison. The following precautions should be observed:
(1) Yards into which newly-dipped sheep are to be turned should
first be cleared of all green food, hay, and even fresh litter; if
perfectly empty they are still safer. (2) When the dipping is finished,
the yard should be cleaned, washed, and swept, and any unused ooze
should at once be poured down a drain which will not contaminate
food or premises used by any animals. (3) Dipped sheep should
remain in an open, exposed place, as on dry ground. (4)
Overcrowding should be avoided, and every facility given for rapid
drying, which is greatly facilitated by selecting fine, clear, dry
weather for dipping. (5) On no account should sheep be returned to
their grazings until they are dry and all risk of dripping is passed.
The feeling of the United States Bureau of Agriculture towards
arsenical dips is shown by the following:
Suggestion as to danger.—The formulæ given above are copied
from the writings of men who have had wide experience in dipping,
but this Bureau assumes no responsibility for the efficacy of the dips
given, or for their correct proportions. Furthermore, as long as
efficacious non-poisonous dips are to be had, we see no necessity for
running the risks attendant upon the use of poisonous dips.

Carbolic Dips.

This class of dips kills the scab mites very quickly, but
unfortunately the wash soon leaves the sheep, which is consequently
not protected from reinfection in the pastures. If, therefore, a
carbolic dip is selected, it is well to add flowers of sulphur (1 lb. to
every 6 gallons) as a protection against reinfection.
The advantages of carbolic dips are that they act more rapidly than
the tobacco or sulphur dips, and that the prepared carbolic dips are
very easily mixed in the bath. They also seem, according to Gillette,
to have a greater effect on the eggs of the parasites than either the
sulphur or the tobacco dips. The great disadvantages of this class of
dips are—first, in some of the proprietary dips, that the farmer is
uncertain regarding the strength of material he is using; second, the
sheep receive a greater set-back than they do with either lime and
sulphur or tobacco.
Fig. 260.—An advanced case of common scab.

The United States Bureau of Agriculture is inclined to be extremely

conservative in regard to them, and to advise their manufacturers to
prepare them in a guaranteed strength with more explicit directions
for use than are to be found in the present circulars.
One of the prominent proprietary carbolic dips was formerly
recognised as one of the three official dips in New South Wales, but it
has now been erased from the list. In Cape Town carbolic dips are
not much used, and in the official reports little is said concerning
them.
The United States Bureau of Animal Industry gives the following
advice as regards dipping:
(1.) Select a dip containing sulphur. If a prepared “dip” is used
which does not contain sulphur, it is always safer to add about 16½
lbs. of sifted flowers of sulphur to every 100 gallons of water,
especially if, after dipping, the sheep have to be returned to the old
pastures.
Fig. 261.—An American sheep-dipping plant in operation.

(2.) Shear all the sheep at one time, and immediately after
shearing confine them to one-half the farm for two to four weeks.
Many persons prefer to dip immediately after shearing.
(3.) At the end of this time dip every sheep (and every goat also, if
there are any on the farm).
(4.) Ten days later dip the entire flock a second time.
(5.) After the second dipping, place the flock on the portion of the
farm from which they have been excluded during the previous four
or five weeks.
(6.) Use the dip at a temperature of 100° to 110° Fahr.
(7.) Keep each sheep in the dip for two minutes by the watch—do
not guess at the time—and duck its head at least once.
(8.) Be careful in dipping rams, as they are more likely to be
overcome in the dip than are the ewes.